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How- ever generic toradol 10mg mastercard, attractive as it may be, it must be recognised Definition that this proposition has not echoed as much, and the term upper motor neurone syndrome continues Spasticity and stretch reflex exaggeration to be used in the literature. The tonic stretch reflex has been shown pathways involved by the lesion are different after 558 Pathophysiology of movement disorders cerebral and spinal lesions, it is not surprising that contracting muscle, and is only demonstrable clin- the pathophysiology of spasticity is different after ically for the quadriceps muscles, where the range stroke and spinal cord injury (pp. There are other decreaseintheresistancetostretchthatoccurswhen features of spasticity, such as clonus and the clasp- a dynamic reflex response subsides as movement knife phenomenon, but these are not invariably slowsorceases. Thus, the relaxation of a vigorous reflex con- In neurological practice, the crucial question about traction stretches muscle spindle endings and can spasticity is the extent to which it contributes to produce a volley that, given the hyperactivity of the the motor impairment and limitation of activity in reflex arc, is sufficient to trigger another reflex con- patients with a corticofugal syndrome. The presence of clonus is directly related assumed that a voluntary movement that stretches to the tendon jerk hyperreflexia, and whether it can a spastic muscle might be expected to produce be elicited depends on the skill of the examiner who reflex activity that would oppose the movement. As clonus subsides, the spin- depends both on the exaggeration of the stretch dle discharge produced by relaxation of the twitch reflex and changes in the transmission in spinal contractiongraduallybecomesdispersed. Spasticity 559 Spastic restraint–adebated proposition reflex threshold (Powers, Marder-Meyer & Rymer, 1988), increased stretch reflex gain (Thilmann, The contribution of spasticity to motor impair- Fellows & Garms, 1991), but no evidence for abnor- ment has been the subject of vigorous discussion, mal stretch reflex (Dietz et al. However, the prevailing view concluded that the increased resistance to stretch is that the exaggeration of stretch reflexes in some of spastic muscles mainly results from changes in of these patients may give rise to crucial restraint non-neuralfactors(see pp. Accordingly, ferent results may be obtained in patients with dif- the usefulness of reducing spasticity is now gener- ferent lesions of the central nervous system, and/or ally accepted (using, e. Patients with spinal cord lesions Stroke patients In patients with spinal cord lesions, in particular In stroke patients, there is evidence that the in spinal cord compression, chronic myelopathies increased resistance to stretch in the triceps surae or hereditary spastic paraparesis, there is evi- is due to mechanical rather than reflex causes (Perry dence that exaggerated stretch reflexes can disrupt et al. Thatreductionofspasticitywillimprove in favour of a neural origin of spastic hyperto- gait remains to be firmly established (Landau, 2003; nia than of changes in the muscle itself. More Cramer, 2004) and, on the contrary, its reduction recently, unwanted stretch reflex activity in the mightbecounterproductiveasspasticityoftenhelps antagonisttriggeredbythedynamicconcentriccon- support the body during locomotion (see Dietz, traction of the agonist has been shown to limit the 2003). Conflicting results have been obtained con- amplitude and/or to slow down the movement of cerning the resistance opposed by the biceps brachii knee muscles (Knutsson, Martensson & Gransberg,˚ to voluntary elbow extension: decreased stretch 1997). However, the exaggeration of the brate rigidity immediately follows the causal lesion, tonic stretch reflex has only a low correlation with while spasticity takes days, often weeks to develop. Moreover, the This gives time for rearrangements to occur at spinal increased resistance to stretch is also, and perhaps level (see pp.

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These effects include inhibition of endogenous highly bound (98%) to plasma proteins and serum half- sex hormones and sperm formation through negative life varies (eg toradol 10 mg on-line, 8 days for IM testosterone cypionate, feedback of pituitary luteinizing hormone (LH) and 9 hours for oral fluoxymesterone). About 90% of a dose is • Male sex hormones given to women antagonize or reduce excreted in urine as conjugates of testosterone and its the effects of female sex hormones. It is given orally, has a half-life of 4 to 5 hours, and is lining of the uterus. This characteris- ° Naturally occurring androgens are given by injec- tic limits the clinical usefulness of these drugs in tion because they are metabolized rapidly by the women and children. Some esters of testosterone sexual development may occur if these drugs are given have been modified to slow the rate of metabolism to young children. For example, intramuscu- lar (IM) testosterone cypionate and testosterone enanthate have slow onsets of action and last 2 to Mechanism of Action 4 weeks. As a result, doses as high as 400 mg/day may ported to the nucleus, where it activates ribonucleic and be needed to produce adequate blood levels for full deoxyribonucleic acid production and stimulates cellular syn- replacement therapy. With male sex hormones, the most clear-cut indication for use is to treat androgen deficiency states (eg, hypogonadism, cryptorchidism, impotence, oligospermia) in boys and men. Individual Androgens Hypogonadism may result from hypothalamic-pituitary or testicular dysfunction. In prepubertal boys, administration of Clinical indications, routes, and dosage ranges are listed in the drugs stimulates the development of masculine character- Drugs at a Glance: Androgens. In postpubertal men who become androgen deficient, the hormones re-establish and maintain masculine characteristics and functions. HERBAL OR DIETARY In women, danazol (Danocrine) may be used to prevent or SUPPLEMENTS treat endometriosis or fibrocystic breast disease. Anabolic steroids are more often abused for body-building purposes Androstenedione and DHEA, androgens produced by the than used for therapeutic effects. They are marketed as safe, natural, alter- cancer and some types of anemia as indications for use, an- native androgens for building muscles.

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With analgesic–antipyretic–anti-inflammatory and antigout agents quality toradol 10 mg, observe for: (1) Gastrointestinal problems—anorexia, nausea, vomiting, These are common reactions, more likely with aspirin, indomethacin, diarrhea, bleeding, ulceration piroxicam, sulindac, tolmetin, colchicine, and sulfinpyrazone and less likely with acetaminophen, celecoxib, diflunisal, etodolac, feno- profen, ibuprofen, naproxen, rofecoxib, and valdecoxib. Most likely to occur in patients with a history of nasal polyps, asthma, or rhinitis. May result in severe symptoms, including potentially fatal bronchospasm. A few cases have been reported with COX-2 inhibitors, mechanism unknown. With triptan antimigraine drugs, observe for: Most adverse effects are mild and transient. However, because of (1) Chest tightness or pain, hypertension, drowsiness, dizzi- their vasoconstrictive effects, they may cause or aggravate angina ness, nausea, fatigue, paresthesias pectoris and hypertension. With ergot antimigraine drugs, observe for: (1) Nausea, vomiting, diarrhea These drugs have a direct effect on the vomiting center of the brain and stimulate contraction of gastrointestinal smooth muscle. Acute poisoning is rare; chronic poisoning is usually a iting, dizziness, thirst, convulsions, weak pulse, confusion, result of overdosage. Circulatory impairments may result from angina-like chest pain, transient tachycardia or bradycar- vasoconstriction and vascular insufficiency. Large doses also dia, muscle weakness and pain, cyanosis, gangrene of the damage capillary endothelium and may cause thrombosis and oc- extremities clusion. Gangrene of extremities rarely occurs with usual doses unless peripheral vascular disease or other contraindications are also present. Drugs that increase effects of aspirin and other NSAIDs: (1) Acidifying agents (eg, ascorbic acid) Acidify urine and thereby decrease the urinary excretion rate of salicylates (2) Alcohol Increases gastric irritation and occult blood loss (3) Anticoagulants, oral Increase risk of bleeding substantially.