Post-ictal blood pressure in aneurysmal subarachnoid haemorrhage.

A prospective study in which the effect of the post-ictal systemic blood pressure levels on the outcome following surgically treated aneurysmal subarachnoid haemorrhage (SAH) in 325 patients is reported. No differentiation was made between pre-existing essential and prolonged reactive hypertension. A significant association was found between the trend for rising diastolic blood pressure levels and the tendency towards a poor outcome. There was a similar trend for rising systolic blood pressure levels which did not reach statistical significance. Patients with definite hypertension (blood pressure of 160/95 mmHg or greater) were 1.6 times as likely to have a poor outcome than were those with lower blood pressures.

Recurrent aneurysmal subarachnoid haemorrhage: incidence, timing and effects. A re-appraisal in a surgical series.

A series of 510 patients with proven aneurysmal subarachnoid haemorrhage (SAH) is reported. The incidence of recurrent haemorrhage during the period awaiting surgery was 13.7%. There was no significant difference in incidence between good and poor grade patients. Following rebleeding there was an immediate mortality of 34% in good grade patients and 52% in poor grade patients. In the long term only 44.4% of good grade and 8% of poor grade patients made a good recovery following a second bleed as compared to 70.6% and 52.8% respectively for those who did not rehaemorrhage.

Dipyridamole and postoperative ischemic deficits in aneurysmal subarachnoid hemorrhage.

Recent evidence has suggested that the delayed cerebral ischemic deficits that often follow surgery for aneurysmal subarachnoid hemorrhage (SAH) may be due to a proliferative vasculopathy. This vascular pathology may result from an interaction between the platelets and the vessel wall. A single-blind controlled trial of dipyridamole administration in 677 patients presenting with SAH (of whom 348 came to surgery) was undertaken to test the hypothesis that the modification of platelet behavior might reduce the incidence of ischemic deficits. Blind independent assessment of the outcome in the surgical group based on the Glasgow Outcome Scale and the specific neurological deficits revealed no significant differences between the control and treatment groups.

Biochemical evidence of selective nerve cell changes in the normal ageing human and rat brain.

Atrophy with ageing of human whole brain, entire temporal lobe, and caudate nucleus was assessed in autopsy specimens, by biochemical techniques. Only the caudate nucleus showed changes. Markers for several neurotransmitter systems were also examined for changes with age. In neocortex and temporal lobe of human brain, small decreases were detected in markers of cholinergic nerve terminals, whereas a large decrease (79%) occurred in the caudate nucleus. Findings were similar in striatum from 3--33-month-old rats. No change occurred in binding of [3H]quinuclidinyl benzilate by human samples. Markers of serotonergic terminals were also unchanged in human and rat brain. By contrast, binding of [3H]lysergic acid diethylamide and [3H]serotonin was decreased (32-81%) in human neocortex and temporal lobe, but not in caudate nucleus. A 43% loss of a marker of gamma-aminobutyrate terminals occurred in human neocortex, while [3H]muscimol binding increased (179%). No changes were detected in markers of catecholamine synapses in temporal lobe or rat striatum. Hence, with human ageing there appears to be a loss of markers of gamma-aminobutyrate neurones intrinsic to neocortex and acetylcholine cells intrinsic to the caudate nucleus, as well as a change in postsynaptic serotonin receptors in neocortex. These losses are accompanied by relative preservation of markers of ascending projections from basal forebrain and brain stem.

Biochemical assessment of serotonergic and cholinergic dysfunction and cerebral atrophy in Alzheimer's disease.

Markers of serotonin synapses in entire temporal lobe and frontal and temporal neocortex were examined for changes in Alzheimer's disease by use of both neurosurgical and autopsy samples. Uptake of [3H]serotonin, binding of [3H]imipramine, and content of indolamines were all significantly reduced, indicating that serotonin nerve terminals are affected. Binding of [3H]serotonin was also reduced, whereas that of [3H]quinuclidinyl benzilate, [3H]muscimol, and [3H]dihydroalprenolol were unaltered. When the Alzheimer's samples were subdivided according to age, the reduction in [3H]serotonin binding was a feature of only autopsy samples from younger patients. In contrast, presynaptic cholinergic activity was reduced in all groups of Alzheimer's samples, including neurosurgical specimens. Five markers, thought to reflect cerebral atrophy, cytoplasm, nerve cell membrane, and neuronal perikarya were measured in the entire temporal lobe. In Alzheimer's disease the reductions (mean 25%, range 20-35%) were thought to be too large to be due only to loss of structures associated with the presumed cholinergic perikarya in the basal forebrain and monoamine neurones in the brain stem.

Choline acetyltransferase activity and histopathology of frontal neocortex from biopsies of demented patients.

Cortical biopsies were taken from the frontal lobe of 25 patients with presenile dementia. Choline acetyltransferase (ChAT) activity, and in some specimens the high affinity uptake of choline, was used to estimate loss of cholinergic nerve terminals. Of the 15 samples with varying degrees of histological evidence of Alzheimer's disease (AD) 14 were from clinically suspected examples of the disease. There was significant loss of ChAT in 10 of the 15 compared with control and the mean activity was also highly significantly reduced (to 41% of control). The deficit was found in patients examined within a year of onset of symptoms. In 6 biopsies from clinically suspected cases of AD without diagnostic histological features there was loss of activity in only one, subsequently shown to have Jakob-Creutzfeldt disease. The remaining samples were two of vascular dementia (no loss of ChAT), one probable disorder of white matter (no loss of activity) and one undiagnosed disorder (with loss of ChAT activity). Thus most patients without histologically demonstrated AD had no evidence of a presynaptic cholinergic defect. It was concluded that suspected cases of AD particularly suitable for putative cholinergic therapy were those with an onset of the disease at 55 to 65 and an absence of family history.

Cerebral lymphoma: clinical radiological correlation.

Twenty patients with primary malignant lymphoma of the brain are described. This tumour tends to involve deep, central structures with subependymal spread and there is a high incidence (30%) of multifocal disease. Many cases present a clinical picture suggesting the location and by inference the possible nature of the tumour: early mental change, somnolence and headache are prominent. In the case of a solitary lymphoma, the computed tomographic appearance is sometimes similar to that of a meningioma whereas, in multifocal disease, confusion with metastases is almost invariable. With CT, it should be possible to reduce the frequency of misdiagnosis, and thus avoid overlooking a potentially radiosensitive lesion.

Accelerated ageing or selective neuronal loss as an important cause of dementia?

Extensive biochemical analysis of whole temporal lobe from cases of dementia and controls suggests that Alzheimer's disease is a primary degenerative nerve-cell disorder and not the result of accelerated ageing. There is selective loss of neocortical cholinergic neurones. Transmitter systems apart from the cholinergic system appears to be affected, but to a lesser extent, and there are no significant changes in the caudate nucleus. The change in cholinergic neurones has been confirmed in biopsy samples.