Nerve compression, membrane excitability, and symptoms of carpal tunnel syndrome.

INTRODUCTION: In this study we investigated the changes in axonal excitability and the generation of neurological symptoms in response to focal nerve compression (FNC) of the median nerve in carpal tunnel syndrome (CTS). METHODS: Sensory excitability recordings were undertaken in 11 CTS patients with FNC being applied at the wrist using a custom-designed electrode. RESULTS: During FNC, refractoriness increased significantly (62.4 ± 3.4%; P < 0.001), associated with a rapid reduction in superexcitability (16.9 ± 2.8%; P < 0.001) and sensory nerve action potential amplitude (SNAP) (32.4 ± 3.9%; P < 0.001), consistent with axonal depolarization. Associated with these changes, paresthesiae steadily increased throughout FNC, as did numbness. Reductions in SNAP amplitude and superexcitability developed more rapidly for CTS patients during FNC compared with controls, and these changes were associated with more marked symptoms. CONCLUSIONS: Axonal responses to compression are impaired in CTS. This may suggest a greater reliance on axonal membrane Na(+) /K(+) -ATPase function.

Changes in human sensory axonal excitability induced by focal nerve compression.

The aim of the present study was to establish the changes in nerve excitability and symptom generation associated with the application of focal nerve compression (FNC). FNC was applied at the wrist by means of a custom-designed electrode in 10 healthy subjects, and was maintained for 24 min. Symptoms of paraesthesiae and signs of numbness were recorded every 30 s. Despite apparently minimal changes in axonal threshold, FNC was associated with prolongation in latency by 14.5 +/- 2.1% (P < 0.001) and reduction in compound sensory action potential (CSAP) amplitude by 34.3 +/- 5.1% (P < 0.001), with two subjects developing conduction block. The reduction in CSAP was associated with abolition of superexcitability, and an increase in refractoriness of 295.2 +/- 55.5% (P < 0.005) and strength-duration time constant (SDTC) by 48.1 +/- 10.3% (P < 0.005), all consistent with axonal depolarization. With release of FNC, threshold rapidly increased above pre-compression levels (P < 0.01), consistent with the development of axonal hyperpolarization. Associated with these changes in axonal excitability, paraesthesiae and numbness steadily increased throughout FNC and reached a peak at the termination of FNC, followed by a gradual recovery on release of FNC. When compared to previous studies that utilised the effects of more generalised limb ischaemia, the changes in axonal excitability recorded during FNC were qualitatively and quantitatively alike, suggesting that similar biophysical mechanisms contributed to the changes observed with both manoeuvres.

Ischaemic sensitivity of axons in carpal tunnel syndrome.

Although carpal tunnel syndrome (CTS) is the most common human entrapment neuropathy characterized by paraesthesiae and numbness with nocturnal exacerbation, the mechanisms underlying the generation of these symptoms remain unclear. Consequently, the aim of the present study was to investigate the relationship between changes in axonal excitability and the development of neurological symptoms in response to an ischaemic insult in CTS patients. Sensory and motor excitability were measured in 10 CTS patients and compared with 10 healthy controls, with participants asked to report symptom generation and intensity during the development of limb ischaemia. To induce ischaemia, a sphygmomanometer was inflated above the elbow and maintained at 200 mmHg for 10 min. During ischaemia there were decreases in axonal threshold, with less overall reduction in CTS patients when compared with controls. Associated with these differences in threshold, both sensory (p < 0.001) and motor (p < 0.05) refractoriness increased dramatically in CTS patients. This prominent increase in refractoriness was accompanied by a significant reduction in compound sensory action potentials and compound motor action potentials amplitudes for CTS patients when compared with controls (p < 0.05). These changes in axonal excitability resulted in a higher intensity of numbness and paraesthesiae reported by CTS patients during ischaemia. The present study has established differences in the nerve excitability and symptom development during ischaemia for patients with mild and moderate CTS, and may suggest that axons in the median nerve of CTS patients have an altered functional capacity to respond to an ischaemic insult, further contributing to nocturnal exacerbation of their symptoms.