HLA antigens and intracranial aneurysms.

The frequencies of the HLA-A, -B and -DR were determined in a group of 59 transplant donors who died from subarachnoid haemorrhage within three days following the rupture of intracranial aneurysm (the SAH group) and compared with those of a control group consisting of 389 donors who died from other causes. The only significant difference was in the increased frequency in the SAH group of non-typed ("empty")-DR loci in association with the DR7 phenotype. The most probable explanation of this finding is that in the SAH group the frequency of DR7 homozygotes is several times higher than in the general population, and that bearing the DR7 allele in homozygotic form is associated with a very high risk of developing potentially fatal intracranial aneurysmal haemorrhage.

The possible role of endothelium in prevention of rebleeding in experimental subarachnoid hemorrhage (SAH).

Experiments were performed on six male cats under nitrous oxide in oxygen anesthesia. Animals were paralysed and artificially ventilated. Subarachnoid hemorrhage (SAH) was produced by basilar artery puncture following clivectomy. After 10 minutes (3 cats) and 60 minutes (3 cats) the basilar artery was dissected and fixed for electronmicroscopic examination. Ultrastructural examinations revealed in the cytoplasm of the endothelial cells on the side of the vessel lumen, the presence of spherical or flattened cylindrical structures identified as Weibel-Palade bodies. In the endothelium of the proximal segment, 10 and 60 minutes after puncture, the number of these electron-dense bodies increased, and was higher than in the corresponding distal segment. The possible role of the Weibel-Palade bodies in SAH after-effects is discussed.

[Management of intracranial vasospasm in rupture of cerebral aneurysm]. / Postepowanie w stanach skurczu naczyn wewnatrzczaszkowych w przebiegu pekniecia tetniaka mózgu.

This paper describes the methods of prevention of delayed neurological deficit (DND) in patients with subarachnoid haemorrhage (SAH) due to ruptured intracranial aneurysm. To prevent the decrease in the cerebral flow, vasodilators, inhibitors of platelet aggregation and synthesis of endogenous prostaglandins, stimulators of prostacyclin synthesis of its analogue should be applied. It is also recommended to use the inhibitors of phosphodiesterase, blockers of serotonin and of calcium channel (particularly nimodipine). Therapy with the immunosuppressive drugs helps to prevent DND. With all those therapeutical methods DND is still a serious complication following SAH.

[Spasm of intracranial arteries or spastic syndrome in ruptured cerebral aneurysm?]. / Skurcz tetnic wewnatrzczaszkowych, czy zespól skurczu w przebiegu pekniecia tetniaka mózgu?

Cerebral vasospasm is the most serious complication of intracranial hemorrhage rupture. For example, the resulting neurological deficits affect more than 30 thousand patients in North America. Subarachnoid hemorrhage is accompanied by the release of more than 50 endogenous substances, most possessing vasoconstrictory activities. There are many theories explaining the pathogenesis of vasospasm following SAH. The most popular is the theory of direct vasoconstrictory activity of releasing substances on a vessel wall. The other one describes the narrowing of vessel lumen as a result of angiopathic process. The other theories include the vasoactive, neurotoxic and ++immuno-aggressive concepts of neurological deficit in following aneurysm rupture. The relationship between the vasospasm and the neurological deficit is also discussed.

Cyclosporine A prevents neurological deterioration of patients with SAH--a preliminary report.

In the present study we found that the neurological outcome in patients anaesthetized for early clipping (up to 72 h after SAH) of a ruptured aneurysm and treated with cyclosporine A was significantly better than the neurological state of control patients without immuno-suppressive treatment. The results justify the presumption that auto-immune reactions are involved in the deterioration of the postoperative neurological state of patients with SAH after rupture of an intracranial aneurysm. Supplementing a standard surgical and pharmacological treatment with cyclosporine A seems to reduce the undesirable neurological consequences of the immunologically, induced vascular disturbance after SAH.

Immunomodulators interfere with angiopathy but not vasospasm after subarachnoid haemorrhage in rabbits.

The present study deals with the effects of immunomodulators on the morphology of intracerebral arterial walls in rabbits with experimental subarachnoid haemorrhage (SAH). Immunostimulators:thymostimuline and inosine dimethylamino-isopropanol-p-acetamido-benzoate were found to aggravate the angiopathic changes, whereas immunosuppressive drugs-cyclosporine A and azathioprine appeared to prevent the damage. The authors consider the possibility of using immunosuppressive drugs in patients with ruptured intracranial aneurysms.

An electron immunocytochemical study of the basilar artery in rabbits after subarachnoid haemorrhage (SAH): a preliminary report.

Vascular endothelial cells of the basilar artery and secretory axons of the neurohypophysis from rabbits after experimental subarachnoid haemorrhage were investigated by postembedding peroxidase--anti-peroxidase technique for electron microscopy to detection of vasopressin (VP). The results indicate an lack of VP-positive endothelial cells in basilar artery, while VP-positive secretory granules were commonly present in the neurohypophysis. The results are discussed in terms of pathophysiological aspect of subarachnoid haemorrhage.

Immunological method for prediction of progress in neurological deficit in patients with intracranial aneurysm rupture.

Skin tests of nonspecific antigens (immunoskin test Sevac) were performed on patients suffering from intracranial aneurysms, scheduled for surgical clipping. It was found that high antibody titre correlated well with the severity and progress of neurological deficit developing after surgery. This deficit was absent in patients who exhibited low antibody titre in response to the skin test before surgery. These results indicate that the immunological processes may play a role in the development of neurological deficit after neurosurgical procedures. Thus the skin test employed may have prognostic value in predicting neurological deficit following intracranial aneurysm surgery.