Can a B12 Deficiency Cause Tremors?

Vitamin B12 deficiency can cause tremors, and the link is well established in the medical literature. Both adults and infants who are deficient in B12 may develop tremor along with other involuntary movements such as chorea, dystonia, and symptoms resembling Parkinson’s disease.¹ These neurological signs sometimes appear before any blood-related problems show up, which means tremor can be the first clue that something is wrong. The relationship between B12 and the nervous system runs deeper than many people realize, and getting it right early makes a meaningful difference in how fully someone recovers.

The Range of Movement Problems B12 Deficiency Can Produce

Tremor is just one entry on a longer list of involuntary movements tied to B12 deficiency. Published case reports and reviews describe patients developing chorea (irregular, flowing jerky movements), myoclonus (sudden muscle twitches), dystonia (sustained muscle contractions that pull a limb or the trunk into an abnormal posture), and full-blown parkinsonism with slowness, rigidity, and resting tremor.¹ Some patients present with only one type of movement disorder; others develop a combination. This variety is one reason B12 deficiency can be tricky to spot on clinical grounds alone. A person with a new tremor, for instance, may be evaluated for Parkinson’s disease or essential tremor while the underlying nutritional cause goes unchecked.

A case report from the Philippines described a patient who developed orthostatic tremor, a distinctive shaking in the legs that appears almost immediately upon standing. Workup revealed megaloblastic anemia and a B12 level below 150 pg/L. After intramuscular methylcobalamin injections given every other day, the tremor gradually resolved.² Orthostatic tremor is uncommon and usually attributed to other neurological causes, so a nutritional deficiency would not be the first thing most clinicians think of. That is exactly the kind of scenario where awareness of the B12 connection matters.

How B12 Deficiency Damages the Nervous System

B12 plays a central role in maintaining the myelin sheath, the fatty insulation that wraps around nerve fibers and allows electrical signals to travel quickly and accurately. When B12 is missing for long enough, that insulation starts to break down. The result is demyelination and, eventually, actual loss of the nerve fibers themselves, in both the brain and spinal cord as well as peripheral nerves.³ This damage can produce a wide spectrum of symptoms ranging from tingling and numbness in the hands and feet to difficulty walking, cognitive changes, and the movement disorders described above.

In infants and young children, the stakes are even higher. Lack of B12 during pregnancy or early life can severely delay myelination of the developing brain, as demonstrated on cranial MRI scans.⁴ Because the young nervous system is still being built, the window for damage is wider and the consequences can be more severe if treatment is delayed.

Subacute Combined Degeneration and Its Overlap With Tremor

The most classically recognized neurological complication of B12 deficiency is subacute combined degeneration, a condition that primarily hits the posterior and lateral columns of the spinal cord. It tends to cause sensory ataxia, meaning the brain loses accurate information about where the limbs are in space, leading to unsteadiness and a clumsy, wide-based walk. One recent case report linked this condition to autoimmune gastritis that had quietly destroyed the stomach’s ability to absorb B12, even though endoscopy did not show obvious damage.⁵

Subacute combined degeneration and movement disorders like tremor can coexist. A person might notice shaky hands and simultaneously feel that their balance is off or that their feet feel numb. The spinal cord damage shows up on MRI as symmetrical bright spots in the posterior columns, a finding that, while not unique to B12 deficiency, should prompt checking B12 levels quickly because early treatment can reverse much of the damage.⁶

Infantile Tremor Syndrome

In parts of the world where vegetarian diets are common and complementary feeding may be delayed, infants can develop a specific condition called infantile tremor syndrome. The hallmarks are tremors, skin darkening, sparse hair, irritability, and developmental regression, all in a baby who has been exclusively breastfed beyond the period when breast milk alone can supply adequate B12. A published case described a nine-month-old girl with grade 2 malnutrition, macrocytic anemia, and a serum B12 of 205 pg/dL who was diagnosed with infantile tremor syndrome and treated with B12 plus nutritional supplementation.⁷

More broadly, movement disorders in children caused by metabolic problems, including B12-related ones, are considered treatable emergencies because supplementation can reverse the symptoms when started early.⁸ A mother who is herself B12-deficient, whether from diet, undiagnosed pernicious anemia, or another cause, may produce breast milk that is too low in B12 to support her infant’s rapidly developing nervous system. Screening the mother and the child when tremor or developmental delay appears in a breastfed infant is a straightforward step that can prevent lasting harm.

When B12 Deficiency Looks Like Parkinson’s Disease

Some of the most dramatic case reports describe patients who are initially evaluated for Parkinson’s disease only to discover that their slowness, rigidity, and tremor are caused by severe B12 deficiency. The term used in the literature is acute parkinsonism, and it has been reported to resolve with B12 replacement.⁹ This is a critical distinction because Parkinson’s disease itself is a progressive neurodegenerative condition with no cure, while B12-related parkinsonism can potentially be reversed entirely if caught in time.

The overlap does not end there. Research has also explored whether B12 levels play a role in people who do have true Parkinson’s disease, since low B12 is common in that population and may worsen existing neurological symptoms. The practical takeaway is that anyone presenting with new tremor and parkinsonian features should have their B12 checked. It is a cheap, fast blood test, and the cost of missing a treatable cause is high.

Who Is at Risk for B12 Deficiency

B12 comes almost exclusively from animal-sourced foods, so strict vegans and vegetarians are at elevated risk unless they supplement. But diet is only one piece. Several common medical situations can deplete B12 or block its absorption:

Metformin use: Multiple observational studies and meta-analyses have found that long-term metformin therapy, especially at higher doses, is associated with an increased risk of B12 deficiency.¹⁰ Given how widely metformin is prescribed for type 2 diabetes, this is a substantial population.
Autoimmune gastritis and pernicious anemia: The immune system attacks the stomach cells that produce intrinsic factor, a protein required for B12 absorption. This can develop silently and may not show dramatic changes on endoscopy.⁵
Gastric surgery: Weight-loss surgeries that bypass or remove portions of the stomach reduce the area available for B12 absorption.
Older age: Stomach acid production tends to decline with age, making it harder to liberate B12 from food proteins. This is why deficiency becomes more common after 60 even in meat-eaters.
Nitrous oxide exposure: Recreational or repeated medical use of nitrous oxide inactivates the body’s stores of B12, sometimes causing rapid neurological deterioration in someone whose levels were already borderline.

The diversity of risk factors means that B12 deficiency is not confined to any single demographic. A 35-year-old taking metformin, a 70-year-old with undiagnosed pernicious anemia, and a breastfed infant of a vegan mother can all end up in the same place neurologically.

Why a Normal B12 Level Does Not Always Rule It Out

One of the trickiest aspects of diagnosing B12-related tremor and other neurological symptoms is that a standard serum B12 test can come back in the normal range while the body is still functionally deficient. The total amount of B12 circulating in the blood does not necessarily reflect how much is actually available inside cells where it is needed.¹¹ This concept, sometimes called functional B12 deficiency, has led to growing interest in additional markers.

Two metabolites, methylmalonic acid and homocysteine, rise when B12-dependent biochemical pathways stall. Measuring them can improve diagnostic sensitivity in patients whose standard B12 number looks reassuring but whose symptoms suggest otherwise.¹² However, these markers are not perfectly specific to B12, as both can be elevated in kidney disease and other conditions. So interpretation still requires clinical judgment. The key message for anyone experiencing unexplained tremor or neurological symptoms is that a single normal B12 reading should not be the end of the investigation if suspicion remains high.

Copper Deficiency and Other Look-Alikes

B12 deficiency is not the only nutritional cause of myelopathy and movement problems. Copper deficiency can produce clinical signs and symptoms that are essentially indistinguishable from B12 deficiency, including spinal cord damage and sensory problems.¹³ This overlap matters because zinc supplementation, which is common and available over the counter, can deplete copper over time. Someone who takes high-dose zinc for immune support or for a different medical reason and then develops numbness, gait problems, or tremor might have their B12 checked but never have their copper measured.

Other conditions on the differential list for someone presenting with tremor and spinal cord findings include multiple sclerosis, HIV-associated myelopathy, and syphilis. The symmetrical posterior cord lesions seen on MRI in B12 deficiency look similar to those in some of these other diseases, which is why the imaging alone is not enough to confirm the diagnosis.⁶ Blood work, clinical history, and sometimes additional metabolic testing are all needed to pin down the cause.

Recovery After Treatment

The good news is that B12-related movement disorders, including tremor, typically respond well to B12 supplementation. In most published cases, symptoms improve with treatment, and some patients experience complete resolution.¹ How fully you recover and how quickly depends in large part on how long the deficiency lasted and how severe the nerve damage had become before treatment started.¹⁴

Mild cases caught early, where the myelin damage is still largely reversible, tend to bounce back within weeks to a few months of starting injections or high-dose oral supplementation. More advanced cases, particularly those with significant spinal cord involvement, may see partial improvement but retain some residual symptoms. This is one of the strongest arguments for checking B12 whenever unexplained neurological symptoms appear: the window for full recovery narrows with time.

One quirk worth knowing about is that some patients develop or temporarily worsen movement symptoms shortly after starting B12 injections rather than before. The literature notes that involuntary movements may become apparent only a few days after parenteral replacement therapy has begun.¹ The exact reason for this paradoxical early worsening is not fully understood, but it is generally transient. If you start B12 injections and notice new twitching or shaking, it does not necessarily mean the treatment is making things worse. It may reflect a temporary phase as damaged neural circuits begin to reactivate.

Inherited Disorders of B12 Metabolism

Most discussions of B12 deficiency focus on dietary intake or absorption problems, but a separate category exists: genetic conditions that impair the body’s ability to process B12 even when intake is adequate. These inherited cobalamin metabolism defects can present in infancy or early childhood with severe neurological problems, including demyelination and axonal loss in both the central and peripheral nervous systems.³ The neurological manifestations in these children can be diverse and severe, sometimes appearing before any changes show up in standard blood counts.

These conditions are rare, but they matter because the treatment is often still B12 supplementation, sometimes in specific forms or combined with other cofactors. Recognizing them requires a high index of suspicion, especially when an infant or young child develops neurological regression, movement abnormalities, or failure to thrive without an obvious dietary explanation. Specialized metabolic testing, including urine organic acids and plasma amino acid panels, can point toward a specific genetic defect. For families affected by these conditions, early and sustained treatment is the difference between progressive disability and relatively normal development.

Practical Steps If You Suspect a B12-Related Tremor

If you or someone you know has developed a new tremor, especially alongside any combination of numbness, balance trouble, fatigue, or cognitive fog, getting B12 levels checked is a reasonable first move. Mention any risk factors to your doctor: a vegetarian or vegan diet, metformin use, a history of stomach surgery, heavy antacid use, or older age. If the standard serum B12 comes back in the low-normal range and symptoms persist, ask about methylmalonic acid testing to look for functional deficiency.¹²

For infants, pediatricians should consider B12 status in any exclusively breastfed baby showing developmental regression, tremors, or irritability, particularly if the mother follows a plant-based diet or has her own risk factors for deficiency. Supplementing the mother during pregnancy and breastfeeding is a straightforward preventive strategy that pediatric and neurological guidelines increasingly emphasize.⁸ The stakes are high enough, and the test simple enough, that a low threshold for checking is hard to argue against.

1
PubMed. Involuntary movements due to vitamin B12 deficiency
2
Philippine Journal of Neurology. Vitamin B12 Deficiency Presenting as Slow Orthostatic Tremor: A Case Report
3
PubMed Central. Inherited disorders of cobalamin metabolism in childhood: biochemical and clinical perspectives
4
PubMed. Retardation of myelination due to dietary vitamin B12 deficiency: cranial MRI findings
5
Journal of the Korean Neurological Association. Subacute Combined Degeneration due to Vitamin B12 Deficiency with Serologic Evidence of Autoimmune Gastritis and Non-specific Endoscopic Findings
6
PubMed Central. Spinal MR imaging in Vitamin B12 deficiency: Case series; differential diagnosis of symmetrical posterior spinal cord lesions
7
PubMed Central. Infantile Tremor Syndrome With Movement Disorder: Current Perspective
8
PubMed Central. Vitamin-Responsive Movement Disorders in Children
9
PubMed Central. Parkinson’s disease and vitamins: a focus on vitamin B12
10
PubMed Central. Long-term metformin therapy and vitamin B12 deficiency: An association to bear in mind
11
International Journal of Innovative Technologies in Social Science. NORMAL SERUM VITAMIN B12 LEVELS IN SYMPTOMATIC PATIENTS: DIAGNOSTIC VALUE OF METHYLMALONIC ACID AND HOMOCYSTEINE IN FUNCTIONAL DEFICIENCY
12
PubMed Central. Vitamin B12 deficiency: testing and treatment
13
PubMed. Metabolic and toxic causes of myelopathy
14
PubMed Central. Diagnosis, Treatment and Long-Term Management of Vitamin B12 Deficiency in Adults: A Delphi Expert Consensus