Department of Ophthalmology, Royal Victoria Infirmary, Newcastle upon Tyne, United Kingdom.
Address correspondence to Ranjeet J. Pandit, MRCP, FRCOphth, Department of Ophthalmology, Royal Victoria Infirmary, Queen Victoria Road, Newcastle upon Tyne, NE1 4LP, England, UK; E-mail: Ranjeet.Pandit@nuth.nhs.uk
Transient Horner syndrome can be a manifestation of acute carotid artery dissection (1). We describe 2 patients in whom this syndrome was transient or incomplete and in whom pharmacologic testing with cocaine played an important role in confirming Horner syndrome at different stages in the disease when all physical signs of oculosympathetic paresis were absent.
Case 1. A 56-year-old decorator with a 3-day history of right periocular pain. His wife had noticed that his right pupil was smaller than his left pupil, but the anisocoria had resolved after 2 days. He had been plastering a ceiling that week, but there was no history of trauma.
He took 50 mg atenolol daily for hypertension but was otherwise in good health. He did not smoke. Ophthalmological and neurological examinations were normal. There was no anisocoria in light or dark, ptosis, or hemifacial anhidrosis. Blood pressure was 165/95 mm Hg. He was prescribed analgesics and advised to rest.
Two days later, he returned with a report of experiencing sudden and complete loss of vision in the right eye for 1 minute. He now had constant holocranial headache that was preventing him from sleep. He also complained of an unpleasant metallic taste and loss of taste sensation. Examination now showed a 1 mm right ptosis but no anisocoria in light or dark. There was sensory loss over the right side of the forehead and impaired taste over the anterior third of the tongue but no other neurological signs. Topical instillation of 10% cocaine drops confirmed a right oculosympathetic deficit.
MRI showed increased signal in the wall of the right internal carotid artery (ICA), consistent with a dissection which extended from the ICA origin to the cavernous sinus (Fig. 1). Anticoagulation treatment consisted of intravenous heparin followed by warfarin (target international normalized ratio 2.5-3.5). Good control of blood pressure was achieved after increasing the dose of atenolol to 100 mg daily.
After 3 months, he was asymptomatic and the ophthalmic examination was normal. Warfarin was discontinued after 6 months, and he was started on 75 mg aspirin daily to continue indefinitely.
Case 2. A 44-year-old man reported a 4-day history of right ptosis and miosis and mild right frontal headache. He had been on a drinking binge the night before the onset of these symptoms. He mentioned that his right upper lid would usually droop for a few days after drinking excessively, but he had not noted the pupil abnormality previously.
Emergency room examination showed a 2 mm right ptosis and a 2-mm anisocoria (right pupil smaller). The degree of anisocoria was greater in dim light. There were no other abnormal signs. Blood pressure was 130/87 mm Hg.
Two days later, neuro-ophthalmologic examination disclosed that headache, ptosis, and miosis had resolved but he mentioned that he had had brief episodes of drooping of the right upper lid. He reported that he had been monitoring his blood pressure and had found that after alcohol bingeing, it was as high as 150/97 mm Hg at a time when he would develop transient right upper lid ptosis. When he was not drinking heavily, he stated that his blood pressure was normal.
MRI showed a right ICA dissection with a mural thrombus extending from 5 cm distal to the carotid bifurcation to the skull base and corresponding narrowing of the lumen with a dissecting aneurysm (Fig. 2). He was treated with 75 mg aspirin daily and advised to avoid alcohol and heavy exercise.
Three months later, he was asymptomatic and examination was entirely normal. However, a cocaine test at this stage confirmed a right oculosympathetic deficit. Repeat MRA 3 months later showed complete resolution of the dissection (Fig. 2).
Our cases confirm the existence of a clinically transient but pharmacologically confirmed Horner syndrome, a phenomenon reported only once before (1). Our Case 2 illustrates that a positive cocaine test may persist for months after the Horner syndrome has clinically resolved. These cases highlight the importance of pharmacological testing when an oculosympathetic deficit is suspected even if there is a lack of anisocoria in light or dark.
1. Leira EC,
Bendixen BH, Kardon RH, Adams HP Jr. Brief, transient Homer's syndrome can be the hallmark of a carotid artery dissection. Neurology. 1998;50:289-290.