0036-9330/03/4803/060 SCot Mid J 2003; 48 i 091.092 @ 2003 Scottish Medical Journal CLAUDE'S SYNDROME IN ASSOCIATION WITH POSTERIOR CEREBRAL ARTERY STENOSIS T Dhanjal, M Waltm, N MacMillan * University Department of Medicineand "Department of Radiology. WesternInfirmary. Glasgow Abstract: Background: m report a case of a 6/ year oldman with midbrain infarction causing Claude'ssyndrome attributable to stenosis of the posterior arebralarury. Casedescription: Thepatimt presmudwitha pupil-sparing lift thirdnerve palsy andcontralateral ataxia. A background history of treaudhyperunsion andcigaretu smoking wasobtained. Magnttic resonance imaging rmaled an area of infarction involving the lift medial midbrain. Magnttic resonance angiography revealed significant sunosis of the lift posterior «rebral artery. Antiplatela therapy wasinstituudandthe patitntmade a satisfactory movery. Conclusions: Thisisthefirst reporttd case of Claude's syndrome arising in association withstenosis of the posterior cerebra! arttry.Intracranial large vessel disease should be considered asa potmtialaetiologicfactorin patimts with similarmidbrain ischaemia. Keywords: Midbrain infarction, posterior arebralarury stenosis Case report 61 year-old man was admitted to our hospital because of ataxia and diplopia. He gave a 24 hour history of extreme gait ataxia and diplopia which was maximal on horizontal gaze to the right. A past history of type 2 diabetes, essential hypertension and chronic obstructive pulmonary disease was obtained. Examination revealed a palsy of the left oculomotor nerve with sparing of the pupil. The gait was ataxic and dysdiadochokinesis was present on examination of the right arm. Neurological examination was otherwise normal. On cardiovascular examination the patient was in sinus rhythm with blood pressure of 176 / 89 mmHg. No clinical evidence of valvular heart disease or cardiac failure was apparent. Magnetic resonance imaging of brain was performed ... (figure 1 and figure 2). A trans-thoracic echocardiograph revealed left ventricular hypertrophy and mild left ventricular systolic dysfunction but no obvious cardioembolic source. Antiplareler therapy with aspirin was initiated and further secondary preventative treatment with antihypertensive therapy was commenced after an interval of seven days. The patient remains in a rehabilitation facility one month after ictus. No new neurological symptoms attributable to the posterior cerebral artery stenosis have occurred. A infarction on the right involving a portion of the crossing of the superior cerebellar peduncles and the medial half of the red nucleus. The medial longitudinal fasciculus was also involved however more rostrally, the oculomotor fibres and the entire red nucleus were infarcted. Disagreement arises over the involvement of the red nucleus. Coppola! and Kremer' both describe the syndrome with Claude's original red nucleus involvement. Indeed, major neuro-opthalmology textbooks have attributed Claude's syndrome to a lesion of the red nucleus." However, a recent review of six patients by Seo et al. demonstrated well-localised lesions on MRI in the midbrain, below the level of the red nucleus with only minimal involvement in one case.' There conclusion stated that the red nucleus contributes little to the syndrome with the major pathology lying within the superior cerebellar peduncle, caudal to the red nucleus. The magnetic resonance images in our case do not demonstrate involvement of the red nucleus and thus support the theory that red nucleus involvement in not Fig 1 T2 Weighted magnetic resonance image of midbrain. Medial midbrain infarction is demonstrated. Discussion There is a clear correlation between ischaemia in the ventromedial midbrain and the clinical presentation of Claude's syndrome in this case. Claude's syndrome has been the subject of relatively few case reports, and there is some disagreement over the precise localisation of the culprit lesion. In 1912, the French psychiatrist and neurologist Henri Claude (1869-1945) described a house painter who developed a right oculomotor nerve palsy with contralateral asynergy and extreme gait ataxia. I The pathological examination demonstrated a paramedian mesencephalic Correspondence to Dr T Dhanjal, University Department of Medicine. Western Infirmary, Glasgow G11 6NT 91 Claude s syndrome mandatory for the clinical manifestations of Claude's syndrome. It should be noted however that magnetic resonance imaging abnormalities may not correlate completely with the results of detailed neuropathological examination. Our patient is unique as this is the first description of a case of Claude's syndrome as a consequence of confirmed posterior cerebral artery (PCA) stenosis. PCA territory infarction is uncommon, accounting for only 5-10% of entries in most stroke registries. The few large series of PC-i\ infarction described in the lirerarurev? suggest that the majority of cases of PCA territory infarction are attributable to embolic disease, while arherorhrornboric lesions of the PCA are implicated in fewer than 10% of patients'? A number of strategies to treat intracranial atherosclerotic stenosis are currently under evaluation," and this case emphasizes the need for thorough clinical and radiologic assessment of patients with midbrain infarction. Stenosis of the PCA should be considered as a potential aetiological factor in such patients. REFERENCES 1 Claude H, Loyez M. Ramolllssement du noyau rouge. Rev Neurol (Paris) 1912; 24: 49-51. 2 Coppola RJ, Freedman H. Bilateral Claude syndrome: clinical and neuropathological study. BUckeyeOsteopathic Physician 1991; 60: 4-6. 3 Kremer C, Baumgartner RW. 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