Carpal tunnel syndrome (CTS) has been an interest of mine for several years, so I was very pleased to be asked to be a participant on this panel.
Carpal tunnel syndrome is precisely defined as a “compressive peripheral neuropathy of the median nerve at the wrist.” It is the most common of the peripheral neuropathies and the incidence of reported cases is increasing annually. Compression of the median nerve at the wrist causes numbness, burning, and ultimately tingling of the first three fingers. Symptoms usually occur during the night or early morning. There also may be pain proximal to the carpal tunnel along the median nerve distribution, diminished sensation, clumsiness, and weakness in hand grasp.
Treatments for CTS may include surgical relief of the transverse carpal ligament in order to decompress tunnel pressure, steroid injections, and hand splinting. Understanding the applied anatomy of the structures involved in this injury leads to a fuller understanding and appreciation of how this syndrome has gained the attention of the medical community and why the work we do is so effective for this condition.
For convenience’s sake, the nervous system is spoken of as being two parts: the central nervous system, which includes the brain and spinal cord, and the peripheral nervous system, consisting of the cranial nerves (except the optic), the spinal nerves with their roots and branches, the peripheral nerves, and the peripheral components of the autonomic nervous system. The two systems could more appropriately be considered as one since they do form a continuous tissue tract-a single organ, as it were. The connective tissues that make up as well as support and house the central and peripheral nervous system are viewed as being continuous even though they have different formats, i.e. the dura matter which covers and protects the brain and spinal cord, and the epineurium which covers and protects the peripheral nerves. The neurons are comprised of a cell body, dendrites, and an axon. They are interconnected both electrically and chemically. Electrically, the impulses that are generated in a sensory nerve ending in the skin are conducted along the axon of the neuron and are received in the brain. Chemically, we have identified the same neurotransmitters at synaptic junctions of both the peripheral and centrally located neurons.
The tissues that make up the nervous system perform and function in one of two ways-either for impulse conduction or for support and protection. Those tissues associated with impulse conduction include the axons, the myelin, and the Schwanncells. The tissues that support and protect the impulse-conducting elements in the central nervous system are the neuroglia and the meninges (a term which designates the dural, arachnoid, and pial layers). The peripheral nerves have their own named connective tissue elements. Figure I diagrams a myelinated and an unmyelinated neuron. As previously said, a neuron consists of a cell body (perikaryon), the thin threadlike processes of the dendrite, and usually one axon. The bottom diagram shows a single axon enwrapped by layers of myelin which are produced by the Schwann cell. Protective layers of connective tissue surround this impulse-conducting unit. In the unmyelinated fiber above, one Schwann cell is associated with a number of axons.
A single axon can extend over long distances in the body. For instance, an axon located in the dorsal root ganglion of a lumbar nerve will travel through the pelvis and lower limb to reach its target terminal in the foot. Many nerve fibers united or bundled together are called fascicles. Within a cross section of a multi-fascicular nerve segment (Figure 2) are seen the designated connective tissue tubes and sheathsthat surround, separate and guide the nerve fibers to and from their destinations. The loose aerolar mesoneurium wraps the nerve trunks. Bundles of fascicles are surrounded by layers of epineurium and each fascicle is ensheathed by a thin layer or perineurium. Individual nerve fibers containing axons possess an endoneurial membrane which surrounds the axon and functions to provide a constant internal fluid pressure and environment. These fibrous tissues are functionally designed to protect and cushion the delicate impulse conducting neural elements from excess compression and tensile force. In fact the greatest portion of neural tissue components consists of fascial and connective tissue. There is a very good reason for this, especially in the peripheral nerves which lie outside the armored protection of the cranium and spinal column.
The peripheral nerves travel a very torturous route through the limbs and trunk. They not only interface with various unyielding structures, they also have to adapt to marked changes in the length of the nerve bed. Millesi and his colleagues worked out that from full wrist and elbow flexion to full wrist and elbow extension, the median nerve has to adapt to a nerve bed that increases in length by 20%.’ Factors that can cause injury to a nerve may be unyielding bony projections or the sharp edges of the fibro-osseous tunnels through which the nerves must pass. Although nerves are very extensible, they can reach a limit that will restrict certain combinations of movement. Figure 3 demonstrates the slump position which, as seen here, determines the amount of possible knee extension. Full knee extension can only be gained when the head is extended.
It is easy to see how extending a nerve over several joints can produce neural tension and also intraneural pressure. The intraneural pressure will increase when tension is applied and the cross-sectional area is decreased. Consider what happens in activities where the body is taken to extreme ranges of movement such as ballet or basketball or figure skating. The nerve manages all these wonderful movements by virtue of the connective tissues.
The health and viability of the nerve is dependent upon adequate blood flow for transport of all the nutritive metabolites and the waste products of metabolism. From these examples it is clear that pathology to the nervous system can stem from either mechanical or vascular factors. Currently it is thought that the incidence of vascular factors, may predominate. Actually, there is a symbiotic relationship that exists with the neuron, the vascular system, and the connective tissue support structures.
Nerve cells typically contain two major components, the nucleus and the fluid medium of cytoplasm. These components are separated from the surrounding fluids by a cell membrane. The cytoplasm is 70-85% water. Dissolved or suspended within the water are the essential chemicals, enzymes, and the highly organized physical structures called organelles, all of which are vital to the health and function of the cell. Because of the fluid nature of water these essential factors are allowed to diffuse or flow from one part of the cell to another. The cytoplasm of the neurotic is termed axoplasm. The axoplasm provides a specialized transport system that insures passage of all substances throughout the entire length of the axon. Lundborg determined that the volume of axoplasmic material found along the length of a single axon may be thousands of times as great as is found in the cell body.’ Other researchers determined that the axoplasmic material of mammals has a viscosity about five times that of water.’ The transport mechanisms within the axon must provide a constant and controlled axoplasmic flow along its entire length. There are many different axonal transport systems within a single axon. Three of these have been identified, each moving at a specific directional flow (Figure 4). Axoplasmic flow that moves from the cell body toward its target tissues is termed antegrade flow; that which moves from the target tissue back to the cell body is known as retrograde flow. Neurotransmitters and transmitter vesicles are carried by a fast integrate transport system that travels at approximately 400 mm per day. These are the substances used in transmission of impulses at the synaptic junctions where neurons are linked to one another. Cytoskeletal material such as microtubules and neurofila-ments are carried in the slow (1-6mm per day) antegrade transport system and are responsible for maintenance of the structure of the axon. The retrograde system transports recycled transmitter vesicles and growth promoting factors from the terminal endings back to the cell body at a rate of 200mm per day. The complexity and sophistication of these transport mechanisms continue to elude the researchers. In the area of neurological sciences, Lundborg has hypothesized that force-generating enzymes and transport filaments may play a part.” We do know that an uninterrupted supply of energy from the blood supply is a vital factor.
Knowledge of these systems is important to the understanding of the symptoms that develop along the nerve pathway following injury. This bidirectional transport system of the nerve has been shown to be present by applying a tourniquet-type pressure around the nerve. The nerve will swell both proximally and distally to the point of pressure. Symptoms can present at any point along the neural pathway regardless of the injury or compression site. It is frequently necessary to treat other than the local area of complaint. This was an important tenet that Dr. Rolf experienced and taught. It is referred to in the medical literature today as the “double crush” or “multiple crush” syndrome.
The “double crush” concept was introduced by Upton and McComas in 1973 after they had examined 115 patients with either carpal tunnel lesions or lesions of the ulnar nerve at the el-bow.’ Their results confirmed that over two-thirds of the patients examined proved to also have electrophysiological and clinical evidence of cervical lesions. The authors proposed that minor serial impingements along a peripheral nerve could have an effect and cause a distal entrapment neuropathy. Many clinical and electrophysiological studies have followed, with evidence to support the concept.
Figure 5 illustrates the mechanism of the “double crush syndrome”. Figure 5 (A) exhibits a normal intervertebral foramen, exiting spinal nerve, and axoplasmic flow through the length of the nerve to its destination at the carpal tunnel. There are no impingements in any part of this system. In (B), there is mild compression at the carpal tunnel; however, a normal neural pathway exists and no impingements are present along the length of the nerve through the limb. There are no symptoms, but there is already some pathology present. In (C) an impingement is shown at the cervical nerve root with a mild compression at the tunnel as in (B). There are carpal tunnel symptoms present even though the main impingement is located at the intervertebral foramen. In (D) there is a normal cervical spine and severe carpal tunnel compression demonstrating a true symptomatic carpal tunnel. In (E) a systemic etiological factor is present-a mild carpal tunnel compression, and no impingement in the neural pathway, but this person is diabetic and symptomatic.
When treating a patient with carpal tunnel syndrome we have to wonder: Is the problem in the tissue? Is the problem in the nerve? Or is the cervical spine or some other more proximal place of entrapment responsible? Pathological processes that lead to adverse tension syndromes can be extraneural or intraneural or both. We need to know something about the client’s history in order to rule some of these factors in or out of the evaluation.
The peripheral nerves carry three distinct and functionally specific fiber types: motor (efferent) fibers; sensory (afferent) fibers; and sympathetic autonomic fibers which innervate blood vessels, hair follicles, and sweat glands of the skin. A spinal nerve contains sensory, motor, and autonomic fibers to one degree or another. There are more or less of one kind of fiber, depending on the functional aspect of the nerve. Autonomic fibers will be found in both sensory and motor nerves. There are no purely motor or purely sensory spinal nerves.
The nerves of the upper limb take origin from the spinal cord segments which forms the brachial plexus (Figure 6). Each of the terminal nerve branches is composed of fibers that have made their way to their final, more distal destinations from various spinal segments through the multiple branching of the plexus. The median nerve receives contributions from C5, 6, 7, 8, and TI. The radial nerve is also contributed to by all of these spinal roots. The ulnar nerve usually gets C8 and T1 distribution.
The dermatome map (Figure 7 on following page) identifies which nerve segments supply the sensory innervation to specific superficial (cutaneous) areas of the body. Sensory (afferent) symptoms such as pain, numbness, and tingling of a specific skin area are then linked to the sensory nerve that supplies that particular dermatomal representation. The radial, ulnar, median and musculo-cutaneous nerves are represented in the arm, forearm, and hand. The hand is served by the radial, ulnar, and median nerves, with the median nerve principal since it carries sensation from the palmar aspect of the thumb, index, and middle fingers. Sensory receptors for touch, temperature, pain, vibration, and pressure are abundant in the thumb and index finger. The opposition of the thumb and the first and second fingers is where we investigate almost everything. Losing sensation in this area of the hand can be devastating for the patient.
The motor (efferent) nerves that power extrinsic muscles of the wrist and hand receive impulses from the radial, ulnar, and median nerves. These muscles are found in the arm and forearm. The muscles that are intrinsic to the hand itself are served by the motor fibers of the median and ulnar nerves. Both nerves enter the hand on its palmar aspect, each passing through a tunnel at the wrist, the radio-carpal joint. The median nerve is accompanied by the tendons of the forearm muscles that transverse the wrist on the way to their distal attachments in the hand. As thetendons and the median nerve cross the carpus, they are held in place, close to the joint axis, by string bands of fibrous tissue called retinaculae. These fibrous bands form the roof of the carpal tunnel.
The structure and position of the carpal bones are important in understanding the mechanics of the carpal tunnel (Figure 8). The retinaculae form two strong bands that spanthe wrist and are attached to the carpal bones. The proximal band is attached from the tubercle of the scaphoid to the pisiform. The pisiform is a sesamoid bone contained within the tendon of the flexor carpi ulnaris. When the wrist is flexed and this muscle is tensed, the band is pulled taut. When the muscle is lax, there is some give at the proximal band of this ligament.
The distal band of the carpal ligament spans the carpus between the tubercle of the trapezium and the hook of the hamate, forming a rigid and unyielding band that crosses the arched form of the carpals. The tunnel narrows and there is less space available beneath the distal carpal row. The contents of the tunnel are shown in Figure 9. The flexor carpi radialis tendon passes under part of the transverse carpal ligament, but is in a tunnel of its own, as is the ulnar nerve, as it passes between the hook of the hamate and the pisiform. The mediannerve is located immediately beneath the transverse carpal ligament and is surrounded by soft tissue, fat, and fluids, and synovial shedons. Unhampered gliding movement of the multi jointed carpals and the flexor tendons held beneath the fibrous tunnel roof is provided by this viscous fluid milieu.
The provision of essential nutritive metabolites necessary for healthy nerve function requires that adequate blood flow passes into and out of the carpal tunnel. Sunderland postulated that by way of a series of pressure gradients the blood flow was moved through each of the structures contained with the restricted tunnel area. By way of this mechanism blood flows into the tun-aths of the ten-nel-into the nerve-and then out of the tunnel. Changes or reversals in these pressure gradients will restrict the fluid flow and cause swelling and ultimately tissue damage. Figure 10 illustrates a gradual degrading process of the nerve within the tunnel as the pressure increases over time.
As the median nerve traverses the forearm it drops off the motor fibers that innervate the massive extrinsic finger and thumb flexors. When it reaches the wrist, it is composed largely of sensory fibers, plus the remaining motor fibers that will serve the muscles of the then are eminence and the lateral two lumbricals. Within the nerve the sensory fibers are usually located around the periphery while the motor fibers are more centrally placed. The median nerve passes directly under the restrictive bands of the transverse carpal (retinacular) ligament and, since pressure from a compressive force first affects the outermost portion of a nerve, sensory symptoms will usually be the first to present. Compression of the motor fibers will cause a wasting of the muscles they supply. Atrophy of the thenar muscles will occur from repetitive and cumulative compression of the median nerve at the wrist.
The blood supplying the contents of the carpal tunnel and in particular the median nerve is derived from a branch of the ulnar artery, which is proximal to the carpal tunnel, and from a branch of the superficial palmar arch which is distal to the tunnel (Figure 11). Flexion or extension of the wrist and fingers causes compression of the small proximal aerterial branch and an increase of pressure within the tunnel. Intermittent flexion or extension movements allow adequate blood flow to proceed; however, prolonged periods of these movements without relaxation, or static and prolonged positions in flexion or extension will result in an increase in tunnel pressure. Neurological symptoms are bound to follow. Interruption of blood flow regardless of the site of vessel entrapment or compression will compromise the supply to any tunnel location it supplies. For instance, when the subclavian artery is compressed in the area of the thoracic outlet it will affect blood flow to any nerve it supplies that is distal to it.
A neutral pressure within the carpal tunnel is ideal. In full extension of the wrist, the pressure is three times what it is in flexion. All activities performed with the wrist held in extension-such as computer work-will cause much more compression at the tunnel than a flexed position. However, both wrist positions produce pressure within the tunnel. It is evident that splinting the hand in neutral position is often effective in treating carpal tunnel symptoms.
We can generalize and say that the nerves are continually in a tunnel in their course through the soft tissue, and there are various pressure gradients along any segment of the nerve. Also, thewalls of the tunnel are continually changing, whether it’s at the carpal tunnel or somewhere along the nerve pathway.
Physicians who diagnose patients with neurovascular compression syndromes must consider all of these multiple factors for each individual case. A thorough family and work history are imperative to a complete clinical evaluation. More and more work-related entities are being identified as causative factors. Our role as health providers in treatment and prevention of CTS becomes clearer as we learn from our colleagues who are working in industrial settings.
1 Millesi, H., The Nerve Gap: Theory and Clinical Practice, Hand Clinics 4: 651-663, 1986
2 Lundborg, G., Nerve. Injury and Repair, Churchill Livingston, Edinburgh, 1988
3 Haak, R.A., Kleinhaus, F.W, and Ochs, S., The viscosity of mammalian nerve axoplasm measured by electron spin resonance, Jounal of Physiology 263: 115-137, 1976
4 Lundborg, op. cit.
5 Upton, – A.R.M., McComas A.J., The Double Nerve Crush in Nerve Entrapment Syndromes, Lancet 2: 359-362, 1973
The following figures are reproduced with permission:
Figure 1: From Butler: Mobilization of the Nervous System, ©1991, Churchill Livingstone, New York
Figure 2: From Butler: Mobilization of the Nervous System, ©1991, Churchill Livingstone, New York
Figure 3: From Butler: Mobilization of the Nervous System, ©1991, Churchill Livingstone, New York
Figure 4: From Butler: Mobilization of the Nervous System, ©1991, Churchill Livingstone, New York
Figure 5: From Butler: Mobilization of the Nervous System, ©1991, Churchill Livingstone, New York
Figure 6: From Haymaker, Webb & Woodhall, Barnes: Peripheral Nerve Injuries, ©1953, WB. Saunders, Philadelphia
Figure 7: From Sunderland: Nerves and Nerve Damage, ©1968, E. & S. Trungstone LTD, Edinburgh & London
Figure 8: From Cailliet: Hand Pain and Imapirment, ED4, ©1994, RA Davis Company, Philadelphia, PA
Figure 9: Kristen McNew ©1995
Figure 10: From Cailliet: Hand Pain and Imapirment, ED4, ©1994, RA Davis Company, Philadelphia, PA
Figure 11: From Butler: Mobilization of the Nervous System, ©1991, Churchill Livingstone, New Yorka
Figure 12: From Cailliet: Hand Pain and Imapirment, ED4, ©1994, RA Davis Company, Philadelphia, PA