[Pseudochoreoathetosis as manifestation of cervical cord lesion. Case report]. / Pseudochoreoatetoza jako objaw uszkodzenia rdzenia kregowego w odcinku szyjnym. Opis przypadków.

The involuntary movements of choreoathetotic type are commonly regarded as a sign of basal ganglia lesion. However, such movements can also occur in pathological processes involving the cervical spinal cord. This condition is referred to as pseudochoreoathetosis. Involuntary movements can be related to lack of proper coordination between agonist and antagonist muscles, their simultaneous activation due to impairment of reciprocal inhibition. The characteristic feature of pseudochoreoathetosis is proprioceptive sensory loss. In this paper we present 4 patients who developed various involuntary limb movements in early stage of the disease. Lesions in the cervical spinal cord were confirmed by MRI. In case 1 the cause was astrocytoma, in cases 2 and 3--demyelination, in case 4 the precise character of the lesion could not be established. Pseudochoreoathetosis is a rare condition which often remains unrecognized. The presented cases emphasise the importance of early and correct diagnosis leading to proper therapeutical procedure.

Modulation of lymphocyte-fibroblast interactions by 2-chloro-2'-deoxyadenosine (2-CdA) in subarachnoid hemorrhage.

The adherence to monolayers of human fibroblasts of chromium-51 labelled peripheral blood mononuclear cells (PBMC) from normal subjects, and from patients after single or multiple subarachnoid hemorrhage (SAH), and the effect of 2-CdA on cell adhesion have been quantified. The fraction of cells adhering to fibroblasts were the lowest for multiple SAH patients and the highest for normal subjects, which can be explained by depletion of activated lymphocytes from peripheral blood of SAH patients. 2-CdA decreased the fraction of adhering cells isolated from normal subjects, did not change the adherence of cells from single SAH patients and increased the fraction of adhering cells isolated from multiple SAH patients. We conclude that the influence of 2-CdA on the adherence of PBMC to fibroblasts is inversely related to the degree of immune system activation.

2-Chloro-2' deoxyadenosine prevents angiopathic changes in cerebral arteries in experimental SAH in rabbits.

We compared the morphology of the basilar artery walls in rabbits with experimental subarachnoid haemorrhage (SAH) without and with concomitant treatment with a novel immunosuppressive drug, 2-chloro-2'-deoxyadenosine (2 CdA). The treatment was successful in the prevention of the angiopathic changes, most likely due to its ability to inhibit lymphocyte activation in response to mitogenic signals. Since lymphocyte (and monocyte?) activation may play an important role in the development of the delayed neurological deficits in patients following SAH, the use of 2 CdA to prevent these deficits shall be considered.

A strategy for analyzing multiple parameters with application to aneurysmal SAH patients all of them clipped but treated with and without cyclosporine.

The study evaluated the effectiveness of the combination of nimodipine and cyclosporine A vs nimodipine alone in the prevention of delayed neurologic deficit in 82 (31 plus 51) patients in whom intracranial aneurysms were clipped within 72 h after subarachnoid haemorrhage. The tests performed included examination of the neurological condition before and after operation, angiography of cerebral arteries to visualize vasospasm, and analysis of the distribution and amount of blood in the brain fluids and/or tissue according to Fisher's scale. Inclusion of cyclosporine A in the treatment was clearly beneficial for the neurological condition. While cyclosporine A did not appear to produce a statistically significant improvement as evaluated by the chi-square test, a positive result was obtained following analysis of the correlation coefficients after Pearson in combination with the logistic log-linear regression analysis. The results argue against the utility of the chi-square test for verifying clinical data obtained in a limited number of patients.

Impaired in vitro proliferative response of suppressor lymphocytes in patients with subarachnoid haemorrhage from ruptured intracranial aneurysm.

Proliferative response to mitogens concanavalin A, phytohemagglutinin and pokeweed mitogen, and other chosen indicators of the activity of the immune system were assayed in peripheral blood mononuclear cells isolated from blood of patients with subarachnoid haemorrhage from ruptured aneurysm. Healthy blood donors served as control group. The SAH group displayed impaired response to concanavalin A, which is a mitogen specific for suppressor cells. It is suggested that the impaired activity of suppressor cells pre-existed in patients with subarachnoid haemorrhage, and after intracranial bleeding it might have contributed to the development of late neurological deficits.

Successful prevention of neurological deficit in SAH patients with 2-chlorodeoxyadenosine.

Twenty patients suffering from subarachnoid haemorrhage due to ruptured intracranial aneurysm and operated on within 72 h after SAH were treated with an experimental immunosuppressive drug 2-chlorodeoxyadenosine (2-CDA), dose 0.05 mg/kg/day i.v. for 7 days. The 2-CDA treatment was started immediately after angiographic confirmation of ruptured aneurysm, and the standard pharmacological treatment (nimodipine and steroids) was also given. 50% of patients were severely threatened by "delayed vasospasm" or late neurological deficit (Fisher's score 3 or 4). The neurological outcome (assessed 8-12 weeks after SAH) was good (GOS = 1) in 70%, and fair (moderate disability, GOS = 2) in 25%. A single case of severe disability (GOS = 3), as well as two cases of less than perfect outcome (GOS = 2), were related to unusual pre- or intraoperative complications. We conclude that the low doses of 2-CDA can be considered as a valuable adjunct to the standard pharmacotherapy of SAH patients operated on early.

Is vascular angiopathy following intracranial aneurysm rupture immunologically mediated?

Immunofluorescence studies showed the presence of IgM and/or C3 in the endothelium of intracranial aneurysms in 5 out of 6 patients with subarachnoid haemorrhage (SAH). In none of them were the immune deposits found in the gyrus rectus. Cortical tissue of 4 epileptic patients which served as a control give negative results. Serum studies on femoral artery wall used as an antigenic substrate did not reveal circulating antibodies of the IgM or IgG class. Our studies strongly suggest that the IgM and/or C3 immune deposits located in the endothelium of intracranial arteries may play a role in post SAH neurological complications.

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.

[A method of bilateral craniofacial approach in the surgical treatment of cancer of the nose and paranasal sinuses]. / Metoda dwustronnego dostepu czaszkowo-twarzowego w leczeniu chirurgicznym nowotworów nosa i zatok przynosowych.

The authors presented the two sides craniofacial method in surgical intervention of nasal and paranasal sinus cancers. The detailed indication, technique and complications of this method were also described as well as the own case as an example.

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.

Acute surgery in intracranial aneurysms. Experience with 100 cases.

In the last 3.5 years (up to August 1988) out of 450 patients with surgically treated intracranial aneurysms in 100 cases (22%) acute surgery was performed (up to 72 h after SAH). Patients in grade I-III (WFNS scale) were operated upon. In all the cases there were supratentorial aneurysms. CSF drainage during the operation was used routinely and nimodipine topically, in intravenous infusion and orally was applied. In all the cases, but one, the aneurysms was clipped. Follow-up--1 year. Assessment of the results was done using the Glasgow Outcome Scale (GOS). Full recovery was obtained in 78 patients and further 5 patients are independent. There were 14 deaths, in 7 patients due to postoperative vasospasm. Symptomatic ischaemia developed in 25 patients, however, in 15 of them it was fully reversible, due to the possibility of aggressive antivasospastic treatment (hypervolaemia, induced arterial hypertension). The relatively worse results were obtained in patients with chronic arterial hypertension.

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.