Case Reports

A Spontaneous Internal Carotid Artery Dissection Presenting With Headache and Miosis

A 56-year-old man presented for evaluation of right-sided headache and pain behind his right eye.

Emergency Medicine. 2016 July;48(7):300-304 | 10.12788/emed.2016.0035

Author(s):

Sandra Deane, MD

Michael A. Gil, PA-C

Francis L. Counselman, MD

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References

1. CADISS trial investigators, Markus HS, Hayter E, et al. Antiplatelet treatment compared with anticoagulation treatment for cervical artery dissection (CADISS): a randomised trial. Lancet Neurol. 2015;14(4):361-367.

2. Thanvi B, Munshi SK, Dawson SL, Robinson TG. Carotid and vertebral artery dissection syndromes. Postgrad Med J. 2005;81(956):383-388.

3. Lucas C, Moulin T, Deplanque D, Tatu L, Chavot D. Stroke patterns of internal carotid artery dissection in 40 patients. Stroke. 1998;29(12):2646-2648.

4. Schievink WI, Mokri B, O’Fallon WM. Recurrent spontaneous cervical-artery dissection. N Engl J Med. 1994;330(6):393-397.

5. Biousse V, D’Anglejan-Chatillon J, Touboul PJ, Amarenco P, Bousser MG. Time course of symptoms in extracranial carotid artery dissections. A series of 80 patients. Stroke. 1995;26(2):235-239.

6. Kasravi N, Leung A, Silver I, Burneo JG. Dissection of the internal carotid artery causing Horner syndrome and palsy of cranial nerve XII. CMAJ. 2010;182(9):E373-E377.

1. Borgman CJ. Horner syndrome secondary to internal carotid artery dissection after a short-distance endurance run: a case study and review. J Optom. 2012;5:209-216.

2. Mohler ER III, Fairman RM. Management of symptomatic carotid atherosclerotic disease. UpToDate Web site. http://www.uptodate.com/contents/management-of-symptomatic-carotid-atherosclerotic-disease. Updated February 24, 2016. Accessed May 6, 2016.

3. Mann J. Anisocoria guidemap. Life in the Fastlane Web site. http://lifeinthefastlane.com/resources/jeff-manns-em-guidemaps/anisocoria-guidemap/. Accessed March 15, 2016.

10. Kedar S, Biousse V, Newman NJ. Horner syndrome. UpToDate Web site. http://www.uptodate.com/contents/horner-syndrome. Updated July 14, 2015. Accessed May 6, 2016.

11. Vertinsky AT, Schwartz NE, Fischbein NJ, Rosenberg J, Albers GW, Zaharchuk G. Comparison of multidetector CT angiography and MR imaging of cervical artery dissection. AJNR Am J Neuroradiol. 2008;29(9):1753-1760.

12. Pham MH, Rahme RJ, Arnaout O, et al. Endovascular stenting of extracranial carotid and vertebral artery dissections: a systematic review of the literature. Neurosurgery. 2011;68(4):856-866.

13. Caplan LR. Dissections of brain-supplying arteries. Nat Clin Pract Neurol. 2008;4(1):34-42.

14. Schievink WI. Spontaneous dissection of the carotid and vertebral arteries. N Engl J Med. 2001;344(12):898-906.

Internal carotid artery dissection (ICAD) is an uncommon cause of stroke that typically occurs in the setting of (often minor) trauma but can also occur spontaneously. Patients with ICAD typically present with ipsilateral head, face, or neck pain. In approximately half of ICAD cases, an acute partial, painful Horner syndrome is present on examination. Although computed tomography angiography (CTA) is currently the imaging study of choice, magnetic resonance imaging/magnetic resonance angiography (MRI/MRA) and Doppler ultrasound can also be used. Management options include thrombolysis, antiplatelet or anticoagulation therapy, and endovascular or surgical intervention.

Case

A 56-year-old man with a history of migraines presented to the ED with a chief complaint of a 4-day history of right-sided headache. He stated that the pain felt different from his usual migraines and was located behind his right eye. Prior to presentation at the ED, the patient had initially visited an urgent care facility for evaluation. The physician who evaluated the patient at the urgent care facility noted the patient’s left eye appeared dilated and referred him to the ED for evaluation.

The patient further stated that the day prior to presentation, one of his friends had also remarked that the patient’s left eye appeared to be enlarged. The patient denied any visual disturbances, focal weakness, nausea, vomiting, neck pain, or stiffness. His medical history was significant for paroxysmal atrial flutter and hypertension. Regarding medications, the patient was taking dronedarone, clonazepam, omeprazole, and metoprolol.

On physical examination, the patient’s vital signs were: blood pressure, 162/109 mm Hg; heart rate, 85 beats/minute and regular; respiratory rate, 18 breaths/minute; and temperature, 98.6°F. Oxygen saturation was 98% on room air. The patient appeared to be in no acute distress. Ocular examination revealed a dilated left pupil of approximately 5 to 6 mm, and a right pupil measuring approximately 3 mm. Both pupils reacted to light, and the extraocular muscles were intact. The patient’s face appeared symmetrical and had intact sensation. He had normal speech, midline tongue, and good bilateral shoulder shrug. The neck examination revealed normal range of motion with full flexion, without jugular vein distention, lymphadenopathy, or palpable thyroid. The cardiovascular, lung, and abdominal examinations were all normal. The neurological examination showed the patient to be awake, alert, and oriented to person, place, and time. He exhibited 5/5 motor strength in all four extremities, normal gait, and normal finger-to-nose performance; his reflexes were 2+ and symmetrical.

The emergency physician (EP) ordered a stat noncontrast CT scan of the head, complete blood count (CBC), and basic metabolic panel (BMP). The CT scan of the head was interpreted by the radiologist as “no acute intracranial abnormality,” and the CBC and the BMP were normal. Since the EP was concerned about a carotid artery aneurysm or dissection, he ordered a CTA of the head and neck (Figures 1 and 2). The CTA was read as:

Long segment dissection of postbulbar cervical segment of right internal carotid artery, very likely extending into the intracranial segment with critical stenosis at the junction of the high cervical segment and proximal petrous segment. Preserved runoff circulation to the anterior and middle cerebral arteries with robust capacity for collateral support in the context of patent anterior and posterior communicating arteries.

Based on the radiology report, the EP consulted with vascular surgery services, and ordered a Doppler study of the ICAs. The Doppler study demonstrated “arterial thrombus in the right distal extracranial internal carotid artery with hemodynamics suggestive of a distal occlusion/significant obstruction.” The patient was started on an intravenous (IV) heparin drip and admitted to the hospital. Three days later he experienced sudden onset of left arm weakness. An emergent CTA of the head and neck revealed an embolic occlusion of mid-to-distal M1 segment of the right middle cerebral artery. The patient was immediately evaluated by interventional radiology for possible clot removal; however, based on his rapid neurological improvement, he was instead treated medically with aspirin and clopidogrel and continued to show significant neurological improvement. He was discharged home on hospital day 8 on both antiplatelet agents with minimal neurological deficit.

Discussion

Even though ICAD accounts for only 1% to 2% of all strokes, it is responsible for 10% to 25% of strokes in young and middle-aged adults.^1-3 The peak incidence for ICAD is in the fifth decade, and it affects men and women equally.⁴ The extracranial portion of the ICA is the most commonly affected vessel (>90%); dissections of the intracranial portion are associated with greater neurological deficits and have a poorer prognosis.^2,5 Cerebral ischemia resulting from a dissection of the extracranial ICA may occur days to weeks after the onset of local symptoms such as head or neck pain, Horner syndrome, or tinnitus.⁵