Acute progressive bilateral carpal tunnel syndrome after upper respiratory tract infection.

Abstract: This report describes the case of a 32-year-old male presenting with acute progressive bilateral carpal tunnel syndrome after a benign upper respiratory tract infection. Serial nerve conduction studies confirmed progressive entrapment of the median nerves in the carpal tunnel to the point of axonal damage. Surgical decompression relieved the entrapment, and nerve conduction studies improved.

Key Words: carpal tunnel syndrome, EMG in carpal tunnel syndrome, median nerve entrapment, postviral disease.

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Carpel tunnel syndrome (CTS) is a common disorder that comprises a set of symptoms associated with entrapment of the median nerve in the carpel tunnel. The entrapment is usually chronic in nature and slowly progressive; however, acute compression of the median nerve has been reported secondary to wrist trauma, local infection, and rheumatologic and hematologic disorders. (1)

Case Report

A healthy, 32-year-old male presented with acute painful paresthesias in the first three digits of both hands 1 week after a mild upper respiratory tract infection. No history of weakness or sensory symptoms in the arms or hands was noted. On examination, he had hyperesthesia in the sensory dermatomes of both median nerves, a positive Tinel sign in the wrists, and a mild decrease in thumb abduction bilaterally. Nerve conduction studies revealed moderate delay in the distal motor latencies and severe delay in the distal sensory latency of both median nerves with severe decrease in the motor and sensory amplitudes bilaterally and decrease in the sensory conduction velocities (Fig. and Table 1). Normal motor and sensory conduction neurographies in both ulnar nerves were noted. An absent median nerve F-response on the left side and a delayed response on the right side were also noted. Motor and sensory nerve conduction studies of the peroneal, posterior tibial, and sural nerves and the posterior tibial F-responses were normal in both lower extremities (Table 2). No denervation activity was detected by needle EMG examination of the abductor pollicis brevis muscles in both hands.

Screening blood tests including chemistry panel, complete blood count, erythrocyte sedimentation rate, thyroid stimulating hormone, and antinuclear antibodies were normal. The patient was started on 20 mg prednisone daily. A 1-week follow-up revealed progression of symptoms and worsening of the nerve conduction studies, with loss of the median sensory response on the left side and severe decrease in the motor and sensory amplitudes (Fig. and Table 1). Fibrillation and positive sharp waves were seen in the abductor pollicis brevis muscles bilaterally. Steroids were increased to 40 mg daily. Repeat nerve conduction studies after 1 week revealed loss of motor and sensory responses in the left median nerves with profuse denervation and early neurogenic changes in both abductor pollicis brevis muscles (Fig. and Table 1). Again, the nerve conduction studies of the ulnar, peroneal, and posterior tibial and sural nerves and their F-responses were normal. Concentric needle EMG examination of the proximal and distal muscles of the arms, other than the abductor pollicis brevis muscles, and the muscles of the legs were normal excluding the possibility of a brachial plexitis, radiculitis, or polyneuritis. The patient was referred to surgery. He underwent bilateral decompression of the median nerves. Intraoperative findings revealed edematous median nerves compressed under the flexor retinaculum. The latter was cut until adequate decompression of the median nerves was confirmed. Small epineurotomy and external neurolysis were performed. After surgery, the patient had gradual improvement in sensory and motor hand function. The nerve conduction studies improved partially on reexamination (Table 1).

Discussion

Acute CTS has been described in wrist trauma, (2) hemophilic disorders, (3) as a complication of oral anticoagulant therapy, (4) in some rheumatologic disorders, (5) and in a variety of infections. (6)

The first two cases of acute CTS secondary to pyogenic infection were described in 1955. (7) Rubella virus, Borrelia species, and Mycobacterium tuberculosis are the most frequent of these rare infectious causes. (6) Samii et al (8) described three cases of bilateral acute carpel tunnel syndrome associated with parvovirus B19 infection, as evidenced by serologic data and, in one case, by detection of parvovirus B19 DNA in blood by polymerase chain reaction. A single case of guinea worm (Dracunculus medinensis) infection causing CTS has been described. (9) CTS has also been reported with a filarial infection alone (10) and in a combined case of loiasis, schistosomiasis, and trypanosomiasis. (11)

[FIGURE 1 OMITTED]

In infection-associated CTS, the underlying cause is not suspected before surgical exploration. (8) As such cases respond well to appropriate treatment, infection should be considered in the differential diagnosis of acute CTS, particularly when there is no history of trauma or other obvious cause.

In our case, a prior upper respiratory tract infection is considered to be the cause of the acute bilateral CTS. The neurologic deficits resulted from progressive edema of the median nerves in the carpal tunnel, resulting in acute entrapment and eventual focal demyelination and axonal damage. The rapid progression of the edema was resistant to oral steroid therapy. Nerve conduction studies confirmed progressive entrapment of the median nerves, reflecting the clinical symptomatology. The persistence of normal conduction studies in the bilateral ulnar nerves and the lower extremity motor and sensory nerves, as well as the posterior tibial F-responses throughout the patient's illness, argues against a generalized polyneuropathy (such as acute inflammatory demyelinating polyneuropathy) and further emphasizes the fact that the patient had focal, progressive, median nerve entrapment in the carpal tunnels. After decompression, the patient improved dramatically, and nerve conduction studies performed 3 months later revealed amelioration of the motor and sensory compound action muscle potentials (Fig.).

In cases of acute progressive postviral CTS, close clinical follow-up with nerve conduction studies is advisable, and early decompression is recommended in cases that do not resolve spontaneously or when there is evidence of axonal degeneration.

References

1. Szabo RM. Acute carpal tunnel syndrome. Hand Clin 1998;14:419-429.

2. Mack GR, McPherson SA, Lutz RB. Acute median neuropathy after wrist trauma: the role of emergent carpal tunnel release. Clin Orthop 1994;300:141-146.

3. Dumontier C, Sautet A, Man M, et al. Entrapment and compartment syndromes of the upper limb in haemophilia. J Hand Surg 1994;19:427-429.

4. Black PRM, Flowers MJ, Saleh M. Acute carpal tunnel syndrome as a complication of oral anticoagulation therapy. J Hand Surg 1997;22:50-51.

5. Chiu KY, Ng WF, Wong WB, et al. Acute carpal tunnel syndrome caused by pseudogout. J Hand Surg 1992;17:299-302.

6. Mascola JR, Rickman LS. Infectious causes of carpal tunnel syndrome: case report and review. Rev Inf Dis 1999;13:1911-1917.

7. Bailey D, Carter JFB. Median nerve palsy associated with acute infection of the hand. Lancet 1955;2668:530-532.

8. Samii K, Cassinotti P, de Freudenreich J, et al. Acute carpal tunnel syndrome associated with human parvovirus B19 infection. Clin Inf Dis 1996;22:162-164.

9. Balasubramanian V, Ramamurthi B. An unusual cause of guinea worm infestation: report of a case. J Neurosurg 1965;23:537-538.

10. Gallagher B, Khalifa M, Van Heerden P, et al. Acute carpal tunnel syndrome due to filarial infection. Pathol Res Pract 2002;198:65-67.

11. Scott JA, Davidson RN, Moody AH, et al. Diagnosing multiple parasitic infections: trypanosomiasis, loiasis, and schistosomiasis in a single case. Scand J Infect Dis 1991;23:777-780.

Men naturally despise those who court them, but respect those who do not
give way to them.
--Thucydides

Ihab I. El Hajj, MD, Mohamad I. Harb, MD, and Raja A. Sawaya, MD

From the Department of Internal Medicine, Division of Neurology, American University of Beirut Medical Center, Beirut, Lebanon.

Reprint requests to Raja Sawaya, MD, Department of Internal Medicine, Division of Neurology, American University of Beirut Medical Center, PO Box 113-6044/C-27, Beirut, Lebanon. Email: [e-mail]

Accepted May 26, 2005.

RELATED ARTICLE: Key Points

* Bilateral carpal tunnel syndrome is a rare condition in young patients.

* Postinfectious carpal tunnel syndrome has been reported in a few cases.

* EMG is the gold standard in diagnosing carpal tunnel syndrome.

* Treatment of acute carpal tunnel syndrome depends on the severity and progression of the entrapment.

Table 1. Neurography of median nerves before and after surgery (a)

                Nov. 17   Nov. 24   Dec. 2    Mar. 1
                DL   Amp  DL   Amp  DL   Amp  DL   Amp

Median motor
  Left          4.7  2.9  4    0.8  0    0    5.3   3.5
  Right         4.7  2.6  4.4  1.6  4.8  3.2  4     4.2
Median sensory
  Left          4    6.1  0    0    0    0    3.1   6
  Right         4    6.7  3.6  3.9  3.7  4.2  3    22

(a) DL, Distal latency in milliseconds; Amp, amplitude in millivolts
(motor)/in microvolts (sensory).

Table 2. Neurography of the nerves of the upper and lower extremities on
admission date (a)

Nov 17             Nerve    DL   Amp   CV

Median left        Motor    4.7   2.9  51
                   Sensory  4     6.1  39
Median right       Motor    4.7   2.6  50
                   Sensory  4     6.7  38
Ulnar left         Motor    2.7   9.5  59
                   Sensory  2.5  72.3  48
Ulnar right        Motor    2.6  13    57
                   Sensory  2.5  71    50
Peroneal left               4    10    49
Peroneal right              4.6   8    48
Post tibial left            4.6  15.5  49
Post tibial right           4    10.4  48
Sural left                  2.8  19    48
Sural right                 3.4  18    38

(a) DL, Distal latency in milliseconds; Amp, amplitude in millivolts
(motor)/in microvolts (sensory); CV, conduction velocity in m/sec.