tardive dyskinesia/ضمور

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Brain atrophy and intellectual impairment in tardive dyskinesia.

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Fourteen chronic schizophrenic patients with tardive dyskinesia (TD) and 13 without TD were given psychological tests and CT scans. The low density rate (LDR), i.e., the ratio of the X-ray absorption (corresponding nearly to that of cerebrospinal fluid) of a brain lesion to the X-ray absorption of

Caudate atrophy in irreversible tardive dyskinesia (a pneumoencephalographic study).

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Pneumoencephalography done under standard conditions on 5 patients with tardive dyskinesia and 3 matched controls revealed evidence of caudate atrophy in 3 of the dyskinetic patients. The same 3 patients proved refractory to treatment of their dyskinesia. It is concluded that tardive dyskinesia is a

CT abnormalities in tardive dyskinesia.

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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

Tardive dyskinesia: clinical correlation with computed tomography in patients aged less than 60 years.

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In a prevalence study of 335 psychiatric in-patients 49 patients (14.6%) with tardive dyskinesia were found. In view of the high prevalence of spontaneous dyskinetic syndromes in elderly patients only patients under 60 years were included (n = 21; mean age: 44.9). Clinical rating was performed with

Neuroradiological covariates of drug-induced parkinsonism and tardive dyskinesia in schizophrenia.

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Computed tomographic (CT) studies have demonstrated structural brain abnormalities including cortical atrophy and enlarged lateral ventricles in a subset of schizophrenic patients including those with abnormal involuntary movements. In the following series of studies, we present our findings

Caudate nucleus morphology in tardive dyskinesia.

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OBJECTIVE The objective of this project was to test whether there are differences in the size of the caudate nucleus in schizophrenic in-patients with and without tardive dyskinesia. METHODS The study was cross-sectional in design, examining group differences between institutionalised schizophrenic

Increased S100B serum levels in schizophrenic patients with tardive dyskinesia: association with dyskinetic movements.

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Several studies show that calcium-binding protein S100B is increased in schizophrenia and may be involved in the pathogenesis of tardive dyskinesia (TD). We therefore compared serum S100B levels in normal controls (n=60), schizophrenic patients with (n=32) and without TD (n=50). Assessments included

Taste disorder in facial onset sensory and motor neuronopathy: a case report.

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Taste disorder is a common symptom in the general population. Several studies have shown that patients with neurological disorders, such as amyotrophic lateral sclerosis and Parkinson's disease, develop taste disturbance. Facial onset sensory and motor neuronopathy (FOSMN) is a rare

Familial psychosis and vulnerability to tardive dyskinesia.

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The demography, course of illness, cognitive dysfunction and neurological consequences of long term treatment of 11 family pairs with long history of chronic schizophrenic illness were studied. There was concordance for the presence of tardive dyskinesia in 6 pairs; each of 2 brother-brother pairs;

Cognitive dysfunction in chronic schizophrenia followed prospectively over 10 years and its longitudinal relationship to the emergence of tardive dyskinesia.

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Basic cognitive function was assessed at initial and at 5- and 10-year follow-up assessments among 41 primarily middle-aged in-patients manifesting the severest form of schizophrenia; additionally, the presence and severity of tardive dyskinesia was evaluated on each occasion. Overall, there was a

Vitamin E for antipsychotic-induced tardive dyskinesia.

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Antipsychotic (neuroleptic) medication is used extensively to treat people with chronic mental illnesses. Its use, however, is associated with adverse effects, including movement disorders such as tardive dyskinesia (TD) - a problem often seen as repetitive involuntary movements around the mouth and

Noradrenergic and neuroradiological abnormalities in tardive dyskinesia.

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Previous studies suggest that catecholaminergic overactivity and structural brain damage may contribute to the pathogenesis of tardive dyskinesia (TD). Although dopaminergic (DA) mechanisms, specifically postsynaptic receptor supersensitivity, have been extensively studied, equally plausible

Can the supersensitivity of rodents to dopamine be regarded as a model of tardive dyskinesia?

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1. The paper presents arguments derived from both, clinical work and animal experiments, for or against the traditional hypothesis suggesting that tardive dyskinesia (TD) is caused by supersensitivity to dopamine. The main aim of this study was to answer the question posed in the title - whether the

Valbenazine for the treatment of tardive dyskinesia.

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BACKGROUND Tardive dyskinesia (TD) is a hyperkinetic movement disorder that may result from treatment with antipsychotics or other dopamine receptor blocking agents. Underlying pathophysiology is incompletely understood but since the 1970s dopamine depleting agents have been used to reduce

Treatment of neurolept-induced tardive dyskinesia.

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Tardive dyskinesia (TDK) includes orobuccolingual movements and "piano-playing" movements of the limbs. It is a movement disorder of delayed onset that can occur in the setting of neuroleptic treatment as well as in other diseases and following treatment with other drugs. The specific

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