Neurological disorders in vitamin B12 deficiency

Abstract

The review discusses thesteps of vitamin B12 metabolism and its role in maintaining of neurological functions. The term "vitamin B12 (cobalamin)" refers to several substances (cobalamins) of a very similar structure. Cobalamin enters the body with animal products. On the peripherу cobalamin circulates only in binding with proteins transcobalamin I and II (complex cobalamin-transcobalamin II is designated as “holotranscobalamin”). Holotranscobalamin is absorbed by different cells, whereas transcobalamin I-binded vitamin B12 - only by liver and kidneys. Two forms of cobalamin were identified as coenzymes of cellular reactions which are methylcobalamin (in cytoplasm) and hydroxyadenosylcobalamin (in mitochondria). The main causes of cobalamin deficiency are related to inadequate intake of animal products, autoimmune gastritis, pancreatic insufficiency, terminal ileum disease, syndrome of intestinal bacterial overgrowth. Relative deficiency may be seen in excessive binding of vitamin B12 to transcobalamin I. Cobalamin deficiency most significantly affects functions of blood, nervous system and inflammatory response. Anemia occurs in 13-15% of cases; macrocytosis is an early sign. The average size of neutrophils and monocytes is the most sensitive marker of megaloblastic hematopoiesis. The demands in vitamin B12 are particularly high in nervous tissue. Hypovitaminosis is accompanied by pathological lesions both in white and gray brain matter. Several types of neurological manifestations are described: subacute combined degeneration of spinal cord (funicular myelinosis), sensomotor polyneuropathy, optic nerve neuropathy, cognitive disorders. The whole range of neuropsychiatric disorders with vitamin B12 deficiency has not been studied well enough. Due to certain diagnostic difficulties they are often regarded as "cryptogenic", "reactive", "vascular» origin. Normal or decreased total plasma cobalamin level could not a reliable marker of vitamin deficiency. In difficult cases the content of holotranscobalamin, methylmalonic acid / homocysteine, and folate in the blood serum should be investigated besides carefully analysis of clinical manifestations.

Clinical and MRI Differences Between Patients With Subacute Combined Degeneration of the Spinal Cord Related vs. Unrelated to Recreational Nitrous Oxide Use: A Retrospective Study

“…Because the human body usually contains a large reserve of VB12 related to the enterohepatic circulation and renal reabsorption, the clinical signs/symptoms of SCD appear only after years of insufficient VB12 intake (10). Therefore, classical SCD is often secondary to gastrointestinal surgeries, a long-term vegetarian diet, or a chronic digestive disease such as atrophic gastritis (11,12). Our current study found that the number of patients with SCD related to N 2 O use who were admitted to our hospital over the last 5 years was comparable to the number of patients with classical SCD, which indicates that recreational N 2 O use has become one of the main causes of SCD in China, especially in young patients.…”

Side effects of long-term use of proton pump inhibitors: practical considerations

“…Vitamin B12: in order to be absorbed in the terminal ileum, vit B12 has to be detached from food proteins and then be complexed with the intrinsic factor secreted from gastric parietal cells; for this to happen, gastric acid and pepsin are required, thus this absorption process is reduced in PPIs users [37]. Furthermore, hypochloridria induced by PPIs treatment is associated with bacterial overgrowth, and since vit B12 may be consumed by bacteria for metabolic processes [38], the bioavailability of this vitamin could be reduced [39].…”

“…Therefore, reduced serum levels of vit B12 cause megaloblastic anaemia and, less frequently, neurological symptoms, such as symmetrical paraesthesia with loss of cutaneous sensation in a 'glove and stocking' distribution, impaired vibration sense and proprioception, and ataxia with positive Romberg's sign. Some patients also develop poor vision, orthostatic dizziness, loss of taste or smell, urinary or faecal incontinence and impotence [38,42]. Moreover, it has been observed that vit B12 deficiency can also be present in Alzheimer's disease (AD).…”

The beneficial role of vitamin B12 in injury induced by ischemia-reperfusion: Beyond scavenging superoxide?

“…Transcobalamin I is also present in the circulation and binds to B12. However, only livers and kidneys can uptake B12 bound with transcobalamin I [ 8 ]. Clearly, intestinal absorption, circulation, cellular uptake, and function of dietary B12 requires complex systems which involve multiple binding proteins, cell surface receptors, lysosomal transfer, and converting enzymes [ 9 ].…”