Canadian Journal of Neurological Sciences 

About: Canadian Journal of Neurological Sciences is an academic journal published by Cambridge University Press. The journal publishes majorly in the area(s): Medicine & Population. It has an ISSN identifier of 0317-1671. Over the lifetime, 5688 publications have been published receiving 105450 citations. The journal is also known as: The Canadian journal of neurological sciences.

The Impact of Fatigue on Patients with Multiple Sclerosis

Abstract: Although fatigue is recognized as a symptom of MS, there have been insufficient methods for evaluating this symptom We administered the Fatigue Impact Scale to 85 MS patients and 20 hypertensive patients Neurologic impairment, mental health, and general health status were also assessed MS patients reported significantly higher fatigue impact than hypertensive patients Most MS patients reported fatigue as either their worst (14%), or one of their worst (55%) symptoms Disease classification and neurologic impairment had little bearing on Fatigue Impact Scale scores in the MS sample The best predictive models for mental health and general health status in the MS sample both included the Fatigue Impact Scale as a significant factor This study demonstrates that: 1) fatigue is a very prevalent and severe problem in MS, 2) fatigue impact cannot be predicted by clinical measures of neurologic impairment, 3) fatigue has a significant effect on the mental health and general health status of MS patients

Accuracy of clinical diagnosis in parkinsonism--a prospective study.

Abstract: Clinical diagnosis of Parkinson's syndrome (PS) is reasonably easy in most cases but the distinction between different variants of PS may be difficult in early cases. The correct diagnosis is not only important for counselling and management of patients but also in conducting pharmacological and epidemiological studies. There is very little critical literature on the pathological verification of the clinical diagnosis in PS. We report our 22 years experience to address that issue. Between 1968 and 1990, 65 PS patients came to autopsy. Complete data are available in 59 (M-50, F-19) cases. The initial diagnosis made by a qualified neurologist was idiopathic Parkinson's disease (IPD) in 43 cases. Of those 28 (65%) had Lewy body pathology. After a mean duration of 12 years the final diagnosis was IPD in 41 cases which was confirmed in 31 (76%). The IPD could not be clinically distinguished from cases with severe substantia nigra neuronal loss without inclusions or from those with neurofibrillary tangle inclusions and neuronal loss at the anatomical sites typically involved in IPD. All progressive supra-nuclear palsy, olivopontocerebellar atrophy, Jakob-Creutzfeldt's disease and the majority of the multiple system atrophy cases were diagnosed correctly during life. The correct clinical diagnosis in most non-IPD variants of PS was possible within 5 years of onset (range: 2 months to 18 years). We recommend that studies aimed at including only the IPD cases restrict the enrollment to those cases that have had PS motor manifestations for five years or longer duration.

Frontal behavioral inventory: diagnostic criteria for frontal lobe dementia.

Abstract: Objective To utilize the diagnostic criteria of frontal lobe dementia (FLD) Methods We studied 12 patients with FLD diagnosed clinically, with radiological confirmation in 10 and autopsy confirmation in 2; sixteen patients with Alzheimer's disease matched for stage and severity to FLD and 11 patients with depressive dementia were used as control groups A 24-item Frontal Behavioral Inventory (FBI) using the most relevant behavioral manifestations of FLD was administered in these populations Results FLD patient scores on the FBI were much higher compared with control groups (AD and DD) Item analysis showed loss of insight, indifference, distractibility, personal neglect and apathy as the most frequent negative symptoms Perseveration, disinhibition, inappropriateness, impulsivity, and irresponsibility were the most significant positive symptoms An operational definition of FLD included a minimum FBI score of 27 Only one false positive was shown in the depressive group and none among the AD group, indicating little overlap between patient groups, and a high discriminating value of the FBI Conclusions The FBI appears to be a useful diagnostic instrument and a method to operate the behavioral criteria of FLD Further prospective studies are warranted to establish validity

3-Nitropropionic acid-exogenous animal neurotoxin and possible human striatal toxin.

Abstract: 3-Nitropropionic acid (3-NPA) — a suicide inhibitor of succinate dehydrogenase — is a widely distributed plant and fungal neurotoxin known to induce damage to basal ganglia, hippocampus, spinal tracts and peripheral nerves in animals. Recent reports from Northern China indicate that 3-NPA is also likely to be responsible for the development of putaminal necrosis with delayed dystonia in children after ingestion of mildewed sugar cane. This article discusses the role of 3-NPA in the causation of the disease in China, its neurotoxic effects in animals and the potential role for this compound as a probe of selective neuronal vulnerability.

Immune system response in Alzheimer's disease.

Abstract: Involvement of the immune system in the pathogenesis of Alzheimer's disease was demonstrated in two ways: by the attachment of complement proteins to diseased tissue, and by the activation of cells associated with the immune system. Alzheimer brain tissue was stained immunohistochemically by antibodies to components of the classical, but not the alternative, complement pathway. Antibodies to C1q, C3d, and C4d stained senile plaques, dystrophic neurites, neuropil threads and some tangled neurons. Antibodies to a neoantigenic site on the C5b-9 membrane attack complex stained dystrophic neurites and many tangled neurons, but not senile plaques. Antibodies to Factor P and fraction Bb of Factor B, which are specific for the alternative complement pathway, did not stain Alzheimer brain tissue. The cellular immune response was evaluated by the presence of reactive microglia and by the infiltration of small numbers of T-cells into diseased brain tissue. Reactive microglia were identified by antibodies to HLA-DR, a class II major histocompatibility complex glycoprotein, and by enhanced staining with antibodies to leukocyte common antigen and the Fc gamma RI and Fc gamma RII receptors. T-cells were identified by antibodies to leukocyte common antigen, as well as the CD4 and CD8 surface proteins. Double immunostaining with antibodies to GFAP and MHC class I or class II antigens established that astrocytes, which are GFAP positive, do not express MHC antigens in Alzheimer's disease. Endothelial cells express MHC class I antigens while reactive microglia and some leukocytes express class II antigen.