SUMMARY The ability to recognise gestures was studied in 65 left-hemispheric stroke patients whose lesions were located by CT scan. In the acute stage (first month) frontal lobe and basal ganglia were frequently involved in patients showing inability to recognise gestures. In the later (third to fourth month) and chronic stages ( >6 months) parietal lobe involvement was important; lesions causing gesture recognition impairment were larger, had more extensive and frequent parietal involvement and produced less temporal lobe damage than those causing aural comprehension defects. These findings are discussed in the light of recent models of cerebral localisation of complex functions.Several studies have demonstrated that some aphasics do not recognise gestures.1-5 This disturbance correlates with comprehension impairment,'24 alexia34 and constructional apraxia.4 Gesture recognition impairment in aphasics has been attributed to asymbolia,l to an impairment of "semantic understanding",2 to damage to a "symbolic unit" that relates gestures to the corresponding objects4 following "plausability" rules,5 or due to loss of visuokinesthetic motor engrams of gestures.4None of these previous studies addressed the question of the anatomical localisation of the lesions that cause impairment of gesture identification. In a previous work, we found that this disturbance of gesture recognition was more common and severe in global, transcortical and Wemicke's aphasics, independent of the severity of auditory comprehension impairment.4 This could reflect the major role of posterior left hemispheric areas for gesture identification. The strong correlation found with.constructional apraxia could indicate a more extensive involvement of the parietal lobe in aphasic patients displaying defective gesture recognition. These suggestions were investigated in the present study. MethodThe study was of 65 adult right-handed patients, 41 males and 24 females (mean age 56-4 ± 11.6 years) who had suffered a single ischaemic cerebrovascular accident of the left hemisphere. Patients with intracerebral haematomas, cerebral infarct associated with subarachnoid haemorrhage and those in whom CT scan showed multiple or bilateral lesions, or diffuse white matter hypodensity suggestive of arteriosclerotic subcortical encephalopathy6 were not included in this series. Thirty-two patients were tested during the 1st month after stroke (acute patients), 37 during the 3rd-4th months after stroke (recent patients) and 44 in the six or more months after stroke (chronic patients). Thirty-three patients were observed in more than one period (acute, recent and chronic stages, 18 patients; acute and recent, eight patients; recent and chronic, six patients; acute and chronic, one patient).
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