Migrainous infarction in an adult: evaluation with serial diffusion-weighted images and cerebral blood flow studies.

We report the case of a 64-year-old man with migrainous infarction, giving special attention to chronological changes in neuroimaging findings. Five days after the onset, diffusion-weighted imaging showed slightly high intensity, and the apparent diffusion coefficient map showed increased diffusion in the right occipital lobe, which indicated vasogenic edema. Perfusion magnetic resonance imaging (MRI) and MR angiography demonstrated hyperperfusion of the ipsilateral hemisphere. Follow-up MRI showed irreversible brain damage. These images may reflect chronological changes in cerebral edema due to prolonged hyperperfusion with migraine.

[A case of spinal cord infarction caused by cervical disc herniation].

A 40-year-old previously healthy female was diagnosed with acute progressive paraparesis. Neurological examination revealed bilateral four-limb weakness predominant in the distal part of the upper limbs and superficial sensory impairment below the cervical region. T2-weighted image on MRI showed an area of hyperintensity in the gray matter of the cervical cord with disc herniation at the C4/C5 vertebral level. Laboratory investigation showed no evidence of infections, autoimmune, inflammatory, or neoplastic causes. A follow-up MRI study 3 days after admission showed that the region of hyperintensity was had enlarged without contrast enhancement. Spinal angiography was performed 21 days after admission and demonstrated that the anterior spinal artery originated from the fourth segment of the left vertebral artery and occluded at the level of C4/C5, which coincided with the location of disc herniation. We hypothesized that she developed anterior spinal artery syndrome which caused disc herniation. Although we frequently encountered disc herniation, there are few cases developed spinal cord infarction. We discuss the etiology and pathogenetic relation between disc herniation and spinal cord infarction.

Dissecting aneurysms involving both anterior cerebral artery and aorta.

Non-traumatic intracranial dissecting aneurysm (IDA) has been recently reported with increasing frequency and is recognized as a possible cause of subarachnoid hemorrhage. However, the pathogenesis of this disease is still unclear. Cystic medial necrosis (CMN) is known to be a cause of aortic dissection, especially in Marfan's syndrome. Presented herein is the case of a 49-year-old man who had IDA of the right anterior cerebral artery and abdominal aortic dissection without Marfan's syndrome. Histological examination showed medial degenerative changes with the accumulation of acid mucopolysaccharides in various intra- and extracranial arteries. Coexistence of dissecting aneurysms in the anterior cerebral artery and aorta suggests the presence of underlying pathogenesis that is common to these two dissection processes.

Preoperative extracranial carotid artery examination with ultrasonography in patients undergoing coronary artery bypass grafting in Japan.

PURPOSE: We investigated the incidence, degree, and plaque characteristics of extracranial carotid stenosis with carotid ultrasonography (CUS) in patients undergoing coronary artery bypass grafting (CABG). MATERIALS AND METHODS: Preoperative CUS was performed on 221 patients (442 carotid arteries) undergoing CABG. The degree of extracranial carotid stenosis was calculated based on the area stenosis, and it was classified into six grades as follows: grade (G) 0, G1 (1%-29%), G2 (30%-49%), G3 (50%-69%), G4 (70%-99%), and G5 (occlusion). RESULTS: The incidence of G4 was 4.1% and G5 1.6%. There were 48 arteries rated G3 or G4. Hypoechoic plaque was detected in 28 of the 48 arteries (58%), and heterogeneous plaque was detected in 37 arteries (73%). Ulcerative plaque was detected in 27 arteries (56%); when comparing the G3 and G4 groups, ulcerative plaque was found more frequently in G4 than in G3 (14/18 vs 13/30 arteries, P < 0.02). CONCLUSION: Our study demonstrated that patients undergoing CABG with extracranial severe carotid stenosis tend to have heterogeneous, hypoechoic, and ulcerative plaque. We believe that preoperative CUS should be used to evaluate the plaque characteristics of extracranial carotid stenosis.

[Extracranial carotid artery disease assessed by contrast enhanced three-dimensional MR angiography: correlation with carotid ultrasonography].

PURPOSE: To evaluate the imaging features of extracranial carotid stenosis and to compare the findings with contrast enhanced three-dimensional MR angiography(CE 3D-MRA) with those of carotid ultrasonography(CUS). MATERIALS AND METHODS: Both studies were performed in 24 patients(48 carotid arteries) with extracranial carotid arteriosclerotic stenosis. Based on the CUS findings, the degree of stenosis was classified into four grades: normal, mild; 1-39%, moderate; 40-69%, severe; and 70-99%, occlusion. The presence or absence of ulceration, as well as high-grade turbulence (HGT) at the stenotic portion, was also assessed by CUS. Furthermore, according to the findings of CE 3D-MRA, stenosis was again classified into four types: normal(n = 4), narrow(n = 26), signal void(n = 10), and occlusion(n = 8). RESULTS: Both studies correctly identified occlusion in 8 arteries. Of 19 arteries that were classified as having mild or moderate stenosis on CUS, 16(84%) were narrow on CE 3D-MRA. On the other hand, of 20 arteries classified as showing severe stenosis on CUS, 10(50%) and 10(50%) were classified as the narrow type and signal-void type, respectively, on CE 3D-MRA. Signal void was only seen in the severe stenosis group. Ulceration was detected more frequently in the signal-void type than in the narrow type (7/10 vs. 5/10). In addition, the incidence of HGT in the signal-void type was significantly higher than that in the narrow type(9/10 vs. 3/10: p < 0.02). CONCLUSION: CE 3D-MRA shows the features of extracranial carotid stenosis more reliably than CUS. In addition, signal void detected on CE 3D-MRA may reflect severe carotid stenosis with HGT.