Brachial Plexus injuries, or brachial plexopathies, are considered among the most devastating of neurological injuries. Numerous mechanisms of injury leading to these afflictions exist, including traction injuries (falls, sports injuries, obstetric), compression injuries (crutches, pack straps, surgical malpositioning), lacerations from penetrating trauma, ischemia, and neoplastic disease. Since most nerves of the brachial plexus are mixed nerves containing both motor and sensory components, patients usually present with some combination of weakness and sensory deficit in the upper extremity, within the distribution of the injured root, trunk, cord, or branch of the brachial plexus. Thorough history and physical examination are the first steps in evaluation of brachial plexopathies and provide valuable clues as to the anatomical location of the injury, as well as the extent of the injury. Based on a provisional diagnosis derived from the physical exam, radiographic imaging and electrodiagnostic studies are then used to further pinpoint the location and severity of injury. Here, we focus on the use of electromyography and nerve conduction studies in the diagnosis and prognostication of brachial plexopathies.
The brachial plexus is an interwoven “netting” of nerves, which are bundles of axons belonging to nerve cells or neurons. These specific neuronal cells originate in in the dorsal horn (sensory) and ventral horn (motor) of the spinal cord from the C5-T1 levels. Nerve roots are mixed nerves containing both sensory and motor axons and are the first bundles of axons which leave the spinal cord and exit the spinal canal. Weaving of these fibers first forms trunks, then divisions, cords, and finally, the terminal nerve branches. The five terminal nerve branches are, the axillary, musculocutaneous, median, radial, and ulnar nerves.
Roots emerge from the spinal canal and travel laterally between the anterior and middle scalene muscles, and deep to the trapezius muscle. After a short distance the 5 roots (C5-T1) merge to form three trunks (superior, middle, inferior). These trunks travel laterally superficial to the first rib and beneath or deep to the clavicle. As these trunks pass under the clavicle to enter the axilla, each trunk divides into two divisions to form six total divisions (three anterior and three posterior). These six divisions then shortly merge to form three cords, which are named for their position relative to the axillary artery (medial, lateral, posterior). Finally, as the cords travel to exit the axilla and enter the arm medial to the humerus, they divide into the five terminal branches or nerves supplying the upper extremity: the axillary, musculocutaneous, median, radial, and ulnar nerves. Lesions along any region of the brachial plexus will produce characteristic presentations of sensory deficit and weakness that can be elicited in the history and physical exam and must be ascertained prior to electrodiagnostic evaluation.
There are many different mechanisms of injury to the brachial plexus. The most common of which is avulsion injury. Iatrogenic surgical trauma, penetrating trauma, compression injuries, ischemia, and neoplastic invasion are less common but possible mechanisms as well.
The area of the brachial plexus most commonly injured is the supraclavicular zone. This is due to the fact that this zone is the most anatomically exposed portion and is most susceptible to avulsion injury due to excessive cervical or upper extremity motion during traumatic mechanisms of injury. Upper roots (C5-C7) and upper trunk are most commonly affected, usually secondary to violent lateral flexion of the head away from the ipsilateral shoulder, or violent head rotation away from the ipsilateral shoulder. A common example of this is Erb’s palsy secondary to birth trauma. Lower root avulsion is far less common and is due to violent abduction of the ipsilateral arm above the head, such as when hanging from the arm from an elevated height. Supraclavicular injuries typically present with “Erb’s Palsy”, or an internally rotated and adducted shoulder, with a pronated forearm. Infraclavicular injuries present with “Klumpke’s Palsy”, or “claw hand deformity” with unopposed forearm supination, extension at the wrist and metacarpophalangeal joints, with flexion at the interphalangeal joints.
Penetrating and compressive trauma can affect any exposed portion of the brachial plexus. Examples of this include penetrating trauma in the arm affecting terminal nerve branches, compressive injuries in the infraclavicular region secondary to crutch use, or in the supraclavicular region secondary to strap compression from packs.
Clinical presentation will depend on the nerve(s) affected, therefore, in depth knowledge of the function of each terminal nerve, as well as the anatomical contribution of the brachial plexus to that particular distribution, is vital to understanding the origin of the pathology along the plexus:
Knowing these anatomical contributions and deficits allows the examiner to use the presenting history and physical as a starting point. Electrodiagnosis can then be used to trace backwards along the affected distribution in order to pinpoint the exact location. For more detail on this technique see the “technique” section below.
Electrodiagnostic studies may be used to confirm, localize, prognosticate, age, and grade severity of neurological injuries and/or diseases. They can also be used to differentiate axonal vs demyelinating lesions, motor vs sensory vs autonomic lesions, and diffuse vs focal vs multifocal lesions. It may also be used to differentiate myopathies from neuromuscular junction disorders and traumatic injuries. The specifics of how each of these is accomplished is beyond the scope of this discussion. Of note, lesions which are limited to A-delta and C fibers will most commonly produce completely normal electrodiagnostic studies. 
There are no absolute contraindications to electrodiagnostic studies. Electrodiagnosis has even been deemed safe in pregnant patients to date. These are generally well tolerated by the patient, however, a certain subset of patients will be “electrically sensitive” and will not tolerate the procedure well. The following are relative contraindications to the procedure:
Commercially available EMG and NCS machines are available and typically contain the following components:
Electrodiagnostic evaluation is typically broken down into three components: nerve conduction studies (NCS), electromyography (EMG), and somatosensory evoked potentials (SSEP). Nerve conduction studies are accomplished by using two skin surface electrodes, one which electrically stimulates and another which records the electrical response downstream along the nerve. These studies are further divided into motor and sensory components. The motor component is accomplished by stimulating motor nerves and recording compound muscle action potentials (CMAPs) which are produced as a result. In a similar fashion, the sensory component is accomplished by stimulating sensory nerves and recording sensory nerve action potentials (SNAPs) which are produced in response. Parameters recorded include the amplitude of action potentials, as well as the latency of the elicited response. The amplitude is a measure of the intensity of the response, while latency is the interval of time from stimulation to response. Once obtained, latency can be used along with the measured distance between the stimulating electrode and the recording electrode, to calculate the conduction velocity of the nerve fibers being studied. This velocity is typically expressed in meters per second (m/s). Measurements in the affected limb are then compared to the normal limb. Decreased amplitude, increased latency, and decreased conduction velocity are all considered pathologic findings and may indicate an injury somewhere between the stimulating electrode and the recording electrode. By moving the electrodes along the length of skin over a nerve, the precise location of neurological lesion can be pinpointed.
The second electrodiagnostic study typically performed in evaluation of brachial plexopathies is electromyography (EMG). This is accomplished by placing a small, disposable, recording needle electrode through the skin and into the muscle. The needle is then used to record the level of electrical activity within the muscle by measuring motor unit action potentials (MUAPs). While this evaluation produces a graphing of electrical activity, electromyographic evaluation tends to be more subjective and is therefore more dependent on the experience of the examiner than nerve conduction studies are. Recordings of activity are made upon insertion of the needle, while the muscle of interest is at rest, and during varying levels of contraction effort produced by the patient. Reduced levels of MUAPs suggest a neuropathic process, while increased MUAPs suggest myopathy or neuromuscular junction pathology. Fibrillation potentials are abnormal spontaneous electrical discharges recorded from muscle tissue. Their presence on EMG suggests axonal injury of the motor nerve distribution under study. Fibrillation potentials develop approximately three weeks after nerve injury in distal muscles. If no electrical activity is seen on voluntary effort made by the patient, this indicates a total injury or completely severed nerve. Any electrical activity suggests surviving axons within the nerve. Nerve regeneration can also be detected by EMG if adequate time is allowed post-injury. The presence of unstable polyphasic units suggests an underlying process of ongoing nerve regeneration. Finally, presence of large amplitude, long duration motor units suggests mature re-innervation.
The final electrodiagnostic study typically used is somatosensory evoked potential (SSEP) measurement. While NCS and EMG are useful for measuring post-ganglionic injuries such as plexopathies, SSEP’s assess the entire sensory tract from periphery to cortex. They are useful in differentiating pre-ganglionic (central) central from post-ganglionic (peripheral) injuries. Integrity of the dorsal column, medial lemniscus, thalamus, or sensory cortex may be assessed. This is accomplished by producing a supramaximal stimulus in the distal nerves and measuring responses over the various central anatomical areas. SSEP’s are useful when it is unclear whether a lesion is peripheral or central, or when localizing a central lesion.
When under electrodiagnostic study, lesions along the brachial plexus are typically localized to terminal branch nerves, cords, the superior trunk, or nerve roots. Note that lesions are not typically localized to the level of divisions, or the inferior or middle trunks. This is because no terminal branches arise directly from these areas of the brachial plexus. Localization of a lesion begins with identification of the affected terminal nerve distribution, which is based the presentation of loss of function:
Once the physical exam is completed nerve conduction testing in the distribution of the suspected injury begins. Attenuated amplitudes and/or increased latency of SNAPs or CMAPs in the area between the stimulating and recording electrodes indicates a lesion is present somewhere within that area. By moving the electrodes closer together/further apart, or more proximally/distally along the forearm, the sensory nerve or motor nerve lesion can be pinpointed. Electromyography is then performed within the specific muscles innervated by the distribution of the suspected lesion. Presence of fibrillation potentials or complete loss of MUAPs upon patient effort suggests a neurological lesion in the nerve supplying that muscle. If a peripheral lesion cannot be identified using these methods, this suggests a central lesion, and SSEP’s may be used to pinpoint the anatomical location of the suspected central lesion. Radiographic studies such as MRI may also be used in correlation to help support the diagnosis.
The clinical significance of electrodiagnostic studies is primarily diagnostic and prognostic in nature. These studies are used by physicians to confirm, localize, prognosticate, age, and grade severity of neurological injuries and/or diseases. Often times neurological diseases manifest with nebulous presentations. Electrodiagnosis is one tool physicians may use to differentate diseases which may have similar or subtle presentations. In brachial plexopathies specifically, nerve conduction and EMG studies help to localize lesions and provide one further diagnositic test to either support or refute a suspected lesion. These studies can also be completed in series in order to track the recovery process after an injury, and may be used in concert with imaging studies to guide decision making processes regarding interventional managment such as surgical decompression, or reimplantation procedures. In this way electrodiagnosis can be used by physicians to guide the management of the patient.
With patient-centered, team-oriented care in mind, the electrodiagnostician contributes by providing an additional mode of diagnosis and prognostication of neurological injuries and disease. Patient referral usually begins with a primary care provider, neurologist, pain medicine physician or neurosurgeon who wishes to obtain more diagnostic insight as to a patient's disease. The patient is referred to a the electrodiagnostician, who is usually a physician in the field of neurology, PM&R, or pain medicine. A single provider is required to complete the study, although a nurse may be present for patient comfort and monitoring for patient safety. Although meta-analyses and randomized controlled clinical trials evaluating the level of support of NCD's and EMG in the diagnosis of brachial plexopathies are limited, one review and meta-analysis of the use of electrodiagnosis in neurological disorders found Level C, Class 3 support for its use. 
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