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Clin Aud II Handout
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Card number_____ 1
card fld "Info"
Syllabus for Clinical
Audiology II — CD 5706
ABR (mostly)
and ENG
Instructor:
Martin 58
Robert de Jonge, Ph.D.,
Text:
•Handbook of Auditory Evoked Responses (1992), James W. Hall III
Supplemental Texts:
•Handbook of Balance Function Testing (1997), Gary P. Jacobson, Craig W. Newman, Jack M.
Kartush
•Contemporary Perspectives in Hearing Assessment (1999) edited by FE Musiek and WF
Rintelmann, Allyn and Bacon.
Exams/Assignments: There will be two exams, each will be multiple choice or short answer essay.
The final is not comprehensive. Also, you will keep a journal of your practical experiences in
performing the ENG battery and evoked potentials. The purpose of the journal is to demonstrate
what you have learned, to document the testing you have accomplished, and to demonstrate that you
can administer the procedures and interpret the results. Initial inspection of the journal will occur at
midterm. Completed journals will be due at final exam time.
Class Attendance: Attendance policy is consistent with University policy. In addition, four absences
are allowed for whatever reason (approved or not, at your discretion). Beyond this the final grade is
reduced by 1/4 of a letter grade for each additional absence. The final grade will be increased by 1/4
for each of the allowed absences that is not used. Perfect attendance improves performance by one
full letter grade.
Class goals: The general purpose of the class is to provide:
1. An overview of the anatomy and physiology of the balance system;
2. An introduction to the evaluation of the balance system through electronystagmography (ocular
motility, positional and positioning, and caloric testing);
3. An introduction to the electrophysiological evaluation of the auditory system: primarily the
auditory brainstem response (ABR), but also including electrocochleography (EcochG), auditory
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middle latency response (MLR), the auditory late response (ALR), P300 response, and mismatch (or
mismatched) negativity (MMN);
4. An understanding of the ENG and evoked potential test protocols, and an ability to perform and
interpret the tests.
Topics
ENG
•Anatomy and physiology of the vestibular system and ocular motor system. Read chapters 2 and 3
in Jacobson et al.
•Ocular motility testing. Read chapters 5 and 6 in Jacobson et al.
•Positional and positioning testing. Read chapter 7 in Jacobson et al.
•Caloric testing. Read chapters 8 and 9 in Jacobson et al.
Evoked Potentials
•An overview of EcochG, ABR, MLR, ALR, P300, and MMN. Read Hall's chapter 1, and the portion
of chapter 8 in Musiek and Rintelmann dealing with MMN.
•Test protocols and procedures: practical suggestions for patient preparation, equipment setup,
testing, and cleanup. Read Hall's chapter 8.
•Waveform analysis: peak picking. Read the "Introduction" and the section on "Conventional
Waveform Analysis," Hall's chapter 6, pages 221-242.
•Peripheral auditory assessment: the effect of degree and configuration of hearing loss on AERs.
Read Hall's chapter 11.
•Neurodiagnosis of eighth nerve, cerebellopontine angle, and extraaxial pathology. Read Hall's
chapter 12.
card fld "Other Readings…"
•ENG Workbook (1983) by Charles W. Stockwell, University Park Press.
This is an excellent resource for someone new to performing and interpreting the ENG battery. Each
of the tests (eg, saccade, gaze, tracking, etc.) is presented in the order normally performed. Examples
are given of normal findings and typical abnormal results. Questions are posed to test your
understanding, and answers are given.
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•Laboratory Exercises in Auditory Evoked Potentials (1997) by John A. Ferraro, Singular Publishing
Group.
This is also an excellent resource for someone new to evoked potential testing. The manual contains
descriptions for each of the protocols, examples of results that are commonly obtained, and practical
suggestions for collecting data and modifying procedures — for example, collect ABRs at different
stimulation rates (21.3/sec, 33.3/sec, and 66.3/sec) and observe the effect on waveform morphology.
•Contemporary Perspectives in Hearing Assessment (1999) edited by FE Musiek and WF
Rintelmann, Allyn and Bacon.
This is a comprehensive textbook for graduate audiology similar to the Handbook of Clinical
Audiology edited by Katz. For a more concise introduction (as compared to Hall's text) to evoked
potentials, see chapters 7 and 8: "Short-latency auditory evoked potentials: Electrocochleography and
auditory brainstem response" by JD Durrant and JA Ferraro, and "Auditory middle and late
potentials" by FE Musiek and WW Lee. Musiek and Lee also discuss the MMN, which is absent from
Hall's text.
•Make use of the equipment manuals that accompany the evoked potential/ENG systems.
card fld "Introduction…"
I want you to be confident in using our equipment for performing the ENG battery and acquiring
ERPs (event related potentials), especially the ABR but also some experience with EcochG, the middle
latency, and late responses.
Some of your lab time, at the beginning, can be during class time, but most will have to be outside of
class.
Use a journaling system to document what you have done and your understanding of the
procedures. Your grade for the journal will depend on the amount of testing you do, the
completeness of your descriptions, and how well your material is presented (i.e., readability,
organization, and ease of understanding).
•A general introduction to the balance system and enough of a description of the ENG battery to get
you started using the equipment.
•An overview of the ENG software and hardware. Each of you can gain experience in using the ENG
software/hardware to perform the test, and each of you can serve as test subjects. Initially, it's very
helpful to gain experience in a "friendly," more leisurely environment, with cooperative subjects
having normal balance systems.
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•An overview of the early (ABR and EcochG), middle (MLR), and late potentials (ALR, P300, and
MMN) with an emphasis on ABR. Again, my goal is to provide enough of a perspective to provide a
context for getting started using our equipment.
•An introduction to using the clinic equipment (Biologic Traveler LT and Intelligent Hearing
Systems) and running the hardware/software. As with ENG, I want you to have ample time to
become comfortable with using the equipment.
•After we've become more familiar with the equipment, and have started testing, we can explore the
details of each of the ENG tests.
•After we've started measuring evoked potentials, we can begin a more in-depth coverage of issues
relating to the ABR:
- Effects of nonpathologic subject factors on the ABR (i.e., age, gender, temperature, drugs and
medications, etc.).
- The effects of stimulus and acquisition factors on the ABR (i.e., polarity, repetition rate,
presentation level, click vs. tone burst, filtering, electrode location, etc.).
- Threshold evaluation in the difficult to test, especially the pediatric population, and related issues
like chloral hydrate sedation.
- Neonatal hearing screening protocols.
- Evaluating, testing for retrocochlear pathology.
- Understanding the effects of peripheral hearing loss (conductive, cochlear, audiometric
configuration) on ABR morphology.
Miscellaneous
•Breaking up into groups. For access to the different "stations" (IHS, Biologic Traveler LT, and
Micromedical M1500B) it will probably be beneficial to break up into smaller working groups.
•Midwest Ear Institute (north of St. Lukes's hospital) does platform posturography, and we might be
able to visit and observe testing.
cd fld "Practicals…"
The practicals will graded with the same weight as an exam (100 points total):
•30 points total, 15 each, two ENG evaluations. Describe results and your interpretation.
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•20 points total, 10 each, two ABR evaluations using alternating clicks at a standard rate, for each ear.
•10 points. ABR results for the right and left ear of a subject show the effect of stimulus polarity.
•10 points. ABR results for one ear showing the latency-intensity function (LIF) for Wave V at 10 dB
intervals, beginning at 90 dB nHL.
•10 points. Demonstrate the effects of click rate (on the 80 dB nHL) ABR, from approximately 10/sec
to 90/sec at 10/sec intervals. Comment on the effect of click rate on Wave V latency.
•10 points. Determine the ABR for tone pips at 500, 1000, 2000 and 4000 Hz. Use a 80 dB nHL.
•10 points. Develop a LIF for bone conduction clicks using a normal click rate.
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card fld "Overview"
An overview of the human balance
system
•In general, the balance system has
evolved to give people the ability to
control their
- posture, and
- motion
in relation to their surroundings.
•This control is possible because of a very sophisticated central system, the
- brainstem, which serves as a multisensory integration and coordination center, and
- the cerebellum, a programming and regulation center for coordinated motor output
•Typically, the balance system functions automatically at a subconscious level. Under unusual
circumstances (alerting or arousal mediated by the reticular formation of the brainstem) it becomes
conscious. The cerebral cortex becomes involved (dizziness or nausea are the perceptions), usually as
a consequence of sensory conflict.
The three components of the balance system…
1. Vestibular system. The nonauditory portion of the inner ear, the 3 semicircular canals (angular
acceleration of the head) and the utricular and saccular maculae (linear acceleration in the horizontal
and vertical planes, including gravity).
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- The VOR (vestibulo-ocular reflex). Output from the vestibular nuclei controls the eye muscles,
allowing the image on the retina to remain centered on the fovea.
- The VSR (vestibulo-spinal reflex) maintains muscle tonus for adequate posture, control of muscle
groups for maintaining the center of gravity over the base.
2. The optic system provides visual information about the body in relation to the environment, allows
the eyes to track moving objects.
3. Proprioceptive system. Superficial and deep sensations for special receptors in the skin, muscles,
tendons, and joints record changes in pressure, tension, gravity, and inertia. These changes activate
muscle groups to maintain stability. Ankle torque (the angle the lower leg makes with the foot) is an
important input.
•Together, these three systems form a very complex (and redundant) monitoring and feedback
system. Theoretically, near normal balance can be maintained with only the proprioceptive system
and one other system.
- Adequate balance can be maintained with no vestibular output. However, difficulty can occur in
certain environments; i.e., low light or uneven surfaces. Individuals with bilateral vestibular deficit
do experience significant difficulty, even when fully compensated (eg, dizziness during head
movements, especially when walking; oscillopsia).
•Disease can produce balance symptoms by creating abnormal sensory input (usually this is paretic,
as in the case of vestibular nerve tumor). The central vestibular control centers can adjust (recalibrate) this abnormal input to return the system to a state of normalcy. The disease will be
compensated, the patient symptomless.
- Compensation is much more difficult if the lesion is not stable.
- Experiments with "prism goggles" and "reversed worlds" demonstrate the dramatic ability of the
CNS to compensate.
- Vestibular rehabilitation exercises (often performed by PTs) promote compensation by inducing
movements that provoke the symptoms of dizziness.
- Medications (like meclizine or Antivert, Valium) that suppress dizziness (by suppressing the CNS)
interfere with compensation.
•Disease can also generate balance symptoms by interfering with the CNS centers that integrate
sensory input.
- These lesions are not as amenable to compensation.
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card fld "Symptoms"
Symptoms of balance disorders
•Depending upon which systems are affected, symptoms of balance disorders can result from either:
1. Abnormal sensory input or integration of input, or
2. Insufficient, inadequate, or uncoordinated motor output.
And, the symptoms may be different depending upon which system is affected.
1. Inadequate integration or abnormal input of sensory information may be associated with vertigo,
dizziness, or clouding of consciousness:
•Vertigo is a subjective experience of a disturbance of the individual in relation to his surroundings, a
hallucination of motion. Usually this is caused by peripheral disorders (end organ or vestibular
nerve): labyrinthitis, Ménière's disease, ototoxicity, trauma, neuritis, acoustic neuroma, etc.
- Subjective vertigo: patient is moving relative to his or her surroundings.
- Objective vertigo: the external world appears to be moving.
- The sensation of vertigo can be rotary, falling, being pushed forward (pulsion), or other sensations
of inadequate orientation.
•Dizziness may also be referred to as wooziness, giddiness, being light-headed. It is different from
vertigo, but patient's "expressive power of language" is often poor in this area. Some use dizziness
and vertigo as synonyms.
- Orthostatic hypotension is a common cause of dizziness, caused by lack of cerebral blood flow.
•Clouding of consciousness is a changing sensorium, vague sense of world taking on unreal aspects;
like the aura associated with Ménière's disease or migraine.
Dizziness or clouding of consciousness may be related to a myriad of conditions: tumors, vascular
disorders (hypertension, hypotension, atherosclerosis, cardiovascular disease, anemia), infections
(encephalitis, febrile disease), psychosomatic disorders, endocrine disorders, metabolic disorders
(like diabetes), drug intoxication, etc.
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All these symptoms may be related to effects on the visual (e.g., train pulling out of station),
vestibular, or proprioceptive (multiple sclerosis) systems — or a combination, like motion sickness
evoked by reading in a car. The sensory conflict (vestibular and proprioceptive systems tell your CNS
you are in motion, the visual system says you're stationary) evokes the sensation.
2. Inadequate motor output usually does not result in these symptoms (especially vertigo) but results
in poor muscle control, difficulty sitting, standing, walking, or ataxia, a general incoordination:
An inability to coordinate muscle activity during
voluntary movement, so that smooth movements
occur. Most often due to disorders of the
cerebellum or the posterior columns of the
spinal cord; may involve the limbs, head, or
trunk
•All of the symptoms involving abnormal sensory input (or integration) are very subjective (usually
not even conscious) so they are very difficult to document, measure, or quantify.
- One objective aspect of the experience is amenable to quantification, the eye movement associated
with nystagmus.
card fld "Nystagmus"
Nystagmus
•Nystagmus is usually thought of as involuntary, repetitive, saccadic (jerky) movements of the eyes.
Both eyes move slowly in one direction, then rapidly snap back to midline.
- Nystagmus has a slow phase and a fast phase. The direction of the beating is referenced by the
direction of the fast phase.
- If you were to spin to your right (at say, 30°/sec), your eyes would move to your left (at 30°/sec,
the speed of the slow phase) until the deviation was too extreme. Then your eyes would rapidly
move back to midline.
- Nystagmus refers to so many different phenomena that it can be hard to make a precise definition.
- Nystagmus can be voluntary; some people can consciously mimic involuntary nystagmus.
Nystagmus can also be undulating or pendular and not contain the typical fast component.
Different schemes for categorizing nystagmus. There are many, depending upon what is to be
emphasized:
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1. Physiological or pathological nystagmus.
- Very tiny nystagmoid movements are physiological (normal, that is). They prevent retinal
adaptation by constantly sweeping the image over the fovea.
- Pathological nystagmus is abnormally intense eye movements brought about by organic lesions, or
other changes (like drug-induced nystagmus).
2. Nystagmus categorized by the system involved in producing it: vestibular nystagmus or ocular
nystagmus (e.g., optokinetic nystagmus).
3. The direction of the nystagmus (referenced by the fast phase): right beating or left beating,
upbeating or downbeating. Or the plane of the nystagmus: horizontal, vertical, or rotary (Note:
vertical or rotary nystagmus measued during the diagnostic evaluation is usually a CNS symptom).
4. When it becomes apparent: congenital or acquired nystagmus.
5. The pathology associated with the nystagmus, like amblyopic nystagmus that is found in people
with very poor vision (not due to CNS defect or refractive error).
6. Whether it is induced or spontaneous; induced nystagmus may be categorized by the manner in
which it's induced: caloric nystagmus, gaze nystagmus, end-point nystagmus, OKN (also called OPK,
optokinetic) nystagmus.
7. Central versus peripheral nystagmus; where the lesion is located causing the nystagmus.
•Nystagmus can result from lesions in either of the three systems, can change forms, be normal or
pathological, peripheral or central, can occur in many planes/directions, can be spontaneous or
induced, strong or weak.
- These differences can be useful as diagnostic tools, site-of-lesion tools.
Clinical techniques for measuring nystagmus
•Direct observation has some advantages: it's easy to perform, no equipment costs. Disadvantages
are that it cannot be quantified, it's insensitive to small changes (so a strong stimulus must be used).
- A major disadvantage is that it permits ocular fixation which causes the nystagmus to be
suppressed.
- Direct observation can be performed with Frenzel's glasses, 15+ diopter lenses which fit into
internally illuminated goggles. This suppresses fixation (but not completely), the eyes are magnified
allowing smaller movements to be detected, but there's no quantitative data.
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•Photoelectronystagmography (PENG). Infrared cameras coupled to computer software can track
eye movements. Monitors allow the eyes to be prominently displayed, videorecording can create a
permanent record of actual movements. Rotary nystagmus is easier to observe. No inconvenience
associated with skin preparation and electrode placement.
- PENG records very small eye movements (0.1° versus 1° with ENG); it's the most sensitive method
(of the commonly used clinical techniques). Subjects eyes must remain open.
- Range is limited to about 20°
•Electro-oculography (ENG) uses electrodes placed around the eyes, relies on the corneo-retinal
potential (≈ 50 - 100 µV). It's cheap, non-invasive, most commonly used method.
- Measures eye deviations of up to 40°
Card number_____ 3
card fld "Note"
For horizontal nystagmus, the
convention is that upward deflections
of the pen signify movement of the eye
to the right, downward deflections
movement of the eye to the left.
For vertical nystagmus, upward
deflection of the pen indicates
movement of the eye upward, downward pen deflections movement of the eye down.
card fld "Recording Nystagmus"
Procedures for Recording Nystagmus
•The corneo-retinal potential is the basis for recording nystagmus.
- It's a bioelectric potential (a dipole) existing between the cornea (+) and the retina (-), exists as a
consequence of metabolic activity, and is small (≈ 50 µV, or so).
- The CRP varies between individuals, fluctuates daily, is influenced by emotion, massage of the
eyelids, acapnea (decreased CO2), anoxia, retinal ischemia, drugs, and light and darkness (potential
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increases with illumination, to a point). Variations can produce changes in CRP of up to 400 µV,
greatly affecting calibration.
•Recording electrodes are basically devices for picking up the CRP. The strength of the signal
increases as the cornea moves closer to the electrode.
- Electrode size, form, and material composition can vary (EEG, ECG, or AEP electroded). ENG
elecrodes are usually silver-silver chloride pellets embedded in a plastic material separated form the
skin by a perforated grid. Contact is made with the skin via electrolyte paste (a semifluid gel). They
are held in place with an adhesive collar. They can stay in place for hours.
•Electrode sensitivity is important since the CRP is so small. It's affected by:
- Light adaptation. The CRP diminishes in the dark, increases with illumination, but also adapts
(diminishes) with bright light. So a dimly lit room is preferable.
- Electrode impedance, which should be low (electrode - skin impedance of 5 kΩ or less). Skin
impedance can be decreased by cleaning skin of make-up, removing oils, gentle abrasion (exfoliation)
with an abrasive pumice-like scrub, alcohol, or even gentle scraping with a needle (caution: infection
control).
- Electrode size. Larger electrodes pick up more signal from a greater skin surface (better
sensitivity), but too large electrodes interfere with eye movements. Sizes are 0.3 to 1.5 cm, 0.5 cm
being typical.
•Amplitude calibration of the recorder needs to be performed on each patient, and generally
between each test (because of variability in CRP, skin impedance, etc.). The goal is to determine how
eye movement corresponds to pen deflection (or the computerized equivalent of pen deflection).
- Amplitude. Since the eyes rotate about an axis, amplitude is measured in degree of eye deflection,
in the horizontal and vertical plane, using calibration lights on a light bar.
- The convention is for recorder gain to be adjusted so that 10° of eye movement corresponds to 1.0
cm of pen deflection.
- The convention is for recorder polarity to be adjusted so that upward pen deflections correspond to
movements of the eye either upward (in vertical channel) or rightward (in the horizontal channel).
- Eye blinks show up as spikes in the vertical channel (Bell's phenomenon: eyes rotate upward and
converge, inhibit nystagmus). Rotary nystagmus shows up as simultaneous nystagmus in the
horizontal and vertical channels.
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- Spacing (distance of light bar from nasion) of the light bar is important to avoid ocular
convergence. Since the distance the spot of light moves on the light bar is fixed, the calibration angle
changes with spacing. We use a 1.0 meter spacing (you can use the meter stick).
- Sensitivity of the recording is limited by "noise" (muscle potentials, EEG activity): usually 1- 2° of
eye deflection can be measured.
•Recorder characteristics. Recorders should be sensitive (25 to 500 µV/cm of pen deflection), have a
high input impedance (so they don't load the system they're measuring), have a high common mode
rejection ratio (> 80 dB, to eliminate the same signal present at the two electrodes, like the 60 Hz line
voltage).
- Paper speed is usually set to 10 mm/sec. Nystagmus occurs at 1 to 3 beats/sec.
- Frequency response should be about 0.05 Hz to 15 Hz. An f2 = 15 Hz reduces high frequency
contamination from EEG and muscle potentials, and an f1 = 0.05 Hz limits baseline drift.
- AC or DC coupling? DC coupled means f1 = 0 Hz. For example, if the system is DC coupled, when
the eyes move 15° to the right, the pen will deflect 15 mm and remain deflected. If the system is AC
coupled, the pen will deflect 15 mm, then slowly return to baseline.
- The time constant (T) is the time it takes to decay to 1/3 of its original value
T = 1/(2*pi*f1) ≈ 3 sec for 0.05 Hz
•Intensity or "strength" of the nystagmus. There are many aspects of the nystagmus that could be
measured: amplitude, number of beats, frequency of beats, speed of the fast phase, speed of the slow
phase, duration of the nystagmus.
- Generally, speed of the slow phase, slow phase velocity, is thought to best represent the "intensity"
of the response.
•Caloric Irrigation apparatus, basic equipment considerations.
- Caloric irrigation is used to stimulate the peripheral vestibular system (mostly the horizontal
semicircular canal). Water or air can be used. Water can be used in either an open or closed loop
system (the water circulates through a small balloon, or bladder). We use an open loop system. It's
cheaper, but more messy and the plumbing can clog, but it can provide a very effective, stable
stimulus.
- The temperature and the amount of water determines the intensity of the stimulus. A warm and
cool stimulus is used: 250 ml of 44°C (111.2°F) — or 30°C (86°F) — water is delivered to the superior,
posterior portion of the eardrum for 40 sec. This is ± 7°C relative to normal body temperature of 37°C.
The flow rate is 6.25 ml/sec.
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- The most common protocol is the alternate binaural bithermal caloric test. Warm and cool
irrigations are performed on each ear, with a brief rest period.
- The warm and cool water are maintained in separate tanks, large enough to perform many
irrigations (2 - 3 gallons), including flushng the system prior to the irrigation (to ensure water is at the
correct temperature). The water is pumped to the ear through flexible, insulated tubing about 6 feet
long. A footswitch is useful to initiate the irrigation.
- Calibration should be performed to check the temperature (at the tip, not in the reservoir), amount
(graduated cylinder), and duration of water (simple watch).
Card number_____ 4
card fld "Note"
The patient distance from the light bar
(R) is critical for proper calibration. For a
1.0 meter distance, the lights should be
separated by 10.55" for a 15° angle.
0.268 = tan(15°)
For R = 1.0 meter,
X = 0.268*39.37 = 10.55"
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card fld "Note"
Some points:
•The ENG evaluation is basically a
compilation of various site-of-lesion
tests. The major purpose of the
evaluation is to find objective evidence related to the patient's symptoms, and to determine site-oflesion.
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- At the end of the evaluation, the major goal is to determine if the pathology is peripheral (and
whether the lesion is right or left side) or central (sometimes a right-left distinction can be made).
- A peripheral lesion is defined as either end-organ or VIII nerve.
The ENG evaluation has some limitations:
•Localization is less refined than audiometry where end-organ pathology can be distinguished from
VIII nerve pathology.
•Several ENG abnormalities (specific test results) can be caused by either peripheral or central
lesions, they are termed "non-specific."
•Nystagmus, the event measured, is but one of a myriad of symptoms. Pathology can sometimes be
present, but not involve this symptom. For central findings, there may be ≈ 25% false negative rate.
•Even in cases of end-organ vestibular pathology, if the lateral semicircular canal is spared, results
can be normal.
•As with any site-of-lesion procedure, false positives and negatives occur (Calorics are about 85%
sensitive to acoustic neuromas, but the false alarm rate is about 33%). So, to minimize this problem,
no single component of the battery is usually taken out of context.
•When thinking about each of the tests, try to remember the procedures used (the protocol) and then
try to describe the findings as either normal, peripheral, central, or non-specific.
Card number_____ 12
card fld "Spontaneous Nystagmus"
Spontaneous Nystagmus
•Spontaneous nystagmus (no stimulus
is needed to elicit it) if present is
recorded with eyes both closed and
open when gaze is directed forward
(0°).
- Nystagmus, if present, is recorded (for about 30 sec, eyes open; 30 sec eyes closed) with the patient
either sitting (usually) or supine (gaze nystagmus could be confused with positional nystagmus) with
the eyes in the midline.
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- With eyes closed, an alerting task may be needed to keep the subject alert and to keep him or her
from being able to suppress nystagmus.
•Normal findings. No nystagmus is measured, except for these exceptions:
- Voluntary nystagmus.
- Bell's phenomenon, vertical deviation of the eyes upon closure. Instead of using eyes closed, a
completely darkened room (difficult to implement) can be used to avoid Bell's phenomenon.
- Low amplitude square wave jerks are not uncommon in normals.
•Peripheral findings. A peripheral finding may (but not necessarily) be indicated by the presence of
ocular or vestibular nystagmus.
- Ocular nystagmus is usually easy to determine by the case history. 95% of ocular nystagmus is
congenital; 4% results from blindness or post-blindness (eyesight restored as in cataract operation);
1% are rare types such as occupational or miner's nystagmus from working in low light conditions
that chronically abuse eyes.
- Vestibular nystagmus can be due to peripheral or central pathology involving the vestibular
system, so the presence of vestibular nystagmus is a non-specific finding. To be vestibular
nystagmus, the nystagmus must:
1. have a well defined slow and fast phase;
2. be primarily horizontal;
3. be suppressed by visual fixation.
- A fixation index (is usually computed during the calorics) can be computed as the ratio of eye
velocity with eyes open to eyes closed (Normal findings are about 50%:
FI = 100* (Eyes Open / Eyes Closed)
- If the vestibular nystagmus is < 7.5°/sec it is of questionable pathological significance. If it's greater
than 7.5°/sec it is a non-specific finding.
- Spontaneous nystagmus usually beats away from the side affected; i.e., toward the right side with
a paretic left semicircular canal.
- Vigorous head shaking ("no," for 10 sec) may bring out a latent, compensated peripheral vestibular
nystagmus.
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•Central findings: A diagnosis of central pathology is made by elimination: noting that a nystagmus
is present but rule out normal, ocular, or vestibular nystagmus. Two major signs of central
spontaneous nystagmus are:
- Vertical (or horizontal) nystagmus that is not suppressed by visual fixation;
- A nystagmus that changes directions depending upon whether the eyes are open or closed.
card fld "Gaze Nystagmus"
Gaze Nystagmus
•Gaze nystagmus is measured with the eyes open. Some try to measure it with eyes closed, but it's
hard for the subject to maintain proper gaze angle. Gaze nystagmus is defined as nystagmus that is
not present when the eyes are in the midline, but is present when the eyes are rotated 20° or 30°
(usually 30°), right or left, in the horizontal or vertical plane, and held there for 10 sec.
- The nystagmus can be either horizontal or vertical.
Procedure
•The patient is instructed to keep head still and gaze steadily at the ± 30° spot on the light bar,
horizontally then vertically.
Results
•Normal findings. Normals show no gaze nystagmus, but at extreme eye deviations (40° or more,
rarely 30°) 40% to 50% of normals will show "end-point nystagmus," which is not to be regarded as
gaze nystagmus.
•Peripheral findings. Gaze nystagmus is not a characteristic of peripheral lesions, but:
- A unilateral gaze nystagmus (present when eyes are deviated in just one direction, right or left)
may be due to an intense (peripheral) vestibular type spontaneous nystagmus, provided that when
the patient closes his eyes (and they return to midline) a spontaneous (> 8°/sec) nystagmus occurs
that beats in the same direction as the gaze nystagmus. Alexander's law states that nystagmus is
enhanced when gaze is directed toward the direction of the fast phase of the spontaneous nystagmus
(also called a first-degree nystagmus). A second-degree nystagmus exists if this nystagmus also is
present on central gaze. A third-degree nystagmus is nystagmus present in all gaze positions.
•Central findings. Gaze nystagmus is usually a central sign, providing peripheral ocular and
oculomotor pathology can be ruled out. Central disorders, especially those involving the cerebellum,
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interfere with the pattern of neural firing required to maintain the eye deviated (the LED spot on the
fovea) against the elastic restoring force of the eye muscles. Different varieties of central gaze
nystagmus include:
- Vertical ( present when eyes are deviated up or down, not necessarily beating vertically)
nystagmus indicates brainstem pathology. If it's present without horizontal gaze nystagmus it
suggests an upper pons or midbrain lesion that is bilateral or on the midline.
- Unilateral gaze nystagmus is a central finding (rule out vestibular nystagmus), and is usually a
brainstem lesion.
- Bilateral and equal gaze nystagmus is central (but, rule out drugs like barbiturates).
- Bilateral unequal gaze nystagmus strongly indicates a central (usually brainstem) lesion, since
drugs produce bilateral equal gaze nystagmus.
- Rebound nystagmus is also related to brainstem or cerebellar disease. Although there is initially no
spontaneous nystagmus, after the eyes return to midline a nystagmus (at least 3 beats) appears which
eventually dissipates. Normals exhibit rebound nystagmus for larger eccentricities (45°) held for
prolonged periods (30 sec).
- Bruhn's nystagmus is associated with cerebellar lesions. No nystagmus is present on center gaze,
but nystagmus is present on right and left gaze, but asymmetrical (greater in magnitude on one side).
card fld "Saccade"
Ocular dysmetria test (aka Calibration or Fixed Saccade test)
•Ocular dysmetria is the inability to direct eye movement smoothly, rapidly, and accurately to a
target (like a spot of light suddenly appearing at a particular azimuth). If eye movements are
abnormal, they may be:
- Saccadic, the movement is not smooth, but jerky (multiple-step saccades);
- Exhibit "refixation": the eyes move past the target, correct the error, then come back (over-shoot, or
hypermetric saccades) or they stop short and then incrementally move to the target (under-shoot, or
hypometric saccades). These patterns can be either unilateral or bilateral.
- Ocular flutter: several overshoots to the target, each overshoot is followed by a saccade in the
opposite direction which put the eye approximately on target.
- Glissades: The eyes slow down appreciably before reaching the target.
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- One eye may move briskly to the target while the trailing eye moves sluggishly. This can happen in
one direction brought about by a lesion in the medial longitudinal fasciculus (unilateral internuclear
ophthalmoplegia) or in both directions (bilateral internuclear ophthalmoplegia).
- Saccadic slowing: Both eyes move slowly, sluggishly to the target.
- The presence of these patterns indicates ocular dysmetria.
Procedure:
•The test was originally performed as part of the calibration procedure. The patient is instructed to
keep the head still and alternately gaze back and forth to two spots (or LED lights) subtending a 20°
angle. Dwell time on the spots is about 3 sec. The presence of over-shoots is the most common
finding.
Results:
•Normal/Peripheral results are expected to show none of the above patterns. Less than 50% of the
calibrations show overshoot. Normals, if fatigued by repeated eye movements may show saccadic
slowing.
•Central: More that 50% of the calibrations showing overshoot is a common CNS finding. Any of the
above patterns also indicate CNS pathology. Several lesions can produce ocular dysmetria: ocular
muscle or nerve weakness, visual field deficits (following stroke), basal ganglia disorders (like
Parkinsonism), brainstem disease, and cerebellar pathology.
Random Saccade
•Under computer control/measurement, it is possible to randomly vary (in time and location, within
25°) the target. Relevant parameters measured are latency (from target movement to initiation of eye
movement), velocity (which is a function of eye deviation), and accuracy (hyper- and hypometria).
- Latency is not a useful parameter with the fixed saccade procedure (the subject can anticipate the
target). Also, lesions causing effects only at different eye speeds won't be detected.
•Generally, CNS lesions can increase latency (but latency is also subject to patient state), and reduce
velocity and accuracy. Graphic displays plot the patient's performance relative to normative data.
card fld "Pursuit"
Sinusoidal tracking (aka smooth pursuit)
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•The sinusoidal tracking test measures the ability of the cortical visual pursuit system to track a
smoothly moving object (a swinging pendulum, sinusoidally moving LED spot). The pursuit system
is usually tested at different speeds (we use 0.1, 0.2, and 0.4 Hz) with peak amplitudes of 20°.
- Predictive pursuit is controlled by frontal cortex.
- Random pursuit is controlled by occipito-parietal- temporal cortex.
•Pursuit data are analyzed in terms of gain, phase, and acceleration. Pursuit data may also be
contaminated by gaze or spontaneous nystagmus.
Results:
•Normal/Peripheral show a smooth sine wave pattern equal in amplitude (gain) and phase to the
stimulus, except for a few brief deviations.
•Central lesions show abnormal tracking (poorly formed, broken up "shaky" tracings) which are
associated with cerebral cortex lesions, brainstem, or cerebellar disorders. These are similar (and may
have the same etiology) to the multi-step saccades, ocular dysmetria seen in the saccade test.
card fld "Optokinetic"
Optokinetic Nystagmus (OPK, OKN)
•The test for OKN is basically an evaluation of the central visual system, testing for oculomotor
pathology. The cortical pursuit system tracks objects and its purpose is to maintain image stability on
the fovea (track foveal targets). The subcortical OKN system tracks objects in the peripheral visual
field.
- Smaller objects tend to measure the pursuit system. Full-field stimuli measure the OKN system.
- OKN is usually measured in the horizontal plane, seldom in the vertical plane.
Procedure:
•OKN is elicited in a number of different ways: a revolving drum (manual or motorized, patient's
head inside or outside) with alternating black and white stripes, projection system, light bar, or
simply cloth or tape moved in front of the patient's eyes.
- Some researchers feel small objects simply duplicate the pursuit test.
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- A slow (15 or 20°/sec) and fast rate (40°/sec) of stripe movement is used for about 20 sec. The
faster rate taxes the OKN system. The stripes move to the right and then to the left.
- Our system uses a light bar that moves LED lines at 0.05 and 0.1 Hz.
Results:
•Normal. Normally, and with most cases of peripheral lesions the eye velocity mirrors the rate of
drum revolution up to 60-90°/sec.
- The slow phase moves smoothly in the same direction as stripe movement. The fast phase is
opposite.
- The patient may adopt one of two strategies, resulting in "look" or "stare" nystagmus. With look
nystagmus (a single stripe is picked out, followed to the end, another is picked up) the pursuit system
in mainly involved and the nystagmus is high amplitude and low frequency.
- Stare nystagmus invokes the OKN system, is higher in frequency and lower in amplitude, and is
the preferred method.
Abnormal responses usually involve poorly formed, jerky (saccadic nystagmus) tracking or an
attenuated eye velocity.
- The saccadic nystagmus is usually present in one direction more than in the other, and it becomes
more apparent as the system is taxed by higher velocity stripe movement.
- Often the saccadic nystagmus is similar to the deficit shown by the pursuit system.
- Attenuated eye velocity, which is greater in one direction than the other, is called optokinetic
directional preponderance (OKN-DP). Normally |OKN-DP| ≤ 10%. If R and L represent slow phase
eye velocity in the right and left directions, then
OKN-DP = 100 * (R - L)/(R+ L)
•Peripheral. Results are usually the same as normal. A poorly formed asymmetry could be related to
an intense vestibular-type spontaneous nystagmus. It's appearance can be similar to that seen with
gaze nystagmus.
•Central. Poorly formed asymmetry is a central sign. |OKN-DP| > 10% is a central sign.
- Rule out vestibular spontaneous nystagmus.
- Rule out peripheral ocular or oculomotor pathology.
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Some points:
•OKN asymmetry occuring with abnormal gaze testing suggests brainstem and/or cerebellar
pathology.
- Lateralizing significance is poor, but the gaze nystagmus tends to beat away from the side with the
lesion.
•OKN asymmetry coupled with normal gaze tests suggests a cerebral hemisphere lesion toward the
side with which the predominant OKN response beats.
•As with gaze nystagmus, an OKN asymmetry which only occures in the vertical plane suggests
central pathology. If the OKN asymmetry is predominantly or entirely vertical it usually indicates
higher midbrain lesions. But this can be caused by cerebral hemisphere damage if the pathology is
diffuse and severe.
•Optokinetic inversion, aka "reverse OKN" (slow phases move in the opposite direction of the
stripes), can occur in some patients with congenital nystagmus. Pseudoinversion also occurs in these
patients, but the slow phase velocities have more of an exponential appearance.
•Optokinetic after nystagmus (OKAN) is OKN that persists after the OKN stimulus stops. It is small
(<10°/sec) and persists for a short time (about 15 sec). It may be abnormally small, asymmetrical, or
hyperactive. It can occur in disorders of the OKN system or the peripheral/central vestibular system.
- OKAN is difficult to measure. It is highly variable, even within the same individual, and requires a
completely dark room. OKAN is often not measured or used diagnostically.
Card number_____ 13
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Card number_____ 14
card fld "Dix-Hallpike BPPV"
Hallpike test for benign paroxysmal
positional vertigo (BPPV)
•The Hallpike test (positioning test) is
similar to the positional test, except
that the emphasis is upon the movement to the position (rather than the assumption of the position).
Procedure
•From a sitting position with the head angled 45° to the right (or to the left), the patient is moved
rapidly to the head hanging right (or to the left) position. It's important to provide adequate support
for the back and neck.
- Nystagmus is recorded for usually no more than 60 sec.
- If nystagmus is found, then the movement is repeated to see it the response fatigues.
•The Hallpike is considered positive if a nystagmus is induced and if it's different (in intensity or
direction) from the corresponding position of the positional test. The nystagmus induced is usually
rotary or has a large vertical component. So, it's important to record eye movement in the vertical
plane, too.
Results:
•Normal: no nystagmus, a negative Hallpike except for maybe 2-3 beats.
•Peripheral: A peripheral lesion is indicated by a "classical response" that conforms to Dix and
Hallpike's (1952) description. The response must contain all four components:
1. Latent period. The response emerges after 1-8 sec following assumption of the position (Coats
considers this component to not be mandatory; he would still consider it a classical response).
2. Limited duration. The response lasts for no longer than 10-40 sec.
3. Response fatigues. It becomes less intense with repeated maneuvers.
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4. Dizziness. Patient becomes dizzy (vertiginous).
A "non-classical response" is defined as one that doesn't meet one of the four criteria. A non-classical
response is non-specific, so it could be peripheral.
•Central: A non-classical response could be central.
•The classical response is presumed to be related to either dislodged utricular otoconia that are either
free-floating (canalolithiasis) or adherent (cupulolithiathis) to the cupula of the posterior semicircular
canal. Some points:
- The condition is most common in the elderly.
- 15% of patients with post-traumatic dizziness may show a classical response.
- Many patients with chronic middle ear pathology who complain of episodic dizziness show a
classical response (labyrinthine fistula?).
- Occasionally, this response is seem following stapes surgery and is thought to be related to
manipulation of the utricle or saccule.
- There are repositioning procedures available for moving the otoconia away from the posterior
canal and back to the utricle.
Card number_____ 15
card fld "Positionals"
Positional nystagmus
•Positional nystagmus is nystagmus
that is brought about by the (gradual)
assumption of one or more positions
other than sitting.
Procedure
•The patient is brought slowly to different positions (different researchers/clinicians suggest
different positions): supine with the head turned right, supine with the head turned to the left, supine
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with the head hanging, body turned and lying on the right side, body turned lying on the left side. A
significant positional nystagmus is:
- The intensity is >5°/sec, or
- If the intensity is <5°/sec then it must persist for at least 30 sec.
- But nystagmus that is <7.5°/sec is of questionable pathological significance (i.e., it may be present
but indicates nothing serious, or treatment needed.
•Positional nystagmus is often categorized in one of the 3 types that is currently based on Aschan’s
(1957) modification of Nylen’s (1950) classification:
- Type I (direction changing): The nystagmus beats in different direction for different positions; at
least one position must have a different direction.
- Type II (direction fixed): The nystagmus beats in the same direction for all positions.
- Type III (transient): The nystagmus appears as a short-lived burst of activity.
•Type I nystagmus shows a slight statistical tendency to be associated with central pathology, Type II
a slight statistical tendency to be associated with peripheral pathology. Type III may be an early sign
of acoustic neuroma (speculative).
- Normal: no nystagmus (<5°/sec, duration less that 30 sec).
- Peripheral: non-specific
- Central: non-specific
•Often the positionals are not diagnostic. The presence of a documented response provides objective
evidence to support the patient's subjectively reported symptoms.
Card number_____ 16
card fld "Caloric Testing"
Caloric testing: The FitzgeraldHallpike Caloric Test (1942) or the
Alternating (or Alternate) Binaural
Bithermal Caloric Test
•This is one of the more informative
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tests of the battery since it can provide information about the status of the peripheral vestibular
system and any ear asymmetry.
Procedure:
•The patient is placed in a supine position with the head elevated 30° to position the lateral
semicircular canal vertically. The ear canal is inspected, excess wax removed, and the tympanic
membrane (TM) is inspected for perforations (a contraindication). Tympanometry is also useful.
•Under otoscopy a probe is inserted into the ear canal and a stream of water is directed to the
posterior superior quadrant of the TM. The patient's eyes are closed.
- Each ear is irrigated for 40 sec (250 ml) of water at 30° and 44°C (the warm, which initially feels hot,
and cool irrigations). These are not considered "minimal stimuli." A rest interval of 5-8 minutes is
required between irrigations to allow the labyrinth to return to a normal state.
- The labyrinth doesn't respond immediately to the caloric stimulus. There is a latency. Usually there
is no need to begin recording until approximately 30 sec into the irrigation, or until after the irrigation
is completed (to save paper or disk space).
•During the test it's important to employ mental alerting tasks to inhibit suppression of the
nystagmus. A number of variable can influence the nystagmus yield:
- Emotional factors: The general emotional state of the patient - motivation, apprehension, and
rapport. To reduce anxiety you should explain the test situation, what you are going to do, the
patient's perceptions.
- Environmental factors: Visual cues, unexpected noises, other distractions can inhibit nystagmus.
Try to eliminate distractions.
- Endogenous factors: The state of wakefulness is important, headache, other body sensations,
intellectual capacity, severe deafness, etc. Drug intake: alcohol, barbiturates, antihistamines,
antidepressants, Valium, Antivert, caffeine, diet pills, aspirin — any non-essential medications
should be avoided.
- To maintain a state of wakefulness, design a mental alerting task apropriate for the individual:
simple conversation, chat about family or friends, simple arithmetic, etc. Some researchers have
suggested tape recording a series of questions appropriate for various mental age levels.
Evaluating caloric responses:
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•SSC (or SPV) is calculated for the most intense 10 sec portion of each of the 4 irrigations: RW, RC,
LW, LC. Generally, the absolute magnitude of the SSC is quite variable across individuals, so the
subjects serves as his/her own control and the two ears are compared.
- At the peak of the caloric response (or shortly after) the subject is told to open his or her eyes and
fixate (on a finger held 1 meter away, or an LED from the quad light). Nystagmus should attenuate
appreciably. Three or more representative beats can be used to estimate eye velocity. The subject is
told to close the eyes and nystagmus is recorded until the response abates (up to about 3 minutes
from initiating the irrigation).
•Conclusions from the caloric evaluation are based upon four variables: UW (unilateral weakness),
DP (directional preponderance), BW (bilateral weakness), and the Fixation Index (FI) or FFS (failure
of fixation suppression).
- UW is the right ear percentage of the total response minus left ear percentage of the total response.
- DP is the right beating percentage of the total response minus left beating percentage of the total
response.
- BW is calculated as the average of the total response.
- FI is the percentage of the eyes open response to the eyes closed response. FFS is the percent
reduction of the closed eye response when eyes are open and fixated. FI is computed for each caloric
condition (or at least one right beating and one left beating condition).
Typical Findings:
•Normals: The average magnitude of SSC is 22°/sec with a standard deviation of 6°/sec. The 95%
range is from about 10°/sec to 34°/sec. Note: regarding the following sifnificance levels, different
experts have slightly different cut-offs.
- UW: The two ears should be the same within 20%.
- DP: Normals show equal DP within 20%, 20 - 30% is questionable.
- BW: No bilateral weakness. The average of the two ears should be greater than 7.5°/sec.
- FFS: normal nystagmus is suppressed by > 20%.
•Peripheral lesions: Peripheral lesions tend to attenuate output from the affected ear.
- UW is the major sign of a peripheral lesion. UW >20% indicates a peripheral lesion on the weak
side.
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- DP > 30% is significant, 20 to 30% is questionable. DP is often seen beating away from the affected
side because of an intense spontaneous nystagmus. However, nystagmus can also beat way from the
affected side without spontaneous nystagmus..
- BW < 7.5°/sec can be due to bilateral peripheral damage, as in streptomycin ototoxicity. BW is
most often dues to peripheral damage, and if central oculomotor pathology is ruled out, it's
considered a peripheral sign.
- FFS: Peripheral lesion show at least 20% suppression or more (some research suggests that FI > the
60% to 70% range is pathological).
•Central lesions:
- UW: Central disorders cannot produce UW; the ears should be the same within 20%.
- DP > 30% can be caused by central lesions. But since it can be produced by peripheral lesions it's
considered non-specific. However, if DP occurs without UW it would suggest a central lesion. The
direction of the preponderance in central lesion is not related to the side of the lesion.
- BW < 7.5°/sec can be caused by central pathology that interferes with the VOR. Even though BW is
usually caused by peripheral pathology, BW is a non-specific finding.
- FFS is a central sign if the nystagmus is suppressed by less than 20% (FI = 80%). Caution: this can
be caused by sedation or by people wearing new and uncomfortable contact lenses.
Card number_____ 17
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Card number_____ 18
card fld "Problems"
Saccades
•Calibration tracings (fixed saccades)
using dc and 0.05 Hz high-pass filter.
Normal saccades.
See Problem 1
•Problem 3 shows normal saccades
with a small amount of overshoot.
Problem 4 shows multi-step saccades
related to CNS disorder.
See Problem 3-4
•Problem 6 shows bilateral hypermetric saccades. Problem 7 shows unilateral hypermetric saccades
(the rightward saccades). Hypermetric saccades are usually associated with cerebellar pathology.
See Problem 6-7
•In problem 15, the saccades are normal, but show a slowing down as the eyes reach the target
(glissades). The patient in problem 16 has bilateral internuclear opthalmoplegia (INO).
See Problem 15-16
•The patient in problem 17 has unilateral INO (when the eyes move to the right). Problem 18 shows
saccadic slowing. This is similar to INO, except for the absence of glissades.
See Problem 17-18
Spontaneous Nystagmus/Gaze Nystagmus
•In problem 22 the eyes are closed (midline) and spontaneous nystagmus is present (12°/sec),
probably due to a peripheral vestibular lesion. Problem 23 is similar, but the recording is noisy.
Problem 24 illustrates a normal patient with square wave jerks.
See Problem 22-24
•The patient in problem 25 is normal, but the eyeblinks make the tracing in the horizontal channel
appear to have spontaneous nystagmus. Problem 26 is similar, but the patient has right beating
spontaneous nystagmus.
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See Problem 25-26
•This patient has left beating spontaneous nystagmus which is suppressed by visual fixation. The
most likely explanation would be a recent, paretic, right vestibular end organ or nerve lesion — but it
could be an irritative lesion on the left side. It is possible that it could be a central vestibular lesion but
with these lesions the nystagmus is usually not suppressed by visual fixation.
See Problem 29
•This is similar to the patient in problem 29 (same etiologic significance), except the spontaneous
nystagmus is stronger, and is also present on left gaze. This is first degree nystagmus (Alexander's
Law).
See Problem 30
•This patient's left beating nystagmus is not suppressed by visual fixation (the amplitude is less, but
eye velocity is about the same). The lack of suppression indicates a CNS lesion.
See Problem 32
•This patient has downbeating vertical nystagmus which is enhanced by downward gaze. This is a
CNS finding, perhaps a lesion in the cerebellum or lower brainstem.
See Problem 40
Tracking test (sinusoidal pursuit)
•Patients 44 and 45 show normal tracking (patient 44 is looking around a bit). Patient 46 is abnormal.
He has saccadic pursuit (jerky) when the target is moving rapidly to the left. It indicates a CNS lesion
(but, rule out intense left beating spontaneous nystagmus from an acute peripheral vestibular lesion).
See Problem 44-46
•Patients 47 and 48 are both abnormal, having bilateral saccadic pursuit (CNS lesion). Patient 49 is
equivocal.
See Problem 47-49
Optokinetic test
•Normal OKN.
See Problem 55
•This patient's left slow phase eye velocity is reduced, compared to the right eye velocity. This OKN
asymmetry indicates a CNS lesion.
See Problem 57
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•OKN is normal except the OKN is saccadic for the stripes moving rapidly to the left, taxing the
central system, revealing the lesion.
See Problem 60
Positional test
•This patient has direction changing positional nystagmus. It is right beating with the right ear
down, left beating with the left ear down (absent when sitting or supine). This is geotropic
nystagmus. It beats toward the ground. It is a non-specific finding (peripheral or central vestibular
lesion). It could also be caused by recent alcohol ingestion.
See Problem 66
•This patient is similar to patient 66 (there is a geotropic nystagmus), except there is also a strong left
beating spontaneous nystagmus present in the sitting and supine positions. The spontaneous
nystagmus enhances the left ear down (left beating) nystagmus, diminishes the right ear down (right
beating) nystagmus.
See Problem 69
Calorics
•Normal caloric responses.
See Problem 77
See Problem 77-Answer
•The patient has a right unilateral weakness. RW and RC eye velocities are lower than LW and LC.
This suggests a right peripheral (paretic) vestibular lesion.
See Problem 79
See Problem 79-Answer
•This patient has a UW on the right and a DP to the left. The UW suggests a right peripheral lesion.
The DP could be due to either peripheral or central causes and is non-specific. DP in the absence of
UW suggests a CNS lesion.
See Problem 86
See Problem 86-Answer
•The FI is normal, suggesting an intact central system.
See Problem 104
See Problem 104-Answer
•The FI is too high indicating FFS. This is evidence of a CNS lesion.
See Problem 105
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See Problem 105-Answer
Card number_____ 19
card fld "Overview"
General
•A variety of evoked potentials (EPs) have
been found, beginning at a latency of
about 1 msec to approximately 300 msec.
•EPs are recorded by placing scalp
electrodes on the surface of the head,
presenting stimuli (usually clicks, tone
pips, or tone bursts), and recording the
electrical activity produced by the EP generators.
•The EP generators include electrical activity in the cochlea, and electrical activity produced by
dendrites and axons occurring in fiber tracts and nuclei located in the auditory brainstem and cortex.
- Often these potentials are very small, embedded in noise (EEG and muscle potentials), and must be
computer averaged to be seen.
•The EP waveform (a graph of voltage versus time) emerges as a series of peaks and valleys. Each
peak is usually generated by a particular anatomic site. Earlier peaks come from locations more
caudally, later peaks more rostrally. Each peak has a label (like wave V of the ABR, Pa of the AMLR,
P2 of the ALR).
- Recordings are set up with a certain time frame in mind (like 0 to 10 msec for the ABR, 0 to 60 msec
for the AMLR, 0 to 600 msec for the ALR).
- The response is analyzed by noting the presence or absence of the peaks, shifts in absolute latency
(relative to normal) of the peaks, shifts in relative latency of the peaks (relative to each other) and
occasionally the amplitude of the peaks (or the amplitude of one peak relative to the other). Interaural
peak latencies also can be compared (like wave V latencies between the RE and LE for suspected VIII
N. tumor).
- Delays in peaks are often associated with pathology (like tumors, MS, increased intracranial
pressure).
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•Generally, the magnitude of the EP response increases (and latencies decrease) as the stimulus
intensity increases. Decreasing stimulus intensity and gradually observing the diminution of the EP
response is used to determine hearing threshold.
•A variety of factors relating to the subject (pathological and nonpathological), the stimulus, and how
the EP response is acquired will influence the recordings. So each EP has a specific protocol which
should be followed.
Electrocochleography (EcochG)
•The EcochG response occurs early, within the first 2 msec following stimulus onset. The response
contains first the cochlear microphonic (CM), followed by the summating potential (SP), and finally
the N1 (whole nerve or compound action potential).
- CM and SP are cochlear potentials. With alternating clicks, CM will be 180° out of phase and
cancelled (and not observed). SP seems to be sensitive to the presence of endolymphatic hydrops as
seen in Ménière's disease (MD/ELH).
- N1 is wave 1 of the ABR.
•EcochG amplitude is greatly affected by the proximity of the electrode to the cochlea. A
transtympanic (TT) needle electrode resting on the promontory records the best response, followed
by the wick electrode resting on the eardrum ("TYMPtrode"), followed by the "TIPtrode" (a gold foil
ear canal electrode covering the foam eartip of the tubephone).
- The TT, TYMPtrode, or TIPtrode is usually set up as the reference electrode, the active electrode is
placed on the contralateral earlobe.
•EcochG can be used for determining hearing sensitivity with either clicks or frequency specific tone
bursts.
- Alternating clicks (or tone pips at 2-2-1 cycles for rise-plateau-fall time) are presented at 7.1/sec:
75-90 dB nHL. The lower click rate enhances definition of wave I.
- Filter settings are 10 - 1500 Hz, gain is 75,000 times (or more depending on electrode type), and
each tracing is an average of at least 50 to more than 1500 sweeps (more sweeps for the less sensitive
electrode locations). Analysis time is usually 5 or 15 msec (longer for simultaneously recording the
ABR).
•The SP/AP ratio is used for documenting the presence of MD/ELH. SP/AP > 50% suggests
MD/ELH. Or, an ear difference in excess of 30% suggests MD/ELH.
Auditory brainstem response (ABR)
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•The ABR is the most commonly measured EP. It is used for both threshold determination and tumor
detection. Wave I (if measurable) is present at a normal latency; subsequent waves are delayed.
- Wave I: Distal end of cochlear nerve.
- Wave II: Proximal end of cochlear nerve.
- Wave III: Cochlear nucleus.
- Wave IV: Superior olivary complex.
- Wave V: Lateral lemniscus.
- Wave VI: Inferior colliculus.
•A typical recording uses an ipsilateral earlobe (A1/A2) to high forehead (Fz) montage with the
ground electrode on the contralateral earlobe. Fz is termed the active electrode (non-inverting) and
the ipsilateral earlobe is the reference (inverting) electrode.
- Alternating (or rarefacting or condensation) clicks are presented at 19.1/sec: 75 dB nHL (up to
37.7/sec is acceptable). Higher click rates stress the CANS, possibly revealing pathology not obvious
at slower rates.
- Filter settings are 150 - 3000 Hz, gain is 100,000 times, and each tracing is an average of at least 1024
sweeps (2048 is better for low amplitude EPs from low stimulus levels). Analysis time is usually 10 to
15 msec (longer for young children, conductive losses, low presentation levels).
•Peak picking.
- Each tracing is immediately replicated, to assess reliability. The peak must be present in both
tracings.
- The presence of a peak can be ambiguous. If there is a peak, at the proper time, then it probably is a
peak.
- Determining the exact location of the peak can be ambiguous. Moving a few pixels over can change
values by a SD. Picking a shoulder of wave V vs. the peak affects absolute and relative latencies.
About the ABR parameters…
•A vertex to nape of neck is a better location for enhancing wave V amplitude, due to the vertical
orientation of the neural generators.
- A horizontal montage enhances wave I due to the horizontal orientation of the cochlear nerves.
•Reducing click rate improves thequality of the tracing (say, 11.1/sec) in a "fragile" CANS. Increasing
click rate degrades quality, and increases latency (beyond about 30-40/sec).
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•Sometimes better ABR waveforms are obtained for rarefacting (usually) or condensation clicks; if
you have no ABR, repeat test using rarefacting clicks
•Increasing the number of samples averaged improves quality, but increasing from 100 to 1000
samples produces the same improvement as going from 1000 to 10,000 — however, the increase in
time to complete test is excessive.
•Choosing the presentation level.
- Present clicks at 75 dB nHL, or higher, at least 15 to 20 dB SL re: audiogram threshold at 3000 to
4000 Hz, or at the limits (usually 95 to 100 dB nHL).
- Try to avoid an unnecessarily high level. It may tense the patient, and create PAM artifact.
Interpreting the ABR:
•A retrocochlear interpretation is generally based upon the effects the lesion has upon transmission
time. But, remember to consider effects (non-retrocochlear) peripheral hearing loss can have on the
ABR.
•Retrocochlear pathology.
- Complete absence of the ABR is not uncommon.
- Normal Wave I, no subsequent waves. With high frequency loss, usually there is no wave I.
- Abnormal interaural latency difference (ILD), usually an ILD > 2/2.5/3 SD (usually this is .3 to .45
msec).
- Abnormal interpeak latencies (IPL, or interwave intervals, IWI). Wave I is normal, but subsequent
waves are delayed. From Ferraro (1997):
I - III is 1.7 to 2.7 msec,
III - V is 1.5 to 2.1 msec,
I - V is 2.5 to 4.5 msec,
Interaural IPLs > 0.2 msec are abnormal.
•Wave morphology may be abnormal: reduced amplitudes or wave V smaller amplitude than wave
I.
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•The Effects of peripheral hearing loss.
- Conductive hearing loss will increase all waves, but IPLs should not be affected. Interpret Wave V
latency as if the presentation level were reduced by the ABG.
- Cochlear hearing loss will increase the latency of all waves, similar to conductive hearing loss.
Precipitous hearing loss (very poor high frequency sensitivity) adds to the latency by the time it takes
the traveling wave to travel to apical regions of the basilar membrane. You can:
- Subtract 0.1 msec (from wave V latency) for every 10 dB audiogram threshold is poorer than 50
dB @ 4000 Hz (Selters & Brackmann, 1977).
- Subtract 0.1 msec (from wave V latency) for every 10 dB audiogram threshold is poorer than 30
dB @ 4000 Hz (Rosenhamer et al., 1981).
- Or you can adjust the presentation level and interpret wave V ILD normally:
PTA for 1000, 2000,
and 4000 Hz
0-19
20-39
40-59
60-79
Click Intensity Level
70
80
90
100
•If you can interpret the ABR in such a way that it is normal, it probably is normal.
The auditory middle latency response (AMLR)
•The main component of the MLR is Pa which occurs at about 25-30 msec. Pa is generated by
projections from the medial geniculate body to the auditory cortex (thalamo-cortical projections).
•The MLR is sensitive to subject state and drugs. The patient must be alert. The response is elicited
unreliably in children younger than 8 - 10 years.
•The MLR can be used for neurodiagnosis (including CAPD) and audiometry using tone pips.
•Montage for recording the AMLR varies depending upon whether the goal is neurodiagnosis or
audiometry. Audiometry uses linked ipsilateral and contralateral earlobes (Ai/Ac) to high forehead
(Fz) montage with the ground electrode Fpz. A neurodiagnostic goal places the active electrodes over
the site where the MLR is generated (C5 for the left, C6 for the right referenced to Ai/Ac).
- For neurodiagnosis, alternating clicks are presented at 7.1/sec or slower (in the case of a poor
response, or for young children) at 70 dB nHL (high levels may elicit the postauricular muscle reflex,
PAM). For audiometry, clicks or tone pips (2-1-2 rise-plateau-fall) are presented at different levels.
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- Filter settings are 10 - 1500 Hz, gain is 75,000 times, and each tracing is an average of at least 1024
sweeps. Analysis time is usually 60 to 100 msec.
The auditory late response (ALR), P300, and MMN
•The prominent components N1 and P2 (P2 occurs at 150 - 200 msec) are generated by the auditory
cortex. Presence of the ALR is evidence of normal cortical functioning (neurodiagnosis, CAPD).
•Montage for recording the ALR uses a high forehead (Fz) active electrode referenced to either the
ipsi or contralateral earlobe (Ai or Ac). Also, a montage like that used for recording the AMLR can be
used.
- Alternating 1000 Hz tone bursts (10 msec rise-fall, 30 msec plateau) are presented at 1.1/sec at 70
dB nHL.
- Filter settings are 1 - 30 Hz, gain is 50,000 times, and each tracing is an average of at least 250
sweeps. Analysis time is usually 600 msec.
•As with the MLR, the ALR is sensitive to subject state and drugs.
•The P300 and mismatched negativity MMN responses are recorded using a protocol similar to the
ALR, except two stimuli are used in an "oddball" paradigm. Whether the P300 response is measured
or the MMN depends upon the instruction given to the patient.
- 1000 Hz tone burst is the frequent stimulus, and the 2000 Hz tone burst is the rare (deviant) or
oddball stimulus. The rare stimulus is mixed at random (15-20%) with the frequent.
- For recording P300, the subject is instructed to attend to the oddball stimuli, count them. For
recording the MMN, no such instruction is given. But patients must remain alert.
- Separate computer averages are maintained for the rare and frequent stimuli. The average for the
frequent stimuli is simply the ALR (P1, N1, P2, N2).
- With P300 instructions: The average for the rare stimuli contains both the ALR (P1, N1, P2, N2)
plus a new wave P3 (or P300) occurring at 300 msec.
- With MMN instructions: The average for the rare stimuli minus the average for the frequent
stimuli yields the MMN response.
•The MMN response is a small negative deflection occurring at 150 -250 msec. The MMN latency is
shortest for adults, longest for infants. The MMN can even be recorded in newborns.
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•The MMN response derives from auditory cortex and is evidence of pre-attentional discrimination
by the auditory system.
•P300 is generated by medial temporal lobe cortex in the region of the hippocampus. The P300
provides evidence that the patient is consciously aware of stimuli differences.
•The P300 is described as an endogenous response (the EcochG, ABR, MLR, ALR are exogenous)
because its presence requires active subject participation.
Card number_____ 20
Card number_____ 21
Card number_____ 22
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card fld "ABR Case MCL"
MCL is an 11 month old girl, born 2 months prematurely, weighing 1 lb 6 oz. Etiology of the hearing
loss is unknown.
Card number_____ 23
card fld "ABR Case CR"
CR is a 43 yo male with a history of
sudden hearing loss and tinnitus 2
weeks prior to the evaluation. Caloric
UW was found on the right side. A
small 1.5 cm tumor was found on the
right side.
Card number_____ 24
card fld "ABR Case JD"
JD is a 27 yo female presenting with
unsteadiness, severe headaches, and
an episode of knife-like pain in the
eyes followed by inability to focus.
ENG suggested a central disorder.
Subsequently, she was diagnosed with
multiple sclerosis.
Card number_____ 25
card fld "ABR Case JTL"
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JTL is a 27 yo male complaining of difficulty hearing co-workers at the plant. Neurological and
otological evaluations were negative. ABR was normal for 80 dB nHL clicks, LIF was normal. JTL was
malingering.
Card number_____ 26
card fld "ABR Case TKR"
TKR is a 41 yo male with a history
consistent with Ménière's disease.
ABR LIF is consistent with cochlear
pathology. RE and LE comparisons are
normal with clicks presented at a high
enough level to eliminate effects of the
peripheral hearing loss.
Card number_____ 27
card fld "ABR Case KCL"
KCL is a 57 yo male with the chief
complaint of left-sided headache and
deep jaw pain. ABRs, administered at
80 dB nHL to both ears, showed
significant wave V delay for the left
ear. The ear difference in hearing loss
was not taken into account when
interpreting the ABR. Periodic
monitoring with CT scan was
recommended. A repeat ABR, at an
appropriate level, indicated cochlear pathology for the left ear.