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The article discusses a study on surgical decompression for space-occupying hemispheric infarction. Highlights include surgical decompression with hemicraniectomy and duraplasty, the use of modified Rankin scale in the study, and the degree of disability or dependence in daily activities of patients with a neurologic condition.

A prospective study focused on whether vestibular symptoms are seen in acute hemispheric strokes, and if so, the frequency and lateralization of causative lesions on MRI. Among 668 patients with hemispheric infarction, we prospectively included those with chief complaints of acute vestibular symptoms, such as vertigo/dizziness, nausea/vomiting and gait instability, in the "VS" group. We also retrospectively reviewed MRI of all stroke patients, and included cases with the findings of parieto-insular vestibular cortex (PIVC) or temporo-periSylvian vestibular cortex (TPSVC) lesion by diffusion-weighted MRI, in the "PIVC" group. Eight patients were found to belong to the VS group, and six other patients to the PIVC group. In the VS group, six patients had the responsible lesion on the right hemisphere, in the middle cerebral artery (MCA) territory except one case and two on the left MCA territory, particularly in the insula, retro-insular region, superior/middle temporal gyrus, angular gyrus, supra-marginal gyrus, putamen and hippocampus/para-hippocampal gyrus. In contrast, none of the six other patients of the PIVC group had vestibular symptoms. One of them had a lesion in the right hemisphere and five in the left hemisphere. Four lesions were located in the insular area and two within the temporal lobe. In conclusion, cerebral hemispheric infarction limited to the PIVC or TPSVC does not necessarily cause vertigo. However, unilateral hemispheric infarctions, restricted to the areas belonging to the vestibular cortical network may cause vestibular symptoms. The lesions responsible for vestibular symptoms are located more often in the right hemisphere. [ABSTRACT FROM AUTHOR]

Background: Decompressive hemicraniectomy reduces secondary brain injury related to brain edema and increased intracranial pressure (ICP) in patients with malignant middle cerebral artery infarction (MMI). However, a substantial proportion of patients still die despite hemicraniectomy due to refractory brain swelling. Objective: We aim to investigate whether ICP measured immediately after hemicraniectomy may indicate decompression effects and predict survival in patients with MMI. Methods: We included 25 patients with MMI who underwent ICP monitoring and brain computed tomography within the first hour of hemicraniectomy. Midline shifts were measured as radiological surrogates of decompression. The Glasgow Coma Scale and pupillary enlargements during the first day after hemicraniectomy were assessed as clinical surrogates of decompression. Long-term survival status at 6 months was used as the final outcome. We analyzed the relationships between early ICP and findings of midline shift, Glasgow Coma Scale, pupillary enlargement, and survival. Results: Initial ICP was correlated with mean ICP (P < .001) and maximal ICP (P < .001) during the first postoperative day. Intracranial pressure was associated with midline shifts (P = .009), lower Glasgow Coma Scale scores (P = .025), and the pupillary enlargement (P = .015). Sixteen (64.0%) patients survived at 6 months. In a Cox proportional hazard model, elevated ICP was associated with mortality at 6 months (hazard ratio: 1.13; 95% confidence interval: 1.03-1.24; P = .008). Conclusion: Increase in ICP soon after hemicraniectomy was associated with midline shift, poor neurological status, and mortality in patients with MMI. Measurements of ICP soon after hemicraniectomy may permit earlier interventions as well as more refined clinical assessments. [ABSTRACT FROM AUTHOR]

The purpose of this study was to determine whether the auditory cortex is sensitive to cortical insults and to determine the specificity of the insults in three clinical situations with different cortical involvement. Auditory-evoked magnetic fields of ten normal subjects, 8 patients with right hemispheric infarction, 11 with chronic dizziness, and 2 with moyamoya disease were measured. To analyze the abnormality of auditory neural networks, the magnitude ratio and the angle difference (Δθ) between response vectors, which were determined from maximum current arrows corresponding to the N100m peak for contralateral and ipsilateral stimuli were used. A normal range of the parameters was defined so that abnormal values could be determined. Of the three parameters, Δθ was the most sensitive: 4 patients with right hemispheric infarction, 4 with chronic dizziness, and 1 with moyamoya disease had abnormal Δθ. The electrical activity in the patients with such abnormal Δθs had a circular current pattern. These findings suggest that right infarction lesions sometime affect the left auditory neural network, dizziness is caused by abnormal neural networks between the vestibular cortical area and the auditory cortex or by an imbalance between left and right auditory-cortex activities, and moyamoya-disease patients have almost normal auditory-electrical activity. [Copyright &y& Elsevier]

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