BOWLER, JV and WADE, JPH and JONES, BE and NIJRAN, K and JEWKES, RF and CUMING, R and STEINER, TJ (1995) CONTRIBUTION OF DIASCHISIS TO THE CLINICAL DEFICIT IN HUMAN CEREBRAL INFARCTION. STROKE , 26 (6) 1000 - 1006.
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Background and Purpose Regions of decreased cerebral blood flow are often seen on single-photon emission computed tomography (SPECT) after stroke and have been widely reported to add to the clinical deficit. However, such reports have not distinguished between correlation and causation. We analyzed 124 serial SPECT scans performed in 50 patients to assess the role of diaschisis in the clinical deficit after stroke.Methods SPECT with the use of Tc-99m-hexamethylpropyleneamine oxime (Tc-99m-HMPAO) was performed in a prospective, unselected series of 50 patients with cerebral infarcts studied at a median of 1.1, 6.8, and 95 days after ictus. Patients were also assessed with the use of the Canadian Neurological Scale, the Barthel Index, a neuropsychological evaluation, and infarct volume measurement.Results One hundred twenty-four serial SPECT scans were done in 50 patients. Diaschisis was identified at 168 sites. There was insufficient correlation between diaschisis and the clinical measurements to support the suggestion that diaschisis independently causes clinical deficits beyond those due to the infarct itself. Unlike the clinical status, diaschisis showed little tendency to resolve during the 3-month follow-up period of the study. Several of the instances of correlation were shown to be of a noncausal kind, with both the diaschisis and the clinical deficit being due to the lesion directly; there was no known mechanism for the diaschisis to cause the clinical deficit.Conclusions Diaschisis does not independently add to the clinical deficit after stroke. It is more likely that it simply represents Dart of the damage done by the stroke.
|Title:||CONTRIBUTION OF DIASCHISIS TO THE CLINICAL DEFICIT IN HUMAN CEREBRAL INFARCTION|
|Keywords:||DIASCHISIS, STROKE OUTCOME, TOMOGRAPHY, EMISSION COMPUTED, CROSSED CEREBELLAR DIASCHISIS, POSITRON EMISSION TOMOGRAPHY, BLOOD-FLOW, GLUCOSE-UTILIZATION, TRANSHEMISPHERIC DIASCHISIS, HEMISPHERIC INFARCTION, NEOCORTICAL ABLATIONS, 2-DEOXYGLUCOSE UPTAKE, THALAMIC INFARCTION, SUBCORTICAL STROKE|
|UCL classification:||UCL > School of Life and Medical Sciences > Faculty of Brain Sciences > Institute of Neurology|
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