• M Hoffmann.
• Department of Neurology, The Nelson Mandela Medical School, University of Natal, Durban, South Africa. mhoff2@pop.uky.edu
• Neurorehabil Neural Repair. 2001 Jan 1; 15 (2): 113-27.

ObjectiveDespite spectacular success of animal model neuroprotective therapy in stroke, these agents have been uniformly unsuccessful in humans. One possible explanation is the crudity of cerebral measurement by insensitive of stroke scales comprising scant or absent higher cortical-function parameters and the heterogeneity of stroke syndromes and etiology. We sought to determine the frequency and extent of cognitive disorders after stroke and their relation to stroke risk factors, syndromes, lesion site, and etiology.MethodsWe used hospital-based consecutive stroke cases. A tiered, hierarchic, cerebrovascular investigative protocol and a battery of predefined, validated bedside higher cortical function deficit (HCFD) tests with comparison to neuropsychological. Quantification according to the World Health Organization levels of disease model was achieved by a clinical neurologic deficit scale, etiologic scale, and disability scale.ResultsStroke deficit, disability and etiology: In patients evaluated (n = 1,000), the admission Canadian Neurological Scale deficit grading was mild, 11.5-9.5 (n = 696); moderate, 9.5-5.5 (n = 204); and severe, 5.0-0 (n = 86); with correlation to Rankin scale of independent (n = 467), mild disability (n = 345) and severe disability (n = 174) with moderate agreement (kappa = 0.54) between the two measurements. The etiologic subtypes included large-vessel atherothrombosis (n = 264), small-vessel atherothrombosis (n = 262), cardioembolic (n = 122), other (dissection, vasculitis, prothrombotic states; n = 253), and unknown (n = 99). Cognitive Data: 1. One or more higher cortical function abnormalities was detected in 607 (63.5%) of 955 nondrowsy patients. The most numerous categories were aphasias (25.2%), apraxias (14.5%), amnesias (11.6%), and frontal network syndromes (9.2%), with the other categories less frequent (3%). Cognitive impairment occurred without elementary neurologic deficits (motor, sensory, or visual impairment) in 137 (22.5%) of 608. The cardioembolic, other, and unknown stroke mechanistic groups differed significantly from the other groups in terms of HCFD (p = 0.01) frequency. HCFD did not differ between younger (younger than 49 years) and older patients (p = 0.194). 3. Univariate and multivariate analyses of risk factors and likelihood of developing an HCFD revealed increasing age, black race, being overweight, and recent infection to be independent variables (p = 0.05). 4. In 76 patients, neuropsychological testing was performed and comparison with the HCFD test revealed a sensitivity of 80.2% (CI, 72-88%) and specificity of 100%.Conclusions1. Cognitive impairment is present in the majority of all types of stroke. 2. Cognitive impairment may be the sole presentation of stroke, unaccompanied by long-tract signs. 3. Stroke etiologic subtype differed significantly among the subgroups, but in comparison of young versus older patients, no significant differences in HCFD frequency were recorded. 4. Risk factors for developing cognitive impairment in the indigenous stroke population included increasing age, black race, overweight body habitus, and recent infection.

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