Laboratory Diagnosis of Neurogenic TOS
Doctors find the clinical diagnosis of neurogenic TOS quite challenging. And following the diagnosis, treatment can be prolonged and incomplete. Early diagnosis and treatment improves the chance of a good outcome. Therefore, doctors have searched for good diagnostic tests for the diagnosis of neurogenic TOS. One such test is the EMG/NCV. Learn about the EMG, and the importance of the EMG in the history of TOS.
What is EMG/NCV?
EMG/NCV stands for electromyography and nerve conduction velocity. EMG and NCV are two components of a group of tests known as electrophysiologic testing. Electrophysiologic testing evaluates the electrical activity and function of nerves and muscles.
As you likely know, doctors have trouble diagnosing many patients with neurogenic TOS. In the past, many doctors used EMG in an effort to improve their diagnostic accuracy.
EMG/NCV tests nerve and muscle function, and does not assess anatomy. The test consists of two parts:
1. Electromyography (EMG)
Normal muscles naturally have a low level of baseline electrical activity. This baseline electrical activity increases under active contraction. EMG measures the electrical activity of the selected muscles. It is performed by inserting small needles into the muscles of interest, and recording the electrical activity at baseline and with contraction.
EMG can help to distinguish between abnormal electrical activity caused by muscle disease and abnormal electrical activity caused by disease of the nerve, or by disease at the neuromuscular junction (where the nerve inserts into the muscle).
2. Nerve conduction velocity (NCV)
Two electrodes are placed over the peripheral nerve being studied. A small electrical impulse is applied to the proximal electrode (the electrode nearer the spinal cord), and the impulse travels distally along the nerve (moving away from the spinal cord), where it is measured by the second electrode. The distance between the two electrodes is measured, the delay between the impulses is measured, and the velocity of the impulse within the nerve is calculated from these two measurements.
How is EMG/NCV used to diagnose peripheral neuropathies?
We will use the diagnosis of carpal tunnel syndrome (CTS) as an example. Carpal tunnel syndrome occurs when there is compression of the median nerve as it crosses the wrist through the carpal tunnel. The median nerve sends motor nerve ﬁbers to the muscles of the thumb, and carries sensory nerve ﬁbers from the thumb and several fingers back to the spinal cord.
Small needles are placed in the muscles at the base of the thumb. EMG then records electrical activity in these muscles at rest and during contraction. For the NCV, two electrodes are placed over the median nerve, one in the forearm, and one in the wrist. An electrical impulse is sent through the forearm electrode and measured at the distal electrode. The speed and quality of conduction along the median nerve is then recorded and assessed.
In this setting, EMG/NCV works well. Specifically, it works well because:
- The median nerve is small and not very complex.
- The median nerve is superficial and easy to access.
- The pathway of the median nerve is straight, without branching.
- The impulse can be sent in a normal direction along the nerve.
- Most of the median nerve fibers are motor fibers, which are assessed by both EMG and NCV.
- The muscles served by the median nerve are localized to one small muscle group.
How is EMG/NCV used to diagnose patients with neurogenic TOS?
Unfortunately, EMG/NCV cannot be performed or assessed in the same manner in patients with neurogenic TOS. Due to the anatomic complexity, location, and function of the brachial plexus, doctors must modify the usual methods of EMG/NCV:
- The brachial plexus is quite complex.
- The brachial plexus is deep, and cannot be accessed with any anatomic reliability.
- The branching pattern of the brachial plexus is complex, and often varies between patients. Even within a given part of the brachial plexus, different patients have different components of the contributing nerve roots.
- The NCV impulse cannot be sent in the normal direction along the nerve.
- The brachial plexus comprises large numbers of motor fibers, sensory fibers, and autonomic fibers.
- The muscles served by the brachial plexus are numerous and spread over the entire upper extremity.
To overcome these challenges, doctors have used specialized ‘F-wave’ NCV tests. For an F-wave test, a supramaximal impulse (above the normal threshold of the nerve) is applied to the nerve at the proximal electrode. This impulse travels distally along the nerve towards the fingers, but a portion of the impulse also travels in a retrograde direction (towards the spinal cord). The impulse must be supramaximal, as the nerve does not normal conduct the impulse in the backwards direction. Thus, the impulse is significantly weakened in this direction. This impulse travels through part of the brachial plexus to the spinal cord. Within the spinal cord, the impulse stimulates other neurons. These neurons then generate weaker impulses that leave the spinal cord in the normal direction. These impulses travel through the brachial plexus and can be measured by the distal electrode. Unfortunately, F-waves have been shown to be insensitive and non-speciﬁc in patients with neurogenic TOS:
- The impulse is weakened and degraded by the direction it takes against normal nerve conduction.
- The impulse is diluted by being spread throughout all components of the brachial plexus.
- When the impulse reaches the spinal cord, multiple other neurons are stimulated, causing a loss of focus on the nerves of interest.
- As the second impulse leaves the spinal cord, it is again diluted as it is spread throughout the brachial plexus.
- EMG cannot be focused on a single, small muscle group. It would have to be performed on all muscles of the upper extremity to find an abnormality. Even then, damage to the brachial plexus might be spread broadly, limiting the chance of a measurable change in any one muscle group. Motor nerve changes are more likely to become detectable when there is chronic and advanced damage to the motor nerve fibers of a muscle. However, such changes represent end-stage damage, and patients with such damage are unlikely to recover function.
Given the limitations of the typical EMG/NCV, doctors have developed other electrophysiologic tests. Besides the F-wave, these include ulnar sensory nerve action potential (SNAP) and ulnar nerve somatosensory evoked potentials (SSEP). Unfortunately, sensitivity and specificity of these tests remains limited.
A common sense analogy
Let’s use a common sense analogy to explain the limitations of EMG/NCV in patients with neurogenic TOS. Firstly, consider the brachial plexus as an imaginary transoceanic telephone cable: there are a very large number of steel or copper wires, some with insulation and some without. There are optical fibers in the cable. Some wires transmit a strong signal, others transmit a weak signal. Overall, the component wires and fibers are of a number of different sizes, resistances, and other physical qualities. Since the cable is transoceanic, it is exposed to damage from salt water and fishing nets. Over time, if salt water seeps through the outer insulation, progressive damage would occur. First, the small wires at the margins would be damaged. Wires without insulation would suffer damage early, those with insulation later. Over time, more of the central wires would suffer damage. Larger wires with thicker insulation would last the longest without damage.
The wires in the cable arise and terminate in multiple destinations on each side of the cable. Some of the wires connect a small building on one side of the ocean with a small building on the other side. Some wires connect a large business on one side with a large business on the other. Some wires are used for internet, others for military use. Some send signals in one direction, while others send signals in the opposite direction. The transoceanic cable is large, complex and vital for communication and function.
Now, imagine you have a ship with an electrical probe, and you want to diagnose technical problems in the cable. The probe can be maneuvered to the cable at any point, and can assess the signals it carries at that point. Let’s start by dropping the probe near one shore, to a small branch of the cable going to a small building. The cable contains a few hundred wires, most of which are the same size and structure, they all transmit a strong signal, and the cable is in shallow water. You can measure this relatively simple signal, and find damage early in the process. That is analogous to EMG/NCV of the median nerve.
Now let’s go the cable twenty miles offshore. You drop the probe, and get a complex signal from thousands of wires, which are composed of many different materials, have different sizes and insulation. You would have a difficult time separating out a few damaged wires from the thousands of other signals that are still normal. Certainly, you could tell if the transoceanic cable were completely cut, or if it was severely damaged. But you would want to repair it before the damage is severe.
Now suppose that an undersea landslide has buried the cable. You cannot get the probe to the buried portion. Instead, you can transmit a signal to the cable at an unburied segment, and then record the weak signal after it bounces back from the faraway shore destinations. As you might expect, it would be hard to overcome these technical challenges. The odds are stacked against you.
This latter situation is analogous to EMG/NCV of the brachial plexus. Remember that the brachial plexus branches in a complex manner. Many different types of nerve fibers with different sizes and types of insulation pass through the brachial plexus. Some pass peripherally, and some pass centrally. Damage occurs to smaller fibers near the periphery, especially those without myelin insulation. Thus, patients experience sensory symptoms early. Larger and more central, myelinated motor nerves are damages later. Since EMG/NCV focuses on motor nerve fibers, it will show damage later. And just like our last analogy, the odds are stacked against EMG/NCV when assessing the brachial plexus.
So how does this affect patients with neurogenic TOS?
The limitations of EMG/NCV affect patients with neurogenic TOS in two significant ways.
1. Inappropriate reliance on EMG/NCV
Some doctors still use EMG/NCV in patients with the potential diagnosis of neurogenic TOS. This creates problems for a few reasons. Firstly, EMG/NCV cannot diagnose neurogenic TOS, nor can it rule out neurogenic TOS. Second, a false negative EMG/NCV may steer doctors away from considering the diagnosis any further. In this situation, the doctor may not consider other diagnostic tests. Third, some doctors and insurance companies insist on EMG/NCV to exclude or diagnose other conditions, such as carpal tunnel syndrome. However, the presence of carpal tunnel syndrome does not rule out neurogenic TOS. Due to a phenomenon known as multiple crush syndrome, patients with neurogenic TOS may appear to have carpal tunnel syndrome or cubital tunnel syndrome. In fact, these distal symptoms are actually caused by compression of the brachial plexus. The medical literature shows that many patients are diagnosed with carpal tunnel syndrome and treated surgically, only to develop recurrent symptoms from compression of the brachial plexus.
Most TOS authorities agree that routine EMG/NCV does not play an important role in diagnosing or ruling out neurogenic TOS.
2. Dismissing TOS as controversial
This is a topic we love to discuss, but hate to hear. We will go into great detail in other sections of our website. However, you should know the basics of the story.
In the 1980s and 1990s, Dr. Asa Wilbourn of the Cleveland Clinic, a neurologist, published several articles in which patients presenting with neurogenic thoracic outlet syndrome had normal EMG/NCV studies in his laboratory. Dr. Wilbourn concluded that these negative results proved that neurogenic TOS was “highly overdiagnosed,” and that many of these patients ended up with “unnecessary and potentially harmful surgery.” He coined the term ‘disputed TOS’ to describe those patients with the clinical presentation of neurogenic TOS, but with a negative EMG/NCV.
Over the same period, Dr. David Roos, a surgeon in Denver, Colorado, published several papers detailing his surgical experience with patients with neurogenic thoracic outlet syndrome. Dr. Roos had helped to pioneer the transaxillary surgical approach to treating neurogenic thoracic outlet syndrome, and had described and categorized soft tissue anomalies in the thoracic outlet in these patients in great detail. He confirmed these anatomic findings in studies of cadavers. Dr. Roos had operated on thousands of patients for neurogenic TOS, with a high success rate and a very low complication rate.
While the two doctors argued through published letters in esteemed medical journals, the results of this argument still echo today. Many otherwise well-informed doctors insist that neurogenic TOS is ‘disputed’ or controversial. It is not. There are thousands of peer-reviewed articles in medical journals. TOS is regularly diagnosed and treated at esteemed academic centers throughout the world. But many doctors don’t learn about TOS because they wrongly believe it is controversial. Unfortunately, patients with TOS pay the price for this unnecessary confusion.
TOS is real and important. Patients and doctors need to take TOS seriously.