what is RNS and what the techniques to perform this test in the lab. Its significance in the evaluation and diagnosis of NMJ disorders like MG, LEMBS etc..
what is RNS and what the techniques to perform this test in the lab. Its significance in the evaluation and diagnosis of NMJ disorders like MG, LEMBS etc..
This presentation describes the common conditions, anatomy and the ideal ways to do and perform nerve conduction studies in lower limbs. It is nicely depicted with self explanatory pictures.
NCS are done by placing electrodes on the skin and stimulating the nerves through electrical impulses. To study motor nerves, electrodes are placed over a muscle that receives its innervation from the nerve you want to test (stimulate).
This presentation is an introduction to the principles of Nerve Conduction Study and is entirely sourced from the book by David C Preston and Barbara E Shapiro: Electromyography and Neuromuscular disorders, 3rd Edition
This presentation describes the common conditions, anatomy and the ideal ways to do and perform nerve conduction studies in lower limbs. It is nicely depicted with self explanatory pictures.
NCS are done by placing electrodes on the skin and stimulating the nerves through electrical impulses. To study motor nerves, electrodes are placed over a muscle that receives its innervation from the nerve you want to test (stimulate).
This presentation is an introduction to the principles of Nerve Conduction Study and is entirely sourced from the book by David C Preston and Barbara E Shapiro: Electromyography and Neuromuscular disorders, 3rd Edition
Axons of the peripheral nervous system have the potential for regeneration, after they are severed.
Axons of the peripheral nervous system have the potential for regeneration, after they are severed.
Nerve Conduction Studies and Electromyography for Beginners to understand basic procedure and interpretations.
It can be used as a basic guideline and advance interpretation can be easily understood after you read it.
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Chapter 6
1. CHAPTER 6 -
THE ELECTRODIAGNOSTIC
EXAMINATION OF THE SPINAL CORD
2. I. Brief review of the spinal cord anatomy
II. Electrodiagnostic examination
A. Nerve conduction studies
A. Motor NCS
B. Sensory NCS
C. Mixed NCS
B. Needle electrode examination
C. Special tests
III. Pathophysiology
A. EDX changes with spinal cord disorders
B. Coeexisting Spinal Cord and Peripheral Nerve Lesions
C. Specific Spinal Cord disorders
OUTLINE
5. The basic EDX:
A. Nerve conduction study (NCS) – motor, sensory and mixed
B. Needle electrode examination (NEE)
C. Special studies – F-wave, H-reflex
II. THE ELECTRODIAGNOSTIC
EXAMINATION (EDX)
6. 1. Motor NCS
A mixed nerve or a “pure” motor
nerve is stimulated at one or two
points along its course while the
resulting response generated by a
muscle it innervates is recorded,
preferably with surface electrodes
Compound muscle action potential
(CMAP) – a function not only of the
motor nerve fibers stimulated, but
also of the muscle fibers that
produced it, and of the intervening
neuromuscular junctions
Thus, it assesses motor nerve
fibers only indirectly
A. NERVE CONDUCTION STUDIES
7. 2. Sensory NCS
Directly assesses the sensory
component of mixed nerves,
or “pure” sensory nerves
Sensory nerve action
potentials (SNAP) is indicative
of an abnormality of the
peripheral sensory fibers or of
the DRGs from which they
derive
No magnification effect =
microvolts
A. NERVE CONDUCTION STUDIES
8. Several measurable components of an NCS
Amplitude
Duration
Latency
Conduction velocity
A. NERVE CONDUCTION STUDIES
9. Amplitude
Height of the response
Measured from baseline to
peak OR peak-peak
Indicator of:
the number of axons capable of being
stimulated
Conducting impulses between the
stimulating and recording points
Relative rate of conduction along those
axons (together with the duration)
It conveys information regarding
the status of neuromuscular
transmission and of the muscle
fibers of the recorded muscles
(in motor NCS)
Recorded in millivolts (CMAPs)
or microvolts (SNAPs)
A. NERVE CONDUCTION STUDIES
10. Duration:
Time period between the onset and termination of the response
Measured in milliseconds
Indicator of the relative rates of conduction
Related to amplitude – as the duration increased, the amplitude
must decrease if the area under the curve is to remain constant
A. NERVE CONDUCTION STUDIES
11. Distal or Peak Latency
A RATE measurement
Determined from the moment of stimulation to either the onset of
the response (distal latency) or to the peak of response (peak
latency)
A. NERVE CONDUCTION STUDIES
12. Conduction Velocity
A RATE measurement
Obtained by stimulating the nerve at two points along its course,
subtracting the latency elicited on distal stimulation (distal latency)
from that obtained on proximal stimulation (proximal latency), then
dividing the difference (in ms) into the distance (in mm) between the
two stimulation points
Measured in meters per second
A. NERVE CONDUCTION STUDIES
13. Essentially assesses the entire motor unit from the AHCs to
the muscle fibers peripherally
Three phases:
Insertion
Rest phase
MUAP activation
B. NEEDLE ELECTRODE EXAMINATION
(NEE)
14. Insertion Phase
Refers not only to the single instance in which the needle
recording electrode is thrust through the skin into a particular
muscle, but also to each of the several times it is advanced
within that muscle
B. NEEDLE ELECTRODE EXAMINATION
(NEE)
15. At-Rest Phase
The needle is held fixed in a muscle that is not being
contracted
Various types of abnormal potentials can be observed,
collectively called spontaneous activities
Fibrillation potentials
Most commonly seen
Non-specific in nature
Produced by a single denervated muscle fibers
Fasciculation potentials
Generated by motor units or portions of motor units
Larger than the typical fibrillation potentials
Motor unit must be intact to generate fasciculation potentials
Evidence of motor unit irritation (versus motor unit disintegration)
Fire irregularly
B. NEEDLE ELECTRODE EXAMINATION
(NEE)
16. At-Rest Phase
Complex repetitive discharges
Caused by repetitive firing of a group of muscle fibers, two of which
serve as primary and secondary pace makers, respectively
Non-specific
Rarely seen with any disorder of less than 6 months duration
B. NEEDLE ELECTRODE EXAMINATION
(NEE)
17. Motor Unit Action Potential Activation Phase
The patient voluntarily contracts the muscle in which the
needle recording electrode has been inserted
2 MUAP firing patterns
Reduced MUAP recruitment
A significant number of motor units in the muscle being assessed by NEE do not fire on
attempted AHC activation
Unequivocal evidence of LMN lesion, and its severity has high correlation with the clinical
weakness of the recorded muscle
If the MUAPs are firing in substantially decreased numbers at 25 to 35 Hx, the
muscle will appear weak on clinical examination
If only one or two MUAPs fire on maximal activation at faster than 10 Hz, the
muscle will essentially be paralyzed
Incomplete MUAP activation
Seen whenever the patient is requested to vigourously contract the muscle and the MUAPs
fire in reduced numbers, but at a slow-to-moderate rate
Not a sign of LMN lesion – can be from pain, conversion reaction, malingering
B. NEEDLE ELECTRODE EXAMINATION
(NEE)
18. F-waves
Caused by stimulation-induced impulses traveling anti-dromically
along motor axons, causing the AHCs to backfire and thereby sending
impulses back down the motor axons to the recorded muscle
Assess solely motor axons and their parent AHC within the spinal
cord
Elicited by supramaximal stimulation
H-reflexes
A spinal monosynaptic reflex initiated by nerve stimulation
Elicited by submaximal stimulation of a mixed nerve
Very sensitive in two PNS disorders: S1 radiculopathy and generalized
polyneuropathies
C. SPECIAL STUDIES
19. The large myelinated axons assessed by EDX have only two
reactions:
Axon degeneration (axon loss)
Nerve fibers are interrupted at the lesion site and the entire distal portion
of the nerve fibers undergo Wallerian Degeneration
Focal demyelination
The only alteration to the nerve fiber is that the myelin at the lesion site is
damaged to varying degrees
Portion distal to the point of the lesion are intact and conduction is
normal in all respects distal to the focal demyelinating injury
III. PATHOPHYSIOLOGY
20. Superior to the level of the lesion
Generally all aspects of the EDX examination are NORMAL
At the level of the lesion
Motor axons
CMAPs are low in amplitude
Reduced MUAP recruitment with chronic neurogenic changes
Sensory axons
SNAPs are low in amplitude, unelicitable, normal in SCD that affect AHCs
only
Inferior to the level of the lesion
Motor NCS – normal
Sensory NCS – normal
NEE – abnormal MUAP activation
Fibrillation potentials – should not be observed
ELECTRODIAGNOSTIC CHANGES WITH
SPINAL CORD INJURIES
21. These may involve nerve fibers derived from spinal cord
segments situated rostral or caudal to the involved segments,
or from the damage segments themselves
Superior to an SCD:
Crutch palsy – infraclavicular plexopathy caused by excessive
pressure placed on terminal nerves in the axilla as the result of
crutches that are ill fitted or used improperly
Ulnar neuropathies
Carpal tunnel syndrome – wheelchair users
At the level of and SCD
Trauma, ischemia
Caudal to the SCD
Traction and compression
Most commonly involved: ulnar nerve along the elbow in quadriplegic
patients and common peroneal nerve at the fibular head in both
quad and para patients
COEXISTING SPINAL CORD AND
PERIPHERAL NERVE LESIONS
22. Anterior Horn Cell Diseases
Poliomyelitis and Post-polio syndrome
Acute Polio
SNAPS are normal
CMAPS are normal, low in amplitude or unelicitable depending on the segment involved and
the muscle being elicited
NEE – fibrillation potentials and reduced MUAP recruitment are noted in muscles innervated
by the involved segments
MUAPs are normal in configuration because there are no collateral sprouting yet
Remote poliomyelitis (at least 12 months duration)
SNAPs are normal
Unelicitable or very low amplitude CMAPs
May be normal – indicative of the total number of muscle fibers in the
recorded muscle responding to the stimulus rather than the the total number
of nerve fibers supplying the recorded muscles reflects the substantial
amount of collateral sprouting
NEE – fibrillation and fasciulation may be seen
Post-polio syndrome
No distinctive EDX changes (same as in remote polio)
SOME SPECIFIC SPINAL CORD
DISORDERS
23. Anterior Horn Cell Diseases
Amyotrophic Lateral Sclerosis
Characteristically manifests UMN as well as LMN changes
Often begins in the C8-T1 segments (unilateral or bilateral painless hand
wasting) or L5 spinal cord segment (painless foot drop)
SNAPS are normal for age
CMAPS are normal or abnormal depending on whether the appropriate
segments are involved and the severity of axon loss)
NEE: goal is to find widespread fibrillation potentials and chronic
neurogenic MUAP changes with at least some fasciculation potentials
SOME SPECIFIC SPINAL CORD
DISORDERS
24. Anterior Horn Cell Diseases
Kennedy’s Disease
Sex-linked recessive AHC disorder involving sensory and motor neurons in
both bulbar and spinal cord segments
NCS suggests pure sensory polyneuropathy or neuronopathy
NEE abnormalities indicative of very chronic AHC disease (prominent
MUAP changes with sparse numbers of fibrillation potentials)
SOME SPECIFIC SPINAL CORD
DISORDERS
25. Spinal Cord Injuries
The EDX examination has a limited role in the initial assessment of
these injuries
Can be helpful in demonstrating the presence or absence of
coexisting plexopathies
SOME SPECIFIC SPINAL CORD
DISORDERS
26. Intraspinal Canal Neoplasms
Radicular pain is the common reason for referral for EDX
examination
EDX findings typically are nonspecific in regard to etiology but their
presence frequently initiates the appropriate neuroimaging studies
SOME SPECIFIC SPINAL CORD
DISORDERS
27. There are 3 basic parts of the EDX
NCS
NEE
Special tests
EDX can differentiate a spinal cord injurry and a peripheral
nerve lesion
EDX examination can help differentiate or confirm a pathology
SUMMARY
The spinal cord, on cross section, consists of grey matter surrounded by white matter. The grey matter is in the form of a letter H with the dorsal (or posterior) segments (or horns) containing sensory fibers, and the ventral (or anterior )semgnets ocntaining the alpha motor neurons or anterior horn cells, whose very long peripheral extensions, labeled axons, comprise the somatic motor portion of the PNS.
The cell bodies of origin of the motor axons are within the spinal cord. In contrast, the cell bodies of origin of the sensory fibers are situated in ganglia, called dorsal root ganglia, which are located on the very distal portion of the primary sensory roots, at the entrance to or within the intervertebral froamina.
Let’s review the somatic portion of the peripheral nervous system.
A motor unit is made up of a motor neuron and the skeletal muscle fibers innervated by that motor neuron’s axonal terminals.
On the sensory side, unipolar cell bodies located in the dorsal root ganglion DRGs send one process centrally into the spinal cord (pregangliotic component) and another peripherally (postganglionic component), the latter being the somatic sensory axon.
From each spinal cord segment both somatic motor and sensory axons originate. A myotome contains all the muscles innervated by a single spinal cord segment, whereas a dermatome is the cutaneous sensory area supplied by a single spinal cord segment.
We now move on to the components of a basic electrodiagnostic examination, which we will refer to from this point on as EDX.
These are: NCS, NEE, Special studies
For every motor axon capable of conducting impulses, hundreds of muscle fibers are depolarized (depending on the innervation ratio).
This results in a striking “magnification” of the nerve action potentials. So CMAPs are large enough to be measured in millivolts
The major liability is that a low amplitude or unelicitable CMAP is not necessarily evidence of a disorder of the motor component of the PNS. Instead, the cause could reside in the NMJ or the muscle fibers themselves.
Physical factors, (limb edema); phyiologic factors (advanced patient age, in phase cancellation of responses) and anatomic factors (cutaneous nerves being quite superficial and thus vulnerable to minor trauma) can compromise recording SNAPS in otherwise normal individuals.
For the purpose of completion,
Everytime an NCS is performed, the response that results contains several measurable components, each one of which provides information regarding the anatomic and physiologic status of the nerve fibers being assessed.
Amplitude
Height of the response
Measured from baseline to peak OR peak-peak
Indicator of the number of axons capable of being stimulated and of conducting impulses between the stimulating and recording points
A reflection of the relative rate of conduction along those axons (together with the duration)
It conveys information regarding the status of neuromuscular transmission and of the muscle fibers of the recorded muscles (in motor NCS)
Recorded in millivolts (CMAPs) or microvolts (SNAPs)
Motor NCS – distal latency
Sensory NCS – peak or distal latency
Demyelinating process (not axonal loss)
Whenever a needle recording electrode is advanced in any normally innervated, healthy muscle, a brief burst of electrical activity is generated, which persists for approximately one-third of a second. This is labeled normal insertional activity.
During the insertional phase, electrical activity generated by needle advancement is assessed in regard to its presence or absence and if present whether it is accompanied or followed abnromal discharged
Snap, crackle pop- young mesomorphic males, considered a normal variant
Insertional postive sharp waves –
Myotonic discharge – insertional and spontaneous activity seen in certain myopathies
FIBRILLATION POTENTIALS
- Non-specific – can be seen in lower motor neuron diseases, myopathic disorders, neuromuscular transmission abnormalities, UMN
- Regularly firing potentials are generated by otherwise healthy single muscle fibers that lost their nerve supply at least 2 to 3 weeks previously. Initially, the denervated muscle fibers individually begin to produce fibrillation potentials only in an unsustained fashion, and after being injured by the needle recording electrode (referred to as insertional positive sharp waves). Within several days, the denervated muscle fibers start to produce such potentials spontaneously and in a sustained manner.
Can be positive sharp waves or a biphasic spike appearance
FASCICULATION POTENTIALS
Can be seen in any PNS disorder, In fact, they are relatively uncommon and most often limited to those that are causing focal demyelination and are chronic in nature. In regard to spinal canal disorders, fasciulation potentiasl may occur with almost any of them, including intramedullary neoplasmsa nd rediculopathies, although they rarely have any diagnostic significance in these instances. The sole exception is one of the AHC disorders, ALS, in which their presence is nearly mandatory for daingosis
The most common situation in which fasiculation potentials appear, however, is the benighn fasciulation syndrome – consists solely of an otherwise halthy person’s expereinceing widesperead, persistent fasciculations, and often cramps as well
COMPLEX REPETITIVE DISCHARGES
- Can be seen with both neurogenic and myopathic disorders
FIBRILLATION POTENTIALS
- Non-specific – can be seen in lower motor neuron diseases, myopathic disorders, neuromuscular transmission abnormalities, UMN
- Regularly firing potentials are generated by otherwise healthy single muscle fibers that lost their nerve supply at least 2 to 3 weeks previously. Initially, the denervated muscle fibers individually begin to produce fibrillation potentials only in an unsustained fashion, and after being injured by the needle recording electrode (referred to as insertional positive sharp waves). Within several days, the denervated muscle fibers start to produce such potentials spontaneously and in a sustained manner.
Can be positive sharp waves or a biphasic spike appearance
FASCICULATION POTENTIALS
Can be seen in any PNS disorder, In fact, they are relatively uncommon and most often limited to those that are causing focal demyelination and are chronic in nature. In regard to spinal canal disorders, fasciulation potentiasl may occur with almost any of them, including intramedullary neoplasmsa nd rediculopathies, although they rarely have any diagnostic significance in these instances. The sole exception is one of the AHC disorders, ALS, in which their presence is nearly mandatory for daingosis
The most common situation in which fasiculation potentials appear, however, is the benighn fasciulation syndrome – consists solely of an otherwise halthy person’s expereinceing widesperead, persistent fasciculations, and often cramps as well
COMPLEX REPETITIVE DISCHARGES
- Can be seen with both neurogenic and myopathic disorders
Reduced MUAP recruitment
A significant number of motor units in the muscle being assessed by NEE do not fire on attempted AHC activation, either because the AHC or motor axon of the motor unit has degeneerated or the AHC is unable to initiate an impule, or conduction is blocked along the axon
AXONAL DEGENERATION
On NCS, if the nerve is stimulated proximal and distal to the site of injury while recording further distally, a conduction block patter is observed. The evoked response on stimulating distal to the lesion is normal, or low in amplitue, and the response on stimulating proximal to it is even lower in amplitude or unelicitable, depending on wehter the lesion is partial or complete. This type of conduction block is called AXON DISCONTINUITY BLOCK – seen because those portions of the axons comprising the distal stump, although in the early stages of degeneration, are still capable of conducting impulses
This is a Short lived phenomenon because by 10 to 11 days post injury, all distal stump fibers have degenerated sufficiently that they are incapable of transmitting impulses. By day 7 post injury CMAPs can’t be elicited. The SNAP amplitude usually do not begin to drop until approximately 5 days after injury and then nadir at 10 to 11 days.
CONDUCTION FAILURE PATTERN
amplitudes of cmaps are uniformly low, whereas complete lesions, they are uniformly unelicitable
most common pattern of ncs seen following focal nerve injuries
kasi nearly all are assessed 10 or more days after onset
Reduced muap recuritment
Fibrillation potentials appear 2-2.5 weeks after lesion onset
Chrnoinc neurogenic muap changes if lesion is of several months duration
FOCAL DEMYELINATION
CAN MANIFEST AS SLOWING OR BLOCKING
IN CONDUCTION SLOWING – CAN BE FOCAL OR SYNCRONIZED SLOWING (NERVE IMPULSES TRAVERSING ALL THE LARGE MYELINATED NERVE FIBERS ARE SLOWED TO THE SAME DEGREE) or DESYNCHRONIZED OR DIFFERENTIAL SLOWING (THE FASTEST CONDUCTING FIBERS ARE NOT AFFECTED BUT CONDUCTION ALONG ALL THE OTHERS IS SLOWED TO VARIOUS DEGREES
We will now describe the EDX manifestation seen under three different circumstances.
All aspects of EDX exam are normal when spinal cord segments cpehalad to a focal SCD are assesseed.
CMAP
Lower amplitude
Not unelicitable – you’re still able to elicit a reaction because muscles receive innervation from more than one spinal cord segment
Inferior to the level of the lesion
Motor NCS normal; CMAP low in amplitude due to atrophy
Snesory NCS should be normal
NEE: no MUAPs at all on voluntary effort or a substanitally decreased number, firing at a slow rate showing incomplete muap activation
Fibrillation potentials are not observed because the muscles sampled are paretic or paralyzed because of a UMN rather than a LMN disorder
EDX exams are also useful in evaluating coexisting peripheral nerve lesions with spinal cord disease. These neuropathies can compromise the independent functioning of these patients.
Remote Poliomyelitis
CMAPs are misleading
Fasiculation potentials are more widespread in weak muscles
Fasiculation potentials are more widespread in weak muscles
Fasiculation potentials are more widespread in weak muscles
Fasiculation potentials are more widespread in weak muscles