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CONTINUING EDUCATION Common Clinical Encounters: Do We Really Know Them? By Ted Venema, PhD IHS offers a diversity of options for obtaining continuing education credit: seminars and classroom training, institutional courses, online studies, and distance learning programs. This article represents yet another opportunity. Upon successful completion of the accompanying test on page 12, you will earn one continuing education credit. (Please check with your licensing board to verify acceptance of continuing education credit for this activity.) This article and test are also available on the IHS website at www.ihsinfo.org. A s those working in the hearing healthcare field, it is our duty for the purposes of rehabilitation to walk with the knowledge of how the ear works. We are the ones who, during our clinical encounters, counsel and educate patients, caregivers, and sometimes physicians. Yet, can we explain the basis for many of our daily common clinical encounters? What Exactly is the Occlusion Effect, and Why Do We Get It The typical definition of the occlusion effect is that one’s own voice sounds louder when one’s ear is plugged. After all, this is why hearing aids have vents. But we get the occlusion effect because low-frequency, bone-conducted sounds Occlusion Effect: Low-Frequency, Bone Conducted Sounds are Louder When the Ear is Plugged Figure 1. The mass of the skull is shown in gray, and the outer ear canal is shown in beige. When occluded (red), the low-frequency energy cannot escape, and so it is forced toward the cochlea. This results in a louder perception of sound when the ear is plugged. THE HEARING PROFESSIONAL are louder for the plugged ear. Mass resonates with low frequencies and stiffness resonates with higher frequencies. The mass of the skull resonate with the lows of one’s own voice. This, in turn, vibrates the cartilaginous portion of the outer ear canal. When the ear is plugged, this added resonance cannot escape (Figure 1). It has nowhere else to go but through the middle ear and into the cochlea, hence the occlusion effect. When listening to your own voice on a recording, you hear yourself as others hear you through air conduction alone. When you hear yourself talking, you hear by air and by bone conduction, and you perceive much more lowfrequency sound. The low frequencies are by far the loudest portion of speech. These lows cause the skull to resonate. It’s these low frequencies that are heard most loudly when we experience the occlusion effect. Say “s” while repeatedly plugging and unplugging your ear. Now try the same thing while saying a lower frequency sound like “mmm.” You should notice a robust effect with the “mmm” but not with the “s.” The Bing tuning fork test is based on the occlusion effect. It compares the sound of a low-frequency tuning fork held against the mastoid bone while the outer ear canal is repeatedly plugged and unplugged. The fork is normally louder when the ear is plugged. With conductive hearing loss, the occlusion effect is less. Plugging the ear still blocks the low-frequency bone conducted sound from escaping, but the middle ear pathology prevents the blocked sound from passing through the middle ear and going on to the Ted Venema, PhD, is a professor of the Hearing Instrument Specialist Program at Conestoga College in Ontario, Canada. He earned his bachelor’s degree at Calvin College and his master’s degree in audiology at Western Washington University, and his PhD at the University of Oklahoma. Venema also served as a volunteer on IHS’s education committee, the International Institute for Hearing Instruments Studies. 5 CONTINUING EDUCATION cochlea. The Bing test can also be done simply by using one’s own voice, as indicated above. What Does Ear Canal Resonance Offer to the Understanding of Speech Look at the combined resonances offered by the outer ear canal and the concha (Figure 2). Figure 3. The middle ear increases the pressure of incoming sound, mainly due to the larger size of the eardrum relative to that of the stapes. Another pressure increase is due to the leverage action of the ossicular chain. The manubrium of the malleus (green) is slightly longer than the long process of the incus (blue). The fulcrum is the straight line running through the head of the malleus and the short process of the incus. Figure 2. Note how the open adult ear canal has a resonance between 1500 and 4000 Hz. The peak occurs at about 2700 Hz. These frequencies are most important for discerning what word is spoken. The odd shape of the outer ear causes these resonances. The most important frequencies for understanding speech lie roughly between 1000–4000Hz. As Figure 2 shows, the outer ear creates an added 15–20 dB gain for these allimportant speech sounds. The connection between speech and hearing here is unmistakable. The shape of this resonance also has a lot to do with the shape of noise-induced hearing loss (NIHL). The three middle ear ossicles are strangely twisted because in this way, they can provide the leverage action that further increases sound pressure by 1.3:1. The length of the manubrium of the malleus is about 1.3 times the length of the long process of the incus. Lastly, the buckling action of the TM increases the pressure of airborne sound by 2:1 (Figure 4). The movement of the TM surface varies between the annulus (outer ring) and umbo (center where the manubrium of the malleus ends), and the areas in between. This is the buckling action. Why Do Mammals Have Middle Ears The cochlea is filled with perilymph fluid in the scala vestibule, and the footplate of the stapes sits inside the oval window. Most of the pressure of sound waves carried through air bounces off fluids. Imagine your head under water in a swimming pool. If one were standing on the edge of the pool talking to you, you wouldn’t hear a word. Almost all of the sound will bounce off the surface of the water. Something has to help airborne sound puncture or penetrate the fluid-filled cochlea, and that is purpose of the middle ear. The middle ear increases the pressure of airborne sound in three ways: the size of the eardrum relative to that of the stapes, the leverage action of the ossicular chain, and the buckling action of the eardrum or tympanic membrane (TM). The TM has 17 times the useful surface area as the footplate of the stapes (Figure 3). Pressure is force over an area; when sound pressure upon the relatively large area of the TM is converged upon the much smaller stapes footplate, the pressure is increased by 17:1. 6 Figure 4. The TM is held fast by its outer ring, the annulus, and so it cannot be displaced there. TM movement is greatest between the umbo and annulus. Less displacement at the umbo means more force at the umbo. This buckling action increases pressure by 2:1. The impact of all these sound pressure increases can be seen by multiplying the factors together: 17 @ 1.3 @ 2 = about 44:1. A 10:1 sound pressure increase corresponds to a 20 dB increase. A 100:1 pressure increase is a 40 dB increase, etc. A 44:1 pressure increase is somewhere between a 20 and a 40 dB increase. Actually, the middle ear offers an increase of close to 30–33 dB. OCTOBER • NOVEMBER • DECEMBER 2010 CONTINUING EDUCATION If the Middle Ear Makes Up 33 dB, Why Can a Conductive Hearing Loss be More Than That We have all seen flat conductive hearing losses of 50–60 dB HL. When the oval window is pushed inward, the round window bulges. Cochlear fluid does not compress so easily, so if the round window could not bulge outward, the oval window could not push inward. Otitis media might result in this, because complete fluid buildup in the middle ear space would prevent the round window from bulging outward. Otosclerosis might also prevent the oval window from being pushed inward. Without oval/round window actions, conductive hearing loss can well surpass the 33 dB that the middle ear adds to incoming sounds. The Rinne tuning fork test is based upon the dB increase offered by the middle ear. When the tuning fork is held first against the mastoid bone and then held near the outer ear, the sound of the tuning fork held near the outer ear is normally heard loudest. This is because air conduction involves the outer, middle, and inner ears. It is a much more efficient way to hear than hearing by simple bone conduction. Louder hearing by air conduction should occur for both normal hearing and with SNHL. A healthy middle ear makes up 33 dB, and the Rinne test is a simple and eloquent demonstration of this increase. Why Are Hearing Thresholds in dB Sound Pressure Level Shaped as a Curve The dB increases offered by the middle ear are different for different frequencies. The resonances of the outer and middle ears combined together form the curve of human hearing threshold, as shown in Figure 5. At quiet inputs, the ear is most sensitive to frequencies between 500 to 4000 Hz. Thresholds of 0 dB HL, across the seven audiometric octave frequencies, therefore represent very different SPLs. 30 30 Total Ear Canal & Concha 20 Middle Ear 20 + 10 10 0 250 500 1000 2000 4000 8000 500 1000 2000 4000 8000 Our hearing sensitivity 40 = 0 250 Note how important speech Hz’s emphasized dB 25 SPL 10 0 125 250 500 1000 Hz 2000 4000 8000 Figure 5. The outer ear (top left) and middle ear (top right) together contribute to the equal loudness curve (bottom). This curve actually represents the sensitivity of one ear under a headphone; 0 dB HL on the audiogram. THE HEARING PROFESSIONAL Why Does Carhart’s Notch Appear with Otosclerosis The term sclerosis means “hardening.” Otosclerosis is actually a growth of soft porous bone tissue around the oval window and stapes. Therefore, some have called the pathology otospongiosis. A decrease in bone conduction thresholds, mostly at 2000 Hz (Carhart’s notch), is commonly noted as a trademark for otosclerosis (Figure 6). Figure 6. Carhart’s notch is not an indication of cochlear hair cell damage. It is an artifact of the way we test bone conduction. The drop in bone scores is most pronounced at 2000 Hz, which is also the resonance of the middle ear ossicles. Carhart’s notch does not, however, truly represent a drop in cochlear sensitivity at 2000 Hz. Otosclerosis simply changes the contributions of the ossicular chain to normal bone conduction testing. There are actually three elements that contribute to normal 0 dB HL bone conduction thresholds: 1) distortional bone conduction—hair cell stimulation caused by vibration of the skull with the bone oscillator; 2) inertial bone conduction—the tiny lag in ossicular chain movement when the skull is vibrating; and 3) osseotympanic bone conduction—the tiny vibration of the air column in the outer ear canal which can move the TM. With otosclerosis, the stapes is fixated in the oval window and so both inertial and osseotympanic bone conduction are compromised. The most obvious result is at 2000 Hz, the resonant frequency of the middle ear ossicles. Acoustic Reflexes: Why Do We Have Them Acoustic reflex (AR) testing used to be performed more frequently, and it should still be routinely performed today. Here’s why. The brain-going parts of the AR are the outer and middle ears, the cochlea, the VIII nerve, and the low brain stem. The ear-going parts of the AR are the low brain stem, and the VII and V nerves. These connect to the stapedius and tensor tympani muscles of the middle ear, respectively. We often think of ARs as nature’s protection device against loud sounds because loud sounds “set them 7 CONTINUING EDUCATION off.” Note, however, that ARs are most robust for low frequencies (500 and 1000 Hz). They reduce the intensity of low-frequency sounds by about 15 dB. Recall that vowels are loudest and lowest in frequency. Therefore, they stimulate the AR when we speak. The AR allows us to hear important high-frequency sounds by reducing the lowfrequency sounds that would otherwise easily mask them. ARs occur while we talk; in fact, they occur about 1/20th of a second before we begin to speak. It appears that the AR enables us to better hear high-frequency sounds while we speak. ARs can also be thought of as a non-behavioral test of inner hair cells (IHCs). Normal IHCs and OHCs are shown in Figure 7. Normal Inner & Outer Hair Cells Picture by R. Harrison (1988) Charles C.Thomas, Publisher Springfield IL Figure 7. An electron microscope photograph shows normal healthy human IHCs and OHCs. Damaged hair cells, especially OHCs, are shown in Figure 8. OHC damage often precedes IHC damage. OHC damage often results in moderate sensorineural hearing loss (SNHL), while severe-profound SNHL is associated with both OHC and IHC damage. All things being equal, IHCs are known to be responsible for poor speech discrimination. OHCs help IHCs to sense soft incoming Damaged sounds, but their damage will not normally result in as poor speech discrimination. Two people who have a similar 50 dB flat SNHL may have very different speech discrimination. Chances are, the person with good speech discrimination will have ARs present (at reduced sensation levels); the person with poor speech discrimination will most likely have absent ARs. Why Do High Frequencies Stimulate the Base of the Cochlea and Low Frequencies Stimulate the Apex The cochlea is an incredibly complex organ that changes fluid motion into electricity. High frequencies stimulate the basilar membrane near the base of the cochlea, and that low frequencies stimulate the basilar membrane near the apex of the cochlea. Why does this occur? Some mistakenly think it is because high frequencies have relatively short sound waves, and so their traveling waves are also short; low frequencies have relatively long sound waves, and so their traveling waves are also longer. This concept is fundamentally false because sound waves in air have little in common with cochlear traveling waves. The basilar membrane is the “floor” upon which the hair cells sit. It is sandwiched between the scala tympani and the scala media. All cochlear traveling waves involve the basilar membrane. Consider that a 250 Hz tone has a wave about 4.5 feet in length. The entire length of the basilar membrane, however, is just over an inch! There is no way these lengths of airborne sound waves can enter the cochlea. The real reason is that the basilar membrane is narrow at the base and wide at the apex of the cochlea. We actually have three rows of OHCs at the base of the cochlea, and five rows of OHCs at the apex. High frequencies stimulate the base of the cochlea because the basilar membrane has less mass and more stiffness near the base. Low frequencies stimulate the apex because the basilar membrane there has more mass there, and it is more flaccid (Figure 9). Because Basilar Membrane (hair cell “floor”) Hair Cells Helicotrema Scala Vestibuli Oval Window Reissner’s Membrane (mostly outer) Scala Media Promotory Basilar Membrane Picture by Engstrom (1988) Copyright by Widex Figure 8. An electron microscope photograph shows damaged hair cells. Note that most damage is confined to the OHCs, as is typically the case. 8 Scala Tympani Round Window From: Compression for Clinicians, 2ed,Venema, T., Thomson Delmar, 2006 Figure 9. At the narrow apex (left), the basilar membrane widens. At the wide base (right), the basilar membrane narrows. These physical mass and stiffness qualities of the basilar membrane determine the peak of the cochlear traveling wave. OCTOBER • NOVEMBER • DECEMBER 2010 CONTINUING EDUCATION We also know the traveling wave has an “active” component (Figure 10). Here, the traveling wave is amplified and also sharpened. These are the contributions of the OHCs. Their natural cochlear amplification of the wave enables us to hear soft sounds below the levels of conversational speech. The sharpening of the wave also enables us to distinguish among frequencies that are close together. Outer Hair Cells Sharpen the Peak! They are the “muscles” of the cochlea They usually get damaged first Apex Lows Base Basilar Membrane Highs Figure 10. A dull, rounded traveling wave occurs with OHC damage. First, soft sounds are no longer audible; second, the resolution required to separate or distinguish among frequencies close together is diminished. OHCs tend to die first, resulting in a moderate degree of SNHL. This degree is consistent with presbycusis. Why does NIHL Drop at 4000 Hz and Improve at 8000 Hz The audiometric configuration of NIHL (Figure 12) is unique. One reason this occurs is that the AR is most robust for low frequencies, and so low frequencies tend to be most protected. The noise presented by a gun, however, happens faster than the reaction time of the AR, and so the damage is done before the AR occurs. Poorer blood supply to the 4000 Hz region of hair cells is another reason why NIHL is most pronounced at 4000 Hz. Another reason is that the stapes footplate motion creates a particular fluid motion in the cochlea with negative effects on the hair cells there. Another reason, however, is the complementary shape of NIHL and the outer ear resonances (Figure 2). Noise tends to damage hair cells approximately a half-octave higher than the frequency of the noise itself. Since the outer ear resonance adds 15–20 dB of gain to incoming sounds, noise is constantly filtered through this resonance. The peak seen at 2700 Hz can simply be pushed upwards half an octave, and flipped upside-down, at about 4000 Hz. Noise Induced Hearing Loss (NIHL) Noise tends to –10 125 250 500 1000 2000 4000 8000 0 damage hair cells 10 20 1/2 octave higher 30 40 People with OHC damage most often have a reduced ability to distinguish between frequencies that are close together. No wonder people who wear hearing aids commonly report difficulty when listening to speech in background noise (Figure 11). 50 60 70 80 90 100 110 120 It’s the “sharpening” thing that’s the main challenge This is why hearing aids for ears aren’t like glasses for eyes Natural shape of fluid wave: 2 peaks from 2 tones close in Hz Hair cell damage results in: smaller rounded peaks Hearing aids make wave bigger: but cannot sharpen it Figure 11. OHC damage removes the “active” component of the normal traveling waves that might occur with two stimuli close together in frequency (top panel). The middle panel shows traveling waves with reduced amplification and sharpness. The bottom panel shows what happens to the middle wave with amplification. The amplitude is restored, but not the sharpness. THE HEARING PROFESSIONAL Figure 12. NIHL has a shape that looks like the typical REUR flipped upside-down, and shifted to the right about half an octave. Why Does Ménière’s Disease Typically Present with a Rising Audiogram Ménière’s is associated with an excess of endolymph fluid inside the scala media of the cochlea. The membranous boundaries or walls of the scala media are the basilar membrane and Reissner’s membrane. These separate the scala media from the scala vestibuli and the scala tympani. Recall the unique shape of the basilar membrane. An excess of fluid buildup inside the scala media will tend to bulge its membranous walls where they are largest and most flaccid. Excess pressure of endolymph will thus become most evident at the apex of the cochlea, and will mostly affect the low-frequency hair cells. This results in Ménière’s disease having a rising reverse audiogram (Figure 13). 9 CONTINUING EDUCATION Meniere’s Disease: Why A Rising, Reverse SNHL? Apical basilar membrane 250 500 1000 Basal basilar membrane 2000 4000 8000 Hz Endolymphatic hydrops 0 10 (too much fluid 20 in scala media) 30 40 Causes less stiff 50 apical BM to 60 be affected more 70 by excess pressure 80 90 100 110 Figure 13. An excess of endolymph fluid pressure will bulge the basilar membrane mostly at the apex. This mechanically compromises traveling wave motion and hair cell excitation mostly at the apex, causing a low-frequency SNHL. Figure created by the author. How Does the Asymmetrical Traveling Wave Shape Show Itself With Cochlear Dead Spots The traveling wave shown in Figure 10 has an asymmetrical shape. Its peak is closer to the steep front of the wave than to the more shallow “tail.” The steep peak always faces the apex (low frequencies). The asymmetrical traveling wave shape is also seen in Figure 14. This creates what is known as the “upward spread of masking.” A loud rumbling of a truck will easily mask the soft chirping of a canary, but a loud chirping of a canary will not mask the soft rumbling of a truck. Loud, low-frequency stimulation creates a traveling wave with a large peak near the apex, and a shallow tail sloping toward the base. The soft chirp of a canary makes a small traveling wave with a peak confined near the base. The tail of the traveling wave produced by the loud truck will easily cover the wave produced by the soft chirping of a canary. Low-frequency background noise thus easily masks soft high-frequency consonants of speech. Loud high-frequency sounds, however, may very well make larger traveling wave peaks with higher amplitudes, but the steep wave front of these waves still remain fairly confined to the base of the cochlea. The asymmetrical traveling wave also has implications for audiometry. With normal high-frequency hearing, a profound low-frequency hearing loss will look like a moderate reverse or rising audiogram (Figure 15). Low-frequency stimulation into a completely dead low-frequency hair cell region along the basilar membrane produces a traveling wave with a large amplitude peak in the dead hair cell region. The shallow tail of the same wave easily extends into the living mid-frequency hair cell region. Mid-frequency hair cells will thus become stimulated, and the person will raise his/her hand indicating he/she heard the tone. This is why low-frequency cochlear dead spots are associated with moderate reverse audiograms. Moderate Reverse SNHL; Hearing Through Remote Hair Cells? Apex Base 250 500 1000 2000 4000 8000 Hz 0 10 20 30 40 50 60 70 80 90 100 110 Upward Spread of Masking Concept Intense Low-Hz traveling wave moves entire Basilar Membrane Intense High-Hz traveling wave moves Basilar Membrane only at base Basilar Membrane Displacement Basilar Membrane Envelopes Figure 14. Traveling wave envelopes are shown for a low-frequency tone stimulus (red) and a high-frequency tone stimulus (blue). A soft high-frequency tone will produce a small traveling wave that will fit inside of the low-frequency traveling wave. A soft low-frequency tone, however, will produce a traveling wave that will not fit inside the highfrequency traveling wave. 10 Figure 15. Moderate Reverse SNHL is often a “signature” of actual profound low-frequency hearing loss. Note how the “tail” of the traveling wave here creeps into the mid-frequency regions. With normal low-frequency hearing, a profound highfrequency hearing loss might look like a steep, precipitously dropping audiogram (Figure 16). The high-frequency hearing loss, however, must be severe in degree. To appreciate why, imagine intense high-frequency stimulation into a completely dead high-frequency hair cell region along the basilar membrane. This produces a traveling wave with a large amplitude peak in the dead high-frequency region. In this case, however, only a tiny piece of the steep front of the same wave can extend into the normal mid-frequency region. With progressively higher frequencies, the peak of the traveling wave occurs further and further inside the dead hair cell region. Due to the steep shape of the front of the traveling wave, dramatic increases of high-frequency stimulation are required in order for the steep front to extend into the healthy mid-frequency hair cell regions. This is why high-frequency cochlear dead spots are associated with severe precipitous audiograms. OCTOBER • NOVEMBER • DECEMBER 2010 CONTINUING EDUCATION As the old saying goes, “one can help the dying, but not the dead.” Summary It is the job of hearing healthcare professionals to elucidate and explain how the ear works for purposes of rehabilitation. The specifics of the cochlea anatomy and physiology, and how its complex inner workings translate into clinical phenomena, are part of the professionals’ education. That knowledge and ability to communicate that knowledge during clinical activities is the hearing aid specialists’ best marketing tool to patients, their caregivers, and physicians. THP All figures within this article were created by the author. Figure 16. Severe-profound precipitous high-frequency SNHL is often a “signature” of actual profound high-frequency hearing loss. Note how the front of the traveling wave here creeps into the midfrequency regions. Implications for amplification: amplify moderate reverse and severe precipitous audiograms with care. Applying a lot of output into dead areas will not do much to rehabilitate the client. Clinicians might do well to amplify the transitions of these audiograms, not the worst thresholds. This article was adapted and reprinted with permission of AudiologyOnline. View the original article, and earn CEUs from hundreds of other text-based, live, and recorded courses from the leading experts in audiology for $99/year at AudiologyOnline. To register, visit www.audiology online.com or call 1.800.753.2160. References Musiek, F. E. (1983). Assessment of central auditory dysfunction: The dichotic digit test revisited. Ear and Hearing, 4, 79–83. Venema, T. H. (2006). Compression for Clinicians (2nd edition). NY: Thomson Delmar Learning. Protect your patients’ hearing aid Generate more revenue Strengthen long term dispenser-patient relationships Call for your copy of the quiz at 1-800-525-7936 www.discoveryrepair.com THE HEARING PROFESSIONAL 11 IHS Continuing Education Test: Common Clinical Encounters: Do We Really Know Them? For continuing education credit, complete this test and send the answer section at the bottom of the page to: International Hearing Society 16880 Middlebelt Rd., Ste. 4, Livonia, MI 48154 • After your test has been graded, you will receive a copy of the correct answers and a certificate of completion. • All questions regarding the examination must be in writing and directed to IHS. • Credit: IHS designates this professional development activity for one (1) continuing education credit. • Fees: $29.00 IHS member $59.00 non-member (Payment in U.S. funds only.) 1. The resonance of the adult outer ear canal lies roughly between: a. 125–8000 Hz b. 500–2000 Hz c. 1500–4000 Hz d. 2000–6000 Hz e. 500–4000 Hz 6. The middle ear provides about a ____ dB increase to incoming sound. a. 17 b. 3.3 c. 44 d. 33 e. 2.1 2. Noise induced hearing loss occurs about ____octave higher than the resonance of the outer ear canal. a. 1/2 b. 1/3 c. 1/4 d. 2 e. none of the above 7. Carhart’s notch is a: a. drop in air conduction thresholds at 2000Hz b. drop in bone conduction thresholds at 2000Hz c. improvement in air conduction thresholds at 2000Hz d. improvement in bone conduction thresholds at 2000Hz e. none of the above 3. In the cochlea, there are ____ rows of outer hair cells at the base and ____ rows at the apex. a. 5/3 b. 3/5 c. 3/4 d. 4/3 e. none of the above 4. This tuning fork test is based on the occlusion effect. a. Rinne b. Weber c. Bing d. Schwabach e. Venema 5. This tuning fork test demonstrates the SPL increase provided by the middle ear. a. Rinne b. Weber c. Bing d. Schwabach e. Venema 8. At the base of the cochlea, the floor upon which the hair cells stand (basilar membrane) has: a. more mass and less stiffness b. more stiffness and less mass c. more mass and more stiffness d. less mass and less stiffness e. more inner hair cells 9. The following is true about the traveling wave: a. short steep wave front faces the apex of the cochlea b. short steep wave front faces the base of the cochlea c. long shallow wave front faces the apex of the cochlea d. long shallow wave front faces the base of the cochlea e. speed increases as it approaches the apex of the cochlea 10. Which of the following statements about acoustic reflexes (ARs) is FALSE? a. ARs are more robust for low frequencies b. when they contract, ARs reduce low frequency sounds by approximately 15 dB c. they occur when we talk d. they cause upward spread of masking ! COMMON CLINICAL ENCOUNTERS: DO WE REALLY KNOW THEM? Name ANSWER SECTION Address City (Circle the correct response from the test questions above.) State/Province Zip/Postal Code 1. a b c d e 6. a b c d e 2. a b c d e 7. a b c d e Last Four Digits of SS/SI# 3. a b c d e 8. a b c d e Professional and/or Academic Credentials: 4. a b c d e 9. a b c d e (PHOTOCOPY THIS FORM AS NEEDED) Please check one: M $29.00 (IHS member) M $59.00 (non-member) 5. a b c d e 10. a b c d Email Office Telephone 12 OCTOBER • NOVEMBER • DECEMBER 2010