Expression of S100 protein and protective effect of arundic acid on the rat brain in chronic cerebral hypoperfusion.

S100 protein is expressed primarily by astroglia in the brain, and accumulates in and around the ischemic lesions. Arundic acid, a novel astroglia-modulating agent, is neuroprotective in acute cerebral infarction, whereas the protective effects remain unknown during chronic cerebral hypoperfusion. Rats undergoing chronic cerebral hypoperfusion were subjected to a bilateral ligation of the common carotid arteries, and were allowed to survive for 3, 7 and 14 days.

Matrix metalloproteinase-2 plays a critical role in the pathogenesis of white matter lesions after chronic cerebral hypoperfusion in rodents.

Background And Purpose: Cerebrovascular white matter (WM) lesions contribute to cognitive impairment and motor dysfunction in the elderly. A disruption of the blood-brain barrier (BBB) is believed to be a critical early event leading to these WM lesions. Previous studies have suggested the involvement of matrix metalloproteinase-2 (MMP-2) in BBB disruptions and the upregulation of MMP-2 after chronic cerebral hypoperfusion in a rat model.

Hypersomnia caused by isolated angiitis of the CNS.

A 42-year-old woman presented gradual development of hypersomnia and memory disturbance. T2-weighted and FLAIR MRI scans revealed a high intensity abnormality in the hypothalamus. Stereotactic brain biopsy specimen revealed prominent infiltration of the lymphocytes in the vessel walls.

[A patient with primary Sjögren's syndrome featuring polyneuropathy and oculomotor paralysis and associated with asymptomatic left middle cerebral artery stenosis].

We report a case of primary Sjögren's syndrome (primary SjS) with polyneuropathy and right oculomotor paralysis associated with middle cerebral artery stenosis. A 39-year-old woman developed progressive numbness and clumsiness of the limbs. Two months later, right third cranial palsy manifested itself and she was admitted to our hospital.