Electrodiagnostic Evaluation of Brachial Plexopathies

Anatomy and Physiology

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 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 that leave the spinal cord and exit the spinal canal. The 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 posteriors). 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.[1]

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.[1][2][3][4]

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.[5][6]

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[1]:

• Axillary: C5-C6 root and posterior cord origin. Innervates deltoid and teres minor muscles. Sensory innervation to the superior lateral cutaneous nerve. Deficits after injury include paralysis of these muscles, resulting in loss of abduction of the arm at the shoulder from 15-90 degrees, and sensory deficit over the upper lateral arm superficial to the deltoid muscle.
• Musculocutaneous: C5-C7 root and lateral cord origin. Innervates the coracobrachialis, biceps brachii, and brachialis muscles. Sensory innervation to the lateral cutaneous nerve of the forearm. Deficits after injury include loss of flexion of the arm at the elbow, loss of supination of the forearm, and sensory deficit over the lateral aspect of the forearm.
• Median: C5-T1, lateral cord, and medial cord origin. Innervation to all forearm flexor muscles except flexor carpi ulnaris, and the part of flexor digitorum profundus which supplies digits 4 and 5. The median nerve also supplies the first and second lumbrical muscles, as well as the muscles of the thenar eminence, via the recurrent thenar branch. Sensory innervation is to the palmar aspect of the first three and half of the fourth digit. A proximal median nerve injury results in loss of forearm pronation, weakness in wrist flexion, loss of flexion in the first three digits, loss of opposition and abduction of the thumb, and sensory loss over the palmar aspect of the first three and a half digits. There is an “ape hand” deformity at rest, and a “benediction sign” when attempting to form a fist.
• Ulnar: C8-T1 and medial cord origin. Innervation to flexor carpi ulnaris, flexor digitorum profundus (medial half), hypothenar muscles, and the third and fourth digital lumbricals. Sensory innervation is to the palmar and dorsal cutaneous branches of the hand, which supply sensory innervation to the entire medial 1.5 digits. Deficits after proximal injury include weakness of flexion of the wrist, loss of flexion in the 4 and 5 digits, and sensory loss over the entire medial 1.5 digits. “Claw hand” deformity is typically seen at rest.
• Radial: C5-T1 and posterior cord origin. Innervation to triceps brachii, brachioradialis, and extensor muscles of the forearm. Sensory innervation is to posterior cutaneous, inferior lateral cutaneous, and posterior-lateral cutaneous nerves. Deficits after proximal injury include loss of extension of the forearm, weakness of supination, and loss of extension of the hand and fingers. The sensory deficit is over the lateral arm, much of the posterior aspect of the forearm, radial half of the dorsum of the hand, and dorsal aspect of the radial 3 ½ digits.

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 back along with the affected distribution in order to pinpoint the exact location. For more detail on this technique see the “technique” section below.

Indications

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 are beyond the scope of this discussion. Of note, lesions that are limited to A-delta and C fibers will most commonly produce completely normal electrodiagnostic studies. [7][8]

Contraindications

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:

• Infection at the site of needle insertion for EMG. Sites of superficial infection should be avoided.
• Electrical sensitivity. Delivery of electrical impulses during electrodiagnostic studies is safe and generally well tolerated. In patients with indwelling pacemaker wires or central lines, leak currents have the potential to reach the heart directly resulting in arrhythmia. Electrical stimulation near these devices should be avoided.[9]
• Areas, where edema/lymphedema is present, have been postulated to have a higher rate of infection and are generally avoided, although no cases reports of lymphoedema-related complications of EMG have been reported.
• The most common reported complication of EMG is pain at the site of needle insertion. Some patients simply will not tolerate the pain of electrode needle insertion. [10]
• Patients who are on chronic anticoagulation or those who have a coagulation disorder are predisposed to excessive bleeding. In these patients, needle insertion should be limited to superficial muscles.[11]

Equipment

Commercially available EMG and NCS machines are available and typically contain the following components:

• Computer- for processing and graphing of electrical signals.
• Speakers- produce audible feedback directly related to levels of electrical activity.
• Printer- for graphical read-outs
• Amplifier- amplifies minute electrical activity to a level that can be recorded and interpreted.
• Stimulator- produces the applied electrical stimulus.
• Surface electrodes- for stimulation and recording of electrical impulses along skin during NCS.
• Disposable needle electrodes- for recording electrical impulses during EMG.

Technique or Treatment

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 the 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 a neurological lesion can be pinpointed.[12][13]

The second electrodiagnostic study typically performed in the 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 the 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, the presence of large-amplitude, long-duration motor units suggests mature re-innervation.[12][13]

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, SSEPs assess the entire sensory tract from the periphery to the cortex. They are useful in differentiating pre-ganglionic (central) central from post-ganglionic (peripheral) injuries. The 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. SSEPs are useful when it is unclear whether a lesion is peripheral or central, or when localizing a central lesion.[12][13]

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 the identification of the affected terminal nerve distribution, which is based on the presentation of loss of function[14][15][16]:

• C5 root- Dorsal Scapular Nerve
• C5, C6, +/- C7- Long Thoracic Nerve
• Upper Trunk- Suprascapular Nerve
• Lateral Cord- Musculocutaneous, Lateral Pectoral, Lateral Antebrachial Cutaneous Nerves.
• Medial Cord- Ulnar, Medial Pectoral, Medial Brachial Cutaneous, Medial Antebrachial Cutaneous Nerves.
• Combined Lateral and Medial Cord- Median Nerve
• Posterior cord- Axillary, Radial, Upper Subscapular, Lower Subscapular, Thoracodorsal Nerves.

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 indicate 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. The 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 SSEPs 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.[17][18][19]

Complications

• Mild discomfort, tenderness, or bruising at the site of study is most common.[10]
• Infection at the site of needle insertion has rarely been reported.
• Serious bleeding and hematoma are very rarely reported. However, in anticoagulated patients, coagulation studies (PT/INR, aPTT) are recommended.[20]
• Complications during pregnancy have not been reported in electrodiagnostic studies.
• There are no known reported cases of neural injury directly due to EMG/NCS.
• Pneumothorax is the most serious complication of truncal muscle EMG but is very rarely reported.[21]
• Implanted deep brain stimulators and vagal nerve stimulators produce electrical activity that renders EMG studies useless. Prior planning with primary providers is necessary in order to have these devices turned off during EMG. [22]

Clinical Significance

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 the severity of neurological injuries and/or diseases. Often times neurological diseases manifest with nebulous presentations. Electrodiagnosis is one tool physicians may use to differentiate between diseases that may have similar or subtle presentations. In brachial plexopathies specifically, nerve conduction and EMG studies help to localize lesions and provide one further diagnostic 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 management such as surgical decompression, or reimplantation procedures. In this way, electrodiagnosis can be used by physicians to guide the management of the patient.

Enhancing Healthcare Team Outcomes

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 an 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 NCDs 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. [23]