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[A clinico-MRI study of extrapyramidal symptoms in multiple system atrophy--linear hyperintensity in the outer margin of the putamen].

We did a clinico-MRI study concerning extrapyramidal symptoms and T2-weighted MRI findings of the putamen in twenty patients with multiple system atrophy (MSA) as well as twenty-five with idiopathic Parkinson's disease. Nine out of twenty MSA patients showed extrapyramidal symptoms. And we could not observe cerebellar ataxia in two of these patients because of severe rigidity and akinesia. Eight out of nine MSA patients with extrapyramidal symptoms showed linear hyperintensity in the outer margin of the putamen. This abnormal intensity was bilateral and symmetric in most patients. However, in MSA patients without extrapyramidal symptoms, only one patient showed the linear hyperintensity. We could not find such abnormal intensity in any patients with Parkinson's disease. On proton density MRI, the signal intensity in the lesion was higher than that in the gray matter, which leads the speculation that the hyperintensity is gliosis of the putamen or increased extracellular fluid space caused by severe shrinkage of the putamen. This characteristic MRI finding is useful to distinguish MSA with extrapyramidal symptoms from Parkinson's disease.

Aged↗

[Magnetic resonance in Hallevorden-Spatz disease].

The Hallevorden-Spatz disease should be suspected in children or young people with motor, pyramidal or extrapyramidal symptomatology and deterioration of superior functions specially upon the existence of family history. Pathognomonic diagnosis may only be obtained by necropsy but magnetic resonance images, although not pathognomic, are sufficiently characteristics to strongly support the diagnosis. Four cases of Hallevorden-Spatz disease are presented with special emphasis on the MR images characteristic of this disease.

Adolescent↗

Compazine.

Explore the source record for details and available documents.

Adult↗

Cocaine-induced sensitization of metabolic activity in extrapyramidal circuits involves prior dopamine D1-like receptor stimulation.

Chronic cocaine treatment leads to the development of behavioral sensitization in experimental animals. The neural circuitry underlying sensitization was studied using the quantitative 2-deoxyglucose technique, with a modification of a rapid procedure that produces locomotor and neurochemical sensitization. Acute cocaine treatment, administered by i.p. injection, increased the regional cerebral metabolic rate for glucose (rCMRglc) in various extrapyramidal regions, compared with saline vehicle treatment, as previously reported. Repeated cocaine treatment further increased rCMRglc in the entopeduncular nucleus and the substantia nigra pars reticulata, producing a sensitized metabolic response only in regions innervated by direct striatonigral neurons. Repeated cocaine treatment also increased rCMRglc in the nucleus accumbens, hippocampus, dentate gyrus and laterodorsal thalamus, as well as sensory and motor cortices, compared with saline vehicle treatment. The pharmacology underlying this sensitized metabolic response to cocaine was investigated by administering either dopamine D1- or D2-like receptor agonists on the first treatment day, followed by cocaine on the final day. Prior treatment with quinpirole (0.2 mg/kg, i.p.), a D2-like receptor agonist, produced metabolic responses that were significantly lower than those produced by repeated cocaine treatment in the entopeduncular nucleus and substantia nigra pars reticulata, similar to those of acute cocaine treatment. In contrast, prior treatment with SKF 38393 (2.0 mg/kg, l.p.), a partial D1-like receptor agonist, increased rCMRglc in the entopeduncular nucleus and substantia nigra pars reticulata, although not as much as did repeated cocaine treatment. These data suggest that the development of metabolic sensitization in striatonigral circuits involves prior D1-like receptor activation.

Animals↗

[Extrapyramidal signs in Alzheimer's disease].

Extrapyramidal signs were assessed in 112 patients satisfying NINCDS/ADRDA criteria for probable Alzheimer's disease. They were present in 50% of the patients. The most common features of them were bradykinesia and rigidity. Resting tremor was rarely encountered. There were no significant differences in age of onset, symptom duration, presence of primitive reflexes and psychotic symptoms between cases with and without extrapyramidal signs, while the presence of extrapyramidal signs was associated with statistically significant greater dementia severity.

Age of Onset↗

[Risperidone in the treatment of chronic schizophrenia: multicenter study comparative to haloperidol].

OBJECTIVE: This study was designed to compare the efficacy and safety of five different doses of risperidone with a fixed dose of haloperidol in patients with chronic schizophrenia. METHOD: After a 1-week single-blind, placebo washout phase, 99 chronic schizophrenic patients were randomly assigned to double-blind treatment with 1, 4, 8, 12 or 16 mg risperidone or 10 mg haloperidol daily for 8 weeks. Efficacy was assessed throughout the study by the Positive and Negative Syndrome Scale (PANSS) for schizophrenia, and Clinical Global Impression (CGI). Safety assessments included the Extrapyramidal Symptom Ratinf Scale (ESRS) UKU Side Effect Rating Scale, vital signs, body weight, ECG and laboratory screening. RESULTS: Risperidone had a bell-shaped dose-response curve, with optimal therapeutic responses occurring at a daily dose of 8 mg. The therapeutic response to haloperidol was similar to that seen with risperidone 16 mg. Risperidone was associated with significantly less extrapyramidal symptoms than haloperidol, as assessed by the ESRS. The effect was mirrored by the requirement for antiparkinson rescue medication. Furthermore, the overall incidence of adverse events was markedly lower with the optimum dose of risperidone than with haloperidol. CONCLUSIONS: Risperidone is at least as effective as haloperidol for the treatment of chronic schizophrenia. Moreover, risperidone is associated with an improved adverse event profile and significantly less extrapyramidal symptoms which will have beneficial implications on patient quality of life and compliance. These results are in agreement with the results from the international multicenter trial.

Adult↗

Clinical, morphological, biochemical, and neuroradiological features of mitochondrial encephalomyopathies. Presentation of 19 patients.

Nineteen patients (9 females, 10 males) with mitochondrial encephalomyopathies (ME) were studied. The diagnosis was established according to clinical and histopathological criteria. Leading clinical features were chronic progressive external ophthalmoplegia (CPEO) and muscle weakness in 95% of the patients. Pigmentary retinopathy was seen in 63%, and was always associated with CPEO. Hypacusis was present in 47% and cerebellar ataxia in 63% of patients. Clinical or electrophysiological signs of involvement of the central nervous system (CNS) were found in 21% of the patients. In muscle biopsy ragged red fibers were the predominant histopathological findings (100% of the patients), while COX-negative fibers were seen in 74%, deletions of the mitochondrial DNA in 42%, and defects of the respiratory chain in 32% of the patients. Increased blood lactate levels were found in 79% of the patients. Needle electromyography revealed myopathic features in 74%, features of denervation in 16%, and was normal in the remainder. Imaging studies showed cerebral atrophy in 58%, cerebellar atrophy in 16%, and hyperintense lesions of the white matter, pyramidal tract or extrapyramidal system in 16% of the cases. It is concluded that the clinical manifestations of ME can be very variable. Diagnosis of ME should be always considered in young patients presenting with CPEO and muscle weakness. In most cases, diagnosis can be made by a few selected investigations, while detection of genetic abnormalities may lead to the diagnosis in the remaining cases.

Adult↗

New drugs for schizophrenia: an update for family physicians.

The prognosis in patients with schizophrenia is worsened the longer the duration of psychosis before institution of effective antipsychotic therapy and the greater the number of psychotic relapses. Use of traditional antipsychotic medications has been limited by their substantial side effects and failure to achieve long-term control of symptoms in some cases. New "atypical" antipsychotic drugs show promise for the treatment of resistant cases of schizophrenia and improvement in patient tolerance and compliance. These medications have been more successful than traditional antipsychotic drugs in treating the negative symptoms of schizophrenia, such as social withdrawal and apathy. The atypical antipsychotic drugs produce fewer extrapyramidal side effects and no tardive dyskinesia or dystonia. However, they are associated with induction of neuroleptic malignant syndrome, and clozapine can produce fatal agranulocytosis. Atypical antipsychotic drugs on the market currently include clozapine, risperidone and olanzapine. Use of these medications in selected patients who do not benefit from, or cannot tolerate, traditional agents is an important step in improving the lives of patients with schizophrenia.

Antipsychotic Agents↗

Hereditary cerebellar cortical and extrapyramidal nuclear abiotrophy in Kerry Blue Terriers.

Ten Kerry Blue terriers from a kennel in New York and 3 from a kennel in California developed clinical signs of a progressive cerebellar disorder, with its onset between 9 and 16 weeks of age. In 9 sequential necropsies, progressive cerebellar cortical degeneration, with loss of Purkinje's cells, was demonstrated. As the disease progressed, there was bilateral symmetric degeneration of the olivary nuclei followed by degeneration of the substantia nigra and caudate nucleus, bilaterally. The California and New York dogs were related, and an autosomal recessive inheritance was proposed for the disease.

Animals↗

[Cranial acupuncture in the treatment of spasticity. Clinical results].

Hospitals in communist China perfected a new acupuncture technique about 3 yrs ago, whereby needles are placed in the scalp to stimulate the cortical centres below. This method is particularly indicated in subjects with neurological damage. Results observed in 45 subjects with cerebral vasculopathy at the neurological clinic of Pisa University and the reflexotherapy service of the University of Turin were encouraging and suggest that clinical experimentation should be attempted on a wider scale.

Acupuncture Therapy↗

[Testing basic visual functions in the evaluation of extrapyramidal side effects of antipsychotic agents].

One of the cornerstones of antipsychotic therapy is the evaluation of the effective dose that cause minimal extrapyramidal side effects. It is known that the visual system (e. g. the retina) contains dopaminergic cells similarly to the striatum where dopaminergic blockade is crucial in the induction of extrapyramidal symptoms. This rises the possibility that striatal functions can be tested by the evaluation of certain visual functions. This study compared the visual contrast-sensitivity of 20 schizophrenic patients on antipsychotic medication (9 patients were on risperidone, 9 on haloperidol, and 1-1 on zuclopenthixol and fluanxol treatment) to that of normal control subjects, and found significant impairment in the former group. The contrast-sensitivity impairments correlated with the severity of extrapyramidal symptoms. These results suggest that contrast-sensitivity measurements can be useful in the evaluation of neuroleptic threshold in the clinical practice.

Adult↗

[Changes in the ultrastructure of the motor zone of the cortex and various areas of the rats pyramidal system in acute toxic action of phenazepam].

As it was revealed by electron microscopic study, phenazepam (benzodiazepine representative) administered to rats in acute toxic dose caused astrocyte processes swelling mainly in reticular portion of substantia nigra and cerebral areas with high density of GABAergic synapses in initial intoxication stage (one hour after the drug introduction). Following 24 hrs changes of axodendritic and axo-somatic synapse postsynaptic part were detected similar to those of myoneural synapses induced by anti-cholinesterase agents, which allows to suggest the contribution of the increased intracellular calcium ions content. Specific benzodiazepine receptor agonist-flumazenil, introduced 30 min later than phenazepam leaded to the decrease of ultrastructural changes in postsynaptic part of the synapses in reticular zone of substantia nigra. Thus toxic effect of drugs that cause prolonged activity of peripheral and central synapses postsynaptic part results in the alike ultrastructural changes irrespective of their mediator type and is likely to be connected with the growth of intracellular calcium concentration.

Animals↗

[Extrapyramidal toxicity caused by metoclopramide and clebopride: study of voluntary notifications of adverse effects to the Spanish Drug Surveillance System].

OBJECTIVE: To clarify if there is any basis for the hypothesis that Clebopride leads to more extrapyramidal reactions than Metoclopramide. DESIGN: Observational, longitudinal, retrospective and comparative study of two series of cases. SETTING: The entire Spanish healthcare system. PATIENTS: Those notified to the Spanish Drug watch system as possibly having suffered an adverse reaction to Metoclopramide (n = 98) or Clebopride (n = 123) between 1/1/1990 and 10/6/1997. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: 84.3% of suspected adverse reactions to Clebopride and 51.6% of those to Metoclopramide had a non-hospital precedence (P < 0.001). In 48.0% of suspected adverse reactions to Metoclopramide and 72.4% of those to Clebopride, there was extrapyramidal toxicity (P = 0.021). CONCLUSIONS: There is a basis for the hypothesis that Clebopride causes more extrapyramidal reactions than Metoclopramide. It was reasonable to realize a study based on this hypothesis.

Adult↗