Ocular manifestations of internal carotid artery dissection

An Internal Carotid Artery Dissection Masquerading as Optic Neuritis: A Case Report

“…The headache being the most common of the ICAD triad has also been shown to respond well to analgesics like sumatriptan [ 11 ] thereby making it even harder to diagnose. The monocular drop in visual acuity from ICAD can range from transient to permanent and results from ischaemic optic neuropathy (ION), central retinal artery occlusion (CRAO)/branch retinal artery occlusion (BRAO), or ophthalmic artery occlusion (OIS) [ 12 ].…”

“…The site of ischaemic damage is used in the classification of ION as fundoscopic examination helps to delineate the site involved - anterior ischaemic optic neuropathy (AION) if the initial fundic examination shows disc oedema, and posterior (retrobulbar) ischaemic optic neuropathy (PION) if there is no initial disc oedema but subsequent examination exhibits optic disc atrophy [ 14 ]. Giant cell arthritis and nonarterial ION make up 90% of the causes of ION while only 4% of ION occurs due to ICAD [ 12 , 15 ]. CRAO/BRAO can result from an occlusion or decrease in perfusion of the central retinal artery.…”

Central retinal artery occlusion secondary to presumed traumatic carotid artery dissection in a healthy child

“…Vertebral and Internal carotid arteries are critical cervical arteries. Any injury that may eventually occur to these vascular structures can lead to vessel thrombosis and dissection, leading to complications such as cerebral ischemia, stroke, blindness, or death [ 1 ].…”

Central retinal artery occlusion and internal carotid artery dissection after COVID-19 nasopharyngeal swab testing

“…Transient monocular visual loss has been reported in 6% to 38%. Less frequent ocular manifestations are oculomotor nerve palsy and permanent visual loss secondary to ischemic optic neuropathy, CRAO or ocular ischemic syndrome [4] , [5] . CRAO is a rare complication of ICAD and its pathophysiologic mechanism is believed to be from haemodynamic compromise with ocular hypoperfusion or, less frequently, secondary to thromboembolic phenomena originated from the dissected area [6] .…”

“…CRAO is a rare complication of ICAD and its pathophysiologic mechanism is believed to be from haemodynamic compromise with ocular hypoperfusion or, less frequently, secondary to thromboembolic phenomena originated from the dissected area [6] . CRAO due to ICAD is usually associated with other ophthalmologic or neurologic manifestations and cervical or facial pain [5] . There are few cases with an isolated CRAO secondary to ICAD reported to date as is the case of our patient [3] , [6] , [7] .…”