Of 2,130 consecutive patients admitted to two hospitals with acute brain infarction, we examined 11 patients (0.52%) with medial medullary infarction. The infarcts documented by MRI were unilateral in 9 patients and bilateral in 2 patients, and located in the anteromedial arterial territory of the upper or middle part of the medulla. Atherosclerosis of the vertebral arteries was the predominant vascular pathology. The vertebral artery was occluded at its terminal portion in 7 patients. Nine patients had hypertension, and 8 of these had additional risk factors. Male gender (10 patients) and smoking habits (7 patients) were more prevalent compared with patients with pontine infarction. One patient had a medial medullary infarction attributed to dissection of the vertebral arteries following blunt head injury. Limb weakness was the major symptom in all patients, and gaze-evoked nystagmus was also frequent (6 patients). Tongue weakness ipsilateral to the infarct, the classic sign of medial medullary syndrome, was evident in only 3 patients. The outcome was usually excellent.
This study indicated that the nocturnal blood pressure dip in patients treated with antihypertensive agents may accelerate the increase in ischemic brain lesions.
Background and Purpose: Recurrent embolization is a serious problem in acute cardioembolic stroke. However, the clinical features and predisposing factors of recurrent embolization have not been fully elucidated.Methods: Subjects were 227 consecutive patients (128 men and 99 women, aged 68.6+13.2 years) with acute cardioembolic stroke who did not receive anticoagulant therapy during the first 14 days after stroke onset. We assigned the subjects to two groups according to the occurrence or nonoccurrence of recurrent attacks within 14 days of the stroke onset. We assessed their clinical features, coagulation study results, and underlying heart disease.Results: Recurrent brain or systemic embolization during the first 14 days after onset was noted in 46 patients (20.3%, group A) but not in the other 181 (group B). Recurrent embolization was more frequently
Background and Purpose:We describe the first case of bilateral medial medullary infarction demonstrated by magnetic resonance imaging. We discuss the relation between this lesion and the oculomotor signs that were observed clinically.Case Description: A 71-year-old man initially presented with pure motor hemiparesis, which progressed to complete quadriplegia. He also developed nearly complete vertical and horizontal ophthalmoplegia. Magnetic resonance imaging revealed upper medial medullary infarctions bilaterally that extended to the pontomedullary junction.Conclusions: We propose that the vertical oculomotor disorders resulted from involvement of the oculomotor system in the caudal brain stem, especially the caudal paramedian pontine reticular formations on both sides. (Stroke 1992;23:1657-1659 KEY WORDS • cerebral infarction • cerebrovascular disorders • magnetic resonance imaging • medulla oblongata • ocular disease I nfarction of the medial medulla oblongata has been rarely reported, even during the era of magnetic resonance imaging (MRI), a technology that can detect small lesions in the posterior fossa.1 Because of the rarity of this syndrome, clinical features such as disturbance of oculomotor control are still controversial. We report the first case, to our knowledge, in which bilateral medial medullary infarction was clearly demonstrated by MRI and discuss the relation between this anatomic lesion and the oculomotor signs appearing in this patient.Case Report A 71-year-old man with a history of hypertension and smoking awoke with a right hemiparesis. He was admitted to our hospital the day after symptoms began. On admission, his pulse rate was 80 beats per minute, blood pressure was 202/110 mm Hg, and respirations were 18 per minute and regular. He was alert, with normal higher cortical function. His speech was dysarthric. The visual fields were intact; pupils were equal, with a normal light reflex; and ocular movements were full and smooth, without nystagmus. A mild right hemiparesis was present involving the face and tongue. The rightsided deep tendon reflexes were slightly increased. There were no sensory deficits to touch, pain, temper-
Hashimoto's encephalopathy (HE) is a steroid-responsive autoimmune encephalopathy associated with Hashimoto thyroiditis. We herein report a case of HE manifesting “smoldering” limbic encephalitis with persisting symptoms and abnormalities on examinations. Although our patient experienced partial clinical remission after treatment, hippocampal hypermetabolism on [ 18 F] fluorodeoxyglucose positron emission tomography (FDG-PET) and subclinical seizures on video electroencephalography persisted. Hypermetabolism on FDG-PET was improved by additional prednisolone therapy. Thus, as with other autoimmune limbic encephalitis cases, HE can take a course of “smoldering” encephalitis. FDG-PET and electroencephalogram findings can reflect the disease activity degree in such patients, although with certain neurophysiological and biochemical distinctions.
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