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NCV and EMG.pptx
- 1.
- 2. Objective To familiarize NerveConduction Studies & Needle Electromyography as diagnostic tools and interpret its findings EMG & NCV 2
- 3. Contents 1. Background 2. BasicInstrumentations 3. Sensory and Motor Nerve Conduction Studies 4. Late responses 5. Electromyography 6. Clinical Interpretations EMG & NCV 3
- 4. Electrodiagnosis • Electrodiagnosis isthe field of study that uses electrical technology to study human neurophysiology. (Adam et al, 2020) Types • Conventional Electrodiagnostic Test • Modern Diagnostic Tests EMG & NCV 4
- 5. Conventional Electrodiagnostic Test StrengthDuration Curve EMG & NCV 5 Rheobase Test Chronaxie Test Faradic/Galvanic Test Reaction of Degeneration Test Pulse Ratio Accommodation Galvanic Tetanus Ratio
- 6. Modern Electrodiagnostic Test Electromyography(EMG) EMG & NCV 6 Nerve Conduction Velocity (NCV) Late Response Repetitive Nerve Stimulation Evoked Potential Studies
- 7. Indication of EMG& NCV 1. Suspected Neuromuscular diseases • Nerve root pathology • Nerve/Plexus pathology • Neuromuscular junction pathology • Muscle pathology 2. Follow up EMG & NCV 7 Jay M Weiss, Lyn D Weiss. Easy EMG. Boston (USA): Elsevier; 2016.
- 8.
- 9. Electrodes EMG & NCV9 Surface Electrodes Disc Ring Ground
- 10. Electrodes EMG & NCV10 Stimulating Electrodes
- 11. Electrodes EMG & NCV11 Concentric Monopolar Bipolar Concentric Needle Electrodes
- 12. Processing Unit Amplifier Filter Signal Averager Analogto Digital Conversion EMG & NCV 12
- 13. Display System 1. VideoComputer screen 2. Audio System Sweep speed: Horizontal screen= milliseconds Sensitivity: vertical axis= response amplitude EMG & NCV 13
- 14. Nerve Condition Studies Testused to measure the speed of the electrical activity of a nerve Nerve conduction studies can test sensory or motor nerve fibers and can determine both the speed of conduction as well as the amplitude of the electrical signal evoked following stimulation of a nerve. (Julie K et al, 2016) EMG & NCV 14
- 15. Nerve Condition Studies Types 1.Sensory Nerve Condition Studies 2. Motor Nerve Conduction Studies 3. Late Responses- (F- wave & H- reflex) 4. Repetitive Nerve Stimulation EMG & NCV 15
- 16. Nerve Condition Studies Advantage 1.Differentiate Axonal loss from demyelination 2. Localizes the site of injury 3. Can assess severity of nerve lesion 4. Can distinguish the type of nerve lesion 5. Non invasive technique EMG & NCV 16 Jay M Weiss, Lyn D Weiss. Easy EMG. Boston (USA): Elsevier; 2016.
- 17. Nerve Condition Studies Limitations 1.Routine studies primarily evaluate distal nerves 2. Very Mild axon loss without demyelination may not be detected. 3. Some deeper nerve branches cannot be easily tested. 4. It does not evaluate small fibers EMG & NCV 17 Jun Kimura. Electrodiagnosis in Nerve and Muscles fourth edition. Kyoto (JAP): oxford; 2012.
- 18. Nerve Condition Studies PatientPreparation: Informed Consent Examine skin Relaxed comfortable position True Nerve length Maintain skin temperature Clean the skin with alcohol swab EMG & NCV 18
- 19. Nerve Condition Studies Stimulation: EMG& NCV 19 Orthodromic Stimulation Antidromic Stimulation Physiological direction
- 20. Nerve Condition Studies DistanceMeasurement: EMG & NCV 20
- 21. Sensory Nerve ConditionStudies Basic Principle of Nerve Stimulation 1. Sensory nerve is stimulated at one point where as Motor nerve is stimulated at least 2 points along its course 2. Supramaximal stimulation is applied for Sensory Nerve Action Potential (SNAP) and Compound Motor Action Potential (CMAP) 3. Cathode pole of electrode (Black) should be placed near to the active electrode EMG & NCV 21 Jun Kimura. Electrodiagnosis in Nerve and Muscles fourth edition. Kyoto (JAP): oxford; 2012.
- 22. Sensory Nerve ConditionStudies Electrode Placement : Sensory NCV EMG & NCV 22 Electrode Site Active (Recording) Over the nerve Reference 3-4 cm apart from Active electrode Stimulating electrode Along the course of nerve to be stimulated Ground Between Active and stimulating Electrode
- 23. Motor Nerve ConditionStudies Electrode Placement: Motor NCV EMG & NCV 23 Electrode Site Active (Recording) Over the muscle belly (motor point) Reference (E2 or G2) Nearby Tendon or bone away from the muscle Stimulating electrode Along the course of nerve to be stimulated Ground Between Active and stimulating Electrode
- 24. Nerve Condition Studies SensoryNerve Action Potential (SNAP) EMG & NCV 24 Compound Motor Action Potential (CMAP)
- 25. Nerve Condition Studies 1.Latency: Time taken electrical impulse to travel from the stimulation site to the recording site Sensory Nerve: Depends upon the speed of conduction of the fastest fiber and distance between stimulus to active electrodes Motor Nerve: Depends upon the speed of conduction of the fastest fiber , distance between stimulus to active electrodes, neuromuscular transmission time and propagation time along the muscle membrane. EMG & NCV 25
- 26. Nerve Condition Studies 2.Duration : Measured from initial negative peak to return to baseline Suggest the number of nerve fiber EMG & NCV 26
- 27. Nerve Condition Studies 3.Amplitude: Measured from baseline to negative peak or negative peak to positive peak Suggest the density of nerve fiber in Sensory NCS and number of motor units in Motor NCS. EMG & NCV 27
- 28. Nerve Condition Studies 4.Nerve Conduction Velocity (NCV): EMG & NCV 28 Distance between Active and stimulating electrode onset latency SNCV = Distance between proximal and distal Stimulating site Proximal latency- distal latency MNCV =
- 29. Normative value :Amplitude EMG& NCV 29 Sensory NCV Nerve Amplitude (micro Volt) Nerve Amplitude (micro Volt) Median (S) >20.0 Sural (S) >10.0 Ulnar (S) >18.0 Lat Femoral Cutaneous 10-25 Radial (S) >10.0 Superficial fibular (S) 10-26 Motor NCV Nerve Amplitude (m Volt) Nerve Amplitude (m Volt) Median (M) >4.0 Fibular >2.0 Ulnar (M) >4.0 Medial Plantar >3.0 Radial (M) >3.0 Lateral plantar >3.0
- 30. Normative Value :NCV EMG& NCV 30 Sensory CV Nerve Velocity (m/s) Nerve Velocity (m/s) Median (S) >45.0 Sural (S) >36.0 Ulnar (S) >45.0 Lat Femoral Cutaneous > 44 Radial (S) >44.0 Superficial fibular (S) 45.5-56.9 Motor CV Nerve Velocity (m/s) Nerve Velocity (m/s) Median (M) >50.0 Fibular >40.0 Ulnar (M) >50.0 Medial Plantar > 40.0 Radial (M) >50.0 Lateral plantar >40.0
- 31. Normative Value :DistalLatency EMG & NCV 31 Sensory CV Nerve Latency (ms) Nerve Latency (ms) Median (S) <1.9 Sural (S) <3.8 Ulnar (S) <3.1 Lat Femoral Cutaneous <2.6 Radial (S) <3.4 Superficial fibular (S) <2.4 Motor CV Nerve Velocity (m/s) Nerve Velocity (m/s) Median (M) <4.2 Fibular <5.5 Ulnar (M) <3.4 Medial Plantar <6.0 Radial (M) <2.9 Lateral plantar <6.0
- 32. To Memorize EMG &NCV 32 Nerve Upper limb Lower Limb Latency <4.0 ms <6.0 ms Sensory Amplitude >10.0 µV >10.0 µV Motor Amplitude >4.0 mV >3.0 mV NCV 40-50 m/s 35-45 m/s
- 33. H Reflex EMG &NCV 33 Monosynaptic reflex Assess proximal lesions Submaximal stimulation Involves sensory and motor neurons Reflex arch of H Reflex: • Ia sensory fiber • Spinal cord and its interneuron • Efferent motor fiber Supramaximal stimulation: No H- reflex
- 34. H Reflex EMG &NCV 34 Normal value in Soleus H reflex in adults • Latency (ms): 30.3 ± 1.7 • Amplitude (mV): 9.8 ± 6.1 • M-wave (mV): 24.6 ±6.6 • HM ratio: 0.4 ± 0.2 Clinical Implications • Evaluates proximal sensory & motor pathways • GBS: absent, delayed or dispersed • S1 radiculopathy: delayed or absent
- 35. F Wave EMG &NCV 35 Supramaximal stimulation No reflex arch Evaluates Root or plexus abnormalities Neuropathy myopathy Helpful in diagnosis of GBS Thoracic outlet syndrome Brachial plexus injury Radiculopathies with more than one root involved
- 36. F Wave EMG &NCV 36 Properties 1. Latency (ms): 16.3 ± 1.9 2. Amplitude(mV): 0.2 ± 0.1 3. Duration (ms): 7.6 ± 1.4 4. F –M ratio: 0.8-0.2 5. Chronodispersion: 2.5 ±1.1
- 37. Interpretation of NCVStudies EMG & NCV 37 Normal Axonal Degeneration Demyelinating Wrist Elbow
- 38. Gullian Barre Syndrome EMG& NCV 38 INCREASED REDUCTION PROXIMAL LATENCY CMAP AMPLITUDE
- 39. Diabetic neuropathy EMG &NCV 39 DISTAL LATENCY CMAP AMPLITUDE SNAP AMPLITUDE NORMAL OR NEAR NORMAL REDUCTION REDUCTION
- 40. Radiculopathy EMG & NCV40 CMAP AMPLITUDE F WAVE H REFLEX REDUCED/ABSENT REDUCTION REDUCED/ABSENT
- 41. Pronater teres syndrome EMG& NCV 41 PROXIMAL LATENCY AT FOREARM DISTAL LATENCY AT WRIST CMAP AMPLITUDE FOREARM WRIST PROLONGED NORMAL NORMAL
- 42. Variables affecting NCVStudies EMG & NCV 42 Physiological Variables Technical variables Age Stimulating system Temperature Recording System Upper limb vs Lower limb Inadvertent stimulation of another nerve Gender Anomalous innervation of muscles
- 43. Electromyography (EMG) • Recordingof action potential of muscle fibers firing singly or in a group, near the needle electrode in a muscles (Mishra & Kalita, 2014) • EMG test the integrity of entire motor system, which consists of upper and lower motor neurons, neuromuscular junction and muscles (Kimura, 2016) • Performed as an extension of physical examination rather than laboratory procedure. EMG & NCV 43
- 44. Electromyography (EMG) EMG &NCV 44 NEEDLE EMG SURFACE EMG
- 45. Special Precautions forEMG • Morbid Obesity • Thin Individuals • Bleeding disorders • Aseptic precaution EMG & NCV 45
- 46. Contraindication for EMG •Recent systemic infectious diseases • Recent muscle biopsy • Localized inflammation • Skin lesions EMG & NCV 46
- 47. EMG Procedure • Preparationof patient • Select the muscles to be tested • Locate the site of needle insertion • Insert the needle quickly • Sharp Motor Unit Potential (MUP) on minimal voluntary contraction confirms that needle is in proper position. If MUP is not sharp, reposition the needle EMG & NCV 47
- 48. Neuropathy vs Myopathy EMG& NCV 48 Neuropathy Myopathy Number of motor neuron decreases Muscle fibers are destroyed Deprived muscles fibers get collateral from viable motor neuron Decreased number of muscle fibers supplied by a single motor neuron Increased number of muscle fibers supplied by a single motor neuron Decrease in size of motor unit Amplitude and duration of Motor unit action potential increases Amplitude and duration of Motor unit action potential decreases
- 49. EMG Analysis 1. InsertionalActivity 2. Muscles at Rest 3. Motor Unit Analysis on mild voluntary contraction 4. Maximum voluntary contraction • Recruitment pattern • Interference pattern EMG & NCV 49
- 50.
- 51.
- 52. Insertional activity Insertional activitySeen in Increased Early stage of denervation Acute myositis Inflammatory myopathies Decreased Atrophied muscles Fibrosed muscles Needle electrode is not in muscle tissue EMG & NCV 52
- 53. Examination of Musclesat Rest 1.No activity 2. Endplate region: 1. Miniature Endplate Potentials (MEEP) 2. Endplate spike 3. Spontaneous Activity EMG & NCV 53
- 54. Examination of Musclesat Rest Endplate region: EMG & NCV 54
- 55. Spontaneous Activity Originated fromMuscle Fibers Originated from motor neuron 1.Fibrillation Potentials (Fibs) 2.Positive sharp waves (PSW) 3.Myotonic Discharge 4.Complex repetitive discharges 1.Myokymic discharge 2.Cramps 3.Neuromyotonic discharge 4.Fasciculation 5.Fibrillation Potentials (Fibs) EMG & NCV 55
- 56. Spontaneous activities 1. PositiveSharp Wave EMG & NCV 56 Seen in: 1. Mainly on Lower Motor Neuron Lesion 2. Also seen in Myopathies
- 57. Spontaneous activities EMG &NCV 57 2. Fibrillation Potential Seen in 1. LMNL 2. Myopathies
- 58. Spontaneous activities Positive SharpWave and Fibrillation Potential EMG & NCV 58
- 59. Spontaneous Activity 3. ComplexRepetitive Discharge (CRD) EMG & NCV 59 Seen in Myogenic conditions Polymyositis Muscular dystrophies Neurogenic Conditions Poliomyelitis ALS Chronic radiculopathies Chronic neuropathies
- 60. Spontaneous Activity 3. ComplexRepetitive Discharge (CRD) EMG & NCV 60
- 61. Abnormal Spontaneous Activity Seenin Myotonic dystrophy Polymyositis Chronic radiculopathy EMG & NCV 61 4. Myotonic discharge
- 62. Abnormal Spontaneous Activity EMG& NCV 62 4. Myotonic discharge
- 63. Abnormal Spontaneous Activity 5.Myokymic discharge EMG & NCV 63 Seen in Facial Muscles: Bells palsy Multiple sclerosis Polyradiculopathy Limb muscles Chronic nerve lesions
- 64. Abnormal Spontaneous Activity 5.Myokymic discharge EMG & NCV 64
- 65. Abnormal Spontaneous Activity 6.Fasciculation EMG & NCV 65 Seen in Small twitch Irritation of AHC Chronic peripheral nerve lesions Nerve root compression Muscle spasm or cramps ALS and PMA (motor neuron diseases)
- 66. Abnormal Spontaneous Activity 6.Fasciculation EMG & NCV 66
- 67. Motor Unit ActionPotential (MUAP) • Analysis of MUAP done with minimal contraction of muscles EMG & NCV 67
- 68. Motor Unit ActionPotential (MUAP) Component Normative value Amplitude 4 µV to 5 mV Duration 2 ms to 17 ms Rise time Upto 500 ms Frequency 1 Hz- 60 Hz Phase Mono to Four phases (Bi-phasic or Tri- phasic) Sound Clear, sharp EMG & NCV 68
- 69. Motor Unit ActionPotential (MUAP) EMG & NCV 69
- 70. Motor Unit ActionPotential (MUAP) EMG & NCV 70 Amplitude and Duration Increased in Neuropathy Decreased in myopathy
- 71. Motor Unit ActionPotential (MUAP) EMG & NCV 71 Phases Normal triphasic Polyphasic + Longer Duration Neurogenic abnormalities + Shorter Myopathic
- 72. Examination of Musclesat Maximum Voluntary Contraction • Change in electrical activity during progressively increasing contraction to maximal contraction 1. Recruitment 2. Interference pattern EMG & NCV 72
- 73. Recruitment & Interference •The motor unit start firing in a regular pattern at 5 Hz EMG & NCV 73 Normal Neurogenic Myopathic
- 74. Normal Interference Pattern EMG& NCV 74
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- 77. EMG finding inDMD EMG & NCV 77 DECREASED/ ABSENT Fibrillation Potential, Positive sharp waves Low amplitude, Short duration, Polyphasic Low amplitude and Reduced Insertional Activity Spontaneous Activity Motor Unit Potential Interference
- 78. EMG finding inGullian Barre Syndrome EMG & NCV 78 Increased Fasciculation or Myokymic High amplitude, long duration, Polyphasic High amplitude and Reduced Insertional Activity Spontaneous Activity Motor Unit Potential Interference
- 79. Role of EMGand NCV Tests in Physiotherapy EMG & NCV 79 EVALUATE TREATMENT OUTCOME NEUROMUSCULOSKELETAL ASSESSMENT PLAN PHYSIOTHERAPY INTERVENTION
- 80. Take Home Message 1.NCV : demyelinating and axonal neuropathy 2. Late responses (F wave and H-reflex) : Radiculopathy and proximal neuropathy 3. Electromyography studies differentiates myopathy with neuropathy 4. All these tests are extensions of physical examinations 5. Findings of Electrodiagnosis tests can be valuable to plan physiotherapy interventions based on severity and type of neuromusculoskeletal injuries EMG & NCV 80
- 81. THANK YOU EMG &NCV 81
Editor's Notes
- #11 Has two Electrodes: Cathode/ Negative pole/Black Anode/Positive/ Red Cathode is placed towards the direction of stimulation (except F wave) Supramaximal stimulation: 10-12% Constant Current Stimulator and Constant Voltage Stimulator
- #17 Severity of lesion: neuropraxia, Axonotmesis and Neurotmesis type of nerve lesion : sensory, motor or mixed
- #18 4: only fast fibers, myelinated fibers
- #19 Examine skin: for sensitivity and integrity True Nerve length: For Ulnar nerve, flexed elbow Maintain skin temperature: at 34 degree Celsius.
- #22 Motor NCV :The distance between two points should be at least 10 cm Normal Supramaximal stimulation for MNCV: 20-50 mA, SNCV: 5-30 mA Motor nerve is stimulated at least 2 points along its course : NMJ and muscle depolarizn time Cathode pole of stimulating electrode should be placed close to the active electrode : prevents hyperpolarization effect of anode and anodal conduction block
- #25 CMAP: summative AP of motor units, more amplitude (mV), longer duration SNAP: summative AP of sensory N fibers, less amplitude (µV), shorter duration
- #28 Skin Temp : 32 degree Celsius UE, 30 degree for LE Side to side amplitude difference of >50 % or 20 % amplitude drop distal to proximal is significant
- #30 Skin Temp : 32 degree Celsius UE, 30 degree for LE Side to side amplitude difference of >50 % or 20 % amplitude drop distal to proximal is significant
- #31 Skin Temp : 32 degree Celsius UE, 30 degree for LE Side to side amplitude difference of >50 % or 20 % amplitude drop distal to proximal is significant
- #32 Skin Temp : 32 degree Celsius UE, 30 degree for LE, 8 cm distal stim site Side to side amplitude difference of >50 % or 20 % amplitude drop distal to proximal is significant
- #33 Skin Temp : 32 degree Celsius UE, 30 degree for LE, distal latency 8 CM Side to side amplitude difference of >50 % or 20 % amplitude drop distal to proximal is significant
- #34 Electrodes: Active: Gastrosoleus, Reference: TA, Stimulating: Popliteal fossa (for S1 radiculopathy) H reflex UE: Flexor carpi radialis, Median nerve at cubital fossa (C6-C7) radiculopathy H reflex disappear when stimulation is further increased Significance: Assess proximal lessions, becomes abnormal early in radiculopathy, assess preganglionic lesion Before 2 years Seen in every muscles Shorter conduction time of S1 due to less dispersion of Ia fiber of nerve
- #36 Obtained from any distal muscles Depolarization of axon hillock—depolarization of dendrite—in turn depolarization of axon hillock select portion of these alpha motor neurons, (roughly 5-10% of available motor neurons), 'backfire' or rebound Only few (10%) of motor neuron particpitaes in F wave Explores only the motor component of peripheral nerve Small amplitude response occurring 20-60 ms after direct muscle response (m-wave)
- #37 Chronodispersion: diff bw minimum and max latencies in series (50-60) of F wave F-M ratio: latencies of F wave: M wave Persistence: no of response occurrence divided by no of stimuli
- #38 50-75 % decrease in CMAP amplitude: moderate axon loss 75%: severe axonal loss Absent CMAP: no viable axon
- #39 Primarily Demyelinating Neuropathy Proximal weakness Mainly affecting motor nerves
- #40 Mainly axonal degeneration, distally
- #42 Neuropraxia Compression of Median nerve at pronater teres, without conduction block
- #43 Age: Infant has half NCV than adult: immature myelin sheet After 60 yrs NCV decreases: degeneration of nerve Temperature: Decrease in temp=latency increases, NCV decreases and amplitude increases Due to closure of ca channel 1 degree fall in temp incrases 0.3 ms latency Increasing temp (29-38), NCV increases by 5 % Idol skin temp : 34 degree Upper limb Vs lower limb Shorter UL nerve has longer internodal distance, large diameter of axon= increases NCV Longer LL nerve have many branches and lower temp than UL Male NCV<Female NCV (Fat increases core temp in female)
- #45 Surface EMG assesses muscle function by recording muscle activity from the surface above the muscle on the skin. Surface EMG can be recorded by multiple electrodes. Limitations: Recordings are restricted to superficial muscles Uses: Kinesological Assessments, Research purpose and Biofeedback.
- #46 Morbid obesity: difficult to localize specific muscles Thin individuals: not to insert needle deep to avoid injury to other tissues ( thoracis-lung)
- #48 Needle location: slightly away from motor point to avoid end plate noise
- #50 Insertional activity: caused by mechanical damage to muscles Spontaneou activity: muscles at rest
- #51 Short burst of electrical activity (clusters of sharp positive and negative spike) lasts for < 300ms Insertional activity: caused by mechanical damage to muscles causing depolarization Sound: Crisp (wringing the paper)
- #52 Increased: electrical activity lasts longer than 300 ms, due to unstable or excitable muscle fiber membrane Decreased: shorter
- #53 Inflammatory myopathies Polymyositis, dermatomyositis Fibrosed muscles: muscular dystrophy diseases ( due to unsynhronous opening and closing of na-K channel) Denervation: acetylcholineesterage inhibition
- #54 Miniature Endplate Potential (MEEP): spont release of ach , creates a small current short duration, irregular, small amplitude (10-20 microvolt) Endplate spike: large amount of ach release, produces short depolarizn single muscle fiber depolarization, biphasic, initial negative defletion, 100-200 microvolt, 3-5 msec Pain
- #55 Endplate region: activity seen when the needle is in endplate region of a muscle fiber Miniature Endplate Potential (MEEP): spont release of ach , creates a small current short duration (1-2 ms), irregular, small amplitude (10-20 microvolt) Endplate spike: large amount of ach release, produces short depolarizn single muscle fiber depolarization, biphasic, initial negative defletion, 100-200 microvolt, 3-5 msec Pain
- #57 PSW: small amplitude (20-100 µV) Mono or biphasic(primary +ve defln) , 0.5-15 Hz Arises from spont depolarization of a single muscle fiber Sound: dull thud; Appears earlier than Fibs after injury LMNL: AHC ds, Radiculopathies, PNI, Polyneuropathies with axonal degeneration Myopathies: Muscular dystrophies, polymyositis
- #58 Fibs: rate: small amplitude 10-300µV; biphasic (initial positive) @ 05-10 hz, Arises from spont depolarization of a single muscle fiber Sound: rain hitting a tin roof LMNL: AHC ds, Radiculopathies, PNI, Polyneuropathies with axonal degeneration Myopathies: Muscular dystrophies, polymyositis
- #59 PSW: dull thud; Appears earlier than Fibs after injury FIBS: rain hitting roofs
- #60 CRD: local muscle arrhythmias, repetitive and regular firing of group of muscle fibers appear and disappear suddenly Suggests ongoing reinnervation originated by the spont depolarization of a single fiber, followed by ephaptic spread (cell to cell)to an adjacent muscle fiber. Frequency: 10-100 Hz, Amplitude: 50 microvolt-500 microvolt Sound: motorboat Usually seen in injury greater than 6 months (chronic neurogenic conditions and myopathies
- #61 CRD: local muscle arrhythmias, repetitive and regular firing of group of muscle fibers Simple or complex spike pattern that appear suddenly and disappear Suggests ongoing reinnervation originated by the spont depolarization of a single fiber, followed by ephaptic spread (cell to cell)to an adjacent muscle fiber. Frequency: 10-100 Hz, Amplitude: 50 microvolt-500 microvolt Sound: motorboat Usually seen in injury greater than 6 months (chronic neurogenic conditions and myopathies
- #62 myotonic:, waxing and waning appearance @ 20-100 hz rate: 20-100 hz Two forms of waves: psw morphology or Brief spikes pattern of biphasic or triphasic potentials originated by the spont depolarization of a single fiber, followed by ephaptic spread (cell to cell)to an adjacent muscle fiber. Sound: dive bomber Seen in myotonic dystrophy, polymyositis, chronic radiculopathy
- #63 myotonic: rate: 20-100 hz, waxing and waning appearance Two forms of waves: psw morphology or Brief spikes pattern of biphasic or triphasic potentials originated by the spont depolarization of a single fiber, followed by ephaptic spread (cell to cell)to an adjacent muscle fiber. Sound: dive bomber (military aircraft) Seen in myotonic dystrophy, polymyositis, chronic radiculopathy
- #64 Regular firing pattern and rhythms: 5-10 Hz Due to hyperexcitability of peripheral nerve motor axons Sound: soldier marching
- #65 Regular firing pattern and rhythms: 5-10 Hz Due to hyperexcitability of peripheral nerve motor axons Sound: soldier marching
- #66 Occurs randomly and irregularly @ 1 Hz-500 Hz Signals Originate from spinal cord or peripheral nerve lesion causing contrctn of ms Due to involuntary asynchronous contraction of bundles of ms fibers or a whole motor unit Can occur in healthy individual or in diseases Can be seen with naked eye Sound: low pitched dump
- #67 Occurs randomly and irregularly @ 1 Hz-500 Hz Signals Originate from spinal cord or peripheral nerve lesion causing contrctn of ms Due to involuntary asynchronous contraction of bundles of ms fibers or a whole motor unit Can occur in healthy individual or in diseases Can be seen with naked eye Sound: low pitched dump
- #69 Amplitude: measured from most positive to most negative peak; reflects muscle fiber density close to needle; Rise Time: time lag from initial positive defletion to subsequent negative upward peak: Distance between needle and MU Duration: initial departure from baseline to final return to baseline, Degree of synchrony between muscle fibers Phases: peaks crossing baseline, Normal has 3 peaks, more than 4_ polyphasics
- #70 Clear, sharp Sound
- #72 Normal Polyphasic seen in : Upto 30 % in Monopolar & 15 % in concentric needle AP of one muscle fiber: represents individual components of phase Myopathic: reflects Regeneration of fibers & increase in fiber density in myopathies Neuropathic: Regeneration of axons in neuropathies
- #73 Recruitment: Interference
- #74 On voluntary contraction, smaller muscles fibers recruited first then larger: Henneman principle
- #79 Myokymia: Due to hyperexcitability of peripheral nerve motor axons
- #80 Neuromusculoskeletal assessment: type of lesion, severity Active stage of disease: energy conservations technique Recovery stage: gradual increase in treatment Neuropraxia, Axonotmesis: