The prognosis for patients in poor neurological grade (WFNS grades IV and V) after subarachnoid haemorrhage (SAH) is grave. Previous reports of such patients have analysed outcome without defining either the cause or the course of the depressed level of consciousness. We report a retrospective study of the outcome of 62 consecutive patients in poor grade after SAH analysed with respect to their clinical course and the predominant computed tomographic feature. Neuroradiological findings were (1) intracranial haematoma, (2) hydrocephalus with or without intraventricular haemorrhage (IVH) and (3) SAH alone. Sixteen patients (25.8%) had a Glasgow Coma Score (GCS) < or = 12 on admission to hospital and subsequently deteriorated. The predominant computed tomographic feature of these patients was hydrocephalus/IVH. Twelve patients (19.4%) had a GCS < or = 12 on admission and subsequently improved without intervention; all had SAH on computed tomography (CT) on admission. Thirty-four patients (54.8%) had a GCS < or = 12 on admission and did not improve or improved only after emergency surgical intervention. Haematoma (44%) and hydrocephalus/IVH (47%) were the predominant CT features in this group. The overall mortality in the 62 patients was 44%. Fifty-two per cent of patients achieved a good outcome or were moderately disabled. Patients harbouring an intracerebral haematoma had a significantly poorer prognosis when compared with the other groups. Patients in poor neurological grade after SAH are a heterogenous group both clinically and neuroradiologically. Management approaches must consider the cause of clinical deterioration and the related CT findings.

To address the question of managing subarachnoid haemorrhage (SAH) in the older patient, the management and outcome of 199 consecutive patients aged > or = 60 years with a confirmed diagnosis of subarachnoid haemorrhage (n = 186) or an unruptured intracranial aneurysm (n = 13) were reviewed. In seven patients, the cause of the SAH was an arterio-venous malformation and these were excluded from further analysis. Angiography was performed in 141 patients with a complication rate of 2.1%. Angiography was not performed in 51 patients and, in this cohort, the in-patient mortality rate was 68.6% and only 27.5% had a favourable outcome at discharge. Operation was not performed in 21 patients with demonstrated aneurysms for a variety of reasons. In this group, the in-patient mortality rate was 47.6% and 38.1% had a favourable outcome at discharge. Eighty-one patients in good neurological grade underwent surgery for a ruptured aneurysm and six patients underwent surgery for a symptomatic unruptured aneurysm. The surgical mortality was 1.1% and a favourable outcome at discharge was achieved in 83.9% of patients. Thirty-three patients were angiographic negative and there was a favourable outcome in 97% of this group. The management mortality in these selected patients admitted to the Department of Clinical Neurosciences was 24.4% and a favourable outcome was recorded in 66.2% of patients. Long-term follow-up (median 40 months, range 3-120 months) was obtained in 97% of discharged patients. The probability of survival at 60 months for patients in good condition at discharge was 0.826 (95% confidence interval 0.722-0.894).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute subdural haematoma secondary to a ruptured intracranial aneurysm may lead to coma or sudden death. We describe five cases encountered in our department over the last 3 years emphasizing the differential diagnosis and approaches to management.

Previous studies have suggested that only a small proportion (< 15%) of comatose head-injured patients whose initial computerized tomography (CT) scan was normal or did not show a mass lesion, midline shift, or abnormal basal cisterns develop intracranial hypertension. The aim of the present study was to re-examine this finding against a background of more intensive monitoring and data acquisition. Eight severely head-injured patients with a Glasgow Coma Scale score of 8 or less, whose admission CT scan did not show a mass lesion, midline shift, or effaced basal cisterns, underwent minute-to-minute recordings of arterial blood pressure, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) derived from blood pressure minus ICP. Intracranial hypertension (ICP > or = 20 mm Hg lasting longer than 5 minutes) was recorded in seven of the eight patients; in five cases the rise was pronounced in terms of both magnitude (ICP > or = 30 mm Hg) and duration. Reduced CPP (< or = 60 mm Hg lasting longer than 5 minutes) was recorded in five patients. Severely head-injured (comatose) patients whose initial CT scan is normal or does not show a mass lesion, midline shift, or abnormal cisterns nevertheless remain at substantial risk of developing significant secondary cerebral insults due to elevated ICP and reduced CPP. The authors recommend continuous ICP and blood pressure monitoring with derivation of CPP in all comatose head-injured patients.

The accuracy with which the ventrolateral thalamic nucleus could be targetted using the BRW stereotactic system and unreformatted axial CT imaging was evaluated in cadaver brains mounted in a skull. Ball bearings (1.82 mm diameter) were placed in the nuclei ventro intermedius (Vim), ventro oralis anterior (Voa) and posterior (Vop) and the brains then sectioned, the locations of the ball bearings relative to the anterior (AC) and posterior commissures (PC) measured and evaluated with reference to a Schaltenbrandt and Bailey stereotactic atlas. Targetting of the ventrolateral thalamic region was frequently accurate (77%) but because of errors in estimation of the AC-PC plane (mean forward angulation of 9 degrees) some ball bearings were placed too deeply in the Fields of and Forel, zona incerta and rostral subthalamic nucleus. Ventrolateral thalamotomy using the BRW stereotactic system and unreformatted axial CT imaging was undertaken in six patients with tremor due to a range of pathologies. The tremor was abolished or altered in four patients whilst no lesion was made in the other two patients since no site that reduced the tremor, could be located. The surgical and clinical implications of this study are discussed.