Vitamin B12 deficiency is a very rare cause of reversible dementia, especially as a sole cause. It consists of global cognitive dysfunction with slowness, lack of concentration, and memory failures. Psychiatric manifestations are frequent: depression, mania, and paranoid psychosis with visual and auditory hallucinations. We present a patient with progressive cognitive decline of six months’ evolution associated with vitamin B12 deficiency, which completely reversed with vitamin treatment.
Below, a case study conducted by Dr. Miguel Damián Junco Bonet (2014) will be presented. ISEP’s Master’s in Aging and Dementias contributes part of its content through clinical cases like the one presented.
A 50-year-old male patient, married, self-employed, who presented an insidious onset with memory lapses, apathy, and depression. Inappropriate behaviors, delusional ideas of persecution, and spatial disorientation progressively appeared, which led him to stop working. In the last weeks, urinary incontinence and gait disturbance with frequent falls were added, which was the reason for his hospitalization.
Among his medical history, he had suffered from hypertension for 12 years, for which he was treated with enalapril 20 mg, one tablet twice daily. The admission mental examination showed marked bradypsychia, with apathy and a suspicious attitude. There was temporo-spatial disorientation, imitation and perseveration behaviors. Memory failure, with confabulations and false recognitions. In addition, acalculia was demonstrated. His language was laconic, without aphasia or dysarthria. The neurological examination showed gait ataxia that prevented ambulation. He presented osteotendinous hyperreflexia and deep sensibility alterations.
Studies performed:
-Neuropsychological evaluation: Folstein Mini-Mental State Exam: 16/30; Raven’s Colored Progressive Matrices Test: 9/36. In word learning, his performance was 29/100 words, with a recognition of 9/10. In semantic (or categorical) memory: five elements (lower range).
-Laboratory Tests: Hemoglobin 89 g/l. Hematocrit 29vol l/l. The vitamin B12 level was 0 pg/ml (normal >179 pg)
-Computed axial tomography of the skull (CT scan): did not reveal involutive elements greater than expected for the patient’s age.
-Digestive endoscopy with gastric biopsy: revealed gastric metaplasia.
Possible diagnoses were considered: dementia due to vitamin B12 deficiency, frontotemporal dementia, and, less likely, Alzheimer’s type dementia.
During hospitalization, the patient presented nocturnal agitation with visual and auditory hallucinations that required major tranquilizers. It was noteworthy that during his neuropsychological evaluation, he showed fluctuations in performance, which suggested pseudodementia.
Treatment with vitamin B12 was started, 5000 units intramuscularly daily for 10 days and then weekly.
Observed progress:
– Evolution of the Mini-Mental State Exam during and after hospitalization. An improvement was observed in all test items, but with significant day-to-day fluctuations in attention and calculation. The evolution of the complete blood count was favorable in relation to the start of vitamin B12 treatment.
– The patient gradually recovered orientation and memory. At his first check-up, one month after discharge, the Mini-Mental State Exam score was 30/30. He presented minimal difficulty in gait and distal paresthesias.
– Two months after the start of treatment, in a new neuropsychological evaluation, he obtained 30/36 points in colored progressive matrices; in word learning he reached 86/100 words, with 9/10 in recall at 10 minutes and 10/10 in recognition. In semantic memory (animals) he recalled 18 words in 60 seconds (60th percentile, upper-middle range); in word recall with P he achieved 25 in 3 minutes (60th percentile, upper-middle range). In the Stroop test (frontal function) there was no interference. The complete blood count normalized.
– The gastric biopsy was repeated and showed atrophic gastritis. The patient returned to work.
This patient represented one of the few truly reversible cases of dementia. His recovery allows ruling out degenerative dementias, such as frontotemporal dementia, which was suspected due to early behavioral alterations. The evolution also allowed ruling out Creutzfeldt-Jakob disease, and the study of Cerebrospinal Fluid (CSF) ruled out other causes of subacute dementias, such as chronic meningitis or carcinomatous meningeal infiltration.
The good response of the neurological condition to vitamin B12 treatment, which coincided with the improvement of the complete blood count, allowed concluding that the dementia was caused by cyanocobalamin deficiency.
Cyanocobalamin participates in a series of biochemical reactions involving the methylation of various metabolites. The neurological damage that occurs in its deficiency can be a consequence of vascular alterations associated with elevated homocysteine, alterations in methylmalonyl CoA mutase, or defects in methylation reactions. These latter alter the basic myelin protein, which prevents its correct conformation or accelerates its destruction. Both small vessel vascular damage and myelination failures (especially of subcortical white matter) can explain cognitive alterations. From a neuropsychological point of view, the existence of behavioral disorders, difficulty walking, apathy, the presence of bradypsychia, and performance fluctuations, suggest a fronto-subcortical dementia in this patient.
The importance of cyanocobalamin deficiency as a cause of dementia is debated. A study showed that elderly individuals with B12 deficiency had cognitive impairment in the absence of hematological manifestations and that in many cases, though not all, cognitive disorders reversed when vitamin levels were corrected (Lindenbaum, et al., 1988). However, other studies in histologically confirmed Alzheimer’s disease patients have described lower serum vitamin B12 levels and an association between behavioral alterations and vitamin levels.
Finally, in the usual study of patients with probable Alzheimer’s disease, it is common to find subnormal vitamin B12 levels, without its administration evidently modifying the clinical picture. It is possible that this is due to isolated clinical observations; that the deficiency was never as severe as in the case of the patient described above (plasma level was 0 pg/ml), or that the deficiency had already caused irreversible damage. The latter seems unlikely considering the ease with which such severe dementia as this patient’s reversed. Furthermore, in vegetarians, it is common to find subnormal B12 levels, which do not necessarily have effects on the nervous system.
Training in dementias is nowadays a necessity for health professionals. The increase in the geriatric population uncovers new treatments in the field of neurosciences every day. ISEP’s master’s in dementias addresses this need and is aimed at professionals in contact with the aging population such as doctors, nurses, psychologists, speech therapists, and occupational therapists.