Differentiation of Acute Cortical and Subcortical Ischemic Stroke by Risk Factors and Clinical Examination Findings
Department of Neurology, University of Wisconsin-Madison Medical School 53792-5132, USA. Neuroepidemiology
(Impact Factor: 2.56).
02/1998; 17(2):80-9. DOI: 10.1159/000026157
Differentiation between acute cortical and subcortical ischemic stroke may be problematic when cortical stroke presents without obvious cortical deficits such as aphasia, neglect or hemianopia. This study explores stroke risk factors and clinical variables that may assist in this differentiation.
Records of consecutive patients with acute ischemic stroke, examined within 72 h of symptom onset, were reviewed. Stroke type was verified by clinical course and follow-up imaging. Stroke risk factors and acute examination findings were compared by odds ratios and positive predictive values for cortical and subcortical stroke.
For 355 patients studied, 237 had cortical stroke and 118 had subcortical stroke. Odds ratios for cortical stroke were highest for atrial fibrillation by EKG (OR = 4.77, CI = 2.08-10.94), recent hospitalization (OR = 4.51, CI = 2.39-8.53) and nonalert mental status (OR = 4.50, CI = 2.29-8.87). Possible cardioembolic condition, ischemic heart disease and peripheral vascular disease were also significant, but hypertension, age and diabetes mellitus were not significantly different for the stroke subtypes. Cortical deficits were absent in 19.4% of cortical stroke patients on initial examination. Predictive models were generated based on the presence or absence of cortical deficits and the interaction of significant risk factors with degree of motor deficit.
There are clinical features that, in addition to initial examination, may help differentiate cortical from subcortical ischemic stroke. These features may be relevant to both diagnostic and therapeutic approaches to acute stroke.
Available from: Seong Hoon Lim
- "In these studies, the size of the lesion in the brain was not related to functional outcome  . Few studies have reported on the relationships between brain lesions and functional recovery   . "
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ABSTRACT: Although studies have demonstrated that several specific brain lesions are related to the severity of functional outcomes, the effects of specific brain lesions are not yet clear. This study investigated the effects of hemorrhagic stroke lesions on motor recovery. Eleven subjects with hemorrhagic stroke were assessed. Using the Fugl-Meyer Assessment and functional ambulation category, clinical motor and sensory impairments were tested four times in total: initially within 2 weeks and 1, 3, and 6 months after the onset of stroke. Brain lesions and size were evaluated using MRIcron, SPM8, and Talairach Daemon software. Trunk control, motor function in the lower limbs, and sensory function improved significantly within 3 months, after which the change was no longer significant. Upper limb function and gait were unchanged within 1 month but improved significantly 3 months after onset and continued to improve for 6 months. Involvement of the anterior putamen, internal capsule, thalamus, periventricular white matter, and premotor cortex was related to poor upper limb recovery in patients with hemorrhagic stroke. These results should be useful for planning rehabilitation strategies and understanding the prognosis of hemorrhagic stroke.
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ABSTRACT: Classically in neurology, aphasia and neglect were accepted as reliable markers of cortical lesions. The actual prognostic values of aphasia and neglect have yet to be formally tested. This analysis sought to determine the predictive accuracy of aphasia and/or neglect in acute stroke for cortical infarction. Data from the RANTTAS investigation of tirilazad mesylate in stroke patients were reanalyzed, comparing acute National Institutes of Health Stroke Scale (NIHSS) measures of aphasia and neglect to lesion location on day 7-10 CT scans. Correlations between the presence of aphasia and/or neglect and the presence of a cortical lesion were only in the moderate range, and positive predictive values were far from perfect, as would be expected. 'Subcortical' aphasia or neglect was more likely in large, subcortical lesions. Aphasia and neglect, as determined in the acute setting by the NIHSS, are only moderately associated with cortical infarct identified on follow-up CT scans. If selective neuroprotection is envisioned for acute stroke patients, more accurate markers of cortical infarction may be needed.
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ABSTRACT: To investigate the association between different kinds of ischemic lesions and cerebrovascular reactivity (CR) and to evaluate their relationships with the major risk factors for stroke.
We evaluated CR using the breath-holding index technique during bilateral transcranial Doppler monitoring of flow velocity in the middle cerebral arteries of 41 consecutive patients attending our clinic for a recent, first-ever, ischemic stroke and in 15 control subjects. Based on the location of the lesion determined by computed tomography, the following 3 types of infarctions were identified: cortical (or territorial), single subcortical, and subcortical with multiple silent subcortical infarctions. Patients with a condition of severe carotid artery stenosis or occlusion, which in itself could account for altered CR, were excluded from this study. All physiological and pathologic conditions that could possibly cause an impairment in CR were recorded.
The breath-holding index was significantly lower in the multiple subcortical infarctions group than in the control subjects (P < .001), single subcortical infarctions group (P < .01), and cortical infarctions group (P < .01). In all of the groups male sex (P < .05) and a history of hypertension (P < .05), regardless of whether hypertension was treated, correlated with low CR. The multiple regression analysis indicated that the only significant factor able to influence the breath-holding index was the type of lesion.
Nonstenotic patients with first-ever stroke who had a recent symptomatic subcortical infarction associated with multiple silent infarctions seem to have an impaired cerebrovascular reserve capacity. The strong association of subcortical infarctions with multiple silent infarctions with low CR indicates the role of small vessel vasculopathy and hypoperfusion as possible pathogenetic mechanisms of subcortical infarctions with multiple silent infarctions.
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