eMedicine Specialties > Neurology > Movement and Neurodegenerative Diseases

Vitamin B-12 Associated Neurological Diseases: Treatment & Medication

Author: Niranjan N Singh, MD, DNB, Fellow in Neurophysiology, Department of Neurology, St Louis University School of Medicine
Coauthor(s): Florian P Thomas, MD, MA, PhD, Drmed, Director, Spinal Cord Injury Unit, St Louis Veterans Affairs Medical Center; Associate Program Director, Associate Professor, Departments of Neurology, Molecular Virology, and Molecular Microbiology and Immunology, St Louis University School of Medicine; Alan L Diamond, DO, Movement Disorder Fellow, Department of Neurology, Baylor College of Medicine; René Diamond, DO, Resident, Internal Medicine, Saint Louis University School of Medicine
Contributor Information and Disclosures

Updated: Jan 29, 2008

Treatment

Medical Care

  • Establish the diagnosis and etiology of vitamin B-12 deficiency and treat with adequate doses.
  • The consequences of vitamin B-12 deficiency, encephalopathy, myelopathy, and peripheral and optic neuropathy require adequate medical care.
  • Physical therapy and occupational therapy are needed to improve gait, balance, and arm function. Patients may require canes or a walker for ambulation and safety.
  • In patients with encephalopathy, neuropsychological interventions may improve cognition, social functioning, and interpersonal relationships.
  • Patients with PA are at increased risk for gastric carcinoma, colorectal adenocarcinoma, and carcinoid tumors and must be monitored.

Consultations

Consultations with a gastroenterologist, a hematologist, and a neurologist must be considered.

Diet

When the cause of vitamin B-12 deficiency is low intake, recommend that patients eat food that contains vitamin B-12 such as meat, eggs, cheese, and yogurt. Supplementation is required when religious or cultural restrictions render dietary changes impossible.

Activity

In most patients with vitamin B-12–associated neuropathy/myelopathy, no restriction on physical activity is necessary unless weakness or gait ataxia is severe. Also, severe encephalopathy may lead to 24-hour supervision. In severe anemia or congestive heart failure, the patient should limit strenuous exercise.

Medication

Standard treatment in patients with vitamin B-12 deficiency consists of parenteral or oral cobalamin. The hematologic abnormalities may respond to folate, but the neurologic manifestations only respond to cobalamin.

Numerous treatment regimens have been proposed, including cobalamin 1000 mcg IM/SC daily for 5 days followed by 1000 mcg/wk for 5 weeks, then 100-1000 mcg/mo for life.

Because 1% of cobalamin is absorbed by passive diffusion, administration of large oral doses is an alternative; 1000 mcg daily yields a daily absorption of 10 mcg, which exceeds the 2-mcg recommended daily allowance (RDA) requirement.

In addition to cobalamin replacement, oral IF supplementation is being evaluated. Supplementation with SAM or methionine-rich diets are being studied for N 2 O-induced myeloneuropathies.

Diagnosis and treatment of tapeworm infection and celiac and Crohn diseases can improve intestinal vitamin B-12 malabsorption. With blind loop syndrome, tetracycline can normalize the intestinal flora and vitamin B-12 absorption.

Dietary supplements

Cyanocobalamin is used to replenish the deficiency caused by any of the etiologies described.


Cyanocobalamin or vitamin B-12 (Berubigen, Cyanoject)

Most stable and available form of vitamin B-12. Absorbed rapidly to the organism from IM or SC applications.
Oral cyanocobalamin can replace parenteral formulations. Is effective in PA because 1% of free cobalamin is absorbed via diffusion rather than requiring the presence of IF.

Adult

Parenteral administration: 1000 mcg/d IM/SC for 5 d or 1000 mcg IM 2 times per wk for 2 wk, then 1000 mcg/wk IM/SC for 5 wk, then 100-1000 mcg IM/SC every mo
Oral administration: 1000-2000 mcg PO qd for life

Pediatric

Parenteral administration:
1000 mcg IM qd for 2 wk; congenital disorders require lifelong replacement of 1000 mcg every mo

Oral administration:<12 years: Not established
>12 years: Administer as in adults

Colchicine, paraaminosalicylic acid, and excessive ingestion of alcohol may produce malabsorption of vitamin B-12; chloramphenicol may reduce cobalamin efficacy through interference with erythrocyte maturation

Documented hypersensitivity; Leber disease, ie, hereditary optic nerve atrophy (patients may experience severe and swift optic atrophy when treated with vitamin B-12); severe megaloblastic anemia (hypokalemia and sudden death may occur)

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Very rarely patients report adverse effects (most commonly asthenia, headache, pruritus, diarrhea, and dizziness); serious reactions such as anaphylaxis and vascular thrombosis may occur; severe hypokalemia may result after correction of megaloblastic anemia because of increased cellular potassium requirements


Folic acid (Folvite)

Folate supplementation can reverse the hematologic abnormalities, but the neurologic manifestations only respond to cobalamin.

Adult

1 mg PO/IM/SC qd

Pediatric

<12 years: Not established
>12 years: 1 mg PO/IM/SC qd

Increase in seizure frequency and subtherapeutic levels of phenytoin reported when used concurrently

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Benzyl alcohol may be contained in some products as a preservative (associated with a fatal gasping syndrome in premature infants); resistance to treatment may occur in patients with alcoholism and deficiencies of other vitamins

More on Vitamin B-12 Associated Neurological Diseases

Overview: Vitamin B-12 Associated Neurological Diseases
Differential Diagnoses & Workup: Vitamin B-12 Associated Neurological Diseases
Treatment & Medication: Vitamin B-12 Associated Neurological Diseases
Follow-up: Vitamin B-12 Associated Neurological Diseases
Multimedia: Vitamin B-12 Associated Neurological Diseases
References
[ CLOSE WINDOW ]

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Further Reading

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Keywords

vitamin B-12 deficiency, cobalamin deficiency, subacute combined spinal degeneration, pernicious anemia, PA, vitamin B-12 associated neurologic diseases, vitamin B-12 associated neurological diseases

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Contributor Information and Disclosures

Author

Niranjan N Singh, MD, DNB, Fellow in Neurophysiology, Department of Neurology, St Louis University School of Medicine
Niranjan N Singh, MD, DNB is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.

Coauthor(s)

Florian P Thomas, MD, MA, PhD, Drmed, Director, Spinal Cord Injury Unit, St Louis Veterans Affairs Medical Center; Associate Program Director, Associate Professor, Departments of Neurology, Molecular Virology, and Molecular Microbiology and Immunology, St Louis University School of Medicine
Florian P Thomas, MD, MA, PhD, Drmed is a member of the following medical societies: American Academy of Neurology and National Multiple Sclerosis Society
Disclosure: Nothing to disclose.

Alan L Diamond, DO, Movement Disorder Fellow, Department of Neurology, Baylor College of Medicine
Alan L Diamond, DO is a member of the following medical societies: American Academy of Neurology, American Medical Association, American Osteopathic Association, and American Society of Neuroimaging
Disclosure: Nothing to disclose.

René Diamond, DO, Resident, Internal Medicine, Saint Louis University School of Medicine
René Diamond, DO is a member of the following medical societies: American Medical Student Association/Foundation and American Osteopathic Association
Disclosure: Nothing to disclose.

Medical Editor

Christopher Luzzio, MD, Clinical Assistant Professor, Department of Neurology, University of Wisconsin at Madison
Christopher Luzzio, MD is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Nestor Galvez-Jimenez, MD, Program Director of Movement Disorders, Department of Neurology, Division of Medicine, Director of Neurology Residency Training Program, Cleveland Clinic Florida
Nestor Galvez-Jimenez, MD is a member of the following medical societies: American Academy of Neurology, American College of Physicians, and Movement Disorders Society
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Nicholas Y Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Neurology
Disclosure: Nothing to disclose.

 
 
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