The best way to understand carpal tunnel syndrome is to start by understanding the carpal tunnel. As its name implies, it is an actual tunnel, with a floor, two walls, and a roof. The carpal bones of the wrist make up the floor and both walls of the carpal tunnel, and the roof is a tough, rigid sheet of connective tissue called the transverse carpal ligament. The tunnel is 2-4 cm long, and 10 structures travel through it to get from the forearm to the hand: nine flexor tendons and the median nerve (Figure 4-1).
NEWS FLASH
Carpal tunnel syndrome is actually a vascular problem!
Yes, it’s true. Compressive neuropathies are the result of compromised blood flow.
Question: What tissue in the human body is most sensitive to ischemia?
Answer: Nerve (muscle is a close second).
Why? Just remember membrane physiology. Both nerve and muscle have electrically active cell membranes. They have ATP-driven transmembrane pumps that are hard at work pumping charged ions across the cell membrane against both electrical and concentration gradients (Figure 4-A).
That takes a lot of energy! When a nerve fires, that energy is released. It’s like setting off a mousetrap: Transmembrane channels snap open, allowing the ions to rush back into the cell, depolarizing the cell membrane. This creates the action potential that nerves use to transmit electrical impulses down their axons. A fraction of a second later, all of these mousetraps need to be reset, a job for the ATP-driven transmembrane pumps. Running these pumps 24/7 is an expensive proposition. It requires a great deal of energy, which requires a rich blood supply, and that blood supply can be compromised by pressure. (Press your thumb firmly into your palm. The skin blanches because the pressure drives the blood out of the tissue. Release your thumb, and the skin turns pink again as the blood flow normalizes.) Pressure on the carpal tunnel compromises blood flow in the small vessels that nourish the axons of the median nerve. Under even transient ischemic conditions, the transmembrane pumps run out of fuel and quit working. The nerve starts to malfunction, which we perceive as numbness, tingling, and paresthesias. Most of us have experienced this firsthand. If you sit too long on the hard edge of a toilet seat, your leg will go numb from pressure and local ischemia as your sciatic nerve is pinched between the toilet seat and your femur bone. Relieve the pressure and sensation returns to normal.
Question: What tissue in the human body is least sensitive to ischemia?
Answer: Connective tissue, specifically cartilage, ligaments, and tendons.
Tendons are like cables. They are built for strength. Their job is to attach our muscles to our bones and to transmit muscle forces to bone. To keep them strong, they are essentially pure collagen, with very few cells and very few blood vessels in them. The few cells that do exist in tendon tissue (chondrocytes and specialized fibroblasts) are the most metabolically thrifty cells in the human body. They are used to living in ridiculously harsh conditions, exposed to the stress and strain of extreme mechanical forces and the metabolic stress of a severely hypoxic environment. How tough are these connective tissue cells? Viable chondrocytes can be harvested from a person’s body days, even weeks, after the person has died!
Although the flexor tendons and median nerve look similar (long, slender, rope-like tissues), they could not be more different physiologically (see sidebar). The biggest difference is their ability to tolerate ischemia. To operate properly, nerve tissue needs a healthy blood supply. In carpal tunnel syndrome, increased pressures in the carpal tunnel resulting from swelling and inflammation compress the nerve and decrease blood flow to its axons and their hungry, ATP-burning transmembrane ion pumps. Without an adequate blood supply to fuel these pumps, the nerve starts to malfunction, resulting in numbness, tingling, and paresthesias (see sidebar). As you would predict, these symptoms should only appear in the tissues serviced by the median nerve, which classically include the palm side of the thumb, index, and middle fingers, as well as the lateral side of the ring finger, though some person-to-person variation in this pattern exists (Figure 4-2). Neurologic symptoms in other distributions about the hand are likely NOT carpal tunnel syndrome (Box 4-1). Unfortunately, it is rare for patients to offer a precise history of symptoms in the exact median nerve distribution. It can be hard for them to discern/remember the exact distribution of their symptoms when they are giving their history.
Box 4-1. Carpal Tunnel Syndrome Is NOT:
Wrist pain (arthritis?)
Glove-like distribution of symptoms (neuropathy?)
Symptoms on the dorsal side of the hand (radial nerve issue?)
Symptoms in the small and ring fingers (ulnar nerve issue?)
Symptoms that radiate up the arm (cervical radiculopathy?)
In their history, we expect these patients to complain of numbness, tingling, and paresthesias in the median nerve distribution. There are also physical exam findings we can expect. An ischemic median nerve in the carpal tunnel has an unstable axon membrane potential, which we can depolarize by tapping on the nerve. This test, done by tapping over the palmer surface of the carpal tunnel, is called Tinel’s sign, and it is considered positive if tapping there produces numbness and tingling in the median nerve distribution. The other two provocative tests are done by increasing pressure in the carpal tunnel, either by pressing firmly onto the transverse carpal ligament (median nerve compression test) or by “kinking” the tunnel by bending the wrist (Phalen’s test, Figure 4-3). To better understand how Phalen’s test works, roll a sheet of paper into a tube, then bend the tube 90 degrees. The “kink” that you create in the paper tube when you bend it demonstrates how Phalen’s test compromises the dimensions of the carpal tunnel. When Phalen’s test is positive, the patient complains of increased neurologic symptoms in the median nerve distribution within 30-60 seconds after starting the test.
Another physical exam finding worth looking for is atrophy of the thinner muscles at the base of the thumb (Figure 4-4). Muscle atrophy is a consequence of long-term denervation of the muscles serviced by the median nerve. When seen, it indicates a chronic case of severe carpal tunnel syndrome. If you see a patient with these muscle atrophy changes, beware: The chances for success with medical or surgical treatment are poor. In typical cases of carpal tunnel syndrome, the goal of treatment is to eliminate the neurologic symptoms. In these severe chronic cases with visible muscle atrophy, nerve damage is likely irreversible, and the goal of treatment is to arrest the progression of the disease and prevent any further nerve and muscle damage.
These simple in-office physical exam tests are quick and easy to perform, but they aren’t always that reliable. Their sensitivity and specificity are only about 50%. Unfortunately, there is no perfect “gold standard” physical exam test.
In all cases of carpal tunnel syndrome, the treatment—surgical or nonsurgical—is to decrease elevated pressure in the carpal tunnel. Increased carpal tunnel pressures can be the result of fluid retention (as seen with pregnancy or thyroid dysfunction) or inflammation (due to arthritis, overuse, or trauma).
As discussed previously, these increased pressures can be exacerbated by bending the wrist, which “kinks” the carpal tunnel. Often, the first stage in treatment combines nonsteroidal anti-inflammatory drugs (NSAIDs) with a wrist brace (Figure 4-5) to keep the wrist straight. Many patients complain that their symptoms are worse at night because humans tend to sleep with their wrists bent. For those patients, the braces need only be used at night and can be discontinued when or if symptoms resolve. If these measures are not successful, then a reasonable next step might be a cortisone injection. A cortisone injection is a safe and effective way of introducing a potent anti-inflammatory medication directly into the carpal tunnel (refer to Chapter 9 to learn this simple injection technique). Within 10 days of the injection, we expect to see one of the following results:
The patient is permanently better. This is unusual, but it can happen. Corticosteroids can cause local atrophy of adipose tissue, and if the cortisone injection decompresses the carpal tunnel by decreasing the volume of fat in the tunnel, it could solve the problem permanently.
The patient gets better, but the symptoms return months later. The fact that the symptoms improved indicates that we have the correct diagnosis and that the nerve injury is reversible. Because the consensus “rule of thumb” is that cortisone injections can only be repeated in the same location once every 4 months, we have the option of reinjecting if 4 or more months have passed. We all have patients in our practices who have episodes of carpal tunnel syndrome once every few years. For those patients, the option of treating them with an injection each time they have a new recurrence is a reasonable way to manage their condition.
The patient gets better, but only for a short time—less than 4 months. This is the patient for whom surgery makes good sense. The fact that their symptoms improved proves to us that we have the correct diagnosis and that the nerve injury is reversible. This is critical. Carpal tunnel surgery is one of the most successful surgeries in all of orthopedics, but there are two types of patient who have poor results: (a) patients who do not have carpal tunnel syndrome (see Box 4-1) and (b) patients who have carpal tunnel syndrome, but it is so advanced that the nerve damage is irreversible. These two types of patients do not get better with surgery. So, the cortisone injection can help us treat carpal tunnel symptoms and predict which patients have the potential to improve with surgery. I find the results of a carpal tunnel cortisone injection to be sufficient in making the diagnosis, but most surgeons will require electromyographic (EMG) testing prior to surgery.
The patient gets no relief at all from the injection. Even a few hours of relief after a cortisone injection confirms the diagnosis of carpal tunnel syndrome and the reversibility of the nerve damage. If patients do not get better, not even for a short period after the injection, then either (a) they do not have carpal tunnel syndrome or (b) they have it, but it is so advanced that the nerve damage is irreversible. These are the patients for whom ordering EMG or nerve conduction studies makes sense. If studies show they do not have carpal tunnel syndrome, we need to come up with some other explanation (see Box 4-1), and EMG or nerve conduction studies can often help. If studies show they do have carpal tunnel syndrome, then we might consider a carpal tunnel release, but we must warn the patient that the symptoms are not likely to resolve and that the purpose of releasing the carpal tunnel is to arrest further progression of the disease.
Unfortunately, braces, cortisone injections, and other conservative treatment options offer only temporary relief for most patients, and it is common for carpal tunnel syndrome to worsen over time. For patients who don’t get adequate relief with nonoperative treatment, the carpal tunnel release operation is a safe and simple solution.
The surgical solution for carpal tunnel syndrome is to surgically divide the transverse carpal ligament (Figure 4-6). The divided transverse carpal ligament will open, and the gap will be bridged by a layer of blood, which will eventually form a bridge of scar tissue that reconnects the gap, resulting in an effective “lengthening” of the transverse carpal ligament (Figure 4-7). The operation increases the volume of the carpal tunnel, taking pressure off the median nerve, and restoring blood flow through the small vessels that nourish the nerve, allowing it to function properly again.
Ulnar nerve entrapment at the elbow (cubital tunnel syndrome) is similar to carpal tunnel syndrome, but it involves the compression of a different nerve (the ulnar nerve) in a different location (the cubital tunnel of the elbow) (see sidebar). The ulnar nerve enjoys a relatively free and comfortable journey from its origins in the brachial plexus in the neck and shoulder area all the way to its most distal innervation targets: the tips of the ring and small fingers. The narrowest, or tightest, section along this pathway is the place where it rounds the corner of the elbow. Here, the ulnar nerve passes through the 2- to 3-inch long cubital tunnel, the floor and walls of which are the humerus and ulna bones and the roof of which is a dense, firm sheet of connective tissue (Figure 4-8).
THE “SQUEEZE ZONE” CONCEPT
Cubital tunnel syndrome and carpal tunnel syndrome (see previous section) both illustrate conditions in which nerve dysfunction results from peripheral nerve axon compression. The mechanism and physiology of this phenomenon are detailed in the sidebar in the section on carpal tunnel syndrome. It is important to understand that for nerve compression to occur, the nerve has to be fixed against some unyielding structure. In carpal tunnel syndrome, it is the carpal bones and the transverse carpal ligament. In cubital tunnel syndrome, it is the medial epicondyle of the humerus, the olecranon process of the ulna bone, and the fascia. The axons of our peripheral nerves travel many inches, often several feet, as they span the distance between their origins (the cell bodies in the spinal cord) to their destinations, for example, the tips of our fingers or toes. Most of that distance is “free and clear,” surrounded by soft, flexible fat and muscle. Rarely, there will be a short section along the pathway of the nerve where the nerve passes through a rigid space, such as the carpal tunnel in the wrist or the cubital tunnel in the elbow. Other examples include the area on the lateral side of the knee where the peroneal nerve is tethered to the proximal head of the fibula bone, and the arcade of Froshe where the radial nerve can be trapped by a rigid band of connective tissue in the proximal forearm. These are areas where nerve compression can occur. Any other place along the path of the nerve, the nerve is free to move aside if something tries to push against it. If you hold a garden hose up in the air with one hand and push against it with the other, it just moves away and the water continues to flow. However, if you stand on a hose that is lying on the sidewalk, it will collapse (compress), and the flow through the hose will decrease to a trickle. Mass effects from inflamed tissue, a hematoma, an intervertebral disk (in the case of the spine) are not likely to cause nerve compression unless they happen to be pressing against the nerve at a place where the nerve is not free to move out of the way.
Inflammation in this area can cause compression of the ulnar nerve, resulting in pain, numbness, tingling, and paresthesias in the small and ring fingers. A patient with a history of these complaints could also have a C8 or T1 cervical radiculopathy, thoracic outlet syndrome, or ulnar nerve compression at the wrist, but the most common cause of this pattern of neurologic symptoms is cubital tunnel syndrome.
In patients with ulnar nerve entrapment at the elbow, tapping over the cubital tunnel (Tinel’s sign) will often create an electrical, shooting sensation into the ring and small fingers, but beware, this test can be positive in normal, asymptomatic patients. If it is negative, and you still suspect cubital tunnel syndrome, I recommend proceeding with conservative treatment. If the patient does not improve, then consider ordering an EMG. Chronic cases may demonstrate wasting of the interosseous muscles of the hand.
Electrodiagnostic studies (EMGs, nerve conduction studies) can be helpful in distinguishing cubital tunnel syndrome from a cervical radiculopathy, thoracic outlet syndrome, or ulnar nerve entrapment at the wrist. When positive, these studies will show a slowing in ulnar nerve conduction across the cubital tunnel.
Often, the ulnar nerve is compressed by local inflammatory changes in the cubital tunnel; therefore, NSAIDs can sometimes help. Another useful treatment option is an elbow pad (Figure 4-9). The bony prominences around the elbow are common sites of minor contusions in daily life, and those contusions contribute to inflammation. Resting the medial side of the elbow on the hard surface of a desk or table, or the armrest of a car can inflame the cubital tunnel. The elbow pad affords some protection against these everyday occurrences. It also bunches up when the elbow is flexed, limiting elbow flexion and the stretch the ulnar nerve experiences in the cubital tunnel when the elbow is put in the deep flexion position. Patients who have symptoms at night when they sleep with their elbows in the deep flexed position can feel relief by wearing an elbow pad at night.
PHYSIOLOGY OF RECOVERY AFTER NERVE DECOMPRESSION SURGERY
For any nerve decompression surgery, recovery can take months. Some of the axons may have died from nerve compression, and those axons will have to grow back down the length of the nerve to reach their innervation targets. This process, called Wallerian degeneration and regeneration, typically occurs at a rate of a millimeter a day (about an inch of axon growth a month). For that reason, results tend to be better for decompressing nerves that have a short distance to regenerate (such as the median nerve in the carpal tunnel) than nerves that have longer distances (such as the ulnar nerve in the cubital tunnel).
In cases that do not respond to conservative management, surgery can also be an option. In the most commonly used surgery for cubital tunnel syndrome, the nerve is transposed (moved) out of the cubital tunnel and repositioned more toward the center of the antecubital fossa (Figure 4-10). By “taking a shortcut” across the corner of the elbow, there is less tension on the ulnar nerve, especially in deep flexion, and the nerve is freed from the firm, unyielding confines of the cubital tunnel (Figure 4-10 inset). Like most surgical procedures, surgery is indicated if conservative treatment fails. The surgical results of cubital tunnel surgery are not as good as they are for carpal tunnel release. Resolution of symptoms takes longer and is less likely to occur in this operation (see sidebar).