Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some of the symptoms and signs of hypothyroidism and hyperthyroidism in elderly patients may be mistakenly attributed to "old age." Weight loss, muscle weakness, tremor, angina, congestive heart failure--all signs of hyperthyroidism--are also concomitants of aging. Fatigue, sluggishness, withdrawal behavior, senile atrophic skin changes--all signs of hypothroidism--are also a part of the normal aging process. Although screening elderly people for thyroid disease is economically unsound, the physician should maintain a high index of suspicion of its presence. Laboratory tests must be interpreted with extra care. Values of 131I uptake, serum T4 and T3, thyroid-stimulating hormone, and thyrotropin-releasing hormone are all helpful in diagnosis. Thyroid disease is easily treated in elderly patients, and results often are dramatic. Propranolol is effective in thyrotoxic patients when symptoms require prompt relief. The definitive treatment, however, is 131I; antithyroid drugs are difficult to manage. Hypothyroidism is easily treated with T4.
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PMID:How thyroid disease presents in the elderly. 2 76

Two patients had ocular myasthenia gravis coexistent with Hashimoto's thyroiditis. A 37-year-old woman presented with diplopia and displayed a head tremor and thyroid enlargement. Thyroid function tests showed an elevated thyroid stimulating hormone (TSH). A quantitative Tensilon test yeilded a "perverse" response and a needle biopsy indicated Hashimoto's disease. A 26-year-old woman presented with diplopia and subsequently developed blepharoptosis and thyroid enlargement. Examination revealed Cogan's eyelid twitch sign, a paradoxical quantitative Tensilon test, and laboratory studies revealed normal thyroid function tests. Treatment was directed at each disease entity separately. Ocular myasthenia gravis was managed with an anticholinesterase agent in combination with oral corticosteroids that provided additional control. Suppressive therapy with desiccated thyroid hormone reduced the size of the thyroid gland, diminished the signs and symptoms of hypothyroidism, and lowered the levels of TSH, possibly decreasing the risk of thyroid carcinoma. Both patients showed gratifying responses to therapy.
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PMID:Ocular myasthenia gravis and Hashimoto's thyroiditis. 117 40

A 42-year-old woman who presented phenytoin intoxication induced by acute hypothyroidism was reported. She had a 29-year history of hypothyroidism and a 18-year history of epilepsy. She was treated with phenytoin (PHT) 100 mg, mephobarbital (MPB) 200 mg, valproic acid (VPA) 400 mg and thyroid powder 100 mg daily for 2 years. She had no medical problem until she noticed gait disturbance and diplopia which appeared 1 month after sudden withdrawal of thyroid powder. On admission, she was somnolent and somewhat disoriented. She had nystagmus in horizontal direction of gaze. Her speech was slurred and she could not sit nor stand due to trunkal ataxia. There was prominent intentional tremor in finger-nose test and heel-shin test showed severe ataxia. Blood cell count and blood chemistry examinations were normal. Serum PHT, phenobarbital (PB) levels were elevated as to 26.4, 36.4 micrograms/ml, respectively. VPA level was low. The endocrinological examinations revealed primary hypothyroidism. EEG showed generalized slow background, but cranial MRI, EMG, SEP and ECG were normal. Thyroxine (T4) administration was started soon, and in the course of thyroid hormone replacement, her cerebellar symptoms gradually improved and serum PHT level decreased even to the subtherapeutical level with the same amount of antiepileptic drugs treatment. By the 40th day of admission, thyroid function became normal and cerebellar signs disappeared, however, she needed 200 mg PHT daily to obtain good control of epilepsy. Cerebellar symptoms of this patient were thought to be PHT intoxication rather than ataxia caused by hypothyroidism itself from the viewpoint of clinical manifestations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of phenytoin intoxication induced by hypothyroidism]. 193 66

Associations between hyperthyroidism and Parkinson disease have been reported. The treatment of the hyperthyroid state seems to improve the extrapyramidal symptomatology. We report a case of a woman suffering from Parkinson disease and hypothyroidism. The treatment with thyroxine increased parkinsonian tremor. Dopamine regulation of TSH circadian and pulsatile release is not clear. These observations stress the possible role of thyroid hormones in regulating dopaminergic metabolism.
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PMID:[Dysthyroidism and Parkinson's disease]. 222 22

Amiodarone is a powerful anti-arrhythmic drug. However, its use is somewhat limited by side-effects. No study examining side-effects specifically in elderly patients exists. We have reviewed noncardiac side-effects in 61 elderly patients on long-term oral amiodarone treatment (follow-up 3-66 months). The most troublesome side-effect was hypothyroidism (nine patients, 15%). No cases of frank hyperthyroidism were seen. Elevation of aspartate transaminase (AST) was common (16 patients, 26%), but generally mild and transient. Photosensitivity occurred in six patients (10%). Corneal deposits were common but gave rise to symptoms in only one patient. Two patients reported tremor. Hypothyroidism appeared to be more common and photosensitivity less common than in previously reported series in younger adults. Possible reasons for this are discussed. It is our policy to continue to prescribe amiodarone to elderly patients, regulate monitoring for adverse effects is however mandatory.
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PMID:Noncardiac side-effects of long-term oral amiodarone in the elderly. 336 37

With the increasing use of amiodarone, several unwanted effects have been recognized. We reviewed 140 patients treated with amiodarone over a 5-year period in an attempt to identify patients at risk, to assess the incidence of these effects and their possible relation to dose, and to determine their outcome. The most common effect was photosensitivity (57% of patients responding to a questionnaire), whereas asymptomatic corneal microdeposits were found in all patients undergoing ophthalmologic examination. In contrast, symptomatic eye changes (colored halos) and slate-gray skin pigmentation were rare. Of the metabolic alterations, the rise in hepatic enzymes correlated with dose and plasma drug and metabolite concentrations (r = 0.59, p less than 0.001; r = 0.62, p less than 0.001, respectively) but was not associated with clinical disease. This relation to dose was not evident in patients developing clinical thyroid abnormalities (two hypothyroidism, two hyperthyroidism), all of whom had normal thyroid function prior to therapy. Four of the five hypothyroid patients were over 70 years of age. No patients developed peripheral neuropathy, but tremor and sleeplessness were common complaints (30% and 28% of patients, respectively) that responded to a decrease in dose. One patient with an abnormal chest x-ray film prior to therapy developed pulmonary fibrosis. We suggest the restricted use of high doses of amiodarone for protracted periods. Patients at particular risk are the older age group (hypothyroidism) and those with abnormal lung function prior to therapy who may be predisposed to pulmonary alveolitis. Most of the observed unwanted effects resolve when amiodarone is decreased in dose or discontinued.
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PMID:Side effects and possible contraindications of amiodarone use. 661 38

In a recent paper (Barbeau and Pourcher, 1982) we demonstrated that so-called "idiopathic" Parkinson's disease is not a homogeneous entity, and defined the existence of a sub-group of patients with genetic parkinsonism. To investigate this last possibility, and to uncover possible metabolic clues as to the etiology of such cases, we carried out a prospective study of 50 kindreds with "familial" parkinsonism. Two control groups were similarly studied: 50 kindreds with essential tremor (neurological control group) and 50 kindreds originating from spouses of the previous patients (non neurological control group). We uncovered two main patterns of genetic transmission within the parkinsonian patients: a parkinsonism related to dominant essential tremor (34 kindreds; 10% of all Parkinsonians) and a recessive "akineto-rigid syndrome" (10 kindreds; 3-4% of all Parkinsonians). A further 4 kindreds assumed a pseudo-dominant pattern but were probably recessive. Finally 2 kindreds were obviously other entities presenting as "phenocopies" of Parkinson's disease. Metabolically, hyperthyroidism appeared to be more frequent in essential tremor and "essential-tremor related parkinsonism" kindreds, while hypothyroidism and possibly hypoparathyroidism (post surgery) seemed more frequent in the recessive akineto-rigid syndrome kindreds.
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PMID:A prospective study of 50 cases of familial Parkinson's disease. 683 26

For decades, the preparation of a hyperthyroid patient for surgery took several weeks or months utilizing thyroid blocking agents and iodine. In 1973, a preliminary report of 20 patients with hyperthyroidism treated with propranolol and thyroidectomy was presented. It was found that a thyrotoxic patient could be prepared for surgery, in an emergency, by intravenous propranolol in less than an hour, or electively by oral propranolol within 24 hours. Since then, 140 additional patients have been similarly treated. It continues to be true at this institution that propranolol, a beta-adrenergic blocking agent, effectively neutralizes the symptoms of autonomic hyperactivity, including sweating, tremor, fever, dilation of blood vessels, and increased pulse rate without significantly affecting thyroid function. An average dose of 160 mg/day was used, with a range of 40 to 320 mg/day. In none of these patients was iodine used; in fact, its use with propranolol is considered unnecessary. A subtotal, near total, or total thyroidectomy was done in all patients, resulting in a 55% incidence of hypothyroidism. There was no postoperative thyroid storm, nerve injury, or permanent hypoparathyroidism. It is believed that the administration of propranolol alone provides a rapid, safe, and effective preparation of the thyrotoxic patient for thyroidal or extrathyroidal surgical procedures during the perioperative period.
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PMID:Propranolol and thyroidectomy in the treatment of thyrotoxicosis. 708 68

This is the first reported case of dystonia with a partial deletion of the long arm (q) of chromosome 18. Neurologic findings in the 18q- syndrome include mental retardation, seizures, nystagmus, incoordination, tremor, and chorea. A 36-year-old woman with an 18q terminal deletion [karyotype 46,XX,del(18)(q22.2)] had hypothyroidism, diabetes mellitus, borderline intelligence, short stature, short neck, sensorineural hearing loss, and sensorimotor axonal neuropathy. Parents' karyotypes were normal. She had had incoordination and writing difficulty since childhood. Posturing and tremor of the head began at age 16, followed by arm tremors. She had jaw deviation and tremor, neck tremor with retrocollis, involuntary pronation of the right arm, coarse postural and severe action tremor, and tight pen grip with dystonic wrist extension on writing. The 18q- syndrome should be added to the list of genetic causes of secondary dystonia. A karyotype analysis should be considered in secondary dystonias, particularly when there are associated features such as short stature and endocrinopathies.
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PMID:Dystonia in a patient with deletion of 18q. 756 32

Lithium is the recommended treatment for the prophylaxis of bipolar affective disorder. The drug is also effective in the prophylactic treatment of recurrent unipolar depression, although many psychiatrists prefer to use antidepressant drugs for this indication. The efficacy of lithium is well established in the short term treatment of mania, although neuroleptic drugs are required at the start of treatment for more severely disturbed patients. Lithium augmentation of antidepressant drugs is increasingly popular for the treatment of resistant depression. It is now common practice to maintain serum lithium concentrations in the range 0.5 to 0.8 mmol/L, which is generally as effective as higher concentrations while reducing the incidence of adverse effects and intoxication. Some individuals may nevertheless require higher serum concentrations. Most adverse effects such as tremor and gastrointestinal upset are usually minor and often transient. There is no good evidence of nephrotoxicity with long term treatment, but persistent polyuria can occur. Hypothyroidism, with or without goitre, can occur uncommonly during long term lithium therapy. Prescribers should be alert to, and patients should be educated about, the predisposing factors and early symptoms relating to lithium intoxication. Specialist mood disorder clinics can facilitate safer and more effective lithium treatment.
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PMID:Lithium. Current status in psychiatric disorders. 769 9


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