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. The presenting symptoms and signs of ICA dissection (ICAD) are variable and can be due to direct local involvement of neural structures (e.g., oculosympathetic plexus causing the ipsilateral Horner syndrome) or indirect distal ischemia to brain or eye (e.g., transient ischemic attack or stroke) from thromboembolic disease
. A distortion of the sense of taste (i.e., dysgeusia) in ICAD, however, is not as widely known as presenting symptoms especially among ophthalmologists. We present a case of TMVL associated with dysgeusia and describe the clinical presentation, localizing topographic anatomy, pathogenesis, and significance of dysgeusia to ophthalmologists evaluating patients with possible ICAD.
A 55-year-old white man presented with 2 episodes of TMVL of the left eye (OS) over 2 weeks associated with a “bitter taste in his mouth.” He had been dining in a restaurant with his wife and complained to the restaurant manager about the taste of the food. He was seen at an outside clinic for eye pain and headache, which was diagnosed as “sinusitis” and treated with antibiotics. His medical history was significant for hypertension and hyperlipidemia. He had prior spine surgery for degenerative disc disease. He had no ocular history or allergies. His family history was noncontributory. His medications were amlodipine, vitamin C, CoQ10, losartan, and rosuvastatin.
His vision was 20/20 in both eyes. There was no temporal artery nodularity or tenderness. Pupils were briskly reactive bilaterally with neither anisocoria nor relative afferent pupillary defect. Anterior segment and fundus examinations were normal. The patient had resolution of his TMVL but persistent dysgeusia.
The patient was admitted to the stroke team at Houston Methodist Hospital. Noncontrast computed tomography (CT) of head was normal. Magnetic resonance imaging of the head was normal, including diffusion-weighted imaging. Electrocardiogram and cardiac echocardiogram were normal. Routine laboratory studies were normal, including complete blood count. Serum erythrocyte sedimentation rate was 12 mm/hr and C-reactive protein measured 0.65 mg/dL.
Contrast CT angiogram (CTA) of the head and neck showed a dissection of the distal cervical and proximal petrous portions of the left ICA (Fig. 1A–C). The patient was started on intravenous heparin. He had initially been on corticosteroids, which were discontinued. A digital subtraction catheter arteriogram showed a small intraluminal thrombus distal to the petrous left ICAD, but no other hemodynamic insufficiency was seen in the intracranial circulation. The patient was transitioned from heparin to apixaban (Eliquis) before discharge. The patient returned for follow-up 3 months later and had a normal eye examination and complete resolution of his dysgeusia and TMVL episodes.
Patients with TMVL should undergo timely evaluation for embolic or nonembolic etiologies of ischemia. In older patients, evaluation and testing for giant cell arteritis is recommended (e.g., serum erythrocyte sedimentation rate and C-reactive protein, temporal artery biopsy). All patients with ischemic TMVL should undergo a full stroke work-up, including neuroimaging (e.g., acute noncontrast CT of the brain followed by magnetic resonance imaging including diffusion-weighted imaging of the brain. Vascular imaging (e.g., CT or MR angiography) of the head and neck is recommended to evaluate for vascular etiologies, including carotid dissection. In addition, echocardiogram, electrocardiogram, and a carotid Doppler are generally indicated. Older age (more than 65 years), higher blood pressure, longer duration of symptoms, and the presence of comorbidities like diabetes raise the risk of a subsequent stroke in the next 2–7 days
and are typically cervical in location. Greater than 90% of ICADs arise within 2 cm cranial to the carotid bifurcation in the cervical section (C2) of the ICA, and approximately half of these extend into the petrous portion of the ICA (C3)
The presenting symptoms of ICAD include direct local effects (e.g., neck pain, Horner syndrome) and indirect distal effects, which are ischemic thromboembolic or hypoperfusion in nature. The most common ischemic symptoms in ICAD are hemispheric transient ischemic attacks, hemispheric cerebral infarction, and TMVL (i.e., amaurosis fugax)
. Head or facial pain (specifically in the orbital region) or ipsilateral eye pain (as seen in our case) can occur even though the ICAD is located in the neck. This referred pain results from the general visceral afferent (GVA) pain carried on the vagus being perceived by the general somatic afferent (GSA) of the trigeminal nerve nucleus in the brainstem
. This type of referred pain is similar to the false localizing left arm pain (GSA) in myocardial infarction (GVA) or the referred visceral pain of appendicitis or kidney stones (GVA) in the back or abdomen (GSA).
ICAD can also produce lower cranial nerve palsies, specifically cranial nerves IX, X, XI, and XII
Ophthalmologists should be aware of the interesting combination of symptoms of TMVL and dysgeusia in ipsilateral ICAD. This is especially important in patients with TMVL who often have completely normal eye examinations. Patients with an ICAD may present to ophthalmology with symptoms and signs of direct compression (Horner syndrome) or indirect distal thromboembolic/hypoperfusion events (transient ischemic attacks/TMVL). Although the combination of Horner syndrome and TMVL is a well-known constellation for ipsilateral ICAD, the combination of TMVL and dysgeusia is also a highly suggestive symptom complex for ICAD of the petrous ICA even without the Horner syndrome.
The authors have no proprietary or commercial interest in any materials discussed in this article.