Greathouse Assignment (1) PDF

1. Did you complete this assignment independently? - Yes. 2. What are characteristics of patients who would be appropriate for referral for electrodiagnostic studies? - Electrophysiological testing is a valuable tool for confirming findings from a thorough physical exami...

1. Did you complete this assignment independently? - Yes. 2. What are characteristics of patients who would be appropriate for referral for electrodiagnostic studies? - Electrophysiological testing is a valuable tool for confirming findings from a thorough physical examination. It can also detect neurological injuries in patients who may not exhibit deficits during a neurological exam. Suitable candidates for testing typically present with specific symptoms such as localized pain, numbness, tingling, weakness, or abnormalities in sensory, reflex, or vascular function. A comprehensive review of systems, including relevant medical history and evaluation for cranial nerve dysfunction, is essential. It\'s important to note that EMG and NCS focus on assessing lower motor neuron disorders, such as those involving the anterior horn cells, nerve roots, plexuses, peripheral nerves, or neuromuscular junctions. They do not evaluate central nervous system conditions. 3. What exam findings may suggest that there is an issue in the myelin? - Prolonged distal latency in sensory or motor nerve conduction studies may indicate focal demyelination, often accompanied by a reduced amplitude of SNAP or CMAP. Additionally, slowed nerve conduction velocity over a localized segment or multiple longer segments can also suggest demyelination. 4. What exam findings may suggest that there is an issue in the axon? - In sensory or motor nerve conduction studies, axonal injury or degeneration is often characterized by prolonged distal latency and reduced amplitude in SNAP or CMAP. On electromyography, findings such as increased insertional activity, abnormal spontaneous activity at rest, decreased interference patterns, and polyphasic motor unit action potentials further show the presence of axonal injury or degeneration. 5. What is the difference between a sensory study and the motor study and why do we do both? - A sensory study evaluates sensory nerve action potentials to assess the sensory function of nerves, including their ability to transmit information related to touch, temperature, and pain. A motor study examines muscle action potentials motor evoked action potentials and compound muscle action potentials to evaluate the signals sent to muscles that enable movement. - Performing both types of studies provides a comprehensive understanding of nerve function, as sensory and motor roles are essential for daily activities. Certain conditions may affect either the sensory or motor components of nerves Testing both functions ensures an accurate diagnosis, which is crucial for developing effective treatment plans and prognoses. 6. Compare and contrast latency and nerve conduction velocity. - Latency, measured in milliseconds, refers to the time between the application of a stimulus and the resulting response. Nerve conduction velocity represents the speed at which an action potential travels along a nerve and is measured in meters per second. 7. How can an exam be modified to target assessment of the neuromuscular junction? - Nerve conduction velocity for the chemical transmission at the neuromuscular junction cannot be measured directly. Instead, NCV is calculated for nerve segments located proximal to the NMJ, such as the median nerve above the wrist. 8. How does the duration, shape, and size of MAUPs compare in normal muscle and myopathy? - MAUP's in normal muscle 1. Duration: 5-15 msec 2. Shape: initial, main spike (\< 15 fibers), terminal part 3. Size: 300 to 10,000 MV 4. Type 1: 300 to 1000 MV 5. Type 2: 1000 to 5000 MV 6. 2-3 phases - MAUP's in myopathy 7. Duration: \> 15 msec if neuropathic and \5 phases 9. Size: \> 10,000 MV 10. Result of axonal sprouting, neuropathic 9. Explain the following findings and include potential clinical results: - Positive Sharp Waves (PSWs): 11. Biphasic, positive-negative potentials recorded from a resting muscle fiber. 12. Represent single muscle fiber discharges from an injured or unstable muscle fiber membrane. 13. Auditory description: sounds like a \"thud\" or \"plop.\" 14. Clinical significance: may indicate conditions such as: 15. Denervated muscles, Polymyositis, Dermatomyositis, Progressive muscular dystrophy, Motor neuron diseases - Fibrillations: 16. Electrical activity associated with spontaneous contraction of a single muscle fiber. 17. Result from biochemical and histological abnormalities, appearing up to 2 weeks after nerve damage. 18. Manifest as increased insertional activity and abnormal spontaneous electrical activity at rest. 19. Indicate instability of the muscle fiber membrane or axonal denervation. 20. Auditory description: sounds like clicking or a manual typewriter. - Fasciculations: 21. Electrical potentials associated with random, spontaneous contractions of a group of muscle fibers or an entire motor unit. 22. Can have positive or negative deflections with two or more phases. 23. Auditory description: sounds like a pop. - Interference Pattern: 24. A summated response of motor unit action potentials during increased effort. 25. Non-uniform and incomplete patterns indicate axon loss from conditions such as: 1. Nerve injuries, Radiculopathies, Neuropathies, Loss of anterior horn cells, Conduction block. - Myotonic Changes: 26. Bursts of discharging potentials that wax and wane, representing recurring single fiber potentials from an injured muscle fiber. 27. Auditory description: sounds like a waxing and waning motorcycle or chainsaw. 28. Observed in conditions such as: 2. Myotonia congenita, Myotonic dystrophy, Paramyotonia congenita, Hyperkalemic periodic paralysis 10. What is the order of recruitment in normal muscle? - Recruitment begins with low-threshold, small-amplitude, and short-duration Type I motor unit action potentials. As recruitment continues, it progresses to higher-threshold, larger-amplitude, and longer-duration Type II MUAPs. 11. What are limitations of electrophysiologic testing? - There are several limitations to nerve conduction studies and electromyography. Not all components of the peripheral nervous system are assessed, such as the sympathetic system. NCS primarily evaluates only large, myelinated nerve fibers, focusing on sensory and motor fibers, and does not assess temperature or pain fibers. Additionally, many nerves are not amenable to NCS. Needle EMG only assesses Type I and Type II muscle fibers, and it does not evaluate central nervous system issues. Technical limitations include factors like equipment quality, room temperature, patient and provider characteristics, the ability to achieve a muscle membrane resting state, patient cooperation, accurate distance measurements, and the length of time since injury or symptom onset. 12. Explain the difference between neurapraxia, axonotmesis, and neurotmesis. - Neurapraxia 29. Conduction loss (temporary or transient block) without structural loss of the axon -- mildest form of nerve block. 30. Cause - Etiology 3. compression of nerve 4. ischemia caused by inappropriate arterial blood supply - Axonotmesis 31. Axon loss neuropathic process (axonopathy) 32. loss of axons at site of lesion 33. effects continuity of distal nerve segment followed by denervation-induced muscle weakness and/or atrophy 34. Wallerian degeneration distal to the site of the injury 35. conduction ceases immediately across the site of nerve injury in the axons involved - Neurotmesis 36. Injury separates the entire nerve, including the supporting connective tissue. 37. endoneurium, perineurium, and epineurium 38. Without surgical intervention, regeneration proceeds slowly (if at all), resulting in an incomplete and poorly organized repair. 13. Explain EMG and NCS findings for the following pathologies: - Radiculopathy 39. EMG - sequence of findings 5. Increased insertional activity & presence of fibs and PWs at rest = denervation 6. Decreased recruitment and interference pattern of MUPs 40. NCV - normal (until later stages of disease) 7. may affect CMAP amplitude secondary to atrophy 8. sensory NCS normal (pre-ganglionic) - Polyneuropathy 41. NCS 9. Reduced Amplitudes of Compound Muscle Action Potentials 10. Slowed Conduction Velocities 11. Prolonged Distal Latencies 42. EMG 12. Reduced Recruitment of Motor Units: 13. Fibrillation Potentials and Positive Sharp Waves 14. Reduced Motor Unit Action Potential (MUAP) Amplitudes - Mononeuropathy 43. normal NCS distal to lesion 44. prolonged latency of the CMAP or SNAP proximal to the lesion 45. conduction block, if present, during acute stages, will also diminish the amplitude of the CMAP or SNAP 46. EMG -- normal - NMJ Disease 47. Myasthenia Gravis 15. normal NCS and EMGs 48. Myasthenic Syndrome 16. NCS - normal sensory, +/- decrease amplitude of CMAP 17. EMG - SFEMG most helpful - Plexopathy 49. EMG - denervation (Increased insertional activity; Rest - Fibs, PWs; loss of MUPs on voluntary contraction) 50. NCV - slowing of conduction across site of injury - Motor Neuron Disease 51. EMG 18. loss of motor neurons = decreased recruitment and interference pattern; decreased amplitude (early stages) 19. Increased insertional activity 52. NCV 20. normal motor conduction studies (may slow as disease progresses and/or decrease in MUAP amplitude secondary to axon loss) 21. muscle atrophy on PE 22. normal sensory conduction studies - Myopathy 53. EMG -- triad of myopathy 23. fibs and PWs at rest 24. complex repetitive discharges (CRDs) 25. SLAPPS 54. NCS studies 55. motor studies are typically normal -- amplitude CMAP may be reduced due to decreased \# muscle fibers and atrophy 56. sensory studies are typically normal 14. Compare and contrast neuropathy and myopathy presentations.  - Neuropathy 57. Injury or disease of the nerve 26. motor neuron (AHC) 27. axon = axonopathy 28. myelin sheath = myelinopathy 29. neuromuscular junction (myoneural) 58. EMG 30. MUPs 1. Increased duration (\> 15 msec) 2. Increased amplitude (\> 10 mV) 3. Decreased recruitment and number of MUPs 59. NCS 31. slowed NCV and prolonged latencies (demyelinating); decreased amplitude (axonal loss) - Myopathy 60. Injury or disease of muscle 32. genetically determined disorders 33. toxic (metabolic or endocrine) 34. Inflammatory 61. EMG 35. MUPs 4. Decreased duration ( \< 5 msec) 5. Decreased amplitude ( \< 300 µV) 62. NCS 36. normal motor and sensory studies