Amitriptyline chemical structure
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Endep

Amitriptyline hydrochloride (sold as Elavil®, Tryptanol®, Endep®) is a tricyclic antidepressant drug. It is a white, odorless, crystalline compound which is freely soluble in water and usually dispensed in tablet form. The empirical formula of its hydrochloride salt is C20H23N·HCl. more...

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Mechanism of Action

Amitriptyline affects serotonin and noradrenaline reuptake almost equally.

Uses

Approved

Amitriptyline is approved for the treatment of endogenous depression and involutional melancholia (depression of late life, which is no longer seen as a disease in its own right), and reactive depression and for depression secondary to alcoholism and schizophrenia.

Unapproved/Off-Label/Investigational

Amitriptyline may be prescribed for other conditions such chronic pain, postherpetic neuralgia (persistent pain following a shingles attack), fibromyalgia, interstitial cystitis, or irritable bowel syndrome.

A randomized controlled trial published in June of 2005 found that amitriptyline was effective in functional dyspepsia refractory to famotidine and mosapride combination therapy.

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Stroke rehabilitation - includes patient information sheets
From American Family Physician, 4/1/97 by M. Prabhakar Reddy

Each year approximately 550,000 people in the United States suffer a stroke. Of these individuals, 150,000 die and 300,000 are left disabled.[1] Due to better medical control of risk factors, improved treatment and changes in health-related behavior, the mortality rate for stroke has decreased considerably over the past 30 years.[2] However, the incidence of new cases of stroke has not decreased at the same rate.[3] The net result is an increased number of stoke survivors with chronic disabilities.

About 3 million Americans are currently living with varying degrees of disability from strokes.[1] The annual cost of stroke in the United States is estimated to exceed $30 billion, with much of the economic burden attributed to disabilities that prevent stroke survivors from returning to their previous level of function.[4] Rehabilitation is believed to decrease the long-term economic cost of stroke.[5,6]

Stroke Rehabilitation and Survival

It has been argued that if a stroke patient is discharged home after rehabilitation and survives 22 months or longer, then stroke rehabilitation is cost-effective and beneficial. Seventy-five percent of stroke patients are able to return home after completing a comprehensive rehabilitation program, and their mean duration of survival after the stroke is 7.5 years.[7]

Goals of Stroke Rehabilitation

and Patient Selection

The goals of stroke rehabilitation are to restore lost abilities as much as possible, to prevent stroke-related complications, to improve the patient's quality of life and to educate the patient and family about how to prevent recurrent stroke.

Approximately 10 percent of stroke survivors are without disability and are able to function independently. These patients do not require rehabilitation. Another 10 percent of patients are institutionalized because of markedly severe disability and are unable to achieve functional independence in a home setting regardless of how many rehabilitation services are provided. The remaining 80 percent of stroke survivors have mild to moderately severe disability and benefit from intense rehabilitation.[8]

Rehabilitation efforts should be initiated 24 to 48 hours after the onset of a stroke. The family physician works closely with a rehabilitation specialist during the acute care, rehabilitation and community reintegration of a stroke patient (Table 1).

Predictors of Functional Outcome

Factors that negatively or positively affect stroke recovery are listed in Table 4. Younger patients generally do better than older patients, who often have multiple medical problems. The longer the interval between the onset of stroke and the initiation of active rehabilitation, the less favorable the functional outcome. The earlier the neurologic recovery, the better the prognosis. The functional prognosis is poor in patients with recurrent stroke.

If seizures do occur, phenytoin Dilantin) is the drug of choice. However, phenytoin levels should be monitored carefully, since overmedication may cause lethargy and balance problems.

When a temporary increase in neurologic deficits (Todd's paralysis) occurs due to a seizure, the event may be misdiagnosed as another stroke.

CENTRAL PAIN SYNDROME

Central pain syndrome rarely occurs following a stroke, but when it does, it is difficult to manage. The syndrome is most likely caused by the brain lesion. Therefore, the pain is described as central in origin. The pain is usually diffuse and intense. It has a burning, tingling, stinging, shooting or, at times, aching quality.

The management of central pain syndrome includes avoiding situations that may stimulate the pain. Thus, it is important to prevent and treat infections, spasticity, contractures, bowel or bladder complications, and pressure sores. Psychotherapy, relaxation training and biofeedback may be helpful. Neurotropic medications such as amitriptyline (Elavil, Endep, Triavil) and anticonvulsant medications such as phenytoinmay be useful.[18]

DEPRESSION

Significant clinical depression occurs in 30 to 60 percent of stroke patients.[26] The rate of depression is considerably higher in elderly stroke patients than in the healthy elderly population.

Initial depression is related to the location of the stroke in the cortex. Social dysfunction and the level of functional impairment appear to be responsible for the reactive depression that can occur six months to one year after a stroke. Depression occurs more frequently and is more severe in patients who have had a left hemisphere stroke, particularly when the stroke occurred close to the frontal lobe.[27]

Regardless of whether the cause is organic or psychosocial, stroke-related depression responds fairly well to a combination of antidepressant medications and psychotherapy.

Measures to Prevent Recurrent Stroke

Patients who have had one stroke are at five times greater risk of having another stroke. Thus, the prevention of recurrent stroke is an important part of the stroke rehabilitation program.[28]

Preventive measures include the identification and control of risk factors, especially hypertension, cigarette smoking and a sedentary lifestyle. Oral anticoagulants help prevent embolic strokes in patients with atrial fibrillation or prosthetic cardiac valves. Aspirin and ticlopidine (Ticlid) have been found to be effective in preventing recurrent stroke.(29)

Surgical measures to prevent recurrent stroke include carotid endarterectomy in patients with carotid artery stenosis of greater than 70 percent and procedures to clip an intracranial aneurysm or to resect an arteriovenous malformation.

REFERENCES

[1.] Post-stroke rehabilitation: assessment, referral and patient management. In: Clinical practice guidelines. Rockville, Md.: U.S. Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, 1995; AHCPR publication no. 95-0662.

[2.] Shahar E, McGovem PG, Sprafka JM, Pankow JS, Doliszny KM, Luepker RV, et al. Improved survival of stroke patients during the 1980s. Stroke 1995; 26:1-6.

[3.] Modan B, Wagener DK. Some epidemiological aspects of stroke: mortality/morbidity trends, age, sex, race, socioeconomic status. Stroke 1992;23; 1230-6.

[4.] Cost of stroke. Stroke Clin Updates 1994:V(3):9-12.

[5.] Jorgensen HS, Nakayama H, Raaschou HO, Larsen K, Hubbe P, Olsen TS. The effect of a stroke unit: reductions in mortality, discharge rate to nursing home, length of hospital stay, and cost. A community-based study. Stroke 1995;26:1178-82.

[6.] Wentworth DA, Atkinson RP. Implementation of an acute stroke program decreases hospitalization costs and length of stav. Stroke 1996;27:1040-3.

[7.] Lehmann JF, DeLateur BJ, Fowler RS Jr, Warren CG, Arnhold R, Schertzer G, et al. Stroke rehabilitation: outcome and prediction. Arch Phvs Med Rehabil 1975;56:383-9.

[8.] Report of the joint Committee for Stroke Facilities. I. Epidemiology for stroke facilities planning. Stroke 1972;3:359-71.

[9.] Kelly-Hayes M, Wolf PA, Kase CS, Gresham GE, Kannel WB, D'Agostine RB. Time course of functional recovery after stroke: the Framingham Study. J Neurol Rehabil 1989;3:65-70.

[10.] Andrews K, Brocklehurst JC, Richards B, Laycock PJ. The rate of recovery from stroke - and its measurement Int Rehabil Med 1981;3:155-61.

[11.] Ferrucci L, Bandinelli S, Guralnik JM, Lamponi M, Bertini C, Falchini M, et al. Recovery of functional status after stroke. A postrehabilitation follow-up study. Stroke 1993;24:200-5.

[12.] Bach y Rita P. Central nervous system lesions: sprouting and unmasking in rehabilitation. Arch Phys Med Rehabil 1981;62:413-7.

[13.] Jongbloed L. Prediction of function after stroke: a critical review. Stroke 1986;17:765-76.

[14.] Feigenson JS, McDowell FH, Meese P, McCarthy ML, Greenberg SD. Factors influencing outcome and length of stay in a stroke rehabilitation unit. Part 1. Analysis of 248 unscreened patients - medical and functional prognostic indicators. Stroke 1977;8:651-6.

[15.] Dove HG, Schneider KC, Wallace JD. Evaluating and predicting outcome of acute cerebral vascular accident. Stroke 1984;15:858-64.

[16.] Granger CV, Hamilton BB, Fiedler RC. Discharge outcome after stroke rehabilitation. Stroke 1992; 23:978-82.

[17.] Kalra L, Yu G, Wilson K, Roots P Medical complications during stroke rehabilitation. Stroke 1995; 26:990-4.

[18.] Roth EJ. Medical complications encountered in stroke rehabilitation. Phys Med Rehabil Clin North Am 1991;2:563-78.

[19.] Roth EJ, Noll SF. Stroke rehabilitation. 2. Comorbidities and complications. Arch Phys Med Rehabil 1994;75:S42-6.

[20.] Censori B, Manara O, Agostinis C, Camerlingo M, Casto L, Galavotti B, et al. Dementia after first stroke. Stroke 1996;27:1205-10.

[21.] Bounds JV, Wiebers DO, Whisnant JP, Okazaki H. Mechanisms and timing of deaths from cerebral infarction. Stroke 1981;12:474-7.

[22.] Horner J, Massey EW. Silent aspiration following stroke. Neurology 1988;38:317-9.

[23.] Reddy MP. Decubitus ulcers: principles of prevention and management. Geriatrics 1983;38:55-6,59-61.

[24.] Roy C. Shoulder pain in hemiplegia: a literature review. Clin Rehabil 1988;2:35-44.

[25.] DeVincenzo DK, Watkins S. Accidental falls in a rehabilitation setting. Rehabil Nurs 1987;12:248-52.

[26.] Robinson RG, Starr LB, Price TR. A two year longitudinal study of mood disorders following stroke: prevalence and duration at six months follow-up. Br J Psychiatry 1984;1 44:256-62.

[27.] Downhill JE jr, Robinson RG. Longitudinal assessment of depression and cognitive impairment following stroke. J Nerv Ment Dis 1994;182:425-31.

[28.] Goldberg G. Secondarv stroke prevention. Phys Med Rehabil Clin North Am 1991:;2517-28.

[29.] Harbison JW. Ticlopidine versus aspirin for the prevention of recurrent stroke. Analysis of patients with minor stroke from the Ticlopidine Aspirin Stroke Study. Stroke 1992;23:1723-7.

The Authors

M. PRABHAKAR REDDY, M.D. is in private rehabilitation medicine practice in Reno, Nev., where he also serves as medical director of the comprehensive medical rehabilitation unit at Saint Mary's Regional Medical Center. Dr. Reddy graduated from the Kakatiya Medical College of Osmania University, India, and completed a residency in physical medicine and rehabilitation at New York Medical College, New York City.

VINAY REDDY, M.D. is a resident in internal medicine at the University of Nevada School of Medicine, Reno, where he also earned his medical degree.

COPYRIGHT 1997 American Academy of Family Physicians
COPYRIGHT 2004 Gale Group

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