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Delayed improvement of cognitive function after folic acid supplementation in an elderly patient with low folate levels‐related dementia: a case report

Dear Editor, It is estimated that symptoms of dementia presenting in 12% of patients are treatable or reversible. Low levels of vitamins, such as vitamin B12 and folate, are common causes of reversible dementia. Reversible dementia with cognitive impairment or behaviour symptoms can be resolved once the primary aetiology is treated. However, there is still limited evidence about the reversibility of dementia by folic acid supplementation. Besides, the time taken for cognitive function improvement after folic acid supplementation is an important issue. Herein, we report the delayed improvement of cognitive function after folic acid supplementation in an elderly patient with low folate levels-related dementia. A 65-year-old man with schizoaffective disorder was admitted to our acute psychiatric ward due to auditory hallucinatory and aggressive behaviour. During admission, impaired recent memory and declined self-care function were observed. Therefore, a series of examinations were arranged to explore the cause of these signs. The blood test results were normal, except for the level of serum folate, which was low (0.8 ng/mL, normal range: 2–20 ng/mL). The Cognitive Abilities Screening Instrument (CASI) score was 65 (3 years ago: 90), and the clinical dementia rating (CDR) score was 2. Furthermore, there was no systemic disease or intoxication or withdrawal from any pharmacological or toxic agent. According to these findings, we suspected low folate status to be the cause of dementia. Subsequently, the patient was treated with folic acid at 5 mg/day. After supplementation with folic acid for 2 months, the level of serum folate was within the normal limit (8.6 ng/mL). Therefore, we discontinued the administration of folic acid. Although the level of serum folate was within the normal limit, his cognitive function did not improve quickly. After 9 months, the CASI score returned to 93, and the CDR score returned to 0.5. This report presents a case of delayed improvement of cognitive function after folic acid supplementation in an elderly patient with low folate levels-related dementia; the response of cognition to folic acid therapy was observed after about 9 months. In a previous study, the neurological response to folic acid therapy was observed to be slow—over many weeks and months. This is because of the efficient blood–brain barrier mechanism for this vitamin which limits entry. Besides, the improvement should be detected within 2–3 months. However, this case reminds us that it could take a longer amount of time to detect the effect of folic acid treatment on cognition. The CASI score in this patient decreased to 65 because of low folate levels and returned to 93 after folic acid therapy. Therefore, recognizing and treating reversible dementia as early as possible can benefit the outcome of patients. Therefore, serum folate tests should be conducted routinely in patients with cognitive impairment. To conclude, clinicians should pay attention to identifying the causes of dementia. In this case, folic acid therapy was successful in treating dementia caused by folate deficiency. Additionally, a longer follow-up is needed, as demonstrated by the delayed improvement of cognition in this elderly patient.