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.
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.
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.
There are many potential causes of sensory loss. These can basically be divided into central and peripheral.
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.
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.
13-1. What is the first step in evaluating the patient with “numbness”?
13-2. What is important about the distribution of the symptoms?
13-3. What conclusions can you draw regarding patient having large areas of diminished sensitivity?
13-4. What is the role of identifying precipitants for the symptoms?
13-5. What is Tinel sign and why is it important?
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)?
13-7. What kind of sensory symptoms are common in panic, high anxiety states and hyperventilation?
13-8. What reflex is helpful to test ophthalmic sensation?
13-9. What is the common sensory loss from damage to the spinal cord?
13-10. What infectious process is a common cause of localized paresthesia in the elderly?
13-11. What characteristics suggest the presence of hysterical sensory loss?
13-12. What is the pattern of sensory loss seen in diffuse damage to peripheral nerves (polyneuropathy)?
13-13. What distribution of sensory deficit would you expect in demyelinating disease?
13-14. What distribution of sensory deficit would you expect in entrapment neuropathy?
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?
13-16. What is the likely implication of the patient with sensory loss on the same side of the face and body?
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)?
13-18. What is the most sensitive confirmatory laboratory test for entrapment neuropathy?
13-19. What laboratory test for can test central conduction along sensory pathways?
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?