Ncs

basics of nerve conduction study

1. Nerve Conduction Study Dr Archana Verma Guide: Dr Neha Rai

2. Overview History Introduction Basic anatomy and physiology NCS Motor Sensory Patterns Axonal loss Demyelination Conduction block Special conditions Late responses Blink reflex Repetitive nerve stimulation Anomalous innervations Artifacts and technical factors

3. History* 1771- Galvani * electrical stimulation of muscular tissue produces contraction and force 1852- Herman von Helmholz # measured nerve conduction velocities in human subjects 1922- Gasser and Erlanger* cathode ray oscilloscope an recording equipment 1940- Weddell , Hodes , Dawson and Scott # Electromyography ( EMG) and NCSs became a practical tool with the publications of Weddell, Hodes , Dawson and Scott . * Mohamed Kazamel , History of Electromyography (EMG) and Nerve Conduction Studies (NCS ): A Tribute to the Founding Fathers (P05.259 ), Neurology February 12, 2013 vol. 80 no. 7 Supplement P05.259 # Rossitza I, EMG and Nerve Conduction Studies in Clinical Practice ,. January/February 2010 | Practical Neurology

4. Electrodiagnostic study An extension of clinical examination. It includes NCS EMG RNST Late responses Blink reflex

5. localization

6. Cardinal rules

7. Patient encounter

8. Anatomy

9. A = MNAP A = CMAP, SNAP A  

10. Physiology (What ) Saltatory conduction

11. Recording (How) Volume conduction Wave form morphology Near field and far field potential

12. Nerve conduction study V CMAP SNAP MNAP

13. Motor conduction study (CMAP) Latency - reflects fastest conducting motor fibers. Amplitude – reflects number of depolarizing muscle fibers. Area - reflects number of depolarizing muscle fibers. Duration - is a measure of synchrony. Conduction velocity -reflects fastest conducting motor fibers. Distance between proximal and distal stimulation/ time Time= PL - DL

14. Sensory conduction study (SNAP) Onset latency Peak latency Amplitude Duration Conduction velocity Difference from CMAP 1. Two latencies 2. Distal stimulation only for conduction velocity calculation.

15. ONSET VS PEAK LATENCY ONSET PEAK Time for stimulus to initial negative deflection. Stimulus to midpoint of first negative peak. Represents fastest conducting fibers. Population represented not known. Used in calculating conduction velocity. - Inter examiner variation. No (normal values exist)

16. MOTOR VS SENSORY CONDUCTION TABLE SNAP

17. MIXED CONDUCTION STUDY (MNAP) Sensory muscle afferent 1 a fibres are recorded only in this study. Done in median ,ulnar or distal tibial nerve. 1a fibres are earliest affected in demyelinating and entrapment neuropathies. Settings used same as SNAP.

18. ANTIDROMIC VS ORTHODROMIC 1.Superior 2.Higher amplitude SNAP 3.For recording very small potentials 4.Less subject to noise and artifacts. 5.Followed by large volume conducted motor potential 6.Misinterpretation error

19. LESIONS PROXIMAL TO DRG RESULTS IN NORMAL SNAP Lesions of sensory nerve root/ spinalcord /brain causes normal SNAP. Because DRG and peripheral nerve is preserved. Insensate limb with normal SNAP signifies lesions proximal to DRG

20. TEMPORAL DISPERSION AND PHASE CANCELLATION Increase in duration and decrease in amplitude and area More prominent with proximal stimulation in sensory studies. Less prominent with motor studies. In demyelinating lesions temporal dispersion and phase cancellation become prominent for motor fibers. .

21. PRINCIPLES OF STIMULATION 1. USE SUPRA MAXIMAL STIMULATION OPTIMISE STIMULATION

22. Important basic patterns V NEUROPATHIC AXONAL LOSS DEMYELINATION CONDUCTION BLOCK MYOPATHIC NMJ

23. Axonal loss DEFINITION decrease in amplitude normal or decreased CV (never < 75% of lower normal ) normal or prolonged distal latency.(never > 130% of upper normal) EXCEPTION Hyperacute axonal loss (nerve transection/nerve infarction)

24. Demyelination DEFINITION marked slowing of CV (< 75% of lower normal) marked prolongation of DL(> 130% of upper normal) or both. Any M/S/Mixed CV < 35m/s in upper limb or < 30m/s in lower limb EXCEPTION regenerating nerve fibers after complete axonal injury

25. Conduction block A feature of acquired demyelinating disease DEFINITION 1.> 50% drop in area/amplitude between proximal and distal stimulation sites. EXCEPTION tibial nerve up to 50% drop may be normal with popliteal fossa stimulation Demyelination associated with amplitude decrease is suggestive of 1.Axonal loss 2.Conduction block

26. Abnormal temporal dispersion DEFINITION 1.drop in CMAP amplitude or area > 20% and < 50% 2.or increase in CMAP duration > 15%. 3 . in axilla / erb’s point > 40% (amplitude/area) and > 30% (duration ) 4. At proximal stimulation site.

27. Conduction block at non entrapment sites differentiate between acquired and inherited demyelinating conditions. 1.inherited- uniform slowing of CV 2.acquired – conduction blocks , abnormal temporal dispersion decreased CV

28. Late responses V F response H reflex Axon reflex

29. Late responses To study more proximal Nerve segments

30. F response F = Foot Not a true reflex (no synapse) Represents a small CMAP Normal in conditions affecting sensory nerves only. Orthodromic motor response Antidromic F response   F Response Afferent Motor Efferent Motor Synapse No Nerves studied All Stimulation Supramaximal Configuration Usually polyphasic Amplitude 1–5% CMAP Varies with each simulation

31. F response Minimal F wave latency- most reliable and most useful Chrono dispersion Persistence F estimate   F Response Major uses Early Guillain – Barré syndrome C8–T1, L5–S1 radiculopathy Polyneuropathy Internal control (entrapment neuropathy) Normal values ≤32 ms median/ulnar * ≤56 ms peroneal/ tibial * Compare to F estimate Compare symptomatic to asymptomatic side Chronodispersion <4 ms (median/ulnar) <6 ms (peroneal/ tibial ) Persistence >50% F estimate= 2D/CV X 10 +1 +DL

32. F response Limitations 1. F responses may be absent in sleeping or sedated patients 2.F responses may be absent with low-amplitude distal CMAPs 3. Picks up C8-T1 and L5-S1 radiculopathies mainly. 4. Can’t pick up sensory radiculopathy. May be enhanced by Jendrassik maneuver

33. H reflex   H Reflex Afferent Sensory ( Ia muscle spindle) Efferent Motor Synapse Yes Nerves studied Tibial –soleus (median-FCR, femoral-quads) Stimulation Submaximal, long duration pulse (1 ms ) Configuration Triphasic and stable At low stimulation intensity, H is present without M As stimulation is increased, H and M increase At high stimulation, H decreases and M increases H = Hoffman,1918 True reflex

34.   H Reflex Major uses Early polyneuropathy S1 radiculopathy Early Guillain – Barré syndrome Tibial and sciatic neuropathy, sacral plexopathy Normal values ≤34 ms * Leg length nomogram Height nomogram ≤1.5  ms difference side to side H/M ratio ≤50% Miscellaneous Electrical correlate of the ankle jerk Must be present if ankle jerk is present May be present even if ankle jerk is absent May be enhanced by Jendrassik maneuver   H Reflex Measurements     Minimal latency H/M ratio (maximal H/maximal M amplitude )

35. H reflex

36. Axon reflex Not a true reflex Seen in reinnervated muscle with submaximal stimulation Suggestive of ephaptic spread of stimulus Found in 1.reinnervation following axon loss 2.GBS

37. Blink reflex Electrical correlate of clinical corneal reflex True reflex Detects lesions of 5 th , 7 th ,pons , medulla . R1= disynaptic = V1 Vm 7 th nucleus with ipsilateral 7 th R2= multisynaptic = V1 Vs ipsi & contra 7 th nucleus and nerve

38. Blink reflex A: Normal pattern B: Incomplete right trigeminal lesion C: Complete right trigeminal lesion. D: Incomplete right facial lesion. E: Complete right facial lesion . F: Right mid- pontine lesion G: Right medullary lesion H: Demyelinating peripheral polyneuropathy .

39. Anomalous innervation V Martin gruber anastomosis Accessory peroneal nerve Riche Cannieu anastomosis

40. Martin gruber anastomosis 1.Ulnar study: pseudo conduction block between wrist and BE 2.Ulnar study: pseudo conduction block between BE and A E

41. Martin gruber anastomosis 3 .Ulnar study: pseudo conduction block between wrist and BE recording FDI 4.Median study: increased CMAP proximally

42. Martin gruber anastomosis 5.MGA & CTS : Positive proximal deflection and factitiously fast CV 6. Needle EMG and MGA

43. Accessory Peroneal Nerve

44. Artifacts and technical factors

45. THANKS