Chapter 13 - Evaluation of the patient with "numbness"


Sensory complaints, and particularly the complaint of “numbness,” are common in neurologic patients. However, evaluation of such sensory problems can be quite frustrating and difficult, particularly due to the subjective nature of the symptom and the range of conditions that can cause it. Additionally, high levels of somatic awareness amongst patients with psychiatric illness make this a common symptom in psychiatric disorders. The evaluation is further complicated by frequent complaints of numbness and tingling amongst patients with certain chronic and diffuse pain problems, such as fibromyalgia. Therefore, it is essential that the evaluation proceed systematically, but always in the context of patient's presentation and associated signs and symptoms.


The history in the patient with “numbness” is extremely important. First of all, as with most neurologic complaints, you must determine what the patient means by “numbness.” Some patients are describing loss of sensitivity (anesthesia or hypesthesia) or distorted sensations (paresthesia), which is often described as tingling. Actual loss of sensitivity is more likely to represent true damage to sensory pathways in the nervous system, while paresthesia has a much broader differential. Dysesthesia, that is the perception of an unpleasant (often burning) sensation or allodynia (the perception of innocuous stimuli as being painful) may result from damage to the nervous system or, more commonly, be the manifestation of an underlying painful condition.

In addition to gaining appreciation for what the patient means by “numbness,” there are several questions that must be answered by the history. Onset: when did the symptom begin? Precipitants: was there anything that caused it or worsens it? Progression: has it been steady, progressive or does it wax and wane? Distribution: where are the symptoms and are there sharp borders? Associated symptoms: are there additional accompanying symptoms that are present? Other diseases: does the patient have symptoms of other underlying diseases? These are important considerations in diagnosis and bear further discussion.


The examination should be focused on detecting any areas of diminished sensation and the borders of this distribution. The main interest here is an attempt to define a pattern suggestive of a particular location of damage to the nervous system. It is good to have a reference available showing the approximate sensory distribution of peripheral nerves as well as nerve roots while examining patients. Broad or vague, sensory complaints with inconsistent distribution and borders are more likely to result from distorted sensory perceptions that often occur in patients with psychological distress or diffuse, chronic pain. In many such cases, you may be able to confirm of the nature of the paresthesia by magnifying or provoking the distal symptoms with maneuvers that do not directly impact the nervous system. For example, the patient complaining of paresthesias resulting from a chronic pain problem (such as fibromyalgia), will usually have “numbness” or paresthesias that are magnified by compression of painful sites in muscles, even when these maneuvers completely avoid pressing on nerves or stretching them. This finding requires evaluation of the chronic pain problem and not the “numbness.”

Sensory changes that follow artificial boundaries such as the hairline or jawline are also suggestive of hysterical sensory loss. Other findings, on examination that are suggestive of hysterical sensory loss include vibratory sensation loss across the midline of the skull, pelvis or sternum. This is because vibration of these midline osseous structures is transmitted bilaterally.

The examination may be useful in demonstrating whether the sensory loss is to all modalities, or whether there is some selectivity. For example, temperature and pin sensation are transmitted along small-diameter nerve fibers and then up the spinothalamic tract. The ability to detect vibration is transmitted via large-diameter, heavily myelinated nerve fibers and then the dorsal column-medial lemniscus tracts. Selective loss of sensation can aid in localization of damage and in understanding its mechanism.

On occasion, reflexes and other responses to simulation can be used to objectify what is fundamentally a subjective exam. The corneal reflex is a good test of trigeminal (ophthalmic) sensory loss. The reaction of the patient to unexpected stimulation with a sharp object can often confirm whether sensations are lost.

Certain laboratory studies may be helpful. Peripheral conduction along sensory pathways can be quantified with nerve conduction studies. This is particularly helpful for the evaluation of trauma or compressive neuropathies. Somatosensory evoked potentials can examine the entire sensory pathway for large diameter sensory fiber input all the way from the periphery to the cerebral cortex and often shows abnormalities in patients with disease of the dorsal column-medial lemniscus tracts of the CNS (such as with multiple sclerosis). However, despite these laboratory aids, the evaluation of the sensory system largely depends on patient cooperation and is fundamentally subjective.


Once the history and exam are completed, and once you are convinced that some sensory component of the nervous system is damaged, various factors need to be weighed to reach a conclusion about the cause.


The pattern of numbness may help define its origin. Numbness confined to a specific nerve or nerve root distribution (see the maps of dermatomes and peripheral nerve sensory innervation) lead to consideration of peripheral nerve or nerve root damage. Loss of sensation on one side of the body is more likely to result from central nervous system damage and if the sensory loss also involves the same side of the face, you can be sure that the cause is located above the level of the pons.

When there is a clear sensory level (a line on the body, below which sensations are lost), a spinal cord lesion must be suspected. Loss of sensation over the upper limbs or upper part of the trunk bilaterally, with preservation over the lower limbs and buttocks, suggests an expanding intraspinal mass. This so-called “sacral sparing” is seen with intraspinal tumors or syrinxes. Numbness over one side of the face, while being a relatively common presentation of psychiatric disease, can also be caused by damage to the lateral part of the brain stem, or upper spinal cord (spinal tract of the trigeminal). Lateral brain stem damage can also produce a picture of sensory decrease on one side of the head and on the opposite side of the body.

Numbness over the face is a relatively common hysterical presentation, reflecting psychiatric disease. This is especially true with perioral paresthesias. Often, the symptoms in these cases do not follow known anatomical nerve distributions and may appear at times of particular stress.

The distribution of symptoms may be helpful in another way. A progression of sensory complaints, particularly tingling, from one region of the body to adjacent regions (which has been described as a "march" of symptoms) is common in migraine and may be seen with focal seizures affecting the sensory cortex. Such a march of symptoms may be very helpful and distinguishing transient sensory changes due to these conditions from transient sensory loss due to stroke or transient ischemic attack.


The identification of clear precipitants for symptoms may be the best indicator of cause and often suggests a particular location of injury as well as a mechanism. This may be very clear, such as with trauma, or may be more subtle, due to the effect of activities or intercurrent illness. When symptoms are intermittent, the specific conditions under which symptoms are present may be the most important factor in diagnosis. For example, the production of distal paresthesias by neck movement or by particular neck positions suggests compressive lesions in the cervical region (nerve roots or spinal cord). Being awakened from sleep by symptoms, usually with the limb in an unusual position, suggests either local compression of a nerve or compression of the circulation to the limb. Common examples include median nerve compressive neuropathy at the wrist or ulnar nerve compression at the elbow. Also, the axillary artery can be occluded in the “thoracic outlet” by certain limb positions, resulting in ischemia of the entire limb.

Associated symptoms

The presence of associated symptoms may be also quite helpful in evaluation. For example, if the symptoms precede or accompany a migraine headache, they are likely to be part of an aura. On the other hand, if they are associated with the situation that provokes extreme anxiety, and particularly if the symptoms are perioral or in the fingers, they are quite likely to be associated with a panic attack and hyperventilation. Of course, if there are other signs or symptoms that would lead to consideration of such conditions as stroke or multiple sclerosis exacerbation, diagnosis may be facilitated.

Clinical setting

Of course, diagnosis of the cause of numbness must take place in the context of the complete presentation. For example, other associated neurologic symptoms may lead to diagnosis. Additionally, a predilection of a particular patient to certain neurologic conditions based on their age, sex or other factors, must be considered. For example, recent localized, but persistent tingling in an elderly patient should raise the suspicion of early zoster. Any tingling in one limb should be intensively investigated for peripheral entrapment or thoracic outlet syndrome. The presence of vascular risk factors, such as age, hypertension, diabetes mellitus and dyslipidemia, increase the likelihood of stroke as a cause.

Etiologies of "numbness"

There are many potential causes of sensory loss. These can basically be divided into central and peripheral.

Peripheral causes

Disorders affecting the peripheral elements of the nervous system are the more common causes of numbness and tingling. They also tend to be associated with more localized symptoms and sharper borders between normal and abnormal sensation.

Generalized polyneuropathy as well as more focal entrapment neuropathies are quite common in neurologic practice. The polyneuropathies tend to produce distal and symmetrical sensory loss starting in the feet. Only much later does it tend to affect the fingers. Differential diagnosis for polyneuropathy is discussed in a later chapter though a table of possible causes is provided here.

The peripheral entrapment neuropathies are also quite common. The distribution of symptoms is the principal mode of recognition of the specific nerve injury, and the specific positions and activities that exacerbate symptoms are important clues to mechanism. Pain is variable and is not particularly helpful in diagnosis. Tinel sign may give strong evidence of the precise location of the nerve damage though provocative measures (such as Phalen maneuver for carpal tunnel syndrome) may be more specific.

Radiculopathies tend to produce relatively localized numbness or tingling in the distal extremities. This is because each dermatome is completely overlapped by adjacent dermatomes. There are only relatively small "autonomous zones" where only a single nerve root supplies the region. Therefore, “numbness” tends to be found only in small areas of the distal limbs. Of course there may be associated signs of damage to motor nerve fibers as well.

Brachial plexus lesions affect broader areas of the limb, overlapping the distributions of individual nerves or roots. With rare exception, they have motor signs and symptoms in addition to the sensory loss.

Central causes

There are many conditions affecting the central nervous system that can produce “numbness.” Spinal cord disease often produces bilateral symptoms with a sensory level, below which the sensation is lost (due to tract damage). The causes of spinal cord damage generally are either extrinsic compressions (extramedullary) or conditions that intrinsically damage the spinal cord (intramedullary). The general differential diagnosis of myelopathy is shown in this table.

Above the foramen magnum, conditions that can cause “numbness” range from cerebral vascular disease through tumors, demyelinating lesions (such as multiple sclerosis) and infectious lesions. Typically, the symptoms are unilateral, specifically affecting the contralateral side of the body. Transient phenomena, such as migraine (where symptoms spread over the body over a period of minutes) and transient ischemic attacks should be considered. To a large extent, the tempo and timing of onset of symptoms, as well as their distribution are critical factors in guiding the investigation.


In summary, the evaluation of numbness can be quite frustrating due to its subjective nature. Many patients with psychiatric disease or chronic pain complain of abnormal sensations, so this must be kept in mind during evaluation. Objective tests, such as the corneal reflex or electrodiagnostic testing can sometimes confirm the sensory loss. But ultimately the pattern of symptoms, associated symptoms and precipitants of symptoms will be the most important determinant of whether the “numbness” is likely to result from nervous system damage. These factors, along with consideration of the other health-related risk factors will be most important to the accurate assessment of the symptom of “numbness.”


Define the following terms:

conscious proprioception, agnosia (sterioagnosia), graphesthesia, dermatome, sclerotome, myotome, radiculopathy, myelopathy, anesthesia/hypoesthesia, hyperpathia, allodynia, hyperesthesia, dysesthesia, paresthesia, polyneuropathy, subjective.
Conscious proprioception is the ability to tell where a body part is in space. It is largely based on joint position sense.
Agnosia (sterioagnosia) is the inability to recognize what a sensation is despite relatively normal perception of the sensation. When it is tactile it is termed sterioagnosia (or asteriognosis). It would be the inability to determine the denomination of a coin despite normal ability to perceive it, for example.
Graphesthesia is the ability to identify letters or figures traced on the skin (without looking).
Dermatome is the area of skin supplied by a nerve root.
Sclerotome is the area of bone and joints supplied by a single nerve root.
Myotome is the muscles supplied by a single nerve root.
Radiculopathy is damage to a nerve root (radiculitis is irritation).
Myelopathy is damage to the spinal cord from any cause.
Anesthesia/hypoesthesia is loss (or decrease) in sensation.
Hyperpathia is the exaggerated perception of normally painful stimuli.
Allodynia is the perception of normally innocuous stimuli as being painful.
Hyperesthesia is excessive sensitivity to any modality.
Dysesthesia is the perception of the pain when no stimulus is present.
Paresthesia is the abnormal perception of a sensation in the absence of any stimulus.
Polyneuropathy is generalized damage to peripheral nerves. This is usually due to a systemic cause.
The sensory exam is by definition subjective, that is, relies on the patient's report.

13-1. What is the first step in evaluating the patient with “numbness”?

13-1. You must determine what the patient is referring to as numbness. Is it paresthesia, or a decrease in sensitivity that they are describing? Most cases of tingling do not result from central nervous system damage (other than a migraine or seizure). Most tingling results from peripheral nervous system problems.

13-2. What is important about the distribution of the symptoms?

13-2. The distribution of numbness is very important since this is key to localizing the lesion. Lost sensitivity is confined to within the distribution of the neural structure responsible. If the symptoms are intermittent, you must assess the reliability of the patient in localizing the symptom that they had.

13-3. What conclusions can you draw regarding patient having large areas of diminished sensitivity?

13-3. Loss of sensitivity covering large areas of the body (especially on one side, and especially involving the face and hand) is the best suggestion of central nervous system involvement.

13-4. What is the role of identifying precipitants for the symptoms?

13-4. This is the best indicator of cause.

13-5. What is Tinel sign and why is it important?

13-5. This is the generation of paresthesias in the distribution of a nerve following a light tap with a reflex hammer. This suggests an excessive excitability of nerve due to some focal damage. It is quite sensitive, but not very specific for conditions such as entrapment neuropathy. It is very useful for localizing a lesion.

13-6. What is suggested by the presence of a "march" of sensory symptoms (paresthesias that progress from one area of the body to adjacent regions over time measured in minutes)?

13-6. This most commonly indicates migraine or a sensory seizure. This does not occur with cerebrovascular disease and is strong evidence against stroke or TIA.

13-7. What kind of sensory symptoms are common in panic, high anxiety states and hyperventilation?

13-7. Perioral and finger tingling are common in these states. This is particular true if the patient was distraught or under high stress levels at the time.

13-8. What reflex is helpful to test ophthalmic sensation?

13-8. Loss of sensations on the upper face can usually be quantified by corneal reflex (or by electrically testing blink reflex).

13-9. What is the common sensory loss from damage to the spinal cord?

13-9. Spinal cord lesions often result in sensory level (loss of sensations below lesion) due to damage to ascending sensory tracts. .This loss (especially of pain sensation) usually begins at least several segments below the level of the lesion of the tract.

13-10. What infectious process is a common cause of localized paresthesia in the elderly?

13-10. Recent tingling in an older patient should raise the suspicion of early zoster.

13-11. What characteristics suggest the presence of hysterical sensory loss?

13-11. Numbness of the face is a common hysterical presentation. This often follows artificial boundaries (such as the jaw line or the hair line). Additionally, patients often report significant differences in vibratory sense across the midline of bones that span the midline (such as the skull, sternum or pelvis).

13-12. What is the pattern of sensory loss seen in diffuse damage to peripheral nerves (polyneuropathy)?

13-12. Diffuse peripheral nerve injury (polyneuropathy) results in stocking (and, later, glove) sensory loss.

13-13. What distribution of sensory deficit would you expect in demyelinating disease?

13-13. Demyelination can produce virtually any pattern of sensory change. However, the region of sensory loss is not likely to be highly localized because tract damage in the CNS usually produces large regions of sensory change.

13-14. What distribution of sensory deficit would you expect in entrapment neuropathy?

13-14. In entrapment neuropathy, the region of sensory decrease should be confined to the distribution of the nerve. Usually, the further the nerve damage is toward the periphery, the sharper the boundary between normal and abnormal sensation. Any tingling in one upper limb should be intensively investigated for peripheral entrapment or thoracic outlet syndrome. It is noteworthy that pain from peripheral entrapment may be experienced well beyond the distribution of the nerve.

13-15. What is the likely implication of the patient with sensory decrease (esp. pain and temperature) on one side of the face and the other side of the body?

13-15. This pattern results from injury to the brain stem (particularly the lateral brain stem, due to damage to the spinothalamic tract and to the spinal tract of the trigeminal nerve).

13-16. What is the likely implication of the patient with sensory loss on the same side of the face and body?

13-16. This pattern results from a lesion rostral to the midbrain (such as the thalamus or sensory cortex).

13-17. What is the significance of a “suspended sensory loss” (loss of a modality, usually pain and temperature sense, on both sides of the upper body with preservation below)?

13-17. This pattern is highly suggestive of an intramedullary spinal cord lesion.

13-18. What is the most sensitive confirmatory laboratory test for entrapment neuropathy?

13-18. Nerve conduction studies are quite sensitive and objective in testing for suspected peripheral neuropathy or peripheral entrapment neuropathy.

13-19. What laboratory test for can test central conduction along sensory pathways?

13-19. Somatosensory evoked potentials test large diameter fibers and dorsal column-medial lemniscus function.

13-20. Your patient with chronic pain compains of paresthesias in a large area of a painful limb. How can you determine whether this is simply related to their pain?

13-20. If this is simply a pain-related phenomenon, the motor and reflex exam should be normal. Also, you should be able to reproduce (or exacerbate) the patient's paresthesia by pressure over painful sites that are not directly over nerve trunks.
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