Abstract:
Backround
Stroke can affect any part of the brain and often includes multiple functional areas, making it
particularly challenging to predict neurological status based on lesion characteristics. Although
the location of the lesion clearly plays a role in its neurological impact, many brain functions
are not anatomically distinct. Activation studies have confirmed that normal brain function
often require an intact network of anatomically distinct areas working in concert. Glasgow
coma scale is a valid, reproducible scale that measures one major neurological deficit.
However, this is a clinical assessment. There is currently no radiological method to
systematically quantify the effect of complex spatial pattern of brain injury on the severity of
neurological function! dysfunction. In the current study, the relationship between Glasgow
coma scale and acute infarct volume as determined by Brain CT scan, is investigate. The aim
is to see, if infarct volume can be used to assess neurological severity after an acute episode of
stroke.
Objectives
To determine the correlation between brain infarct volume and the neurological deficit in
patients with an acute episode of stroke in Muhimbili National Hospital between July 2009 to
December 2009.
Materials and methods
This was a cross-sectional study of 74 patients with an acute episode of stroke seen at
Muhimbili National Hospital Radiology department between July 2009 to December 2009,
who underwent Brain C'I' scan examination and Glasgow coma scale within 48 hrs of stroke
onset. The Glasgow coma scale was recorded prospectively by the admitting doctor at the time
of acute presentation and this was used to determine neurological deficit. Acute stroke was
confirmed by Brain CT scan, read by Muhimbili National Hospital Radiologist.
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Stroke volume was calculated from the product of infarct diameter, the greatest perpendicular
diameter to this and the thickness of the brain lesion estimated from the thickness of the CT
slices. The result was then divided by two.
Correlation analysis was performed for volume scores versus Glasgow coma scale scores by
computing Person correlation coefficient. P<0.05 was considered to be statistically significant.
Results
There was a poor correlation between infarct volume and Glasgow coma scale with a
correlation coefficient ofr = -0.547; P 0.01. This defines a weak linear association. It showed
the regression Hest as t = -5.550 with 95% confidence interval- 1.024- -2.172 and regression
correlation coefficient of r2 = 0.300; p<O.OOl. Hence infarct volume proved to be a poor
predictor of Glasgow coma scale.
Conclusion and recommendations.
From this study, we can conclude that calculated stroke volume alone cannot be used to
estimate stroke severity in patients with acute stroke. Future work with larger data sets and by
incorporating knowledge of the sophisticated networks that connect different brain regions is
required. Such studies in different patients cohorts would also address reproducibility and
reliability of the current findings.