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4 Articles in Volume 2, Issue #6
A Conceptual Model of Pain: Measurement and Diagnosis
Carpal Tunnel Syndrome as a Neuropathic Condition
Chronic Insomnia and Pain
Identifying Pain-Drug Abusers and Addicts

Carpal Tunnel Syndrome as a Neuropathic Condition

Characterized by hand and wrist pain, CTS is a symptomatic distal median nerve neuropathy at the wrist and is the most commonly encountered entrapment neuropathy.

Carpal tunnel syndrome (CTS) was first described by Sir James Paget in 1863, and subsequently Dr. George Phalen described the classic Phalen’s sign in 1949.1 It occurs in 10% of the general population, and up to 50% in industrial settings. There is a female predisposition (by a factor of 3:1), more often occurs in obese middle-aged individuals (58%), more likely affecting their dominant hand, but may occur bilaterally. This entrapment is rarely familial. It is also associated with pregnancy (due to edema; 10-20%), rheumatologic diseases including rheumatoid arthritis (with tenosynovitis of the wrist), systemic lupus erythematosus, ankylosing spondylitis, eosinophilic fasciitis,2 diabetes mellitus, other ischemic polyneuropathies (may occur with arteriovenous shunts or peripheral vascular disease of the upper extremity), hypothyroidism with myxedema, acromegaly with boney enlargement, hyperparathyroidism, toxic shock syndrome, amyloidosis and multiple myeloma.1 Most commonly, it occurs following repetitive stress or overuse, but this condition may occur following trauma (direct or secondary to compression from a hematoma or old wrist fracture with callous deformity), and with soft tissue compression (lipoma, flexor tendon synovitis, ganglion cyst, or gouty tophi).3

Anatomy

Carpal tunnel anatomy (Figure 1) includes: medially — pisiform and hook of hamate; laterally — trapezium, scaphoid; posteriorly — lunate and capitate; and anteriorly — 9 flexor tendons (one of these tendons, namely the flexor digitorum sublimus may rarely have congenital hypertrophy), and are bound by the transverse carpal ligament and flexor retinaculum. The palmaris longus tendon lies more superficial (anterior) to the carpal tunnel.1 The median mixed (sensory and motor fibers) nerve transverses this tunnel just distal to the wrist crease and innervates the abductor pollicis brevis, Opponens and superficial head of the flexor pollicis brevis. Upon rare occasion, there is a congenital or idiopathic enlargement of the median nerve at this site. The CTS lesion usually occurs at 2-4 cm distal to the palmar wrist crease with compression of sensory branch 1 cm distal to the motor compression. The smallest crossectional area is 2-2.5 cm distal to the wrist crease. With caliper measurements, the ratio of the antero-posterior thickness to the width > 0.7 (Johnson index), increases the incidence of CTS. Within the carpal tunnel, the median nerve branches to the median recurrent nerve (turns backward into transverse ligament) innervating the abductor pollicis brevis, provides sensation to digits 1 through 3 and the radial portion of digit 4, and a distal motor branch innervates the lumbrical muscles of digits 2 and 3.3

Figure 1. Carpal tunnel anatomy1

Presentation

The common symptoms of CTS include hand pain, numbness, or paresthesias of median nerve distribution (more often to digits 1- 3, but not the thenar skin because it is innervated by the palmar cutaneous branch which branches proximal to carpal tunnel). It is often associated with nocturnal awakening, and may have a sclerotomal deep aching pattern into the thenar region. The symptoms are usually intensified with repetitive wrist flexion including driving, reading, keyboarding, handicrafts, and with vibration (jack hammering). There may be volar (anterior) hand and wrist pain, as well as referral into the proximal forearm, elbow, arm or shoulder. There may be a sensation of swelling, with occasional autonomic symptoms which may include vasomotor instability or Reynaud’s syndrome. An acute traumatic presentation due to sudden forceful extension of the wrist with motor vehicle accidents, industrial injuries or sports may result in a greater likelihood of thenar weakness due to conduction block (neuropraxia). Lacerations of the wrist may result in complete or partial transection of the median nerve (neurotmesis) and flexor tendons. In chronic cases, there is a sensory predominance with the insidious onset of thenar weakness with atrophy (though the deep head of flexor pollicis brevis is spared due to ulnar nerve innervation). The patient may describe clumsiness or dropping objects.3

Extremes of wrist flexion and extension in a constricted canal as the result of high force, high repetition, vibration or awkward posture (also observed with dystonia, athetosis or catatonia) and temperature extremes are the most common ergonomic risk factors of CTS. The patient may report partial alleviation of their symptoms with shaking out hands (flick sign), placing their wrist in a neutral position and with elevation. Often, patients will present asymptomatically with “distal median neuropathy,” especially in the elderly and diabetics.4

Some patients with CTS may experience a disproportionate level of pain from their condition. Often, they may have a superimposed problem including repetitive strain of the forearm with lateral epicondylitis, arthritis/arthralgias of the hand and wrist, or their symptoms may be associated with a myofascial pain syndrome.

Further, differential diagnosis may include lesions of the musculoskeletal, peripheral and central nervous system. CTS may be coexisting, superimposed with or mimicked by these conditions (see Table 1).

Differential Diagnosis of CTS
  • Cervical radiculopathy — C6-7 sensory, C8-T1 motor5
  • Brachial plexopathy, thoracic outlet syndrome (thenar weakness predominates, with sensory symptoms of dermatomal C8)3
  • Motor neuron disease (may initially present with distal motor weakness with hyperreflexia and fasciculations without sensory deficits)
  • Median neuropathy, with more proximal or distal entrapments, or predisposed due to “double crush” entrapment predilection - pronator syndrome (entrapment at the head of the pronator teres and flexor sublimus), anterior interosseous nerve syndrome, supracondylar process syndrome (ligament of Struthers or lacertus fibrosis), pseudo-CTS (distal forearm entrapment under flexor digitorum sublimus to digit 2 just proximal to the carpal tunnel), Palmaris longus anomalous distal muscle belly causing direct median nerve compression, distal digital nerve entrapments at the deep transverse metacarpal ligament due to trauma, arthritis, or tumor.3
  • Complex regional syndrome type 1 (reflex sympathetic dystrophy)5
  • Complex regional syndrome type 2 with nerve injury (causalgia)5
  • Peripheral neuropathy6
  • Central nervous system dysfunction including lacunar cerebrovascular accidents, spinal cord lesions or multiple sclerosis5
  • Radial artery thrombosis5
  • Wrist/finger flexor tendonitis including deQuevains tenosynovitis5
  • Wrist/thumb arthritis/arthralgia including, avascular necrosis of the lunate5
  • Flexor tendon ganglion synovial cyst5
  • Myofascial pain mimicry: brachioradialis, extensor carpi radialis longus and brevis, extensor digitorum communis, extensor carpi ulnaris, palmaris longus, flexor carpi radialis, pronator teres, opponens pollicis and adductor pollicis, scalenii, brachialis, infraspinatus, subscapularis, and teres major which may cause sensory referral patterns into the wrist and hand7
  • Psychogenic or nonorganic etiologies

Table 1.

Physical Exam

The physical exam for CTS includes sensory deficits of palmar digits 1-3 and radial aspect of digit 4 to vibration, pressure, proprioception, sharp or deep lacinating pain (type A beta fibers), cold temperature, localized touch, pin or sharp lacinating pain (type A delta fibers), hot temperature, diffuse pain and touch (type C fibers),7 with reduced 2 point discrimination (greater than 5 mm), sensitivity over carpal tunnel (150 mm Hg compression for more than 30 sec), Tinel’s sign (percussion over the carpal tunnel ligament for up to a 45% specificity), Phalen’s sign (>60 sec in maximum wrist flexion with a 75% sensitivity) or with wrist hyperextension (reverse Phalen’s sign) resulting in duplication of the sensory symptoms. A tethered median stress test is a very sensitive evocative maneuver, with the second digit hyperextended through palmar pressure, while the wrist is extended and the forearm is supinated. There may be weakness of the thenar eminence (thumb flexion, opposition and abduction) and lumbricals (digits 2 and 3) sometimes associated with atrophy or fasciculations. Additional examination should include a full musculoskeletal exam of the neck, shoulder, elbow and fingers, with neurological evaluation of the upper extremities, and a palpatory exam of the upper torso to evaluate for other coexisting or superimposed findings which may assist in the differential diagnosis.4

Neurophysiologic diagnostic testing functionally evaluates the sensory and motor components of the median nerve.

The initial treatment of CTS usually consists of avoidance of precipitating events and ergonomic modifications (especially with computer typing workstations) and may require avoidant activities for up to 3 months to determine a response.

Electrodiagnostic Testing

Traditional electrodiagnostic testing (Table 2), including nerve conduction velocity (NCV) and electromyography (EMG), has been used to confirm a diagnosis as an extension of the physical examination, though the testing has its limitations. Normal testing does not fully exclude a diagnosis of CTS. Sensory NCV is most sensitive part of the test but it preferentially evaluates the largest fibers (A delta). Motor NCV evaluates the large myelinated alpha motor neurons to detect demyelinization (conduction delay), and if more profound, neuropraxia (conduction block), and if severe weakness, axontmesis (dennervation). Needle electromyography (EMG) can evaluate motor unit interference patterns (weakness is related to increased frequency of firing and a reduction of the number of recruited motor units), and for reinnervation (polyphasicity as a result of asynchronous conduction of the muscle fibers making up a motor unit) and nascient potentials. Insertional activity with muscle membrane instability (positive sharp waves and fibrillation potentials) evaluates the effects of dennervation which may have a lag of up to 21 days after injury. Occasionally, motor unit fasciculations can be associated with dennervation. Electrodiagnostic testing may be used to exclude other neurological diagnoses.1,3,5,8 There is a specificity of 90% and a sensitivity of 73% in symptomatic hands, but asymptomatic patients commonly had abnormalities. The prevalence for bilateral distal median neuropathy was 55%, and 4% with CTS had only motor abnormalities. The diagnostic criteria include absolute motor and sensory distal latency prolongation (usually with normal NCV proximally), and/ or amplitude reduction, as well as comparison of the ulnar and radial nerves on the same hand and the median nerve of the opposite limb. The measurements may need to be modified for children, with normative correction for longer limbs, older individuals and with cooler temperatures.5 An inching technique has been described to exactly localize the lesion and for definitive evaluation of neuropraxia.3 A mild electrodiagnostic abnormality usually affects the sensory fibers with sparing of the motor fibers. A moderate finding includes sensory and motor abnormalities of conduction without EMG abnormalities. A severely affected CTS includes profound sensory and motor NCV abnormalities with EMG evidence of dennervation.4

Published Criteria for NCV Abnormalities in CTS1,3,6,9
Median Sensory NCV abnormalities in CTS (surface skin temp >33°C)
Antidromic stimulation is stimulation proximal to recording electrode. Orthodromic stimulation is stimulation distal to recording electrode (physiologic direction).
SNAP = sensory nerve action potential

Median distal SNAP peak latency > 3.4 ms (14 cm stimulation site)

  • Median midpalmar SNAP peak latency > 1.8 ms (7 cm stimulation site) with amp <50 uV
  • Ulnar/median SNAP peak latency > 0.2 ms (8 cm stimulation site antidromically across carpal tunnel) or >0.4 ms dig to wrist (14 cm)
  • Radial/median SNAP peak latency >0.5ms (10 cm stimulation site) antidromically
  • SNAP amp <20 uV (orthodromic), <25 uV (antidromic)

Combined Assessments (sensory)

  • Combined sensory index (sum of three latency differences) for mild CTS
  • 1. Median-ulnar mid palmar difference
  • 2. Median-ulnar sensory digit 4
  • 3. Median-radial sensory digit 1 (Bactrian sign)

Median Motor NCV abnormalities for CTS

  • Forearm NCV >49 m/s to exclude median neuropathy (may have retrograde slowing in severe CTS)
  • Amplitude difference elbow/ wrist >20% +/- temporal dispersion
  • Compound motor action potential amplitude <4 mV
  • Distal latency >3.9 ms

Comparative hands for CTS

  • Right to left difference > l.0 ms median motor latency
  • Same hand ulnar- median motor latency difference > 1.8 ms
  • Thenar compound motor action potential (CMAP) < 4mV or < 50% of contralateral hand

Combined Assessments (motor)

  • Terminal motor latency index = distal latency distance in mm/ (NCV in m/s of proximal segment x terminal latency in ms)
  • Less than 0.34 is abnormal
  • 11% had proximal NCV motor slowing felt to be related to retrograde nerve fiber degeneration

Table 2.

Electrodiagnostic testing performed after successful CTS release surgery may show improvement but not necessarily result in normalization of NCV results.1 An anomalous Martin Gruber anastomosis (median to ulnar crossover in the forearm seen in 15% of the population) may falsely elevate median nerve proximal conduction across the forearm with an abnormally appearing waveform with proximal stimulation and reduce the motor amplitude response at the wrist. Thenar motor innervation anomalies may affect interpretation of the EMG, particularly if the ulnar motor nerve predominately innervates several of the thenar muscles.1 Other electrodiagnostic tests including somatosensory evoked responses, magnetic evoked stimulation and F waves are not clinically useful for this condition, but may be considered if additional testing is required to evaluate for other neurological lesions.

Functional Imaging

Functional imaging studies used to evaluate CTS may include thermography (for small myelinated or unmyelinated fibers assessing vasomotor or autonomic changes). Quantitative sensory testing (QST) using a neurometer can assess electrical current perception thresholds which can correlate with larger fiber function at higher frequencies or the smaller fibers (including pain, temperature and touch) at the lower frequencies. Static and dynamic two point discrimination can accurately assess sensory function and can also be used to monitor progress during recovery from trauma or surgery.4

Anatomic Imaging

Other anatomic imaging of CTS include diagnostic ultrasonography (may be used dynamically with wrist motions or to evaluate median nerve hypertrophy), MRI or 3-D CAT scan. Radiographs can evaluate for boney lesions including arthritis, tumor or fracture. Pathologically, the median nerve will have loss of the epineurium with flattening, and edema, with loss of the surrounding fat in the carpal tunnel.4

Treatment Modalities

Treatment for CTS, presenting as simple or complex, spans the range of modalities from avoidance of precipitating events to surgical intervention. In the case of complex presentation with comorbidity of coexisting conditions, a comprehensive multidisciplinary pain program is required.

Avoidance

The initial treatment of CTS usually consists of avoidance of precipitating events and ergonomic modifications (especially with computer typing workstations) and may require avoidant activities for up to 3 months to determine a response. A resting wrist (or cock up) splint fitted in neutral or slightly extended position of the wrist is best worn at night, at a minimum, and preferably in the daytime (or during activities that evoke the symptoms) for at least 6 wks for all degrees of CTS. The patient may require alternating use of splints if they have bilateral CTS. Splints have been shown to reduce intracarpal tunnel pressure and avoid traction stress to median nerve.

Pharmacology

Pyridoxine (especially with elderly and females on oral contraceptives) in doses up to 300 mg/d and, riboflavin (50 mg/d) may help with nerve regrowth, and NSAID’s or COX-2 selective agents may be used to reduce the associated median neuritis, arthritis or tenosynovitis in the carpal tunnel region. Diuretics may be used in those with edema susceptibility. One must also treat co-morbidity (including thyroid dysfunction, diabetes, rheumatologic diseases, avoidance of alcohol, and weight reduction).4 In those patients with a significant component of neuropathic pain, considerations may be made for tricyclic antidepressants (i.e. amitriptyline) or anticonvulsants (i.e. gabipentin). In those patients with hypersensitivity, considerations should be made for topical local anesthetics, capsaicin or doxepin.

An injection (1 cc of a lipid soluble corticosteroid using a 25-27 gauge 1.5 cm needle for 1-3 injections over 8 weeks) is given just ulnar to the palmaris longus tendon and proximal to the volar wrist crease angled at 30’ and aimed distally so as to avoid a direct intraneural injection of the median nerve. A mixture of local anesthetic may be combined for retrospective localization of the injection site resulting in transient numbness in the median nerve distribution and to minimize soreness.9,10 A single steroid injection has been completely effective in 28%, though there may be relapses requiring additional injections 9-15 months later.

Physical Medicine

Physical medicine modalities including underwater ultrasound followed by passive stretch of the transverse carpal ligament, wrist mobilization with range of motion, neural stretch, iontophoresis (with steroids or local anesthetics) may be performed by both occupational (some have additional expertise as a certified hand therapists) and physical therapists.4 In many individuals, the pain generator may also include a superimposed myofascial pain syndrome; therefore, myofascial releases to the upper extremity, in conjunction with trigger point injections should be considered.6 For edema control, centrifugal massage, wrapping or compression sleeves may be considered. Chiropractic adjustments or osteopathic wrist manipulation have also been beneficial.11 A hand function evaluation may be helpful to identify the specific motor and sensory deficits followed by exercises which may include neurofacilatory proprioception, and thenar strengthening (functional electrical stimulation may also be considered), along with patient education for energy conservation, avoidance of repetitive strain and job modification with adaptive equipment. Integrative medicine approaches including magnetic wrist supports and acupuncture have been used. Further, recent studies have shown that lifestyle changes with general conditioning are more important than vocational changes in those patients with CTS.9

Multidisciplinary Pain Program

Patients experiencing symptom-amplified or complex presentation with co-morbidities require a multidisciplinary pain program for successful outcome. Such a program includes the concerted application of select pharmacotherapeutics, physical medicine, and psychosocial counseling.

Pharmacotherapeutics may include psychotropics, analgesics, clonidine, tizanidine or muscle relaxant medications. Physical medicine therapies may include additional treatment (i.e. customized splints, paraffin baths or desensitization massage) as well as general conditioning exercises (with modifications to avoid stress to the wrist) and modalities applied to other affected regions including the neck and upper extremity, supplemented with myofascial injections. Psychosocial counseling for pain coping strategies, lifestyle changes and vocational options is important in those dysfunctional individuals with CTS with symptom magnification. Occasionally, patients require diagnostic (and subsequently therapeutic) peripheral nerve and stellate ganglion blocks to further characterize the pain generator(s).

Surgical Intervention

If conservative management is unsuccessful (> 3-6 months) or there is progression of symptoms, CTS decompressive surgery should be considered taking into account the age, general health, severity of objective findings and symptom correlation. Unfortunately, there is a suboptimal correlation between the extent of electrodiagnostic abnormalities and symptoms. In studies, surgical intervention was considered successful in 69%- 90%, with a more limited response in those with greater severity or longer duration of symptoms, older age, males, or coexisting morbidity. Endoscopic releases have been recently advocated because of a significantly shorter postoperative period, but there is a greater risk of inadvertent injury to median nerve due to poor visualization during the procedure. Pre-emptive analgesia with COX-2 selective agents along with topical local anesthetics has been helpful in minimizing postoperative pain. Surgical complications occur in 2% and may include infection, cutaneous neuroma, traumatic nerve injury, complex regional pain syndrome type 2, bleeding, failed decompression, bowing of the flexor tendons with loss of grasp and residual pain over the incision due to a scar hypertrophy.4,9,10

Summary

CTS is a common presentation and represents a challenge to physicians because of its many different manifestations. Electrodiagnostic testing is currently the most common method of confirming a diagnosis. The treatment options should be carefully correlated with the patient’s presentation, including symptoms and functional deficits, along with physical and objective findings. Conservative management including anti-inflammatories, wrist splints, steroid injections and physical medicine modalities should be considered first. Surgical options in selected patients can be curative, but there are significant numbers who continue to have residual problems. Industrial-related CTS may complicate treatment because of disincentives including time loss compensation, job dissatisfaction or lack of reasonable accommodation. Therefore, the prognosis for successful resolution of their symptoms is diminished. These patients frequently require a comprehensive multidisciplinary pain program with active participation. Additional research is necessary to prevent this condition from commonly occurring in the workplace.

Last updated on: July 30, 2019
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