Transcript Brachial Plexopathies - VCU Physical Medicine & Rehabilitation

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
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Closed
–Traction Injuries
–Radiation
–Tumor (1^2^)
–Surgical Positioning
–Brachial Neuropathy
–Thoracic Outlet Syn.
–Hematoma
–Blunt trauma/Fx’s
Open
Neurovascular
Gunshot Wound
Laceration
Surgical Trauma
Needles
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 C56 (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
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Shoulder dislocations
Humeral neck fractures
GSW or misplaced needles
General anesthesia, neuralgic amyotrophy
BP Injuries (cont.)
• Musculocutaneous Nerve
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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
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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 Concussionneuropraxia)
• 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
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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
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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