Chronic Median Nerve Compression Research Articles

Ultrasound examination predicts 6-month progression in carpal tunnel syndrome patients.

Carpal tunnel syndrome (CTS) is a peripheral neuropathy resulting from chronic median nerve compression. Chronic compression leads to neurological changes that are quantified through nerve conduction studies (NCS). Although NCS represents the gold standard in CTS assessment, they provide limited prognostic value. Several studies have identified ultrasound as a tool in diagnosing and potentially predicting the progression of CTS in patients. The purpose of this study was to evaluate the predictive value of ultrasound examination in CTS patients. Twenty patients recruited at their first visit with the neurologist completed two NCS and ultrasound examinations approximately 6 months apart. Ultrasound examination consisted of B-mode, pulse-wave Doppler and colour Doppler ultrasound videos and images to quantify median nerve cross-sectional area, intraneural blood flow velocity in three wrist postures (15° flexion, neutral, and 30° extension), and displacement of the flexor digitorum superficialis (FDS) tendon and the adjacent subsynovial connective tissue (SSCT) of the middle finger during repetitive finger flexion-extension cycles. A questionnaire was administered to assess the work-relatedness of CTS. Linear regression analyses revealed that intraneural blood flow velocity (R2 = 0.36, p = .03), assessed in wrist flexion, and relative FDS-SSCT displacement (R2 = 0.27, p = .04) and shear strain index (R2 = 0.28, p = .04) were significant predictors of nerve sensory and motor changes at 6 months. Results suggest the possibility of using a battery of ultrasound measures as viable markers to predict median nerve functional changes within 6 months.

Brain remodeling after chronic median nerve compression in a rat model.

Carpal tunnel syndrome is the most common compressive neuropathy, presenting with sensorimotor dysfunction. In carpal tunnel syndrome patients, irregular afferent signals on functional magnetic resonance imaging are associated with changes in neural plasticity during peripheral nerve injury. However, it is difficult to obtain multi-point neuroimaging data of the brain in the clinic. In the present study, a rat model of median nerve compression was established by median nerve ligation, i.e., carpal tunnel syndrome model. Sensory cortex remodeling was determined by functional magnetic resonance imaging between normal rats and carpal tunnel syndrome models at 2 weeks and 2 months after operation. Stimulation of bilateral paws by electricity for 30 seconds, alternating with 30 seconds of rest period (repeatedly 3 times), resulted in activation of the contralateral sensorimotor cortex in normal rats. When carpal tunnel syndrome rats received this stimulation, the contralateral cerebral hemisphere was markedly activated at 2 weeks after operation, including the primary motor cortex, cerebellum, and thalamus. Moreover, this activation was not visible at 2 months after operation. These findings suggest that significant remodeling of the cerebral cortex appears at 2 weeks and 2 months after median nerve compression.

ASYMPTOMATIC CALCIUM PYROPHOSPHATE DIHYDRATE DEPOSITION DISEASE CAUSING CARPAL TUNNEL SYNDROME: CASE REPORT

Calcium pyrophosphate dihydrate deposition disease typically involves the wrist joint in the form of calcifications of the triangular fibrocartilage and the distal radioulnar joint. We describe an 87-year-old male who presented to us with asymptomatic form of deposition with multiple flexor tendon calcifications causing chronic median nerve compression. Simple carpal tunnel decompression relieved his median nerve symptoms.

Abstracts of the 8th Meeting of the Italian Peripheral Nerve Study Group: 5

We studied the effect of chronic compression of median nerve at wrist on cutaneous innervation. Two‐mm punch biopsies were obtained from third fingertip in 40 patients (32 female and 8 male, age range 30–74 years) with carpal tunnel syndrome. Patients with diabetes and other metabolic or endocrinological disorders or with electrophysiological findings of a diffuse neuropathy were excluded. By means of immunohistochemical techniques and confocal microscopy we counted epidermal nerve fibers, Meissner corpuscles and myelinated papillary endings. All patients underwent electrophysiological study and quantitative sensory testing using Semmes‐Weinstein monofilaments for tactile threshold and Medoc TSA II Neurosensory analyzer for thermal threshold evaluation. Morphological and functional data were compared with age and sex matched controls. We observed abnormalities of epidermal nerve fibers, mechanoreceptors and their myelinated afferents in all patients. These abnormalities ranged from mild to marked and appeared more severe in patients with a longer disease duration and a slower conduction velocity along the median nerve.

Moving objects with clumsy fingers: how predictive is grip force control in patients with impaired manual sensibility?

Anticipatory grip force adjustments to movement-induced load fluctuations of a hand-held object suggest that motion planning is based on an internal forward model of both the external object properties and the dynamics of the own motor apparatus. However, the central nervous system also refers to real time sensory feedback from the grasping digits in order to achieve a highly economical coupling between grip force and the actual loading requirements. We analyzed grip force control during vertical point-to-point arm movements with a hand-held instrumented object in 9 patients with moderately impaired tactile sensibility of the grasping digits due to chronic median nerve compression (n = 3), axonal (n = 3) and demyelinating sensory polyneuropathy (n = 3) in comparison to 9 healthy age- and sex-matched control subjects. Point-to-point arm movements started and ended with the object being held stationary at rest. Load force changes arose from inertial loads related to the movement. A maximum of load force occurred early in upward and near the end of downward movements. Compared to healthy controls, patients with impaired manual sensibility generated similar static grip forces during stationary holding of the object and similar force ratios between maximum grip and load force. These findings reflect effective grip force scaling in relation to the movement-induced loads despite reduced afferent feedback from the grasping digits. For both groups the maxima of grip and load force coincided very closely in time, indicating that the temporal regulation of the grip force profile with the load profile was processed with a similar high precision. In addition, linear regression analyses between grip and load forces during movement-related load increase and load decrease phases revealed a similar precise temporo-spatial coupling between grip and load forces for patients and controls. Our results suggest that the precise and anticipatory adjustment of the grip force profile to the load force profile arising from voluntary arm movements with a hand-held object is centrally mediated and less under sensory feedback control. As suggested by previous investigations, the efficient scaling of the grip force magnitude in relation to the movement-induced loads may be intact when deficits of tactile sensibility from the grasping fingers are moderate.

Effects of chronic median nerve compression at the wrist on sensation and manual skills.

The aim of this study was to analyse the functional impairments caused by chronic median nerve compression at the wrist on hand sensation and manual skill. Hand function was assessed in 11 patients (8 women and 3 men) with severe carpal tunnel syndrome (CTS) and compared with that of an age- and sex-matched control group. Apart from CTS, the subjects were healthy and the electrodiagnostic examination was normal. The pressure and vibration detection thresholds of the index finger were partially impaired and statistically different (P<0.05) when compared with controls, suggesting a reduction of tactile acuity in the territory of the median nerve. The thermal thresholds were identical in both groups, suggesting that the small-diameter fibres were not affected. When a small object was lifted and positioned in space, the coordination between the grip force and the vertical lifting force did not seem to be affected in our patients. They were able to modify their grip force according to the friction between the fingertips and the object, i.e. the more slippery the object, the higher the grip force. The unimanual Purdue Pegboard subtest results suggest that digital dexterity was also not significantly perturbed in our sample of CTS patients when compared with controls. Despite the severe abnormalities of median nerve conduction, our results suggest that chronic median nerve compression occurring in CTS induces partial impairment of tactile sensibility with minor impact on grasp force regulation and digital dexterity.

An Immunohistochemical Study on Cutaneous Sensory Receptors after Chronic Median Nerve Compression in Man

Carpal tunnel syndrome represents the most frequent chronic compressive neuropathy in man and hence may be investigated as a spontaneous model of peripheral nerve damage and repair. In the present report the fate of nerve fibers in the digital skin after long-lasting median nerve compression has been investigated immunohistochemically in comparison to normal digital skin, with special consideration to sensory endings and encapsulated receptors. The presence has been documented of the neurospecific marker PGP 9.5, the glia-associated protein S-100, and the neuropeptides CGRP and CPON which are mainly associated with the sensory and sympathetic nerve fibers respectively. The morphology and distribution of nerve fibers and corpuscles appeared comparable to that of normal digital skin; a reduction in the density of sensory receptors has, however, been observed, although not to the degree that was expected to explain the clinical deficits. It has been also demonstrated that at least part of the CGRP-containing sensory and CPON-containing sympathetic axons may survive unaltered even in patients with a long clinical history of profound sensorial impairment. An apparent discrepancy between the maintenance of nerve fibers and the sensory disturbances and the frequent observation of prompt postoperative recovery even after years of compression results from this investigation. The correlation of immunohistochemical observations and functional scores may not be considered conclusive. It must, however, be discussed if the sensorial impairment in this syndrome might have, at least in some cases, not only an anatomical but also an electrophysiological basis.

Internal neurolysis and flexor tenosynovectomy: adjuncts in the treatment of chronic median nerve compression at the wrist in hemodialysis patients.

This retrospective clinical study reports our results with surgical treatment of chronic median nerve compression at the wrist in 27 hemodialysis patients with a mean follow-up of 22 months. Due to the high incidence of amyloidosis in our patient population, an extensive tenosynovectomy was done in all patients. Statistically significantly (P = .03) better results were obtained when a microsurgical internal neurolysis was added to the procedure, than simple decompression alone (82% vs. 63% good to excellent results).

An electron microscope study of chronic median nerve compression in the guinea pig.

In guinea-pigs with chronic median nerve compression at the wrist the electron microscopic changes at level of the lesion and both proximal and distal to it have been studied. At the level of the lesion in animals with prolonged motor latency there was a loss of large myelinated fibres. Remaining large fibres had disproportionately thin myelin sheaths or were demyelinated. Regenerating clusters containing myelinated fibres were present. Evidence of degeneration and regeneration of unmyelinated fibres was present in the more severely affected nerves of this group. Distal to the wrist myelinated fibre density recovered, with regenerating clusters and many axons having disproportionately thin myelin sheaths. Midforearm and upper arm levels were normal.