Serum Vitamin B12 Will Most Likely Confirm the Diagnosis
The answer is (b) serum vitamin B12, as this patient's clinical presentation—progressive gait disturbance, paresthesia, absent lower extremity reflexes, and loss of position/vibration sense in a bedbound elderly patient on chronic metformin and pantoprazole—is classic for subacute combined degeneration from vitamin B12 deficiency.
Clinical Reasoning
Key Diagnostic Features Present
This patient demonstrates the hallmark triad of B12 deficiency myeloneuropathy:
- Posterior column dysfunction: Loss of position and vibration sense bilaterally in fingers and toes 1, 2
- Peripheral neuropathy: Progressive paresthesia with reduced/absent deep tendon reflexes, more pronounced in lower extremities 3
- Cognitive impairment: Forgetfulness reported by family, consistent with the neuropsychiatric manifestations seen in 38% of B12-deficient patients 3
The progressive nature over 4 months leading to being bedbound represents severe, untreated deficiency 4.
Medication-Induced Risk Factors
Both of this patient's chronic medications are established causes of B12 deficiency:
- Metformin: Impairs B12 absorption through effects on intrinsic factor and ileal uptake 5
- Pantoprazole: Reduces gastric acid necessary for B12 release from food proteins, causing B12 non-dissociation syndrome—the second most common cause of B12 deficiency in elderly patients after pernicious anemia 2
Why Not the Other Options?
MRI lumbar spine (option a) would be appropriate for cauda equina syndrome, but this patient lacks the key features: no bowel/bladder dysfunction, no saddle anesthesia, and the sensory loss is length-dependent (affecting both hands and feet equally) rather than dermatomal 6. The bilateral upper extremity involvement argues against a purely spinal cord lesion 6.
CT head (option c) would not explain the peripheral neuropathy findings or the specific posterior column signs 7. While chronic subdural hematoma can cause gait impairment in elderly patients, it doesn't produce the characteristic sensory examination findings seen here 7.
Neurocognitive testing (option d) may eventually be useful but won't confirm the underlying etiology 6. The forgetfulness is likely secondary to the metabolic derangement rather than a primary neurodegenerative process 3.
Expected Laboratory Findings
Serum B12 <300 pg/mL confirms deficiency and correlates with neurological improvement after treatment 8. Importantly, 17.5% of patients with B12 deficiency have normal hemoglobin and MCV, so the absence of anemia does not exclude the diagnosis 3. The bone marrow would show megaloblastic changes if examined 2, 3.
Treatment Response as Diagnostic Confirmation
Studies consistently show that 54-100% of patients with B12 deficiency-related neurological symptoms improve within 1-6 months of parenteral B12 replacement 8, 4, 3. This therapeutic response further confirms the diagnosis when B12 levels are low.
Critical Pitfall to Avoid
The most dangerous error would be delaying B12 testing because of normal CBC parameters. Neurological manifestations can occur before or without hematological abnormalities 4, 3. Early diagnosis and treatment are essential to prevent permanent neurological damage, as the condition is often reversible if caught early 1, 3.