Two Cases of Partial Oculomotor Nerve Palsy due to Midbrain Infarction

Traditionally, monocular parital oculomotor pareses are localized to the cavernous sinus or retro-orbital region and are usually caused by diabetes mellitus, aneurysms of the internal carotid artery, inflammation by vrial infection or autoimmune diseases, neuropathy or neuromuscular disesases. Although rare, the monocular partial oculomotor paresis also can be caused by lesions of ventral midbrain because of their particular topographic arrangement. We present 2 cases with fascicular oculomotor nerve involvement from midbrain lesion, who presented with monocular partial ocu-lomotor nerve palsy. One patient showed partial ptosis and slow saccadic movement of the right eye. The other patient showed parital ptosis and limitation of adduction and elevation in the left eye. They had normal pupil size and light reflexes. Brain magnetic resonance images showed focal infarction in the fascicular portion of the oculomotor nerve.

Decision of Shunt Insertion Based on Electroencephalography and Stump Pressure During Carotid Endarterectomy

BACKGROUND: Carotid endarterectomy (CEA) is an effective treatment for the prevention of stroke in patients with high grade carotid stenosis. Electroencephalographic (EEG) monitoring and measurement of stump pressure are the most widely used methods for assessing the risk of cerebral ischemia during CEA. We designed this study to assess the usefulness of EEG and stump pressure for shunt insertion during CEA. METHODS: Nineteen patients were enrolled from January, 1996 to April, 1999. We calculated the percent of carotid stenosis in the patients by the NASCET (North American Symptomatic Carotid Endarterectomy Trial) criteria. The inclusion criteria of the CEA were high grade stenosis (>70%), or moderate stenosis (>50%) with ulcerated plaque. Intra-operative monitoring by using stump pres-sure, and an EEG was performed in 19 operations. RESULTS: The number of patients with asymptomatic and sympto-matic carotid stenosis were 6 and 13 respectively. Shunt during the operations was used in 12 patients; nine had both significant EEG changes and low stump pressures, two had only low stump pressure, one patient had only a significant EEG change. The peri-operative complications of mortality and stroke were found in one case. In the other patients, there no stroke recurrences during the mean follow-up period of 24 months. CONCLUSIONS: EEG and stump pressure may be useful in deciding shunt insertion during CEA for detecting ischemic changes.