At 38-weeks gestation a 31-year-old primigravida presented with diplopia on left gaze of 1- day duration. The diplopia was worse for far objects. She had unilateral throbbing headache similar to her previous migraines for 3 days prior to admission, associated with two to three episodes of vomitting per day, which were similar to her previous migraine attacks. There was no history of fever, photophobia or phonophobia.
She had an uneventful follow-up in antenatal clinic throughout the pregnancy. Her blood pressure was normal at the 13 week, 20 week and 33 week follow up visits. Her urinalysis was normal and she was not diabetic. There was no significant past medical or family history. She was non-smoker, non-alcoholic and there was no history of substance abuse. Preeclampsia was ruled out and she was referred to neurology with above history on the same day of admission.
On examination, she was alert and oriented. Her blood pressure was 106/65. There was complete paralysis of the left lateral rectus muscle. She had hyper-reflexia in all four limbs (Deep tendon reflexes were 3+). Rest of the neurologic examination was normal. MRI brain showed a non-enhancing, central, symmetrical, pontine T2 hyper-intensity which also showed evidence of restricted diffusion [Figure 1a and b] consistent with central pontine myelinolysis (CPM). The MRI of orbits, MR angiogram and MR venogram were unremarkable.
Blood investigations including full blood count, ESR, renal, liver and thyroid function tests, folate, Vitamin B12, calcium and phosphate were normal. Serial daily electrolytes did not reveal any derangement. Toxicology and autoimmune workup included were negative.
Lumbar puncture opening pressure was normal and CSF was unremarkable. (WBC = 0; Proteins = 0.24g/; Glucose normal; Gram stain, bacterial culture, fungal smear and culture, TB-PCR and TB-culture negative, oligoclonal bands negative).
Patient underwent Caesarean section. A healthy baby weighing 3180 g was delivered. Considering the diagnosis of CPM due to typical lesion, absence of obvious secondary cause and mild symptoms and signs, she was observed without any specific treatment. She gradually improved and the left eye abduction movement had recovered to about 50% at the time of discharge 4 days after the delivery. At 2-week follow-up after discharge, she was asymptomatic and her VI nerve palsy had fully recovered. A repeated MRI at this time showed complete resolution of the previous changes. [Figure 2]