Chapter 6
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This document discusses the electrodiagnostic examination of the spinal cord. It begins with an overview of spinal cord anatomy and the different components of an electrodiagnostic examination, including nerve conduction studies to assess motor and sensory fibers, and needle electromyography. It then covers the pathophysiology of different spinal cord disorders and how they present on electrodiagnostic testing, such as abnormal findings occurring at, above, or below the level of a spinal cord lesion. Specific spinal cord conditions like ALS, polio, and spinal cord injuries are also reviewed. The document provides detailed information on interpreting electrodiagnostic results in the context of spinal cord and nerve root disorders.
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
- 3. I. SPINAL CORD ANATOMY
- 4. I. SPINAL CORD ANATOMY
- 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
- 28. FIN CHAPTER 6 - THE ELECTRODIAGNOSTIC EXAMINATION OF THE SPINAL CORD
Editor's Notes
- #4: 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.
- #5: 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.
- #6: 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
- #7: 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.
- #8: 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.
- #9: For the purpose of completion,
- #10: 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
- #11: 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)
- #13: Motor NCS – distal latency Sensory NCS – peak or distal latency
- #14: Demyelinating process (not axonal loss)
- #16: 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
- #17: 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
- #18: 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
- #19: 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
- #21: 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
- #22: 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
- #23: 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.
- #24: Remote Poliomyelitis CMAPs are misleading
- #25: Fasiculation potentials are more widespread in weak muscles
- #26: Fasiculation potentials are more widespread in weak muscles
- #27: Fasiculation potentials are more widespread in weak muscles
- #28: Fasiculation potentials are more widespread in weak muscles