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)

The effects of L-type calcium channel blockers and stimulants on naloxone-precipitated withdrawal in mice acutely dependent on morphine were evaluated. Verapamil (10-80 mg/kg), diltiazem (20-120 mg/kg) and nicardipine (20-160 mg/kg), when administered subcutaneously, produced a dose-dependent reduction in forepaw tremor and weight loss during the abstinence reaction; jumping was also reduced by all three drugs, although the effect was not statistically significant in the case of nicardipine. By contrast, the calcium agonist Bay K 8644 (0.5-2 mg/kg, SC) increased forepaw tremor and weight loss, although this latter effect did not reach statistical significance. The effects of the calcium channel active drugs on the rotarod test were also explored, no correlation appearing with the results observed in abstinence (except for the jumping response), which suggests that the withdrawal results are not influenced by motor incoordination or unspecific CNS depression. These findings suggest that L-type calcium channels probably play an important role in withdrawal after acute morphine dependence. Taken together with other observations in chronic models, these results show that calcium channels are similarly involved in morphine abstinence after acute and chronic dependence, in contrast to the differences in the content and uptake of neuronal calcium induced by morphine under both conditions.
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PMID:Differential effects of L-type calcium channel blockers and stimulants on naloxone-precipitated withdrawal in mice acutely dependent on morphine. 171 13

Psoroptes sp. mites were isolated from two llamas (Lama glama), a 4-mo-old male and its dam, in Washington. Mites were restricted to the ears and were responsible for head-shaking and incoordination. Infestations were treated successfully with a subcutaneous injection of ivermectin at 0.2 mg/kg of body weight and with 2 drops of ivermectin diluted in saline given topically in each ear. This is the first known report of Psoroptes sp. in llamas in the United States.
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PMID:Psoroptes sp. in two llamas (Lama glama) in Washington. 173 60

Systemic administration of the selective D1 antagonist, SCH 23390, caused significant motor changes in healthy African green monkeys. The effects included the parkinsonian signs of motor freezing, incoordination, bradykinesia, poverty of movement, tremor and depressed blink rate. SCH 23390 administered to MPTP-treated monkeys increased existing parkinsonism. The results are of particular interest in light of recent data that demonstrate the effectiveness of dihydrexidine, a full D1 agonist, in alleviating parkinsonism in MPTP-treated monkeys. These data implicate D1 receptors in the functions impaired by Parkinson's disease and suggest the possibility of parkinsonian side effects in the clinical use of this or similar D1 antagonists as treatments for psychiatric disorders.
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PMID:The D1 receptor antagonist, SCH 23390, induces signs of parkinsonism in African green monkeys. 183 30

Spasmodic dysphonia is a disturbance of phonation with laryngeal spasms. We report voice and neurologic examination findings in 45 subjects. Neurologic abnormalities were found in 32 subjects (71.1%). Rapid alternating movement abnormalities, weakness, and tremor were common. Incoordination and spasticity were rare. Lower extremity findings were frequent. Abnormalities were bilateral. Spasmodic dysphonia severity was related to age. Type, severity, and duration of vocal symptoms were not different for subjects with or without neurologic abnormalities. Vocal tremor was more frequent in neurologically abnormal subjects. Involvement of a pallidothalamic-supplementary motor area system could account for neurologic findings, brain imaging findings, and clinical heterogeneity. The view emerging is that spasmodic dysphonia is a manifestation of disordered motor control involving systems of neurons rather than single anatomical sites.
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PMID:Heterogeneity in spasmodic dysphonia. Neurologic and voice findings. 200 Nov 89

This study presents the main clinical findings on 200 AIDS patients at Kilimanjaro Christian Medical Centre in the northern zone of Tanzania, with detailed neurological findings on 135 out of 200 cases and 53 controls. Results show that 21 out of 200 (10.5%) had an obvious focal neurological disorder, including cranial nerve palsies, hemiparesis and paraparesis. Ninety-seven out of 135 (72%) had less obviously detectable neurological disorders, versus 36% of controls (P less than 0.005). Most frequent were AIDS dementia complex (54%), retinopathy (23%), areflexia (21%), pyramidal tract signs (19%) and tremor and incoordination (19%). Frontal lobe release signs (FLRS) were found in 103 out of 135 (76%) patients, versus 36% of controls (P less than 0.005). Advanced and terminal AIDS cases were more likely to have neurological disorders than early AIDS patients. A further study on 87 non-AIDS patients with acute unexplained neurological disorders showed 10 out of 87 to be HIV seropositive. Three case studies are presented. This study suggests that neurological disorders are among the main clinical features of AIDS and HIV disease in Africa.
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PMID:Neurological disorders in AIDS and HIV disease in the northern zone of Tanzania. 250 33

Sixty-four outpatients with major affective disorder according to DSM-III and on continuous lithium treatment for an average duration of 7.8 years were first investigated in 1980 and then followed for 7 years. The predictive value of patients' attitudes to their lithium, the prognostic influence of psychiatric status, side effects, and anamnestic and laboratory data including lithium parameters were studied. At the end of the 7-year follow-up, 61% of the patients were still on lithium maintenance treatment, 25% had discontinued lithium for clinical reasons, and 14% of the patients had died. Side effects of lithium were the major clinical reason for discontinuing treatment, while attitudes towards medication were of minor importance. Approximately one fourth of the patients who discontinued lithium were differentiated from those who continued treatment by showing a high frequency of the neurologic side effects incoordination, paresthesia, and disturbed sensibility in addition to having more severe tremor. In yet another fourth of those who discontinued for clinical reasons, lithium was stopped by the treating psychiatrist as maximal urine osmolality values were considered to be too low. These patients did not show any signs of clinically significant impairment of renal functions. Their psychiatric status was excellent in terms of extremely low CPRS scores. The patients who died during the follow-up period were differentiated from those who continued treatment by a much higher frequency of alcohol and drug abuse prior to the initiation of lithium therapy. The total number of side effects and the number of severe side effects were significantly larger than in continuers on lithium. The most common causes of death were cardiovascular disease and suicide. In no case was the cause of death attributed to lithium therapy.
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PMID:Factors associated with discontinuation of long-term lithium treatment. 251 Apr 58

Tremorgenic mycotoxins are fungal secondary metabolites with a specific effect on the central nervous system (CNS). Except for a few toxins that are produced by Claviceps paspali, a plant parasitic fungus, most tremorgenic mycotoxins are synthesized by common saprophytic moulds of the genera Penicillium and Aspergillus. Since these compounds produce sustained tremor in the abscence of other neurotoxic effects, several authors have suggested that they are the causative agents of a number of naturally occurring incoordination syndromes in ruminants. The nature of the tremor produced by these compounds in laboratory animals is clinically indistinguishable from that occurring naturally. In particular, the most implicated tremorgenic mycotoxins are those that contain a single nitrogen atom in their molecules. Although individual compounds within this group are produced by unrelated fungal species, they all contain a similar biologically active chemical moiety. To date, their mechanism of action is unknown, and their role in neuropharmacology has not yet been defined. However, the presence of a GABA-like conformation within their active nucleus and the limited torsional flexibility of this moiety suggest that they are partial agonists of GABA (gamma-aminobutyric acid). A hypothetical mode of action of these toxins at the GABA receptor sites is presented and discussed.
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PMID:Fungal tremorgens: the mechanism of action of single nitrogen containing toxins--a hypothesis. 269 1

Three patients from two families had an unusual phenotypical variant of late-onset hexosaminidase-A deficiency. The clinical picture was dominated by spinal motor neuron involvement mimicking juvenile-onset spinal muscular atrophy. Atypical features included prominent muscle cramps, postural and action tremor, recurrent psychosis, incoordination, corticospinal and corticobulbar involvement, and dysarthria. The presence of these atypical features in patients whose lower motor neuron involvement would otherwise be consistent with juvenile-onset spinal muscular atrophy should raise the suspicion of the presence of hexosaminidase-A deficiency and GM2 gangliosidosis that can be proved by appropriate enzyme assays.
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PMID:Hexosaminidase-A deficiency presenting as atypical juvenile-onset spinal muscular atrophy. 293 15

Ethanol, a highly lipid-soluble compound, appears to exert its effects through interactions with the cell membrane. Cell membrane alterations indirectly affect the functioning of membrane-associated proteins, which function as channels, carriers, enzymes and receptors. For example, studies suggest that ethanol exerts an effect upon the gamma-aminobutyric acid (GABA)-benzodiazepine-chloride ionophore receptor complex, thereby accounting for the biochemical and clinical similarities between ethanol, benzodiazepines and barbiturates. The patient with acute ethanol poisoning may present with symptoms ranging from slurred speech, ataxia and incoordination to coma, potentially resulting in respiratory depression and death. At blood alcohol concentrations of greater than 250 mg% (250 mg% = 250 mg/dl = 2.5 g/L = 0.250%), the patient is usually at risk of coma. Children and alcohol-naive adults may experience severe toxicity at blood alcohol concentrations less than 100 mg%, whereas alcoholics may demonstrate significant impairment only at concentrations greater than 300 mg%. Upon presentation of a patient suspected of acute ethanol poisoning, cardiovascular and respiratory stabilisation should be assured. Thiamine (vitamin B1) and then dextrose should be administered, and the blood alcohol concentration measured. Subsequent to stabilisation, alternative aetiologies for the signs and symptoms observed should be considered. There are presently no agents available for clinical use that will reverse the acute effects of ethanol. Treatment consists of supportive care and close observation until the blood alcohol concentration decreases to a non-toxic level. In the non-dependent adult, ethanol is metabolised at the rate of approximately 15 mg%/hour. Haemodialysis may be considered in cases of a severely ill child or comatose adult. Follow-up may include referral for counselling for alcohol abuse, suicide attempts, or parental neglect (in children). The ethanol withdrawal syndrome may be observed in the ethanol-dependent patient within 8 hours of the last drink, with blood alcohol concentrations in excess of 200 mg%. Symptoms consist of tremor, nausea and vomiting, increased blood pressure and heart rate, paroxysmal sweats, depression, and anxiety. Alterations in the GABA-benzodiazepine-chloride receptor complex, noradrenergic overactivity, and hypothalamic-pituitary-adrenal axis stimulation are suggested explanations for withdrawal symptomatology.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute ethanol poisoning and the ethanol withdrawal syndrome. 304 Dec 44

The establishment of, and sex differences in, physical dependence on methaqualone (MQ) in rats were studied by the drug-admixed food (DAF) method. Female and male rats were treated with MQ-admixed food on the same schedule of gradually increasing doses (0.5 and 1 to 6 mg of methaqualone/g of food). Only female rats showed hypothermia from MQ at 1 and 2 mg/g and motor incoordination from MQ at 4 and 6 mg/g of food. Moreover, after MQ withdrawal, severe withdrawal signs, including convulsions and death, were observed in female rats, but not in male rats. We also instituted a different schedule of graded increases in dose (1 and 2 to 10 and 12 mg/g of food) to develop physical dependence on MQ in male rats. Under this schedule male rats exhibited a hypothermia and severe motor incoordination from MQ 6 and 8 mg/g of food condition. After MQ withdrawal, various severe signs of MQ withdrawal occurred, including tremor, convulsions and death. These results demonstrate that severe physical dependence on MQ in both sexes can be established using the DAF method, and that there are marked sex differences in the physical dependence on MQ.
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PMID:Sex differences in physical dependence on methaqualone in the rat. 317 79


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