SLIDE CONTENT — BRACHIAL PLEXUS (First Half, ~20 Slides)

SLIDE 1: Title Slide

SLIDE 2: Overview — What is the Brachial Plexus?

• Contains approximately 100,000–160,000 nerve fibers
• Originates from C5 to T1 nerve roots
• Provides motor and sensory supply to the shoulder girdle, upper trunk, and upper limb
• Also supplies autonomic fibers to the inferior cervical ganglion

SLIDE 3: Five Components of the Brachial Plexus

1. Roots — Five roots: C5, C6, C7, C8, T1
2. Trunks — Upper, Middle, Lower
3. Divisions — Two divisions from each trunk (anterior and posterior)
4. Cords — Three cords: Lateral, Medial, Posterior
5. Terminal Nerves — Final branches supplying the limb

SLIDE 4: Roots — Location & Anatomy

• Roots are situated between scalenus anterior and scalenus medius muscles
• Located deep to the sternocleidomastoid muscles
• C5–C6 → Upper trunk
• C7 → Middle trunk
• C8–T1 → Lower trunk
• Root-level branches: Dorsal scapular nerve (C5), Long thoracic nerve (C5–C7)

SLIDE 5: Trunks of the Brachial Plexus

• Upper trunk: Anterior rami of C5 and C6
• Middle trunk: C7
• Lower trunk: C8 and T1
• Trunks commence from the lateral border of the scaleni
• Each trunk divides into anterior and posterior divisions
• At trunk level: Suprascapular nerve is the only branch, arising from the upper trunk (supplies supraspinatus and infraspinatus)

SLIDE 6: Cords — Formation

• All posterior divisions unite → Posterior cord
• Anterior divisions of upper + middle trunk → Lateral cord
• Anterior division of lower trunk → Medial cord

SLIDE 7: Branches of the Medial Cord

• Medial pectoral nerve
• Medial brachial cutaneous nerve
• Medial antebrachial cutaneous nerve
• Ulnar nerve
• Medial head of the median nerve

SLIDE 8: Branches of the Lateral & Posterior Cords

• Musculocutaneous nerve
• Lateral head of median nerve
• Lateral pectoral nerve

• Subscapular nerves
• Thoracodorsal nerve
• Axillary nerve
• Radial nerve

SLIDE 9: Clinically Relevant Localizing Points

1. C5–C7 anterior primary rami — assessed by EMG of rhomboids (C5) and serratus anterior (C5–C7). Abnormality = lesion proximal to upper/middle trunk
2. C8–T1 level: No branching at this level; mixed spinal nerve contains preganglionic sympathetic fibers — involvement causes Horner syndrome → localizes lesion proximal to lower trunk
3. Pectoral nerves — derived from most proximal cord; used to differentiate diffuse supraclavicular from infraclavicular lesions

SLIDE 10: Supraclavicular vs. Infraclavicular — Key Distinction

SLIDE 11: Brachial Plexopathy — Introduction

• Brachial plexus is highly vulnerable to traction injury — situated between two mobile structures (neck and shoulder)
• Also liable to injury due to its superficial location
• Surrounding structural diseases can also affect the plexus
• Supraclavicular and infraclavicular plexopathy differ in incidence, severity, and prognosis

SLIDE 12: Supraclavicular Brachial Plexopathy

• Most common form of brachial plexopathy
• 3–7 times more common than infraclavicular
• Out of 31 possible permutations, 5 clinically important presentations:
  • C5–C6 (Upper trunk)
  • C5–C7
  • C8–T1 (Lower trunk)
  • C7–T1
  • C5–T1 (Complete)
• Upper plexus lesions (C5–C6 / upper trunk) are the most common subgroup

SLIDE 13: Causes of Supraclavicular Plexopathy

• Obstetric injury
• Post-anesthetic paralysis
• Neuralgic amyotrophy (Parsonage-Turner syndrome)
• Pack palsy
• Burner syndrome
• Pancoast syndrome
• Metastatic plexopathy
• Neurogenic thoracic outlet syndrome
• Post-median sternotomy

SLIDE 14: Upper Plexus Lesion (C5–C6 / Upper Trunk)

• Upper limb hangs beside trunk
• Extended at the elbow
• Adducted and internally rotated at shoulder
• Palm visible from the rear
• Weakness of: Rhomboids, serratus anterior, supraspinatus, infraspinatus, deltoid, biceps brachialis, brachioradialis
• Sensory loss: Restricted to over deltoid, outer arm, and forearm

SLIDE 15: Lower Plexus Lesion (C8–T1 / Lower Trunk)

• Wasted medial forearm and hand
• Weakness of all ulnar innervated muscles
• Weakness of median innervated hand muscles
• Weakness of muscles with anterior interosseous nerve supply
• Weakness of some radial innervated muscles (extensor pollicis indicis proprius, extensor pollicis brevis)
• Sensory loss: Medial aspect of forearm, extending up to arm or hand (4th and 5th digits)
• Horner syndrome suggests C8–T1 root lesion

SLIDE 16: Prognosis — Upper vs. Lower Plexus

1. Pathology is usually demyelinating → complete recovery more likely
2. Location of injury is nearer to muscles → reinnervation more complete
3. Lesions are usually extraforaminal → amenable to surgery

• These advantages are lacking
• Hence they have poor recovery

SLIDE 17: Infraclavicular Brachial Plexopathy

• Less common than supraclavicular
• Affects the cord or nerve or both
• A cord lesion typically produces deficits in the distribution of two or more peripheral nerves

SLIDE 18: Infraclavicular — Cord-Specific Deficits

SLIDE 19: Common Causes of Brachial Plexopathy (Table 3.21)

• Fall from height (especially on shoulder)
• Trauma, Sports injuries
• Motor vehicle accident
• Obstetric palsy
• Cardiac surgery / median sternotomy

• Pack strip palsy (supraclavicular)
• Crutch (infraclavicular)
• Hematoma, aneurysm, vascular malformation

SLIDE 20: Neurophysiological Assessment — Aim & Questions

1. Is brachial plexopathy present?
2. Where is it located — supraclavicular or infraclavicular?
3. Is it partial or complete?
4. Is nerve continuity maintained (neurapraxia, axonotmesis) or lost (neurotmesis)?
5. Which part is involved — upper (C5, C6, C7) or lower (C8, T1)?
6. Preganglionic or postganglionic?
7. What are associated comorbidities?
8. Is the patient likely to benefit from surgery?
9. What is the prognosis?

SLIDE 21: Neurophysiological Tests Used

1. Nerve Conduction Studies — helps localize lesion immediately after injury; baseline studies best at ~3 weeks post-injury (Wallerian degeneration)
2. F Waves
3. Somatosensory Evoked Potentials (SEPs)
4. Needle EMG — at one time shows degenerative changes; serial studies demonstrate clinically significant regeneration and help determine axonotmesis vs. neurotmesis

SLIDE 22: Pathophysiological Response After Brachial Plexus Lesion

• Limited pathophysiological response: axonal loss + Wallerian degeneration
• Motor fibers: Conduction failure noted by Day 7
• Sensory fibers: Conduction failure noted by Day 11
• Demyelinating changes result in conduction block and conduction slowing
• EMG + NCS together: Differentiate neurapraxia from more severe grades of injury

SUPRACLAVICULAR PLEXUS ASSESSMENT — PPT CONTENT (~20 Slides)

SLIDE 1: Title Slide

SLIDE 2: Why Neurophysiological Assessment?

• Size and complexity of brachial plexus lesions demand clinical AND neurophysiological expertise
• No single EMG or nerve conduction study is diagnostic alone
• An extensive evaluation is justified for:
  • Localization
  • Defining pathophysiology
  • Determining severity
• Brachial plexus lesions are regional — they do not generally affect all elements
• Electrodiagnostic testing should be relevant and focused to screen the lesion

SLIDE 3: Key Questions the Assessment Must Answer

1. Is brachial plexopathy present?
2. Where is it located — supraclavicular or infraclavicular?
3. Is it partial or complete?
4. Is nerve continuity maintained (neurapraxia, axonotmesis) or lost (neurotmesis)?
5. Which part is involved — upper (C5, C6, C7) or lower (C8, T1)?
6. Preganglionic or postganglionic?
7. What are associated comorbidities?
8. Is the patient likely to benefit from surgery?
9. What is the prognosis?

SLIDE 4: Neurophysiological Tests Used

1. Nerve Conduction Studies (NCS)
2. F Waves
3. Somatosensory Evoked Potentials (SEPs)
4. Needle EMG

SLIDE 5: Nerve Conduction Studies — Basics

• Conduction in brachial plexus measured by stimulating Erb's point using surface or needle stimulation
• Needle stimulation is preferred to avoid:
  • Risk of pneumothorax
  • Transmitting infections
• Surface stimulation → stimulates adjacent nerves (volume conduction) — reduced by needle recordings or collision technique

SLIDE 6: Muscles Used in Nerve Conduction (Localization Value)

• Reference: Gassel, 1964
• Latency should always be compared with the uninvolved side, keeping electrode distance equal

SLIDE 7: Amplitude vs. Latency — What to Measure

• Latency measurements are not reliable due to volume conduction in surface recording and restricted recording area with needle electrodes
• A right-to-left latency difference exceeding 0.6 ms is a better indicator than absolute latency in unilateral lesions (Kimura, 1989)
• Amplitude of CMAP: Stimulating median/ulnar nerve at wrist and recording from hand muscle gives indication about axon loss; same applies to SNAPs
• Latency measurements of triceps are not reliable due to vertical orientation of the endplate (McComas et al., 1984)

SLIDE 8: NCS Timing After Brachial Plexus Injury

• NCS may help localize lesion immediately after injury
• However, baseline EMG studies are best performed ~3 weeks post-injury by which time Wallerian degeneration is likely to occur
• CMAP: Begins declining by Day 2, lowest by Day 7
• SNAP: Starts declining by Day 5, lowest by Day 11
• Needle EMG: Reveals fibrillations after 3 weeks; motor unit dropout seen immediately but not apparent in mildly affected patients

SLIDE 9: Clinico-neurophysiological Correlation

• Decline in CMAP is proportional to muscle weakness
• Decline in SNAP is proportional to proprioceptive sensory loss
• Demyelinating lesion with conduction block → weakness disproportionate to CMAP and dropout of MUP
• Lesions distal to dorsal root ganglia → reduced SNAP and CMAP
• Preganglionic lesions after 11 days → reduced CMAP but normal SNAP
• Sensitive indicator of axon loss = fibrillations for motor; reduction of SNAP amplitude for sensory

SLIDE 10: Preganglionic vs. Postganglionic — NCS Key Point

• SNAPs will be present in preganglionic lesions when an anesthetic finger is stimulated but absent in postganglionic or combined pre- and postganglionic lesions
• Great sensory overlap in index and middle fingers and thumb — interpretation of SNAPs must be done cautiously in C5, C6, C7 lesions

SLIDE 11: Nerves Assessed in NCS for Supraclavicular Lesions

• Median, Ulnar, Radial — already well described
• Additional nerves important for supraclavicular assessment:
  • Suprascapular nerve
  • Long thoracic nerve
  • Axillary nerve
  • Musculocutaneous nerve
  • Lateral antebrachial cutaneous (LABC) nerve
  • Medial antebrachial cutaneous (MABC) nerve

SLIDE 12: F Waves — Role in Assessment

• F waves assess conduction in the proximal portion of nerves, plexus, or roots
• Useful in assessing plexopathies
• However, F waves do not have much localizing value in brachial plexopathies
• Used as supplementary data — not a standalone test

SLIDE 13: Somatosensory Evoked Potentials (SEPs) — Overview

• Obtained by stimulating various nerves — usually median or ulnar
• Recorded from:
  • Erb's point
  • Posterior cervical spine
  • Contralateral somatosensory cortex
• SEPs are more complex than sensory nerve conduction and provide no extra advantage in routine evaluation
• Intraoperative SEPs are valuable — can assess C5 fibers (not evaluated by SNCS or conventional SEPs)

SLIDE 14: Intraoperative SEPs — Surgical Application

• Intraoperative action potentials performed during surgical exploration of brachial plexus 3–4 months after injury
• Stimulating and recording across the site of lesion allows evaluation of conduction through brachial plexus
• If nerve action potentials can be recorded → substantial number of large fibers traversing the lesion site remain intact
• Unrecordable action potential = indication for resection; spontaneous recovery is unlikely (Kline et al., 1986)

SLIDE 15: Needle EMG — Role and Advantage

• Needle EMG can detect the minimal amount of axon loss
• Helps evaluate several nerves that cannot be evaluated by NCS
• Can reveal minimal residual innervation with severe but incomplete axon loss
• Shows early reinnervation before it is clinically apparent
• Chronicity of lesion determined by changes in MUP configuration
• Fibrillations in paraspinal muscles suggest root involvement (paraspinal muscles derive their innervation from posterior primary rami)

SLIDE 16: EMG — Timing and Extent

• Presence of fibrillations = sensitive indicator of axon loss
• Takes ~3 weeks to appear
• For optimal information:
  • EMG examination should be extensive
  • Sufficient NCS should be performed to evaluate motor and sensory fibers of brachial plexus
  • At least two muscles supplied by each motor component of brachial plexus must be included in EMG
• Evaluation of "non-standard" nerve conduction should be carried out to evaluate upper and middle trunks as well as lateral and posterior cords

SLIDE 17: Summary — Supraclavicular Plexus Assessment Overview

• Brachial plexus lesions are regional → testing must be relevant and focused
• Upper plexus (C5–C6): No sensory nerves for C5 dorsal root ganglia or postsynaptic fibers
• Middle plexus (C7): Sensory nerves evaluating it are median nerve recording from index and middle fingers
• Lower plexus (C8–T1): Ulnar sensory conduction from little finger assesses C8 dorsal root ganglia, postganglionic fibers, and lower trunk

SLIDE 18: Upper Plexus Assessment (C5–C6) — Sensory NCS

• No sensory nerves for C5 dorsal root ganglia or its postsynaptic fibers
• LABC nerve and median SNCS from thumb → assess C6 dorsal root ganglia and postganglionic fibers
• Should be carried out bilaterally
• Side-to-side difference >50% suggests abnormality
• Superficial radial NCS and median NCS from index finger also assess upper plexus elements — though less reliably:
  • Superficial radial: 60% sensitivity
  • Median NCS from index finger: 20% sensitivity (Ferrante and Wilbourn, 1995)

SLIDE 19: Upper Plexus Assessment (C5–C6) — Motor NCS & EMG

• Musculocutaneous motor NCS recording from biceps
• Axillary recording from deltoid → evaluate upper plexus elements; compare with unaffected side

• C5,6 Radial muscles
• C5,6 Axillary muscles
• C6 Median innervated muscles
• Levator scapulae, rhomboid, serratus anterior, spinati → helpful in defining proximal extent of lesion

SLIDE 20: Middle Plexus Assessment (C7)

• Middle plexus contains fibers from C7 root
• Sensory nerves evaluating it:
  • Median nerve recording from index finger — about 80% sensitivity
  • Median nerve recording from middle finger — about 70% sensitivity
  • Superficial radial nerve evaluates it in ~40% of instances
• Motor NCS: Radial motor NCS from extensor digitorum communis or anconeus can be evaluated
• Needle EMG from selected muscles:
  • Triceps, anconeus, pronator teres, flexor carpi radialis
• Isolated middle plexopathies are rare → should prompt a search for adjacent upper and lower plexus lesions

SLIDE 21: Lower Plexus Assessment (C8–T1)

• Lower plexus contains fibers from C8 and T1 roots
• Ulnar sensory NCS recording from little finger → assesses C8 dorsal root ganglia, postganglionic fibers, and lower trunk
• MABC nerve study → assesses the corresponding T1 structures
• These two studies are complimentary at prenerve trunk level
• Ulnar cutaneous nerve study is superfluous if the same brachial plexus lesion as the ulnar study is already present (Ferrante and Wilbourn, 1995)
• Ulnar motor NCS recording from abductor digiti minimi and median recording from abductor pollicis brevis → evaluate lower brachial plexus
• Radial motor NCS from extensor indicis proprius → excludes medial cord lesion; involvement excludes lower trunk lesion

SLIDE 22: Three Motor NCS for Pretrunk vs. Lower Plexus Differentiation

1. Radial — evaluates solely C8 root
2. Ulnar — evaluates C8 root predominantly, and median T1 root almost solely
3. Ulnar recording from first dorsal interosseous — reflects same lower plexus elements as abductor digiti minimi; however, lower plexopathies may affect these two CMAPs differently — hence both are often needed

• EMG needed to evaluate muscles innervated by C6 T1 median, C8 T1 ulnar, and C8 radial motor fibers

SLIDE 23: Reinnervation — Key Features

• As time passes, features of reinnervation become apparent
• Axonal growth rate: ~2.5 cm/month
• Collateral sprouting occurs if axons are intact
• Degree of reinnervation depends on:
  • Distance of injury from the muscle
  • Severity of axonal loss
• Time distance factor is crucial
• A denervated muscle fiber survives 18–24 months without reinnervation
• Distance of 2 ft is critical — sensory recovery is possible even later

ADVANCED SUPRACLAVICULAR PLEXUS ASSESSMENT — 10 High-Level Slides

SLIDE 1: Preganglionic vs. Postganglionic Lesions — Electrophysiological Dissection

• Dorsal root ganglion (DRG) = the deciding landmark
• Preganglionic lesion = injury proximal to DRG (avulsion from spinal cord)
• Postganglionic lesion = injury distal to DRG

SLIDE 2: Wallerian Degeneration Timeline — Precision Electrophysiology

SLIDE 3: The SNAP Paradox in C5–C6 Root Avulsions — Why Sensory NCS Can Mislead

• C5 root avulsion → no SNAP abnormality because there is no C5 sensory nerve accessible for testing
• C6 assessment requires LABC nerve and median SNCS from thumb — these assess C6 DRG and postganglionic fibers
• A >50% side-to-side amplitude difference = significant
• Superficial radial NCS from index finger detects C6 abnormality in only 60% of cases
• Median NCS from index finger detects it in only 20% of cases

SLIDE 4: Conduction Block vs. Axonal Loss — How to Differentiate Electrophysiologically

• CMAP amplitude reduced or absent when stimulating proximal to lesion
• CMAP normal or preserved when stimulating distal to lesion
• SNAP normal
• No fibrillations on EMG (no Wallerian degeneration)
• Weakness disproportionately severe relative to CMAP reduction
• MUP dropout present

• CMAP reduced both proximal AND distal to lesion (after Day 7)
• SNAP reduced (if postganglionic)
• Fibrillations present at 3 weeks
• CMAP reduction proportional to weakness

SLIDE 5: Serial Neurophysiological Evaluation — The Only Way to Determine Axonotmesis vs. Neurotmesis

• Recordable NAP across lesion → large fibers traversing intact → do NOT resect
• Unrecordable NAP → indication for resection; spontaneous recovery unlikely (Kline et al., 1986)

SLIDE 6: EMG Strategy for Defining Proximal Extent — Systematic Root-by-Root Mapping

• Paraspinal muscle fibrillations = root-level involvement (posterior primary rami)
• Rhomboid fibrillations (dorsal scapular nerve, C5) = most proximal supraclavicular marker
• Serratus anterior fibrillations (long thoracic nerve, C5–C7) = confirms root/trunk-level lesion

SLIDE 7: The C7 Middle Plexus Lesion — Why It Is a Diagnostic Trap

• Sensory nerve detection rates are low — median recording from index finger: 80%, middle finger: 70%, superficial radial: 40%
• C7 contributes to multiple nerves — median, radial, and ulnar — making isolated deficits unclear
• C7 is the root of symmetry — C6 and C8 on either side have similar contributions, masking C7 deficits

• Radial motor NCS from extensor digitorum communis or anconeus (pure C7 muscle)
• Anconeus NCS is highly specific for C7 root

• Triceps (most reliable C7 indicator)
• Anconeus
• Pronator teres
• FCR

SLIDE 8: Reinnervation Electrophysiology — Detecting Recovery Before It Is Clinically Visible

• If nascent MUPs appear on EMG at 3–6 months → do not operate, spontaneous recovery underway
• If no MUPs and unrecordable intraoperative NAP → proceed with surgical exploration and grafting
• EMG thus directly guides the surgical decision window

• At 2.5 cm/month → injury at nerve root level, 30 cm from target muscle → reinnervation expected at ~12 months
• If no EMG evidence of reinnervation by expected time → reassess surgical candidacy

SLIDE 9: Intraoperative Neurophysiology — Supraclavicular Surgical Decision-Making

• Surgical exploration of brachial plexus at 3–4 months post-injury (after Wallerian degeneration is complete and clinical plateau established)

• Stimulate and record across the site of lesion using direct nerve action potential recording
• Assesses C5 fibers — otherwise not evaluable by conventional SNCS or SEPs

SLIDE 10: Prognostic Electrophysiology — Integrating All Parameters to Predict Outcome

• Preserved or mildly reduced SNAP amplitude (postganglionic, demyelinating)
• Conduction block pattern (neurapraxia) — complete recovery expected
• Early appearance of nascent MUPs (3–6 months)
• Recordable NAP intraoperatively
• No paraspinal fibrillations (extraforaminal location)
• Upper plexus (C5–C6) lesions — location nearer to muscles, more complete reinnervation

• Normal SNAP with absent CMAP + paraspinal fibrillations = preganglionic avulsion — surgical repair not possible
• Unrecordable NAP intraoperatively
• Lower plexus (C8–T1) involvement — lacks advantages of upper plexus (deeper, longer reinnervation distance, often intraforaminal)
• Absent fibrillations persisting beyond 18–24 months = irreversible muscle fibrosis
• Horner syndrome = C8–T1 root avulsion with sympathetic chain involvement

SUPRACLAVICULAR PLEXUS ASSESSMENT — EXPERT LEVEL (8 Slides)

SLIDE 1: Dorsal Root Ganglion as the Electrophysiological Fulcrum — The Anatomical Basis of the SNAP Paradox and Its Exceptions

• A preganglionic avulsion severs the central process only
• The peripheral process remains trophically supported by the intact DRG
• Therefore: SNAP is preserved despite complete clinical anesthesia — Wallerian degeneration does NOT occur peripherally

• If SNAP is used as the sole determinant of postganglionic lesion → C5–C6 avulsions will be systematically misclassified as postganglionic
• C5 has no accessible sensory nerve — there is no sensory NCS for C5 DRG or its postsynaptic fibers whatsoever
• C6 via LABC and median thumb SNCS: detects postganglionic C6 pathology — but a normal result does NOT exclude intradural C6 root avulsion

1. Paraspinal fibrillations (posterior primary ramus involvement)
2. Absent cortical SEP with normal peripheral SNAP
3. Horner syndrome (preganglionic sympathetic disruption at C8–T1)
4. Rhomboid + serratus anterior denervation (branches arise before scalene triangle)
5. Absent NAP intraoperatively with normal distal SNAP

SLIDE 2: Dissecting the Wallerian Degeneration Gradient — Why Single-Timepoint NCS Is Epistemically Insufficient in Supraclavicular Injuries

• Supraclavicular lesions involve long proximal segments — Wallerian degeneration travels a greater distance distally
• If NCS is performed between Day 2–5 post-injury: CMAP may already be declining but SNAP appears normal — this falsely mimics a motor-only or preganglionic pattern
• If NCS is performed before Day 2: both CMAP and SNAP appear entirely normal despite complete axonal disruption

• In mixed traction injuries, proximal conduction block (neurapraxia component) coexists with distal axonal degeneration (axonotmesis component)
• Stimulating distal to block before Day 7 gives a normal CMAP amplitude — falsely suggesting intact axons
• This is the "false normal window" — a highly dangerous period for prognostic conclusions

SLIDE 3: The C7 Root — Electrodiagnostic Ambiguity Arising from Bilateral Symmetrical Contribution and Multi-Nerve Overlap

• Median from index finger: 80% — but index finger also receives C6 contribution
• Median from middle finger: 70% — middle finger is the most "C7-pure" sensory territory, yet 30% cases are missed
• Superficial radial NCS: only 40% — large individual variation in C7 contribution to radial sensory territory

• C7 maintains a unique symmetry — two roots above (C5, C6) and two below (C8, T1)
• This same symmetry is maintained in sensory supply: middle digit (C7) has one digit on each side (C6 = index, C8 = ring)
• Cross-innervation from adjacent roots means C7 lesions are buffered by C6 and C8 contributions → SNAP abnormalities are attenuated or absent even in complete C7 axonotmesis

• Anconeus is the most C7-specific muscle for EMG — but radial motor NCS from EDC evaluates C7,8 combined — cannot isolate C7
• FCR is the most reliable median-innervated C7 muscle — but also receives C6

SLIDE 4: Clinico-Neurophysiological Dissociation — When Weakness and CMAP Amplitude Are Not Proportional and What It Reveals

• Mechanism: Conduction block proximal to stimulation site
• Stimulating distally bypasses the block → CMAP appears normal or near-normal
• But motor axons are not conducting across the lesion → clinical weakness is severe
• Diagnosis: Neurapraxia/demyelinating injury with conduction block
• Prognosis: Excellent — remyelination expected

• Mechanism: Collateral reinnervation already underway
• Surviving axons have sprouted to reinnervate denervated muscle fibers
• CMAP does not capture the full functional recovery because it reflects total axon count, not reinnervation efficiency
• EMG will show large-amplitude long-duration polyphasic MUPs (collateral sprouting signature)

• Most dangerous dissociation
• In fresh injury: false normal window (Day 0–7)
• In established injury with normal SNAP: preganglionic avulsion
• Postganglionic with absent CMAP + normal SNAP in C5–C6 is anatomically impossible after Day 11

SLIDE 5: Paraspinal EMG — The Most Proximal Electrophysiological Anchor and Its Interpretive Limitations

• They are innervated exclusively by posterior primary rami — the first branches off the spinal nerve, arising before the nerve enters the scalene triangle
• Fibrillations in paraspinal muscles = lesion at or proximal to nerve root exit = intradural or at intervertebral foramen level
• This is the only muscle group that definitively confirms root-level pathology in supraclavicular injuries

• C5 paraspinals: Cervical levels C4–C5 (confirmed by level-specific needle placement under fluoroscopy in research settings)
• C6 paraspinals: C5–C6
• C7 paraspinals: C6–C7
• C8–T1 paraspinals: C7–T1

1. Cervical spondylosis causes paraspinal fibrillations without plexopathy — must be excluded clinically and radiologically
2. Bilateral paraspinal fibrillations suggest spondylotic radiculopathy rather than traumatic plexopathy
3. Paraspinal fibrillations may be absent in preganglionic avulsion if the posterior root avulses cleanly without involving the posterior primary ramus — this is rare but documented
4. Paraspinal EMG is technically demanding — needle placement too superficial misses deep paraspinal fibers; incorrect level placement gives false localization

SLIDE 6: Intraoperative Nerve Action Potential Recording — The Electrophysiological-Surgical Interface

• Axonotmesis (intact endoneurial tubes, spontaneous recovery expected) from
• Neurotmesis in continuity (endoneurial disruption with neuroma formation, no spontaneous recovery)

• Stimulate proximal nerve stump; record from distal stump across the neuroma/lesion in continuity
• A recordable NAP = large-caliber myelinated fibers traversing the lesion = axonotmesis = do NOT resect
• An unrecordable NAP = no fibers crossing = neurotmesis in continuity = resect and graft

• Performed at 3–4 months post-injury
• Before this: Wallerian degeneration incomplete, regenerating axons have not yet reached the lesion site — NAP will be absent even in axonotmesis → false unrecordable
• After 6 months: Target muscle end-plates begin irreversible degeneration — delay reduces surgical outcome

• Stimulating individual root stumps while recording cortical SEP assesses C5 root viability — impossible preoperatively (no C5 sensory nerve accessible for surface SNCS)
• This directly guides whether to attempt nerve root reimplantation vs. nerve transfer

SLIDE 7: Collateral Sprouting vs. Axonal Regeneration — How EMG Distinguishes Two Entirely Different Recovery Mechanisms

• Injured axon regrows from proximal stump toward target
• Rate: 2.5 cm/month
• EMG signature: Nascent MUPs — small amplitude (<300 µV), short duration (<5 ms), highly polyphasic, unstable (varying morphology on consecutive discharges)
• Appears at time predicted by distance ÷ 2.5 cm/month from lesion to muscle
• Signifies the axon has reached the muscle and early neuromuscular junctions are forming

• Intact surviving axons sprout terminal branches to reinnervate denervated but adjacent muscle fibers
• No new axons — existing axons expand their territory
• EMG signature: Giant MUPs — large amplitude (>5 mV), long duration (>15 ms), polyphasic
• Appears earlier than axonal regeneration
• Signifies surviving axon rescue of denervated fibers — partial lesion

SLIDE 8: Integrated Prognostic Algorithm — Synthesizing NCS, EMG, SEP, and Intraoperative NAP into a Definitive Supraclavicular Management Decision

• SNAP preserved + paraspinal fibrillations + absent cortical SEP = Preganglionic avulsion → surgery not restorative via direct repair → plan nerve transfer (contralateral C7, phrenic, intercostal, accessory nerve)
• SNAP reduced + no paraspinal fibrillations = Postganglionic → proceed to Tier 2

• Conduction block pattern (CMAP reduction proximal > distal, normal SNAP, no fibrillations) = Neurapraxia → conservative management, full recovery expected
• Reduced CMAP + reduced SNAP + fibrillations = Axonotmesis or neurotmesis → proceed to Tier 3

• Nascent MUPs appearing on schedule (distance ÷ 2.5 cm/month) = Axonotmesis confirmed → continue conservative, reassess at 6 months
• No nascent MUPs, no clinical improvement by Month 3–4 = Neurotmesis suspected → proceed to Tier 4

• Recordable NAP = axonotmesis confirmed → neurolysis only, no resection
• Unrecordable NAP = neurotmesis in continuity → resect neuroma, interpositional nerve graft
• Absent NAP with preganglionic SEP pattern = avulsion confirmed → nerve transfer

• Target muscle >60 cm from lesion (2-ft rule) → axonal regeneration cannot arrive before end-plate degeneration (18–24 months) → primary repair futile → nerve transfer to local motor branch preferred to minimize regeneration distance

SUPRACLAVICULAR NCS — EXPERT INTEGRATION: 8 NEW SLIDES

SLIDE 1: Spinal Nerve Root Stimulation Technique — Why Needle Placement Geometry Determines Which Trunk You Are Actually Testing

• Positioning needle caudal to C7 spinous process activates C6, C7, C8, and T1 spinal nerves simultaneously for evaluation of the posterior cord
• A metal plate or disk electrode placed at this position can achieve similar results in experienced hands

SLIDE 2: Table 6-7 Decoded — Nerve Conduction Times from Erb's Point and What the Variance Reveals About Plexus Physiology

• Supraspinatus latency (2.6–2.7 ms) is the shortest of all shoulder girdle muscles — the suprascapular nerve takes the most direct course from Erb's point
• Triceps latency increases nonlinearly with distance — this is because the triceps endplate zone is vertically oriented, innervated by longer nerve branches; latency changes do not follow linear distance-velocity calculations
• Biceps and deltoid endplates are horizontally oriented in the middle of the fiber — point of recording does NOT affect latency as much as in triceps
• The same problem applies to infraspinatus and supraspinatus — these principles must be understood before interpreting prolonged latencies as pathological

SLIDE 3: Table 6-8 — Latency Across the Plexus with Nerve Root Stimulation: The Definitive Plexus Segmental Conduction Reference

• The lower trunk/medial cord has the shortest mean latency (4.7 ms) despite the longer distance to ADQ — reflecting the large-caliber, fast-conducting ulnar fibers of the lower trunk
• The upper trunk has the longest mean (5.3 ms) because musculocutaneous fibers to biceps are smaller caliber than ulnar fibers
• SD of 0.4–0.5 ms: a side-to-side difference exceeding 0.6 ms is pathological — this cutoff (Kimura, 1989) is derived from the SD range and represents >1.5 SD difference

• Table 6-8 provides segmental latency across the plexus — i.e., from the root to the recording muscle — subtracting the distal latency of the ulnar nerve
• This isolates the plexus conduction time exclusively — peripheral nerve conduction time is removed from the calculation
• This is why Table 6-8 values are NOT the same as Table 6-7: Table 6-7 measures total Erb's-to-muscle time; Table 6-8 subtracts distal nerve latency to give only the plexus segment time

SLIDE 4: The Latency vs. Amplitude Debate in Brachial Plexus NCS — Why Amplitude Wins and Latency Misleads in Axonal Injuries

• In axonal degeneration, remaining surviving axons are the fastest-conducting large-diameter fibers — they tend to show relatively normal conduction velocity and normal latency
• The lost axons are the slow ones and the fast ones equally — but remaining fast axons dominate the latency measurement
• Result: Latency criteria rarely provide useful information in axonal degeneration — the measured latency appears deceptively normal

• Amplitude of CMAP and SNAP directly reflects the number of conducting axons
• Amplitude preservation above one-half compared to the normal side suggests limited distal degeneration and good prognosis
• Amplitude has considerable variability between subjects and between the two sides of the same individual — this is why side-to-side comparison is mandatory, not absolute values
• An intramuscular needle with restricted recording radius does not register the overall size of CMAP — must use surface electrodes for CMAP amplitude measurement; needle is used for latency precision only

• Latency prolongation → demyelination → neurapraxia → good prognosis
• Amplitude reduction with normal latency → axonal loss → axonotmesis/neurotmesis → prognosis depends on degree
• Both latency prolongation AND amplitude reduction → mixed lesion → assess each component separately

SLIDE 5: The Collision Technique — Advanced NCS Methodology for Eliminating Volume-Conducted Interference in Brachial Plexus Recording

• Volume-conducted potentials from co-activated muscles interfere with accurate recording of the intended signal — even with the electrode placed over a specific intrinsic hand muscle
• This is especially problematic when stimulating at Erb's point: thenar and hypothenar muscles are activated simultaneously as a volume effect
• The intended CMAP from a specific muscle (e.g., biceps) is contaminated by potentials from adjacent co-activated muscles

1. Stimulate at Erb's point (proximal stimulus) — activates all plexus fibers
2. Simultaneously apply a second, distal stimulus to the specific nerve NOT under consideration
3. The antidromic impulse from the distal stimulus travels proximally and collides with and annihilates the orthodromic impulse from the proximal stimulus in the non-target nerve
4. Result: Only the target nerve's signal reaches the muscle — volume conduction from non-target muscles is eliminated

• Without collision technique, CMAP recorded from biceps may contain contributions from brachioradialis, brachialis, and medial head contributions — overestimating amplitude in partial lesions
• In a partial upper trunk lesion where only some C5 fascicles are injured, the collision technique correctly identifies the reduced biceps CMAP — without it, contamination from preserved lateral cord fibers gives a falsely reassuring amplitude

SLIDE 6: Why the Triceps Endplate Zone Geometry Uniquely Invalidates Latency Comparison in Posterior Cord Assessment

• Endplates are horizontally oriented in the middle of the muscle fibers
• The point of recording does NOT affect latency significantly regardless of where the recording electrode is placed along the muscle
• Side-to-side latency comparison is reliable

• Endplate zone is vertically oriented — the distal portion of the muscle is innervated by longer nerve branches
• Latency of recorded response increases with increasing distance from the stimulus point in a nonlinear fashion
• This nonlinearity reflects irregularly spaced points of innervation along the endplate zone

• If recording electrode on the triceps is placed 2 cm more distally than on the contralateral side → artificially prolonged latency that mimics posterior cord conduction slowing
• Standard protocol: Equalize the distance between stimulating and recording electrodes on both sides — this is the only way to make triceps latency comparison valid
• Failure to equalize distances is the most common source of false-positive posterior cord latency abnormality

SLIDE 7: Musculocutaneous Nerve — The Master Probe for Upper Trunk and Lateral Cord Integrity

• It is a pure C5–C6 derivative via the lateral cord
• It has both motor (biceps, brachialis, coracobrachialis) and sensory (LABC — lateral antebrachial cutaneous nerve) components — providing simultaneous motor and sensory evaluation of the same root-trunk-cord pathway

1. The axilla — between the axillary artery medially and the coracobrachialis muscle laterally
2. Posterior cervical triangle — 3 to 6 cm above the clavicle, just behind the sternocleidomastoid muscle

• Both surface electrodes and needle electrodes are adequate for stimulation
• Recording from biceps brachii for CMAP

• Stimulating both in the axilla AND at Erb's point allows calculation of conduction velocity across the proximal segment
• If conduction velocity is slowed between Erb's point and axilla → lateral cord/upper trunk demyelination
• If CMAP amplitude drops between axilla stimulation and Erb's stimulation → proximal axonal loss or conduction block localized to the plexus segment

• Recorded orthodromically from the forearm
• Provides direct assessment of C6 postganglionic sensory axons
• Side-to-side amplitude difference >50% = significant abnormality
• This is the most sensitive sensory nerve for C5–C6 supraclavicular lesion detection — more reliable than median thumb SNCS in isolation

SLIDE 8: Integrating Normative Data with Pathological Patterns — A Precision Diagnostic Matrix for Upper, Posterior, and Lower Trunk Supraclavicular Lesions

• Any amplitude preservation >50% of normal side = limited axonal degeneration = good prognosis marker
• Latency prolongation alone (amplitude intact) = pure demyelination = neurapraxia, complete recovery expected
• Latency normal + amplitude severely reduced = axonal loss — prognosis depends on serial EMG

(Root-needle NCS latency across plexus from Table 6-8) + (Side-to-side amplitude comparison) + (Collision technique for CMAP purity) + (LABC + median thumb SNCS for C6 postganglionic status) + (Paraspinal EMG for preganglionic exclusion) + (Serial EMG for nascent MUP detection) = Complete supraclavicular electrophysiological characterization

SUPRACLAVICULAR NCS — EXPERT LEVEL: 6 SLIDES

SLIDE 1: Spinal Nerve Root Stimulation Technique — Needle Geometry Determines Root Selectivity

• C5 spinous process sits at the level of C6 vertebral body exit foramen due to angulation
• Needle placed 1 cm too medial at C5 level co-stimulates C4 → produces a "normal C5 response" by activating C4 collaterals even in complete C5 root avulsion
• Needle stimulation avoids volume conduction and adjacent nerve activation but carries a small risk of pneumothorax — the reason surface stimulation remains common despite its limitations

SLIDE 2: Normative Reference Data — Tables 6-7 and 6-8 as Diagnostic Anchors

• Table 6-7 = total Erb's-to-muscle time (includes peripheral nerve segment)
• Table 6-8 = plexus conduction time only — distal ulnar nerve latency is subtracted, isolating the plexus segment exclusively
• The lower trunk has the shortest plexus latency (4.7 ms) despite longest distance to ADQ — reflecting large-caliber fast-conducting ulnar fibers

SLIDE 3: Latency vs. Amplitude — Why Amplitude Is the Dominant Prognostic Parameter and Latency Misleads in Axonal Injuries

• Surviving axons after axonal degeneration are the fastest-conducting large-diameter fibers — they maintain near-normal conduction velocity
• Lost axons include slow AND fast fibers, but the remaining fast fibers dominate the measured latency
• Result: Latency appears deceptively normal in established axonal loss — it rarely provides useful information in axonal degeneration

• CMAP/SNAP amplitude directly reflects total number of conducting axons
• Amplitude preservation >50% of contralateral side = limited axonal degeneration = good prognosis
• Amplitude is affected by considerable individual variability → side-to-side comparison is mandatory; absolute values are unreliable
• For CMAP amplitude: must use surface electrodes — intramuscular needle has a restricted recording radius and does NOT register overall CMAP size

SLIDE 4: The Triceps Endplate Zone Anomaly — Why Posterior Cord Latency Comparison Requires Distance Equalization

• Endplates are horizontally oriented in the middle of the fibers
• Recording electrode position along the muscle does NOT significantly affect latency
• Side-to-side latency comparison is inherently reliable

• Endplate zone is vertically oriented, with the distal portion innervated by longer nerve branches
• Latency of the recorded response increases nonlinearly with distance from the stimulus point
• This nonlinearity reflects irregularly spaced innervation points along the vertical endplate zone
• Same problem applies to infraspinatus and supraspinatus due to their complex 3D muscle folding

SLIDE 5: Musculocutaneous Nerve — Dual-Component Upper Trunk and Lateral Cord Probe

• Motor component → biceps, brachialis, coracobrachialis
• Sensory component → LABC (lateral antebrachial cutaneous nerve)

1. Axilla — between axillary artery medially and coracobrachialis laterally
2. Posterior cervical triangle — 3–6 cm above clavicle, just behind the sternocleidomastoid

• Either surface or needle electrodes are adequate; recording from biceps brachii

• Stimulate at both axilla AND Erb's point
• Amplitude drop between axilla stimulation and Erb's stimulation = conduction block localized to the plexus segment (not peripheral nerve)
• Velocity slowing between the two sites = demyelination at upper trunk/lateral cord level

• Side-to-side amplitude difference >50% = significant C6 postganglionic abnormality
• More sensitive than median thumb SNCS for detecting C5–C6 supraclavicular lesions
• Combined with median thumb SNCS: if both are abnormal → confirmed postganglionic C6 pathology; if both are normal despite clinical anesthesia → preganglionic C6 avulsion

• Biceps → upper trunk and lateral cord
• Triceps → posterior cord
• Ulnar-innervated intrinsic hand muscles → lower trunk and medial cord

SLIDE 6: Precision Diagnostic Matrix — Integrating Root Stimulation, Normative Data, Amplitude Rules, and EMG into a Unified Supraclavicular Decision Framework

• LABC + median thumb SNCS abnormal → postganglionic → proceed to surgical timeline
• LABC + median thumb SNCS normal with clinical anesthesia → preganglionic → nerve transfer planning, NOT direct repair

• Nascent MUPs by expected date (lesion-to-muscle distance ÷ 2.5 cm/month) → axonotmesis → conservative
• No nascent MUPs → neurotmesis suspected → intraoperative NAP

• Recordable NAP → neurolysis only
• Unrecordable NAP → resect and graft (Kline et al., 1986)

(Table 6-8 plexus latency) + (Side-to-side amplitude, 0.6 ms rule) + (Collision technique for CMAP purity) + (LABC and median thumb SNCS for preganglionic exclusion) + (Paraspinal EMG) + (Serial EMG nascent MUP timeline) + (Intraoperative NAP if needed) = Complete supraclavicular electrophysiological characterization

SUPRACLAVICULAR NCS — 6 SLIDES (CONDENSED)

SLIDE 1: Root Stimulation Technique & Collision Method

• 1–2 cm lateral to C5 spinous process → activates C5 & C6 (upper trunk + lateral cord)
• Slightly caudal to C7 spinous process → activates C8 & T1 (lower trunk + medial cord)
• Between both points → activates C6, C7, C8 (posterior cord)

• C5 spinous process ≠ C5 foraminal level (angulation offset) → 1 cm too medial = C4 co-stimulation = false normal in C5 avulsion
• Surface stimulation at Erb's point → volume conduction contamination from co-activated muscles

• Second distal stimulus applied to non-target nerve
• Antidromic impulse collides with and annihilates Erb's-evoked signal in that nerve
• Only target nerve CMAP survives → eliminates false amplitude inflation in partial lesions

SLIDE 2: Normative Reference Data — Tables 6-7 & 6-8

• Supraspinatus: 2.6–2.7 ms (shortest — most direct suprascapular nerve course)
• Biceps: 4.6–5.0 ms | Deltoid: 4.3–4.4 ms | Triceps: 4.5–5.3 ms

• Lower trunk has shortest plexus latency despite longest distance → large-caliber fast ulnar fibers
• 0.6 ms side-to-side difference = pathological (Kimura, 1989) — derived from SD of 0.4–0.5 ms

SLIDE 3: Latency vs. Amplitude — Why Amplitude Wins

• Surviving axons = fastest large-diameter fibers → latency appears deceptively normal
• Latency rarely provides useful information in axonal degeneration

• Directly reflects total conducting axon count
• >50% amplitude preservation vs. contralateral = limited degeneration = good prognosis
• Must use surface electrodes — needle has restricted recording radius, does not capture full CMAP

SLIDE 4: Triceps Endplate Zone — The Posterior Cord Latency Trap

• Endplate zone is vertically oriented; distal portion innervated by longer branches
• Latency increases nonlinearly with distance from stimulus → irregularly spaced innervation points
• Same issue applies to supraspinatus and infraspinatus

SLIDE 5: Musculocutaneous Nerve — Dual-Component C5–C6 Probe

• Pure C5–C6, lateral cord derivative
• Motor (biceps) + sensory (LABC) from the same root-trunk-cord axis simultaneously

• Axilla (between axillary artery and coracobrachialis)
• Posterior cervical triangle, 3–6 cm above clavicle, behind SCM

• Amplitude drop: axilla→Erb's = conduction block localized to plexus segment
• Velocity slowing between sites = demyelination at upper trunk/lateral cord level

• Side-to-side amplitude >50% difference = significant C6 postganglionic pathology
• Normal LABC + normal median thumb SNCS + clinical anesthesia = preganglionic C6 avulsion — no direct repair possible, plan nerve transfer

• Biceps → upper trunk/lateral cord
• Triceps → posterior cord
• Ulnar intrinsics → lower trunk/medial cord

SLIDE 6: Unified Supraclavicular Decision Matrix

1. LABC + median thumb SNCS abnormal → postganglionic → surgical timeline
2. Both normal despite anesthesia → preganglionic → nerve transfer, not direct repair
3. Serial EMG nascent MUPs on time (distance ÷ 2.5 cm/month) → axonotmesis → wait
4. No MUPs by expected time → intraoperative NAP at 3–4 months
5. Recordable NAP → neurolysis only | Unrecordable NAP → resect and graft (Kline, 1986)