Vitamin B12 deficiency and dementia: what one unusual case revealed

Vitamin B12 deficiency and dementia can sometimes appear remarkably similar. A 61-year-old woman gradually developed memory problems, loss of independence, hallucinations and epileptic seizures. The cause was identified only five years after her symptoms began: her body was unable to absorb vitamin B12 normally.

The case was published in BMJ Case Reports in 2019. It was not a clinical trial or evidence for a new treatment for dementia, but a detailed report of one patient with an unusual combination of neuropsychiatric symptoms.

The woman had been born in Cape Verde and had lived alone for many years. Her relatives noticed a progressive change in her behaviour. She stopped cooking and maintaining her home, neglected personal hygiene, sometimes walked naked in public and appeared to speak to people who were not there.

After moving to Portugal to live with her sister, she experienced a seizure involving loss of consciousness and tonic-clonic movements. A head CT showed no structural abnormality, and her routine blood tests appeared normal. Antiseizure treatment prevented further episodes for a time, but her cognitive and psychiatric symptoms continued.

She became lost when outside, struggled to remember familiar things and was disoriented in time and place. She reported seeing and hearing deceased relatives and believed that members of her family intended to poison her.

Why a normal blood count did not rule it out

Further testing found a vitamin B12 concentration below 117 pmol/L and an elevated homocysteine level of 15.3 μmol/L. Yet her red blood cell count, haemoglobin concentration and mean corpuscular volume were all normal.

This was a central feature of the case. Vitamin B12 deficiency is often associated with megaloblastic anaemia, in which the production of red blood cells is disrupted. Neurological and psychiatric symptoms, however, can develop before obvious abnormalities appear in a routine blood count.

The patient tested positive for antibodies against intrinsic factor and gastric parietal cells. A biopsy also showed chronic atrophic gastritis. Together, these findings supported a diagnosis of pernicious anaemia, an autoimmune disorder that prevents the digestive system from absorbing vitamin B12 efficiently.

This means that descriptions of the case as the result of a “simple dietary change” are inaccurate. Eating more B12-rich food would not have corrected the underlying absorption problem. The patient required injections that delivered the vitamin without relying on the gastrointestinal tract.

Vitamin B12 is involved in DNA synthesis, nervous-system function and the maintenance of myelin, the insulating material surrounding nerve fibres. Prolonged deficiency can disrupt nerve signalling, and some damage may eventually become permanent. In this patient, however, a substantial part of the cognitive impairment remained reversible.

What changed after treatment

The patient was initially given the antipsychotic drug olanzapine. Once pernicious anaemia had been diagnosed, she received parenteral cyanocobalamin: 1 mg daily for six days, weekly for the next six weeks and monthly thereafter. Carbamazepine treatment for seizures was continued.

Her cognitive and functional condition improved dramatically after B12 replacement began. She became oriented in time and place, her speech became coherent, and her behaviour became organised. She was again able to cook, help around the house, shop independently and manage ordinary daily activities.

The outcome was nevertheless not a complete cure. Her hallucinations and delusions initially resolved while she was taking olanzapine but returned six months after the drug was withdrawn. Another antipsychotic was then required. A seizure also recurred after she stopped taking carbamazepine on her own.

Vitamin replacement therefore produced a striking recovery in cognition and independence, but psychosis and susceptibility to seizures did not disappear completely. At the time of the report, she remained on monthly B12 injections and continued antiseizure treatment.

What the case actually shows

Because this is a single case report, it cannot establish how often vitamin B12 deficiency causes dementia-like symptoms or how frequently treatment leads to comparable recovery. It also does not suggest that common neurodegenerative dementias can generally be reversed with vitamin supplements.

Its clinical lesson is more specific. Potentially reversible metabolic causes should be investigated when cognitive deterioration occurs alongside atypical psychosis or seizures. Severe vitamin B12 deficiency can affect the nervous system even when haemoglobin and other routine blood measurements remain normal.

Five years without the correct diagnosis did not prevent this patient from recovering much of her cognitive and functional ability. The symptoms that persisted, however, also illustrate why identifying and treating vitamin B12 deficiency as early as possible remains important.