**Transcript of Cyberseminar**

**Mild TBI Diagnosis and Management Strategies**

**Diagnosis and Treatment of Vestibular Disorders in mTBI**

**Presenters: Faith W. Akin, Ph.D.,  Jorge M Serrador, PhD**

**November 12, 2013**

*This is an unedited transcript of this session. As such, it may contain omissions or errors due to sound quality or misinterpretation. For clarification or verification of any points in the transcript, please refer to the audio version posted at www.hsrd.research.va.gov/cyberseminars/catalog-archive.cfm or contact Jorge.Serrador@va.gov or faith.akin@va.gov*

*Moderator:*It's a pleasure today to have a discussion of vestibular consequences of mTBI, with an emphasis on diagnosis and treatment of vestibular disorders.  Our experts are Jorge Serrador, who is with the War Related Injury Study Center in East Orange New Jersey, and Associate Professor at Rutgers; and Faith Akin, who is at the VA Medical Center in Mountain Home.  With that, we'll turn it over to the slides.  Thank you very much.  

*Presenter:*Okay, thank you Dr. Depalma; also for the invitation to speak at today's cyber seminar, and to the conference coordinators at HSRND.  I guess I should make sure everybody hears me first.  

*Moderator:*Yes, we can hear you.  

*Presenter:*Okay, great.  My plan for this presentation today is to provide some background on dizziness and head injury, and then review some methods of clinical vestibular assessment, and then share with you some preliminary data from an ongoing VA-funded study at Mountain Home, designed to examine vestibular consequences of mild traumatic brain injury and blast exposure.  

Here's my disclaimer.  I'd like to begin with a poll question, to get an idea of the audience that we have today, so please indicate your primary role in VHA.  

*Moderator:*Faith, just as people are responding here, we did get one comment, and if you could speak a little louder.  Unfortunately,  not everyone has great computers.

*Presenter:*Is that better?

*Moderator:*That should be better.  Not everyone has great computer speakers, so sometimes a little louder helps.  Thank you.

*Presenter:*Sure.  It looks like the majority of our audience are clinicians.  I think that looks like that's about it on the poll, so 79-80 percent are clinicians, and then about six percent are less in other categories.  

*Moderator:*Okay great, thank you.

*Presenter:*The relationship between dizziness and war related head injuries is well known.  Robert Barany that you see in this slide, was an Austrian physician who won the Nobel Prize in Medicine for his work on the vestibular system.  In World War I, he joined the Austrian army as a civilian surgeon and provided care to wounded soldiers with head injury.  Ironically, he was later in a Russian prisoner of war camp when he learned that he had won the Nobel Prize.  Then later, in the early 1960s, Caveness and Nielson reported that approximately half of 400 veterans who sustained head injuries in the Korean conflict complained of dizziness or vertigo.  Today, there are numerous journal articles describing symptoms of dizziness and vertigo in individuals with war related head injury.  

I'll review some of these a little later in the presentation.  A glance at the literature reveals that the incidence of dizziness associated with head injury ranges from 15 to 78 percent, and that wide range may be due to differences across studies and definitions of head trauma or head injury, or differences in the quality of symptoms.  For example, some studies look at vertigo specifically, whereas others might look at imbalance.  Numerous studies have also reported that the symptoms of dizziness last for six months or longer following head trauma and blast exposure.  This long term chronic nature of these symptoms is a real troubling aspect of working with these patients.

To give you some background on the vestibular system, it's one of three sensory systems.  Let me find my cursor here.  It's one of three sensory systems that contribute to balance.  This information from these three sensory systems, vision, vestibular, proprioception or somatosensory is processed or tuned up at the level of the brainstem in the cerebellum, and then it results in these motor or perceptual outputs.  The two types of motor outputs are postural changes, to keep upright balance and to help us move through our environment, and eye movement to keep gaze steady when our head is in motion.

There are two types of vestibular sensory organs: semicircular canals and otolith organs in the inner ear.  The otolith organs, which I'll come back to in a few minutes, and then the semicircular canals that you can see are positioned at right angles to each other.  They're paired with canals on either side of the head.  These three canals sense angular acceleration or head rotation in three dimensions.  During activation of these sensory—or these semicircular canals, head rotation causes inertia of fluid, or endolymph in the canal, to activate sensory cells in the vestibular system.  The activation of these sensory cells produces an electrical signal that's relayed to the eye muscles.  You can see right here, via the vestibule-ocular reflex shown in this figure.  

The purpose of the VOR is to keep gaze steady when the head is in motion.  In most clinical tests of vestibular function, the VOR response is measured during vestibular stimulation, to determine if the vestibular system is functioning adequately.  Two tests of – traditionally clinical vestibular assessment has included binaural bithermal caloric test and the rotary chair test.  These are both tests of horizontal semicircular canal function.  The patient wears video goggles, so that the clinician can measure the output of the VOR during stimulation of the horizontal canals.  

The caloric test, this happens when we place water or air in the—into the ear canal, causing this temperature gradient that induces indolent flow in the horizontal canal.  In the rotary chair that you see here in the figure, the patient is secured upright, and then the chair rotates clockwise and counter-clockwise about the Y axis, to stimulate the horizontal canal.  Both of these tests have been the predominant measure of vestibular function in studies examining the effective head injury on the vestibular system.

Ocular motor function tests are used to uncover eye movement abnormalities that may interfere with the interpretation of vestibular  tests.  In these tests, they may include a gaze-evoked nystagmus, smooth pursuit, tracking saccades, optokinetic nystagmus, and fixation suppression.  In general, ocular motor abnormalities suggest possible central pathology or brainstem/cerebellar abnormalities.

In addition to the three semicircular canals, the two other vestibular organs called otolith organs include the utricle, which is closest to the semicircular canals, and lies in the horizontal plane; and the saccule, which lies in the vertical plane, when the head is upright.  The otolith organs contribute to postural and gaze stability by providing sensory input regarding linear acceleration of the head and head tilt or changes in gravity.  In this photo—this inset photograph, you can see otoconia that are calcium carbonate crystals, imbedded in the otolithic membrane of the otolith organs.  They serve to increase the density of the organ, so that it's gravity sensitive.

In some individuals, following head injury, these otoconia become detached, most likely here in the utricle, and migrate into the semicircular canals, causing symptoms of benign paroxysmal positioning vertigo, or BPPV.  BPPV is characterized by recurrent brief episodes of vertigo associated with changes in head position, like looking up or rolling over in bed.  BPPV is the most common peripheral vestibular disorder, and although the etiology of BPPV is often idiopathic, head trauma is the most common known cause of BPPV, and 10 to 25 percent of patients with head trauma develop BPPV.  That's been shown in numerous studies.  The presumed mechanism of BPPV is canalithiasis, or free floating otoconial debris in the endolymph, which causes endolymph flow and activation of the VOR, inducing nystagmus and vertigo.  This canalithiasis theory is the basis for modern treatment approaches for BPPV.  

The treatment is performed by placing the patient in a series of positions that you can see here in this figure, with the goal of moving the otoconia out of the semicircular canal, and into the vestibule.  Canalith repositioning therapy, or the modified Epley maneuver is the standard treatment for BPPV, and its efficacy is well established.  In fact, there are two clinical practice guidelines that are both available at the end of this presentation in the references.  One is published by the American Academy of Neurology, and one developed by the American Academy of Otolaryngology Head and Neck Surgery, and they're worth taking a look at if you're treating patients with BPPV.

Recently, clinical tests have been developed to measure otolith organ function, and these fall into two general categories: vestibular evoked myogenic potentials or VEMPs, and the measurement of ocular torsion or subjective visual vertical during off-axis rotation or centrifugation, using a modified rotary chair.  For this presentation, I will focus on the use of VEMPs ad a test of otolith function.  

VEMPs are short latency electromyograms evoked by high level sound or vibration stimuli.  They're recorded from surface electrodes placed over the tonically contracted muscles.  There's two types of VEMPs: cervical VEMPs or cVEMPs that are recorded from the sternocleidomastoid muscle; and the ocular VEMP that's recorded from the inferior oblique extra-ocular muscles.  This slide shows a cVEMP recording, measured from the activated SCM muscle, right here, during the presentation of a fairly loud, brief, low-frequency tone, presented through an insert earphone on the same side as that activated SCM muscle.  

The cVEMP waveform consists of an early positive negative component that's dependent on the integrity of the vestibular afferents.  Neurophysiological and clinical data indicate that the cVEMPS are mediated through a pathway that includes the saccule in the inferior branch of the vestibular nerve.  Clinical interpretation of the VEMPs – the cVEMPs – is focused primarily on inter-ear amplitude or threshold asymmetry.  In patients with saccular or inferior vestibular nerve involvement, cVEMPs are typically absent or have reduced amplitude.

This slide shows an oVEMP or ocular VEMP recording, measured from the activated inferior oblique muscles, using bone conduction vibration placed on the forehead.  Note that this participant is gazing up to activate the eye muscles.  Recent evidence indicates that these oVEMPs elicited using bone conduction stimuli are mediated by a pathway that includes the utricle and superior vestibular division of the vestibular nerve, and is a contralateral pathway to the inferior oblique muscles of the eyes.  

In patients with utricular or superior vestibular nerve disorders, oVEMPs are typically absent or have decreased amplitude.  In addition to vestibular site of lesion tests, balance and postural control can be measured clinically, too.  Postural control is modulated via the vestibulospinal reflexes.  The lateral vestibulospinal tract receives the majority of input from the otolith organs and cerebellum, and it aids in contraction of the anti-gravity muscles in the lower extremities.  The medial vestibular spinal tract projects bilaterally down the spinal cord and controls the position of the head, neck and eyes, in response to changes in posture.  

Balance can be assessed using static or dynamic tests of balance function.  The sensory organization test or the SOT test, assesses the integration of sensory information for static balance by measuring postural sway under conditions in which visual and somatosensory feedback is altered.  When the vision and somatosensory inputs are altered, input from the vestibular system is critical to maintaining stability.

This table summarizes several studies that examine vestibular function tests in individuals with TBI, and that's shown in these dark blue rows, and in studies that examined the effect of a blast exposure on vestibular function, the light blue rows.  I've only included studies in this table in which the percentage of individuals or number of individuals with normal or abnormal findings were reported, so rather than group mean.  Note that all seven studies assess vestibular function using tests of horizontal canal function.  The number of individuals with abnormal findings on these tests range from zero to fifty-one  percent.  In contrast, only three of the seven studies included otolith organ testing, and the number of individuals with abnormal otolith findings range from 17 to 54 percent.

With the exception of Scherer et al, the incidence of ocular motor abnormalities is fairly low, so less than ten percent.  Gait or balance was measured in three of the seven studies, and the number of abnormal findings ranged from four to thirty-seven percent.  

Like I said, we're in the midst of an ongoing clinical trial at Mountain Home, examining the vestibular consequences of mild TBI and blast exposure, and we've recruited participants who complain of dizziness or imbalance related to history of mild TBI and/or blast exposure.  In addition, we're recruiting a control group that will eventually be age matched.  I'm going to share with you some of our preliminary data.

This table shows the characteristics of our TBI blast and control groups.  You can see that the TBI blast participants are a little older than the control groups.  The mini mental state exam was used to screen for cognitive impairment, and there was little difference between groups.  Most of the participants in the TBI blast group have PTSD, tinnitus and hearing loss.  A few of the control participants had hearing loss.  

This table shows the characteristics of symptoms reported by the TBI blast group.  The most common symptom was imbalance and light headedness, with approximately half of the participants reporting vertigo or lateropulsion, which is the sensation of being pulled to one side.  

As you can see from this upper table on this slide, most of the veterans have been exposed to multiple blasts; most of them five or more, and several participants in this group reported hundreds of blast exposures.  It's difficult to identify the time since the blast exposure or mild TBI.  Instead, we ask the participants to share the time since the worst exposure or incident, and that’s shown in this lower table.  When we removed four participants who reported that it had been 20 years or more since the blast exposure or head injury, the range was six months to ten years, with the average time since the worst exposure, five years and nine months.

This bar graph shows the percentage of normal findings for ocular motor tests for each group, and the TBI blast group test findings are represented by blue bars and the control group by green bars.  Although a few participants in the TBI blast group had abnormal saccades—and that was typically low or slow velocity—most of the participants in both groups had normal findings on the ocular motor testing.

This bar graph shows the percentage of normal findings for tests of peripheral vestibular function for the TBI blast and control groups.  Interestingly, all control participants, and most of the TBI blast group had normal horizontal canal superior vestibular function, based on caloric and rotary chair tests.  A preliminary analysis revealed the cVEMP—the cervical VEMP—was the only peripheral vestibular test that was significantly different between groups.  These findings suggest a higher incidence of saccular inferior vestibular nerve dysfunction in the TBI blast group, compared to the control group.

These findings are supported by histological studies, and cVEMP studies in human and animals, that suggest that the saccule may be particularly susceptible to noise or blast-related damage.  In fact, if you examine the proximity of the saccule right here, to the footplate of the stapes, and the drawing on these findings are not surprising.

This bar graph shows a percentage of normal findings for several tests of gait imbalance for both groups.  These data represent four measures of gait and balance: the equilibrium score on the sensory organization test; the dynamic gait index, which is a clinical test that was developed to measure postural stability with changing task demands, such as head turns and pivot turns during walking; the functional ambulation profile, which is an integrated variable to provide a single numerical representation of gait; and the preferred gait velocity, which is based on age-normative values.

The TBI blast group showed a significantly higher frequency of abnormality on all the gait and balance tests, except this functional ambulation profile, which was the same in both groups.  I'd like to conclude with a case study of a 22-year-old male, who complained of imbalance and lightheadedness with onset one year ago.  He had a history of over 300 blast exposures.  He worked as security for an explosive ordinance clearance team.  He was diagnosed with mild traumatic brain injury and PTSD.  He had noise-induced sensorineural hearing loss that was worse on the right side, and constant tinnitus in both ears.

His ocular motor tests were within normal limits.  The caloric test revealed normal and symmetrical nystagmic responses.  The rotary chair test was within normal limits for gain, asymmetry and Phase.  These findings suggest that the horizontal semi-circular canal and superior vestibular nerve are intact.  Otolith testing revealed an abnormal cVEMP on the right side, with—which is consistent with a right saccular inferior vestibular nerve dysfunction.  In contrast, ocular VEMPs were present and symmetrical on both sides.  It suggests the utricle and superior vestibular pathway is intact.  The only peripheral vestibular abnormality was seen on the cVEMP, and suggested saccular or otolith involvement.

All measures of gait and balance were abnormal, so the SOT revealed an equilibrium score of 55.  He scored a 19 out of a possible 24 on the dynamic gait index.  The functional ambulation profile equaled 88.  We considered an FAP less than 95 as abnormal.  Finally, gait velocity was abnormally slow for his age.  

Where do we go from here?  First, we need to include otolith assessment for individuals with dizziness following mild traumatic brain injury and blast.  Most of the clinical settings across the country use tests of horizontal semicircular canal function only, and otolith testing should be a component of any clinical protocol for assessing dizziness related to mild traumatic brain injury and blast exposure.  We need to determine the functional consequences and effective rehab for individuals with otolith organ dysfunction.  

Most of the studies examining effective vestibular loss in postular stability have only included measures of horizontal semicircular canal function, so we don't have a clear clinical picture of the effect of otolith disorders on postural stability and gait.  Similarly, vestibular exercises that are used to improve gait stability are based on VOR dysfunction, and so it's not clear if those exercises are effective in patients with otolith organ loss.  

Finally, an underlying assumption in some of the literature is that the symptoms of dizziness or imbalance related to head injury or blast-induced overpressures are often due to central vestibular, or CNS involvement.  Our preliminary data in other studies however, suggests that central vestibular function, at least using ocular motor tests, is usually within normal limits in this group of patients.  We probably need a more sensitive measure of CNS abnormality to study the effect of mTBI and blast and dizziness.  In our ongoing study, we're collaborating with some investigators at Wayne State University in the use of experimental imaging protocols to determine the relationship between dizziness and imbalance on the CNS.  We hope to have those data available in the near future.  

Here are some references, if you are interested in further reading about any of the vestibular assessment techniques that I've described.  I want to acknowledge my colleagues in VA rehabilitation research and development for their support of our work.  Thank you for your attention.

*Moderator:*Jorge, if you are speaking, we actually can't hear you.  I think you may be muted.

*Presenter:*All right.  I'm here.

*Moderator:*Perfect.  

*Presenter:*Okay, so we'll get on to the second part, which is I'm looking at more related to research—current research we're doing on possible effects of blast in mild TBI on vestibular function, and so Faith did a fantastic job of introducing everything, so I can get right into it.  I have this poll question, just out of curiosity, as to what people think about.  Okay, looks like Faith set us up quite well.  Everybody's—there's a lot of concerned with otolith function, both unilateral especially, and then bilateral.  I'm going to now go into what we have found in some of our work.

Okay, so first thing I always like to talk about is what does vestibular dysfunction look like, and we don’t have—I don't have a human video, but I have a dog video.  Heidi, if you could play the video.  This is a dog after an immediate acute event, so what you can see in the video is clear—there's a clear head tilt.  The dog is having a very hard time even doing normal gait.  There's the leaning to one side, and so it's quite obvious that this dog has a vestibular issue.  Heidi, if we can stop that video.  

Now if you want to play the chronic video.  What happens after a dog—or after there's some time to adapt.  Here we go, same dog a couple months later, and what you can see is that even though, if you look closely, you can see this little—still has a little head tilt, and there's clearly not a fully normal gait.  The dog is really running around and doing things.  Okay, you can stop that video, too.  The reason I point that out is that one of the things that we have to be aware of is that there's a lot of compensation that's possible with vestibular loss.  Individuals may not look like they really have vestibular problems, but may have underlying problems that's not showing up.

All right, now let's wait till the slides come back up.  What we were interested in was when we look at underlying vestibular function in individuals that don't necessarily have clear symptoms, clear problems, would we find—but have a history of blast exposure and head injury—could we—would we actually see that they in fact, do have underlying problems.  We started looking at posturography and looking vestibular ocular reflex in this individuals to try to determine what level of vestibular dysfunction they might have.  Here is some posturography data that we did on a group of veterans.  We had healthy controls, which is the first bar.  It appears that the colors got screwed up a little bit, so the first part is—let me use the pointer here, okay.  

The first bar is the healthy controls.  Next bar is the healthy veterans, and then the third bar is the individuals with blast exposure-slash-possible mild TBI.  What we see is that if you look at the condition where they have somatosensory and vestibular, and vision, they're all doing great.  When we take away the vision and the somatosensory by having them conditioned by where their eyes are closed and they're on a movable platform, we see that there is definitely decrements in performance in both the healthy veterans and the healthy controls.  We see there's more of a decrement in the blast-exposed group, but there's quite a range, quite a stand deviation there.  

Again, when we look at the vestibular score based on that posturography, we see there's quite a—it's lower, but there's quite a range again.  We wanted to assess ocular torsion in this group.  The way we do that—if you can play the presentation video for me Heidi, please—is we actually look at—we do infrared images in the dark of the eye.  What you can see here is we can actually look at the features on the eye, and we can watch it as we tilt an individual back and forth.

Now, note this is actually seven minutes, this protocol, so they're being tilted really slowly, but there's an ocular torsion *[inaudible]* actually move—rotate within the socket.  You can see that feature is going back and forth with the tilt from one side of that line to the other side of the line.  We can actually measure that feature with software, and figure out how much of that ocular torsion they have.

Now we go back to the slides.  What that allows us to do is assess sort of how much otolith input they seem to be getting from that tilt.  The idea is if we're doing that in slow, plus or minus 20 degrees, they're not getting a lot of somatosensory information because it's so slow—and it's totally in the dark, so there's no vision—can we get an associated assessment of otolith function.  What we found that was really surprising was that when we looked at the ocular counter-roll during that, we found that in individuals that had no history of blast or head injury, we got about 0.12.  When we looked at individuals with just blast, but no associated head injury, we got slightly higher.  Then we actually got the highest level in those with both blast and head injury, which was very surprising to me.

We started looking at that a little bit more, and so we wanted to assess unilateral function.  Can you play the unilateral video for me Heidi please?  What we see in unilateral—to assess unilateral function, we put them on a rotating—a *[inaudible 00:32:42]* rotating chair, where they start spinning on center.  If you watch the earrings in this video, what you'll see is the earrings come out as the rotates up equally on either side.  Both ears are getting angular acceleration from the rotation.  Then we can actually slide the chair five centimeters, and you can see the one earring no longer is getting any angular acceleration, but the other ear is, which allows us to give a stimulus to only one ear at a time.  

We now slide the chair back the other direction, and you see now this ear is not getting any acceleration, but this ear is getting a clear acceleratory force due to the rotation.  This allows us to do an assessment of each otolith independently, the left and right otolith.  If we go back to the slides, what we found when we started to asses unilateral function in these same individuals was that this is an example of an individual.  What you see is—we look at the degrees of ocular counter-roll.  When the chair is on center here, so zero, what happens is—let me get the pointer, there we go.  As the chair goes off center by 50 millimeters or five centimeters, you get a compensatory ocular counter-roll in the opposite direction.  You can see it's about two degrees.

Then we move the chair from that, from the one side to the other side, and what you see is we get another counter-roll response, but now there's about four degrees of counter-roll on that side.  We come back, still around two degrees; come back, around four degrees; and then back and two degrees.  What you can see, this is an individual where they have twice the counter-roll on one side that they do on the other, so clear unilateral difference.  In fact, when we then take the –we look at that same data that we did from that sinusoidal roll tilt on that chair, where they're getting both—input from both otoliths, and we see that higher level of blast—or higher level in the blast/head exposure group—head injury group—what we see when we look at the unilateral centrifugation, where we just compare the best to the worst side, we find that it was similar in the group that had none.  It was similar in the group with just the blast exposure.  In that group that had had a blast and the head injury, what we found is there was a big difference from one side to the other, so there was clear unilateral differences.  

In fact, when we sort of plot these individuals as differences in ocular counter-roll between the sides—so if we look at the counter-roll as a percentage, what you see here is that lots of people were sort of below 30 percent in the none, blast and the blast/head injury group, but there was definitely a group of individuals—about half the ones that had a blast with the head injury—that had a big difference between sides.  That said to us that even though they had high ocular counter-roll when we did the sinusoidal tilt, they clearly had a unilateral deficit that wasn't coming out when we got that bilateral input.  

These long term effects of blast exposure are still not understood, but it definitely does seem like there seems to—there could possibly be some underlying unilateral otolith dysfunction, and so we were interested in working on some new treatments for that.  We decided to look at can we improve vestibular function, and so I'm going to talk about an unusual thing called stochastic noise.  

Is noise always a bad thing?  Right now, we have a famous picture, and normally, if I had an audience, I'd be like what is that picture of?  I'd let you guys guess.  If we add noise to that picture, it becomes pretty clear, that's Big Ben.  If we add more noise, it starts to get muddy again.  The idea around stochastic noise is your adding just the right amount of noise to improve your ability to detect the underlying signal.  In fact, in the interest of time, I'll kind of skip over—there's been quite a little bit of data that's used stochastic noise in other physiological systems.  

We decided to use it in the vestibular system, and the way I was thinking it probably works is if you look at activity in a nerve or let's say membrane potential in a nerve, and there's a stimulus that you put on it that will increase the membrane potential, but if it doesn't get to the firing threshold, the nerve won't fire and your brain will not sense that stimulus.  Now if we—just applying noise—and say this is noise.  It's a low-level noise that's going to change the membrane potential and bounce it around—it never gets to that firing potential, so it never actually fires the nerve when it's just operating by itself.

If we then add the noise on top of the actual stimulus, you'll see a base line when the noise is bouncing around; it's not reaching the threshold, so not firing.  Then when we provide a vestibular input that noise gets added onto that below threshold value that we had before, and now it bumps it above the threshold, and that nerve will fire, and you'll sense that stimulus.  It allows you to sense a stimulus that you couldn’t sense before, but does not affect your sort of base line function.  Does it really work?  

What we did is we did the same tile that I'd showed you before, where we were going—tilting back and forth, plus-or-minus 25 degrees and here's an example of one subject, where it had a very low counter-roll response, so you can see there wasn't much—less than one degree going back and forth during the tilt.  We applied the noise, which they can't feel because it's so low-level electrical galvanic stimulation.  We did electrodes over the mastoid process, and we applied low-level electrical stimulation, usually about 0.2 milliamps, and you can see in this individual there's a big increase in their ocular counter-roll response.  We got a much higher ocular counter-roll with noise.  In fact, you look at all of the subjects, what you see is, no matter what their base line ocular counter-roll or torsion was, that they tended to go up with the application of the stimulation, or that low-level stimulation they can't feel.

Some people had huge increases.  Some people had very little.  Some people had a slight decrease, which probably means we had the wrong level of noise, but we definitely could enhance that noise, and so the question is does that improvement in ocular counter-roll, or this vestibular ocular reflex result in functional improvements.  What you can see here again is a subject where we did Sham stimulation, so they thought the stim was on, but it wasn't.  You can see that that's the grey line, so you can see they had lots of sway.  Then this is the anteroposterior mediolateral sway.  Then we did stim, and you can see they had a lot less sway during that stimulation.  That same level of stim that we were able to improve ocular counter-roll, also reduced the area of their sway.  

If we look at the equilibrium score with their eyes closed on an unstable surface, we can see that when you compare the control condition of sham condition to the stim condition, there was a significant improvement in equilibrium scores with the stochastic noise stimulation.  There was also a significant increase in the stand time.

Based on that, we're going to have you guys pull again the same questions and see what you think based on what you're seeing so far.   That's good, so you can see.  What's really interesting about this, I think especially, is that neither Dr.  Akin or I had previously talked about our work until this webinar, and so we both seem to be finding this unilateral otolith dysfunction in this group that we were—or I'd not expected.  It definitely seems to be something to look for.  

Okay, since we're a little short on time, why don't we move on.  That definitely gives you an idea—you seem to get the idea.  Then, so in summary, the work that we've been doing here, is basically, we've been trying to assess whether there's unilateral otolith damage in these mild TBI flash blast exposure veterans, or veterans with blast exposure-slash-mild TBI.  What we are finding, it does seem to have—there is a level of unilateral damage.  We're finding it's pretty high so far, about 50 percent of the group that we've done so far; and that these deficits may be masked during these bilateral tests.  If we do a traditional tilt test to look at ocular counter-roll, if we do something that's really where they can use both inputs, we may not see it.  The unilateral test, like the unilateral centrifugation, or the VEMPs, as Dr. Akin was talking about, are sort of necessary for us to see these unilateral differences.   

We're working on a new application of subsensory galvanic vestibular stimulation that people can't feel—so it's completely subsensory, they don't know it's on—with a specific type of noise that may actually improve that vestibular ocular reflex, and balance—and my help alleviate some of the symptoms that the veterans with this sort of vestibular dysfunction, both bilateral and unilateral, may have.  

All right.  I think that is it.

*Moderator:*Okay, fantastic.  We do have some pending questions out here, but for the audience, if you do have any questions that came up, please type those into the Q&A screen in Adobe Connect, located at the lower right hand corner of your monitor.  We are just going to start going through the questions we've received now.  The ones we have now, I believe all came in while Faith was speaking, so Jorge, you can take a break here until those start rolling in for you.

*Presenter:*All right.  

*Moderator:*The first question we have here, a question regarding treatment for abnormal otolith dysfunction from a physical therapist's perspective.

*Presenter:*Yeah, that's a great question and we don't really know the answer to it.  Most of the—most treatment—most vestibular exercises are based on what we know about adaptation—vestibular adaptation in the horizontal canals.  We really don't know how—as much information about how the otoliths adapt.  We don't really know the effectiveness of traditional vestibular exercises for otolith patients.  One thing we know is these patients have symptoms that last a long time, and that's not a typical pattern in patients that have horizontal canal dysfunction.  It kind of suggests that there may be some other treatment because I think most of those patients probably would have adapted if it had been just involvement of the horizontal canal.  That's a question that we're asking and wondering about as well.

*Moderator:*Great, thank you.  The next question I have here, what would cause the lateropulsion in those patients with TBI?

*Presenter:*The theory would be—the theory is that whatever organ that is affected in the vestibular system, so if the canals are involved, then you would expect that the patient may experience vertigo because those organs sense head rotation.  In contrast, if the otolith organs were involved, a patient may feel like they're being pulled to one side.  They may also sense kind of general imbalance or lightheadedness, which is typically what we see with those patients.  It's kind of the classic answer or description would be that's a patient with an otolith disorder.

*Moderator:*Great, thank you.  The next question , what is the role of the vestibular cortex in these patients with complaints of dizziness.

*Presenter:*Yeah, that's a good question.  It's difficult to really test the vestibular cortex because it's primarily a reflex.  There's really not a good—there's not a test for that because if you map the vestibular response, a majority of it is brainstem.  Although there's some parts—there are some central projections, the majority of it is a reflex.  I don't know how you would test that at this point.  We're trying to look at some sites that we kind of are assuming that there may be some projections to in our imaging study, but it's been—it's a little too early to look at that data, so good question.

*Moderator:*Okay, thank you.  The next question that we have, since you are turning the head with the cVEMP testing, is it also possible that the positive finding implicates a cervicogenic etiology for the sensation of dizziness, since the other tests were normal?

*Presenter:*Yeah, that's a good question.  It could be anywhere along that pathway, so an absent cervical VEMP would be—could occur if there's any type of lesion anywhere along that pathway.  That pathway includes the saccule, projections to the inferior vestibular nerve, to the vestibular nuclei, and to the medial vestibular spinal tract, and then the accessory nucleus, and then the motor neurons on the sternocleidomastoid muscle.  Anywhere along that pathway that could disrupt—or a disruption anywhere along that pathway, could result in an absent VEMP, so sure, I think that is possible.

*Moderator:*Okay, thank you.   The next question, how would we separate psychogenic vertigo due to PTSD, and pure complaints of dizziness?

*Presenter:*That's a good question.  That's actually a question that we had—probably one of the motivating factors for this study for us because we know that with PTSD, dizziness and balance problems can occur.  If we looked through some of the studies that have been done, some—a lot of them didn't include objective measurements of vestibular function.  They were just questionnaires like symptoms of dizziness, or how that dizziness affected everyday life, which it's not that they're not important, but they're not objective measures of vestibular function.  I think the most important way to separate that is by looking at objective measures of vestibular laboratory tests.  

*Moderator:*Okay, great.  Thank you.  The next question, if the cVEMP is not available for testing, what is recommended to help establish the diagnosis of otolith disorders?

*Presenter:*That's a good question  I think it does take instrumentation.  I don't know that it would be very—it would be difficult to measure otolith function.  People have used static subject visual vertical, but that's not that sensitive to just otolith organ function.  It can also occur with central vestibular abnormalities.  Unfortunately, you really would need the instrumentation to measure vestibular evoked myogenic potentials, but the instrumentation is just—you can use commercially available evoked potential units.  Most clinics have those if they're doing like auditory brainstem response testing.  

*Moderator:*Okay, great, thank you.  The next question here, are any clinicians other than research, applying oVEMP and roll, tilt and centrifugation tests in their vestibular test battery?

*Presenter:*Good question.  I don't know—none that I know of.  

*Presenter:*Yeah, I think the—I'm not really familiar—now for clinicians, I know that—yeah, not really.  Some of them use it as an additional, but not as a standard test bat.  

*Moderator:*Before this next question, I just want to remind people that I am not a subject expert, and I apologize in advance that I am going to butcher what I'm going to say here.  The next question here, are cervical proprioception differences looked at all in SCM otolith saccule study?

*Presenter:*I think that might be similar to an earlier question that you asked about cervicogenic dizziness.

*Moderator:*Okay.   Yeah, once again, since I'm not a subject expert, you could ask the exact same question in two different ways and I'd have no idea.  If you want to skip that one because it was covered, we can go move on.

*Presenter:*Okay.  I’m not sure exactly, okay.

*Moderator:*The next question, you discovered VEMPSs—I'm sorry, you discussed VEMPs, but do you recommend the use of step velocity testing in evaluating otolith function, and is it as sensitive as cVEMPs?

*Presenter:*Step velocity testing really measures the horizontal semicircular canal VOR function, so it's an abrupt acceleration.  Usually the chair rotates quickly about the ya axis.  We do that, but not as a test of otolith function.  We use it as a test of horizontal canal function.  I don't know if you want to add to that, Jorge.

*Presenter:*No , I totally agree with that.  

*Moderator:*Okay, thank you.  The next question, how should I counsel my PT counterparts on how to treat these patients, meaning mild TBI patients with abnormal otolith test findings.

*Presenter:*Yeah, that's a good question.  I mean those are the questions that we're asking in our lab, and we really just need more work in this area, I think until we can answer some of those.  There's just not a lot of work, particularly looking at the effect of blast and TBI on otolith organ function.  It is an issue that I think particularly affects VA because of the population that we see here.  I don't have the answer.  I wish I did.  I'm trying to get the answer, but its taking a lot of time.  If colleagues were—if we had other people, like Jorge said, we had no idea that we were both looking at the same part of the vestibular system and finding the same thing, so I'm encouraged to hear that there's at least another lab that's kind of thinking about this and looking at some of the same things that we've been looking at.  Maybe we can answer that down the road.  Jorge, maybe you have an idea right now.  

*Presenter:*No.  In fact, I mean that's why we're working on this stimulator idea because we're trying to see if we can develop this stimulator as sort of a prosthetic device that would allow for improvement in function in those that have impaired function.   We actually just got a DOD grant to try to develop this as a restorative device.  Hopefully, in a few years, we'll have an idea as to whether this could be used as a long term treatment or not.  At this moment in time, I'm in the same boat.  I don’t have any great advice on how you can treat this.

*Moderator:*Okay, thank you.  The next question that we have, are you testing the oculomotor pathways in torsion when you say they are normal?  They would be abnormal in torsion if the graviceptive pathways are effective.

*Presenter:*We are doing a standard VNG, so we are checking the oculomotor pathways to make sure that they are functioning, and that the normal ocular control systems are intact, before we do the torsion, so that's kind of our double check, to make sure that there is proper ocular control.  

*Moderator:*Okay, thank you.  The next question here, are the effects you observed either decreased or exacerbated by comorbid psychiatric conditions like depression, panic disorder, alcohol use?  Also,  would you consider the effects you found to be biomarkers of the presence of mTBI?

*Presenter:*Was that directed towards me?  

*Moderator:*I'm not sure.

*Presenter:*Why don't you start?

*Moderator:*Yeah, I mean certainly we are currently also looking at PTSD, sort of to see what role that may have, which we haven't found has had a—thus far, have not found has a huge effect on the—from the ocular—from the otolith function perspective.  We are also screening our subjects to make sure that they're not—that they currently don't have alcohol issues.  These subjects were relatively healthy with a history of mild TBI, rather than being mild TBI patients that were having current symptom problems and all that kind of stuff.  That's why we were kind of interested in the group that might be compensated, but may still have underlying damage, and that might be part of the issues.  None of them had—we did measure depression, and none of them had depression.  

*Moderator:*Okay, thank you.  The next question here is directed to Dr.  Serrador.  Did you find any carryover adaptation or sensitization with the use of subsensory TBS over time?

*Presenter:*That's a great question.  That's part of our grant we just got.  We're going to do a six-week protocol to see whether there is any.  We have not found—so we found when we compare the sham control situation, it doesn't seem to matter as far as the improvement goes, whether we do sham first and then control, or whether we do control and then sham.  These are 30-second balance assessments.  What we find is—and the same thing when we do it within the chair, the ocular counter-roll, is that basically it seems to be an on-off kind of response.  When we turn it on, it improves the balance, it improves the ocular counter-roll.  When we turn it off, it goes back to its original levels.  

*Moderator:*Okay, great.  Thank you.  The next question here, what kind of hearing loss are you seeing with the subjects used in the study?

*Presenter:*Do you want me to answer that?

*Presenter:*Yeah, I think that's your question.

*Presenter:*Yeah, I can just tell you that we haven't—like I said, this is an ongoing study, so we just looked at some preliminary data just for this session.  I haven't really quantified that.  I just counted normal hearing—patients with abnormal hearing or normal hearing.  Most of them are high-frequency sensorineural—most of them are not severe, but yeah, noise-induced hearing loss pattern.  They're fairly young, most of them, so they're not—it's not usually a severe hearing loss, so mild to moderate high frequency sensorineural hearing loss.

*Moderator:*Okay, great.  Thank you.  The next question here, can we help provide patients or data for your research?

*Presenter:*What a great question.

*Presenter:*Yeah.

*Presenter:*That's great.

*Presenter:*Sure.  

*Presenter:*If you are in the New Jersey area, and you have patients that are interested in participating, you can look up the War Related Illness and Injury Study Center.  There's a 1-800 number.  They can certainly call and ask about current research studies, and we'd be happy to have them come in.  We don't really  have a travel budget that would allow us to travel people, but we—if they're in the local area—and I would encourage any of you that are interested in—if you have complicated patients that have chronic multi-symptom illness, that's actually one of the specialties of the center, and it is sort of a referral center, so you can send patients here for further workups if you like.  That's the War Related Illness and Injury Study Center.  Okay, Faith, now your turn.

*Presenter:*Yeah, so if you're closer to the Southeast, and you'd like to refer them to us, we're in the northeast corner of Tennessee.  If you're in Virginia, North Carolina, Kentucky, Tennessee, South Carolina area, please give us a call.  We have seen patients from as far away as Maryland.  Sometimes we can work out some travel arrangements.  

*Moderator:*Fantastic.  Thank you.  Now just for the audience, I know that we are at the top of the hour.  This session is scheduled until 15 minutes past the hour, but I know a lot of people are only able to take an hour for the session.  We are recording the session, and we will make that available in our catalog after the session today.  If you do need to leave, if you have another appointment, we are recording this, and we will have this available for you to catch within a few days.  Okay, the next question that we have here, how much more time will it take to perform these new tests on a per-patient basis?

*Presenter:*I can speak for—VEMPs are fairly quick.  They take—it takes the longest amount of time to place electrodes, and so maybe 30, 45 minutes for both cervical and ocular VEMPs at the very most.  

*Presenter:*If you have a rotating chair that has the capability to do the unilateral, it's—it depends—30 minutes to an hour, depending on sort of how extensive you want to try to do the unilateral testing, but around the same.  

*Moderator:*Okay, great.  Thank you.  The next question, were the subjects in these studies tested for overlying BPPV?

*Presenter:*Yes, in ours, yeah.

*Presenter:*Yes.

*Presenter:*None of our—interestingly, none of ours had BPPV, and that's probably because that's detected fairly early on, and treated.  Most of our patients were several years post the TBI or blast exposure, and so none of our patients had BPPV.  

*Presenter:*I have the exact same answer, yes.  None of ours had it, and same thing.  Ours are several years post-exposure usually, so they probably were treated if they had had it.  

*Moderator:*Great, thank you.  The next question here, was hearing compared with service entrance exams?

*Presenter:*No.

*Presenter:*We didn't do hearing assessments.

*Moderator:*Okay.  Next question here, is there a treatment protocol you suggest  for tinnitus?

*Presenter:*I'm not going to go down that road.  That's not my area of expertise.  There are many people that could probably answer that in the VA.  The person that you might want to contact is Jim Henry at the National Center for Auditory Research.  

*Presenter:*Yeah, I'm not an expert.  

*Moderator:*I know that we have recently had a couple of sessions on tinnitus, and that you can find those archive recordings in the HSRND cyber seminar catalog archives.  There should be some really good information out there about this.

*Presenter:*Great.

*Moderator:*Okay, the next question that we have here, was the incidence of tinnitus greater than other TBI patients without vestibular difficulties?

*Presenter:*We haven't looked at our data in that way yet, other than just simply what was the incidence in the TBI blast group.  I will say when we had designed this study, we were planning on having for groups of subjects, the control group, TBI alone, blast alone, and TBI and blast.  Almost all our subjects are in the TBI blast group, so we weren't able to really separate those like we had hoped we would be able to.

*Moderator:*Okay, thank you.  That actually is all of the questions that we have today.  I don't know if either of you—or Ralph, if you're still on the call—if any of you have any final remarks you'd like to make before we close things out today.

*Presenter:*No, just thank you to you, Heidi, for your help.

*Presenter:*Yeah, thank you so much.  This was very smooth and easy to do.  Thanks for handling my many videos.

*Moderator:*We do our best to make things run as smoothly as possible, okay.

*Presenter:*You did a great job.

*Moderator:*You guys did a fantastic job.  I have the easy part here, so—but for our audience, we really want to thank everyone for joining us for today's HSRND cyber seminar.  As I close the session out, you will be prompted with a feedback survey.  If you could take a few moments to fill that out, we would very much appreciate that.  We do pass all of that information on to our presenters, and I'm sure they would love to read your feedback for today.  Faith, Jorge, both of you, thank you so much for taking the time to prepare and present today.  I'm sorry about the hiccup the first time around, but things—it looks like things went very well today.  Thank you very much to both of you.  

*Presenter:*Thank you.

*Moderator:*For the audience, we hope to see you at a future HSRND cyber seminar.  Thank you everyone for joining us today.

*Presenter:*All right.  Thanks, bye.

*Presenter:*Bye-bye.

*Moderator:*Thank you.  

*[End of Audio]*

Page 1 of 17