Transcript EMG and NCV for upper extremity diagnosis

EMG, NCV and SSEP for
evaluating and diagnosing
upper extremity neuromuscular
disorders
Dr. David Stannard
•
•
•
•
Dr. David Stannard D.C., FCCO(C), FACO, FABES.
Doctor of Chiropractic (Research Honors)
Chiropractic Orthopedic Specialist
Fellow of the College of Chiropractic
Orthopedists (Canada)
• DABCO
• Fellow of the North American Academy of
Impairment Rating Physicians
• Fellow of the American Board of
Electrodiagnostic Specialties
Additional post graduate training
• Completed advanced training in acupuncture
• Completed advanced training in vestibular
disorders, diagnosis, treatment and
rehabilitation
• Completed the electrodiagnosis program and
performed EDX studies for 1 ½ years
• Recently completed the Diplomate Neurology
program and is currently board eligible.
• Hospital privileges at the Medicine Hat
Regional Hospital for 5 years.
• WCB authorized provider
• Appointed Independent Medical Consultant
(IMC) as registered by the Alberta Insurance
Bureau.
• Operates a full orthopedic rehabilitative clinic
including casting and bracing of fractures.
Appointments
Appointments include Canadian Director for the
North American Academy of Impairment Rating
Physicians. (10 years to current)
Currently serves as Director for The Pain Society
of Alberta– a multi-disciplinary medical society.
Qualified as an expert witness in the Alberta
judicial courts system.
Publications and presentations
• Adverse Effects of Diagnostic Ultrasound, A
Review. Journal of Chiropractic Research and
Clinical Investigation 1990. (Peer reviewed
journal).
• Rigid Lumbar Orthosis (Masters Thesis) poster
presentations to the International Society for the
Study of the Lumbar Spine (2003).
• The Tempromandibular apparatus: a commonly
overlooked source of head pain. (manuscript in
progress)
Electrodiagnosis
• Electrodiagnostic (EDX) studies play a key role
in the evaluation of patients with
neuromuscular disorders.
• Among these studies are nerve conduction
studies (NCV), repetitive stimulation, late
responses (F-wave and H reflex), SSEP, blink
reflexes and needle electromyography (EMG),
in addition to a variety of other specialized
examinations.
NCV’s and EMG
• NCV’s and needle EMG form the core of the
EDX study. These studies are performed first
and usually yield the greatest diagnostic value.
• Performed and interpreted correctly, EDX
studies yield critical information about
underlying neuromuscular disorders and allow
use of other diagnostic imaging or laboratory
tests in an appropriate and efficient manner.
EDX looks at function of the nervous
system
• The specialized nerve tests like EMG, NCV and
SSEP are designed to investigate and diagnose
the functioning of the nervous system; while
imaging studies like the CT scans or MRI scans
look at the structure or anatomy of a
particular body part or organ.
What is an NCV
• NCV, or Nerve Conduction Velocity, is an
electrical diagnostic test that provides
information about abnormal conditions in the
nerves. Nerves are stimulated with small
electrical impulses by one electrode while
other electrodes detect the electrical impulse
"down-stream" from the first electrode.
NCV wave form may look like this
Interpreting NCV
• When interpreting NCV, the distance between
electrodes and the time it takes for electrical
impulses to travel between electrodes are
used to calculate the speed of impulse
transmission. Slower than normal speed could
indicate nerve damage from direct trauma,
demyelination, diabetic or peripheral
neuropathy, viral nerve infection or nerve
entrapment diseases like the Carpal Tunnel
Syndrome among other conditions.
What is EMG?
• EMG, or Electromyography is a technique for
evaluating and recording the electrical activity
produced by muscles. An electromyogram
detects the tiny amount of electricity
generated by muscle cells when they are
activated by the nerves connected to them.
Types of EMG
• There are two types of EMG: intramuscular
EMG and surface EMG. The intramuscular
EMG is the most common. It involves inserting
a needle electrode through the skin into the
muscle that is being studied. Surface EMG
(SEMG) involves placing electrodes on the skin
over the muscle to detect the electrical
activity of the muscle. It is not used as often
because it provides less useful information
than the intramuscular EMG.
EMG
• EMGs can detect abnormal muscle electrical
activity in many diseases and conditions,
including inflammation of muscles, pinched
nerves, damage to nerves in the arms and legs,
disc herniation, and degenerative diseases such
as muscular dystrophy, Lou Gehrig's disease and
Myesthenia gravis, among others. The EMG helps
doctors distinguish between muscle conditions
that begin in the muscle and nerve disorders that
cause muscle weakness.
EDX supports dx and appropriate care
• The information gained from EDX studies
often lead to specific chiropractic treatment
strategies, medical treatment or surgery.
•
EDX support your clinical examination
• In practice, EDX studies serve as an extension
of the clinical examination and should always
be considered as such.
EDX Quantitates Nerve and/or Muscle
Injury
•
•
•
•
•
•
Provides Useful Data Regarding Nerve
Injury
Site
Type
Severity
Duration
Prognosis
Goals of EDX Testing
•
|
|
•
Location
Severity
•
________|____________|_________
•
|
|
|
|
• Muscle
NMJ
Nerve Anterior Horn
Nerve Conduction Studies
• Studies of the waveforms generated in the
• peripheral nervous system.
• – Motor nerve conduction (CMAP)
• Stimulation of a peripheral nerve while
recording from a muscle innervated by that
nerve.
• Sensory nerve conduction (SNAP)
• Stimulation a mixed nerve while recording from a
mixed or cutaneous nerve
Terminology
•
•
•
•
LATENCY (DL)
Interval between the onset of a stimulus and the onset of a response.
AMPLITUDE (AMP)
The maximum voltage difference between two point. It is proportional to the
number and size of nerve fibers that are depolarized.
Provides an estimate of the amount of nerve tissue that is electrically active
DURATION
The time from onset to termination.
Total duration measures the dispersion of all components.
Measures the differences in conduction of the nerve fibers
CONDUCTION VELOCITY (CV)
The “speed” at which the nerve fibers are carrying the electrical stimulus
between two sites.
Comparison of conduction between two segments of the same nerve can localize
a lesion.
Types of nerve conduction
studies
• Sensory: typically antidromic
- Commonly examined nerves: Sural, ulnar,
median, occasionally radial, superficial
peroneal or lateral femoral cutaneous nerve.
Sensory NCS Parameters
• Onset and peak latencies
Conduction velocity determined by velocity
of a very few fast fibers
• Amplitude
determined by the number of large sensory
fibers activated
Motor Nerve Conductions
• Vital part of EDX as this important for
identifying demyelination and compression
• Need to do proximal and distal studies to
evaluate for conduction velocity, conduction
block, temporal dispersion
• Typical nerves: ulnar, median, peroneal, and
tibial.
• Less common: radial, femoral, phrenic, spinal
accessory, facial.
F-waves and H-reflex
• Useful for identifying proximal segmental
Demyelination
• Can only be done when motor amplitude is >
1 mV
• Dependent on patient’s height.
F wave and H reflex
F waves
• Motor F wave studies proximal roots: Antidromic motor
to the anterior horn of the spinal cord; orthodromically
to the muscle.
• Pure motor test.
• A prolonged asymmetric F waves suggest a proximal
root lesion.
• Clinical application best for plexopathy.
– Quite prolonged in demyelination, AIDP, mild
prolongation in axonal injury.
• Less sensitive than EMG for radiculopathy since only
short segment of nerve is demyelinated in
radiculopathy.
F - wave
Abnormal demyelinating PN F-wave
H REFLEX
• Reflex loop: Orthodromic sensory and motor
- Utilized to assess for radiculopathy of S1, *C6/7
• S1; Popliteal fossa, record in Medial Gastrocnemeus
• C6/7; Median nerve at wrist, record at Flexor Carpi
Radialis
• Unilateral delay, absent suggests tibial, sciatic, sacral
plexus, cord, S1 motor or sensory roots.
– Once abnormal, may not normalize;
– Often absent in polyneuropathy or > 60 years of age.
Example of a H – Reflex
Needle Electromyography: Techniques
• Needle electrode is inserted into the muscle
• Needle is disposable, single use
• Multiple muscles are accessible for
examination
• Combination of muscles tested
- Dependent upon clinical question
- Level of discomfort is mild
Needle Electromyography: Data
•
•
•
•
•
Insertional Activity
Spontaneous Activity
Motor Unit Configuration
Motor Unit Recruitment
Interference Pattern
EMG data
Needle EMG
• Insertion activity increases within a few days
of muscle denervation, whereas abnormal
spontaneous activity takes 2‐4(3) weeks to
develop, depending on the distance between
the nerve lesion and the muscle
• Abnormal spontaneous activity and increased
insertion activity are not pathognomonic of
denervation, may occur in certain disorders
of muscle or the neuromuscular junction
EMG: Recruitment
• When a muscle is voluntarily contracted a single motor
unit may fire.
• As the muscle is further contracted more motor units
are added or recruited.
• Normally, recruitment of additional motor units occurs
at relatively low levels of effort
• If there is a loss of MUAPs with any disease process
then recruitment is reduced.
• Loss of nerve axons
• Conduction block at the neuromuscular junction
• Sufficient loss of muscle fibers
EMG
• The electromyographic findings may provide a
guide to the time of onset of the lesion and to
its chronicity.
• If a patient reports that a wrist drop has
developed immediately after an operative
procedure and needle electromyography
performed shortly thereafter reveals abnormal
spontaneous activity (fibrillation potentials and
positive sharp waves) in the extensor muscle of
the wrist, it is likely that the lesion is at least 2‐3
weeks old and therefore it preceded the surgery.
EMG motor unit configuration
• Similarly, the presence of long‐duration,
large‐amplitude, polyphasic motor unit
potentials indicates that the denervation
occurred several weeks or more before
surgery because some reinnervation has
occurred.
When to order EDX
•
•
•
•
Mononeuropathy
Mononeuropathy Multiplex
Polyneuropathies
Cranial neuropathies (Trigeminal
Mononeuropathy (blink reflex)
• Radiculopathy
• Plexopathy (Brachial or Lumbosacral)
• Myopathy
EDX Findings; Polyneuropathy
• Axonal
Sensory +/‐ Motor
Normal CV
Normal DL
Reduced to absent Amp.
Normal F‐Wave (if amp. > 1MV)
Needle EMG in motor or sensorimotor;
Denervation and reinnervation changes (slowly
progressive can show only reinnervation
changes)
EDX Findings; Polyneuropathy
• Demyelinating
Motor + Sensory change
Slow NCV
Conduction Block
Distal Latency: Long
Slow F‐waves
Amplitude: Normal to reduced (late)
Needle EMG: Normal (late with axonal loss
Denervation and/or reinnervation).
Most common causes of
polyneuropathy
•
•
•
•
•
1) diabetic (fasting blood sugar, Hb A1C)
2) thyroid (TSH, total, free, TPO, T antibodies)
3) Anemia (aplastic)
4) Vit deficiencies (B12, Folate, B1, B6)
5) Infections (CBC white cell count,viral panel,
Lyme; HSV1,2; cytomegalovirus; EBV; HIV)
• 6) Neoplastic (Athena labs has a neoplastic
study.)
• 7) Autoimmune (Mag/Sulfatide, GM, Gallop)
• 8) Inherited (HMSN )
PAINFUL NEUROPATHIES:
Differential Diagnosis
• Toxic
Alcohol
Metals: Thallium; Arsenic
Medications: cis‐platinum; Disulfiram;
Ifosfamide; Nitrofurantoin; Dilantin;
Perhexiline; Taxol; Thalidomide; Vinca
alkaloids
PAINFUL NEUROPATHIES:
Differential Diagnosis
• Immune
- Acute onset
1) Guillain Barré - Diffuse pain during acute course;
Distal pain with incomplete recovery; Immobility.
2) Acute panautonomic
- Anti‐Sulfatide Antibody associated polyneuropathies
- Connective tissue diseases
- HIV (DILS)
- M‐protein
- Ganglionopathies: Sjögren's; Paraneoplastic (Hu)
PAINFUL NEUROPATHIES:
Differential Diagnosis
•
Hereditary
- α‐galactosidase (Fabry's)
- GM2 gangliosidosis: Late‐onset
- Sensory Neuropathy I Lancinating pains
- Motor‐Sensory Neuropathy I & II Foot deformity
- Burning feet syndrome
- Amyloidosis - Polyneuropathy: Pain & Paraesthesias in legs
Carpal tunnel syndrome: Pain in hands
- Porphyria
- Restless legs syndromes: Some with PNS involvement
- Hereditary (Acromelalgia) : 12q
- HSN 1
- HMSN 5
- CMT 2
- Huntington disease‐like 1
- Also: Renal failure
PAINFUL NEUROPATHIES:
Differential Diagnosis
• Metabolic
- Diabetic: Acute: Lumbar or Thoracic radiculopathy; Distal sensory.
Chronic: "Small fiber"neuropathy.
- Alcoholic: Acute
- Pellagra ( niacin)
- Beriberi (thiamine)
- Strachan syndrome (Cuban neuropathy)
- Post gastroplasty
- Hypertriglyceridemia
- Chronic mountain sickness
Idiopathic
- Distal sensory polyneuropathy syndromes
- Erythromelalgia
Mononeuritis multiplex
PAINFUL NEUROPATHIES:
Differential Diagnosis
•
Motor disorders with pain
- Diabetic amyotrophy
- Polio
Infections:
- Polio; HIV
• Localized disorders
- Nerve lesions:
Trigeminal
Brachial plexus
Lumbosacral plexopathy
Thoracic outlet syndrome
Median
Posterior tibial (Tarsal tunnel syndrome)
Radiculopathies: Upper & Lower Extremities
Painful neuropathies differential dx.
- Burning mouth syndrome
- Diabetic Amyotrophy
- Reflex Sympathetic Dystrophy (Complex
regional pain syndrome)
- Infections: Herpes zoster
- Neoplastic infiltration: Burning pain with
dysesthesia in area of sensory loss
- Post surgical localized pain syndromes
PAINFUL NEUROPATHIES:
Differential Diagnosis
• Acute onset of pain & paresthesias
- Acute porphyria
- Toxic: Thallium; Arsenic; Perhexiline; Vinca
alkaloids
- Guillain‐Barré
Diabetes and PNS Diseases
• Symmetric Polyneuropathies
Chronic
- Distal sensory +/- Autonomic
- Autonomic
- Sensory-motor
Acute
- Painful
- Reversible
PNS diseases
Asymmetric neuropathies
- Lumbosacral plexopathy
- Mononeuropathies i.e., CTS
- Mononeuritis multiplex
Predisposition to immune PN
- CIDP
- Diabetic amyotrophy
- Perineuritis
- Muscle infarction
Common Mononeuropathies
• Median at the Wrist (CTS)
• Ulnar at the Elbow (Tardy Ulnar Palsy)
• Peroneal Palsy at the Fibular Head
Plexopathy: Selected Etiologies
•
•
•
•
Compression - (CABG)
Inflammatory - (Parsonage‐Turner Syndrome)
Radiation Injury - (Radiotherapy)
Traumatic Injury - (Traction, laceration,
missile)
• Ischemia - (Diabetic amyotrophy)
Carpal Tunnel Syndrome
- prolongation of the median nerve motor/sensory
latency upon stimulation at the wrist ("terminal" or
"distal" latency),
- normal median motor conduction velocity in the
forearm,
- slow median sensory conduction velocity across the
wrist,
- normal motor and sensory NCS of the ulnar nerve
(not involved in CTS). NCS are positive in 91‐98% of
patients with clinical CTS
- Diagnosed by comparing Median to Ulnar sensory
and motor DL’s.
Case study of right hand dominant pt.
• A 78 year old female presented with cervical pain, bilateral forearm pain,
and bilateral hand pain ongoing for 3 months and slowly worsening. No
associated inciting trauma or specific causative event. The forearm and
hand pain occurred all day and night, and possibly worse at night but “not
really different day or night”. The extremity pain pattern was poorly
defined by the patient and she felt it may involve the entire hand however
the lateral hand and general forearm was most noticeable. There were no
defined exacerbating factors as the pain was “pretty well constant day and
night”. She could not recall finding remission with any position and over
the counter NSAIDs were “not very helpful”. Significant orthopedic tests
to the cervical spine showed Spurling’s test at the L and R ; and cervical
extension to be provocative. DTR”s at the biceps triceps and
brachioradialis were 2+ during L and R challenges. Allen’s test at the L and
R demonstrated a normal response.
Case Study (cont)
• Phalen’s, reverse Phalen’s and Tinal tap was not
provocative at the L and R. Two point touch was
diminished at the thumb and index finger at the L and
R. Tenderness with slight increased symptoms was
noted during palpation at the pronator teres L and R.
No abnormalities were palpated over the medial
epicondyle. Jamar dynamometer grip strength testing
demonstrated 6 kg right and 8 kg left. Radiographs of
the C-sp showed moderate to severe disc degeneration
with IVF encroachment at mid and lower levels of the
cervical spine. The patient was using a night splint at
both wrists/hands for the last 3 weeks with no effect.
Trial of treatment
• Pt had a trial of treatment involving cervical
mobilization, myofascial release techniques,
manual traction, active release techniques at
the pronator teres, volar forearm and carpal
tunnel areas. Mobilizations at the carpals and
transverse retinaculum stretches were done.
Electrotherapy and ultrasound was also used.
The pt was given home based exercises at the
cervical spine and CTS exercises.
Treatment had no effect
• The patient was unresponsive to a variety of
physiologic, chiropractic, bracing, ergonomic
and therapeutic endeavors.
Referral for a trial of cortisone
• Pt was referred to a pain management
specialist for cortisone injections at the carpal
tunnel left and right for therapeutic and
diagnostic purposes.
• This had no effect.
Where do we go from here?
• Possible diagnostic work up needed: MRI of
the C-sp? Blood tests to R/O possible causes
of peripheral polyneuropathy?
Electrodiagnostic studies?
EDX
• Electro diagnostic studies would be the most
prudent test to order and would provide the
most diagnostically accurate information as it can
differentiate and Dx spinal nerve root lesion,
brachial plexus lesion, peripheral neuropathy
such as demyelination, and conduction block
such as carpal tunnel syndrome. Plus if a carpal
tunnel syndrome is confirmed, then an Edx study
is needed and is the gold standard for a surgeon
to perform a carpal tunnel release.
Results
• Results of the EDX: Demonstrated increased
latency at the median nerve at the wrist, with
decreased conduction velocity and decreased
NCV amplitude. SNAPS showed increased latency
and decreased amplitude. EMG was significant
for denervation at the APB showing spontaneous
activity and increased insertional activity.
Cervical paraspinal EMG was normal. All other
cord level muscles emg was done C5-T1 were
normal. Diagnostic impression: moderate
/severe median neuropathy at the wrist at the
left and right.
Case study #2
• A 35 year old male smoker presented with severe cervical
pain, right shoulder girdle pain, and radiations into the right
upper extremity. The pain intensity was high with a
burning and sharp throbbing nature. Symptoms had been
ongoing for a few months and pt was unsure of inciting
trauma or causation. He did have a bad chest cold for a few
weeks prior to his symptoms with a lot of coughing, and
sneezing which his doctor told him was viral and “would
not give him antibiotics” for that. He thought the coughing
bothered his neck and lying in bed a lot watching tv with his
head propped up. He had sought the treatment of a
general chiropractor for one month with poor effect for a
diagnosis of “a rib out of place”.
Examination
• Upon examination, the right upper extremity
was held in the dependant position. There
was weakness in right shoulder abduction and
external rotation, elbow flexion and there was
winging of the scapula. Active and passive
shoulder girdle movements were acutely
painful. Spurling’s test was provocative during
R challenges as was cervical extension.
Case study #2
Case Study #2
• Note atrophy of the supraspinatus,
infraspinatus and deltoid. There was
numbness described at the lateral shoulder
and lateral forearm/hand including the thumb
and index finger. DTR’s were decreased at the
biceps and brachioradialis 1+ at the right.
Cervical radiographs were taken and revealed
mild disc degeneration at C5-T1 spinal levels.
Where do we go from here?
• MRI of the C-sp? Chest films R/O pancoast
tumor? Shoulder films? EDX? Ultrasound of
the shoulder to R/O rotator cuff disease? MRI
of the shoulder?
What is your diagnostic impression?
• Electrodiagnosis should also be considered
initially to confirm neuropathic diagnosis and
to rule out various other conditions (eg,
cervical spine disease, radiculopathy,
neuropathy, amyotrophic lateral sclerosis, etc).
Diagnosis
• EDX confirmed Parsonage Turner syndrome (Brachial
Plexus Amyotrophy) at the right.
• The paraspinal emg was normal ruling out cervical
nerve root disease, as well as the levator scapula (C5
nerve root). EMG showed muscles innervated by the
upper plexus but involving different peripheral nerves
were involved including suprascapular nerve, axillary
nerve, long thoracic nerve, musculocutaneous and
radial. These muscles showed denervation such as
sharp’s and fibs. CMAP’s and SNAP’s were normal at
the distal nerves.
Parsonage Turner Syndrome
• Pts often present with symptoms following a
viral infection although many other inciting
factors have been associated. Some studies
show 20-50% have a history of viral illness or
vaccination that occurred days or weeks to the
onset of symptoms. Some studies also note
trauma, severe exercise, and surgery as a
probable cause.
Thank-you
• Thank – you for allowing me to present this
information to you!!