We report 2 patients who had clinical and neuroimaging signs of spontaneous intracranial hypotension and who developed cerebral sinus venous thrombosis. This sequence of events – known after dural puncture but not in spontaneous intracranial hypotension – was suggested by the change in the pattern of headache, from a postural to a permanent and increasing one. The diagnostic and therapeutic difficulties that this complication raises are discussed.

Omega-3 polyunsaturated fatty acids (OPFA) have beneficial effects on inflammatory reactions and production of cytokines. They decrease the release of 5HT by platelets and possess vasorelaxant activity. This led them to be tried in the prophylactic treatment of migraine. After 4 weeks of a single-blind placebo run-in period, patients were randomized and treated in double-blind condition by placebo or OPFA 6 g a day for 16 weeks, followed by a 4-week placebo run-out period. The intention to treat population included 196 patients. Those who received all four treatment periods included 96 patients taking OPFA and 87 taking placebo. The primary efficacy analysis was the number of migraine attacks during the last 4 weeks of treatment. During this period, the mean number of attacks was 1.20 +/- 1.40 in the OPFA group and 1.26 +/- 1.11 in the placebo group (NS). The total number of attacks during the 4-month period of the study was significantly different between groups: 7.05 in the placebo group, 5.95 in the OPFA group (P = 0.036). Mean intensity, mean duration of the attacks and rescue medication use, were not significantly different between the two groups. Except for a significant difference against OPFA for eructations, the tolerance was satisfying. Despite a run-in placebo period of 1 month, a very strong placebo effect was observed in this trial: 45% reduction of the attacks between run-in and 4-month treatment period (55% in the OPFA group, P = 0.058). Finally, this large study did not confirm two previous studies based on a small number of patients.

Microangiopathy of the inner ear, retina, and brain was first described in 1979 by John O. Susac. Since then, approximately 60 cases have been reported. Otolaryngologists must be aware of this syndrome, in which cochleovestibular symptoms are an important part of the diagnosis. In this article, we report a new case of Susac syndrome and discuss the diagnosis, physiopathologic characteristics, and treatment of this disease.

Background and Purpose-We report a case of facial diplegia complicating a bilateral internal carotid artery dissection. Case Description-A 49-year-old patient presented with unilateral headache and oculosympathetic paresis. Cerebral angiography revealed a bilateral internal carotid artery dissection. A few days later, the patient developed a facial diplegia that regressed after arterial recanalization. An arterial anatomic variation may explain this ischemic complication of carotid dissection. Conclusions-Double carotid dissection should be included among the causes of bilateral seventh nerve palsy. (Stroke.1999;30:681-686.)Key Words: carotid artery dissection Ⅲ cerebral blood flow Ⅲ facial paralysis C ommon clinical presentation and possible ischemic complications of internal carotid artery (ICA) dissections vary. Cranial nerve palsies seem to occur in this pathological condition, appearing in Ͼ10% of the cases. 1 Several cranial nerve palsies have been described, 1,2 especially lower cranial nerves syndromes and ocular motor nerves syndromes, probably owing to transient impairment of the cranial nerves' blood supply. We describe the first reported case of facial diplegia resulting from a bilateral ICA dissection. Anatomic variation of the blood supply of the seventh cranial nerve may explain this finding. Case ReportA 49-year-old right-handed-man was referred for a left hemicrania associated with a left ptosis. His past medical history was significant for resolved poliomyelitis, a thoracic zoster eruption, and a schwannoma of the right pneumogastric nerve. He had experienced right-sided tinnitus for the past 2 years.Five days before admission, while he was on holiday, without having participated in any unusual sports activity, he experienced a left periorbital pain followed by left hemicrania and neck pain, which persisted up to his admission and fluctuated in intensity. He noticed a left ptosis 2 days later. At admission, he had left hemicrania, neck pain, and left oculosympathetic paresis. His blood pressure was 130/80 mm Hg, and the remainder of the clinical examination was normal. The erythrocyte sedimentation rate was 25 mm/h, without dysglobulinemia or nuclear antibodies. Other routine laboratory investigations and extensive coagulation studies were normal. There were neither clinical nor histological signs of a specific elastictissue disease. Brain MRI and MR angiography demonstrated bilateral dissection of the ICA, with more severe narrowing of the left ICA (Figure 1). Intravenous heparin sodium was initiated. Cerebral angiography, performed 2 days later, with selective catheterization of carotid and vertebral arteries, confirmed extensive dissection of both ICAs (Figures 2A and 2B). Both ICA territories were partially filled by the posterior circulation through the posterior communicating arteries ( Figure 2C). There was no vascular abnormality to suggest a fibromuscular dysplasia, and renal arteries were normal. Eight days after admission, a neck ultrasound examination and transcranial Doppler (TCD) ...

Omega-3 polyunsaturated fatty acids (OPFA) have beneficial effects on inflammatory reactions and production of cytokines. They decrease the release of 5HT by platelets and possess vasorelaxant activity. This led them to be tried in the prophylactic treatment of migraine. After 4 weeks of a single-blind placebo run-in period, patients were randomized and treated in double-blind condition by placebo or OPFA 6 g a day for 16 weeks, followed by a 4-week placebo run-out period. The intention to treat population included 196 patients. Those who received all four treatment periods included 96 patients taking OPFA and 87 taking placebo. The primary efficacy analysis was the number of migraine attacks during the last 4 weeks of treatment. During this period, the mean number of attacks was 1.20 +/- 1.40 in the OPFA group and 1.26 +/- 1.11 in the placebo group (NS). The total number of attacks during the 4-month period of the study was significantly different between groups: 7.05 in the placebo group, 5.95 in the OPFA group (P = 0.036). Mean intensity, mean duration of the attacks and rescue medication use, were not significantly different between the two groups. Except for a significant difference against OPFA for eructations, the tolerance was satisfying. Despite a run-in placebo period of 1 month, a very strong placebo effect was observed in this trial: 45% reduction of the attacks between run-in and 4-month treatment period (55% in the OPFA group, P = 0.058). Finally, this large study did not confirm two previous studies based on a small number of patients.