Williams GP, Lukaris A, Hawksworth NR
Eye. 2007 Jan;21(1):139-40
Publication year: 2007


A 46-year-old man presented with a droopy left upper-lid associated with headache, facial, and neck pain. He was otherwise well and a nonsmoker.

Examination revealed 2 mm of left ptosis, anisocoria (see Figure 1) and facial anhidrosis. Acuity was 6/4 in each eye. The blood pressure was markedly elevated (250/140). He had hypertensive retinopathic changes but ocular and systemic examinations were otherwise unremarkable. Although index of suspicion for carotid artery dissection was low, urgent ultrasound Doppler’s of the carotid/vertebral circulations and computed tomography scanning with contrast of the head/neck were performed and excluded this possibility.

A weak adrenaline solution (1 : 1000) was instilled to ascertain if a preganglionic or postganglionic Horner’s was present. This resulted in no change in pupil size, confirming a preganglionic lesion or central Horner’s syndrome.

Chest radiography and electrocardiography revealed cardiomegaly and left ventricular hypertrophy. He was referred to the medical team for further investigation/management. Subsequent echocardiography confirmed left ventricular hypertrophy. He was found to have elevated serum lipids and creatinine (at 164 μmol/l). All other investigations were normal. Hypertension and hypercholesterolaemia were controlled medically and Aspirin commenced.

Although the presence of a Horner’s syndrome was irrefutable on clinical grounds (Figure 1), full pharmacological testing with 4% cocaine eyedrops (unavailable in ‘out of hours’ practice), would have completed the investigations.1 After 1 month, the central Horner’s syndrome had completely resolved. Our patient had sustained a transient ischaemic attack affecting the preganglionic neuron in the ocular sympathetic chain. Given the absence of brainstem signs we suspect the lesion was near the posterolateral hypothalamus, the origin of the ocular sympathetic chain. This area is supplied by small vessels known as the posteriomedial penetrating arteries, which arise variably from the Circle of Willis, posterior and middle cerebral arteries. Treatment involves modification of the cardiovascular risk profile—as in this case.

Although hypertension has been described with Horner syndrome, this was in relation to carotid dissection.2 This is a life-threatening emergency which may manifest in numerous ways in association with Horner syndrome.3 To our knowledge this is the first reported case of transient central Horner syndrome associated with hypertension.