Abstract

Thiamine (vitamin B1) deficiency can occur secondary to malnutrition, which is associated with multiple etiologies, from imbalanced dietary habits to significant gastrointestinal nutritional losses such as recurrent vomiting or diarrhea. Thiamine deficiency can manifest as dry or wet Beriberi, Wernicke encephalopathy, or Korsakoff syndrome.
We present a case of a 26-year-old female who presented to the emergency department with bilateral lower limb weakness of five-day duration. It was associated with peripheral vision loss, inability to maintain eye contact, and altered mental status.  She is a known case of morbid obesity post-laparoscopic sleeve gastrectomy on 21st of August 2024, and multiple hospital admissions post-laparoscopic sleeve gastrectomy due to recurrent nausea and vomiting, poor oral intake, and abdominal pain. Her vitals were within the normal limits. Neurological examination revealed Glasgow coma scale of 15/15 with altered mental state, power of 4+/5 in all upper limb muscle groups, and lower limb power of 3/5 proximally and 4-/5 distally. She had brisk deep tendon reflexes in both upper limbs, absent reflexes and downgoing plantar reflexes in both lower limbs. She had normal sensory assessment and normal extraocular movements. Slit lamp exam revealed abnormal bilateral ocular movements.
Lumbar puncture was done for her. Cerebrospinal fluid (CSF) analysis results were only significant for elevated CSF proteins (54 mg/dL; normal 15045 mg/dL) with no white blood cells seen. CSF meningitis and encephalitis panels, oligoclonal bands, aquaporin-4 antibodies (neuromyelitis optica or NMO-IgG), myelin oligodendrocyte glycoprotein (MOG) antibodies, and angiotensin-converting enzyme levels were all negative. Blood tests were significant for abnormally low vitamin B1 levels. Copper, zinc, magnesium, and ammonia levels were within normal ranges. Vitamins B9 (folic acid) and B12 were elevated secondary to over-supplementation from her previous admissions. Autoimmune antibodies - including vasculitis antibodies - and lupus anticoagulant tests were negative. Multiple imaging studies of the brain and spine, and nerve conduction studies were done. All were unremarkable with no evidence of demyelination appreciated.
The patient was diagnosed with nutritional myeloneuropathy secondary to thiamine deficiency due to her recurrent loss of nutrients by vomiting and decreased nutritional intake. The patient was treated with dietary modifications, regular intravenous thiamine infusion followed by regular intramuscular administration of vitamins B1, B6, and B12, increased protein, vitamin, and mineral intake, and physiotherapy. Vitamins B1, B6, and B12 were switched to oral tablets later. With vitamin supplementation and physiotherapy, her weakness has significantly improved, and her vitamin B1 levels returned to normal.
This case emphasises the importance of considering nutritional deficiencies as a differential of neuropathies, especially with certain risk factors such as poor nutritional intake status, gastrointestinal operations or losses.