Paresthesia and Dysesthesia
Rosemarie Cannarella
Paresthesia and dysesthesia are symptoms of peripheral nerve dysfunction caused by ectopic nerve pulses generated in these fibers. They are unphysiologic evocations of elementary physiologic sensations.
Approach.
Paresthesias are experienced in the absence of any specific stimuli; dysesthesias are a result of specific stimulus. Patients find these unusual sensations difficult to describe, and may use many descriptions as listed below.
A. Sensory phenomena can be divided into two categories.
1. Positive phenomena. These include tingling, pins and needles, pricking, bandlike sensations, lighteninglike shooting feelings (lacinations), aching, drawing, pulling, crawling, tightening, burning, searing, electrical, and raw (1). Pain may or may not be perceived. These sensations are not always accompanied by a sensory deficit on examination.
2. Negative phenomena describe a decrease or loss of feeling in a particular distribution (1). These sensations are generally accompanied by abnormal findings, and include terms such as hypoesthesia, analgesia, hyperesthesia, and hyperpathia. Dry skin, motor weakness, orthostasis, autonomic dysfunction, and cold extremity are other forms of negative symptoms.
B. Special concerns. Acute onset of paresthesia that persists can indicate a structural problem (transient ischemic attack, stroke).
History
A. Do these sensations occur in a special nerve distribution or in a certain anatomic location? Do they occur in response to a stimulus? Are they intermittent, or persistent and continuous? Was onset acute or insidious? How have the symptoms progressed? Any chronic medical illnesses?
1. Glove and stocking distribution: suggests diabetes, vitamin B12 or folate deficiency, alcohol, or intoxications (heavy metals, industrial chemicals or medications).
2. Dermatomal distribution: suggests herpes zoster, vasculitis.
3. Other distributions: nonspecific pattern suggests idiopathic paresthesia, whereas extremity pattern suggests hyperventilation.
B. Is there an exposure to solvents, pesticides, heavy metals, or recent viral illness? Is there abuse of alcohol or symptoms of systemic dysfunction or chronic illness?
C. Would the patient otherwise feel in good health if free of the paresthesia? The answer to this question provides an idea of the patient’s general health and a clue to a systemic illness.
D. Is this a sensation that is unfamiliar to the patient (dysesthesia) or a familiar pain “like a toothache” (nerve trunk pain-aching sensation)?
E. What makes it better or worse (dysesthesia—worse after activity, little makes it better; nerve root pain—better with rest, worse with movement, nerve stretch, or palpation)?
F. What is the distribution of the pain (dysesthesia—cutaneous or subcutaneous; symmetrical distally; nerve trunk origin—deep and relatively proximal) (2)?
Physical examination
A. General examination. Perform a thorough examination and check for hypertension, tachypnea, and tachycardia.
B. Nervous system. Perform a sensory examination in the area of complaint: touch, pinprick, heat or cold, proprioception, and motor examination, including deep tendon reflexes.
1. Decreased sharp touch and thermal sensation suggest small fiber neuropathies (spinothalmic tract syringomyelia).
2. Decreased position sense, vibratory, or motor dysfunction but retention of most other cutaneous sensations are found with large fiber neuropathies.
3. Sometimes paresthesias alone do not suggest their origins, but when combined with other neurologic deficits, the cause becomes more clear.
4. Are the signs symmetrical? Do they occur in a graded fashion (polyneuropathy), somewhat asymmetric findings or multifocal signs (multiple mononeuropathy), or damaged individual cutaneous nerves?
C. Look for other physical signs of chronic disease such as alcoholism, diabetes, malnutrition, pulmonary disease, and acquired immunodeficiency syndrome.
D. Avoid testing a patient who is extremely fatigued (unreliable sensory examination). An overly cooperative patient may read too much into an examination and may discern very small differences that are not clinically significant. Do not prompt too much—give general directives.
Testing
(2–4)
A. Clinical laboratory tests that may be useful include complete blood count; liver, renal, and thyroid function tests; sedimentation rate; antinuclear antibodies; vitamin B12; and folate. Perform heavy metals and toxin assays if the history is suggestive.
B. The electromyelogram or nerve conduction study is the gold standard in assessing the origin of the neuropathy associated with the paresthesia, if indeed one exists. It can differentiate between axonal and demyelinating causes.
C. A nerve biopsy is most useful in suspected inflammatory disorders (vasculitis, amyloidosis). It is also useful in suspected, selected small-fiber neuropathies, and in undiagnosed chronic neuropathy where significant debilitation has occurred.
Diagnostic assessment
The positive phenomena of paresthesia and dysesthesia do not necessarily mean a devastating diagnosis. They can be troublesome with no clinical diagnosis or be harbingers of peripheral neuropathy. The negative phenomena usually are a more ominous sign. Positive phenomena can act as troublesome symptoms that have no clinical diagnosis or as harbingers of more complicated syndromes of the peripheral neuropathies. If there is a documented neurologic deficit, especially once the motor system becomes involved, then it is more imperative to make a diagnosis. The most frequent neuropathy seen in clinical practice is the diabetic neuropathy (5). The real emergent diagnosis is that of Guillian-Barré syndrome, in which paresthesia can rapidly progress to full motor loss within days. Important is the association of symptoms to true sensory or motor deficits, systemic illness, toxin or medication exposure, or the rapidity of worsening symptoms.
References
1. Asbury A. Numbness, tingling and sensory loss. In: Braunwald E, Fauci AS, Isselbacher DL, et al., ed. Harrison’s Principles of internal medicine, 14th ed. New York: McGraw-Hill, 1998:2457–2469.
2. Asbury AK, Thomas PK. Peripheral nerve disorders. Cambridge: Butterworth Heinemann, 1995:8.
3. Bradley W, Daroff R, Fenichel G, Marsden CD. Neurology in clinical practice, 2nd ed. Vols. I and II. Boston: Butterworth Heineman, 1996.
4. Haerer AF. The neurologic examination, 5th ed. Philadelphia: JB Lippincott, 1992.
5. Poncelet AN. An algorithm for the evaluation of peripheral neuropathy. Am Fam Physician 1998;57(4):755–760.
Book Source Details
- Book Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
- Author(s): Robert B. Taylor (editor)
- Year of Publication: 2000
- Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2000 Lippincott Williams & Wilkins.
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Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2008 Williams & Wilkins.
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