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. A patient is presented with progressive cognitive decline of six months’ evolution associated with vitamin B12 deficiency, which completely reversed with treatment with that vitamin.
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 with an insidious onset of memory failures, apathy, and depression. Inappropriate behaviors, persecutory delusions, and spatial disorientation progressively appeared, which led him to leave his job. In recent 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 arterial hypertension for 12 years, for which he was treated with enalapril 20 mg, one tablet twice a day. The admission mental examination showed marked bradypsychia, with apathy and a suspicious attitude. There was temporo-spatial disorientation, imitation behaviors, and perseveration. 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 alterations in deep sensitivity.
Studies performed:
-Neuropsychological evaluation: Folstein Minimental test: 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 29 vol l/l. Vitamin B12 level was 0 pg/ml (normal >179 pg)
-Computed axial tomography of the skull (CAT): did not reveal involutive elements greater than those 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 presented fluctuations in performance, which suggested pseudodementia.
Treatment with vitamin B12, 5000 units intramuscularly daily for 10 days and then weekly, was initiated.
Observed progress:
– Evolution of the Minimental test during and after hospitalization. An improvement was observed in all test items, but with significant fluctuations in attention and calculation from one day to the next. The evolution of the blood count was favorable in relation to the start of vitamin B12 treatment.
– The patient gradually recovered orientation and memory. In his first check-up, one month after discharge, the Minimental test was 30/30. He presented minimal difficulty in walking 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 blood count normalized.
– The gastric biopsy was repeated and showed atrophic gastritis. The patient returned to work.
This patient represented one of the few cases of truly reversible 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 meningeal carcinomatous infiltration.
The good response of the neurological condition to vitamin B12 treatment, which coincided with the improvement of the 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 fluctuations in performance, allow proposing a fronto-subcortical dementia in this patient.
The importance of cyanocobalamin deficiency as a cause of dementia is debated. One study showed that elderly people 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 patients with histologically confirmed Alzheimer’s disease 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 levels of vitamin B12, without its administration significantly 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 (the 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 that of this patient reversed. Furthermore, in vegetarians, it is common to find subnormal levels of B12, which do not necessarily have effects on the nervous system.
Dementia training is today a necessity for health professionals. The increase in the geriatric population discovers new treatments in the field of neurosciences every day. ISEP’s master’s in dementias responds to this need and is aimed at professionals in contact with the aging population such as doctors, nurses, psychologists, speech therapists, and occupational therapists.