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BRACHIAL PLEXUS NEUROPATHYBackground

Trauma accounts for a large proportion of brachial plexopathies. The mechanism of aninjury and the magnitude, rate, and direction of deforming forces ultimately determine theextent and location of a traumatic brachial plexopathy.

A lesion of the brachial plexus can result in motor, sensory, and sympatheticdisturbances. 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 brachialplexus as it progresses distally, injuries to it may result in diverse paralyses, anesthesias, andparesthesias, depending on the exact level of injury and the extent of injury to the variouselements at that level.

Definition

A generalized term for insult in the brachial plexus. Trauma is the most common causeof brachial plexus injury. Closed injury can occur from traction from the head and neck areforcibly bend away from the shoulder or in association with fractures of the clavicle orshoulders. Open injuries can occur with knife or missile wounds often the patient has otherserious injuries which can delay identification of the brachial plexus injury. Traumatic injuriescan affect multiple trunks and cords or even avulsion injuries to the roots and individualnerves.

Epidemiology

FrequencyThe 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 isundetermined, primarily because of significant underreporting. Prospective studies performedat 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 hadmultiple trauma to the head and skeletal system.

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

http://www.medscape.com/viewarticle/576005

http://www.medscape.com/viewarticle/576005



RaceNo race predilection is reported for traumatic brachial plexopathy.

SexIn 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.

EtiologyPathology can occur from: (a) focal crush, (b) stretch, (c) transection, or (d) peripheral

neuropathies.

Mechanism of injuryTraction injury Most common cause of brachial

plexopathy

Predominantly supraclavicular orother plexus palsy

Predisposing factors: wide range ofmotion of shoulder, cervical roots lacksprotective epineural and perinerualsheaths and have poor tensile strength.

Most common specific causes: birthinjury and sports injuries andmotorcycle accidents causing shouldertrauma “ Pack Palsy”due to shulderdepression combined with lateral neckflexion puts traction force in upperplexus especially C5-C6 or C5-C7

Excessive hyperabduction also causebrachial plexus injury

Infraclavicular involvent requires moresevere traction force

Obstetrics paralysis Is a specific type of traction injuryfollowing a stretch of the neck-shoulder angle during birth.

Result in erb-duchenne palsy (upper



plexus) or klumpke’s paralysis (loerplexusinvolvment)

Motor deficits predominate

Sensory deficits mild

Most often involve right plexus since

head is often turn to the left duringbirth

most cases result in neupraxia sorecovery good

klumpkes poorer prognosis since itoften involves rot avulsion

Trauma sharp lacerations better potential forrecovery (after repair) comparedtoblunt lacerations that cut & stretch thenerve

traumatic hematoma may be the one

responsible for the nerve compressionIatrogenic injury Less common in the brachial plexus

compared to lumbar plexus

Most frequent cause of stretchinjury→spreding of a sternum-splittingthoracotomy

Most common cause of directinjury→transaxillary surgery forthoracic outlet syndrome; axillarylymph node removal; deep cervicalexploration

Neoplastic Usually due to direct extension or

metastasis

Most commonly from lung and breastcancer

Usually insidious onset with UE pain& paresthesia & localized tendernessproximally

PancoastSyndrome- combination offindings (shoulder radiating pain, armparesthesia & weakeness & hornerssyndrome) associated with brachial

plexus injury dueto direct extension ofan apical lung tumor; usually C8-T1/lower trunk distribution

May also occur following neck oraxillary surgery, chemotherapy &radiation therapy of a neoplasm



Anatomy

The brachial plexus is a somatic nerve plexus formed by intercommunications among theventral rami of thelower four cervical nerves ( C 5 - C 8) and the first thoracic nerve (T 1). It isresponsible 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 thearea of the axilla( armpit) (which is supplied by the intercostobrachial nerve), an area just abovethe point of the shoulder (supplied by supraclavicular nerves) and the dorsal scapular areawhich 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 formthree 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 musclesThe 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 the posterior 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 andthen passes downward between biceps and brachialis muscles. It appears at the lateralmargin of the biceps tendon and pierces the deep fascia just above the elbow and it runsdown 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 themedial of the arm. The nerve pierces the medial fascial septum accompanied by thesuperior ulnar collateral artery and enters the posterior compartment of the arm andpasses 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 & 1/2digits ( the 5th. and 1/2 of the 4th. digits)

Radial nerve-Originate from the posterior cord of the brachial plexus in the axilla. (C5-T1) 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 thelateral and medial heads of the triceps. It pierces the lateral fascial septum above theelbow and continues downward into the cubital fossa in front of muscles. In the spiralgroove the nerve is accompanied by the profunda vessels, and it lies directly in contactwith the shaft of the humerus. Innervates the extensor muscles of the elbow, wrist andfingers.

Axillary Nerve- Originate from the posterior cord (C5,C6) Motor innervation is deltoidand teres minor muscles that act on the shoulder joint. Sensory innervation is from theskin just below the point of the shoulder.

COMPONENTS OF PERIPHERAL NERVE

Cell body- performs metabolic work that sustains the nerve’s primary function:signalconduction

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 energyexpenditure

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 morelikely than women and older men to develop a rare brachial plexus condition known asParsonage-Turner syndrome, which can cause shoulder paralysis.



Clinical Manifestations

NumbnessBPN 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 aninability to detect pain.

Abnormal SensationsSometimes 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 andhand.

WeaknessA 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 SyndromeHorner 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 aninjury 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 dueto cervical rib abnormality.(I) Erb's Palsy involves C5-6, upper arm paralysis, may involve rhomboids, levatorscapulae, 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 ofhand, 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 totalavulsion of nerve is possible.

Peripheral nerve injury may result in motor, sensory, and/or sympathetic impairments. Inaddition, pain may be a symptom of nerve tension or compression because the connective tissueand vascular structures surrounding and in the peripheral nerves are innervated and the

http://www.healthline.com/human-body-maps/wrist

http://www.healthline.com/human-body-maps/wrist



peripheral nerve function is sensitive to hypoxic states. Knowing the mechanism of injury andthe clinical signs and symptoms help the clinician determine the potential outcome for thepatient and develop a plan of care.

Mechanisms of Nerve Injury

Nerves are mobile and capable of considerable torsion and lengthening owing to theirarrangement. Yet they are susceptible to various types of injury including.

Compression (sustained pressure applied externally suchas tourniquet or internally suchas from bone, tumor, or soft tissue impingement resulting in mechanical or ischemicinjury)

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 theinsult. Biomechanical injuries to the peripheral nervous system result most commonly fromfriction, compression, and stretch. Secondary injury can be from blood or edema. Compressiveforces can affect the microcirculation of the nerve, causing venous congestion and reduction ofaxoplasmic 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. Siteswhere 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 anabrupt 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 symptomsderived from adverse tension on the nervous system. Results may be intraneural and/orextraneural.

Intraneural. Pathology that affects the conducting tissues (e.g., hypoxia ordemyelination) or connective tissues of the nerve (e.g., scarring of epineurium orirritation 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 relationto surrounding tissues.

DEMYELINATION

Definition



This is a nerve injury that can cause motor and sensory abnormalities in which themyelin is impaired but the axon remains intact. The membrane capacitance increases due to theloss of myelin insulation, thus hindering saltatory conduction. The trophic factors of the nerveare 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 internodaldistances, it can cause an improved but slower than normal conduction velocity.

AXONAL INJURY

DefinitionAn 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 DegenerationDescription: 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 4–5 days postfocal or multifocal nerve

damage. It completes in 7 days for motor nerves or 11 days for sensory nerves. The axondegenerates distally from the site of injury, leaving the proximal portion intact

EtiologyPathology 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 motorunit and innervates denervated muscle fibers of an injured motor unit. The sprouts connectwith smaller terminal branches, thinner myelin, and weaker neuromuscular junctions. Increasedfiber 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 withpoor firing synchronicity, secondary to the immature terminal sprouts. This results inpolyphasic waveforms with increased amplitudes.

– Axonal Regrowth

Description: This is a process of repair in which the axon will regrow down its original pathwaytoward its muscle fibers. It will travel approximately 1 mm/day or 1 inch/month if the supportingconnective tissue remains intact. These axons will have a decreased diameter, thinner myelin,



and shorter internodal distance. With reinnervation, low amplitude, long duration, andpolyphasic potentials known as nascent potentials are formed. If the connective tissue is notintact to guide proper nerve re-growth, a neuroma can form with failure to reach the final endorgan.

– Collateral Sprouting vs. Axonal Regrowth

If an axon regrows to innervate its original muscle fibers and collateral sprouting to these fibershas occurred, the recovery process possessing the largest axon, thickest myelin, and strongestneuromuscular junction will prevail and keep the muscle fibers.

NERVE INJURY CLASSIFICATIONNerve 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 substructuresand the effect on prognosis.

• Seddon Classification



Sunderland Classification

Pathophysiology of Brachial Plexus Neuropathy

nerves in your upper shoulder areabecomes damaged

severe pain and decreased sensation in this area

BRACHIAL PLEXUS NEUROPATHY

pressure

from tumors

pressure

from tumors

other

stretching

injuries

birth trauma direct injury



Differential Diagnosis:

Differential Diagnoses

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

numbnessHorner’s

Syndrome

Abnormal

SensationsWeakness

http://emedicine.medscape.com/article/315632-overview












PT Management

Management Guidelines- Recovery from Peripheral Nerve INJURY1. 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 ofnn 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 anddistal 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 RECOVERY1. Duration of the paralysis2. Age (px)3. Type of nn involved4. Level at which nn is injured5. 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 havecentral and peripheral anticholinergic effects, as well as sedative effects, and block the active

reuptake of norepinephrine and serotonin. The multifactorial mechanism of analgesia couldinclude improved sleep, an altered perception of pain, and an increased pain threshold. Theefficacy 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. Tricyclicantidepressants 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 shouldreconstructive 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

IER’s NPTE review and study guide,by O’ SULLIVAN and Siegelman Handbook of Orthopaedic Surgery by Brashear Physical Medicine and Rehabilitation by BraddomNeck and shoulder pain by Calliethttp://emedicine.medscape.com/article/316888-differential

http://emedicine.medscape.com/article/316888-differential

http://emedicine.medscape.com/article/316888-differential



Brachial PlexusNeuropathy

Submitted by:David, Jonette

Eje, Kim T.Carillo, Carlo R.

Garganera, WarlitoMission, Ruth MarizSaluta, Maria JurelleMendiola, Jen Alex

Submitted to:Sir Glynn FuentesPT Staff In-charge

August 14, 2013

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