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Biomedical subjects

A Kertesz

Publications and source records attributed to A Kertesz.

119 records · Page 7Linked to original sources
PubMed1972

Enlargement of the Sylvian aqueduct: a sequel of head injuries.

A review of pneumoencephalography and clinical data in a large group of patients has shown that severe head injury may be followed by a consistent clinical-radiological syndrome. A prolonged period of unconsciousness is a characteristic initial feature of this syndrome. Clinically there is ataxia and dysarthria and, often, abnormal movements and oculomotor dysfunction. The characteristic radiological feature is an enlargement of the aqueduct of Sylvius. The clinical picture, together with the enlargement of the aqueduct, suggests that loss of neuronal and axonal substance in the midbrain is the probable pathology.

Adult↗
PubMed1970

Subacute sclerosing panencephalitis. Studies of two cases treated with 5-bromo-2-Deoxyuridine.

Two cases of subacute sclerosing panencephalitis treated with 5-bromo-2-deoxyuridine (BUDR) are reported. Both cases had a classical presentation with motor and mental deterioration, myoclonic jerks, paretic colloidal gold curve in CSF and periodic bursts of the EEG. The diagnosis was confirmed by brain biopsy with light and electron microscopic findings. Immunological studies revealed markedly elevated serum and CSF measles antibodies on serial determinations by the virus neutralization, complement fixation and hemagglutination inhibition techniques. Both cases were treated with 100 mg./kg./day of BUDR, intravenously, for five days, and Case 2 received a second course of treatment. Only minimal side effects were experienced from the use of BUDR; clinical symptoms showed sustained improvement in Case 1 and no further deterioration in Case 2. Both patients survived for more than 16 months. More extensive controlled trials with antiviral agents for the treatment of subacute sclerosing panencephalitis appear to be justified.

Antibodies↗
PubMedDate not supplied

A Canadian cohort study of cognitive impairment and related dementias (ACCORD): study methods and baseline results.

The overall objective of the Canadian Collaborative Cohort of Related Dementias (ACCORD) study is to describe the diagnostic distribution, natural history and treatment outcomes of individuals referred from the community to dementia clinics in Canada. Between 1997 and 1999, an inception cohort of 1,136 subjects entered into this longitudinal study. At the baseline assessment, 10.9% of the subjects were classified as "not cognitively impaired" (NCI), 30.1% as "cognitively impaired not demented" (CIND), and 59% as demented. A subclassification of CIND included amnestic 25.1%, vascular cognitive impairment 18.1%, psychiatric 17.2%, neurologic 7.3%, medical/toxic metabolic 3.5%, mixed 7.6% and not specified 19.0%. The percentage of the cohort referred with dementia increased progressively each decade, while the proportions of CIND and NCI decreased. Within the dementia group, Alzheimer's disease accounted for 47.2% of the subjects, mixed dementias 33.7%, vascular dementia 8.7%, frontotemporal degenerations 5.4%, dementia with Lewy bodies 2.5%, and unclassifiable 1.8%. The ACCORD cohort will allow a detailed study of the longitudinal course of CIND, and the longer-term outcomes of both treated and untreated dementia subjects.

Adult↗
PubMedDate not supplied

Spasticity measurement in stroke: a pilot study.

The ability to objectively measure spasticity, related to cerebral stroke, is important in the rehabilitation therapies since many therapeutic modalities have been developed over the years to reduce spasticity. The unproven clinical expectation is that function would be improved were spasticity to be reduced. Unfortunately, the ability to measure spasticity to conduct efficacy studies of spasticity-reducing therapies is not possible. This relates to the multi-variable nature of the spastic syndrome with the result that no clinical measurement technique has been proven to be sensitive, valid and reliable. Therefore, it is important to develop a research-oriented spasticity measurement system to meet this need. We describe the current development of such a system. Details of our pilot study of a reflex excitability technique, designed to measure certain components of cerebral spasticity, are presented. The technique combined biomechanical and electrophysiological measures to investigate a homogenous stroke sample (n = 6); it incorporated the H-reflex in soleus, during passive ankle movements, as a measure of faulty neural inhibition. This component significantly (p < .05) differentiated the stroke sample from a matched, healthy control group (n = 6). Evocation of a cutaneous reflex in soleus was a condition that was problematic and it had to be dropped from the protocol. Joint stiffness, which is thought to affect measures of spasticity during passive movement, did not contaminate the measures. Further research in this direction is required to delineate and measure other neural components of spasticity while taking into account related non-neural variables. The final objective in this line of research is to develop a valid, reliable and sensitive spasticity measurement system that could be used to judge the efficacy of physical neurorehabilitation treatments currently employed to reduce spasticity following stroke.

Aged↗
PubMedDate not supplied

A reflex technique to measure presynaptic inhibition in cerebral stroke.

The purpose of this study was to evaluate the feasibility of reflex excitability measurement techniques in the partial measurement of spasticity related to cerebral stroke. Techniques involved the testing of the soleus H-reflex at specific ankle positions during passive dorsiflexing movements with and without background plantarflexing contractions; conditions attempted to simulate the terminal stance phase of gait. Testing of 12 stroke subjects, having cerebrovascular lesions related only to occlusion of the middle cerebral artery, demonstrated significantly (p < 0.01) less inhibition of the H-reflex during passive ankle dorsiflexion compared to 12 matched, healthy controls. However, evocation of the H-reflex during a low-level, voluntary plantarflexing contraction concomitant with passive dorsiflexion, did not reflect a statistical difference between the two groups. The two conditions were thought to each represent measures of faulty presynaptic inhibition as indicators of cerebral spasticity. A Chi-square calculation of sensitivity for the passive ankle movement without background plantarflexing contraction condition, was shown to significantly differentiate (p < 0.05) between the stroke and normal groups. A positive, but weak, correlation was found for stroke subjects between this reflex measure and the Ashworth clinical measure of spasticity (r = 0.49). Although stroke subjects exhibited increased joint stiffness when the full range of passive ankle dorsiflexion movement was considered, in comparison to the matched healthy control subjects, no significant increase in passive stiffness was found at the joint position of the reflex evocation. Size of the cerebral lesion, as determined from CT or MRI scan, was not related to the spasticity measures. Therefore, in a homogeneous stroke sample, a component of cerebral spasticity i.e., faculty Ia presynaptic inhibition, has been measured during a simulated functional movement in the lower extremity and was shown to differentiate this group from a matched, healthy, control sample. Joint stiffness did not contaminate the measures.

Aged↗