- Because early compressive radiculopathy might be expected to cause focal, predominantly sensory demyelination F-waves will be normal. Only a radiculopathy with significant injury to a large proportion of the motor fibres would be expected to decrease response.

- If there is a severe C8 radiculopathy the F-response might still be normal due to the T1 component (and similarly in the lower limb)

H-Reflex

• Named after Paul Hoffman who developed the test in 1918

• Can be elicited from many motor nerves before age 2 – after that age – only tibial

• True reflex

o Afferent – Ia muscle spindle

o Synapse

o Efferent – alpha motor neuron

• Evoked by low amplitude, long (1ms) stimulus

• Procedure

o Recording electrode just under ¾ of the way down from popliteal fossa to Achilles tendon (2-3 FB below point where gastroc meets soleus).

o Stimulate popliteal fossa with cathode placed proximally

o Low intensity, 2sec between stimuli

o If response cannot be obtained try – slightly plantarflexing ankle or Jendrassik manoeuvre

o As stimulus increases H reflex increases in amplitude and decreases in latency

o At higher stimulus an M-reponse appears, this also travels up the motor fibre, collides with and reduces the H-response

o Take the H-reponse with the shortest latency and measure maximal amplitude

• Normal values

o <34ms (varies according to height and age, use nomogram)

o <1.5ms difference between sides

o H/M amplitude ratio <50%

• Major uses:

o Early polyneuropathy

o S1 radiculopathy

o Early GBS

o Tibial and sciatic neuropathy, sacral plexopathy

Test

• Nerves often used

• Sensory and motor

• Median, ulnar, radial

• Sensory

• Sural, superficial peroneal, facial and accessory

• Motor

• Peroneal and tibial

•

Interpretation

	Demyelination	Axonal
CMAP amplitude	Normal	Small
Conduction block	Present	Non-present
Distal motor latency	Prolonged	Normal/slightly prolonged
Motor conduction velocity	Reduced	Normal/slightly reduced
Sensory response	Small absent	Small absent
F-wave	Prolonged	Normal/slightly prolonged

EMG

Summary

Insertional activity

• Burst of discharge on insertion of the needle

• Muscle fibres responding to structural damage/deformation from needle

• Decreased or absent – inexcitable fibres

o Fibrotic/atrophic muscle

o Familial periodic paralysis

• Prolonged – hyperexcitable fibres

o Denervation

o Myotonic disorder

o Myositis

Spontaneous activity

Activity occurring when the muscle is at rest, activity over which the patient has no control
Normal muscle should be electrically silent

Endplate noise

• Low amplitude, monophasic, negative potentials

• Motor end plate potentials

• Rate: 20-40Hz

• Sound: Seashell

• Cause: Normal endplate

Endplate Spikes

• Source: single muscle fibre

o Firing due to irritation of terminal axon twigs by needle

• Initial negative deflection (c.f. fibrillations)

• Pattern: Irregular (sputtering)

• Rate: 5-50Hz

• Sound: sputtering, like fate in frying pan.

Fibrillation and positive sharp waves

• Are the same thing - Fibrillation – upwards deflections, PSWs – downwards deflections.

• Source: result from spontaneous firing of individual muscle fibres.

• Myopathies - if there is fibre splitting, part of the fibre becomes functionally denervated

• Occur as fibres become hyper-excitable when they lose their nerve supply and overexpress Ach receptors.

• Causes:

o Denervation

o Some muscle disease – esp. inflammatory myopathies

o Severe NMJ disease – e.g. botulism (rarely)

• Fibrillation

o Brief initial positive spike, then brief negative

o 1-5ms

o Low amplitude 10-100uV

o Very Regular 0.5-10Hz – may slow (c.f. endplate spikes – very irregular)

o Get smaller with more chronic denervation

o Sound – rain on roof

• Positive sharp waves

o Brief initial positive, long negative

o Low amplitude 10-100uV

o Caused by needle deforming muscle fibre

o Occasional discharges in distal muscles acceptable as normal

• Grading

o 0 - None

o +1 – Single trains in at least 2 areas

o +2 – Moderate number in 3 or more areas

o +3 – Many in all areas

o +4 – full interference pattern

Complex repetitive discharge

• Source: Depolarisation of single muscle fibre, followed by ephaptic spread to adjacent fibres, generates circuit

• Sound: Machine

• Rate: High frequency 5-100Hz

• Pattern: Perfectly regular, unless overdriven

• Usually identical each time

• Causes:

o Denervation – usually chronic rather than acute, such that group atrophy has occurred to allow denervated fibres to lie next to each other

o Some acute muscle disease with denervation

Myotonic discharges

• Source: Single muscle fibre

• Pattern:

o Waxing and waning of frequency and amplitude

• Rate: 20-150Hz

• Sound: Revving engine, Dive bomber

• Causes:

o Myotonic dystrophy

o Myotonia congenita

o Paramyotonia congenita

o Other myopathies: Acid maltase, polymyositis, myotubular myopathy

o Hyperkalaemic periodic paralysis

o Denervation (rarely)

Fasciculation

• Source: spontaneous firing of part or whole of motor unit

• Probably arise in the terminal braches of the motor nerve

• Morphology of normal CMAP (or abnormal if there is reinnervation)

• Rate:

o Often very slow (1-2Hz – c.f. minimum 4-5Hz of voluntary activity)

o Overall range 0.1-10Hz

• Pattern: Irregular

• Sound: Corn popping

• Causes: Occur in neurogenic conditions

Doublets/Multiplets

• Grouped fasciculations

• Same significance as fasciculations except are characteristically seen in hypocalcaemia

Myokymia

• Grouped fasciculations

• Rhythmic grouped spontaneous firing of the same motor unit

• Spontaneous depolarisation or ephaptic transmission along demyelinated segments of nerves

• Rate:

o Intraburst 5-60Hz

o Interburst 1-5Hz

• Sound: Marching soldiers

• Causes:

o Radiation injury (usually brachial plexus)

o GBS (Facial)

o MS (facial)

o Pontine tumours (Facial)

o Hypocalcaemia

o Timber rattlesnake venom

o Rarely also seen in:

- GBS (limbs)

- CIDP

- Nerve entrapments

- Radiculopathy

Cramps

• Painful, involuntary contractions of muscle that tend to occur when muscle is in shortened position and contracting

• Source: High frequency discharges of motor axons/motor units

• Rate: 40-75Hz

Neuromyotonic discharges

• Involuntary spontaneous discharge of motor units and their axons

• Rate: Very high frequency 150-250Hz

• Pattern: Decrementing, repetitive discharge of a single motor unit

• Sound: Pinging

• Cause:

o Neuomyotonic syndromes (Isaac’s syndrome etc)

o Extremely chronic neuropathic disease (e.g. polio and SMA)

o Hereditary neuromyotonia

Voluntary Activity

• Analyse:

o Morphology

- Duration

- Polyphasia

- Amplitude

o Stability

o Firing Pattern

- Activation

- Recruitment

- Interference

Morphology

Duration

• Parameter that best reflects number of muscle fibres in motor unit

• Typical 5-15ms

• Increased with age

• Decreases with increased temperature

• Increased in distal muscles

• Sound – duration is inversely proportional to pitch (dull to crisp)

Polyphasia

• Measure of synchrony

• Nonspecific

• Normal:

o 2-4phases

o <5-10% of MUAPs polyphasic

o Except deltoid: normal <25%

• Sound: high frequency clicking

Amplitude

• Measured from negative to positive peak

• Normal 0.1-2mV

• Increased size with motor unit synchrony

• Sound: proportional to volume

Stability

• Measure of the similarity of the morphology of an individual MUAP each time it fires

• Lack of stability correlates with impaired NMJ function

Firing Pattern

Activation

• Ability to increase firing rate

• Causes:

o Central disease – CNS – MS/stroke

o Reluctance to activate due to pain

Recruitment

• Ability to recruit more MUAPs as the firing rate and force increase

• First motor unit starts with rate of 5Hz, by 10Hz a second unite should activate and so on.

• 5:1 ratio

• Decreased recruitment

o Loss of MUAP axons

o Conduction block

Early recruitment

• Too many units firing for the degree of force being generated (examiner needs to be judging amount of force)

• Seen when there is dropout of individual muscle fibres (Myopathies/NMJ blockade)

• Each MUAP generates less force, therefore more units needed early

Common patterns

EMG

NCS

MUAP Morphology

MUAP Firing Pattern

Spontaneous

Motor

Sensory

Dur.

Amp.

Pha.

Act.

Recr.

Fibs/PSW

Amp

F-M

Amp

Neuropathic-axonal

Acute (several days – few weeks)

N/I

N/D

N/I

N/D

Subacute (several weeks)

I++

N/I

N/D

N/I

N/D

Chronic (inactive: months-yrs)

N/D

N/I

N/D

N/I

N/D

N/I

N/D

Neuropathic-demyelinating

Proximal lesion - slowing

Distal-N

Prox- D

I++

Proximal lesion – with block

Distal-N

Prox- D

I++

Distal Lesion – slowing

N/D

I++

D++

Distal lesion - block

I++

D++

Early reinnervation after severe denervation

D++

N/I

N/D

N/I

D++

N/D

N/I

Myopathic

Acute

N/Early

N/+/Myotonia

N/D

Chronic (with denervating features)

D/I

N/Early

N/+/CRDs

N/D

Endstage

D/I

D++

N/D

NMJ disorders

Increased jitter

PreS-N

PostS-D

Intermittent block

N/D

N/I

N/Early

I+

Severe block

D++

I++

CNS disorders

D++

o L5-S1 nerve root lesion fibs and PSWs develop after:

- 10-14days - Paraspinal muscles

- 2-3 weeks - Proximal thigh

- 3-4 weeks - Leg

- 5-6 weeks – distal leg/foot

o If it is a distal lesion, near NMJ, then may only take a few days to develop.

	Immediate	Hyperacute <3 days	Acute >1Wk to <3-6 Wk	Subacute >1 Wk to < 3-6 Wk	Subacute/Chronic >2-3 Months to Many months	Chronic Years
Clinical findings	Abnormal	Abnormal	Abnormal	Abnormal	Abnormal	Abnormal/Normal
NCS	Normal	Normal	Abnormal	Abnormal	Abnormal	Abnormal/Normal
MUAP recruitment	Decreased	Decreased	Decreased	Decreased	Decreased	Decreased
Spontaneous activity	Normal	Normal	Normal/ abnormal	Abnormal	Abnormal	Normal
MUAP morphology	Normal	Normal	Normal	Normal	Reinnervated	Reinnervated