The medical term for abnormal sensations is “paresthesia,” and it includes a wide range of experiences: numbness (reduced ability to feel), tingling (the “pins and needles” sensation), burning, prickling, crawling sensations, and heightened sensitivity to touch. These sensations most commonly affect the hands and feet but can occur anywhere in the body.

While temporary numbness or tingling — like when your foot “falls asleep” from sitting in one position too long — is harmless, persistent or recurring symptoms often indicate peripheral neuropathy: damage to or dysfunction of the peripheral nerves that carry sensory information from your body to your brain. Many causes of peripheral neuropathy are metabolic or nutritional and are readily detected through blood tests.

This article explores why numbness and tingling happen, what underlying conditions might be responsible, and what blood tests can reveal about the health of your nerves.

Understanding Numbness and Tingling

Your peripheral nervous system is an intricate network of nerves that extends from your spinal cord to every part of your body. Think of it as the body’s communication network — millions of nerve fibers carrying signals back and forth between your brain and the rest of your body. These nerves carry three types of signals: sensory information (touch, temperature, pain, position sense) traveling from body to brain; motor commands traveling from brain to muscles; and autonomic signals controlling involuntary functions like heart rate, blood pressure, digestion, sweating, and bladder function.

When peripheral nerves are damaged or dysfunctional, sensory symptoms are often the first to appear — sometimes years before motor symptoms develop. The sensory nerves are particularly vulnerable because many have very long fibers extending from the spinal cord to the toes, making them susceptible to metabolic insults along their entire length. Understanding the pattern of your symptoms provides important clues about the underlying cause and helps guide appropriate testing.

Types of abnormal sensations:

Numbness (hypoesthesia): Reduced ability to feel touch, pressure, temperature, or pain. The area may feel “dead,” as if it’s been injected with novocaine, or as if it’s covered with a thick layer of fabric or glove. Numbness can range from subtle decreased sensation to complete lack of feeling. This is a “negative” symptom — loss of normal sensation. Numbness can be dangerous because it reduces awareness of injuries — people with numb feet may not notice cuts, blisters, burns, or even broken bones.

Tingling (paresthesia): The classic “pins and needles” sensation, similar to what happens when a limb “falls asleep” after being in one position too long. Unlike that temporary situation, pathological tingling persists or recurs without obvious positional cause. May be constant or intermittent, mild or intense. Often described as prickling, buzzing, electric, fizzing, crawling, or like static electricity running through the skin. This is a “positive” symptom — abnormal sensation rather than loss of sensation.

Burning: A sensation of heat or burning without actual temperature change — the skin feels like it’s on fire or scalded, yet appears normal and isn’t actually warm. Common in certain types of neuropathy, particularly diabetic small fiber neuropathy and inflammatory neuropathies. Can be extremely distressing and difficult to treat.

Electric shock sensations: Brief, sharp, shooting pains that feel like electrical jolts traveling along a nerve pathway. May be spontaneous or triggered by movement, touch, or even temperature change. Can be startling and frightening when they occur unexpectedly.

Heightened sensitivity (hyperesthesia/allodynia): Increased sensitivity where normal, innocuous touch feels exaggerated, uncomfortable, or frankly painful. The light brush of clothing against skin may be uncomfortable; the pressure of bedsheets may be intolerable. This represents disordered pain processing by damaged nerves.

Abnormal temperature perception: Feeling cold when the temperature is normal, or misinterpreting temperature signals. Some people feel like they’re walking on ice when their feet are actually at room temperature. Others may not perceive heat properly, creating risk for burns.

Loss of position sense (proprioception): Difficulty knowing where your limbs are in space without looking at them. You may not know where your foot is landing when you walk unless you watch it. This causes particular difficulty walking in the dark, on uneven surfaces, or with eyes closed. May cause a sensation of “walking on cotton” or feeling like the ground is unsteady beneath you.

Tightness or band-like sensations: Feeling of bands wrapped tightly around limbs, or of wearing a sock or glove that’s too tight, even when barefoot or bare-handed.

Patterns that suggest specific causes:

“Stocking-glove” distribution: Symptoms that start in the toes and gradually progress up the feet to the ankles, calves, and eventually thighs — or start in the fingertips and progress up through the hands and forearms — following a pattern like putting on stockings and gloves. This symmetric, length-dependent pattern is the hallmark of metabolic and toxic neuropathies, including diabetic neuropathy, B12 deficiency, thyroid dysfunction, kidney disease, and alcoholic neuropathy. The longest nerves are affected first because they’re most vulnerable to metabolic insults — there’s simply more nerve length to be damaged, and the far ends of nerves are most vulnerable to problems with their blood supply and metabolic support.

Asymmetric or patchy distribution: Symptoms affecting one limb more than another, affecting one area while sparing the corresponding area on the other side, or affecting different areas unpredictably. This pattern may suggest nerve entrapment (compression of a nerve at a specific point), mononeuropathy multiplex (damage to multiple individual nerves), vasculitis (inflammation of blood vessels supplying nerves), or certain inflammatory conditions.

Single nerve distribution: Numbness or tingling confined to a specific anatomical pattern that corresponds to one nerve’s sensory territory. Examples include the thumb, index finger, middle finger, and half of the ring finger (median nerve, as in carpal tunnel syndrome), the little finger and adjacent half of the ring finger (ulnar nerve), the outer forearm and thumb base (radial nerve), or a band-like area on the outer thigh (lateral femoral cutaneous nerve). This pattern strongly suggests nerve compression or entrapment at a specific location.

Dermatomal pattern: Symptoms following a band-like distribution around the trunk or down a limb, corresponding to the territory supplied by a single spinal nerve root. This suggests radiculopathy — compression of a nerve root as it exits the spine, typically from disc herniation, spinal stenosis, or arthritic changes. The pattern follows predictable paths: C6 radiculopathy affects the thumb side of the forearm and hand; L5 radiculopathy affects the outer calf and top of the foot, and so on.

Both sensory and motor involvement: When numbness is accompanied by weakness, muscle wasting (atrophy), fasciculations (visible muscle twitching), or difficulty with fine motor tasks like buttoning shirts, more extensive nerve damage is likely. Motor involvement suggests either more severe neuropathy or different underlying causes.

When to be concerned:

Many people experience occasional temporary numbness or tingling — from sleeping on an arm, sitting cross-legged too long, or leaning on an elbow. This typically resolves within minutes once position is changed. Seek medical evaluation for numbness and tingling that:

• Persists for more than a few days without obvious cause (like an awkward sleeping position)
• Is progressive — gradually spreading to larger areas or moving up a limb over weeks to months
• Affects both sides of the body symmetrically (this pattern suggests a systemic cause that blood tests can often identify)
• Is accompanied by weakness or difficulty with coordination or balance
• Affects bladder or bowel function (urgent — may indicate spinal cord involvement)
• Follows an injury, especially to the neck or back
• Is accompanied by other symptoms like unexplained fatigue, weight loss, or fever
• Significantly interferes with daily activities or sleep

Emergency warning signs:

Seek immediate medical care if numbness or tingling:

• Comes on suddenly with weakness on one side of the body, facial drooping, difficulty speaking, vision changes, or severe headache — these are possible signs of stroke and require emergency evaluation
• Affects the genital area, buttocks, or inner thighs (“saddle area”) with bladder or bowel dysfunction — this pattern suggests cauda equina syndrome, compression of the nerve roots at the base of the spine, which is a surgical emergency requiring immediate treatment to prevent permanent damage
• Rapidly progresses up the legs with weakness over days — possible Guillain-Barré syndrome, an acute inflammatory neuropathy that can affect breathing and requires hospital monitoring
• Occurs after significant neck or back injury — may indicate spinal cord or nerve damage
• Is accompanied by severe pain, especially new severe back pain — could indicate serious spinal pathology

Diabetes and Prediabetes: The Leading Cause

Diabetic peripheral neuropathy is the most common cause of peripheral neuropathy in developed countries, affecting an estimated 50% of people with diabetes at some point during their lives. For many people, peripheral neuropathy is what brings them to the doctor where diabetes is then discovered — the nerve damage was the first obvious symptom of a disease that had been silently progressing.

But here’s what many people don’t realize: neuropathy can develop during prediabetes — sometimes years before blood sugar levels reach the diabetic threshold. In fact, studies show that 10-30% of people with unexplained neuropathy have impaired glucose tolerance (prediabetes) when properly tested. This means that waiting until someone has frank diabetes to consider blood sugar as a cause of neuropathy misses a significant opportunity for early intervention.

How high blood sugar damages nerves:

The relationship between elevated blood sugar and nerve damage involves multiple interconnected mechanisms that researchers are still working to fully understand:

• Polyol pathway activation: When blood glucose is high, excess glucose is converted to sorbitol through an enzyme called aldose reductase. Sorbitol accumulates inside nerve cells, drawing in water and causing osmotic damage. This also depletes other important molecules (myo-inositol, taurine) needed for normal nerve function.
• Advanced glycation end products (AGEs): Chronic hyperglycemia causes glucose to attach non-enzymatically to proteins, lipids, and nucleic acids, forming AGEs. These modified molecules don’t function properly and accumulate in nerve tissue, directly damaging nerve structure and triggering inflammation.
• Microvascular damage: High blood sugar damages the tiny blood vessels (vasa nervorum) that supply oxygen and nutrients to nerve fibers. Just as diabetes damages blood vessels in the eyes (retinopathy) and kidneys (nephropathy), it damages vessels feeding nerves. Impaired blood flow leads to nerve ischemia — essentially, the nerves are slowly starving.
• Oxidative stress: Hyperglycemia dramatically increases production of reactive oxygen species (free radicals) that damage nerve cell membranes, proteins, mitochondria, and DNA. The nervous system is particularly vulnerable to oxidative damage.
• Inflammation: Chronic hyperglycemia triggers inflammatory pathways that contribute to nerve damage. Elevated inflammatory markers are found in people with diabetic neuropathy.
• Impaired nerve repair mechanisms: Under normal conditions, nerves have some capacity for repair and regeneration. High blood sugar interferes with these repair processes, so damage accumulates rather than being corrected.
• Protein kinase C activation: High glucose activates this enzyme, which affects blood flow, basement membrane thickness, and multiple aspects of cell function that contribute to nerve damage.

Characteristics of diabetic neuropathy:

• Classic stocking-glove pattern: Symptoms typically begin in the toes and gradually progress up the feet and lower legs. When symptoms reach the knee level, hands often start to become involved. This length-dependent pattern reflects the vulnerability of the longest nerve fibers — they have the most length to be damaged and the greatest metabolic demands.
• Sensory symptoms predominate initially: Numbness, tingling, burning, prickling, and pain are usually the earliest symptoms. The burning pain of diabetic neuropathy can be particularly severe and distressing, often worse at night and interfering with sleep.
• Multiple sensory modalities affected: Light touch, temperature perception, pin-prick sensation, and vibration sense may all be affected. Loss of vibration sense (tested with a tuning fork) is often one of the earliest findings.
• Gradual, insidious onset: Symptoms develop slowly over months to years, not suddenly. Many people don’t notice the progression until significant damage has occurred. Some people have substantial nerve damage with minimal symptoms.
• Loss of protective sensation: As neuropathy progresses, the ability to feel pain and temperature diminishes — and this is actually dangerous. Normally, pain protects us by alerting us to injury. With numb feet, cuts, blisters, burns, or pressure ulcers may go unnoticed, leading to serious infections and, in severe cases, amputation. This is why foot care is so critical in diabetes.
• Autonomic involvement: Diabetic neuropathy can also affect the autonomic nerves, causing a constellation of symptoms: orthostatic hypotension (dizziness on standing from blood pressure dysregulation), gastroparesis (delayed stomach emptying causing nausea, bloating, early satiety), bladder dysfunction (incomplete emptying, overflow incontinence), erectile dysfunction in men, abnormal sweating (often decreased in feet but excessive in upper body), and cardiac autonomic neuropathy (which affects heart rate variability and increases cardiac risk).
• Treatment-induced neuropathy: Paradoxically, some people develop or experience worsening neuropathy when blood sugar is brought under rapid control — called “treatment-induced neuropathy of diabetes” or sometimes “insulin neuritis.” This is typically self-limited but can be distressing. It underscores that gradual rather than abrupt blood sugar normalization may be preferable.

Prediabetes and neuropathy:

The conventional view that neuropathy only occurs after years of established diabetes has been overturned by research showing nerve damage begins earlier in the disease process. The metabolic dysfunction of prediabetes — not just glucose elevation but also insulin resistance, increased oxidative stress, inflammation, dyslipidemia, and hypertension — creates a toxic environment for nerves even when fasting glucose and HbA1c are only mildly elevated.

Studies using glucose tolerance testing have found that a significant percentage of people with “idiopathic” neuropathy (neuropathy of unknown cause) actually have impaired glucose tolerance that wouldn’t be detected by fasting glucose or HbA1c alone. This has important implications:

• More comprehensive glucose testing (including glucose tolerance tests) may be warranted in unexplained neuropathy
• Prediabetes should be taken seriously as a cause of neuropathy, not dismissed as “not diabetes yet”
• Early intervention with lifestyle changes (weight loss, exercise, dietary modification) can often reverse prediabetes and may slow or halt neuropathy progression
• This represents a window of opportunity before both full diabetes and more severe neuropathy develop

What to test:

Fasting glucose — screens for diabetes and prediabetes, but may miss people with normal fasting glucose but abnormal post-meal responses.

HbA1c — reflects average blood sugar over 2-3 months. More reliable than a single glucose measurement for detecting chronic elevation. HbA1c is now used for diabetes diagnosis.

Fasting insulin — identifies insulin resistance, which may be present even when glucose is still normal. Elevated fasting insulin indicates metabolic dysfunction that may contribute to nerve damage through mechanisms beyond glucose toxicity alone.

An oral glucose tolerance test (measuring glucose before and after drinking a standard glucose solution) may be recommended by your healthcare provider if standard tests are normal but there’s strong clinical suspicion of glucose intolerance. This test can reveal abnormal glucose handling that fasting tests miss.

Vitamin B12 Deficiency: A Critical Cause

Vitamin B12 deficiency is one of the most important causes of peripheral neuropathy to identify — and one that’s frequently missed or diagnosed late. It’s important because B12 deficiency is common (particularly in certain populations), it’s easily treatable with supplementation, and if left untreated, it can cause permanent, irreversible nerve damage. Early diagnosis can mean the difference between complete recovery and lasting disability.

B12 is essential for maintaining the myelin sheath — the insulating layer around nerves that allows rapid, efficient signal transmission. Think of myelin like the insulation around electrical wires; without it, signals “leak” and transmission slows or fails. B12 is also critical for DNA synthesis and for maintaining the integrity of nerve fibers themselves. Without adequate B12, both the myelin sheath and the nerve fibers deteriorate.

How B12 deficiency causes neuropathy:

• Demyelination: B12 is required for the synthesis and maintenance of myelin. When B12 is deficient, myelin production falters and existing myelin breaks down. This slows nerve conduction velocity and eventually damages the underlying nerve axons themselves. Demyelination is initially patchy but becomes more widespread as deficiency persists.
• Subacute combined degeneration of the spinal cord: Severe or prolonged B12 deficiency can affect not just peripheral nerves but the spinal cord itself, causing a characteristic syndrome involving the posterior columns (which carry position sense and vibration sensation) and lateral columns (which carry motor signals). This causes a combination of sensory loss, weakness, and balance problems that can become permanent.
• Methylation defects: B12 is a cofactor for enzymes involved in methylation reactions critical for nerve function. Deficiency disrupts these metabolic processes, affecting neurotransmitter synthesis and nerve membrane maintenance.
• Elevated homocysteine and methylmalonic acid: Without adequate B12, these metabolic intermediates accumulate and may directly contribute to nerve damage.

Characteristics of B12 deficiency neuropathy:

• Sensory symptoms: Numbness, tingling, pins and needles, and burning sensations. The distribution is typically symmetric, often described as stocking-glove, but B12 deficiency neuropathy sometimes affects the hands more prominently than typical diabetic neuropathy — when someone presents with hand numbness before or more severely than feet, B12 deficiency should be strongly considered.
• Loss of position sense (proprioception): Difficulty knowing where your limbs are in space without looking at them. This is a hallmark of B12 deficiency and reflects damage to the dorsal columns of the spinal cord. People may describe feeling like they’re “walking on pillows” or that the ground feels unsteady.
• Balance problems and gait disturbance: The combination of impaired position sense and damage to motor pathways causes unsteadiness. People have particular difficulty walking in the dark (when they can’t use vision to compensate for lost proprioception), on uneven surfaces, or with eyes closed. The gait may become wide-based and ataxic (uncoordinated). The classic Romberg sign — swaying or falling when standing with feet together and eyes closed — indicates dorsal column dysfunction.
• Can occur without anemia: This is absolutely crucial and often leads to delayed diagnosis. The neurological manifestations of B12 deficiency can develop before blood count changes appear — sometimes by months or even years. Waiting for macrocytic anemia (large red blood cells) before testing B12 may result in preventable, potentially permanent nerve damage. The nervous system is more sensitive to B12 deficiency than the blood-forming system.
• Cognitive symptoms: B12 deficiency affects the brain as well as peripheral nerves, causing memory problems, difficulty concentrating, mental slowness, confusion, personality changes, and in severe cases, dementia and psychosis. These may be mistaken for Alzheimer’s disease or other forms of dementia.
• Other symptoms: Glossitis (smooth, sore tongue), fatigue, weakness, and mood changes including depression may accompany the neurological findings.

Who’s at risk for B12 deficiency:

• Vegetarians and vegans: Vitamin B12 is found almost exclusively in animal products — meat, fish, eggs, and dairy. Without supplementation or fortified foods, plant-based diets inevitably lead to B12 deficiency, though it may take years to deplete body stores.
• Older adults: Stomach acid production decreases with age (a condition called atrophic gastritis), and gastric acid is needed to release B12 from food proteins. Additionally, intrinsic factor production may decline. Up to 30% of older adults have reduced B12 absorption. B12 deficiency should always be considered in older people with cognitive decline or neurological symptoms.
• People taking certain medications: Metformin (widely used for diabetes) significantly reduces B12 absorption — long-term metformin users should have B12 monitored. Proton pump inhibitors (omeprazole, pantoprazole) and H2 blockers (ranitidine, famotidine) for acid reflux also impair B12 absorption by reducing stomach acid. Long-term use of these medications is a significant risk factor.
• Pernicious anemia: An autoimmune condition in which antibodies destroy the parietal cells of the stomach that produce intrinsic factor — a protein essential for B12 absorption in the small intestine. Without intrinsic factor, B12 cannot be absorbed regardless of dietary intake. This requires lifelong B12 supplementation, typically by injection.
• Gastrointestinal conditions and surgeries: Celiac disease, Crohn’s disease (especially affecting the ileum where B12 is absorbed), gastric bypass surgery, other bariatric procedures, and any condition affecting the stomach or terminal ileum can cause B12 malabsorption.
• Alcohol use disorder: Chronic heavy alcohol use impairs B12 absorption and utilization, and is often accompanied by poor dietary intake.
• Genetic conditions: Rare genetic disorders can affect B12 metabolism or transport.

What to test:

Vitamin B12 — the direct measurement of circulating B12. However, interpretation can be tricky: B12 levels in the “low-normal” range may still be functionally insufficient for some people, as blood levels don’t always reflect tissue status. Different laboratories use different reference ranges.

Methylmalonic acid (MMA) — becomes elevated when B12 is functionally insufficient at the cellular level, even if serum B12 appears borderline or even “normal.” Elevated MMA confirms B12 deficiency and is considered more sensitive than B12 measurement alone. This test is particularly valuable when B12 is in the low-normal or indeterminate range.

Homocysteine — also elevated in B12 deficiency (and folate deficiency). Another functional marker of B12 status. Elevated homocysteine with elevated MMA strongly suggests B12 deficiency; elevated homocysteine with normal MMA suggests folate deficiency.

Complete blood count — may show macrocytic anemia (MCV elevated, indicating large red blood cells) in B12 deficiency. However, remember that neurological symptoms can precede anemia — a normal CBC does not rule out B12 deficiency.

Anti-intrinsic factor antibodies and anti-parietal cell antibodies can help diagnose pernicious anemia if B12 deficiency is confirmed.

Other Vitamin and Nutritional Deficiencies

Several other nutritional deficiencies can cause or contribute to peripheral neuropathy.

Vitamin B6 (Pyridoxine):

B6 is involved in neurotransmitter synthesis and nerve function. Both deficiency and excess can cause neuropathy:

• Deficiency: Uncommon but can occur with poor diet, alcoholism, certain medications (isoniazid), and malabsorption. Causes sensory neuropathy.
• Toxicity: More common than deficiency. High-dose B6 supplementation (typically exceeding 200mg daily for extended periods) can paradoxically cause sensory neuropathy. Symptoms usually improve when supplementation is stopped.

Vitamin B1 (Thiamine):

Thiamine deficiency causes beriberi, which includes peripheral neuropathy. In developed countries, thiamine deficiency occurs primarily with:

• Chronic alcohol use (the most common cause)
• Bariatric surgery
• Severe malnutrition
• Prolonged vomiting (including hyperemesis gravidarum)

Vitamin E:

Vitamin E deficiency is rare but can cause progressive neuropathy and balance problems. It occurs with severe fat malabsorption syndromes or rare genetic conditions affecting vitamin E transport.

Copper:

Copper deficiency causes a neuropathy similar to B12 deficiency, affecting both sensory nerves and spinal cord. It can occur with:

• Excessive zinc supplementation (zinc interferes with copper absorption)
• Gastric bypass surgery
• Malabsorption syndromes

Folate:

Folate deficiency can contribute to neuropathy, though less commonly than B12. It often co-occurs with B12 deficiency. Folate is important for nerve function and DNA synthesis.

What to test:

Vitamin B6 — if deficiency or toxicity suspected

Thiamine (B1) — especially with alcohol use history or bariatric surgery

Folate — often tested alongside B12

Copper — if zinc supplementation or malabsorption

Thyroid Dysfunction

Both hypothyroidism and hyperthyroidism can cause peripheral neuropathy, though hypothyroidism is more commonly associated with nerve symptoms.

Hypothyroidism and neuropathy:

Hypothyroidism causes neuropathy through several mechanisms:

• Metabolic effects: Thyroid hormone affects nerve metabolism. Deficiency impairs nerve function and repair.
• Myxedema: The accumulation of mucopolysaccharides in tissues can compress nerves. Carpal tunnel syndrome (compression of the median nerve at the wrist) is particularly common in hypothyroidism.
• Slowed nerve conduction: Hypothyroidism reduces the speed at which nerves conduct signals.

Hypothyroid neuropathy typically presents with:

• Numbness and tingling in hands and feet
• Carpal tunnel syndrome symptoms (numbness in thumb, index, middle finger; worse at night)
• Muscle aches and weakness
• Slowed reflexes

These symptoms usually improve with thyroid hormone replacement, though recovery may take months.

Hyperthyroidism:

Hyperthyroidism less commonly causes neuropathy but can contribute to:

• Muscle weakness (thyrotoxic myopathy)
• Tremor
• Rarely, peripheral neuropathy

What to test:

TSH — the primary screening test

Free T4 and Free T3 if TSH is abnormal

TPO antibodies — identifies autoimmune thyroid disease

Other Conditions Causing Numbness and Tingling

Kidney disease:

Chronic kidney disease causes uremic neuropathy in up to 60% of people with advanced kidney failure. When kidneys fail to adequately filter blood, metabolic waste products (uremic toxins) accumulate that healthy kidneys would normally excrete. These toxins are directly harmful to peripheral nerves. The neuropathy is typically symmetric, sensorimotor (affecting both sensation and some motor function), and affects legs more than arms. Symptoms include numbness, tingling, burning sensations, and restless legs syndrome. Uremic neuropathy tends to improve with dialysis or kidney transplantation, confirming that the accumulated toxins are responsible.

Creatinine and eGFR assess kidney function and should be checked as part of any neuropathy evaluation.

Liver disease:

Chronic liver disease can cause peripheral neuropathy through several mechanisms including accumulation of toxins and associated nutritional deficiencies (particularly B vitamins). Hepatitis C infection can cause neuropathy through associated cryoglobulinemia.

Autoimmune conditions:

Several autoimmune conditions can cause peripheral neuropathy:

• Guillain-Barré syndrome: Acute inflammatory neuropathy causing rapidly progressive weakness and sensory symptoms — a medical emergency.
• Chronic inflammatory demyelinating polyneuropathy (CIDP): The chronic counterpart to Guillain-Barré, developing gradually over months.
• Rheumatoid arthritis, lupus, Sjögren’s syndrome: Systemic autoimmune conditions that can include neuropathy. Sjögren’s is particularly associated with small fiber neuropathy.
• Vasculitis: Inflammation of blood vessels supplying nerves can cause ischemic nerve damage.

Tests for autoimmune causes may include ANA, ESR, CRP, and specific antibody panels.

Infections:

• HIV: Can cause neuropathy directly or through treatment medications
• Hepatitis C: Associated with cryoglobulinemia causing neuropathy
• Lyme disease: Can cause various neurological symptoms including neuropathy
• Shingles: Postherpetic neuralgia causes persistent pain and abnormal sensation after the rash heals

Alcohol:

Alcoholic neuropathy is common in people with chronic heavy alcohol use, resulting from both the direct neurotoxic effects of alcohol and associated nutritional deficiencies (particularly thiamine and other B vitamins). Symptoms are typically symmetric, affecting legs more than arms, with burning pain, numbness, and weakness. Stopping alcohol and supplementing B vitamins can halt progression.

Medications and toxins:

Many medications can cause peripheral neuropathy:

• Chemotherapy drugs (platinum compounds, taxanes, vinca alkaloids)
• Some antibiotics (metronidazole, fluoroquinolones, nitrofurantoin)
• Amiodarone (heart medication)
• High-dose vitamin B6 (paradoxically, excess B6 causes neuropathy)
• Some HIV medications

Industrial toxins (lead, mercury, arsenic) can also cause neuropathy.

Nerve compression syndromes:

• Carpal tunnel syndrome: Median nerve compression at the wrist — numbness in thumb, index, middle finger. Often worse at night. Very common, associated with hypothyroidism, diabetes, and repetitive hand use.
• Cubital tunnel syndrome: Ulnar nerve compression at the elbow — numbness in little finger and ring finger.
• Tarsal tunnel syndrome: Tibial nerve compression at ankle — numbness in sole of foot.
• Meralgia paresthetica: Lateral femoral cutaneous nerve compression — numbness and burning in outer thigh.

These are diagnosed primarily by history, examination, and nerve conduction studies rather than blood tests, though blood tests can identify underlying conditions (hypothyroidism, diabetes) that increase compression risk.

The Testing Strategy for Numbness and Tingling

Blood tests can identify many metabolic, nutritional, and systemic causes of peripheral neuropathy. The appropriate tests depend on the clinical picture.

Core tests for peripheral neuropathy evaluation:

Blood sugar:

• Fasting glucose
• HbA1c

Vitamin B12:

• Vitamin B12
• Methylmalonic acid if B12 borderline

Thyroid function:

• TSH

Complete blood count:

• CBC — may show macrocytic anemia (B12/folate deficiency) or other abnormalities

Kidney and liver function:

• Creatinine, eGFR
• Liver enzymes

Additional tests based on clinical suspicion:

• Folate
• Thiamine (B1) — if alcohol use or malnutrition
• Vitamin B6 — if deficiency or toxicity suspected
• Copper — if zinc supplementation or malabsorption
• Homocysteine — functional marker for B12/folate
• Inflammatory markers (ESR, CRP) — if autoimmune cause suspected
• Hepatitis B and C serologies
• HIV testing
• Serum protein electrophoresis — screens for monoclonal gammopathy

What to Do With the Results

If diabetes or prediabetes is found:

Strict blood sugar control is essential to slow neuropathy progression. Lifestyle modifications (diet, exercise, weight loss) are fundamental; medications may be needed. Early intervention in prediabetes may prevent or reverse neuropathy. Pain management may be needed for symptomatic relief.

If B12 deficiency is found:

B12 supplementation can halt progression and often leads to improvement. The route (oral vs. injection) depends on the cause of deficiency. Neurological recovery may take months and may be incomplete if deficiency was severe or prolonged — this is why early detection matters.

If thyroid dysfunction is found:

Treating hypothyroidism with thyroid hormone replacement often improves neuropathy symptoms over weeks to months. Carpal tunnel symptoms may also improve as tissue swelling resolves.

If other deficiencies are found:

Appropriate supplementation and addressing underlying causes (malabsorption, alcohol use, medication effects) are the mainstays of treatment.

When Tests Are Normal

Normal blood tests narrow the possibilities but don’t rule out all causes of numbness and tingling:

• Nerve compression syndromes: Carpal tunnel, cubital tunnel, and other entrapment neuropathies are diagnosed clinically and with nerve conduction studies, not blood tests.
• Idiopathic small fiber neuropathy: A form of neuropathy affecting small nerve fibers that may not be detected by standard tests. Diagnosed with specialized testing (skin biopsy).
• Radiculopathy: Nerve root compression from disc herniation or spinal stenosis. Diagnosed with imaging (MRI).
• Early or mild neuropathy: Blood tests may be normal in very early stages.
• Genetic neuropathies: Inherited conditions like Charcot-Marie-Tooth disease.

If blood tests are normal but symptoms persist, further evaluation with nerve conduction studies, imaging, or specialist referral may be warranted.

Protecting Your Nerves

Whether or not a specific cause is identified, these strategies support nerve health and may slow progression or help prevent neuropathy from developing:

• Control blood sugar: This is the single most important factor for preventing and managing diabetic neuropathy. Even if you don’t have diabetes, avoiding chronic blood sugar spikes protects nerves. Eat balanced meals with protein and fiber at every meal; limit refined carbohydrates and sugary foods that cause glucose spikes; get regular physical activity (which improves insulin sensitivity); maintain a healthy weight. If you have prediabetes, lifestyle changes can reverse it and protect your nerves.
• Ensure adequate B vitamins: Eat a varied diet including animal products (meat, fish, eggs, dairy) which are primary sources of B12. If vegetarian or vegan, supplementation is essential. If you take metformin or acid-blocking medications long-term, discuss B12 monitoring with your provider. Be cautious with high-dose B6 supplements — doses above 100mg daily can paradoxically cause neuropathy.
• Limit alcohol: Alcohol is directly toxic to nerves and also depletes B vitamins essential for nerve health. Moderation or abstinence protects nerve health. If you have neuropathy and drink heavily, stopping alcohol is crucial.
• Don’t smoke: Smoking impairs circulation to peripheral nerves and worsens neuropathy from any cause. Smoking also increases diabetes risk. Quitting provides both immediate and long-term nerve health benefits.
• Exercise regularly: Physical activity improves circulation, helps control blood sugar, reduces inflammation, and may directly support nerve health. Both aerobic exercise and strength training are beneficial. If neuropathy affects your balance, choose safe activities like swimming or cycling.
• Protect extremities if you have neuropathy: Check feet daily for cuts, blisters, or redness you might not feel. Wear well-fitting, protective shoes. Be careful with hot water and heating pads — you may not sense dangerous temperatures. Moisturize dry skin to prevent cracking.
• Maintain healthy weight: Obesity is associated with both diabetes and nerve compression syndromes. Weight loss improves blood sugar control and reduces mechanical compression on nerves.
• Review medications: If you develop neuropathy symptoms while on medications, discuss with your provider whether any might be contributing. Never stop medications without medical guidance, but alternatives may exist.
• Manage underlying conditions: If you have diabetes, thyroid disease, kidney disease, or other chronic conditions, optimal management protects nerve health.

The Bottom Line

Numbness and tingling that persist or progress often signal peripheral nerve dysfunction with identifiable — and frequently treatable — underlying causes. The good news is that blood tests can detect many of the most common metabolic and nutritional causes, and early treatment can often halt progression and allow nerves to recover.

Blood sugar problems (diabetes and prediabetes) are the leading cause of peripheral neuropathy and can begin causing nerve damage before blood sugar reaches diabetic levels. Vitamin B12 deficiency is another critical cause — common, easily treated, but capable of causing permanent damage if missed. Thyroid dysfunction, other nutritional deficiencies, kidney disease, and various conditions can also damage peripheral nerves.

The pattern of symptoms provides crucial diagnostic information. Symmetric “stocking-glove” numbness starting in the feet strongly suggests a metabolic cause that blood tests can identify. Asymmetric symptoms or single-nerve patterns suggest localized problems like nerve compression.

If you’re experiencing persistent numbness, tingling, or other abnormal sensations, don’t ignore them. Early identification and treatment of the underlying cause offers the best chance of halting progression and allowing nerve recovery. Peripheral nerves have some capacity to regenerate when the damaging factor is removed — but this window closes as damage becomes severe. Blood testing can put you on the path to preserving your nerve function.

Remember that the causes of numbness and tingling range from completely benign (temporary compression from awkward positions) to serious conditions requiring immediate attention. Persistent, progressive, or concerning symptoms deserve medical evaluation. A combination of careful symptom assessment and appropriate blood testing can identify most treatable causes and guide you toward effective management.

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Key Takeaways

• Numbness and tingling often signal peripheral neuropathy — damage to or dysfunction of the peripheral nerves that carry sensory information from your body to your brain
• Diabetes and prediabetes are the leading causes — nerve damage can begin before diabetes is diagnosed, making blood sugar testing essential in any neuropathy evaluation
• B12 deficiency is a critical cause to identify — it’s common, easily treatable, but can cause permanent neurological damage if missed; importantly, nerve symptoms can precede anemia
• The pattern of symptoms matters diagnostically — symmetric “stocking-glove” distribution strongly suggests metabolic causes; asymmetric or single-nerve patterns suggest compression or focal injury
• Thyroid dysfunction can cause neuropathy — hypothyroidism is particularly associated with carpal tunnel syndrome and generalized nerve symptoms
• Many medications can cause neuropathy — chemotherapy, certain antibiotics, and high-dose B6 are among the culprits; review all medications with your healthcare provider
• Nerve compression syndromes are common — carpal tunnel and other entrapments cause localized numbness and are diagnosed clinically, not with blood tests
• Early treatment can prevent permanent damage — peripheral nerves have some capacity to recover when the underlying cause is addressed, but this window closes with prolonged damage
• Normal blood tests narrow possibilities — they rule out metabolic causes, allowing focus on structural or other issues that require different evaluation
• Lifestyle factors significantly impact nerve health — blood sugar control, B vitamin adequacy, limiting alcohol, not smoking, exercise, and healthy weight all protect peripheral nerves
• B12 deficiency is a critical cause to identify — it’s common, treatable, and can cause permanent damage if missed
• The pattern matters — symmetric “stocking-glove” distribution suggests metabolic causes; asymmetric patterns suggest nerve compression
• Thyroid dysfunction can cause neuropathy — hypothyroidism is associated with carpal tunnel and other nerve symptoms
• Many medications can cause neuropathy — review all medications with your healthcare provider
• Nerve compression syndromes are common — carpal tunnel and other entrapments are diagnosed clinically, not with blood tests
• Early treatment can prevent permanent damage — nerves can recover if the underlying cause is addressed in time
• Normal blood tests narrow possibilities — but further evaluation may be needed if symptoms persist
• Lifestyle factors matter — blood sugar control, B vitamins, limiting alcohol, and not smoking all protect nerve health