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Background and Purpose: To address the increasing need to counsel patients about treatment indications for unruptured intracranial aneurysms (UIA), we endeavored to develop a consensus on assessment of UIAs among a group of specialists from diverse fields involved in research and treatment of UIAs., Methods: After composition of the research group, a Delphi consensus was initiated to identify and rate all features, which may be relevant to assess UIAs and their treatment by using ranking scales and analysis of inter-rater agreement (IRA) for each factor. IRA was categorized as very high, high, moderate, or low., Results: Ultimately, 39 specialists from 4 specialties agreed (high or very high IRAs) on the following key factors for or against UIA treatment decisions: (1) patient age, life expectancy, and comorbid diseases; (2) previous subarachnoid hemorrhage from a different aneurysm, family history for UIA or subarachnoid hemorrhage, nicotine use; (3) UIA size, location, and lobulation; (4) UIA growth or de novo formation on serial imaging; (5) clinical symptoms (cranial nerve deficit, mass effect, and thromboembolic events from UIAs); and (6) risk factors for UIA treatment (patient age and life expectancy, UIA size, and estimated risk of treatment). However, IRAs for features rated with low relevance were also generally low, which underlined the existing controversy about the natural history of UIAs., Conclusions: Our results highlight that neurovascular specialists currently consider many features as important when evaluating UIAs but also highlight that the appreciation of natural history of UIAs remains uncertain, even within a group of highly informed individuals.

The Physiological and Operative Severity Score for enUmeration of Mortality and morbidity (POSSUM) scoring systems have been designed for comparative audit and have been well validated in general and vascular surgery. The Portsmouth predictor equation (P-POSSUM) was highly predictive of mortality in a study of elective craniotomies for neurosurgery but has yet to be validated in spinal, peripheral nerve or acute cranial neurosurgery. The West Australian Categorisation of Operative Severity (WA classification) was created for all neurosurgical procedures. Case notes and laboratory results of 531 consecutive patients undergoing neurosurgery were reviewed retrospectively. All POSSUM variables were collected and the POSSUM and P-POSSUM mortality equations were applied. The observed mortality rate was 4.52% and the WA P-POSSUM predicted mortality rate was 4.58% (p>0.951). The WA P-POSSUM rate was more predictive than either the WA POSSUM rate (10.9%, p<0.0001) or the previously proposed elective craniotomy P-POSSUM classification (5.8%, p<0.198). We concluded that the P-POSSUM model with WA classification has the potential to be used in mortality audits for general neurosurgery. By quantifying preoperative risk, P-POSSUM might provide a useful denominator to observed death rates for meaningful comparison of individual neurosurgeons and between departments.

Neuroprotective activity with magnesium associated with animal models of cerebral ischaemia, seizure, perinatal hypoxia/ischaemia, subarachnoid haemorrhage and traumatic brain injury has provided the justification for clinical stroke trials. However, the recent IMAGES stroke clinical trial found magnesium to be largely ineffective. Hence, due to the negative stroke trial outcome, current FAST-MAG trial and our own experience with magnesium in cerebral ischaemia animal models, we thought it prudent to review these preclinical and clinical studies. We reviewed nine studies describing the use of magnesium following global cerebral ischaemia and fourteen following focal cerebral ischaemia. Four global ischaemia and six focal ischaemia studies did not show a significant neuroprotective effect with magnesium. In the majority of positive magnesium studies animal body temperature was not monitored post-ischaemia. Thus the effects of post-ischaemic hypothermia cannot be ruled out as a confounding factor in positive magnesium cerebral ischaemia studies. Moreover, data from our own laboratory indicates that magnesium is only neuroprotective when combined with post-ischaemic hypothermia. These data provide a possible explanation of why the IMAGES trial was largely unsuccessful, as current stroke patient management does not involve hypothermia induction. Future preclinical and clinical cerebral ischaemia trials with magnesium should consider combining treatment with mild hypothermia.

We present an elderly patient with an unusual extensive multifocal central nervous system mass lesion, with dramatic imaging changes but only minor disturbance of cerebral function. Cerebral biopsy revealed an unexpected finding of severe cerebral amyloid angiopathy with secondary florid vasculitic appearances, which is a very rare but recognised association. Immunosuppression has produced significant sustained clinical and radiological remission.

Chondromyxoid fibroma of bone (CMF) is a rare benign primary bone neoplasm accounting for less than 0.5% of all primary bone neoplasms. The spine is an uncommon site for this tumour, with forty-two cases reported in the modern English literature. They have clinical features similar to CMF arising at other sites. Local recurrence is well documented. We report an incidentally discovered lytic lesion of the C2 vertebra. The patient underwent stereotactic CT guided trans-oral curettage of the lesion with iliac bone graft and anterior fusion of C2 and C3. Microscopic examination of the surgical specimen demonstrated CMF. This is the second reported case of this rare tumour in this location. We review the literature and the unique radiological and pathological features and management of spinal CMF. Local recurrence of spinal CMF and its management is also discussed in light of the five previously reported cases of local spinal recurrence.

Preconditioning describes a variety of treatments that induce neurons to become more resistant to a subsequent ischemic insult. How preconditioned neurons adapt to subsequent ischemic stress is not fully understood, but is likely to involve multiple protective mechanisms. We hypothesized hypoxic preconditioning induces protection by a coordinated up-regulation of antioxidant enzyme activity. To test this hypothesis, we developed two in vitro models of ischemia/reperfusion, involving oxygen-glucose deprivation (OGD) where neuronal cell death was predominantly by necrosis (necrotic model) or programmed cell death (PCD model). Hypoxic preconditioning 24 h prior to OGD significantly reduced cell death from 83% to 22% in the necrotic model and 68% to 11% in the PCD model. Consistent with the hypothesis, the activity of the antioxidant enzymes glutathione peroxidase, glutathione reductase, and Mn superoxide dismutase were significantly increased by 54%, 73% and 32%, respectively, in neuronal cultures subjected to hypoxic preconditioning. Furthermore, superoxide and hydrogen peroxide concentrations following OGD were significantly lower in the PCD model that had been subjected to hypoxic preconditioning.

Studies on the neuroprotective effect of magnesium treatment in animal models of focal and global cerebral ischemia have produced inconsistent results. Nevertheless, two magnesium acute stroke phase III trials (IMAGES and FAST-MAG) have either been completed or are planned. Therefore, we decided to re-evaluate the efficacy of magnesium following focal cerebral ischaemia in rats. Two experiments were carried out in two independent laboratories based in Australia. Both used the intraluminal thread method to induce focal cerebral ischemia in the rat. In the Perth study the middle cerebral artery (MCA) was occluded for 45 min and body temperature was controlled during and after ischemia. In the Canberra laboratory the MCA was occluded for 2 h and body temperature was only controlled during surgery. Three different doses (180, 360, or 720 micromol/kg) of MgSO4 in the Perth study and two different MgSO4 doses (370 or 740 micromol/kg) in the Canberra study were intravenously or intra-arterially administered immediately before ischemia. Control animals were given an equal volume of normal saline just before ischemia in both studies. Twenty-four or 72 h post-ischemia, infarct volume was determined following 2',3',5'-triphenyl-2H-tetrazolium chloride (TTC) staining. No significant differences (P > 0.05) in total, cortical and striatal infarct volumes between saline and MgSO4 treated animals were observed in either study. We conclude MgSO4 does not reduce infarct volume when administered before focal cerebral ischemia in rats.

A case of glioblastoma with leptomeningeal spread after control of the primary lesion by radiation therapy. A discussion is made regarding leptomeningeal metastatic disease with reference to the literature., (Copyright 2002 Elsevier Science Ltd.)

We report the case of a 32-year-old South Korean male who presented with bilateral leg weakness, spastic gait and associated sensory loss from below the T5 dermatome. MRI and CT scans of the spine confirmed the presence of calcified ligamentum flavum from T1-T6. A thoracic laminectomy resulted in an excellent post-operative recovery with full return of all functions. This case review will discuss the differences that exist between ossification of the posterior longitudinal ligament (OPLL) and ossification of the ligamentum flavum (OLF), but also the similarities at a molecular and possibly at a genetic level. We have reviewed the reported literature of patients presenting with progressive lower limb spacity due to OLF, and an excellent outcome is achieved using decompressive laminectomy., (Copyright 2002 Published by Elsevier Science Ltd.)

Objective: We aimed to determine an effective dose schedule for intravenously administered magnesium, to establish its neuroprotective efficacy in both pre- and postischemic treatment paradigms, and to compare the neuroprotective properties of MgSO(4) and MgCl(2)., Methods: Rats that had been subjected to the bilateral carotid artery occlusion plus hypotension model of transient forebrain cerebral ischemia received either an intravenously administered loading dose (LD) of 360 micromol/kg MgSO(4) only or an intravenously administered LD of 360 micromol/kg followed by a 48-hour intravenous infusion of MgSO(4) at either 60, 120, 240, or 480 micromol/kg/h. For evaluation of the efficacy of MgSO(4) after ischemia, the dose (LD, 360 micromol/kg; infusion, 120 micromol/kg/h) that provided maximal neuroprotection before ischemia was administered 4, 8, 12, or 24 hours after ischemia. MgCl(2) (LD, 360 micromol/kg; infusion, 120 micromol/kg/h) was administered before and 8 hours after ischemia. At 7 days after ischemia, hippocampal CA1 neurons were histologically examined for protection., Results: Animals that received the LD only demonstrated 33% hippocampal CA1 neuronal survival. Animals that received the LD followed by continuous infusion of MgSO(4) at either 60, 120, 240, or 480 micromol/kg/h demonstrated 30, 80, 16, and less than 5% CA1 neuronal survival, respectively. MgSO(4) treatment commencing at 4, 8, 12, or 24 hours resulted in 82, 71, 52, and 33% CA1 neuronal survival, respectively. Preischemic and 8-hour postischemic administration of MgCl(2) resulted in 50% and less than 5% CA1 neuronal survival, respectively., Conclusion: These results demonstrate a neuroprotective intravenous dose of MgSO(4), which is effective when administered before or late after ischemia, and a previously uncharacterized dose-response curve for MgSO(4).

Driver (sham-operated) and tester (ischemic) hippocampal cDNAs were subtracted, and the resulting ischemia-induced upregulated gene expression was verified by northern analysis. cDNAs isolated corresponded to (1) genes known to be upregulated following ischemia, (hsc70, hsp90, hsp105 and trkB) and (2) a gene not previously implicated with cerebral ischemia, sodium calcium exchanger (ncx). Furthermore, upregulation of these genes was demonstrated following preconditioning transient global ischemia.

Pituitary carcinomas, currently defined as primary adenohypophyseal neoplasms with evidence of either brain invasion or metastatic spread, are exceptionally rare. A case of corticotroph pituitary carcinoma is reported. A 17-year-old female first presented with an invasive and clinically non-functioning pituitary macroadenoma. The primary pituitary lesion lacked atypical histological features and retrospective immunohistochemical studies confirmed its corticotrophic nature. Repeated episodes of local recurrence followed together with the acquisition of severe Cushing's disease. Local disease control was not obtained despite repeated surgical decompression and courses of radiation therapy. Systemic dissemination with multiple bone metastases became manifest eleven years after the first presentation. Atypical histological features and Crooke's hyaline change were evident in both the recurrent and metastatic disease. She remains alive at last follow-up with severe complications relating to persisting sellar and metastatic disease and ongoing endocrine dysfunction. A further 32 cases of pituitary corticotroph carcinoma reported in English are reviewed to highlight the clinicopathological features of this rare form of pituitary neoplasm. Difficulties associated with the diagnosis and management of pituitary carcinoma are also discussed.

Cavernous haemangiomas (cavernomas) are uncommon vascular malformations of the central nervous system (CNS). They occur in both sporadic and familial forms and may involve any site in the CNS. Spinal cavernomas are less common than intracerebral lesion s, and examples in the spinal epidural space are rare. A case of a solitary sporadic spinal extradural cavernoma in a 41 year old male which presented as progressive lower limb numbness and weakness is reported. The literature regarding spinal cavernomas is reviewed and the symptomatology, diagnostic evaluation, pathology, management and prognosis of these lesions are discussed., (Copyright 2001 Harcourt Publishers Ltd.)

1. Transient forebrain ischemia in adult rats, induced by 10 min of bilateral carotid occlusion and an arterial hypotension of 40 mmHg, caused substantial damage not only to CA-1 neurons in hippocampus but also to epithelial cells in lateral ventricle choroid plexus. 2. When transient forebrain ischemia was followed by reperfusion (recovery) intervals of 0 to 12 hr, there was moderate to severe damage to many frond regions of the choroidal epithelium. In some areas, epithelial debris was sloughed into cerebrospinal fluid (CSF). Although some epithelial cells were disrupted and necrotic, their neighbors exhibited normal morphology. This patchy response to ischemia was probably due to regional differences in reperfusion or cellular metabolism. 3. Between 12 and 24 hr postischemia, there was marked restoration of the Na+, K+, water content, and ultrastructure of the choroid plexus epithelium. Since there was no microscopical evidence for mitosis, we postulate that healthy epithelial cells either were compressed together on the villus or migrated from the choroid plexus stalk to more distal regions, in order to "fill in gaps" along the basal lamina caused by necrotic epithelial cell disintegration. 4. Epithelial cells of mammalian choroid plexus synthesize and secrete many growth factors and other peptides that are of trophic benefit following injury to regions of the cerebroventricular system. For example, several growth factors are upregulated in choroid plexus after ischemic and traumatic insults to the central nervous system. 5. The presence of numerous types of growth factor receptors in choroid plexus allows growth factor mediation of recovery processes by autocrine and paracrine mechanisms. 6. The capability of choroid plexus after acute ischemia to recover its barrier and CSF formation functions is an important factor in stabilizing brain fluid balance. 7. Moreover, growth factors secreted by choroid plexus into CSF are distributed by diffusion and convection into brain tissue near the ventricular system, e.g., hippocampus. By this endocrine-like mechanism, growth factors are conveyed throughout the choroid plexus-CSF-brain nexus and can consequently promote repair of ischemia-damaged tissue in the ventricular wall and underlying brain.

A 28-year-old Caucasian woman presented with a 12 month history of secondary amenorrhoea, polyuria and polydipsia with fatigue and weight loss. Investigations revealed panhypopituitarism, diabetes insipidus, an intrasellar mass and papilloedema, thought to be due to benign intracranial hypertension. She was treated conservatively. However, a repeat magnetic resonance image showed enlargement of the pituitary mass with compression of the optic nerves. The pituitary abscess was drained by a transsphenoidal approach. Postoperatively the patient received antibiotics with no recurrence of the pituitary abscess. Copyright 1999 Harcourt Publishers Ltd.

Transient cerebral ischaemia accompanies a number of disease processes, including stroke, subarachnoid haemorrhage and head injury, that have a profound social and economic impact on our community. The development of neuroprotective agents that reduce the morbidity associated with these diverse conditions requires an understanding of the mechanisms of neuronal death following cerebral ischaemia. There is increasing evidence that a significant proportion of neurons die following ischaemia by a process called apoptosis. Apoptosis involves the activation of a highly regulated series of intracellular events in which the neuron actively participates in its own death. Genes such as bcl-2 and proteolytic enzymes such as the caspases, which have been shown to play an important role in apoptotic cell death in other cell types, are now being investigated for their role in apoptotic neuronal death. This review will focus on current knowledge of the intracellular pathways of apoptosis, with particular reference to their role in ischaemic neuronal death.

Although transforming growth factor-beta (TGF-beta) is known to be multifunctional in many physiological systems, its role in the brain is undergoing elucidation. The situation is made more complex by the presence of multiple isoforms, which may be differentially regulated and have various activities in each particular cell type. Because neurons are dependent on neurotrophic factors for survival, we utilized a rat model of transient forebrain ischemia (TFI) to test the hypothesis that TGF-beta isoforms are important in the hippocampal response to injury. Northern blot analysis demonstrated a differential and temporal alteration in TGF-beta isoform expression following TFI. In-situ hybridization experiments revealed that at day 1 following TFI, there was a strong neuronal increase in the TGF beta-1 transcript but a reciprocal decrease in TGF-beta 2 and -beta 3 transcript levels. Immunohistochemical analysis of all three TGF-beta s demonstrated at day 1 following TFI a loss of the immunoreactive proteins in the vulnerable CA-1 hippocampal neurons, but protein preservation in the CA-2-4 neurons which are more resistant to the ischemic insult. At 3-5 days following TFI, significant extraneuronal changes in TGF-beta isoform expression were also detected. Double-staining experiments with antibody to glial fibrillary acidic protein (GFAP) as a marker for astrocytes, and lectin isolectin B4 Griffonia simplicifolia for microglia, demonstrated increased expression of all TGF-beta isoforms in astrocytes but not microglia. Taken together, these results suggest that the TGF-beta peptides in neurons and astrocytes are important endogenous mediators in the CNS response to ischemic injury.

Meningiomas arise from the arachnoidal cells surrounding the brain and are one of the most common tumors of the central nervous system. These tumors are known to be hormonally modulated and may occur in association with breast carcinoma. Overexpression of the erbB-2 oncogene product and mutation of the tumor suppressor p53 gene are considered causal driving forces in the pathogenesis of adenocarcinomas of the breast. To determine whether abnormal expression of these genes also plays a role in the pathogenesis of meningiomas, we analyzed the expression of the erbB-2 and p53 proteins in 17 atypical and 35 typical meningioma tissue specimens by immunohistochemistry. The staining intensity was assigned a relative value of 0 to 5+, where 5+ denoted confluent immunoreactivity, 4+ to 1+ denoted varying degrees of focal positivity, and 0 denoted no evidence of staining. Levels of p53 and erbB-2 immunohistochemical staining were then correlated with tumor histology. For p53 immunoreactivity, typical meningiomas had a median staining score of 1.0, compared to 4.0 for atypical meningiomas (P < 0.0001, Mann-Whitney U test). For erbB-2 immunoreactivity, typical meningiomas had a median staining score of 5.0 compared to 1.0 for atypical meningiomas (P < 0.0001, Mann-Whitney U test). The inverse relationship between levels of erbB-2 and p53 immunoreactivity was found to be statistically significant (P < 0.0001, ANOVA). Expression of the erbB-2 protein was not associated with gene amplification or the presence of activating mutation in the transmembrane region of the protein. These findings may improve our understanding of the molecular events that occur in the neoplastic transformation of meningothelial cells. The patterns of erB-2 and p53 immunoreactivity may prove to be useful markers with which to identify potentially more malignant meningiomas.

A multicenter, randomized, blinded, placebo-controlled trial was conducted to study the possible role of intracisternally administered fibrinolytic agent recombinant tissue plasminogen activator (rt-PA) in preventing delayed onset cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH). The target population was patients with ruptured saccular aneurysms causing severe SAH, placing them at high risk for vasospasm. Treatment consisted of a single 10 ml intraoperative injection of either vehicle buffer solution or rt-PA (1 mg/ml) into the opened basal subarachnoid cisterns immediately following aneurysm clipping. The major efficacy endpoint in this trial was angiographic vasospasm, and the major safety concern was intracranial hemorrhage. One hundred patients were randomized, 49 to placebo and 51 to rt-PA treatment. Baseline population characteristics were similar between the two groups. Severity of intracranial hemorrhage on computed tomographic scans was also similar between groups: 87.2% of both placebo and rt-PA treated patients had thick subarachnoid clots, and the rates for intracerebral and intraventricular hemorrhage were, respectively, 16.3% and 22.5% for placebo and 23.5% and 21.6% for rt-PA. Nine randomized patients did not receive treatment in the operating room, and in 8 this was due to conditions felt unsafe for the administration of a fibrinolytic agent. The overall incidence of angiographic vasospasm measured between the seventh and eleventh day following SAH was similar between the two groups, with arterial narrowing detected in 74.4% of dosed placebo patients and 64.6% of rt-PA treated patients. However, there was a trend toward lesser degrees of vasospasm in the rt-PA treated group. The rates for no or mild, moderate, and severe vasospasm were 69%, 16% and 15% in the rt-PA treated group, versus 42%, 35% and 23% in the placebo group (P = 0.07). When only those patients with thick subarachnoid clots were considered at the treating centers, there was a 56% relative risk reduction of severe vasospasm in the rt-PA treated group, which was significant (P = 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Patients with symptomatic aneurysms that are not excluded from the cerebral circulation have a poor prognosis. Standard treatment is surgical exploration with direct clipping of the aneurysm. Because of their large size or relationship to the base of the skull, some aneurysms may not be suitable for direct surgical clipping and may require alternative treatment modalities. A prospective clinical and radiological study of seven patients treated with the endovascular placement of platinum-Dacron microcoils to exclude the aneurysm from the cerebral circulation is reported. The seven patients ranged in age from 37 to 63 years; four were women. At completion of the endovascular procedure, total occlusion of the aneurysm with preservation of the parent artery had been achieved in four patients and 90% occlusion of the aneurysm in two. In the seventh patient, occlusion of the internal carotid artery resulted in the patient's death. At the 6-month follow-up review, both patients with an aneurysm less than 20 mm in size had persistent aneurysm thrombosis; however, the two patients with giant aneurysms had partial recanalization. Both required repeat thrombosis of their aneurysm with the placement of additional microcoils, one at 6 weeks and one at 6 months. These two patients have persistent aneurysm thrombosis at 12 months following their second procedure. The patient mortality rate for this study was 14%, while the procedure mortality/morbidity rate was 9%. It is concluded that thrombotic aneurysm therapy of difficult aneurysms is a safe procedure and will have a place in the treatment of selected aneurysms.

The traditional surgical management of complex craniofacial injuries is performed in three stages: immediate craniotomy, orbitofacial repair in 7 to 10 days, and cranioplasty delayed 6 to 12 months because of the perceived risks of infection and prolonged anesthesia in the head-injured patient. Cosmetic considerations have always played a secondary role; however, there are reports that suggest that bone fragments and grafts can be safely placed even in contaminated wounds. In addition, advances in neuroanesthetic technique allow for prolonged administration of anesthesia without untoward effects on the patient. The purpose of this prospective study was to determine if early single-stage repair of complex craniofacial injuries could be accomplished with acceptable morbidity and mortality. In this study, 13 patients (9 men, 4 women) ranging in age from 3 to 53 years, with Glascow Coma Scale scores of 10 to 15, all had a combined single-stage repair of their complex craniofacial injuries within 24 hours of their trauma. After initial assessment and resuscitation, all patients were evaluated with computerized tomography of the face and head before surgery. Bicoronal skin flaps were used for maximum exposure for frontal sinus exenteration as well as dural repair, cortical debridement, and calvarial reconstruction. Dural grafts were necessary in 12 of 13 patients (92%), and supplementary bone grafting was required in 9 of 13 patients (69%), of which 3 of the 9 (33%) had iliac bone grafts, where split calvarial grafts were used in the other 6 of 9 (67%). No artificial cranioplasty material was used.(ABSTRACT TRUNCATED AT 250 WORDS)

Intramedullary spinal abscesses are rare and potentially devastating lesions. A heightened clinical awareness of patients at risk is essential for an early diagnosis and intervention to improve the prognosis of these patients. The first case of spinal abscess was described in 1830, and only 63 cases have been reported subsequently. Intraspinal epidermoids also are unusual lesions. These tumors were reported first in 1829 and represent less than 1% of all intraspinal tumors. We present a case of a 2-year-old girl who had rapidly progressive paraplegia with urinary and bowel retention and was found to have an intramedullary epidermoid and an intramedullary abscess as a result of a dermal sinus. The association of an intramedullary abscess and epidermoid tumor, two rare lesions, has not been reported previously. We also review the literature related to both intramedullary epidermoids and intramedullary abscesses of the spinal cord. Advances in sectional imaging as described should help lead to an early and safe diagnosis of these rare but often debilitating lesions. This case illustrates the importance of a complete neurological assessment of all patients with a congenital dermal sinus because of the potential for intradural extension and the frequent association with other dysraphic abnormalities. Prophylactic surgery is indicated in many cases to prevent dangerous and recurrent infections of the central nervous system.

Microdialysis is used in vivo for measuring compounds in brain interstitial fluid. The authors describe another application of this technique to the central nervous system, namely microprobe dialysis in the cisterna magna to study the dynamics of ion transport and cerebrospinal fluid (CSF) formation in the rat. The choroid plexus is the major source of CSF, which is produced by active transport of Na from blood into the cerebral ventricles. Formation of CSF is directly proportional to the blood-to-CSF transport of Na. By injecting 22Na into the systemic circulation and quantifying its movement into CSF by microdialysis, one can reliably estimate alterations in the rate of CSF formation. The sensitivity of this system was determined by administering acetazolamide, a standard inhibitor of CSF production. Because acetazolamide is known to decrease CSF formation by 40% to 50%, the cisternal microdialysis system in animals treated with this drug should detect a corresponding decrease in the amount of 22Na dialyzed. This hypothesis is supported by the 22Na uptake curves for control versus treated animals: that is, by the acetazolamide-induced average diminution of about 45% in both the rate and extent of tracer accession to dialysate. Bumetanide, a loop diuretic, reduced by 30% the 22Na entry into dialysate. Microprobe dialysis of fluid in the cisterna magna is thus a minimally invasive and economical method for evaluating effects of drugs and hormones on the choroid plexus-CSF system.

A seven-year-old girl sustained a gunshot wound to the chest and spine. Evaluation of a persistent pleural effusion demonstrated a subarachnoid-pleural fistula. Surgical closure of the dural defect resulted in resolution of the fistula. Traumatic subarachnoid-pleural fistulae are rare. The diagnosis is reached by an awareness of fistula formation from penetrating or blunt trauma to the chest.

Patients suffering from a subarachnoid hemorrhage who were admitted to the Neurosurgical Unit of the Royal Perth Hospital during the period 1971 to 1979 were assessed with regard to the effectiveness of preoperative treatment with epsilon-aminocaproic acid, kanamycin, and reserpine. Forty-two patients who were treated with epsilon-aminocaproic acid had a rebleed rate of 2.3% compared to 1 9.7% rebleed rate in appropriately selected controls. Patients treated with kanamycin and reserpine had a preoperative cerebral vasospasm rate of 32% compared to a 26% rate in controls; however, kanamycin and reserpine were found useful for decreasing the postoperative complications of cerebral vasospasm.

The grade of cerebral function on admission, the clinical outcome and the initial computerized tomographic (CT) scan of 52 patients with subarachnoid haemorrhage have been reviewed. The presence of widespread haemorrhage, hydrocephalus, haematoma and ischaemia on the initial CT scan is associated with poor neurological outcome in this series, irrespective to the initial neurological grading.

The present work reports that simple oxidizing agents are capable of inducing isotonic contraction of rat aorta in vitro, and that the concentration of agent required depends on its oxidizing potential. Conversely a reducing agent will reverse a muscular contraction induced by oxidizing agents.

Spinal epidural abscess is an unusual disease in the pediatric age group, requires early diagnosis and prompt surgical drainage to insure a good clinical outcome. Back pain and fever are usually the only presenting symptoms occurring before precipitous neurologic deterioration. The causative organism is most often Staphylococcus aureus, which presumably is spread to the epidural space hematogenously. Diagnosis is facilitated by computed tomography (CT) scan, but the entire spine must be imaged by either myelography or magnetic resonance imaging (MRI) to assess for skip lesions.

A family incorporating 2 interesting variants of trigeminal and glossopharyngeal neuralgia is presented. The familial occurrence of these cranial neuralgias spanning 3 generations is very unusual. In the case of glossopharyngeal neuralgia it has not been documented previously. Furthermore, the coincidence of trigeminal and glossopharyngeal neuralgia in the same person is quite exceptional, despite the anatomical contiguity of the sensory territories of the fifth and ninth cranial nerves. These features suggest firstly that there must be an important constitutional factor in the aetiology of the cranial neuralgia, and secondly that in many cases there is a centronuclear rather than cranial nerve ganglionic pathogenesis of the pain.

Fifty-one children who were clumsy because of perceptual disabilities and/or defects of motor organization were surveyed with computerized axial tomographic (CT) head scanning and compared to 33 controls by using both linear measurements and visual appraisal of the scans. Thirty-nine percent of these so-called clumsy children described as having developmental apraxia and agnosia, compared to 9% of the controls, were either abnormal or normal variants. These presumed abnormalities included ventricular dilatation, peripheral atrophy and parenchymal lesions. The Evans Ratio and Intercaudate Distance in the clumsy children were not significantly different from the controls, but the Ventricular Area Index was found to be very significantly different in the two groups.

Twenty-four clumsy children of whom 13 had matched controls were reappraised eight years after their original assessment. The findings indicate that developmental clumsiness generally has a favourable prognosis. Mild and moderate degrees of clumsiness improved to normality, but severe degrees of clumsiness had a less favourable outcome only in regard to motor proficiencies. Clumsiness seemed not to have bearing, either on social class or on the subsequent pursuit of sporting activities. Although there was a lower level of academic achievement in the clumsy children, who also chose careers which were less manually exacting, these observations did not reach statistical significance. Maturational lag might be the aetiology in mild developmental clumsiness, whereas structural lesions involving the cerebral cortex may be present in more severely afflicted children. These findings should be considered when counseling clumsy children, both academically and vocationally.

Cerebral blood flow (CBF) was measured during the 1st week of subarachnoid hemorrhage in 46 patients who were in a good clinical grade and had a proven ruptured intracranial aneurysm. The mean initial CBF in patients who developed cerebral ischemia was 42 ml/min-1/100 gm brain-1, which was significantly lower than in patients who did not develop cerebral ischemia (49 ml/min-1/100 gm brain-1). This reduced CBF was not secondary to raised intracranial pressure or angiographic spasm. Patients with a reduced CBF (less than 50 ml/min-1/100 gm brain-1) and diffuse subarachnoid blood on computerized tomography had a very high incidence (78%) of cerebral ischemia, despite a good clinical grade at the time of measurement. Serial CBF measurements are of value in monitoring the evolution of cerebral vasospasm.

2 women with acute anterior poliomyelitis affecting the upper limb girdles in early childhood later developed thoracic outlet syndromes, 1 of them bilaterally. It is thought that the poliomyelitis was a contributory factor in each case by allowing undue descent of the shoulder girdles, although cervical ribs were also present in the second case. This association had not been recorded previously. Both patients obtained substantial relief from anterior scalenotomy, indicating that previous involvement of the shoulder girdle by poliomyelitis does not negate the efficacy of this operative procedure.

We analysed 360 patients who presented with a proven subarachnoid haemorrhage during the period 1971-78. The most common cause was a cerebral aneurysm (75%), with the anterior communicating artery being the most common site for a ruptured aneurysm. Overall mortality rate before surgical intervention was 28%. During the period of study, 106 Grade 1 patients underwent direct clipping of their aneurysms; this procedure was associated with a 6.6% mortality rate. Delayed surgical intervention was associated with a lower surgical mortality rate.

Standard neurosurgical management mandates prompt evacuation of all epidural hematomas to obtain a low incidence of mortality and morbidity. This dogma has recently been challenged. A number of authors have suggested that in selected cases small and moderate epidural hematomas may be managed conservatively with a normal outcome and without risk to the patient. The goal of this study was to define the clinical parameters that may aide in the management of patients with small epidural hematomas who were clinically asymptomatic at initial presentation because there was no clinical evidence of raised intracranial pressure or focal compression. A prospective study was conducted of 22 patients (17 males and five females) aged from 1 to 71 years, who had a small epidural hematoma diagnosed within 24 hours of trauma and were managed expectantly. Of these, 32% subsequently required evacuation of the epidural hematoma 1 to 10 days after the initial trauma. Analysis of the patients revealed that age, sex, Glasgow Coma Scale score, and initial size of the hematoma are not risk factors for deterioration. However, deterioration was seen in 55% of patients with a skull fracture transversing a meningeal artery, vein, or major sinus, and in 43% of those undergoing computerized tomography (CT) within 6 hours of trauma. In contrast, only 13% of patients in whom the diagnosis of a small epidural hematoma was delayed over 6 hours subsequently required evacuation of the epidural collection. Of patients with both risk factors, 71% required evacuation of the epidural hematoma. None of the patients suffered neurological sequelae attributable to this management protocol. It was concluded that patients with a small epidural hematoma, a fracture overlaying a major vessel or major sinus, and/or who are diagnosed less than 6 hours after trauma are at risk of subsequent deterioration and may require evacuation. Conversely, patients without these risk factors may be managed conservatively with repeat CT and careful neurological observation, because of the low risk of delayed deterioration.