A 73–year–old woman presented with one week of bilateral hand weakness and increasing confusion. She had a baseline Alzheimer’s dementia, but her family reported that her confusion markedly increased in the prior week, with a noticeable progression of dementia in the previous four months. With the exception of decreased strength in both upper extremities, her physical examination revealed no focal neurologic deficits. Her cranial nerves were normal, as were her cardiac, pulmonary and abdominal examinations. There were no skin abnormalities. Her electrolytes were normal, and a head and spinal MRI showed no abnormalities. Her hemoglobin was 7.4 g/dL with an MCV of 110. Based upon the coexistance of the anemia and the neurologic abnormalities, a Vitamin B12 level ordered, realing a level of 130; a methylmalonic acid test confirmed the diagnosis of Vitamin B12 dficiency. She was diagnosed with B12 deficiency leading to bilateral upper extremity parasthesias and weakness and acute–on–chronic dementia. Upon supplementation, her neurologic deficits resolved, and her mental status returned to her prior baseline.
Hospitalists are frequently tasked with the management of the geriatric patient. Distinguishing reversible causes of delirium and progressive dementia from baseline dementia can be challenging. It is therefore important that the hospitalist is aware of the reversible causes of dementia. The differential diagnosis is broad and includes stroke/ transient–ischemic–attacks, hypoglycemia, electrolyte imbalances and vitamin deficiencies. Cobalamin (Vitamin B12) deficiency in the elderly is frequently overlooked, as it is often asymptomatic. However, the deficiency can also present with symptoms of gastrointestinal, psychiatric, and neurologic impairment. Psychiatric manifestations include delirium, dementia, and hallucinations; neurologic symptoms include parasthesias and neuropathies. Parasthesias are typically the presenting symptom, but can worsen to gait ataxia, decreased vibration/proprioception, and positive Romberg’s sign. If the patient is noncommunicative or bed–bound, however, these early signs and symptoms may be missed by the evaluating physician. Malnutrition, in addition to atrophy of the epithelial lining of the tongue and stomach, predispose to the condition, and should raise the pretest probability for the deficiency.
Cobalamin is required for the methylation of homocysteine in the S–adenosylmethione pathway, which is needed for the synthesis of neurotransmitters such as acetylcholine. Decreased methylation secondary to low cobalamin prevents neuron repair, leading to parasthesias, dementia, and depression, all of which were seen in this patient. Further, low cobalamin levels lead to elevated homocysteine levels, thereby worsening cognitive function.