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

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SLIDE 1: Title Slide

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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

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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

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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)

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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)

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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

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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

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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

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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

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SLIDE 10: Supraclavicular vs. Infraclavicular — Key Distinction

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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

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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

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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

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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

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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

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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

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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

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SLIDE 18: Infraclavicular — Cord-Specific Deficits

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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

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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?

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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

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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

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SUPRACLAVICULAR PLEXUS ASSESSMENT — PPT CONTENT (~20 Slides)

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SLIDE 1: Title Slide

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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

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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?

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SLIDE 4: Neurophysiological Tests Used

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

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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

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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

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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)

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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

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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

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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

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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

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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

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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)

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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)

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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)

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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

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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

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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)

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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

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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

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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

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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

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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

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