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30 Cards in this Set
- Front
- Back
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EMG/NCS of neuropathy can answer three broad questions about the neuropathy. What are these?
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EMG/NCS of neuropathy answers the three broad questions of chronicity, severity and whether the lesion is axonal or demyelinating.
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Does Wallerian degeneration happen sooner for motor or sensory nerves?
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(233) Motor. Think Slow Sensory.
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3. What is the range of days that it takes for Wallerian degeneration of Slow Sensory nerves to take place?
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) Wallerian degeneration of Slow Sensory nerves takes 6 to 10 days. Slow Sensory nerves take una Semana to degenerate.
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What is the range of days that it takes for Wallerian degeneration of motor nerves to take place?
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(233) Wallerian degeneration of motor nerves takes 3 to 5 days. Motor nerves take half the time to degenerate compared to the Slow Sensory Semana. 3-5 days is the Motor Midpoint of the Sensory Semana.
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Wallerian degeneration from partial transection of a motor nerve may cause some slowing due to loss of the fastest fibers. However a pure axonal lesion will not cause slowing to the demyelinating range. What is the threshold percentage of normal conduction velocity below which demyelination must be invoked as a cause?
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(233) Demyelination must be invoked as a cause if the conduction velocity is less than 75% of the lower limits of normal
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What is the threshold percentage of normal distal latency above which demyelination must be invoked as a cause?
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(233) Demyelination must be invoked as a cause if the distal latency is more than 130% of the upper limits of normal
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Immediately after a partial motor nerve transection, characterize EMG findings in a weak muscle.
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(234) Immediately after a partial motor nerve transection, NCS distal to the lesion are normal. However EMG in a weak muscle should show reduced recruitment.
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How long after denervation at the nerve root does it take for abnormal spontaneous activity to develop in paraspinals?
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(234) 10-14 days
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How long after denervation at the nerve root does it take for abnormal spontaneous activity to develop in proximal thigh muscles?
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(234) 2-3 weeks
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How long after denervation at the nerve root does it take for abnormal spontaneous activity to develop in distal leg and foot?
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(234) 5-6 weeks
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Does it take longer for abnormal spontaneous activity to develop in paraspinals after radiculopathy or in deltoid with botulism?
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(234) Abnormal spontaneous activity occurs first in botulism; it may take just a few days. This illustrates the principle that the length of time it takes for abnormal spontaneous activity to begin depends directly on the distance from the nerve lesion to the muscle. Because botulism’s lesion is just proximal to the neuromuscular junction, fibs develop in just a few days.
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Reinnervation takes months. What aspect of the NCS changes most with reinnervation?
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(234) amplitudes may increase
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What aspect of EMG first changes with reinnervation via the process of collateral sprouting?
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(234) In partial axonal loss injuries, collateral sprouting results in MUAPs that are polyphasic with longer durations and greater amplitudes.
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What is the rough time frame for abnormal spontaneous activity to cease in an injury that will successfully reinnervate?
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(234) months to years
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Your patient regained some but not all strength after a partial nerve transection many years ago. Abnormal spontaneous activity is no longer present. MUAP morphology is normal. What abnormality would you expect to find on EMG?
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(234) With the reduced strength, you would expect to see decreased recruitment, even if all other findings have normalized
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Weakness from a purely demyelinating lesion implies that you should find what phenomena on NCS?
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(235) Weakness from a purely demyelinating lesion implies that you should find conduction block because not all the signal reaches the muscle.
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Weakness is the sign that corresponds to conduction block of a motor nerve. What is a sign that corresponds to conduction block of a sensory nerve?
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Conduction block of a sensory nerve results in fixed numbness. Pure slowing may result in a perception of altered sensation, but not in fixed numbness.
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You suspect sensory nerve demyelination and note depressed and absent reflexes on exam. Does this imply conduction block of sensory nerves?
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235) Pure slowing of sensory nerves may result in depressed or absent reflexes; conduction block is not necessary to cause this finding.
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The finding of conduction block from demyelination provides three types of information. Does it imply a good or poor prognosis for recovery?
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(235) Conduction block from demyelination implies a good prognosis for recovery.
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In addition to implying good prognosis for recovery, conduction block at an entrapment site can localize the pathology. The third way conduction block can be informative is in a patient with polyneuropathy. What do you conclude in a polyneuropathy patient with conduction block at non-entrapment sites?
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(235) Conduction block at non-entrapment sites in polyneuropathy is consistent with acquired rather than hereditary polyneuropathies. Hereditary polyneuropathies result in uniform slowing.
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What histologic structure is damaged in pseudo conduction block?
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(236) Pseudo conduction block looks like conduction block on NCS but is caused by damage to the axon.
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Up to how long after an axonal motor injury might you find pseudo conduction block?
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(236) You may find pseudo conduction block before Wallerian degeneration occurs. For motor nerves this is the 3-5 day motor midpoint of the slow sensory semana
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What are the EMG findings of a purely demyelinating lesion resulting in conduction block?
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In a pure demyelinating lesion with conduction block, the only abnormality on needle EMG is reduced recruitment.
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24. What are the EMG findings of a purely demyelinating lesion resulting in slowing without conduction block?
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236) In a pure demyelinating lesion without weakness and its EMG correlate of conduction block, needle EMG is normal.
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Are pure demyelinating lesions common or uncommon?
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236) Pure demyelinating lesions are uncommon. Most demyelinating lesions have some secondary axonal loss, regardless of etiology and whether they meet the criteria for conduction block. Such cases demonstrate a combination of axonal and demyelinating changes on EMG/NCS, but it is usually still possible to determine if the primary pathology is demyelination or axonal loss.
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Your patient suffered partial axonal loss less than 3 days ago. He has a hyperacute picture on NCS/EMG. Motor NCS show pseudo-conduction block. What would you expect to find on late responses?
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237) In a hyperacute partial axonal loss injury, late responses are usually normal unless the nerve has been completely transected.
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Your patient suffered partial axonal loss less than 3 days ago. He has a hyperacute picture on NCS/EMG. What findings do you expect on needle EMG?
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In a hyperacute partial axonal loss injury, on needle EMG you expect to find only reduced recruitment.
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What pattern is difficult to distinguish from hyperacute axonal loss?
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237) It is difficult to distinguish hyperacute axonal loss from acute demyelination with conduction block.
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After completing your H&P and EMG/NCS, you aren’t sure if the lesion is due to hyperacute axonal loss or acute demyelination with conduction block. What is your plan to distinguish between the two diagnoses with their quite different prognoses?
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237) To distinguish between hyperacute axonal loss and acute demyelination with conduction block, repeat the NCS in a week. This gives time for Wallerian degeneration to occur. After Wallerian degeneration, the two syndromes will test differently.
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Acute axonal loss pattern has the NCS findings you would expect after Wallerian degeneration: amplitudes are decreased with relatively normal conduction velocity and distal latency. EMG findings show only decreased recruitment. What is the range of time after injury in which you would expect to see this pattern?
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237) This pattern of acute axonal loss is between the events of Wallerian degeneration and the start of abnormal spontaneous activity. As such, it begins a 3-5 days after injury and ends 2-6 weeks after injury
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