The document discusses the motor unit and electromyography (EMG). It describes how EMG can be used to examine muscle activity and motor unit recruitment patterns. Minimal muscle contraction activates few motor units, while increased tension recruits more units in a set order based on size. EMG can provide information about normal motor unit firing rates and patterns, as well as abnormalities seen in various neurological and muscular diseases. The effects of age, temperature, fatigue, disuse and other factors on EMG readings are also reviewed.

1. The Motor Unit &
Electromyography
Stanley J. Myers, Bhagwan T. Shahani, and
Frans L. Bruyninckx
Reading Downey and Darling’s Chapter 14

2. Interference pattern &
recruitment
 Needle emg examination of a normal
skeletal muscle at rest reveals an
isoelectric baseline
 Recruitment :
◦ Successive activation of the same &
additional motor units with increasing
strength of voluntary muscle contraction

3. Interference pattern &
recruitment
 Minimal voluntary contraction  1 or
several motor units are activated  low
amplitude
 As tension increase  firing frequency
of the individual potential increase
 Motor unit potentials tended to
increase in amplitude with heightened
tension during isometric contraction
(Studies of the human rectus femoris &
gastrocnemius)

4. Interference pattern &
recruitment
Order of recruitment :
 S type (slow-fatigue , type I) :
◦ Low strength of contraction  few motor units are active
slow rate of discharge & low amplitude
◦ Low-treshold, early activated unit produce relatively small
forces used for fine motor control & postural adjustment.
 Increasing tension  increases the frequency of
discharge by the active motor unit & recruitment of
previously inactive units
 FF (fast-fatigue) or FR (fatigue-resistant) type :
◦ Higher threshold units, larger force contribution
 Motor units are recruited in order of size, from small to
large.

5. Interference Pattern & Recruitment
 Normal, smooth, clinically sustained
contraction of a muscle, motor units fire
at a rate and in relation to each other 
smooth, continous, nonjerky contraction.
 Recruitment interval :
◦ Interdischarge interval between two
consecutive discharge of a MUAP at the point
at which a second motor unit potential is
recruited with gradually increasing strength of
voluntary muscle contraction

6. Interference Pattern &
Recruitment
 Recruitment frequency (firing rate)
◦ Firing rate of a MUAP when a different
MUAP first appears, with gradually
increasing strength of voluntary muscle
contraction
◦ The reciprocal of the recruitment interval
◦ Quantitative measures
◦ Most accurately evaluated when a fixed,
low-level percentage of max voluntary
contraction (MVC) of a particular muscle
(25-30%) is maintained

8. Interference Pattern &
Recruitment
 In neuropathic disease:
◦ First unit usually firing more rapidly at the
moment when the second is recruited.
◦ the recruitment interval is shortened
◦ Recruitment frequency is increased
 In myopathic disease :
◦ first unit is firing more slowly at the moment
when the second unit is recruited
 Ratio of the average firing rate to the
number of active units (N < 5:1)

9. Interference Pattern &
Recruitment
 It appears that recruitmet has a more
important role in grading of activity than
does changing the frequency, except at
very low and very high contraction
strenghts
 Under most condition (25-75% MVC),
the fastest units respond at frequencies
between 25-35 Hz.
 Over the tension range of 5-60% MVC,
the firing starts and stops abruptly and
frequency increases, but not in
proportion to strength

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13. Effect of age
 The normal mean duration of the
muscle action potential increases with
age.
 Decrease in the propagation velocity
of the impulse over the muscle fiber.
 Peterson & Kugelberg :
◦ in young persons normal values are
obtained from the first-recruited low-
treshold muscle action potentials
◦ Aging may selectively destroy muscle
fibers with the largest calibers and lowest
tresholds.

14. Effect of age
Stalberg & Thiele :
 Study on EDC muscle in subject aged
10-89 years
 Fiber density increases slowly
throughout life and progress faster
after age 70 years
 Impairment of nerve and
neuromuscular impulse transmission
increases at the same time 
degenerative loss of motor neurons
with aging was compensated for by

15. Effect of age
 Motor unit density in the m tibialis
anterior decreased with age 
indicate loss of motor units with
increasing age
 Distal muscles show more extensive
changes than proximal ones, & not all
muscles are uniformly affected
 There was no evidenc for loss of
motor neurons p to age 60, but
beyond that age, there was evidence
for a diminishing motor neuron
population

16. Effect of temperature
 For every 1 ° reduction :
◦ Mean duration of the muscle action potential increases
10-30%
◦ Mean amplitude decreases by 2-5%
 The number of polyphasic potentials can increase
as much as 10-fold with a 10% decrease in
temperature
 Temperature coefficient of the propagation
velocity  prolongation of duration
 The slower propagation velocity of the impulse
over the muscle fiber and the terminal nerve fibers
can cause temporal dispersion of fibers within the
motor unit

17. Fatigue
• Neuromuscular fatique :
 Any reduction in the force-generating
capacity of the total neuromuscular system,
regardless of the force required in any given
situation
 Increased of force caused by:
◦ Activation of more motor units
◦ Greater frequency of discharge
 Fatiguing muscle :
◦ Relative force developed
◦ Sum of electrical activity remain linearly
related until the level of mechanical activity
cannot be maintained

18. Fatigue
 EMG results recorded with surface
electrode:
◦ Increased amplitude of the summated
potentials
◦ Decreased frequency
 Jerky firing pattern
 Needle EMG :
◦ Discharges of fibers from different motor
units tend to group during fatiguing muscle
work
◦ Increase in total number of active motor
units
◦ Individual MUAPs are decreased in
amplitude, duration is little changed.
◦ Number of polyphasic potentials is
increased (incomplete synchronization

19. Effect of disuse
 In muscle with disuse atrophy,
polyphasic potensials accounted for
25% of all action potentials, normal
muscle 1-3%
 A reduction or increase in duration of
MUAPs occasionally is noted.

20. Clinical Applications
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Lower Motor Neuron Disease
 EMG has certain general characteristics:
- ↑ Insertional activity, fibrilation potentials, and
PSW, fasciculation potentials
- ↑ amplitude & average duration of MUAPs
together with ↑ incidence of polyphasic
potentials
- ↓ number of MUAPs observed during full
effort
 Axonal sprouting : Collateral regeneration
consists of the ingrowth of branches from
intact nerve fibers to adjacent denervated
muscle fibers.

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Anterior Horn Cell Disorders
- Poliomyelitis, ALS, the progressive SMA
(e.g., Werdnig-Hoffman disease), & in
hereditary degenerative conditions (Charcot-
Marie Tooth disease)
- Fibrilation potentials  common
- Fasciculation potentialsmay be seen
- The degree of spontaneous activity
diminishes with chronicity & reinnervation
- Most MUAPs have prolonged duration &
pronounced ↑ amplitude

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Nerve Root & Plexus Lesions
- Causes denervation in the involved
segments
- Manifested by fibrilllation potentials &
occasional fasciculation, reduced numbers
of MUAPs under voluntary control, and
complex polyphasic units, increased
duration.
- Acute phase: electrical silence with
fibrilation potential and PSWWallerian
degeneration

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Peripheral Nerve Disorders
- Physiological block (neuropraxia) 
characterized by electrical silence at rest,
no voluntary action potentials if block is
complete & reduced number of normal
potentials if the block is partial.
- Fibrilation & PSW noted approximately of
10 days after the injury.
- Voluntary MUP first seen with return of
function are of low amplitude, long duration
& polyphasic  caused by early terminal
reinnervation of a reduced unit.
- In peripheral neuropathy both axonal
degeneration and demyelination can
occur.

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Motor End-Plate Disturbances
- A defect in transmission across the NMJ,
as in myasthenia gravis, characterized by
a decrease amplitude of the successively
evoked potentials on repeated low-
frequency stimulation.
- Change in amplitude by blocking of
excitation at the end-plate to a variable
number of muscle fibers supplied by the
neuron with fibers recovering at different
rates.
- MG: autoimune disease which the defect
is at the postsynaptic junction.

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Myashenic Syndrome (Lambert-Eaton
Myasthenic Syndrome)
- The weak, resting patient becomes weaker
with continuing muscle contraction or
stimulation after an initial period of enhanced
strength.
- The defect is in the presynaptic region

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Myopathy
- Fibrillation potentials mechanism is not
completely clear
- In progressive muscular dystrophy and
hyperkalemic periodic paralysis these
spontaneous discharges  related to the
increase in excitability resulting from low
levels of intracellular potassium also the
degenerating muscle fibers may lose their
terminal innervation
- Complex repetitive discharge noted in
myositis
- Low amplitude, short duration

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Myotonia
- Abnormally sustained contraction & difficulty
in relaxation.
- EMG:
Repetittive high-frequency, waxing & waning
discharges (positive waves or biphasic
potentials whose initial deflection is positive)

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Upper Motor Neuron Lession
- Hoefer & Putnam  study in spastic
condition : voluntary contraction show
decreased frequency & amplitude.
- EMG finding of PSW & fibrilation
potentials
- A number of theories proposed to explain
 transsynaptic neuronal degeneration,
membrane instability, & antifibrilation
factor.

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33. Synchronization
 Is demonstrated when action potentials
are obtained simultaneously from 2 or
more widely separated recording
electrodes
 The cause is not clear 
◦ intraspinal mechanism for synchronization
of dicharge rhythm in a number of different
motor units supplied by the same spinal
segment
◦ In a given muscle single units of large area
are responsible

34. Study
 Spinal cords of 47 subjects , 13-95 years
, died suddenly, were examined
 There was no evidence for loss of motor
neurons up to age 60, but beyond that
age, although individual counts varied
considerably, there was evidence for a
diminishing motor neuron population.
 > age 60  only 50% of younger
subjects
 Clinical weakness usually is not noted
until 40-60% of muscle fibers have been
lost.

35. Chapter 2 Neurons and Associated Cells
33
Figure 2.11: Degeneration and
regeneration of peripheral somatic
motor nerve fibers. (A) Several
days after transection (at the wedge). Note
the central chromatolysis and eccentric
nuclei,
increase in number of neurolemma cells,
and fragmentation of myelin sheaths. (B)
Several weeks
later, the neurolemma cord receives
regenerating axis cylinders from the
transected fibers and collateral
branches from the adjacent normal fiber.
(C) Several months later, collateral
branches of axis
cylinders that failed to innervate motor end
plates degenerate. The regenerated
portions of the fibers
contain more internodes than before:
hence, they conduct nerve impulses more

38. Interference Pattern &
Recruitment
 Recruitment has a more important role
in grading of activity
 25-75% MVC : the fastest units
respond at frequency 25-35 Hz
 Over the tension range of 5-60%
MVC, The firing stars and stop
abruptly, frequency increases, but not
in propotion to strenght

39. Interference Pattern &
Recruitment
 For example : in one motor unit  the
firing commenced at 20 Hz when the
tension was 15% of MCV & increased
with the tension rise, but only to 30 Hz
 Units that are active at tensions below
5% of MVC usually have a lower
starting frequency (5-7 Hz) and
greater frequency range, irregular
discharge rates,even during constant
contraction