BACKGROUND: Dyskinesia is a movement disorder categorized by involuntary movement of muscle. Although dyskinesia can be brought on by taking medications, it can also be a symptom of a variety of diseases. Antiepileptic drug-induced involuntary movements have been well researched. Rare reports have been made for dyskinesia, a type of dystonia caused by phenytoin. The mechanism of its occurrence must be succinctly studied.
METHODS: A 53-year-old Asian patient taking phenytoin (100 mg twice daily) experienced symptoms of perioral muscle involuntary movement, impaired speech, and generalized tremors and was admitted to the hospital. Brain magnetic resonance imaging showed significant development of encephalomalacia and porencephaly. The serum phenytoin levels were in the toxic range (33 g/ml). These were suggestive of phenytoin-induced dyskinesia. Levetiracetam and clonazepam were initiated, and the patient showed significant improvement in the symptoms.
CONCLUSIONS: This case presented a substantial reference value for the differential diagnosis and treatment prognosis of phenytoin-induced dyskinesia. The phenytoin-induced dyskinesia in this patient was successfully reversed with prompt identification and treatment. According to the case study\'s findings, such people may benefit from periodic therapeutic drug monitoring.

BACKGROUND: Benztropine is an anticholinergic drug used as a therapy for Parkinson\'s disease and treatment for extrapyramidal side effects. While tardive dyskinesia is an involuntary movement disorder that often occurs gradually after long-term use of medications, it does not commonly present acutely.
METHODS: A 31-year-old White woman experiencing psychosis presented with spontaneous, acute-onset dyskinesia induced with the withdrawal of benztropine. She had been followed in our academic outpatient clinic for medication management and intermittent psychotherapy.
CONCLUSIONS: The pathophysiology of tardive dyskinesia is not fully understood, but several hypotheses exist, including the involvement of changes in basal ganglia neuronal systems. To our knowledge, this is the first case report to document acute-onset dyskinesia associated with the withdrawal of benztropine.
CONCLUSIONS: his case report, which describes an atypical response to discontinuing benztropine, might offer the scientific community potential clues to better understand the pathophysiology of tardive dyskinesia.

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Tardive dyskinesia is defined as involuntary athetoid or choreiform movements that develop due to the use of neuroleptic drugs for at least a few months. Tongue, lower face, jaw, upper and lower extremities are the most affected parts of the body in tardive dyskinesia. Quality of life is negatively affected because of the low remission rates. Besides tardive dyskinesia, involuntary movements may appear after discontinuation, change or a reduction in the dose of antipsychotic medications, which is called withdrawal-emergent dyskinesia (WED). Unlike tardive dyskinesia, the involuntary movements involve mainly the neck, trunk, and limbs and regress in shorter period of time in WED. A consensus has not yet been reached for the treatment of WED. Restarting the previous antipsychotic agent with slow titration or switching to an atypical antipsychotic with low affinity for dopamine D2 receptors are among the primary options for treatment. As WED is one of the predictors of tardive dyskinesia development, early detection and treatment is believed to have positive effect on the quality of life. In this report, the case of a patient followed up for bipolar disorder type I (BD-I) and started on clozapine for WED after discontinuation of haloperidol on account of adverse effects is discussed. It is necessary for clinicians to consider these types of complications when discontinuing or changing treatment. Further research is needed in order to reach a common approach for the treatment of WED.

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Belly dancer syndrome, also called belly dance syndrome or belly dancer dyskinesia, is a kind of abdominal dyskinesia with painful sensation. Its etiology is still unclear and there are few studies reporting its association with antipsychotics. Quetiapine is an atypical antipsychotic that causes lower risk of extrapyramidal symptoms than typical antipsychotics. Here, we presented the first case of belly dancer syndrome in a 71-year-old woman with major depressive disorder after short-term use of quetiapine.

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BACKGROUND: Sodium valproate (VPA) and lamotrigine (LTG) are widely used antiepileptic drugs, disabling postural, and action tremors after using LTG with VPA were reported in 1993. However, in this study, we describe a patient in whom disabling resting-type tremor induced by 2-year use of VPA and LTG.
METHODS: A 50-year old man was referred to department of neurology because of involuntary upper limbs resting-type tremor with high amplitude that had begun 6 months previously and progressively worsened, and he could not work on the day of visit. Furthermore, he had been treated with VPA, LTG, and benzhexol for 2 years as he suffered from twitch of eyelids and facial region, and amantadine, monolithic compound preparation (flupentixol and melitracen) were added in the last 2 months because of tremor and anxiety. However, the treatment had no benefit on improving involuntary movements of the patient.
METHODS: Drug-induced disabling tremor was diagnosed.
RESULTS: LTG, amantadine, and VPA were withdrawn, the remaining 2 drugs, benzhexol and compound preparation (flupentixol and melitracen), were continued to use, and the patient improved in 2.5 months after discontinuation of 3 drugs. There was no recurrence at 6 months follow-up.
CONCLUSIONS: Considering the wide and long-term utilization of VPA and LTG, healthcare providers should be aware of them as a possible cause of tremor. When necessary, an attempt of discontinuing the suspected drugs should be made to confirm the diagnosis, instead of symptomatic treatment, especially when the adverse event was severe and fatal.

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