Edaravone, a novel free radical scavenger, demonstrates neuroprotective effects by inhibiting vascular endothelial cell injury and ameliorating neuronal damage in ischemic brain models. The present study was undertaken to verify its therapeutic efficacy following acute ischemic stroke. We performed a multicenter, randomized, placebo-controlled, double-blind study on acute ischemic stroke patients commencing within 72 h of onset. Edaravone was infused at a dose of 30 mg, twice a day, for 14 days. At discharge within 3 months or at 3 months after onset, the functional outcome was evaluated using the modified Rankin Scale. Two hundred and fifty-two patients were initially enrolled. Of these, 125 were allocated to the edaravone group and 125 to the placebo group for analysis. Two patients were excluded because of subarachnoid hemorrhage and disseminated intravascular coagulation. A significant improvement in functional outcome was observed in the edaravone group as evaluated by the modified Rankin Scale (p = 0.0382). Edaravone represents a neuroprotective agent which is potentially useful for treating acute ischemic stroke, since it can exert significant effects on functional outcome as compared with placebo.

In a prospective study of 70 patients with infarcts in the posterior circulation admitted consecutively to a population-based primary-care center, we assessed infarct location and etiology using magnetic resonance imaging, three-dimensional time-of-flight magnetic resonance angiography, and noninvasive cardiac tests. The brainstem (mainly the paramedian pons) was the most commonly infarcted site (41/70, 59%), followed by the cerebellum (33/70, 47%). Combined supra- and infratentorial multiple vertebrobasilar infarcts occurred in 11 patients (16%). Overall, 27 patients (39%) had > or = 50% stenosis or occlusion of the basilar artery. There were other large-artery lesions in 19 patients (27%), including vertebral (V2-V4) stenosis or occlusion (in seven) and dolichoectatic vertebral/basilar arteries (in 12). Fifteen of the 70 patients had a potential cardiac source of embolism, which coexisted with large-artery disease in more than one-third of the cases. Cerebellar infarct without concomitant brainstem or occipital infarct was associated with cardioembolism (67%), while isolated paramedian pontine or midbrain infarct was associated with basilar artery stenosis (71%), suggesting in situ occlusion of the mouth of the perforators off the stenosed basilar artery. After exclusion of other potential causes of stroke, presumed small-artery disease associated with chronic hypertension remained the likely etiology in only 11 patients (16%), but these infarcts were not associated with any of the classical lacunar syndromes. Our findings emphasize the high frequency of severe intracranial large-artery disease in posterior circulation infarcts.

Seventeen patients with hemiataxia as a manifestation of thalamic infarction were studied. Hemiataxia had the main clinical characteristics of a "cerebellar type" of ataxia, though it never occurred in isolation, being associated with ipsilateral sensory disturbance (hemiataxia-hypaesthesia) in 7 patients, with ipsilateral sensory disturbance and hemiparesis (hypaesthetic ataxic hemiparesis) in 8 patients, and with hemiparesis (ataxic hemiparesis) in 2 patients. Recovery was good, and in all patients the sensory and motor disturbances improved or cleared before the hemiataxia. All patients had an infarct involving the lateral part of the thalamus (thalamogeniculate territory in 16, tuberothalamic territory in 1), also affecting the posterior limb of the internal capsule (PLIC) in 7 patients. Hemiataxia seemed linked to involvement of the caudal part of the ventral lateral nucleus of the thalamus or the immediately adjacent medial part of the PLIC. These structures are near the corticospinal pathways and the ventral posterior nucleus of the thalamus, explaining why hemiataxia is associated with hemiparesis or hypaesthesia in this type of infarct.

Thalamic stroke commonly occurs in young adults. and its mechanism is often undetermined. Increased awareness of this type of stroke in young adults should lead to better delineation of its clinical features, course, and management.

Temporal bone thickness and texture are independent predictors of TCD insonation failure in Amerindians.