David Rempel, MD, MPH
David Rempel is Professor of Medicine at the University of California, San Francisco, Professor of Bioengineering at UC Berkeley, and director of the ergonomics graduate training program at UC Berkeley. The research of his group has focused on understanding mechanisms of injury to tendon and nerve due to cyclical loading and the application of this information to the design of tools and work in order to prevent musculoskeletal disorders. His recent research has involved workplace intervention studies in the garment, dental, construction, and office sectors. The publications of the group and a description of the graduate training program are at : http://ergo.berkeley.edu/
Consensus is lacking on the precise role of workplace biomechanical factors in the causation of CTS. Epidemiologic studies are limited in their ability to clarify the dose-response relationships because the
Indicateur épidémiologique mesurant la fréquence de survenue d'une maladie pendant une période donnée En savoir plus... ) of CTS is low, the exposure patterns at work and home are complex, and there is lack of agreement on measuring and aggregating biomechanical exposures (van Rijn 2009). However, some light can be shed on the relationship between biomechanical factors and the pathophysiology of activity-related CTS by examining findings from human and animal physiologic studies. Human histologic and intraoperative studies provide insights into the tissue changes in synovium and nerve and the location of damage. Animal studies provide support for the mechanism of injury. And human studies of carpal tunnel pressure provide detailed information on the relationships between biomechanical factors and a mediator of injury : elevated intracarpal pressure.
We know that patients with CTS have elevated fluid pressure in the carpal tunnel compared to healthy controls. Furthermore, we know that in patients with CTS and in healthy subjects, the pressure in the tunnel can increase by external compression or by moving the wrist toward posture extremes. The pressure remains elevated for as long as the wrist is manipulated because there is no lymphatic drainage.
The role of elevated fluid pressure in causing peripheral nerve injury is supported by animal studies. Powell and Meyers (1986) applied small inflatable cuffs around the rat sciatic nerve for just two hours then examined the nerve one month later. Pressures of 0 or 10 mm Hg had little effect while pressures of 30 mm Hg caused subperineurnal edema and demyelination and pressures of 80 mm Hg led to epineural fibrosis.
So understanding how hand postures and loads increase carpal tunnel pressure may provide insights into how to prevent CTS in the workplace. A physiologic model is gaining support that explains the relationship between hand postures and tunnel pressures. The model considers the carpal tunnel as a closed compartment. The boundaries are stiff enough to sustain an elevated fluid pressure. As the boundaries change with changes in wrist and finger the tunnel pressure changes. Half the contents of the tunnel are stiff flexor tendons that traverse the tunnel. These will not deform but they move within the tunnel with changes in finger loading (Yoshii 2009). The other half is the tenosynovium that surrounds the tendons and the median nerve. The tenosynovium is a gel-like material that can sustain a fluid pressure gradient within the tunnel. Therefore, the pressure in one region of the tunnel may be different from another region.
The tunnel is narrowest at the hook of the hamate. Intraoperative studies of patients with CTS report that the greatest narrowing of the median nerve occurs at the level of the hook of the hamate and the nerve is enlarged just proximal to the hook. A recent primate model of CTS revealed that repetitive, forceful grasping for several weeks not only caused nerve slowing but also caused enlargement of the median nerve in the location similar to that seen in humans.
Several laboratories have been mapping the relationships between hand/wrist postures, forearm rotation, fingertip loading and carpal tunnel pressure. Pressure is increased by wrist extension or flexion. Supination and full pronation increase pressure. Fingertip loading increases CTP. External compression increases CTP. But there are large between-subject differences. Some of these differences may be due to differences in methods of measuring pressure. For example, small changes in the location of the pressure sensor within the carpal tunnel may have a large influence on the pressure pattern.
Understanding the relationship between hand and wrist postures and fingertip loading and carpal tunnel pressure may provide guidelines for improving the design of work to prevent CTS. A study of pinching found a relatively linear relationship between pinch force and carpal tunnel pressure with pinch forces of 5N or 10 N associated with pressures of 30 and 40 mmHg, respectively. For pronation/supination, the lowest carpal tunnel pressure is at 45 degrees pronation. For finger flexion, the pressure is lowest at 45 degrees MCP ( Fermer MCP
Maladies à caractère professionnel En savoir plus... ) flexion.
The proposed model suggests that tools and hand tasks be designed so that the mean pressure in the tunnel is as low as possible or stays below some pressure associated with tissue injury. We recently proposed that, based on an injury threshold of 30 mmHg, the mean wrist postures that protect 75% of the population are 32.7 extension, 48.6 flexion, 21.8 radial deviation, and 14.5 ulnar deviation (Keir 2007). Similar guidelines could be developed for pinch force, finger postures, and wrist contact stress.
This approach may provide guidance for static postures and loading but the hand is active at work. Hand activity is dynamic and the pressures in the carpal tunnel can change rapidly. For example, pressure is elevated during a material handling task, similar to that of grocery clerk checker, when an object is gripped. But the pressure rapidly drops when the object is released. For keyboard work the mean pressure is primarily determined by wrist posture and contact stress during keying ; this can be considered a static load. The dynamic act of keying increases the mean pressure by an additional 5 mmHg but the pressure fluctuates.
Determining the relationships between nerve compression pressure, compression time, and recovery time that prevent an ischemic reperfusion injury of the synovium or nerve is a ripe area for research. Is the primary determinant of injury the exposure duration to peak pressures, to mean pressures, or an inadequate time to some minimal pressure that allows for tissue perfusion ? A study of the rat sciatic nerve exposed it to static and cyclic pressures. Nerve function was influenced by mean tissue pressure not peak pressure. But do pressure patterns that cause an acute change in nerve function also initiate the more serious changes of demyelination or fibrosis ?
Keywords : Mechanism, Early prevention, CTS
Keir PJ, Bach JM, Hudes M, Rempel DM. Guidelines for wrist posture based on carpal tunnel pressure thresholds. Human Factors 2007 ; 49:88-89.
Powell HC, Myers RR. Pathology of experimental nerve compression. Laboratory Investigation. 1986 ; 55 ;91–100.
van Rijn RM, Huisstede BMA, Koes BW, Burdof A. Associations between work-related factors and the carpal tunnel syndrome – a systematic review. Scand J Work Environ Health 2009 ; 35:19-36.