Effect of Intrathecal Urokinase Infusion on Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage.

BACKGROUND: Vasospasm following an aneurysmal subarachnoid hemorrhage (SAH) causes serious neurological complications, despite surgical clipping of the aneurysm. Intrathecal urokinase (UK) infusion has been shown to effectively prevent symptomatic vasospasm in patients who have undergone endovascular obliteration of the ruptured aneurysms. OBJECTIVE: To investigate whether intrathecal UK infusion can prevent symptomatic vasospasm in patients undergoing surgical or endovascular treatment. METHODS: A total of 90 patients with severe aneurysmal SAH were enrolled and assigned to a surgical neck clipping (n = 56) or an endovascular coil embolization (n = 34) groups. After treatment, UK infusion from the lumbar drain was repeated in 32 patients in the surgical neck clipping group (group B) and all in the endovascular coil embolization group (group C) until complete resolution of the SAH was observed on computed tomography. The remaining 24 of the surgical neck clipping group, without UK infusion, were assigned to group A. RESULTS: Symptomatic vasospasm occurred in 7 (29.2%) patients in group A, 2 (6.3%) in group B, and none in group C (group A vs. group B [P = 0.02]; group B vs. group C [P = 0.14]). Excellent clinical outcomes (modified Rankin score, 0 or 1) were observed in 37.5%, 59.4%, and 76.5% of patients in group A, B, and C, respectively (group A vs. group B [P = 0.11]). CONCLUSION: Clearance of SAH via intrathecal UK infusion significantly reduced symptomatic vasospasm in patients in both UK groups, resulting in better clinical outcomes.

Surgical treatment of arteriovenous malformation in a patient with human immunodeficiency virus infection and hemophilia a: case report.

This case illustrates surgical treatment of an arteriovenous malformation (AVM) in a patient with hemophilia A also infected with human immunodeficiency virus (HIV). A 31-year-old man was admitted to our hospital with right parietal intracerebral hemorrhage. He had previously been diagnosed with hemophilia A and HIV. Carotid angiography revealed an AVM. As the hematoma enlarged and clinical symptoms progressed, we resected the hematoma and the AVM while providing supplemental infusion of Factor VIII before, during, and after the operation. The patient did not experience abnormal postoperative bleeding, and he was discharged with mild motor weakness of the left lower extremity. We discuss the surgical indications, risk, and patient management in relation to hemophilia and HIV infection.

A non-enzymatic derived arachidonyl peroxide, 8-iso-prostaglandin F2 alpha, in cerebrospinal fluid of patients with aneurysmal subarachnoid hemorrhage participates in the pathogenesis of delayed cerebral vasospasm.

We performed serial measurements of 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha), a non-enzymatic derived arachidonyl peroxide, in the cerebrospinal fluid (CSF) of 34 patients with subarachnoid hemorrhage (SAH). Patients were treated with open or endovascular surgery within 48 h of onset. Delayed cerebral vasospasm was verified by the presence of a low-density area on CT scan indicating focal cerebral infarction occurring after symptomatic delayed vasospasm. Concentrations of 8-iso-PGF2alpha in the CSF of 15 patients exhibiting delayed cerebral vasospasm were compared with those of 19 patients who did not exhibit vasospasm. The concentrations of 8-iso-PGF2alpha in the CSF of patients showing vasospasm were 42.4+/-37.1 pg/ml (mean+/-S.D., n=12) on Days 0-2, 66.4+/-41.0 pg/ml (n=14) on Days 3-5, 118.5+/-89.9 pg/ml (n=15) on Days 6-8, 86.2+/-70.2 pg/ml (n=11) on Days 9-11, 48.8+/-31.8 pg/ml (n=10) on Days 12-14, 27.8+/-20.1 pg/ml (n=7) after Day 20, while the concentrations in patients not showing vasospasm were 24.8+/-12.0 pg/ml (n=18) on Days 0-2, 25.7+/-15.2 pg/ml (n=19) on Days 3-5, 47.5+/-52.3 pg/ml (n=18) on Days 6-8, 56.7+/-72.0 pg/ml (n=13) on Days 9-11, 34.2+/-53.1 pg/ml (n=15) on Days 12-14, 20.1+/-18.2 pg/ml (n=10) after Day 20. CSF concentrations of 8-iso-PGF2alpha on Days 3-5 and Days 6-8 were significantly higher in patients showing vasospasm as compared to patients not showing vasospasm. CSF levels of 8-iso-PGF2alpha in patients showing vasospasm gradually increased in the days after onset of SAH and peaked on Days 6-8. Levels returned to normal after Day 20. These values on Days 3-5, Days 6-8, and Days 9-11 were significantly higher than the value after Day 20. Considering these data and the biological activities of 8-iso-PGF2alpha, such as development of inflammation, membrane perturbation and vasoconstriction, we conclude that 8-iso-PGF2alpha may play a role in delayed cerebral vasospasm after SAH.

[MR imaging study of edema along the optic tract in patient with Rathke's cleft cyst].

We report an 80-year-old woman who was admitted to our hospital with symptoms due to diabetes insipidus. Magnetic resonance (MR) imaging demonstrated a sellar/suprasellar cystic lesion with marginal enhancement and the thick pituitary stalk. The MR imaging depicted edema spreading along the optic tract on fluid-attenuated inversion recovery (FLAIR) images. Upon neurological examination at the time of admission, there were no abnormal findings affecting the field of vision or visual acuity. In endocrinological examination, the basal plasma values of pituitary hormones were within normal range except for that of prolactin, which was 47.9 ng/ml. The preoperative diagnosis was craniopharyngioma, and the intrasellar mass was partially removed by the endoscopic transnasal transsphenoidal approach. Postoperative histopathological examination revealed Rathke's cleft cyst associated with squamous metaplasia. Lymphocytic infiltration was also confirmed in both the anterior and posterior pituitary lobe. The postoperative course was satisfactory. Edema spreading along the optic tract was reported as a characteristic MR imaging finding for diagnosis of craniopharyngiomas or optic nerve glioma. However, it is suggested that edema of the optic pathway seems to be caused not only by craniopharyngioma but also other suprasellar lesions. It was a rare case of secondary lymphocytic hypophysitis caused by Rathke's cleft with edema along the optic tract.