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Purpose: This study was designed to determine whether, among Japanese patients receiving medical treatment for carotid stenosis, symptomatic carotid stenosis was more strongly associated with subsequent neurological events than asymptomatic carotid stenosis., Methods: We consecutively registered Japanese patients with carotid stenosis of 50% or more as evaluated by digital subtraction angiography who were treated medically. We reviewed medical records regarding previous neurological events as well as other stroke risk factors and underlying diseases at admission. We monitored the occurrence and date of stroke and death after the first evaluation. We also attempted to obtain information from patients or their family members by means of a questionnaire or telephone survey., Results: Among 67 patients with carotid stenosis of 50% or more who were treated medically, follow-up was completed in 62 subjects (56 men, 6 women; median age, 72 years; mean follow-up period, 37.3 months). The number of patients with subsequent stroke with symptomatic carotid stenosis was five, while that with asymptomatic stenosis was four. A significantly higher rate of subsequent stroke was observed in patients with symptomatic carotid stenosis compared with those with asymptomatic stenosis (p=0.012). Cox proportional hazards model indicated that symptomatic carotid stenosis was significantly correlated with future neurologic events (p=0.019)., Conclusion: In a Japanese population with carotid stenosis treated medically, symptomatic carotid stenosis is associated with future stroke more frequently than asymptomatic carotid stenosis., (© 2011 The Japanese Society of Internal Medicine)

A 65-year-old woman with poorly controlled diabetes presented bilateral miosis, bilateral abducens nerve palsy, and left hemiparesis. On MRI, cavernous sinus thrombosis, subdural empyema and hemorrhagic infarction in the frontotemporal lobe were detected. Cerebral angiogram revealed filling defect in the cavernous sinus with venous congestion but no involvement of internal carotid artery. Postmortem examination demonstrated hemorrhagic infarction in the right frontotemporal lobe as well as hemorrhagic necrosis of the pituitary gland. It should be noted that venous congestion due to cavernous sinus thrombosis may cause these complications.

A 54-year-old Japanese woman with a 6-year history of systemic lupus erythematosus (SLE) was admitted to our hospital suffering from acute blindness in her right eye. Her condition recovered after steroid pulse therapy, however, 18 months later she suffered from nuchal pain for 2 weeks after which right hemiparesis with urinary incontinence developed. A spinal magnetic resonance imaging (MRI) revealed cord swelling from C2 to C7. She was diagnosed with neuromyelitis optica (NMO) and intravenous steroid administrations were immediately commenced. Her condition promptly improved. This case was unique because the steroid treatment was quite effective for this case of myelitis, which had passed the acute phase. We supposed that, because most of the lesion was not necrotic or demyelinated, but rather showed edematous change caused by vasculitis based on autoimmune pathogenesis, the symptoms progressed rather gradually and improved promptly in response to glucocorticoid treatment.

We report a patient who developed reversible posterior leukoencephalopathy syndrome (RPLS) in puerperium without preeclampsia-eclampsia or chronic hypertension. The woman suddenly complained of visual loss and headache 10 days after delivery caused by edematous lesions mainly distributed in the bilateral occipital lobe. Apparent diffusion coefficient map was useful for distinction of this vasogenic edema from cytotoxic edema due to brain infarction. Under the diagnosis of RPLS, we successfully treated her disease using a trinitroglycerin as an antihypertensive, a hyperosmolar agent, methylprednisolone, and a free radical scavenger. Postpartum women may have the risk of development of RPLS even without preeclampsia-eclampsia. Vascular endothelial dysfunction may trigger RPLS, in addition to acute and modest increase in systemic pressure.