An experimental model of tardive dyskinesia

Summary There are numerous clinical and experimental similarities between amine induced stereotyped behavior and tardive dyskinesia. The results presented here show that chronic pretreatment of guinea pigs with chlorpromazine produces a persistent reduction in the amounts of amphetamine or apomorphine needed to induce stereotyped behavior. It is suggested that chlorpromazine pretreatment may alter the sensitivity of the striatal dopaminergic receptors to dopamine. The alteration in receptor site responsiveness produced by prolonged chlorpromazine pretreatment may be analogous to the neuroleptic induced tardive dyskinesias. The same dopaminergic mechanism may underlie both the amine stereotyped behavior seen in animals and tardive dyskinesias in man, while lingual-facial-buccal dyskinesias may be the human equivalent of the stereotypies seen in animals when the dopaminergic response in the striatum is increased.Dr.Rubovits is a resident in the Department of Psychiatry, University of Maryland Hospital, Baltimore, Maryland.     

Risk factors for tardive dystonia: a case-control comparison with tardive dyskinesia

The objective of this study was to determine the putative risk factors for the development of tardive dystonia (TDt) in contrast with tardive dyskinesia (TD). Fifteen TDt patients seen in the Movement Disorders Clinic were compared with 2 groups of 15 TD controls each. The first control group was drawn from the Clinic and matched with the TDt cases for severity, using degree of dysfunction as the matching variable. The second control group comprised mild TD cases drawn from a separate study of drug-induced movement disorders in chronic schizophrenia and were matched for age and sex with the TDt cases. A number of demographic, treatment-related, diagnosis-related and historical variables suggested in the literature were examined. Most risk factors for TDt that have been suggested by previous studies were not supported. The first control group was significantly older than the TDt cases. The TDt patients had a more frequent past history of acute drug-induced dystonia and of postural tremor prior to the onset of the mental illness, although only the former reached statistical significance. The results suggested that TDt and TD do not differ in most putative risk factors, although the small sample size increases the likelihood of a type II error. It is inconclusive on the role of young age and male sex as risk factors. TDt cases may, however, be individuals vulnerable to the development of dystonia, with neuroleptics probably bringing out such a vulnerability. This finding needs to be examined in larger studies.     

Duloxetine-related tardive dystonia and tardive dyskinesia: a case report

Tardive dyskinesia and tardive dystonia are caused by dopamine receptor blocking agents, mostly antipsychotics and sometimes antidepressants or calcium channel blockers. Duloxetine-related tardive syndrome is rarely reported in the literature. We report one case of tardive dystonia and tardive dyskinesia occurring in a 58-year-old female with major depressive disorder, who developed distressing oral dyskinesia, mandibular dystonia with trismus and dystonia over left neck after treatment of duloxetine (30–60 mg per day) for 18 months. Despite discontinuation of duloxetine, she only obtained partial remission. Even though this association has been rarely reported, duloxetine may pose a potential risk of inducing tardive syndrome. Clinicians should cautiously detect early signs of movement abnormality when prescribing antidepressants.     

Screening for tardive dyskinesia

A program of routine Abnormal Involuntary Movement Scale (AIMS) examinations is contrasted with a referral system for detection of tardive dyskinesia in an outpatient schizophrenia clinic. Routine clinical use of the AIMS examination may have improved the early detection of tardive dyskinesia, which could result in a decrease in the morbidity associated with this disorder. Routine AIMS examinations also facilitated repeat discussions with patients about tardive dyskinesia, which provide an opportunity to obtain ongoing informed consent for treatment with neuroleptics.     

Metoclopramide-induced tardive dyskinesia: a case report

A case of tardive dyskinesia developed in a patient who had been treated with metoclopramide for 8 months. Acute extrapyramidal side effects are also possible with this medication. Guidelines for the use of metoclopramide are presented with special emphasis on patients with renal insufficiency and the elderly. The importance of consultation-liaison psychiatrists' familiarity with the neurologic side effects of this commonly prescribed drug used in general medical practice is emphasized.     

Clozapine-induced tardive dyskinesia: a case report

PURPOSE: Clozapine is indicated in the treatment of patients with tardive dyskinesia. However, there have been some reports of movement disorders associated with clozapine treatment in the literature. The authors report a patient who developed tardive dyskinesia 1 year after initiation of clozapine treatment. CASE: The patient was a 65-year-old male with diagnosis of schizophrenia who had used multiple typical and atypical antipsychotics for 30 years. Clozapine treatment was initiated for his resistant symptoms. He developed buccolingual dyskinesia of moderate severity, which started 1 year after the initiation of clozapine treatment and did not ameliorate during follow-up. CONCLUSION: This case may contribute to existing knowledge by raising the possibility that clozapine can induce dyskinesia.     

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.     

Bereitschaftspotential in tardive dyskinesia

The bereitschaftspotential or motor readiness potential is a slow negative electroencephalographic wave occurring 150-1500 ms prior to the onset of a voluntary movement. It was measured in 33 subjects: 11 normal controls, 11 medicated schizophrenics with no tardive dyskinesia or evidence of drug-induced parkinsonism, and 11 patients with tardive dyskinesia. The bereitschaftspotential amplitude was more than two times larger in patients with tardive dyskinesia than in normal controls or schizophrenic patients without tardive dyskinesia. The increased amplitude correlated with the degree of severity of the tardive dyskinesia as measured on the Abnormal Involuntary Movement Scale (AIMS). The finding of the increased bereitschaftspotential amplitude in tardive dyskinesia, taken together with earlier findings of low amplitude in Parkinson's disease, suggests that this potential may reflect the level of dopaminergic activity in the basal ganglia.     

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 )     

褪黑素治疗迟发性运动障碍的随机对照研究

目的 观察褪黑素治疗慢性精神分裂症患者迟发性运动障碍(TD)的临床疗效和不良反应.方法 选择76例有迟发性运动障碍的精神分裂症住院患者,按照入组顺序用随机数字表将患者分为褪黑素治疗组(以下简称褪黑素组,39例)和对照组(37例).褪黑素组患者每晚服用褪黑素1次(9 mg/次),对照组患者只维持常规治疗;观察期均为12周.76例患者治疗前和治疗第4,8,12周末盲法采用异常不自主运动量表(AIMS)评定TD疗效,采用治疗中需处理的不良反应症状量表(TESS)评定不良反应.结果 治疗第4,8,12周末,对照组患者AIMS总分较治疗前的差异均无统计学意义(配对t检验,P均>0.05);褪黑素组患者AIMS总分均较治疗前显著降低,差异有统计学意义(配对t检验,P均<0.05),治疗第12周末舌部、上肢的TD症状较治疗前显著降低,差异均有统计学意义(配对t检验,P均<0.05).治疗第8,12周末两组AIMS总分差异有统计学意义(t检验,P<0.05).褪黑素组和对照组治疗各时点TESS总分与治疗前比较,褪黑素组患者治疗第4,8,12周末较治疗前均显著降低,差异均有统计学意义(配对t检验,P均<0.05);而对照组及两组间的差异均无统计学意义(t检验,P均>0.05).结论 褪黑素治疗慢性精神分裂症患者TD有效,对舌和上肢的症状效果明显,无不良反应.