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.