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)

Risperidone is an antipsychotic drug used for the treatment of schizophrenia. It was expected that this atypical neuroleptic agent would not cause dystonia or neuroleptic malignant syndrome (NMS) owing to its unique mechanism of action with attenuated anti-dopaminergic activity and more potent antiserotoninergic activity. We report the case of a geriatric patient in whom signs and symptoms consistent with NMS developed after 3 weeks of risperidone therapy. The patient presented with fever, mental status changes, tremor, and rigidity. His laboratory findings were significant for increased serum creatine phosphokinase, hypernatremia, and metabolic acidosis. There have been few reported cases of risperidone-induced NMS. Health care providers should be aware of the risk of risperidone-induced NMS.
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PMID:Risperidone-induced neuroleptic malignant syndrome. 936 May 86

The purpose of this study was to assess the effects of an anticholinergic (trihexyphenidyl) antiparkinsonian medication on the Mini-Mental State Examination (MMSE) and the Cambridge Cognitive Examination (CAMCOG) scores in long-term institutionalized elderly patients with schizophrenia. Seventeen schizophrenic (DSM-III-R) inpatients on long-term medication who had received trihexyphenidyl for at least 6 consecutive months were compared for MMSE scores, CAMCOG scores, and other demographic and clinical variables with 14 patients not receiving any anticholinergic agent for the same time period. Results showed that age, years of education, illness duration, length of current hospital stay, the Manchester Scale scores, and chlorpromazine daily equivalent dose in mg were not different in the two groups compared. Extrapyramidal signs such as tremor, rigidity, and bradykinesia were more frequent in trihexyphenidyl receivers. The scores of MMSE (p < .007) and CAMCOG (p < .005) and CAMCOG subscales of orientation (p < .03), language (p < .01), and memory (p < .002) were significantly lower among trihexyphenidyl receivers, as was the Social and Occupational Functioning Assessment Scale score (p < .05). In addition, the MMSE and CAMCOG scores were significantly lower for patients receiving 10 mg of trihexyphenidyl a day compared with those receiving 5 mg/day and nonusers. It is suggested that trihexyphenidyl in usual clinical doses may impair total MMSE and CAMCOG scores as well as some of the CAMCOG subscales in this patient population. However, only a prospective study, preferably double-blind and controlled, with measures of change will validate this conclusion.
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PMID:Effects of trihexyphenidyl on MMSE and CAMCOG scores of medicated elderly patients with schizophrenia. 962 29

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

The aetiology and treatment of Parkinsonism is currently conceptualised within a dopamine (DA) deficiency-repletion framework. Loss of striatal DA is thought to cause motor impairment of which tremor, bradykinaesia and rigidity are prominent features. Repletion of deficient DA should at least minimise parkinsonian signs and symptoms. In Section 2, based on extensive pre-clinical and clinical findings, the instability of this approach to Parkinsonism is scrutinised as the existing negative findings challenging the DA deficiency hypothesis are reviewed and reinterpreted. In Section 3 it is suggested that Parkinsonism is due to a DA excess far from the striatum in the area of the posterior lateral hypothalamus (PLH) and the substantia nigra (SN). This unique area, around the diencephalon/mesencephalon border (DCMCB), is packed with many ascending and descending fibres which undergo functional transformation during degeneration, collectively labelled 'orphan neurones'. These malformed cells remain functional resulting in pathological release of transmitter and perpetual neurotoxicity. Orphan neurone formation is commonly observed in the PLH of animals and in man exhibiting Parkinsonism. The mechanism by which orphan neurones impair motor function is analogous to that seen in the diseased human heart. From this perspective, to conceptualise orphan neurones at the DCMCB as 'Time bombs in the brain' is neither fanciful nor unrealistic [E.M. Stricker, M.J. Zigmond, Comments on effects of nigro-striatal dopamine lesions, Appetite 5 (1984) 266-267] as the DA excess phenomenon demands a different therapeutic approach for the management of Parkinsonism. In Section 4 the focus is on this novel concept of treatment strategies by concentrating on non-invasive, pharmacological and surgical modification of functional orphan neurones as they affect adjacent systems. The Orphan neurone/DA excess hypothesis permits a more comprehensive and defendable interpretation of the interrelationship between Parkinsonism and schizophrenia and other related disorders.
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PMID:Orphan neurones and amine excess: the functional neuropathology of Parkinsonism and neuropsychiatric disease. 972 69

(5R,6R)6-(3-propylthio-1,2,5-thiadiazol-4-yl)-1-azabicyclo[3 .2.1]octane (PTAC) is a potent muscarinic receptor ligand with high affinity for central muscarinic receptors and no or substantially less affinity for a large number of other receptors or binding sites including dopamine receptors. The ligand exhibits partial agonist effects at muscarinic M2 and M4 receptors and antagonist effects at muscarinic M1, M3 and M5 receptors. PTAC inhibited conditioned avoidance responding, dopamine receptor agonist-induced behavior and D-amphetamine-induced FOS protein M5 expression in the nucleus accumbens without inducing catalepsy, tremor or salivation at pharmacologically relevant doses. The effect of PTAC on conditioned avoidance responding and dopamine receptor agonist-induced behavior was antagonized by the acetylcholine receptor antagonist scopolamine. The compound selectively inhibited dopamine cell firing (acute administration) as well as the number of spontaneously active dopamine cells (chronic administration) in the limbic ventral tegmental area (A10) relative to the non-limbic substantia nigra, pars compacta (A9). The results demonstrate that PTAC exhibits functional dopamine receptor antagonism despite its lack of affinity for the dopamine receptors and indicate that muscarinic receptor partial agonists may be an important new approach in the medical treatment of schizophrenia.
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PMID:Unexpected antipsychotic-like activity with the muscarinic receptor ligand (5R,6R)6-(3-propylthio-1,2,5-thiadiazol-4-yl)-1-azabicyclo[3.2.1]octane . 977 40

A survey of the prescribing of psychotropic drugs was carried out at the Psychiatric Hospital of Bahrain. This retrospective study on 60 inpatients of the Long Stay Ward revealed a man:woman ratio of 2.7. 91% of the men and 88% of the women were over 40 years old. 44 of the 60 patients had a diagnosis of schizophrenia, the rest had dementia, depression, schizoaffective disorders, drug-induced psychosis, general paralysis or Huntington's chorea. 95% of patients received antipsychotic drugs. Thioridazine was the most common drug followed by chlorpromazine. The mean number of drugs/patient was 1.7, with 41.7% of patients receiving only 1 drug. Tardive dyskinesia was observed in 11 patients and 9 experienced varying degrees of tremor. The findings confirm that psychiatric illness treated by psychiatrists need not lead to polypharmacy. As a consequence, its treatment may be less likely to result in adverse reactions than when patients are treated by general practitioners.
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PMID:Utilisation of psychotropic drugs in patients of the long stay ward. 1014 30

A combination of clozapine and lithium can be used in the treatment of refractory schizophrenia, schizoaffective disorder and bipolar disorder with rapid cycling. We report a patient with refractory bipolar disorder who developed side-effects after combination therapy with clozapine and lithium at usual therapeutic dosages. Reversible neurotoxicity developed twice during the therapeutic course, once with the restarting of lithium, the other with increasing the dose of lithium, despite the lithium concentrations being less than 0.5 mEq/l. Neurotoxicity manifested as ataxia, coarse tremor, myoclonus, facial spasm and increased deep tendon reflex. While the mechanism causing toxicity is not clear, interaction between the serotonergic effect of clozapine and lithium may be the cause. This report is evidence that a combination of clozapine and lithium may increase the risk of neurotoxicity. We suggest the need to keep clozapine and lithium at lower dosages and closely monitor their side-effects as necessary when these drugs are used concomitantly.
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PMID:Reversible neurotoxicity induced by a combination of clozapine and lithium: a case report. 1022 8

Our experience with atypical antipsychotics in patients with PD is that their motor effects are not predictable. The multiple reports concerning clozapine's beneficial effects on tremor, dystonia, nocturnal akathisia, and dyskinesias all underscore this observation. However, the appearance of even minor degrees of parkinsonism in normal volunteers or schizophrenics should suggest that an antipsychotic will not be well-tolerated in patients with PD. The treatment of PD is probably the most stringent test of a drug's freedom from parkinsonian side effects. The data from trials in schizophrenia concerning parkinsonian effects cannot always be confidently interpreted. Virtually all subjects in these trials have been treated with typical neuroleptics until shortly before study entry. Because the parkinsonian side effects of these drugs may persist for several months, patients may still show declining levels of parkinsonism even when placed on a drug that induces it if this effect is milder than that induced by the pre-study neuroleptic. Depending on the pre-study drug used and the duration of the study, distinguishing placebo from a low-potency neuroleptic may be impossible. Furthermore, the standard measure of parkinsonism in psychiatric studies is the Simpson-Angus scale which is heavily weighted toward rigidity and may underscore bradykinesia, gait, and posture abnormalities. The prolactin response to an antipsychotic drug may turn out to be a good predictor of its freedom from parkinsonian side effects. That would fit with the data presented above of clozapine and quetiapine having less parkinsonian effects, olanzapine having more but variable effects and risperidone being poorly tolerated. With the data presented above, comprising a current review of all reports of the use of atypical antipsychotics in PD that we could locate, we can say little with certainty. The only drug with confirmed benefit without worsening parkinsonism is clozapine. Open-label trials involving over 400 patients and two multicenter, placebo-controlled, double-blind trials have demonstrated that it is effective in treating the psychosis. It improves tremor, does not worsen other motor functions to any significant extent, and is safe at low doses. Limited data provide conflicting information on both risperidone and olanzapine. Quetiapine seems to be well-tolerated with some, but definitely less, worsening of PD motor features than risperidone and olanzapine. Based on the current literature, our personal experience, and anecdotal experience of other PD specialists which we solicited, we will venture our own interpretation and recommendations. We think risperidone is poorly tolerated and should be used only as a last resort; that olanzapine is better than risperidone but will, in a majority of patients with PD, worsen motor function. We are optimistic, but not yet convinced, that quetiapine may prove to be as effective and better tolerated than clozapine. It will not require cumbersome monitoring because it does not induce a blood dyscrasia. We therefore recommend that DP be treated in the following manner. First, the anti-PD medications should be simplified and reduced as much as tolerated. We think, in general, side effects multiply more with increasing numbers of drugs than with drug dose, so that patients are more likely to tolerate a higher dose of levodopa than a lower dose of levodopa combined with other adjunctive anti-PD medications. In reducing anti-PD medications, we recommend tapering and stopping, if necessary, the drugs with the highest risk-to-benefit ratio first. Anticholinergics are stopped first, then selegiline, dopamine agonists, amantadine, and finally COMT inhibitors, which have no psychotomimetic action of their own. Finally, levodopa is reduced. Generally, a point is reached at which the anti-PD medications cannot be reduced without jeopardizing motor function. If psychosis persists at this point, then an antipsychotic is added. (ABS
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PMID:Atypical antipsychotics in the treatment of drug-induced psychosis in Parkinson's disease. 1075 67

This open-label clinical study was conducted for patients with schizophrenia in order to investigate the efficacy, safety and optimal dose of olanzapine. One hundred and fifty-six of the 159 enrolled patients were included in the analysis set. For the primary efficacy measure, the Final Global Improvement Rating (FGIR) score, 15.4% of patients had remarkable improvement, 58.3% of patients had moderate improvement or more, 79.5% of patients had slight improvement or more, and 10.3% of patients had increase in disease symptomatology (worsening). Results from the Brief Psychiatric Rating Scale (BPRS) in all individual items were improved from baseline. Olanzapine was effective not only against positive psychotic symptoms but also against negative symptoms. This was consistent with results from the Positive and Negative Syndrome Scale (PANSS). For the majority of patients, a dose range of 7.5-10.0mg/day, as a lower bound on the minimally effective dose, was suggested by the results of the dose to first response based on improvement in Global Improvement Rating (GIR) analyses. The ratio of olanzapine dose to equivalent haloperidol dose was estimated at 1.2 :1. The most commonly reported treatment-emergent signs and symptoms (TESS) occurring at a frequency of 10% or more were insomnia, weight increase, excitement, sleepiness, anxiety, malaise and dull headaches. There was a low incidence of extrapyramidal treatment-emergent signs and symptoms; the most commonly reported were akathisia (6.4%), tremor (5.8%) and muscle rigidity (2.6%).
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PMID:Olanzapine optimal dose: results of an open-label multicenter study in schizophrenic patients. Olanzapine Late-Phase II Study Group. 1099 65

Clozapine is known to be beneficial for the treatment of dopamine agonist-induced psychotic states in patients with Parkinson's disease (PD). Many reports have suggested that it may also be efficacious for the treatment of parkinsonian tremor. We describe a patient with schizophrenia in whom early-onset PD appeared after treatment with antipsychotic drugs. When the parkinsonian symptoms proved resistant to anticholinergic agents, we introduced a trial with up to 50 mg clozapine daily, which yielded a prompt and dramatic response. Thereafter, the parkinsonian symptoms reappeared each time the patient discontinued clozapine and rapidly disappeared on its repeat initiation. There was also a marked improvement in his psychotic and depressive symptoms. This report suggests that some patients with concomitant schizophrenia and PD-a difficult treatment challenge-may benefit from clozapine treatment alone for both disorders.
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PMID:Low-dose clozapine for the treatment of Parkinson's disease in a patient with schizophrenia. 1130 50


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