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.

Background and Purpose: Phenylpropanolamine (PPA) has been associated with an increased risk of intracranial hemorrhage (ICH). The aim of this study was to assess the association between PPA intake and ICH in a Mexican population. Methods: We included all patients with ICH aged 18 to 51 years, with no known structural etiology, diagnosed from January 1991 to December 2000. Three to 4 controls per patient matched by sex, age (within 5 years) and place of residence were included. Patients and controls were asked about use of cold medication or appetite suppressant medications within the previous year before the interview. We considered a PPA related hemorrhage when there was a temporal relationship between the use of medication and the development of the hemorrhage, and when other causes could be ruled out. Associated risks for PPA use and other possibly related variables were estimated. Results: 177 patients (mean age 39 ± 12 years) were included; 58 (33%) were diagnosed with subarachnoid hemorrhage (SAH) and 119 (67%) with ICH. 41.2% (73 of 177) of patients had documented use of PPA within the past year and 10 (5.7%) of them had a temporal relationship between ingestion of PPA and ICH. In control subjects 42.4% (422 of 996) had been exposed to PPA and none of them developed hemorrhage. The time from PPA exposure to the onset of ICH varied from 30 minutes to 24 hours. The risk of PPA exposure for hemorrhage was not significant in cases or controls, OR 0.95 (95% CI, 0.68 to 1.34; p = 0.77). No subjects (cases or controls) reported use of PPA as an appetite suppressant. Conclusions: We found no association between ingestion of PPA and cerebral hemorrhage with respect to ingestion of PPA in the previous year. When recent use was looked at an apparent risk was evident.

Neurosyphilis is increasing due to a rise in the number of cases of syphilis in cocaine/crack addicts and in patients with HIV infection. Neurosyphilis is an example of a unique group of chronic CNS diseases that may cause either a degenerative or a vasculitic process, where the main pathogenic event is ''endarteritis obliterans'' of terminal arterioles. In meningovascular neurosyphilis, the most commonly involved artery is the middle cerebral artery. It generally presents with a prodromic phase, weeks or months before the onset of identifiable vascular syndromes. When there is focal inflammation the clinical picture is characterized by hemiplegia, whereas in the case of multifocal involvement of small intracranial arteries, it presents with a slowly progressive loss of cognitive functioning and personality changes. Since neurological deficits once established may only slightly improve with treatment, the goal of therapy is to halt the progression of the disease. Intravenous aqueous crystallin penicillin G is the most accepted treatment. HIV-infected patients have shown accelerated development of neurosyphilis, and it is suggested that coinfection with HIV alters the course of Treponema pallidum infection. Atypical manifestations of neurosyphilis have been reported among HIV patients, including fulminant presentation, rapid progression, atypical serological findings, and failure of conventional doses of penicillin to eradicate infection.

Background: There is no information on transcranial Doppler (TCD) failures due to poor insonation among native inhabitants of Latin America. Methods: Seventy Ecuadorian natives and 70 age- and sex-matched individuals of European origin underwent TCD. The same investigators performed all exams using the same equipment and protocol. Using the McNemar's test for correlated proportions, we compared TCD failures related to poor insonation across ethnic groups. Results: Out of 140 participants, 56 (40%) had one or more suboptimal/absent acoustic windows. These persons were older (p = 0.01) and were more often women (p < 0.0001) than those with all optimal windows (irrespective of race/ethnicity). In the matched-pair analysis, Amerindians were more likely to have suboptimal/absent acoustic windows than individuals of European origin (OR: 2.8, 95% CI: 1.3-6.5, p = 0.006). Conclusion: Amerindians are almost three times more likely to have insonation failures related to poor acoustic windows than their European counterparts.