Shoulder and Elbow

Brachial Neuritis

The Problem

Brachial Plexopathy

The brachial plexus (BP) is a complicated anatomical structure formed by the lower cervical and upper thoracic nerve roots. Fascicles from these roots intermix inside the plexus to ultimately form the nerves of the upper extremity. The diagnosis of brachial plexopathy can be very challenging, requiring extensive knowledge of the anatomy of the plexus as well as various clinical presentations of the syndrome. Ultimately, NCS and EMG are needed to precisely localize the lesion within the brachial plexus, establish possible etiologies and determine the severity of the damage (especially important in case of trauma).

Anatomy

The BP is situated between the lower neck and the axilla, starting behind the scalene muscle proximally and behind the clavicle and the pectoralis muscle distally. The plexus originates from the C5 to T1 nerve roots and consists of trunks, divisions and cords generated by intermixing of these roots to ultimately end in peripheral nerves. The roots and the nerves are not considered part of the brachial plexus. The upper trunk is formed by the C5 and C6 roots, the middle trunk is the continuation of the C7 root and the lower trunk is formed by the C8 and T1 roots. C4 proximally and T2 distally can occasionally contribute to the plexus reflecting recognized anatomic variations.

Each trunk then divides into an anterior and posterior division. The divisions generate the cords distal to the clavicle. The posterior divisions of all the trunks form the posterior cord; the anterior division of the upper and middle trunk form the lateral cord; the anterior division of the lower trunk forms the medial cord.

All the nerves of the upper extremity originate from the trunks or the cords. Two important nerves originate directly from the roots and proximal to the plexus: dorsal scapular (C5 +/- C4 innervating the rhomboid muscle) and the long thoracic (C5-C6 –C7 innervating the serratus anterior muscle).

Clinical Presentation

Brachial plexopathies can present in a variety of clinical patterns depending on the portion of the plexus involved. See Table 1.

Panplexus: A complete lesion of the plexus results in weakness, sensory loss and absent reflexes in the entire upper extremity. As only the plexus is involved and not the cervical roots, the serratus anterior and the rhomboid muscles are the only spared muscles as they are innervated by nerves that emerge proximal to the plexus. This can be tested clinically and proven electrodiagnostically with EMG and is helpful in differentiating a severe plexus lesion from one involving the cervical roots.

Upper trunk plexopathy: The upper trunk is formed by the C5 and C6 roots. The muscles affected will be the ones with exclusive or partial C5 and C6 innervation: deltoid, biceps, brachioradialis, supraspinatus, infraspinatus and partially triceps and pronator teres (C6 and C7 innervation). The sensory loss will be in the lateral arm, forearm and hand in the distribution of the axillary, lateral cutaneous antebrachii and median and radial sensory branches to the thumb. The biceps and brachioradialis reflexes will be decreased or absent but the triceps reflex is spared.

Middle trunk plexopathy: Middle trunk plexopathies are very rare. They mimic a C7 radiculopathy and the muscles primarily affected are triceps, pronator teres and flexor carpi radialis. The sensory abnormalities involve the posterior forearm and the middle finger in and overlapping median and radial sensory distribution. The triceps reflex is absent but the other upper extremity reflexes are preserved.

Lower trunk plexopathy: The lower trunk is formed by the C8 and T1 roots. The lower trunk ultimately forms the ulnar nerve, the sensory branches of the medial arm and forearm and sends “ motor contributions” via the posterior division to the median (abductor pollicis brevis (APB), flexor pollicis longus (FPL), and flexor digitorum profundus (FDP) muscles) and radial nerves (extensor indicis proprius (EIP) and extensor pollicis brevis (EPB) muscles). A lower trunk plexopathy will cause weakness of the entire hand and sensory loss in the medial arm, forearm and hand. There will be no reflex abnormalities.

Lateral cord plexopathy: The lateral cord is formed by the anterior divisions of the upper and middle trunks of the brachial plexus and includes nerves originating from the C5, C6 and C7 roots. It originates the musculocutaneous nerve and a section of the median nerve with contributions from C6 and C7. The affected muscles are the pronator teres (pronation of the forearm), flexor carpi radialis (FCR) (wrist flexion) and the biceps brachii (elbow flexion). The sensory loss involves the lateral forearm and lateral hand (lateral cutaneous antebrachial nerve and sensory portion of the median nerve). The only absent reflex is the biceps reflex.

Posterior cord plexopathy: The posterior cord is formed by the posterior divisions of the upper, middle and lower trunks of the brachial plexus. It originates the axillary, radial and thoracodorsal nerves. The affected muscles are the deltoid (shoulder abduction), latissimus dorsi (arm adduction) and all the radial innervated muscles (elbow, wrist and fingers extensors) thus causing elbow extension weakness and wrist drop. The sensory loss is in the distribution of the axillary and radial nerves. The only absent reflex is the triceps reflex.

Medial cord plexopathy: The medial cord is the extension of the anterior division of the lower trunk after it divides into the anterior and posterior divisions; the posterior division is incorporated into the posterior cord and therefore lesions of the medial cord are almost identical with lesions of the lower trunk with the exception of the spared C8 innervated radial muscles (EIP, EPB; index and thumb extension). The affected muscles include all of the ulnar and median hand muscles and the C8-T1 innervated portions (digit flexors) of the median nerve. The sensory loss is identical with lower trunk lesions involving the medial arm, forearm and medial hand (digits 4 and 5). There are no reflex abnormalities.

Common Brachial Plexopathies

Traumatic brachial plexopathies

Trauma is the most common cause of brachial plexopathy and occur primarily as a result of motor vehicle accidents, penetrating wounds (gun shot, knives) or traction injury in newborns at the time of delivery.

If the head and neck are pulled away from the shoulder during the injury, an upper trunk plexopathy will result (also known as Erb’s palsy). Muscles innervated by C5 and C6 roots will be affected and there will be weakness of arm abduction, elbow flexion and forearm supination.

If the arm and shoulder are pulled up during the injury, a lower trunk plexopathy will result. Muscles innervated by the C8 and T1 roots will be affected causing severe weakness, atrophy and sensory loss of the hand (also known as Klumpke’s palsy). The arm will be spared.

High-speed motor vehicle accidents and severe traction injuries may result in a combined injury of the plexus (plexopathy) and cervical roots (root avulsion). With root avulsion, the motor roots are physically separated from the anterior horn cell in the spinal cord and there is virtually no chance of recovery. Electrodiagnostic studies using nerve conduction, EMG and somatosensory evoked potentials will help differentiate root avulsion from brachial plexopathy.

Brachial plexitis (neuralgic amyotrophy)

Brachial plexitis is a common and frequently underdiagnosed inflammatory condition of the brachial plexus. It can affect the whole plexus or individual nerves. It is also known as Parsonage Turner syndrome or brachial amyotrophy.

Typically, the onset of symptoms is preceded by a viral illness or immunization for 1-2 weeks. Subsequently an intense neuropathic pain develops in the affected arm followed 1-2 weeks later by weakness and atrophy in the affected arm in the distribution of the affected nerves. By the time the weakness develops the pain disappears and a residual sensory loss may be noticed in the affected nerves’ distribution. Any nerve of the brachial plexus may be affected by the condition. It is not uncommon for the brachial plexitis to involve individual nerves emerging proximal to the brachial plexus (for example, long thoracic nerve presenting with scapular winging due to serratus anterior weakness).

The brachial plexitis episodes are mostly unilateral and sporadic. Recurrences and bilateral occurrences are rare. Gradual recovery is the usual course but mild residual deficits are not uncommon.

Post–operative brachial plexopathy

This is one of the complications that can occur in the setting of chest surgery in which chest wall retraction is used (for example, coronary artery bypass surgery) or in the setting of prolonged spine surgeries where the arms are maintained away from the body for a long period of time. This type of positioning causes traction with or without ischemia of the lower trunk of the brachial plexus. The patients will notice weakness in the C8 – T1 innervated muscles (hand muscles, long fingers flexors and even extensors of the index and thumb) and numbness in the medial aspect of the arm, forearm and hand with digits 4 and 5 involved. There can be significant neuropathic pain. Shoulder surgery can also be a cause of brachial plexopathy and is usually the result of prolonged traction or positioning. The pattern of involvement can be quite variable. In this setting it is important to differentiate these causes from direct injury to the plexus from surgical instruments.

Recovery over the course of several months is usually the rule as the mechanism of injury is mostly nerve stretching and compression, affecting mostly the myelin layer of the nerves without disruption of the nerves’ basal lamina. If significant ischemia takes place and axonal damage occurs the recovery is less complete and more protracted. If the basal lamina of the nerves is disrupted, the nerve recovery will no longer be possible and there will be significant residual deficit in the C8 and T1 distribution. Occasionally, there will also be residual pain in the affected territory that can be chronic and refractory to treatment.

Radiation plexopathy

Radiation plexopathy is an insidious, progressive brachial plexopathy that presents years after exposure to radiation. It occurs in patients with tumors of the breast, neck or lung that have been treated with rather large doses of radiation (more than 5000 rads) and whose radiation ports included the axillary and periaxillary regions.

When symptoms of progressive weakness, paresthesias and pain develop in a brachial plexus distribution in a patient treated with radiation for malignancy in the same area, the differential diagnosis includes brachial plexopathy from radiation versus brachial plexopathy from recurrent tumor. Clinically, with direct neoplastic invasion of the plexus, prominent pain and a Horner syndrome (ipsilateral ptosis, pupillary myosis and hemifacial anhydrosis) are much more common. In the radiation plexitis the symptoms are less prominent and more insidious and are dominated by paresthesias and numbness. Diagnostically, gadolinium MRI of the brachial plexus will show enhancing masses in the case of tumor invasion of the plexus, while electrodiagnostic studies will show specific myokimic EMG discharges in the affected muscles in the case of radiation plexopathy.

Brachial plexopathy due to regional compression

The brachial plexus can be compromised by local compression and invasion from nearby tumors (Pancoast tumor of the lung), by local compression by enlarged metastatic lymph nodes (in lymphomas, breast and lung cancers) or by nerve sheath tumors (schwannomas, neurofibromas, etc). More rarely, local vascular malformations (aneurysms, arteriovenous malformations) or a rudimentary cervical rib will also compress sections of the brachial plexus and cause neurogenic symptoms. Clinically, brachial plexopathy related to direct tumor invasion or local compression is usually associated with prominent pain and slowly evolving weakness, atrophy and sensory loss. Horner’s syndrome may be present if the lower trunk is involved.

Thoracic Outlet Syndrome

Neurogenic thoracic outlet syndrome (TOS) is a partial brachial plexopathy caused by mechanical irritation of the lower trunk by a rudimentary cervical rib connected via a fibrous band to the first thoracic rib. It is quite rare and it manifests as a typical lower trunk plexopathy with weakness and atrophy of the hand muscles and of the long finger flexors (FPL and FDP) as well as numbness in the medial aspect of the arm, forearm and hand. Clinically, the thenar atrophy seems to be more prominent than the hypothenar atrophy, probably because the thenar muscles are innervated mostly by the T1 root which is more involved in the TOS. Electrodiagnostic studies will help differentiate the true neurogenic TOS from the much more common ulnar neuropathy or C8/ T1 radiculopathy.

Diagnostic evaluation of the brachial plexus pathology

The purpose of diagnostic evaluation of brachial plexopathy is to confirm, localize and grade the severity of the lesion as well as to determine the prognosis for recovery.

Imaging studies are useful as confirmatory and localizing tools. MRI of the brachial plexus with and without contrast is the most useful imaging technique. It will show abnormal signal on T2 sequences in most etiologies and enhancement on post contrast T1 sequences in etiologies with a primary or secondary inflammatory mechanism.

Electrodiagnostic studies are the most useful diagnostic tool in confirming, localizing and establishing severity and prognosis for recovery of brachial plexus lesions. In addition, they should exclude the possibility of radiculopathy or multiple peripheral nerve lesions mimicking a brachial plexopathy.

The electromyographer should always perform a clinical neurological evaluation prior to the electrodiagnostic test in order to have an appropriate clinical suspicion for the pathology to be investigated by the study.

Electrodiagnostic studies of the brachial plexus include nerve conduction studies (NCS) and electromyography (EMG). Somatosensory evoked potential studies (SSEP) can be added if root avulsion is to be excluded.

Several features of nerve conduction studies are invaluable in separating a root lesion versus a brachial plexus lesion. If axonal damage takes place distal to the dorsal root ganglion which hosts the sensory neuron cell body, the sensory nerve action potential (SNAP) will be abnormal or absent as the damage to the nerves of the plexus will disconnect some of the dendrite from the cell body and cause Wallerian degeneration in the nerve. Conversely, if axonal or compressive damage takes place proximal to the dorsal root ganglion (in the nerve root region) the sensory nerve action potential will remain normal (because the sensory neuronal body and its peripheral dendrite are intact) but the patient will have authentic sensory changes in the clinical neurological examination due to the interruption of the sensory pathway by the sensory root lesion. The motor action potential (CMAP) recorded in the affected territory will be affected if a sizeable lesion is present in the motor root or in the motor nerve as both lesions will be distal to the motor neuron cell body located in the anterior horn of the spinal cord. However, the routine motor NCS only records CMAPs in the C8 and T1 distribution (ulnar and median nerves) and are not very sensitive for more proximal lesions of the brachial plexus. Conversely, the routine sensory NCS span the entire distribution of the brachial plexus and are very helpful in localization.

Nerve conduction studies

The SNAPs performed in the upper extremity include median, ulnar, radial, medial cutaneous antebrachial and lateral cutaneous antebrachial nerves. They are all easily performed. In severe cases the SNAPs in the distribution of the affected section of the brachial plexus are absent. In milder cases the SNAPs are present but a dysfunction is only visible when they are compared with the contralateral SNAPs in a side-to-side comparison.

The motor nerve conduction studies (median and ulnar) are only useful in brachial plexopathies involving the lower trunk or the medial cord. In this situation, the CMAPs are either absent or significantly reduced in size on the affected side when compared with the contralateral responses. F responses of the median and ulnar nerves are also absent, delayed or prolonged on the affected side. The radial motor study is useful in suspected lesions of the middle trunk or the posterior cord. Proximal stimulation of motor nerves is usually not indicated in brachial plexopathy as most lesions are axonal and conduction block or proximal demyelination are not part of the presenting pathology.

Electromyography

Electromyography is usually straightforward and helpful in the diagnosis of brachial plexopathy. A sufficient number of the muscles should be sampled to represent all trunks, cords and nerves and to allow isolation of the affected section of the plexus. The affected muscles show active denervation, motor unit remodeling and loss in recruitment, as well as unusual spontaneous discharges (myokimia). Adding the more proximal muscles that are innervated directly from the nerve roots (paraspinals, serratus anterior and rhomboids) is very helpful in differentiating a root from a plexus lesion. In a plexus lesion the proximal muscles should be unaffected as they emerge proximally to the plexus. They can however be occasionally denervated in brachial plexitis of viral origin. Myokimic discharges and fasciculations are useful markers of radiation plexopathy and they help distinguish it from plexopathy caused by direct tumor invasion.

EMG is also useful in establishing the severity of the lesion and the prognosis for recovery. Very poor or absent recruitment in the setting of good clinical effort from the patient is a marker of a severe lesion. If the basal lamina of the nerve has been destroyed there will be no spontaneous regeneration of the nerve and consideration should be given to surgical exploration, nerve grafts or tendon transfers. If the lesion is acute (1-3 months from the injury) it is useful to wait and repeat the EMG study 3-6 months later, before making any surgical decisions. The signs of true reinnervation can be seen on EMG in the form of nascent motor units (small, polyphasic units which fire fast on recruitment) and are detectable on EMG a few months before clinical improvement is noticed.

If the basal lamina of the affected nerves is preserved (as demonstrated by reduced but not absent recruitment) time should be allowed for true spontaneous reinnervation to occur before any decision for surgical intervention is made.

Last but not least, as it takes several days for Wallerian nerve degeneration to occur, a nerve conduction abnormality may not be detected if the NCS is performed too early from the time of the injury. It is useful to wait at least a week before referring the patient for a NCS study. Additionally, due to the same process of Wallerian degeneration, denervation potentials may not be seen in the most distal muscles for 2-3 weeks. Loss of recruitment can be seen immediately in severe lesions and it will match the clinical weakness of the patient in the respective muscles; however, if the loss is subtle it may not be appreciated easily on EMG and the confirmatory presence of denervation potentials is needed for diagnosis. Therefore, given the above considerations, the ideal time for an electrodiagnostic study in suspected cases of brachial plexopathy is 3 to 4 weeks from the onset of symptoms or the time of injury.

Outcomes/Evidence in the Literature

Preston, David C., Shapiro, Barbara E. "Electromyography and neuromuscular disorders". Elsevier Saunders Publisher. 2005.

Michael, O’Brien. "Aids to the examination of the peripheral nervous system". Elsevier health sciences Publisher. 2010.

Staal, A., van Gijn, J., Spaans, F. "Mononeuropathies: Examination, diagnosis, and treatment". WB Saunders publisher. 1999.

Aldo, Perotto. "Anatomical guide for the electromyographer; the limbs and the trunk". by Charles C. Thomas. Publisher. 1994.

Jasper, DAube. "Clinical Neurophysiology". Oxford University Press Publisher. 2002.

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