Tailor each patient’s rehabilitation program to be as unique as each injury.
Distinguish between pre and post-ganglionic injury because there is little chance of spontaneous recovery in preganglionic avulsion injuries without surgical intervention.
Injury to the long thoracic nerve or the dorsal scapular nerve suggest a more proximal injury because both originate at the root level.
Supraclavicular plexopathies (frequently due to traction injuries) are more common, more severe, and with variable outcome.
Positions that help avoid pain lend themselves to contracture development and prevention is paramount to optimal functional outcomes.
Many orthotic braces exist to accommodate each unique plexus injury and reduction of pain appears to be the strongest motivator for brace compliance.
Pain management aims to help with participation in rehabilitation.
Chronic neuropathic pain as a result of plexus injury will lead to central neural changes that increase the pain response.
Significant recovery after nerve grafting can take more than 18 months for functional improvement.
For some, amputation and prosthetic restoration may be an option, but this is not a treatment for neuropathic pain.
Brachial plexus injuries can have devastating effects on the physical capabilities of patients. These lesions can result in loss of function, significant pain, and psychological distress that handicap the patient financially and diminish the patient’s quality of life.
The rehabilitation care of a patient with brachial plexopathy is too complex to be provided by a single individual. Rehabilitation of an individual with a brachial plexus injury is a team effort that requires the close collaboration of many health care specialists. The rehabilitation effort is usually coordinated by a physiatrist (Physical Medicine and Rehabilitation physician), but this role could be accomplished by another physician specialist with the appropriate knowledge, skill, experience and interest in overseeing the rehabilitation process. In addition to the physiatrist, other physician team members typically include a neurosurgeon, orthopedic surgeon, and plastic surgeon specialized in hand and upper limb surgery. A number of other non-physician health care specialists, depending on the specific needs of an individual patient, will also be part of the rehabilitation team. These other members can be occupational therapists, physical therapists, rehabilitation nurses, psychologists, social workers, vocational rehabilitation counselors and/or case managers, to list a few. The various specialists who make up a patient’s rehabilitation team may vary throughout the course of the patient’s rehabilitation care, depending on the particular treatment focus or the patient’s care needs at any given time.
In order to provide appropriate rehabilitation strategies for brachial plexus injuries, team members must have a thorough understanding of the anatomy and physiology of the brachial plexus and the functional neuromuscular assessment of the upper extremity. The rehabilitation strategy must be individualized, and this plan can only be established once a thorough evaluation of the patient has occurred. The evaluation requires a detailed history and physical examination with particular emphasis on the musculoskeletal and neurologic examination of the involved upper extremity. The physician should obtain information regarding active and passive range of motion, presence or absence of voluntary muscle contraction including detailed manual muscle testing, distribution of preserved, altered or absent sensation, and the presence or absence of other physical findings such as a Horner’s sign. This information is critical for identifying the location and severity of the plexus lesion, as well as the functional deficits that will need to be addressed by the rehabilitation team. Additional specialized diagnostic studies such as imaging and electrodiagnostic studies will provide additional helpful information regarding location, severity and prognosis. All of this information must be taken into account when planning a patient’s rehabilitation program.
Establishing whether a plexus injury is neurapraxic, axonotmetic, neurotmetic, pre-ganglionic or post-ganglionic will determine different prognoses and different rehabilitation management plans. A rehabilitation plan for brachial plexopathy must be derived based on an accurate assessment of the patient’s physical findings, identification of the location and extent of the lesion, and understanding of likely prognosis for recovery. When this is known, then all the team members can contribute to the development of a rational rehabilitation program. Discussion regarding anatomy, clinical evaluation, imaging and electrodiagnosis of the brachial plexus will only be limited in this chapter because they are covered in greater detail elsewhere in this text.
The majority of brachial plexus injuries are traumatic and patients with brachial plexus injuries may sustain multiple traumatic injuries that impair communication and make participation in a thorough physical exam difficult. These patients may have other injuries such as skeletal trauma and/or traumatic brain injury that will require additional rehabilitation efforts specific to these problems. In addition to delaying or obscuring the identification of an underlying plexus injury, these other injuries may also complicate the rehabilitation of the plexus injury. This chapter will focus solely on the rehabilitation of an isolated brachial plexus injury without other associated impairments in need of rehabilitation.
Anatomy and physiology
The brachial plexus is commonly formed from the C5 through T1 nerve roots and extends from the spinal cord to the axilla. The plexus may be pre-fixed or post-fixed and receive contributions from the C4 or T2 nerve roots respectively. There are five separate identifiable sections of the brachial plexus: roots, trunks, divisions, cords, and terminal branches or nerves. The dorsal and ventral rootlets exit the spinal cord and fuse to form the dorsal and ventral roots ( Figure 21.1 ). The percentage of sensory and motor fibers composing each root varies. The largest percentage of motor fibers is found in the C5 and C6 roots; C7 and T1 have the least. The greatest number of sensory fibers is found in the C7 root, followed in descending order by C6, C8, T1, and C5. The brachial plexus also carries sympathetic fibers. The dorsal root ganglion is comprised of the cell bodies of the sensory nerves and lies within the confines of the spinal canal and foramen.
The C5 and C6 roots merge to form the upper trunk and the C8 and T1 roots merge to form the lower trunk. C7 becomes the middle trunk. The point at which C5 and C6 merge (Erb’s point) marks the location at which the suprascapular nerve emerges. Each trunk then divides into anterior and posterior divisions and passes beneath the clavicle. The posterior divisions merge to become the posterior cord, and the anterior divisions of the upper and middle trunk merge to form the lateral cord. The anterior division from the lower trunk forms the medial cord ( Figure 21.2 ). The cords are named for their relationship to the second segment of the axillary artery, to which they are typically bound.
The posterior cord forms the axillary nerve and the radial nerve. The lateral cord splits into two terminal branches: the musculocutaneous nerve and the lateral cord contribution to the median nerve. The medial cord contributes to the median nerve as well as to the ulnar nerve.
A few terminal nerve branches come off the roots, trunks, and cords of the plexus. The branches off the C5 root include a branch to the phrenic nerve, the dorsal scapular nerve (rhomboid muscles), and the long thoracic nerve (serratus anterior muscle). The branches off C6 and C7 roots also contribute to the long thoracic nerve (serratus anterior muscle). The branches off the upper trunk include the suprascapular nerve (supraspinatus and infraspinatus muscles) and the nerve to the subclavius muscle. The lateral cord gives off the lateral pectoral nerve (pectoralis major); while the posterior and medial cords each have three branches. The posterior cord gives off branches (proximal to distal) that include the upper subscapular nerve, thoracodorsal nerve, and the lower subscapular nerve. The medial cord gives off the medial pectoral nerve, the medial antebrachial cutaneous nerve, and the medial brachial cutaneous nerve. By noting loss of function to these muscles, one can pinpoint the level of brachial plexus injury.
A preganglionic injury is when the spinal roots are injured proximal to the dorsal root ganglion and may be avulsed from the spinal cord. Preganglionic injuries can be separated into central avulsions, in which the nerve is avulsed directly from the spinal cord, and intradural ruptures, in which rootlets rupture proximal to the dorsal root ganglion. An injury distal to the dorsal root ganglion is called postganglionic. Distinguishing between a preganglionic and a postganglionic injury is important when considering the implications for prognosis. It is possible that traumatic brachial plexus injuries may include damage to both pre and post-ganglionic portions of the plexus, which can further complicate assessment of prognosis. There is little potential for spontaneous recovery of preganglionic avulsion injuries. These injuries will require some type of surgical intervention to improve function. A complete avulsion injury of all the roots contributing to the plexus has more limited options for surgical intervention to improve nerve function. Spontaneous recovery may occur following a postganglionic injury or may need surgery to improve function depending on the degree of injury (neurapraxia, axonotmesis, or neurotmesis).
Neurapraxia is a conduction block at the site of injury without macroscopic injury to the nerve. There may be a demyelinating injury, but Wallerian degeneration does not occur. As soon as the block is resolved, nerve function to the target organ will normalize. The recovery time may extend from hours to months, depending on the extent and severity of the injury to the myelin covering. Nerve conduction studies will show no conduction across the area of injury but will show normal sensory and motor conduction distal to the area of injury; this finding is unique to neurapraxias. In axonotmesis, the axon is disrupted, but the epineurium and perineurium remain intact. Wallerian degeneration will occur distal to the injury and generally will be complete over the course of 7 to 10 days. Regeneration from the surviving proximal axon stump is still possible and can occur at a rate of 1 to 4 mm per day. In neurotmesis, the entire nerve trunk is ruptured and axonal continuity is lost and spontaneous recovery will not occur. Without surgical intervention, this injury pattern will heal as a nonfunctional neuroma.
Classification of plexopathies
It is difficult to ascertain the number of brachial plexus injuries that occur per year. With the advent of extreme sports, high energy motor sports and increased numbers of individuals surviving motor vehicle accidents, the number is increasing. Most brachial plexus injuries occur in males aged 15 to 25 years. The rule of “seven seventies” is based on experience with over 1,000 patients with brachial plexus injuries. Approximately 70% of traumatic brachial plexus injuries occurred secondary to motor vehicle accidents; of these, approximately 70% involved motorcycles or bicycles. Of the cycle riders, approximately 70% had multiple injuries. Overall, 70% had supraclavicular lesions; of those, 70% had at least one root avulsed. At least 70% of patients with a root avulsion also have avulsions of the lower roots (C7, C8, or T1). Finally, of patients with lower root avulsion, nearly 70% will experience persistent pain.
Brachial plexopathies are best classified according to the region involved, such as supraclavicular (root and trunks), retroclavicular (divisions), and infraclavicular (cords and terminal nerves) sites. Although this approach is anatomically simple, it has considerable clinical utility because the incidence, severity, prognosis, and lesion type vary among these regions.
In general, supraclavicular plexopathies are more common, more frequently due to closed traction (which can produce lengthy lesions), usually more severe (because greater force is required to produce them), and typically associated with a worse outcome. The supraclavicular plexus is further divided into upper (C5 and C6 roots and upper trunk), middle (C7 root and middle trunk), and lower (C8 and T1 roots and lower trunk) portions; this is a clinically relevant distinction. Patients with upper trunk plexopathies tend to recover more completely because, in general, these lesions may more commonly have some degree of demyelinating conduction block, the muscles they innervate are in closer proximity, making recovery of muscle function more likely whether following spontaneous nerve regeneration or following surgical repair compared to those muscles innervated by the lower trunk of the plexus that have the worse recovery potential. The infraclavicular plexus is not subdivided because lesions affecting it do not show significant regional differences in incidence, severity, prognosis, or lesion type.
Because most brachial plexopathies are axon loss in nature, neurologic examination frequently discloses weakness and sensory loss. With supraclavicular lesions, the pattern of sensory and motor loss is segmental—dermatomal and myotomal, whereas infraclavicular plexopathies produce nonsegmental patterns that resemble those observed with involvement of one or more terminal nerves.
Having the patient identify the cause of injury, location of injury, any noted weakness, sensory changes, and functional difficulties will help to focus the history, physical exam and subsequent diagnostic evaluation. Forceful injuries with contralateral neck flexion and ipsilateral shoulder depression should raises suspicion of a traction injury to the upper trunk of the plexus. On the other hand, a fall or blow against an arm abducted to 90 degrees or more that further forcefully abducts the arm may result in injury to the lower trunk of the plexus. Pain is often associated with plexus lesions whether from direct nerve injury or surrounding local tissue trauma. Over time, pain may become chronic and neuropathic in character. Pain may be severe to the point that its control may become the primary and overriding concern for patients with brachial plexus injury. It is important to have the patient try to provide information regarding the character and location of the pain so that it can be properly managed.
The physician should be suspicious of a brachial plexus injury when examining a patient with severe head, neck, shoulder girdle and proximal upper extremity injury. The examiner should record active and passive ranges of motion, sensory levels, as well as the presence or absence of reflexes. Acutely, inspection of the extremity should not demonstrate significant changes in muscle bulk or passive joint motion, but with time, atrophy of the involved muscles together with limitation of passive joint motion may become apparent. Detailed muscle testing of the shoulder girdle and upper extremity muscles of involved extremity should be compared to the opposite side. Table 21.1 summarizes key myotomes to examine.
|C5||Shoulder abduction, extension, and external rotation; some elbow flexion|
|C6||Elbow flexion, forearm pronation and supination, some wrist extension|
|C7||Diffuse loss of function in the extremity without complete paralysis of a specific muscle group, elbow extension, consistently supplies the latissimus dorsi|
|C8||Finger extensors, finger flexors, wrist flexors, hand intrinsics|
The distribution of absent muscle function, weakness or normal strength will help identify the site and extent of injury to the plexus ( Table 21.1 ). A thorough knowledge of muscle anatomy is necessary to evaluate an upper extremity with plexus injury because residual muscle function may only be at Trace (or 1 MRC scale) levels that require precise localization and palpation of the muscle to assess for presence of a voluntary muscle contraction. Sensory examination is extremely important. The presence or absence of sensation should further help pinpoint the location and degree of involvement of the plexus. Deep pressure sensation may be the only clue to the continuity of a nerve with no motor function; testing can be made by by full pinch to the nail base and pull the patient’s finger outward. Any burning suggests continuity of the nerve tested. When no burning is elicited, these examination findings are less helpful because neurapraxia can persist for more than 6 months. Sensory examination of dermatomes to help identify a precise root level, however, can be unreliable because of overlap from other nerves or anatomic variation.
Certain findings suggest preganglionic injury on clinical examination. For example, the patient should be examined for the presence of Horner syndrome, consisting of miosis (small pupil), enophthalmos (sinking of the orbit), ptosis (lid droop), and anhydrosis (dry eyes), which is suggestive of a root avulsion at the C8-T1 level ( Figure 21.3 ). Injury to the long thoracic nerve or the dorsal scapular nerve suggests a higher (more proximal) level of injury because both nerves originate at the root level. Elevation of the diaphragm on the side of injury suggests phrenic nerve involvement and proximal root level injury to the upper plexus.
When evaluating the patient with brachial plexus injury, it is important to consider additional points during the examination as these may have significant management and rehabilitation considerations. With head, neck and shoulder trauma resulting in plexus injury, there may be a concomitant spinal cord injury, and the trunk and lower limbs should be examined for the presence of altered strength, sensory levels, increased reflexes, and pathologic reflexes. Muscles innervated by nerves adjacent to but not originating from the brachial plexus should be evaluated, as the nerves supplying these muscles may have been injured as well. This includes the spinal accessory nerve innervating the trapezius and sternocleidomastoid, the phrenic nerve innervating the diaphragm and cervical plexus innervating the levator scapuli. Involvement of any of these nerves will have both functional and surgical management implications. It is also important to assess the vascular status of the involved upper extremity because injury to adjacent vascular structures such as the axillary artery can occur especially with infraclavicular plexus lesions.
Various diagnostic procedures will complement the history and physical examination of the patient with brachial plexus injury to help refine the location, extent and prognosis of the injury. These studies may include electrodiagnostic studies (nerve conduction and electromyography) and imaging (MRI, CT, myelography and ultrasound). With this information, the patient’s care team will be able to define an appropriate treatment and rehabilitation program to facilitate recovery of function.
Rehabilitation of adults with brachial plexopathy
For all patients with lesions involving the brachial plexus, there are a number of general rehabilitation considerations that should be addressed for all patients regardless of etiology, location, extent of involvement, or the chronicity of the plexopathy. These include the following: 1. maintaining range of motion of the joints of the extremity, 2. support of the extremity with particular attention to any weak or paralyzed joint, 3. preserving or improving strength in weak muscles, 4. preventing edema in a weak or paralyzed extremity, 5. addressing activities of daily living issues, 6. education regarding proper use of the uninvolved upper extremity to prevent development of musculoskeletal symptoms of overuse, and 7. pain management.
Range of motion
Patients with injury to the upper trunk of the brachial plexus will typically have weakness or complete paralysis of muscles about the shoulder, weakness of supinators of the forearm and some weakness of forearm pronation and wrist flexion. Lower trunk lesions will have loss of motor function distally in the extremity by affecting mostly the hand muscles. A pan plexus injury will involve the entire extremity. Depending on the pattern of weakness or paralysis in the extremity following a plexus injury, a patient may have either an imbalance or total lack of muscle function about a joint. This can lead to total flaccidity about a joint and result in contracture from prolonged abnormal positioning. This can occur either from the improper use of splinting/orthotics or from a patient positioning the extremity in a preferred position for prolonged periods of time. Joint and soft tissue contractures can also occur when there is imbalance of agonist/antagonist muscles about a joint with the contracture favoring the direction of motion of the stronger muscle(s). Because the time for recovery from a plexus injury may be long, development of contractures is a real concern. The presence of joint and soft tissue contractures may limit any residual extremity function and hinder recovery of function when reinnervation is occurring.
Seeing a patient with a plexus injury during the acute phase of the injury has its advantages. Contractures are easier to prevent than to treat. Therapy to maintain range of motion can start before there has been time for a significant contracture to develop. The therapist can teach the patient or the patient’s family the appropriate exercises to maintain range of motion in the extremity. During the time of acute injury management, performance of these exercises may be limited due to pain and/or due to medical or surgical contraindications associated with management of other injuries. It is important to begin range of motion as soon as medically or surgically appropriate because contractures can develop in as quickly as within one or two weeks.
Patients who are not seen until sometime after the onset of their plexus lesion and have already developed contractures represent a more difficult problem. Aggressive and frequent prolonged stretching under the direction of a skilled therapist (occupational or physical) will be necessary to reduce the contracture and gain joint and soft tissue range of motion. Therapeutic modalities, typically those that provide heat to the soft tissues and joint capsule such as hot packs, whirlpool, diathermy or therapeutic ultrasound, can be utilized prior to exercising the joint to increase the elasticity of the tissues being stretched. As plexus patients with weakness are likely to have altered sensation, one must be careful with thermo therapy modalities to avoid burns. The patient will need to continue with an aggressive home exercise and positioning program to counteract the contracture or formal therapy will be of little benefit. Often passive positioning or dynamic splinting will be required as part of the contracture reduction program to provide prolonged stretch to the contracted joint. Use of neurolytic agents such as Botox or phenol may help balancing agonist/antagonist muscle forces about the joint by weakening a stronger muscle that is facilitating the contracture. Mobilization of a contracture under anesthesia or surgical release of a contracture may at times be necessary for patients with contractures who do not respond to the previously mentioned treatment approaches. Contractures can significantly limit function or inhibit recovery associated with a recovering nerve function. Again, it is better to prevent than treat a contracture.
As previously mentioned, injury to the upper trunk of the brachial plexus is among the more common of plexus injuries. With upper trunk lesions, there is weakness or paralysis of the shoulder girdle musculature particularly the rotator cuff, deltoid and long head of the biceps brachii muscles, all of which can result in subluxation of the glenohumeral joint due to the distractive forces of the weight of the upper extremity. If left unattended over time, this subluxation of the joint can become quite pronounced. It is not unusual to have a palpable gap of several finger breadths between the acromion and the head of the humerus when examining the joint ( Figure 21.4 ).