Case presentation: 
Here we present a 47 years old, right-handed male, who is a strict vegetarian, without known past medical or surgical history, who presented to the emergency department of our hospital with sudden onset three days history of unsteady gait with imbalance associated with bilateral lower limb numbness, from the soles of the feet to his knees. He denied any back or neck pain, with no urinary symptoms [No urinary or fecal incontinence or retention], no numbness in the saddle area. He has had no similar episodes in the past, with no Fever or constitutional symptoms. There was no history of preceding trauma. The patient denied taking any supplements or exposure to heavy metals.
Upon initial assessment, his vitals were RR 20, BP 14578, HR 84, 98% on RA, Temp 36.9 degrees. Complete neurological exam yielded higher mental function, intact, alert, conscious, and oriented to time, place, and person. Cranial nerve examination, including a fundus exam, was normal with no nystagmus. Motor exam of upper/lower limb normal 5/5 as per MRC grade, with deep tendon reflexes (DTR) +2 in the upper limb, and +1 in the ankle, with flexor plantar. The sensory exam showed an impaired sense of proprioception and vibration to the knee, intact in the upper limb, and the rest of the sensory modality intact with no sensory level. Cerebellar examination showed cautious gait with significantly impaired lower limb coordination, evident by dysmetria and impaired heel to chin. There were no detectable cerebellar signs in the upper limbs. Special tests revealed positive Romberg’s sign, with negative Spurling’s and straight leg raise or lasègue sign. The findings above were more suggestive of sensory ataxia.
Initial Laboratory assessment showed normal hemoglobin of 13.6, with hyperchromic, macrocytosis of red blood cells on peripheral smear, mean corpuscular volume, mean corpuscular hemoglobin, 105.7 fl, and 36.8 pg, 34.8 respectively. A plain non-enhanced computed tomography (CT) head was unremarkable. The patient was given an emergency Intra-muscular B12 1000mcg/ml injection before further blood samples were taken for B12 levels. Hence, B12 level was falsely elevated of a value 1476 pg/ml (187-1,058 pg/ml). However, the rest of the work showed a normal folate level of 76 and an elevated homocysteine level of 78.0, correlating with Vitamin B12 deficiency. Pernicious anemia screening was unrevealing, and it was attributed to his vegan diet.
Magnetic resonance imaging (MRI) of the head and whole spine was performed. It showed lower thoracic spinal cord posterior para-median relatively symmetrical intramedullary areas of signal abnormality extending opposed D11 and D12 vertebral levels high T2 signal intensity associated with restricted diffusion pattern in the DWI that raised the possibility of subacute cord ischemia vs. subacute combined degeneration secondary to vitamin B12 deficiency. Noted also Multilevel cervical posterior disc bulges with partial neural compromise are more significant at the C5-6 level. However, this does not correlate with his current presentation.
Diagnosis of subacute combined degeneration of the spinal cord was made, and he was placed on intramuscular methylcobalamin (1000 μg daily) for five days. During his admission, he showed improvement and ambulating with minimal assistance. The patient was discharged home on oral 2000mg Q-weekly B12 supplements and regular follow-up, which the patient has numbness has resolved and was able to walk without any assistance.