Anemia’s association with gastrointestinal and neurological abnormalities in brain, spinal cord, and peripheral nerves has been documented extensively.
In 1877, Gardner and Osler termed pernicious anemia for patients with arm numbness and tool use difficulties.
Echtenstein (1884) linked PA to spinal cord disease via tabes dorsalis, while Lichtheim (1887) and Minnich (1892) identified histologic differences in both.
Vitamin B12 is important for biological processes in the nervous system with deficiency linked to neurological and psychiatric disorders.
B12 helps neurotransmitter production for brain function and mood and is essential for DNA synthesis in rapidly dividing cells.
Vitamin B12 converts homocysteine to methionine is necessary for S-adenosylmethionine from B12 deficiency harms nerves.
Epidemiology
Vitamin B-12 deficiency prevalence is hard to determine due to various causes, with 300,000 to 3 million affected.
The prevalence of vitamin B-12 deficiency is 3-16% below 200 pg/mL and 21% in geriatrics with levels above 300 pg/mL and elevated HC and MMA.
Chronic diarrhea subgroup has a 39% rate, but the link between vitamin B-12 deficiency and neurologic disease is unclear.
Elevated HC increases risks for coronary artery, cerebrovascular, and peripheral vascular diseases, with 10% of vascular disease risk associated.
PA prevalence is higher in white individuals and lower in Hispanic and black individuals.
Anatomy
Pathophysiology
Vitamin B-12 deficiency from malabsorption occurs in 2-5 years, while vegetarian dietary inadequacy takes 10-20 years.
After ingestion, low stomach pH releases cobalamin from proteins, which then binds to gastric R binder and travels to the intestines for digestion.
Free cobalamin binds to gastric intrinsic factor with hydrochloric acid secretion. The cobalamin-IF complex binds to cublin in the distal ileum that enables energy-dependent internalization.
The cobalamin-TCII complex enters portal blood absorbed by liver then lysosomal degradation releases cobalamin in the cytoplasm.
Etiology
The causes of Vit.B-12 associated neurological disease are:
Dietary deficiency
Malabsorption
Impaired transport
Malabsorption syndromes
Genetics
Prognostic Factors
Vitamin B-12 therapy prevent progression and improves neurological deficits in younger patients with milder conditions.
A review of 57 subacute combined degeneration patients found specific signs linked to better prognoses.
Spinal MRI showing less than 7 segments involved indicates better prognosis with cord swelling. Clinical improvement is strongest in the initial 2 months.
Clinical History
Clinical History:
Collect details including presenting symptoms, dietary and medical history to understand clinical history of patient.
Physical Examination
Psychiatric Examination
Neurological Examination
Musculoskeletal Examination
Hematologic Examination
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Neurosyphilis
Toxic Neuropathy
Multiple Sclerosis
Tropical Myeloneuropathies
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Treatment Paradigm:
Neurologically impaired patients required extra care in skilled nursing units and outpatient follow-up.
Hospitalization is needed only for life-threatening anemia or severe neurologic deficits during therapy.
Diagnose vitamin B-12 deficiency and treat appropriately to prevent serious consequences including encephalopathy and neuropathy.
Physical and occupational therapies enhance gait, balance, and arm function.
Tests for vitamin B-12 deficiencies in elderly patients is important for proper diagnosis and treatment.
Periodic vitamin B-12 testing is essential for certain gastrointestinal patients.
»
Home » CAD » Vitamin B-12 Associated Neurological Diseases
Vitamin B-12 Associated Neurological Diseases
Updated :
December 18, 2024
Anemia’s association with gastrointestinal and neurological abnormalities in brain, spinal cord, and peripheral nerves has been documented extensively.
In 1877, Gardner and Osler termed pernicious anemia for patients with arm numbness and tool use difficulties.
Echtenstein (1884) linked PA to spinal cord disease via tabes dorsalis, while Lichtheim (1887) and Minnich (1892) identified histologic differences in both.
Vitamin B12 is important for biological processes in the nervous system with deficiency linked to neurological and psychiatric disorders.
B12 helps neurotransmitter production for brain function and mood and is essential for DNA synthesis in rapidly dividing cells.
Vitamin B12 converts homocysteine to methionine is necessary for S-adenosylmethionine from B12 deficiency harms nerves.
Vitamin B-12 deficiency prevalence is hard to determine due to various causes, with 300,000 to 3 million affected.
The prevalence of vitamin B-12 deficiency is 3-16% below 200 pg/mL and 21% in geriatrics with levels above 300 pg/mL and elevated HC and MMA.
Chronic diarrhea subgroup has a 39% rate, but the link between vitamin B-12 deficiency and neurologic disease is unclear.
Elevated HC increases risks for coronary artery, cerebrovascular, and peripheral vascular diseases, with 10% of vascular disease risk associated.
PA prevalence is higher in white individuals and lower in Hispanic and black individuals.
Vitamin B-12 deficiency from malabsorption occurs in 2-5 years, while vegetarian dietary inadequacy takes 10-20 years.
After ingestion, low stomach pH releases cobalamin from proteins, which then binds to gastric R binder and travels to the intestines for digestion.
Free cobalamin binds to gastric intrinsic factor with hydrochloric acid secretion. The cobalamin-IF complex binds to cublin in the distal ileum that enables energy-dependent internalization.
The cobalamin-TCII complex enters portal blood absorbed by liver then lysosomal degradation releases cobalamin in the cytoplasm.
The causes of Vit.B-12 associated neurological disease are:
Dietary deficiency
Malabsorption
Impaired transport
Malabsorption syndromes
Vitamin B-12 therapy prevent progression and improves neurological deficits in younger patients with milder conditions.
A review of 57 subacute combined degeneration patients found specific signs linked to better prognoses.
Spinal MRI showing less than 7 segments involved indicates better prognosis with cord swelling. Clinical improvement is strongest in the initial 2 months.
Clinical History:
Collect details including presenting symptoms, dietary and medical history to understand clinical history of patient.
Psychiatric Examination
Neurological Examination
Musculoskeletal Examination
Hematologic Examination
Neurosyphilis
Toxic Neuropathy
Multiple Sclerosis
Tropical Myeloneuropathies
Treatment Paradigm:
Neurologically impaired patients required extra care in skilled nursing units and outpatient follow-up.
Hospitalization is needed only for life-threatening anemia or severe neurologic deficits during therapy.
Diagnose vitamin B-12 deficiency and treat appropriately to prevent serious consequences including encephalopathy and neuropathy.
Physical and occupational therapies enhance gait, balance, and arm function.
Tests for vitamin B-12 deficiencies in elderly patients is important for proper diagnosis and treatment.
Periodic vitamin B-12 testing is essential for certain gastrointestinal patients.
Neurology
Distractions should be minimized to help focus and reduce confusion.
Use chairs with armrests and firm cushions for easy standing position.
Family and caregivers should be encouraged to be involved in recovery and daily assistance.
Install home monitoring systems or personal emergency response devices as part of emergency aid.
Proper awareness about vitamin B-12 associated neurological disease should be provided and its related causes with management strategies.
Appointments with a neurologist and preventing recurrence of disorder is an ongoing life-long effort.
Neurology
Cyanocobalamin:
It has metabolic functions including protein synthesis and carbohydrate metabolism.
Folic acid:
It enhances elimination of formic acid in methanol toxicity to folate dehydrogenase.
Neurology
Procedural interventions target causes, recovery, and complications of B12 deficiency.
Intervention therapies include vitamin B12 replacement therapy, endoscopic procedure, and plasma exchange.
Neurology
In the initial diagnosis phase, the focus should be on rapidly replenished Vitamin B12 levels and prevent progression of neurological damage.
Pharmacologic therapy is effective in the treatment phase as it includes the use of dietary supplements.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and interventional therapies.
The regular follow-up visits with the neurologist are scheduled to check the improvement of patients along with treatment response.
Anemia’s association with gastrointestinal and neurological abnormalities in brain, spinal cord, and peripheral nerves has been documented extensively.
In 1877, Gardner and Osler termed pernicious anemia for patients with arm numbness and tool use difficulties.
Echtenstein (1884) linked PA to spinal cord disease via tabes dorsalis, while Lichtheim (1887) and Minnich (1892) identified histologic differences in both.
Vitamin B12 is important for biological processes in the nervous system with deficiency linked to neurological and psychiatric disorders.
B12 helps neurotransmitter production for brain function and mood and is essential for DNA synthesis in rapidly dividing cells.
Vitamin B12 converts homocysteine to methionine is necessary for S-adenosylmethionine from B12 deficiency harms nerves.
Vitamin B-12 deficiency prevalence is hard to determine due to various causes, with 300,000 to 3 million affected.
The prevalence of vitamin B-12 deficiency is 3-16% below 200 pg/mL and 21% in geriatrics with levels above 300 pg/mL and elevated HC and MMA.
Chronic diarrhea subgroup has a 39% rate, but the link between vitamin B-12 deficiency and neurologic disease is unclear.
Elevated HC increases risks for coronary artery, cerebrovascular, and peripheral vascular diseases, with 10% of vascular disease risk associated.
PA prevalence is higher in white individuals and lower in Hispanic and black individuals.
Vitamin B-12 deficiency from malabsorption occurs in 2-5 years, while vegetarian dietary inadequacy takes 10-20 years.
After ingestion, low stomach pH releases cobalamin from proteins, which then binds to gastric R binder and travels to the intestines for digestion.
Free cobalamin binds to gastric intrinsic factor with hydrochloric acid secretion. The cobalamin-IF complex binds to cublin in the distal ileum that enables energy-dependent internalization.
The cobalamin-TCII complex enters portal blood absorbed by liver then lysosomal degradation releases cobalamin in the cytoplasm.
The causes of Vit.B-12 associated neurological disease are:
Dietary deficiency
Malabsorption
Impaired transport
Malabsorption syndromes
Vitamin B-12 therapy prevent progression and improves neurological deficits in younger patients with milder conditions.
A review of 57 subacute combined degeneration patients found specific signs linked to better prognoses.
Spinal MRI showing less than 7 segments involved indicates better prognosis with cord swelling. Clinical improvement is strongest in the initial 2 months.
Clinical History:
Collect details including presenting symptoms, dietary and medical history to understand clinical history of patient.
Psychiatric Examination
Neurological Examination
Musculoskeletal Examination
Hematologic Examination
Neurosyphilis
Toxic Neuropathy
Multiple Sclerosis
Tropical Myeloneuropathies
Treatment Paradigm:
Neurologically impaired patients required extra care in skilled nursing units and outpatient follow-up.
Hospitalization is needed only for life-threatening anemia or severe neurologic deficits during therapy.
Diagnose vitamin B-12 deficiency and treat appropriately to prevent serious consequences including encephalopathy and neuropathy.
Physical and occupational therapies enhance gait, balance, and arm function.
Tests for vitamin B-12 deficiencies in elderly patients is important for proper diagnosis and treatment.
Periodic vitamin B-12 testing is essential for certain gastrointestinal patients.
Neurology
Distractions should be minimized to help focus and reduce confusion.
Use chairs with armrests and firm cushions for easy standing position.
Family and caregivers should be encouraged to be involved in recovery and daily assistance.
Install home monitoring systems or personal emergency response devices as part of emergency aid.
Proper awareness about vitamin B-12 associated neurological disease should be provided and its related causes with management strategies.
Appointments with a neurologist and preventing recurrence of disorder is an ongoing life-long effort.
Neurology
Cyanocobalamin:
It has metabolic functions including protein synthesis and carbohydrate metabolism.
Folic acid:
It enhances elimination of formic acid in methanol toxicity to folate dehydrogenase.
Neurology
Procedural interventions target causes, recovery, and complications of B12 deficiency.
Intervention therapies include vitamin B12 replacement therapy, endoscopic procedure, and plasma exchange.
Neurology
In the initial diagnosis phase, the focus should be on rapidly replenished Vitamin B12 levels and prevent progression of neurological damage.
Pharmacologic therapy is effective in the treatment phase as it includes the use of dietary supplements.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and interventional therapies.
The regular follow-up visits with the neurologist are scheduled to check the improvement of patients along with treatment response.
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