Abstract

Sirs: The third cranial (oculomotor) nerve divides into superior and inferior divisions or rami within the superior orbital fissure or anterior cavernous sinus, the former branch supplying levator palpebrae superioris and superior rectus, the latter the medial rectus, inferior rectus and inferior oblique muscles. Selective involvement of these muscle groups may thus be of localising value. However, superior and inferior divisional palsies have occasionally been reported with more proximal lesions, most usually in the fascicular portion of the oculomotor nerve, and of vascular aetiology [1, 4–8]. A patient with superior division palsy associated with metastatic infiltration in the subarachnoid space is reported. A previously healthy 46-year-old right handed man presented with a two week history of right frontal headache. This was constant, sharp and aching in character, and more noticeable at night, but not exacerbated with coughing or bending. He also gave a six day history of double vision on upgaze, with vertical separation of images, but without eye pain or visual impairment. There was no history of hypertension or diabetes mellitus; he smoked 20 cigarettes a day. On examination there was a right partial ptosis, but no proptosis. Visual acuity was 6/9 bilaterally uncorrected. There was no miosis and pupillary responses to light and accommodation were normal. There was limited elevation of the right eye on attempted upgaze with concurrent diplopia in both the primary position and abduction, but not in adduction, indicating isolated superior rectus weakness. Eye movements were otherwise normal. There was no fatiguability of extraocular, bulbar, or limb muscles. There was no limb wasting, alteration in tone, weakness, incoordination or reflex abnormality. General medical examination was normal; blood pressure was 110/70mm Hg. The following investigations were normal or negative: full blood count, differential, urea and electrolytes, liver-related tests, serum glucose (random = 5.5 mmol/l); chest radiograph. Magnetic resonance imaging of the brain showed multiple areas of increased signal on T2-weighted scans, within the anterior temporal lobes, basal ganglia, and at the foramen magnum. Following gadolinium injection, there was extensive surface enhancement of the meninges over the brainstem, including a lesion ventral to the midbrain on the right at the point where the oculomotor nerve emerges from the brainstem into the subarachnoid space (Fig. 1a, b). Appearances were suggestive of malignant metastatic disease, rather than granulomatous or infective infiltration. No lesion was seen within the ventral midbrain, cavernous sinus, or superior orbital fissure. Cerebrospinal fluid was examined twice, showing an elevated white cell count (20 and 60/μl; mostly lymphocytes) and protein (2.49 and 3.18 g/l) with normal glucose ratio. On neither occasion were neoplastic cells seen on cytological examination. Posterior fossa craniectomy was performed to remove the foramen magnum lesion. Histology showed a poorly differentiated highly malignant nonlymphoid tumour with neuroendocrine differentiation; lung was thought the most likely primary site. He was referred for chemotherapy but died shortly thereafter, just over two months after the first presentation. Permission for autopsy was not granted. The clinical observation of ptosis and elevator paresis in abduction suggests selective involvement of levator palpebrae superioris and LETTER TO THE EDITORS

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