Severity Of Involuntary Movements Research Articles

Associations between polymorphisms in the cannabinoid receptor 1 gene, cognitive impairments and tardive dyskinesia in a Chinese population with schizophrenia

ObjectiveTardive dyskinesia (TD) is a medically induced movement disorder that occurs as a result of long-term use of antipsychotic medications, commonly seen in patients with schizophrenia (SCZ). The study aimed to investigate the relationship between single nucleotide polymorphisms (SNPs) of the CNR1 gene, TD and cognitive impairments in a Chinese population with SCZ. MethodsA total of 216 SCZ patients were recruited. The participants were divided into TD and without TD (WTD) groups using the Schooler-Kane International Diagnostic Criteria. The severity of TD was assessed using the Abnormal Involuntary Movement Scale (AIMS). Cognitive function was assessed using the Repeatable Battery for Assessment of Neuropsychological Status (RBANS) scale. Hardy-Weinberg equilibrium tests, chained disequilibrium analyses and haplotype analyses were performed using SHE-sis software. To explore the main effects of TD diagnosis, genotype and cognitive function, as well as interaction effects, analysis of covariance (ANCOVA) was employed. ResultsThe prevalence of TD was approximately 27.3%. Significant differences were observed in the rs806368 CT genotype and rs806370 TC genotype within the hypercongenic pattern between the male TD and WTD groups (OR = 2.508, 95% CI: 1.055–5.961, p = 0.037; OR = 2.552, 95% CI: 1.073–6.069, p = 0.034). Among TD patients, those carrying the rs806368 CC genotype exhibited higher limb trunk scores (p < 0.05). Moreover, there was a statistically significant difference in visuospatial/construction between the TD and WTD groups (p = 0.04), and a borderline significant difference in visuospatial/construction when considering the interaction between TD diagnosis and genotype at the rs806368 locus (p = 0.05). ConclusionCNR1 rs806368 and rs806370 polymorphisms may play a role in TD susceptibility. Additionally, CNR1 gene polymorphisms were associated with the severity of involuntary movements and cognitive impairments in TD patients.

Expanding phenomenologic heterogeneity of tardive syndromes: Time for an updated assessment tool

Tardive syndromes (TDS) are a group of hyperkinetic and hypokinetic movement disorders that occurs after exposure to dopamine receptor blocking agents such as antipsychotic and antiemetic drugs. The Abnormal Involuntary Movement Scale (AIMS) is a widely used instrument that has become the standard for assessment of tardive dyskinesia (TDD), the most common form of TDS. However, the AIMS has a number of clinimetric limitations and was designed primarily to assess the anatomic distribution and severity of involuntary movements without regard to phenomenology. To build on recent advances in understanding and treatment of TDS, re-evaluation and revision of the AIMS that could aid both clinical practice and research may be worthwhile. Challenges, such as retaining the efficiency of the current AIMS, incorporating evaluation of impairment in daily activities, and re-training clinicians for a revised examination procedure and rating instrument, are very likely surmountable.

Dysfunctional inhibitory control in Parkinson's disease patients with levodopa-induced dyskinesias.

Chronic dopamine replacement therapies in Parkinson's disease can induce side effects, such as levodopa-induced dyskinesias and impulse control disorders. A dysfunction of inhibitory brain networks has been related to both disorders; however, there is no clear behavioral evidence supporting this hypothesis. We aimed to determine whether PD patients with levodopa-induced dyskinesias show features of increased impulsivity in parallel with altered motor inhibition. Two matched samples of Parkinson's disease patients with (n = 14) or without (n = 14) levodopa-induced dyskinesias and a control group (n = 10) participated in the study. All groups were evaluated by the Barratt Impulsiveness Scale-11 to assess impulsivity traits. Furthermore, participants performed a stop signal task to evaluate reactive-motor inhibition and a Go/NoGo task to evaluate proactive-inhibitory control. PD patients were tested both in OFF and ON levodopa medication. Parkinson's disease patients with levodopa-induced dyskinesias showed higher impulsivity scores than PD patients without levodopa-induced dyskinesias. Dyskinetic patients presented also delayed stop signal reaction times indicating a worse performance in reactive inhibition. The slowness in inhibiting a motor command correlated with the impulsiveness scores. Furthermore, in the dyskinetic group, a positive correlation was found between stop reaction times and the severity of involuntary movements. Under the effect of levodopa, all patients were faster but dyskinetic patients were significantly less accurate in proactive inhibition. Inhibitory control is compromised in dyskinetic patients in parallel with increased impulsivity, revealing an impairment of motor and behavioral inhibitory control in Parkinson's disease patients with levodopa-induced dyskinesias.

Unawareness of deficits in Huntington's disease.

People with Huntington's disease (HD) may show reduced awareness of physical and mental changes in themselves. This article reviews the evidence for loss of awareness (anosognosia) in an attempt to elucidate its characteristics and possible underlying mechanisms. It is shown that defective awareness occurs across domains. People with HD may under-report the presence or severity of involuntary movements, under-estimate cognitive impairment and deny behavioural change. Nevertheless, awareness is not all or none. Moreover, it may be affected differentially for different symptom domains and emerge at different stages of disease, raising the possibility of distinct contributory mechanisms. Findings of an inverse relationship between insight and severity of disease suggest that cognitive impairment, in particular executive dysfunction, may be an important contributory factor. Evidence has accrued to support this argument. However, cognitive impairment cannot fully account for patients' lack of awareness of involuntary movements. Findings that patients accurately report consequences but not the experience of involuntary movements, and better acknowledge their presence when watching videotapes of themselves suggests that physiological factors play an important role. The putative role of denial as a coping mechanism is discussed. Recognition by clinicians of deficient self-awareness is crucial because of its implications for diagnosis and optimal clinical management of HD.

Involuntary movements and their correlates in first-episode psychoses

Involuntary movements and their correlates in first-episode psychoses

I10 In vivo evidence of decreased nigrostriatal terminals in Huntington's disease: a SPECT study

BackgroundHuntington's disease (HD) is pathologically characterised by a selective neurodegeneration of vulnerable populations of neurons, with an early marked neuronal loss and atrophy in the neostriatum. Dopaminergic innervations of neostriatal...

Increased serum levels of CCL11/eotaxin in schizophrenia

Background Inflammatory and immune alterations occur and may be relevant in patients with schizophrenia. Chemokines are a subgroup of cytokines that play a major role in the recruitment of determined subsets of leukocytes into tissues. To date no study has evaluated whether levels of chemokines are altered in patients with schizophrenia. Objective To evaluate serum levels of CC and CXC chemokines of schizophrenic patients and age- and gender-matched controls. Methods Forty male institutionalized schizophrenic patients (mean ± SD age, 52.3 ± 9.9) and 20 asymptomatic matched controls were recruited for this study. Severity of symptoms was assessed using BPRS, PANSS and AIMS. All patients were under typical antipsychotic treatment. Serum concentrations of chemokines were measured by ELISA. Results There was no statistical difference in serum levels of CCL2, CCL3, CCL24, CXCL9 and CXCL10 between controls and patients. Serum levels of CCL11 were increased in schizophrenic patients when compared to controls. Serum levels of chemokines were not correlated with the length of disease or hospitalization and the severity of involuntary movements, positive and/or negative symptoms. Conclusion CCL11 is a ligand for CCR3, a receptor expressed preferentially on Th2 lymphocytes, mast cells and eosinophils. Higher serum levels of CCL11 in schizophrenia reinforce the view that this disease may be associated with a Th1/Th2 imbalance with a shift toward a Th2 immune response.

Kraepelinian and non-Kraepelinian schizophrenia subgroup differences in cerebral metabolic rate

We studied two subtypes of schizophrenia, the Kraepelinian subtype ( n=10) characterized by an unremitting and severe course and the non-Kraepelinian subtype ( n=17) characterized by a remitting course and some periods of self-care. Patients were assessed with positron emission tomography (PET) with 18F-deoxyglucose (FDG) and high-resolution magnetic resonance imaging (MRI). A group of 32 age- and sex-matched normal volunteers served as comparison subjects. During the FDG tracer uptake period, patients performed a serial verbal learning task. MR images were segmented into gray, white and cerebrospinal fluid regions, and warped to average normal coordinates. PET images were coregistered to the MR images and similarly warped for analysis. Kraepelinian subtype patients were characterized by lower metabolic rates in the temporal lobe and cingulate gyrus, and lower fronto/occipital ratios than non-Kraepelinian subtype patients. Exploratory statistical probability mapping also revealed lower metabolic rates in the right striatum in Kraepelinian versus non-Kraepelinian patients. These differences could not be attributed to differences in age, symptom severity, task performance during FDG uptake, or severity of involuntary movements. Factor analysis of the cortical surface identified significantly lower temporal lobe metabolic rates in Kraepelinian patients than non-Kraepelinian patients. A combined frontal/temporal deficit or greater cortical change may be associated with poorer longitudinal course.

Cognitive impairment, clinical course and treatment history in out-patients with bipolar affective disorder: relationship to tardive dyskinesia.

Clinical, neuropsychological and psychopharmacological characteristics were investigated for their ability to distinguish individuals with and without involuntary movements (tardive dyskinesia), among a population of 40 out-patients with bipolar affective disorder and a history of exposure to neuroleptics and lithium. Impaired performance on a test of cognitive flexibility bore the primary association with both the presence and the severity of involuntary movements. The additional relationships identified emphasized further that individual vulnerability to involuntary movements appeared to be associated not with greater duration or dosage of treatment, but with features of the bipolar illness, including number and type of affective episodes, for which that treatment was prescribed.

Correlation between facial involuntary movements and abnormalities of blink and corneal reflexes in Huntington's chorea.

Blink and corneal reflexes were studied in 11 patients with Huntington's chorea and the results compared with the severity of the disease. The latency of the R2 component of the blink reflex was delayed and the duration of R2 and of the corneal reflex (CR) prolonged. A greater habituation of the R2 component was found in the patients with involuntary movements in the face, and in some patients a long-lasting depression of R2 was present. A correlation was found between: (a) severity of involuntary face movements and R2 and CR latency and (b) severity of involuntary movements in the neck and latency of R2.

Transdihydrolisuride in parkinsonism.

The semisynthetic lisuride derivative transdihydrolisuride (terguride, TDHL) is an effective antiparkinsonian drug. In animals, TDHL appears to possess mixed dopamine agonist-antagonist effects, but this may not be the case in man. Single doses of TDHL were given to 21 subjects with parkinsonism. Overall, TDHL 0.25-0.5 mg caused dose-related improvement in parkinsonism for periods of up to 6 h, although 8 of 21 subjects showed no improvement or deterioration with TDHL 0.5-1 mg. In three patients with levodopa-induced psychosis, the addition of TDHL 0.75 mg daily for 5-10 days did not alter the psychotic state. In three subjects with levodopa-induced dyskinesias, the addition of TDHL 0.75 mg daily for 14 days resulted in a slight increase in the severity of involuntary movements. Side-effects of TDHL, sickness and hypotension, were similar to those observed with levodopa. Transdihydrolisuride caused prolonged inhibition of prolactin release, but unlike levodopa did not elevate plasma growth hormone levels. Additionally, TDHL did cause considerable sedation. These results may be due to combined effects of TDHL on nondopamine as well as dopamine neurotransmitter systems, rather than to partial or incomplete dopamine agonist effects.

Serotonergic functions in man.

Abundant preclinical evidence suggests that serotonin-containing neural systems may participate in the regulation of both extrapyramidal and neuroendocrine function. In an attempt to examine these possibilities in man, patients with various neurologic disorders received drugs believed to facilitate or inhibit serotonergic function. Extrapyramidal signs in patients with parkinsonism or Huntington's disease showed no consistent change with L-tryptophan or parachlorophenylalanine. Unexpectedly, L-5-hydroxytryptophan, given in combination with a peripheral decarboxylase inhibitor, caused a worsening of parkinsonian akinesia and rigidity. Fenfluramine, at doses which appeared to diminish central serotonin but not dopamine turnover, had no consistent effect on the severity of involuntary movements in patients with Huntington's chorea, but did produce a significant rise in plasma prolactin.