Chapter 6

CHAPTER 6 - THE ELECTRODIAGNOSTIC

EXAMINATION OF THE SPINAL CORD

I. Brief review of the spinal cord anatomyII. Electrodiagnostic examination

A. Nerve conduction studiesA. Motor NCSB. Sensory NCSC. Mixed NCS

B. Needle electrode examinationC. Special tests

III. PathophysiologyA. EDX changes with spinal cord disordersB. Coeexisting Spinal Cord and Peripheral Nerve LesionsC. Specific Spinal Cord disorders

OUTLINE

I. SPINAL CORD ANATOMY

I. SPINAL CORD ANATOMY

The basic EDX:A. Nerve conduction study (NCS) – motor, sensory and mixedB. Needle electrode examination (NEE)C. Special studies – F-wave, H-reflex

II. THE ELECTRODIAGNOSTIC EXAMINATION (EDX)

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

2. Sensory NCSDirectly 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


Several measurable components of an NCS Amplitude Duration Latency Conduction velocity


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)


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


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)


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


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)

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


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


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


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 fi ring in substantially decreased numbers at 25 to 35 Hx,

the muscle will appear weak on clinical examination If only one or two MUAPs fi re 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


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 stimulationH-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

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

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

These may involve nerve fi bers 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

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

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


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)


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


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


There are 3 basic parts of the EDX NCS NEE Special tests

EDX can diff erentiate a spinal cord injurry and a peripheral nerve lesion

EDX examination can help diff erentiate or confirm a pathology

SUMMARY

FIN

CHAPTER 6 - THE ELECTRODIAGNOSTIC

EXAMINATION OF THE SPINAL CORD

Health & Medicine

Chapter 6