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)

Four age groups of healthy men; 20-29, 30-39, 40-49, and 50-59 years (N = 12 per group), drank 0.68 g of ethanol/kg body weight as neat whisky in the morning after an overnight (10 hr) fast. The concentration of ethanol in fingertip blood, various signs and symptoms of intoxication, body-sway (open and closed eyes), hand-tremor, positional alcohol nystagmus (PAN) and roving ocular movements (ROM) were measured at 30-60 min intervals after drinking. Body-sway and hand-tremor increased with advancing age in tests made before the ingestion of alcohol (P < 0.05). After drinking alcohol, body-sway and hand-tremor increased in the four age groups (P < 0.05), being most pronounced at or near the time of reaching the peak blood alcohol concentration (BAC). The initial impairment subsided when the post-absorptive phase of ethanol kinetics commenced. At 60 min post-drinking, body-sway was most pronounced in men aged 40-49 years when their eyes were closed (P < 0.05). Otherwise, age-related differences in alcohol impairment in the other age groups were not statistically significant. Positional alcohol nystagmus (PAN) developed mainly during the acute phase of intoxication, decreasing in intensity as the time after drinking progressed. Roving ocular movements (ROM) were most apparent during the post-absorptive phase (120-420 min). We conclude that the acute effects of a moderate dose of ethanol on sensory and motor functions are not much different in men aged between 20 and 59 years.
Alcohol Alcohol 1994 Mar
PMID:Age-related differences in the effects of ethanol on performance and behaviour in healthy men. 808 May 98

We examined 678 essential tremor patients in specialty, university, and private practice clinics. The mean age of patients was 65.2 years with a similar number of men and women. Six percent of patients were left-handed. A positive family history of tremor was reported in more than 60% of patients. Alcohol ingestion was reported to decrease tremor in 74% of patients who were cognizant of the effect of alcohol on tremor. Mean age at tremor onset was 45.3 years. An earlier onset of tremor was observed in those patients having a positive family history of tremor. Tremor affected the hands in 90% of patients, head in 50%, voice in 30%, and legs and chin in 15%. Functional disability was common and impairment at work occurred in 18%. Propranolol and primidone were the most frequently used drugs and were effective in 40% of patients. Six and one-tenth percent of essential tremor patients had concomitant Parkinson's disease, 6.9% had a coexisting dystonia, and 1.8% had myoclonus. It is concluded that the frequency of Parkinson's disease in essential tremor is more than would be reported in the general population and that other movement disorders are infrequently observed in essential tremor.
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PMID:The relationship of essential tremor to other movement disorders: report on 678 patients. Essential Tremor Study Group. 821 Feb 29

Alcohol withdrawal delirium (AWD) requires treatment with an adequate sedative, anticonvulsant, and antipsychotic agent next to general intensive care measures. Optimal medication should have a rapid onset of action and the possibility of parenteral application. A specific antagonist should be available. Flunitrazepam is a benzodiazepine that fulfills all these criteria. Twenty five patients suffering from AWD (mean age 45 years) took part in an open trial and underwent treatment with infusions of flunitrazepam (concentration: 8 mg/250 ml NaCl; speed, 250 ml/hr). Psychopathological, vegetative, and vital parameters were assessed every hour. All patients survived. They were treated with a mean total dose (SD) of 83.9 (45.4) mg of flunitrazepam (1.3 mg/kg body weight), which induced sedation 13.2 (5.3) min after the initiation of intravenous treatment. The mean duration of AWD (85.1 +/- 39.4 hr) corresponded to other studies, whereas the frequency of preexisting and concomitant diseases was higher (92%) in our patients. A patient who suffered from bronchitis and had a nasopharyngeal tamponade showed severe respiratory depression after having received 4 mg of flunitrazepam. This complication remitted immediately when 0.5 mg of flumazenil was given intravenously. No epileptic manifestation was observed during the treatment or after discontinuation of flunitrazepam. Vegetative and psychopathological symptoms (tremor, sweating, hallucinations, confusion, and restlessness) remitted rapidly. Our data suggest that intravenous flunitrazepam can be an efficacious and safe alternative to traditional treatment strategies of AWD.
Alcohol Clin Exp Res 1993 Aug
PMID:Intravenous flunitrazepam in the treatment of alcohol withdrawal delirium. 821 8

We reported two cases of acute alcoholic myopathy associated with rhabdomyolysis. The first case was 62 year-old man, who had been drinking every day for 40 years. Following diarrhea, he had psychic symptoms, and was admitted to our hospital. He was in a state of delirium. Tremor in extremities, dysarthria and weakness of lower extremities were observed. Neither swelling nor grasping pain were seen in any muscles. Laboratory data showed severe hypokalemia and high levels of serum muscle enzymes and myoglobin. An increase of lactate and pyruvate was not seen in ischemic exercise test performed at the acute or the recovery phase. It was suggested that glycolysis in muscles was suppressed in this case. The second case was 43 year-old man, who had been drinking every day for 27 years. Rapidly progressive weakness of both lower extremities was seen, and he was admitted to our hospital. Grasping pain of both legs and proximal muscle weakness of extremities were observed. Laboratory date showed normokalemia and high levels of serum muscle enzymes and myoglobin. Muscle biopsy showed no abnormal findings in histology and electron microscopy. Although the pathogenesis of acute alcoholic myopathy is unknown, suppression of muscle glycolysis enzyme caused by ethanol may play an important role in the first case.
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PMID:[Two cases of acute alcoholic myopathy associated with rhabdomyolysis]. 829 65

The concentration-time profiles of ethanol were determined for capillary blood, end-expired breath, and saliva after 21 healthy men ingested ethanol at 0.68 g/kg body weight. Near the time of obtaining body fluids, the volunteers estimated their feelings of intoxication, and body sway (with open and closed eyes), hand tremor, positional alcohol nystagmus (PAN), and roving ocular movements (ROM) were quantitatively recorded. The concentration-time profiles of ethanol in blood, breath, and saliva agreed well within individuals but there were large variations between subjects. The mean saliva-ethanol profiles ran slightly above those for blood and breath. Subjective ratings of intoxication and impairment of body function (standing steadiness and hand steadiness) were highest at the time of reaching the peak concentrations of ethanol in body fluids. PAN was evident in most subjects between 60 and 120 min after the start of drinking, whereas ROM appeared mainly during the postabsorptive phase of ethanol kinetics (120-420 min). The blood ethanol concentration thresholds were between 500 and 700 mg/L (50-70 mg/dL) when the diminished performance had recovered to baseline values.
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PMID:Pharmacokinetics of ethanol in saliva: comparison with blood and breath alcohol profiles, subjective feelings of intoxication, and diminished performance. 837 57

omega-Conotoxin and ethanol produce similar actions on in vitro calcium channel functions. The present study was designed to determine their possible behavioral interaction. omega-Conotoxin injected ICV at either 0.1 microgram or 0.3 microgram, produced an increase in spontaneous and evoked tremor activity in male Sprague-Dawley rats. The tremor was present at 30 min and continued at least 4 h after injection. At 4 h post ICV injection, animals were given an IP injection of ethanol (3 g/kg body weight). Although no blood alcohol differences were observed between groups, rats injected with omega-conotoxin showed a concentration-dependent increase in sleep times: Saline controls slept for an average of 84.7 +/- 16.7 min, 0.1 and 0.3 microgram conotoxin treated animals slept for 121.3 +/- 16.2 and 211.1 +/- 30.7 min, respectively. These results extend the class of calcium channel blockers capable of producing a behavioral interaction with ethanol.
Alcohol
PMID:Omega-conotoxin increases sleep time following ethanol injection. 844 94

Behavioral effects induced by 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT; i.e., lower lip retraction, flat body posture, and forepaw treading) were examined in rats during ethanol withdrawal following a 2-week period of access to a liquid diet containing 9% (v/v) ethanol. After an 18 h withdrawal period, tolerance to 8-OH-DPAT-induced flat body posture and, conversely, sensitization to the effects of 8-OH-DPAT on lower lip retraction were observed in the 9% ethanol group as compared to control rats fed an isocaloric diet. In contrast, 8-OH-DPAT-induced forepaw treading in the 9% ethanol group was not significantly different in comparison to control rats. Plasma corticosterone levels were significantly higher in the ethanol-exposed group than in control animals, an effect which was not additive with the increase in corticosterone levels normally observed after the administration of low doses of 8-OH-DPAT. Altered flat body posture and lower lip retraction responses to a submaximal dose of 8-OH-DPAT (2.5 mg/kg i.p.) were still observed as late as 3 days after withdrawal of the 9% ethanol liquid diet, but were no longer apparent at 7 days. Interestingly, prominent ethanol withdrawal signs such as tremor and rigidity, while occurring on the first day, were completely absent on the third day. Taken together, these results indicate that chronic ethanol exposure differentially alters sensitivity to several pharmacological effects of the 5-HT1A receptor ligand 8-OH-DPAT. They further support the involvement of 5-HT (5-hydroxytryptamine, serotonin) systems in alcohol abuse and therapeutic interventions using 5-HT1A ligands.
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PMID:Modification of behavioral effects of 8-hydroxy-2-(di-n-propylamino)tetralin following chronic ethanol consumption in the rat: evidence for the involvement of 5-HT1A receptors in ethanol dependence. 852 4

We used H2 15O positron emission tomography (PET) to investigate the effect of ethyl alcohol on regional cerebral blood flow in 6 patients with alcohol-responsive essential tremor and 6 age-matched control subjects. The patients were scanned while at rest and during involuntary postural tremor of the extended right arm. Normal control subjects were scanned at rest and during passive wrist oscillation of the right arm at tremor frequency. Regional cerebral blood flow associated with these conditions was measured before and after oral administration of 2 to 3 units of alcohol. The mean blood alcohol level was 35.3 +/- 20.0 mg/dl in the patient group and caused marked suppression of tremor; it was 33.9 +/- 12.9 mg/dl in the control group. Similar to previous PET studies on essential tremor patients, tremor compared with rest was associated with bilateral cerebellar activation including the cerebellar vermis. This pattern of activation differed from passive wrist oscillation where ipsilateral cerebellar activation was observed. Ethanol ingestion led to bilateral decreases of cerebellar blood flow in both tremor patients and normal subjects, and this was associated with suppression of tremor in the patients. Alcohol-associated increases of regional cerebral blood flow were observed in the inferior olivary nuclei in the patients but not in the control subjects. We conclude that alcohol-induced suppression of essential tremor is mediated via a reduction of cerebellar synaptic overactivity resulting in increased afferent input to the inferior olivary nuclei.
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PMID:The effect of ethanol on alcohol-responsive essential tremor: a positron emission tomography study. 900 8

A growing number of studies have implicated the hypothalamic-pituitary-adrenal (HPA) axis in acute and chronic alcoholization and in ethanol withdrawal. In order to study the ethanol/HPA axis interaction during alcohol withdrawal, we performed experiments using adrenalectomized (ADX) male rats alcoholized by a chronic pulmonary alcoholization procedure. Eight hours after the 3 weeks of the alcoholization procedure, the rats were evaluated for a tremor activity. In order to reduce the great variability of the withdrawal tremors, we estimated the supersensitivity of the withdrawn rats to the tremorogenic compound harmine. We also studied the effect of a hydrocortisone treatment given in the drinking bottle during the alcoholization procedure on the harmine-induced tremors of ADX and sham rats. Alcohol withdrawal resulted in increased tremor response to 10 mg/kg harmine, and a protective effect of adrenalectomy on this effect was observed. Hydrocortisone administration to ADX or sham rats did not affect the tremor profile of the alcohol withdrawn rats.
Alcohol Alcohol 1996 Mar
PMID:Adrenalectomy protects ethanol-withdrawn rats from harmine-induced tremor. 873 13

Despite the existence of a well-defined abstinence syndrome in offspring of opiate-dependent mothers, the mechanisms involved in neonatal abstinence remain unclear. The goal of the present study was to determine the contribution of noradrenergic neurons in the opiate abstinence syndrome in neonatal rats (10 days old). First, the ability of the alpha 2-adrenergic agonist, clonidine to attenuate the symptoms of neonatal opiate abstinence precipitated by naloxone was determined. Secondly, the activity of noradrenergic neurons was determined by measuring postmortem levels of 3-methoxy-4-hydroxyphenylglycol (MHPG) in the hypothalamus, hippocampus and cortex in opiate-abstinent pups. Neonatal opiate abstinence was characterized by an increased incidence of wall climbing, tremors and mouthing. Acute treatment with morphine and naloxone in chronic saline-treated pups also produced the tremor, albeit less severe than in pups treated chronically with morphine. Clonidine (0.2 mg/kg) attenuated the expression of tremor and mouthing in neonates, but increased wall climbing. Clonidine elicited wall climbing in opiate-naive neonates. Treatment with morphine followed by naltrexone increased MHPG levels in all of the brain areas examined, irrespective of the chronic treatment, but naltrexone treatment elicited a larger increase in MHPG levels in pups treated chronically with morphine. Acute morphine treatment increased MHPG levels only in the hypothalamus. The results of the present study provide behavioral and neurochemical data supporting the hypothesis that noradrenergic hyperactivity plays a role in neonatal opiate abstinence.
Drug Alcohol Depend 1996 May
PMID:Role of noradrenergic hyperactivity in neonatal opiate abstinence. 879 9


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