EMG in Neurogenic Disorders

Neurogenic disorders — diseases of the motor neuron, motor root, plexus, or peripheral nerve — produce characteristic EMG patterns that localize and characterize the pathology. The combination of denervation signs (fibrillations and positive sharp waves), motor unit changes (large polyphasic MUAPs of reinnervation), reduced recruitment, and distribution across muscle groups translates clinical weakness into specific anatomic localization. This page covers EMG patterns in motor neuron disease, radiculopathy, plexopathy, mononeuropathy, and polyneuropathy.

The Neurogenic EMG Pattern

1. Denervation signs: fibrillation potentials and positive sharp waves (acute neurogenic).
2. Reinnervation signs: large polyphasic, long-duration MUAPs (chronic neurogenic).
3. Reduced recruitment: few motor units firing at high rates with mild effort.
4. Distribution: specific to anatomic level (myotomal for radiculopathy; peripheral nerve for mononeuropathy; multifocal/widespread for MND/ALS).

Acute vs Chronic Distinguishing Features

Motor Neuron Disease (ALS)

EMG Features

• Fasciculations: spontaneous, coarse, irregular, low-frequency, often persistent.
• Fibrillations and PSWs: in multiple muscle groups.
• Large polyphasic MUAPs: reinnervation.
• Reduced recruitment: with high firing rates.
• Distribution: multiple regions affected per EFNS/El Escorial criteria.

EFNS Criteria for ALS (Awaji Criteria)

• Need evidence of upper and lower motor neuron involvement.
• Lower motor neuron: denervation + reinnervation EMG findings.
• Distribution requirements:
  • 4 anatomic regions: bulbar (genioglossus, masseter), cervical (deltoid, biceps, triceps), thoracic (paraspinal), lumbar (vastus lateralis, tibialis anterior).
  • Need findings in 2+ regions for “definite” ALS.

Distinguishing ALS from Mimickers

• Multifocal motor neuropathy: has motor conduction block on NCS; sensory NCS preserved; IVIG-responsive; anti-GM1 often positive.
• Cervical/lumbar radiculopathy: distribution by myotome; paraspinal involvement; no fasciculations typically.
• Inclusion body myositis: also shows fibs and polyphasic MUAPs (mixed myopathic/neurogenic); progressive; histologic features distinct.
• Post-poliomyelitis syndrome: history of polio; older patients; chronic stable then progressive.
• Spinal muscular atrophy (adult onset): usually milder progression; family history.

Radiculopathy

EMG Features

• Fibrillations and PSWs: in muscles supplied by the affected root.
• Paraspinal muscle involvement: key distinguishing feature from plexopathy (paraspinal muscles innervated by the dorsal primary ramus of the same root level).
• MUAP: normal acutely; large polyphasic chronically.
• Recruitment: reduced in affected muscles.

Myotomal Mapping (Common Roots)

Acute vs Chronic Radiculopathy

• Acute (<3 weeks): may not have fibs yet; clinical exam more sensitive.
• Subacute (3 weeks–3 months): fibs and PSWs in affected myotome.
• Chronic: large polyphasic MUAPs; fibs may resolve.
• Old radiculopathy: residual large MUAPs without fibs; stable.

EMG vs MRI for Radiculopathy

• Some patients have radiographic disc herniation without clinical/electrophysiologic radiculopathy.
• Some patients have electrophysiologic radiculopathy without obvious imaging findings (rare).
• EMG defines the functional level; MRI defines the structural lesion.
• Concordant EMG and MRI strengthen surgical decision-making.

Plexopathy

Brachial Plexus

• Findings in multiple muscle groups supplied by the affected plexus segment.
• Paraspinal muscles spared (paraspinal supplied by dorsal primary ramus from root, proximal to plexus).
• Distribution helps localize:
  • Upper trunk (C5-C6): biceps, supraspinatus, infraspinatus.
  • Middle trunk (C7): triceps, latissimus.
  • Lower trunk (C8-T1): intrinsic hand muscles.
  • Lateral cord: median, musculocutaneous.
  • Posterior cord: radial, axillary.
  • Medial cord: ulnar, medial portion of median.

Lumbosacral Plexus

• Findings in femoral nerve distribution (psoas, quadriceps).
• Sciatic nerve distribution (hamstrings, leg muscles).
• Combinations suggesting plexus level.
• Paraspinal sparing distinguishes from root.

Specific Plexopathies

• Parsonage-Turner syndrome (neuralgic amyotrophy): acute brachial plexopathy, often post-vaccine or post-infection; involves upper trunk predominantly; characteristic burning shoulder pain followed by weakness.
• Diabetic amyotrophy: asymmetric proximal leg weakness; multifocal in lumbosacral plexus and roots.
• Radiation plexopathy: chronic, often years after radiation; myokymia common; sensory more than motor.
• Traumatic plexopathy: motor vehicle accident, stretch injury; localized to specific plexus segment.

Mononeuropathy

Median Nerve at the Wrist (CTS)

• Most common mononeuropathy.
• Findings in APB (abductor pollicis brevis): fibs in advanced cases, polyphasic MUAPs in chronic, reduced recruitment.
• Normal innervation in proximal median territory (pronator, FCR).
• NCS: prolonged median motor distal latency; sensory studies most sensitive.

Ulnar Nerve at the Elbow

• Findings in ulnar-innervated muscles distal to elbow: FCU, FDP IV/V, intrinsic hand muscles.
• Sparing of FCU may occur (innervated proximally to elbow).
• NCS: slow CV across elbow; conduction block possible.

Radial Nerve

• Spiral groove: findings in radial-innervated muscles (extensors of wrist and fingers).
• Posterior interosseous: similar but spares triceps and brachioradialis.
• Sparing of triceps suggests injury at or distal to spiral groove.

Peroneal Neuropathy at Fibular Head

• Findings in tibialis anterior, peroneus longus, EDB.
• Sparing of biceps femoris (innervated by sciatic above peroneal branch).
• NCS: slow CV across fibular head; conduction block.

Femoral Neuropathy

• Findings in quadriceps and iliopsoas (when accessible).
• Sparing of hip adductors (obturator nerve).
• Sensory loss in anterior thigh.

Polyneuropathy

Length-Dependent Polyneuropathy

• EMG findings predominantly in distal muscles.
• Often combined with NCS findings (reduced sural, reduced peroneal CMAP).
• Examples: diabetic, alcoholic, idiopathic distal symmetric.
• EMG complementary to NCS for severity and localization.

Non-Length-Dependent (Mononeuritis Multiplex)

• EMG shows findings in multiple individual nerves’ distributions.
• Often vasculitic; biopsy may be indicated.

Acute vs Chronic Polyneuropathy

• Acute (GBS): EMG less helpful in first weeks; NCS more sensitive (F-waves prolonged).
• Chronic axonal: characteristic findings of chronic denervation/reinnervation.
• Demyelinating: NCS findings more prominent than EMG.

Specific EMG Patterns

Critical Illness Myopathy/Neuropathy

• Common in ICU patients.
• Myopathy: small polyphasic MUAPs, early recruitment.
• Neuropathy: fibs and PSWs.
• Often coexist.
• EMG distinguishes from primary muscle or nerve disease.

Post-Poliomyelitis Syndrome

• Decades after polio.
• Progressive weakness in previously affected muscles.
• EMG: large polyphasic MUAPs (reinnervation), some fibs, reduced recruitment.
• Distinguish from chronic ALS by history and slower progression.

Spinal Muscular Atrophy

• SMN1 mutation; hereditary.
• Variable phenotypes (SMA1: infantile to SMA4: adult).
• EMG: fasciculations, fibrillations, chronic neurogenic.
• Genetic confirmation.

Hereditary Motor Sensory Neuropathy (CMT)

• EMG and NCS combined characterize the type:
  • CMT1: demyelinating; uniformly slow conduction.
  • CMT2: axonal.
  • CMT4 subtypes: various.
  • HSMN-X: X-linked.
• EMG shows chronic neurogenic distally predominant.
• Family history common.

Reporting

A neurogenic EMG report should include:

• Muscles examined and findings in each (insertional, spontaneous, MUAP, recruitment).
• Specific localization (myotome, peripheral nerve, plexus level).
• Acute vs chronic.
• Differential of likely etiologies.
• Recommendations for further evaluation (imaging, lab, genetic, etc.).

🔍 Did You Know?

The classic teaching that paraspinal muscle EMG abnormalities distinguish radiculopathy from plexopathy derives from the fact that paraspinal muscles are innervated by the dorsal primary ramus of the spinal nerve, which leaves the spinal canal immediately at the root level — before the nerve branches form the plexus. A C7 root lesion produces denervation in BOTH the cervical paraspinal muscles AND the C7-innervated limb muscles (triceps, pronator teres). A brachial plexopathy at the middle trunk affects the limb muscles but spares the paraspinal. This anatomic principle has made paraspinal EMG one of the most useful localizing tools in clinical electrodiagnosis. The clinical pearls: (1) paraspinal denervation indicates a lesion at the level of the root or proximal; (2) absence of paraspinal involvement in a patient with limb denervation suggests plexopathy or peripheral nerve lesion; (3) lumbar paraspinal EMG can localize lumbosacral radiculopathies versus plexopathy. The technique requires expertise — paraspinal muscles are deep, near the spine, and risk pneumothorax with poor technique (especially thoracic). For practicing electrodiagnosticians, the routine inclusion of paraspinal sampling in any suspected radiculopathy work-up substantially improves diagnostic confidence and localization accuracy. The same principle generalizes: knowing the anatomy of innervation at each muscle is what allows EMG to localize beyond what clinical examination alone reveals.

Pitfalls and Pearls

• Neurogenic EMG pattern: fibs/PSWs + large polyphasic MUAPs + reduced recruitment.
• Acute neurogenic: fibs only (2–3 weeks post-injury); MUAPs normal initially.
• Chronic neurogenic: large polyphasic MUAPs (reinnervation); fibs may be absent.
• ALS pattern: fasciculations + fibs + large MUAPs + reduced recruitment in multiple regions.
• Awaji criteria: ALS diagnosis based on regions involved.
• Radiculopathy: fibs in myotome + paraspinal muscles.
• Plexopathy: limb findings without paraspinal; localization by anatomic level.
• Mononeuropathy: findings localized to specific nerve distribution.
• Parsonage-Turner: acute brachial plexopathy; upper trunk predominant; pain then weakness.
• Diabetic amyotrophy: asymmetric proximal leg weakness; multifocal in lumbosacral plexus/roots.
• MMN distinguished from ALS: motor conduction block; preserved sensory NCS; anti-GM1.
• CIDP: combine motor + sensory NCS findings with EMG patterns.
• EMG timing: 2–3 weeks for fibs to develop; serial studies often useful.
• Critical illness myo/neuropathy: common in ICU; distinguish from primary disease.
• Hereditary neuropathies: family history + EMG/NCS pattern + genetic testing.
• EMG and NCS are complementary: cannot fully evaluate peripheral nerve disease with one alone.
• Distribution pattern: essential for localization (myotome, dermatome, nerve, plexus).

References

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3. de Carvalho M, Dengler R, Eisen A, et al. Electrodiagnostic criteria for diagnosis of ALS. Clin Neurophysiol. 2008;119(3):497-503.
4. Aminoff MJ, ed. Aminoff’s Electrodiagnosis in Clinical Neurology. 6th ed. Elsevier; 2012.
5. Daube JR, Rubin DI. Needle electromyography. Muscle Nerve. 2009;39(2):244-270.