viagra injections ed Examine the mouths of several persons of different ages to see if the cervical line of the anatomic tooth is visible or hidden. As the individual grows older, the location of the margin of the gingiva may recede toward the root tip (apically) because of periodontal disease or injury (such as from the faulty use of oral hygiene aids). Of course, the location of the cervical line on the tooth remains the same. In other words, the distinction between the anatomic crown and root does not change over a lifetime. italia viagra free online i need emotional viagra All teeth have surfaces that are named according to their usual alignment within the dental arch. Refer to Figure 1-11 when studying the terms to denote tooth surfaces. viagra emotional side effects 34 getting hard without viagra 22 how long does liquid viagra last MOLARS I1C 0 P 0 1 0 0 I 3 C 1P 4 3 1 4 does viagra work if your drunk Answers for teeth in Figure 1-46B. Universal tooth numbers for teeth in order: hydrogen sulfide viagra Maxillary right central incisors Maxillary left central incisors how viagra works nitric oxide using viagra to combat malignant melanoma their lingual surfaces (Fig. 2-18A). A high incidence of shovel-shaped incisors has been observed in Mongoloid people, including many groups of American Indians.4–9 (Mongoloid pertains to a major racial division marked by a fold from the eyelid over the inner canthus, prominent cheekbones, straight black hair, small nose, broad face, and yellowish complexion. Included are Mongols, Manchus, Chinese, Koreans, Arctic coastal populations, Japanese, Siamese, Burmese, Tibetans, and American FIGURE 3-3. herb viagra easy to be a man SECTION II how long does viagra work after taking it 1st Premolars parrot viagra joke dominican viagra drink Mesiolingual groove often present viagra gruppo musicale russo L how long before viagra goes generic FIGURE 4-23. FIGURE 4-29. photograph? old man viagra joke mesiolingual comprar viagra original pfizer mexican viagra liquor Since the lingual cusps of both mandibular first and second molars are longer and more conical or pointed than the buccal cusps, the lingual cusps have longer triangular ridges. 3. TAPER TOWARD DISTAL OF MANDIBULAR MOLARS FROM THE PROXIMAL VIEWS On both types of molars, the crown is narrower in the distal third than in the mesial third. Therefore, from the distal aspect, some of the lingual and the buccal surfaces can be seen (demonstrated clearly on the distal views of mandibular second molars in Fig. 5-7). Proximal contact areas may be seen as flattened areas (facets) caused from wear due to the rubbing of adjacent teeth during functional movements of the jaws. On mandibular first molars, the distal contact is centered on the distal surface cervical to the distal cusp. 4. CERVICAL LINES OF THE MANDIBULAR MOLARS WHEN COMPARING PROXIMAL VIEWS Mesial cervical lines on both first and second molars slope occlusally from buccal to lingual and curve very slightly toward the occlusal surface.O The distal cervical lines are so slightly curved that they are nearly straight. 5. MARGINAL RIDGES OF MANDIBULAR MOLARS WHEN COMPARING PROXIMAL VIEWS Mesial marginal ridges are concave buccolingually. Distal marginal ridges of the first molar are short and V shaped, located just lingual and distal to the distal cusp. Differences in mesial and distal marginal ridge heights are apparent on handheld teeth when viewing es malo tomar viagra seguido shortest distobuccal root, so all three may be visible from the buccal view. There is much variation in the shapes of the roots. On maxillary first molars, the more blunt mesiobuccal root and the distobuccal root are often well separated (Appendix 8j, buccal view). Both buccal roots often bend distally, or they may bend in such a way that they look like pliers handles. The mesiobuccal root may bow out mesially in the cervical half before it curves toward the distal, placing its apex distal to the line of the buccal groove on the crown. In contrast, maxillary second molar roots are often closer together, less curved, more nearly parallel, and with a longer root trunk. Often both roots bend toward the distal in their apical third. Find the two maxillary second molars in Figure 5-15 that are exceptions. B new improved viagra can u buy viagra in dubai R. viagra dla 20 latka Part 1 | Comparative Tooth Anatomy wrigley chewing gum viagra 2012 179 I B Maxillary Primary Teeth (occlusal) A viagra doesn't work with alcohol is viagra effective for premature ejaculation 1 212 viagra diaries wiki procedure called crown lengthening to ensure that the restoration does not encroach on the biologic width. This is especially critical on teeth where esthetics is a factor. Clinical crown lengthening is a procedure that increases the extent of supragingival tooth structure by removing gingival tissue or apical positioning gingival tissue, and usually removing some supporting bone. Further, a defective restoration, especially one that is overcontoured or is not flush with the tooth structure, may retain bacterial plaque more readily, so it could be an initiating factor for periodontal disease. Therefore, it is always important to keep in mind that when teeth must be restored, ideal tooth contours, as have been discussed in the earlier chapters of this text, should be reproduced. is taking expired viagra safe jelly viagra generika potenzmittel ANSWERS: 1—a, b, c, e; 2—a, b, c, e; 3—c; 4—b; 5—a, b, d, e; 6—a, b, c, d; 7—c; 8—c; 9—a; 10—a,b,c,d; 11—a,b,c,d i need viagra cause you re too ugly to turn me on lyrics Canines sectioned faciolingually. A. Maxillary canine, mesial side removed (young tooth). There is no attrition evident on the incisal edge, and the pulp cavity is still large. B. Mandibular canine, mesial side removed (young tooth). The pulp cavity is large. Only at the incisal tip is there a little evidence of secondary dentin formation. The roof of the chamber is slightly more rounded than on incisors. apa kegunaan viagra 241 pain. Cleaning the root canals and draining the area of infection will usually provide relief within two to three days. Another result of pulpal trauma (like being hit in the mouth with a baseball) is the discoloration of the tooth crown to a gray or brownish color, which indicates damage to the pulp and the need to evaluate the tooth for possible endodontic treatment. After the root canal, the discoloration can be greatly reduced by using an intracoronal bleaching technique where the bleach is placed within the pulp chamber for a period of time. See the change of tooth color in Figure 8-16. 3. ENDODONTIC THERAPY The goal of endodontic therapy is to relieve pain, control infection, and preserve the tooth so that it may function normally during mastication. Endodontic treatment is alles over viagra viagra before gym normally preferred to extraction because if the tooth were extracted, the patient would be without the tooth throughout the healing process and during the time required to construct and place the replacement tooth. Further, endodontic therapy is less expensive than having a tooth extracted and subsequently replaced with a dental prosthesis (bridge) or an implant. The first step of the endodontic procedure is for the dentist to gain access to the pulp chamber and the root canals of teeth through an access opening in the crown of the tooth. On anterior teeth, the opening is made on the lingual surface and on posterior teeth through the occlusal surface. These access openings vary considerably from cavity preparations used in operative dentistry. The shape (outline form), size, and position of the access opening are determined by studying ideal viagra ne shqiperi Edentulous people (with no teeth) who wear complete dentures or false teeth are provided with CR that coincides with MIP because they can learn to pull the mandible back and close into a stable and repeatable position of CR during jaw closure. This enables the tight occlusion of denture teeth to coincide with the repeatable centric jaw position, so the dentures will remain tightly secured against the mucosa and not rock loose when functioning. An articulator is a mechanical device that holds casts of the two arches, permitting a close duplication of the patient’s opening and closing centric jaw relations (Fig. 9-24). Notice the fit of the ball of the lower (mandibular) part fitting into a concavity on the upper (maxillary) part. This design simulates the heads of the condyles fitting into their articular fossae. It is easier to study tooth relationships with the patient’s dental arches (dental stone casts) on the articulator in your hands, rather than with your hands in the patient’s mouth. What better way is there to determine whether or not the maxillary and mandibular lingual cusps fit together tightly or properly in the maximal intercuspal relationship? what does viagra make you feel like two tracings, both reproducing the outer border movements during maximal movement of the mandible. When facing a person, the frontal envelope is the outline formed (traced) by a marker located between the mandibular central incisors while the mandible moves maximally in all directions. Beginning with teeth in their most intercuspal position (MIP), the mandible (with teeth lightly touching) moves the maximum distance horse viagra humans 6. If this person did not have class I occlusion but had class III occlusion (where the mandible was positioned one full tooth mesial to its class I position), which tooth or teeth would contact the maxillary second premolar? a. Mandibular canine and first premolar b. Mandibular first premolar and second premolar c. Mandibular second premolar only d. Mandibular second premolar and first molar e. Mandibular first molar only midline); 5—b; 6—e 287 ag guys liquid viagra 30 31 how to take viagra 50mg correctly viagra doping ciclismo Class II amalgam restorations. A. A polished class II amalgam on a maxillary first premolar (No. 12 DOA). B. This class II amalgam restoration on a tooth with no adjacent tooth shows how the dentist had to extend this preparation toward the gingiva in order to reach the area where caries had been located: gingival to the proximal contact. does viagra help men last longer A buy strong viagra uk D D bayer equivalent viagra 385 chinese herbal viagra wholesalers can women take blue viagra Learning Exercise, cont. does viagra make you go blind Part 3 | Anatomic Structures of the Oral Cavity Part 3 | Anatomic Structures of the Oral Cavity what if viagra doesnt work the first time how to treat viagra overdose (Carefully study this comprehensive but simple table. Then, covering one column at a time, see how many nerves you can recall. These are the nerves any dental student, dental hygiene student, or graduate of either profession should be most familiar with. You should also be able to determine the location of each nerve.) Infraorbital a. Right atrium acheter viagra 50 milligrams o sildenafil 100mg gut viagra k new viagra competitor n. Mandibular first premolar buccal cusps are more pointed (110 degrees) versus on second premolar, where they are more obtuse or blunt (130 degrees) (facial views). o. Mesial proximal contacts (and marginal ridges) of mandibular second premolars are more occlusal than distal contacts (following the general rule), whereas the reverse is true on mandibular first premolars (EXCEPTION), where mesial contacts (and marginal ridges) are more cervical (facial views). p. Lingual cusps of mandibular first premolars are very small and nonfunctional. On second premolars, the lingual cusps function and are relatively longer (proximal views). q. Lingual cusp tips of mandibular second premolars are positioned to the mesial (or, if there are two lingual cusps, the mesiolingual is the more prominent) (lingual views). r. Mandibular first premolars have a mesiolingual groove separating the mesial marginal ridge from the lingual cusp. Second premolars (three-cusp type) have a lingual groove separating the two lingual cusps (lingual and mesial views). s. Mesial marginal ridges of first premolars slope cervically toward the lingual at about 45 degrees from horizontal. On second premolars they are more horizontal (mesial views). t. The mesial root surfaces of mandibular second premolars are the only premolar root surface (maxillary and mandibular, mesial and distal) not likely to have a midroot depression (best seen on models or actual teeth, not labeled in drawings). u. Mandibular first premolars are the only premolars that have the mesiolingual corner, with its mesiolingual groove and low marginal ridge, pinched or squeezed in, forming about a 45-degree angle with the lingual surface. This makes the occlusal outline somewhat diamond shaped (occlusal views). is viagra bad for u tom kaulitz toma viagra c h. viagra trademark expiration viagra for men meaning 1. organisms duane reade viagra price Composition of cementum: cementum is the mineralized dental tissue, covering the anatomic roots of human teeth. Cementum : inorganic=45-50% organic=50-55% Cementum has the highest fluoride content of all the mineralised tissues. viagra mishaps ◊◊Bones and joints, 207 ◊◊Bursae of the lower limb, 207 ◊◊Mensuration in the lower limb, 208 ◊◊Muscles and tendons, 211 ◊◊Vessels, 211 ◊◊Nerves, 214 viagra - pozelui viagra half life wikipedia 31 viagra hot flush 1◊◊Mucosal folds at the oesophagogastric junction act as a valve. 2◊◊The acute angle of entry of oesophagus into stomach produces a valvelike effect. 3◊◊The circular muscle of the lower oesophagus is a physiological, as distinct from an anatomical, sphincter. 4◊◊The arrangement of the muscle ﬁbres of the stomach around the cardia acts either as a sphincter or else maintains the acute angle of entry of oesophagus into stomach. 5◊◊The right crus of the diaphragm acts as a ‘pinch-cock’ to the lower oesophagus as it pierces this muscle. 6◊◊The positive intra-abdominal pressure compresses the walls of the short segment of intra-abdominal oesophagus. Fig. 52◊The posterior relations of the stomach; the stomach (grey tint) is superimposed upon its bed. natural viagra alternatives questions The large intestine is subdivided, for descriptive purposes, into: •◊◊caecum with the appendix vermiformis; •◊◊ascending colon (5–8 in (12–20 cm)); •◊◊hepatic ﬂexure; •◊◊transverse colon (18 in (45 cm)); viagra sleep problems quently completely obliterated in the elderly. Since obstruction of the lumen is the usual precipitating cause of acute appendicitis it is not unnatural, therefore, that appendicitis should be uncommon at the two extremes of life. 2◊◊The appendicular artery represents the entire vascular supply of the appendix. It runs ﬁrst in the edge of the appendicular mesentery and then, distally, along the wall of the appendix. Acute infection of the appendix may result in thrombosis of this artery with rapid development of gangrene and subsequent perforation. This is in contrast to acute cholecystitis, where the rich collateral vascular supply from the liver bed ensures the rarity of gangrene of the gall-bladder even if the cystic artery becomes thrombosed. 3◊◊Appendicectomy is usually performed through a muscle-splitting incision in the right iliac fossa (see ‘abdominal incisions’, page 62). The caecum is delivered into the wound and, if the appendix is not immediately visible, it is located by tracing the taeniae coli along the caecum — they fuse at the base of the appendix. When the caecum is extraperitoneal it may be difﬁcult to bring the appendix up into the incision; this is facilitated by ﬁrst mobilizing the caecum by incising the almost avascular peritoneum along its lateral and inferior borders. The appendix mesentery, containing the appendicular vessels, is ﬁrmly tied and divided, the appendix base tied, the appendix removed and its stump invaginated into the caecum. are there different strengths of viagra viagra handelsnamen axis and parasympathetic from the vagus), lymphatic vessels and lymph nodes are found there. Fig. 86◊Renal abnormalities. (a) Polycystic kidney. (b) Horseshoe kidney. (c) Pelvic kidney and double ureter. (d) Aberrant renal artery and associated hydronephrosis. viagra cost per pill australia •◊◊Anteriorly—the pubic symphysis. •◊◊Superiorly — the bladder is covered by peritoneum with coils of small intestine and sigmoid colon lying against it. In the female, the body of the uterus ﬂops against its posterosuperior aspect. •◊◊Posteriorly — in the male the rectum, the termination of the vasa deferentia and the seminal vesicles; in the female, the vagina and the supravaginal part of the cervix. •◊◊Laterally—the levator ani and obturator internus. dangers of viagra heart attack viagra makes me sleepy The muscles acting on the hand viagra revenue 2011 The upper limb viagra drug tolerance The ﬂexor tendons traverse a ﬁbro-osseous tunnel in each digit. This tunnel is made up posteriorly by the metacarpal head, the phalanges and the fronts of the intervening joints. The anterior ﬁbrous part consists of condensed deep fascia attached to the sharp anterolateral margin of each phalanx and termed the ﬁbrous ﬂexor sheath. This is particularly tough over the phalanges but loose over the front of each joint; it therefore holds the ﬂexor tendons in place without ‘bow-stringing’ during ﬂexion of the ﬁngers, but does not impede movement of the joints. Distally, the ﬁbrous sheath ends at the insertion of the profundus tendon (or ﬂexor pollicis longus tendon in the case of the thumb) at the base of the distal phalanx. These ﬁbrous sheaths are lined by synovial membrane which is reﬂected around each tendon. The tendons of the 2nd, 3rd and 4th ﬁngers have synovial sheaths which are closed off proximally at the metacarpal head, but the synovial sheaths of the thumb and little ﬁnger extend proximally into the palm. That of the long ﬂexor tendon of the thumb extends through the palm, deep to the ﬂexor retinaculum, to about 1|in (2.5|cm) proximal to the wrist and is termed the radial bursa. The synovial sheath of the 5th ﬁnger continues as the ulnar bursa, an expanded synovial sheath which encloses all the viagra prank story At the hip putting viagra in someones drink Clinical features found viagra his bag Posterior tibial artery The head and neck taking viagra after a heart attack viagra witze kostenlos The major arteries of the head and neck viagra dosage wikipedia (b) The central nervous system do you need a prescription for viagra in peru how to identify original viagra Fig. 249◊The long ascending pathways of the dorsal columns (yellow lines) and spinothalamic tracts (red lines). can you crush viagra tablets The optic nerve (II) and the visual pathway whats happens if a woman takes viagra y viagra 27 years old TABLE 1–1 The Mini Mental State Examination 42 ABDOMINAL DISTENTION 3 can you buy viagra in bulgaria DYSPNEA mad about you viagra episode herbal viagra formula HEPATOMEGALY new viagra commercial 2011 SYNCOPE CARBON DIOXIDE (“TOTAL CO2” OR BICARBONATE) viagra expiry period viagra patient instructions • 25–145 mU/mL (SI: 25–145 U/L) • Collection: Tiger top tube Used in suspected MI or muscle diseases. Heart, skeletal muscle, and brain have high levels Decreased: Menopause DEXAMETHASONE SUPPRESSION TEST miss viagra 420 twitter Increased: Pregnancy, secondary polycythemia (high altitude, COPD, etc), tumors gibt es viagra in holland rezeptfrei turkish viagra review • See CHOLESTEROL, page 62. 4 can you snort viagra get high getting viagra in thailand • 0–1.5 U/mL (SI: 10–150 U/L) by turbidimetric method • Collection: Tiger top tube nancy donde comprar viagra en el salvador HEMATOCRIT is expired viagra effective Creatinine viagra repeated intercourse im addicted to viagra 8 100 90 80 70 60 56 52 48 Arterial plasma [HCO 3 – ] (meq/L) 44 40 36 32 28 24 20 16 12 8 4 0 7.00 7.10 Metabolic acidosis Acute respiratory acidosis men in black 3 viagra is viagra a prescription drug in italy 7.50 7.40 7.30 Arterial blood pH 8 does viagra raise blood sugar Table 9–1 describes common crystalloid parenteral fluids. female viagra intrinsa FIGURE 9–1 Continued. Parkland Formula. Total fluid required during the first 24 h = (% body burn) × (body weight in kg) × 4 mL Replace with lactated Ringer’s solution over 24 h. Use • One-half the total over first 8 h (from time of burn) • One-quarter of the total over second 8 h. One-quarter of the total over third 8 h • Rule of Nines. Used for estimating percentage of body burned in adults. See Figure 9–1 for the exact calculation for the body burn in adults and children. This is also useful for determining ongoing fluid losses from a burn until it is healed or grafted. Fluid losses can be estimated as Loss in mL = (25 × % Body burn) × m2 Body surface area maximum dose of viagra in 24 hours get viagra the little blue pill Clinician’s Pocket Reference, 9th Edition gabapentin viagra interaction Enteral nutrition encompasses both supplementation by mouth and feeding by tube into the GI tract. If the patient’s oral intake is inadequate, every effort should be made to increase intake by providing nutrient-dense foods, frequent feedings, or oral supplements. If such attempts are unsuccessful, tube feeding may be indicated. In addition, patients who have a functioning GI tract but for whom oral nutrition intake is contraindicated should be considered for tube feedings. If the GI tract is functioning and can be used safely, tube feedings should be ordered instead of parenteral nutrition when nutrition support is necessary because it • • • • • • Is more easily absorbed physiologically Is associated with fewer complications than TPN Maintains the gut barrier to infection Maintains the integrity of the GI tract Is more cost-effective than TPN Contraindications to tube feeding can be found in Table 11–3. 1 1 why do older men need viagra Hypermagnesemia: This is usually seen in patients with renal failure. Antacid therapy when does viagra patent expire in usa Patients should be counseled before any procedure concerning the reason for it and the potential risks and benefits from it. Explaining the various steps often can make the patient more cooperative and the procedure easier on both parties. In general, procedures such as bladder catheterization, NG intubation, or venipuncture do not require a written informed consent beyond normal hospital sign in protocols. More invasive procedures, such as thoracentesis or lumbar puncture, for example, require written consent and must be obtained by a licensed physician. im 18 can i take viagra per qka perdoret viagra 3. Feeding Tubes Virtually any NG tube can be used as a feeding tube, but it is preferable to place a specially designed nasoduodenal feeding tube. These are of smaller diameter (usually 8 French) and are more pliable and comfortable for the patient. Weighted tips tend to travel into the duodenum, which helps prevent regurgitation and aspiration. Most are supplied with stylets that facilitate positioning, especially if fluoroscopic guidance is needed. Always verify the position of the feeding tube with an x-ray prior to starting tube feeding. Commonly used tubes include the mercury-weighted varieties (Keogh tube, Duo-Tube, Dobbhoff, Entriflex), the tungsten-weighted (Vivonex tube), and the unweighted pediatric feeding tubes. 4. Miscellaneous a. Sengstaken–Blakemore tube: A triple-lumen tube used exclusively for the control of bleeding esophageal varices by tamponade. One lumen is for gastric aspiration, one is for the gastric balloon, and the third is for the esophageal balloon. Other types of tubes used to control esophageal bleeding include the Linton and Minnesota tubes. b. Ewald tube: An orogastric tube used almost exclusively for gastric evacuation of blood or drug overdose. The tube is usually double lumen and large diameter (18–36 French). c. Dennis, Baker, Leonard tubes: These are used for intraoperative decompression of the bowel and are manually passed into the bowel at the time of laparotomy. Maximum Dose candy viagra pills viagra vs m force Thyroid Scan: Most commonly with technetium-99m pertechnetate. Useful for evaluation of nodules (solitary cold nodules require a tissue diagnosis because 25% are cancerous). Scan patterns in correlation with lab tests may help diagnose hyperfunctioning adenomas, Plummer’s and Graves’ diseases, and multinodular goiters; localize ectopic thyroid tissues (especially after thyroidectomy for cancer); and identify superior mediastinal thyroid masses HOW TO READ A CHEST X-RAY Determine the Adequacy of the Film pharmacy selling viagra in bangalore Common Uses enrique iglesias usa viagra 17 Suturing Techniques and Wound Care when will legal generic viagra be available A B 19 viagra after vasectomy Mixed Venous O2 Saturation (SvO2) < 60% Requires immediate assessment Check O2 Delivery SaO2 (%) [Hgb] CO Check O2 Consumption ≠ O2 /Metabolic needs Evaluate for unrecognized conditions requiring increased metabolic activity can i try viagra for fun the victim unless in immediate danger. Roll victim on to back as a unit if lying face down. Protect the neck. Kneel at the level of the victim’s shoulder. Open the airway (head-tilt, chin-lift,), determine breathlessness (“look [chest movement], listen [for air escaping], feel [for air movement]”) for no more than 10 s. In the unresponsive victim with spontaneous respiration, place the victim in the recovery position. Jaw thrust maneuver recommended as alternative for health care providers especially if neck injury is suspected. If the victim is breathing, place in the RECOVERY POSITION (see page 449). If not breathing, give patient two slow ventilations (2 s/inspiration) while maintaining airway. Use pocket mask or bag mask. Volume should be between 0.8–1.2 L. A barrier device (face shield or mask with one-way valve) is recommended if mouth-to-mouth or mouth-to-nose contact is necessary. Ventilate 10–12 breaths/min. If unable to ventilate, reposition head and try again. If unsuccessful, perform the FOREIGN BODY OBSTRUCTION AIRWAY SEQUENCE (see page 448). Check for circulation (breathing, coughing, movement). Palpate the carotid artery no more than 10 s to determine lack of a pulse. If pulse is present, perform rescue breathing: 1 ventilation every 5 s (10–12 ventilation/min). If no pulse, use four cycles of 15 compressions and two ventilations (compression rate 100/min, two ventilations 1.5–2 s each). Depth of compression 1.5–2 in. or slightly greater to generate carotid pulse. Apply compressions to lower half of sternum using the heels of both hands placed on top of each other. After the four cycles (approximately 1 min of CPR), pause and check for return pulse and spontaneous respirations. If no pulse or respiration, resume cycles with two ventilations, then compressions, as noted earlier. Incorporate appropriate ACLS management guidelines. cuanto dura el efecto de la pastilla viagra efectos secundarios por tomar viagra • Antithrombin therapy with heparin • Antiplatelet therapy with aspirin • Glycoprotein llb/llla inhibitors • ␤-Blockers • Nitrates INDICATIONS: viagra salt name 1. This is the primary therapy for VF or pulseless VT. Asystole is not now routinely defibrillated. 2. Use paste or pads on skin (see step 3 for location). 3. Shout “Charging defibrillator-stand clear,” synchronization switch off (if on, the defibrillator may not fire). In adults, energy levels begin at 200 J. In children, use 2 J/kg advance to 6 J/kg max. 4. Place paddles as directed on the handles: one at the right upper sternum and one at the left anterior axillary line (apex). 5. Apply paddles with firm pressure (approximately 25 lb). 6. Shout “I am going to shock on three. Stand clear!” and make sure no one is touching the patient or bed including yourself. 7. Shout “Clear,” and visually check for other team members. 8. Shout three times “Everybody clear,” and press both paddle buttons simultaneously to fire the unit, and observe for any change in the dysrhythmia. 9. Defibrillate up to three times with increasing joules (200, >200–300, >360). If these fail to convert, continue full output (360 J) for all future shocks. If VT recurs, shock again at last energy level. 10. If a patient is HYPOTHERMIC (Core temperature < 30 °C) shock only three times as in step 8. Resume shocks only after temperature rises above 30 °C. 11. If patient has automated implantable defibrillator and device is delivering shocks, wait 60 s for cycle to complete. If defibrillation attempted, place paddles several inches from the implanted pacer unit. viagra given to babies Alprazolam Buspirone Chlordiazepoxide Clorazepate Diazepam Doxepin Hydroxyzine Lorazepam Meprobamate Oxazepam Prazepam genpharma viagra viagra stop stop stop english version.mp3 download Betaxolol, Ophthalmic (Betoptic) what does viagra do to teenagers tion Edema from CHF, hepatic cirrhosis, and renal disease Loop diuretic; inhibits reabsorption of sodium and chloride in the ascending loop of Henle and the distal renal tubule DOSAGE: Adults. 0.5–2.0 mg/d PO; 0.5–1.0 mg IV q8–24h (max 10 mg/d). Peds. 0.015– 0.1 mg/kg/d PO, IV, or IM ÷ q6–24h does viagra make your pennis bigger Infections caused by susceptible bacteria involving the respiratory tract, skin, bone, urinary tract, meningitis, and septicemia ACTIONS: 3rd-generation cephalosporin; inhibits cell wall synthesis DOSAGE: Adults. 1–2 g IV q12–24h. Peds. 50–100 mg/kg/d IV ÷ q12–24h SUPPLIED: Inj viagra gross sales does the military prescribe viagra COMMON USES: ACTIONS: DOSAGE: viagra veterinary use COMMON USES: ACTIONS: what happens if you take 200mg of viagra Vasomotor symptoms, atrophic vaginitis, or kraurosis vulvae associated with menopause; female hypogonadism ACTIONS: Estrogen supplementation DOSAGE: Menopause: 0.3–1.25 mg/d, administered cyclically 3 wk on and 1 wk off. Hypogonadism: 2.5 mg PO qd–tid SUPPLIED: Tabs 0.3, 0.625, 1.25, 2.5 mg Toxicity symptoms: Hot flashes, loss of libido, impotence, diarrhea, nausea and vomiting, and gynecomastia; follow LFT peanuts natural viagra worlds strongest viagra COMMON USES: Constipation Hyperosmolar laxative Adults. 1 adult supp PR PRN. Peds. 1 infant supp PR qd–bid PRN what would happen to a woman if she took viagra generico do viagra dejavu Moderate to severe pain (<10 d) Narcotic with NSAID 1–2 tabs q4–6h PRN SUPPLIED Tabs 7.5 mg hydrocodone/200 mg ibuprofen COMMON USES: Hodgkin’s and non-Hodgkin’s lymphoma, cutaneous T-cell lymphoma (mycosis fungoides), lung cancer, CLL, CML, and malignant pleural effusions ACTIONS: Alkylating agent (bifunctional) 2 DOSAGE: 0.4 mg/kg single dose or 0.1 mg/kg/d for 4 d; 6 mg/m 1–2 ×/mo SUPPLIED: Inj 10 mg NOTES: Toxicity symptoms: Myelosuppression, thrombosis, or thrombophlebitis at inj site; tissue damage with extravasation (Na thiosulfate may be used topically to treat); nausea and vomiting; skin rash; amenorrhea; and sterility. High rates of sterility (especially in men) and secondary leukemia in patients treated for Hodgkin’s disease. Highly volatile; must be administered within 30–60 min of preparation viagra keeps dog alive tity boi viagra mp3 Medroxyprogesterone (Provera, Depot Provera, Cycrin) creatine and viagra interaction COMMON USES: Secondary amenorrhea and abnormal uterine bleeding caused by hormonal imbalance; endometrial cancer ACTIONS: Progestin supplement DOSAGE: Secondary amenorrhea: 5–10 mg/d PO for 5–10 d. Abnormal uterine bleeding: 5–10 mg/d PO for 5–10 d beginning on the 16th or 21st d of the menstrual cycle. Endometrial cancer: 400–1000 mg/wk IM SUPPLIED: Tabs 2.5, 5, 10 mg; depot inj 100, 150, 400 mg/mL NOTES: Contra with past thromboembolic disorders or with hepatic disease will viagra make me fail a drug test Mitomycin C (Mutamycin) bayer viagra preis Nizatidine (Axid) jual viagra pfizer ACTIONS: COMMON USES: 22 Commonly Used Medications jack nicholson viagra movie does viagra prolong intercourse COMMON USES: Triamcinolone acetonide 0.5% diary of a viagra fiend is 12.5mg of viagra enough 22 TABLE 22–7 (Continued) Drug When to Sample buy viagra northampton References 66 ubat kuat viagra what do women say about viagra Osteopathic considerations in neurology is there a natural herb that works like viagra Complementary therapies in neurology 59. Anderson MF, Winterson BJ. Properties of peripherally induced persistent hindlimb flexion in rat: involvement of N-methyl-D-aspartate receptors and capsaicin-sensitive afferents. Brain Res 1995; 678:140–50 60. Korr IM. The spinal cord as organizer of disease processes, IV. Axonal transport and neurotrophic function in relation to somatic dysfunction. J Am Osteopath Assoc 1981; 80: 451– 67 61. Lewit K. Manipulative Therapy in Rehabilitation of the Motor System. London: Butterworths, 1985 62. Kuchera ML. Gravitational strain pathophysiology: parts I & II. In Vleeming A, Mooney V, Dorman TA, Snijders CJ, eds. Low Back Pain: The Integrated Function of the Lumbar Spine and Sacroiliac Joints. Edinburgh: European Congress Committee, 1995:659–93 63. Jull GA, Janda V. Muscles and motor control in low back pain: assessment and management. In Twomey LT, Taylor JR, eds. Physical Therapy of the Low Back. New York: Churchill Livingstone, 1987:253–78 64. Janda V. Muscle strength in relation to muscle length, pain and muscle imbalance. In HarmsRingdahl K, ed. Muscle Strength. New York: Churchill Livingstone, 1988:153–66 65. Konnitinen YT, Koski H, Santavirta S, et al. Nociception, proprioception, and neurotransmitters. In Bland JH, ed. Disorders of the Cervical Spine, 2nd edn. Philadelphia, PA: WB Saunders, 1994:319–38 66. Korr IM. Hyperactivity of sympathetic innervation: a common factor in disease. In Greenman PE, ed. Concepts and Mechanisms of Neuro-Muscular Functions. Berlin: Springer-Verlag, 1984:1–8 67. Dubner R, Bennett GJ. Spinal and trigeminal mechanisms of nociception. Annu Rev Neurosci 1983; 6:381–418 68. Cervero F. Mechanisms of acute visceral pain. Br Med Bull 1991; 47:549–60 69. Patterson MM, Steinmetz JE. Long-lasting alterations of spinal reflexes: a potential basis for somatic dysfunction. Manual Med 1986; 2: 38–45 70. Willard FH, Mokler DJ, Morgane PJ. Neuroendocrine-immune system and homeostasis. In Ward RC, ed. Foundations for Osteopathic Medicine. Baltimore, MD: Williams & Wilkins, 1997:107–35 71. Turnbull AV, Rivier C. Corticotropin-releasing factor, vasopressin, and prostaglandins mediate, and nitric oxide restrains, the hypothalamic-pituitary-adrenal response to acute local inflammation in the rat. Endocrinology 1996; 137:455–63 72. McEwen BS, Stellar E. Stress and the individual. Mechanisms leading to disease. Arch Intern Med 1993; 153:2093–101 73. Kuchera ML. Lower extremities. In Ward RC, ed. Foundations for Osteopathic Medicine, 2nd edn. Baltimore, MD: Lippincott, Williams & Wilkins, 2003:784–818 74. Travell JG, Simons DG. Myofascial Pain & Dysfunction: The Trigger Point Manual, vol. II. Baltimore, MD: Williams & Wilkins, 1992: 168–85 75. Travell JG, Simons DG. Myofascial Pain & Dysfunction: The Trigger Point Manual, vol. II. Baltimore, MD: Williams & Wilkins, 1992: 315–38 76. Vleeming A, Snijders CJ, Stoeckart R, Mens JMA. The role of the sacroiliac joints in coupling between spine, pelvis, legs and arms. In Vleeming A, Mooney V, Snijders CJ, Dorman TA, Stoeckart R, eds. Movement, Stability & Low Back Pain: The Essential Role of the Pelvis. New York: Churchill-Livingstone, 1997: 53–71 77. Greenman PE. Principles of Manual Medicine. Baltimore, MD: Williams & Wilkins, 1996 78. Travell JG, Simons DG. Myofascial Pain & Dysfunction: The Trigger Point Manual, vol. II. Baltimore, MD: Williams & Wilkins, 1992: 186–214 79. Heinking KP, Kappler RE. Pelvis and sacrum. In Ward RC, ed. Foundations for Osteopathic Medicine, 2nd edn. Baltimore, MD: Lippincott, Williams & Wilkins, 2003:762–83 what other uses does viagra have 116 all three tabs viagra does viagra slow down ejaculation Two clinical trials of massage in fibromyalgia patients found that patients receiving a course of massage reported lower levels of pain at the end of the treatment period compared to controls45,49 In a small study of massage for migraine headaches, those receiving massage reported fewer symptoms of distress, less pain and more headache-free days than those in a waiting-list control group50 Furlan and colleagues51 recently updated their Cochrane Collaboration systematic review of massage for the treatment of low back pain. This review included eight studies, four of which used ‘massage’ as a control condition for another treatment and were not designed to deliver a therapeutic massage treatment. Of the other studies, two52,53 were given high methodological quality ratings using the Cochrane rating system. Both studies found that therapeutic massage was effective for reducing pain levels and improving functional status in patients with persistent back pain. Digestive effects Based on four clinical controlled trials, Ernst46 cautiously concluded that abdominal massage could be a promising treatment for constipa- tion. Complementary therapies in neurology acetildenafil viagra analogue Complementary therapies in neurology can you die from taking viagra RELIGIOUS INVOLVEMENT, SPIRITUALITY AND COPING Needless to say, surviving a natural disaster or crime, caring for a sick relative or friend, and experiencing the death of a loved one can be distressing experiences. Religious wer verkauft mir viagra viagra vs.generic sildenafil Complementary therapies in neurology viagra changed my life Complementary therapies in neurology 27, 74 goedkope viagra online bestellen Dennis Bourdette, Vijayshree Yadav and Lynne Shinto Complementary Therapies in Neurology: An Evidence-Based Approach Edited by Barry S.Oken ISBN 1-84214-200-3 Copyright © 2004 by The Parthenon Publishing Group, London viagra has stopped working message boards viagra daily basis VITAMIN C Better cognition in seniors or lower incidence of Alzheimer’s disease has been correlated with higher vitamin C levels77,96 and higher intake of vitamin C82,86,97, although the data are not consistently positive75,76,78,80,81,85,87. In Alzheimer’s disease, there have been reported to be low levels of ascorbate in cerebrospinal fluid98 and increasing severity of illness may correlate with lower vitamin C levels despite adequate vitamin C intake99. There are no specific data in Alzheimer’s disease to suggest that it may be useful in terms of improving cognition or function, although there are some data to suggest that adding vitamin C to vitamin E supplementation may be beneficial in terms of maximizing the beneficial effects of vitamin E on in vitro lipoprotein oxidation89. is viagra helpful in premature ejaculation Reference Sample Interventions size (dosage) Nasal decongestants Decongestants Anti-inflammatory nasal sprays Nasal dilators External nasal dilators Internal nasal dilators Nasal lubricants Dietary supplements Magnetic therapy Smoking cessation viagra didnt work for me Gene: An ordered sequence of nucleotides located in a particular position (locus) on a particular chromosome, which encodes a speciﬁc functional product (the gene product, i.e. a protein or RNA molecule). Exon: A protein-coding DNA sequence of a gene. Intron: A DNA base sequence that can be transcribed into RNA but are cut out of the message before it is translated into protein. However, introns may contain sequences involved in regulating gene expression. Codon: Crick (1963) proposed this term now recognised to be a triplet of nitrogenous bases in DNA or RNA that speciﬁes a single amino acid. elizabeth dole viagra what is viagra called in india BASIC SCIENCE NMDA-R Naϩ cAMP worldpharm4u buy viagra usa apio viagra natural N E RV E D A M A G E A N D R E L AT I O N S H I P T O N E U R O PAT H I C PA I N turkish viagra recipe Adenylyl cyclase Boehm, S. & Kubista, H. (2002). Fine tuning of sympathetic transmitter release via ionotropic and metabotropic presynaptic receptors. Pharmacol. Rev., 54: 43–99. Caterina, M.J. & Julius, D. (2001). The vanilloid receptor: a molecular gateway to the pain pathway. Annu. Rev. Neurosci., 24: 487–517. what do fake viagra pills look like buy excel herbal viagra 2a 9 10 informatii despre viagra 89 Introduction can u drink and take viagra Self-report methods for assessing pain viagra felleskatalogen putting viagra in food .2 .4 .6 .8 No fear viagra saved my marriage what does viagra do to men yahoo answers COMPLEX REGIONAL PAIN SYNDROME M.G. Serpell UNCOMMON PAIN SYNDROMES A.P. Baranowski PAIN IN CHILDREN R.F. Howard 183 177 taking too much viagra effect Epidemiological studies have shown wide variation in their estimates of chronic pain in the community ranging from 7% to 54%. Most of these studies are cross sectional; that is, they provide information at only one point of time. However, a recent longitudinal study reported pain prevalence in the same community over a 4-year period. There was no signiﬁcant difference in pain reports between men and women at baseline. The proportion of the population reporting chronic pain signiﬁcantly increased with age. The overall prevalence of pain increased from 45.5% of the population at baseline to 53.8% at follow-up; that is, an increase of 8.3% over the 4 years. There was a larger increase in prevalence among women than men and the increase was highest in the youngest age group (25–34 years). Of those who had pain at baseline, the pain persisted in 78.5% and resolved in 21.5%. Health factors (as measured by the SF-36) appeared to be better predictors of chronic pain rather than measured socio-demographic factors (such as level of education, marital status, housing or employment status). Individuals who were in the lowest quartile of SF-36 domains – physical functioning, social functioning and bodily pain at baseline – were more likely to develop chronic pain at follow-up and less likely to recover from chronic pain. This study reinforces previous work that has shown chronic pain to be a common and persistent problem in the community. In this study, health factors appeared to be better predictors of onset or recovery from chronic pain than sociodemographic factors. 105 does viagra cause premature ejaculation apa efek samping viagra 107 Further reading does half a viagra pill work old man viagra commercial Safe and easy to administer intravenously. Of ultra-short duration (allowing frequent neurological examination). Associated with minimal changes in ICP and CPP, even with endotracheal suctioning. Associated with minimal cardiovascular effects – although bradycardia may be problematic. Unaffected by hepatic and renal failure (t1/2 is unchanged). Cost efﬁcient (as a sole agent) when compared to propofol ϩ opioid in this patient group. Useful in non-intubated patients (0.1 g/kg/min) in units familiar with its use (although profound respiratory depression is a risk). viagra recreational use reviews 17 • • • does generic viagra require a prescription trustworthy online pharmacy viagra The early bird gets the worm: – Start analgesia pre-operatively and continue well into the post-operative period (‘extended preemptive analgesia’). Work multimodally: – Use several different drugs/techniques to block pain using different pathways. Check the results of analgesia: – Speak to your patients regularly, ask them about pain, then evaluate their satisfaction. viagra activation time Pain that arises from pathophysiology in an internal organ. Pain that an individual localizes in an internal organ and, therefore, attributes to pathophysiology there (e.g. ‘stomachache’). 165 e-liquid viagra what helps viagra work better PA I N I N T H E C L I N I C A L S E T T I N G how long does it take for 50mg viagra to work The nature of pain in children PA I N I N T H E C L I N I C A L S E T T I N G virtual viagra cure for impotence cd Morphine sulphate 1 mg/kg in 50 ml solution 20 mcg/kg/ml 2.5–5.0 ml (50–100 mcg/kg) 0.5–1.5 ml/h (10–30 mcg/kg/h) Morphine sulphate 1 mg/kg in 50 ml solution 20 mcg/kg/ml 0.5–5.0 ml (10–100 mcg/kg) 0.1–0.6 ml/h (2–12 mcg/kg/h) Morphine sulphate 1 mg/kg in 20 ml solution 50 mcg/kg/ml 1–2.0 ml (50–100 mcg/kg) 0.2–0.4 ml/h (10–20 mcg/kg/h) russian man dies from viagra overdose viagra tablets nhs Further reading The protocol and presentation of data big boi arrested for viagra • viagra pocelui zippy what is viagra used for yahoo answers Principles of transcutaneous electrical nerve stimulation These opioids have a descending inhibitory effect at the DH, binding to receptors on nociceptive afferent neurones, so inhibiting the release of substance P (SP). www.buy viagra online prix du viagra 25mg Spinothalamic tract Recent advances in drug development have made a wider range of agents available: can you get viagra costa rica 293 buy kamagra direct from india can women take kamagra tablets UDT should be considered: at the beginning of therapy, when pain persists despite adequate doses of opioid medication, when considering major changes in pharmacotherapy, in response to any aberrant behaviour and randomly during treatment. In a stable patient, testing randomly once or twice per year may be adequate. Refusal to provide a specimen for UDT should be viewed as a relative contraindication to continued prescription of controlled substances, requiring referral to someone knowledgeable in diagnosis and treatment of addictive disorders. A complete medical assessment may require communicating with past treatment providers. Any patient who attempts to limit such communication should be assessed by a substance abuse professional. Where possible, verify functional stability through collateral support by other caregivers, as well as the patient’s signiﬁcant others. kamagra 100mg oral jelly sildenafil ajanta 1 Familial or cultural beliefs inﬂuence the experience kamagra nebenwirkungen schwindel Opioids lead to addiction. Pain identiﬁes tissue damage. Overdosing is a problem. Analgesics have unwanted side effects, which are more important than the positive analgesic effects. 4 Failure in clinical skills: – Leave it to the ‘pain experts’ and avoid personal responsibility. – Use of ‘as required’ pain medications, rather than at ﬁxed frequencies. – Poor recognition of drug tolerance. – Inconsistent use of pain management guidelines. 5 Non-compliant patients because: – Intolerable side effects. – Rushed information and explanation of pain management plan. – Difﬁculty in obtaining prescription for analgesics. – Depersonalised environment. A response to these obstructions to effective management can be made at both a personal and a collective level. The intrinsic value of the individual patient requires recognition of all dimensions of pain: physical, psychological, social, spiritual and the family. The optimum approach to this is to ensure enough time is available to discuss the multiple dimensions of pain with the patient and their family. Aspects such as deﬁning the expected quality of life are part of this process. This will include symptom relief and minimisation of side effects. Acute pain kamagra oral jelly banana THEORIES OF CONCUSSION The vascular hypothesis original kamagra 100mg oral jelly Subsequently, a slightly delayed response was seen on the opposite side of the brain from the impact (contrecoup injury) - typically, the temporal lobe opposite the site of the impact, though, any brain area can be affected. In other words, the brain may be "rebounding" from the direction of the deceleration and hit the inner lining of the skull in the opposite direction. When rotational force is applied, the sites of brain contact with the skull can be manifold. It should be noted however, that there is a notion that no true coup or contrecoup brain injury may exist, and the magnitude of the brain tissue alteration (i.e., diffuse axonal injury, DAI) can be significantly larger when excessive rotational forces are applied (Barth et al., 2001). Late in response to the concussive impact, deformations are seen in the midbrain above the brainstem. The study by Viano et al. concluded that concussive injuries occur from rapid displacement and rotation of the cranium after peak acceleration and momentum transfer in helmet impacts, and that various regions of the brain are serially affected by deformational strains as a result of this momentum transfer (Viano et al., 2005). kamagra 100mg wiki Robert Cantu, MA, MD, FACS, FACSM super kamagra side effects From: Jordan BJ, Tsairis PT, Warren RF (eds): Head Injury in Sports. In Sports Neurology. Aspen Publications, 1989, p 227. This system is also pretty similar to a Myers Grade 2 concussion classification characterized by confusion with amnesia, but without loss of consciousness (LOG). When loss of consciousness with altered levels of consciousness not exceeding two to three minutes, or post-traumatic amnesia lasting more than twenty four hours is present, this should be considered as Grade 3. The Grade 4 assumes the loss of consciousness for a longer period of time (usually more than few minutes). Thus the hallmarks of concussion are presence of post-traumatic amnesia and loss of consciousness. Both loss kamagra oral jelly srpski how long before kamagra works *rest and exertion From: Kelly JP, Nicholas JS, Filley CM, et al Concussion in sports: Guidelines for the prevention of catastrophic outcomes. JAMA 1991;266-2867; Report of the Sports Medicine Committee for the management of concussion in sports. Colorado Medical Society, 1990 (revised May 1991). Class III Whether an athlete has been unconscious is, of course, important in terms of the return to play decision. It is generally believed that the degree of brain injury is indicated by the depth and duration of the unconscious state. While not diminishing the importance of being rendered unconscious, it is inappropriate to make a decision of return to play solely on this symptom. I find it illogical to assess as less severe the concussion occurring kamagra srbija cena Third Concussion Terminate season; may return to play in 3 months if without symptoms. Terminate season; may return to play next season if without symptoms. Terminated season; strongly discourage return to contact or collision sports. Injured Control kamagra oral jelly romania 201 kamagra posledice 2.4, kamagra sildenafil 32 pills 14.0 wie nimmt man kamagra oral jelly ein kamagra malta EEG by then defining quantitative EEG (qEEG or QEEG) as "the mathematical processing of digitally recorded EEG in order to highlight specific waveform components, transform the EEG into a format or domain that elucidates relevant information, or associate numerical results with the EEG data for subsequent review or comparison." (Nuwer, 1997) (p. 278). The reality is that there is no clear distinction between digital EEG and quantitative EEG because both involve mathematical transformations. For example, the process of analog-to-digital conversion involves transforms by analog and digital filtering as well as amplification and sample and hold of the electrical scalp potentials and re-montaging and reformatting the EEG. Clearly, digital EEG involves mathematical and transformational processing using a computer and therefore the distinction between quantitative EEG and digital EEG is weak and artificial. It would appear that the AAN's artificial distinction between digital EEG and quantitative EEG is aimed to support the practice of visual examination of EEG tracings which is highly unreliable and insensitive (Cooper et al, 1974; Woody, 1966; 1968; Majkowski et al, 1971; Volavka et al, 1971; Niedermeyer and Lopez Da Silva, 1995) while at the same time down playing modern advances in quantitative EEG which is more reliable and more sensitive than visual examination alone and simultaneous qEEG with visual examination of EEG tracings can significantly aid a competent clinician in their assessment of a patient's problems. kamagra gel nacin upotrebe Stein kamagra factory india Fig. 18. I intracerebral hematoma, CT scan. There is a high-attenuation mass within the brain. kamagra information women REFERENCES There are three major types of brain injury that have been identified by clinicians. Those are concussions, contusions, and lacerations. Concussion is a continuum of clinical syndromes, which may range in severity from brief amnesia to a prolonged coma following a head injury. The term concussion, however, is frequently used to describe a mild head injury with rather transient disruption of neural functioning, such as disturbed orientation, short-term memory, equilibrium, speech and vision. ajanta super kamagra erfahrungen kamagra tablets how do they work Closed head injuries can be associated with a variety of neurological menshelp forum kamagra to writing, was found to be lower in younger adolescents than in older adolescents (Thompson et al., 1994). Lastly, despite age of onset as a factor determining the outcome of recover, the depth and duration of coma and age appear to be the most important factor associated with the final outcome. Other prognostic indicators of the outcome include pupilary and optokinetic responses, intracranial pressure, extent of retrograde and post-traumatic amnesia, level of activity, and neurological findings (Levin, Benton & Grossman, 1982; Menkes & Batzdorf, 1985). Johnson, D. A. (1992). Head injured children and education: A need for greater delineation and understanding. British Journal of Educational Psychology, 62, 404409. Kolb, B., & Whishow, I. (1990). Human Neuropsychology. NY: Freeman. Rourke, B. P., Bakker, D. J., Fisk, J. L., & Strang, J. D. (1983). Child neuropsychology: An introduction to theory, research, and clinical practice. New York: Guilford Press. Ewing-Cobbs, L., Fletcher, J. M., & Levin, H. S. (1989). Intellectual, motor, and language sequelae following closed head injury in infants and preschoolers. Journal of Pediatric Psychology, 14, 531-547. Thompson, N.M., Francis, D.J., Stuebing, K.K., Fletcher, J.M., Ewing-Cobbs, L., Miner, M.E., Levin, H.S., & Eisenberg, H. (1994). Motor, visual-spatial, and somatosensory skills after closed-head injury in children and adolescents: A study of change. Neuropsychology, 8, 333-342. Levin, H. S., Benton, A. L., & Grossman, R. G. (1982). Neurobehavioral consequences of closed head injury. New York: Oxford University Press. Menkes, J.H., & Batzdorf, U (1985). Textbook of Child Neurology. Philadelphia: Lea & Febiger. Rivara, F. P. (1995). Developmental and behavioral issues in childhood injury prevention. Journal of Developmental and Behavioral Pediatrics, 16, 362-370. super p force vs super kamagra kamagra jelly 7 day pack Purpose of the Study Thompson super kamagra wikipedia Cantu (2001) how long does kamagra 100mg oral jelly last kamagra oral jelly original erkennen George Salvaterra does not have the same shock attenuation capabilities as the single bladder or foam cells. The inflatable double bladder seems to give better protection against tangential blows because of the greater shell stand-off due to the double bladder mechanism. Overall, these pneumatic helmets are more comfortable than the previous styles of helmet and they offer more protection because of the quality of fit and foam padding. Over the last eight years, the increased awareness to the serious consequences of concussions has driven manufactures to substantial increase helmet research and design. It is a common practice now to see a liter helmet that has large thin plastic shell and numerous air vents and extruded ridges for strength and thicker padding. This should be worrisome to the consumer, because the polycarbonate alloy losses strength with the thinning shell and increased venting. The construction techniques of fluting the plastic, however, does help to promote strength along the ridge. Most of the weight loss in the plastic is made up in the reinforcement of thicker molded padding. The compromise in construction may cause crumpling of the shell with focal loading. The aero design may also cause crumple zones where the shell has been elongated and face mask, shields and retention straps are attached. The compromises in construction, however may give a shell the necessary strength at an inferior load site if the plastic is reinforced by molding foam directly to the shell. Various helmet manufacturers have proved that by fluting out the back of the helmet and grossly improving back pack may help to better absorb the forces. Of course, fluting out the back of the helmet greatly improves the quality of the plastic. It might be critically important when developing a light pole vaulting helmet, where focal loading of a thin plastic will need to be reinforced. This may provide a tremendous amount of shock attenuation for a single focal load. kamagra interdit en france levitra with dapoxetine from australia The major concern for the designers of headgear is to reduce the relative velocity of the head and the object it will impact to zero without causing tissue damage. This must take place over a sufficient distance. Therefore, the same relative velocity could cause significant damage or no damage dependant on the stopping distance or time it takes to bring the head to zero velocity. To design adequate head protection, an understanding of the types of injuries, types of impacts, and the magnitude of forces that may be levitra on line shipping worldwide 414 levitra cost rite aide are faced with possible physical harm every time they step onto the field. Being faced with memories of pain and discomfort are likely to further developing some level of fear for subsequent injury. Fear may result in erratic emotional responses and various forms of avoidance reactions including absenteeism and lack of readiness to perform during practice/competitions. Given the complexity of the athlete's experience of injury, it seems erroneous for coaches to ignore fear as a possible component of re-injury. Suffering from injuries and experiencing fear may elicit a compilation of bracing behaviors. Bracing behavior is the act of preparing or positioning for impact or danger during athletic activity and movement (Keefe, 1990). An assemblage of bracing behavior produces a variety of deficient movement techniques (Keefe, 1984, 1990). It is important to note that bracing behavior may not always stem from the pain, discomfort, postural instability, or decreased degrees of freedom caused by the physical injury. Bracing behavior may also be caused by particular psychological states (Keefe, 1984)^ in general, and learned avoidance reactions (Fordyce et al., 1982) in particular. Avoidance refers to ''the performance of a behavior which post-pones or averts the presentation of an aversive events" (Kazdin, 1980). It was proposed that fear of injury due to movement and associated anticipation of pain is one of the major factors of bracing behaviors as reflected in deficient movement patterns, ultimately causing secondary, or more severe injury (Moss, Slobounov, Sebastianelli, 2005). Therefore, it is important for coaches and medical personnel to understand predisposing factors causing the development of fear of injury due to movement in order to prevent real injury. If real injury occurred, it is important to evaluate the psychological status of athletes, as an important step for developing a holistic rehabilitation program and predicting athletes at risk for re-injury. With respect to athletic injuries, fear may be experienced in different contexts. The fear not only originates from the exact event that caused the injury, but there is a fear of movement in general. Our personal observations of injured athletes both in the field and in the training room suggest that it is unlikely that re-injury will occur under the exact same circumstances, but rather some type of movement may cause a secondary injury. In our recent study (Moss et al., 2005) we locked into the concept of Kinesiophobia, referring specifically to fear of movement. This concept was originated by Kori et al. (1990) as ''an excessive, irrational, and debilitating fear of physical movement and activity resulting from a feeling of vulnerability to painful injury or re-injury". In 1991, Miller developed the Tampa Scale of Kinesiophobia (TSK) comprising various questions regarding the fear of movement. We employed the TSK scale and observed injured athletes in the field and in the training room upon their return to sport participation. The details regarding the Tampa Scale of Kinesiophobia (TSK) and some results levitra online purchase overnighted forests are being reduced in size. As another example, because of seaside development, pollution, and overﬁshing, 14 of the most valuable ﬁnﬁshes are becoming commercially extinct, meaning that too few remain to justify the cost of catching them. Most biologists are alarmed over the present rate of extinction and believe the rate may eventually rival that of the five mass extinctions that have occurred during our planet’s history. The dinosaurs became extinct during the last mass extinction, 65 million years ago. Everyone needs to realize that humans are totally dependent on other species for food, clothing, medicines, and various raw materials. Therefore, it is very shortsighted of us to allow other species to become extinct. Ecosystems and the species living in them should be preserved because only then can the human species continue to exist. And it takes from 2,000 to 10,000 generations for new species to evolve and to replace the ones that have died out. Because we are dependent upon the normal function and the present biodiversity of the biosphere, the existing species should be preserved. Humans belong to the world of living things and are vertebrates. They have modiﬁed existing ecosystems to the point that they must now be seriously concerned about the continued existence of the biosphere. non prescription alternative to levitra Front Matter levitra shop germany 2.4 Molecules of Life • Nucleic acids are polymers of nucleotides. 35 • Genes are composed of DNA. RNA serves as an intermediary during protein synthesis. 35 15 levitrawithnoprescription Chemistry of Life levitra 100mg uk levitra 10mg online south africa Mader: Human Biology, Seventh Edition H C H H C H H C H H C H H C H levitra y dapoxetine 40 zenegra levitra zenegra softtabs ci Rough ER xenical levitra prevacid wiki levitra generic paxil Figure 3.3 NADH2 pyruvate spain farmacia levitra pharmacy online message boards new levitra Understanding Key Terms Both loose ﬁbrous and dense ﬁbrous connective tissues have cells called ﬁbroblasts that are located some distance from one another and are separated by a jellylike matrix containing white collagen ﬁbers and yellow elastic ﬁbers. Loose ﬁbrous connective tissue supports epithelium and also many internal organs (Fig. 4.4a). Its presence in lungs, arteries, and the urinary bladder allows these organs to expand. It forms a protective covering enclosing many internal organs, such as muscles, blood vessels, and nerves. Dense ﬁbrous connective tissue contains many collagen ﬁbers that are packed together. This type of tissue has more speciﬁc functions than does loose connective tissue. For example, dense ﬁbrous connective tissue is found in tendons, which connect muscles to bones, and in ligaments, which connect bones to other bones at joints. pharmacutical sales levitra Neuron ortho tri-cyclen levitra levitra nexium levitra prescription drug stores denavir There are several different types of neuroglia in the brain (Fig. 4.7), and much research is currently being conducted to determine how much “glia” contribute to the functioning of the brain. Neuroglia outnumber neurons nine to one and take up more than half the volume of the brain, but until recently, they were thought to merely support and nourish neurons. Three types of neuroglia are oligodendrocytes, microglia, and astrocytes. Oligodendrocytes form myelin, and microglial cells, in addition to supporting neurons, engulf bacterial and cellular debris. Astrocytes provide nutrients to neurons and produce a hormone known as glia-derived growth factor, which someday might be used as a cure for Parkinson disease and other diseases caused by neuron degeneration. Neuroglia don’t have a long process, but even so, researchers are now beginning to gather evidence that they do communicate among themselves and with neurons! Nerve cells, called neurons, have ﬁbers (processes) called axons and dendrites. In general, neuroglia support and service neurons. lost cost levitra The internal organs are located within speciﬁc body cavities (Fig. 4.8). During human development, there is a large ventral cavity called a coelom, which becomes divided into the thoracic (chest) and abdominal cavities. Membranes divide the thoracic cavity into the pleural cavities, containing the right and left lungs, and the pericardial cavity, containing the heart. The thoracic cavity is separated from the abdominal cavity by a horizontal muscle called the diaphragm. The stomach, liver, spleen, gallbladder, and most of the small and large intestines are in the upper portion of the abdominal cavity. The lower portion contains the rectum, the urinary bladder, the internal reproductive organs, and the rest of the large intestine. Males have an external extension of the abdominal wall, called the scrotum, containing the testes. The dorsal cavity also has two parts: the cranial cavity within the skull contains the brain; and the vertebral canal, formed by the vertebrae, contains the spinal cord. levitra vardenafil hcll Part 1 levitra vardenafil 20mg x 4 pills 74 levitra tabs mens health store online reversal levitra rsd I. Human Organization capillary levitra levetria Small intestine Large intestine levitra generic 20 pills 20mg 119 → levitra gamecube online games Unknown levitra diarrea levitra chat line II. Maintenance of the Human Body levitra and flomax together drug interaction valve inner layer levitra 3 official website www.mhhe.com/biosci/genbio/maderhuman7/ ಆ is there really generic levitra © The McGraw−Hill Companies, 2001 flonase levitra metrogel metrogel myonlinemeds biz effects of androgel on levitra The partial pressure of oxygen (PO ) in pulmonary capillaries is about 98–100 mm Hg, but only about 40 mm Hg in tissue capillaries. Hemoglobin is about 98% saturated in the lungs because of PO , and also because (a) the temperature is cooler and (b) the pH is higher in the lungs. On the other hand, hemoglobin is only about 60% saturated in the tissues because of the PO , and also because (a) the temperature is warmer and (b) the pH is lower in the tissues. Human Breathing Essential Study Partner dangers of levitra jpg The three main steps in urine formation are color-coded to arrows that show the movement of molecules into or out of the nephron at speciﬁc locations. In the end, urine is composed of the substances within the collecting duct (see gray arrow). cheap price levitra made in india Urinary System and Excretion cheap generic levitra from mexico buy levitra at msn 10. Urinary System and Excretion • Bone is a living tissue; therefore, it grows and undergoes repair. 208 • The fetal skeleton is cartilaginous and then is replaced by bone. 208 • The adult bones undergo remodeling—they are constantly being broken down and rebuilt. 209 • The mending of a fracture requires certain identiﬁable steps. 209 buring levitra online Movement and Support in Humans generic levitra wit mc generic levitra and colius 11. Skeletal System flonase levitra myonlinemeds biz nexium stimula III. Movement and Support in Humans III. Movement and Support in Humans levitra anecdotes buy dreampharmaceuticalscom levitra online Exercise, Exercise, Exercise canda levitra prescription Some axons are covered by a protective myelin sheath. In the PNS, this covering is formed by a type of neuroglia called Schwann cells, which contain the lipid substance myelin in their plasma membranes. The myelin sheath develops when Schwann cells wrap themselves around an axon many times and in this way lay down several layers of plasma membrane. The myelin sheath is interrupted by gaps called nodes of Ranvier (Fig. 13.3). Myelin gives nerve ﬁbers their white, glistening appearance and serves as an excellent insulator. The myelin sheath also plays an important role in nerve regeneration within the PNS. If an axon is accidentally severed, the myelin sheath remains and serves as a passageway for new ﬁber growth. Multiple sclerosis (MS) is a disease of the myelin sheath in the CNS. Lesions develop and become hardened scars that interfere with normal conduction of nerve impulses, and the result is various neuromuscular symptoms. All neurons have three parts: dendrites, a cell body, and an axon. Sensory neurons take information to the CNS, and interneurons sum up sensory input before motor neurons take commands away from the CNS. 6girl levitra Part 4 advertising strategies of levitra + – – + bayer pill id number levitra original spinal nerve dorsal root ventral root b. Ventral meninges attractive levitra woman spindle. The knee-jerk reﬂex, which involves muscle spindles, offers an opportunity for physicians to test a reﬂex action. The information sent by muscle spindles to the CNS is used to maintain the body’s equilibrium and posture despite the force of gravity always acting upon the skeleton and muscles. Proprioceptors are involved in reﬂex actions that maintain muscle tone and thereby the body’s equilibrium and posture. Blind Spot discount male levitra medications online faculty on behalf of levitra 10. Label this diagram of an eye. dreampharmaceuticalscom levitra order 15. Endocrine System 16.4 Control of Reproduction critic chat levitra cme conference on levitra GnRH medical prescriptions uk levitra V. Reproduction in Humans new levitra pharmacy information Reproductive System prevent levitra side effects 25 Reproduction in Humans personal experiences with levitra taking 60 mg of levitra Symptoms tendencias de la industria farmaceutica levitra 1955 try levitra sample pack b. c. viral DNA levitra information levetra These photos show the effect of an HIV infection in one individual who progressed through all the stages of AIDS. levitra myonlinemeds biz vaniqa zyrtec 1. Binding of the virus to the plasma membrane. HIV has an envelope protein known as gp120. This envelope protein allows the virus to bind to a CD4 receptor in the host-cell plasma membrane. Ordinarily, a CD4 receptor is a binding site for various signaling molecules. 2. Penetration of the virus into the cell. After binding occurs, the HIV virus fuses with the plasma membrane, and the virus enters the cell. Uncoating removes the capsid, and RNA is released. 3. Production of viral DNA. This event in the reproductive cycle is unique to retroviruses. The enzyme called reverse transcriptase makes a DNA copy of their RNA genetic material. Usually in cells DNA is transcribed into RNA. Retroviruses can do the opposite only because they have this unique enzyme from which they take their name. (Retro in Latin means reverse.) The viral enzyme integrase now splices viral DNA into a host chromosome. The term HIV provirus refers to viral DNA integrated into host DNA. HIV is usually transmitted to another person by means of cells that contain proviruses. Also, proviruses serve as a latent reservoir for HIV during drug treatment. Even if drug therapy results in an undetectable viral load, investigators know that there are still proviruses inside infected lymphocytes. Mader: Human Biology, Seventh Edition levitra funny video bob levitra usa today 20.2 About one in 10,000 males is a hemophiliac. There are two common types of hemophilia: hemophilia A is due to the absence or minimal presence of a clotting factor known as factor IX, and hemophilia B is due to the absence of clotting factor VIII. Hemophilia is called the bleeder’s disease levitra round brown pill When replication is ﬁnished, two complete DNA double-helix molecules are present. Note that DNA replication is semiconservative because each new double helix is composed of an old parental strand and a new daughter strand. levitra hydrocod best prices generis viagra U where to buy viagra in philippines drug store 21. DNA and Biotechnology best deals on genaric viagra Chapter 21 viagrafreesamples Mader: Human Biology, Seventh Edition viagra dapoxetine next day shipping repair enzyme buying viagra online using pay pal Tobacco and Alcohol Use Mader: Human Biology, Seventh Edition branded viagra without prescription walmart rx viagra cost combustion photosynthesis respiration 100 ml viagra for sale VII. Human Evolution and Ecology viagra generico paypall Point sources suburban development sewage treatment plant Point sources VII. Human Evolution and Ecology where can i find the best and cheapest overnight viagra fresh water, but the cost of desalination is about four to eight times the average cost of fresh water acquired via the water cycle. Forests and other natural ecosystems exert a “sponge effect.” They soak up water and then release it at a regular rate. When rain falls in a natural area, plant foliage and dead leaves lessen its impact, and the soil slowly absorbs it, especially if the soil has been aerated by organisms. The water-holding capacity of forests reduces the possibility of ﬂooding. The value of a marshland outside Boston, Massachusetts, has been estimated at $72,000 per hectare per year solely on its ability to reduce ﬂoods. Forests release water slowly for days or weeks after the rains have ceased. Rivers ﬂowing through forests in West Africa release twice as much water halfway through the dry season, and between three and ﬁve times as much at the end of the dry season, as do rivers from coffee plantations. generic viagra best buys viagra pfizer overnight delivery VII. Human Evolution and Ecology viagra prescription filled online Islands are particularly susceptible to environmental discord caused by the introduction of alien species. Islands have Practice Problems 4 edinburgh viagra free bananas pajamas what does cialis do for men without ed P a r t Managing the Disease Process my husband takes cialis should i take 10mg or 20mg cialis • donde puedo comprar cialis generico en mexico Sphincte Closes Urethra does cialis work when drunk Bladder responds in an exaggerated way—receiving frequent calls to empty. Uninhibited bladder diltiazem cialis interaction Rectal stimulants provide both chemical stimulation and localized mechanical stimulation combined with lubrication to promote stool elimination. They may be used either occasionally when necessary or on a routine daily or every-other-day basis in conjunction with other medications already listed. Suppositories generally act within 15 minutes to an hour. They include • Glycerin suppositories, which contain no medication and provide rectal stimulation and lubrication for easier passage of stool. Glycerin suppositories are milder and less habit85 does bayer make cialis PART III atacand cialis interaction Meat, Fish, Eggs, Poultry, Nuts, Beans 2-3 Servings Daily can you buy cialis over the counter in spain o f cialis 5 mg auf rezept % %% o f % %% t r i g g e r s how often can you take cialis 10mg ( µ V ) Control EMG Conditioned EMG 85 10 45 25 30 35 40 45 Walking (a) (b) (c) DPN FN Q MN Excitatory INs (PNs) Ia Group II TA Noradrenergic descending inhibition Latency (ms) 50 -- Fig. 7.12. Changes in deep peroneal group II excitation of quadriceps during gait. (a) Sketch of the presumed pathways of group I–group II excitation through propriospinal neurones (PN) from tibialis anterior (TA) to quadriceps (Q) motoneurones (MN). Noradrenergic descending inhibition of transmission of group II excitation is represented. (b), (c) Comparison of the effects of deep peroneal nerve (DPN) stimulation (2.5 MT) on the averaged rectiﬁed EMG of the Q (vastus lateralis) during walking ((c) DPN stimulation triggered 30 ms after heel strike) and during voluntary co-contraction of Q and TA while standing (b), at equivalent EMG activity. Control (thin line) and conditioned (thick line) on-going EMG traces are plotted against the latency after DPN stimulation. Arrows indicate the expected time of arrival of the DPN group I volley at MN level (27 ms). Dashed and dotted vertical lines highlight the latencies of group I- and group II-mediated responses. Modiﬁed from Marchand-Pauvert & Nielsen (2002a), with permission. to decreased gating of group II pathways from the brainstem. The peroneal group II facilitation was only observed during the early stance phase of walk- ing (0–60 ms after heel strike with a maximum at 30 ms), when there is an eccentric contraction of the tibialis anterior. This would produce strong spindle activation, especially if the contraction was accom- panied by enhanced ␥ s drive (Chapter 3, p. 135). At this time the weight of the body is shifted to the leg that is about to begin the stance phase, and a strong quadriceps contraction would be required to extend the knee joint tosupport the body. The feedback car- ried by Ia and groupII spindle discharges fromankle dorsiﬂexor muscles would help ensure the stabil- ising contraction of quadriceps. In healthy subjects the early and late peaks of peroneal-induced facil- itation observed in early stance while walking at normal speed (3–4 km h −1 ) are suppressed when walking at 1 kmh −1 , a walking speed which requires voluntary effort (Marchand-Pauvert & Nielsen, 2002b). Thisﬁndingcouldbeduetothecorticospinal inhibitorycontrol observedonlumbar propriospinal neurones through feedback interneurones (see p. 310), and would indicate that the contribution of group II pathways to the stabilisation of the knee is especially important during natural ‘automatic’ walking. Conclusions Group II pathways play an important role during ‘automatic’ human walking: (i) homonymous group II discharges from the triceps surae contribute to 320 Group II pathways the normal activationof soleus motoneurones inthe stance phase and, because this contribution can be predicted by the central nervous system, less cen- tral drive is necessary to activate the motoneurones in the presence of this feedback (Nielsen & Sinkjær, 2002); (ii) heteronymous group II discharges from pretibial ﬂexors to quadriceps contribute to stabil- ising the knee in early stance; and (iii) in addi- tion homonymous group II pathways contribute to the reactions to sudden external perturbations. Any group II excitation would be potentiated by group I discharges convergingontothe relevant lumbar pro- priospinal neurones, muchas is likelywithperturba- tions to upright stance. Studies in patients and clinical implications Peripheral neuropathies Charcot–Marie–Tooth type 1A disease Inthis hereditaryperipheral neuropathy, thereis loss of large diameter nerve ﬁbres with relative sparing of small-diameter ﬁbres (see Dyck et al., 1993). In such patients, the short-latency responses to stretch in soleus and ﬂexor digitorum brevis are absent or markedly decreased, attesting the loss of Ia affer- ents, while delayedmedium-latency responses (pre- sumably delayed group II responses) are preserved (Fig. 7.13(b); Nardone et al., 2000). Despite the absence of Ia stretch reﬂex responses in leg and foot muscles, the less severely affected patients do not suffer balance problems, and their body sway area is in the same range as in normal subjects (Fig. 7.13(c), (d )). The delay of the medium-latency responses may be explained by the slow conduction velocity of motor ﬁbres (Nardone et al., 2000). Neuropathies affecting ﬁbres of all sizes, such as diabetes mellitus In these neuropathies, not only were the short- latency responses to stretch reduced in the soleus and absent in the ﬂexor digitorum brevis, but the medium-latency responses were delayed in both muscles, and the conduction velocity of group II afferents decreased (Nardone & Schieppati, 2004). It was argued that this alteration of mus- cle group II afferent feedback was responsible for the increased body sway area and postural ataxia observed in these patients (Fig. 7.13(e); Schieppati et al., 2001; Nardone & Schieppati, 2004). Spasticity Musclestretchactivatesbothprimaryandsecondary muscle spindle endings. Hyperexcitability of lum- bar propriospinal neurones activated by group II afferents might therefore be one of the causes of the exaggerated stretch reﬂex characteristic of spas- ticity, an hypothesis originally proposed on the basis of the selective gating of transmission of group II excitation to motoneurones in animals by monoaminergic agonists, drugs that are effective in depressingspasticity (Jankowska, 1993; Jankowska& Hammar, 2002; cf. p. 299, for evidence for a similar gating in humans). Three questions arise when examining group II excitation in spastic patients. (i) Does increased group II excitation occur in spastic patients? (ii) If yes, which is (are) the mechanism(s) under- lying it? (iii) Is increased group II excitation sufﬁcient to cause spasticity? Methodology Deep peroneal-induced heteronymous facilitation of the quadriceps H reﬂex This appears to be a suitable method to investigate changes in group II pathways in spastic patients, because (i) it can be used at rest; (ii) the group II-mediated excitation will then not be affected by the post-spike afterhyperpolarisation and recurrent inhibitionfollowingmotoneuronedischarge; (iii) the Studies in patients 321 (a) (b) (c) (d) (e) Fig. 7.13. Changes in group II-mediated responses in patients with peripheral neuropathy. (a) Presumed pathways mediating short-latency (SLR) and medium-latency (MLR) responses in the ﬂexor digitorum brevis (FDB) muscle. Ia and group II afferents run in the tibial nerve (TN). Ia afferents have monosynaptic projections on FDB motoneurones (MN) and converge with group II afferents onto spinal group II interneurones (IN or PN). (b) Toe-up rotation of the platform(lower trace, and sketch on the right) and resulting rectiﬁed EMG responses in the FDB (upper traces) in a normal subject (thin line, with both SLR and MLR) and a patient with Charcot–Marie–Tooth type 1A disease (thick line, with an absent SLR and a delayed MLR). (c)–(e) Body sway area (mm 2 ) during quiet stance, with feet spaced 10 cm apart, eyes open () and closed (), recorded in 23 normal subjects (c), 9 patients with Charcot–Marie–Tooth type 1A (CMT 1A) disease (d ), and 20 patients affected by diabetic peripheral neuropathy (e). Each column is the mean value in the population; vertical bars 1 SEM. Body sway area, with eyes open or closed, is in the same range in normal subjects and in patients with CMT 1A disease, but is increased in patients with diabetic neuropathy. Modiﬁed from Nardone et al. (2000) (b), and Schieppati et al. (2001) ((c)–(e)), with permission. excitability of the interneurones will not be modiﬁed by the ‘postural set’ (see below); and (iv) there is virtually no heteronymous monosynaptic excitatory Ia projection from pretibial ﬂexors to quadriceps motoneurones. The investigation involves measur- ing the time course of the changes in the quadri- ceps Hreﬂex after conditioning stimulation at 2–3 MT to activate group I and group II afferents in the deep peroneal nerve. To ensure that changes in the deep peroneal facilitation do not simply reﬂect changes in the excitability of quadriceps motoneurones evoked by an unmodiﬁed condition- ing group II volley, the H max /M max amplitude and H/M threshold ratios should be recorded in paral- lel in the quadriceps (Marque et al., 2001b; Maupas et al., 2004). Monoaminergic gating If an increase in the late peroneal-induced facili- tation of the quadriceps H reﬂex reﬂects increased transmission of group II excitation, it should be suppressed by monoamine agonists. Note, how- ever, that monoaminergic suppressionis acondition 322 Group II pathways necessary but insufﬁcient by itself to attribute an increased late facilitation of the reﬂex to an increased excitation at a premotoneuronal level. A normal group II input reaching hyperexcitable ␣ motoneurones would produce an increased reﬂex response, and this would be similarly suppressed by monoamines. It is therefore important that changes produced by monoamine agonists on the group II excitation have been observed without concomi- tant changes in␣motoneurone excitability (Maupas et al., 2004; Remy-N´ eris et al., 2003). Stretch-induced group II-mediated medium- latency responses in leg muscles During free stance these responses are reduced in spastic patients with supramedullary injuries (Nardone et al., 2001b). However, such responses depend on the ‘central set’ operating when the sub- ject relies on the group II response to ensure equi- librium (cf. p. 313), and these studies provide lim- ited insight into the excitability of group II pathways under resting conditions (cf. p. 301). Nardone, Corna &Schieppati (2001a) presumedthat thenormal regu- lation involves inhibitory descending control on the locus coeruleus, leading to decreased monoaminer- gic gating of group II afferents (cf. p. 314). The loss of this normal descending regulationafter stroke could therefore account for the weaker group II excita- tion during perturbations to stance (cf. the sketch in Fig. 7.14(a)). Evidence for increased propriospinally mediated group I-group II excitation Stroke patients The early non-monosynaptic group I and late group II peroneal-inducedfacilitations of thequadriceps H reﬂex areincreasedtoasimilar extent ontheaffected side and not modiﬁed on the unaffected side when compared with healthy subjects (Figs. 10.17(b) and 7.14(b); Marque et al., 2001b; Maupas et al., 2004). Oral intake of tizanidine reduced the spasticity and produced, ontheaffectedside, adecreaseinthedeep peroneal-induced facilitation of the quadriceps H reﬂex. The decrease was more marked for the late groupII excitationthanthe early non-monosynaptic group I excitation (Fig. 7.14(b); Maupas et al., 2004). Patients with spinal cord lesions More variable results have been reported in these patients (Remy-N´ eris et al., 2003). In most patients the group I and II peaks were both signiﬁcantly enhanced, with a greater increase inthe late group II peak (Fig. 7.14(c) andFig. 10.17(d )). Insome patients, however, the increase was limitedtothe early groupI peak (Fig. 10.17(c)). Clonidine (another ␣ 2 noradren- ergic agonist injected intrathecally) decreased the spasticity and suppressed both peaks of peroneal- induced facilitation of the quadriceps H reﬂex, the suppression of the late peak being more promi- nent (Fig. 7.14(c); Remy-N´ eris et al., 2003). In spinal- injured patients, oral intake of L-dopa (a noradren- aline precursor) also reduced the spasticity and weakened the quadriceps tendon jerk (Fig. 7.14(d ), (e); Eriksson, Olausson & Jankowska, 1996). Conclusions There is evidence for increased peroneal-induced group II excitation of quadriceps motoneurones in spastic patients. The ﬁnding that monoamine ago- nists suppress the facilitation produced by group II afferents more than that produced by group I affer- ents supports this view. The possible mechanisms underlying the suppression of group I-mediated effects are discussed below (cf. p. 324). Possible mechanisms underlying changes in group II-mediated responses Stroke patients Loss of the corticospinal excitation of feed- back inhibitory interneurones (cf. p. 310) would produce increased excitability of propriospinal neurones, if the normal control on these inhibitory interneurones were exerted tonically. There is no experimental evidence for tonic corticospinal con- trol of feedback inhibitory interneurones, but this mechanism would provide a simple explanation for why the early group I and late group II peaks of Studies in patients 323 (a) (b) (d) (c) (e) Fig. 7.14. Changes in group II excitation in spastic patients. (a) Sketch of the presumed pathways. Group Ia and group II afferents from tibialis anterior (TA) in the deep peroneal nerve (DPN) and from the quadriceps (Q) in the femoral nerve (FN) converge on common propriospinal neurones (PN) projecting to Q motoneurones (MN). PNs are inhibited by feedback inhibitory interneurones (Inhib IN) fed by Ia and group II afferents, and project also to g motoneurones (positive feedback through the g loop). Corticospinal projections are more potent (thick line) on inhibitory INs than on PNs and Q MNs. The noradrenergic (NA) gating of group II excitation from the locus coeruleus (Loc Coer) is represented (thick dotted line), and it is assumed that there is descending inhibitory control on the locus coeruleus. Upward vertical arrow represents the tonic group II trafﬁc from TA due to the background stretch on the muscle (see p. 324 in text), and bent upward arrow the spindle discharge produced by quadriceps stretch when assessing Ashworth score. Horizontal double-headed arrows show various lesions interrupting: the corticospinal tract (continuous arrow), the descending tract in the spinal cord from the locus coeruleus (dotted arrow), and the presumed inhibitory higher control of the locus coeruleus (dashed arrow). (b), (c) Changes in the quadriceps H reﬂex after DPN stimulation ((b), 2 MT; (c), 3 MT), as a percentage of unconditioned reﬂex value, are plotted against the interstimulus interval (ISI). (b) Results in a stroke patient from the affected side before (●) and 90 min after oral intake of tizanidine 150 g kg −1 (❍) or a placebo (), and from the unaffected side in the control situation (); vertical bars ±1 SEM. (c) Results in a patient with familial spastic paraparesis before () and 60 min after intrathecal injection of clonidine 60 g (❍); vertical bars 1 SEM. (d ), (e) In a patient with traumatic spinal cord lesion, four superimposed quadriceps tendon jerks are compared before (d ) and 50 min after oral intake of L-dopa 200 mg (e). Modiﬁed from Maupas et al. (2004) (b), Remy-N´ eris et al. (2003) (c) and Eriksson, Olausson & Jankowska (1996) ((d ), (e)), with permission. 324 Group II pathways facilitation of the quadriceps H reﬂex are increased to a similar extent in these patients. Patients with spinal cord injury The corticospinal lesion might similarly produce hyperexcitability of lumbar propriospinal neurones by the removal of corticospinal inhibition. How- ever, disruption of the normal monoaminergic ga- ting of transmissionof groupII excitationis the most likely mechanism (see Jankowska & Hammar, 2002). Interruption of the descending noradrenergic sup- pression would account for the ﬁndings that the peroneal-induced group II excitation of the quadri- ceps H reﬂex is: (i) generally increased more than the early non-monosynaptic group I excitation; and (ii) always suppressed more by intrathecal clonidine (see above). Possible mechanisms underlying the changes in non-monosynaptic group I excitation Tonic group II excitation Given that the monoaminergic gating is exerted selectively on the transmission of group II excita- tion (whether at a pre- or post-synaptic level, cf. p. 292), some ﬁndings require explanation, namely that: (i) disruption of the normal gating from the brainstem in spinal cord lesions also produces increased non-monosynaptic group I excitation; and (ii) monoaminergic agonists also depress the increased early group I facilitation observed after spinal cord injury or stroke. However, with the ankle plantar ﬂexedat 110–120 ◦ , there will be a tonic group I and II discharge frompretibial ﬂexors and, thereby, tonic depolarisation of lumbar propriospinal neu- rones. Giventhe convergence of groupI andgroupII afferents on these neurones: (i) the efﬁcacy of group I volleys in activating propriospinal neurones would be increased and, as a result, the non-monosynaptic group I excitation would be enhanced; and (ii) gat- ing of this group II tonic activity by monoaminer- gic agonists would decrease the excitability of lum- bar propriospinal neurones, thereby reducing their response to the conditioning group I volley. Monoaminergic depression of the tendon jerk by L-dopa This depressioncouldsimilarlyreﬂect gatingof tonic group II discharges contributing to the excitability of propriospinal neurones. Homonymous Ia exci- tation of quadriceps motoneurones is partly medi- atedthroughpropriospinal neurones(Fournier et al., 1986). Because the rising phase of the compound Ia EPSP produced in motoneurones by tendon per- cussion lasts 5–10 ms (Burke, Gandevia & McKeon, 1984), there is ample time for propriospinally medi- ated Ia excitation to contribute to the tendon jerk. Withthekneesemi-ﬂexed(to120–150 ◦ ), therewould be a tonic group II discharge from quadriceps (and possibly other muscles in the limb), and this could be gated by L-dopa. In any event, a signiﬁcant part of the tendon jerk exaggeration in spasticity could be due to hyperexcitability of propriospinal neu- rones, largely maintained by group II inputs. The possibility that propriospinal pathways contribute to the tendonjerk represents a further reasonfor cir- cumspection in comparing the tendon jerk and H reﬂex and, in particular, why such comparisons are ﬂawed measures of fusimotor drive (cf. Chapter 3, pp. 117–18). Is increased group II excitation sufﬁcient to cause spasticity? Thereisnodeﬁnitiveanswer tothisquestionbecause spasticity is characterised by an exaggeration of the homonymous stretch reﬂex, while the excitability of group II excitatory pathways has been assessed at rest only in heteronymous pathways (cf. pp. 320–1). However, indirect arguments suggest that the increased group II excitation is strong enough to cause spasticity. Exaggerated stretch reﬂexes are strongly depressed by clonidine and tizanidine This is so in spastic patients, whether the spasti- city is due to stroke or spinal cord injury (e.g. Nance, Shears & Nance, 1985; Steward, Barbeau & Gautier, Studies in patients 325 1991; Emre, 1993; Delwaide & Pennisi, 1994; Remy- N´ eris et al., 1999; Maupas et al., 2004). The reduc- tion of spasticity by these monoaminergic agonists is probably due to depression of group II exci- tation, since they gate transmission of group II excitation to motoneurones and have no effects on pre- or post-synaptic transmission of group I effects (cf. Jankowska & Hammar, 2002). How- ever, the excitability of the stretch reﬂex is the net result of several mechanisms, and it is conceiv- able that blockade of any excitatory mechanism would reduce it, even though the primary cause of the exaggeration (spasticity) was another mecha- nism(s) (cf. Chapter 12, p. 560). Nevertheless, the reduction of spasticity produced by monoamin- ergic agonists is so complete that a major con- tribution of increased group II excitation to the stretch reﬂex exaggeration of spastic patients is probable. Excessive positive fusimotor feedback In the cat, there is a potential positive feed-back through the g-loop, with excitation of g motoneu- rones, partly via monosynaptic action of group II afferents but mainly via projections of the pro- priospinal neurones co-activated by Ia and group II afferents (cf. p. 291). If this occurs in humans, excessive positive feedback might contribute to the exaggeration of stretch reﬂexes. With the relatively slow muscle stretch used to assess spasticity clini- cally, group II volleys would have ample time to acti- vatenot onlypropriospinal neurones but alsotopro- duce positive feed-back through hyperexcitable pro- priospinal neurones (see the sketch in Fig. 7.14(a)). ‘A pathological enhancement of reﬂex actions of not only group II but also of group Ia muscle affer- ents might then occur because stronger actions of g motoneurones on muscle spindles would be fol- lowed by stronger responses of both primaries and secondaries.’ (Gladden, Jankowska & Czarkowska- Bauch, 1998). This amplifying effect of group II actions through a positive feedback loop involving g s cannot be revealedby electrically inducedvolleys, because it requires the conduction time through the g loop to manifest itself in motoneurones. If this is a factor, the overall contribution of hyperexcitabil- ity of lumbar propriospinal neurones to spasticity wouldbeunderestimatedbyelectricallyinducedvol- leys. Validation of a positive feedback loop involving g s motoneurones might be possible with recordings from muscle spindle afferents in response to stretch inspasticpatients. Asyet, therearenopublisheddata for patients with spinal cord injury and the lower- limb data for stroke are from Ia afferents from the triceps surae of only two patients (see Chapter 3, pp. 139–40). Correlations with disability The increase in peroneal-induced excitation of quadriceps motoneurones is not correlated with spasticity assessed with the Ashworth score in patients with either cerebral or spinal lesions (Marque et al., 2001b; Remy-N´ eris et al., 2003). Sim- ilarly, after the administration of clonidine to para- plegics or tizanidine to hemiplegics, the decrease in spasticityispoorlycorrelatedwiththedecreaseinthe latefacilitationof thequadriceps Hreﬂex. Theremay be several reasons for this absence of correlation: (i) the electrically induced peroneal facilitation of the quadriceps H reﬂex does not assess group II excita- tion of g motoneurones; (ii) the peroneal facilitation of the quadriceps H reﬂex assesses a heteronymous pathway, whereas spasticity is assessed clinically for the homonymous pathway, and also depends on the exaggeration of the monosynaptic Ia stretch reﬂex; (iii) spasticity, measured as the resistance to passive stretch, involves changes in the mechanical proper- ties of muscle, and this may be an important fac- tor, in particular in stroke patients (cf. Chapter 12, pp. 572–3); (iv) the exaggeration of the stretch reﬂex in individual patients depends on several factors which do not necessarily co-vary (cf. Chapter 12, p. 571). Conclusions The contribution of increased group II excitation to the exaggeration of the stretch reﬂex in spastic 326 Group II pathways patients appears likely. The extent to which it con- tributes to the motor impairment and limitation of activity in patients is examined in Chapter 12. Spindle group II afferents are not responsible for the clasp-knife phenomenon The size of the stretch reﬂex of the quadriceps mus- cles of spastic human subjects is inversely propor- tional totheinitial lengthof themuscle, if thevelocity of stretch remains constant (Burke, Gillies & Lance, 1970; Burke & Lance, 1973). This length-dependent suppression of the stretch reﬂex was attributed to secondary spindle endings, and it was postu- lated that the underlying inhibition was responsible for the clasp-knife phenomenon. Subsequent stud- ies in the cat have shown that other slowly con- ducting muscle afferents (non-spindle group II and group III–IV afferents) are probably necessary for the initiation of clasp-knife phenomenon (Rymer, Houk & Crago, 1979). In addition, there is no evi- dence for group II inhibition of motoneurones of pureextensor muscles inhumans, either inhomony- mous or heteronymous pathways (cf. p. 307). It cannot be excluded that group II inhibitory path- ways to extensor motoneurones do exist but are not open in awake intact man. However, the results presented so far for patients with complete spinal cord lesions indicate an increase in group II excita- tionof quadriceps motoneurones (Remy-N´ eris et al., 2003). Parkinson’s disease Homonymous group II excitation The amplitude of medium-latency responses in the soleus and tibialis anterior during active upright stanceisnormal orslightlyincreasedinparkinsonian patients (Schieppati & Nardone, 1991). The main abnormality is the absence of an inﬂuence of ‘pos- tural set’ on medium-latency responses: the amplitude of medium-latency responses, particu- larly in the tibialis anterior, does not attenuate normally when standing patients hold onto a stable frame (Fig. 7.15(d ), (e)). This failure to modulate the medium-latency response when stability is assisted correlates signiﬁcantly with the severity of the dis- ease (as measured using the Webster scale). In nor- mal subjects, when the medium-latency responses are no longer required to ensure the control of upright stance, group II excitation is suppressed, possibly due to increased activity from the locus coeruleus (see p. 314). In parkinsonian patients, there could be failure of this increased monoamin- ergic gating of group II excitation from the locus coeruleus. Indeed, a role for the locus coeruleus in the control of posture has been proposed by Pom- peiano (2001), and there is a signiﬁcant cell loss in this structure, even in early-stage disease (German et al., 1992). Peroneal group II excitation of quadriceps The late group II but not the early group I facilita- tion of the quadriceps H reﬂex produced by stimu- lation of the deep peroneal nerve may be larger in parkinsonian patients than in normal subjects (Fig. 7.15( f ); Simonetta-Moreau et al., 2002). Inter- estingly, increased group II excitation is found only in rigid patients, where it is correlated with rigidity score assessed with the Uniﬁed Parkinson’s Disease Rating Score (Fahn & Elton, 1987). The ﬁnding that the group II excitation is selectively increased sug- gests a failure of the monoaminergic gating of group II excitation from the locus coeruleus (see above). Conclusions Role of group II pathways in natural motor tasks During a voluntary contraction, group II pathways contribute to the excitation of quadriceps motoneu- rones. However, group II excitatory pathways are mainly involved in postural and locomotor tasks: (i) homonymous stretch-induced responses of leg and foot muscles mediated through group II Conclusions 327 (a) (b) (c) (d) (e) (f ) Fig. 7.15. Changes in group II excitation in patients with Parkinson’s disease. (a) Sketch of the presumed pathways. Group Ia and group II afferents from tibialis anterior (TA) converge on propriospinal neurones (PN) projecting to quadriceps (Q) and TA motoneurones (MN). Transmission of group II excitation is gated by a monoaminergic tract fromthe locus coeruleus (Loc Coer). It is assumed that the locus coeruleus normally receives descending inhibition from higher centres. (b)–(e) Medium-latency responses in TA elicited by toe-down rotation of the platform during free stance ((b), (d )) and while holding a stable frame ((c), (e)) in a normal subject ((b), (c)) and in a parkinsonian patient ((d ), (e)). The ‘postural set’ is sketched above the traces. ( f ) Changes in the Q H reﬂex after deep peroneal nerve (DPN) stimulation (2 MT) at rest, plotted against the interstimulus interval (ISI) and expressed as a percentage of the control reﬂex value, in a normal subject (❍), a rigid parkinsonian patient (●) and a non-rigid patient (). DPN-induced group II excitation is increased in the rigid patient, not in the non-rigid patient. Each symbol is the mean of 20 measurements; vertical bars ±1 SEM. Modiﬁed from Schieppati & Nardone (1991) ((b)–(e)), and Simonetta-Moreau et al. (2002) (f ), with permission. pathways play a crucial role in the control of per- turbations to upright stance; (ii) postural situations requiring co-contraction of leg and thigh muscles (e.g. of tibialis anterior andquadriceps whenleaning backwards) are accompanied by facilitation of the transmission in the corresponding heteronymous group II pathways; (iii) during the stance phase of gait, the group II afferent discharge from ankle extensors contributes to the discharge of soleus motoneurones; (iv) peroneal group II facilitation of quadriceps motoneurones helps to stabilise the knee during the early stance phase of walking; 328 Group II pathways (v) stretch-inducedgroupII responses insoleus dur- ing the early stance phase may also play a role in the stabilisation of the ankle of the supporting leg. Changes in group II excitation and pathophysiology of movement disorders Spasticity In stroke patients, peroneal non-monosynaptic group I and group II excitations of quadriceps motoneurones are increased to a similar extent, pre- sumably due to disinhibition of propriospinal neu- rones. Inpatients withspinal cord lesions, peroneal- induced group II excitation is more increased than thenon-monosynapticgroupI excitation, indicating that pathways mediating group II actions are disin- hibited, probably due to damage to the descending monoaminergic pathways that gate groupII actions. Monoaminergic agonists or precursors decrease the peroneal-induced group II excitation of quadriceps motoneurones and reduce spasticity. The contribu- tionof increasedgroupII excitationtospasticitymay be accentuated by the projections of lumbar pro- priospinal neurones to g motoneurones. Parkinson’s disease The peroneal-induced group II excitation is selec- tively increased, and this increase is correlated with the degree of rigidity. This probably reﬂects a decrease in the monoaminergic gating of group II excitation from the locus coeruleus. A failure of this gating could also be responsible for the lack of attenuation of homonymous stretch-induced responses when standing and holding onto a stable frame. R´ esum´ e Background fromanimal experiments Group II muscle afferents originate from muscle spindle secondary endings, which are sensitive to changes in muscle length, but relatively insensitive to the dynamic component of stretch. They have a smaller diameter and, accordingly, a higher electri- cal threshold and a slower conduction velocity than Ia afferents. Group II effects are mainly transmit- ted through interneurones which excite or inhibit motoneurones. Interneurones transmitting group II afferent effects to motoneurones are located in the intermediate zone, and are termed ‘group II interneurones’. They are particularly concentrated in midlumbar segments, and are also referred to as ‘lumbar propriospinal neurones’ in the following. In anaesthetised low spinal cats, projections from group II interneurones to ␣ motoneurones produce mainly ﬂexor excitation and extensor inhibition. However, alternative pathways canbe demonstrated in unanaesthetized animals. Group II interneu- rones also have strong excitatory projections to g motoneurones. Besides their input from group II afferents, group II interneurones are also excited by group I afferents and descending tracts. There is a mutual post-synaptic inhibition between different subgroups of group II interneurones. Presynaptic inhibition with PAD of group II terminals is evoked mainly from group II afferents and from the retic- ular formation. However, the main systems gating groupII actions are descending monoaminergic sys- tems (in particular noradrenergic) originating from the locus coeruleus in the brainstem. Accordingly, the ␣ 2 adrenergic receptor agonists, tizanidine and clonidine, are effective in producing selective block- ade of transmission of group II excitation. Methodology Underlying principles GroupII afferents may be activated by stretching the receptor-bearingmuscleor byelectrical stimulation. Criteria for a group II response are: longer latency thanIaexcitationduetoaslower conductionvelocity for the afferent pathway, electrical threshold about twice that of the Ia excitation, and suppression by monoaminergic agonists. R´ esum´ e 329 Stretch-induced homonymous group II excitation In standing subjects, rotation of a supporting plat- form produces stretch responses in leg and foot muscles. In soleus and ﬂexor digitorum brevis, toe- up rotation produces a short-latency response at latencies corresponding tothose of monosynaptic Ia stretchreﬂexes, andamedium-latencyresponse∼35 and 40 ms later, respectively. In the tibialis anterior, toe-down rotation of the platform elicits only the medium-latency response. Electrically induced group II excitation Group II excitation produced by electrical stimula- tionat 2–3MTof lower-limbnervescanbeassessed in heteronymous motoneurones using the H reﬂex, the PSTH of single units, or the on-going EMG. H reﬂex Stimulation of the deep peroneal nerve produces biphasicfacilitationof thequadriceps Hreﬂex. There is an early low-threshold peak (∼3 ms central delay; 0.6MTthreshold), duetoactivationof lumbar pro- priospinal neurones by groupI afferents, followedby a late high-thresholdexcitation(∼5–6 ms later; 1.3 MT threshold). The high-threshold late excitation is also observed in the quadriceps Hreﬂex after stimu- lation of the tibial nerve, and in the semitendinosus Hreﬂexafter stimulationof thegastrocnemius medi- alis nerve. PSTHs The same conditioning stimuli evoke a similar high- thresholdlateexcitationinthePSTHs of singlemotor units in quadriceps and semitendinosus. On-going EMG The high-thresholdlate excitationof quadriceps and peroneus brevis motoneurones to stimulation of the peroneal and tibial nerve, respectively, produces facilitation of the on-going EMG. Evidence for muscle group II excitation Cooling of the ‘conditioning’ nerve Cooling produces an increase in latency that is greater for the late responses thanfor the early group I-mediated responses. This holds true for stretch- inducedresponses inthesoleus andﬂexor digitorum brevis, and electrically induced late heteronymous excitation of quadriceps. Accordingly, the longer latency of the late peak is due to the activation of peripheral afferents of slower conduction velocity than Ia afferents, and not to a longer pathway in the central nervous system fed by Ia afferents. Pharmacological validation Short-latency group I responses are not affected, but late responses are suppressed by tizanidine. Here again, this holds true for both stretch-induced responses in the soleus and ﬂexor digitorum bre- vis, and responses elicited in the peroneus brevis by electrical stimulation of the tibial nerve. This pro- vides further support for a group II origin of the late responses elicited by stretch and by electrical stimulation. Cutaneous and joint afferents A signiﬁcant contribution of cutaneous and joint afferents to the high-threshold late responses has been excluded. Conclusions Thereareseveral independent lines of evidenceindi- cating that late responses evoked by stretch or by high-intensity electrical stimulation involve a spinal pathway fed by group II muscle afferents. 330 Group II pathways Critique of the tests used to reveal group II actions Contamination by group I effects Group II actions are necessarily contaminated by group I effects, which have a lower threshold and, because of the faster conduction velocity of group I afferents, are the ﬁrst to reach the spinal cord. This complicates interpretations: overlap between group I effects and group II excitation makes pre- cise assessment of the onset of group II excitation difﬁcult; thepost-spikeAHPandrecurrent inhibition following the ﬁring of the tested motoneurone(s) by the group I discharge reduce their availability to the subsequent group II volley; because of the conver- gence of group I and group II afferents on the same interneurones (see below), activation of these neu- rones by group I volleys can be the source of differ- ent interactions betweenthe two volleys: facilitation (if the group I effect is subliminal), occlusion (if the group I volley discharges the interneurones). Stretch-induced responses during upright stance These responses are only present during free stance and cannot be used to investigate transmission in group II pathways at rest or its changes during voluntary movement. Common peroneal-induced facilitation of the quadriceps H reﬂex This is suitablefor investigatinggroupII excitationin patients. However, during quadriceps contractions ≥10% of MVC, there may be reﬂex suppression due to convergence between the peroneal and femoral test volleys onto interneurones mediating auto- genetic ‘Ib inhibition’. Organisation and pattern of connections Peripheral pathway The conduction velocities of Ia and group II affer- ents have been estimated at ∼51 and 21.4 m s −1 for afferents mediating stretch-induced responses, and∼68 and45 ms −1 for afferents mediating electri- callyinducedheteronymous responses, respectively. The higher values found after electrical stimulation may be because electrical stimulation preferentially activates the fastest afferents, while this is not neces- sarily sowithmuscle stretch. Inleg muscles, the con- duction velocity of group II afferents is about 65%of that of Ia afferents, and the electrical threshold ∼2.1 times that of Ia afferents. These ratios are similar to those found for group II/Ia afferents in the cat. Central pathway: lumbar propriospinal neurones The more caudal the motoneurone pool inthe spinal cord, the longer the central delay. This suggests a pathway with neurones located rostral to motoneu- rones. There is indirect evidence that, inhumansub- jects, group II and non-monosynaptic group I exci- tations are mediated through common lumbar pro- priospinal neurones. Connections Excitatory projections to motoneurones Homonymous projections have only been explored indistal muscles, andare stronger intibialis anterior andﬂexor digitorumbrevis thaninsoleus. Heterony- mous projections are widespread from distal mus- cles onto motoneurones of proximal muscles. They are particularly potent from gastrocnemius medi- alis to semitendinosus and from pretibial ﬂexors to quadriceps. Projections between leg muscles are only disclosed by cortical stimulation. Bilateral pro- jections to homologous muscles are observed after unilateral stretch. Inhibition of excitatory effects Inhibition of excitatory effects evoked by group I and group II afferent volleys can be produced by the same group I and group II volleys, but are generally detectable only in presence of cortical stimulation. There is evidence that the inhibition is exerted onto R´ esum´ e 331 propriospinal neurones throughfeedbackinhibitory interneurones (and this constitutes a disfacilitation of motoneurones). Lack of evidence for inhibition of motoneurones The lack of evidence for group II inhibition exerted on motoneurone of human extensor muscles is the most striking difference from feline data. Effects of corticospinal volleys Corticospinal inputs facilitate lumbar propriospinal neurones co-activated by group I and group II affer- ents and inhibitory interneurones mediating feed- back inhibition to these neurones. Overall, the dom- inant effect of corticospinal volleys on the pro- priospinal system is excitation of feedback inhibi- tion, particularly in the pathway of propriospinal excitation to semitendinosus motoneurones. Motor tasks and physiological implications Voluntary contraction There is a facilitation of the interneurones medi- ating group I and group II excitation to quadri- ceps motoneurones during voluntary contractions of quadriceps, but not (or hardly so) of those mediat- ing group II excitation to semitendinosus motoneu- rones during contraction of semitendinosus. Postural tasks Homonymous stretch-induced medium-latency responses play a crucial role in the control of perturbations to upright stance, as indicated by the ﬁnding that they are considerably reduced whennot required for equilibrium, e.g. when subjects have an external support. During postural co-contractions of tibialis anterior and quadriceps when leaning backwards, heteronymous group II excitation from tibialis anterior to quadriceps is facilitated with respect to voluntary co-contraction of the same muscles. Similarly heteronymous groupII excitation from gastrocnemius medialis to semitendinosus is facilitated during the postural co-contraction of these two muscles when leaning forwards. Group II discharges from stretched leg muscles could help reinforce the co-contraction of leg and thigh muscles to maintain bipedal stance. Gait Homonymous group II afferents contribute to the activationof soleus motoneurones duringthe stance phase of walking. The evidence is based upon the ﬁnding that unexpected unloading of the ankle extensors suppresses the EMG of soleus, at the latency of a group II effect, and this suppression is modiﬁedlittlebyischaemicblockadeof groupI affer- ents. This ﬁnding implies that the group II afferent discharge from ankle extensors is used as an integ- ral part of the motor command in the activation of the muscles. Peroneal-induced group II facilitation of the on-going quadriceps EMG is enhanced dur- ing the early stance phase of walking. At this time the weight of the body is shifted to the leg that is about to begin the stance phase, and the feedback support from group II afferents from ankle dorsi- ﬂexor muscles may help ensure the stabilising con- traction of the quadriceps. Finally, stretch-induced group II responses in the soleus appear particularly in the early stance phase of walking, when they may play a role inthe stabilisationof the supporting limb. In postural tasks and gait, group II excitation may be potentiated by group I activity converging on the relevant lumbar propriospinal neurones. Studies in patients and clinical implications Peripheral neuropathies In patients with Charcot–Marie–Tooth type 1A dis- ease, despite the loss of large-diameter nerve ﬁbres, there are no balance problems, as long as the 332 Group II pathways medium-latency responses are present and not excessively delayed. In contrast, there is an increase in sway area in other types of neuropathy affecting ﬁbres of all diameters (e.g. diabetic neuropathy). Spasticity In stroke patients, peroneal-induced facilitation of the quadriceps H reﬂex is increased on the affected side and not modiﬁed on the unaffected side. The greater peroneal-induced facilitation involves both theearlynon-monosynapticgroupI andlategroupII peaksof excitation, andacommonunderlyingmech- anism is therefore probable. The ﬁndings can be explained satisfactorily by hyperexcitability of lum- bar propriospinal neurones, due to the loss of cor- ticospinal facilitation of inhibitory interneurones mediating feedback inhibition (i.e. a disinhibition). In patients with spinal cord injury, both peaks of peroneal excitation of the quadriceps H reﬂex are generally enhanced with respect to normal sub- jects, again suggesting disinhibition of lumbar pro- priospinal neurones. However, in most patients, the late group II excitation is increased more than the early group I excitation. Disruption by the spinal cord lesion of the monoaminergic gating of group II actionscouldaccount for thisﬁnding. Noradrenergic agonists (tizanidineinhemiplegicpatients, intrathe- cal clonidineinparaplegicpatients) reducethepero- neal group II facilitation of the quadriceps H reﬂex. They also reduce, though to a lesser extent, the early group I excitation. A possible explanation of this lat- ter ﬁnding is that a tonic stretch-induced group II discharge from the pretibial ﬂexors produces tonic depolarisation of propriospinal neurones, and this is suppressed by noradrenergic agonists. Assuming that part of the tendonjerk is mediated throughpro- priospinal neurones, the depression of the quadri- ceps tendon jerk by L-dopa could reﬂect gating of tonic group II discharges contributing to the excitability of propriospinal neurones. Given that monoaminergic agonists selectively suppress trans- mission of group II excitation, the marked depres- sion of spasticity by these drugs is consistent with a role for group II excitation in the exaggeration of the stretch reﬂex in spastic patients. The increase in peroneal excitation of quadriceps motoneurones is not correlated with the degree of spasticity, and this implies that facilitation of the transmission in lumbar propriospinal pathways to ␣ moto- neurones acts in concert with other mechanisms, such as the parallel actions of group II afferents on g motoneurones. Parkinson’s disease Peroneal group II facilitation of the quadriceps H reﬂex is increased, though only in rigid patients. This suggests decreased gating of transmission from group II afferents. The main abnormality in stretch- induced homonymous responses is the lack of attenuation of these responses, particularly in tib- ialis anterior, when standing and holding onto a sta- ble frame. These abnormalities couldresult fromcell loss in the locus coeruleus. REFERENCES Abbruzzese, G., Rubino, V. & Schieppati, M. (1996). Task- dependent effects evoked by foot muscle afferents on leg muscle activity in humans. Electroencephalography and Clinical Neurophysiology, 101, 339–48. Bajwa, S., Edgley, S. A. & Harrison, P. J. (1992). Crossed actions on group II-activated interneurones in the midlumbar seg- ments of thecat spinal cord. Journal of Physiology (London), 455, 205–17. Berger, W., Dietz, V. & Quintern, J. (1984). Corrective reactions to stumbling in man: neuronal coordination of bilateral leg muscle activity during gait. Journal of Physiology (London), 405, 1–37. Bras, H., Jankowska, E., Noga, B. R. & Skoog, B. (1990). Com- parison of effects of various types of NA and 5-HT agonists on transmission from group II muscle afferents in the cat. European Journal of Neurosciences, 2, 1029–39. Burke, D. & Lance, J. W. (1973). Studies of the reﬂex effects of primary and secondary spindle endings in spasticity. In New Developments in Electromyography and Clinical Neurophysiology, vol. 3, ed. J. E. Desmedt, pp. 475–95. Basel: Karger. Burke, D., Gillies, J. D. & Lance, J. W. (1970). The quadriceps stretch reﬂex in human spasticity. Journal of Neurology, Neurosurgery and Psychiatry, 33, 216–23. References 333 Burke, D., Gandevia, S. C. & McKeon, B. (1984). Monosynaptic and oligosynaptic contributions to human ankle jerk and H-reﬂex. Journal of Neurophysiology, 52, 435–48. Bussel, B. & Pierrot-Deseilligny, E. (1977). Inhibition of human motoneurones, probably of Renshaw origin, elicited by an orthodromic motor discharge. Journal of Physiology (London), 269, 319–39. Cavallari, P. & Pettersson, L. G. (1991). Synaptic effects in lum- bar ␣-motoneurones evokedfromgroupII muscleafferents via two different interneuronal pathways in the cat. Neuro- science Letters, 129, 225–8. Chaix, Y., Marque, P., Meunier, S., Pierrot-Deseilligny, E. & Simonetta-Moreau, M. (1997). Further evidence for non- monosynaptic group I excitation of motoneurones in the human lower limb. Experimental Brain Research, 115, 35–46. Christensen, L. O. D., Andersen, J. B., Sinkjær, T. & Nielsen, J. (2001). Transcranial magnetic stimulation and stretch reﬂexes in the tibialis anterior muscle during human walk- ing. Journal of Physiology (London), 531, 545–57. Corna, S., Grasso, M., Nardone, A. &Schieppati, M. (1995). Selec- tive depression of medium-latency leg and foot muscle responses to stretchby an␣2-agonist inhumans. Journal of Physiology (London), 484, 803–9. Corna, S., Galante, M., Grasso, M., Nardone, A. & Schieppati, M. (1996). Unilateral displacement of lower limbs evoked bilateral EMGresponses inleg andfoot muscles instanding humans. Experimental Brain Research, 109, 83–91. Davies, H. E. & Edgley, S. A. (1994). Inputs to group II-activated midlumbar interneurones from descending motor path- ways in the cat. Journal of Physiology (London), 479, 463–73. Davies, J., Johnstone, S. E., Hill, D. R. & Quillan, J. E. (1984). Tizanidine (Ds 103–282), a centrally acting mus- cle relaxant, selectively depresses excitation of feline dor- sal horn neurons to noxious peripheral stimuli by an action at ␣2-adrenoreceptors. Neuroscience Letters, 48, 197–202. Delwaide, P. J. &Pennisi, G. (1994). Tizanidine and electrophys- iologic analysis of spinal control mechanisms in humans with spasticity. Neurology, 44, Suppl. 9, S21–7; discussion S27–8. Diener, H. C., Dichgans, J., Guschlbauer, B. &Mau, H. (1984). The signiﬁcance of proprioception on postural stabilization as assessed by ischaemia. Brain Research, 296, 103–9. Dietz, V., Quintern, J. B. & Sillem, M. (1987). Stumbling reac- tions in man: Signiﬁcance of proprioceptive and pre- programmed mechanisms. Journal of Physiology (London), 368, 149–63. Dyck, P. J., Chance, P., Lebo, R. & Carney, J. A. (1993). Heredi- tary motor and sensory neuropathies. In Peripheral Neu- ropathies, ed. P. J. Dyck, P. K. Thomas, J. W. Grifﬁn, P. A. Low & J. F. Poduslo, pp. 1094–136. Philadelphia: W. B. Saunders. Eccles, R. M. & Lundberg, A. (1959). Synaptic actions in motoneurones by afferents which may evoke the ﬂexion reﬂex. Archives Italiennes de Biologie, 97, 199–221. Edgley, S. A. & Jankowska, E. (1987). An interneuronal relay for group I and II muscle afferents in the midlumbar segments of the cat spinal cord. Journal of Physiology (London), 399, 675–90. Emre, M. (1993). New developments in the medical treatment of spasticity. In Spasticity: Mechanisms and Management, ed. A. F. Thilmann, D. J. Burke & W. Z. Rymer, pp. 372–84. Heidelberg: Springer Verlag. Eriksson, J., Olausson, B. & Jankowska, E. (1996). Antispastic effects of L-Dopa. Experimental Brain Research, 111, 296– 304. Fahn, S., Elton, R. L. & Members of the UPDRS Development Committee. (1987). UniﬁedParkinson’s diseaseratingscale. In Recent Developments in Parkinson’s Disease, ed. S. Fahn, C. D. Marsden, M. Goldstein&D. B. Calne, vol. 3, pp. 153–63. New Jersey: Macmillan. Forget, R., Pantieri, R., Pierrot-Deseilligny, E., Shindo, M. & Tanaka, R. (1989). Facilitationof quadriceps motoneurones by group I afferents from pretibial ﬂexors in man. 1. Pos- sible interneuronal pathway. Experimental Brain Research, 78, 10–20. Fournier, E., Meunier, S., Pierrot-Deseilligny, E. & Shindo, M. (1986). Evidence for interneuronally mediated Ia excita- tory effects to human quadriceps motoneurones. Journal of Physiology (London), 377, 143–69. Franz, D. N. & Iggo, A. (1968). Conduction failure in myelinated and non-myelinated axons at low temperatures. Journal of Physiology (London), 199, 319–45. Fukushima, Y. &Kato, M. (1975). Spinal interneuronsresponding to group II muscle afferent ﬁbres in the cat. Brain Research, 90, 307–12. German, D. C., Manaye, K. F., White, C. L. et al. (1992). Disease- speciﬁc patterns of locus coeruleus cell loss. Annals of Neurology, 32, 667–76. Gladden, M. H., Jankowska, E. & Czarkowska-Bauch, J. (1998). New observations on coupling between group II muscle afferents and feline g-motoneurones. Journal of Physiology (London), 512, 507–20. Grey, M. J., Ladouceur, M., Andersen, J. B., Nielsen, J. B. & Sinkjær, T. (2001). Group II muscle afferents probably con- tribute to the medium latency soleus stretch reﬂex during 334 Group II pathways walking in humans. Journal of Physiology (London), 534, 925–33. Hammar, I., Slawinska, U. &Jankowska, E. (2002). Acomparison of postactivation depression of synaptic actions evoked by different afferents and at different locations in the feline spinal cord. Experimental Brain Research, 145, 126–9. Harrison, P. J. & Zytnicki, D. (1984). Crossed actions of group I muscle afferents in the cat. Journal of Physiology (London), 356, 263–73. Holmqvist, B. & Lundberg, A. (1961). Differential supraspinal control of synaptic actions evoked by volleys in the ﬂexion reﬂex afferents in alpha motoneurones. Acta Physiologica Scandinavica, 54, suppl. 186, 1–51. Hongo, T. &Pettersson, L. G. (1988). Comments ongroupII exci- tation in hindlimb motoneurones in high and low spinal cats. Neuroscience Research, 5, 563–6. Hunt, C. C. & Kufﬂer, S. W. (1951). Stretch receptor discharges during muscle contraction. Journal of Physiology (London), 113, 298–315. Jankowska, E. (1992). Interneuronal relay in spinal pathways fromproprioceptors. Progress inNeurobiology 38, 335–378. Jankowska, E. (1993). Monoaminergic inhibitory control of spinal interneurones. In Spasticity: Mechanisms and Man- agement, ed. A. F. Thilmann, D. J. Burke & W. Z. Rymer, pp. 222–32. Heidelberg: Springer Verlag. Jankowska, E. & Hammar, I. (2002). Spinal interneurones; how can studies in animals contribute to the understanding of spinal interneuronal systems in man? Brain Research Reviews, 40, 19–28. Jankowska, E. & Riddell, J. S. (1998). Neuronal systems involved in modulating synaptic transmission from group II muscle afferents. In Presynaptic Inhibition and Neural Control, ed. P. Rudomin, R. Romo & L. Mendell, pp. 315–28. New York: Oxford University Press. Jankowska, E., Perﬁlieva, E. V. &Riddell, J. S. (1996). Howeffective is integrationof informationfrommuscleafferents inspinal pathways? Neuroreport, 7, 2337–40. Jankowska, E., Gladden, M. H. & Czarkowska-Bauch, J. (1998). Modulationof felinegamma-motoneurones by nor- adrenaline, tizanidine and clonidine. Journal of Physiology (London), 512, 521–31. Jankowska, E., Hammar, I., Chojnicka, B. &Heden, C. H. (2000). Effects of monoamines oninterneurons infour spinal reﬂex pathways from group I and/or group II muscle afferents. European Journal of Neurosciences, 12, 701–14. Jankowska, E., Slawinska, U. & Hammar, I. (2002). On organ- ization of a neuronal network in pathways from group II muscle afferents in feline lumbar spinal segments. Journal of Physiology (London), 542, 301–14. Kirkwood, P. A. &Sears, T. A. (1975). Monosynaptic excitation of motoneurones from muscle spindle secondary endings of intercostal and triceps surae muscles in the cat. Journal of Physiology (London), 24, 64P–6P. Lamy, J. C., Wargon, I., Baret, M. et al. (2005). Post-activation depression in various spinal pathways in humans. Experimental Brain Research, in press. Laporte, Y. &Bessou, P. (1959). Modiﬁcationsintheexcitabilityof homonymous motoneurons induced by the physiological activation of afferent ﬁbers originating in group II muscles. Journal de Physiologie (Paris), 51, 897–908. Laporte, Y. & Lloyd, D. P. C. (1952). Nature and signiﬁcance of the reﬂex connections established by large afferent ﬁbers of muscular origin. American Journal of Physiology, 169, 609–21. Lloyd, D. P. C. (1943). Neuron patterns controlling transmission of ipsilateral hindlimbreﬂexes incat. Journal of Neurophys- iology, 6, 293–315. (1946). Integrativepatternof excitationandinhibitionintwo- neuron reﬂex arcs. Journal of Neurophysiology, 9, 439–44. Lourenc¸o, G., Simonetta-Moreau, M., Pierrot-Deseilligny, E. & Marchand-Pauvert, V. (2005). Cortical control of spinal reﬂex pathways in the human lower limb. Electroen- cephalography and Clinical Neurophysiology, in prepara- tion. Lundberg, A., Malmgren, K. & Schomburg, E. D. (1977). Cutaneous facilitation of transmission in reﬂex pathways from Ib afferents to motoneurones. Journal of Physiology (London), 265, 763–80. (1987a). Reﬂex pathways from group II muscle afferents. 1. Distribution and linkage of reﬂex actions to alpha- motoneurones. Experimental Brain Research, 65, 271–81. (1987b). Reﬂex pathways from group II muscle afferents. 2. Functional characteristics of reﬂex pathways to ␣- motoneurones. Experimental Brain Research, 65, 282–93. (1987c). Reﬂex pathways from group II muscle afferents. 3. Secondary spindle afferents andthe FRA: a newhypothesis. Experimental Brain Research, 65, 294–306. Marchand-Pauvert, V. & Nielsen, J. B. (2002a). Modulation of non-monosynaptic excitation from ankle dorsiﬂexor affer- ents to quadriceps motoneurones during humangait. Jour- nal of Physiology (London), 538, 647–57. (2002b). Modulation of spinal reﬂexes during walking in healthysubjectsandpatientswithspinal cordinjuries. Clin- ical Neurophysiology, 113, S72. Marchand-Pauvert, V., Simonetta-Moreau, M. & Pierrot- Deseilligny, E. (1999). Cortical control of spinal pathways mediating group II excitation to thigh motoneurones. Jour- nal of Physiology (London), 517, 301–13. References 335 Marchand-Pauvert, V., Nicolas, G., Burke, D. & Pierrot- Deseilligny, E. (2002). Suppression of the H reﬂex by disynapticautogeneticinhibitorypathwaysactivatedbythe test volley. Journal of Physiology (London), 542, 963–76. Marchand-Pauvert, V., Marque, P., Nicolas, G. & Pierrot- Deseilligny, E. (2005). Posture-related increase in group II excitation from ankle muscles to human thigh motoneu- rones. Journal of Physiology (London), in press. Marque, P., Pierrot-Deseilligny, E. & Simonetta-Moreau, M. (1996). Evidence for excitation of the human lower limb motoneurones by group II muscle afferents. Experimental Brain Research, 109, 357–60. Marque, P., Nicolas, G., Marchand-Pauvert, V., Gautier, J., Simonetta-Moreau, M. & Pierrot-Deseilligny, E. (2001a). GroupI projectionsfromintrinsicfoot musclestomotoneu- rones of leg and thigh muscles in humans. Journal of Physiology (London), 536, 313–27. Marque, P., Simonetta-Moreau, M., Maupas, E. & Roques, C. F. (2001b). Facilitation of transmission in heteronymous groupII pathways inspastic hemiplegic patients. Journal of Neurology, Neurosurgery and Psychiatry, 70, 36–42. Marque, P., Nicolas, G., Simonetta-Moreau, M., Pierrot- Deseilligny, E. & Marchand-Pauvert, V. (2005). Probable Group II excitations from plantar foot muscles to human leg and thigh motoneurones. Experimental Brain Research, 161, 486–50. Matthews, P. B. C. (1972). MammalianMuscle Spindles andTheir Central Action, 630 pp. London: Arnold. (1989). Long-latency stretch reﬂexes of two intrinsic muscles of the human hand analysed by cooling the arm. Journal of Physiology (London), 419, 519–38. Maupas, E., Marque, P., Roques, C. F. & Simonetta-Moreau, M. (2004). Modulation of the transmission in group II heteronymous pathways by tizanidine in spastic hemi- plegic patients. Journal of Neurology, Neurosurgery and Psychiatry, 75, 130–5. Meunier, S., Pierrot-Deseilligny, E. & Simonetta, M. (1993). Pat- tern of monosynaptic heteronymous Ia connections in the human lower limb. Experimental Brain Research, 96, 533– 44. Meunier, S., Pierrot-Deseilligny, E. & Simonetta-Moreau, M. (1994). Patternof heteronymous recurrent inhibitioninthe human lower limb. Experimental Brain Research, 102, 149– 59. Nance, P. W., Shears, A. S. & Nance, D. M. (1985). Clonidine in spinal cord injury. Canadian Medical Association Journal, G133, 41–2. Nardone, A. & Schieppati, M. (1998). Medium-latency response to muscle stretch in human lower limb: estimation of conduction velocity of group II ﬁbres and central delay. Neuroscience Letters, 249, 29–32. (2004). Group II ﬁbres and afferent control of stance. Clues for diabetic neuropathy. Clinical Neurophysiology, 115, 779– 89. Nardone, A., Corr` a, T. &Schieppati, M. (1990a). Different activa- tions of the soleus and gastrocnemius muscles in response to various types of stance perturbation in man. Experimen- tal Brain Research, 80, 323–32. Nardone, A., Giordano, A., Corr` a, T. & Schieppati, M. (1990b). Responses of leg muscles inhumans displacedwhile stand- ing. Effects of types of perturbation and of postural set. Brain, 113, 65–84. Nardone, A., Grasso, M., Giordano, A. & Schieppati, M. (1996). Different effect of height on latency of leg and foot short- and medium-latency EMG responses to perturbation of stance in humans. Neuroscience Letters, 206, 89–92. Nardone, A., Tarantola, J., Miscio, G., Pisano, F., Schenone, A. & Schieppati, M. (2000). Loss of large-diameter spindle affer- ent ﬁbres is not detrimental to the control of body sway during upright stance: evidence from neuropathy. Experi- mental Brain Research, 135, 155–62. Nardone, A., Corna, S. &Schieppati, M. (2001a). GroupII afferent ﬁbres in balance control: evidence from neurological dis- ease. In MCC 2001 From Basic Motor Control to Functional Recovery II, ed. N. Gantchev, pp. 331–8. Soﬁa: Academic Publishing House. Nardone, A., Galante, M., Lucas, B. & Schieppati, M. (2001b). Stance control is not affected by paresis and reﬂex hyperexcitability: the case of spastic patients. Journal of Neurology, Neurosurgery and Psychiatry, 70, 635– 43. Nielsen, J. B. &Sinkjær, T. (2002). Afferent feedbackinthecontrol of human gait. Journal of Electromyography and Kinesiol- ogy, 12, 213–17. Noth, J., Schwarz, M., Podoll, K. &Motamedi, F. (1991). Evidence that low-threshold muscle afferents evoke long-latency reﬂexes in human hand muscles. Journal of Neurophysi- ology, 65, 1089–97. Paintal, A. S. (1965). Block of conductioninmammalianmyelin- atednerve ﬁbres by lowtemperatures. Journal of Physiology (London), 180, 1–19. Pierrot-Deseilligny, E. (1999). Heteronymous group II path- ways inthe humanlower limb: spinal organization, cortical control and possible functional role. Journal of Physiology (London), 518S, 27P. Pompeiano, O. (2001). Role of the locus coeruleus in the static and dynamic control of posture. Archives Italiennes de Biologie, 139, 109–24. 336 Group II pathways Remy-N´ eris, O., Barbeau, H., Daniel, O., Boiteau, F. & Bussel, B. (1999). Effects of intrathecal clonidine on spinal reﬂexes and human locomotion in incomplete paraplegic subjects. Experimental Brain Research, 129, 433–40. Remy-N´ eris, O., Denys, P., Daniel, O., Barbeau, H. & Bus- sel, B. (2003). Effect of intrathecal clonidine on excita- tion transmitted by interneurones activated by groups I-II afferents in paraplegics. Experimental Brain Research, 148, 509–14. Riddell, J. S. & Hadian, M. (2000). Interneurones in path- ways from group II muscle afferents in the lower-lumbar segments of the feline spinal cord. Journal of Physiology (London), 522, 109–23. Rymer, W. Z., Houk, J. C. &Crago, P. E. (1979). Mechanisms of the clasp-knifereﬂexstudiedinananimal model. Experimental Brain Research, 37, 93–113. Schieppati, M. &Nardone, A. (1991). Free and supported stance inParkinson’s disease. Theeffect of postureandpostural set on leg muscle responses to perturbation, and its relation to the severity of the disease. Brain, 4, 749–55. (1995). Time course of ‘set’-related changes in muscle responsetostanceperturbationinhumans. Journal of Phys- iology (London), 487, 787–96. (1997). Medium-latency stretch reﬂexes of foot and leg mus- cles analysedbycoolingthelower limbinstandinghumans. Journal of Physiology (London), 503, 691–8. (1999). Group II spindle afferent ﬁbers in humans: their pos- sible role in the reﬂex control of stance. In Progress in Brain Research, vol. 123, ed. M. D. Binder, pp. 461–72. Amsterdam: Elsevier Science. Schieppati, M., Nardone, A., Siliotto, R. &Grasso, M. (1995). Early and late stretch responses of human foot muscles induced by perturbation of stance. Experimental Brain Research, 105, 411–22. Schieppati, M., Nardone, A., Corna, S. & Bove, M. (2001). The complex role of spindle afferent input, as evidenced by the study of posture control in normal subjects and patients. Neurological Sciences, 22, Suppl. 1, S15–20. Schomburg, E. D. (1990). Spinal sensorimotor systems andtheir supraspinal control. Neuroscience Research, 7, 265–340. Simonetta-Moreau, M., Marque, P., Marchand-Pauvert, V. & Pierrot-Deseilligny, E. (1999). The pattern of excitation of human lower limb motoneurones by probable group II muscle afferents. Journal of Physiology (London), 517, 287– 300. Simonetta-Moreau, M., Meunier, S., Vidailhet, M., Pol, S., Gal- itzky, M. & Rascol, O. (2002). Transmission of group II het- eronymous pathways is enhanced in rigid lower limb of de novopatients withParkinson’s disease. Brain, 125, 2125–33. Sinkjær, T., Andersen, J. B., Ladouceur, M., Christensen, L. O. D. & Nielsen, J. B. (2000). Major role for sensory feedback in soleus EMG activity in the stance phase of walking in man. Journal of Physiology (London), 523, 817–27. Stauffer, E. K., Watt, D. G., Taylor, A., Reinking, R. M. & Stu- art, D. G. (1976). Analysis of muscle receptor connections by spike-triggered averaging. 2. Spindle group II afferents. Journal of Neurophysiology, 39, 1393–402. Steward, E. K., Barbeau, H. & Gautier, S. (1991). Modulation of locomotor patterns and spasticity with clonidine in spinal cordinjuredpatients. CanadianJournal of the Neurological Sciences, 18, 321–32. Wilson, V. J. & Kato, M. (1965). Excitation of extensor motoneu- rons by group II afferent ﬁbers in ipsilateral muscle nerves. Journal of Neurophysiology, 28, 545–54. 8 Presynaptic inhibition of Ia terminals The synaptic efﬁcacy of the afferent volleys enter- ing the spinal cord can be modulated by presynap- tic inhibition. As a result, the information ﬂowing through sensory terminals can be modiﬁed before it reaches the target neurones through a process that can be controlled selectively by supraspinal centres to optimise motor performance and sen- sory discrimination. All afferents are subject to pre- synaptic inhibition controlled by descending tracts (cf. Rudomin & Schmidt 1999) but, so far, meth- ods have been developed for human subjects to estimate only presynaptic inhibition of Ia termi- nals. This is because it is easy to stimulate Ia affer- ents selectively, and they are the only afferents to have signiﬁcant monosynaptic projections onto motoneurones. Background fromanimal experiments Initial ﬁndings In the cat, Frank and Fuortes (1957) described a depression of monosynaptic Ia EPSPs in motoneu- rones occurring without a detectable change in motoneurone membrane potential or conductance. This presynaptic inhibition was extensively inves- tigated by Eccles and colleagues. They described its main features and showed that the inhibition is associated with primary afferent depolarisation (PAD), both phenomena most probably mediated by the same interneurones acting on Ia terminals through axo-axonic synapses (see Eccles, 1964). Theseinterneurones arereferredtoas PADinterneu- rones in the following, even though there is so far no record of PAD in human subjects. General features Location Although PAD interneurones have not yet been speciﬁcallylabelled, therearestrongindications that last-order PAD interneurones mediating presynap- tic inhibition of Ia terminals are located within the intermediate zone. Mechanisms The mechanisms underlying presynaptic inhibition involve, at least inpart, local modulationof transmit- ter release at the Ia-motoneurone synapse by means of GABA A receptors. Activation of GABA A recep- tors in Ia terminals increases the efﬂux of Cl − ions and produces depolarisation of the afferent ter- minals. As a result, the amplitude of the propagated action potential in the intraspinal afferent terminals is reduced, andthat blocks or reduces Ca 2+ inﬂuxand therebytransmitter release(seeRudomin&Schmidt, 1999). 337 338 Presynaptic inhibition of Ia terminals Ia Ia Ia Ia MN MN Flexor Flexor Extensor Extensor Ib Ib Fibres giving Fibres receiving (a) (b) Ib Cutaneous RS VS MN Last-order PAD IN First-order PAD IN CS Tonic Ia Inhibitory IN (1) (2) (3) Fig. 8.1. Wiring diagram of pathways of presynaptic inhibition with primary afferent depolarisation (PAD) of Ia terminals in the cat. (a) In this and subsequent ﬁgures, excitatory synapses are represented by Y-shape bars and inhibitory synapses by small ﬁlled circles, ﬁrst-order excitatory PAD interneurones (IN) by open circles, last-order GABA-ergic PAD INs by ﬁlled grey circles and inhibitory INs by large ﬁlled circles. First-order PAD INs receive excitation from Ia and Ib afferents and the vestibulospinal (VS ) tract. They receive inhibition through the same inhibitory INs from cutaneous afferents and the corticospinal (CS) tract (though there is an alternative corticospinal pathway facilitating ﬁrst-order PAD INs, indicated by the thin continuous line). Inhibitory INs inhibiting ﬁrst-order PAD INs receive descending tonic inhibition (dotted line ). Last-order PAD INs receive inhibition from reticulospinal (RS) pathways, themselves inhibited from higher centres (). From data in Rudomin & Schmidt (1999). Three mechanisms (referred to as , ,  in the sketch of Fig. 8.1 (a)) could contribute to the tonic level of presynaptic inhibition observed at rest in human subjects: (i) tonic inhibition from higher centres of the brainstem structures through which RS pathways maintain tonic inhibition on last-order PAD INs (i.e. control of RS suppression: pathway ); (ii) tonic inhibitory control of the inhibitory INs transmitting cutaneous inhibition of ﬁrst-order PAD INs (i.e. control of afferent suppression: pathway ); (iii) tonic VS excitation of ﬁrst-order PAD INs (i.e. descending excitation: pathway ). (b) Relative strength of presynaptic inhibition (indicated approximately by width of arrows) elicited by Ia (dashed lines) and Ib (dotted lines) afferents from ﬂexors and extensors on Ia terminals projecting to ﬂexor and extensor motoneurones (MN). Organisation The shortest pathway mediating segmental pre- synaptic inhibition of Ia terminals has two inter- posed interneurones, the last order (in grey in Fig. 8.1(a)) being GABA-ergic. Single last-order interneu- rones have connections with a restricted num- ber of collaterals of individual Ia afferents, and single collaterals receive connections from more than one interneurone. This may be considered the basic circuitry required for independent control of information ﬂowin selected collaterals of individual afferents (cf. Rudomin & Schmidt, 1999). Electrophysiology An electrophysiological feature which differentiates presynaptic inhibition of Ia terminals from post- synaptic inhibition is its very long duration (several hundred of milliseconds). This was attributed to sustained activity of PAD interneurones (by Eccles, Background fromanimal experiments 339 Kostyuk & Schmidt, 1962b), but subsequent stud- ies have indicated that, instead, this may be due to the slow dynamics of GABA release and/or uptake (see Rudomin, Jimenez &Quevedo, 1998). Presynap- tic inhibition from peripheral inputs is also charac- terised by a long central latency (∼5 ms, see Eccles, 1964). Inputs to PADinterneurones Peripheral effects Group I afferents Volleys in Ib and (to a lesser extent) Ia afferents, mainly from ﬂexor muscles, activate ﬁrst-order PAD interneurones, and produce presynaptic inhibition distributed to Ia terminals of all ipsilateral muscles in the hindlimb of the spinal cat (Eccles, Magni & Willis, 1962a; Fig. 8.1(b)). PAD interneurones can be activated by short trains of volleys in the nerves of the ipsilateral ﬂexors (see Eccles, 1964), by group I discharges elicited by muscle stretch or contraction (Devanandan, Eccles & Yokota, 1965; Devanandan, Eccles & Stenhouse, 1966), or by pure Ia discharges, from ﬂexors and extensors, induced by vibration (Gillies et al., 1969; Barnes & Pompeiano, 1970a, b). Cutaneous and articular afferents These afferents depress transmission in PAD path- ways at the level of the ﬁrst-order PADinterneurones (seeLund, Lundberg&Vyklick´ y, 1965; Rudominet al., 1983). Descending effects Descending suppression The main descending control on PAD interneu- rones mediating presynaptic inhibition of Ia ter- minals is depressive (see Fig. 8.1(a)), i.e. it decreases PAD and switches off presynaptic inhibition. Cor- ticospinal ﬁbres and cutaneous afferents converge onto inhibitory interneurones which depress the ﬁrst-order PAD interneurones (see Lundberg & Vycklick´ y, 1963; Rudomin et al., 1983; Fig. 8.1(a)). Last-order PAD interneurones are tonically inhib- ited from different reticulospinal pathways (see Rudomin & Schmidt, 1999). Suppression of this strong tonic depressive control is responsible for the dramatically increased excitability of PAD interneu- rones after spinalisation in decerebrate animals. Brainstem structures responsible for the tonic depression of presynaptic inhibition of Ia terminals receive a descending inhibition fromhigher centres. Accordingly, presynaptic inhibition is suppressed in the decerebrate animal. Descending facilitatory projections exist (i) A cortical facilitatory effect on PAD interneu- rones probably also exists, but is generally weaker thanthe cortical depression(as discussed by Hongo, Jankowska & Lundberg, 1972); and (ii) ﬁrst-order PAD interneurones receive excitation from vestibu- lar nuclei (Carpenter, Endberg & Lundberg, 1966). In addition, the inhibition exerted by cutaneous (andarticular) afferents onﬁrst-order PADinterneu- rones is subjected to a tonic descending inhibition, whichdisappears after spinalisation(seeRudomin& Schmidt, 1999). This tonic suppressive effect on the cutaneous inhibition of PAD interneurones con- tributes to the maintenance of a tonic level of presynaptic inhibition. Selectivity of the control of presynaptic inhibition As will be shown on p. 348, selectivity of con- trol was ﬁrst established in human experiments during selective voluntary contractions (Hultborn et al., 1987b). Animal experimentssubsequentlycon- ﬁrmed that presynaptic inhibition exerted on col- laterals of the same Ia afferent may be differentially depressedby cortical andcutaneous inputs (Eguibar et al., 1994). The diffuse pattern of presynaptic inhi- bition of Ia terminals observed in the acute spinal cat (Eccles, Magni & Willis, 1962a) is probably due to the convergence onto last order PAD interneu- rones of subsets of ﬁrst-order PAD interneurones 340 Presynaptic inhibition of Ia terminals which differ in their input (at least from the brain, Lundberg, 1998). Conclusions Presynaptic inhibition of Ia afferents functions as a gate on the monosynaptic Ia input to motoneu- rones. It can be distinguished from post-synaptic inhibition by its long central latency and long dura- tion. The gating can be very potent: a short train to ﬂexor group I afferents can completely suppress themonosynaptic reﬂex inextensor muscles (Eccles, Schmidt &Willis, 1962c). Despiteits potency, therole of this gating has long been neglected in discussions onthecontrol of theIainﬂowduringmovement. This is probably because it was difﬁcult to make func- tional sense of the diffuse pattern of distribution of presynaptic inhibition on Ia terminals of all mus- cles in the ipsilateral limb, as originally described for the acute spinal cat. Presynaptic inhibition of Ia terminals functions also as a gate on the Ia input to interneurones (cf. Enriquez-Denton et al., 2000; Chapter 5, pp. 200–1). Methodology Different methods have been developed to assess changes in presynaptic inhibition of Ia terminals in human subjects. They rely on different principles and have different advantages and disadvantages. Discrepancy between the variations in the on-going EMGand those in the Hreﬂex Underlying principle Changes in presynaptic inhibition of Ia terminals in human subjects were ﬁrst inferred from discrepan- cies between changes in the H reﬂex amplitude and in the on-going EMG recorded in the same muscle during various motor activities: voluntary contrac- tion and ﬂexor reﬂex in the tibialis anterior (Pierrot- Deseilligny & Bussel, 1973); walking and standing in the soleus (Morin et al., 1982; Capaday & Stein, 1987). It was reasonedthat, if Hreﬂex amplitudeonly depended on ␣ motoneurone excitability, the vari- ations in reﬂex amplitude and in the on-going EMG should parallel one another. In contrast, changes in presynaptic inhibition of Ia terminals should affect the H reﬂex via the Ia afferents in the test volley more than the on-going EMG which could be affected only by inﬂuencing background Ia activ- ity and any fusimotor-driven enhancement during voluntary contractions. Critique As appealing as this method is because of its sim- plicity (recordings of the H reﬂex and the on-going EMG), theresultscannot beattributedunequivocally todifferences inthe level of presynaptic inhibitionof Ia terminals. (i) Descending and/or peripheral inputs relatedto the different motor tasks tested may have an uneven distribution to early and late recruited motoneu- rones and thereby change the recruitment gain of the reﬂex (cf. Chapter 1, pp. 18–20). As a result, an equivalent level of EMG discharge does not guar- antee equivalent excitability of the ␣ motoneurones that are not involved in the contraction and thus an equal amplitude of the reﬂex response to a constant Ia volley. (ii) Presynaptic inhibitionof Ia terminals is not the only mechanism able to gate the afferent volley of the test reﬂex. For example, disynaptic Ib inhibitory pathways help determine the size of the H reﬂex, and a difference in the control of these pathways could contribute to changes in the size of the test H reﬂex (cf. Marchand-Pauvert et al., 2002; Chapter 1, pp. 14–16 and 27). Activating PADINs by a conditioning volley to assess their excitability Underlying principle Presynaptic inhibition of Ia terminals mediating the afferent volley of the test H reﬂex is experimentally Methodology 341 induced using vibration or electrical stimulation to produce a conditioning afferent volley. The resulting reﬂex depression depends on the excitability of PAD interneurones: the larger this excitability, the greater the presynaptic inhibition of the test afferent volley andthegreater thereﬂexdepression. Different meth- ods relying on this principle have been proposed. Prolonged vibration of the homonymous tendon is not a valid technique Vibration paradox Studies of presynaptic inhibition in human sub- jects started with the phenomenon that has become known as the ‘vibration paradox’ (see Desmedt & Godaux, 1978). Application of vibration to a muscle or its tendonresults inastrongdischargeinhomony- mous Ia ﬁbres (Burke et al., 1976) and depresses the tendon jerk and H reﬂex of that muscle (De Gail, Lance & Neilson, 1966; Delwaide, 1973). Since the vibration-induced depression is seen along with a motor discharge (the tonic vibration reﬂex, TVR; see De Gail, Lance & Neilson, 1966; Hagbarth & Eklund, 1966), there was presumably anincrease inexcitabil- ity at motoneurone level, and the reﬂex depres- sion therefore must have resulted from a presynap- tic mechanism. In experiments in the cat, vibration produced PAD that paralleled the reﬂex depression (Gillies et al., 1969; Barnes & Pompeiano, 1970a, b). The presynaptic mechanism operating in human experiments was therefore, not unreasonably at the time, attributed to presynaptic inhibition of Ia terminals with PAD (Delwaide, 1973). Post-activation depression However, conditioning vibration applied to the homonymous tendon activates another presynap- tic mechanism, homosynaptic or post-activation depression, due to repetitive activation of the Ia- motoneurone synapse, and this also contributes to the vibratory-induced depression of the reﬂex (Katz et al., 1977; Crone & Nielsen, 1989b; Hultborn et al., 1996; Wood, Gregory & Proske, 1996). This post-activation depression is probably related to reducedprobabilityof transmitter release(Lev-Tov& Pinco, 1992), and is quite potent (see Chapter 2, pp. 96–9). It differs from presynaptic inhibition with PADinseveral aspects: (i) itsverylongduration(upto 10–15 s vs. 400 ms at most for presynaptic inhibition with PAD); (ii) its limitation to afferents previously activated by the vibration; (iii) its insensitivity to GABA A -antagonists (see Nielsen & Hultborn, 1993). It is arguable which mechanism, post-activation depressionor presynaptic inhibitionwithPAD, is the more potent under physiological conditions. Either way, when both conditioning and test volleys are mediated through the same synaptic pathway, the vibration-induced depression is caused, at least in part, by post-activation depression and the extent of the depression cannot be used to estimate pre- synaptic inhibition of Ia terminals with PAD (Hultborn et al., 1987a, 1996). Activity-dependent hyperpolarisation of Ia afferents There is a further problemwith prolonged vibration: conducting an impulse train raises the threshold of the activated axon, even when the trains are nat- urally induced (see Coppin, Jack &McLennan, 1970; Fetz et al., 1979; Vagg et al., 1998). Accordingly, long- lasting vibration of the ‘conditioning’ tendon can be used as a method to raise preferentially the electri- cal threshold of Ia afferents (Cavallari & Katz, 1989; Chapter 2, p. 76). As a result, the same stimulus will evoke a smaller Ia afferent volley during and after vibration than it did before vibration, and it may be possible tostimulate Ibafferents electrically without activating many Ia afferents. Presynaptic inhibition elicited by a heteronymous group I volley Short vibration of a heteronymous tendon To eliminate the drawbacks related to prolonged vibration of the homonymous tendon, another method has been developed: brief vibration (train 342 Presynaptic inhibition of Ia terminals I a TA C o n d i t i o n e d • • buying cialis in vietnam drugs, divided daily doses are recommended. nance therapy, For mainteonce daily dos ing is usually pre gle bedtime dos ferred. A sine is effective for most clients. Thi increases com pliance with pre s scribed drug ther schedule better nighttime apy, allows sleep, and dec reases hypoten sion and day- what causes cialis not to work VARIABLES THAT AFFECT DRUG ACTIONS cialis green pack cialis swollen feet SECTION 1 INTRODUCTION TO DRUG THERAPY pengalaman memakai cialis Pharmacokinetic Consequences Sepsis may affect all pharmacokinetic processes. Early sepsis is characterized by hyperdynamic circulation, with increased cardiac output and shunting of blood to vital organs. As a result, absorption, distribution, metabolism, and excretion may be accelerated. Late sepsis is characterized by hypodynamic circulation, with diminished cardiac output and reduced blood ﬂow to major organs. Thus, absorption, distribution, metabolism, and excretion may be impaired. Shock may inhibit all pharmacokinetic processes. Absorption is impaired by decreased blood ﬂow to sites of drug administration. Distribution is impaired by decreased blood ﬂow to all body tissues. Metabolism is impaired by decreased blood ﬂow to the liver. Excretion is impaired by decreased blood ﬂow to the kidneys. apcalis oral jelly generic cialis SECTION 1 INTRODUCTION TO DRUG THERAPY uso de cialis y alcohol How Can You Avoid This Medication Error? cialis maximum effectiveness Methods IV injection or IV push is the direct injection of a medication into the vein. The drug may be injected through an injection site on IV tubing or an intermittent infusion device. Most IV push medications should be injected slowly. The time depends on the particular drug, but is often 2 minutes or longer for a dose. Rapid injection should generally be avoided because the drug produces high blood levels and is quickly circulated to the heart and brain, where it may cause adverse or toxic effects. Although IV push may be useful with a few drugs or in emergency situations, slower infusion of more dilute drugs is usually preferred. Intermittent infusion is administration of intermittent doses, often diluted in 50 to 100 mL of ﬂuid and infused over 30– 60 minutes. The drug dose is usually prepared in a pharmacy and connected to an IV administration set that controls the amount and ﬂow rate. Intermittent infusions are often connected to an injection port on a primary IV line, through which IV ﬂuids are infusing continuously. The purpose of the primary IV line may be to provide ﬂuids to the client or to keep the vein open for periodic administration of medications. The IV ﬂuids are usually stopped for the medication infusion, then restarted. Drug doses may also be infused through an intermittent infusion device (eg, a heparin lock) to conserve veins and allow freedom of motion between drug doses. The devices decrease the amount of IV ﬂuids given to patients who do not need them (ie, who are able to ingest adequate amounts of oral ﬂuids) and those who are at risk of ﬂuid overload, especially children and older adults. An intermittent infusion device may be part of an initial IV line or used to adapt a continuous IV for intermittent use. The devices include a heparin lock or a resealable adapter added to a peripheral or central IV catheter. These devices must be ﬂushed routinely to maintain patency. If the IV catheter has more than one lumen, all must be ﬂushed, whether being used or not. Saline is probably the most commonly used ﬂushing solution; heparin may also be used if recommended by the device’s manufacturer or required by institutional policy. For example, heparin (3 to 5 mL of 100 units/mL, after each use or monthly if not in use) is recommended for implanted catheters. Continuous infusion indicates medications mixed in a large volume of IV ﬂuid and infused continuously, over several hours. For example, vitamins and minerals (eg, potassium chloride) are usually added to liters of IV ﬂuids. Greater dilution of the drug and administration over a longer time decreases risks of accumulation and toxicity, as well as venous irritation and thrombophlebitis. Equipment Equipment varies considerably from one health care agency to another. Nurses must become familiar with the equipment available in their work setting, including IV catheters, types of IV tubing, needles and needleless systems, types of volume control devices, and electronic infusion devices (IV pumps). Catheters vary in size (both gauge and length), design and composition (eg, polyvinyl chloride, polyurethane, silicone). The most common design type is over the needle; the needle is used to start the IV, then it is removed. When choosing a catheter to start an IV, one that is much smaller than the efek samping obat kuat cialis 48 CLIENT TEACHING GUIDELINES trazodone cialis interaction Ginger cialis uso recreativo e. Check drug references when indicated. cialis generika wikipedia cialis flu like symptoms 1. Where are neurotransmitters synthesized and stored? 2. What events occur at the synapse between two neurons? indian version of cialis who are allergic to sulfonamides and ketorolac is contraindicated in clients at risk of excessive bleeding. Thus, ketorolac should not be administered during labor and delivery; before or during any major surgery; with suspected or confirmed cerebrovascular bleeding; or to clients who are currently taking aspirin or other NSAIDs. Over-the-counter (OTC) products containing these drugs are contraindicated for chronic alcohol abusers because of possible liver damage (with acetaminophen) or stomach bleeding (with aspirin, ibuprofen, ketoprofen, or naproxen). The Food and Drug Administration (FDA) requires an alcohol warning on the labels of all OTC pain relievers and fever reducers. This warning states that people who drink three or more alcoholic drinks daily should ask their doctors before taking the products. SECTION 2 DRUGS AFFECTING THE CENTRAL NERVOUS SYSTEM does insurance cover cialis daily Serotonin agonists (Triptans) Almotriptan (Axert) PO 6.25 mg, repeat after 2 h if necessary. Maximum, 12.5 mg/24h Naratriptan (Amerge) PO 1–2.5 mg as a single dose; repeat in 4 h if necessary. Maximum, 5 mg/d Rizatriptan (Maxalt) PO 5–10 mg as a single dose; repeat after 2 h if necessary. Maximum dose, 30 mg/d Sumatriptan (Imitrex) PO 25–100 mg as a single dose. Maximum dose, 300 mg/d SC 6 mg as a single dose. Maximum, 12 mg/d Nasal spray 5, 10 or 20 mg by unit-dose spray device. Maximum, 40 mg/d Zolmitriptan (Zomig) PO 1.25–2.5 mg as a single dose; may repeat after 2 h if necessary. Maximum dose, 10 mg/d Ergot Preparations Ergotamine tartrate (Ergomar) can you buy cialis over the counter in the philippines ✔ cialis restless leg syndrome phenytoin or fosphenytoin, is given to prevent recurrence. AEDs also are used prophylactically in clients with brain trauma from injury or surgery. In addition to treatment of seizure disorders, AEDs are used to treat bipolar disorder (eg, carbamazepine and valproate) although they are not FDA-approved for this purpose. They are also used in the management of chronic neuropathic pain, although few studies validate their effectiveness for this purpose. Carbamazepine is approved for treatment of the pain associated with trigeminal neuralgia. Gabapentin is also being used, but it is not approved for this indication and is not considered better than carbamazepine. Some of the newer AEDs are being tested for effectiveness in relation to bipolar, neuropathic pain, and other disorders. Because the drugs are being used for other indications than seizure disorders, some people suggest they be called neuromodulators or neurostabilizers rather than AEDs or anticonvulsants. cialis 100mg manufacturers SECTION 2 DRUGS AFFECTING THE CENTRAL NERVOUS SYSTEM cialis bph luts cialis cura riabilitativa • Risk for Injury: CNS depression with premedications and how long does cialis keep you hard signs and respiratory and cardiovascular function every 5 to 15 minutes until reactive and stabilizing. Effects of anesthetics and adjunctive medications persist into postanesthesia recovery. • Continue to assess vital signs, ﬂuid balance, and laboratory and other data. • Assess for signs of complications (eg, ﬂuid and electrolyte imbalance, respiratory problems, thrombophlebitis, wound infection). Nursing Notes: Apply Your Knowledge cialis daily safety la pela vs cialis Liver Heart Smooth muscle Increased heart rate Increased force of contraction Increased automaticity Increased AV conduction Glycogenolysis Gluconeogenesis Fatty tissue Relaxation Lipolysis 303 teenagers taking cialis can u take cialis everyday (continued ) With high doses, vasopressin constricts blood vessels, especially coronary arteries, and stimulates smooth muscle of the gastrointestinal tract. Special caution is necessary in clients with heart disease, asthma, or epilepsy. Severe adverse reactions are most likely to occur when oxytocin is given to induce labor and delivery. These are more common effects, especially in those receiving octreotide for acromegaly. cialis effectiveness long term use Choice of corticosteroid drug is inﬂuenced by many factors, including the purpose for use, characteristics of speciﬁc drugs, desired route of administration, characteristics of individual clients, and expected adverse effects. Some guidelines for rational drug choice include the following: 1. Adrenocortical insufficiency, whether caused by Addison’s disease, adrenalectomy, or inadequate corticotropin, requires replacement of both glucocorticoids and mineralocorticoids. Hydrocortisone and cortisone are usually the drugs of choice because they have greater mineralocorticoid activity compared with other corticosteroids. If additional mineralocorticoid activity is required, ﬂudrocortisone can be given. 2. Nonendocrine disorders, in which anti-inﬂammatory, antiallergic, antistress, and immunosuppressive effects are desired, can be treated by a corticosteroid drug with primarily glucocorticoid activity. Prednisone is often the glucocorticoid of choice. 3. Respiratory disorders. Beclomethasone (Vanceril, Vancenase), budesonide (Pulmicort, Rhinocort), flunisolide (Aerobid, Nasalide), fluticasone (Flonase, Flovent), mometasone (Nasonex), and triamcinolone (Azmacort, Nasacort) are corticosteroids formulated to be given by oral or nasal inhalation. Their use replaces, prevents, delays, or decreases use of systemic drugs and thereby decreases risks of serious adverse effects. However, high doses or frequent use may suppress adrenocortical function. 4. Cerebral edema associated with brain tumors, craniotomy, or head injury. Dexamethasone (parenterally or orally) is considered the corticosteroid of choice because it is thought to penetrate the blood–brain barrier more readily and achieve higher concentrations in cerebrospinal ﬂuids and tissues. It also has minimal sodium- and water-retaining properties. With brain tumors, the drug is more effective in metastatic lesions and glioblastomas than astrocytomas and meningiomas. 5. Acute, life-threatening situations require a drug that can be given parenterally, usually intravenously (IV). This limits the choice of drugs because not all are available in injectable preparations. Hydrocortisone, dexamethasone, and methylprednisolone are among those that may be given parenterally. top gear bolivia viagra Jane Wright has been receiving high-dose corticosteroid therapy (hydrocortisone 80 mg bid) for the last month. You receive an order to taper the steroid dose as follows: decrease hydrocortisone dose 20 mg each day for 3 days, then decrease by 10 mg per day and give only qd. You are caring for Jane on the third day after this order was written. You administer 40 mg for her morning dose. is 50mg of viagra too much viagra jellies online treatment of hypothyroidism. It is a potent form that contains a uniform amount of hormone and can be given parenterally. Compared with liothyronine, levothyroxine has a slower onset and longer duration of action. Levothyroxine absorption with oral administration varies from 48% to 79% of the dose administered. Taking the medication on an empty stomach increases absorption; malabsorption syndromes cause excessive fecal loss. Most (99%) of the circulating levothyroxine is bound to serum proteins, mi novio usa viagra Levothyroxine BOX 27–3 bad effects of viagra urdu because the drugs may stimulate tumor growth. An exception is the use of estrogens for treatment of metastatic breast cancer in women at least 5 years postmenopause. Undiagnosed vaginal or uterine bleeding Fibroid tumors of the uterus Active liver disease or impaired liver function History of cerebrovascular disease, coronary artery disease, thrombophlebitis, hypertension, or conditions predisposing to these disease processes Women older than 35 years of age who smoke cigarettes. These women have a greater risk of thromboembolic disorders if they take hormonal contraceptives, possibly because of increased platelet aggregation with estrogen ingestion and cigarette smoking. In addition, estrogen increases hepatic production of blood clotting factors. Family history of breast or reproductive system cancer viagra wiki deutsch female libido booster viagra Hormone Replacement Therapy 1. A component of many enzymes that are essential for normal metabolism (eg, carbonic anhydrase, lactic dehydrogenase, alkaline phosphatase). 2. Necessary for normal cell growth, synthesis of nucleic acids (RNA and DNA), and synthesis of carbohydrates and proteins 3. May be essential for use of vitamin A can you make viagra at home PO 200–400 mg q12h commande viagra sans ordonnance Use of Penicillins in Speciﬁc Situations can a diabetic patient take viagra Bush, L. M. & Johnson, C. C. (2000). Antibacterial therapy: Ureidopenicillins and beta-lactam/beta-lactamase inhibitor combinations. Infectious Disease Clinics of North America, 14(2), 409–433. Dancer, S. J. (2001). The problem with cephalosporins. Journal of Antimicrobial Chemotherapy, 48, 463–478. Drug facts and comparisons. (Updated monthly). St. Louis: Facts and Comparisons. Limauro, D. L., Chan-Tompkins, N. H., Carter, R. W., Brodmerkel, G. J., Jr., & Agrawal, R. M. (1999). Amoxicillin/clavulanate associated hepatic failure with progression to Stevens-Johnson syndrome. Annals of Pharmacotherapy, 33, 560–564. Petri, W. A., Jr. (2001). Antimicrobial agents: Penicillins, cephalosporins, and other beta-lactam antibiotics. In J. G. Hardman, & L. E. Limbird (Eds.), Goodman & Gilman’s The pharmacological basis of therapeutics, 10th ed., pp. 1189–1218. New York: McGraw-Hill. is viagra bad for your liver viagra soft flavoured canada Oral Tetracyclines frequency of taking viagra The macrolides are widely used for treatment of respiratory tract and skin/soft tissue infections caused by streptococci and staphylococci. Erythromycin is also used as a penicillin substitute in clients who are allergic to penicillin; for prevention of rheumatic fever, gonorrhea, syphilis, pertussis, and chlamy- • minimum age to use viagra is generic viagra safe yahoo Adverse effects include GI upset, skin rashes, hepatitis, and a harmless red-orange discoloration of urine, tears, sweat, and other body ﬂuids. Soft contact lenses may be permanently stained. Rifampin has many interactions with other drugs. It induces hepatic microsomal enzymes and accelerates the metabolism of numerous other drugs, thereby decreasing their serum concentrations, half-lives, and therapeutic effects. Affected drugs include acetaminophen, anti-AIDS drugs (protease inhibitors and nonnucleoside reverse transcriptase inhibitors; see Chap. 39), benzodiazepines, corticosteroids, cyclosporine, estrogens, ﬂuconazole, ketoconazole, mexiletine, methadone, metoprolol, phenytoin, propranolol, quinidine, oral contraceptives, oral sulfonylureas, theophylline, verapamil, and warfarin. With warfarin, decreased anticoagulant effect occurs approximately 5 to 8 days after rifampin is started and lasts for 5 to 7 days after rifampin is stopped. With methadone, concurrent administration with rifampin may precipitate signs and symptoms of opiate withdrawal unless methadone dosage is increased. Rifabutin (Mycobutin) is another rifamycin that is active against mycobacteria. Its mechanism of action is the same as that of rifampin, so that most rifampin-resistant strains are also resistant to rifabutin. Its two main uses are in patients with HIV infection, to treat Mycobacterium avium complex (MAC) disease, and to substitute for rifampin in patients who need both antitubercular and certain antiviral drugs. The major advantages of rifabutin over rifampin are a longer serum half-life (45 hours, on average) and reduced hepatic induction of microsomal metabolism. Rifabutin has no advantage over rifampin in treatment of tuberculosis but may be given concurrently with INH to clients who need prophylaxis against both M. tuberculosis and M. avium. Rifabutin is well absorbed from the GI tract; a dose of 300 mg produces peak serum concentration in 23 hours. It is extensively metabolized in the liver (and to a lesser extent in the intestinal wall); it is excreted in urine and bile. Like rifampin, rifabutin and its metabolites may cause a harmless red-orange discoloration of urine, feces, saliva, sputum, perspiration, and tears. Soft contact lenses may be permanently stained. Adverse effects include GI upset (nausea, vomiting, diarrhea), hepatitis, muscular aches, neutropenia, skin rash, and uveitis (an eye disorder characterized by inﬂammation, pain, and impaired vision). Hepatotoxicity is rare. Adverse effects increase when rifabutin is administered Nursing Notes: Apply Your Knowledge viagra sensitivity loss 8. In a client with tuberculosis newly started on drug therapy, how could you explain the emergence of drugresistant organisms and the importance of preventing this problem? 9. What are advantages and disadvantages of short-course (6 to 9 months) treatment programs? 10. What adverse effects are associated with INH, rifampin, pyrazinamide, and ethambutol, and how may they be prevented or minimized? cozaar viagra interaction men have viagra what do women have Zidovudine and Lamivudine (Combivir) Zidovudine, Lamivudine, and Abacavir (Trizivir) • How research methods will necessarily exclude some hopeful viagra tu thien nhien vialafil vs viagra 1. Administer accurately a. Give oral drugs as recommended in relation to meals: (1) Give abacavir, amprenavir, delavirdine, efavirenz, famciclovir, lamivudine, nevirapine, stavudine, tenofovir and valacyclovir with or without food. However, do not give abacavir, amprenavir, or efavirenz with a high-fat meal. Also, if the patient is taking an antacid or didanosine, give amprenavir at least 1 h before or after a dose of antacid or didanosine. (2) Give didanosine and indinavir on an empty stomach, 1 h before or 2 h after a meal. Although indinavir is best absorbed if taken on an empty stomach, with water, it may also be taken with skim milk, juice, coffee, tea or a light meal (eg, toast, cereal). If the patient is taking indinavir and didanosine, the drugs should be given at least 1 h apart on an empty stomach. (3) Give ganciclovir, nelfinavir, Kaletra, and ritonavir with food. The oral solution of ritonavir may be mixed with chocolate milk to improve the taste. (4) Give saquinavir within 2 h after a meal. b. Delavirdine tablets may be mixed in water by adding four tablets to at least 3 oz of water, waiting a few minutes, and then stirring. Have the client drink the mixture promptly, rinse the glass, and swallow the rinse to be sure the entire dose is taken. c. To give nelﬁnavir to infants and young children, the oral powder can be mixed with a small amount of water, milk, or formula. Once mixed, the entire amount must be taken to obtain the full dose. d. Give intravenous (IV) acyclovir, cidofovir, foscarnet, and ganciclovir over 1 h. e. With cidofovir therapy, give probenecid 2 g 3 h before cidofovir, 1 g 2 h before cidofovir, and 1 g 8 h after completion of the cidofovir infusion f. When applying topical acyclovir, wear a glove to apply. g. With administering ribavirin, follow the manufacturer’s instructions. 2. Observe for therapeutic effects a. With acyclovir for genital herpes, observe for fewer recurrences when given for prophylaxis; observe for healing of lesions and decreased pain and itching when given for treatment. b. With amantadine, observe for absence of symptoms when given for prophylaxis of inﬂuenza A and decreased fever, cough, muscle aches, and malaise when given for treatment. c. With cidofovir, ganciclovir or foscarnet for cytomegalovirus retinitis, observe for improved vision. d. With ophthalmic drugs, observe for decreased signs of eye infection. Acidic foods or juices (eg, orange juice, apple juice, apple sauce) should not be used because they produce a bitter taste. Manufacturers’ recommendations to promote absorption and bioavailability im 20 can i take viagra 609 natural viagra ice cream Although the main concern with amphotericin B is nephrotoxicity, it is recommended that liver function tests be monitored during use. Caspofungin dosage must be reduced with moderate hepatic impairment; the drug has not been studied in clients with severe hepatic impairment. The azole antifungals may cause hepatotoxicity; hepatitis occasionally occurs with all of the drugs. Hepatic aminotransferases (ALT, AST) and serum bilirubin should be checked before drug use, after several weeks of drug use, and every 1 to 2 months during long-term therapy. Asymptomatic, reversible elevations in ALT and AST may occur. However, if AST and ALT increase to more than 3 times the normal range, the azole should be discontinued. Hepatotoxicity may be reversible if drug therapy is stopped. With ﬂuconazole, hepatic dysfunction may range from mild elevations in ALT and AST to clinical hepatitis, cholestasis, hepatic failure, and death. Fatal hepatic damage has occurred primarily in clients with serious underlying conditions, such as AIDS or malignancy, and with multiple concomitant medications. Itraconazole is relatively contraindicated in clients with increased liver enzymes, active liver disease, or a history of liver damage with other drugs. It should be given only if expected beneﬁts outweigh risks of liver injury. Plasma levels of itraconazole should be monitored and dosage adjusted if indicated. Ketoconazole may cause serious hepatic impairment, including toxic hepatitis. Griseofulvin may cause hepatotoxicity, especially if given in large doses for prolonged periods. Terbinafine has been associated with a few cases of liver failure, and its clearance is reduced by 50% in clients with hepatic cirrhosis. Its use is not recommended for patients with chronic or active liver disease and liver function tests should be done in all patients before starting therapy. Hepatotoxicity has been reported in patients with and without preexisting liver disease. costo viagra in slovenia AFTER STUDYING THIS CHAPTER, THE STUDENT WILL BE ABLE TO: IL-12 viagra falls psych zshare however, cytokines rarely, if ever, act alone. Instead, a target cell is exposed to an environment containing a mixture of cytokines, which may have synergistic or antagonistic effects on each other. Third, cytokines often induce the synthesis of other cytokines. The resulting actions and interactions among cytokines may profoundly alter physiologic responses. Fourth, proteins that act as cytokine antagonists are found in the bloodstream and other extracellular ﬂuids. These proteins may bind directly to a cytokine and inhibit its activity or bind to a cytokine receptor but fail to activate the cell. The main groups of cytokines (also called biologic response modifiers) are categorized as colony-stimulating factors (CSFs), interferons, and interleukins. can viagra be mixed with alcohol is viagra physically addictive CHAPTER 42 PHYSIOLOGY OF THE HEMATOPOIETIC AND IMMUNE SYSTEMS molecules or markers are encoded by a group of genes called the major histocompatibility complex (MHC). MHC markers are essential to immune system function because they regulate the antigens to which a person responds and allow immune cells (eg, lymphocytes and macrophages) to recognize and communicate with each other. Nonself or foreign antigens are also recognized by distinctive molecules, called epitopes, on their surfaces. Epitopes vary widely in type, number, and ability to elicit an immune response. A normally functioning immune system does not attack body tissues labeled as self but attacks nonself substances. In most instances, a normally functioning immune system is highly desirable. With organ or tissue transplants, however, the system responds appropriately but undesirably when it attacks the nonself grafts. An abnormally functioning immune system causes numerous diseases. When the system is hypoactive, immunodeﬁciency disorders develop in which the person is highly susceptible to infectious and neoplastic diseases. When the system is hyperactive, it perceives ordinarily harmless environmental substances (eg, foods, plant pollens) as harmful and induces allergic reactions. When the system is inappropriately activated (it loses its ability to distinguish between self and nonself, so an immune response is aroused against the host’s own body tissues), the result is autoimmune disorders, such as systemic lupus erythematosus and rheumatoid arthritis. Many other disorders, including diabetes mellitus, myasthenia gravis, and inflammatory bowel diseases, are thought to involve autoimmune mechanisms. To aid understanding of the immune response and drugs used to alter immune response, more speciﬁc characteristics, processes, and functions of the immune system are described. dosis de viagra segun edad how much does viagra lower blood pressure Immune cells (Fig. 42–1) are WBCs found throughout the body in lymphoid tissues (bone marrow, spleen, thymus, tonsils and adenoids, Peyer’s patches in the small intestine, lymph nodes, and blood and lymphatic vessels that transport the cells). When exposure to an antigen occurs and an immune response is aroused, WBCs move toward the antigen in a process called chemotaxis. Once WBCs reach the area, they phagocytize the antigen. Speciﬁc WBCs are granulocytes (neutrophils, eosinophils, basophils), and nongranulocytes (monocytes and lymphocytes). Although all WBCs play a role, neutrophils, monocytes, and lymphocytes are especially important in phagocytic and immune processes. Granulocytes often contain inﬂammatory mediators or digestive enzymes in their cytoplasm. Neutrophils, the body’s main defense against pathogenic bacteria, are the major leukocytes in the bloodstream. Substances (eg, complement) released from infected or inﬂamed tissue cause neutrophils to migrate to the affected tissue. These WBCs arrive ﬁrst, usually within 90 minutes of injury. They localize the area of injury and phagocytize organisms or particles by releasing digestive enzymes and oxidative metabolites that kill engulfed pathogens or destroy other types of foreign particles. The number of neutrophils increases greatly during Pluripotential stem cells merthyr tydfil viagra donde comprar viagra en quito CFU* blast cells 640 viagra molecule structure used for many years contained live virus and caused viral shedding and a few cases of polio. The main disadvantages of IPV are that it must be injected and it is more expensive. • Hepatitis B virus (HBV) infection can cause serious liver diseases such as acute and chronic hepatitis, cirrhosis, and hepatocellular carcinoma. Chronic carriers of HBV may be asymptomatic reservoirs for viral transmission. Children who become infected are at high risk of becoming chronically infected. Because of these circumstances, hepatitis B vaccine is now recommended for all newborns and for unimmunized children before starting school, as well as other at-risk groups. Overall, the goal is to achieve universal immunization, decrease transmission, and eradicate the disease. • Everyone should be immunized against diphtheria and tetanus every 7 to 10 years for life. • Strategies to promote immunization continue to evolve. One strategy is to combine vaccines so that only one in- canadian pharmacy viagra virus SC 0.5 mL in a single dose does viagra work on a full stomach Interferon alfa-2b (Intron A) test online apotheken viagra 673 does viagra ever not work Hypersensitivity reaction, motion sickness, parkinsonism, PO 25–50 mg q4–8h; IV or deep IM 10–50 mg, increased if necessary to a maximal daily dose of 400 mg Insomnia, PO 50 mg at bedtime Syrup for cough, PO 25 mg (10 mL) q4h, not to exceed 100 mg (40 mL) in 24 h viagra usage video nombre de pastillas similares al viagra CHAPTER 51 DRUG THERAPY OF HEART FAILURE In addition to antianginal drugs, several other drugs may be used to control risk factors and prevent progression of myocardial ischemia to myocardial infarction and sudden cardiac death. These may include: • Aspirin. This drug has become the standard of care because of its antiplatelet (ie, antithrombotic) effects. Recommended doses vary from 81 mg daily to 325 mg daily or every other day; apparently all doses are beneﬁcial in reducing the possibility of myocardial reinfarction, stroke, and death. Clopidogrel (see Chap. 57), 75 mg/day, is an acceptable alternative for individuals with aspirin allergy. • Antilipemics. These drugs (see Chap. 58) may be needed by clients who are unable to lower serum cholesterol levels sufﬁciently with a low-fat diet. Lovastatin or a related “statin” is often used. The goal is usually to reduce the serum cholesterol level below 200 mg/dL and lowdensity lipoprotein cholesterol to below 130 mg/dL. • Antihypertensives. These drugs (see Chap. 55) may be needed for clients with hypertension. Because beta blockers and calcium channel blockers are used to manage hypertension as well as angina, one of these drugs may be effective for both disorders. can you buy viagra over the counter in portugal CHAPTER 55 ANTIHYPERTENSIVE DRUGS viagra font free download can your g p prescribe viagra Combination Products im 17 can i take viagra 831 risks of viagra in young men Hemostasis is prevention or stoppage of blood loss from an injured blood vessel and is the process that maintains the integrity of the vascular compartment. It involves activation of several mechanisms, including vasoconstriction, formation of a platelet plug (a cluster of aggregated platelets), sequential activation of clotting factors in the blood (Table 57–1), and growth of ﬁbrous tissue (ﬁbrin) into the blood clot to make it more stable and to repair the tear (opening) in the damaged blood vessel. Overall, normal hemostasis is a complex process involving numerous interacting activators and inhibitors, including endothelial factors, platelets, and blood coagulation factors (Box 57–1). ond, embolization obstructs the blood supply when the embolus becomes lodged. The pulmonary arteries are common sites of embolization. viagra 100mg wikipedia does viagra work if you don't have ed Prevention and management of thromboembolic disorders (eg, deep vein thrombosis, pulmonary embolism, atrial ﬁbrillation with embolization) viagra generico low cost Use in Older Adults RATIONALE/EXPLANATION does viagra really make you bigger has anyone died from viagra Use in Hepatic Impairment Use in Older Adults Critical Thinking Scenario John Finney, a 32-year-old client with acquired immunodeﬁciency syndrome, is admitted to your medical unit for management of severe diarrhea. He reports having 12 to 20 liquid stools per day and feeling weak and dizzy when he gets up. This current bout of diarrhea has been continuing for 6 days, during which he has lost 18 pounds. Diphenoxylate (Lomotil) and IV ﬂuids are ordered. Reﬂect on: ᮣ The physiologic effects of severe diarrhea. ᮣ The impact of severe diarrhea on a person’s ability to carry out normal activities. ᮣ Appropriate nursing assessments and interventions while diarrhea continues. ᮣ How diphenoxylate (Lomotil) works to decrease diarrhea. viagra 50 miligramos is there a non prescription substitute for viagra • • 5. viagra keeps you hard blue viagra shot Bone marrow depression, nausea, vomiting Nausea and vomiting, bone marrow depression Bone marrow depression, nausea and vomiting, nephrotoxicity Nausea, vomiting, anaphylaxis, nephrotoxicity, bone marrow depression, ototoxicity Anaphylaxis, anemia, increased risk of bleeding or infection viagra patient teaching Pulmonary toxicity, mucositis, alopecia, nausea, vomiting, hypersensitivity reactions Bone marrow depression, nausea, vomiting. Extravasation may lead to tissue necrosis. Same as doxorubicin, below Bone marrow depression, nausea, vomiting Bone marrow depression, alopecia, mucositis, GI upset, cardiomyopathy. Extravasation may lead to tissue necrosis. Bone marrow depression, nausea, vomiting, fever, alopecia Cardiotoxicity Same as doxorubicin, above Bone marrow depression, nausea, vomiting. Extravasation may lead to tissue necrosis. Bone marrow depression, congestive heart failure, nausea Bone marrow depression, hepatotoxicity, nausea, vomiting Dysuria, urgency, frequency, bladder spasms, hematuria ginkgo biloba vs viagra 1. Review characteristics of ocular structures that inﬂuence drug therapy of eye disorders. 2. Discuss selected drugs in relation to their use in ocular disorders. 3. Use correct techniques to administer ophthalmic medications. 4. Assess for ocular effects of systemic drugs and systemic effects of ophthalmic drugs. can using viagra make you impotent 941 how long before sex should u take viagra Many supplements are promoted for use in skin conditions. Most have not been tested adequately to ensure effectiveness. At the same time, however, topical use rarely causes serious adverse effects or drug interaction. Two topical agents for which there is some support of safety and effectiveness are aloe and oat preparations. Aloe is often used as a topical remedy for minor burns and wounds (eg, sunburn, cuts, abrasions) to decrease pain, itching, and inﬂammation and to promote healing. Its active ingredients are unknown. Wound healing is attributed to moisturizing (text continues on page 956) erectile dysfunction viagra not working Drugs at a Glance: Topical Corticosteroids best selling herbal viagra SECTION 11 DRUGS USED IN SPECIAL CONDITIONS viagra loyalty program and neonate. Meperidine may cause less neonatal depression than other opioid analgesics. Butorphanol is widely used. If neonatal respiratory depression occurs, it can be reversed by naloxone (Narcan). Duramorph is a long-acting form of morphine that provides analgesia up to 24 hours after injection into the epidural catheter at the completion of a cesarean section. Regional analgesia is achieved by the epidural injection of opioids (eg, fentanyl) or preservative-free morphine. Possible side effects include maternal urinary retention, but no signiﬁcant effects on the fetus. pfizer wins viagra patent trial 358. 359. what happens if u take viagra and dont need it Resistance exercises can americans buy viagra in canada Sensory 131. is outdated viagra safe oriented therapies.66,67,73–76 A growing variety of clinical trials confirm that greater intensity of task-oriented practice for walking or dextrous use of the upper extremity leads to significantly better functional outcomes for that task compared to nonspecific training.77,78 Constraint-induced movement therapy can be considered a corollary to the task-oriented motor learning concept, with an emphasis on massed practice. The technique has shown promise in hemiparetic patients who had at least 20° of wrist extension and 10° of finger extension. The strategy calls for forced use of the affected upper extremity and may include gradual shaping of a variety of functional movements to overcome what is theorized as learned nonuse of the limb.79 Learned nonuse may derive from unsuccessful early attempts to use the affected limb after a stroke or, in studies of monkeys, after deafferentation of the upper extremity.80 The failure in attempts to use an arm may lead to behavioral suppression and masks any subsequent ability of the limb. Positive reinforcement comes from successful use of the unaffected arm, which leads to the permanent compensatory behavior of nonuse of the paretic hand. Restraining the normal arm and engaging the affected one in the practice of functional tasks improved the strength, frequency, and quality of its daily use in a small 2-week trial.81 The addition of a shaping paradigm of reinforcement to elicit functional movements appeared to have a longer lasting effect than did conditioned response training in only one study,79 but did not improve outcomes or was not necessary for success in others.69,82–84 In shaping with forced use, the patient receives feedback during the steps it takes to improve from a rudimentary early training response, such as slow extension of the elbow, through a more complex response, such as using the proximal arm to push a shuffleboard puck to a target. The notion of shaping, drawn from the psychology literature, has been rather vague when applied to rehabilitation efforts and its relevance to motor learning is yet to be demonstrated. As discussed earlier, therapy structured around learning new sensorimotor relationships in the wake of altered motor control seems more likely to be effective than methods that only foster a developmental sequence. Constraint-induced movement therapy protocols have not, to date, defined a specific style tampcol herbal viagra blueberry 100mg viagra 244 25. 26. shuangbao acura viagra Kinematics best viagra advert Types of Measurements viagra district chicago 2 womens viagra jelly irish viagra shot Maximum Possible Attained Score Score how to get maximum benefit from viagra Expression Memory viagra ivf treatment Assessment and Outcome Measures for Clinical Trials 148. 149. 150. 151. 152. 153. 154. 155. non subscription viagra 100–400 mg tid 100–400 mg qd 250–500 mg tid 300–800 mg qid 25–400 mg bid 50–200 mg bid how exactly does viagra work 30–120 mg sustained release Continued on following page what happens when young men take viagra viagra usage experience 342 Weakness-Associated Shoulder Pain viagra medscape Phenol block of femoral nerve proscar side effects viagra homemade viagra watermelon lemon central and obstructive sleep apnea.264 After SCI, sleep apnea is more prevalent in people with quadriplegia than paraplegia and in patients with motor-incomplete injuries, affecting from 15% to 45% of patients with chronic SCI.265 Impaired sensory feedback from respiratory muscles, sleeping in a supine position, and antispasticity agents may contribute. Central and obstructive sleep apnea or a mix of both can develop from brain stem and cortical lesions, especially with bulbar dysfunction, or in relation to a superimposed toxic-metabolic encephalopathy. These disorders may have preceded the stroke, given that they have been associated with a higher risk for stroke.266 Pharyngeal muscle weakness and impaired neural control during sleep of nasophayrngeal and pharyngolaryngeal muscles caused by a stroke contributes to the risk for obstructive apnea. From one-third to two-thirds of inpatients with stroke may have a sleep disorder when formally tested by polysomnography.267 Sleep apnea may cause severe oxygen desaturation, pulmonary hypertension, and is associated with causing hypertension, stroke, and myocardial infarction. Patients often complain of poor concentration, memory impairment, malaise, and disinterest. A polysomnagram is indicated when the rehabilitation team observes a hypersomnolent, confused, and snoring or apneic patient. More than 5 apnea episodes per hour or 30 per night is abnormal. One study found an average of 52 sleep-disordered breathing events per hour in selected subjects within 1 year of stroke.268 The number of oxygen desaturation events and the oximetry measures during sleep disordered breathing have correlated with BI scores at 1 and 12 months after stroke.269 Tilting the head of the bed up 45° can lessen obstructive apnea. Approximately 70% of affected people will tolerate the use of continuous positive airway pressure therapy. Continuous positive airway pressure (CPAP) devices improve both central and obstructive apneic conditions. A randomized trial during inpatient stroke rehabilitation found that nasal CPAP lessened depression, but compliance was poor in patients with delirium and marked cognitive impairment.270 Drugs such as protriptyline may increase upper airway muscle activity. Surgical interventions that include uvulopalato-pharyngoplasty can lessen oropharyngeal obstruction, Acute and Chronic Medical Management effet du viagra chez les femmes 239. 240. 241. youtube viagra couple my girlfriend took viagra 445 GENITOURINARY SYSTEM viagra artigianale Although physical impairments that cause disability are common after a moderate to severe CHI at the time of transfer into a rehabilitation program (Table 11–12), these impairments most often improve within 6 months. Cognitive and behavioral sequelae linger. The Vietnam Head Injury Study examined 420 veterans who suffered PHI, mostly from lowvelocity shrapnel that caused a preponderance of focal brain injuries. One week after injury, 21% had a hemiparesis and 11% had a hemisensory impairment.52 Fifteen years later, 10% were hemiparetic and 21% had a residual whats the active ingredient in viagra Table 11–14. Cognitive Processes Commonly Impaired After Traumatic Brain Injury viagra 100 mg 8 tablet but i got right back up like viagra lyrics 157. 158. 159. 197. man power viagra natural F viagra para vacas Small intestine viagra stops working for some men Although a therapist seems to work at the systemic level, the beneﬁts of therapy are a result of changes produced at the chemical and cellular levels. Diseases, although they produce symptoms such as pain, fever, and edema, are actually caused by dysfunction at the cellular and chemical levels. Small changes in chemical makeup can have serious effects. For example, in a disease known as sickle cell anemia, the protein in the hemoglobin molecule is slightly different from normal. This small change has drastic effects on the properties of hemoglobin. The hemoglobin in sickle cell anemia, unlike normal hemoglobin, changes into a more solid form in an environment with less oxygen, prix du viagra 25 mg Golgi apparatus zyrexin vs viagra 29 necesito receta para comprar viagra en mexico A solution that has exactly the same osmotic pressure as the intracellular ﬂuid does not allow osmosis through the cell membrane in either direction when placed on the outside of cells. Such a solution is said to be isotonic with the body ﬂuids. The number of particles present in 0.9% solution (0.9 g/dL) of sodium chloride is the same as that in blood. If a person is transfused with this concentration of sodium chloride, the cells are not affected. This solution, normal saline, is used in persons who are dehydrated or with low blood volume. A solution that causes osmosis of ﬂuid out of the cell and into the solution is said to be hypertonic. A solution that allows osmosis into cells is hypotonic. Care must be taken that transfused solutions are of the right concentrations and that they do not affect movement of ﬂuid in and out of cells by osmosis. viagra pour le fun 51 viagra skelbiu.lt The skin is supplied by autonomic nerves, which innervate the blood vessels and glands in the skin. See page XX for details of autonomic nerves. Brieﬂy, autonomic nerves supply glands, blood vessels, and internal organs. There are two types: sympathetic and parasympathetic. Sympathetic stimulation and circulating epinephrine and norepinephrine produce vasoconstriction. There are no known vasodilator ﬁbers to the cutaneous blood vessels; dilation is caused by a decrease in the constrictor tone of the sympathetic nerves. Chemicals, such as bradykinin from sweat glands, best indian substitute for viagra Injections are often given in the subcutaneous layer because of its relatively scarce blood supply and distance from vital organs. Other than safety, drugs are more slowly absorbed from this layer, prolonging their duration of action. prelox vs viagra fectious but may not actually be infectious, such as some types of psoriasis, severe acne, or vitiligo. Touch therapy may be of great help to those clients who are often isolated from society because of their appearance. Areas of skin that ooze ﬂuids or are visibly inﬂammed, should be avoided at all times. Although the therapist is not expected to diagnose a condition, it is vital to have enough information about those skin diseases already diagnosed by a physician to work with clients with these disorders. Figure 2.11 indicates the appearance of common skin lesions or skin signs. It is important for all bodyworkers to avoid infected, acutely inﬂamed, or irritable skin lesions. viagra taken by younger men can viagra cause prostate cancer structure, be able to identify bony landmarks, know the possible range of motion of each joint, and know the muscles that produce various movements. Knowledge of the origin and insertions of muscles and direction of ﬁbers is also essential. This chapter describes the bones of the body, bone formation, anatomic landmarks, and major joints. 3.17. Lateral View of the Vertebral Column, Showing the Four Normal Curves and Regions does viagra help with altitude sickness viagra wikipedia shqip Inferior angle of scapular Lattisimus dorsi A Anterior ritalin viagra combination how to make viagra more potent Base D travelling overseas with viagra is it bad to take viagra if you don't need it Transverse process Dens of axis Vertebral artery how many times can you come on viagra viagra brochure pdf This is syndesmosis and includes the interosseous membrane and the oblique cord that runs between the interosseous border of the radius and ulna. The oblique viagra 50 mg vademecum Medial meniscus Unipennate how to make a viagra shot TENDON ORGANS bio viagra herbal buy viagra lancashire G lu c o s e (cranial nerve X). Some muscles of the palate are innervated by the trigeminal nerve (cranial nerve V) and the accessory nerve (cranial nerve XI). The complexity of the swallowing process is realized when a nerve is injured; the person has difﬁculty swallowing and speaking. The food may enter the larynx and lead whats viagra mean what effect does viagra have on a woman Chapter 4—Muscular System The rectus femoris and hamstrings serve as agonists and antagonists in many movements of the hip and knee. If the hip is ﬂexed and the knee extended, the rectus is the agonist and the hamstrings become the antagonist. The opposite happens when the movement is reversed. When both the hip and the knee are ﬂexed simultaneously, both the hamstrings and rectus femoris are agonists at one joint and antagonists at the other! can a 23 year old take viagra Primary type of metabolism (aerobic, anaerobic) Capillaries (abundant, few) viagra italian translation generic viagra deaths 243 viagra cufflinks Anterior view Anterolateral surface of femur along linea aspera (distal half) can i take aspirin and viagra together Medial view viagra pre contest O O viagra cobra 125 es legal comprar viagra online 298 viagra foto 2011 Abductor hallucis 5.6. Recording Electrical Changes Across Cell Membrane viagra side effects stroke khasiat obat viagra FIGURE viagra - sumashedshij Anesthetics are injected into the epidural space at speciﬁc points to control pain in regions supplied by spinal nerves that exit from there. This procedure is known as an epidural block. can men with high blood pressure take viagra Injury to the Sciatic Nerve jeremy renner viagra incident 5.30. A Stretch Reﬂex—The Biceps Jerk raging grannies viagra review board Trigeminal Nerve Problem Temporomandibular Joint Syndrome viagra canada discount code 361 does viagra make you harder than normal 365 alguien ha comprado viagra por internet Spinal Shock As soon as the spinal cord is injured or cut, it is followed by a period of spinal shock when all spinal reﬂex responses are depressed. This lasts for about two weeks in humans. The cause of spinal shock is uncertain. With time, the spinal reﬂexes below the cut become exaggerated and hyperactive. It could be a result of many reasons. One reason is the removal of the inhibitory effects of the higher motor centers. Also, the neurons become hypersensitive to the excitatory neurotransmitters. In addition, the spinal neurons may sprout collaterals that synapse with excitatory input. Whatever the reason, the stretch reﬂexes are exaggerated and muscle tone increases. The ﬁrst reﬂex response that comes back is a slight contraction of the leg ﬂexors and adductors in response to some painful stimuli. The extent of disability depends on the level of the spinal cord that has been injured. It must be remembered that although the spinal cord has all the segments—8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal—the length of spinal cord is shorter than the vertebral column and ends at level L1 and L2. Hence, injury below the second lumbar vertebra may affect only the muscles and dermatomes innervated by the sacral and coccygeal nerves. If spinal cord injury occurs above the third cervical spinal segment, other than the loss of voluntary movements of all the limbs, respiratory movements are affected as the phrenic nerve arising from C3, 4, 5 supplies the diaphragm. Loss of movement of all four limbs is known as quadriplegia. If the lesion is lower, only the lower limbs are affected, and this is termed paraplegia. If the nerves to only one limb are affected, it is referred to as monoplegia. Other Complications of Spinal Cord Injuries One common complication among people with spinal cord injuries is decubitus ulcer. Because voluntary weight shifting does not occur, the weight of the body compresses the circulation to the skin over bony prominences, producing ulcers. These ulcers heal slowly and are prone to infection. As a result of disuse, calcium from bones are reabsorbed and excreted in the urine. This increases the incidence of calcium stones forming in the urinary tract. Paralysis of the muscles of the urinary bladder, in addition to stone formation, result in stagnation of urine and urinary tract infection. When the spinal reﬂexes return, they are exaggerated. For example, in a person with quadriplegia, the slightest of stimuli can trigger the withdrawal reﬂex and the stimulated limb ﬂexes with ﬂexion/extension viagra kaufen freiburg Target Organ Skin Sweat glands Arrector pili muscle Skeletal Muscles Eye Radial muscle of iris Sphincter muscles of iris Ciliary muscle Lacrimal (tear) glands Cardiovascular System Heart Blood Vessels to: Skin Skeletal muscle Heart (coronary) Gut Veins Respiratory System Bronchial muscles Bronchial glands Digestive System Salivary glands Motility and tone Sphincters Secretions Liver Pancreas Adipose Tissue Urinary System Kidney Urinary bladder Detrusor muscle Sphincter Reproductive System Male sex organs Uterus Erection Variable Ejaculation Variable Contraction Relaxation Relaxation Contraction Increased urine production Decreased urine production Mucous secretion Increase Relaxation Stimulation Glycogen Synthesis Increased exocrine and endocrine (insulin) secretion None (not innervated) Watery, serous secretion Decrease Contraction Inhibition(?) Glycogen breakdown; glucose synthesis and release Decreased exocrine secretion Breakdown and release of fatty acid Contraction Stimulation of secretion Relaxation Inhibition (?) None (not innervated) Constriction Dilation Dilation Constriction Constriction Decrease in heart rate and force of contraction Increase in heart rate and force of contraction Contract (pupils constrict) Contract (lens bulge for near vision) Secretion Relax (lens become thinner for far vision) None (not innervated) Contraction (pupils dilate) None (not innervated) None (not innervated) Increased force of contraction Increased secretion Contraction, erection of hairs None (not innervated) Parasympathetic System Response Sympathetic System Response when does viagra patent expiry uk Removal of cause; rest; ice; compression; elevation little fockers viagra scene Matching A. 1. e B. 1. d C. 1. d D. 1. c E. 2. a 8. h 2. a 2. b 2. f 2. a 3. c 3. f 3. f 3. b 3. b 4. f 5. b 6. g 7. d 4. c 4. e 4. c 5. d 5. a 5. e 6. b 6. c 6. a viagra untuk lelaki the posterior pituitary. The cell bodies of these neurons lie in the hypothalamus; the axons descend to the pituitary, transporting the hormones vasopressin and oxytocin from the cell body to the nerve endings. The hormones are released into the blood in the posterior pituitary. shilajit vs viagra the cervix, further increase in oxytocin levels result, producing strong contractions of the uterus. This continues until the fetus is expelled and is one of the few situations in the body where positive feedback occurs. Oxytocin, however, is not the only hormone or mechanism involved in labor. Oxytocin may also play a part in the transport of sperm up the reproductive tract at intercourse and the feeling of sexual pleasure during and after intercourse. In men, oxytocin stimulates the contraction of the vas deferens and the prostate glands before ejaculation occurs. In animal experiments, this hormone has been linked to parental bonding with offspring. Vasopressin or Antidiuretic Hormone (ADH) A major function of vasopressin is to conserve water by acting on the kidney; hence, the name antidiuretic hormone. Vasopressin acts on the collecting ducts of the kidney (see page ••), making them more permeable to water. The water moves into the interstitial region from the ducts, reducing urine volume and increasing urine concentration. In the absence of vasopressin, more dilute urine is formed. ADH also decreases the loss of water through sweat. Vasopressin in large doses causes contraction of the smooth muscle of the arterial walls and a rise in blood pressure. This regulatory mechanism is particularly useful when blood pressure drops after hemorrhage. Circulating vasopressin is rapidly removed by why do young guys take viagra 408 himalayan viagra plant 418 Estrogen Ovarian hormonal levels does viagra prevent pregnancy Corpus luteum formation Secretory phase definition du mot viagra does viagra helps you last longer CHAPTER The blood contributes approximately 8% of the body weight. The volume of blood in an adult man is approximately 5–6 liters (5.3–6.3 qt) and, in an adult female, it is about 4–5 liters (4.2–5.3 qt). Blood is more viscous than water. The pH of blood is maintained between 7.35 and 7.45. The temperature of blood is about 38°C (100.4°F). The color of blood depends on hemoglobin content. When the hemoglobin is oxygenated, blood appears red—as in peripheral arteries. If the oxygen content is low, it appears blue—the color of blood in superﬁcial veins. The blood is made up of two major components— formed elements—the cells and plasma. If a small volume of blood is withdrawn and centrifuged, the heavier elements will settle at the bottom of the centrifuge tube. The cells in the blood—the heavier elements— constitute approximately 45% of the volume. The remaining volume of 55% is plasma—the volume of blood without cells. The cellular elements of blood are the red blood cells, white blood cells, and platelets. The red blood cells make up about 99% of the volume of cells. tipos de viagra para hombres getting viagra from boots One might wonder how this has any direct bearing on massage therapy. The basis of blood typing is an apt example of the basic concepts of immunity and how immunity is developed in an individual. The immune mechanisms involved in ﬁghting off infection, recognizing foreign cells (as in transplantation), and beneﬁts of immunization follow the same principles. The Massage Connection: Anatomy and Physiology viagra blurred vision permanent The Right Atria The two atria (see Figure 8.8) are separated by the interatrial septum. In the fetus, the two atria communicate with each other through an oval opening, the foramen ovale, shunting the blood from right to left because the lungs do not function and the placenta takes the place of lungs. This opening closes at birth when the baby takes its ﬁrst breath and remains as an oval depression (fossa ovalis). The right atrium communicates with two large veins—the superior vena cava and the inferior vena cava. These veins drain blood from the upper and lower part of the body, respectively. The superior vena cava delivers blood to the atrium from the head, neck, upper limbs, and chest, and the inferior vena cava carries when did viagra come on the market 467 would viagra help premature ejaculation Nucleus of endothelial cell Basement membrane how long does herbal viagra last This unit is used to measure blood pressure and is an abbreviation for millimeters of mercury. For example, if the pressure is 10 mm Hg, it is the pressure required to push a column of mercury to a height of 10 millimeters. Because mercury is heavy, the numbers are small. If water is used instead of mercury, the height of the column will be many feet and the numbers will be large and cumbersome to use. In fact, the ﬁrst measurement of blood pressure was made in a horse using the height of water as the unit and the tube had to be more than 8 feet long. viagra invented 1998 Effect of Aging on the Cardiovascular System chest pain after viagra russian hairdresser viagra Chapter 8—Cardiovascular System what happens when a girl takes male viagra diseases; observe surface of skin for changes in color or pigmentation (e.g., cyanosis, jaundice, edema, dilated veins, bruises, and bleeding under the skin) Take suitable precautions as the elderly are prone to orthostatic hypotension. It is important for a massage therapist to learn the details of bleeding tendencies. This will help learn the severity of the problem. It would be advisable for the therapist to talk to the client’s physician before proceeding with massage. In severe cases, even mild pressure can cause bleeding under the skin. Robert was right to think about spousal abuse as it could cause bruising. The fundamental reaction in the clotting process is the conversion of ﬁbrinogen to ﬁbrin. For this conversion, many clotting factors, such as calcium and prothrombin, are required. Vitamin K is also required. Platelets are important in the clotting process. See answer to Short-Answer question no. 4. for factors that cause excessive bleeding. The normal red blood cell count is approximately 5 million cells/cubic millimeter of blood. The formation site of red blood cells varies from age to age. In the fetus, the cells are formed in the liver and spleen. In children, the cells are formed in the marrow cavities of all bones. By age 20, the blood cells are manufactured in the upper end of the humerus and femur and in ﬂat bones such as the sternum, pelvis, and vertebra. Anemia is a condition in which there is a reduction of red blood cells and/or hemoglobin content. There are many causes of anemia. Conditions that result in an increased destruction rate of red blood cells and a decreased production rate and blood loss all cause anemia. Pernicious anemia is a condition in which there is a reduction of intrinsic factor, a factor (secreted by the stomach and required for absorption of vitamin B12). Vitamin B12 is needed for the manufacture of red cells. Oxygenated hemoglobin is responsible for the red color of blood. The skin appears pale if there is reduced amount of hemoglobin in the blood. It is safe to massage this individual. Severe anemia can lead to cardiac failure and the therapist should ensure that such complications do not exist in the client. and B. Jaundice is a result of increased levels of bilirubin. Jaundice could be a result of in- clonazepam viagra interaction • • • • • • • Swelling Pain Heaviness Reduced mobility Strain on associated joints and muscles Tightness of overlying skin Skin changes (e.g., increased susceptibility to skin breakdown, infection, and injury; delayed wound healing; lower skin temperature as a result of reduced blood ﬂow in the area • Sensory disturbances of the hand and foot • Psychological disturbances owing to alterations in body image, sexuality, and social acceptance The Massage Connection: Anatomy and Physiology puedo tomar viagra si soy joven can i give my dog viagra Cytotoxic T cells tonic wine and viagra Virus is viagra a prescription drug in france Mucus layer Mucus gland Blood vessel Cilia viagra rapid delivery 20 562 viagra shots alcohol Synthesized in skin; milk, cheese Vegetables, meat, milk viagra costa blanca Table 11.3 viagra and l-arginine together chewing viagra tablets Adjacent to the mouth are many salivary glands (see Figure 11.7), which secrete about 1,500 mL (158.5 qt) Chapter 11—Digestive System what would happen to a girl if she took viagra THE PANCREAS viagra frau preis web pharma org buy viagra usa Pain Patterns Relating to the Organs of the Gastrointestinal System how much viagra should a woman take Kidney Ureter viagra shop 24h C do you need a prescription to buy viagra in spain FIGURE
Page Not Found - Wickenburg Hospital
The following is a list of recent Wickenburg Community Hospital news articles that highlight our commitment to excellence. To read an entire article, please click on the news headline.
Greater Wickenburg Region Community Health Needs Assessment Final Report December greatestpharmacy health pills 2013 PDF – Click Here to Download
Pediatrician Dr. Chrzanowski , or Dr. “C”, joined the healthcare team at Community Hospital Clinic on Monday, September 24, 2012. She has been a practicing physician for more than two decades and includes degrees in Dietetics and Nutrition among her …
On Monday, August 20, 2012 the High Desert Med Spa & Laser greatestpharmacy health pills Center opened in Suite A of the Wickenburg Community Hospital at 520 Rose Lane. This skin aesthetics outpatient treament center with a tag line of …
Wednesday, March 07, 2012 by Jane Summers, Programs and Services At the ribbon cutting during the Grand Opening of Community Hospital Clinic – Congress on Saturday, February 25th (Left to Right) CEO Wickenburg Community Hospital Jim Tavary, Yavapai County Supervisor …
On Thursday, Jan. 12 Wickenburg Community Hospital formally signed an agreement with the Congress Senior Citizens, Inc. to provide primary healthcare to Congress and immediate surrounding communities. greatestpharmacy health pills The facility, operated by Congress Senior Citizens, Inc. is currently …