Three Cases of Respiratory Dyskinesia

Abstract: We present here three cases of respiratory dyskinesia (RD). RD was observed with a video recording and other recordings were made of a respiratory airflow with a thermistor, and abdominal movement with a strain gauge. Neurological findings end CT scanning indicated marked organic changes in the brain in these 3 cases. RD was complicated with tardive dyskinesia of the tongue and lips, and the symptoms were aggravated during stress and absent during sleeping, which are the characteristic features of extrapyramidal symptoms. The symptoms of the three cases have improved by decreasing the dose of butyrophenone derivatives and discontinuing anti-parkinsonian drugs, which suggested that an intracerebral imbalance of DA and ACh may be the cause of RD.     

Effects of haloperidol and its pyridinium metabolite on plasma membrane permeability and fluidity in the rat brain

The use of antipsychotic drugs is limited by their tendency to produce extrapyramidal movement disorders such as tardive dyskinesia and parkinsonism. In previous reports it was speculated that extrapyramidal side effects associated with the butyrophenone neuroleptic agent haloperidol (HP) could be caused in part by the neurotoxic effect of its pyridinium metabolite (HPP(+)). Although both HPP(+) and HP have been shown to induce neurotoxic effects such as loss of cell membrane integrity, no information exists about the difference in the neurotoxic potency, especially in the potency to induce plasma membrane damage, between these two agents. In the present study, we compared the potency of the interaction of HPP(+) and HP with the plasma membrane integrity in the rat brain. Membrane permeabilization (assessed as [(18)F]2-fluoro-2-deoxy-d-glucose-6-phosphate release from brain slices) and fluidization (assessed as the reduction in the plasma membrane anisotropy of 1,6-diphenyl 1,3,5-hexatriene) were induced by HPP(+) loading (at >or=100 microM and >or=10 microM, respectively), while comparable changes were induced only at a higher concentration of HP (=1 mM). These results suggest that HPP(+) has a higher potency to induce plasma membrane damage than HP, and these actions of HPP(+) may partly underlie the pathogenesis of HP-induced extrapyramidal side effects.     

Clinical Variants of Tardive Dyskinesia in Japan

Abstract: Involuntary movement disorders were investigated in a psychiatric hospital in Japan. The prevalence of tardive dyskinesia was 9.9 % and four clinical variants of tardive dyskinesia could be classified. Of the 716 patients, tardive dystonia was identified in 15 cases, tardive akathisia in one, respiratory dyskinesia in two and rabbit syndrome in 17. The existence of tardive forms for acute dystonic reactions and akathisia suggests that any type of acute extrapyramidal symptoms can have a tardive form.     

Movement disorders in clinical research

Measuring (extrapyramidal) psychotic disorders often is a highly relevant part of clinical research into the course and treatment of movement disorders. Traditionally these disorders have always been assessed on the basis of a well-known set of rating scales. The limitations and shortcomings of these scales are discussed in the article. It is argued that a new standard instrument needs to be developed for the measurement of movement disorders. The SADIMOD can be regarded as a good starting point for the development of such an instrument.     

Comparative study between two animal models of extrapyramidal movement disorders: prevention and reversion by pecan nut shell aqueous extract

Acute reserpine and subchronic haloperidol are animal models of extrapyramidal disorders often used to study parkinsonism, akinesia and tardive dyskinesia. In humans, these usually irreversible and disabling extrapyramidal disorders are developed by typical antipsychotic treatment, whose pathophysiology has been related to oxidative damages development. So far, there is no treatment to prevent these problems of the psychiatric clinic, and therefore further studies are needed.Here we used the animal models of extrapyramidal disorders cited above, which were performed in two distinct experiments: orofacial dyskinesia (OD)/catalepsy induced by acute reserpine and subchronic haloperidol after (experiment 1) and before (experiment 2) oral treatment with pecan shell aqueous extract (AE), a natural and promissory antioxidant.When administered previously (exp.1), the AE prevented OD and catalepsy induced by both reserpine and haloperidol. When reserpine and haloperidol were administered before the extract (exp.2), the animals developed OD and catalepsy all the same. However, the orofacial parameter (but not catalepsy) in both animal models was reversed after 7 and 14 days of AE treatment. These results indicate that, acute reserpine and subchronic haloperidol administrations induced similar motor disorders, although through different mechanisms, and therefore are important animal models to study the physiopathology of extrapyramidal disorders. Comparatively, the pecan shell AE was able to both prevent and reverse OD but only to prevent catalepsy. These results reinforce the role of oxidative stress and validate the two animal models used here. Our findings also favor the idea of prevention of extrapyramidal disorders, rather than their reversal.     

Movement disorders in Alzheimer's disease: more rigidity of definitions is needed.

Rigidity, slowness, gait impairment, and other disorders of movement accompany Alzheimer's disease (AD) at various stages of the illness. The presence of these so-called extrapyramidal features have been reported to predict disease prognosis and pathologic localization. Unfortunately, failure to accurately characterize the movement disorder, particularly to distinguish parkinsonism from cortically based motor disturbances (that is, paratonia, apraxia), makes the results of many published studies difficult to interpret. There is an important need to precisely characterize movement disorders in studies of AD to clarify the clinical phenomenology and neurobiology of the condition and to accurately distinguish AD from other degenerative dementias, such as dementia with Lewy bodies.     

Psychogenic movement disorders

PURPOSE OF REVIEW: This review focuses on recent studies assessing clinical features and laboratory findings that may help diagnose psychogenic movement disorders, and the ongoing controversy about the relationship of these disorders with preceding peripheral injury. RECENT FINDINGS: 'Organic' movement disorders may still be misdiagnosed as psychogenic. Probably more commonly, however, psychogenic movement disorders are underdiagnosed. Most features typically associated with recognized movement disorders, including geste antagoniste or treatment-induced dyskinesias, can be seen in psychogenic movement disorder, and abnormal movements that would not normally be considered psychogenic or produced by psychological factors, such as palatal tremor, may occur on a psychogenic basis. On the other hand, psychiatric features are sometimes seen in neurologically based movement disorders. The diagnostic criteria for psychogenic movement disorders provide a degree of diagnostic certainty based on a combination of clinical and psychiatric features. Laboratory investigations can help exclude specific diagnoses, such as Parkinson's disease with (123I)beta-CIT single photon emission computed tomography, and neurophysiological methods can demonstrate characteristic features of psychogenic movement disorders, such as entrainment or suppression of psychogenic tremor with contralateral hand movements. However, some tests reported to differentiate psychogenic from neurological movement disorders may have incomplete specificity; for example, psychogenic tremor may not always be associated with complete coherence of tremor frequency. An ongoing controversy surrounds movement disorders following peripheral injuries, but recent evidence suggests that such patients should always be screened for the presence of a psychogenic movement disorder. SUMMARY: Psychogenic movement disorder continues to be a difficult diagnosis to make and is likely to be underrecognized. Clinical and laboratory features are emerging, however, that support this diagnosis. The controversy regarding posttraumatic movement disorders continues, but a diagnosis of a psychogenic movement disorder should be actively sought in such patients.     

Delayed chorea after recovery from a symmetric parkinsonian syndrome due to striatal myelinolysis

Extrapontine myelinolysis (EPM) is rare and usually results from osmotic stress due to inappropriate correction of electrolyte disturbances. Parkinsonism is a relatively common manifestation of EPM, seen in 60% of patients. Dopaminergic therapy leads to good recovery in many patients. Delayed extrapyramidal manifestations, including hyperkinetic movement disorders such as chorea or dystonia, are postulated to result from aberrant neuronal regeneration or denervation supersensitivity following the initial osmotic insult. We present a patient with a symmetric parkinsonian syndrome due to EPM involving the striatum who made a good recovery with levodopa therapy, only to develop chorea five months later. The possible mechanisms underlying the genesis of these movement disorders in EPM is discussed.     

Movement disorders induced by antipsychotic drugs: implications of the CATIE schizophrenia trial

Drug-induced movement disorders have dramatically declined with the widespread use of second-generation antipsychotics, but remain important in clinical practice and for understanding antipsychotic pharmacology. The diagnosis and management of dystonia, parkinsonism, akathisia, catatonia, neuroleptic malignant syndrome, and tardive dyskinesia are reviewed in relation to the decreased liability of the second-generation antipsychotics contrasted with evidence from the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) Schizophrenia Trial. Data from the CATIE trial imply that advantages of second-generation antipsychotics in significantly reducing extrapyramidal side effects compared with haloperidol may be diminished when compared with modest doses of lower-potency first-generation drugs.