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)

All major symptoms of Parkinson's disease, i.e., rigidity, tremor, hypokinesia and postural instability are induced by an impaired dopaminergic neurotransmission in the nigro-striatal pathway. Levodopa pioneered the symptomatic therapy of Parkinson's disease. While it is effective on the motor symptoms, long-term levodopa therapy often results in dyskinesia, motor fluctuations and psychosis. Coadministration of levodopa and dopamine agonists, bromocriptine and pergolide, decreases these adverse side effects. Anticholinergics and amantadine are often effective as adjuvant drugs for the early stage of patients with Parkinson's disease. Furthermore, L-threo-DOPS, nor-adrenergic precursor drug, is sometimes effective for the advanced stage of Parkinson's disease. Thus coadministration of multiple antiparkinsonian drugs, rather than single therapy of levodopa, is useful for the long-term treatment of Parkinson's disease.
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PMID:[Treatment of Parkinson's disease with multiple drugs]. 901 24

The use of ondansetron, a selective serotonin 5-HT3 receptor antagonist, is well established in patients with nausea and vomiting associated with cancer chemotherapy, radiotherapy or anaesthesia and surgery. The wide distribution of 5-HT3 receptors in the body and the role of these receptors in disease have provided the rationale for investigation of ondansetron in novel applications. Preliminary data have shown ondansetron to have clinical benefit in patients with nausea and vomiting associated with drug overdosage or poisoning, anti-infective or antidepressant therapies, uraemia or neurological trauma, and in patients with pruritus. Patients with gastrointestinal motility disorders (e.g. carcinoid syndrome, irritable bowel syndrome, diarrhoea associated with cryptosporidiosis or diabetes, and chronic refractory diarrhoea) have also shown some improvement when treated with ondansetron, as have patients with certain pain or CNS-related disorders [e.g. alcohol (ethanol) dependence, opiate withdrawal, vertigo, cerebellar tremor and Parkinson's disease treatment-related psychosis]. In contrast to conventional antiemetics, ondansetron is generally well tolerated with a lower incidence of sedation and only isolated case reports of extrapyramidal reactions. Furthermore, unlike dopamine receptor-blocking neuroleptics, ondansetron does not appear to worsen the symptoms of Parkinson's disease. Thus, in addition to its established indications, preliminary results suggest that ondansetron may be beneficial in a number of novel applications. This drug may represent a treatment alternative in patients with refractory disease, or an effective treatment of conditions for which current therapies are either poorly tolerated or not available. Further investigation of ondansetron in a range of potential new applications appears to be warranted.
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PMID:Ondansetron. A review of its pharmacology and preliminary clinical findings in novel applications. 911 22

Hypoglycemia is often associated with typical, but not specific symptoms. A differentiation is made between neuroglucopenic symptoms (e.g., confusion, somnolence) on the one hand, and those that arise as a result of the counterregulatory response of the sympathetic nervous system (e.g., tremor, sweating), on the other. The diagnosis of hypoglycemia can cause considerable problems, in particular when only isolated single symptoms present (e.g., confusion, psychosis, seizures, coma). For the elective clarification of recurrent hypoglycemia, further diagnostic examinations (e.g., fasting with determination of hormones, measurement of insulin) are employed in addition to the patient's history. For differential diagnostic considerations not only organic causes, but also adverse drug reactions and a factitious genesis must be excluded. In the event of an emergency (e.g., hypoglycemic coma) the usual form of treatment is the administration of glucoses or glucagon.
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PMID:[Hypoglycemia. Symptoms, differential diagnosis, therapy]. 917 11

Clozapine, the only commercially available atypical neuroleptic, is approved for the treatment of schizophrenic patients who are unresponsive to or intolerant of typical neuroleptics. It has an unusual pharmacologic profile compared with standard neuroleptics, and it follows that clinical response to this drug is also different. It has shattered the notion that a drug must be capable of inducing or worsening parkinsonism to be a potent antipsychotic. Based on these findings, it is being used increasingly by neurologists for psychiatric and nonpsychiatric problems in patients with movement disorders. The most common use for clozapine among neurologists is in the management of drug-induced psychosis in Parkinson's disease (PD). This problem has been a source of increased morbidity and mortality in PD because of a lack of adequate therapeutic intervention. At this time, because of success in numerous open trials, with improvement of > 80% of patients, clozapine therapy for psychosis in PD is becoming the standard of care. It also appears to be of value in the management of some motor features of PD, including tremors and dyskinesia and possibly even sensory symptoms such as akathisia and pain. The literature also suggests that clozapine may be of potential benefit in hyperkinetic movement disorders including essential tremor, Huntington's disease, and tardive dyskinesia. We review the current data concerning the use of clozapine in patients with these movement disorders and others.
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PMID:The emerging role of clozapine in the treatment of movement disorders. 925 Oct 65

L-DOPA, the precursor of dopamine, remains most effective in the treatment of patients with Parkinson's disease, but prolonged L-DOPA treatment often produces adverse effects, including dyskinesia and psychosis. Dopamine receptors can be divided into two major subtypes, D1 and D2. Might both subtypes of the dopamine receptor be equally relevant to amelioration of parkinsonian symptoms and responsible for the adverse side effects? To address this question, the effects of D1 or D2 receptor agonists alone and in joint administration were examined in MPTP-induced parkinsonian monkeys. The parkinsonian symptoms, such as tremor, bradykinesia and rigidity, and the adverse side effects, such as hyperactivity and aggressiveness, were evaluated independently using different behavioral criteria. The results showed that antiparkinsonian effects can be exerted either by the D1 agonist (SKF 82958) alone or by the D2 agonist (quinpirole) alone, whereas hyperactivity and aggressiveness manifested by dopamine agonists require coactivation of the D1 and D2 receptors. Thus, the antiparkinsonian effect can be dissociated from the adverse effect by therapeutic strategy. It is implied that imbalances in activation of the D1 and D2 receptors may provide a favorable approach for long-term treatment of parkinsonian patients with dopamine drugs.
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PMID:Differential therapeutic effects of dopamine D1 and D2 agonists in MPTP-induced parkinsonian monkeys: clinical implications. 927 96

This study reports the case of a 16-year-old male who presented with a history of prominent psychotic symptoms and paranoid delusions which overshadowed subtle signs and symptoms of cognitive and motor dysfunction. Intensive neurobehavioral and biochemical investigations eventually led to the diagnosis of Niemann-Pick disease, type C (NPC), an autosomal recessively inherited storage disease that is associated with the accumulation of cholesterol in lysosomes and difficulties in the processing of exogenously derived cholesterol. Clues to the presence of a neurological disorder included: a history of insidiously declining academic and athletic performance which antedated the onset of psychosis; abnormalities on mental status examination, including psychomotor slowing, memory difficulties, and impairment of higher attentional functions; physical findings of subtle downgaze impairment, mild symmetrical hyperreflexia, and lower-extremity hypertonia with flexor plantar responses, marked impairment of upper-extremity rapid alternating movements, action tremor, and bilateral posturing with stress gait maneuvers. This case demonstrates the importance of careful and persistent neurodiagnostic evaluation in adolescents with psychotic presentations, particularly when cognitive and motor deterioration is suspected, and even when head CT and MRI scans are judged to be normal.
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PMID:Psychosis as a presentation of physical disease in adolescence: a case of Niemann-Pick disease, type C. 948 3

Tiagabine is a gamma-aminobutyric acid (GABA) uptake inhibitor which is structurally related to nipecotic acid but has an improved ability to cross the blood-brain barrier. Clinical trials have shown that tiagabine is effective as add-on therapy in the management of patients with refractory partial epilepsy. In short term studies of this indication, tiagabine < or = 64 mg/day for 7 to 12 weeks reduced the complex partial and simple partial seizure frequency by > or = 50% in 8 to 31 and 28.2 to 37% of patients, respectively. Tiagabine appeared to produce a sustained reduction in seizure frequency in studies of up to 12 months' duration. Data from preliminary studies are currently insufficient to confirm the usefulness of tiagabine when used as monotherapy or in the treatment of children with epilepsy. Further studies are, therefore, necessary to more fully elucidate the efficacy of the drug in these settings. Adverse events associated with tiagabine are primarily CNS-related and include dizziness, asthenia, nonspecific nervousness and tremor. Skin rash or psychosis occurred with similar frequencies among tiagabine- and placebo-treated patients. With long term administration (> or = 1 year for many patients), the profile and incidence of adverse events was similar to that for short term therapy. Tiagabine does not appear to affect the hepatic metabolism of other drugs such as carbamazepine and phenytoin. Possible disadvantages of tiagabine include its short plasma elimination half-life, necessitating 2 to 4 times daily administration, and its inducible hepatic metabolism. Thus, tiagabine is a new antiepileptic agent with a novel mechanism of action, which has demonstrated efficacy in the adjunctive treatment of patients with refractory partial epilepsy. Further investigation of the efficacy of tiagabine is expected to provide a clearer definition of its place in the treatment of epilepsy and its relative merits in relation to other antiepileptic drugs.
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PMID:Tiagabine. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic potential in the management of epilepsy. 953 May 48

We conducted a multicentered, retrospective review of clozapine's (CZP) effects on a range of psychiatric, sleep, cognitive, motor, and sensory disorders in Parkinson's disease (PD). Therapeutic outcomes and adverse events were compared with varying prescribing practices at participating sites. The medical records of 172 consecutive PD patients treated with CZP at four movement disorder clinics were reviewed. Low-dose CZP improved psychiatric symptoms of psychosis, anxiety, depression, hypersexuality, sleep disturbance, and akathisia. Tremor, torticollis, limb dystonia, and pain showed modest rates of improvement. Twenty-three percent of patients withdrew as a result of adverse events or treatment failure. Inpatient CZP initiation did not improve therapeutic efficacy, or reduce adverse events or the withdrawal rate. Low-dose CZP in the outpatient setting is generally an effective and well-tolerated treatment for many of the psychiatric, sleep, motor, and sensory disturbances common to late-stage PD.
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PMID:Clozapine use in Parkinson's disease: a retrospective analysis of a large multicentered clinical experience. 961 25

Quetiapine is an atypical antipsychotic with clozapine-like pharmacology but without associated agranulocytosis. We report our complete experience with quetiapine for the treatment of drug-induced psychosis (DIP) in Parkinson's disease (PD). Thirty-five patients with PD and DIP aged 75 years (range, 58-89) with a mean PD duration of 8.4 years on an average of 427 mg levodopa per day received a mean dose of 40.6 mg quetiapine daily. Twenty of 24 neuroleptic-naive patients reported marked improvement of psychosis without a decline in motor function as assessed by the Unified Parkinson's Disease Rating Scale (UPDRS-motor). Ten patients had a baseline and 4-week follow-up assessment using the Mini-Mental Status Examination (MMSE) and Brief Psychiatric Rating Scale (BPRS). The improvement in BPRS score (32.6 versus 22.8) was clinically and statistically significant (p = 0.024). Three of 24 were unable to tolerate quetiapine because of orthostatic hypotension, headache, nausea, and persistence of hallucinations. One patient died of an unrelated cause. We also tried to switch 11 psychiatrically stable patients on clozapine (eight) and olanzapine (three). Five patients made this transition without a loss of effect as measured on BPRS and MMSE. Six did not (five on clozapine, one on olanzapine) because of confusion, erratic behavior, and increased hallucinations. No crossover failure had worsened PD except for increased tremor in one. Quetiapine is useful and well-tolerated as a first drug to treat DIP in PD but must be used cautiously to replace other atypical antipsychotic drugs.
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PMID:Quetiapine for the treatment of drug-induced psychosis in Parkinson's disease. 1034 74

Acute injection of the cannabinoid agonist HU 210 (6.25-100 microg/kg, i.p.) dose-dependently inhibited rat locomotor activity and rearing, while subchronic treatment with the drug (once daily for 7 days) at the same doses only diminished locomotion. Acute but not subchronic administration of HU 210 (12.5-50 microg/kg, i.p.) potently counteracted acute and subchronic cocaine (15 mg/kg, i.p.)-induced hyperlocomotion and enhanced rearing. The acute cannabinoid (6.25-100 microg/kg, i.p.) also inhibited locomotor activity, stereotyped behaviour and shaking elicited by the D1/D2 agonist CQP 201-403 (500 microg/kg, i.p.). On the contrary, subchronic treatments with HU 210 enhanced CQP 201-403-induced locomotor activity and potently stimulated escape attempts. Discussion centers on the influence of cannabinoids on experimental models of psychosis.
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PMID:Influence of the cannabinoid agonist HU 210 on cocaine- and CQP 201-403-induced behavioural effects in rat. 1046 48


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