Biomedical subjects
Publications and source records attributed to L Symon.
Cavernoma and suprasellar meningioma are rarely associated. We describe a patient, whose recovery after removal of the meningioma was complicated by haemorrhage from the cavernoma. This occurrence has not been previously reported.
The purpose of this study was to examine the effects of blockade (sulpiride) and activation (quinpirole) of dopaminergic D2 (DA2) receptors on brain lesions subsequent to excessive activation of glutamate (GLU) receptors. Striatal lesions were produced by direct injection of quinolinic acid, an endogenous GLU receptor agonist. Sulpiride (100 mg kg-1 i.p., 30 min before quinolinic acid injection and 1 h after) significantly (p < or = 0.05) reduced the volume of the lesion by around 20%. Quinpirole (1.25 mg kg-1 i.p., 30 min before quinolinic acid injection) had no effect. The protective action of DA2 receptor blockade strongly suggests that quinolinic acid-induced excitotoxicity may be partly modulated by DA2 receptors.
Experimental evidence conveys clear suggestions that early reperfusion following at least focal cerebral ischemia in the primate is accompanied by a return of function demonstrably suspended during the ischemic period. Complete and permanent arrest of the cerebral circulation has been known within seconds to lead to depression of brain electrical activity, and within minutes to gross disruption of the normal energy metabolism with failure of ionic homeostatic mechanisms. There is irreversible cell change and death within 5 to 10 minutes. Very much more protracted periods of ischemia have been shown more recently to be associated with potential viability of neuronal function, and in clinical neurosurgery we have known for years that patients with established cerebral vascular occlusion and a dense neurological deficit may show quite evident improvement over months or years. In these protracted recoveries, the potential for re-learning in nervous circuits may play a part, but in more acute circumstances, for example in the progressive recovery from vasospasm, re-learning is clearly not a factor, and this demonstrates quite evidently that neurons at one moment apparently non-functioning, can again within a few minutes recover function even after hours of apparent suppression. The experimental evidence is fairly well known. In this symposium and elsewhere we have presented a model of experimental occlusion of the middle cerebral artery in primates demonstrating irreversible recovery of electrical function after some 20 minutes of middle cerebral artery occlusion, and reversible recovery of ionic homeostasis after periods of up to an hour.(ABSTRACT TRUNCATED AT 250 WORDS)
Fifty-one cases of posterior fossa haemangioblastoma have been seen in our department over a period of 23 years. Seven cases were associated with spinal cord lesions and one with a supratentorial lesion. There were 22 cases of Lindau's disease (43%). The onset was earlier and recurrences commoner than in isolated cases. In 10 cases the development of new tumours in different parts of the central nervous system (CNS) required re-operation, demonstrating the multicentric nature of this disease. The majority of the tumours occupying the fourth ventricle or medulla oblongata (8 cases) were macroscopically solid and had higher post-operative morbidity than the cystic tumours in the cerebellum. The recent development of magnetic resonance imaging (MRI) provides accurate anatomical information of the lesions (especially those of the brain stem and spinal cord) even while asymptomatic. The brilliant enhancement of these tumours on MRI with Gadolinium-diethyline-triamine-pentaacetic acid (Gd-DTPA) has proved to be particularly useful.
A microdialysis probe is described that can simultaneously monitor indices of electrical activity, ionic homeostasis and changes in the composition of the extracellular fluid at the same brain site in anaesthetised laboratory animals. The probe is no larger than its conventional counterpart and avoids tissue injury problems due to implantation of separate recording electrodes. Examples are given of its application to the study of changes following probe implantation, cerebral ischaemia and local high K(+)-induced depolarisation.
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Changes in the extracellular levels of excitatory and inhibitory amino acid transmitters were studied in the rat striatum during penumbral ischaemia using intracerebral microdialysis. Effects of penumbral forebrain ischaemia were compared with those of ischaemia with sustained anoxic depolarisation and K+ (100 mM). Comparisons were also made between different groups of animals at 2 and 24 h after dialysis probe implantation. The K+ stimulus did not provoke any release of excitatory amino acids in the 24-h group, probably reflecting a decrease of functional synapses adjacent to the probe. During 30 min of penumbral ischaemia, excitatory amino acids did not reach critical concentrations in the extracellular fluid, and increases in levels of inhibitory/modulatory amino acids were similar. On the other hand, severe transient ischaemia resulted in massive synchronous release of many neuroactive excitatory and inhibitory compounds, in both the 2- and 24-h groups. These and other data suggest that changes during severe ischaemia may arise from both neurotransmitter and metabolic pools. It is concluded that ischaemic damage in the penumbra may not be related to extracellular neuroactive amino acid changes generated within this region.
Generalised neurotransmitter overflow into the extracellular space on cerebral ischaemia has been widely reported and implicated in events leading to subsequent neuronal death. As little is known about the effect of depth of ischaemia on these changes, we have subjected anaesthetised rats to a sequence of four challenges [high K+ stimulus, moderate (penumbral) ischaemia, severe ischaemia, cardiac arrest] and have concurrently monitored both electrophysiological parameters and changes in extracellular dopamine, serotonin, and their metabolites in the striatum. Of particular relevance to human stroke therapy was penumbral ischaemia, where ionic homeostasis was maintained even though electrical function was lost. All challenges increased extracellular monoamines, although levels were significantly greater when ischaemia was severe enough to produce sustained anoxic depolarisation. Baseline levels were rapidly restored during recovery phases. Acidic monoamine metabolites decreased significantly during each insult, returning to basal levels during reperfusion after moderate ischaemia, and to significantly higher levels after severe ischaemia. Results indicate that sustained anoxic depolarisation may be a critical factor in determining outcome after ischaemia, being associated with significantly greater release of monoamines, and impairment of electrical function recovery.
The effect of a previous K+ stimulation on striatal extracellular monoamine levels during global ischaemia, under simulated penumbral conditions, was investigated. Rats were implanted with microdialysis probes in both striata, monoamine release was stimulated unilaterally by adding K+ (100 mM, 20 min) to the artificial CSF perfused through one probe, and bilateral partial ischaemia was imposed after monoamine levels had returned to basal values or below. Resultant increases in dialysate levels of dopamine and 5-hydroxytryptamine were markedly and significantly greater on the side previously exposed to K+, even though electrophysiological measurements indicated similarly severe ischaemia on both sides. Associated monoamine metabolite changes did not differ significantly between the two sides. There was no evidence of greater neuronal loss in the K(+)-stimulated striata 7 days after ischaemia. However, striatal tissue probably exposed to the highest concentrations of K+ could not be examined because of extensive gliosis around the probe.
We have measured changes in the levels of dopamine (DA), 5-hydroxytryptamine (5-HT), and their metabolites in striatal dialysates during 30 min of global ischaemia under simulated penumbral conditions, and compared these with neurological assessments over the following 7 days and histological damage at the end of this period. On the basis of dialysate DA levels during ischaemia, the animals fell into two subgroups; group I, with little or no DA increase (less than three times basal); and group II, with a much larger increase (greater than 30 times basal). Changes in 5-HT, though of lesser magnitude, showed a similar pattern. These findings may indicate that the amine changes depend on a critical reduction of blood flow within the range obtained by our experimental procedure. Levels of deaminated metabolites fell in all ischaemic animals, with comparable decreases of 3,4-dihydroxyphenylacetic acid plus homovanillic acid in both groups. Decreases of 5-hydroxyindoleacetic acid were greater in group II than in group I, but the relative differences between the groups were much less marked than those of 5-HT. These neurochemical findings suggest that moderate ischaemia affects extracellular amine and deaminated metabolite levels by different mechanisms. Only one of the ischaemic rats (a member of group II) showed a marked neurological deficit, but histological damage, as indicated by neuronal loss and gliosis in vulnerable structures, was apparent in all ischaemic animals. Although damage tended to be greater in animals with marked increases in extracellular monoamines, differences were not significant.(ABSTRACT TRUNCATED AT 250 WORDS)
Two further cases of Creutzfeldt-Jakob disease (CJD) in association with cadaveric dura mater grafts are described. The clinical features of all such reported cases resemble more closely those of sporadic CJD, in contrast with kuru and the cases of CJD which have arisen after therapy with human pituitary-derived growth hormone. This observation may reflect the route of inoculation of the agent.
Twelve patients with facial nerve neurinoma have been treated at The National Hospital, Queen Square, London, during the last 20 years. Nine tumours lay in the middle fossa arising from the area of the geniculate ganglion, two lay in the posterior fossa arising from the segment of the facial nerve in the internal auditory canal, and one tumour arose from the vertical segment of the facial nerve with extracranial extension through the stylomastoid foramen. Two patients had neurofibromatosis. The clinical and radiographic features of those tumours, the operative approaches employed, and the postoperative outcome are described. Complete tumour excision was achieved in all patients; all 12 remain free of recurrence 3-80 months after surgery. Facial nerve function was restored at least in part in all cases by transposition with end-to-end anastomosis, placement of a cable graft from the sural nerve or hypoglosso-facial anastomosis. The major determinant of the outcome of facial nerve function was the duration of preoperative facial paralysis, the results being invariably poor when this was of long duration.
Seventy-three patients with posterior fossa meningioma were operated upon between July 1975 and September 1992. The authors attempt a simple classification of these tumours. Fifty-five were women (average age: 48 years) and 18 were men (average age: 52 years). Frequently, there was gait disturbance except in tentorial meningioma where headache was the most common symptom. The most common physical finding was a cranial nerve deficit (77%). All patients underwent CT and angiography. More recently, MRI was used and found very helpful. Surgical approaches used were either a suboccipital craniectomy, a subtemporal craniotomy or a combined suboccipital-subtemporal approach. Tumour resection was complete in 57 (78%) cases. There were no operative deaths. Thirty-three per cent of patients were left with permanent deficits: mainly cranial nerve deficit (47%). Seventy-seven per cent of patients out of the 57 who could be followed up are functioning independently, 21% of these having no neurological deficit. With proper neuroradiological evaluation, good selection of patients and microneurosurgical techniques posterior fossa meningiomas can be completely excised with an acceptable complication rate.
The common method of presentation of intracranial aneurysms is at the time of their rupture (with subarachnoid haemorrhage) or on the occasion of their compression of neighbouring structures. While giant aneurysms may occasionally present with subarachnoid haemorrhage, their more common methods of presentation are due to their space occupying and neighbourhood effects. Giant aneurysms are commonly defined as those with a diameter larger than 2.5 cm. Previously this diameter was assessed either by arteriography, so that size meant internal diameter, or by the displacement of surrounding structures, as for example, small perforating vessels, which could be attributed positively to the presence of a larger mass. Before CT scanning however, the factor of a very considerable larger aneurysm, partly occluded by clot could occasionally cause unexpected operative difficulty. The advent of CT scan and now especially MR imaging has made the prediction of the size of the aneurysm much easier and the extent of the intra-aneurysmal clot also clearly definable. This paper describes one surgeon's experience with 64 giant cerebral aneurysms operated on in the last 10 years (Table 1). It has emerged from this experience that the most satisfactory method of handling the lesion is to remove the intra-aneurysmal clot and clip the neck of the aneurysm, and the steps necessary to secure this laudable design from the burden of the paper.
Based on an own material of 64 cases a survey is given on the management of giant intracranial aneurysms. Essential investigations are as well CT and Magnetic Resonance Scanning as detailed angiographic studies. With regard to the operative handling the following questions are discussed: approach; use of temporary vascular occlusion and related monitoring; preparation of the aneurysm neck for occlusion. In cases without recent subarachnoid haemorrhage morbidity and mortality were less than 10%. It was 15% in cases where recent haemorrhage had occurred.
In 7 baboons maintained under propofol anaesthesia, pyramidal tract responses were related to the corresponding peripheral EMG evoked by electrical stimulation of the motor cortex under conditions of focal cortical ischaemia. Pyramidal responses were recorded epidurally at the C5 level and the EMG was recorded from the contralateral hand or foot muscle using subdermal needle electrodes. Cortical ischaemia was produced by transorbital occlusion of the common anterior cerebral artery, and regional cortical blood flow was measured by the hydrogen clearance method. In the normally perfused brain, the later I waves of the C5 response required a lower stimulus strength to elicit them than the earlier I1 wave. It was more difficult to record the EMG from the hand than from the foot following stimulation of the corresponding cortex even though the C5 responses were always obtained in both cases. With moderate ischaemia, the later I waves were selectively abolished, leaving the D and I1 waves. EMG amplitude was significantly correlated with cortical blood flow (r = 0.88, P less than 0.005), and the threshold of cortical flow for the EMG was 10-13 ml/100 g/min. Our results indicate that changes in amplitude of the late I waves and particularly of the EMG are sensitive indicators of cortical ischaemia.
The role of motor evoked potentials in the management of a case of presumed hysterical paraplegia precipitated by spinal injury in a man with a previous history of surgery for scoliosis is presented. Motor evoked potentials were elicited with magnetic stimulation 12 days after injury and were within normal limits. The presence of normal motor electrophysiology and observation by the patient of involuntary movement of the lower limbs during stimulation greatly facilitated the patient's management. These findings are discussed with reference to current diagnostic investigations in the presence of a suspected diagnosis of hysterical paraplegia.
A 36 year old man developed slowly progressive unilateral visual loss due to a cystic lesion of the intraorbital optic nerve. Pathologically the lesion was an epithelium lined cyst entirely within the atrophic nerve. The cyst lining consisted of columnar epithelium partly pseudostratified and ciliated with evidence of mucin secretion, and was immunoactive for cytokeratin but not glial fibrillary acidic protein. This lesion is considered to be similar to neuroenteric cysts that have been reported elsewhere in the nervous system, and the immunocytochemical results are consistent with a heterotopia derived from the primitive ectoderm of the stomatodeum.