1/393. risperidone-induced rabbit syndrome: an unusual movement disorder caused by an atypical antipsychotic. Rabbit syndrome is a rare side effect of chronic neuroleptic administration characterized by rapid, fine, rhythmic movements of the mouth along a vertical axis. It gains its name from an unusual resemblance to the chewing and puckering motions of the rabbit. It is generally thought to be an extra-pyramidal side effect, in part due to its rapid response to anti-cholinergic medication. This is the first case report of risperidone, an atypical antipsychotic, inducing the syndrome. The theoretical implications for the classification of the syndrome along the spectrum of neuroleptic-induced movement disorders are discussed. ( info) |
2/393. diazepam in the treatment of tardive dyskinesia. Preliminary observations. Three patients, aged 23-33 years, with the diagnosis of schizophrenia, developed symptoms of tardive dyskinesia while receiving neuroleptic treatment, mostly with haloperidol. Existential problems and emotional upset seemed contributory. diazepam was found effective in controlling dyskinesia. Its therapeutic effect seemed not to be related to sedation. Some implications of the reported observations are mentioned. ( info) |
3/393. Anticonvulsant-induced dyskinesias: a comparison with dyskinesias induced by neuroleptics. anticonvulsants cause dyskinesias more commonly than has been appreciated. Diphenylhydantoin (DPH), carbamazepine, primidone, and phenobarbitone may cause asterixis. DPH, but not other anticonvulsants, may cause orofacial dyskinesias, limb chorea, and dystonia in intoxicated patients. These dyskinesias are similar to those caused by neuroleptic drugs and may be related to dopamine antagonistic properties possessed by DPH. ( info) |
4/393. Case report: complications of rehabilitation using osseointegrated implants--tardive dyskinesia. The oral rehabilitation of patients using osseointegrated dental implants is a well established treatment modality. However complications can arise during the provision of treatment. This case report describes the management of a patient exhibiting tardive dyskinesia with an implant stabilised mandibular overdenture. Complications of the treatment and their resolution are discussed. ( info) |
5/393. Antipsychotic-induced life-threatening 'esophageal dyskinesia'. We report two patients with lingual dyskinesia and complaints of food regurgitation following long-term antipsychotic therapy. Esophageal contrast radiography revealed dyskinetic movements extending from the pharynx to the upper portion of the esophagus. The elevation of intraesophageal pressure was confirmed by esophageal manometry. The dyskinetic movements almost disappeared along with improvement of lingual dyskinesia following the administration of sulpiride in one patient. Another patient suddenly died due to asphyxiation of foods before the beginning of treatment. We termed this life-threatening movement, 'esophageal dyskinesia'. It should be emphasized that 'esophageal dyskinesia' associated with lingual dyskinesia is a potentially fatal adverse reaction to antipsychotic therapy. ( info) |
6/393. From off-period dystonia to peak-dose chorea. The clinical spectrum of varying subthalamic nucleus activity. The effect of chronic bilateral high-frequency stimulation of the subthalamic nucleus (STN) on levodopa-induced dyskinaesias was investigated in eight patients with fluctuating Parkinson's disease complicated by functionally disabling off-period dystonia. All of the patients also had severe diphasic and peak-dose chorea, so that it was possible to study the effect of high-frequency stimulation on the different types of levodopa-induced dyskinaesias. Off-period fixed dystonia was reduced by 90% and off-period pain by 66%. After acute levodopa challenge, high-frequency stimulation of the STN reduced diphasic mobile dystonia by 50% and peak-dose choreic dyskinaesias by 30%. The effect of bilateral high-frequency stimulation of the STN on the Unified Parkinson's disease Rating Scale motor score had the same magnitude as the preoperative effect of levodopa. This allowed the levodopa dose to be reduced by 47%. The combination of reduced medication and continuous high-frequency stimulation of the STN reduced the duration of on-period diphasic and peak-dose dyskinaesias by 52% and the intensity by 68%. Acute high-frequency stimulation of the STN mimics an acute levodopa challenge, concerning both parkinsonism and dyskinaesias, and suppresses off-period dystonia. Increasing the voltage can induce repetitive dystonic dyskinaesias, mimicking diphasic levodopa-induced dyskinaesias. A further increase in voltage leads to a shift from a diphasic-pattern dystonia to a peak-dose pattern choreodystonia. Chronic high-frequency stimulation of the STN also mimics the benefit of levodopa on parkinsonism and improves all kinds of levodopa-induced dyskinaesias to varying degrees. Off-period dystonia, associated with neuronal hyperactivity in the STN is directly affected by stimulation and disappears immediately. The effect of chronic high-frequency stimulation of the STN on diphasic and peak-dose dyskinaesias is more complex and is related directly to the functional inhibition of the STN and indirectly to the replacement of the pulsatile dopaminergic stimulation by continuous functional inhibition of the STN. Chronic high-frequency stimulation of the STN allows a very gradual increase in stimulation parameters with increasing beneficial effect on parkinsonism while reducing the threshold for the elicitation of stimulation-induced dyskinaesias. In parallel with improvement of parkinsonism, the levodopa dose can be gradually decreased. As diphasic dystonic dyskinaesias are improved to a greater degree than peak-dose dyskinaesias, both direct and indirect mechanisms may be involved. Peak-dose choreatic dyskinaesias, associated with little evidence of parkinsonism and thus with low neuronal activity in the STN, are improved, mostly indirectly. Fixed off-period dystonia, mobile diphasic dystonia and peak-dose choreodystonia seem to represent a continuous clinical spectrum reflecting a continuous spectrum of underlying activity patterns of STN neurons. ( info) |
7/393. Improvement of tardive dyskinesia following treatment with olanzapine. This case illustrates a marked improvement of tardive dyskinesia in a 59-year-old male patient with delusional disorder with a long history of neuroleptic exposure, following treatment with olanzapine. ( info) |
8/393. Use of clonazepam in an elderly bipolar patient with tardive dyskinesia: a case report. Tardive dyskinesia (TD) is an adverse effect of long-term neuroleptic use. An effective treatment for TD is needed, especially if chronic neuroleptic therapy is indicated. The treatment of TD in the elderly is not well established. We present here the case of an 81-year-old male with TD who had a significant reduction in dyskinetic and dystonic movements when treated with clonazepam. ( info) |
9/393. Dyskinesia induced by phenytoin. phenytoin is an effective antiepileptic drug, although, it can be associated with many side effects, including dyskinesia. OBJECTIVE: To describe the clinical characteristics of phenytoin induced dyskinesia. methods: We investigated the occurrence of involuntary movements in patients followed at our adult and pediatric epilepsy clinics during the period of one year. RESULTS: Three patients presented with phenytoin-induced dyskinesia: one adult with axial and orofacial dyskinesia, and two children with choreoathetosis. They did not have other signs of phenytoin intoxication and had complete recovery after phenytoin withdrawal. CONCLUSION: phenytoin induced dyskinesia may occur during either chronic or initial treatment and with normal serum phenytoin levels. However, it occurs most often in patients on polytherapy, usually after increasing dosage and with toxic serum levels. Other signs of phenytoin intoxication may be present in these patients, but often the dyskinesia is the only side effect, which may delay the diagnosis and treatment. The clinical characteristics of the involuntary movements vary and may be focal or generalized, most often characterized by choreoathetosis and dyskinesias. These may last for hours, days or even years, but frequently disappear completely after phenytoin withdrawal. ( info) |
10/393. Late-onset adrenoleukodystrophy associated with long-standing psychiatric symptoms. BACKGROUND: It is not commonly appreciated that patients with adrenoleukodystrophy (ALD) can first present in adulthood with psychiatric symptoms. METHOD: This case study involved a 31-year-old man who was referred for a neuropsychiatric assessment of tardive dyskinesia and treatment-resistant psychosis. Upon neurologic examination, he was found to have spasticity, marked hyperreflexia with clonus, and bilateral Babinski signs. T2-weighted magnetic resonance imaging demonstrated severe white matter disease. Metabolic screening revealed abnormalities of very long chain fatty acids consistent with the diagnosis of ALD. These results prompted us to review the literature on late-onset ALD with attention to (1) the nature of the associated psychiatric and neurologic symptoms, (2) the neuroimaging abnormalities associated with this disorder, and (3) treatment considerations. RESULTS: Individuals with adult-onset ALD may initially present with psychiatric symptomatology. Most commonly, these patients manifest signs of mania including disinhibition, impulsivity, increased spending, hypersexuality, loudness, and perseveration. ALD patients will often have upper motor neuron findings on neurologic examination. Despite the name of the disease, patients with ALD may not have clinical evidence of adrenal dysfunction. neuroimaging reveals diffuse, confluent white matter lesions that typically originate in the parieto-occipital region. Both neuroleptic and anticholinergic medications may result in significant side effects with little resolution of the underlying psychiatric symptoms. CONCLUSION: This case study and review of the literature illustrate the importance of performing neurologic and radiological examinations on all psychiatric patients with chronic illnesses. We emphasize the importance of reexamining and reimaging patients who are not responding to standard treatment. The clinical problem of "treatment resistance" should be seen as an indication that other diagnoses, such as an underlying metabolic disorder, need to be considered. ( info) |