Amaurosis Fugax Caused by Neurocysticercosis

Abstract

To The Editors: Neurocysticercosis (NCC) is the most common parasitic disease of the central nervous system caused by the larval stage of the pork tapeworm Taenia solium. We present here an unusual, interesting manifestation of NCC in a young boy as episodic, transient vision loss mimicking a transient ischemic attack. A previously healthy, 11-year-old boy presented with 2 episodes of acute-onset, bilateral, painless, loss of vision lasting for around 10 minutes each in the past 2 days. The episodes were followed by vomiting and gradual recovery of vision over the next few minutes. There was no associated headache, loss of postural tone, impairment of consciousness, tonic-clonic activity or focal deficits. There was no history of fever, head trauma, recurrent headaches, vertigo, dizziness or similar episodes in the past. There was a family history of epilepsy and intellectual disability in the paternal cousin. Detailed neurological and other system examination was unremarkable. Fundus examination showed normal disc and macula. A clinical diagnosis of amaurosis fugax was considered and the underlying etiologies suspected were transient ischemic attack and occipital epilepsy. Electroencephalogram showed persistent, arrhythmic, focal delta slowing over the right occipital area suggestive of an underlying structural pathology (Figure, Supplemental Digital Content, https://links.lww.com/INF/B780). Magnetic resonance imaging of the brain revealed right occipital ring-enhancing lesion with peri-lesional edema consistent with NCC (Fig. 1). Based on the clinico-radiological scenario, a presumptive diagnosis of NCC with symptomatic occipital epilepsy was considered and the child was started on antiepileptics (phenytoin 5 mg/kg/d) and oral prednisolone (2 mg/kg/d) followed by albendazole 15 mg/kg/d for 1 week. There was no recurrence of symptoms and the lesion disappeared after 6 months in repeat neuroimaging.FIGURE 1: Magnetic resonance imaging of the brain T2-weighted axial section showing right occipital neurocysticercosis with scolex (arrow) and peri-lesional edema (arrowhead).Vision loss in NCC can be multifactorial such as secondary optic atrophy due to hydrocephalus and papilloedema, optic nerve or chiasmal damage by inflammation and compression from adjacent cysts and retrochiasmal lesions including cortical blindness due to vasculitic cerebral infarction.1 The episode of transient blindness, however, reflects a transient dysfunction of visual cortex due to the cysticercal granuloma that triggered an occipital seizure with spread of seizure activity to both hemispheres, resulting in transient, bilateral blindness. This is termed ictal amaurosis and is a known manifestation of occipital lobe seizures. The cause of the occipital seizure may be a mass lesion (tumor, abscess, chronic granulomatous lesion, intracranial parasites, arteriovenous malformation) or idiopathic. Close clinical mimics are transient ischemic attacks due to thrombo-embolic phenomenon and idiopathic occipital epilepsy in children. Sometimes, the association of visual auras misleads the clinician to the possibility of migraine with aura till a neuroimaging reveals the cysticercal occipital granuloma.2 Transient cortical blindness in a 4-year-old boy with underlying NCC has been described.3 Being a treatable and preventable entity, it seems prudent to consider NCC in children from endemic regions who present with sudden onset neurological or cognitive disorders including unusual clinical manifestations such as amaurosis fugax. Additionally, neuroimaging is recommended in suspected cases of occipital epilepsies to rule out structural lesions such as NCC. Pratibha Singhi, MD, Arushi Gahlot Saini, MD Naveen Sankhyan, MD, DM Pediatric Neurology and Neurodevelopment Department of Pediatrics Postgraduate Institute of Medical Education and Research Chandigarh, India.