Background and Purpose-We sought to determine the clinical and neuroradiological features of intracranial vertebrobasilar artery dissection. Methods-The clinical features and MR findings of 31 patients (20 men and 11 women) with intracranial vertebrobasilar artery dissections confirmed by vertebral angiography were analyzed retrospectively. The vertebral angiography revealed the double lumen sign in 11 patients (13 arteries) and the pearl and string sign in 20 patients (28 arteries). Results-The patients ranged in age from 25 to 82 years (mean, 54.8 years). Clinical symptoms due to ischemic cerebellar and/or brain stem lesions were common, but in 3 cases the dissections were discovered incidentally while an unrelated disorder was investigated. Headache, which has been emphasized as the only specific clinical sign of vertebrobasilar artery dissection, was found in 55% of the patients. Intramural hematoma on T1-weighted images has been emphasized as a specific MR finding. The positive rate of intramural hematoma was 32%. Double lumen on 3-dimensional (3-D) spoiled gradient-recalled acquisition (SPGR) images after the injection of contrast medium was identified in 87% of the patients. The 3-D SPGR imaging method is considered useful for the screening of vertebrobasilar artery dissection. Conclusions-Intracranial vertebrobasilar artery dissection is probably much more frequent than previously considered.Such patients may present no or only minor symptoms. Neuroradiological screening for posterior circulation requires MR examinations, including contrast-enhanced 3-D SPGR. Angiography may be necessary for the definite diagnosis of intracranial vertebrobasilar artery dissection because the sensitivity of the finding of intramural hematoma is not satisfactory.

Background and Purpose: We have encountered a peculiar atrophic change in the midbrain in some patients with parkinsonian syndromes. We discovered these patients had vertical supranuclear gaze-palsy, an eye movement disorder. The purpose of this study was to elucidate whether this atrophic pattern of the midbrain (which we have termed morning glory sign) is related to the vertical eye movement disorder, in particular to progressive supranuclear palsy (PSP).Methods: We reviewed T 2 -weighted axial images obtained from 42 patients with parkinsonian syndromes, includingˆve patients with PSP, 23 patients with Parkinson's disease, and 14 patients with multiple system atrophy (MSA). We focused on a speciˆc atrophy of the midbrain, the morning glory sign, which is a concavity of the lateral margin of the tegmentum of the midbrain.Results: The morning glory sign was detected in four of theˆve patients with PSP and in one (striatonigral degeneration; SND) of the14 patients with MSA. All morning glory sign patients had vertical supranuclear gaze-palsy, as did the one PSP patient without the morning glory sign. Vertical supranuclear gaze-palsy was seen in no other patients (23 patients with Parkinson's disease and 13 patients with MSA) who lacked the morning glory sign.Conclusions: Morphologically, the morning glory sign is believed to be related to vertical supranuclear gaze-palsy. This sign should be considered a useful clue when diagnosing PSP.

We performed a histopathological study of two human brains to look at dilated Virchow-Robin (V-R) spaces in the anterior perforated substance and putamen. We measured the diameter of 74 arteries in 54 dilated V-R spaces. In 28 patients without neurological deficits we ascertained the characteristic location of dilated V-R spaces in the anterior perforated substance and basal ganglia on MRI, measuring the distance from 64 foci of cerebrospinal fluid signal intensity to the centre of the mamillary body on 1 mm thick images. In the histopathological study, the mean diameter of the arteries was 39.0 +/- 36.0 microns. Dilatation of the V-R space was observed from the end of the indentation of the pial membrane towards the brain surface along the perforating artery. In the MR images, the mean distance from the dilated V-R space to the mamillary body was 10.0 +/- 4.5 mm. The V-R space was confined to a fixed level in the lower part of the basal ganglia, and not found near the brain surface.

The objective of the present study was to examine the association between a polymorphism of the aldehyde dehydrogenase 2 (ALDH2) gene and lacunar infarcts of the brain. We conducted a population-based, cross-sectional study on residents from two age groups (61- and 72-year olds). A total of 376 subjects participated in the study, which included brain magnetic resonance image and genetic analysis of the ALDH2 gene. Of the 61- and 72-year-old subjects, 46.4% and 64.3%, respectively, had one or more lacunar infarcts. The average number of infarcts also increased from 2.0 to 2.8 in men and from 2.3 to 3.5 in women. No significant association between the ALDH2 genotype and the presence of lacunar infarction (> or =1) was found. However, in subjects with lacunar infarction, the genotype of ALDH2 *1/*1 was associated with a larger number of the lesion ['single' versus 'multiple' odds ratio (OR) 3.73, 95%CI: 1.43-9.74] in men. The OR was comparable even after adjusting for alcohol consumption, tobacco habits, age, hypertension, hypercholesterolemia, and diabetes mellitus (DM) (OR 3.88; 95% CI: 1.10-13.66). In women, there was no significant association between the ALDH2 genotypes and lacunar infarcts. The present study revealed that the ALDH2 *1/*1 genotype was significantly associated with the prevalence of multiple lacunar infarcts in Japanese men.