A 36-year-old female with diabetes mellitus, hypertension, and hypothyroidism underwent a cesarean section a few weeks prior to admission and a gastric sleeve procedure 1 year before that.
Two days before admission to hospital, the patient developed ascending numbness followed by weakness, which progressed over 2 days. It interfered with her movement, making her bed bound. She reported a 1-day history of subjective fever and diarrhea a week before the onset of symptoms, which subsided spontaneously. Weakness was not associated with double vision, shortness of breath, slurred speech, abnormal movement, or confusion. She did not have fever, diarrhea, or abdominal pain and did not have similar attacks previously.
She lost approximately 40 kg in 2 months; she did not receive any vitamin supplementation after surgery. The patient reported vomiting three to four times daily postoperatively until a month before her presentation.
Examination showed that the cranial nerves were intact with no motor or sensory abnormalities. Her UL and LL tone was normal. There was a symmetrical decrease in power in her ULs both proximally and distally. LL power was also decreased. Her reflexes were diminished but elicitable, but her plantar response was mute with various maneuvers. The sensory examination was unremarkable and her coordination was intact.
The patient was admitted to hospital as a case of postbariatric surgery myeloneuropathy or GBS. IVIG was given for a complete course of five continuous days. Thiamine loading and maintenance were given parentally. Vitamin B12 and D levels were within normal limits. She was discharged with persistent weakness to undergo rehabilitation. No MRI or NCS was done at admission.
She presented again with the same concern and was admitted to neurology inpatient services. An MRI scan of the entire spine was performed, which showed early dorsal spine spondylitic changes with small anterior osteophytes at the lower dorsal spine. An EMG/NCS was also done, showing pure motor neuropathy and myopathic changes at proximal muscle and a normal sensory picture, suggestive of acute motor axonal neuropathy for early Guillain-Barre syndrome.
She continued to receive vitamin supplementation and physiotherapy. Plasma exchange was discussed but declined by the family. She will require ongoing extensive neurorehabilitation at a dedicated center at King Faisal Specialist Hospital and Research Centre or King Fahad Medical City in Riyadh.