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Objectives Several plaque and lesion characteristics have been associated with an increased risk for procedural stroke during or shortly after carotid artery stenting (CAS). While technical advancements in stent design and cerebral protection devices (CPD) may help reduce the procedural stroke risk, and anatomy remains important, tailoring stenting procedures according to plaque and lesion characteristics might be a useful strategy in reducing stroke associated with CAS. In this descriptive report of the ongoing Asymptomatic Carotid Surgery Trial-2 (ACST-2), it was assessed whether choice for stent and use or type of CPD was influenced by plaque and lesion characteristics. Materials and methods Trial patients who underwent CAS between 2008 and 2015 were included in this study. Chi-square statistics were used to study the effects of plaque echolucency, ipsilateral preocclusive disease (90–99%), and contralateral high-grade stenosis (>50%) or occlusion of the carotid artery on interventionalists' choice for stent and CPD. Differences in treatment preference between specialties were also analysed. Results In this study, 831 patients from 88 ACST-2 centres were included. Almost all procedures were performed by either interventional radiologists (50%) or vascular surgeons (45%). Plaque echolucency, ipsilateral preocclusive disease (90–99%), and significant contralateral stenosis (>50%) or occlusion did not affect the choice of stent or either the use of cerebral protection and type of CPD employed (i.e., filter/flow reversal). Vascular surgeons used a CPD significantly more often than interventional radiologists (98.6% vs. 76.3%; p < .001), but this choice did not appear to be dependent on patient characteristics. Conclusions In ACST-2, plaque characteristics and severity of stenosis did not primarily determine interventionalists' choice of stent or use or type of CPD, suggesting that other factors, such as vascular anatomy or personal and centre preference, may be more important. Stent and CPD use was highly heterogeneous among participating European centres.

Neurovascular compression (NC) seems to have been confirmed as the major cause of classical trigeminal neuralgia (TN). In spite of the large number of surgically positive cases, however, there are still cases where no vascular compression of the trigeminal nerve can be found. To evaluate whether NC could be demonstrated preoperatively, high-resolution magnetic resonance angiography (MRA) was performed in 287 consecutive patients with TN and persistent idiopathic facial pain (PIFP) on a 0.5-T and a 1-T MR unit. Depending on the clinical symptoms, the TN cases were divided into typical TN and trigeminal neuralgia with non-neuralgic interparoxysmal pain (TNWIP) groups. Microvascular decompression (MVD) was performed in 103 of the MRA-positive cases. The patients were followed up postoperatively for from 1 to 10 years. The clinical symptoms were compared with the imaging results. The value of MRA was assessed on the basis of the clinical symptoms and surgical findings. The outcome of MVD was graded as excellent, good or poor. The clinical symptoms were compared with the type of vascular compression and the outcome of MVD. The MRA image was positive in 161 (56%) of the 287 cases. There were significant differences between the clinical groups: 66.5% of the typical TN group, 47.5% of the TNWIP group and 3.4% of the PIFP group were positive. The quality of the MR unit significantly determined the ratio of positive/negative MRA results. The surgical findings corresponded with the MRA images. Six patients from the MRA-negative group were operated on for selective rhizotomy and no NC was found. Venous compression of the trigeminal nerve was observed in a significantly higher proportion in the background of TNWIP than in that of typical TN on MRA imaging (24.1% and 0.8%, respectively) and also during MVD (31.2% and 1.2%, respectively). Four years following the MVD, 69% of the patients gave an excellent, 23% a good and 8% a poor result. The rate of some kind of recurrence of pain was 20% in the typical TN and 44% in TNWIP group. The rate of recurrence was 57% when pure venous compression was present. The only patient who was operated on from the PIFP group did not react to the MVD. The clinical symptoms and preoperative MRA performed by at least a 1-T MR unit furnish considerable information, which can play a role in the planning of the treatment of TN.

Aim: Many investigators have proved the usefulness of acetazolamide provocation and the carbon dioxide test for assessment of the local cerebrovascular reactivity by measurement of the regional cerebral blood flow in patients with occlusive cerebrovascular disease. Data originating from a comparison of these two different vasomotor stimuli as concerns the differences in sensitivity to them in various parts of the central nervous system are scarce. Our aim was to compare the cerebral blood flow responses to hypercapnic and acetazolamide stimuli in different brain regions. Methods: The cerebral blood flow was measured in the cerebrum (cortex and caudate nucleus) and cerebellum (cortex), as measured by a hydrogen clearance method in anaesthetized, artificially ventilated rabbits. Results: In normocapnia, the cerebral blood flow values in the cerebrum and the cerebellum differed significantly. The cerebral blood flow responses to both vasodilatory stimuli were to be significantly higher in the cerebrum than in the cerebellum, but the relative increases, i.e. the mean relative reactivities, were similar in the different regions measured. Conclusion: The regional dissimilarity might explain to some extent the different sensitivities of the various brain areas to sudden blood pressure changes (infarction or haemorrhage). The results further suggest that heterogeneity in cerebrovascular reactivity should be considered in the assessment of vasoreactivity in patients with occlusive cerebrovascular disease. Since the comparison of the carbon dioxide and acetazolamide – induced cerebrovascular reactivities revealed a strong linear relationship, it was concluded that acetazolamide provocation is equivalent to the carbon dioxide test in the evaluation of cerebrovascular reactivity.

The terms moyamoya disease, moyamoya syndrome and moyamoya phenomenon can be found dispersed throughout the literature. The diagnostic criteria for moyamoya disease are: (1) stenosis or occlusion of the anterior cerebral, middle cerebral and internal carotid arteries, (2) an abnormal vascular network near these arteries and (3) bilateral findings. When only the two first conditions are present, the term moyamoya syndrome is used. The incidence of moyamoya disease is high in the Mongol race, although the moyamoya syndrome is more frequently reported among Caucasians. In the last two decades 41 cases of moyamoya were diagnosed in two Hungarian and two Scandinavian hospitals, respectively. Thirty-one patients were operated on 12 unilaterally and 19 bilaterally--either with extracranial/intracranial bypass (29 cases) or with encephalomyosynangiosis (2 cases). After a mean follow-up of seven years, 67.7% of the operated cases were symptom-free or neurologically improved. The majority of the patients had moyamoya disease and turned out to be of Finno-Ugric or Lapplandish ancestry. These people originally migrated from the East and belong to the Ural-Altaic family. Our findings suggest that while the moyamoya syndrome is found in different races, the moyamoya disease may be limited to people of Eastern (Mongol) origin. Revascularization surgery may be of benefit to patients with moyamoya.

ZusammenfassungBei 29 Patienten (3 Kontrollpersonen, 26 Patienten mit zerebrovaskulärer Erkrankung) wurde prospektiv die Hirn-SPECT mit 99mTC-HMPAO und bei 20 Patienten (3 Kontrollpersonen, 17 Patienten mit ZVK) die transkranielle Dopplersonographie (TCD) vor und nach i. v. Gabe von Azetazolamid durchgeführt. Die Sensitivität der Hirn-SPECT erhöhte sich mit Azetazolamid von 62% auf 77%. Bei Patienten mit reversiblem neurologischem Defizit wurde eine Verbesserung von 50% auf 71 %, bei Patienten mit persistierendem Defizit von 75% auf 83% beobachtet. Die Ergebnisse der Hirn-SPECT und der TCD stimmten in der Beurteilung der zerebro-vaskulären Reservekapazität in 91% der Hemisphären überein. Die Korrelation zwischen den beiden Methoden war statistisch signifikant.

Very great confusion exists as regards terminology of neural tumours and their c1assification. Many apellations and comments have been applied to each of these tumours since the beginning of the century. This confusion is further aggravated by the difficulties of histological diagnosis and by the persistent uncertainty as to the precise origin of these tumours in the nerve tissue. Harkin and Redd (1968) c1assified the tumours into five categories: 1. Neoplasms of nerve sheath origino A. Benign primary nerve sheath tumours. 1. Schwannoma (neurilemmoma). 2. Neurofibroma. B. Malignant primary nerve sheath tumours. 1. Malignant schwannoma. 2. Nerve sheath fibrosarcoma. lI. Neoplasms of nerve cell origino 1. Neuroblastoma. 2. Ganglioneuroma. 3. Pheochromocytoma. lII. Tumours metastatic to peripheral nerves. IV. Neoplasms of non-neural origino 1. Lipofibromatosis. 2. Intraneurallipoma, haemangioma, ganglion. V. Non-neoplasms (traumatic neuroma, compressive neuroma). The neuropathologists c1assify more tumour types into the category of peripheral nerve tumours. Consequently the aboye mentioned list should be completed with the granular cell tumours, with the melanotic neuroectodermal tumours, with the chemodectomas as well as with the tumours of APUD (Amine Precursor Uptake and Decarboxylation) cell origino It seems to be agreed by all present-day authors that three main types of peripheral nerve tumours exist, all arising from the Schwann-cell and secondarily from the fibroblasts of the endoneurium and perineurium: schwannomas (neurilemmomas), neurofibromas and nerve tumours malignant from the outset (neurofibrosarcomas). These are the peripheral nerve tumours with which a neurosurgeon must be familiar.

We describe a 23-year-old girl with an extremely uncommon form of cerebral venous drainage and cerebellar leptomeningeal angiomatosis as a possible variant of the Sturge-Weber syndrome. Extensive congenital port-wine stains all over the body, hypoplastic left renal and subclavian and iliac veins, cardiomegaly and ptosis and hypoplasia of the left kidney had been recognised in early childhood. She rapidly developed signs of intracranial hypertension. CT and MRI showed a right medial temporal lesion. Angiography revealed cerebellar pial angiomatosis with enlarged medullary veins and no functioning sigmoid sinuses or jugular veins. Cerebral venous drainage was via enlarged ophthalmic veins. Although the intracranial venous abnormalities were characteristic of the Sturge-Weber syndrome anomalies beyond the encephalofacial territory suggested a more complex developmental abnormality.

Surgical management of giant and complex posterior circulation aneurysms continues to be a technically difficult task with high operative morbidity. To minimize morbidity we have used cardiopulmonary bypass and circulatory arrest for the treatment of a giant basilar aneurysm. A 48-year-old woman presented with sudden headache. Magnetic resonance angiography revealed a giant basilar aneurysm. On the 2nd hospital day she developed right sided hemiparesis and cranial nerve deficits as a result of the second rupture of the aneurysm. The aneurysm was successfully treated and no significant neurological complications were related to this technique. This initial experience indicates that patients with giant posterior circulation aneurysm that cannot be treated using conventional techniques might benefit from a surgical approach that included the use of deep hypothermic circulatory arrest.

The authors evaluated the follow-up results of microvascular decompression (sec. Janetta) in 8 patients with hemifacial spasm (HFS). Indication was based on there dimensional time of flight magnetic resonance angiography with 0.5T Elscint Gyrex V Dix equipment. Contrast material was administered in every case and maximum intensity projection and thin slice reconstruction were performed in three standard directions. Vascular contact with the facial nerve in the entry zone was identified on the symptomatic side in 10 patients. No contact was detected in 2 cases. Microvascular decompression was performed in 8 cases. The surgical and neuroradiological findings were identical in every cases. Five patients were completely free of HFS immediately after surgery, and another 2 patients became free of HFS during the next few weeks. Only 1 patient had uncured symptoms. In conclusion, the authors suggest that microvascular decompression of the facial nerve may evolve as the method of choice if vascular contact is proved by 3D TOF MRA.

Cholesterol-granuloma is a pseudotumoral mass that is believed to enlarge by a self-perpetuating sequence of repeated hemorrhages and reparative tissue reaction. Albeit an almost ubiquitous phenomenon throughout the body, cholesterol-granuloma has recently been appreciated as a distinctive lesion mimicking or associated with craniopharyngiomas. Upon review of a surgical series of 15 purported craniopharyngiomas, the authors identified 3 such occurrences. All were characterized by a predominance of slit-like cholesterol clefts with multi-nucleated giant cells embedded in a fibrotic stroma permeated with lipid laden macrophages, lymphocytes, as well as organizing hemorrhage. Non-craniopharyngioma specific cuboidal epithelium was present in one case. The mean age of patients--all males--with cholesterol-granuloma was 26 years, and all but one had an intrasellar tumor component. Clinical symptoms referrable to hypopituitarism predominated. At variance with the above, patients with adamantinomatous or papillary craniopharyngiomas were 23.5 and 46 years old, respectively, and presented with neurological deficits or ones due to hypothalamic involvement by their tumors. With marginal central nervous tissue present in 53 percent of the specimens, 75 percent of adamantinomatous craniopharyngiomas, but only 12 percent of cholesterol-granulomas showed invasive growth. At present cholesterol-granulomas are conceived as a clinicopathologically distinctive lesion of uncertain origin. They most probably represent a clinically relevant entity in the ontogenesis of adamantinomatous craniopharyngiomas with predisposing factors yet to be elucidated.

Rhabdoid meningioma is a recently recognized clinicopathologic entity characterized histologically by cytoplasmic aggregates of intermediate filaments, and clinically by the propensity of such tumors to pursue an aggressive course. The authors report on clinical, radiologic and pathologic findings in three cases of rhabdoid meningioma identified in a retrospective surgical series of 204 meningothelial tumors. Patients included two females, aged 39 and 55 years, and a 54-year-old male. In the first two cases the tumors were located on the right and left lesser sphenoid wing, respectively; in the third case, the right cerebellopontine angle was affected. All three neoplasms evolved on a background on transitional meningioma and were conspicuous for dis-cohesive tumor cells and suppression of syncytical architecture. Immunohistochemistry and ultrastructural examination confirmed the meningothelial origin of inclusion-bearing rhabdoid cells. Although none of the tumors showed evidence of histologic anaplasia and Ki-67 labeling indices remained inferior to 2%, infiltrative growth into adjacent brain was noted in all three cases. On follow-up ranging from 8 months to 6 years, the patients remained either disease-free or alive with nonprogressive residual tumor. On account of their clinical behavior, well-differentiated rhabdoid meningiomas will be accommodated in the category of atypical meningiomas (WHO grade II). Their pathogenesis is likely to involve disrupted cytoskeletal integration of cell motility and proliferation, of which the rhabdoid phenotype may possibly represent a morphologic correlate.

FDG-PET studies permit an assessment of the degree of brain tumour malignancy and detection of tumour recurrence. MIBI-SPECT also affords promising results in this respect. In this work, the diagnostic value of MIBI-SPECT was compared with that of FDG-PET for the determination of primary brain tumours malignancy and the detection of recurrent brain tumours. SPECT and PET examination were carried out within a week in 14 patients (12 males, 2 females, mean age: 40 years, range 16-61 years) with brain tumours. Seven patients had a primary tumour, and in a further 7 MRI or the clinical signs and symptoms let to a suspicion of tumour recurrence. All tumours were verified histologically to be gliomas of grades I-IV. The SPECT and PET images were analysed visually and semiquantitatively. In 3 of the investigated 7 primary glioma patients, there was a visibly enhanced MIBI-positive cases, only one had an increased FDG uptake. In 4 of the 7 tumour recurrence cases, either the MIBI or the FDG uptake was visibly increased. All of these were histologically high-grade gliomas. In the remaining low grade tumours (primary of recurrent), neither MIBI nor FDG revealed a pathologically increased uptake. The intensity of radiopharmaceutical uptake at the site of the tumours was visually and semiquantitatively higher for MIBI that for FDG. It is concluded that MIBI-SPECT is a valuable and simple tool for evaluation of the biological characteristics of brain tumours, showing increased uptake of MIBI according to the malignancy and tumour recurrence of brain tumours.

The experience with a series of 28 posterior fossa exploration and microvascular decompression for trigeminal neuralgia is presented. All the patients were treated with carbamazepine previously and some of them were operated on by destructive methods. The diagnostic work-up consisted of an accurate history, CT or MRI in all cases, and recently (in 17 cases) the vascular compression of the trigeminal nerve was demonstrated directly by MR angiography in the plane of the trigeminal nerve. Microvascular decompression was performed through a suboccipital retromastoid craniotomy. At the operations 21 arterial, 4 venous, 2 combined (arterial + venous) and 1 arachnoid band compression were found. The mean follow up was 30 months. Immediate pain relief was achieved in all cases but one, and there were two recurrences 6 and 12 months later (both of them were venous compression), which have been controllable medically since then. There were 3 permanent hypaesthesia of the face (one of them loss of corneal reflex), 2 hypacusis, 1 cerebrospinal fluid leakage and 1 cerebellar edema as complications. Microvascular decompression is a safe and effective treatment for trigeminal neuralgia and advised if the medical treatment is failed, the patient suitable for general anaesthesia, and there is the evidence of vascular compression of trigeminal nerve on MR angiography.

We describe a case of a patient with a syndrome of paradoxical worsening of a dural-sinus cavernous arteriovenous malformation which was an iatrogenic consequence of previous embolization of the basal branches of a dural shunt with Yvalon. It is presumed that the thrombogenousYvalon reached the basal branches of the medial meningeal artery of the superior ophthalmic vein, where it caused a complete thrombosis. The compromised ocular and orbital venous outflow caused a dramatic worsening of the ocular congestive symptoms: venous stasis retinopathy with dilated veins, flame and dot-shaped hemorrhages and secondary increase in intraocular pressure. The diagnosis of thrombosis of the entire superior ophthalmic vein was confirmed by color Doppler imaging. The pathomechanism is discussed. Although the ocular pathology is usually self-limiting after establishment of the collateral venous outflow channels, because of serious congestive ocular symptoms, argon laser photocoagulation and conservative antiglaucomatous local therapy were applied. In this patient, shortly after establishing the orbital collateral venous draining channels, the ocular symptoms improved. There was no other complication during the one-year follow-up.

The detection of vasospasm plays an important role for the definition of the strategy of treatment in patients with subarachnoid hemorrhage (SAH). Besides the invasive contrast angiography, the non-invasive 99m-Tc-HMPAO brain perfusion SPECT and transcranial Doppler sonography (TCD) are recently used for this purpose. For the investigation of the possibilities of the last two methods, comparative studies were performed in 29 SAH patients in the subacute phase of the disease. In the detection of regional brain ischaemia the sensitivity of the SPECT study was 90%, the specificity was 28% and the accuracy was 50%, the corresponding values of TCD were 82%, 71% and 75%. In patients, in whom chronic neurological symptoms, or morphological abnormalities could be excluded, the specificity of the SPECT study was 67% at unchanged sensitivity. Based on the results it is concluded, that the brain perfusion SPECT and the TCD investigation are useful methods for the detection of vasospasm after SAH. The combination of the two methods is recommended for the correct diagnosis of vasospasm in SAH. Further investigations are necessary to clarify the prognostic impact of the result of these investigations.

The dysembryoplastic neuroepithelial tumor is a benign central nervous system neoplasm of children and young adults manifesting almost exclusively in complex partial seizures. The authors report the case of an 8-year-old boy presenting with characteristic clinical and radiologic features who subsequently underwent surgery. Light microscopic, immunohistochemical and ultrastructural traits of the tumor are described demonstrating pluripotential differentiation of tumor cells and architectural features suggesting a dysontogenic lesion. A brief literature review on the biology and histologic diagnosis of the dysembryoplastic neuroepithelial tumor is provided. Although this uncommon tumor accounts for only a minority of intracranial neoplasms, its pathogenetic role has to be considered in the differential diagnosis of temporal lobe epilepsies. This is the first report on this recently described, rare neoplastic condition in Hungary.

A case of pigmented choroid plexus papilloma removed from the 4th ventricle of a 43-year-old man is reported. The tumor showed histologic, immunophenotypic, and ultrastructural features of neoplastic choroid plexus epithelium. There was no evidence of melanosomal activity or neurosecretion. The pigment consisted of an intimate association of lipofuscin and neuromelanin, indicating autocatalytic peroxydation of the former as a putative way of melaninogenesis. The low proliferation rate of the tumor together with immunohistochemical evidence of inactivation of p53 protein suggest a delayed turnover of neoplastic cells as a possible source of lipofuscin accumulation.

The developmental and morphological characteristics, clinical course, diagnostic and therapeutic possibilities of cavernous angiomas of the central nervous system are summarized on the basis of the literature. The clinical courses of 27 patients with cavernous angiomas are presented. The surgical treatment of cavernous angiomas has had a good outcome when the indications and microsurgical principles were adhered to. Special attention should be paid to cavernous angiomas located near or inside the ventricles because of the danger they may cause.

500 lumbosacral plain x-ray injured patients and 1000 myelography of patients suffering from low back pain and nerve root sign were reviewed to evaluate the rate of transitional lumbosacral vertebra. This anomaly appeared in 4.6% in the normal population. The rate of the transitional vertebra in patients with nerve root syndrome was double (8.4%) whereas that with lumbar disc herniation four time as many as in the normal population. The data demonstrate that the asymmetrical anomalies have more clinical significance. The authors consider, that the role of the transitional vertebra is twofold: it can be consider primary in low back and sciatic pain, but in the formation of lumbar disc herniation is secondary. They find the analysis of the lumbosacral plain x-ray is necessary even in cases with CT and MRI.

Cerebral blood flow velocity was measured by transcranial Doppler sonography at rest and during cerebral vasodilatation evoked with acetazolamide in 14 patients before and after carotid endarterectomy. Before surgery the vasoreactivity in the affected middle cerebral artery territories was reduced and abnormal (asymptomatic side: 35.9 +/- 25.6% [mean +/- SD; n = 14]; symptomatic side: 25.6 +/- 10.7%), but the difference between the two hemispheres was not significant however, vasoreactivity was normalized 5 days after surgery (asymptomatic side: 46.9 +/- 22.3% symptomatic side: 58.9 +/- 23%) (p0.001). The increase in cerebral reserve capacity and changes in Gosling's index of pulsatility correlated significantly in both hemispheres (p0.02). This findings indicate an improved perfusion reserve on the fifth day following carotid endarterectomy in patients with an internal carotid artery diameter reduction of at least 70%.

To determine the relationship between the dynamics of mean arterial blood pressure (MABP) elevation and possible changes in the cochlear microcirculation the cochlear blood flow (CBF) was measured in guinea pigs by a laser Doppler method. The MABP was elevated at rates ranging from 0.02 mmHg/s to 4 mmHg/s by intravenous infusions of norepinephrine or epinephrine in various concentrations. A fall in MABP was induced by exsanguination of the animals. The purpose of the experiments was to record the time of onset and course of an expected autoregulation in the cochlea in response to slow or rapid changes in MABP. The data suggest that there is no short-term autoregulation in the cochlear microcirculation reflecting the increase of the MABP, but a slight compensation occurs when the MABP declines. These latter changes could be attributed to the high CO2 sensitivity of the cochlear blood vessels.

Brain perfusion (rCBF) (99mTc--HMPAO) and blood volume (rCBV) (99mTc--RBC) investigations were performed by SPECT on 13 patients with intracranial AVM. In each cases the rCBF revealed a decreased tracer uptake at the site of the AVM. In the rCBV SPECT, abnormal AVM structures with increased radioactivity were detected in 92% of cases. In all of the patients surgical resection of the AVM was also carried out. In the cases where the rCBF disturbance was equal or larger than the rCBV abnormality the surgical complications were more frequent it was concluded that combined rCBF--rCBV method is suitable to detect the AVM-s, and to clarify their haemodynamic effects. It is helpful in planning the surgical intervention, and in the follow-up.

Thirty-two patients suffering from occlusive cerebrovascular disease were investigated by means of 99mTc-HMPAO brain SPECT before and one month after EC-IC bypass operation. The regional cerebral blood flow was unchanged postoperatively in 19 patients, increased in 7 cases, and deteriorated in 6 patients. One patient died in the postoperative period and in another no follow-up SPECT could be performed. It is concluded that the regional cerebral blood flow, even in the absence of a morphological deficit on CT, was not improved by the operation in the majority of cases.

Clinical experience based on regional cerebral blood flow investigations with 99mTc HMPAO SPECT in 164 patients is reported. The pharmacokinetics of the 99mTc HMPAO are summarised, and the important indications of the investigations are interpreted in case reports (stroke, surgical solution of intracavernous aneurysm, Alzheimer and multiinfarct types of dementias). The literature data suggest that the diagnostic possibilities with this method are good in other diseases too, this area is surveyed briefly.

The present studies were performed to determine the response of the brain water and electrolytes to acute hypoosmolality and hyperosmolality in animals with intact skull and dura, in comparison with those subjected to extensive bilateral or unilateral craniectomy and dural opening. Four to 5 weeks following extensive unilateral or bilateral craniectomy and dural opening in rats, a 50 mosm/kg decrease in plasma osmolality was produced by systemic administration of distilled water ("water intoxication"), or a 28 mosm/kg increase in plasma osmolality was produced by systemic administration of either 1 M NaCl or 1 M mannitol in 0.34 M NaCl. Tissue water, Na, and K contents were determined after 120 minutes. Tissue water accumulation or water loss was proportional to the decrease or increase in plasma osmolality. However, the tissue water accumulation following "water intoxication" was less (40% of the predicted value) than that predicted for ideal osmotic behaviour. The brain tissue was also found to shrink less than predicted on the basis of ideal osmotic behaviour (40% of the predicted value after mannitol treatment, and 60% after NaCl administration). This non-ideal osmotic response of the brain tissue is consistent with the finding in other studies and indicated a significant degree of volume regulation. Water and electrolyte changes were not different in operated and non-operated animals, demonstrating no effects of extensive skull and dura defects on tissue volume regulation under hypo- and hyperosmolar conditions of a degree that may be encountered under clinical circumstances.(ABSTRACT TRUNCATED AT 250 WORDS)

In 1981 Marcus Raichle put forward the hypothesis that a central neuroendocrine system regulates the brain ion and water homeostasis38. In this presentation I would like to summarize briefly the available data—including our own results—in support of this hypothesis. The hypothesis supposes that three cell groups (brain capillary endothelial cells, secretory cells of the choroid plexus, and astroglia) regulate the internal ionic environment of the brain38. A unique element of this hypothesis is that the regulation of the ion and volume homeostasis of the brain is orchestrated by a central neuroendocrine system capable of affecting all three cell types38.

Two series of patients (814 cases altogether) with ruptured intracranial aneurysms are analyzed in order to try to outline the clinical significance of space-occupying intracerebral haematomas (ICH) which may accompany SAH. In particular the question of whether intracerebral clots are or are not to be taken into account in planning emergency surgery is debated. From the reported series, it would appear that ICH after aneurysm rupture seldom lead to increasing intracranial hypertension warranting urgent surgery. This evolution was observed in approximately 5% of patients with expanding ICH. In 35% the intracerebral effusions were associated with irreversible lesions and in 20% the initial symptomatology definitely improved. Finally, in a relatively high percentage of cases (about 40%) ICH lacked of clinical significance.

The observations presented are based on 11 patients who had suffered from stroke caused by internal carotid occlusion. In all cases an anastomosis between the superficial temporal artery (STA) and a cortical temporal branch of the middle cerebral artery (MCA) was done. This resulted in a considerable additional blood supply from the external carotid to the affected middle cerebral circulation. The extent of the territory of the MCA irrigated by the STA depends upon the different anatomical configurations of the MCA. There was a considerable improvement in neurological status even in the chronic post-stroke stage. A topographical correlation between the postoperative angiographically identified increase of rCBF and the recovery or considerable improvement of neurological functions was not ascertained.

Es wird uber einen Fall von sog. kongenitaler extraduraler Zyste berichtet. Das histologische Bild der Zysten wand bietet keinen sicheren Anhaltspunkt fur die Erklarung des Entstehungsmechanismus dieser Zysten.

To prevent cerebrovascular insufficiency resulting from stenosis or occlusion of the carotid or middle cerebral artery (MCA) if they have no adequate collateral circulation, a new, effective collateral vascular pathway was first used in 1967 by Donaghy and Yasargil and was termed STA-MCA anastomosis.(4).

Post-hemorrhagic hydrocephalus was studied in two homogeneous series including 410 patients, 320 of whom had ruptured intracranial aneurysms. Ventricular dilatation was more frequently observed in the patients with subarachnoid hemorrhage from ruptured aneurysm (44%) than in those in whom no vascular malformation was detected by the four vessel angiography (21%). Moreover, hydrocephalus was over twice as frequent in high grading (76-64%) than in low grade patients (31-35%). Ventricular dilatation was revealed in 58-52% of A.Co.A., in 39-30% of C.I.A. and in 20-21% of M.C.A. Altogether 51 patients underwent continuous ventricular drainage (EVD): 54% improved significantly, but fatal recurrent hemorrhage took place on drainage in half of them. On these grounds, it would appear that EVD may be indicated only in grade IV and, occasionally, in Grade III patients on condition that early radical surgery is carried out as soon as significant improvement is attained, without waiting for an entirely satisfactory grading. In this way, devastating hemorrhages on drainage could be prevented in the last patients of our series. Chronic disturbances of CSF dynamics calling for permanent shunting proved exceedingly rare in our patients.

The present paper summarizes our experiences with intraoperative fluorescein angiography in 50 external carotid artery-internal carotid artery bypass operations. This technique has provided precise localization of the ischemic lesion and aided in selecting the sites and direction of the anastomoses to be performed, as well as in checking the patency of the anastomoses and the area supplied by them. A comparison of X-ray angiography with fluorescein angiography indicates the reliability of the latter in the estimation of the area supplied by the anastomosis.

The rapid development of vascular surgery in recent years has created technical conditions for performing preventive reconstructive operations on cerebral arteries. This raises an urgent demand for the diagnosis of vascular lesions at an early phase of their development, when there has not yet been any irreversible damage of brain structure and function.

The significance of the combination of two or more vascular lesions (stenoses and occlusions) causing disturbances in the cerebral circulation has long been understood. Therefore, it is not surprising that, in one fifth of the patients with internal carotid occlusion a severe stenosis can be found in the contralateral internal carotid artery. This seriously influences the natural history of the disease.

Ventricular dilatation following SAH, particularly caused by aneurysm rupture, has long been debated. We have recently (Papo et al. 1984) dealt with post-haemorrhagic hydrocephalus in its different aspects. In the present report we discuss the role played by hypertensive hydrocephalus in producing clinical deterioration in the acute stage after intracranial aneurysm rupture.

Considerable evidence indicates that regulation of the ionic environment of the brain is coordinated by a central neuroendocrine system capable of affecting the capillary endothelium, the choroid plexus, and the astroglia. All three cell groups are responsible for precise control of brain volume through adjustment of cell water and electrolyte content. With these considerations in mind, we have attempted to elucidate the possible involvement of the central vasopressin (AVP) and atrial natriuretic factor (ANF) systems in the regulation of the water and ion homeostasis of the brain tissue of rats: Vasopressin-positive vascular connections, investigated by immuno-electronhistochemistry, were found in close or direct contact with brain microvessels. Central administration of AVP (125 ng) or DDAVP (0.5 micrograms), with or without an accompanying water load, brought about a 1-1.3% water accumulation. Brain oedema caused by experimental subarachnoid haemorrhage had a different course in Wistar and Brattleboro DI rats, the latter being unable to synthetize AVP. These findings suggest that the centrally released AVP leads to brain water accumulation by increasing the water permeability of capillaries, and may facilitate the production of brain oedema in various pathological conditions. On the other hand, central administration of synthetic rat ANF (2 micrograms) prevented the water accumulation elicited in rat brain by systemic hypoosmolar fluid load, and led to a significant sodium loss from the nervous tissue by altering the capillary sodium permeability. The better understanding of these hormone receptors and their manipulations have exciting clinical implications.

A microsurgical anastomosis between the superficial temporal artery and a cortical branch of the middle cerebral artery was carried out in 11 cases with internal carotid occlusion. This treatment was attempted following angiography of the intra- and extracranial cerebral arteries. After the microsurgical procedure for creating an extra-intracranial arterial anastomosis selective angiography of the homolateral external carotid circulation was performed. The analyses of the serial arteriograms showed, that a) a considerable blood supply from the external carotid circulation through the additional collateral pathway to the territory of the middle cerebral artery is possible, b) the extent of the area of the middle cerebral artery supplied by the superficial temporal artery is not only dependant upon a pressure gradient between the external carotid and the middle cerebral artery circulation, but also by the different anatomical variations of the middle cerebral artery.

Imprints of haematoxilin-eosin and Giemsa-stained, 33 surgically removed different intracranial tumors were examined. In case of sufficient number of cells and adequate clinical data, the cytological examination was suitable to quick intraoperative diagnosis in majority of cases. Its demonstration on GFAP smear facilitates the diagnosing of gliomas.