Comprehensive Notes on the Peripheral Nervous System

Peripheral Nervous System (PNS)

  • Includes somatic motor and sensory components of cranial and spinal nerves.
    • Arising from neurons in the brainstem, spinal cord, or dorsal root ganglia.
  • Also includes peripheral aspects of the Autonomic Nervous System (ANS).
  • Axons from these components form peripheral nerves.

Disorders of the PNS

  • Broadly divided into:
    • Neuropathies: Pathology confined to the nerve.
    • Myopathies: Pathology occurs in the muscle.
  • Subdivided further by anatomic involvement site.
  • Signs/symptoms relate to motor, sensory, and ANS systems.

Motor Involvement (Lower Motor Neuron - LMN)

  • Occurs when affecting:
    • Alpha motor neuron cell body (anterior horn cell) in spinal cord/brainstem.
    • Axons from anterior horn cell forming spinal, peripheral, and cranial nerves.
    • Motor endplate of the axon.
    • Muscle fibers innervated by motor nerve axon.

Sensory Fiber Involvement

  • Occurs with lesions in:
    • Dorsal root ganglion (cell body).
    • Nerve root proximal to ganglia.
    • Distal fibers of the peripheral nerve.

Autonomic Nervous System (ANS) Involvement

  • Motor fibers (preganglionic or postganglionic): Affects involuntary motor function of organs.
  • Sensory fibers: Alters transmission of unconscious sensory functions (e.g., baroreceptors, receptors signaling irritants, distention, hypoxia) into the CNS.

Structure of Nerves in PNS

  • Supported and covered by connective tissue coverings.
    • Endoneurium: Innermost, surrounds each individual axon.
    • Perineurium: Middle layer, envelopes groups (fascicles) of axons; maintains the blood-nerve barrier.
    • Epineurium: Outermost layer, surrounds the entire nerve, providing cushioning.
  • Axolemma: Phospholipid membrane forming the axon's surface.
  • Schwann cells: Lie between the axolemma and endoneurium.
    • Communicate with axons throughout life via molecular signaling.

Myelination

  • Large-diameter axons (> 1 \mu m): Schwann cells wrap membranes to create myelin.
  • Small-diameter axons: Schwann cells envelop and support nonmyelinated fibers.
  • Myelin provides electrical insulation for rapid saltatory conduction.
  • Myelin causes sodium channels to cluster at nodes of Ranvier, reinforcing conduction.
  • Smallest axons: Schwann cells provide support for unmyelinated fibers; action potentials conducted via local circuit conduction.
  • Only ~25% of fibers in peripheral nerve are myelinated.
  • Normal action potential propagation requires sufficient energy, supplied by vascular plexus between connective tissue layers.

Vascular Supply

  • Each peripheral nerve receives an artery penetrating the epineurium.
    • Branches extend into perineurium as arterioles, then endoneurium as capillaries.
  • Vessels appear coiled in shortened limb positions, uncoiling after movement.
  • Rich vascular supply makes peripheral nerves relatively resistant to ischemia.

Peripheral Nervous System Changes with Aging

  • May represent normal growth/development continuum or pathologic processes superimposed on aging.
  • Animal models used due to difficulty of studying human peripheral nerves in vivo.
  • Age does not affect fascicle size/number.
  • Perineurium and epineurium thicken with age; endoneurium often becomes fibrosed (increased collagen).
  • Cross-sectional area decreases slightly with age due to reduced numbers of unmyelinated and myelinated fibers.
  • Ventral root fibers (controlling motion) more affected than dorsal root fibers (controlling sensation).
  • Blood vessels may become atherosclerotic; occlusion contributes to nerve fiber loss.
  • Decreases in protein production may cause myelin deterioration.
  • Shorter internodes are seen in myelinated fibers, suggesting demyelination-remyelination occurs.
  • Structural alteration in myelination may diminish vibratory sense appreciation.

ANS Dysfunction in Elderly

  • More common; related to nervous system changes.
  • Cell bodies show chromatolysis and lipofuscin accumulation (diminished toxin removal).
  • Loss of cell bodies observed in sympathetic ganglia, along with unmyelinated fiber loss in peripheral nerves.
  • Sympathetic control of dermal vasculature declines, diminishing wound repair efficiency.
  • TENS (Transcutaneous Electrical Nerve Stimulation) improved vascular response in aging animal model.
  • Peripheral activity of sympathetic nerves affected by low-frequency electrical stimulation.

Motor Endplate and Sensory Receptor Changes

  • Age-related changes occur in the motor endplate as early as the third decade of life, but not in all muscles.
  • Density and morphology of sensory receptors are altered in the elderly.
  • Altered axonal myelination slows Nerve Conduction Velocities (NCVs).
  • Loss of fibers decreases the amplitude of the potential.
  • Decreased protein production and intraaxonal transport by cytoskeletal elements in peripheral nerve.
  • Electromyographic (EMG) studies show loss of motor units and signs of reinnervation.
  • Morphologic changes observed after age 60 manifest as decreased strength and sensory changes.

Clinical Presentation in Healthy Elderly

  • May suggest peripheral neuropathy (numbness, tingling in hands/feet, mild diffuse weakness – especially in distal hand muscles).
  • Sensory alterations may lead to poor balance and gait instability.
  • Increased sensory thresholds on examination.

Causes of Aging Neuropathy

  • Combination of factors:
    • Loss of motor and sensory cell bodies.
    • "Dying-back" condition (neurons support limited number of fibers/receptors).
    • Chronic compression/repetitive trauma over lifetime.
    • Coexisting medical conditions, atherosclerosis, nutritional deficiencies.

Response to Injury in Aging PNS

  • Wallerian degeneration is delayed, and regeneration takes longer due to slower trophic factor secretion.
  • Density of regenerating axons is less.
  • Collateral sprouting is reduced, limiting function recovery in partial nerve injury.

Response to Injury in General (PNS)

  • Peripheral nerve damage from heredity, trauma, infections, toxins, and metabolism.
  • Limited response: fibers either demyelinate or degenerate.
  • Segmental demyelination: Occurs with external nerve compression or disease; myelin is lost in segments, leaving the axon intact but bare.
  • Degeneration: Occurs in disorders affecting the axon directly (physical injury, disease).
  • More severe involvement causes axonal degeneration distal to lesion (anterograde or Wallerian degeneration). Begins immediately and completes in a few weeks.
  • Neuropathic diseases affecting the axon/cell body typically affect longest nerve fibers first (length-dependent), beginning distally and progressing proximally.
  • Conditions affecting only myelin cause segmental demyelination in sensory/motor fibers.
  • Disruption of action potential conduction from proprioceptors/mechanoreceptors causes sensory changes.
  • Neuropathies affecting myelin cause demyelination of motor nerves to muscle and preganglionic fibers of the ANS, creating weakness, proprioceptive/tactile changes, and autonomic involvement.

Classification of Nerve Injury (Traumatic)

  • Two systems based on structural and functional changes:

    • Seddon:
      • Neurapraxia
      • Axonotmesis
      • Neurotmesis
    • Sunderland: classified into 5 categories, based on axonal and connective tissue covering involvement.

Neurapraxia

  • Segmental demyelination, slowing/blocking action potential conduction at the demyelination point.
  • Often occurs after nerve compression inducing mild ischemia.
  • If segmental demyelination occurs due to the disease process, the response can be termed a myelinopathy.
  • Conduction is normal above/below compression point; muscle does not atrophy (axon remains intact).

Axonotmesis

  • Axon is damaged, but connective tissue coverings remain intact.
  • Prolonged compression producing infarction and necrosis.
  • In the presence of disease, Wallerian degeneration creates an axonopathy, which is analogous to axonotmesis.

Neurotmesis

  • Most severe: complete severance of axon and disruption of supporting connective tissue coverings.
  • Caused by gunshot/stab wounds or avulsion injuries.

Wallerian Degeneration

  • Occurs when axonal continuity is lost (axonotmesis or neurotmesis).
  • Axons distal to lesion degenerate.
  • Muscle fibers atrophy rapidly because they depend on nerve cell body for nourishment/trophic control.

Regeneration after Segmental Demyelination

  • Molecular signaling causes remaining Schwann cells to divide mitotically.
  • Newborn Schwann cells move to envelop the denuded segment and begin forming myelin.
  • Shorter internodal distance occurs with remyelination; nerve conduction velocity may not return to normal, even though muscle contracts normally

Regeneration after Axonal/Wallerian Degeneration

  • Possible if nerve cell body remains viable.
  • New axons sprout from proximal end of damaged axons.
  • Successful functional regeneration requires alignment of proximal/distal ends of connective tissue tube.
    • Occurs in axonotmesis because coverings remain intact.
    • Less likely in neurotmesis without surgical intervention.
    • Without surgery, axonal sprouts may enter nearby soft tissue (neuroma) or grow down incorrect endoneurial tube (nonfunctional reinnervation).
  • Once axon establishes distal contact (muscle or sensory receptor), remyelination begins.
  • In partial axonal degeneration, adjacent noninvolved axons produce collateral sprouts that innervate muscle fibers before damaged axons can reinnervate.
  • Results in enlarged motor unit for neuron with collateral sprouts.

Classification of Neuropathy

  • Classified by rate of onset, type/size of nerve fibers involved, distribution pattern, or pathology.
  • Mononeuropathy: Single peripheral nerve affected (commonly from trauma).
  • Polyneuropathy: Several peripheral nerves involved.
  • Radiculoneuropathy: Nerve root involvement as it emerges from the spinal cord.
  • Polyradiculitis: Several nerve roots involved (inflammatory response from infections).

Myopathy

  • Involvement of muscle itself.
  • Follows different clinical pattern than nerve involvement.
  • Typically reflected by proximal weakness, wasting, and hypotonia without sensory impairments.

Signs and Symptoms of Peripheral Dysfunction

  • Aid in localization of the level/levels of involvement.
  • Sensory loss follows peripheral nerve distribution or dermatomal pattern (spinal nerve/dorsal root ganglia affected).
  • Motor involvement causes paresis/paralysis in muscles innervated by that nerve distal to the lesion or weakness occurs in all the muscles receiving axons from that spinal level (a myotomal pattern).
  • Individuals with only peripheral nerve involvement will have no signs or symptoms of CNS dysfunction.

Classic Pattern of Involvement

  • Distal sensory deficits (longest nerves involved first).
  • Often sensory: tingling, prickling, burning, or bandlike dysesthesias and paresthesias in the feet.
  • If multiple nerves involved: glove-and-stocking distribution (dying-back of longest fibers).
  • Motor nerve involvement: distal weakness and abnormalities of tone (hypotonicity/flaccidity).
  • Weakness of dorsiflexors or plantar flexors.
  • Deep Tendon Reflexes (DTRs) are diminished or absent distally affected first.
  • Rapid atrophy occurs with axonal degeneration, along with electrophysiologic changes.
  • Prolonged paralysis gives rise to secondary complications such as contracture formation and edema.
  • Muscle tenderness or cramping may be associated with muscle diseases.
  • In a myopathy, the weakness tends to be proximal; in neuropathy, motor symptoms tend to first occur distally.

ANS Fiber Involvement

  • Preganglionic fibers (myelinated) affected by segmental demyelination.
  • In axonal degeneration: changes in vascular control and sweating.
  • Laceration of median nerve in the hand: smooth skin that does not sweat or wrinkle.
  • Systemic metabolic cause: hypotension with cardiac irregularities.

Pathogenesis and Diagnosis of Peripheral Dysfunction

  • Trauma, inherited disorders, environmental toxins, and nutritional disorders may affect the myelin (myelinopathy), axon (axonopathy), or cell body of a peripheral nerve.
  • The anatomic region/regions affected determine the severity of involvement and amount of function lost.

Hereditary Neuropathies

  • Can be the primary disorder or part of a greater multisystem disorder.

Charcot-Marie-Tooth Disease (CMT)

  • Also known as hereditary motor and sensory neuropathy or peroneal muscular atrophy.
  • Most common inherited disorder affecting motor and sensory nerves.
  • Initially involves the fibular (peroneal) nerve, affecting muscles in the foot and lower leg.
  • Later progresses to muscles of the forearms and hands.
  • Clinically characterized by distal limb muscle wasting and weakness, usually with skeletal deformities, distal sensory loss, and abnormalities of DTRs. (same clinical phenotype among different disorders)
Incidence
  • Relatively common (1 in 2500 persons in the US).
  • Onset can occur in childhood or adulthood.
Etiology
  • Genetically heterogeneous neuropathy inherited as autosomal dominant, autosomal recessive, or X-linked pattern.
  • Over 50 loci defects on chromosomes identified through DNA testing.
  • Chromosomal defects create duplication, deletion, or point mutations in genetic code for proteins involved in myelination.
CMT1
  • The most common autosomal dominant pattern, subdivided into CMT1A, 1B, and 1C.
  • CMT1A: accounts for 70% of all CMT1 cases; caused by DNA duplication on chromosome 17 for peripheral myelin protein 22 (PMP22), creating segmental demyelination of the fibular (peroneal) nerve.
CMT2
  • Has chromosomal abnormalities mapped to chromosomes 1, 8, and X. On chromosome 1, CMT2 is associated with a mutation in human myelin protein zero (P0), which has been associated recently with axonal dysfunction.
  • Associated with axonal degeneration.
  • Onset varies between the second and seventh decades; less involvement in small muscles of the hands than CMT1.
Pathology
  • Mutations in proteins (PMP, P0, and connexin) associated with Schwann cell myelination create extensive demyelination along with a hypertrophic onion bulb formation.
  • CMT2 is associated with genetic mutations that disrupt neurofilament assembly and thus affect axonal transport, creating axonal involvement.
Clinical Manifestations
  • Nearly impossible to tell CMT1 from CMT2 clinically.
  • In CMT1 some members of a family with the genetic mutation may have greater signs of the disorder than others, who have only minor involvement. (variable expressivity).
  • X-linked form: men are affected and have signs of both demyelination and axonal degeneration.
  • Slowly progressive disorder; CMT1 begins in childhood, but onset may be difficult to determine.
  • Clinical signs: distally symmetric muscle weakness, atrophy, diminished DTRs.
  • Feet have pes cavus (high arch) deformities and hammer toes.
  • Client will have weakness of the dorsiflexors and evertors (peroneal musculature) and will ambulate with a foot drop (steppage) gait pattern.
  • As CMT progresses, involvement will be seen distally in the upper extremities: Weakness and wasting of the intrinsic muscles of the hand occur, followed by progressive wasting in the forearms.
  • Proprioception is lost in the feet and ankles, and cutaneous sensation is diminished in the foot and lower legs. Sensory loss is minimal in CMT2. Sensory symptoms can include tingling and burning in the feet and legs, as well as impaired proprioception
  • Legs take on the shape of an inverted champagne bottle because normal muscle bulk is maintained above the knees.
Medical Management
  • Diagnosis by history and clinical examination, hereditary picture, electrophysiologic studies, and nerve biopsy.
  • Diagnosis of CMT can be confirmed using gel electrophoresis to detect duplication, deletions, or sequence variations in genes.
    • Electrophysiologic testing reveals underlying axonal degeneration. Slowed motor nerve conduction does not have a linear correlation with the clinical severity of the disease.
  • Both motor and sensory NCVs will be slowed in CMT1 but are normal or only slightly slowed in CMT2. Abnormalities of electrophysiologic studies in CMT2 will be a decreased amplitude of the potential, indicating axonal loss.
Treatment
  • No specific treatment to alter its course (inherited disorder).
  • Treatment is symptomatic to ensure function is maintained safely.
  • Foot drop and hand deformities can be helped by orthotic devices.
  • Range-of-Motion (ROM) exercises to prevent contractures.
Prognosis
  • Slowly progressive disorder: If unmanaged, contracture formation resulting from weakness will create further gait abnormalities, with clients reporting an increased number of falls.
  • Clients may develop problems with writing and handling objects.
  • Individuals with CMT should be cautioned that some medications have been reported to cause exacerbation of CMT.
  • A database of the drugs that should be avoided is maintained by CMT North America.
Special Implications for the PTA: CMT
  • Goal is to minimize deformity and maximize function.
  • Physical therapist assistant (PTA) should anticipate that deformities will arise from the imbalance between the tibialis anterior and peroneus longus and the tibialis posterior and peroneus brevis, which leads to a pes cavus and varus deformity, respectively.
  • This weakness may be combined with diminished or lost proprioception and some degree of cutaneous involvement that can lead to an unsteady gait. These problems should be addressed with stretching, ROM exercises, and bracing to improve ambulation.

Mechanical Injuries: Compression and Entrapment Syndromes

  • Proximity of peripheral nerves to bony, muscular, and vascular structures can cause entrapment neuropathies
  • Traction: As tension exceeds 10%–20% of the axon's resting length, the axon's internal slack within fascicles is eliminated and structural damage occurs.

Carpal Tunnel Syndrome (CTS):

  • The most common entrapment neuropathy in the United States.
  • Compression of the median nerve within the carpal tunnel at the wrist.
  • Characterized by general signs and symptoms of neuropathies: pain, tingling, numbness, paresthesia, and later, muscular weakness in the distribution of the median nerve.
Incidence
  • 3.5 cases per 1000 individuals per year (US).
  • 70% of all CTS cases occur in women.
  • 500,000 surgeries annually for CTS.
  • Surgery peaks in women between 45-55 years and in men older than 65 years.
Etiology
  • Any disorder that increases the volume of the contents of the carpal tunnel or that decreases the volume of the carpal tunnel will create a sustained rise in pressure within the tunnel that impinges on the median nerve.
  • CTS is also more than 2.5 times more likely in obese individuals (body mass index >29).
  • Risk Factors: people with rheumatoid tenosynovitis, edema, pregnancy, hypothyroidism, and post-Colles’ fractures.
Association with Occupation
  • Positive association between a combination of factors: force and repetition and/or force and posture.
  • Older patients have a different pattern of risk factors.
Pathogenesis
  • Normal tissue pressures are 7–8mm Hg. In CTS, these pressures rise above 30mm Hg, when wrist flexion or extension occurs. Pressures go as high as 90mm Hg when the wrist is fully flexed and up to 79.5mm Hg when the wrist is extended.
  • Unrelieved compression creates initial neurapraxia with segmental demyelination of axons.
Clinical Manifestations
  • Sensory symptoms in the median nerve distribution.
  • Pain may be located distally in the forearm or wrist and radiate into the thumb, index, and middle fingers. It may also radiate into the arm, shoulder, and neck.
  • Nocturnal pain is the hallmark of CTS.
  • Diminished two-point discrimination, diminished ability to perceive vibration and elevation of threshold in Semmes–Weinstein monofilament testing routinely occur.
  • Thenar weakness is seen in advanced cases.
  • Combined loss of grip strength, inability to pinch, and sensory loss cause clumsiness in the hands.
Medical Management
  • Diagnosis:
    • Provocation tests: Phalen's test, Tinel's test, carpal compression test, and the flick sign tests are used to replicate CTS symptoms.
    • Distal motor and sensory latencies and sensory NCV across the carpal tunnel are most frequently administered.
    • Ultrasonography is more helpful in estimating the severity of symptoms and nerve conduction deficit.
Treatment
  • For clients with mild symptoms, conservative management is generally instituted including steroid injection into the carpal canal to provide initial relief of symptoms.
  • Early management also addresses ergonomic measures and modification of the client's occupation.
  • Wearing of wrist splints to immobilize the wrist near neutral to minimize carpal tunnel pressures and client education are also instituted.
  • Surgical intervention is advocated for persons without resolution of symptoms following a traditional conservative approach for 2–3 months.
Prognosis
  • Relates directly to the severity of the nerve entrapment at diagnosis, clinical cause, and mode of treatment.

Sciatica

Incidence and Etiology
  • Radiculopathy occurring most often in individuals between the ages of 40 and 60 years in which the nerve root is affected, most typically by compression. Of those developing lumbosacral radiculopathy, 10%–25% develop symptoms that last more than 6 weeks.
Pathogenesis
  • Herniation of the intervertebral disk can impinge on the nerve root or structures innervated by the recurrent sinuvertebral nerve to cause pain.
Clinical Manifestations
  • When sensory fibers are affected, the pain will radiate into one or both legs.
  • Coughing, sitting, and sneezing worsen the pain.
  • Inflammatory chemical mediators released into the epidural space affect nearby nerve roots, without any direct compression of those roots.
Medical Management
  • Diagnosis: MRI is preferred to computed tomography (CT) scanning for lumbar spine imaging; however, because 60% of people without back symptoms have disk bulging on MRI, protrusion and bulges may not correlate with symptoms.
Treatment
  • Has shown that selective epidural injection of steroids at target nerve roots through the intervertebral foramina has offered short -term benefits for pain relief, as has the use of nonsteroidal antiinflammatory drugs (NSAIDs).
Prognosis
  • Subjects who were evaluated 1 year after diskectomy had recovery in unmyelinated and small myelinated fibers; the function of larger myelinated fibers did not improve.
Special Implications for the PTA: Sciatica
  • It has been recommended that physical therapy interventions emphasize the use of joint mobilizations and exercise for improvements in health in people with sciatica.
  • Outcome assessments such as the Oswestry Disability Index and the Patient-Specific Functional Scale should be used to quantify more meaningful functional changes in the quality of life of the individual with physical therapy intervention.

Idiopathic Facial Paralysis/Bell's Palsy

Incidence
  • A common clinical condition in which the facial nerve is unilaterally affected.
  • It affects 20 of 100,000 people each year.
  • Most common in persons between the ages of 15 and 45 years.
Etiology and Pathogenesis
  • Increasing evidence indicates that the primary cause of Bell's palsy is a latent herpes virus (herpes simplex type 1/herpes zoster) that has been reactivated.
  • Pain suggests that this disorder is a product of an inflammatory response.
  • Any agent that causes inflammation and swelling creates a compression that initially causes demyelination or axonal degeneration.
Clinical Manifestations
  • A unilateral facial paralysis develops rapidly, often overnight.
  • Paralysis of the muscles of facial expression on one side creates an asymmetric facial appearance.
  • If the lesion is proximal to where the fibers of the chorda tympani enter the facial nerve, the client will experience loss of taste on the affected side.
  • If the autonomic fibers are involved, the client will experience dry eye (lack of tearing) and will produce less but thicker saliva.
Medical Management
  • Diagnosis: Ask the client to wrinkle the forehead, close the eyes tightly, smile, and whistle while you observe for facial asymmetry.
  • Tests of facial nerve excitability will also indicate whether the paralysis is complete.
  • The LMN involvement of the facial nerve can be differentiated from an upper motor neuron (UMN) involvement.
Treatment
  • Treatment should begin as soon as possible and no later than 10 days after the onset of signs of paralysis.
  • Treatment with antiviral medications, such as acyclovir or acyclovir paired with corticosteroids, may aid in recovery.
Prognosis
  • Ninety-four percent of individuals with incomplete involvement make a full recovery, generally within 3 weeks.
  • Plastic surgery, using fascial slings to replace active muscle contraction, can help restore facial function when recovery does not occur.
  • Experiment animal use have indicated that electrical stimulation suppresses neuronal sprouting, some scientists have proposed that electrical stimulation should not be used.

Tardy Ulnar Palsy/Retroepicondylar Palsy

Anatomy
  • The ulnar nerve arises from the lower trunk of the brachial plexus and carries fibers from C8 and T1 nerve roots. At the elbow, it passes behind the medial epicondyle and then passes between the two heads of the flexor carpi ulnaris.
Etiology
  • Ulnar nerve palsy is a common complication of fractures (elbow region).
  • A late or tardy ulnar palsy may occur years after a fracture and is associated with callus formation or a valgus deformity of the elbow.
Pathogenesis
  • Recurrent microtrauma associated with fracture causes recurrent cubital subluxations, as well as entrapment at the entrance or exit of the cubital tunnel.
  • Compression will initially cause neurapraxia with demyelination of the nerve; if the pressure goes unrelieved, this will progress to axonotmesis, with denervation occurring below the level of the elbow.
Clinical Manifestations
  • Expect a claw hand deformity with metacarpophalangeal (MCP) extension and interphalangeal (IP) flexion of the ring and little fingers because of the unopposed action of the extensor muscle group. Paralysis of the FCU produces a radial deviation of the hand when wrist flexion is attempted.
Medical Management
  • NCV studies are helpful only when sufficient nerve damage has occurred to produce definite strength or sensory changes in the hand.
  • To relieve the compression, either decompression, the preferred method (medial epicondylectomy), or transposition of the ulnar nerve to the anterior aspect of the elbow is performed.
  • Symptomatically, the claw hand deformity should be treated with a splint that blocks MCP hyperextension (lumbrical bar) and allows the extensor digitorum to extend the IP joints.
Prognosis
  • Decompression surgery should have a complete restoration of function quickly, but recovery after transposition surgery may take up to 6 months.

Thoracic Outlet Syndrome (TOS)

Definition
  • Entrapment syndrome caused by pressure from structures in the thoracic outlet on fibers of the brachial plexus at some point between the interscalene triangle and the inferior border of the axilla. In addition, vascular symptoms can occur because of pressure on the subclavian artery.
Etiology
  • Neurologic structures becoming entrapped, arterial and venous structures also may be affected individually or in combination.
  • Practically, TOS can be divided into three groups: neurogenic (compression of brachial plexus), vascular (compression of the subclavian artery and/or vein), and disputed (nonspecific TOS with chronic pain and symptoms of brachial plexus involvement).
Pathogenesis
  • Chronic compression of nerve roots or proximal plexus and arteries between the clavicle and first rib or impinging musculature results in edema and ischemia in the nerves. Causes segmental demyelination and axonotmesis.
Clinical Manifestations
  • Signs and symptoms reflect the structures that have been compressed.
  • When the nerves are compressed, most people report paresthesias and pain in the arm; most often these are nocturnal.
  • If the lower plexus is compromised (C7 to T1), pain and numbness occur in the posterior neck and shoulder, medial arm and forearm, and radiate into the ulnar innervated digits of the hand.
Medical Management
  • There is no universally accepted reliable diagnostic test for TOS, Adson's maneuver appears among the most effective.
  • NCV allows the examiner to pinpoint the lesion, either because of a change in amplitude or a slowing in conduction velocity.
Treatment
  • The initial treatment of the person with TOS is conservative when symptoms are mild to moderate in severity.
  • Surgical management of TOS is reserved for cases that are refractory to postural and exercise correction and those with vascular compromise.
Prognosis
  • Factors that are associated with long-term disability include preoperative depression, single status, and less than high school education.