Brachial Plexopathies by yadd8eQB

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									Brachial Plexopathies


  William McKinley, MD
   Associate Professor
  Department of PM&R
      Incidence & Prevalence
• 10% of all peripheral nervous system
  lesions involve brachial plexus
• 14% of upper extremity neurological
  disorders due to brachial plexopathy
• Bimodal Distribution
  –Obstetric: male/female 1:1, R>L
  –Age 20-30 y/o males 2^MVA, knife/bullet
  wounds - unilateral dominant limb
                 Etiologies
–      Closed                  Open
    –Traction Injuries      Neurovascular
    –Radiation              Gunshot Wound
    –Tumor (1^2^)           Laceration
    –Surgical Positioning   Surgical Trauma
    –Brachial Neuropathy    Needles
    –Thoracic Outlet Syn.
    –Hematoma
    –Blunt trauma/Fx’s
              BP Anatomy
• Anatomy
  –Ventral Rami C5-T1
  –Prefixed (C4) or Postfixed (T2)
  –RTDCB, “Palindrome” (53635)
  –Preganglionic vs postganglionic
  –Supraclavicular (roots & trunks) vs
  Infraclavicular (cords & branches)
  –cords are named (lateral, posterior, medial)
  by their relationship to the axillary art.
  –Lateral cord (C5, 6, 7), Medial cord (C8,
  T1), Posterior cord (C5, 6, 7, 8 & T1)
     BP Injuries: Classification
• Supraclavicular (roots & trunk)
• Root Avulsions
  – Poor prognosis
  – affects posterior primary rami (pasaspinal m’s)
  – Sensory NCS potentials normal
• Proximal Root Nerve Lesion
  –Dorsal Scapular Nerve
  –Long Thoracic Nerve
  –Suprascapular Nerve
          BP Injuries (cont.)
• Upper Trunk “Erb-Duchenne”
  –Most common BP Injury
  –Weakness at shoulder, EF, sensory loss
  C5-6 (Positioning: Add & IR)
  –Prognosis: Best
  –Causes: Trauma, Traction
  –Obstetrical
  –Brachial Neuropathy
• Lower Trunk “Dejurine-Klumpe”
  –Clinical: Horners
  –Metastatic Tumor, Pancoast Tumor
            BP Injuries (cont.)
• Infraclavicular (Cords/Branches)
• Axillary Nerve
  –   Shoulder dislocations
  –   Humeral neck fractures
  –   GSW or misplaced needles
  –   General anesthesia, neuralgic amyotrophy
            BP Injuries (cont.)
• Musculocutaneous Nerve
  –   Anterior shoulder dislocation
  –   arm extension
  –   Weight lifting
  –   Malpositioning
  –   Neuralgic Amyotrophy
• Radial Nerve
  – GSW or trauma to axilla
  – Improper crutch fitting
          BP Injuries (cont.)
• Median Nerve
• Ulnar Nerve
  – Thoracic Outlet Syndrome (TOS) (NCS-ulnar,
    sensory, motor and median motor
    abnormalities)
• Panplexopthy
  –Causes: Trauma, Severe Traction
  –Metastasis/Radiation
• Prognosis: Poor
          Mechanism of Injury
•   Traction/Stretch - trauma, positioning
•   Contusion/compression - trauma, tumor
•   Laceration - trauma, bullet, knife
•   Ischemia - trauma, vascular
   Preganglionic vs Postganglionic
• Preganglionic = prox. to “sensory” dorsal root
  gang. (distal to “motor” ant. horn cell)
  – Nerve Root Avulsion -Conn. Tissue Covers spinal
    nerve, traction force transferred to dura = root rupture!
    –Ventral roots move vulnerable - sensation often
    spared, motor lost
    –78% of BP result in some root avulsion
    –C8 and T1 are more susceptiple (lack c.t.)
  – Root avulsion = Poor prognosis!
  – Sensation lost... but sensory NCS is Normal
  – Paraspinal M’s abnormal on EMG
  – Positive “Axon reflex test”
         Etiologies of Injury
• Closed trauma - MVA (motorcycle), back
  pack palsy, fractures (humerus, shoulder)
• Burners (“stingers”) - sports
• Birth Injuries
  –Supraclavicular
  –Occurring during L&D (not forceps)
• Perioperative
  –Etiology: traction and positioning
  –Primarily upper plexus
  –Good prognosis
                Etiologies (cont.)
• Violence-related
  –Knife, bullets (Laceration or Concussion-
  neuropraxia)
• Primary tumors: usually benign (Schwannomas)
• Metastatic tumors
  –Lung and breast (also lymphoma and sarcoma)
  – Lung (pancoast tumor - C8, T1, lymphadenopathy)
    •Radiation therapy
       –Greater than 6 but less than 24 months
       –Unlikely with less than 6000 R
       –Radiation plexopathy favors upper trunk. Mestatatic
         Neuralgic Amyotrophy
• Described by Parsonage & Turner in 1948
• Characteristics: Acute onset of shoulder pain of
  a deep, stabbing, burning nature, aggravated by
  shoulder movement, muscles may be tender on
  exam. pain may radiate to the trapezius, arm,
  forearm or hand. Intense pain last up to 3 weeks
  and is then replaced by dull ache that may persist
  for months. Within 2 weeks the patients c/o
  weakness involving the painful limb- many
  associate pain subsiding as weakness begins.
  Muscle wasting occurs rapidly.
         Neuralgic Amyotrophy
• Synonyms
  –Brachial
  Neuropathy/Plexitis/Neuritis/Plexopathy
  –Parsonage-Turner syndrome
• Incidence: 1.64 per 100,000 population
• Male: 2:1
• Age of Onset: usually 20-40 years (3 mo - 74
  years reported)
• Antecedent or Associated Illness: Roughly
  45% patients
  –Serum Inoculation Sickness
  –Typhus, Variola, Diptheria, Influenza,
  Triple Vaccine & Tetanus Toxiod
• Weakness
  –Shoulder Girdle (C5, 6) - 50%
  –Single Peripheral Nerve - 10%
  •Radial LT, Axillary, SS, Phrenic
• Senory Deficits: 67%
   –Axillary N and Lateral Antebrachial
  Cutaneous N
• Bilateral: 33% (right 54%)
• Histopathology: wallerian degeneration
  from axonal loss
• Prognosis: Good
• Natural History: Functional recovery 36%
  first year, 75% second year, 89% third year
• Rehabilitation: no therapies effectively alter
  eventual outcome
   –Daily PROM is important to prevent
  contractions
 Pathophysiology of BP Lesions
• Neuropraxia: Conduction Block
  –Ischemic: short duration, recovery minute
  to hours
  –Demyelinative: physical damage to
  segment of myelin, necessitating
  remyelination. Denervation (axon loss) does
  not ensue; several weeks to months to
  recover
  –Good prognosis
• Axonotmesis: Axonal Loss without
  “supporting” Structural (conn. tissue)
  Damage
  –Axon distal to injury site undergoes
  degeneration.
  –Restored function often occurs: nerve
  length and extent of damage are
  considerations to recovery
•
• Neurotmesis: Axon Loss with supporting
  Structural Damage
  –Axon, Endoneurium, Perineurium,
  Epineurium destroyed.
  –Axons may regenerate along aberrant
  pathways, misdirection of motor and
  sensory nerves, scarring impedes nerve
  regrowth.
  –Poor prognosis
         History & Physical
• Expertise in anatomy and functional
  anatomy prerequisite!
• Hx: mechanism of injury, change of sx, pain
• Observation: Horners synd (ptosis, myosis),
  winging of scapula, atrophy, skin changes
• Exam: motor, sensory, DTR, ROM, tinnels,
  vascular
• Additional studies: EMG/NCS, Xray
        Differential Diagnosis
• Peripheral nerve injuries
• Radiculopathies
• SCI
    Radiologic (and other) Studies
•   Electromyography
•   C-Spine, shoulder xrays
•   MRI
•   Myelography
•   Axon reflex testing
    –Histamine “Triple response of Bonney”
    –Vasodilation, wheal, flare
    –NL in “preganglionic (poor prog)
    –ABNL in “post” (better prog)
     Electrodiagnostic Eval of
      Brachial Plexus Injury
• Summary
  –motor and sensory potential (esp
  amplitude) and needle EMG (PSW, Fibs)
  are most sensative indicators of axonal loss
  –Paraspinal EMG usually normal.
  Abnormalities indicate preganglonic injury
  (radiculopathy, SCI)
  –SSEP, F-waves and H-reflexes (LS Plexus)
  may be delayed or absent b/c depend on
  proximal conduction
• –Poor Prognosis: preganglionic,
  panplexopathy
• Conduction Block
  –Drop in CMAP amplitude exceeding 20%
  without temporal dispersion
  –Failure of afferent and efferent impulse
  propagation across affected site
  –Prognosis evaluation at appx 10 days to 2
  weeks
• –SNAP, CMAP, NCV, EMG should be
  normal
  –Decreased recruitment may be present
  with increasing force production
• Demyelination
  –Slowing of NCV 25-30%
  –Increased temporal dispersion
• Axonal Loss
  –Wallerian degeneration ensues
  –Sensory loss evidenced by decreased
  amplitude or loss of potential, but
  preganglionic lesions, like radics, have
  preserved SNAP with sensory loss which
  has poor prognosis. 7-10 days SNAP’s
  disappear.
• –Compound Motor Action Potential has
  decreased amplitude that precedes SNAP
  changes secondary to sensory nerve lack of
  NMJ, which disintegrates at 6-7 days. It is
  important to compare side amplitude
  difference. (>50% signifies axon loss)
• –EMG Shows spontaneously depolarization
  evidenced by fibrillations and positive sharp
  waves that can occur at 7-10 days in
  muscles close to the injury and 4-6 weeks in
  muscles distal from lesion. Increased
  insertional activity and decreased
  recruitment also present.
  –NCS may be normal until late
    Conservative Management
• Strengthening, ROM
• Sling for protection and subluxation
• One-handed activities
• Complicated braces ( ? usefulness)
• Pain management (begin early, do not
  amputate, meds), stellate ganglion blocks
• Edema control
• Psychological counseling
• Vocational support
         Surgical Treatment:
           Generalizations
• No surgery for preganglionic injuries
• Surgical treatment in closed “total” (whole
  plexus) supraclavicular injuries
• Timing: 6-12 months
• Alternative: amputation plus arthrodesis
  plus prosthesis
• C8-T1 - defer to surgical reconstruction
• C5-7 - better prognosis, shoulder
  arthrodesis plus tendon transfer
      Lumbosacral Plexopathy
• Lumbar plexus L1-3(4)
  –Terminal nerves - femoral, obturator
  –Sensory loss: L1-3(4)
  –Weakness: hip flexors, knee extensors, hip
  adductors
  –Differentiate from femoral nerve injury
  (no hip adductor weakness)
• Sacral plexus (L4-S2)
  –Terminal nerves - sciatic (tibial &
  peroneal), Gluteal (superior & inferior)
  –Differentiate from sciatic n injury (no hip
  abductor/extensor weakness)
  –May include anal sphincter muscles
• Etiology: pelvic injury, retroperitoneal
  hematoma, neoplasm, RT, traction,
  idiopathic

								
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