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275 Cards in this Set
- Front
- Back
For neuronal injury, what is considered "brief" ischemia
|
6 hours or less
|
|
General pathologic changes that occur in nerve with brief ischemia
|
- no structural changes to nerve
- may be surrounding edema |
|
Which fibers are most effected by crush/tourniquet injury?
|
larger fibers more than smaller
|
|
Complete conduction block occurs when internodal conduction times exceed _____
|
500-600 microseconds
|
|
Why does significant demyelination result in complete conduction block instead of just severe slowing?
|
sodium channels are focused at nodes of Ranvier and not available along the section of demyelinated axon
|
|
Pathological changes in muscle after neurapraxic lesions
|
- few direct changes
- may have disuse atrophy if more prolonged |
|
Axonal changes in axonotmesis at 2 days, 3 days and 8 days after injury
|
2 days:
- leakage of intra-axonal fluid from severed nerve - swelling of distal nerve segment - disapearance of neurofibrils in the distal segment 3 days: - fragmentation of axon and myelin - digestion of myeline components Day 8: - axon digested - Schwann cells attempt to bridge the gap between 2 segments |
|
Cell body changes in axonotmesis at 48 hours and 2-3 weeks
|
48 hours:
- Nissl bodies break apart 2-3 weeks: - nucleus and nucleolus displaced eccentrically |
|
What is the ideal timing for electrodiagnostic studies after peripheral nerve trauma?
|
- 3-4 weeks in general (fibrillations apparent on EMG)
- at 7-10 days may be able to differentiate conduction block from axonotmesis - 2 months post injury if lesion documented surgically and EMG is just to document recovery |
|
Changes in CMAP in neurapraxic lesions immediately after injury
|
normal distal to site of lesion and smaller/absent CMAP proximal to the lesion
|
|
When evaluating CMAP along a peripheral nerve, what change in amplitude with distance would be clearly abnormal?
|
greater than 20% drop over 25cm or less
|
|
Give 2 reasons for slowing in a neurapraxic lesion
|
- loss of fast conducting fibers
- demylintion of surviving fibers |
|
Changes in CMAP in neurapraxic lesions should resolve within what time frame
|
a couple of months
|
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How do traumatic peripheral nerve lesions with axonotmesis look different on electrodiagnostics than on those with neurotmesis?
|
they look the same because differences are in the surrounding tissue
|
|
Changes in CMAP within the first few days of a nerve injury with axonotmesis
|
looks the same as in neurapraxic lesions (normal distal to site of lesion and smaller/absent CMAP proximal to the lesion)
|
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At what point after trauma can you distinguish neurapraxic lesion from axonotmeis/neurotmesis?
|
After Wallerian degeneration has occured (about 9 days)
|
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Changes in CMAP 10 days after a traumatic nerve injury with axonotmesis
|
CMAP with stimulation distal to the lesion will fall (Wallerian degeneration)
|
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In traumatic axonotmesis/neurotmesis, which fails first, NMJ transmission or nerve excitability?
|
NMJ transmission
|
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Inherent side to side variability in normals in CMAP amplitudes
|
30-50%
|
|
Limitations of using CMAP amplitude to estimate number of surviving fibers after axonotmesis/neurotmesis
|
- inherent 30-50% side to side difference
- can only use early in injury before sprouting occurs |
|
Percentage of axon loss estimations in mixed lesions in axonotmesis/neurotmesis are best done by...
|
comparing CMAP amplitude from distal stimulation with that obtained contralaterally
|
|
Conduction block estimates in in mixed lesions in axonotmesis/neurotmesis are best done by
|
comparing amplitudes or areas obtain proximal and distal to the lesion
|
|
F-waves are dependent on ___% of axons to elicit a resonse
|
3-5%
|
|
Usefullness of F-waves in evaluation of traumatic nerve injuries
|
variable; may be useful in evaluation brachial plexus injuries where difficult to stimulate above and below the lesion
|
|
Which has a greater amplitude drop with distance of recording: CMAPs or SNAPs?
|
SNAPs
|
|
Factors that make SNAP amplitude decrease with distance
|
- temporal dispersion
- phase cancellation |
|
Expected amplitude drop in SNAP over a 25cm distance
|
often 50-70%
|
|
Compare the timing of when you can see changes in sensory vs. motor nerve conduction in axonotmesis/neurotmesis
|
- 9 days for motor
- 11 days for sensory * because NMJ transmission fails earlier than nerve conduction |
|
Changes on needle EMG in neurapraxic lesions with complete conduction block
|
- No MUAPs on recruitment imemdiately after injury
- fibrillation potentials are controversial |
|
Are NCSs very sensitive for picking up minimal axon loss?
|
No
|
|
Changes on needle EMG in neurapraxic lesions with incomplete conduction block
|
Reduced recruitment (decreased # of MUAPs firing more rapidly)
|
|
Are there morophology changes in MUAPs at any time after neurapraxic injuries?
|
No, there's no axon loss so there's no sprouting
|
|
Timing of onset of fibrillation potential and positive sharp after axonotmesis/neurotmesis injuries
|
* depends on length of nerve
- 10-14 days for short distal stump - 21-30 days for longer distal stump (such as hand muscles in brachial plexopathy) |
|
In general, what happens to fibillation potential size over time?
|
It decreases
|
|
Describe the specific changes that happen in fibrillation potentials over time with axonotmesis/neurotmesis injuries
|
- first few months: several hundred microvolts
- 1 year old: less than 100 microvolts |
|
What happens to fibrillation potential frequency as a muscle is reinnervated? Is this generally clinically useful?
|
- decrease
- usually not useful (difficult to quantify, may be from muscle atrophy) |
|
Does direct muscle injury cause fibrillation potentials?
|
Yes
|
|
How long can fibrillation potentials from direct muscle injury last
|
large range, but reported after biopsy to 11 months
|
|
What are the general changes in MUAP morphology that occur after axonal sprouting?
|
- amplitude: increase
- duration: prolonged - polyphasic units: increased% |
|
When does axonal spouting occur after axonotmesis/neurotmesis injuries?
|
- 4 days on pathological evaluation
- Seen on single fiber EMG studies at 3 weeks post-injury |
|
After complete axonal loss, what are the first needle EMG findings of recovery?
|
MUAPs with:
- small amplitude - polyphasic - unstable |
|
Which comes first with recovery after axonotmesis/neurotmesis injuries, EMG findings or clinical findings?
|
EMG findings usually occur before clinically evident voluntary movement
|
|
General approach to localizing traumatic nerve injuries
|
- detecting focal slowing or conduction block on NCSs
- pattern of denervation on EMG |
|
Which type of traumatic nerve injuries can be well localized with NCS?
|
- able to stimulate above and below the lesion
- partial or complete neurapraxia or very acute axonal injuries |
|
A patient has absent sensation but intact SNAPs after a traumatic nerve lesion...in general, where is the injury?
|
proximal to the dorsal root ganglia
|
|
Trying to localize a traumatic nerve lesion based on nerve branching needs to also consider...
|
intraneural topography
|
|
Main electrodiagnostic tests used to differentiate root and plexus lesions in the brachial plexus
|
Paraspinal EMG and SNAPs
|
|
Describe the general order of mechanisms for recovery that contribute to increased functional muscle strength after a traumatic nerve injury
|
- resolution of conduction block
- distal axon sprouting - muscle fiber hypertrophy - axon regeneration |
|
What limits the time that motor axonal regrowth can be expected to give functionally significant recovery?
|
18-24 months
After this the muscle has atrophied too much to respond even if nerve regrows |
|
Remyelination after a neuropraxic lesion may take several _____
|
months
|
|
How fast can recovery occur after a Sunderland second degree traumatic nerve lesion?
|
- axons traverse segment in 8-15 days then regenerate along distal nerve segment at 1-5mm/day
|
|
Mixed traumatic nerve injuries often have a _____ phase recovery
|
2: initially fast phase, then slower
|
|
General prognosis of recovery in axonotmesis based on CMAP
|
* compare to contralateral side
<10% poor 10-30% good; not always complete >30% excellent (based on facial nerve; may even be more liberal in limbs) |
|
How long should you wait to look for evidence of reinnervation in previously completely dennervatedmuscle near the site of a peripheral nerve traumatic lesion?
|
2-4 months
|
|
General steps involved in sensory recovery after traumatic peripheral nerve lesion
|
- resolution of conduction block
- redistribution of sensory function - axonal regeneration |
|
When is immediate surgical reconstruction indicated for traumatic peripheral nerve lesions?
|
sharp nerve laceration in who the nerve end are likely otherwise uninjured, complete injury
|
|
When is early (1 month)surgical reconstruction indicated for traumatic peripheral nerve lesions?
|
blunt trauma or avulsion with complete nerve disruption; sharp lesions that were not taken care of immediately
Usually only with complete lesions |
|
In patients with axonotmesis with some spontaneous recovery, which is better: the natural recovery or recovery after surgical intervention
|
usually natural recovery course is better
|
|
When is delayed (3-6 months) surgical reconstruction indicated for traumatic peripheral nerve lesions?
|
when not clear if there is nerve continuity (traction injuries)
|
|
Nerve grafting 6 or more months after injury has a ____ surgical outcome
|
poor
|
|
When is late (1+years) surgical reconstruction indicated for traumatic peripheral nerve lesions?
|
usually no functional recovery; may be done for pain control
|
|
How is the relative electrical magnititude mismatch between the motor neuron and muscle overcome?
|
By chemical transmission
|
|
How many times is the neuron's electrical signal amplified after transmission to the muscle?
|
Over 100-fold
|
|
What is the chemical transmitter at the neuromuscular junction?
|
acetylcholine
|
|
Where is acetylcholine synthesized in nerve motor neurons?
|
in the nerve terminal
|
|
Acetylcholine is synthesized from _____ and ____ by the enzyme _____
|
synthesized from acetyl coenzyme-A and choline by the enzyme choline acetyltransferase
|
|
What are the 3 "compartments" of acetylcholine in the nerve terminal?
|
- reserve
- mobilization store - synthesis |
|
A quanta of acetylcholine likely contains how many molecules of acetylcholine?
|
Several thousand
|
|
The site on the motor neuron where Ach vesicles fuse is also called the _____ _____
|
active zone
|
|
Frequency of Ach quanta released by the motor neuron is dependent on
|
1. extracellular caldium concentration
2. temperature |
|
Where are post-synaptic Ach receptors concentrated on muscle fibers?
|
At the crests of the post-synaptic folds across from the pre-synaptic active zones
|
|
Each Ach receptor requires the binding of how many molecules of Ach?
|
2
|
|
What is a MEPP?
|
- miniature endplate potential: postsynaptic nonpropagating depolarization
|
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Acetylcholine is broken down by the enzyme _____ into ____ and ____
|
brokendown by the enzyme aceylcholinesterase into acetic acid and choline
|
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The action of Ach on the post-synaptic membrane is normally terminated within _____
|
a few milliseconds
|
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Depolarization of the nerve terminal causes an _____ of calcium
|
influx
|
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How many quanta are likely released after depolarization of a motor neuron?
|
around 100
|
|
Aproximate number of Ach receptor activated by Ach release from a depolarized motor neuron
|
100,000 Ach receptors
|
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What is an EPP?
|
endplate potential; non-propagating depolarization of post-synaptic membrane (larger than MEPPs)
|
|
If an end plate potential exceeds the threshold for activation, what happens?
|
action potential propagated in both directions along the non-junctional muscle membrane
|
|
Generally speaking, what path does the action potential take to trigger muscle contraction?
|
along the membrane to transverse tubule system and voltage-sensitive calcium influx triggers mechanical cotnraction of the muscle fiber
|
|
What is the "safety factor" of neuromuscular transmission?
|
normally an excess of Ach is released and many more Ach receptors are activation beyond what would be needed for muscle contraction
|
|
Often often is myasthenia gravis associated with thymoma?
|
15% of patients
|
|
Reflexes in myasthenia gravis are
|
normal
|
|
Sensation in myasthenia gravis is
|
normal
|
|
Clinical presentation of myasthenia gravis is typically
|
Asymmetric weakness and fatiguability of extracular, bulbar, nuchal or limb muscles.
|
|
Antibodies in myasthenia gravis are directed at
|
Ach receptors; immune complexes are localized to the post-synaptic membrane
|
|
Antibodies to Ach receptors are detected in ____% of patients with myasthenia gravis
|
80%
|
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The number of Ach receptors on the post-synaptic membrane in myasthenia gravis is ____
|
decreased
|
|
Decreased number of Ach receptors in myasthenia gravis correlates with what electrodiagnostic finding?
|
MEPP amplitude in myasthenia gravis is about 1/5 of normal
|
|
Frequency of MEPPs is a function of what part of the synapse?
|
Pre-synaptic
|
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Frequency of MEPPs in myasthenia gravis is ____
|
normal
|
|
Presynaptic Ach content and synaptic vesicles in myasthenia gravis are _____
|
normal
|
|
What effects do anticholinesterases (cholinesterase inhibitors) have on EPPs?
|
- increased amplitude
- increased duration - increased chance that EPP with reach threshold to cause an action potential |
|
70% of cases of Lambert-Eaton Myasthenic syndrome are associated with _____
|
oat cell carcinoma of the lung
|
|
Typical muscle presentation of Lambert-Eaton Myasthenic syndrome
|
weakness/fatigability of proximal limb muscles with relative sparing of extraoccular and bulbar muscles
|
|
Reflexes in Lambert-Eaton Myasthenic syndrome
|
hyporeflexic
|
|
Lambert-Eaton Myasthenic syndrome is associated with what mucosal symptom?
|
dry mouth
|
|
On electron microscopy, what is disrupted in Lambert-Eaton Myasthenic syndrome?
|
The active zone is disrupted with decreased number of vesicles
|
|
MEPP amplitude in Lambert-Eaton Myasthenic syndrome is
|
normal
|
|
Main problems in Lambert-Eaton Myasthenic syndrome
|
Presynaptic; fewer Ach quanta are released
|
|
EPPs in Lambert-Eaton Myasthenic syndrome are
|
small
|
|
MEPP frequency in Lambert-Eaton Myasthenic syndrome is
|
normal
|
|
In Lambert-Eaton Myasthenic syndrome the decrease in EPP size is proportional to
|
decreased number of active zone particles
|
|
General definifion of congenital myasthenia
|
Collection of syndromes; muscle weakness and fatigue from birth, family history, no autoimmune myasthenia gravis in the mother and no Ach receptor antibodies in the child
|
|
In general, immunotherapy in congeital myasthenia is
|
not effective
|
|
Responses to anticholinesteraes in congenital myasthenia is
|
variable
|
|
Familial infantile myasthenia usually presents with
|
severe respiratory and feeding problems
|
|
Proposed pathology for congential myasthenias
|
- deficient presynaptic Ach storage
- deficient presynaptic Ach mobilization - deficient presynaptic Ach resynthesis - reduced number of Ach receptors - altered affinity of Ach ligands for receptors |
|
Botulism is ____ mediated
|
toxin
|
|
Organism causing botulism
|
Clostridium botulinum
|
|
Typical presentation of infant botulism
|
- fail to suck/feed
- constipation - weakness/hypotonia |
|
Typical presentation of botulism in adults
|
descending paralysis, starting with the eyes
|
|
Extent of autonomic cholingergic involvement with botulism is determined by
|
the type of toxin
|
|
The onset of paralysis in botulism is faster in...
|
- nerves with high rate of firing
- increased temperature |
|
Target of botulism toxin
|
irreversibly blocks Ach release; prevents vesicle fusion by some unknown mechanism
|
|
MEPP amplitude after botox A
|
normal; eventually decreased with huge doses
|
|
MEPP frequency after botox A
|
greatly reduced
|
|
Number of Ach quanta released after botox A is _____
|
greatly reduced
|
|
Ach synthesis in botulism is
|
normal
|
|
Postsynaptic Ach sensitivity in botulism is
|
normal
|
|
Recovery after botulism requires
|
- sprouting of new nerve terminals
- formation of new neuromuscular junctions |
|
General definition of single fiber EMG
|
monitors action potentials of single muscle fibers extracellularly
|
|
Basic requirements of single fiber EMG (what do you need)?
|
- time base with resolution to microseconds
- stable trigger - delay line - method to record and count potentials |
|
Duration of single fiber action potentials
|
1 millisecond
|
|
Peak-to-peak rise time of single fiber action potentials
|
100-200 microseconds
|
|
Amplitude of single fiber action potentials
|
1-5 microvolts
|
|
Muscle fiber density in neuromuscular disorders
|
usually normal
|
|
In normal muscle, pairs of potentials will be recorded about ____% of the time
|
30%
|
|
On normal EMG what does recording a pair of potentials indicate
|
That you are recording 2 muscle fibers innervated by the same motor axon
|
|
What is the general definition of jitter
|
The variability in the interpotential interval between discharges
|
|
Normal jitter is between
|
10-60 microseconds
|
|
How is jitter usually expressed?
|
as the mean consecutive difference (MCD)
|
|
What produces most normal jitter?
|
fluctuations in the time the EPPs take to reach threshold for action potentials
|
|
In general, when is jitter increased?
|
- when the safety factor of neuromuscular transmission is lessened
- size of EPPs decreased - rise time of EPPs decreased |
|
At low rates of firing, increased jitter is a nonspecific measure of
|
neuromuscular dysfunction
|
|
What is blocking (related to jitter)
|
When one of the paired potentials fails to appear with the other
|
|
What is the underlying mechanism for blocking (related to jitter)
|
The EPP for the potential that did not show up, failed to reach threshold and therefore did not cause an action potential
|
|
Blocking is the single fiber EMG manifestation of clinical _____ and _____
|
fatigue and weakness
|
|
What is the most sensitive EMG finding of impaired neuromuscular transmission
|
increased jitter (although it's nonspecific)
|
|
In normal people, how does age influence jitter
|
Normal people over the age of 50 have increased jitter and blocking
|
|
What is abnormal jitter in the extensor digitorum muscle of the forearm?
|
- more than 1 in 20 pairs has MCD above 55 microseconds OR
- mean MCD of the 20 pairs is greater than 35 microseconds |
|
Relation of jitter and firing rate in myasthenia gravis
|
increased jitter with increasing firing rate
|
|
Relation of jitter and firing rate in Lambert-Eaton myasthenic syndrome
|
decreased jitter with increasing firing rate
|
|
Relation of jitter and firing rate in botulism
|
decreased jitter with increasing firing rate
|
|
When is Ach supply depleted most prominantly during repetitive nerve stimulation in the normal nerve?
|
the first few stimuli when stimulated at 1-4 Hz (after that mobilization stores have replenish the supply)
|
|
What is the effect of calcium on repetitive stimuli less than 200milliseconds apart?
|
Calcium from previous impulse still around to help facilitate transmission
|
|
Why does facilitation through calcium of neurotransmission decreased at 50Hz and 200Hz?
|
50: impulses begin to overlap each other
200: exceeds refractory period of muscle and nerve |
|
Optimal stimulation rate for calcium facilitation in Lambert-Eaton myasthenic syndrome and botulism
|
40-50 Hz
|
|
Why is a drop in MUAP amplitude on routine EMG not a good indicator of NMJ disease?
|
Because the change is more likely to be from needle movement than blocking
|
|
Why can amplitude increase again after 5 or so repetitive stimuli during EMG study in myasthenia gravis at rest?
|
Presumably Ach mobilization has caught up with the depletion
|
|
Voluntary exercise typically creates a stimulation rate of ___ Hz
|
20-50 Hz
|
|
Tetanic external stimulus is delivered at ___Hz
|
50 Hz
|
|
What is postactivation potentiation in myasthenia gravis?
|
The size and areas of evoke response may be larger and the decrement less immediately after exercise secondary to calcium facilitation
|
|
What is psedofacilitation is comparison to postactivation potentiation?
|
Increased amplitude after exercise because of greater synchronization; area of the response remains the same.
|
|
What is post-activation exhaustion in myasthenia gravis?
|
A few minutes after exercise the size of the response is smaller and the decrement with repeat stimulation greater
|
|
Post-activation exhaustion in myasthenia gravis is attributed to
|
receptor desensitization
|
|
Often the only electrodiagnostic finding in mild myasthenia gravis may be
|
post activation exhaustion (measure every minute after exercise for 5 minutes)
|
|
Is repetitive nerve stimulation a sensitive test for myasthenia gravis?
|
No.
For example ~30% of patients with definitive MG may have normal repetitive nerve stimulation findings |
|
Is repetitive nerve stimulation a sensitive test for Lambert-Eaton myasthenic syndrome?
|
Yes
|
|
CMAP at rest in Lambert-Eaton myasthenic syndrome is usually ____% of normal
|
10%
|
|
2 electrodiagnostic hallmarks of Lambert-Eaton myasthenic syndrome
|
- postactivation potentiation
- low amplitude initial response |
|
What happens to the initial/early response in Lambert-Eaton myasthenic syndrome with slow stimulation?
|
Further Ach depletion occurs and there is a decremental response
|
|
If postactivation potentiation is greater than 200%, what 4 conditions should you think of?
|
- Lambert-Eaton myasthenic syndrome
- botulism - hypermagnesemia - hypocalcemia |
|
In Lambert-Eaton myasthenic syndrome, what muscle typically display the typical electrodiagnostic findings?
|
ALL limb muscles
|
|
Do decremental responses with slow rates of stimulation typically occur in botulism?
|
No
|
|
Electrodiagnostic findings typical of moderate botulism
|
- postactivation potentiation
- incremental responses to high rates of stimulation * indicate that neurotransmitter release can be increased with repeated stimulation |
|
Electrodiagnostic findings typical of severe botulism
|
- small initial response
- no post-activation potentiation - no incremental response |
|
In botulism, which muscles typically show electrodiagnostic abnormalities?
|
Variable
|
|
Why is repetitive nerve stimulation often a useful test in botulism?
|
Electrodiagnostic changes are usually evident several days before toxin can be identified in the lab
|
|
Regular EMG findings typical for infantile botulism
|
Within a few day, see short-duration low amplitude polyphasic motor units with spontaneous activity
|
|
What are the guidelines for holding medications prior to testing for NMJ disorders
|
hold anticholinesterase medications for 24 hours prior to test if it does not compromise the patient's swallow or respiratory status
|
|
Why does cooling improve transmission in NMJ disorders?
|
- acetylcholinesterase activity is less when colder
|
|
Does limb temperature matter in repetitive nerve stimulation?
|
Yes, NMJ transmission may appear falsely normal if the patient is cold
|
|
In myasthenia gravis, which muscles are more likely to show abnormalities on repetitive nerve stimulation: distal or proximal?
|
proximal (think of proximal muscles as being warmer)
|
|
What kind of stimulation do you use in repetitive nerve stimulation for NMJ disorders?
|
Supramaximal at 25% greater than the stimulus where no change in amplitude is observed
|
|
In general, what stimulus do you deliver during repetitive nerve stimulation?
|
At least 4 supramaximal stimuli at a rate of 2-3 Hz
|
|
In general, how long do you wait between trains of stimuli in repetitive nerve stimulation?
|
15 seconds
|
|
What % change for decrement in repetitive nerve stimulation is considered abnormal
|
5% likely
10% certainly |
|
List the levels and numbers for spinal roots
|
C 8
T 12 L 5 S 5 Cox 1 |
|
Where are the cell bodies of the nerves that form the ventral roots of the spinal nerve?
|
In the anterior and lateral gray columns
|
|
Where are the cell bodies of the dorsal roots of the spinal nerve?
|
In the dorsal root ganglia
|
|
Where does the dorsal root ganglia lie anatomically?
|
In the ostium of the bony intervertebral foramina
|
|
What do the posterior primary rami of the spinal nerves supply?
|
segmental paraspinal muscles and skin
|
|
What are the rules for where the cervical nerve roots exit compared to vertebral level?
|
C1-C7 exit superiorly, C8 exits below C7 vertebral body
|
|
What are the rules for where the thoracic and lumbar nerve roots exit compared to vertebral level?
|
exit at below the vertebral level of the same number
|
|
The sensory fibers composing the cauda equina are __-ganglionic
|
pre-ganglionic
|
|
Radiculopathy in patients under 40-50 years old is usually from
|
intervertebral disk protrusions or ruptures
|
|
Radiculopathy in patients over 50 years old is usually from
|
osseoligamentous hypertrophy
|
|
What are the most common motor vs. sensory presentations of radiculopathy
|
sensory > mixed > motor
|
|
How does conduction block in radiulopathy usually manifest clinically?
|
short-lived but profound weakness
|
|
What is the presumed mechanism of slowing in radiculopathy when deep tendon reflexes are lost but there is no weakness or sensory loss?
|
desynchronized or differential slowing
|
|
What is more characteristic of radiculopathy: subtotal or total root involvement?
|
subtotal root involvement
|
|
Single motor and sensory NCS in radiculopathy are usually _____
|
normal
|
|
When there is nerve damage proximal to the DRG, nerve degeneration proceeds in which direction?
|
proximally
|
|
Why are SNAPs normal in radiculopathies?
|
because the injury is proximal to the DRG
|
|
What is the only abnormality on NCS that may occur with radiculopathy
|
decreased amplitude of the CMAP if there is axon degeneration
|
|
Why are CMAPs on NCS usually normal in single level radiculopathy?
|
- incomplete nerve root involvement
- muscles innervated by more than one root |
|
Abnormal H-wave latency criteria that reflect S1 radiculopathy
|
1.0-1.8 ms side to side difference, or outside of normal predicted by nomogram
|
|
Abnormal H-wave amplitude criteria that reflect S1 radiculopathy
|
side-to-side reduction of amplitude of 50% or unable to elicit response
|
|
5 limitations of using H-waves in the diagnosis of radiculopathy
|
- only S1 used
- may be normal with radic - abnromal H-wave does not equal radic - once H-waves lost, often remain so - often unelictable bilaterally in polyneuropathy |
|
H-waves in normal people over the age of 60 are often
|
unelictable bilaterally
|
|
F-waves are generally ___% of the size of the direct muscle response
|
less than 5%
|
|
For F-waves, minimal latency is assumed to represent
|
conduction time along one of the largest diameter motor fibers in the stimulated nerve
|
|
Are SEPs helpful in the diagnosis of radiculopathy?
|
Usually not, relatively insensitive
|
|
In the evaluation of radiculopathy, the needle electrode examination (NEE) is primarily evaluating what?
|
motor root fibers for the occurance of axon loss
|
|
How many muscles are required in a "radiculopathy screen."
|
5-7 including paraspinals
|
|
Ideally, what are consititues a positive needle screen for radiculopathy?
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Findings in 2 or more muscles that receive innervation from the same root
- ideally via different peripheral nerves - neighboring myotomes normal |
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What is the deepest paraspinal muscle?
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The multifidus
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Which paraspinal muscle is the only one considered to have monosegmental innervation?
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The multifidus
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In general, paraspinal muscle sampling in radiculopathy screen should be done at and ___ the level of the lesion
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below
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Effect of age on spontaneous fibrillation potentials seen in paraspinals of normals
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increase with age, especially over 40
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% of normal people with fibrillation potentials in paraspinals
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15-50%, increases with age
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List conditions other than radiculopathy that may cause fibrillation potentials in the paraspinal muscles
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- motor neuron disease
- muscle trauma (LP, steroid injections, surgery) - tumors - toxic/inflammatory myopathies - diabetes |
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The inside of a muscle cell is relatively ______ in charge compared to the outside
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negative
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Why can you detect voltage in a depolarizing cell?
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No longer a perfect balance of +/- charges in the region of depolarization and thus can detect a voltage difference
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Key ions for detecting voltage change in EMG?
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Na+ and K+
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Voltage = ()x()
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Voltage = Current x Impedence
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In EMG what is the zero reference?
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the ground
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The magnitude and polarity of a recorded EMG potential depend on what 4 key factors?
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- charge density near the membrane
- distance from depolarization - properties of the medium - location of measurement |
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What is Fourier analysis?
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It's a frequency analysis that characterizes a waveform by its frequency components
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CMAPs are ____ duration
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long
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SNAPs are ____ duration
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short
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Give 3 examples for waveforms that have fast changing components (high frequency)
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- Fibrilations
- Polyphasic motor units - single fiber EMG |
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Give 4 examples for waveforms that have slow changing components (low frequency)
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- CMAPs
- SNAPs - the positive part of positive sharp waves - SEPs |
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Give 3 common general sources for electrical noise on EMG
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- radio
- 60 Hz - electrical equipment |
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The signal for EMG is typically amplified ______ times
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50-250,000
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What is the voltage requirement for a signal to be respresented reasonably in analog?
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1-10 volts
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Define gain
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electrical amplification of the signal
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Define sensitivity
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display resolution
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Why do we use a differential or instrumentation amplifier?
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to reject environmental noise
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Define common mode signal
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signal that appears with equal amplitude at both the recording and reference electrodes
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What is the common mode rejection ratio?
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for the amplifier: the gain of the physiologic potential/the gain of the noise signal
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What common mode rejection ratio do you want in an EMG amplifier?
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at least 90 dB
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What is the main function of filters in EMG?
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noise attenuation
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Why is the low frequency filter in single fiber EMG increased to 500 Hz?
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To filter out more distant motor units
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What does a filter setting really mean?
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The point where 1/2 of the energy is removed
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Do filters cause phase shift?
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yes
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Where is phase shift from filters the most pronounced?
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near the filter limit
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What are the typical filter settings for motor NCS?
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2-10,000 Hz
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What are the typical filter settings for sensory NCS?
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5-2,000 Hz
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What are the typical filter settings for EMG?
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10-10,000 Hz
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What are the typical filter settings for quantitative EMG?
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2-10,000 Hz
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What are the typical filter settings for SSEP?
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5-2,000 Hz
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Lowering the high frequency filter will have what effect on the CMAP?
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- decrease amplitude
- reduce polyphasia |
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Lowering the high frequency filter will have what effect on SNAP?
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- decrease amplitude
- prolong latency |
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Lowering the high frequency filter will have what effect on the triggering of the instrument to record a potential?
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- increase the magnitude of change needed to trigger the recording
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What is the effect of increasing the change needed to trigger an EMG recording?
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Increased onset latency
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Why is the filter range for SNAPs smaller than that for CMAPs?
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More important to reduce noise
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What percentage of SNAP amplitude is lost with typical standard filters?
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10-15%
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Soft tissue acts as what type of filter?
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high frequency
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Increasing the low frequency filter will have what effect on the CMAP?
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- decreased amplitude
- poor tracking of return to baseline so wave form gets distorted - shorter peak latency (returns to baseline sooner) |
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Lowering the high frequency filter will have what effect on the SNAP?
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same effects as on CMAP but less pronounced:
- amplitude loss - wave form distortion - shorter peak latency |
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Lowering the high frequency filter will have what effect on the MUAPs?
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- prolonged duration from trailing negative hump
- decreased amplitude - decreased duration |
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Do most waveforms have significant 60 Hz components?
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yes
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When digitizing a signal, how often should you sample?
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Twice the rate of your highest filter (so if filter is 10K then need to sample at least 20K).
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You need good electrodes for EMGs so that...
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they create stable polarization potentials on the skin that are reliable for analysis
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When the recording electrode is placed right over the motor point the waveform tends to have these characteristics:
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- clean take-off
- biphasic morphology - initially negative |
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SNAPs with the A&R electrodes less than 4cm apart will ____
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have decreased amplitude
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Why do SNAP A&R electrodes need to be at least 4cm apart?
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4cm is the length of nerve that is in a depolarized state assuming a 50m/s conduction velocity and 0.8ms depolarization duration.
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In needle EMG with a monopolar electrode, the impedence of the reference is usually ______ fold lower
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10 fold
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Why does needle EMG with a monopolar electrode have more 60 Hz interferrence?
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The 10 fold difference in impedence at the recording and reference electrodes makes common mode rejection difficult
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Skin reference for monopolar electrodes should be placed...
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over a local bony or tendon site; if lots of interference then place closer to the needle
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Typical tip area of a monopolar electrode
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0.14-0.2mm2
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Typical tip area of a concentric electrode
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0.2-0.9mm2
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The recording area of a concentric electrode is determined by
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- wire diameter
- angle of the bevel |
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What is the diameter of a typical muscle fiber?
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60 micrometers
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Compared to monopolar electrodes, concentric electrodes record _____ amplitudes.
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smaller (about 1/2 as large)
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Compared to monopolar electrodes, concentric electrodes record _____ phasicity
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less
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Compared to monopolar electrodes, concentric electrodes record _____ duration
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similar
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Why is the amplitude recorded by concentric electrodes smaller than monopolar?
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recording surface and proximity of reference to active
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Why is the phasicity recorded by monopolar electrodes more than concentric?
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larger recording distance = less synchrony
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The EMG machine analyzes signal by subtracting...
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active - reference
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The duration of a waveform depends most on what frequency components?
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slow
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Why do we use impedence in EMGs instead of resistence?
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Becuase the current fluctuates (use resistance with stable current like batteries).
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