EMG/Nerve Conduction Studies

• Used for determining localization, axonal vs. demyelinating, muscle vs. nerve
• "If someone is weak, the EMG should always be abnormal"
• EMG
• Measures the electrical activity associated with motor units
• Uncomfortable study for patient
• Provides useful data in neuropathy/myopathy evaluation
• Spontaneous activity – detects acute denervation
• Fibrillation – small, sharp spike that initiates with small positive (downward) deflection
• occur proximally first
• regular firing – "rain-on-a-roof" pattern
• spontaneous discharge of muscle fiber
• Positive waves – downward wave with slow return
• spontaneous discharge of muscle fiber
• Fasciculations – slow, irregular EMG pattern
• spontaneous discharge of motor unit
• Voluntary Activity – Firing characteristic and recruitment
• Activation – amount of activity caused by muscle contraction; denotes CNS pathology
• Recruitment – number of motor units at given firing frequency
• 1/5 is normal (5Hz- 1 motor unit, 10Hz- 2 motor units, 15Hz- 3 motor units)
• increased firing rate causes increased motor unit firing
• Wallerian Degeneration – occurs at 4-7 days
• EMG normal before Wallerian degeneration except for decreased recruitment
• Fibrillations and positive waves occur at 10-14 days (longer for distal muscles)
• Chronic Neurogenic Units
• large, long, polyphasic units with reduced recruitment (fewer units to help out)
• Acute Neurogenic Units – have not yet renervated so only see reduced recruitment (not large units)
• Demyelinating Lesions – decreased recruitment only, slowing of signal recruits more firing
• Myopathic Units – small, short, polyphasic units with early recruitment
• Motor unit potential – myopathy polyphasic – small amplitude, short duration
• Neuropathy – large amplitude, long duration
• Conduction velocity = distance / (distal latency - proximal latency)
• Internodal demyelination – conduction delay
• Segmental demyelination – loss of conduction proximally
• Cut axon
• loss of conduction proximally, unaffected distally immediately after injury
• 7-10 days later – see loss of conduction distally as well due to distal Wallerian degeneration (motor 5-6 days, sensory 10-11 days)
• proximal signal will be dispersed due to different speeds of various sized axon
• 3 weeks – fibrillation potentials indicating denervation of muscle; but it does not give location (radicular vs. peripheral nerve injury)
• best determination of nerve injury – EMG immediately afterwards, then in 7-10 days to determine if there is still an action potential
• Insertional activity
• Electrical response to mechanical damage to the muscle
• Prolonged in acute neuropathies and active myopathies
• Decreased with advanced myelopathy with fibrous or fatty tissue replacement
• Spontaneous activity
• Resting muscle has little or no activity
• Some spontaneous mEPSP from released quanta
• Fibrillation potential – triphasic potential 1-5 msec
• Not visible through the skin
• Caused by deinnervation with increased muscle sensitivity
• Starts 3 weeks after injury
• May display positive sharp wavs
• Fasciculation potential – 3-5 phases lasting 5-15 msec
• Caused by activity in a motor unit
• Visible through the skin
• Associated with nerve irritability, not destruction
• Recruitment
• Initiation of firing of additional motor units from increase in firing rate of active units
• Rapid in myopathy – all units recuited at low levels of force
• Decreased in neuropathy – Total number of motor units is reduced

o EMG in Myopathy

§ Usually no spontaneous activity is seen

§ Diffuse loss of muscle fibers results in motor unites with fewer fibers, thus while the number of units is normal, the electrical activity of the unit is smaller than normal

§ The number of motor unites recruited during contraction is normal, but the motor unites may be smaller than normal with normal or shorter than normal duration

• Active – fibrillations, positive waves
• From deinnervation, inflammation (polymyositis, Duschenne MD)
• Chronic – small EP, rapid recruitment
• Other MDs, congenital and metabolic myopathies

o EMG in Neuropathy

§ Denervated muscle is hyperexcitable, resulting in spontaneous action potentials (fibrillations)

§ With axonal loss, the number of motor units is reduced

§ The remaining axons re-innervate some of the muscle fibers so that the remaining motor units are larger than normal and longer in duration

§ The number of motor unites recruited during contraction is reduced with the units that are recruited larger than normal, longer in duration, and polyphasic in appearance

§ Active – Fasciculations

• Chronic (reinnervation) – large EP, slow recruitment
• Nerve Conduction Velocities
• Records the electrical activity conducted along a nerve which has been electrically stimulated
• Provides useful data in neuropathy evaluation
• Measure sensory nerve action potentials (SNAPS) and compound motor action potentials (CMAPS)
• Amplitude – relates integrity of axons
• Latency – relates speed/state of myelination (if >25% of baseline, indicates demyelination)
• Nerve injury
• CMAP decreases in amplitude in 5 days
• SNAP decreases in amplitude in 9 days (more sensitivity)
• Axonal disease – decreases wave amplitude
• Myelin disease – increases latency (decreased velocity), signal degredation

• M wave – direct motor response to stimulation of a motor nerve
• F wave – caused by supramaximal stimulation of a mixed motor-sensory nerve
• Antidromic impulse to the anterior horn followed by orthodromic impulse back
• Forms a second, smaller action potential with greater latency than direct stimulation
• Can be used to measure conduction in the proximal protion of the nerve
• H reflex – elicited by submaximal stimulation of a sensory fiber
• Sends impulse to the spinal cord that elicits a monosynaptic reflex
• Only works in the calf (Achilles reflex)

o NCV in Myopathy

• Normal study is the usual finding
• NCV in Neuropathy
• Disorders with axonal injury – amplitudes are reduced and conduction velocities may be slightly slowed
• Segmental demyelination with axonal sparing – conduction velocities are slowed and amplitudes are relatively spared (if severe, amplitudes will be reduced)
• Patterns
• Radiculopathy
• SNAPs are always normal since pathology is proximal to the DRG
• CMAPs low (axon from anterior horn cell affected)
• See chronic neurogenic motor units in a myotomal distribution
• Mononeuropathy
• low and slow SNAPs and SMAPs
• neurogenic motor units in a nerve distribution