Traumatic Brachial Plexopathy

In traumatic brachial plexopathy, nerve roots may be avulsed from the cord, or the plexus may be subject to traction or compression. Any injury that increases the distance between the relatively fixed points of the prevertebral fascia and the midforearm may injure the brachial plexus.

Traction or compression may result in ischemia, which initially damages the vasa vasorum. Severe compression injuries can result in intraneural hematomas, which can compress adjacent nerve tissue.

Frequency

United States

The frequency with which traumatic brachial plexopathies occur varies according the etiology and severity of specific injuries. Brachial plexus injuries are estimated to account for 5% of peripheral nerve injuries. However, the true frequency of injuries to the brachial plexus is undetermined, primarily because of significant underreporting. Prospective studies performed at Tulane University revealed a 7.7% incidence of stingers in a group of college football players; however, other sources have reported a 40% incidence.[10]

International

As noted above, frequency varies according to the etiology and severity of the injury.

Mortality/Morbidity

Coexistent musculoskeletal or central nervous system injury, such as spinal cord injury (SCI) or traumatic brain injury (TBI), is common after violent trauma and presents a diagnostic challenge.

Narakas reported that 80% of patients with severe traumatic brachial plexopathy had multiple trauma to the head and skeletal system.[11]

Root avulsion and contusions of the brachial plexus and cord, which are other frequently occurring coexistent, complicating factors, pose additional diagnostic and prognostic challenges.

A hospital-based, multicenter, observational study by Ciaramitaro et al found that out of 107 patients with traumatic brachial plexus injury, 74 (69%) suffered pain, with 60 (56%) specifically having neuropathic pain. The most frequent and severe form of pain was the spontaneous, burning type. No association was found between pain and age, but pain was determined to be related to the severity of peripheral nerve damage. The investigators also found that neuropathic pain led to depression and impaired quality of life.[12]

Similarly, a study by Landers et al indicated that the prevalence of posttraumatic stress disorder (PTSD), depression, and suicidal ideation is high in adults who suffer traumatic brachial plexus injury. Evaluating 21 patients, the investigators reported that seven of them (33.3%) admitted to suicidal ideation, while evidence of PTSD and clinical depression was found in four patients (19.0%) each.[13]

Race

No race predilection is reported for traumatic brachial plexopathy.

Sex

In general, traumatic brachial plexopathy is more prevalent in men than in women because of an association with violent trauma and sports.

• Certain conditions, such as thoracic outlet syndrome (TOS), are statistically more common in women than in men.[14]

• Other regional differences influence sex- and cause-related statistics.

Age

Because of an association with violent trauma and sports-related injuries, traumatic brachial plexopathy is most prevalent in males in their midteens and in men in their early 30s.

History taking should include inquiry into the mechanism of injury, as well as a description of patient symptoms. Common mechanisms of injury involve cervical extension, rotation, lateral bending, and depression or hyperabduction of the shoulder.

Patients should be queried about weakness, sensory loss, paresthesias and dysesthesias, and the location of symptoms in the arm.

The physician should examine the cervical spine, shoulder, clavicle, scapula, and related joints for range of motion (ROM), alignment, and tender points. A thorough neurologic examination of the upper extremity should include manual muscle testing, sensory examination, and an evaluation of deep tendon reflexes.[15]

• The site of injury can be accurately localized with a precise neurologic examination by using the correlative neuroanatomy.

• A sensory examination should include testing for light-touch sensation, pinprick sensation, 2-point discrimination, vibration sensation, and proprioception.

• In an anterior dislocation of the shoulder, the sensory distribution of the axillary and musculocutaneous nerves are tested to detect nerve injury in the early stages.

• Associated problems that require prompt attention can be identified with the following:

  • Evaluation of joint instability and scapular winging

  • Auscultation to detect hemidiaphragmatic paralysis

  • Observation of patterns of muscle weakness and/or atrophy, in which the injured side is compared with the uninvolved side

  • Testing for SCI and TBI

As previously noted, a large proportion of brachial plexopathies are caused by trauma. The mechanism of traumatic injuries and the magnitude, rate, and direction of deforming forces ultimately determine the extent and location of the injury. Mechanisms include traction, penetrating injury, and crushing or compression.

Closed injuries, such as those caused by motor vehicle accidents, industrial accidents, and sports-related trauma, are more common in civilian life than in military life. Violent torsion of the upper limb, either upward or downward, may damage the plexus. Shrapnel injuries and blast injuries, as well as gunshot wounds and knife injuries to the neck or axilla, can cause lesions in the brachial plexus.[16]

Iatrogenic injuries occur during surgery, particularly in procedures involving the following: (1) neck or shoulder, (2) opening of the chest, (3) regional anesthetic blocks, and (4) placement of cannulas. Injuries to the brachial plexus of neonates may occur during birth, as a result of the strain placed on the plexus by a wide separation of the head and shoulder or by forced adduction of the shoulder joint during a difficult delivery.[17, 3]

Electrodiagnosis has become a mainstay in the diagnostic evaluation of brachial plexopathies. Electrodiagnostic tests provide physiologic data about the continuity of pathways and of lesion type and severity. Serial testing is helpful to determine prognosis.[18, 19]

While positive waves and fibrillations (which indicate axonal injury) do not appear for several weeks after injury, sensory nerve action potentials (SNAPs) can be useful within days of injury to distinguish a presynaptic lesion from a postsynaptic lesion. With postsynaptic lesions, SNAPs are absent, whereas they are present with presynaptic ganglionic lesions.[20]

Somatosensory evoked potentials (SSEPs) are also useful to assess proximal lesions, such as root avulsions.[20, 21, 22]

Radiography

Many peripheral nerve injuries can be associated with other soft-tissue or bone injuries that can be detected at radiography.

Radiographs of the injury site help to identify fractures or foreign bodies. For example, fractures of the cervical spine are frequently associated with brachial plexus injuries.

In cases of phrenic nerve paralysis, chest radiographs demonstrate unilateral elevation of the diaphragm.

Midhumeral fractures are associated with radial nerve injuries, and midforearm fractures of the ulna or radius are associated with median or ulnar nerve injuries, respectively.

To rule out bony and ligamentous injuries, all patients with axillary nerve injury should initially undergo radiography of the shoulder and cervical spine.

MRI and CT scanning

Computed tomography (CT) scanning can be used in the investigation of occult fractures that are not depicted on plain radiographs. With myelography, CT scanning can be used to demonstrate root avulsion.[23, 24, 25]

The resolution of the fine anatomic detail of soft tissue is better with magnetic resonance imaging (MRI) than with CT scanning.

Conventional MRI is used to visualize normal and abnormal peripheral nerve structures.[2]  Moreover, in a study by West and colleagues, MRI depicted signal intensity changes in denervated muscle as early as 4 days after clinical symptoms developed.[26] With short-tau inversion recovery (STIR) techniques, signal intensity changes in the thenar muscles were demonstrated on MRI scans of 100% of the patients with clinically advanced carpal tunnel syndrome.

With neurapraxic nerve injuries,[22] the signal intensity in the innervated muscles remains normal on STIR or T2-weighted images. Therefore, after a peripheral nerve injury, early MRI of the muscle can be useful in distinguishing a neurapraxic injury from more severe axonotmesis or neurotmesis.

Because CT scanning and traditional MRI techniques have inherent limitations in their resolution and distinction of peripheral nerves from the surrounding structures, magnetic resonance neurography (MRN) has been developed.

MRN can depict normal and abnormal peripheral nerves in various regions of the body. The injured peripheral nerve can be assessed by orienting the images along the course of the damaged nerve. For example, the loss of signal intensity on T2-weighted images indicates damage to the myelin sheath.

In addition, loss of water content in denervated nerves of the deep muscles can be assessed with MRN when needle electromyography (EMG) is difficult to perform.[2]

The predictive value of MRN in the diagnosis of peripheral nerve trauma has not yet been reliably established.

A retrospective study by Brogan et al found through MRI evaluation that among 280 adults with traumatic brachial plexus injuries, 23 of them (8.2%) had a concomitant full-thickness rotator cuff tear. The investigators therefore proposed that the rotator cuff be imaged in patients with traumatic brachial plexopathy when treatment options are being assessed.[27]

Related Medscape Drugs & Diseases topic:

Brachial Plexus Evaluation with MRI

Clinical threshold testing can be used to evaluate sensory function in peripheral nerves. These tests can be used to determine the level of stimulus necessary to elicit a response.

Semmes-Weinstein monofilaments are fine filaments that exert a discrete amount of pressure on the fingertips. They are used to perform threshold testing. Vibratory senses can be assessed by means of clinical threshold testing with low (30 Hz) to high (256 Hz) frequencies.

At light microscopy, nerves injured with epineurectomy or a crush mechanism have widespread fiber degeneration and myelin debris in the subperineurial region. The centrofascicular areas are relatively preserved compared with the subperineurial regions. The central vessels are preserved mostly within the centrofascicular area of the injured nerve. The thickness of myelin in the axons is decreased after injury, and the internodal length becomes more variable compared with its length before injury. A loss of cross-sectional area without a loss in the muscle fiber count begins within 1 week of denervation.

Physical Therapy

Depending on local expertise, a rehabilitation program may be undertaken with a physical therapist and/or an occupational therapist. The goals are to preserve ROM, improve strength, and manage pain.

Patients should undergo physical therapy to maintain ROM and to optimize the recovery of motor function as muscle reinnervation occurs.

The goal of treatment is to return function to the structures supplied by the damaged nerves and to improve the patient's quality of life. The injured nerve and the exogenous sources of nerve injury are treated.

At the onset of injury, early mobilization and icing are used. In the subacute phase, therapy gradually progresses from passive to active motion and from assisted to active ROM, as tolerated.

Heat, ultrasonography, transcutaneous electrical nerve stimulation (TENS), interferential current stimulation, and/or electrical stimulation are used, depending on the predominant symptoms.

Cervical muscle strengthening and the correction of upper extremity muscle imbalances are included in the protocol as well.

The use of appropriate slings, the protection of extremities and joints, and the prevention of subluxation must be considered.

Cervical pillows or collars may be required for patients with combined lesions of the roots and plexus.

A literature review by de Santana Chagas et al found that in adults with brachial plexus injury, physical therapy most often involved kinesiotherapy (such as ROM exercises, muscle stretching, and strengthening techniques), electrothermal treatment, phototherapy, manual therapy, and sensory reeducation.[28]

Occupational Therapy

During occupational therapy efforts are concentrated on maintaining ROM in the shoulder; fabricating appropriate orthoses to support the function of the hand, elbow, and arm; and addressing edema control and sensory deficits, with testing and therapy.

Occupational therapy may address issues related to the patient's ability to write, type, and find alternate ways of communicating.

Additionally, occupational therapy provides help with retraining for activities of daily living (ADLs), including the use of 1-arm techniques, adaptive equipment, and self-ranging and strengthening exercises.

Recreational Therapy

Recreational therapy should address compensatory strategies and activities that can substitute for altered or lost function in extremities that were required for recreation prior to injury.

Complications may include intractable pain syndromes, such as persistent neuropathy and complex regional pain syndrome type 2 (CRPS II or causalgia), skin damage and infection, significant muscle atrophy, contractures and capsulitis, subluxations, sensory loss, osteopenia, heterotopic ossification, myofascial pain, and depression and anxiety.

Bone dislocation with neurologic deficit requires prompt anatomic reduction to prevent irreversible nerve damage.

The use of analgesics can help patients control pain from nerve injuries. Steroids may help to decrease endoneurial edema associated with nerve injury.

Hyperbaric oxygen decreases vascular compromise of the vasa nervorum, as well as endoneurial edema and pressure. Hyperbaric oxygen is an approved adjunctive treatment for acute traumatic ischemic reperfusion injury.

Ciliary neurotrophic factor (CNTF), which enhances motor neuron survival in vivo and in vitro, is in the investigational stage.

Surgery is reserved for patients in whom symptoms persist despite appropriate conservative treatment.[3, 4, 5, 6, 7, 8] Two important issues to consider before surgery are as follows: (1) whether function can be obtained after the nerve is repaired and (2) whether the potential benefit to the patient outweighs the surgical risks, costs, and loss of productivity. The timing of surgery is important as well.[29]

Other factors to consider are as follows:

• In clean lacerating injuries in which the nerve ends are visible in the wound or when clinical examination reveals obvious motor and sensory deficits from the laceration, immediate primary repair may be indicated.

• In blunt transections resulting from lacerations, delayed repair has a better surgical result.

• Injuries without evidence of early spontaneous recovery, such as those caused by bullets, crushing blows, traction, fractures, or injections, are explored several months after the injury.

• Brachial plexus stretches or contusions are observed for 4 months. If no evidence of recovery is present, the plexus is explored.

• Nerve or tendon transfers may be necessary if nerve repair is unsuccessful.[30, 31]

Brachial plexus injuries are not always reparable. In such cases, neurotizations or nerve transfers may offer a better functional outcome.[9]

Sunderland suggests 2 criteria that must be present before fascicular repair or interfascicular grafting is considered[32] :

• The fascicular bundle must be large enough for suturing.
• The bundle must be sharply localized or sufficiently well defined so that it can be identified and mobilized for repair.

The spinal accessory or long thoracic nerve can be grafted onto distal arm nerve trunks, with some improvement in elbow flexion.

A literature review by Ali et al indicated that in adult upper trunk brachial plexus injuries, the Oberlin nerve transfer procedure is more effective in restoring elbow flexion than nerve grafting or combined grafting/transfer techniques. The study also found that nerve transfer in general is more effective than grafting or combined procedures in restoring shoulder abduction.[33]

Intraoperative care with proper axial orientation of the fascicles, hemostasis, suture material, and suture line tension leads to better outcomes in brachial plexus surgery. Tension of the suture line and inadequate preparation of the nerve stumps are 2 leading causes of regenerative failure across the suture site (resulting in poor recovery of nerve function).

Although there has been controversy over whether brachial plexus reconstruction can effectively restore elbow function in patients over age 50 years who have sustained traumatic brachial plexus injury, a report by Gillis et al indicated that such surgery can benefit these individuals. In the study, patients in this age group underwent nerve grafting, nerve transfer, or free functional muscle transfer, with an average 24-month follow-up. While no cohort members demonstrated a British Medical Research Council flexion grade as high as M3 preoperatively, the majority of patients reached M3 or above postoperatively, although better results were achieved with nerve transfer than with muscle transfer.[34]

Surgical repairs are most effective within 3 months of the injury.[35] Surgical delays in excess of 5 months dramatically decrease the rate of functional return. (However, a study by Wang et al reported that strength and range of motion for the shoulder and elbow continued to improve beyond 2-3 years postsurgery in adult patients who underwent nerve reconstruction for brachial plexus injury.[36] )

When repair does not provide adequate results, planned tendon transfers can increase extremity function.

Rarely, in cases of a complete multilevel injury (eg, flail injury, anesthetic arm), amputation may result in a better functional outcome, because the patient can use the extremity with an appropriate prosthesis. However, the result may be less cosmetically pleasing than would that obtained with other approaches.

Related Medscape Drugs & Diseases article:

Brachial Plexus Hand Surgery

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• Consultations with an orthopedic surgeon and a neurosurgeon are considered in cases in which there has been poor neurologic and functional recovery.

• A complete multidisciplinary rehabilitation assessment is indicated.[37] A consultation with a prosthetic specialist may be required for the fabrication of a temporary or permanent prosthetic device.

• A pain management strategy is of great importance in improving the patient's ability to cope and function and in improving his/her quality of life.

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• In cases of CRPS II, sympathetic (ie, stellate) blockade may be required, along with the appropriate combination of neuropathic and narcotic medications.

• For incomplete, painful injuries, and especially in cases of CRPS II, the use of a spinal cord stimulator on a trial basis may be beneficial. If this trial is successful, the stimulator may be implanted.

• Implantable peripheral nerve stimulators have also been successfully used in some centers.

• The use of an implantable intrathecal device (eg, pump) may be considered in cases in which the employment of oral medications, therapy, and a spinal cord stimulator fail.

Nonsteroidal anti-inflammatory drugs (NSAIDs) and neuropathic pain medications are most commonly used in the treatment of traumatic brachial plexopathy, depending on the symptoms and the length of time since the injury's occurrence. During the acute phase, narcotic analgesics may also be necessary, but they should not be used for long-term pain management. Narcotic medications are also indicated in the acute postoperative period.

Neuropathic pain medications are useful for the relief of dysesthetic pain in the acute and chronic phases. There is no drug of choice, and medications often must be tried in serial fashion to find one that provides optimal relief for the patient.

Class Summary

After acute injury, NSAIDs are particularly helpful in relieving pain related to the injury, including injuries involving soft tissues, such as muscles and ligaments.

Celecoxib (Celebrex)

Inhibits primarily COX-2. COX-2 is considered an inducible isoenzyme, induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, GI toxicity may be decreased. Seek the lowest dose for each patient.

Naproxen (Naprosyn, Aleve)

For relief of mild to moderate pain; naproxen inhibits inflammatory reactions and pain by reducing the activity of cyclooxygenase, which decreases prostaglandin synthesis.

Class Summary

The use of certain antiepileptic drugs, such as the GABA analogue gabapentin (Neurontin), has proven helpful in some cases of neuropathic pain. Anticonvulsants have central and peripheral anticholinergic effects, as well as sedative effects, and block the active reuptake of norepinephrine and serotonin. The multifactorial mechanism of analgesia could include improved sleep, an altered perception of pain, and an increased pain threshold. The efficacy of these drugs can be potentiated with the concomitant use of opiates and NSAIDS. Rarely should these drugs be used in the treatment of acute pain, because they may require a few weeks to become effective.

Gabapentin (Neurontin)

Has anticonvulsant properties and antineuralgic effects; however, the exact mechanism of action is unknown. Gabapentin is structurally related to GABA, but it does not interact with GABA receptors. Titration to effect can take place over several days (300 mg on day 1, 300 mg bid on day 2, and 300 mg tid on day 3).

Class Summary

This is a complex group of drugs that have central and peripheral anticholinergic effects, as well as sedative effects. They have central effects on pain transmission. Tricyclic antidepressants block the active reuptake of norepinephrine and serotonin.

Nortriptyline (Pamelor)

Has demonstrated effectiveness in the treatment of chronic pain. By inhibiting the reuptake of serotonin and/or norepinephrine by the presynaptic neuronal membrane, this drug increases the synaptic concentration of these neurotransmitters in the central nervous system. Pharmacodynamic effects, such as the desensitization of adenyl cyclase and the down-regulation of beta-adrenergic receptors and serotonin receptors, also appear to play a role in nortriptyline's mechanisms of action.

Doxepin (Sinequan, Adapin)

Inhibits histamine and acetylcholine activity; doxepin has proven useful in the treatment of various forms of depression associated with chronic and neuropathic pain.

Class Summary

Narcotics are indicated in the acute injury period and in the postoperative period should reconstructive surgery be required. In rare cases in which patients require long-term opioid use, these patients should use scheduled, longer-acting medications, such as methadone.

Methadone (Dolophine)

Used in the management of severe pain. Methadone inhibits ascending pain pathways, diminishing the perception of and response to pain.

Oxycodone (OxyContin, Roxicodone, OxyIR)

Indicated for the relief of moderate to severe pain.

Oxycodone and acetaminophen (Percocet)

Drug combination indicated for the relief of moderate to severe pain.

Fentanyl citrate (Duragesic)

Potent narcotic analgesic with much shorter half-life than morphine sulfate. Fentanyl citrate is the DOC for conscious sedation analgesia. It is ideal for analgesic action of short duration during anesthesia and for the immediate postoperative period.

Fentanyl citrate is excellent for pain management and sedation with short duration (30-60 min); it is easy to titrate. The drug is easily and quickly reversed with naloxone.

After the initial dose, subsequent doses should not be titrated more frequently than q3h or q6h thereafter.

When the transdermal dosage form used, controlled with 72-h dosing intervals effective in most patients. However, some patients require 48-h dosing intervals.

Hydrocodone and acetaminophen (Lorcet)

Drug combination indicated for moderate to severe pain.

Tramadol (Ultram)

Inhibits ascending pain pathways, altering perception of and response to pain. Tramadol also inhibits the reuptake of norepinephrine and serotonin.

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• Continuation of physical therapy and/or occupational therapy and follow-up with a surgeon and/or orthotist may be needed.

• Vocational rehabilitation and modifications at home and/or work are also assessed.

• In some cases, repeated electrodiagnostic evaluations may be required for prognostication and further treatment planning. These tests can be used to detect early signs of muscle reinnervation several months before clinically evident muscle contractions appear.

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• If physical therapy is not initiated promptly after surgery, denervation can occur and can result in muscle atrophy and fibrosis, joint stiffness, motor endplate atrophy, and trophic skin changes.

• Grant and colleagues do not advocate the traditional treatment, which involves several weeks of immobilization.[38] Instead, the use of a short period to allow healing and adequate strengthening of the repair site is advised.

• Repairs (nerve transfer/neurotization, as well as tendon transfer) are protected by means of relaxed joint posturing for about 3 weeks.

• To prevent disruption of the sutures at the repair site, the patient should avoid strenuous physical activity.

• In nerve transfers, the extremity is immobilized for 4 weeks after surgery, at which time physical therapy is initiated.

• Postoperative clinical examinations are performed every 3 months for the first 2 years after surgery and every 6 months after that.

• At each postoperative visit, the ROM, strength, and sensation in the treated area should be tested, and the results should be documented.

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• A variety of medications may be required, mainly for the management of associated painful states.

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• When indicated, the patient may be admitted to the hospital for orthopedic or neurosurgical procedures.

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• Measures that the patient can use to prevent setbacks and further damage include the following:

  • Protecting the damaged limb from repeat injury and extremes of motion

  • Maintaining the functional ROM

  • Strengthening muscles in the cervical region and limbs

  • Making appropriate modifications in the workplace and/or at home

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• Late complications may include the following:

  • Pain syndromes, such as persistent neuropathy, neuroma, and CRPS II

  • Skin damage and infection

  • Significant muscle atrophy

  • Contracture and capsulitis

  • Subluxation

  • Sensory loss

  • Osteopenia

  • Heterotopic ossification

  • Myofascial pain

  • Depression and anxiety

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• The outcome and prognosis of acute injury varies widely, depending on the type and etiology of injury and the timing of therapy.[5]

  • The extent of injury to neural tissue and the age and medical status of the injured patient are important factors that influence the outcome.

  • Patient compliance and motivation for recovery can also have an important effect on the overall success of therapy.

• With mild neurapraxic lesions, spontaneous recovery may occur only days or weeks after the trauma has occurred; following a gunshot wound, spontaneous recover may occur as late as 11 months later.

• Recovery from axonotmetic injuries usually occurs over months.

  • In axonotmesis, although axons regenerate, functional recovery depends on the associated injuries, the amount of healthy proximal axon that remains after injury, and the age of the patient.

  • Recovery is usually complete unless the injury is so proximal that atrophy of the motor endplate or sensory receptor occurs before the axon can grow back to these organs.

  • In cases of a coexisting root avulsion, the above scenario of a very proximal lesion, resulting in atrophy of the motor endplate or sensory receptor, may be possible. Therefore, healing may be greatly delayed or incomplete.

• In neurotmesis, regeneration occurs, but function rarely returns to its preinjury level.

• Generally, the rate of spontaneous recovery after shotgun wounds is lower than it is with other mechanisms.

• Neural injuries associated with fractures have a greater incidence of spontaneous resolution; generally, recovery is less common with neural injuries secondary to dislocations.

• Lesions resulting from shoulder dislocations heal within 12-45 weeks, depending on severity of the dislocation and, consequently, the type and extent of the associated neural injury or injuries.

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• Educating the patient, family, and rehabilitation team, as well as medical practitioners involved in the patient's postdischarge care, may have several benefits.

  • It facilitates the coordination and planning of services.

  • It hastens the implementation of appropriate interventions.

  • It results in a better recovery.

• Of equal importance is addressing the associated psychological factors, with the aim of improving the following:

  • The patient's mood stability

  • The patient's coping skills

  • Family functioning

  • Pain management

  • Patient motivation

  • Patient participation in therapy

  • Overall outcome