Basic Principles

of Needle electrode EMG

t in a
p t . t ia r a k e n c a n a
“ After Sales Service Is More Important Than Sales “

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Introduction to EMG
• When is EMG testing performed?
− Find the cause of weakness, paralysis, or muscle twitching
− Diseases that damage muscle tissue, nerves, or the
junctions between nerve and muscle (neuromuscular
junctions). These include amyotrophic lateral sclerosis (ALS),
or myasthenia gravis (MG), muscular dsytrophy, etc.

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 What do we express with needle EMG?

• Muscle membrane function - spontaneous

• Muscle fibre characteristics; diameter
• MU organisation
– number of fibres
– grouping
• N-M transmission
• # motor units
– total
– activation; pattern, fullness

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 Steps in EMG analysis
• Insertional activity
—Decreased
—Increased
• at rest - spontaneous activity
– fibs, psw, myotonia, complex rep discharges(CRD)
– fasciculations, myokymia
• at slight voluntary contraction – MUP/Motor units/recruitment
—Manual selection from the 5 seconds recording,
—Triggering selection
—Multi-MUP, automatic recognition and AVG
—shape parameters, stability (jiggle), behaviour
• at strong/maximum contraction - interference pattern
– recruitment, fullness, MUP parameters, sum of motor
unit potentials
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 Spontaneous activity from the muscle
FINDING
• neurotonic discharges
• myokymic discharges
• muscle cramps
• fasciculations
• neurogenic extra discharges
MEASURE AS
• #/ 10 recording sites
• or +, ++, +++, ++++
– few (per time unit)
– moderate
– abundant
• indicated
– spontaneous or
– after provocation

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Spontaneous EMG activity

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 At rest
• No electrical activity, NOTE, muscle position for
complete rest

• EXCEPTIONS (we may hear something!)

– insertion activity
– motor end-plate noise
– nerve spikes
– few positive waves in end-plate region

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 Insertional activity
Decreased
Muscle necrosis
Increased
Neuropathy often before fibrillation
potentials appear
Myopathy
Some healthy muscles
Calf muscles
Thenar muscles

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Normal spontaneous/Insertional activity
Burst of muscle fiber action
potentials provoked by the
movement of the needle
electrode
Duration <100 ms
Not a reliable parameter for
abnormality

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 Abnormal Insertional activity

Reduced
Increased

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 End-plate activity monophasic

Spontaneous electric activity recorded with a needle electrode close to muscle end-plates
Low-amplitude (10-20 μV), short-duration (0.5-1 ms), monophasic (negative) potentials that occur

in a dense, steady pattern and are restricted to a localized area of the muscle
Because of the multitude of different potentials occurring, the exact frequency, although
appearing to be high, cannot be defined
These non-propagated potentials are probably miniature end-plate potentials recorded
extracellularly
 This form of end-plate activity has been referred to as end-plate noise or seashell sound
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 End-plate activity biphasic

Moderate-amplitude (100-300 μV), short-duration (2-4 ms), biphasic (negative-positive)

spike potentials that occur irregularly in short bursts with a high frequency (50-100 Hz),

restricted to a localized area within the muscle.

These propagated potentials are generated by muscle fibers excited by activity in nerve
terminals.
These potentials have been referred to as biphasic spike potentials, end-plate spikes,
and, incorrectly, nerve potentials.

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 Fasciculaiton potentials - significance
Normal in distal intrinsic foot muscles, any age
Benign fasciculation
May be short lasting
Sometimes permanent
Neurogenic disorders
Usually chronic or inactive
Motor neuron disease

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 Fasciculation potentials

Random spontaneous twitching of a group of muscle fibers or motor unit. This twitch
may produce movement of the overlying skin, mucous membrane or digits
The electric activity is called fasciculation potentials

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 Generation of fasciculation potentials

Abnormal spontaneous action potentials generated in the

motor neuron
Fasciculation potentials are generated both centrally and
peripherally in the motoneuron
Initial axon hillock of the axon
Local anesthesia does not block fasciculation in ALS
Muscle has been implicated in benign fasciculation
Also the upper motor neuron has been suggested

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 Fibrillation & PSW

Effects of denervation on muscle fibers

Sensitivity to acetylcholine increases x 100
Decreased resting membrane potential
New sodium channels develop after denervation
Increased sodium conductance
Require usually 2-4 weeks to develop, may be seen after 8-10 days
Muscles close to local nerve lesion are first to show fibrillation potentials
Steroids and cytostatic drugs suppress fibrillation potentials α –
bungarotoxin and ischaemia suppress fibrillation potentials,
acetylcholine receptors play a role
 Acetylcholine receptor hypersensitivity is not the sole cause

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 Fibrillation & PSW Fibrillation potential

The electric activity associated with a spontaneously contracting (fibrillating) muscle fiber
Action potential of a single muscle fiber
The action potentials may occur spontaneously or after movement of the needle electrode
The potentials fire at a constant rate
A small proportion fire irregularly
Potentials are biphasic spikes of short duration (<5 ms) with an initial positive phase and a peak-to-
peak amplitude of less than 1 mV
 Firing rate has a wide range (1-50 Hz) and often decreases just before cessation of an individual
discharge.
A high-pitched regular sound is associated with the discharge of fibrillation potentials and has been
described in the old literature as ”rain on a tin roof” by msyd 17
 Fibrillation & PSW Positive sharp waves

A biphasic, positive-negative potential

Initiated be needle movement
Recurring in a uniform, regular pattern at a rate of 1- 50 Hz; the discharge frequency may
decrease slightly just before cessation of discharge
The initial positive deflection is rapid (<1 ms), its duration is usually less than 5 ms, and the
amplitude is up to 1 mV
The negative phase is of low amplitude, with a duration of 10-100 ms.
Positive sharp waves can be recorded from the damaged area of fibrillating muscle fibers.
The positive sharp waveform is not specific for muscle fiber damage
Its configuration may result from the position of the needle electrode. The electrode triggers an
action potential propagating away from the electrode
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Fibrillation & PSW

Fibrillation potentials and positive sharp waves

Fibrillation

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20
 Fibrillation & PSW

Denervation activity

This term has been used to describe a fibrillation potentials and positive sharp waves
The use of this term is discouraged because fibrillation potentials may occur in
myopathies

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 Fibrillation & PSW

Fibrillation potentials - clinical significance

Occur rarely in healthy muscle

One out of 20 insertions
Neuropathic disorders
Acute or subacute
If initial lesion was severe, also in inactive
Myopathic disorders
Active myopathies
CNS
Following stroke or CNS trauma

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 Fibrillation & PSW

Fibrillation potentials
Quantification: Uppsala
Number of insertions/10 with
fibrillation potentials or positive sharp
waves
Does not take into account the number
of fibrillation potentials at each
insertion
Accurate and reproducible in mild cases
(2-5/10)
Not so reproducible at levels 6-9/10
Quantification: Mayo clinic
Grading Characteristics
0 No fibrillation potentials
1+ Single trains in at least two sites
2+ Moderate number in at least
three or more muscle areas
3+ Many in all muscle regions
4+ Baseline obliterated with
fibrillation potentials

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 Myotonic Myotonic discharges

Repetitive discharge at rates of 20 to 80 Hz are of two different types:

Biphasic (positive negative) spike potentials less than 5 ms in duration resembling
fibrillation potentials
Phositive waves of 5 to 20 ms duration resembling positive sharp waves
Both potential forms are recorded after needle insertion, after voluntary muscle contraction
or after muscle percussion, and are due to independent, repetitive discharges of single
muscle fibers
 The amplitude and frequency of the potentials must both wax and wane to be identified as
myotonic discharges
This change produces a characteristic musical sound due to corresponding change in pitch,
which has been likened to the sound of a “starting motor cycle”

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Myotonic

Myotonic disorders
Progressive myopathy and myotonia
Myotonic dystrophy type 1
Myotonic dystrophy type 2 (Proximal myotonic myopathy)
Main symptom myotonia
Myotonia congenita (Thomsen and Becker)
Myotonia fluctuans
Other myotonias
Chondrodystrophic myotonia
Paramyotonia congenita
Paraneoplastic myotonia
Periodic paralysis
Hyperkalemic periodic paralysis
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Myotonic
Na+ channel function
Channelopathies
Chloride channel
Myotonia congenita (Thomsen)
Myotonia congenita (Becker)
Myotonia levior
Na+ channel function Calcium channel
Hypokalemic periodic paralysis
Myasthenic syndrome
Sodium channel
Myotonia fluctuans
Paramyotonia congenita
Hyperkalemic periodic paralysis
Myotonia permanens
Acetazolamide responsive
myotonia
Potassium channels
Neuromyotonia

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 Myotonic

Myotonic dystrophy - Pathophysiology

Patients with mainly myotonia tend to have normal resting membrane

potential
Patients with severe dystrophy have reduced resting membrane
potential
Cl- conductance varies from low to low normal
K- conductance normal
Patch clamp studies have shown abnormal inactivation of Na+ channels
In myotonic muscular dystrophy, abnormal muscle Na+ currents
underlie
myotonic discharges (Mounsey et al 1995).

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 Neuromyotonia
Clinical syndrome of continuous muscle fiber activity manifested as
continuous muscle rippling and stiffness
The accompanying electric activity may be intermittent or continuous
Terms used to describe related clinical syndromes are continuous
muscle fiber activity, Isaac-Merton syndrome

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 Myotonic

Neuromyotonic discharges
Bursts of motor unit action potentials with originate in the motor axons
firing at high rates (150-300 Hz) for a few seconds, and which often start
and stop abruptly.
The amplitude of the response typically wanes.
Discharges may occur spontaneously or be initiated by needle movement,
voluntary effort and ischemia or percussion of a nerve.
These discharges should be distinguished from myotonic discharges and
complex repetitive discharges

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Myotonic

Neuromyotonia Isacs syndrome

Antibodies agains K+ channels
May be a paraneoplastic phenomenon
Generated in the axons
Respond to phenytoin or carbamazapine

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 complex rep discharges

Complex repetitive discharges

Polyphasic or serrated action potentials that may start spontaneously or after a

needle movement.
Uniform frequency, shape, and amplitude, with abrupt onset, cessation, or change
in shape
Amplitude ranges from 100 μV to 1 mV and frequency of discharge from 5 to 100 Hz
Bizarre high frequency discharge, bizarre repetitive discharge, bizarre repetitive
potential, near constant frequency trains, pseudomyotonic discharge and not
recommended by msyd 31
 complex rep discharges

Generation of complex repetitive discharges

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complex rep discharges

Significance of CRD

Rarely observed in healthy subjects

Myopathies
Polymyositis
Myscle dystrophies
Neuropathies
May be seen in most neuropathies
Chronic
CRD is a non-specific abnormality

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 Myokymia

Myokymia - definition
Motor unit action potentials that fire repetitively and may be
associated with clinical myokymia.
 Two firing patterns have been described
Brief repetitive firing of single units for a brief period (up to a few
seconds) at a uniform rate (2-60 Hz) followed by a brief period of
silence (up to a few seconds)
Less commonly uniform firing rate (1-5 Hz)
Clinically undulating spontaneous movements or contractions of the
muscle

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 Myokymia

Myokymic discharges

Probably generated in the motor axon

Blocked by curare
Spinal anesthesia has no effect
Demyelination seems to be important
Focal myokymia
Brachial plexus lesions following radiation therapy
Facial myokymia
MS
Pontine glioma
GBS, ALS, trigeminal neuralgia
Generalized myokymia (=neuromyotonia??)
Idiopathic or hereditary form
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Myokymic discharges

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 Abnormal spontaneous activity

Muscle fibers Motor units

Fibrillation potentials Fasciculation potentials
Positive sharp waves Neuromyotonia
Myotonic discharges Myokymia
Complex repetitive discharges Cramps

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 Abnormal Spontaneous Activity
Fibrillation potentials: spontaneous depolarizations
Positive sharp waves: same significance as fibrillation potentials
Complex repetitive discharges: depolarization of a single fiber followed by
ephaptic spread (muscle membrane to muscle membrane)
Myotonic Discharge: spontaneous discharge of msucle fiber with waaxing
and waning of amplitude and frequency (rate between 20 and 150)
Fasciculation: Single, spontaneous, involuntary discharge (slow rate 1-2 hz)

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 Grading of PSW/fibs
Very short runs of unsustained P-waves/fibs (<500 ms) should be
interpreted
as increased insertional activity.
1+ fibs/PSW: at least 2 areas of a muscle with sustained fibs/PSWs, clearly
defined visually and by audio
2+ fibs/PSW: fibs/PSWs present in most areas sampled in a muscle
3+ fibs/PSW: fibs/PSWs present in nearly all areas of the muscles sampled,
with many PSWs/fibs at each location
4+ fibs/PSW: complete interference pattern of PSW/fibs
This grading is helpful to the person hearing your report, but this does not
usually make or break a diagnosis. Severity of lesion is usually higher with
higher amounts of active denervation.

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 Generated in the muscle fibre

Seen in end-plate region also in normal muscle: irrgular, with initial negativity

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Generated in the muscle fibre

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Generated in the nerve/motor neurone

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Generated in the nerve/motor neurone

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 Muscle-normal

Insertional activity
• Description: burst of psw or biphasic act, < 300 msec

• Generated by: needle movement

• Seen in: all normal. May be prolonged in denervation

• Not seen in: fibrosis, hyperkal.per.par

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 Muscle-normal

End-plate noise

• Description: low amplitude noise, neg waves

• Generated by: mepp

• Seen in: normal muscle

– at end-plate region
– often accompanied by pain

• Not seen in: denervation

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 Muscle-normal

End-plate spikes

• Description: irregular negative spikes (100-200 uV) in end-plate regions

(often with end-plate noise in the backgound)

• Generated by: needle irritation of terminal nerve activating the muscle fibres

• Seen in: normal end-plate region

• Not seen in: denervation

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 Muscle- abnormal

Fibrillation potentials and positive sharp waves

• Description: Fib: usually regular(> 50%), s.f.a.p, rate 0.5-15 psw: often
irregular discharges or runs

• Generated by: denervated muscle fibres 7-21 days after axonal damage

• Seen in:
– nerve lesions
– axonal neuropathies
– MND
– muscular dystrophies

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 Muscle- abnormal

Myotonic discharges

• Description:s.f.a.p., waxing and waning trains, 20-100 Hz

• Generated by: membrane instability of single muscle fibres

• Seen in:
– myotonic dystrophy
– myotonia congenita
– paramyotonia
– acid maltase deficiency
– hypercalemic per paralysis

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 Muscle- abnormal
Complex repetitive discharges, CRD

• Description: abrupt onset and end of trains (few to hundreds discharges in

each), repeated with regular low (1-20) or high frequency (>50/sec)

• Generated by: ephaptic activation of adjacent denervated muscle fibres

• Seen in:
—polymyositis - post radiation neuropathy
—Duchenne myopathy - Schwartz-Jampel syndrome
—distal her myopathy - ALS
—myxoedema - Her neuropathies
—LG dystrophy - CT

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 Nerve/normal-abnormal

Fasciculations

• Description: variable complexes, 0.1-10 Hz

• Generated by: neurone, axon (terminal), muscle

• Seen in:
– normal (more after exercise) - metabolic disorders
– MND (thyretoxicosis,tetany,
– CJD antiACh-esterase therapy)
– radiculopathy

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 Nerve/normal-abnormal

Double discharges
• Description: extra discharge following 4-50 msec after a regular MUP

• Generated by: repetition of a MUP discharge. The extra discharge comes

within relative refractory period,has reduced amplitude and may block next
discharge

• Seen in:
₋ normal as first discharge after a pause - polymyositis
₋ st p GBS - dystr myotonica
₋ st p radiculopathy

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 Nerve

Myokymia
• Description: irregular bursts, 0.5-10/sec, with 2-10 discharges in each, 20-
80Hz

• Generated by: usually by MUPs (nerve initiation) but sometimes by single

muscle fibers (myogenic)

• Seen in:
– focal: st p Bell palsy, MS (facial myokymia), post-radiation
– segmental: syringomyelia
– generalized: CIDP, thyr.tox, familial parox kinesiogenic ataxia

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 Nerve

Neurotonia
• Description: Doublets, triplets, burts of MUPS 150-300 Hz, few seconds

• Generated by: activity or spont (K-channels?)

• Seen in: neurotonia, chron pnp, paramalign

• Not seen in: myotonia

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 Nerve/normal-abnormal

Muscle cramps
• Description: EMG activity as in voluntary

• Generated by: motor neurone hyperexcitability

• Seen in: all normal, chron neurogenic disorders,

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 Nerve/central

Synkinesia
• Description: involuntary activity triggered by remote vol activity

• Generated by: ephaptic transmission, aberrant innervation, central

hyperexcitability

• Seen in:
– St p Bell palsy
– syrinx
– st p trauma

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Denervation activity
- positive waves and fibrillation potentials

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 Slight contraction

Slight contraction
• Pinch the skin at insertion point (distraction)

• Ask for slight contraction. Move the electrode a little to reach ”focus”,
sharp signals

• Move the needle to new position

– 2 mm deeper
– 2 mm deeper
– out and then new direction—pyramid

• 2-3 skin insertions, total 30 MUPs

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 Slight contraction

Conc needle EMG, signals from 2 - 15 muscle fibres

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Slight contraction

1 normal motor unit

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Slight contraction

Parameters used in MUP analysis

parameter significance measurement
• amplitude # fibres/0.5mm peak-peak
• area # fibres/2 mm within dur
• duration # fibres in 2.5 mm slope criteria
• phases temp dispersion 0-cross + 1
• turns “ change in dir
• rise time closeness to fibre neg-pos peak
• satellites extreme delay late spike
• jiggle n-m transm

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Slight contraction

Multi-MUP, result

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Force contraction

Interference pattern

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Force contraction

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Force contraction

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•Weakness/fatigue
•central
•motor neurone
•peripheral nerve; pnp, focal
•muscle (nm-j, myopathy, periodic weakness)

•Numbness

•Cramps
• myotonia, ben. fasc. syn., neurotonia, stiff p. Syn

•Pain

•ICU
•Critical illness…

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Pattern of EMG changes in Neuropathic Disorders
Immediate: Morphology normal, recruitment decreased or absent
(depending on severity of injury)
Same pattern seen in demyelinating disorders with conduction block
10 days: Spontaneous activity present (wallerian degeneration has taken

place)
After 6 weeks morphology becomes more neuropathic (remodeling has
occurred): nDecreased recruitment, larger amplitude, polyphasic
Satellite potentials: small, short duration, unstable units time locked to
another larger unit
Nascent units: Small amplitude short duration units with decreased
recruitment (recruitment distinguished from myopathic units)

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 Radiculopathy

Typically, sensory nerve studies remain normal, in the relevant

dermatome.
Pathology is proximal to the dorsal root ganglion.
Motor CMAP amplitudes can be reduced.
EMG findings:
Active denervation, reduced recruitment in at least 2 anterior
myotome muscles innervated by that root, likely with paraspinal
active denervation also.

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 Plexopathy
Sensory studies: Most sensitive.
In contrast to radiculopathy, plexopathies
should feature reduced
amplitude/absent SNAPs.
In the dermatome affected:
Upper trunk: median SNAP +
musculocutaneous SNAP
Same for Lateral Cord lesions

Middle trunk: radial SNAP

Same for Posterior Cord lesions

Lower trunk: ulnar SNAP + medial cutaneous forearm SNAP

Same for Medial Cord lesions
EMG: can be severely abnormal, with 3-4+ fibs/no motor
units or
severely reduced recruitment
Paraspinals classically unaffected. by msyd 68
Brachial plexus - tips

- Dorsal scapular nerve arises

at the proximal point of
the upper trunk.
It innervates rhomboids,
which if abnormal
suggests a C5 root lesion.
- Radial muscles + deltoid
suggests a posterior
cord lesion
- Abnormal distal median and
ulnar muscles on EMG,
with normal median sensory
study suggests medial cord.
- Always look at paraspinals
to evaluate root lesion (avulsion)

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 Motor Neuron Disease

ALS, SMA, Kennedy’s disease will all have denervation that

cannot be explained by 1 or 2 single lesions.
One must continue to test additional muscles to rule out
more systemic illness.
E.g. CTS with active denervation in the APB prompts
evaluation of pronator, FDI, and other proximal muscles.
El Escorial criteria: 3 regions, each with 2 muscles showing
active denervation PLUS UMN findings in 3 regions (usually
no EMG correlate for UMN)
Awaji criteria are similar but allow for fasciculations to
count as active denervation

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 Myopathy
EMG reports of myopathy should also include the ideal muscle
biopsy target (if desired). nMost abnormal muscle, with small motor units,
especially if fibs/PSWs present. Ideally, this would be a vastus, biceps, deltoid,
brachioradialis, gastrocnemius, in declining order of preference.
Some myopathies can involve paraspinal muscles only. Difficult, but
possible to bx this site.
Generally perform EMG on one side only, leaving the contralateral
side for biopsy, to avoid EMG needle site affecting the biopsy
Exception: generally vastus medialis findings are assumed present in
vastus lateralis also.
The specific diagnosis of type of myopathy is rarely obvious from EMG
only (e.g. FSHD vs polymyositis). nException: myotonic dystrophy

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 Pattern of EMG changes in
Myopathic Disorders
Myopathy: number of functioning muscle fibers decreased—units smaller,
shorter duration.
Abnormal firing causes polyphasia
Acute: short duration, small amplitude units with normal or early recruitment
Chronic: (some denervation often occurs) long-duration, high amplitude
MUAPS can be seen (often with short-duration, small units)
Recruitment is still normal or early until end stage

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 Pattern of EMG changes in
Myopathic Disorders
Myopathy: number of functioning muscle fibers decreased—units smaller,
shorter duration.
Abnormal firing causes polyphasia
Acute: short duration, small amplitude units with normal or early recruitment
Chronic: (some denervation often occurs) long-duration, high amplitude
MUAPS can be seen (often with short-duration, small units)
Recruitment is still normal or early until end stage

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The classical changes seen in myopathy and neuropathy can now be understood
in a better way. A summary of the current view is given in this table.

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 The Upper Extremity Muscles
Intrinsic Muscles of the Hand

Abductor Digiti Minimi – Hand Abductor Pollicis Brevis First Dorsal Interosseous – Hand
N.Ulnar, C8,T1 N.Median C6,7,8,T1 N.Ulnar, C8,T1
Distal Arm

Anconeus Brachioradialis Extensor Carpi Radialis

N.Radial C6,7,8, N.Radial C6,7,8, N.Radial C6,7,8,
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 The Upper Extremity Muscles

Distal Arm

Extensor Digitorum Communis Extensor Indicis Flexor Carpi Radialis

N.Radial C6,7,8, N.Radial C6,7,8, N.Median C6,7,8,T1

Flexor Carpi Ulnaris Flexor Digitorium Profundus Flexor Pollicis Longus

N.Ulnar, C8,T1 N.Ulnar, C8,T1 N.Inteross Ant. C6,7,8,T1
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 The Upper Extremity Muscles

Distal Arm

Pronator Teres Supinator

N.Median C6,7,8,T1 N.Radial C6,7,8,
Proximal Arm and Shoulder

Biceps Brachii Deltoid – Anterior Deltoid – Middle 77

N.Musculocutaneous C8.T1 N.Axillaris C5
 The Upper Extremity Muscles
Proximal Arm and Shoulder

Infraspinatus Latissimus Dorsi Levator Scapula

N.Suprascapularis C5 N.Thoracodorsalis C7 N.Dorsalis capulae C5

Rhomboids – Major
Pectoralis Major – Clavicular Pectoralis Major – Sternocostal N.Dorsalis capulae C5
N.Thorac Ant Lat C7 N.Thorac Ant Lat C7
78
 The Upper Extremity Muscles

Proximal Arm and Shoulder

Supraspinatus
Rhomboids – Minor Serratus Anterior N.Suprascapularis C5
N.Dorsalis capulae C5 N.Thorac Longus C5,6,7

Triceps Brachii - Long Head

Teres Major Triceps Brachii - Lateral Head
N.Radial C6,7,8, 79
Axillaris C5 N.Radial C6,7,8,
 The Lower Extremity Muscles
Intrinsic Muscles of the Foot

Abductor Digiti Quinti – Foot Abductor Hallucis Extensor Digitorum Brevis

N.Tib Plant Med L4,5,S1,2,3 N.Tib Plant Med L4,5,S1,2,3 N.Peroneous L 4,5, S1.

First Dorsal Interosseous – Foot

N.Tibialis L4,5,S1,2,3 80
 The Lower Extremity Muscles

Distal Leg

Tibial Anterior Extensor Dig.Longus Ext. Hallucis Longus

N.Peroneous L 4,5, S1. N.Peroneous L 4,5, S1. N.Tibialis L4,5,S1,2,3

Peroneous Longus
N.Peroneous L 4,5, S1.
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 The Lower Extremity Muscles
Distal Leg

Soleus
N.Tibialis L4,5,S1,2,3 Gastrocnemius - Medial Head Gastrocnemius - Lateral Head
Thigh and Pelvis N.Tibialis L4,5,S1,2,3 N.Tibialis L4,5,S1,2,3

Gluteus Maximus
Biceps Femoris - Short Head N.Gluteus Ant L5,S1,2
Adductor Longus
N.Tibialis L4,5,S1,2,3
N.Obturatorius L1,2,3,4
0 82
 The Lower Extremity Muscles
Thigh and Pelvis

Gluteus Medius Iliacus Semimembranosus

N.Gluteus Superior L4,5 N.Femoralis L1,2,3,4 N.Tibialis L4,5,S1,2,3

Semitendinosus Vastus Lateralis Vastus Medialis

N.Tibialis L4,5,S1,2,3 N.Femoralis L1,2,3,4 N.Femoralis L1,2,3,4 83
Paraspinal Muscles

Cervical Paraspinals/Trapezius Thoracic Paraspinals Lumbar Paraspinals

N. Accessories/Cervical Spinal Nerve C3,4 Posterior branch of spinal nerve T1,2
Cranial Muscles

Frontalis Masseter Orbicularis Oculi

N.VII N.VII N.VII

84
Cranial Muscles

Orbicularis Oris
N.VII Sternocleidomastoid Tounge – Genioglossus
N.VII N.VII

Trapezius
N. Accessories C3,4 85
Other Muscles

Scalenes Splenius Capitus

86
 Thanks !

t in a
p t . t ia r a k e n c a n a

Neuro Diagnostics 87
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