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Electrodiagnostic approach to peripheral neuropathy
This document discusses electrodiagnostic approaches to peripheral neuropathy. It begins with the anatomy and physiology of peripheral nerves and clinical clues in diagnosis. It then covers electrodiagnostic principles in nerve conduction studies and their use in evaluating various pathologies. Specific examples discussed include mononeuropathy, polyneuropathy, mononeuritis multiplex, and demyelinating vs axonal neuropathies. Case examples are also provided of common conditions like carpal tunnel syndrome, Guillain-Barré syndrome, and chronic inflammatory demyelinating polyneuropathy.
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Electrodiagnostic approach to peripheral neuropathy
- 1. Electro- Diagnostic approachto peripheral neuropathy -Dr. Sachin Adukia
- 2. Content Anatomy ofperipheral nerve Physiology of peripheral nerve Clinical clues in diagnosis of peripheral neuropathy Electrodiagnostic principles in NCS NCS in various pathologies References
- 3. Elements of theperipheral nervous system.
- 4. ANATOMY Neuropathic disordersencompass diseases of: -Neuron cell body (neuronopathy) -anterior horn cell disorders(MND) -dorsal root ganglion disorders (sensory neuronopathy / ganglionopathy) -Peripheral neuropathy -axonal -demyelinating
- 5. Neuropathies subdividedas per diameter of impaired axon: -Large myelinated axons -motor and sensory axons (vibration, light touch, proprioception). -Thinly myelinated axons -sensory axons(touch,pain,temp, pre-ganglionic autonomic) -Small unmyelinated axons -sensory axons(pain,touch, post-ganglionic autonomic)
- 6. ELECTRON MICROSCOPIC VIEWOF A NERVE BIOPSY SPECIMEN 6 UNMYELINATED AXONS MYELINATED AXON
- 7. Role of nervefibers in peripheral neuropathy
- 8. Peripheral neuropathy isdivided into Polyneuropathy: sens-motor involvement; relatively symmetrical with distal to prox gradient. Mononeuropathy-focal involvement of single nerve Mononeuritis multiplex- multiple nerves asymmetrically.
- 9. On the basisof clinical course Acute (< 4 wks) -Subacute (4-8 wks) -Chronic (> 8 wks) On the basis of symptoms: -Pure motor -Pure sensory -Mixed -Autonomic
- 10. HISTORY Positive Sensory Tingling Band like sensation Tightness Paresthesias - spontaneous Dysesthesias - on stimulation Allodynia - on non noxious stimulus Hyperalgesia - on noxious stimulus Deep burning, cutting, gnawing, shooting, jabbing, electric like flashes, nocturnal and at rest Negative sensory Numbness- loss of sensation Cotton wool sensation Walking on ice Feels different Painless ulcerations Foot deformities
- 11. Negative Motor Weaknessin feet toe extensor and hands Tripping, Falls Difficulty in walking Wasting Positive Motor Cramps Fasciculations Tremor Myokymia Autonomic Lightheadedness Orthostatic hypotension Syncope Sweating disturbance Heat intolerance Bladder bowel disturbance Erectile dysfunction Gastroparesis - nausea, early satiety, vomiting Constipation Diarrhoea
- 12. ANATOMIC PATTERNS AXONAL DEMYELINATING Distal> proximal Length dependent Proximal=distal Slow evolution Acute/subacute Distal weakness Distal & proximal weakness Distal areflexia Areflexia Pain – temp loss is > vibration, proprioception Vibration & proprioception > pain & temp Amplitude affected>velocity Velocity > amplitude Axonal degeneration & regeneration Demyelination & remyelination Slow recovery Rapid recovery
- 13. SYMPTOMS SIGNS numbness Diminishedor absent reflexes Pin & needle sensation Decreased joint position sense tingling Decreased vibration sense Poor balance Sensory ataxia Large fiber
- 14. Small fibre neuropathy PAIN-burning, shocklike, stabbing, pricking, shooting, lancinating Allodynia Decreased pinprick sensation Insensitivity to heat and cold Diminished temperature sensation
- 15. APPROACH DISTRIBUTION OF WEAKNESS SINGLENERVE MONONEUROPATHY ULNAR NERVE RADIAL NERVE MULTIPLE NERVES MONONEURITIS MULTIPLEX SYMMETRIC DISTAL > PROXIMAL AXONOPATHY SYMMETRIC PROXIMAL > DISTAL MYELINOPATHY ACUTE CHRONIC AIDP CIDP
- 16. Erlanger Gasser classificationof nerve fibres
- 17. DISORDER LATENCY VELOCITYAMPLITUDE DURATION AXONAL NORMAL (<130%) NORMAL (>75%) DECREASED NORMAL DEMYELINATING PROLONGED (>130%) DECREASED (<75%) <35 in UL <30 in LL NORMAL OR Reduced if Conduction Block PROLONGED (Temporal Dispersion)
- 18. NCS: Basic principles Amplitude: related to the number of axons in a nerve Latency : time dependent ; therefore, most affected in demyelination Conduction velocity: time dependent, thus more affected in demyelination In axonal loss, Large, fast conducting fibers are lost Moderate slowing Demyelination Marked slowing
- 20. Axonal Loss MostNeuropathies LE > UE Distal > proximal Sensory > Motor So a NCS study in axonal Neuropathy shows Low amplitudes, more severe in the legs than arms Loss of sensory responses in legs early on CV slowing but less severe than demyelination Amplitude dependent slowing, ie, CV is reduced because a subpopulation of faster conducting axons have been lost, not because of demyelination of conducting axons.
- 21. Demyelinating Process Hereditary Uniform slowing Across all segments Uniform waveform shape CMAPs Profound slowing Acquired Non-uniform process Non-compressible segments Conduction block Temporal dispersion Increased variability in range of velocities Some nerves affected more than others MMN
- 22. Motor ms mAm/s Latency Amplitude Velocity Median <4.2 >5 >48 Ulnar <4 >5 >48 Deep peroneal <6 >2 >42 Posterior tibial <6 >5 >42 Radial <2.9 >2 >49 Musculocutaneous <5.7 Compare Axillary <4.9 Compare Suprascapular <3.7 Compare Femoral >3 Sensory uV Median <3.4 >15 >48 Ulnar <3.4 >15 >48 LABC <3 >15 >50 MABC <3.2 >10 >50 Superfical peroneal <3.4 >5 >42 Sural <3.4 >5 >42 Sapheneous <3.9 >2 >40
- 23. Limitations conduction velocityand latency measurements are from largest and fastest fibers. Large-diameter fibers have the most myelin and the least electrical resistance faster conduction velocities. NCS study only largest A-alpha fibers poses a problem when strength & vibration and position senses are unaffected but pain and temperature sensations are abnormal: "small fiber neuropathy” small fiber neuropathy may not reveal any abnormalities on NCSs
- 25. Clinical examples Mononeuropathy- CTS, foot drop, wrist drop Polyneuropathy - AIDP, AMAN - CIDP Mononeuritis multiplex
- 26. 67/F, History clumsiness, tingling, and pain in both hands of several months most prominent at night, often awakening her from sleep, or during hand use such as driving. Examination : slight wasting of both thenar eminences. Reflexes were normal. Thumb abduction was weak bilaterally. Sensation was slightly reduced over the finger pads of the thumb, index, middle, and ring fingers. Tinel’s sign –ve on either side Phalen’s maneuver +ve bilaterally after 30 seconds.
- 29. 42/M, persistent leftwrist drop. History: •3 weeks ago he awoke with a nearly complete left wrist drop and finger drop •no pain, but he did notice an area of abnormal sensation on the back side of his hand between the thumb and index finger. •During the subsequent 3 weeks, no improvement occurred. On physical examination •near paralysis of wrist and finger extension (MRC grade 1/5). •Wrist and finger flexion were intact. Elbow flexion and extension were normal. Shoulder abduction was normal. •On sensory examination, numbness over lateral dorsum of the left hand between the thumb and index fingers extending into the proximal phalanges of the index, middle, and ring fingers. •Reflexes: biceps and triceps were normal. Left brachioradialis reflex was absent
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- 33. 52/F, WITH H/OA PERSISTENT RIGHT FOOT DROP WHICH BEGAN SLOWLY 6 MONTHS PREVIOUSLY HISTORY: •INITIALLY- NUMBNESS OVER THE TOP OF THE FOOT AND THE LATERAL CALF F/B RIGHT FOOT DROPPING. DURING THE LAST 2 MONTHS, SLOWLY PROGRESSED TO A NEARLY COMPLETE FOOTDROP. •MORE RECENTLY, SHE NOTED A SENSATION OF TIGHTNESS AND PAIN FROM HER HIP DOWN TO HER KNEE AND INTO HER CALF. ON EXAMINATION •ATROPHY OF THE ANTERIOR COMPARTMENT OF THE RIGHT LEG AND WASTING OF THE RIGHT EDB MUSCLE. IN THE RIGHT LOWER EXTREMITY THERE WAS A COMPLETE FOOTDROP. •TOE AND ANKLE DORSIFLEXION WERE 1/5, AS WAS ANKLE EVERSION. •ANKLE INVERSION ALSO WAS WEAK (4/5). IN ADDITION, TOE FLEXION & KNEE FLEXION WERE WEAK. RIGHT ANKLE JERK WAS ABSENT. TOES WERE DOWNGOING. •SENSORY DISTURBANCE TO LIGHT TOUCH ON THE TOP OF THE FOOT, LATERAL FOOT AND CALF, LATERAL KNEE, AND POSTERIOR CALF ON THE RIGHT SIDE.
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- 39. EDS In AIDP NCS abnormal: 81-100% cases Distal segment may be normal if demyelination is confined to the proximal segment of nerve or root F waves: most sensitive MNCS abnormalities: 80-100% SNCS abnormalities: 56-76% May be the sole abnormality in early GBS
- 40. 32/F, progressive weaknessand numbness. History diarrhea and fever that persisted for several days, and remitted. Ten days ago, she developed pins-and-needles paresthesias in both feet and both hands. Those symptoms were followed by clumsiness of gait and progressive weakness of both arms and legs. Examination bifacial weakness and a mild, diffuse quadriparesis. Depressed Reflexes in arms and absent reflexes in the legs. mild distal sensory loss to pinprick, light touch, and vibration was present in both upper and lower extremities.
- 42. SLOWING OF NCV& PROLONGED DL Slowing of NCV and prolonged DL: Synchronized slowing (all faster conducting axons are affected to same degree) EMG correlate: none
- 43. AMPLITUDE Normal toreduced CMAP amplitudes Normal, reduced or absent SNAP amplitudes Decrease in amplitude in DM is because of: Conduction block Temporal dispersion
- 44. AIDP – MNCS Diffuse slowing of CV (<35 m/sec in UL and <30 m/sec in LL nerves) with variable TD and CB . Generally slowing can be seen in both distal and proximal segments of a nerve. More characteristic of GBS is nonuniform slowing - proximal greater than distal
- 45. AIDP - SENSORYNCS Abnormalities less frequent compared to motor NCS, especially early (<2 weeks) Most frequently seen as reduced/absent SNAP amp. Amp. are relatively preserved in demyelination vs. axonal forms Sensory velocities are less often affected SURAL SPARING Normal sural SNAP OR Relatively preserved sural SNAP amp. compared with at least 2 abnormal SNAPs in UL (median, ulnar and radial) nerves. Characteristic of Demyelinaiton : specific (96%) but modestly sensitive (~50%)
- 46. EARLY EDX. FINDINGSIN AIDP Non diagnostic EDX. findings if symptom duration is < 4-5 days Maximum motor NCS abnormalities observed during the 3rd week and for sensory during 4th week Number of abnormalities found will increase with no. of nerves studied Abnormal H reflex (absent or low amplitude) may be the sole EDX. finding in first 5 days Abnormal F wave* ( prolonged latency or absent) may be the sole EDX. finding in first 5-7 days
- 47. Case 38/M, presentedwith acute onset ascending symmetrical flaccid areflexic quadriparesis alongwith bulbar involvement reaching maximal deficit within 2 days of onset. No preceding AFI or diarrhea
- 49. NCS F and Hare absent
- 50. AMAN selective involvementof motor nerves electrophysiologic pattern of axonal involvement distal motor amplitudes are low initially but may increase rapidly with recovery of function; these findings may reflect reversible conduction failure F waves may be absent but not significantly prolonged There is no sensory nerve involvement no peripheral nerve demyelination. no significant slowing of CV or increase in DL. no temporal dispersion. Kokubun N, Nishibayashi M, Uncini A, et al. Conduction block in acute motor axonal neuropathy. Brain 2010; 133:2897.
- 51. AMAN No featuresof DM as defined in AIDP criteria Decreased CMAP amplitudes <80% of the lower limit of normal (2 or more nerves) Normal sensory conduction AMSAN --do-- --do— Decreased SNAP amplitudes <80% of the lower limit of normal (2 or more nerves) (Ho et al. Neurology 1997;48:695-700)
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- 54. EFNS criteria fordefinite CIDP- 2010
- 55. Case 52/M, withh/o progressive numbness and weakness of 6 months’ duration. History insidious onset of pins-and-needles paresthesias in his toes bilaterally 6 months ago, followed by slow progression up his feet and calves. Recently, a pins-and needles sensation developed in the fingertips. difficulty with dexterity developed, along with a tendency to trip with walking. Examination stocking-glove loss of vibration and pinprick sense. Reflexes diffusely hypoactive and absent at the ankles. Mild distal weakness and atrophy were present on motor examination. A Romberg sign was present. Gait was moderately ataxic.
- 59. Differentiating Demyelinating vsAxonal slowing when CV are borderline Comparing the CV across the same segment of nerve, recording prox. and distal muscles e.g.EDB and TA. Normal – no significant difference in CV. Demyelinating polyneuropathy – usually marked slowing when recording both distal and proximal muscles. Severe axonal polyneuropathy – CV may reach cut off value but CV is usually faster or normal when recording a more proximal muscle i.e. – Distal to prox.CV gradient normalizing proximally is characteristic of axonal polyneuropathies.
- 61.
- 62. MOTOR NCS Alltested nerves show abnormalities, though to different extent. Both distal and proximal segments affected, with proximal being more impaired in 80% cases Marked slowing of NCV with values <35 m/sec in UL and <30 m/sec in LL CB and TD
- 63. SENSORY NCS Symmetric Low or absent SNAPs are a consistent findings. There may be dissociation between SNCS & MNCS findings Sensory sparing patterns. Velocity reductions are less in SNCS compared to MNCS
- 64. F-wave & H-reflex Typically abnormal Absent to markedly prolonged latencies (>150%) F wave chronodispersion (CD): F wave counterpart of TD - measures conduction across large motor fibers. High sensitivity in chronic demyelination CD >9 msec. observed only in CIDP or AIDP But at least 60 F waves must be recorded
- 65. Phenotype – MADSAMneuropathy Sensory and Motor Often painful Hands more than ankles Individual Nerves Stepwise Slowing, CB, TD
- 66. Multifocal acquired demyelinatingsensory and motor neuropathy (MADSAM) CB TD Prolonged DL Slow NCVs Delayed or absent F waves Asymmetric (multifocal) SNAP abnormalities Sensory abnormalities should be carefully looked for to differentiate from MMN CB •Closely resemble MMN CB •Asymmetric (multifocal)
- 67. References Mathey EK,Park SB, Hughes RAC, et alChronic inflammatory demyelinating polyradiculoneuropathy: from pathology to phenotype J Neurol Neurosurg Psychiatry Published Online First: 12 February 2015 Preston DC, Shapiro BE. Electromyography and Neuromuscular Disorders E-Book: Clinical- Electrophysiologic Correlations (Expert Consult-Online). Elsevier Health Sciences; 2012 Nov 1 Daroff RB, Jankovic J, Mazziotta JC, Pomeroy SL. Bradley's Neurology in Clinical Practice E- Book. Elsevier Health Sciences; 2015 Oct 25. Joint Task Force of the EFNS and the PNS. European Federation of Neurological Societies/Peripheral Nerve Society Guideline on management of chronic inflammatory demyelinating polyradiculoneuropathy: report of a joint task force of the European Federation of Neurological Societies and the Peripheral Nerve Society--First Revision. J Peripher Nerv Syst 2010; 15:1. Uncini A, Kuwabara S. Electrodiagnostic criteria for Guillain–Barré syndrome: a critical revision and the need for an update. Clinical neurophysiology. 2012 Aug 1;123(8):1487-95.
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- 69. AXONOPATHIES DEMYELINATING Acute Toxins Axonal GBS Tickparalysis Critical illness neuropathy Acute AIDP Diptheria Subacute/Chronic Metabolic Toxic Hereditary CMT II Systemic disorders Chronic/Relapsing CIDP POEMS Multiple myeloma Paraproteinemia (MGUS) HIV Inherited CMT I, III, X Refsum disease Leukodystrophies
- 70. Motor neuropathies Pure motorneuropathies MMN AMAN MND Predominantly Motor Neuropathies GBS CIDP Porphyric Neuropathy Lead intoxication POEM Syndrome Diabetic Lumbar plexopathy HMSN
- 71. Sensory neuropathies Toxins Sjogren’s syndrome Paraneoplastic syndrome HSN Infections-leprosy,HIV Metabolic-amyloidosis,diabetes.
- 72. Autonomic Neuropathies GBS/AIDP Diabetes Mellitus Porphyria Idiopathic acute panautonomic neuropathy Paraneoplastic HSAN Amyloidosis HIV related Vincristine, amiodarone, cisplatin, organic solvents, metals
- 73. 6 Questions 1) Systemsinvolved Motor, Sensory, Autonomic, Mixed 2) Distribution Distal or Proximal & Distal Focal/Asymmetric or Symmetric 3) Sensory involvement Pain, burning, stabbing or proprioceptive loss With or without sensory loss 4) UMN involvement 5) Temporal profile Acute, Subacute, Chronic 6) Family history Sensory signs without symptoms
- 74. Pattern recognition approachof Peripheral Neuropathy 1) Symmetric proximal and distal weakness with sensory loss - Myelinopathies 2) Symmetric distal weakness with sensory loss - Metabolic, drugs, toxins, HMSN, amyloidosis 3) Asymmetric distal weakness with sensory loss - Multiple nerves (vasculitis, HNPP, leprosy, sarcoid, HIV). Single nerve (compression, radiculopathy) 4) Asymmetric distal weakness without sensory loss - MMNCB, MND (with UMN signs) 5) Asymmetric proximal and distal weakness with sensory loss - plexopathy, HNPP, idiopathic, meningial carcinomatosis) 6) Symmetric sensory loss without weakness -Metabolic (diabetes), cryptogenic, drugs, toxins 7) Symmetric distal sensory loss with UMN signs - B12 deficiency and SCD 8) Proprioceptive loss without weakness – ganglionopathy. 9) Autonomic neuropathy.