“Numbness” can be used by patients to describe various symptoms, including loss of sensation, abnormal sensations, and weakness or paralysis. However, numbness is actually loss of sensation, either partial (hypesthesia) or complete (anesthesia). Numbness may involve the 3 major sensory modalities—light touch, pain and temperature sensation, and position and vibration sensation—to the same or different degrees.

Numbness is often accompanied by abnormal sensations of tingling (pins-and-needles) unrelated to a sensory stimulus (paresthesias). Other manifestations (eg, pain, extremity weakness, nonsensory cranial nerve dysfunction) may also be present depending on the cause. Adverse effects of chronic numbness include difficulty walking and driving and increased risk of falls. In addition, infections, diabetic foot ulcers, and injuries may not be recognized, leading to delayed treatment.


Anatomy: Sensory processing areas within the brain connect with cranial nerves or spinal cord sensory pathways. Sensory fibers exiting the spinal cord join just outside the cord to form dorsal nerve roots (except for C1—see Fig. 1: Spinal Cord Disorders: Spinal nerve.). These 30 dorsal sensory roots join with corresponding motor ventral roots to form spinal nerves. Branches of the cervical and lumbosacral spinal nerves join more distally to form plexuses and then branch into nerve trunks. The intercostal nerves do not form plexuses; these nerves correspond to their segment of origin in the spinal cord. The term peripheral nerve refers to the part of the nerve distal to the nerve root and plexus.

Nerve roots from the most distal spinal cord segments descend within the spinal column below the end of the spinal cord, forming the cauda equina. The cauda equina supplies sensation to the pubic, perineal, and sacral areas (saddle area).

The spinal cord is divided into functional segments (levels) that correspond approximately to the attachments of the pairs of spinal nerve roots. The area of skin supplied mostly by a particular spinal nerve is the dermatome corresponding to that spinal segment (see Fig. 1: Approach to the Neurologic Patient: Sensory dermatomes. ).

Mechanisms: Numbness can occur from dysfunction anywhere along the pathway from the sensory receptors up to and including the cerebral cortex. Common mechanisms include the following:

Ischemia (eg, brain or spinal cord infarction, vasculitis)

Demyelinating disorders (eg, multiple sclerosis, Guillain-Barré syndrome)

Mechanical nerve compression (eg, by tumors or a herniated disk [nucleus pulposus], in carpal tunnel syndrome)

Infections (eg, HIV, leprosy)

Toxins or drugs (eg, heavy metals, certain chemotherapy drugs)

Metabolic disorders (eg, diabetes, chronic kidney disease, thiamin or vitamin B12 deficiency)

Immune-mediated disorders (eg, postinfectious inflammation, such as transverse myelitis)

Degenerative disorders (eg, hereditary neuropathies)


There are many causes of numbness. Although there is some overlap, dividing the causes based on the pattern of numbness can be helpful (see Approach to the Neurologic Patient: Some Causes of Numbness).

Table 5

Some Causes of Numbness

Suggestive Findings
Diagnostic Approach

Unilateral numbness of both limbs*

Cortical dysfunction (eg, stroke, tumor, multiple sclerosis, degenerative brain disorders)
Facial and body sensations lost on the same side, plus loss of cortical sensation (eg, agraphesthesia, astereognosis, extinction)

Usually nonsensory neurologic deficits (eg, weakness, hyperreflexia, ataxia)

Upper brain stem or thalamus dysfunction (eg, stroke, tumor, abscess)
Facial and body sensations lost on the same side

Often cranial nerve deficits (eg, oculomotor nerve palsy on the side opposite the numbness in some upper brain stem strokes)
MRI (preferred for brain stem dysfunction) or CT

Lower brain stem dysfunction (eg, stroke, tumor, degenerative brain disorders)
Facial and body sensations lost on opposite sides (crossed face-body distribution)

Often cranial nerve deficits

Bilateral numbness of the limbs or trunk

Transverse myelopathy† (eg, spinal cord compression, transverse myelitis)
Loss of sensory, motor, and reflex function below a specific spinal segment

Autonomic dysfunction (eg, bowel, bladder, and erectile dysfunction; anhidrosis)

Dorsal column spinal cord dysfunction (eg, multiple sclerosis, vitamin B12 deficiency, tabes dorsalis)
Disproportionate loss of vibration and position sensation

In vitamin B12 deficiency, bilateral and symmetric findings (usually due to spinal cord dysfunction, although peripheral neuropathy may contribute)

Vitamin B12 level, CSF cell count and protein, CSF and blood tests for syphilis

Compression of the cauda equina—also called cauda equina syndrome† (eg, due to a herniated disk or spinal or vertebral metastases)
Numbness affecting primarily the perineum (saddle area)

Often urinary retention, fecal incontinence, and/or loss of sphincter reflexes (eg, anal wink, bulbocavernosus)

Polyneuropathies such as

Axonal polyneuropathies (eg, those associated with drugs, diabetes, chronic kidney disease, metabolic disorders)

Demyelinating polyneuropathies (eg, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, toxic or drug-related demyelinating polyneuropathy—see Peripheral Nervous System and Motor Unit Disorders: Polyneuropathy)
Bilateral, roughly symmetric, mostly distal (stocking-glove distribution) paresthesias and sensory deficits

Sometimes weakness and hyporeflexia (eg, in demyelinating polyneuropathies)

Electrodiagnostic testing

Laboratory testing based on suspected disorder

Multiple mononeuropathy—also called mononeuritis multiplex (eg, associated with connective tissue disorders, infection, or metabolic disorders such as diabetes)
Numbness with or without pain

Usually motor and reflex deficits in the distribution of multiple peripheral nerves, sometimes affecting specific nerves sequentially (but may be clinically indistinguishable from stocking-glove distribution)
Usually electrodiagnostic testing and laboratory testing based on suspected disorder

Numbness of part of a single limb

Radiculopathy‡ (eg, a herniated disk, bone compression due to OA or RA, carcinomatous meningitis, infectious radiculopathy)
Pain (sometimes like an electric shock), sensory, and often motor and/or reflex deficits in a nerve root distribution (see Table 5: Peripheral Nervous System and Motor Unit Disorders: Symptoms of Common Radiculopathies by Cord Level)

Pain possibly worsened by moving the spine or a Valsalva maneuver

Sometimes electrodiagnostic testing

Plexopathy (eg, brachial or lumbar plexopathy, brachial neuritis, thoracic outlet compression syndrome)
Sensory deficits, pain, and motor deficits in part of a limb (sometimes most of a limb) in a distribution larger than that caused by radiculopathy or single mononeuropathy
Electrodiagnostic testing

MRI unless the cause is trauma or suspected brachial neuritis

Single mononeuropathy (eg, carpal, cubital, radial, and tarsal tunnel syndromes; ulnar, radial, and peroneal nerve palsies)
Numbness (with or without pain) and motor and reflex deficits in the distribution of a single peripheral nerve
Clinical evaluation

Sometimes electrodiagnostic testing

*Only a single entire limb may be affected; the trunk may be affected.

†Conus medullaris syndrome is a transverse myelopathy at about the L1 level. Findings are similar to those of cauda equina syndrome.

‡Findings may be bilateral.

OA = osteoarthritis.


Because so many disorders can cause numbness, a sequential evaluation is done. First, the distribution of numbness is used to localize the part of the nervous system that is involved. Then, other clinical features—particularly rate of onset, associated neurologic symptoms and signs, and symmetry—further narrow the differential diagnosis and thus guide further questions and tests to diagnose specific causative disorders.

Although in practice certain elements of the history are typically asked selectively (eg, patients with a typical stroke syndrome are not usually asked at length about risk factors for polyneuropathy and vice versa), many of the potentially relevant components of the history are presented here for informational purposes.

History: History of present illness should include using an open-ended question to ask patients to describe numbness. Symptom onset, duration, and time course should be ascertained. Most important are the location of numbness and associated neurologic symptoms (eg, paresis, dysesthesias, sphincter dysfunction such as incontinence or retention, dysphasia, visual loss, diplopia, dysphagia, cognitive decline). Possible precipitating causes (eg, compression of an extremity, trauma, recent intoxication or sleeping in an awkward position, symptoms of infection) are sought.

Review of systems should identify symptoms of causative disorders. Some examples are back and/or neck pain (osteoarthritis- or RA-associated herniated disk, spinal cord compression), fever and/or rash (infectious neuropathy, infectious radiculopathy, brain infection, rheumatic disorders), headache (brain tumor, stroke, encephalopathy), joint pain (rheumatic disorders), undernutrition (vitamin B12 deficiency), and excessive intake of high-mercury seafood (polyneuropathy).

Past medical history should identify known conditions that can cause numbness, particularly diabetes or chronic kidney disease (polyneuropathy); infections such as HIV, syphilis, or Lyme disease (infectious peripheral neuropathy or brain infection); CAD, atrial fibrillation, atherosclerosis, or smoking (stroke); and osteoarthritis or RA (radiculopathy). Family history should include information about any familial neurologic disorders. Drug and social history should include use of all drugs and substances and occupational exposures to toxins.

Physical examination: A complete neurologic examination (see Approach to the Neurologic Patient: Neurologic Examination) is done, emphasizing the location and neurologic territories of deficits in reflex, motor, and sensory function. In general, reflex testing is the most objective examination, and sensory testing is the most subjective; often, the area of sensory loss cannot be precisely defined.

Red flags: The following findings are of particular concern:

Sudden onset (eg, within minutes or hours) of numbness

Sudden or rapid onset (eg, within hours or days) of weakness


Signs of cauda equina or conus medullaris syndrome (eg, saddle anesthesia, incontinence, loss of anal wink reflex)

Neurologic deficits below a spinal segment

Loss of sensation on both the face and body (on the same side or opposite sides)

Interpretation of findings: The anatomic pattern of symptoms suggests the location of the lesion but is often not specific. In general,

Numbness of part of one limb: Peripheral nervous system lesion

Unilateral numbness of both limbs (with or without the trunk): Brain lesion

Bilateral numbness below a specific dermatomal level: Transverse myelopathy (a spinal cord lesion)

Bilateral numbness not corresponding to a specific dermatomal level: Polyneuropathy, multiple mononeuropathy, or a patchy spinal cord or brain disorder

More specific localizing patterns include the following:

Stocking-glove distribution: When motor signs are minimal or absent, usually an axonal polyneuropathy; when accompanied by weakness and spasticity (eg, hyperreflexia, increased tone, extensor plantar response), sometimes cervical spondylosis or a demyelinating polyneuropathy or demyelinating lesion of the spinal cord

Single dermatomal distribution: Nerve root lesion (radiculopathy)

Single extremity with more than one nerve or nerve root affected: Plexus lesion (plexopathy)

Multiple related or unrelated peripheral nerves: Multiple mononeuropathy

Loss of sensation affecting position and vibration disproportionately: Dysfunction of the dorsal columns or a demyelinating peripheral neuropathy

Saddle area distribution: Conus medullaris syndrome or compression of the cauda equina (cauda equina syndrome)

Crossed face-body distribution (ie, face and body affected on different sides): Lower brain stem lesion

Ipsilateral face and body distribution: Upper brain stem, thalamic, or cortical lesion

Findings that indicate involvement of multiple anatomic areas (eg, both brain and spinal cord lesions) suggest more than one lesion (eg, multiple sclerosis, metastatic tumors, multifocal degenerative brain or spinal cord disorders, or more than one causative disorder.

The rate of symptom onset helps suggest likely pathophysiology:

Nearly instantaneous (usually seconds, occasionally minutes): Ischemic

Hours to days: Infectious or toxic-metabolic

Days to weeks: Infectious, toxic-metabolic, or immune-mediated

Weeks to months: Neoplastic or degenerative

Degree of symmetry also provides clues. Highly symmetric involvement suggests a systemic cause (eg, a metabolic, toxic, drug-related, infectious, or postinfectious cause; vitamin deficiency). Clearly asymmetric involvement suggests a structural cause (eg, tumor, trauma, stroke, peripheral plexus or nerve compression, a focal or multifocal degenerative disorder).

After location of the lesion, rate of onset, and degree of symmetry have been determined, the list of potential specific diagnoses is much smaller, so that focusing on clinical features that differentiate among them is practical (see Table 1). For example, if initial evaluation suggests an axonal polyneuropathy, subsequent evaluation focuses on features of each of the many possible drugs, toxins, and disorders that can cause these polyneuropathies.

Testing: Testing is required unless the diagnosis is clinically obvious and conservative treatment is elected (eg, in some cases of carpal tunnel syndrome, for a herniated disk or traumatic neuropraxia). Test selection is based on anatomic location of the suspected cause:

Peripheral nerves or nerve roots: Nerve conduction studies and electromyography (electrodiagnostic testing)

Brain or spinal cord: MRI

Electrodiagnostic tests can help differentiate between neuropathies and plexopathies (lesions distal to the nerve root) and more proximal lesions (eg, radiculopathies) and between types of polyneuropathies (eg, axonal and demyelinating, hereditary and acquired).

If clinical findings suggest a structural lesion of the brain or spinal cord or a radiculopathy, MRI is usually indicated. CT is usually a second choice but may be particularly helpful if MRI is not available soon enough (eg, in emergencies). However, CT is rarely helpful for brain stem lesions.

After the lesion is localized, subsequent testing can focus on specific disorders (eg, metabolic, infectious, toxic, autoimmune, or other systemic disorders). For example, if findings indicate a polyneuropathy, subsequent tests typically include CBC, electrolytes, renal function tests, rapid plasma reagin test, and measurement of fasting plasma glucose, hemoglobin A1C, vitamin B12, folate, and thyroid-stimulating hormone. Some clinicians include serum protein electrophoresis.


Treatment is directed at the disorder causing numbness.

Patients with insensitive feet, particularly if circulation is impaired, should take precautions to prevent and recognize injury. Socks and well-fitting shoes are needed when walking, and shoes must be inspected for hidden foreign material before wear. The feet should be inspected frequently for ulcers and signs of infection. Patients with insensitive hands or fingers must be alert when handling potentially hot or sharp objects.

Patients with diffuse sensory loss or loss of position sense should be referred to a physical therapist for gait training. Precautions should be taken to prevent falls (see Falls in the Elderly: Prevention). Driving skill should be monitored.

Key Points

Use an open-ended question to ask patients to describe their numbness.

The anatomic pattern and time course of symptoms helps narrow the list of possible diagnoses.

If part of a limb is numb, suspect a peripheral nerve, plexus, or nerve root lesion.

If both limbs are numb on one side, with or without numbness of the trunk on the same side, suspect a brain lesion.

If patients have bilateral numbness below a specific spinal cord segment, particularly with motor and reflex deficits, suspect a transverse myelopathy.

If patients have bilateral numbness not corresponding to a spinal cord segment, suspect a polyneuropathy, multiple mononeuropathy, or a patchy spinal cord or brain lesion.

If numbness occurs in a stocking-glove distribution, suspect an axonal polyneuropathy.

If numbness occurs suddenly, suspect an acute ischemic event.

Usually, first do electrodiagnostic studies for suspected peripheral nervous system causes and MRI for CNS causes.


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