Paresthesias: A Practical Diagnostic Approach - December, 1997 - American Family Physician
 
   

Paresthesias:
A Practical Diagnostic Approach

This section is compiled by Frank M. Painter, D.C.
Send all comments or additions to:
   Frankp@chiro.org
 
   

FROM:   American Family Physician 1997 (Dec);   56 (9):   2253–2260

JERRY T. MCKNIGHT, M.D., and BOBBI B. ADCOCK, M.D.

University of Alabama School of Medicine, Tuscaloosa, Alabama


Paresthesias may be caused by central or peripheral nervous system abnormalities. Central nervous system-induced paresthesias are most commonly caused by ischemia, structural or compressive phenomena, infection, inflammation or degenerative conditions. Peripherally induced paresthesias can be caused by entrapment syndromes, metabolic disturbances, trauma, inflammation, connective tissue diseases, toxins, hereditary conditions, malignancies, nutritional deficiencies and miscellaneous conditions.

Confirming the diagnosis and establishing an etiology may require appropriate laboratory and radiologic studies, or other studies. In most cases, the specific clinical syndromes associated with the paresthesias, coupled with the presenting neurologic findings, provide the physician with a framework for the diagnosis.


Paresthesias are abnormal sensations experienced in the absence of specific stimuli.1(p1234),2 These sensations are usually described as burning, tingling or numb feelings, although they may be described as feelings of cold, warmth, prickling, pins and needles, skin crawling or itching.2 The most common locations of paresthesias are the hands, arms, legs and feet, although paresthesias can be present anywhere on the body. Paresthesias are contrasted with dysesthesias, which are abnormal interpretations of appropriate stimuli.1(p515),2 Paresthesias are common presenting complaints, and diagnosis is usually assisted by knowing the specific clinical presentations associated with various paresthetic syndromes.

TABLE 1

Selected Causes of Paresthesias


Central
Ischemic
Cerebrovascular accident
Transient ischemic attack
Structural
Tumor
Trauma
Infectious
Brain abscess
Encephalitis
Inflammatory
Systemic lupus erythematosus
Nutritional
Vitamin B12 deficiency
Miscellaneous
Multiple sclerosis
Peripheral
Neuropathy (see Table 2)

Pathophysiology and Etiology

The basic pathophysiology of paresthesias is an altered nerve or nerve pathway function. Paresthesias are thought to represent abnormal showers of impulses generated from an ectopic focus3 and can arise from an abnormality anywhere along the sensory pathway, from the peripheral nerves to the sensory cortex.4 Paresthesias can be caused by central nervous system or peripheral nervous system abnormalities. Central nervous system causes include ischemia, obstruction, compression, infection, inflammation and degenerative conditions (Table 1).

The most common causes of peripherally induced paresthesias are neuropathies. Peripheral neuropathies can be caused by metabolic disturbances, entrapment syndromes, trauma, inflammatory conditions, connective tissue disorders, toxic injury, hereditary conditions, malignancy, nutritional deficiencies, infections and miscellaneous causes (Table 2). Some common peripheral neuropathies include those secondary to diabetes, hypothyroidism, vitamin B12 deficiency, alcoholism and nerve entrapment syndromes.5 The most common type of nerve entrapment is carpal tunnel syndrome related to compression of the median nerve at the wrist. Other relatively common peripheral syndromes include ulnar nerve entrapment, tarsal nerve entrapment and lateral femoral cutaneous nerve entrapment6,7 (Table 2).


TABLE 2

Selected Causes of Peripheral Neuropathy


Metabolic/nutritional disturbances
Diabetes
Hypothyroidism
Vitamin B12 deficiency
Alcoholism
Uremia
Amyloidosis
Porphyria

Entrapment syndromes
Carpal tunnel syndrome
Ulnar entrapment syndrome
Thoracic outlet syndrome
Lateral femoral cutaneous syndrome
Peroneal palsy
Tarsal tunnel syndrome

Trauma
Inflammation
Acute idiopathic polyneuritis
Chronic relapsing polyneuropathy
Connective tissue disorders
Polyarteritis nodosa
Autoimmune vasculitis
Rheumatoid arthritis
Systemic lupus erythematosus
Systemic sclerosis
Sjögren's syndrome

Toxins
Chemotherapy
Heavy metals
Medications (didanosine [Videx], zalcitabine [Hivid], stavudine [Zerit])
Industrial exposures
Chronic overdosage of pyridoxine

Hereditary conditions
Charcot-Marie-Tooth disease
Denny-Brown's syndrome
Familial amyloiditic polyneuropathy
Malignancy
Tumor compression
Paraneoplastic syndromes
Lymphomas
Cancer of the lung, stomach, breast or ovary
Plasma cell dyscrasias
Multiple myeloma
Osteoclastic myeloma
Monoclonal gammopathy
Waldenstrom's
macroglobulinema
Miscellaneous
Sarcoidosis
Malnutrition

Infections
Lyme disease
HIV infection
Leprosy

HIV=human immunodeficiency virus.








TABLE 3

Diagnosis of Common Nerve Root Lesions


Nerve root
Disc level
C5
C4-C5
C6
C5-C6
C7
C6-C7
L4
L3-L4
L5
L4-L5
S1
L5-S1







Sensory Lateral border of upper arm Lateral forearm, including thumb, index finger and half of middle finger

Middle finger Medial leg and medial foot Dorsum of foot Lateral foot
Reflex Deltoid tendon Biceps and brachioradialis tendon

Triceps tendon Patellar tendon None Achilles tendon
Muscle Deltoid, biceps Wrist extensors, biceps Triceps, wrist flexors, finger extensors Inversion of foot Dorsiflexion of toes and foot Plantar flexion and eversion of foot


Radiculopathies caused by compression of cervical or lumbar nerve roots are common causes of paresthesias8 (Table 3). Causalgia is an intense, burning type of paresthesia caused by trauma to a nerve (e.g., the median, ulnar, posterior tibial or peroneal nerves).9(p1161) Reflex sympathetic dystrophy is an unusual cause of paresthesias, pain and autonomic dysfunction occurring after minor soft tissue injuries or fractures and usually affecting the distal extremities.10 Toxic injury to nerves may be caused by cancer chemotherapy (e.g., cisplatin [Platinol], vincristin [Oncovin, Vincasar]), heavy metals (e.g., lead, mercury, arsenic), medications (e.g., isoniazid (Laniazid), nitrofurantoin (Furadantin, Macrodantin, Macrobid), gold, hydralazine (Apresoline), industrial exposures (e.g., acrylamide, carbon disulfide, hexacarbons, trichloroethylene) or chronic overdosage of pyridoxine.11 Malignancy, an uncommon cause of neuropathy, should be considered when the diagnosis is elusive. Tumor compression of peripheral nerves, nerve roots, spinal cord or the brain can cause paresthesias. Paraneoplastic syndromes from cancers, particularly small cell carcinoma of the lung, can cause paresthesias.12 Lymphomas and tumors of the lung, stomach, breast and ovary have been associated with neuropathies.13

TABLE 4

Diagnosis of Common Nerve Entrapment Syndromes


Syndrome
Nerve
Associated conditions
History
Physical examination
Carpal tunnel Median nerve at wrist Diabetes, pregnancy, rheumatoid arthritis, hypothyroidism, repetitive wrist movements, sustained hand positions, amyloidosis, acromegaly, multiple myeloma, chronic renal failure, tenosynovitis Intermittent hand pain or paresthesias, especially at night; poor grip/dropping things; decreased fine motor skills Decreased thumb adduction, thenar atrophy, decreased sensation of digits 1, 2 and 3, positive Phalen's sign, positive Tinel's sign
Cubital tunnel Ulnar nerve at elbow Leaning on elbow, shallow ulnar groove, increased forearm flexion/extension, elbow fracture, rheumatoid arthritis, immobilization Elbow pain, hand weakness, numbness of ulnar side of hand Decreased finger abduction, decreased thumb adduction, atrophy of intrinsic hand muscles (if severe), claw hand (if severe), decreased sensation of digits 4 (ulnar side) and 5, positive Tinel's sign at elbow
Meralgia paresthetica Lateral femoral cutaneous nerve Obesity, pregnancy, diabets, increased walking/standing Numbness/pain of lateral thigh Usually no motor deficit, increased light touch and pinprick response over lateral thigh
Tarsal tunnel Posterior tibial nerve Phlebitis, rheumatoid arthritis, fracture Burning/tingling of ankle and sole, increased with ambulation Usually no motor deficit, decreased sensation on plantar foot, positive Tinel's sign of nerve


Diagnosis

The diagnosis of paresthesias is based on the history and physical examination, as well as appropriate laboratory, radiologic and special studies. In most cases the history provides the key to the diagnosis. The physician should be aware of the specific clinical syndromes associated with paresthesias (Table 4). This knowledge, coupled with the presenting neurologic findings, will provide a framework for the diagnosis. The laboratory examination will help further define the diagnosis in many cases but should be tailored for specific diagnoses.

HISTORY

The patient history should document time of onset, duration and location of the paresthesias, and any accompanying pain or motor dysfunction. Additional information should include past medical history, current medical problems, current and past medications, recreational drug use, trauma and toxic exposure.

Family history may reveal a relative with peripheral neuropathy, malignancy, diabetes, thyroid disease or connective tissue disease. An occupational history of repetitive movement, use of vibratory tools or toxin exposure may be important. The history will help the physician determine if the condition is symmetric and primarily motor or sensory. The review of systems will provide information regarding symptoms of systemic disease such as fever, cough or weight loss, which may be associated with neuropathies. Paresthesias accompanied by pain are generally peripheral in nature.

Paresthesias that do not persist are unlikely to be associated with a serious medical problem. Most people have experienced a transient type of paresthesia they describe as "my leg falls asleep." The history should focus on categorizing the area of paresthesia into known medical syndromes (e.g., median nerve entrapment, S1 lumbar radiculopathy or diabetic neuropathy). Knowledge of sensory spinal root distribution and cutaneous nerve distribution is requisite to diagnosing paresthesias (Figures 1 through 3). The physician should understand that these symptoms are often very strange to the patient and, therefore, are difficult to describe.



FIGURE 1. Sensory dermatomes.



FIGURE 2. Cutaneous nerve distribution of the upper limb.




FIGURE 3. Cutaneous nerve distribution of the lower limb.



Diabetic neuropathy generally has a graded, symmetric, distal glove and stocking type of distribution, usually with proximal progression from the toes and feet, although other peripheral neuropathies may display this pattern.14 A specific dermatomal pattern of paresthesias suggests a radiculopaty or herpetic neuralgia. Other notable patterns of paresthesias include areas of specific single nerves (mononeuropathy) or involvement of multiple nerves (mononeuritis multiplex). Paresthesias of multiple somatic locations should alert the physician to the possibility of multiple sclerosis.15

The Authors

JERRY T. MCKNIGHT, M.D.
is associate professor and chair of the Department of Family Medicine at the University of Alabama School of Medicine, Tuscaloosa. Dr. McKnight graduated from the University of Tennessee, Memphis, College of Medicine and completed a residency at the Tuscaloosa Family Practice Residency Program.

BOBBI B. ADCOCK, M.D.
is an assistant professor and director of family medicine predoctoral education in the Department of Family Medicine at the University of Alabama School of Medicine, Tuscaloosa. Dr. Adcock graduated from the University of Mississippi School of Medicine in Jackson and completed a residency at the Tuscaloosa Family Practice Residency Program.

Address correspondence to Jerry T. McKnight, M.D., Department of Family Medicine, University of Alabama School of Medicine, Capstone Medical Center, 700 University Blvd. E., Tuscaloosa, AL 35401.


PHYSICAL EXAMINATION

Patients presenting with complaints of paresthesias should have a complete physical and neurologic examination. The physical examination should be used to help rule out metabolic or systemic causes of neuropathies. The neurologic examination should test for motor and sensory functions, the latter being perhaps the most difficult part of the examination. The primary sensory examination should focus on the patient's response to pain, touch, vibration, joint position and thermal sensation.9(pp130-47) This examination will test major afferent pathways of both primary sensation and cortical sensory function. It is quite possible to have symptoms of paresthesias with no measurable neurologic deficit.

An efficient sensory examination will preclude unreliable results caused by patient fatigue. Pain sensation is generally tested with a pin or needle, and soft touch is adequately tested with a wisp of cotton.16 It is best to begin the examination on a normal part of the body and move toward an area of altered sensation. It may be helpful for the patient to outline the sensory abnormality after the initial examination is completed. This serves to map the area of involvement, with a view toward categorizing the abnormality into a specifically defined syndrome (i.e., dermatomal, nerve, nerve root, or glove and stocking pattern). Sensory mapping may provide information as to a spinal cord lesion or a peripheral nerve abnormality. The proximal sensory examination should be compared with the distal examination, paying special attention to areas of numbness. Symmetric distal sensory loss is compatible with a polyneuropathy.

Vibration is tested using a 128- or 256-cps (cycles per second) tuning fork. The 128-cps tuning fork is standard for vibratory testing. The 256-cps tuning fork is harder for the patient to appreciate but, if the vibration is perceived, a vibratory sensation defect is effectively ruled out. Loss of vibratory sensation occurs relatively early in a peripheral neuropathy such as those related to diabetes, alcoholism, vitamin B12 deficiency or dorsal column disease.

Vibratory sensation is assessed by placing the stem of the tuning fork against several bony prominnces, beginning at the most distal joints. If the patient does not respond in the distal joints, the more proximal joints should be checked. It is important to start with an area of normal sensation to provide the patient with an appropriate reference point. The physician should make sure the patient is responding to the vibration and not the pressure of the instrument by occasionally dampening the vibration and eliciting a response. The examiner can generally feel the same level of vibration as the patient.

Proprioception is tested by grasping the sides of the finger or toe being tested and asking the patient, whose eyes should be closed, to indicate whether the digit is moved into an up or a down position.17 Loss of position sense is associated with a nerve root lesion, a peripheral nerve abnormality or dorsal column disease.

Thermal sensation is tested with test tubes filled with water of various temperatures. Patients with normal thermal sensation should be able to distinguish between stimuli differing by a few degrees.2 Unfortunately, the examiner is relying on a subjective patient response, which is dependent on the patient's level of motivation and intelligence. A sensory loss may not be present in areas of symptoms; likewise, sensory deficits may be detected in asymptomatic areas.

Abnormal findings should be correlated with reflex or motor abnormalities. These abnormalities may suggest a specific nerve, nerve root or spinal cord lesion. Hyperreflexia is suggestive of upper motor neuron disease, while decreased reflexes are associated with spinal nerve segment disease or peripheral nerve injury. A neurologic examination may also reveal signs of a neuropathy or myelopathy that may help determine the etiology of the paresthesia. The extremities may demonstrate trophic changes, changes in skin color or palpable nerves, such as the superficial radial or the posterior auricular nerve, as occurs in patients with hereditary hypertrophic neuropathy.18 Muscle groups, especially the distal musculature, should be assessed for strength and signs of atrophy. Abnormalities of specific muscles or muscle groups are associated with specific nerve lesions.

TABLE 5

Laboratory and Other Studies Useful in Diagnosing Paresthesias


Initial evaluation
Complete blood cell count
Chemistry profile
Urinalysis
Thyrotropin-stimulating hormone
Sedimentation rate

Miscellaneous studies
Folate
Vitamin B12
VDRL
Antinuclear antibodies
Serum immunoelectrophoresis
Nerve conduction velocities
Electromyography
Roentgenograms
Magnetic resonance imaging
Myelography
Computed tomographic scan
Lumbar puncture
Purified protein derivative (PPD)
Heavy metal analysis
Nerve biopsy
Muscle biopsy


LABORATORY EVALUATION

The laboratory examination (Table 5) is a vital aspect in the evaluation of paresthesias. Basic laboratory evaluation should begin with a complete blood cell count, a chemistry profile, a urinalysis and determination of thyrotropin-stimulating hormone and sedimentation rate.19 Depending on the clinical situation, additional serologic tests, including measurement of folate an vitamin B12 levels, VDRL, antinuclear antibodies and serum immunoelectrophoresis, should be considered.19 A purified protein derivative (PPD) tuberculin should be applied, if clinically indicated. Heavy metal analysis of serum for the presence of lead, mercury or arsenic may be necessary. Tests of nerve conduction velocity and electromyography should be ordered if the laboratory tests do not provide a diagnosis.20,21 Radiologic studies should focus on a specific anatomic area, such as evaluation of a suspected lumbar radiculopathy. Evaluation of a suspected herniated disc should include magnetic resonance imaging (MRI), myelography or computed tomography of the affected area.

Radiography of a specific anatomic site may be helpful in evaluating a compressive neuropathy. A chest radiograph may be helpful in ruling out a lung tumor or tuberculosis. MRI is recommended for the evaluation of suspected intracranial lesions, with MRI angiography helpful in diagnosing vascular abnormalities. A lumbar puncture may be necessary to eliminate a diagnosis of tertiary syphilis, carcinomatous meningitis or a central inflammatory cause. A nerve biopsy is helpful in the diagnosis of polyarteritis nodosa, sarcoidosis and amyloidosis.

REFERENCES:

  1. Dorland's Illustrated medical dictionary. 28th ed. Philadelphia: Saunders, 1994

  2. The exteroceptive sensations. In: Haerer AF, ed. DeJong's The neurologic examination. 5th ed. Philadelphia: Lippincott, 1992:47-66

  3. Asbury AK. Numbness, tingling, and sensory loss. In: Isselbacher KJ, Braunwald E, Wilson JD, et al., eds. Harrison's Principles of internal medicine. 13th ed. New York: McGraw-Hill, 1994:133-6

  4. Thompson HG, Rowland LP. Pain and paresthesias. In: Rowland LP, ed. Merritt's Textbook of neurology. 8th ed. Philadelphia: Lea & Febiger, 1989:28-31

  5. Diseases of the peripheral nervous system. In: Scientific American medicine. New York: Scientific American 1994;11:1-15

  6. Dawson DM. Entrapment neuropathies of the upper extremities. N Engl J Med 1993;329:2013-8

  7. Dawson DM, Hallett M, Millender LH, eds. Entrapment neuropathies. 2d ed. Boston: Little, Brown, 1990:93-124

  8. Swanson PD. Signs and symptoms in neurology. In: Disorders of sensation. Philadelphia: Lippincott, 1984:206-302

  9. Adams RD, Victor M, eds. Principles of neurology. 5th ed. New York: McGraw-Hill, 1993

  10. Schwartzman RJ, McLellan TL. Reflex sympathetic dystrophy. A review. Arch Neurol 1987;44:555-61

  11. Donaghy M. Toxic and environmental disorders of the nervous system. In: Walton J, ed. Brain's Diseases of the nervous system. 10th ed. Oxford, England: Oxford University Press, 1993:513-29

  12. Posner JB. Secondary neoplastic disease. In: Asbury AK, McKhann GM, McDonald WI, eds. Diseases of the nervous system: clinical neurobiology. Philadelphia: Saunders, 1992:1093-1104

  13. Posner JB. Paraneoplastic syndromes. In: Asbury AK, McKhann GM, McDonald WI, eds. Diseases of the nervous system: clinical neurobiology. Philadelphia: Saunders, 1992:1105-20

  14. Brown MJ, Asbury AK. Diabetic neuropathy. Ann Neurol 1984;15:2-12

  15. Sibley WA, Poser CM, Alter M. Multiple sclerosis. In: Rowland LP, ed. Merritt's Textbook of neurology. 8th ed. Philadelphia: Lea and Febiger, 1989: 741-60

  16. The nervous system: Techniques of examination. In: Bates B, Bickley LS, Hoekelman RA, eds. A guide to physical examination and histor taking. 6th ed. Philadelphia: Lippincott, 1995:505-40

  17. The neuropsychiatric examination. In: DeGowin RL, ed. DeGowin and DeGowin's bedside diagnostic examination. 5th ed. New York: Macmillan, 1987:780-852

  18. Donaghy M. Hereditary motor and sensory neuropathy. In: Brain's Diseases of the nervous system. 10th ed. Oxford, England: Oxford University Press, 1993:590-2

  19. Collins RD. Illustrated manual of neurologic diagnosis. 2d ed. Philadelphia: Lippincott, 1982:200-1

  20. Levin KH. Common focal mononeuropathies and their electrodiagnosis. J Clin Neurophysiol 1993; 10:181-9

  21. Burke D. Microneurography, impulse condition, and paresthesias. Muscle Nerve 1993;16:1025-32.


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