We present a case of a 14-year-old African boy from Nigeria who presented to the hospital with symptoms of throbbing headaches, vomiting, fever (40.0°C), slurred speech, seizures, hemiparesis, bilateral vision loss, suprapubic pain, and confusion. The symptoms had began 3 days before the hospital visit. The patient’s parents thought the symptoms were of malaria and started him on an antimalarial drug (hydroxychloroquine) and Tylenol for the pain. However, when the patient’s symptoms failed to improve and he complained of not being able to see, he was brought to the hospital for treatment.
Neurological examination upon arrival revealed bilateral vision loss and hemiplegia in the left part of both upper and lower extremities, with loss of sensation. The patient also complained of suprapubic discomfort and had urinary retention which raised a suspicion of a possible urinary tract infection. His immunizations were all up to date, and he had no family history of neurological diseases.
During the physical examination, he was febrile (40.0°C), confused, and oriented only to his name. He had a seizure episode that was relieved with phenytoin. His body mass index was normal (21 kg/m2). Ophthalmological examination revealed normal pupillary light reflexes and no obvious cause of vision loss.
Several diagnostic tests were performed, including blood culture, urinalysis, and cerebrospinal fluid analysis [Table-1]. Serology (enzyme-linked immunoelectrotransfer blot) of blood for cysticercosis antibodies to glycoprotein antigens was positive, suggesting cysticercosis. Head computed tomography (CT) scan showed local soft tissue inflammation due to cyst degeneration [Fig. 1), scolexes in the cerebral cortex, and multiple cysticercus granulomas in the cerebral cortex(Fig. 2). Brain magnetic resonance angiography (MRA) showed a wedge-shaped T1-Weighted hypointense and T2-Weighted hyperintense lesion in the body of the right caudate nucleus. Diffusion of contrast was restricted on diffusion-weighted imaging. The lesion measured 2.3 cm in diameter and was suggestive of an acute/subacute infarct. Multiple T1W hypointense areas with T2W and FLAIR hyperintense areas were seen in the subcortical regions of both the temporal and parietal lobes (Fig. 3). There was no restriction of contrast diffusion on DW1, suggesting white matter changes. A final diagnosis of cysticercal encephalitis with cortical blindness was made.
Management of the patient began with bladder catheterization, which drained 200 ml of cloudy urine and relieved the suprapubic discomfort. Urinalysis showed bacteriuria, and IV levofloxacin 250 mg was administered every 24 h for 3 days. A slow IV infusion of 15 mg/kg phenytoin was also administered to control the seizures. A glucocorticoid (IV methylprednisolone 20 mg every 6 h) was administered at a lower pressure in the brain. An antihelminth drug (oral albendazole 400 mg BID) was also added to the treatment regimen. The patient’s symptoms improved over the course of five days of in-hospital stay. A prescription of oral albendazole at the same dosage was administered to the patient for 10 additional days upon discharge from the hospital.
A repeat brain CT with contrast was performed 3 months after discharge from the hospital, and it showed complete resolution of the lesions [Fig-4]. There was also no further recurrence of the symptoms at the 1-year follow-up visit, and no neurological abnormality was noted during clinical examination of the patient, except for bilateral blindness.