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Internuclear Ophthalmoplegia and Horner's Syndrome Due To 362 Journal of the Royal Society of Medicine Volume 86 June 1993 Internuclear ophthalmoplegia and Her erythrocyte sedimentation rate (ESR) was 105 in the Horner's syndrome due to presumed first hour, the white blood cell count was 11.1 x109/l, giant cell arteritis platelets 475x 109/1, the blood film showed some target cells and ++ rouleaux. Her alkaline phosphatase was 226 and her 7y-glutamine transferase 102. A computerized tomography scan reported atrophic changes in the cerebral hemispheres, and an old infarct was noted in the left temporal lobe. Within Ayman Askari MRCP1 0 M P Jolobe FRCP2 6 days of starting treatment the headache improved remarkably, and in the following 2 months the patient D I Shepherd FRCP2 'Princess Royal Hospital; maintained her progress with no change in the neurological Telford, Shropshire and 2Tameside General Hospital signs. The ESR was 47 within 8 days of admission and 3 by Ashton-under-Lyne, Lancashire day 38 of starting treatment. Keywords: giant cell arteritis; ophthalmoplegia; Horner's syndrome; Discussion ataxic nystagmus Our aim is to draw attention to the association between neuro-ophthalmic signs and presumed GCA. Leukocytosis, abnormal latex fixation test and fever are in keeping with cell arteritis is an inflammatory, the diagnosis. It is likely that many patients with GCA have Giant (GCA) occlusive ophthalmoplegia in the course of their illness and failure arteriopathy of unknown aetiology. It is common in the to detect it may be due to the transient nature of this elderly, with an incidence of 17.4 per 100 000 ofthe popula- manifestation3. Ophthalmoparesis does not always predate tion over 50 years of age1. There is a female preponderance visual loss, but if both conditions are present, the former and it is confined almost exclusively to caucasians. It is precedes the latter in the majority of cases4. In our case, the associated with numerous neurological manifestations, involvement ofthe right medial longitudinal fasciculus with however, neuro-ophthalmological symptoms are the most the sympathetic fibres causing Horner's syndrome and commonly recognized, occurring in up to 40% ofcases in some ophthalmoplegia, represent a rare combination series1. The ocular findings range from amaurosis fugax, Internuclear visual recognized recently5. This finding in our patient, taken permanent loss, scotomas, diplopia and Horner's in last indicates an syndrome2. It is of fundamental importance to recognize together with those the reference, in unusual manifestation of GCA, which has possibly been this condition because it is remediable and the delay overlooked in the past. Although histology was not obtained, diagnosis carries grave consequences. we feel that the presentation, signs and response can only We report a case of internuclear ophthalmoplegia associated be due to an inflammatory vasculitis of which GCA is the with Horner's syndrome induced by presumed GCA which most likely. It is preferable to follow the clinical response was managed successfully. rather than the sedimentation rate in tapering the steroid dose6. Case report An 84-year-old lady presented with an 8 week history of We hope, that in accordance with the experience of others7, that the diplopia, ptosis and miosis will regress headache, dizziness and a recent flu-like illness which was with continuation of steroid therapy. subsiding. She was previously well with no significant past medical history. References On examination she was pyrexial (37.8). In the central 1 Huston KA, Hunder GG, Lie JT, Kennedy RH, Elveback LR. nervous system, the visual acuity was right 6/18 and left Temporal arteritis: a 25-year epidemiologic, clinical and 6/9, she had right partial ptosis and a miotic right pupil. pathologic study. Ann Intern Med 1978;88:162-7 Both pupils reacted to light. There was an internuclear 2 Bromfield EB, Slakter JS. Horner's syndrome in temporal ophthalmoplegia with impaired adduction ofthe right eye, arteritis. Arch Neurol 1988;45:604 some restriction of abduction of the left eye and mild 3 Healy LA, Wilsker KR. Manifestations of giant cell arteritis. Med nystagmus in the abducting eye. Upward gaze produced some Clin N Am 1977;61:261-70 divergence. Tenderness was noted on palpation of right 4 Fisher CM. Ocular palsy in temporal arteritis. Mimm Med temporal scalp region, otoscopy, power and reflexes remained 1959;42:1258-68 5 Trend P, Graham E. Internuclear ophthalmoplegia in giant cell normal. At this stage a presumed working diagnosis ofacute arteritis. J Neurol Neurosurg Psych 1990;53:532-3 GCA was made and prednisolone was started before the 6 Wyngaarden JB, Smith LH Jr, eds. Cecil textbook ofmedicine 17th completion of investigations. edn. London: WB Saunders Co., 1985:1947 7 Meadows SP. Temporal or giant cell arteritis. Proc R Soc Med 1966;59:329-33 Correspondence to: Dr Ayman Askari Work carried out at Tameside General Hospital (Accepted 5 February 1992).
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