A 31-year-old Indian male, not a known case of any medical condition, presented to the emergency department with a 3-day history of sudden onset diplopia and right sided frontal headache.
The headache was constant over the right frontal and retroorbital area, radiating to the nasal side of the right eye, throbbing in nature, not aggravated with light or sound and not associated with any redness or lacrimation. No history of fever, neck stiffness, photophobia, phonophobia, pulsatile tinnitus, seizures, nausea and vomiting. The horizontal diplopia was more prominent upon right lateral gaze and resolved on covering one eye (Binocular diplopia). Left lateral vision was unaffected. No pain on eye movement. Both the headache and horizontal diplopia began simultaneously for the first time.
Patient denied any recent history of travel, viral illness and head injury. There was no similar history of headaches or attacks in the family. Review of systemic and rheumatological systems was insignificant.
Physical examination was significant only for right lateral rectus palsy and left sided horizontal nystagmus. Pupils were equal, round, reactive to light and accommodating. No proptosis, ptosis or facial numbness present. No papilledema appreciated on fundoscopy. Visual acuity, other cranial nerves and upper and lower motor neuron examinations were normal (Fig. 1).
On investigation, full blood count displayed raised WBC’s (13.7 × 109/L) with a left sided neutrophil shift (80.4%), normal lymphocytic count (13.2%), normal hemoglobin (149 g/L) and normal platelets level (246). No elevated inflammatory markers (CRP 0.2 mg/L; ESR 3). Creatinine kinase levels were 742 U/L (normal 35–232). Normal blood glucose levels (5.4 mmol/L). Rheumatological screening showed normal ANA, rheumatoid factor and complement levels. Infectious work up including Lyme and syphilis serologies and CSF analysis were not performed, because patient was not sexually active and no other neurological signs were present.
Pre and post contrast CT brain displayed a very small (5 × 6 mm) well-defined rounded peripherally hyperdense isolated lesion in the right frontal region, with central hypodensity. Lesion was suggestive of neurocysticercosis. No surrounding edema, post contrast enhancement, brain parenchymal lesion or evidence of acute cerebrovascular insult (CVA) visualized. Para nasal sinuses appeared unremarkable. MRI and MRV requested to investigate for potential causes of abducens nerve palsy, corresponded to the same area of calcification seen on the previous CT scan, which was thought to be a calcified granuloma, possibly calcified stage of neurocysticercosis. No new abnormalities or lesions and no evidence of cavernous sinus thrombosis or inflammation were discovered.
Due to the young age of our patient and sudden presentation of the headache and ipsilateral abducens nerve palsy, our differentials revolved around space occupying pathologies compressing the sixth nerve, pseudotumor cerebri, inflammatory or infectious lesions. However, physicals were not suggestive of raised intracranial pressure (normal fundoscopy), labs were normal and brain imaging did not reveal any intracranial pathology apart from the incidental neurocysticercosis located in the right frontal lobe but regardless of the discovery, it does not explain the sixth nerve palsy as it is too small in size to be compressing the nerve and they are also not anatomically related. Hence, we labelled the patient as a case of idiopathic right abducens nerve palsy secondary to an undetermined cause.
Patient was commenced on a 5-day course of Albendazole 400 mg and IV Dexamethasone 8 mg for presumed inflammatory causes. Dexamethasone was gradually tapered and patient was discharged on oral dexamethasone 4 mg (once/day) for 5 days. The headache had resolved during hospital admission but the palsy persisted on discharge.
