No abstract

Eighty-six patients with monosymptomatic optic neuritis of unknown cause were followed prospectively for a median period of 12.9 years. At onset, cerebrospinal fluid (CSF) pleocytosis was present in 46 patients (53%) but oligoclonal immunoglobulin in only 40 (47%) of the patients. The human leukocyte antigen (HLA)-DR2 was present in 45 (52%). Clinically definite multiple sclerosis (MS) was established in 33 patients. Actuarial analysis showed that the cumulative probability of developing MS within 15 years was 45%. Three risk factors were identified: low age and abnormal CSF at onset, and early recurrence of optic neuritis. Female gender, onset in the winter season, and the presence of HLA-DR2 antigen increased the risk for MS, but not significantly. Magnetic resonance imaging detected bilateral discrete white matter lesions, similar to those in MS, in 11 of 25 patients, 7 to 18 years after the isolated attack of optic neuritis. Nine were among the 13 with abnormal CSF and only 2 belonged to the group of 12 with normal CSF (p = 0.01). Normal CSF at the onset of optic neuritis conferred better prognosis but did not preclude the development of MS.

We determined the angiographic presence of extracerebral and intracerebral arterial disease in 122 patients with minor stroke within the carotid territory; we excluded patients with a recognized cardiac source of emboli. Based on clinical features and computed tomographic findings, patients were classified as having lacunar infarcts (n=61), nonlacunar infarcts (n=53), and infarcts of indeterminate type (n=8). Severe carotid bifurcation disease (>50% stenosis or occlusion) was significantly more common in nonlacunar than in lacunar infarcts, on both the ipsilateral (p<0.001) and the contralateral (p<0.01) sides; 79% of the patients with nonlacunar infarcts had severe carotid bifurcation and/or middle cerebral artery disease on the ipsilateral side compared with 3.3% of the patients with lacunar infarcts. Our data underscore the need for classification of patients by the underlying mechanisms in future studies of treatment of ischemic stroke. (Stroke 1989;20:59-64) T ransient ischemic attacks (TIAs) are well recognized as a risk factor for the development of stroke. Patients with minor stroke have a similar risk for further neurologic deterioration 1 but have only rarely been singled out for detailed study. The desirability of establishing the pathogenesis of the cerebral ischemic event has been emphasized in recent reviews.2 -4 A stroke patient should ideally be characterized by the clinical signs and symptoms, by the localization and extent of infarction, and by the underlying vascular abnormality. Whereas in TIA patients the signs and symptoms have usually resolved by the time the patient is seen by a physician and the computed tomogram (CT scan) is most often normal, patients with minor stroke usually can be more fully characterized in these respects.In clinical practice the classification of patients into groups with ischemia due to large-vessel versus small-vessel disease is often difficult but of obvious importance. Large-vessel disease commonly affects the carotid bifurcation, and the ischemic symptoms are caused by artery-to-artery embolism alone or in combination with hemodynamic impairment. 2 -5 Small-vessel disease (lacunar infarction) in the anterior circulation localized to the basal ganglia and adjacent structures is caused by primary disease in the penetrating arterioles and is associated with lacunar syndromes, of which pure motor hemipareFrom the

We describe the acute and long-term prognosis in 43 patients with lateral medullary infarction (LMI) collected from a population-based stroke registry from 1982 to July 1988. Mean age was 63.9 years and median time of follow-up was 33 months. In the acute phase, 5 patients (11.6%) died from respiratory and cardiovascular complications and 2 new strokes occurred, both in the posterior circulation. During follow-up, recurrent vertebrobasilar territory strokes occurred in only 2 patients (a rate of 1.9% per year). The mechanisms of stroke were vertebral artery (VA) branch occlusion, causing a medial medullary syndrome, and basilar artery thrombosis propagating from a contralateral, distal VA stenosis. In the acute phase of LMI, respiratory and cardiovascular events, presumably caused by autonomic dysfunction related to the lateral medullary lesion, are the major hazards. Recurrent posterior circulation strokes were uncommon during follow-up.

Sixty consecutive patients with a ruptured supratentorial aneurysm underwent operation during the acute stage, 56 of them within 72 hours after the first bleed, one on the 4th day, and three on the 5th day. Six patients were classified preoperatively in Hunt and Hess neurological Grade I, 39 in Grade II, 11 in Grade III, and four in Grade IV or V. Nine patients had severe intracerebral hematomas, and one patient had a subdural hematoma. After the aneurysm was clipped, nimodipine was applied to the exposed arterial segments in a 2.5 X 10(-5)M solution for 10 minutes. Subsequently, all patients received a continuous intravenous nimodipine infusion (2 mg/hr) for 7 to 12 days, followed by oral treatment (270 mg/day). Forty-six patients (77%) made a good neurological recovery; the morbidity rate was 22%, and mortality rate 1.5%. Of the 45 patients in good condition (Grades I to II) preoperatively, 38 (84%) made a good neurological recovery. Two patients (3% of the total series) developed a typical picture of cerebral ischemic dysfunction of delayed onset with subsequent fixed neurological deficits. The results favor the opinion that early operative intervention is beneficial in patients in good condition rather than delaying surgery, and indicate that nimodipine provides an additional anti-ischemic effect. The appearance and severity of late angiographic vasospasm did not seem to be affected by nimodipine.