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It has been suggested that blood viscosity is involved in the control of cerebral blood flow (CBF) (Thomas et al. 1977a, b, Humphrey et al. 1979). CBF, using the intravenous Xenon133 technique, blood viscosity and haematocrit were measured in 21 patients with elevated viscosity due to paraproteinaemia and found to be the same as in normal subjects. However, the paraproteinaemic patients were anaemic with a mean haematocrit of 0.342. This degree of anaemia would normally be associated with a high CBF. The paraproteinaemic patients were then compared with a group of 10 anaemic patients with matched haematocrits but without paraprotein bands. The whole blood and plasma viscosities were significantly higher in the paraproteinaemic patients and the CBF was significantly lower. The haematocrit, and therefore oxygen carriage, was similar in the two groups. It is likely that in the anaemia of paraproteinaemia the expected increase in CBF did not occur because of the limiting factor of increased viscosity. This suggests that in this instance viscosity rather than oxygen carriage is a major determinant in the control of CBF. This is further emphasized by the better correlation between CBF and blood viscosity than between CBF and haematocrit. It seems likely that viscosity and oxygen carriage are independent variables in the control of CBF.

The cerebral blood flow is low in primary polycythaemia, and it has been suggested that this is due to the increase in viscosity which accompanies the elevated haematocrit. In the present study cerebral blood flow has been measured by a non-invasive 133Xenon technique in six subjects with an elevated haematocrit secondary to a haemoglobin variant with increased oxygen affinity. Flow was significantly higher than normal and 81 % higher than in 11 subjects of comparable age, matched for haematocrit and viscosity, but without the haemoglobin variant. In patients with this unusual type of polycythaemia, cerebral blood flow is high despite the elevated blood viscosity and the implications of these results are discussed.

The direct cortical response (DCR) and associated local cerebral blood flow was recorded from the primate cerebral cortex during a period of focal ischaemia induced by middle cerebral artery occlusion (MCAO). The DCR was lost when local blood flow fell below 20 ml/100 g/min but began to recover as collateral flow increased. Hypercapnia demonstrated a loss of local vascular reactivity following MCAO, but isovolaemic haemodilution still proved effective in increasing blood flow to these areas. The reduction in blood oxygen content induced by haemodilution did not impair cerebral function but the reduction in whole blood viscosity did exacerbate cerebral susceptibility to hypercapnia-induced intra-cerebral steal.

Two designs of thin film amperometric enzyme biosensor flow cell are described for the on-line measurement of glucose and glutamate concentrations in the extracellular fluid of the brain in conjunction with a microdialysis probe. The biosensors have high sensitivity and speed of response, enabling them to be used in the investigation of short term phenomena. The effects of oxidisable chemical compounds and other interferences on the amperometric current are discussed and strategies for eliminating these effects are described. Whereas the interferences can be adequately overcome with ease for glucose measurements in the millimolar range using platinised carbon paper-based enzyme electrodes, they are much more serious in the case of glutamate, which is present in brain extracellular fluid at much lower concentrations. Results are presented to demonstrate the applicability of two types of biosensor module for in vivo measurements.

A novel method of eliminating interferences which arise from electrochemically active substances is described. The sample solutions are passed through a platinum tube electrode inserted into the sample flow line, where they are subjected to DC pre-electrolysis before delivery to a detector cell containing an enzyme electrode. This method was specifically developed to avoid the interference of monoamines and ascorbic acid when brain extracellular fluid is analysed for glutamate, glucose or lactate using an amperometric enzyme flow-cell. HPLC analysis of the reaction products showed that the pre-oxidation treatment efficiently removes the principal interferents, but leaves unaffected the analyte of interest.

Recent data strongly suggest that repetitive ischemic episodes have an adverse cumulative effect on development of edema and tissue damage. We wanted to assess further whether special risks such as exacerbation of extracellular acidification reflecting progressive exhaustion of the capacity to buffer H+ in the extracellular space are associated with repeated short ischemic insults. We monitored spontaneous electrical activity, extracellular direct-current potential, extracellular H+ activity, and tissue PCO2 in the cerebral cortex of rats subjected to four cycles of 3-minute ischemia produced by four-vessel occlusion with 27-minute reperfusion after each insult. Except for electrical activity, which failed to recover fully from the first ischemic insult, all parameters returned to a level close to normal after each reperfusion. Changes during ischemia did not evolve with repetition of the insult. Electrical silence occurred within approximately 20 seconds after the onset of each ischemic episode and always preceded the steep drop of direct-current potential, indicating ischemic depolarization. Each four-vessel occlusion immediately initiated a steep rise of tissue PCO2 and extracellular H+ activity, with extracellular H+ activity reaching a maximum within approximately 145 seconds. Changes in extracellular H+ activity during each recirculation period consistently included an additional and short-lasting increase associated with repolarization, a rapid decrease closely related to that of tissue PCO2, and a slow progressive return to normal. These results suggest that short, repetitive ischemic episodes severe enough to produce cell membrane depolarization and maximum acidosis of the neuronal microenvironment do not have a deleterious cumulative effect on the studied parameters, in particular, on interstitial acidosis.

A 47-year-old man presented, in 1990, with a short history of left-sided cerebellar ataxia. In 1986 he had undergone excision of a glomus jugulare tumour. A magnetic resonance (MRI) scan demonstrated cerebellar herniation through a defect in his skull base. Surgical repair was undertaken with resolution of his symptoms.

Three cases of surgically verified intramedullary cavernous angioma (cavernoma) of the spinal cord are reported. Intramedullary cavernomas of the cord are quite uncommon and account for between 3 and 12% of all vascular lesions of the spinal cord. Little is known of their natural history, although their tendency to produce haemorrhage and episodic symptomatic worsening is recognized. Our series includes one male and two females whose ages ranged between 31 and 67 years. The most common presenting symptom was pain, which in all cases preceded weakness. In two of our cases, the typical progression of sudden paroxysmal worsening of symptoms accompanied by pain was noted. This was thought to be related to bleeding in the lesion. In this series, an average of 8 years had elapsed after the onset of symptoms before the patients came to surgery. Standard microsurgical technique facilitated removal of the lesions, following which all patients regained preoperative function.

Experimental and clinical data strongly support the concept that brain tissue acidification is a common and major factor responsible for neural tissue damage resulting from inadequate oxygen supply to the brain or head trauma (see Rosner and Becker 1984 for review). Intracellular acidosis has been extensively investigated and nuclear magnetic resonance spectroscopy has provided new insights (Siesjo 1985; Allen et al. 1988), but it is also important to assess the events occurring in the extracellular fluid as it is the neuronal microenvironment where neurotransmitters and drugs are available to receptors. This chapter concentrates on new data related to changes detected in the extracellular fluid.

Attempts at radical excision of craniopharyngioma has been made increasingly possible by the advent of neuroradiological imaging and the use of microscopic technique. Between 1977 and 1993, 62 patients of The National Hospital for Neurology and Neurosurgery, London, have undergone surgical excision of craniopharyngioma by the temporal route, with a small anterior temporal resection. Surgical mortality was 4%. Forty-eight patients (76%) remain well on average follow-up of 34 months. Twelve percent had major complications (hypothalamic damage, subdural haematoma, scalp collections requiring shunt drainage). There were four recurrences in patients where the initial operations were considered as complete microscopic excision. Maximal control of tumour recurrence by removal of all tumour accessible and visible to the surgical microscope is best achieved by radical excision at the first operation.

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.

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)

Although Luschka [2] in 1854 gave a description of what appears to have been an intracranial cavernoma, the first clear description of the entity was in 1928 by Walter Dandy [1]. The true frequency of symptomatic cavernomas remains hard to establish, but they are uncommon and probably represent only some 5%–13% of all CNS vascular anomalies, and estimates for the proposition below the tentorium vary from 10% to 23%. This report deals with our findings in 13 cases of brainstem haematoma related to confirmed cavernoma in 9 and probable cavernoma in the others, 12 lying within the brainstem and 1 in the superior vermis of the cerebellum. All were managed by direct microsurgical approach with evacuation of the haematoma and, in the majority of instances, verification of abnormal vessels consistent with cavernoma within the wall [5].

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.

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.

As Gushing [2] pointed out in 1932, of all the tumors of the suprasellar region, few are as difficult to deal with as craniopharyngiomas. As a result widely varying opinions have been expressed about their management, and although it is well known that the lesions are almost invariably “benign”, most surgical series quoted over the past 20 years attest to the difficult management characteristics of these tumors and their tendency to recur. They carry in general a miserable prognosis. Early surgical experience without the operating microscope showed that as the tumors were followed over a long time recurrence was inevitable despite apparent initial complete resection [6, 8, 10, 11]. Not surprisingly, the poor results of surgery led to aggressive radiotherapy, and following the series reported by Kramer et al. [5] many surgeons inclined to the view that minimal surgical intervention with the aspiration of any associated cyst in establishment of the diagnosis followed by aggressive radiotherapy had better results. Nevertheless, isolated reports [4, 11] have suggested that an aggressive approach remains justified, and our own experience with a total of 36 radically excised cases suggests that radical excision, if possible, is undoubtedly the best method of management. Our series is almost exclusively adult, only 4 of the 36 were below the age of 20 years, and only one was younger than 10.

Acquisition of physiological data pertinent to the state of the function of the central nervous system during neurosurgical procedures is desirable wherever possible. For this information to be truly valuable it is necessary to have an experimental framework within which individual observations can be interpreted. Our clinic has studied the effects of controlled cerebral ischemia on electrophysiological cortical function in the primate and has established the concepts of “the ischemic penumbra” and “flow thresholds.”

Our clinic now has a cumulative experience in operating on over 400 patients with acoustic neuromas. During the past 40 years it has been apparent that there has been a progressive reduction in the morbidity rate of patients being operated on for this condition. This prompted us to investigate means of maximizing the preservation of hearing after surgery for patients with an acoustic neuroma. As our department already had extensive experience in intraoperative electrophysiological monitoring, we explored brainstem auditory evoked potentials (BAEP), electrocochleography (ECoG) and direct eighth nerve recording in an attempt to resolve this problem.

In 1965, Hakim and Adams [28,29] described a syndrome of normal pressure hydrocephalus (NPH). Since then, 25 years have passed, but the search for clarity of diagnosis and reliable indices of the prognostic outcome of shunting procedures still occupies our attention. Beneficial results of diversionary procedures for cerebrospinal fluid (CSF) [1,5,22,44,50,55,56,66] have been obtained by many, but difficulties in sorting out patients and disappointing therapeutic results in other series [4,7,8,11,19,37,43,44,45,48,49,51,53,58,61,64,65] have emphasised the continuing need for careful selection before submitting patients to surgery. Our own experiences and those of other workers of a significant proportion of subdural fluid collection following shunt procedures (approaching 10% in the treatment of patients with little evidence of raised pressure in communicating hydrocephalus) was sufficient to convince us that the apparently simple surgical manoeuvre of insertion of a valve system in every patient with marked degree of ventricular dilatation was not desirable surgical management [36,45,57,63].

1. The aim of this study was to examine the rapid changes in extracellular hydrogen ion activity [( H+]o or pHo) which are associated with depolarization and repolarization subsequent to cerebral ischemia reperfusion. Two parallel studies were performed with different rat models of ischemia: repetitive severe ischemia produced in anesthetized animals by occlusion of the vertebral and carotid arteries and temporary interruption of blood flow in isolated brain. [H+]o and direct current potential (DC potential) were recorded simultaneously in all experiments. Examination of these two parameters was supplemented by recording tissue concentration of carbon dioxide (PtCO2) in the four-vessel occlusion model and assaying major metabolites involved in energy production in experiments with isolated brains. 2. Measurements of [H+]o during ischemia consistently revealed a steady increase of [H+]o on which was superimposed an abrupt and transient fall in [H+]o closely related to the occurrence of the fast negative shift of DC potential characterizing brain-cell depolarization. Analysis of the relationship between the magnitude of the transient fall in H+ and the level of [H+]o at which this occurred showed that the amplitude of the transient fall in H+ increased with tissue acidosis. 3. We propose that this phenomenon is indirect evidence that rapid transfer of acid equivalents occurs across the plasmalemma, concomitantly to its depolarization. Both events probably result from a common cause, i.e., nonspecific increase of the cell-membrane permeability to ions subsequent to opening of membrane channels. 4. Early on during recirculation, an acidotic [H+]o shift associated with membrane repolarization was clearly visible whenever the ionic gradients recovered rapidly.(ABSTRACT TRUNCATED AT 250 WORDS)

We report a patient who developed a transient paraparesis without myoclonus following contrast injection during an intravenous urogram (IVU) who was subsequently shown to have a spinal AVM

Dandy was the first to describe the successful removal of a colloid cyst in 192110. Initially a variety of open surgical approaches were described mainly through the frontal horn of the lateral ventricle or through the corpus callosum and although these were attended by considerable mortality and morbidity in the past12, 13, 23,24, 34, modern microsurgery has revolutionized the management of these conditions1, 27. The two series reported here by classical neurosurgical techniques, from Zurich and London, indicate that complete excision of these tumours may now be achieved with low mortality and morbidity. Since 1975, an increasing number of reports have described aspiration techniques avoiding craniotomy5, 11, 15, 17,29,30,31 and a series from Homburg/Saar is described using these techniques. The ventriculoscope has been employed stereotactically or freehand29 (Calliauw) and a brief description of the modern ventriculoscope is appended from Brussels.

Three patients presenting with visual failure had MRIs with hypersignal extending from the region of the optic chiasm along both optic tracts in 2 cases, and along 1 optic tract in the 3rd. In all patients intrinsic tumor of the chiasm was the most likely diagnosis based on MRI appearances, but all 3 had craniopharyngioma.

Local CBF (LCBF) was compared with the corresponding local tissue concentration of ATP, phosphocreatine (PCr), and lactate in anaesthetized baboons subjected to focal ischaemia produced by middle cerebral artery occlusion (MCAO). LCBF hydrogen electrodes were implanted in cortical regions where MCAO had been previously shown to produce severe and penumbral ischaemia and in posterior regions where blood flow is not altered. Metabolites were assayed in small tissue samples collected either by cryoprobe biopsy in the regions where LCBFs were measured (series 1) or by sampling appropriate regions of the rapidly frozen brain (series 2). Subsequent topographical study of brain tissue pH with umbelliferone was performed in this latter series. The results from these two series are compared and discussed in terms of the more appropriate way to perform simultaneous electrode measurements and analysis of tissue samples for studying focal ischaemia in the primate brain. They confirm that the concentrations of ATP and PCr decrease, and that lactate level increases, with decreasing blood flow. These metabolites tended to change more rapidly below a blood flow threshold, rather than showing a steady decrease as the blood flow was reduced, although the variability of the data precluded us from establishing this with confidence. Topographical study of tissue pH often showed sharp boundaries between zones of very low pH and regions with normal pH.

Multidirectional extension and invasive spread are important features of giant pituitary adenomas. Operability cannot be established merely by determining the size of the most prominent part of the tumour. Detailed radiological evaluation with plain films, computed tomography, angiography, and air studies all contribute to evaluation of the precise anatomy before surgery. In the final decision risks of surgical treatment must be balanced against the patient's age and prospects of long-term useful survival. Unfavourable cases for surgical treatment in our hands were those tumours embedded in the hypothalamus with thalamic and posterior extensions. Partial removal of such cases gave poor results. Where the mass proves soft, radical excision may be possible, but not otherwise. Limited biopsy for histological study, followed by a shunt procedure and x-ray therapy seems still the only recourse.

The authors had supplemented the customary treatment by laminectomy in metastatic spinal compression, with the use of immobilization through posteriorally placed rods. They considered that this enabled more rapid mobilization and had also applied the treatment to benign spinal lesions. They had used the technique in twenty cases of metastatic carcinoma, three cases of primary malignancy to the spine and two benign spinal lesions.

Central conduction time following median nerve stimulation has been recorded in 28 patients with infratentorial space occupying lesions. Fourteen of these (50%) showed a prolonged central conduction time, which invariably involved that segment of the conduction time between the dorsal column nuclei generators and the generation site for P15, which we believe to be the upper brain stem or thalamus. Three other cases showed prolongation of the N14-P15 segments though total central conduction time was within normal limits. One case with marked hydrocephalus showed prolongation both before and after the P15 wave. The possible pathophysiology of prolongation of central conduction time in these cases and the possible neural generation site of P15 are discussed.

Epilepsy is an important problem in the period immediately following intracranial surgery. Rapid control of seizures is important to prevent damage to cerebral neuronal function. A method of managing epilepsy using intravenous chlormethiazole is reported. This regimen has proved to be safe and rapidly effective in the control of post-operative seizures.