Horner Syndrome in Giant Cell Arteritis: Case Series and Review of the Literature

Background: Giant cell arteritis (GCA) is a systemic inflammatory vasculitis that affects medium- and large-sized arteries and can result in permanent vision loss. In rare instances, Horner syndrome has been noticed at the time of GCA diagnosis, although the mechanism of both diagnoses occurring at the same time is not entirely understood. We reviewed 53 charts of all patients diagnosed with biopsy-proven GCA in tertiary neuro-ophthalmology practice to find patients who presented with new onset of Horner syndrome at the time of GCA diagnosis. Methods: Two patients with biopsy-confirmed GCA who presented with concurrent Horner syndrome were found. Data on age, sex, and ophthalmic and neuroradiologic examination findings were collected. Results: Patient 1 was a 67-year-old man who presented with new onset of vertical binocular diplopia and was diagnosed with right fourth cranial nerve palsy. He then developed left ptosis and miosis, and was diagnosed with Horner syndrome by pharmacologic testing. He also had persistently elevated inflammatory markers. Patient 2 was a 71-year-old man who presented with new onset of binocular vertical diplopia, bitemporal headaches, and jaw ache. Both of his inflammatory markers were elevated. On examination, he had left ptosis and myosis, and small comitant left hypertropia. The diagnosis of left Horner syndrome was confirmed on pharmacologic testing and left hypertropia was attributed to skew deviation. Both patients underwent temporal artery biopsy, which confirmed the diagnosis of GCA. Treatment with high dose of oral corticosteroids commenced, and vertical diplopia has completely resolved in both patients. Horner syndrome persisted in Patient 1 and resolved in Patient 2. MRI and MR angiography of the brain and neck were unrevealing in both patients. Conclusions: This case series describes 2 patients with new diagnosis of GCA and concurrent Horner syndrome, with new diagnosis of likely nuclear/fascicular fourth nerve palsy in one patient and skew deviation in the other. In both patients, vasculitis presumptively affected vertebral arteries and their branches supplying the first-order sympathetic neurons in the brainstem. Considering the severe complication of permanent vision loss in GCA, this diagnosis should be considered in older patients presenting with concurrent new onset of Horner syndrome.

Original Contribution Section Editors: Clare Fraser, MD Susan Mollan, MD Horner Syndrome in Giant Cell Arteritis: Case Series and Review of the Literature Irina Sverdlichenko, BHSc, Cindy Lam, MD, Laura Donaldson, MD, PhD, Edward Margolin, MD Background: Giant cell arteritis (GCA) is a systemic inflammatory vasculitis that affects medium- and largesized arteries and can result in permanent vision loss. In rare instances, Horner syndrome has been noticed at the time of GCA diagnosis, although the mechanism of both diagnoses occurring at the same time is not entirely understood. We reviewed 53 charts of all patients diagnosed with biopsy-proven GCA in tertiary neuroophthalmology practice to find patients who presented with new onset of Horner syndrome at the time of GCA diagnosis. Methods: Two patients with biopsy-confirmed GCA who presented with concurrent Horner syndrome were found. Data on age, sex, and ophthalmic and neuroradiologic examination findings were collected. Results: Patient 1 was a 67-year-old man who presented with new onset of vertical binocular diplopia and was diagnosed with right fourth cranial nerve palsy. He then developed left ptosis and miosis, and was diagnosed with Horner syndrome by pharmacologic testing. He also had persistently elevated inflammatory markers. Patient 2 was a 71year-old man who presented with new onset of binocular vertical diplopia, bitemporal headaches, and jaw ache. Both of his inflammatory markers were elevated. On examination, he had left ptosis and myosis, and small comitant left hypertropia. The diagnosis of left Horner syndrome was confirmed on pharmacologic testing and left hypertropia was attributed to skew deviation. Both patients underwent temporal artery biopsy, which confirmed the diagnosis of GCA. Treatment with high dose of oral corticosteroids commenced, and vertical diplopia has completely resolved in both patients. Horner syndrome persisted in Patient 1 University of Toronto, Faculty of Medicine (IS), Toronto, Ontario, Canada; Department of Ophthalmology and Vision Sciences (CL, LD, EM), University of Toronto, Faculty of Medicine, Toronto, Ontario, Canada; and Department of Medicine (EM), Division of Neurology, University of Toronto, Faculty of Medicine, Toronto, Ontario, Canada. The authors report no conflicts of interest. Address correspondence to Edward Margolin, MD, FRCSC, Dipl. ABO Associate Professor, University of Toronto, Department of Ophthalmology and Visual Sciences, Department of Medicine, Division of Neurology Director, Neuro-Ophthalmology and Strabismus Fellowship, 801 Eglinton Avenue West, Suite 301, Toronto, Ontario M5N 1E3, Canada; E-mail: [e-mail] 340 and resolved in Patient 2. MRI and MR angiography of the brain and neck were unrevealing in both patients. Conclusions: This case series describes 2 patients with new diagnosis of GCA and concurrent Horner syndrome, with new diagnosis of likely nuclear/fascicular fourth nerve palsy in one patient and skew deviation in the other. In both patients, vasculitis presumptively affected vertebral arteries and their branches supplying the first-order sympathetic neurons in the brainstem. Considering the severe complication of permanent vision loss in GCA, this diagnosis should be considered in older patients presenting with concurrent new onset of Horner syndrome. Journal of Neuro-Ophthalmology 2022;42:340–345 doi: 10.1097/WNO.0000000000001593 © 2022 by North American Neuro-Ophthalmology Society G iant cell arteritis (GCA) or temporal arteritis (TA) is a systemic inflammatory vasculitis of medium- and large-sized arteries (1). It affects individuals older than age 50 years, and the incidence from population-based studies is estimated to be between 15 and 25 out of 100,000 persons per year (2). GCA is defined by a granulomatous panarteritis with mononuclear cell infiltrates and giant cell formation within the vessel wall (3). This histological characteristic confirms the diagnosis of GCA in biopsy specimens of the temporal artery. Although the superficial temporal branch of the carotid artery is particularly susceptible, arteries at any site can be affected (1). The most common manifestations of GCA include headaches, an abnormal temporal artery with temporal artery pulsation and pain, jaw claudication, scalp tenderness, and constitutional symptoms (2). The most feared complication of TA is arteritic anterior ischemic optic neuropathy, which results in permanent vision loss. As visual impairment is the most devastating symptom, treatment with high-dose corticosteroids needs to be initiated immediately. Although rare, patients with GCA have been reported to present with Horner syndrome (4–9). Horner syndrome results from the disruption of the ipsilateral sympathetic Sverdlichenko et al: J Neuro-Ophthalmol 2022; 42: 340-345 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution nerve supply of the eye and classically presents with unilateral partial ptosis and miosis (10). The oculosympathetic pathway is a three-neuron chain that originates in the hypothalamus and ends with the long ciliary nerves that supply the iris dilator and superior tarsal muscles. A patient with a lesion anywhere along this course can present with Horner syndrome. Given the potential serious complication of irreversible vision loss that may occur with GCA, it is important to recognize that Horner syndrome can be a presenting sign of GCA. Thus, the purpose of this study was to review patients from our practices who were eventually diagnosed with GCA who also had Horner syndrome at the time of GCA diagnosis, discuss the potential etiology of Horner syndrome in patients with GCA, and review available literature on this subject. METHODS This is a retrospective case series of patients with biopsyconfirmed GCA evaluated at tertiary neuro-ophthalmology practices affiliated with the University of Toronto who also received a new diagnosis of Horner syndrome at presentation. 53 charts of patients diagnosed with biopsyproven GCA were reviewed, 2 patients were identified who fulfilled inclusion criteria for the study, and clinical data on age, sex, and ophthalmic and neuroradiologic examination findings were collected. This study was approved by the University of Toronto Research Ethics Board and follows the tenets of the Declaration of Helsinki. RESULTS Case 1 A 67-year-old man was referred for neuro-ophthalmology consultation because of a four-month history of worsening vertical binocular diplopia. He denied headaches, scalp tenderness, jaw claudication, or other neurological symptoms. He had a medical history of polymyalgia rheumatica first diagnosed 7 years before, which was treated with steroids for 4 years. On examination, visual acuity was 20/ 20 in each eye, pupils were round and symmetric, and there was no relative afferent pupillary defect (RAPD). No nystagmus was noted, and extraocular motility was full. A small angle right hypertropia, which was worse on left gaze, right head tilt, and when looking up, was noticed and was attributed to decompensated congenital right fourth cranial nerve palsy. Four months after his initial assessment, the patient presented to an emergency department (ED) with recurrence of vertical diplopia and new mild left upper lid ptosis. He was suspected to have a third cranial nerve palsy; thus, computed tomography (CT) and CT angiography (CTA) of the brain and neck were performed and interpreted as normal. He was then seen by a neurologist, who suspected Sverdlichenko et al: J Neuro-Ophthalmol 2022; 42: 340-345 ocular myasthenia as a culprit for his symptoms and started him on pyridostigmine 30 mg 3 times daily. During a follow-up visit 1 month later, he was still experiencing vertical diplopia and had new onset of right tinnitus. Visual acuity was 20/30–1 in the right eye and 20/ 30 + 2 in the left eye (LE). On alignment testing, there was again right hypertropia, which fits the pattern for the fourth nerve palsy but he now also had left ptosis and slight anisocoria, with the left pupil being 0.5 mm smaller than the right with anisocoria more pronounced in the dark. Instillation of 0.5% apraclonidine resulted in reversal of anisocoria confirming the diagnosis of left Horner syndrome. Erythrocyte sedimentation rate (ESR) was 70 mm/hr and C-reactive protein (CRP) was 10 mg/L. As there was no obvious explanation for elevated inflammatory markers and the angiographic study of the neck was normal, a decision was made to proceed with temporal artery biopsy to rule out GCA. Surprisingly, it revealed active arteritis with disruption of the internal elastic lamina. Treatment with 60 mg of oral prednisone commenced and Mestinon was discontinued. Diplopia resolved several weeks after treatment with high-dose corticosteroids commenced, although the ptosis persisted. Subsequent MRI and MR angiography of the brain and neck to look for presence of vasculitis affecting the vessels supplying the brainstem revealed no evidence of carotid artery dissection and no obvious abnormalities in the vertebral arteries or any intracranial vessels. Case 2 A 71-year-old man was referred for neuro-ophthalmic consultation for 1-week history of acute onset of intermittent binocular vertical diplopia. He also endorsed 1-month history of neck pain and 2-week history of bitemporal headaches and jaw ache. His medical history was significant for hypertension. He had visited an ED twice in the past 2 weeks complaining of head and neck pain. CT head was interpreted as normal and ESR was 42 mm/hr. His jaw pain was attributed to temporomandibular joint inflammation. On examination, visual acuity was 20/20 in each eye, there was no RAPD, but his left pupil was 1 mm smaller than the right with anisocoria more pronounced in the dark. There was mild left nonfatigable upper lid ptosis. Orbicularis oculi strength was normal bilaterally. Extraocular motility was full and he had a flick (1–2 prism diopters) of comitant left hypertropia. Ophthalmoscopy was normal. Instillation of 0.5% apraclonidine led to reversal of the left ptosis and miosis, confirming the diagnosis of left Horner syndrome. ESR was 68 mm/hr, and CRP was 46 mg/L. CTA of the head and neck was normal. Treatment with 60 mg of oral prednisone for presumed diagnosis of GCA commenced. When seen the following day, both diplopia and headache completely resolved and jaw claudication improved. On examination, he still had all the features of left Horner syndrome but was now orthophoric on 341 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution TABLE 1. Overview of case reports on Horner Syndrome and GCA Study Title and Authors Presentation of GCA and Horner Syndrome “Horner syndrome and 77-year-old female with bitemporal ipsilateral abduction headaches, jaw deficit attributed to claudication, weight GCA.” Arunagiri et al loss, myalgia, and 2006 bilateral scalp tenderness Binocular horizontal diplopia and blurry vision Ptosis and miosis of the left eye Reduced abduction of left eye Temporal arterial pulsation absent and scalp tender, but no thickening or nodularity “Internuclear ophthalmoplegia and Horner’s syndrome due to presumed GCA” Askari et al 1993 342 An 84-year-old woman with headaches, dizziness, and flu-like illness Visual acuity was 6/18 in the right eye and 6/9 in the left eye She had right partial ptosis and right miosis There was internuclear ophthalmoplegia with impaired adduction of the right eye, some restriction of abduction in the left eye, and mild nystagmus in the abducting eye Tenderness on palpation of the right temporal scalp Investigations and Diagnosis Localization of Lesion Treatment and Follow-Up Horner syndrome Absence of brainstem, Patient was started on intravenous confirmed by instilling spinal cord signs, methylprednisolone 10% cocaine in both and normal brain 250 mg per day, and eyes MRI argued 80 mg oral prednisone ESR 57 mm/hr, CRP against a per day was initiated. 4.1 mg/L, and platelets preganglionic lesion. She was also started on 475 · 109/L The authors alendronate, calcium suspected MRI brain with contrast with vitamin D, and cavernous sinus was normal and MR ranitidine. Within a lesion because of angiography showed week of initiation of concurrent presence incidental small basilar treatment, she had of Horner syndrome tip aneurysm resolution of diplopia, and ipsilateral Temporal biopsy on left headaches, and abduction deficit. side was consistent temporal pain. Ptosis They believed with GCA and pupillary granulomatous Diagnosis of GCA with abnormality remained inflammation of the concurrent Horner unchanged. Prednisone internal carotid syndrome and left was tapered slowly over artery might have lateral rectus paresis 18 months affected the was made sympathetic fibers as well as the sixth cranial nerve ESR 105 mm/hr, The authors believed it The patient was started on leukocytes 11.1 · 109/ prednisolone and within was involvement of 6 days of initiating the right medial L, and platelets 475 · treatment, headaches longitudinal 109/L improved. In the fasciculus with the CT scan reported atrophic following 2 months, the sympathetic fibers changes in the cerebral patient maintained her that caused Horner hemispheres, and an progress with no syndrome old infarct in the left change in neurological temporal lobe signs Diagnosis of GCA and Horner syndrome was made Sverdlichenko et al: J Neuro-Ophthalmol 2022; 42: 340-345 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution (Continued ) Study Title and Authors Presentation of GCA and Horner Syndrome Investigations and Diagnosis Localization of Lesion Treatment and Follow-Up The patient started on Hemoglobin 11.9 g/dL, Preganglionic prednisone 60 mg after leukocytes 8 · 109/L involvement and presumed diagnosis of presence of Temporal artery biopsy GCA, and this was nystagmus localized showed cellular followed by 15 mg 4 the lesion to the infiltration with giant times daily. Horner brainstem. It was cells and fragmentation syndrome did not believed to be due to of internal elastic resolve over the year brainstem infarct lamina the patient was taking 10% cocaine to the right systemic steroids eye produced sluggish dilation, confirming diagnosis of Horner syndrome 2% hydroxyamphetamine drops to the right eye produced pupil dilation, indicating preganglionic lesion Instillation of 1% “Horner’s syndrome in A 67-year-old woman The authors diagnosed Prednisone therapy was hydroxyamphetamine with headache, TA” Bromfield and initiated at 60 mg oral TA associated with failed to dilate the right ptosis, and miosis of Slakter 1988 daily. The headache postganglionic Horner pupil the right eye resolved within 2 days syndrome. As the Hemoglobin 1.37 g/L, Superficial temporal and ESR rate declined patient did not leukocytes 11.5 · 109/ arteries were to 30 mm/hr within a endorse sweat nontender with week changes, the authors L and ESR 70 mm/hr diminished pulses believed the lesion Carotid studies showed was distal to the mild disease at left carotid bifurcation, bifurcation where sudomotor Right temporal biopsy fibers separate from revealed thickened pupillodilator and artery with narrowed tarsus innervators to lumen follow the external Microscopic section carotid system showed granulomatous infiltration The patient was treated Because of the An 84-year-old man with Test with cocaine 10% “Horner’s syndrome with 60 mg prednisone dilatation provoked failed to dilate the left periorbital pain, due o GCA” Pascualdaily, and the general by 1% phenylephrine pupil fatigue, and jaw Sedano and Roig condition, orbital pain, and spared Phenylephrine 1% in both claudication 1998 and jaw claudication ipsilateral sweating eyes produced left He had left eye ptosis improved, whereas left on the face, this dilatation and miosis Horner syndrome indicated Horner ESR 22 m/hr, hemoglobin Temporal arteries had persisted syndrome with 137 g/L feeble pulses postganglionic CT and MRI cerebral involvement. Jaw scans showed mild claudication in the ventricular dilatation patient suggested with significant arteritic involvement attenuation of the of the facial artery periventricular white matter Angio-MRI of carotid circulation was normal The results of left temporal artery biopsy was consistent with GCA An 81-year-old man with A case of giant-cell history of headaches, arteritis and malaise, scalp Horner’s syndrome” tenderness, and jaw Bell, et al 1980 pain Visual acuity light perception in the right eye, and 6/9 in the left eye Right ptosis and miosis, and swollen right optic disc Palpable, nontender temporal arteries and horizontal jerky nystagmus on lateral gaze Sverdlichenko et al: J Neuro-Ophthalmol 2022; 42: 340-345 343 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution (Continued ) Study Title and Authors “Horner’s syndrome associated with GCA” Shah et al 2007 Presentation of GCA and Horner Syndrome Investigations and Diagnosis Treatment and Follow-Up The authors postulated The patient was started on ESR 9 mm/hr initially; A 67-year-old man with oral prednisolone that the site of the after repeat testing, it headaches, (60 mg), and lesion was small was 44 mm/hr and CRP confusion, weight headaches resolved caliber extracranial 65 mg/L loss, and anergia within 7 days of branches of the On pharmacological The patient later treatment. The ptosis internal carotid testing, the right pupil developed mild ptosis and miosis were still artery that are failed to dilate with 4% and miotic pupil on present 3 weeks later involved with the cocaine and 1% the right side sympathetic carotid hydroxyamphetamine Visual acuity was 6/4 plexus. The GCA was confirmed by bilaterally branches were likely temporal artery biopsy Superficial temporal occluded as they arteries were passed through the thickened but affected wall of the nontender, with carotid artery diminished pulses bilaterally alignment testing. Temporal artery biopsy showed disruption of the internal elastic lamina by infiltrating inflammatory cells and arteritis. MRI and MR angiography of the brain and neck were both normal, demonstrating normal caliber of the vertebral arteries and normal intracranial vasculature. After 3 days of treatment with oral steroids, anisocoria and left upper lid ptosis both resolved. DISCUSSION In this case series, we describe 2 patients diagnosed with GCA who received a concurrent diagnosis of new onset Horner syndrome. Patient 1 also likely had fourth nerve palsy contralateral to the side of the Horner syndrome, suggesting involvement of the sympathetic chain where it runs in close proximity to the fourth cranial nerve nucleus and fascicle in the dorsocaudal midbrain. Patient 2 had a very small comitant ipsilateral hyperdeviation, which likely indicated involvement of the vestibulo-ocular pathway as well as the central oculosympathetic pathway in the brainstem by the vasculitis. Although rare, Horner syndrome has previously been documented in association with GCA (Table 1). Arunagiri et al (5) described a 77-year-old woman with headaches, jaw claudication, scalp tenderness, and weight loss. She also had binocular horizontal diplopia, upper lid ptosis, anisocoria, and ipsilateral abduction deficit. The patient was eventually diagnosed with GCA and concurrent Horner syndrome. A preganglionic lesion was presumed unlikely because of the absence of brainstem and spinal cord signs and a normal brain MRI. The authors suspected a cavernous sinus lesion and thought that granulomatous inflammation affected postganglionic sympathetic fibers and the sixth cranial nerve 344 Localization of Lesion causing concurrent abduction deficit. However, no abnormalities in the area of the cavernous sinus were seen on neuroimaging. Another case was described by Bell et al (4), who reported an 81-year-old patient with preganglionic Horner syndrome and jerky nystagmus associated with GCA. They hypothesized that both the Horner syndrome and nystagmus localized the lesion to the brainstem, and brainstem stroke was hypothesized to have been the cause, although no modern neuroimaging was available at the time of the report. Askari et al (6) reported a patient with what they interpreted as internuclear ophthalmoplegia and Horner syndrome resulting from GCA; however, again, no modern neuroimaging was available to test their hypothesis. Similar case reports have also described patients presenting with postganglionic Horner syndrome and GCA where granulomatous inflammation involving the sympathetic chain was deemed to be the likely culprit; however, none of these papers reported results of neuroimaging (7–9). We hypothesize that in both of our patients, the firstorder sympathetic neurons that originate in the hypothalamus and then travel through the brainstem and spinal cord to synapse in the lower cervical/upper thoracic spinal cord were involved by the vasculitis (10). In case 1, the lesion may have been localized to the dorsal caudal midbrain, as suggested by the presence of presumed nuclear/fascicular fourth nerve palsy. In case 2, we believe first-order sympathetic neurons were affected as well, given the concomitant presence of what was likely a skew deviation. We postulate the GCA affected the small perforator branches of the vertebral arteries supplying the dorsocaudal midbrain and this was beyond the detection of MR angiography. Although GCA predominantly affects Sverdlichenko et al: J Neuro-Ophthalmol 2022; 42: 340-345 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Original Contribution extracranial branches of the internal carotid artery, any artery in the body can be affected and inflammatory infiltrates of lymphocytes and giant cells in GCA producing a gradual occlusion of branches of the vertebral arteries has been described in the past (9). This may subsequently result in ischemia of the sympathetic chain as it passes through the midbrain. A similar mechanism has been described by Shah et al (8), who postulated that postganglionic Horner syndrome in their patient may have resulted from ischemic damage to the sympathetic nerve fibers because of vasculitis affecting vasa nervorum arising from the branches of the internal carotid artery. Another mechanism that has been described to explain the relationship of Horner syndrome and GCA includes direct granulomatous injury of the sympathetic fibers by the vasculitis process (9). In summary, we described 2 patients who presented with Horner syndrome and were later diagnosed with biopsyconfirmed GCA. The most likely culprit was ischemia of the first-order neurons of the sympathetic chain because of vasculitis affecting the vertebral arteries and their branches supplying the brainstem. As the most feared complication of GCA is irreversible vision loss and the need for treatment with corticosteroids is immediate, the diagnosis of GCA should be considered in all older patients presenting with the new onset of Horner syndrome. Thus, in addition to the neuroradiological evaluation of the entire sympathetic chain, we recommend reviewing the history for symptoms of GCA and checking inflammatory markers in all patients older than age 50 years who present with the new onset of Horner syndrome. Sverdlichenko et al: J Neuro-Ophthalmol 2022; 42: 340-345 STATEMENT OF AUTHORSHIP Conception and design: L. Donaldson, C. Lam, I. Sverdlichenko, and E. Margolin. Acquisition of data: L. Donaldson, C. Lam, and E. Margolin. Analysis and interpretation of data: L. Donaldson, C. Lam, I. Sverdlichenko, and E. Margolin. Drafting the manuscript: L. Donaldson, C. Lam, I. Sverdlichenko, and E. Margolin. Revising the manuscript for intellectual content: L. Donaldson, C. Lam, I. 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