vitamin-b-12 and Sensation-Disorders

Topics: Animals; Antineoplastic Agents; Boronic Acids; Bortezomib; Cold Temperature; Drugs, Chinese Herbal; Humans; Hyperalgesia; Organoplatinum Compounds; Oxaliplatin; Paclitaxel; Peripheral Nervous System Diseases; Pyrazines; Sensation Disorders; Vincristine; Vitamin B 12

Topics: Aged; Anemia, Pernicious; Brain; Cognitive Dysfunction; Diagnosis, Differential; Humans; Injections, Intramuscular; Magnetic Resonance Angiography; Magnetic Resonance Imaging; Male; Methylmalonic Acid; Neurologic Examination; Postural Balance; Sensation Disorders; Syphilis Serodiagnosis; Treponema pallidum; Vitamin B 12; Vitamin D Deficiency

Topics: Diagnostic Errors; Female; Humans; Middle Aged; Sensation Disorders; Subacute Combined Degeneration; Vitamin B 12

We describe a 35 year-old man presenting with a four-week history of non-painful limb paraesthesias and unsteady gait causing falls. On examination he had an ataxic gait associated with dorsal column sensory loss. He had a medical history of a partial gastrectomy six years prior and anaemia. He had received monthly intramuscular hydroxycobalamin injections since the gastrectomy. Laboratory tests revealed normal vitamin B12 and holotranscobalamin levels, a reduced serum caeruloplasmin of 0.05 g/L (normal: 0.22-0.58 g/L), a copper-to-caeruloplasmin ratio of 1.9 μmol/L (11.0-22.0 μmol/L) and a reduced 24-hour urinary copper concentration of <0.30 μmol/L (0-0.3 μmol/L). Cerebrospinal fluid analysis, nerve conduction studies, electromyography and visual-evoked responses were unremarkable. MRI revealed abnormal hyperintense signal in the cervical dorsal columns. Hypocupric myelopathy was diagnosed and he was treated with daily oral elemental copper. Three months later, his walking and balance had improved although there was no change noted on MRI.

Topics: Adult; Gait Ataxia; Humans; Longitudinal Studies; Magnetic Resonance Imaging; Male; Sensation Disorders; Spinal Cord; Spinal Cord Diseases; Subacute Combined Degeneration; Vitamin B 12

Combined medullar sclerosis, together with peripheral sensory neuropathies, is the most common neurological manifestation observed in cobalamin deficiency. Biermer's disease is the predominant cause. Other clinical and etiological aspects are nevertheless frequent, although underestimated.. This retrospective study included patients with neurological symptoms and cobalamin (B12 vitamin) deficiency confirmed by laboratory tests collected over a period of 11 years.. Twenty-seven cases were analyzed. Mean age was 47 years and there were 11 women and 16 men. Distribution of the neurological syndromes was: combined medullar sclerosis in 18 patients (67%), sensory neuropathies in 30% of cases and sensory-motor neuropathies in 15%. One patient had fronto-subcortical dementia with good improvement after vitamin replacement. In addition, autonomic dysfunction was noted in six patients (orthostatic symptomatic hypotension and/or urinary dysfunction and/or erectile failure). Dysautonomia revealed cobalamin deficiency in three patients with a good and fast response to the cobalamin therapy in all cases. Biermer's disease was diagnosed in 17 patients (63%) and a likely syndrome of nondissociation of cobalamin in two patients. One patient had Crohn's disease and no etiology was found in seven patients. In five patients (19%), nitrous oxide undoubtedly induced decompensation of latent cobalamin deficiency; four after a general anesthesia and one by chronic professional exposure. Outcome was very good in 46% of patients after vitamin replacement, particularly if treatment was started rapidly.. The findings in this series highlight the frequency of autonomic dysfunction sometimes revealing cobalamin deficiency with a fast and good response to vitamin replacement and the frequency of neurological disorders following decompensation triggered by general anesthesia using nitrous oxide in patients with latent cobalamin deficiency.

Topics: Adolescent; Adult; Aged; Anesthesia, General; Autonomic Nervous System Diseases; Female; Humans; Male; Medulla Oblongata; Middle Aged; Nervous System Diseases; Retrospective Studies; Sclerosis; Sensation Disorders; Vitamin B 12; Vitamin B 12 Deficiency; Vitamins; Young Adult

Vitamin B12 deficiency is an important nutritional disorder causing neurological manifestations of myelopathy, neuropathy and dementia. Sub-acute combined degeneration (SCD) with involvement of the posterior columns in the cervical and thoracic cord is a common presentation of this disorder. In this case report, we describe a 43 year old woman with pernicious anemia and myelopathy with atypical clinical features. The patient presented with motor symptoms, a sensory level and bladder dysfunction. She had severe autonomic disturbances including an episode of unexplained bronchospasm, which has not been previously reported as a manifestation of vitamin B12 deficiency. We review the literature regarding these rarely reported features of vitamin B12 deficiency, and discuss aspects of management of this reversible condition. We emphasize the importance of awareness of autonomic disturbances in B12 deficient individuals.

Topics: Adult; Anemia, Pernicious; Autonomic Nervous System Diseases; Bronchi; Bronchial Spasm; Female; Humans; Leg; Magnetic Resonance Imaging; Muscle, Skeletal; Neural Pathways; Paraparesis; Sensation Disorders; Spinal Cord; Spinal Cord Diseases; Subacute Combined Degeneration; Sympathetic Nervous System; Treatment Outcome; Urinary Bladder, Neurogenic; Vitamin B 12; Vitamin B 12 Deficiency

Topics: Anemia, Pernicious; Cell Phone; Humans; Male; Middle Aged; Sensation Disorders; Vibration; Vitamin B 12; Vitamin B 12 Deficiency

A 55 year old male presented 2 years after a jejuno-iliectomy with weakness of all limbs, paraesthesiae, and difficulty in walking. Clinical examination revealed loss of posterior column sensations. Investigations were suggestive of a deficiency of vitamin B12 and folate. MRI showed a band of hyperintensity on T2 image, in the dorsal portion of the spinal cord.

Topics: Humans; Magnetic Resonance Imaging; Male; Middle Aged; Nerve Degeneration; Sensation Disorders; Spinal Cord; Spinal Cord Diseases; Vitamin B 12; Vitamin B 12 Deficiency

The unknown biochemical basis for neurologic dysfunction in cobalamin deficiency and the frequent divergence between neurologic and hematologic manifestations led us to study homocysteine metabolism in 22 patients with pernicious anemia. Serum levels of total homocysteine (tHcy), methionine, S-adenosylmethionine (AdoMet), cysteine, cysteinylglycine (cys-gly), and glutathione (GSH) were measured. Only levels of tHcy and cysteine were increased and only GSH was decreased in cobalamin deficiency as a whole, compared with 17 control subjects. AdoMet correlated only with methionine levels (P =.015) and cysteine only with cys-gly (P =.007) in healthy subjects, but in cobalamin-deficient patients AdoMet correlated instead with cysteine, cys-gly, and folate levels only (P =.008, P =.03, and P =.03, respectively). Significant differences appeared in clinically subgrouped cobalamin-deficient patients. The 11 patients with neurologic defects had higher mean levels of folate (27.9 versus 15.4 nM), AdoMet (117.2 versus 78.6 nM), cysteine (462 versus 325 microM), and cys-gly (85.0 versus 54.7 microM) than the 11 neurologically unaffected patients. Cobalamin therapy restored all metabolic changes to normal. The results indicate that changes in several metabolic pathways differ in patients with and without neurologic dysfunction. Cysteine levels were the most significant predictors of neurologic dysfunction, but it is unclear if they are direct or indirect indicators of neurotoxicity. The higher AdoMet levels in neurologically affected patients may result from inhibition of glycine N-methyltransferase by those patients' higher folate levels. The origin of the folate differences is unclear and possibly varied. Low AdoMet and GSH levels were independent predictors of anemia.

Topics: Anemia; Anemia, Pernicious; Cysteine; Dipeptides; Folic Acid; Glutathione; Homocysteine; Humans; Memory Disorders; Methionine; Movement Disorders; Nervous System Diseases; Retrospective Studies; S-Adenosylmethionine; Sensation Disorders; Vitamin B 12; Vitamin B 12 Deficiency

Distal sensory peripheral neuropathy (DSPN) has been reported in 5 to 75% of patients with human immunodeficiency virus (HIV) infection, particularly in advanced stages of the disease. Twenty HIV seropositive patients were studied prospectively to determine the frequency of DSPN in clinical stage II and III of the HIV infection, and to investigate the role of vitamin B12 deficiency on the frequency of DSPN in HIV patients. All patients had complete blood count, serum vitamin B12 level, anti-intrinsic factor antibody, Schilling test, and electrodiagnostic studies including nerve conduction studies and concentric needle examination in the lower extremities, and sympathetic skin responses. Only 1 patient (5%) had clinical and electrophysiological evidence of possible DSPN. Of the 6 patients with abnormal Schilling test, only one had DSPN based on distal sensory symptoms, abnormal neurological examination and electrodiagnostic studies. Evidence for possible DSPN was present in 5% of patients with early HIV infection and did not appear to be more frequent in patients with concurrent vitamin B12 deficiency.

Topics: Adult; Electrophysiology; HIV; Humans; Infections; Male; Middle Aged; Motor Neuron Disease; Sensation Disorders; Vitamin B 12

Two cases of severe myeloneuropathy and macrocytic anemia associated with a low serum level of vitamin B12 after prolonged exposure to nitrous oxide are reported. In both cases, the neurological manifestations worsened initially despite B12 supplementation, although in one case the use of methionine seemed to arrest the progression of the disease and accelerate recovery. This offers further support for the biochemical hypothesis of methionine synthetase inhibition by nitrous oxide and reproduces in man previously reported animal studies with methionine. Methionine may be an important first-line therapy in the initial treatment of neuropathy and myeloneuropathy induced by nitrous oxide, and has a hypothetical role in the treatment of subacute combined degeneration of the cord.

Topics: Adult; Anemia, Macrocytic; Female; Humans; Male; Methionine; Nervous System Diseases; Neuromuscular Diseases; Nitrous Oxide; Sensation Disorders; Vitamin B 12