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)

A new antidepressant, amoxapine, which is a dibenzoxazepine deprivative, was compared with amitriptyline in a randomised double-blind trial. Forty-eight patients were included and 41 completed a 4-week treatment. Most of the patients were maintained on 150 mg daily. Assessments were made by the Hamilton Psychiatric Rating Scale for Depression (HAM-D), Nurses' Observation Scale for Inpatient Evaluation (NOSIE), Clinical Global Impression (CGI) scale and Patient's Self-Evaluation. The total HAM-D score was considerably reduced in the majority of the patients. Amitriptyline was the most effective with regard to symptoms included in the factor Sleep Disturbances and-secondary maybe-towards some items included in the factor Somatization. For the remaining items,including the items of the factors Anxiety/Depression and Apathy, the last score was lower in the amoxapine group than in those treated with amitriptyline. Among the unipolar cases the amoxapine treated patients were more satisfied with regard to efficacy (P = 6.3%). The frequency of side effects such as tremor and dizziness was considerably lower in the amoxapine group. In total, the side effects lasted longer in the amitriptyline group. We conclude that amoxapine seems to be an effective antidepressant with a low frequency of side effects.
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PMID:Amoxapine versus amitriptyline in endogenous depression. A double-blind study. 38 Feb 69

Animal data indicate that serotonin (5-HT) is a major neurotransmitter involved in the control of numerous central nervous system functions including mood, aggression, pain, anxiety, sleep, memory, eating behavior, addictive behavior, temperature control, endocrine regulation, and motor behavior. Moreover, there is evidence that abnormalities of 5-HT functions are related to the pathophysiology of diverse neurological conditions including Parkinson's disease, tardive dyskinesia, akathisia, dystonia, Huntington's disease, familial tremor, restless legs syndrome, myoclonus, Gilles de la Tourette's syndrome, multiple sclerosis, sleep disorders, and dementia. The psychiatric disorders of schizophrenia, mania, depression, aggressive and self-injurious behavior, obsessive compulsive disorder, seasonal affective disorder, substance abuse, hypersexuality, anxiety disorders, bulimia, childhood hyperactivity, and behavioral disorders in geriatric patients have been linked to impaired central 5-HT functions. Tryptophan, the natural amino acid precursor in 5-HT biosynthesis, increases 5-HT synthesis in the brain and, therefore, may stimulate 5-HT release and function. Since it is a natural constituent of the diet, tryptophan should have low toxicity and produce few side effects. Based on these advantages, dietary tryptophan supplementation has been used in the management of neuropsychiatric disorders with variable success. This review summarizes current clinical use of tryptophan supplementation in neuropsychiatric disorders.
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PMID:L-tryptophan in neuropsychiatric disorders: a review. 130 30

The aim of this study was to evaluate the safety of zimeldine, a 5-HT reuptake inhibitor, in the long-term treatment of depressive disorders. The study was an open label, multicentre investigation involving 147 patients who were suffering from depressive illness and who needed long-term anti-depressant treatment. Sixty-five patients completed the intended treatment period of 1 year, 75 terminated prematurely, and 7 are still in the programme. The reasons for termination were mainly ineffectiveness of the drug and adverse reactions. During the long-term treatment the most common emergent symptoms were, in order of decreasing frequency, dizziness, dry mouth, sleep disorders, sweating, tremor, nausea and headache. The side-effects were, however, mild and they generally decreased during the treatment period. No new adverse symptoms were reported. In the long-term treatment group, body weight showed a slight mean decrease. Clinical chemistry and cardiovascular investigations were judged to show no changes of clinical importance. It is concluded that zimeldine was shown to be a safe drug in this 1-year treatment programme of depression.
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PMID:The safety of zimeldine in long-term use in depressive illness. 623 Aug 89

In a controlled clinical inpatient trial (n = 93) comparing the efficacy and safety of brofaromine versus tranylcypromine for 6 weeks in treatment-resistant major depressed patients, the two drugs were found to be of comparable afficacy and tolerability. The response rate (a 50% reduction) on the Hamilton Scale for Depression (HAMD) in both groups was about 73%. The most common side effects in the brofaromine group were sleep disorders, hypotension, tremor and dryness of mouth; and in the tranylcypromine group sleep disorders, fatigue, hypotension, tremor and vertigo. Methodological and practical clinical implications of the results are discussed.
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PMID:Brofaromine in treatment-resistant depressed patients--a comparative trial versus tranylcypromine. 800 47

Geniospasm is a hereditary disorder characterized by episodic, usually stress-induced involuntary trembling of the chin. Nineteen families from Europe and the U.S.A. suffering from this disorder have been described since 1894. We present three cases from two newly detected families. There was no evidence of any other nervous system abnormality, although abnormal EEG, sleep disorders, and involvement of other facial muscles have been described in rare cases. Geniospasm is transmitted as an autosomal-dominant trait with high penetrance. It must be differentiated from facial myokymia, palatal tremor, and essential tremor affecting facial muscles. Neurophysiological and molecular mechanisms of this peculiar disorder are unknown.
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PMID:Geniospasm: hereditary chin trembling. 834 Dec 98

Amyloid deposits in leptomeningeal vessels, subarachnoid, subpial, and subependymal cerebrospinal regions, spinal ganglia, peripheral nerves, and some internal organs (predominantly heart and kidney) characterize a dominantly inherited disease in a Hungarian family. We found four definitely and three probably affected members in this family of 56 persons in four generations. Clinical features in all definitely diseased patients include disturbance of memory, psychomotor deceleration, ataxia, and hearing loss. In most patients there was temporary disorientation, migraine-like headache with vomiting, and tremor. Some patients had nystagmus, pyramidal signs with spastic paraparesis, hallucinations, urinary retention, and obstipation. Single patients had facial tics and sleep disorders. Progressive visual disturbance and clinically manifest polyneuropathy were absent. CSF protein was markedly elevated in all patients. CT showed characteristic symmetric calcification along the sylvian fissure; MRI after contrast administration showed prominent enhancement at the surface of the sylvian fissures, brainstem, and cerebellum. Autopsy data was available in three definitely affected patients and in one unaffected family member. Immunohistochemistry identified the amyloid deposits as of the AF (transthyretin, TTR) type; DNA studies revealed a novel TTR missense mutation at codon 18 (TTR Asp18Gly). According to clinical features, pathologic alterations, and molecular studies, this disease is a novel type of systemic familial amyloidosis with disease manifestation clinically restricted to the CNS. It is similar to the oculoleptomeningeal amyloidoses but can be clinically diagnosed by characteristic CTs and the absence of progressive visual impairment.
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PMID:Familial meningocerebrovascular amyloidosis, Hungarian type, with mutant transthyretin (TTR Asp18Gly) 896 Jul 46

The authors prospectively assessed symptoms induced by the interruption of antidepressants in 16 patients (11 women and 5 men), aged from 33 to 85 years (mean = 52.4 +/- 16.4), treated with antidepressants since at least two weeks. All patients were free of alcohol abuse or dependence disorder and of other dependence to psychoactive substances. None of them presented medical illness. Diagnosis were made by separate evaluations by two authors and confirmed with a semistructered assessment instrument: the Schedule for Affective Disorders and Schizophrenia (Lifetime Version). All patients were submitted to a brutal discontinuation of their antidepressant agent. Patients were assessed twice, before the interruption of the antidepressant, and 72 hours later. Effects of antidepressant interruption were assessed by several means. Modification of anxiety and depression were evaluated using the Montgomery Asberg Depression Rating Scale (MADRS) and the Hamilton Anxiety Scale. Symptoms of withdrawal were assessed with Cassano and al.'s scale SESSH including an evaluation of anxiety, agitation, irritability, anergy, difficulty on concentrating, depersonalization, sleep and appetite disorders, muscle pains, nausea, tremor, sweating, altered taste, hyperosmia, paresthesias, photophobia, motor incoordination, dizziness, hyperacousia pain, delirium. Fourteen of the 16 patients (87.5%) presented modifications of their somatic or psychic state 3 days after the interruption of the antidepressant treatment. Most frequent symptoms were: increase in anxiety (31%), increase in irritability (25%), sleep disorders (19%), decrease of anergia and fatigue (19%). Mean scores of anxiety and depression were not significantly modified by the withdrawal. Following TCAs interruption (7 patients) most frequent symptoms were sleep disorders; increase in anxiety, nausea. Among patients withdrawn from SSRIs (6 patients), most frequent symptoms were increase in anxiety, increase in irritability, headache. Patients also presented a decrease of nausea, and of anorexia.
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PMID:[Prospective evaluation of antidepressant discontinuation]. 969 14

Gamma-hydroxybutyrate (GHB), a compound found in the mammalian brain, meets many criteria of a neurotransmitter. Experimentally, GHB has been used as a model for petit mal epilepsy; clinically it has been used as a general anaesthetic, to treat certain sleep disorders and alcoholism. Lately GHB has been abused for its euphoric, sedative and anabolic effects. Coma and seizures following abuse of GHB have been reported, but dependency has received little attention. Adverse effects of GHB include seizure activity and a withdrawal syndrome characterised by insomnia, anxiety and tremor. The present paper reviews the neuropharmacology, potential therapeutic uses and acute adverse effects of GHB, together with a presentation of three cases.
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PMID:[Gamma-hydroxybutyrate--an endogenous substance and an intoxicant]. 988 13

Patients suffering from Parkinson's disease (PD) often report about sleep disorders and excessive daytime sleepiness. To some extent, motor disabilities or neural degeneration of sleep modulating structures may be responsible for these effects. Depressive disorders also contribute to the occurrence of insomnia and daytime sleepiness. Nevertheless, dopaminergic, anticholinergic, and other drugs used in PD have a great impact on sleep/wakefulness mechanisms. They may indirectly improve or worsen sleep by changing motor symptoms such as akinesia, hyperkinesia, or tremor. Although their is only little information on the complex regulation of vigilance, it is well known that monoaminergic and cholinergic drugs could influence it directly. Data from animal experiments and clinical experiences led to the hypothesis of a biphasic influence on sleep by dopaminergic substances: small doses of L-Dopa e. g. appear to improve sleep whilst higher doses led to insomnia. Different dopaminergic receptor types or changes in receptor sensitivity may explain these phenomena. Dopaminergic and anticholinergic drugs suppress REM sleep. Recently, initial data on 'sleep attacks' after pramipexole or ropinirole treatment were published. Our preliminary results using 24 h polygraphic recordings showed excessive daytime sleepiness in patients taking ropinirole and L-Dopa which disappeared when changed to ropinirole monotherapy. Sleepiness did never appear as an irresistible attack. Current hypotheses on this topic are reviewed.
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PMID:Effects of parkinsonian medication on sleep. 1119 13

During the wake-sleep transition and sleep, diverse motor phenomena such as hypnagogic foot tremor may occur in the lower extremities. We investigated the relevance of this phenomenon in 375 consecutive subjects examined polysomnographically in a sleep disorders center. Rhythmic feet movements while falling asleep (RFM) were found in 28 subjects (7.5%). RFM occurred mostly as single, short series with a duration of between 10 and 15 seconds. They had a high night-to-night variability and were detected as rhythmic, oscillating movements of the whole foot or toes. Surface electromyographic (EMG) recordings displayed series of repetitive phasic bursts with a periodicity mostly between 1 and 2 per second. Single EMG burst duration varied between 300 and 700 msec. RFM at highest intensity occurred during presleep wakefulness, and usually persisted in sleep stages 1 and 2. RFM did not have a major sleep-disturbing effect in any of the affected subjects. Due to its high prevalence and the lack of a major sleep-disturbing effect, short series of RFM could be considered a quasiphysiological phenomenon. However, in more severe forms of RFM with evidence of a sleep-disturbing effect, RFM should be considered abnormal.
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PMID:Rhythmic feet movements while falling asleep. 1174 54


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