Clinical and biochemical effects of gamma-vinyl Gaba in tardive dyskinesia.

Clinical and biochemical effects of Gamma-vinyl-Gaba (GVG) have been evaluated in a blind video-controlled study in 10 psychiatric patients (mean age 71 yr) with tardive dyskinesia. CSF free and total Gaba and homocarnosine concentrations increased from three to five fold with GVG treatment. Despite the GVG-induced biological effects on Gaba metabolism, GVG did not consistently improve tardive dyskinesia. Psychomotor side-effects occurred in older patients, who only tolerated GVG dosages of 2-4 g/day.     

糖尿病对迟发性运动障碍的影响

目的：比较迟发性运动障碍（TD）在有糖尿病与无糖尿病的精神障碍患者中的发生率。方法：对1 016例精神障碍患者进行时点调查,分为糖尿病组与非糖尿病组,采用异常不自主运动量表（AIMS）评定患者有无TD及严重程度。结果：TD的总发生率为10.93%。糖尿病组中TD的发生率为18.50%,非糖尿病组中TD的发生率为9.40%,两组比较差异有显著性（χ^2=11.72,P〈0.01）。糖尿病组中TD患者的AIMS平均为（7.97±1.35）分,非糖尿病组中AIMS平均（6.60±2.38）分,两组比较差异有显著性（t=3.79,P〈0.01）。结论：糖尿病可能是TD发生的1个重要易感因素。     

Clinical forms of severe tardive dyskinesia

The authors describe 19 patients with severe tardive dyskinesia, 11 of whom had a diagnosis of affective or schizoaffective disorder rather than schizophrenia. Most patients had been receiving long-term neuroleptic treatment with few interruptions and had received only one or two different neuroleptics. Frequent eye blinking was the most prevalent prodromal sign of tardive dyskinesia (in seven patients). Four subtypes of tardive dyskinesia could be distinguished: choreoathetosis, tardive dystonia, blepharospasm, and tardive akathisia. Optimal pharmacotherapy most often consisted of combinations of neuroleptics, lithium carbonate, benzodiazepines, and antiparkinsonian drugs. However, after an average of 62 months, only five patients had markedly improved.     

Persistent tardive dyskinesia and neuroleptic effects on glucose tolerance

The relations of persistent tardive dyskinesia (TD) to glucose tolerance and family history of type 2 diabetes mellitus (FH-NIDDM) were examined in 22 schizophrenic patients. All patients underwent a standard oral glucose tolerance test (GTT) while receiving haloperidol, and 15 patients also underwent a GTT when drug free. Fasting blood glucose (FBS) was significantly higher in the TD group than in the non-TD group in the medicated condition, but not in the drug-free state. TD and non-TD groups did not differ significantly in postload glucose levels either in the drug-free or in the medicated condition. However, relative to the drug-free state, haloperidol-treated TD patients showed decreased glucose tolerance while non-TD patients showed increased glucose tolerance. Seven (32%) of the 22 patients had an FH-NIDDM. A positive FH-NIDDM was significantly associated with the presence of TD and with higher drug-free FBS. A possible role of melatonin in mediating the TD-augmenting effects of FH-NIDDM and the neuroleptic-induced decrease in glucose tolerance has been proposed.     

A biochemical study of tardive dyskinesia in young male patients

Based on specific criteria, tardive dyskinesia was diagnosed in 6 out of 29 young schizophrenic male inpatients. We compared several biochemical parameters in these six dyskinesia patients with those in six matched controls. The patients with dyskinesia had significantly lower platelet monoamine oxidase activity and significantly higher plasma dopamine-beta-hydroxylase activity as compared with the controls, thus confirming our previous findings in a population of elderly female inpatients. The dyskinetic and nondyskinetic groups did not differ from each other in mean whole blood serotonin concentration and mean serum neuroleptic concentration as measured with a radioreceptor binding assay. Possible significance of our results is discussed.     

Tiapride: effects on tardive dyskinesia and on prolactin plasma concentrations

In a placebo-controlled double-blind crossover study of 21 patients chronically treated with neuroleptics and suffering from tardive dyskinesia, tiapride (600 mg/day, mean plasma level: 682 ng/ml) exhibited a transient efficacy during 12 weeks of treatment, most distinct in the 6th week (p less than 0.01). Tiapride induced an increase of prolactin plasma levels, on the average, from 1,195 to 2,179 microIU/ml (p less than 0.01). Tiapride was well tolerated. Increase of parkinsonism was only mild and not significant. The results underline the difficulty in treating tardive dyskinesia and, thus, confirm the importance of prevention.     

Thiethylperazine and tardive dyskinesia

Over a 14-month period in the outpatient department of a geriatric hospital, 7 female patients over 75 years of age were identified with tardive dyskinesia associated with the use of thiethylperazine. The indication for thiethylperazine treatment had been vertigo or dizziness. 3 of the patients also had symptoms related to cerebral arteriosclerosis and 2 had mild Parkinson's disease without levodopa therapy. None of them were markedly demented nor had chronic psychosis. Tardive dyskinesia appeared after a treatment period of 3 weeks to 6 years. These findings suggest that association of tardive dyskinesia with the use of thiethylperazine is not uncommon in geriatric outpatients.     

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.     

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.