BRACHIAL PLEXUS NEUROPATHY

Background Trauma accounts for a large proportion of brachial plexopathies. The mechanism of an injury and the magnitude, rate, and direction of deforming forces ultimately determine the extent and location of a traumatic brachial plexopathy. A lesion of the brachial plexus can result in motor, sensory, and sympathetic disturbances. Impairments can be transient, as in stinger or burner injuries in football players, or they may result in intractable palsy. Because of the changing arrangement of the brachial plexus as it progresses distally, injuries to it may result in diverse paralyses, anesthesias, and paresthesias, depending on the exact level of injury and the extent of injury to the various elements at that level.

Definition A generalized term for insult in the brachial plexus. Trauma is the most common cause of brachial plexus injury. Closed injury can occur from traction from the head and neck are forcibly bend away from the shoulder or in association with fractures of the clavicle or shoulders. Open injuries can occur with knife or missile wounds often the patient has other serious injuries which can delay identification of the brachial plexus injury. Traumatic injuries can affect multiple trunks and cords or even avulsion injuries to the roots and individual nerves.

Epidemiology Frequency 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. Mortality/Morbidity Coexistent musculoskeletal or central nervous system injury, such as spinal cord injury (SCI) or traumatic brain injury (BI), is common after violent trauma. Narakas reported that 80% of patients with severe traumatic brachial plexopathy had multiple trauma to the head and skeletal system. Root avulsion and contusions of the brachial plexus and cord, which are other frequently occurring coexistent, complicating factors, pose additional diagnostic and prognostic challenges.

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. Other regional differences influence sex- and cause-related statistics. young men are more likely than women and older men to develop a rare brachial plexus condition known as Parsonage-Turner syndrome(shoulder paralysis). 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.

Etiology Pathology can occur from: (a) focal crush, (b) stretch, (c) transection, or (d) peripheral neuropathies. Mechanism of injury Traction injury

Obstetrics paralysis

Most common cause of brachial plexopathy Predominantly supraclavicular or other plexus palsy Predisposing factors: wide range of motion of shoulder, cervical roots lacks protective epineural and perinerual sheaths and have poor tensile strength. Most common specific causes: birth injury and sports injuries and motorcycle accidents causing shoulder trauma Pack Palsydue to shulder depression combined with lateral neck flexion puts traction force in upper plexus especially C5-C6 or C5-C7 Excessive hyperabduction also cause brachial plexus injury Infraclavicular involvent requires more severe traction force Is a specific type of traction injury following a stretch of the neckshoulder angle during birth. Result in erb-duchenne palsy (upper

Trauma

Iatrogenic injury

Neoplastic

plexus) or klumpkes paralysis (loer plexusinvolvment) Motor deficits predominate Sensory deficits mild Most often involve right plexus since head is often turn to the left during birth most cases result in neupraxia so recovery good klumpkes poorer prognosis since it often involves rot avulsion sharp lacerations better potential for recovery (after repair) comparedto blunt lacerations that cut & stretch the nerve traumatic hematoma may be the one responsible for the nerve compression Less common in the brachial plexus compared to lumbar plexus Most frequent cause of stretch injuryspreding of a sternum-splitting thoracotomy Most common cause of direct injurytransaxillary surgery for thoracic outlet syndrome; axillary lymph node removal; deep cervical exploration Usually due to direct extension or metastasis Most commonly from lung and breast cancer Usually insidious onset with UE pain & paresthesia & localized tenderness proximally PancoastSyndrome- combination of findings (shoulder radiating pain, arm paresthesia & weakeness & horners syndrome) associated with brachial plexus injury dueto direct extension of an apical lung tumor; usually C8-T1/ lower trunk distribution May also occur following neck or axillary surgery, chemotherapy & radiation therapy of a neoplasm

Anatomy The brachial plexus is a somatic nerve plexus formed by intercommunications among the ventral rami of thelower four cervical nerves ( C 5 - C 8) and the first thoracic nerve (T 1). It is responsible for the motor innervation to all of the muscles of the upper limb with the exception of the trapezius and levator scapula. It supplies all of the cutaneous innervation of the upper limb with the exception of the area of the axilla( armpit) (which is supplied by the intercostobrachial nerve), an area just above the point of the shoulder (supplied by supraclavicular nerves) and the dorsal scapular area which is supplied by cutaneous branches of dorsal rami.

Roots -The ventral rami of spinal nerves C5 to T1 are referred to as the roots of the plexus. Trunks- Shortly after emerging from the intervertebral foramina , these 5 roots unite to form three trunks. The ventral rami of C5 & C6 unite to form the Upper Trunk. The ventral ramus of C 7 continues as the Middle Trunk. The ventral rami of C 8 & T 1 unite to form the Lower Trunk. Divisions - Each trunk splits into an anterior division and a posterior division. The anterior divisions usually supply flexor muscles The posterior divisions usually supply extensor muscles Cords - The anterior divisions of the upper and middle trunks unite to form thelateral cord. The anterior division of the lower trunk forms the medial cord. All 3 posterior divisions from each of the 3 cords all unite to form theposterior cord. The cords are named according to their position relative to the axillary artery. Terminal Branches- are mixed nerves containing both sensory and motor axons.

Musculocutaneous nn.- Originate from the lateral cord of the brachial plexus(C5,C6,C7) in the axilla. It runs downward and laterally, pierces the coracobrachialis muscle and then passes downward between biceps and brachialis muscles. It appears at the lateral margin of the biceps tendon and pierces the deep fascia just above the elbow and it runs down the lateral aspect of the forearm as the lateral cutaneous nerve of the forearm. Innervates the muscles in the flexor compartment of the arm.Supplies the skin of the front and lateral aspect of the forearm down as far as the root of the thumb. Median nerve-Originate from the medial cord of the brachial plexus in the axilla. (C7,C8,T1). It runs downward on the medial side of the brachial artery as far as the medial of the arm. The nerve pierces the medial fascial septum accompanied by the superior ulnar collateral artery and enters the posterior compartment of the arm and passes behind the medial epicondyle of the humerus. Motor innervation is mainly to

intrinsic muscles of the hand. Sensory innervation is from the medial ( ulnar) 1 & 1/2 digits ( the 5th. and 1/2 of the 4th. digits) Radial nerve-Originate from the posterior cord of the brachial plexus in the axilla. (C5T1) The nerve winds around the back of the arm, first between the long and medial heads of the triceps, then in the spiral groove on the back of the humerus, between the lateral and medial heads of the triceps. It pierces the lateral fascial septum above the elbow and continues downward into the cubital fossa in front of muscles. In the spiral groove the nerve is accompanied by the profunda vessels, and it lies directly in contact with the shaft of the humerus. Innervates the extensor muscles of the elbow, wrist and fingers. Axillary Nerve- Originate from the posterior cord (C5,C6) Motor innervation is deltoid and teres minor muscles that act on the shoulder joint. Sensory innervation is from the skin just below the point of the shoulder.

COMPONENTS OF PERIPHERAL NERVE Cell body- performs metabolic work that sustains the nerves primary function:signal conduction Axon- communicate with distal parts of the body Dendrites- provide synaptic contact with neighboring nerve cells &fibers Nodes of Ranvier- Saltatory conduction, for fast transmission with minimal energy expenditure Schwann cells- provides myelin sheath in PNS(for faster conduction)

COVERING OF A NERVE Endoneurium- covers individual nerve fiber. Contains schwann cells & axon Perineurium- covers nerve fascicles. Primary strengthening connective tissue of the nerve Epineurium- outer connective tissue sheath. Protects nerve from compression

Brachial plexus neuropathy may be associated with: birth defects exposure to toxins inflammatory conditions immune system issues There are no specific risk factors associated with BPN. However, young men are more likely than women and older men to develop a rare brachial plexus condition known as Parsonage-Turner syndrome, which can cause shoulder paralysis.

Clinical Manifestations Numbness BPN can cause numbness in your shoulder, arm, and hand. Severe cases can cause complete loss of sensation. This numbness can cause additional complications related to recurring injury to the affected areas. These complications could go unnoticed due to an inability to detect pain. Abnormal Sensations Sometimes BPN can cause abnormal sensations such as tingling and burning on or near nerves related to the brachial plexus. These types of sensations generally occur in your arm and hand. Weakness A decreased ability to lift your wrist or extend it backward is a common way for BPN to manifest. Weakness in your hands may also indicate BPN. Horner Syndrome Horner syndrome is rare, but it can indicate BPN. Horner syndrome results from an interruption in the nerve signals that control regions of the facial area. It is usually caused by an injury to the nerves of the brachial plexus. Symptoms of Horner syndrome are:

constriction of the pupil (it becomes very small) eyelid drooping inability to sweat (affected facial area)

Pathophysiology A. Traction or compression Injury to unilateral brachial plexus during birth process or due to cervical rib abnormality. (I) Erb's Palsy involves C5-6, upper arm paralysis, may involve rhomboids, levator scapulae, serratus anterior, deltoid, supraspinatus, infraspinatus, biceps brachii, brachioradialis, brachialis, supinator and long extensors of wrist fingers, and thumb. (2) Klumpke's Palsy involves C8-Tl,lower arm paralysis, involves intrinsic muscles of hand, flexors and extensors of wrist and fingers. (3) Erb-Klumpke Palsy, whole arm paralysis. B. Nerve sheath is torn and nerve fibers compressed hemorrhage and edema, although total avulsion of nerve is possible. Peripheral nerve injury may result in motor, sensory, and/or sympathetic impairments. In addition, pain may be a symptom of nerve tension or compression because the connective tissue and vascular structures surrounding and in the peripheral nerves are innervated and the

peripheral nerve function is sensitive to hypoxic states. Knowing the mechanism of injury and the clinical signs and symptoms help the clinician determine the potential outcome for the patient and develop a plan of care. Mechanisms of Nerve Injury Nerves are mobile and capable of considerable torsion and lengthening owing to their arrangement. Yet they are susceptible to various types of injury including. Compression (sustained pressure applied externally suchas tourniquet or internally such as from bone, tumor, or soft tissue impingement resulting in mechanical or ischemic injury) Laceration (knife, gunshot, surgical complication, injection injury) Stretch (excessive tension, tearing from traction forces) Radiation Electricity (lightening strike, electrical malfunction) Injury may be complete or partial and produces symptoms based on the location of the insult. Biomechanical injuries to the peripheral nervous system result most commonly from friction, compression, and stretch. Secondary injury can be from blood or edema. Compressive forces can affect the microcirculation of the nerve, causing venous congestion and reduction of axoplasmic Transport, thus blocking nerve impulses; if sustained, it can cause nerve damage. The endoneurium helps maintain fluid pressure and may provide cushioning for nerves, especially when close to the surface and subject to greater pressure. The insult can be acute from trauma or chronic from repetitive trauma or entrapment. Sites where a peripheral nerve is more vulnerable to compression, friction, or tension include tunnels (soft tissue, bony, fibro-osseus), branches of the nervous system (especially if the nerve has an abrupt angle), points where a nerve is relatively fixed when passing close to rigid structures (across a bony prominence), and at specific tension points. Response to injury can be pathophysiological or pathomechanical, leading to symptoms derived from adverse tension on the nervous system. Results may be intraneural and/or extraneural. Intraneural. Pathology that affects the conducting tissues (e.g., hypoxia or demyelination) or connective tissues of the nerve (e.g., scarring of epineurium or irritation of dura mater) may restrict the elasticity of the nervous system itself. Extraneural. Pathology that affects the nerve bed (e.g., blood), adhesions of epineurium To another tissue (e.g., a ligament), and swelling of tissue adjacent to a nerve (e.g., Foraminal stenosis) may restrict the gross movement of the nervous system in relation to surrounding tissues. DEMYELINATION Definition

This is a nerve injury that can cause motor and sensory abnormalities in which the myelin is impaired but the axon remains intact. The membrane capacitance increases due to the loss of myelin insulation, thus hindering saltatory conduction. The trophic factors of the nerve are maintained and myelin regeneration is possible due to Schwann cell proliferation.

Etiology (a) Compression causing a transient ischemic episode, edema, or myelin invaginations with paranodal intussusception or (b) peripheral neuropathies Remyelination (a) Description: This is a process of repair in which the demyelinated region develops new myelin by the Schwann cells. This new myelin is thinner with shorter internodal distances, it can cause an improved but slower than normal conduction velocity.

AXONAL INJURY Definition An injury to the axon may present in one of two typical forms: axonal degeneration or Wallerian degeneration. Both of these can affect the cell body and cause a central chromatolysis

Axonal Degeneration Description: A nerve injury that begins presenting in a dying back fashion, affecting the nerve in a length-dependent manner. It begins distally and ascends proximally. Wallerian Degeneration (WD) Description: A nerve injury that begins presenting 45 days postfocal or multifocal nerve damage. It completes in 7 days for motor nerves or 11 days for sensory nerves. The axon degenerates distally from the site of injury, leaving the proximal portion intact Etiology Pathology can occur from: (a) focal crush, (b) stretch, (c) transection, or (d) peripheral neuropathies. Recovery Collateral Sprouting Description: This is a process of repair in which a neurite sprouts off the axon of an intact motor unit and innervates denervated muscle fibers of an injured motor unit. The sprouts connect with smaller terminal branches, thinner myelin, and weaker neuromuscular junctions. Increased fiber type grouping occurs as muscle fibers become part of the new motor unit and take on its characteristics, increasing the size of its territory. This remodeling results in motor units with poor firing synchronicity, secondary to the immature terminal sprouts. This results in polyphasic waveforms with increased amplitudes. Axonal Regrowth Description: This is a process of repair in which the axon will regrow down its original pathway toward its muscle fibers. It will travel approximately 1 mm/day or 1 inch/month if the supporting connective tissue remains intact. These axons will have a decreased diameter, thinner myelin,

and shorter internodal distance. With reinnervation, low amplitude, long duration, and polyphasic potentials known as nascent potentials are formed. If the connective tissue is not intact to guide proper nerve re-growth, a neuroma can form with failure to reach the final end organ.

Collateral Sprouting vs. Axonal Regrowth If an axon regrows to innervate its original muscle fibers and collateral sprouting to these fibers has occurred, the recovery process possessing the largest axon, thickest myelin, and strongest neuromuscular junction will prevail and keep the muscle fibers.

NERVE INJURY CLASSIFICATION Nerve injuries are classified using either the Seddon or Sunderland classification systems; both are based on structural and functional changes that occur in the nerve with various degrees of damage. These systems describe the degree of injury to nerve substructures and the effect on prognosis. Seddon Classification

Sunderland Classification

Pathophysiology of Brachial Plexus Neuropathy

BRACHIAL PLEXUS NEUROPATHY

nerves in your upper shoulder area becomes damaged

severe pain and decreased sensation in this area

pressure from tumors

pressure from tumors

other stretching injuries

birth trauma

direct injury

numbness

Horners Syndrome

Abnormal Sensations

Weakness

Differential Diagnosis:

Differential Diagnoses Guillain-Barre Syndrome Multiple Sclerosis Neoplastic Brachial Plexopathy Spinal Cord Injury Spinal Stenosis Syringomyelia Thoracic Outlet Syndrome Traumatic Brain Injury

PT Management Management Guidelines- Recovery from Peripheral Nerve INJURY 1. Acute Phase: immediately after injury or surgery Immobilization: time dictated by surgeon Movement: amount and intensity dictated by type of injury and surgical repair Splinting: or bracing: may be necessary to prevent deformity Patient education: protection of the part 2. Recovery Phase: signs of reinnervation (muscle contraction, increased sensitivity) Motor training: muscle hold in the shortened position Desensitization: multiple texture for sensory stimulation; vibration Descriminative sensory re-education: identification of objects with, then without, visual cues 3. Chronic Phase: reinnervation potential peaked with minimal or no signs of neurological recovery Compensatory function: minimized during the recovery phase but is emphasized when full neurological recovery does not occur Preventive Care: emphasis on lifelong care to involved region

Immobilization Positioning ROM exercise Orthoses Muscle re-education PREs Strengthening of the rotator cuff Scapular stabilization Therapeutic modalities o Cold, heat, TENS

SURGICAL TREATMENT A. SURGICAL EXPLORATION Indication 1st month -(+) complete nn division -(+) Extensive sensory loss -(+) persistent motor loss 3rd month -(+) incomplete nn division but s definite improvement

I. PRIMARY (I ) - performed immediately after injury C/I -(+) open fx -bullet wounds -Contaminated wounds. II. SECONDARY (2) - performed after the original wound has healed/when progress in gradual recovery of nn fxn has been unsatisfactory. B. AUTOGENOUS NERVE GRAFTING -Used when long defect in nn is impossible to bring its two ends together. - c limited success - autogenous -requires that instead of the 1 gap the regenerating axons must bridge 2 (proximal and distal line). - fxnal return C. MICROSURGICAL TECHNIQUES -(+) improve accuracy of nn suture. - careful dissection done under magnification to identify individual nn bundles and permit matching of proximal and distal segments combined c internal(fascicular) and external (epinueral) sutures. D. NEUROLYSIS -freeing of the nn from cicatricial adhesions and constrictions FACTORS AFFECTING POST-OP RECOVERY 1. Duration of the paralysis 2. Age (px) 3. Type of nn involved 4. Level at which nn is injured 5. Degree of 2 change in mm, tendons and joints.

Medication A. Nonsteroidal anti-inflammatory drugs 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) Naproxen (Naprosyn, Aleve)

B. Anticonvulsants 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. Gabapentin (Neurontin) C. Tricyclic antidepressants 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) Doxepin (Sinequan, Adapin) D. Analgesics 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) Oxycodone (OxyContin, Roxicodone, OxyIR) Oxycodone and acetaminophen (Percocet) Fentanyl citrate (Duragesic) Hydrocodone and acetaminophen (Lorcet) Tramadol (Ultram)

References: Therapeutic Exercises by Kisner and Colby 5th Ed. Physical Medicine and Rehabilitation Board Review by Sara J. Cuccurrullo,M.D IERs NPTE review and study guide,by O SULLIVAN and Siegelman Handbook of Orthopaedic Surgery by Brashear Physical Medicine and Rehabilitation by Braddom Neck and shoulder pain by Calliet http://emedicine.medscape.com/article/316888-differential

Brachial Plexus Neuropathy

Submitted by: David, Jonette Eje, Kim T. Carillo, Carlo R. Garganera, Warlito Mission, Ruth Mariz Saluta, Maria Jurelle Mendiola, Jen Alex

Submitted to: Sir Glynn Fuentes PT Staff In-charge

August 14, 2013