The pathophysiology of elevated intracranial pressure in idiopathic intracranial hypertension (IIH) is unclear. Cerebral venous outflow obstruction and elevated intracranial venous pressure may play an etiological role. We examined jugular valve insufficiency as a potential factor contributing to intracranial hypertension. Jugular venous valve function was assessed bilaterally by duplex sonography in 20 consecutive patients with diagnosis of IIH and in 20 healthy controls matched for age, gender and body mass index. Diagnosis of valvular insufficiency was based on reflux duration during a controlled Valsalva maneuver. Intracranial venous outflow was evaluated in 11 patients (MR venography in 10, digital subtraction angiography (DSA) in two cases). As a principle result, valvular insufficiency was significantly more frequent in patients with IIH (70 vs. 30%; p < 0.05). This finding was associated with irregular leaflet structures on B-mode imaging (p < 0.01). Bilateral insufficiency was more frequent in the patient group which, however, was not significant (p = 0.08). In addition, sinovenous outflow obstruction was found in five of six patients that had undergone contrast-enhanced MR venography and DSA. The detection rate was inferior in phase-contrast MR imaging (one of five patients). In conclusion, this study gives evidence that valvular insufficiency may play a causal role in IIH. Obesity is a major risk factor for the disease and weight reduction leads to improvement of symptoms. Possibly, increased intra-abdominal pressure is transmitted into the intracranial venous system, causing intracranial hypertension. Jugular valve insufficiency may facilitate pressure transmission. As transverse sinus stenosis was a concomitant finding, these factors may be complementary.

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This case report gives insight into the mechanism of cerebral venous air embolism. This is the firstcase describing jugular valve insufficiency as the missing link between peripheral air embolism and cerebral venous air entrapment.

The incidence of a significant hemorrhage in the natural history of cavernomas is below 1% per year, but the risk of a second hemorrhage in patients with initial bleeding cavernomas is between 14% and 29%. In the light of these figures, all cavernomas ought to be resected if surgical-related morbidity can be minimized. Stereotactically guided neurosurgery offers the advantage of planning the least traumatic approach before craniotomy due to the knowledge of the exact localisation of the lesion. During a 2-year period 12 patients (age 16-54 years) with intracranial supratentorial cavernomas (size 0.5-1.8 cm) were treated by stereotactically guided microsurgery. The cavernomas were seated in a depth between 0.4 and 4.5 cm. 4 patients had an overt hemorrhage in their history. In six cases a seizure was the first symptom (altogether 8 patients had seizures preoperatively). Two patients were asymptomatic. Standard CRW (Cosman, Roberts, Wells) stereotactic system was used in all cases. The skin incision and the osteoplastic craniotomy (mean diameter 2.8 cm) were planned stereotactically. In 11 patients a transsulcal approach was used. The size of the corticotomy could be limited to less than 1 cm. Using the stereotactic method, all cavernomas were found with a high degree of accuracy. After lesionectomy a total of 1 to 2 mm of the surrounding yellow-stained brain tissue was sucked away because it contains hemosiderin and therefore iron, which may have an epileptogenic effect. No relevant surgical-related neurological morbidity was found in any patient a half year after surgery. Seven out of eight patients were free of seizures. One still had problems.

In SAH patients with vasospasm, a combination therapy of balloon angioplasty and intra-arterial nimodipine resulted in a more than doubled vasodilative effect in the central cerebral arteries compared to the sole infusion of nimodipine. Regarding the ICA and BA arteries, this beneficial effect was even more pronounced. Although there was a tendency of better effects of the BAP-N group, regarding the overall effect in all territories combined, this failed to reach statistical evidence. In cerebral peripheral arteries, no differences were observed, and there was no difference in clinical outcome, too.

In 72 patients with acute subarachnoid haemorrhage (SAH) the relationship between the amount of subarachnoid blood clots detected by initial cranial computed tomography (CCT) up to 48 hours after bleeding and the later development of vasospasm, established by blood flow velocity measurement with transcranial Doppler ultrasound (TCD) was investigated. The serial Doppler examinations started within the first 72 hours after SAH and were carried out every second day up to three weeks. Each Doppler recording was accompanied by a neurological examination. Patients classified as Hunt and Hess grade V were excluded from the study. All patients with remarkable brain oedema in CCT or with intracranial pressure above 25 mmHg were also excluded. Because of the well known age-dependence of vasospasm after SAH, two age groups were formed. A statistically significant correlation (p > 0.05) between blood flow velocities and blood load after SAH was not found. The mean age of the investigated 72 individuals was 48.9 years (14 up to 76 years). 47 patients were younger than 56 years. Linear regression analysis indicated a correlation with a quite low significance level (r = 0.350, p < 0.025) between TCD blood flow velocities and blood load in CCT in these younger subjects. No significant correlation (p > 0.05) between these two variables could be established in the 25 patients older than 55 years. In a second step an intra-individual comparison of side-to-side differences in TCD and CCT was made. There were no significant differences in blood flow velocities between subjects with or without side-to-side differences in cisternal blood load. It is concluded that the amount of blood visible on initial CCT after SAH is not a powerful predictor of cerebral blood flow velocities measured by TCD.

The presented glioma rat model consisting of the C6 cell line and Sprague-Dawley rats as recipients is a well-suited model to investigate surgical techniques and their impact on tumour therapy. However, the site of transplantation, the preparation of cell grafts and the technique of tumour growth evaluation is of utmost importance to achieve reliable results.

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