Presentations on Cuba Health Attacks at SOFWERX-USSOCOM)/J5 Donovan Group Neuroweapon Event on  2018-08-21


Dr. James Giordano




Full transcript of presentation


“Embassy Encephalopathy”: Induced Hearing Loss, Cognitive Dysfunction and Neuropathological Changes - Possible Causes, Mechanisms, and Effects


James Giordano PhD

Departments of Neurology and Biochemistry, Georgetown University Medical Center, Washington, DC, USA


First and foremost I want to thank Lieutenant Colonel Snow for inviting us, certainly the rest of my esteemed colleagues, Drs. Hoffler, Balaban, Canton. Thanks very much to SOFWERX for having us down. Will be back here again in January to spend some time with you. My training, I'm a neuropathologist, I've been doing neuroscience for about 38 years. Very often my colleagues like to call me and jokingly we addressed us this morning, a disruptive neuroscientist because I work in the area primarily of the way neuroscience can be utilized for a variety of different purposes not all of the medical. And certainly on the medical side you can do two things. You can help or you can harm. You can withdraw certain types of care and that can be harmful or the very same things that work on a biological and physiological system through a variety of different anatomical sites can be inductive of things that are at least burdensome, if not threatening and harmful, I d’say probably what we've got here. So as you heard from Dr. Hoffler, he got a call early in 2017 that said “this is Department of State, we've got a problem”. In the middle of 2017, I got a call from Department of State saying “Dr. Giordano we've got a question”. “And the question is what do you think we're doing here, what do you think we've got here, we've got this set of findings and apparently this is going to be some type of problematic issue.”


My work is fairly well known for the term "neural weaponology." Back into 2006 and 2007 we developed a paradigm by which neuroscience could be weaponized and we assessed that on the world stage. In 2008, the National Academies National Research Council came back and said: “You know brain science really is not ready for primetime”. That was a misnomer. Our work in 2009-10 and the work of the Nuffield Council in 2013 demonstrated that not only was brain science viable and a value to be weaponized but in many cases it was already being weaponized based upon older technology that was now taking updates and being put increasingly into a variety of circumstances that would yield individuals to be in harm's way. We're beginning to see a little bit more of this and perhaps this is what we're seeing here. I want to start out with that premise because I'm not gonna point any fingers. I'm not going to make any accusations. However, what I want to do is to work with two things: the explicit findings and the implications those findings give rise to. Particularly in light of the fact that by 2014 the National Academies and National Research Council reconvened and demonstrated that not only were the brain sciences viable but they were in fact of high value and were in use globally as neural weapons.


Characteristically, we take a look at neuralweapons as what we think of is drugs, bugs, toxins and devices. Not all of these things will work directly in the brain, very often they will work on the peripheral nervous system or on the neurosensory organs to then have a feedback effect that are going to disrupt the process of cognition, emotion and behavior. What I want you to remember is that these are not weapons of mass destruction, these are weapons of mass disruption. Where the disruption can be on the level of the individual and then creating a ripple effect not only on that individual and their cohorts but on larger scales socio-economic scales. Geopolitical scales, military scales, keeping that in mind it's very very important to determine a pattern of use with the implication being that something's going on here and this was probably, very probably not an incidental event. Now, could it have been? Yes absolutely. What is the likelihood of that? Think about it. So if we're talking about things that go bump in your brain, there's a lot of different ways to get into your brain.


The primary findings as you heard from Dr. Hoffler were primarily autological findings and vestibular findings, things that happen in the ear and there are two terms I think that become important for you to understand. The first is the idea of otopathology which is there's something wrong there and the second is that this may be adduced to some toxic event. The initial thought was perhaps these individuals were exposed to some compound either an environmental compound or an intentional compound that then caused some type of pharmacological or chemical damage to the organs of the inner ear, whether that organ was the hearing organ, the cochlea or the organs of balance and orientation which are the semicircular canals, the saccule and the ampule. There are a number of different drugs that could do this. So we know that there are certain things that were called damage to the ear, structural damage to the ear, a blow, a pressure wave. There are certain drugs that can create a toxic effect in the ear or components of the ear and what these will then do is they'll affect a variety of the components inclusive of the nerve that emanates from the ear and goes into the spiral ganglion and then up into the brain.


So the idea of an ear brain connection is not far into this type of otopathology and ototoxicity. What are the various signs and symptoms: hearing loss, tinnitus, vertigo, disequilibrium, nausea, visual features, such as nystagmus and oscillopsia which you heard earlier. And then certainly a whole different types of headache and or disruption of cranial functions. There was not only headache but facial pain, unusual sensations and then a loss of attentiveness and cognitive functions that can be accompanying this. Next slide please. What type of things can do this? What type of agents could do this? Well, certainly if we take a look at just defining these into two major categoricals, we have drugs and devices. The drugs that could do this, I have listed for you. The likelihood of this being a drug-induced event is very very low. The reason for that is that the drugs would have to be given repeatedly. Characteristically, I'd have to be giving you the spiked doses that would have another host of effects, we call a constellation of effects. This would be notable and you wouldn't tend to see uniform effects based upon the way the drugs were given. In other words, drugs being given in different doses, at different times might manifest distinct effects in different people but also not had this particular pattern of presentation. So we can take the drugs and say: of those that we would say we're probably most notably those that are anti-tumour drugs like cisplatin and carboplatin. And probably the organic solvents. Once again these drugs are highly toxic. There'd be no way these individuals would present with this symptom alone and not present with another cascade or constellation of symptoms that would be indicative of exposure to these agents.


[5min56s] Which then brings us down to the idea of devices. What type of things could it be.


Well, it could be subsonic stimulation, it could be ultrasonic hypersonic stimulation. it could be a combination of both or it could be some type of microwave or electromagnetic pulse. The idea is that it could be all of these things. These are not mutually exclusive and very often devices can in fact be manufactured that will combine one or more of these different types of phenomenon to induce a percussive effect. This is not foreign as well. We understand that during the 1970s and 1980s a number of countries were examining the idea of electromagnetic pulse devices, sonic devices. Some of these have gone sort of mass-market production, some of these are commercially available even today as Dr. Balaban will illustrate to you. These are purchasable direct off the shelf. Moreover, we know that there have been a lot of dedicated efforts by nation-states and including from non-state actors that have tried to get work in this area, primarily to create weapons of mass disruption. And we see these being used for example with varying success on crowds, small aggregates of people and against individuals. But the problem is, very often, the older technology required fairly large-scale devices to implement this. However, with the sophistication of the tools that we have, we're now able to see this being shrunk down like so many other things. I'm looking at an audience of group of people, a variety of ages. Remember those first cell phones at about the size of a Volkswagen. We felt really good, “yeah I'm on the cell phone” you have to hold it like this. Now take a look at the size of a cell phone. What we see is compartmentalization and shrinkage of technology that increases its viability and utility of application. Next slide please.



[7min23s]This is where we're talking about. Ladies and gentlemen, welcome to your inner year. So if we're looking at the ear, take a look at a slot on the upper left, what we see is that the ear basically has an external meatus, this thing out here and then there's a canal. There is a membrane which is the tympanic membrane, the eardrum to which are connected a series of bones which are called the ossicles. These things will move with a particular stiffness which will then intrude on to the hearing organ which is called the cochlea. So there are really two components of what the ear does. First is that the ear hears naturally. However, we also have to understand that the secondary component of what the ear does is the organs of balance and orientation. These referred to as the vestibular apparatus and they include the semicircular canals or the three looping canals and the saccule and ampule as you see here. Now, these are highly vulnerable organs to a number of different things. They're vulnerable to heat, they're vulnerable to pressure, they're vulnerable to sound. They're also exceedingly vulnerable to any other form of disruption that then caused a head trauma. So it's not unusual individuals have a jaw fracture or a mandibular fracture, maxillary fracture that very often you'll see secondary symptoms occurring as a consequence of inflammation. I'd bring that to you simply to tell you that these are exceedingly small structures that are exceedingly vulnerable to a variety of different injuries and insults. Moreover, take a look at the structure of the inner ear. The inner ear provides a mechanism by which a variety of different pulse stimuli can be amplified. Now, if we're looking at where damage can occur particularly with regard to hearing loss, we're mostly looking at this larger organ here called the cochlea. It's a semi-stiff organ, there's fluid in the middle and we know that various types of auditory stimuli can disrupt the cochlea and its function, sheer the hair cells, induced damage. You would see hearing loss with that. Next slide please.



What types of pathologies would you see, you'd see inflammation both locally and then more distally, you see hair cell damage and hair cell death. These are the organs for example in the cochlea that are sensitive to disruptions of the membrane that then transmitted, transduce the necessary stimuli for hearing. You would see membrane scarring and any of the membranes that were affected. You ‘d begin to see neurological damaging. Realistically, we know that we begin to see neurological damage as a consequence of two things. Number one, that the nerve itself is directly damaged, because of some insult to the nerve. Or number two, we then begin to see is if you're damaging the sensory organs of the inner ear you're seeing changes due to what is called excitotoxicity of the nerve. In other words you're overstimulating that area of the inner ear,you're hyperstimulating the nerve, as the nerve becomes hyperstimulated, you then see a disruption of neurological calcium and with the disruption of calcium you then get something called excitotoxity. Once that nerve becomes excitotoxic, characteristic is to be giving to see changes occurring upstream. This is just basic neuropathology. Next please.



What type of things can do this. Well, again a host of drugs could do these types of things but we have to rule these out because we're not seeing drug like effects. Number one. Number two, we didn't see a constellation of signs and symptoms from these individuals that would be suggestive of some type of pharmaco-toxicology. And number three, the long-term effects really do not match what you would tend to see with either cisplatin or organic toxins. So as a consequence of that we can rule this out. Some of the early hypotheses were well perhaps these individuals were exposed to one or more of these compounds either directly or indirectly. Is it possible? Yes it is possible, might this have been a beta test where there was some priming or synergistic effect where individuals were exposed to low doses of these drugs? Yes. But these drugs were non recoverable as well. Moreover that didn't seem to be any other physiological signs that would suggest that these individuals received a high enough dose of these drugs to do the job. So we can rule these out. Next please.


"Mechanisms of Effect

"Sub-/Ultra-sonic Stimulating Devices"

"Pulsatile/tonic delivery of inaudible sonics"

[10min52s] What about sonic devices and/or electromagnetic pulse and microwave devices. Well, there's a number of different things that could be done here. Realistically, would you see is either pulsatile or tonic delivery of either sound pulse, particular a hypersonic pulse that would begin in the subsonic then translate through the sonic and into the hypersonic range. And/or you can engage some type of electromagnetic pulse, microwave pulsing that could then affect these symptoms in a very similar way, these signs in a very similar way. You would get over stimulation of hair cells, clearly with any type of sonic delivery. You would get hair cell fatigue breakage and death, you would get scarring and denervation.




[11min27] But you would also see that if in fact it was a hypersonic pulse and/or an electromagnetic pulse. You would then begin to cause cavitation in anything that has a fluid medium in it. Which would include any one of the vulnerable organs of the inner ear, the cochlea included. But most notably those that would concentrate this type of an energy pulse mode most directly. In other words, an acoustic or an electromagnetic lens. Are there structures of the inner ear that can do this. Next slide please.


The auditory features you would see if we're just limited to the auditory system would be these.

Note - Slide description:

High frequency hearing loss (~4000 Hz “muna”)

High to low progression  (3-6 KHz spread, with < 1KHz spread)


However this was not noted as you saw in the earlier data. We're ruling out the idea that this was just an auditory assault. Next slide please.


So if you're going to engage the diagnosis for this and you're thinking, well, could there have been some means with focused energy that would then produce the signs and symptoms that we're seeing in these individuals with the statistical significance as was demonstrated here. What might be the viability to do such a thing. Well, you heard that audiological testing suggested that indeed these individuals were exposed to something but there's no long-term audiological or hearing changes. Pharmacological, toxicological recovery early on did not demonstrate that there was in fact any toxic substances or pharmacological poisoning. Cochlear imaging is difficult to do. Biopsy and forensic anatomy can certainly be done after the fact but your most reliable tests are those that are used in neurosensory defect. Those tests that as you saw earlier will determine the function of those nervous systems that are involved, in vestibular apparatus, balance, orientation and position. And in fact that's exactly what we saw. However, there also seemed to be some mild cognitive changes that were initially somewhat high and then tapered off and then some that were a little more progressive and that were more persistent. Is it possible, as you heard earlier, that the primary effect was localized to the inner ear and you're seeing secondary effects, what we call sequelae, with the individual's levels of cognition and emotional challenge then disrupted by the fact that they were highly vertiginous?


Yes, absolutely. I mean look, in a previous life, I flew airplanes for a while. And I got to tell you I mean one of the things that happens if you put individuals in a spin or an unusual altitude, it is exceedingly disorienting. Pilots and aircrew are trained to be able to function cognitively and with emotional stability and unusual environments that disrupt their positional sense. You recognize that. One of the most curious phenomenon is when an individual is exposed to either spinning or tumbling, very often what you'll find is cognitive deficits that will persist for several minutes to hours after that exposure. The longer the exposure, the longer the cognitive deficits occur. What type of cognitive deficits? Most notably with regard to information transfer, information assimilation and synthesis and the ability to then process information in a proactive way. And if you think about it, it almost makes sense. As you heard earlier from Dr. Hopper. It obtains. The issue here is simple. If I have to concentrate very very strongly on orienting my environment to what is up and what is moving around, it becomes exceedingly difficult to do anything else. We can tell you that one of the things we use very often is something called a branny chair. We'll put an individual on a spinning chair and then we'll ask them to do various tasks both during the spin and after the spin. And they become so disoriented as a consequence of loss of their vestibular senses and their positional upright and/or processional surround that their cognitive capabilities seem to be grossly, grossly impacted. Almost to the point that you are now saying this is a cognitive, a full cognitive defect? Now clearly when everything returns back to normal for these individuals, the cognitive defect then tapers it, diffuses it or damps over time.


But you do see similar phenomena with regard to cognitive blunting and cognitive defects in individuals who have profound Meniere's disease, which is an inflammation of the inner ear that then causes vestibular and semicircular disruption. Not only these individuals are positionally disrupted with vertiginous defect and dizziness, but they're also cognitively disrupted because the ability to process information inclusive of things like upright orientation, interactions with others then induces as the neuroscientist Antonio Damacio says a feeling of “what happens”. It is anxiogenic, it produces anxiety. If you've ever been dizzy, if you've ever had vertigo, you know that this is a very unsettling experience. And the phenomenon of that itself can be cognitively blocking. So could this be focused to the inner ear as a primary pathology, that then caused a secondary reactive or manifest changes in individuals ability to process and engage cognitive information transfer and capability? Yes, certainly it could. But could it be more, could it be that in fact you are also seeing an indirect or direct effect on the brain itself? Next please.


[15min59s] This is the idea of targeting the brain by accessing the periphery. Is it possible that what we're seeing here is not only a form of traumatic neurological injury to the ear but a communicating neurological injury that was then able to evoke indirect or direct effects on the brain? How might that happen? Well, again, there are a number of different things that can do this. We've talked about a variety of different pharmacological agents that co-present with some initial ototoxic or auto pathologic effects but realistically are working more in the central nervous system. But once again we can rule these out. The reason being is we're not seeing the recovery of these agents in blood, lymph, cerebrospinal fluid nor are we seeing the constellation of effects in the brain that would be reflective or indicative of this type of pharmacotoxicology.


However, if we then focus more on the devices, there are a number of different things that could work on the brain directly and/or affect the brain indirectly by working through one or more of the sensory portals. These include sonic generators, electromagnetic pulse generators and although not necessarily pertinent to this discussion, something I do want to bring to your attention is nanoparticulate matter and this is becoming increasingly a problem because as Jen Snow and I are working on this is now aerosolysible. The idea of aerosolysible nanobots has become a reality. So the idea of being able to utilize nanoparticulate matter as a neuroweapon now has become in fact real.


[17min25s] What are the possible mechanisms of effect? Whereby you could get an indirect or direct action into what's called the supratentorial space. The space above the tentorial membrane essentially the brain. Well, I think one thing it becomes exceedingly important to understand is that the brain is bathed in fluid, this is called cerebrospinal fluid. The brain is protected by a set of membranes, called the meninges and the meninges are basically threefold. The outermost and the most durable is called the dura mater. There's an in-between membrane that looks very much like the articulations of a spider web and in fact it's called the arachnoid membrane and it is filled with fluid called subarachnoidal fluid. And then this interfaces directly with the surface of the brain which is called the pia mater, the dear mother literally. That layer right on top of the brain is very very thin. The area of the subarachnoidal space is also a very richly vascular area. So what you now have is blood vessels that are interfacing with a fluid space existing in this kind of padded zone that looks like a spider web. So that particular structure itself might lend itself to some type of pressure-damage, inter-cavitation damage if we're looking at the meninges. But it's pretty hard to get those kind of waves at that level of effect through the skull. But what happens if you didn't have to go through the skull. What if you could go in the side door. What if you could create a pressure wave that was amplified through peripheral structures, that could then be communicated directly up into the brain. Essentially, what you're doing is now you don't have to storm the castle to go through the walls, you can literally sneak through the side doors and then go up to the parapets.




Image: Inner ear - Brain. Slide by Dr. Giordano.


[18min54s] Let's go back to the inner ear. This is the inner ear. This is the brain. One more time. This is the inner ear, this is the brain. They live right next door to each other, they communicate, they communicate primarily through this region here. And this region here is called the ductus reunions. And this area here where there's an actual communication that goes from the inner ear space that contains fluid called perilymph into the brain is called the cochlear aqueduct. It is an aqueduct. But what I want you to take a look at is the size differential between this fairly large vestibular space, would be basically called here as the foraminal area, the opening area, sometimes referred to as “the foyer” and the brain space. See the tube? This tube essentially, works as a venturi, it communicates fluid between these two spaces. One of the things we worry about for example for an inner ear infection is the communication of that infection into the brain space that then would produce a meningitis.


[19min56But if we create a pressure wave here, we can disrupt the internal structures in two ways. Number one, primarily by amplifying it through the Venturi effect of creating cavitation in this structure here called the ductus reunienswhich then affects the sacculethe ampulus here, the utriculusAnd/or by then creating an effect that would then communicate upward into the brain space by creating a cavitational wave that goes up through the cochlear aqueduct directly into the cerebrospinal fluid.


Now recall the cerebrospinal fluid bathes the brain. So what you would tend to see is injuries that occur in around the space beginning here, that could then cause a more disruptive effect as you actually disrupt the flow of this fluid. This fluid moves. Any in cavitation this fluid is going to be disruptive and it can create something which is known as “communicating hydrocephalus”. So now what's happening is you're actually getting a change in the level of the fluid because of bubble expansion, bubble collapse. This continues to communicate, it doesn't disrupt the flow of that fluid, but it can produce neurological sequelae, both short and long-term. The other thing that that can then do is that can produce a lot of change in the way the brain resorbs its blood flow, because this particular mechanism also affects the way blood is exchanged between the brain space and the vascular space. But the vascular space is also a portal by which peripheral disruption can then lead to central disruption. Next slide please.


"Mechanisms of Effect

Focused cavitation in fluid media | Perilymph - Sub-arachnoidal media"

[21min11s] So clearly if we're looking at the paralymphatics we can see that once again disruption of the paralymphatics, as we said earlier, can communicate into the brain space. It can also communicate up here into the subarachnoidal space because we know that the paralymphe will communicate with the CSF via that particular aqueduct. But once again we have blood vessels that are embedded within this subarachnoidal membrane that then interfaces directly with the substance of the brain. If we disrupt that fluid around the brain, could we then create a disruptive pressure wave by cavitation into these blood vessels, that would then be communicated into the brain space by both the paralymphatic CSF communication and the blood space? Yes we can. These things are essentially talking together. Next slide.


"Mechanisms of Effect

Direct and/or Communicating Effects"

[21min56sSo if we look at these communications what we can see is that any type of communication here into the subarachnoid space is capable of inducing a variable pressure wave, a cavitation wave, inclusive cavitation damage at a variety of different brain locales. We know that one of the things that this can then do is that can actually disrupt the integrity of the tissue because you're now increasing two things: number one, localized pressure, which then actually creates a traumatic event, which can then lead to axonal shearing and vascular effects which can then disrupt the blood flow to the brain. Disrupt the blood flow to the brain can then lead to microhemorrhagic infarcts, small level blood blood flow disruption, small areas of necrosis in the brain and this would then be more long-term. So clearly one way we could affect the brain through the inner ear is through the fluid medium that occurs via the inner ear directly to the subarachnoid space affecting the fluid medium that surrounds the brain and thereby causing a disruption to the brain structure directly.


Mechanisms of Effect

Focused cavitation in fluid media: Blood


[22min47s] But we can also affect the blood. And there's a number of different ways we can affect the blood. Certainly we can engage the inner ear and most of the pathology we're seeing here with this embassy encephalopathy would suggest that the inner ear provides for us an acoustic or some other form of energetic lens. This is going to concentrate this type of information creating disruption primarily in the vestibular area in and around the foyer that would then affect the saccule and the ampule. This would then disrupt the function of the inner ear, this could produce a cognitive constellation but at the same time could have a secondary disruptive effect, where it's now creating a cavitation wave that spreads throughout the paralymphatic fluid, communicates via Venturi effect up into the cerebrospinal fluid space, disrupts the flow of the cerebrospinal fluid in the subarachnoid space and thereby can also disrupt the vasculature.


But could you disrupt the vasculature directly, could you incur cavitation changes in some area of the vasculature that's going to affect both the inner ear and the brain? Oh yes you can. This is the area in and around the inner ear and what we can see is that there is a direct concentration of blood vessels - once again take a look at the upper left-hand portion of the slide -  this shows the arterial supply to the inner ear, the utricle and the saccule. This is supplied by the anterior vestibular artery which forms a direct connection to the basilar artery which then communicates the cerebral arteries, most notably the middle cerebral artery. The middle cerebral artery branches up into the brain and has what's called here as this lacunar effect, in other words through these deep penetrating arteries that go into the brain space. These are exceedingly small vessels and the concentration of pressure within these vessels is exceedingly important to maintain a variety of neurological responses and cerebral vascular responses. These things will change as a consequence of local pressure and they'll alter the blood flow to maintain stable pressures across the brain space. Brain is highly vulnerable to these types of things. But if you disrupt the flow of arterial blood, you're going to get two things. Number one you get a compensatory arterial response and going to see changes in perfusion that'll occur in the vascular site. If this occurs as a consequence of bubbles what you are essentially producing here is microemboli. Can the microemboli lodge here in these lacunar vessels to create lacunar infarcts, microstrokes? Yes indeed they can. Can you get disruption of the brain space directly by disrupting the arachnoidal membrane, by disrupting the fluid that exists in the arachnoidal membrane by disrupting the fluid of the paralymph in the ear? Yes, you can. Can you do both at the same time? You betcha. What would the effect be? Well, clearly, if you're disrupting the inner ear directly by affecting the foyer, by affecting the utricle and the saccule by virtue of a pressure wave that then creates some type of cavitation within those structures that are fluid filled structures. You are going to disrupt, otolithic effects and you're going to get a change in the balance organs and balance function. Could that lead to problems with regard to cognitive processing? Absolutely. But based upon the structure of the inner ear could you also then begin to cause neurological changes and neurological damage? Yes, that's a possibility as well. You could certainly begin to cause degenerative changes at the innervation of the inner ear that could communicate along the cranial nerves, then have a neurodegenerate change. Is this easy to determine? Not necessarily, but certainly it could be done by virtue of certain types of imaging and certain types of nerve conduction velocity testing.


[25min59] But what if he didn't have to affect the nerve itself and you can get directly into the brain. The same pressure wave that would affect the utriculus and the saccule could indeed create a pressure wave with inside that foyer that would affect two components that would directly and indirectly assess the brain. The first direct effect being the communication through the paralymph of cavitation disruptions that then enter through the cochlear aqueduct to profuse the subarachnoidal space and cause a disruption in cerebrospinal fluid. And the second which would be a disruption of the vasculature here in the arterial blood supply that would then communicate back to the basilar artery and communicate up with cavitation in the blood flow to the brain. So what you see here is converging pathologic effects. Disruptive pathologic effects. Next slide please.


How would look to assess these types of things. You've already heard this, I'm not going to repeat the information. Dr. Hoffer’s group did a wonderful job in neurocognitive testing, neuroimaging, Clearly if you wanted to look a little more deeply, you have to take a look at some of the forensic anatomy (...). But you could also model some of this work, vivo, in vitro and with computer simulations. Which becomes probably the most accurate way to take some simulacrum in a phantom or in some other type of situation that would then model what these effects would be on the mammalian ear and on the mammalian brain. Of course for that our next speaker Dr. Balaban will discuss some of the work that he's done to empirically demonstrate what these findings not only are but could be based upon not only a type of image we see here or the type of image that we would then see if you were to increase the frequency or change some of the electromagnetic pulse. And next slide please.


[27min27s] So based upon that, what's the take-home messages I have for you. Like anything else let's go through a process of elimination. We have to go about this somewhat deductively. Because we have a set of individuals who've suffered this particular constellation of signs and symptoms and we recognize that from that these are the things we're seeing. What types of changes could we be seeing in the peripheral and central organs, neurosensory organs and in fact the brain that might be indicative of this and what could do it. Is it possible that drugs alone could have done that. Well early on in our discussion we ruled that out. Is it possible that ultrasonics could do this. Yes this is very likely and highly probable. Is it possible that electromagnetic pulsing, microwave pulsing, in some way could do that. Very possible, highly probable. Is it also possible there may be some combinatory approach, a beta test if you will to see if we give drug first at a low dose or ultrasonics at a low dose coupled with some type of electromagnetic pulse, microwave dosing in some combinatory form, could these be worked. Quite possible with very positive explanatory value.


In other words if someone put a gun in my ear and said which one do you think is going to produce this constellation of effects that we saw in those individuals who are most affected not only in Cuba but more recently in China, I would tend to think that what you're probably finding is this last one. Whether or not drugs or some other form of pharmaco-toxicologic agent we use I think remains dubious. But certainly there are devices that are widely available that we also have know have been dedicated activities in the neural weapons space by a variety of nation states. They would be capable of doing just this type of thing. The inner ear provides a locus forum for this to then be conducted in such a way to manifest these effects, but it's not the inner ear alone. It could occur through the sinuses both the ethmoid and the sphenoid sinuses. It could occur through the hard palate of the mouth. Any one of the vulnerable amplifying spaces of the head could do it and certainly what becomes important is how such a weapon could then be focused and utilized in those ways to be able to create this effect. Might it be once again that this was something it was serendipitous, sarcastic, that this was some type of vermin protecting agent or device that was simply in those rooms which these individuals were then suspect. Perhaps. Is that likely? Not very. The reason for that would be that many others would have these signs and symptoms, for one, number two there would be some engineering artifact which would then be attributable. Here's the device, this is what was being used for and there would be an attribution or custodial record for that. Absent that, once again by virtue of implication, this is intentional, this is directed, there seems to be a beta test of some type of a viable neuroweapon that utilizes one or more of these modalities for its effect. Next slide please.


That's all I have for you. Clearly what I'd like to leave you with is speculation. Speculation based upon the facts of the case, speculation based upon what we know about the weaponology and or at least the device-ology. Speculation about what we know about what the pathology is and could be and how this would work. So what I'm asking you to do is something quite simple. Take the facts of the case based upon the findings that were presented to you by Dr. Hoffler. Want you to take the level of possibility and probability in terms of what the viable structures are that could communicate such effects in real life terms. And then pair that if you will to our next set of speakers will not only talk about what the empirical findings are that could reproduce this in a model scenario, but how this could also be leveraged geopolitically with regard to the viability of an increasing capability confidence in consideration in neural weaponology. Thank you.




Dr. Michael Hoffer




Full transcript of presentation (derived from the transcript of the full length video).


"Acute presentation of an acquired neurosensory syndrome"
Hoffer M., Levin B., Snapp H., Burkirk J. and Balaban, C.
University of Miami, Miller School of Medicine, University of Pittsburgh


“First of all I'd like to thank the Donovan group, SOFWERX, SOCOM (USSOCOM J5) and the group for inviting us to speak. This is a very important topic and we're honored to be here and present today. So thank you very much. So these are the author affiliations for the group, these are the views of the authors, not the views of the government, not the views of the Navy, not the views of my University. So in February of 2017, I literally got this call: "this is the State Department, we have a problem". So what happened was individuals began experiencing symptoms - late in 2016 - of ear pain, tinnitus, dizziness and cognitive issues. The profiles were: all experienced a loud noise or pressure phenomenon before and during the symptoms. All were members or family members of individuals stationed with the U.S. diplomatic mission in Havana Cuba and the sound was localized and followed the individuals. In fact, if they opened the door to the outside the sound immediately went off.


So thirty five individuals who were symptomatic or at risk were evaluated at our facility, at the University of Miami. Twenty five who were exposed and had symptoms and ten who were not exposed but lived with the individuals who were exposed and were in the houses when the individuals were exposed. We also saw a hundred and five unaffected Embassy members. We evaluated those people in Havana. They were largely selected by the Embassy to see us, however we did ask to see all the Marines who are assigned to the Embassy detail ourselves.


So all the individuals at University of Miami underwent a standard history and physical with an additional targeted neurologic history and physical. They all had eye movement tests that included tests for a nystagmus, smooth pursuit, saccades and anti-saccades, optokinetic response and vergence responses. They all had standard audiometry and then a subset of individuals had additional vestibular testing and additional neuropsychological testing. We were seeing these individuals as patients. Only clinically relevant data were collected and all testing that we did had to be justified and approved by insurance. New individuals we saw were acute and unaffected by the influences of time, variable pre-treatment modalities, compensation - they weren't seeing us for workers comp - and media attention. So when we saw the individuals they did not know what they were supposed to be presenting with, because at that time the media had not publicized what the effects were. So they came to us without the ability to “kind of know” what they should say.


The prevalence of the symptoms in the unaffected groups and the affected group were analyzed with a two-tailed Fisher's Exact test, this is going to be explained, going to be used in the following slides and due to the non Gaussian distribution we used the lower fifth percentile, and the lower one percentile of performance to judge abnormalities. And this is up there because there's been a criticism that some of the tests that we're going to present, people that have anxiety or people that have other disorders have these abnormalities. But not to this degree. So that counters that argument. This is a population study in 140 total,105 in Cuba and 35 in Miami distributed as I reported earlier. So here is the presenting symptoms of the groups. So the affected group you can see, they had a lot of, a great number of them reported dizziness. This is reporting when they saw us in Miami. Cognitive disorders in about half. Hearing loss in one-third. Tinnitus one-third. Ear pain in 20%. And none of the ten individuals who were in the houses at the same time but were not affected had any of those symptoms. In fact, except for headache which is a common symptom in many individuals, the affected group had statistically more symptoms than the unaffected group. Notice said again 96% of the affected group had at least two symptoms and 64% had at least three symptoms. Again, symptoms being dizziness, cognitive disorders, hearing loss, ringing in the ears, pain in the ears or headache.


This is the data by group of the 25 affected individuals. So now we're not talking about the ten that weren’t affected, the 25 that were affected. 88% of them had an abnormal subjective visual vertical testing, 52% of them had abnormal anti-saccade testing, 83% had Chair impulse testing. You can read the slide yourself and 92% had at least one VEMP abnormality.


And let me explain: subjective visual vertical is a test where individuals are told to take an object that's off-center and make it point straight up. Vestibular Evoked Myogenic Potentials (VEMPs) are tests that explore how the organs of gravityception both either the utricle or saccule, how they respond to sound. If you have an abnormal VEMP or an abnormal subjective visual vertical it's telling us that the organs of gravityception, which are the utricle and the saccule, are affected. So what we're seeing is that if you take the subjective visual vertical and the VEMP data, every one of the affected individuals, all 25 of them, had at least one test that was abnormal telling us that their utricle or their saccule in least one year were affected. So the organs that tell you that you're up and down were affected universally in this population. That set of organs is extremely important because that gives you a perception of where you are in space. Not where your head’s turning but how your body is oriented to gravity. And when these organs are affected, when these organs are abnormal in this population and in other vestibular populations, individuals are severely affected. Because if you don't know which way up and down is, you're not really good for anything else. So these are the definitions, again you can read them, but what we want to point out is that we're taking abnormalities that are extreme. So subjective visual vertical abnormalities in the lab are 1.5 to 2.5 degrees, we're only accepting over 3.2 degrees and on down. Cervical VEMP errors abnormal if amplitude is less than 100 microvolts or greater than 35% amplitude asymmetry between the sides, again those are much stricter criteria than the standard vestibular lab uses. So if you see arguments that “well people have these abnormalities with other disorders”, not to this extent. Not to the extent we're reporting. And again that's important because there was a recent article in JAMA where someone said “well lots of people have these abnormalities”, well not to this extent.


So there were also some cognitive and neuropsychological symptoms that Bonnie Levin who's an (...) physician did this data, so I'm reporting her data. Cognitive fog, inattention, problems retrieving information and increased irritability. And when you did the testing they were below the expected level for verbal fluency, for working memory and for sustained attention. They had difficulty with auditory processing and difficulty with increased levels of cognitive load. Now while this pattern of abnormalities can be seen in other populations, at least according to our neuropsychological colleagues, the unique pattern seen here is unique to this group. So we have a unique set of vestibular findings and we have a unique set of neurocognitive or neuropsychological findings, and that combination is not seen in any other group of patients.


The exposure is unknown today, we're going to talk about that a lot this morning. It could be ultrasonic energy, it could be microwave energy, it could be one of a variety of things. Dr. Balaban is going to talk a lot about directed energy, can produce cavitation bubbles. I think Dr. Giordano is gonna speak about this as well. Bubble formation and bubble bursting can produce damage in any hollow space and candidate spaces exist right in the area of those vestibular (...). So I use the term utricle and saccule, I think dr. Giordano’s got a picture of those in his presentation, and those organs sit right next to areas where cavitation can occur. So it makes sense that if I'm getting a sound in and it cavitates in that area it's going to affect those two gravity organs, the utricle and the saccule."





"The aura of mild traumatic brain injury. I use this term because if you really break down the term mild traumatic brain injury, it's simply injury to the brain that is mild and that occurred from trauma. And it's synonymous with concussion, nothing more. So if you say you ‘ve a sprained ankle, you have a sprained ankle. If you say you have MTBI, all of a sudden you're some mystical creature who crawled out out of the lagoon. It doesn't make any sense because again medically, it's just traumatic damage to the brain that's mild. Just like traumatic you know damage to the ankle that is mild.


So one important question we're always asked, we were asked by the State Department, we were asked by DoD, we were asked by CDC and we were asked by NIH is “is this what you saw in these Cuba patients, is this traumatic brain injury. This is the definition of traumatic brain injury as determined by the DoD back in 2005, reaffirmed in 2009 and finally reaffirmed most recently in 2017. Individuals suffer a blow to the head. The individual has a period of altered or loss of consciousness of less than 30 minutes, some groups not the DoD but some groups will accept less than 60 minutes. Individual has a sequela, they have a finding after that. And the same individual does not have intracranial bleeding, does not require surgery for the injury or acquiring an intensive-care state. Essentially, synonymous with concussion. Now I will say that the blow to the head could be either a natural physical contact with the head or could be a pressure sensation. It doesn't have to be physical contact. So that's what the DoD said a year ago and still stands by as their definition for mild traumatic brain injury. Now it doesn't need to be our definition but it's their definition. And it's one that we use in a lot of our work because I was in military for 21 before this, so I'm a good soldier or good sailor. So this is what mild traumatic brain injury looks like.


If you look at people that were injured in a war, this is data from when I was in San Diego. The acute group was collected acutely, when I was deployed in Iraq. These individuals were all within three days of having had an injury in theater usually a blast injury. Subacute group was collected in San Diego when I was there and the chronic group also at San Diego. To give you some idea about how much traumatic brain injury was produced, the number of individuals in the acute group is 88, the number of individuals not shown here in the subacute group, but this is all published data already, is seventy and there's about sixty in the chronic group and that was collected subacute and product in San Diego over a two-month period of time at the height of the war in Iraq. A lot of individuals were coming back with brain injury.


So notice that dizziness is the most common symptom. At all time epochs. Acutely, subacutely and chronically. Different groups of people but again very similar presentations. So notice that dizziness is there 98% of the time almost universally in the acute group and it falls off but not very much. Headache is the next most common. See it at 72 percent, 82 percent long-term. And then you can see vertigo and hearing loss. So for those of you who do vestibular stuff, dizziness in this case was unsteadiness, being off-balance. Vertigo is actually room spinning phenomenon. So there was a lot of off-balance, not as much room spinning and not as much hearing loss. And notice the high prevalence of headache. This is the ROC curve, again published data that from from Carey Balaban and I on our group, where we take a pair of goggles, the same pair of goggles that we applied to the Cuba individuals, Kerry's going to talk about these a little bit later, and these are the key factors: anti-saccade error rates predict dif. saccade error rates and it had even post-testing error rates. Okay notice that the visual vertical, vemp testing are not on there, they're not the key indicators for TBI, they are the key indicators for the group in Cuba. So is this traumatic brain injury? The definitions don't match, the findings don't match. Anti and predictive saccades and head thrust tests are used for MTBI, whereas odourless findings are seen in those with this syndrome, so different findings. There's a much higher incidence of headache in the mild traumatic brain injury, I showed you anywhere from 76 to 82 percent versus the low incidence in this group 32%. And there's a difference in neuropsychological testing outcome as well that Bonnie Levine showed. So I'm not we're not saying this is not MTBI but this does not fit the military definition of MTBI as subscribed a year ago.


[14min08] So what is it. It's an acquired neurosensory dysfunction with essentially universal otolithic disorders, some additional vestibular findings and a unique pattern of cognitive findings. Remember, I described for you that otolithic abnormalities, utricle and saccule, mean that the individual has an abnormal gravity sense. Now, the site of injury could be limited to the inner ear with secondary cognitive dysfunction. Because when you don't know what upright is. Essentially when you're being chased by a tiger in the jungle and you fall down, you ‘re dinner for the tiger. It really doesn't matter if you can balance your checkbook or function cognitively. So it's quite possible, we have data in our lab with Carey and Bonnie as well that show that if you have a dysfunction of what's up and down, you don't have a lot of mental energy left over for cognitive tasks. So the injury could be limited to the inner ear and the cognitive effects may be secondary as simply the inability to know what up and down is. Or there could be injury in multiple parts of the system, that remains to be determined. But we're working on that now because again if you don't know what up and down is, you can't do much cognitively.


Most importantly this is a real physical injury and those truly affected. The 25 individuals we saw had objective findings of a disorder that came acutely from what happened in Cuba. I'm not talking about the word well, I'm not talking about people who presented later somewhere else. I'm talking about people who came to Miami, they didn't know what they should report and they had objective findings. You can't fake a VEMP test, you can't fake a subjective visual vertical. You can fake it but it will be apparent to us that you're faking it. So the tests were real and they were objective. And that's important because the 25 most affected individuals and we're not sure if anyone got affected elsewhere in the world until we do this kind of testing on them, but the 25 affected individuals are often accused of malingering or exaggerating. I can tell you those 25 are not. And that's an important message. Also importantly, these findings suggest the ability to screen potential cases. So otolithic tests, the test for whether you are up and down are easy to transport and quick to perform. And a quick cognitive screen could be easily designed. And these screening techniques are critically important for distinguishing the word well. We already have at least 25 documented cases of word well from the truly affected. And the fact that these findings are known means, I mean it's going to call out groups, they should have been applied to anybody else who complain to this, and we feel that again, we can design a fairly easy screen and Carey is going to show you an additional part of that screen in his talk, to really determine who's affected and who's word well. Because now that it's out there, now that people know what they should complain of, now they know what the symptoms are and this is all almost all lay media attention, they can fake this stuff pretty easily and again we've had 25 people trying to fake it come to us and we've been able to rule them out. In any current or future evaluation of case, you should include at least this short battery as a screening battery, for what's going on.


So I'd like to thank a bunch of people because this work doesn't get done in a vacuum kaskus. We've been doing work with the Office of Naval Research, funded work with that office for many many years. They did not fund this work but they fund similar work. Fred Telischi is my department Chair who allows me to do this stuff and see these patients. Toni (...) is our Vice Chairman who watches all of our finances at Miami. Even more important for allowing me to do this stuff. Danna is my administrative assistant who scheduled all 35 of these patients from Cuba to Miami. Interestingly enough almost all the people who saw these individuals were Cubans that worked in our clinic. Constanza Pelosi is our research director, Aaron Williams is my research coordinator. The nurses, audiologists and support staff at the Miami Hearing Institute were amazing in helping us with these individuals and again we want to thank you for giving us a forum to present this and you know we think this is the true story, there are other stories out there, we know this is the real story of at least the acute individuals. Thank you very much”.