final exam new info Flashcards
(116 cards)
1
Q
electrophotography (ECochG)
A
measurement of an evoked response arising from the cochlea and the 8th nerve
-typically occurring within 2-3 ms after stimulus onset
-wave 1 components of the ABR are viewed
2
Q
what are the three components that we observe in the ECochG
A
cochlear microphonic, summating potential and the compound action potential
3
Q
cochlear microphonic (CM)
A
this originates from the hair cells and is a stimulus dependent response meaning anytime there is displacement of the BM there will be a CM
4
Q
summating potential (SP)
A
viewed as a direct current shift in the baseline of the ECochG recording, usually in the same direction and just prior to the compound AP
5
Q
what makes recording the SP difficult?
A
with greater amounts of HL, the SP becomes harder to identify
6
Q
compound or whole nerve action potential (AP)
A
the potential that we are recording
-the ECochG is wave 1
7
Q
anatomical structures of the ECochG
A
CM: OHCs
SP: IHCs
AP: afferent fibers of CN 8
8
Q
what are the main applications of the ECochG
A
operative monitoring, cochlear hydrops, assessment of hearing, enhancement of wave 1, functional HL, third window disorders and diagnosing ANSD
9
Q
how can the ECochG help with operative monitoring
A
it can give information regarding the health of the 8th nerve
10
Q
relationship between cochlear hydrops and ECochG
A
common pattern is a large SP amplitude relative to AP amplitude
-this occurs due to the increase in endolymph
-however there is variability due to the nature of the disease
11
Q
how can the ECochG help look at cochlear synaptopathy
A
remember, this is the loss of nerve connections between sensory cells and the brain, so it tells us how the nerve is functioning
12
Q
even though the ECochG can help identify third window disorder, it typically is not used. what is the other common test used to help identify these disorders
A
VEMP
13
Q
how is ECochG altered by nonpathological subject factors
A
-latency is prolonged with reduced amplitude in younger children
-attention has no effect
-no drug affects however diazepam has been shown to impact some recordings
14
Q
ECochG type of stimulus
A
typically a click is preferred as it gives a good amplitude, but not good frequency information
-we can use a LF TB if they have a severely sloping corner audio
15
Q
how is the ECochG altered by acquisition factors
A
-epoch of around 10 ms, if too big we lose the fine details
-filters should be wide enough to encompass the frequencies of the signal
16
Q
two main limiting factors with ECochG
A
how much sensory loss the patient has AND how long ago was an active attack with menieres
17
Q
recording parameters of the ECochG
A
inserts, click stimulus, 0.1 ms duration, alternating, 8.1/sec, 95-100 dB nHL with no masking
18
Q
normative data of the ECochG
A
SP/AP ratio greater than 0.5 (50%) abnormal, AP condensation-rarefaction is 0.38
-remember that the high values are abnormal
19
Q
how does rate impact the ECochG recording
A
-lower rates give larger amplitudes
-higher rates give smaller amplitudes
20
Q
CPT coding and billing for ECochG
A
92584
21
Q
auditory steady state response (ASSR)
A
another type of evoked potential that uses a modulated tone, helpful with estimating hearing thresholds
-provides us with an electroacoustic audiogram
-purely assessing hearing
22
Q
how does the ASSR vary from the ABR
A
stimulus: ASSR is a continuous tone with variations, ABR is a transient stimuli
measurement: ASSR is time locked to a period of time, ABR is time locked to a stimulus
detection: ASSR is looking at phase and amplitude, ABR is looking at latency
23
Q
similarities of ASSR and the ABR
A
both are EPs, both recording bioelectric activity and both can be used to estimate thresholds for patients who cannot do behavioral measures
24
Q
differences of ABR and ASSR
A
ASSR can assess both ears at one, ASSR can assess hearing at higher stimulus levels (up to 100-120), ASSR is measured in nanovolts whereas ABR is measured in microvolts
25
neural generators of the ASSR
-at slower modulation rates we are assessing the auditory cortex
-at faster modulation rates we are assessing the brainstem
26
with adult norms and the ASSR, how do these results compare to behavioral results
-better correlation to behavioral thresholds in those that have HL (within 5-20 dB)
-poor correlation to behavioral thresholds in those that have normal hearing (within 10-25 dB)
27
clinical advantages of ASSR
-the usage of frequency specific signals with both AC and BC
-detection is automated and statistically based
28
clinical disadvantages of ASSR
-site of lesion is not possible as we cannot see the actual waveform
-absence of ASSR does not differentiate between profound HL or ANSD
-there is no current billing code for ASSR
29
auditory middle latency response (AMLR)
voltage oscillations occurring between 10 and 80 ms from stimulus onset
-middle latency response (MLR)
30
as we move further up the auditory pathway, these responses take longer. what's the main reason?
these responses become more complicated as there are multiple neural generators and they all have many nerve fibers
31
main differences between early AERS and the mids/late AERs
-alterations impact the amplitude more than latency in mids/lates
-latencies show high natural variability
-mids/lates require a slower recording rate
-mids/lates are more impacted by neuromaturation
-mids/lates are affected by patient state
-mids/lates have more LF content
32
exogenous vs. endogenous responses
exogenous: early and mids ; an obligatory response
endogenous: most lates ; arising from components that depend on cognitive processing
33
endogenous responses, therefore late responses, can help provide clues to the nature of ....
higher cognitive function
-how we know we are no longer looking just at the auditory cortex but also their association areas
34
all AMLR are ____________ responses of the auditory system
low frequency
35
waveform components of the AMLR
-Po (~10ms)
-Na (~18-20ms)
-Pa (~30ms)
-Nb (~40ms)
-Pb (~50ms)
36
AMLR follows the ______ and precedes the ______
ABR ; ALR
37
what is the largest wave of the AMLR
Pa
-the detection increases from birth to adolescence
38
AMLR can be recorded in children as young as 4 years of age when ...
-they are awake
-in certain sleep stages such as 1, rapid eye movement sleep or alpha stage
39
neural generators of AMLR
inferior colliculus, thalamus and auditory cortex
40
one of the biggest problems when recording the AMLR is the myogenic responses. what is the biggest muscle that can impact it?
postauricular muscle (PAM)
-this reflex is vestigial (not useful) response
41
when does the PAM become an issue within the AMLR? how does it appear?
-evoked at high intensity levels (greater than 70 dB HL) with active muscle contraction
-occurs at around 12 to 20 ms, same range as the Na response
-appears as a sharper spike
42
how to differentiate between the PAM and Pa
PAM: less than 20 ms, higher amplitude with a sharper peak
Pa: around 30 ms, shallower with not a sharp peak
43
what is important regarding the Pb (P50) waveform
it is considered the border between AMLR and ALR representing preattentive brain activity
44
sensory gating and the AMLR
the ability of the brain to attenuate irrelevant sensory stimuli to prevent sensory overload in order to respond to a novel stimulus or a change in an ongoing stimulus
-when two stimuli are presented that are identical, the Pb is reduced for the second stimulus as that elicits a diminished response whereas the first stimulus elicits an excitatory response
45
how will sensory gating be impacted if the second stimulus is different (novel) from the first
the P50 for the second stimulus will be larger in amplitude
-in order for this to occur they need to be separated by a short inter stimulus interval of around 500 ms
46
norms for S2/S1 ratio for sensory gating
less than 0.4 in adults implies intact sensory gating
47
in what type of patient population will we see abnormal sensory gating with
-does not occur in patients with schizophrenia
-increased S2/S1 may be seen with Alzheimer's disease, autism or TBIs
48
AMLR recording parameters
-electrode montage is the same as previous recordings, but both R and L sides need to be symmetrical
-filter settings should be bandpass from around 1 to 200 Hz
-rates need to be very slow (nothing greater than 10/second but is the best with 1/second)
-intensity not over 70 dB nHL
-single polarity
-epoch set to 100 ms
49
what type of electrodes will not pick up any asymmetry within the AMLR
vertex or midline
50
artifacts that impact the AMLR
-power line noise
-transducer related stimulus artifact
-eyeblinks and eye movements
-PAM reflex
51
spectral analysis confirms that most of the energy in the AMLR components is in the ____ to ____ Hz region
10 - 50
52
since there is natural variability within the AMLR recording, when would we say it is abnormal
-if absent
-if very small (reduced amplitude)
-if it is not repeatable
53
what are two approaches to measuring the amplitude for the AMLR
-peak to baseline
-peak to trough
54
how can the amplitude of wave 5 be used with the analysis of the AMLR
Pa components of the AMLR is twice the size of the wave 5 component
-so therefore the amplitude of Pa can be considered reduced if it is smaller than the amplitude of wave 5
55
what are two aspects that are more important than latency within the AMLR
amplitude and morphology
56
what are 3 advantages of the AMLR over the ABR
-amplitude is very large, allowing for the comparisons to the ABR
-AMLR is evoked by tone bursts with longer durations
-type of instrumentation is the same for the AMLR as the ABR
57
usage of ALMR with neurodiagnostic
interhemispheric amplitude differences reflect the side of the cortical lesion regardless of which ear is stimulated
-however, this was not noted when the lesion did not affect the temporal lobes
58
usage of AMLR with TBI's
-studies have shown that if patients have a good and present AMLR then a good percentage of them will have a good recovery
-additional studies have shown that the amplitude of Na and Pa have decreased with increased severity of TBI
59
usage of AMLR with (C)APD
have been helpful with evaluating these children as it removes the effects of memory and attention
-however there has been no indicated specific or reliable patterns for (C)APD
-that being said, some typical patterns have included decreased amplitude and increased latency of Na, Nb and Pa
60
usage of AMLR with central deafness
this will result in an abnormal AMLR as the lesion is within the temporal lobe and auditory cortex
61
usage of AMLR with dementia
the only waveform that has been shown to be affected is Pb which is either abnormal or absent
-however, with parkinson's disease this showed greater Pb abnormality than with alzheimer's
62
usage of AMLR with MS
despite the variability of the disorder, these patients do tend to show increased latencies of Pa and Pb or the absence of waveform components
-there has been an increase in sensitivity when using the AMLR with the ABR to identify
63
usage of AMLR with strokes
AMLRs are related to recovery of aphasia as the Nb peak latency recorded during the first few days of the stroke was related to improvement in language scores
64
clinical advantages of the AMLR
-recording is from the auditory cortex
-provides the ability to lateralize auditory cortical dysfunction
-response is present in young children
-feasible with tonal and other complex stimuli
-sensitive to reticular activating system
-suitable for assessing sensory gating
-assesses CI function
65
clinical limitations of the AMLR
-artifact issues
-subject and subject state issues
-variation in normal waveform morphology
-abnormal responses that vary with different recording conditions and not pathologies
-interpretation is limited by an incomplete understanding of AMLR neural generators
66
auditory late responses (ALR)
cortical responses that are evoked by the presentation of auditory stimuli and processed in or near the auditory cortex
-referred to as cortical auditory evoked potential's or cortical event related potentials
67
waveforms of the ALR
described by positive and negative peaks (nomenclature)
68
waveform components seen in the ALR
-P1 or P50 (40-50ms)
-N1 (90-150ms)
-P2 (180-200ms)
-N2 (200-275ms)
69
P1 or P50 of the ALR is believed to be the ....
Pb of the AMLR
70
in the ALR what is the largest component in young children? what is the largest component in older children and adults?
P1/P50 ; P2
71
within the ALR, what is believed to be the first endogenous potential
N2
-the first part of the nonspecific polysensory system
72
what do we know about neural generators of the ALR
the precise location is unknown however there is believed to be severe overlapping in areas of generation
-multiple areas from both primary and secondary auditory cortices
-posterior portion of the superior temporal plane
-lateral temporal lobe and adjacent parietal lobe regions
-frontal motor and/or premotor cortex
73
what does the neuromaturation look like within the ALR
with age, the monophasic P1 response slowly changes to a triphasic P1-N1-P2 waveform that is seen in adults
-P2 wave is adult like around 2 to 3 years
-N2 first appears around 3 years
-full maturity of the ALR is around 12 to 14 years of age
74
ALR recording parameters
-filter of 1 to 100 bandpass filter
-speech like stimuli or a tone burst
-very very slow rate (less than 1/s)
-best responses occur when the patient is awake and alert
75
why is a click a poor choice of stimuli for the ALR
the ALR is generated by slower neurons that reflect changes within timing, frequency and intensity of the stimulus
76
waveform analysis for ALR
N1 latency and the N1-P2 amplitude (comparing the latencies of these two waves)
77
abnormal ALR response
-reduction in amplitude
-polarity reversal for selected components
-total absence of one or more component
-prolonged latency
-absent N1-P2 component
78
how can the ALR help determine management options for older adults
as people grow older, the CNS starts to become slower with processing and loss of neurons
-so based on the results, it can indicate the importance of providing options that go beyond making the signal audible
79
usage of ALR with neuromaturation
P1 changes with age and it is a biomarker of the developing auditory system post exposure to sound
-studies have shown that children implanted younger showed a normal P1 response whereas children implanted later should abnormal P1 responses
80
usage of ALR with HAs/CIs
without auditory stimulation, P1 does not reach normal latencies and morphology of the waveforms is also affected
-when recorded after being aided, it shifted back into the norms for those ages
-when recorded after implantation, the P1 became visible and WNL
81
usage of ALR with auditory training
-children with auditory learning problems who completed auditory training exhibited plasticity of neural encoding of speech sounds at the cortical level
-latency of P1 response can serve as a biomarker for maturation of central auditory pathways post HA/CI usage
82
usage of ALR with ANSD
-children who have shown a normal or delayed P1 had some desynchrony
-children who had abnormal or absent P1 showed greater desynchrony
83
usage of ALR with schizophrenia
most studies have shown waveforms from patients with schizophrenia report a decrease in N1 amplitude with a very slight increase in latency
-additionally suppression or sensory gating does not occur
84
the P300 (P3)
a cognitive or discriminatory auditory evoked response that was first identified in the mid 1960s
-this is a non sensory specific response
-essentially an ALR component but with an extended time frame recorded under special conditions
85
waveform components of the P300
-N1 (90-150ms)
-P2 (180-200ms)
-N2 (200-275ms)
-P3 (250-400ms)
86
neural generators of the P300
these are complex and poorly understood with multiple overlapping sites
-primary auditory cortex
-frontal and temporal cortex
-temporoparietal association areas
-multisensory temporal cortical areas
-may also involve the hippocampus (where memory functions are stored)
87
what is the type of stimulus that we use for the P300
oddball paradigm
-contains a standard stimulus and then the rare/oddball stimulus
-requires attention therefore why we use it for the P3
88
two types of P3 that can be observed
P3a (passive) : in response to changes of the attend or inattentive stimuli
P3b (active) : response to effortful attention
89
in order to get a target response with the P3, when does this happen
when the listener is asked to count from the deviant sound and the non target deviant in unexpected
-the greater the difference between the standard and nonstandard stimuli the larger the amplitude will be
90
P300 recording parameters
-tone bursts
-epoch 500+
-very slow rate (less than 1.1)
-bandpass filter (0.5-100 Hz)
-oddball paradigm
-alternating polarity
-70 dB nHL or less for intensity
91
interpretating the P300
amplitude is around 10-20 microvolts
-described with latency and amplitude but amplitude is the more sensitive response we get
-remember there is great individual variability for the P300
92
what does a larger P300 amplitude indicate
greater inhibition
93
factors that affect the P300
age, drugs, disease conditions, attention
94
neuromaturation and the P300
-will see an adult P300 around 15 years
-recommended to not test before age 6
-decreases in latency and increases in amplitude are notes as they grow
-recorded less reliably with advancing age
95
drugs that can impact the P300
any drug that is a depressant can impact it or those with excitatory conditions
-diazepam can impact it
-anything producing central suppression of brain activity will influence and diminish the recordings
96
absence of the P3 when alertness is not questionable may be evidence of ....
higher level CANS dysfunction such as dementia
97
usage of the P300 with chronic alcoholism
studies have shown that the amplitude of the P300 are lower in alcoholics than non alcoholics
-including when they are not actively drinking
-more pronounced for visual tasks
-also has been reported for children of alcoholics so could be used as a possible predisposition
-low amplitude indicates less CNS inhibition
98
usage of the P300 with (C)APD
most studies have shown that they may be sensitive to the suspected (C)APD however further research is required to establish clinical criteria
99
usage of the P300 with Alzheimer's disease
have shown decrease in amplitude and latency for Alzheimer's but not seen with other dementias
-can identify mild to moderate AD but not severe (due to the inability to attend to the signal)
100
usage of the P300 with schizophrenia
has helped support the idea that it has a biologic basis by showing a typical decreased amplitude
-has also shown that when the symptoms improved, the amplitude went back to baseline
101
usage of the P300 with type 2 diabetes
studies have shown a decrease in amplitude
-concluded that attention and working memory may deteriorate with an increase in glucose levels
102
mismatch negativity (MMN)
a negative wave that is elicits when the standard stimuli response is subtracted from the deviant
-occurs within the 100 to 300 ms
103
neural generators of the MMN
appears to be located within the supratemporal plane near the auditory cortex
-may also have some aspects within the frontal lobe
104
how is the MMN best visualized
as a difference waveform
-meaning it is a subtraction of the response from the standard stimulus from the deviatn stimulus
105
clinical applications of the MMN
-looking at processing abilities of CI (meaning that when they begin to hear the sound it will show a response)
-study of central auditory function
-evaluation of patients who are comatose
-aging population
-patients with parkinsons
-patients with dementia
106
electroneuronography (ENOG)
a neurological noninvasive test used to study the facial nerve in cases of muscle weakness in one side of the face or with bell's palsy
107
what are some facial nerve disorders
bell's palsy, trauma, surgical injury, otitis media as it may invade the IE, mumps, tumors, stroke
-most will resolve on their own
108
clinical usage of the ENOG
determine the course of action for management or to indicate monitoring the statis of the patient
-based upon the finding, it indicates what the next step is
109
what is denervation
loss of nerve supply regardless of the cause
-those areas near the injury are damaged and the loss of function occurs as a result HOWEVER those areas further away from the damage remain functioning
110
what is wallerian degeneration
an active process of degeneration that results when a nerve fiber is cur or crushed and those distal parts degenerates
-begins 24-36 hours after injury
-complete degeneration takes around 72 hours
111
given what we know about degeneration, what is the recommended timeline for testing the facial nerve
typically will want to wait for around 3 days but no later than 21 days for the best prognosis
-wanting to wait around 3 days to ensure that complete degeneration has occurred
112
what are the two ways that we can classify facial nerve injury
-sunderland and seddon injury classification
-house brackmann facial nerve grading
113
how do the results of the ENOG help determine what clinical approach is done for the patient
-if there is at least 10% of function or more then the approach is generally more conservative and will monitor
-if there is less than 10% of function then they will be more aggressive with the management
114
importance of proper instructions for the ENOG
wanting to ensure that the patient knows it will not be painful
-using tapping
-using discomfort
-using movement
115
purpose of intraoperative monitoring
to reduce the risk of debilitating permanent neurologic deficits from surgery
116
modalities for ENOG
somatosensory (SSEP), transcranial motor (TcMEP), spinal nerve electromyogram (EMG), cranial nerve electromyogram (EMG), brainstem auditory evoked potentials, EEG, motor and sensory mapping
