The radiological aspect, pathology, treatment and results of 132 subdural haematomas observed in 100 patients, are discussed. The majority of these cases were characterized by a nonhomogenous CT scan picture, resulting from repeated bleeding in a previous subdural haematoma evolving to chronicity, or in a pre-existent subdural hygroma. Taking aspirin may have constituted a predisposing factor in 16% of our patients, whilst coagulation disturbances, including anticoagulant treatment, were observed in another 6%; ethylism was present in 11%. A traumatic origin was ascertained in 80% of the patients. The treatment consisted of burr hole evacuation and drainage in 91.5% of the haematomas, corresponding to 92% of the patients; it was eventually repeated once or twice in some cases. In 6% of the patients, a subduro-peritoneal drainage had to be placed ultimately and in 2%, a membranectomy had to be performed because the haematoma had become nearly completely fibrous. The necessity for repeated evacuation and eventual subduro-peritoneal drainage seems to depend mainly on a slow brain re-expansion in some elderly people, who are actually more frequently referred. Two patients died; one was deeply comatose and another in poor general condition. Morbidity in the 96 remaining patients, 2 being lost to follow-up, was 11%: 5% related to the haematoma or to the causal trauma, and 6% from other concomitant neurological disease. The functional result was satisfactory in 85%.

The first day of the symposium was devoted to coma (J. Brihaye); the second day dealt with injury scalling (S. Lindgren and G. Stroobandt); the third day was concerned with brain death (E. A. Walker and E. Pillen) but no firm conclusion was reached and another meeting on brain death was planned in near future.

As beta-2 transferrin is almost specific to the cerebrospinal fluid, its detection in rhinorrhea or otorrhea fluids demonstrates the occurrence of CSF fistula. We describe a highly sensitive method based on immunoaffinity-mediated capillary blotting for the detection of this cathodic isoform of transferrin in minute amounts (3 microliters) of rhinorrhea or otorrhea fluids. Application of this method in a series of 10 patients with CSF fistula is reported.

The authors report 3 observations of dural arterio-venous fistula cured by combined neuroradiological and neurosurgical intervention. In the first case, the shunt affected the left lateral sinus. Repeated embolizations failed whilst intracranial hypertension developed, as a consequence of flux in the opposite lateral sinus and in the sagittal sinus. Surgical intervention, consisting in isolation of the transverse sinus, led to complete cure, after a one month delay. In the second case, the shunt was adjacent to the sagittal sinus, right parietal, and had led to an intracerebral haematoma, by rupture of an arterialized cortical vein. Embolizations alone could not cure the fistula which therefore had to be excised. In the third case, the shunt was located in the falx, at the parieto-occipital junction, and was responsible for arterialization of cerebral veins in the right parieto-occipital region. For this reason, after failure of endovascular treatment, the fistula was coagulated, with subsequent complete cure. These three cases illustrate the different types of drainage of such arterio-venous fistula, and their corresponding neurological symptoms and signs, complications and risks, that required a radical-not only clinical, but also anatomical-cure. This aim was achieved when embolizations were accompanied by direct surgical attack.

In the scope of a late intervention policy on ruptured intracranial aneurysms, on D.+12 on an average, we first used tranexamic acid, at moderate doses: 3 g orally or 1.5 g intravenously per day. We, subsequently, added nimodipine, usually 240 mg orally per day or 2 mg intravenously per hour. The medical treatment consisted of amply sufficient hydration, and in systematic and regular administration of analgesics and sedatives. Hypotension was absolutely avoided; if necessary, an antihypertensive treatment was prescribed very cautiously. Phenytoin was regularly given. In the present study, we try to answer the following questions: (1) Can we confirm that the preventive action of tranexamic acid remains as effective, when doses, markedly lower than usually recommended, are used? (2) Does nimodipine prevent the increase of pre-operative ischaemic complications, which should be expected when tranexamic acid is administered? Amongst 101 patients with SAH of proven aneurysmal origin, 84 were treated with tranexamic acid and nimodipine. In 25 patients, an aneurysm was not visualised; 21 received this treatment. For several reasons, only a retrospective study was possible, to evaluate the results of our antifibrinolytic and calcium-blocking therapies, on rebleeding and pre-operative delayed ischaemia. We compared, therefore, similar cases from the literature, with our own cases, taking into consideration the clinical grades, the days of admission and of intervention, the moment of rebleeding and of delayed pre-operative ischaemia, etc. The following impressions emerge: (1) same effectiveness of moderate doses of tranexamic acid; (2) no increase of pre-operative delayed ischaemic complications, in comparison with patients not receiving antifibrinolytics but nimodipine; (3) important role of a devastating initial bleed and of operative complications; (4) difficulty of avoiding rebleeding at D.0, whatever the therapeutic measures, medical and/or surgical.