P129 Retrograde changes in carpal tunnel syndrome

P129 Retrograde changes in carpal tunnel syndrome

Poster Session: Electromyography and Neurography ~ k O W DOSE, SHORT-TERM ORAL PREDNISOLONE IN THE TREATMENT OF CARPAL TUNNEL SYNDROME K. Ozalp, N. Er...

144KB Sizes 0 Downloads 45 Views

Poster Session: Electromyography and Neurography ~ k O W DOSE, SHORT-TERM ORAL PREDNISOLONE IN THE TREATMENT OF CARPAL TUNNEL SYNDROME K. Ozalp, N. Erdo~an, A. Ozge, F. Tunali, N.Y. Ereno~lu. Department of

1st Neurology Haydarpa~a Numune Hospital, lstanbul-Turkey We investigated the effectiveness of short-term, low-dose oral prednisolone treatment on clinical and electrophysiological findings of the treatment of the carpal tunnel syndrome (CTS) which is commonly seen in neuropathy entrapment. Thirty-two hands of 20 female patients (mean age 41 years) with diagnosis of CTS were examined. The patients complained about numbness, hand and finger pain, shoulder and arm pain and weakness. Patients received 10 mg daily single dose prednisolone for eight weeks. Electrophysiological findings were evaluated separately on the 4th and 8th weeks of treatment. In ENMG examination a decrease in DAP amplitude and a reduction in sensory conduction velocity was observed in 32 median nerves. In 27 median nerves CMAP amplitude decreased and in 24 nerves distal motor latency prolonged. At the end of the 4th week a 21% improvement in numbness, and a 26% improvement in pain was obtained. ENMG findings in 25 hands were positive. Among them, sensory conduction velocity, DAP amplitude, CMAP amplitude, and distal motor latency improved in six, three, two, and four hands, respectively. We concluded that short-term (4 weeks) low dose, oral prednisolone administration in mild to moderate patients with CTS can be considered an alternative therapy.

~

THE EFFECT OF PERIPHERAL NERVE COMPRESSIONON PROXIMAL CONDUCTION VELOCITY

J.E. Fox, I.H. Bangash, A.P. Mocroft. Queen Elizabeth Hospital,

Birmingham, B15 2TH and Royal Preston Hospital, Preston, PR2 4HT, UK In a random sample of 100 patients with electrophysiologically proven carpal tunnel syndrome, it has been demonstrated that mean motor conduction velocity in the forearm segment of the median nerve is significantly slower than that in normal controls; 18% of the patients had conduction velocities less than 50 m/sec, compared with 2% of the normal controls. If this difference is due to retrograde changes in the motor axons (rather than to a selective block of conduction in large diameter fibres), it might be expected that the effect would be most marked in the segment of nerve closest to the compression site. Motor conduction velocity has therefore been measured in the median nerve as it passes through the forearm, a) between the antecubital fossa and a point 3-5 cm above the proximal skin crease of the wrist and b) in the distal 3-5 cm of the forearm segment of the median nerve. The ratio of distal:proximal conduction velocities has then been compared in patients and normal controls. The results demonstrate that distal slowing is greater in a significant number of the patient group, supporting the hypothesis that peripheral compression can induce retrograde changes which cause a slowing of conduction that is most marked close to the site of entrapment.

EVALUATIONOF CARPAL TUNNEL SYNDROME USING INTRAFASCICULARNEUROGRAPHY O. Hasegawa, R. Kurita, A. Komiyama, S. Matsumoto, Y. Kubota, M. lint, M. Matsumoto. Yokohama City University, Yokohama, Japan To evaluate quantitatively conduction block and retrograde axonal degeneration in carpal tunnel syndrome (CTS), we applied intrafascicular neurography to 23 CTS hands from 19 patients. The age-matched 46 controls also were subjected to the test. A tungsten microeleetrode was inserted percutaneously into the median nerve trunk at the elbow. Using Neuropack 8, the median nerve was stimulated at the wrist 20 mm proximal to the wrist stria or at the palmar site 20 mm distal to the stria. The peak to peak amplitude of each CNAP was measured. Palm/wrist CNAP amplitude ratios in the patients were reduced to 0.17 4- 0,10 (SD), implying the presence of conduction block, while those in the controls were 0.76 4- 0.10. CNAP amplitudes obtained with stimulation at the wrist also were smaller in the patients (168 4- 106 ~V) than in the controls (386 4- 95/zV), showing the retrograde axonal degeneration in CTS forearms. Following surgery, the palm/wrist CNAP amplitude ratio in 18 CTS hands was restored to 0.38 4- 0.21; however, wrist CNAP amplitude remained small. Improvement in conduction block was correlated well with alleviation of dysesthesia. This study indicates that intrafascicular neurography

307

is useful in assessing both the conduction block and retrograde axonal degeneration accompanied by CTS.

[



RETROGRADE CHANGES IN CARPAL TUNNEL SYNDROME

A.K. Chattopadhyay, R.H. Kandler, J.A. Jarratt. Royal Hallamshire

Hospital, Sheffield, $10 2JE UK Abnormal median nerve conduction proximal to carpal tunnel compression has been described before, but the nature of the underlying pathology is controversial. The following measurements were made from the median nerve in 67 patients with carpal tunnel syndrome (CTS) and 48 control subjects: motor conduction velocity between elbow and wrist (MCVE-W), between axilla and elbow (MCVA-E), and distal latency to abductor pollicis brevis (DL); mixed nerve conduction velocity between wrist and elbow (NCVW-E); mixed nerve action potential amplitude at elbow (NAPE); sensory conduction velocity between digit II and wrist (SCVII-W), and amplitude of the sensory action potential at the wrist (SAPII-W). The mean velocities, MCVE-W and MCVA-E, were slowed (52.7 -4- 6.7 vs 59.4 4- 4.3 m/s; p < 0.001) and (63.6 4- 8.6 vs 67.9 4- 6.7 m/s; p < 0.01 ), and the slowing correlated with prolongation of DL (p < 0.002) and (p < 0.01), respectively. The gradient of the regression line was greater for the forearm than the upper arm segment. The mean value of NCVW-E was reduced when SAPII-W was present (65.8 4- 4.4 vs 67.2 4- 4.3 m/s; p < 0.05), and more so when SAPII-W was absent (62.2 4- 2.5 vs 67.2 4- 4.3 m/s; p < 0.005). The slowing in the mixed nerve also correlated with prolongation of DL (p < 0.01). The amplitude of NAPE was reduced ( 11.7 4- 7.9 vs 17.3 4- 9.0 uV; p < 0.001 ). We confirm the presence of slowed conduction proximal to the wrist in patients with CTS. The changes are proportional to the severity of the lesion. The motor studies imply a gradient of change along the nerve, distal portions being more affected. This could be due to paranodal demyelination. However, the mild slowing is insufficient to account for the reduced amplitude of the nerve action potential which therefore probably denotes co-existent retrograde degeneration.

~-~

F-WAVE LATENCIESIN PATIENTSWITH ACUTE AND CHRONIC SPINAL CORD INJURY

M.E. Keck, A. Curt, V. Dietz. Swiss Paraplegic Center, University

Hospital Balgrist, 8008 Ziirich, Switzerland Objective: To assess the evidence of F-wave latencies in patients with traumatic alpha-motoneuron lesions due to acute and chronic spinal cord injury (SCI). Patients: 66 tetraplegic patients with acute (n = 32) and chronic (n = 34) traumatic cervical SCI were studied. 15 healthy subjects were examined as a control group. Methods: Motor/sensory nerve conduction studies (NCS) and F-waves of the median and ulnar nerves were performed in the two patient groups. The acute tetraplegics were followed monthly during the first 3 months; in addition after 6 months and 1 year after SCI. Results: The motor compound action potentials (MCAP) revealed in about 50% of patients an axonai lesion of both nerves and in 20% even a complete loss of the motor potentials due to wallerian degeneration. The mean MCAP of the tetraplegics with acute and chronic SCI were significantly (p < 0.001) reduced compared to normal subjects. Because the sensory potentials in these patients were normal in both nerves, the loss of motor nerve fibres has to be attributed to intramedullary damage of the alpha-motoneurons. In acute SC160% of the tetraplegics showed a loss of F-wave responses due to spinal shock. However about 3 months after trauma in all patients with preserved motor potentials F-wave responses could be recorded. The mean F-wave latencies showed no significant difference between healthy subjects and tetraplegic patients; the presence of i.e. the F-wave was not related to the severeness of alpha-motoneuron lesion. The follow-up in acute tetraplegics revealed no significant change of MCAP and F-wave latencies over time. Conclusions: F-wave responses are influenced by spinal shock. However, after spinal shock in contrast to MCAP, neither the presence of the F-wave nor the F-latencies are related to the extent of alpha-motoneuron lesion in SCI, unless in the case of a toss of MCAP.