Electroencephalogram in tardive dyskinesia

The electroencephalogram was studied in affective disorder and schizophrenic patients both with and without tardive dyskinesia. There were no significant differences in electroencephalographic changes among the groups. The majority of electroencephalographic abnormalities appear to be drug induced. Tardive dyskinesia is not associated with specific changes in the electroencephalogram.     

Amisulpride-induced tardive dyskinesia

Tardive dyskinesia (TD) is a movement disorder that develops during the course of long-term treatment with neuroleptic agents and is characterized primarily by choreiform and athetotic movements. We report the case of a 34-year-old man suffering from schizophrenia, disorganized type. He received amisulpride (400 mg daily) and the result was much improvement. 20 months later, he was presented with TD, which resolved almost completely after change of treatment to 1200 mg quetiapine without any relapsing. To our knowledge, his is the first case report in the literature of tardive dyskinesia induced by amisulpride.     

Laryngeal tardive dyskinesia

Neuroleptic treatment frequently induces movement disorders, the tardive dyskinesias. These are frequently seen in the orobuccolingual region. Although the beginning of neuroleptic treatment can cause acute dystonia and breathing difficulty, chronic neuroleptic treatment has only rarely been shown to affect the laryngeal musculature. Laryngeal abnormal movements were assessed in 12 patients receiving chronic neuroleptic treatment who showed orobuccolingual abnormal movements. The Abnormal Involuntary Movement Scale was systematically assessed in all patients. Clinical examination revealed that 8 had speech disorders, 8 had breathing difficulties, and 5 had swallowing disorders. Laryngeal endoscopy showed that 10 of the patients had intermittent partial obstruction of the glottis, due to repetitive abnormal adduction of the vocal cords. Percutaneous electromyography of the thyroarytenoid muscles showed spontaneous irregular and prolonged muscular contractions, while the patients were at rest and when speaking. The patients were not aware of these movements. In view of this finding, laryngeal dyskinesia should be considered and studied as a possible side-effect of chronic neuroleptic use.     

Quetiapine in tardive dyskinesia

Tardive dyskinesia (TD) is a potentially irreversible side-effect of antipsychotic medication. Some atypical antipsychotics, by virtue of their better side-effect profile, seem to have an ability to reverse TD. The importance of trying to treat TD has become more urgent in view of the medico-legal implications of Article 3 of the Human Rights Act, 1998 which states that ''no one shall be subjected to inhuman or degrading treatment or punishment'': interpretation of this article was successfully used to win a large out-of-court settlement for a patient with TD in our region. Though clozapine has been used in cases with TD, its role is limited, due to the risk of agranulocytosis. We write about three cases with TD who responded well to quetiapine (Seroquel © , AstraZeneca), and suggest that more robust research be carried out to investigate the initial promise. (Int J Psych Clin Pract 2002; 6: 175-177 )     

Neuroleptic-induced tardive dyskinesia

Prolonged exposure to neuroleptic drugs induces tardive dyskinesia which may be persistent or permanent. Predisposing factors to tardive dyskinesia are not apparent although the aging brain appears more vulnerable. The drug treatment of tardive dyskinesia is at present unsatisfactory. Preventive measures, other than limiting neuroleptic use have not been established. The pathophysiology of tardive dyskinesia may relate to cerebral dopamine overactivity. However, although this may be a primary change responsible for tardive dyskinesia alterations in other neuronal systems such as acetylcholine, 5HT or GABA may be involved.     

Familial tardive dyskinesia

The authors surveyed 500 inpatients receiving long-term neuroleptics; 8 had first-degree family members who were also being treated with long-term neuroleptics and suffering from a psychiatric disorder. The 8 patient-relative pairs showed concordance for the presence or absence of tardive dyskinesia.     

Experimental tardive dyskinesia

In this work, we have attempted to reproduce dyskinesia similar to tardive dyskinesia by two methods. In the first experiment, we have administered to 6 macacca mulatta, haloperidol 0.25 mg/kg daily for six months. During that period we observed in all monkeys, after each dose: restelessness, akinesia and tremor. One monkey developed choreoathetoid movements, which were seen each day after the first month. They disappeared however upon cessation of the drug administration. Only one animal developed a bucco lingual dyskinesia after two months which was still present when they were sacrificed six month after the drug administration was discontinued. At that time, harmaline 3 mg/kg induced a postural tremor in all monkeys suggesting a lesion of the rubro-olivo-cerebello rubral loop. Histological analysis of the brains revealed no gross abnormality. In a second experiment, a left mid-brain electrolytic lesion was performed in twelve monkeys. One monkey, developed a contralateral tremor but five including the trembling one developed a buccolingual dyskinesia which has now lasted more than a year. This dyskinesia is present at rest but increased by dopaminergic agents and blocked by haloperidol. Histological analysis of the brain of one of the monkeys revealed a dorsal lesion involving the region of the nucleus parafascicularis thalami. The substantia nigra was spared.     

Computerized tomography in tardive dyskinesia

Summary Twenty-nine patients with moderate to severe tardive dyskinesia (TD) and 29 age-and sex-matched controls (C) with long-term neuroleptic therapy comparable to that of the patients were all examined using computeized tomography. Significant differences were found between the two groups in the width of the third ventricle (TD>C), the bicaudate distance (TD>C), the computed area of the head of the caudate nucleus (TD相似文献   

CT abnormalities in tardive dyskinesia

Many investigators have suspected neuropathology in tardive dyskinesia (TD) to center in the striatum. Previous computed tomographic (CT) studies of middle-aged and older subjects using linear measurements have reported primarily negative results. The present study attempts to identify neuropathological abnormalities in the periventricular region of young chronic schizophrenics using specific area measurements of in vivo brain imaging. A ratio of frontal horn area to maximal internal skull area (FHBR) was used in an effort to gain sensitivity and give a reliable measure of caudate atrophy. The ventricle-brain ratio (VBR) measurement and a cortical atrophy rating were also done. The TD and non-TD control groups did differ in the CT variables. Negative CT results do not rule out the possibility that more subtle neuropathological abnormalities may be present. Magnetic resonance imaging, with its superior gray/white matter differentiation and its ability to detect subtle differences in tissue, may discover abnormalities in TD.     

High-dose naloxone in tardive dyskinesia

Tardive dyskinesia (TD) is thought to result from nigrostriatal dopaminergic supersensitivity secondary to prolonged neuroleptic exposure. Preclinical studies have demonstrated that the opiate antagonist naloxone can acutely reverse a haloperidol-induced hyperdopaminergic state. In a trial of high-dose naloxone, 20 patients with TD received i.v. naloxone (20 mg, 40 mg, and placebo) under double-blind conditions. At baseline and at regular postdrug intervals, patients were evaluated using a battery of motor, clinical, and neuropsychological measures to study effects on neurological, behavioral, and cognitive functions. There was a significant improvement in involuntary movements at 30 min postnaloxone, together with improvement in clinical ratings at that time point, as well as some cognitive changes. The implications of these findings for the putative functional relationship between dopaminergic and enkephalinergic systems in the nigrostriatal area are discussed.     

Sulpiride in tardive dyskinesia.

The abnormal involuntary movements in tardive dyskinesia can be reduced by the dopamine antagonist drugs, phenothiazines and butyrophenones, but most cause an increase in Parkinsonian signs. Sulpiride, a benzamide derivative, and selective antagonist of D2 receptors had a significantly beneficial effect on most of 15 patients (p less than 0.01). In 12 patients the improvement was marked. The reduction of abnormal movements was observed even with low doses, and it was not necessary to increase the dose of sulpiride above 600 mg daily. There were no significant side effects during the trial nor during an additional three months of treatment.