The Dizziness Group: For those who are floating, boating, falling or flying

[[cs...]]

 

 

A couple of other things pose some questions for me as I start to read the article. First, is benzo-related dizziness considered "damage" in the same way as that referred to in the article? It's not "unilateral vestibular deafferentation (UVD)", nor is it a "lesion", which is another type of vestibular issue. In the Mal de Debarquement article, the authors state that they're not even sure if MdD caused by motion and non-motion-triggered MdD symptoms are related. Similar symptoms can have different causes, and that's obviously the case here.

 

I fully agree Lapis.  Since there’s such a lack of research in Benzodiazaphines, we have to extrapolate.  I agree it makes drawing conclusions difficult , but it doesn’t prevent us from trying to connect the dots.  Prior to posting I noted the traumas.

 

in my very humble opinion, benzdiazaphines inflict some of the worst kind of damage to our nervous systems.  I’m not saying that to scare anyone, because I believe much of the “damage” is reversible.  When one looks at neural circuts, and how dependent all neural circuits are on inhibitory and excitatory signaling, one recognizes how disturbances in these areas can cause physiological deficits in our everyday function.  Is this a trauma to the neural circuit ?  I believe so.  Is a lesion a trauma to the neural circuit?  I think so.  The neural circuit literature refers to these “traumas” as perturbations or stressors on the circuit.  These are things that disrupt the normal way the neurons fire in a phasic fashion, ie in what order they fire and at what frequencies they fire, apart from one another.  This determines the very  physiological function of the circuit and neurological function itself....  (Ie, how we walk, how we move, how we feel emotion, and how we maintain balance, etc).      Losing neurons to a lesion will screw this up, and benzdiazaphines will do this in a more insidious way.

 

Also,,please note that the article focuses on the vestibular compensation system itself and how the stress system affects that,  If your compensation is dysfunctional it makes recovery long, once the trauma has occurred.

 

 

This neural circuits stuff is an area that I have not fully presented in the layman’s thread due to lack of time, but I’ve completed the research.

 

Thanks again for bringing up these very good points

I’m glad you pointed this out.

 

Thanks

 

Hi dm123,

Thanks for your input and for sharing that article. I do hope there's some good news somewhere, though, since it creates a fairly bleak picture for someone like me. I can only hope that the innate healing powers of the body can overcome these traumas.

 

Hi Lapis,

 

I understand.  Just to give you an idea of my encounters with auditory issues during benzdiazaphine use, I developed severe tinnitus during tolerance and it continued throughout many months of the taper.  I hadn’t noticed, but it’s faded quite a bit.  I’ve also got hyperacusis, and have had an earplug in my left ear for over a year (yes I change it frequently:) )

 

Recently, the last few weeks I’ve been removing it several hours a day to start the compensation process.  It’s slow.

 

I know you are familiar with the vestibular neural circuits (there’s so many of them!) but I just wanted to put an image of the VOR circuit from Wikipedia below to illustrate that physiological function is a manifestation of alternating firing of neurons in a circuit at certain frequencies and shifted off phase from one another.  I won’t bore you with the details, but this only works well when inhibitory and excitatory Action potentials of neurons can inhibit and excite each other through feedback loops.  These are called oscillators, and form the foundation of how neural circuits manifest as physiological function.

 

Benzdiazaphines blunt the responsiveness of the circuit, and impose stress on the circuit.  The circuit can still function fairly well up to a point.  At threshold, the circuit crashes and this manifests itself as a severe physiological dysfunction.  In general once the stressors are removed, circuits recover.  Circuits are rarely cooked, ie permanently damaged.

 

The big question is why does a circut remain decompensated and dysfunctional long after benzdiazaphine washout.  That’s where long term plastic and neurogenic changes come in.  During benzdiazaphine wd and washout, it’s possible for these changes to persist after washout.  There are some feedback cycles that prevent recovery, and one is the negative stress feedback cycle.  And the persistent symtoms themselves perpetuate the problem.  Vestibular compensation to restore homeostasis to vestibular and ocular circuits is hampered by chronic negative stress.

 

 

I will leave it at that for now, until i can look at Soto’s work, and others work in more detail.

 

Here’s the simplified VOR circuit.  Note that head rotation is clockwise (L to R) and eye movement reflex  is counterclockwise (R to L) to stabilize gaze and prevent disequilibrium and disorientation.

 

Those scribbles are just some notes to myself.  Bold black shows the + excitatory and - inhibitory action potentials, and Roman numerals designate cranial nerves

If you are on an apple touchscreen you can zoom in to see more detail in the photo below.

 

https://en.m.wikipedia.org/wiki/Vestibulo%E2%80%93ocular_reflex

 

 

 

[[La...]]

Hi dm123,

Thanks for that. I'm not, actually, well-versed in the inner workings of the vestibular system, as I've learned it's rather complicated. Ironically, my father was an ENT surgeon, but he passed away around the time that my symptoms got quite bad. Otherwise, I would've had about a million questions for him!

 

I'm sorry to hear about your tinnitus. It's quite common around here, and I've got it too. I can ignore it, though. I, too, had hyperacusis, but it settled down completely. I couldn't stand the sound of running water, as it just seemed too loud. So strange! I love water!

 

You may be interested in this paper, which differentiates between rotary-type symptoms and push-pull/boat-like motions. According to the author, those symptoms reflect the part of the vestibular system that's likely malfunctioning, i.e. semicircular canals, saccule, utricle (the last two are referred to as the "otolith organs").

 

https://www.hindawi.com/journals/isrn/2014/629049/

 

Here's an excerpt:

 

The neurophysiology of the canals and otolith organs is distinct with unique contributions of each to perceived head position and balance abilities. Therefore, adults with dizziness and imbalance due to otolith organ involvement may present with different symptoms as compared to those with canal dysfunction. Both canals and otolith organs contribute to the perception of head orientation, but each responds to unique stimuli [23–25]. The canals are optimally sensitive to angular acceleration, which explains why patients with pathology affecting the canals report symptoms of spinning (rotary vertigo) [7]. The otolith organs, although less thoroughly studied and understood [8, 12], optimally respond to linear and gravitational acceleration due to translational head movements and head tilts [2, 24]. This could explain why anecdotal reports of feeling like rocking, tilting, walking on pillows, being pushed, feeling drunk, and falling have been used by patients with otolith dysfunction [7, 12]. In addition to perceived orientation, canals and otolith organs both contribute to postural control via vestibulospinal pathways. However, it is thought that the contribution of the otoliths is the main vestibular source for postural control [23, 25]. The vestibulospinal pathways that receive canal input terminate on motor neurons of the cervical cord, whereas those of the otolith organs innervate motor neurons from the cervical through the sacral cord [26]. The otolith organ input facilitates activation of antigravity muscles and modulates the tone of neck, trunk, and limb extensor muscles enabling the maintenance of posture [25]. Consequently, it seems logical to conclude that dysfunction of canals versus that of otolith organs would effect perceived orientation and balance differently. In turn, it would seem reasonable that exercise strategies used in rehabilitation would need to be designed specifically to promote stimulation of residual function of these structures.

 

Vestibular rehabilitation (VR) exercises, which focus on the reduction of complaints of dizziness and imbalance, have been based on diagnoses involving only the canals. VR has emphasized the use of rotational head movement exercises, which optimally stimulates canal function [27]. This may affect the success of intervention because these exercises do not optimally stimulate the otolith organs, and thus, the exercises used may be incomplete or incorrect for individuals with otolith dysfunction. This could explain, at least in part, the variable outcomes of VR that are reported [28, 29]. A prospective, controlled study by Krebs et al. [29] demonstrated that only 60% of patients with unilateral and bilateral P-VeD who performed gaze stability and balance retraining exercises benefited from the VR as indicated by improved gait parameters. Ernst et al. [28] reported that although there was improvement of perceived orientation, gaze stability, and/or postural control following VR in most patients with vestibulopathy, some patients did not have resolution of their symptoms. A prospective study by Enticott et al. [30] found that patients with a mixture of vestibular dysfunctions (canal only, canal and otolith, and otolith only) who performed a variety of head turning and walking tasks over 10 weeks had significant improvement of impairments compared to patients who only performed lower extremity strengthening exercises. Even though perceived disability, balance confidence, and severity of symptoms improved in patients studied by Enticott, patients’ perception of the therapy program’s impact on their symptoms did not improve significantly in the treatment group compared to the control group. By having a more thorough understanding of the qualitative nature of the symptoms of canal versus otolith dysfunction, the diagnosis could be more specific, which could improve the development of optimal intervention for individuals with vestibulopathy. However, to date, this has not been done.

 

 

 

I found an article by Soto-Varela (is that whom you're referring to?), and the title is quite interesting:

 

"Instability Due to Drug-Induced Vestibulotoxicity"

 

https://www.ncbi.nlm.nih.gov/pubmed/27716608

 

Benzos and SSRIs are both considered to be "ototoxic", as are NSAIDs, but none of these meds are specifically referred to in this study. The list of ototoxic meds meds is rather long, though, so there's lots to choose from.

 

There's also this paper, but I believe it's a different Soto this time:

 

https://www.ncbi.nlm.nih.gov/pubmed/24177345

 

2013;23(3):119-37. doi: 10.3233/VES-130494.

 

Neuropharmacological basis of vestibular system disorder treatment.

 

Soto E1, Vega R, Seseña E.

 

Author information

 

1

    Instituto de Fisiología, Universidad Autónoma de Puebla, Puebla, México.

 

Abstract

 

This work reviews the neuropharmacology of the vestibular system, with an emphasis on the mechanism of action of drugs used in the treatment of vestibular disorders. Clinicians are confronted with a rapidly changing field in which advances in the knowledge of ionic channel function and synaptic transmission mechanisms have led to the development of new scientific models for the understanding of vestibular dysfunction and its management. In particular, there have been recent advances in our knowledge of the fundamental mechanisms of vestibular system function and of drug action. In this work, drugs acting on vestibular system have been grouped into two main categories according to their primary mechanisms of action: those with effects on neurotransmitters and neuromodulators dynamics and those that act on voltage-gated ion channels. Particular attention is given in this review to drugs that may provide additional insight into the pathophysiology of vestibular diseases. The critical analysis of the literature reveals that there is a significant lack of information defining the real utility of diverse drugs used in clinical practice. The development of basic studies addressing drug actions at the molecular, cellular and systems level, combined with reliable and well controlled clinical trials, would provide the scientific basis for new strategies for the treatment of vestibular disorders.

 

[[cs...]]

Hi dm123,

Thanks for that. I'm not, actually, well-versed in the inner workings of the vestibular system, as I've learned it's rather complicated. Ironically, my father was an ENT surgeon, but he passed away around the time that my symptoms got quite bad. Otherwise, I would've had about a million questions for him!

 

I'm sorry to hear about your tinnitus. It's quite common around here, and I've got it too. I can ignore it, though. I, too, had hyperacusis, but it settled down completely. I couldn't stand the sound of running water, as it just seemed too loud. So strange! I love water!

 

You may be interested in this paper, which differentiates between rotary-type symptoms and push-pull/boat-like motions. According to the author, those symptoms reflect the part of the vestibular system that's likely malfunctioning, i.e. semicircular canals, saccule, utricle (the last two are referred to as the "otolith organs").

 

https://www.hindawi.com/journals/isrn/2014/629049/

 

Here's an excerpt:

 

The neurophysiology of the canals and otolith organs is distinct with unique contributions of each to perceived head position and balance abilities. Therefore, adults with dizziness and imbalance due to otolith organ involvement may present with different symptoms as compared to those with canal dysfunction. Both canals and otolith organs contribute to the perception of head orientation, but each responds to unique stimuli [23–25]. The canals are optimally sensitive to angular acceleration, which explains why patients with pathology affecting the canals report symptoms of spinning (rotary vertigo) [7]. The otolith organs, although less thoroughly studied and understood [8, 12], optimally respond to linear and gravitational acceleration due to translational head movements and head tilts [2, 24]. This could explain why anecdotal reports of feeling like rocking, tilting, walking on pillows, being pushed, feeling drunk, and falling have been used by patients with otolith dysfunction [7, 12]. In addition to perceived orientation, canals and otolith organs both contribute to postural control via vestibulospinal pathways. However, it is thought that the contribution of the otoliths is the main vestibular source for postural control [23, 25]. The vestibulospinal pathways that receive canal input terminate on motor neurons of the cervical cord, whereas those of the otolith organs innervate motor neurons from the cervical through the sacral cord [26]. The otolith organ input facilitates activation of antigravity muscles and modulates the tone of neck, trunk, and limb extensor muscles enabling the maintenance of posture [25]. Consequently, it seems logical to conclude that dysfunction of canals versus that of otolith organs would effect perceived orientation and balance differently. In turn, it would seem reasonable that exercise strategies used in rehabilitation would need to be designed specifically to promote stimulation of residual function of these structures.

 

Vestibular rehabilitation (VR) exercises, which focus on the reduction of complaints of dizziness and imbalance, have been based on diagnoses involving only the canals. VR has emphasized the use of rotational head movement exercises, which optimally stimulates canal function [27]. This may affect the success of intervention because these exercises do not optimally stimulate the otolith organs, and thus, the exercises used may be incomplete or incorrect for individuals with otolith dysfunction. This could explain, at least in part, the variable outcomes of VR that are reported [28, 29]. A prospective, controlled study by Krebs et al. [29] demonstrated that only 60% of patients with unilateral and bilateral P-VeD who performed gaze stability and balance retraining exercises benefited from the VR as indicated by improved gait parameters. Ernst et al. [28] reported that although there was improvement of perceived orientation, gaze stability, and/or postural control following VR in most patients with vestibulopathy, some patients did not have resolution of their symptoms. A prospective study by Enticott et al. [30] found that patients with a mixture of vestibular dysfunctions (canal only, canal and otolith, and otolith only) who performed a variety of head turning and walking tasks over 10 weeks had significant improvement of impairments compared to patients who only performed lower extremity strengthening exercises. Even though perceived disability, balance confidence, and severity of symptoms improved in patients studied by Enticott, patients’ perception of the therapy program’s impact on their symptoms did not improve significantly in the treatment group compared to the control group. By having a more thorough understanding of the qualitative nature of the symptoms of canal versus otolith dysfunction, the diagnosis could be more specific, which could improve the development of optimal intervention for individuals with vestibulopathy. However, to date, this has not been done.

 

 

 

I found an article by Soto-Varela (is that whom you're referring to?), and the title is quite interesting:

 

"Instability Due to Drug-Induced Vestibulotoxicity"

 

https://www.ncbi.nlm.nih.gov/pubmed/27716608

 

Benzos and SSRIs are both considered to be "ototoxic", as are NSAIDs, but none of these meds are specifically referred to in this study. The list of ototoxic meds meds is rather long, though, so there's lots to choose from.

 

There's also this paper, but I believe it's a different Soto this time:

 

https://www.ncbi.nlm.nih.gov/pubmed/24177345

 

2013;23(3):119-37. doi: 10.3233/VES-130494.

 

Neuropharmacological basis of vestibular system disorder treatment.

 

Soto E1, Vega R, Seseña E.

 

Author information

 

1

    Instituto de Fisiología, Universidad Autónoma de Puebla, Puebla, México.

 

Abstract

 

This work reviews the neuropharmacology of the vestibular system, with an emphasis on the mechanism of action of drugs used in the treatment of vestibular disorders. Clinicians are confronted with a rapidly changing field in which advances in the knowledge of ionic channel function and synaptic transmission mechanisms have led to the development of new scientific models for the understanding of vestibular dysfunction and its management. In particular, there have been recent advances in our knowledge of the fundamental mechanisms of vestibular system function and of drug action. In this work, drugs acting on vestibular system have been grouped into two main categories according to their primary mechanisms of action: those with effects on neurotransmitters and neuromodulators dynamics and those that act on voltage-gated ion channels. Particular attention is given in this review to drugs that may provide additional insight into the pathophysiology of vestibular diseases. The critical analysis of the literature reveals that there is a significant lack of information defining the real utility of diverse drugs used in clinical practice. The development of basic studies addressing drug actions at the molecular, cellular and systems level, combined with reliable and well controlled clinical trials, would provide the scientific basis for new strategies for the treatment of vestibular disorders.

 

 

Hi Lapis

 

Thanks much for that first article.  I’ve download the pdf and will read and dissect it later in the week.  Those excerpts and the abstract look very interesting.

 

By the way, I assume you are more otolith dysfunctional per your symptoms?

 

The ductus semicircularis lateralis ( the circles on the very bottom)on that simple vestibular neural circuit I posted above is the lateral canal of the three.  As we would expect , that VOR circuit is one of many vestibular neural circuits involving rotation.  (And counter lateral eye rotation to stabilize gaze).  I had posted it to illustrate something common of all types neural circuits, which is the complex interplay between inhibitory and excitatory synapses relayed by a network of complex interneurons.  It’s no wonder that benzdiazaphines affect us so profoundly. 

 

Assuming you are mostly otolith dysfunction, I at least know where to focus.  VR is also very interesting.

 

Regarding the Soto, it was actually the second Soto link you posted E Soto, “Neuropharmacological.......”. 

Unfortunately there’s no full access to the link.

 

 

[[La...]]

Hi dm123,

Yes, I wish we had someone around here who could access full studies of certain abstracts. Only a few of them can be accessed for free. Those in the medical profession may have access to online libraries.

 

Here's another abstract that might be useful for you. I read it years ago, and if, indeed, what it's saying is true, then it fleshes out the picture of why the otolith organs are most affected in those of us who have taken benzos. I've never forgotten it, but I haven't come across further info on the the subject. It refers to specific areas of the vestibular system that are suppressed by various medications. I'll highlight a few key lines.

 

Have a look:

 

https://www.ncbi.nlm.nih.gov/pubmed/22517315

 

2012;17(4):235-42. doi: 10.1159/000337273. Epub 2012 Apr 19.

 

Pharmaceutical countermeasures have opposite effects on the utricles and semicircular canals in man.

 

Weerts AP1, De Meyer G, Pauwels G, Vanspauwen R, Dornhoffer JL, Van de Heyning PH, Wuyts FL.

 

Author information

 

1

    Antwerp University Research Centre for Equilibrium and Aerospace (AUREA), Edegem, Belgium.

 

Abstract

 

INTRODUCTION:

 

Sensory conflicts in the vestibular system lead to motion sickness of which space motion sickness (SMS) is a special case. SMS affects up to 70% of the astronauts during the first 3 days in space. The search for effective countermeasures has led to several nonpharmacological and pharmacological approaches. The current study focuses on the effects of lorazepam (1 mg), meclizine (25 mg), promethazine (25 mg), and scopolamine (0.4 mg) on the vestibular system, with special focus on the canal and otolith functions separately.

 

METHODS:

 

The study had a placebo-controlled, single blind, repeated measures design. Sixteen healthy volunteers were subjected to a total of 7 test sessions, the first and last being without intake of medication. Semicircular canal function was evaluated by means of electronystagmography and otolith function with unilateral centrifugation. The horizontal semicircular canal function was characterized by the vestibulo-ocular reflex (VOR) gain measured during earth vertical axis rotation as well as the total caloric response. The function of the utricles was represented by the utricular sensitivity, reflecting the ocular counter roll relative to the virtual induced head tilt.

 

RESULTS:

 

Promethazine significantly decreased the semicircular canal and utricular parameters. Both scopolamine and lorazepam caused only a decrease in the utricular sensitivity, whereas meclizine only decreased the semicircular canal-induced VOR gain.

 

DISCUSSION:

 

The results show that the drugs affected different areas of the vestibular system and that the effects can thus be attributed to the specific pharmacological properties of each drug. Meclizine, as an antihistaminergic and weak anticholinergic drug, only affected the VOR gain, suggesting a central action on the medial vestibular nucleus. The same site of action is suggested for the anticholinergic scopolamine since acetylcholine receptors are present and utricular fibers terminate here. The global vestibular suppression caused by promethazine is probably a consequence of its anticholinergic, antihistaminergic, and antidopaminergic properties. Based on the fact that lorazepam increased the affinity of gamma-aminobutyric acid (GABA) for the GABA(A)-receptor and its effects on the utriculi, the site of action seems to be the lateral vestibular nucleus.

 

CONCLUSION:

 

Meclizine, scopolamine, and lorazepam selectively suppress specific parts of the vestibular system. Selective suppression of different parts of the vestibular system may be more beneficial for alleviating (space) motion sickness than general suppressive agents. Additionally, this knowledge may help the clinician in his therapeutic management of patients with either semicircular canal or otolith dysfunction.

[[...]]

Just dropping off a couple more surveys from the sidebar (if I close my browsers, they'll be gone forever).  I've just skimmed but they're much more comprehensive than the first, and quite interesting reading.

 

Mal de Debarquement Syndrome: a survey on subtypes, misdiagnoses, onset and associated psychological features

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5834551/

 

The above survey actually includes the full questionnaire as a Word attachment.  This part gave me a bit of a lump in the throat, hits the nail on the head:

 

"Throughout both questionnaires, the respondents had the opportunity to add open-ended comments regarding anything they were willing to share about their MdDS experience. A great proportion of respondents expressed a high level of frustration and helplessness related not only to misdiagnoses and unawareness of MdDS in the medical community but also the debilitating nature of this condition and how much their lives had changed, “I regard myself as handicapped now”—SO respondent, “My whole life has significantly changed. I cannot go anywhere without my husband to hold on to. I am unable to travel on public transport on my own. I cannot go shopping on my own without a shopping trolley to hold on to. My whole life has changed.”—MT respondent. Patients also indicated that they were unable to work full time and live a normal life, others expressed their concerns about ageing with the condition, “My life barely resembles what it used to… I no longer travel, cannot see friends or have energy to do anything but work and come home to my family. I don’t go out, can’t physically exert myself, get seriously ill if I do exert myself, and can no longer do most of my hobbies or goals”—MT respondent, “It has changed my life. I am not able to do all the things I once enjoyed.”—SO respondent, “The biggest change to my lifestyle is a reluctance to go out unaccompanied due to the way I feel when I am walking. I feel much more secure with company and somebody to hold to alleviate the feeling of unsteadiness”—SO respondent."

 

 

 

The following questionnaire, Lap, regarding your interest in the role of hormones:

 

Mal de Debarquement Syndrome: A Retrospective Online Questionnaire on the Influences of Gonadal Hormones in Relation to Onset and Symptom Fluctuation

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5992375/

 

 

 

And this from a neuroimaging perspective, and describes the current theories.

 

Perspective: Stepping Stones to Unraveling the Pathophysiology of Mal de Debarquement Syndrome with Neuroimaging

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5816028/

 

 

[[La...]]

Great stuff, abcd! Thanks for posting those. I'll have a look over the next few days or so.

[[La...]]

So, I've just finished reading the first of the three studies that you shared above, abcd. This one:

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5834551/ 

 

Very interesting! However, I'm still stuck on the fact that both SSRIs and benzodiazepines seem to help a number of people (they didn't specify which group and how many in total), but we know that both groups of medications can CAUSE dizziness. The use of medication muddies the water quite a bit, I believe. Both classes of medications can cause profound changes in neurotransmitter activity, and both classes of medication can cause people to feel more, rather than less, anxiety and depression. So, I'd like to see that information explored and applied and made clear. To leave such information out is to miss what might be an explanation for at least some of these people's MdDS.

 

Also, there's no information about any other medications that people might be taking. Many medications are considered to be "ototoxic" and are known to affect balance.

 

One other thing: Awhile back, I shared a Johns Hopkins paper that explains how MRI machines can cause people to feel dizzy. So the use of the fMRI machine to test for some things makes me wonder if there's an understanding of what role the testing machine itself might play.

 

In any case, I'm really pleased to see a larger sample size for this survey vs. the last one. As with all studies, we can see that "more study is required".

 

 

Here's the paragraph about medication:

 

Finally, our study suggests that MdDS is the cause for developing psychological disorders in both its subtypes, which is supported by the fact that antidepressants as well as sedative medications (e.g., benzodiazepines) are found to be helpful in MdDS patients and therefore often prescribed by healthcare professionals [39]. The use of such medication may also have an impact on stress levels, which from our study seems to be responsible for aggravating MdDS symptoms. A further and more detailed examination of the psychological component, psychological symptoms associated to MdDS and effect of stress on MdDS patients should be undertaken.

[[cs...]]

Hi dm123,

Yes, I wish we had someone around here who could access full studies of certain abstracts. Only a few of them can be accessed for free. Those in the medical profession may have access to online libraries.

 

Here's another abstract that might be useful for you. I read it years ago, and if, indeed, what it's saying is true, then it fleshes out the picture of why the otolith organs are most affected in those of us who have taken benzos. I've never forgotten it, but I haven't come across further info on the the subject. It refers to specific areas of the vestibular system that are suppressed by various medications. I'll highlight a few key lines.

 

Have a look:

 

https://www.ncbi.nlm.nih.gov/pubmed/22517315

 

2012;17(4):235-42. doi: 10.1159/000337273. Epub 2012 Apr 19.

 

Pharmaceutical countermeasures have opposite effects on the utricles and semicircular canals in man.

 

Weerts AP1, De Meyer G, Pauwels G, Vanspauwen R, Dornhoffer JL, Van de Heyning PH, Wuyts FL.

 

Author information

 

1

    Antwerp University Research Centre for Equilibrium and Aerospace (AUREA), Edegem, Belgium.

 

Abstract

 

INTRODUCTION:

 

Sensory conflicts in the vestibular system lead to motion sickness of which space motion sickness (SMS) is a special case. SMS affects up to 70% of the astronauts during the first 3 days in space. The search for effective countermeasures has led to several nonpharmacological and pharmacological approaches. The current study focuses on the effects of lorazepam (1 mg), meclizine (25 mg), promethazine (25 mg), and scopolamine (0.4 mg) on the vestibular system, with special focus on the canal and otolith functions separately.

 

METHODS:

 

The study had a placebo-controlled, single blind, repeated measures design. Sixteen healthy volunteers were subjected to a total of 7 test sessions, the first and last being without intake of medication. Semicircular canal function was evaluated by means of electronystagmography and otolith function with unilateral centrifugation. The horizontal semicircular canal function was characterized by the vestibulo-ocular reflex (VOR) gain measured during earth vertical axis rotation as well as the total caloric response. The function of the utricles was represented by the utricular sensitivity, reflecting the ocular counter roll relative to the virtual induced head tilt.

 

RESULTS:

 

Promethazine significantly decreased the semicircular canal and utricular parameters. Both scopolamine and lorazepam caused only a decrease in the utricular sensitivity, whereas meclizine only decreased the semicircular canal-induced VOR gain.

 

DISCUSSION:

 

The results show that the drugs affected different areas of the vestibular system and that the effects can thus be attributed to the specific pharmacological properties of each drug. Meclizine, as an antihistaminergic and weak anticholinergic drug, only affected the VOR gain, suggesting a central action on the medial vestibular nucleus. The same site of action is suggested for the anticholinergic scopolamine since acetylcholine receptors are present and utricular fibers terminate here. The global vestibular suppression caused by promethazine is probably a consequence of its anticholinergic, antihistaminergic, and antidopaminergic properties. Based on the fact that lorazepam increased the affinity of gamma-aminobutyric acid (GABA) for the GABA(A)-receptor and its effects on the utriculi, the site of action seems to be the lateral vestibular nucleus.

 

CONCLUSION:

 

Meclizine, scopolamine, and lorazepam selectively suppress specific parts of the vestibular system. Selective suppression of different parts of the vestibular system may be more beneficial for alleviating (space) motion sickness than general suppressive agents. Additionally, this knowledge may help the clinician in his therapeutic management of patients with either semicircular canal or otolith dysfunction.

 

Thanks Lapis, I’m going to start with this one and then study some more on the neuroanatomy in this area, and then take a look at some of the articles abcd posted above, especially the hormone related one.

[[Fi...]]

How do people cope with this stuff?!  I may have had it this whole time but was too distracted by my other symptoms to notice it as much.  But, now it is very profound and scary.  I don’t know how to cope!!!  Between the Floaty Boaty and Dp/Dr.  My world is disappearing.

 

 

2yrs since forced CT off Klonopin.   

[[cs...]]

So, I've just finished reading the first of the three studies that you shared above, abcd. This one:

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5834551/ 

 

Very interesting! However, I'm still stuck on the fact that both SSRIs and benzodiazepines seem to help a number of people (they didn't specify which group and how many in total), but we know that both groups of medications can CAUSE dizziness. The use of medication muddies the water quite a bit, I believe. Both classes of medications can cause profound changes in neurotransmitter activity, and both classes of medication can cause people to feel more, rather than less, anxiety and depression. So, I'd like to see that information explored and applied and made clear. To leave such information out is to miss what might be an explanation for at least some of these people's MdDS.

 

Also, there's no information about any other medications that people might be taking. Many medications are considered to be "ototoxic" and are known to affect balance.

 

One other thing: Awhile back, I shared a Johns Hopkins paper that explains how MRI machines can cause people to feel dizzy. So the use of the fMRI machine to test for some things makes me wonder if there's an understanding of what role the testing machine itself might play.

 

In any case, I'm really pleased to see a larger sample size for this survey vs. the last one. As with all studies, we can see that "more study is required".

 

 

Here's the paragraph about medication:

 

Finally, our study suggests that MdDS is the cause for developing psychological disorders in both its subtypes, which is supported by the fact that antidepressants as well as sedative medications (e.g., benzodiazepines) are found to be helpful in MdDS patients and therefore often prescribed by healthcare professionals [39]. The use of such medication may also have an impact on stress levels, which from our study seems to be responsible for aggravating MdDS symptoms. A further and more detailed examination of the psychological component, psychological symptoms associated to MdDS and effect of stress on MdDS patients should be undertaken.

 

Hi Lapis I haven’t read up in this article yet, but I noted the words about stress in the quote you pulled from the article.  Specifically

 

“The use of such medication may also have an impact on stress levels, which from our study seems to be responsible for aggravating MdDS symptoms. A further and more detailed examination of the psychological component, psychological symptoms associated to MdDS and effect of stress on MdDS patients should be undertaken.”

 

Benzdiazaphines profoundly destabilize the stress system over time.  Once the stress system becomes destabilized it can be very challenging to stabilize it.  Neuroplastic and neurogenic changes do take place as stress resiliency deteriorates, and one if the things I will do is explore how plastic the neurons are in the vestibulo-occular regions.  If they are plastic then they will be susceptible to this protracted feedback loop.  The olfactory bulb and hippocampus are the most plastic regions of the brain.  As you know with vestibular pathology we are dealing with cortical and brainstem regions of the brain(vestibular nuclei),so one of the things I want to start exploring is just how plastic the vestibular nuclei in brainstem are.  Cortical regions of the brain are revealed as being quite plastic in the lastest latest research.

 

I also wanted to ask you about the incident of your father’s passing.  Was it an extremely stressful event?. You had mentioned your vestibular issues worsened at that time.  Please ignore if too personal a question.

 

 

Best,

Dm123

[[cs...]]

How do people cope with this stuff?!  I may have had it this whole time but was too distracted by my other symptoms to notice it as much.  But, now it is very profound and scary.  I don’t know how to cope!!!  Between the Floaty Boaty and Dp/Dr.  My world is disappearing.

 

 

2yrs since forced CT off Klonopin. 

 

Hi F4Me,

 

I was going to ask the same of this group, but did not want to offend anyone.  How does one cope with constant disequilibrium or even unpredictable sporadic episodes of lengthy dizziness? Can one drive a car?  I can see how this would be challenging with forward and lateral acceleration.  Etc......

[[Fi...]]

How do people cope with this stuff?!  I may have had it this whole time but was too distracted by my other symptoms to notice it as much.  But, now it is very profound and scary.  I don’t know how to cope!!!  Between the Floaty Boaty and Dp/Dr.  My world is disappearing.

 

 

2yrs since forced CT off Klonopin. 

 

Hi F4Me,

 

I was going to ask the same of this group, but did not want to offend anyone.  How does one cope with constant disequilibrium or even unpredictable sporadic episodes of lengthy dizziness? Can one drive a car?  I can see how this would be challenging with forward and lateral acceleration.  Etc......

 

dm123,

Do you have the Floaty Boaty as well?

[[La...]]

Hi,

For me, coping has to do with getting through each day the best I can. No, there's no driving -- actually, it's pretty hard just to walk. I've been using a walker for quite awhile now, but I'm also dealing with significant foot issues, including a slow-healing fracture and intense pain in the other foot. In order to get through it, I read, listen to music, stay in contact with caring people, distract myself as much as possible, do exercises, get physiotherapy, eat healthy food, etc.

 

There are some pretty special people on BB, too, so that helps. I do try to stay away from the most negative posts, if I can, but I totally understand the need to vent and to seek support. We all need that.

 

I don't think there's a magic bullet. There's just the consistent, day-to-day effort to keep one's head in the right place and hope that the body is constantly moving towards healing in the meantime. We know that others have healed from this, so there's reason for hope.

[[Fi...]]

This is just breaking me down.    My gosh. 

[[La...]]

Have you read either of Baylisssa Frederick's books? She, too, was dizzy for quite some time. It helps me to know that she came out the other end, even though she took the same medication I did, and for a longer period of time.

[[cs...]]

How do people cope with this stuff?!  I may have had it this whole time but was too distracted by my other symptoms to notice it as much.  But, now it is very profound and scary.  I don’t know how to cope!!!  Between the Floaty Boaty and Dp/Dr.  My world is disappearing.

 

 

2yrs since forced CT off Klonopin. 

 

 

I was going to ask the same of this group, but did not want to offend anyone.  How does one cope with constant disequilibrium or even unpredictable sporadic episodes of lengthy dizziness? Can one drive a car?  I can see how this would be challenging with forward and lateral acceleration.  Etc......

 

dm123,

Do you have the Floaty Boaty as well?

 

Hi F4Me

 

No I do not, but I have hyperacusis and sporadic tinnitus.  Both are improving .   

 

I’m very interested in this thread.  I’m going to try to read up more on it.

[[La...]]

Hey dm123,

Thanks for your interest. Any info you can share would be much appreciated. The studies that abcd shared are quite interesting, too, so those would be worthwhile checking out. I'm just making my way through the second one. Clearly, there's interest by researchers in Mal de Debarquement Syndrome now, but whether that moniker reflects what we're dealing with here on BB is another question. I'm thankful to see the interest and the research, though.

 

Tinnitus is quite common, and I have it too. I can ignore it, though, although it has been much louder in the past. Really, if I can walk and not be dizzy, then a little tinnitus won't bother me.

[[Fi...]]

Lapis,

 

Yes, I have read Baylissa’s book and spoken to her directly.  She said she actually had more symptoms but the editor wouldn’t let her put them in the book. 

 

Like you, if I could get rid of the dizziness and can handle a little tinnitus.    What gets our attention grows!!!

[[La...]]

Hey F4M,

I'm glad you got to talk to Baylissa. I did so a couple of years ago, and I've kept her in my heart ever since. I hope she gave you a boost!

 

Hang in there!

[[Fi...]]

Lapis,

 

Have there been people that have overcome the dizziness or is an ongoing symptom?  I know that people can have it a varying degrees.  This is such a new symptom for me it really has me very distressed and discouraged.  I can’t be bedridden I have so many people relying on me.

[[La...]]

Yes, for sure, F4M! Unfortunately, people don't always come back to tell us how they're doing, but yes, of course, people get better. It's a symptom that, like the others, should go away. There's no timetable, though, and to my knowledge, no way to speed things up. If people have other compounding factors, then that can make things worse. In my case, I have my foot issues, so that's hugely problematic for me. But I've never stayed in bed. Not one day. It would depress the hell out of me. I get up. I use my walker. I wobble around. I do my exercises. I try to stay mobile. On better days, I have more hope. On other days, I cry.

 

I think we just have to be as strong as we possibly can. Please take good care!

[[Fi...]]

You too Lapis.  Thanks.

[[cs...]]

Hey dm123,

Thanks for your interest. Any info you can share would be much appreciated. The studies that abcd shared are quite interesting, too, so those would be worthwhile checking out. I'm just making my way through the second one. Clearly, there's interest by researchers in Mal de Debarquement Syndrome now, but whether that moniker reflects what we're dealing with here on BB is another question. I'm thankful to see the interest and the research, though.

 

Tinnitus is quite common, and I have it too. I can ignore it, though, although it has been much louder in the past. Really, if I can walk and not be dizzy, then a little tinnitus won't bother me.

 

Hi Lapis,

 

I read the otolith vs. canal vestibular dysfunction article link very very closely.  I’m going to look at the links abcd posted next.

 

Otolith is not only perceived as more severe by vestibular dysfunction patients, but it’s far more relevant to postural control (and you know this all too well having survived some falls)

 

I found the quotes below very interesting , and I’m delving into the vestibular neuroantomy as it pertains to inneervation to the motor neurons via the brainstem from the cervical through the sacral cord.  Looking at a cross section of the brainstem one can clearly differentiate between the vestibular nuclei and the other nuceli.

 

I only bring this up because we know that Benzodiazaphines do affect brainstem neurons, although not as profoundly as other more plastic regions of the brain.

 

Here are some of the quotes

 

Quotes

 

However, it is thought that the contribution of the otoliths is the main vestibular source for postural control [23, 25]. The vestibulospinal pathways that receive canal input terminate on motor neurons of the cervical cord, whereas those of the otolith organs innervate motor neurons from the cervical through the sacral cord [26]. The otolith organ input facilitates activation of antigravity muscles and modulates the tone of neck, trunk, and limb extensor muscles enabling the maintenance of posture [25]. Consequently, it seems logical to conclude that dysfunction of canals versus that of otolith organs would effect perceived orientation and balance differently.

.......

 

No individuals with canal only dysfunction reported falls. This may be attributed to the neurophysiological role that the otolith organs play in modifying tone in antigravity muscles for postural control. Additional support for this theory was demonstrated with the greater severity of perceived limita- tions with daily activities, as measured by DHI, in individuals who had otolith dysfunction, regardless of the presence of canal dysfunction (Groups 2 and 3). In particular, the physical domain scores were significantly higher (worse) scores when all individuals were grouped based on presence of otolith dysfunction, regardless of whether or not the individuals had canal dysfunction (Groups 2 and 3), as compared to those with canal only dysfunction (Group 1). Walking in the market, walking down a sidewalk, and bending over were the items within the physical domain of the DHI that demonstrated the most differences. The findings of greater subjective reports of falls and the limitations with daily activities in this study are supported by evidence of objective impairments of postural control in those with reduced otolith function. Basta et al. [12] demonstrated that sensory organization testing and trunk sway measures during stance and gait activities were impaired in those with otolith only dysfunction as compared to healthy controls. Serrador et al. [33] demonstrated that with age there is a reduction of utricular function as measured by ocular counter rolling, and as a result, individuals can have increased postural sway and be at increased risk of falling.

 

......

 

This study provides support for the predominant functional contribution of the otolith organs to postural control, as was reported by Markham [25]. However, further objective comparison of postural control and balance impair- ments between those with canal versus otolith dysfunction needs to confirm these findings.

 

End quotes

 

 

So, *if * benzdiazaphines do more profoundly affect otolith function ( rather than canal function), perhaps this explains why it is literally so disabling in PWS....being that postural control itself is severely compromised.

 

 

[[La...]]

Exactly, dm123.

 

As I mentioned, I came across this study a number of years ago, and I eventually got in contact with one of the authors. I was asking about vestibular rehabilitation that might be effective for those with otolith issues, and, at the time, there was little she could offer. It seems that the VR mostly addresses canal issues. I recently asked a physiotherapist who has done a small bit of VR training what she learned about helping those with MdDS, and she said that such symptoms were expected to fade away over time. I'm not sure if there have been any updates to that info.

 

People can certainly seek out VR-trained physiotherapists in their areas and find out what options are currently available in terms of symptomatic help. Personally, I'm trying to focus on staying as functional as possible, but on bad days (like yesterday, when I had a 9 out 10 level of dizziness), I'm really at the mercy of the forces that are described in the article. When I try to sit down  on a dizzy day, my body is pushing me forwards, so the internal muscular fight between wanting my hips to go backwards and that intense force going in the opposite direction is excruciating. There's no other word.

 

However, I have the unique situation of having a slow-healing fracture in one foot and a chronic issue in my other foot, so that has complicated my situation a lot. I can only hope that others aren't as badly affected as me. My suggestion to others would be to stay as functional, mobile, flexible and strong as possible. Lying down all day is NOT a good idea, as it leads to further weakness and dysfunction. In my case, the help of a physiotherapist is absolutely essential. Exercises (in lying and sitting) can help. If people can walk (e.g. on a treadmill, around the house, with a cane or walker) or do a stationary bike, then those activities would be helpful too.

 

Thanks for your input, dm123. I'll be interested to hear your thoughts on the articles that abcd posted. Take care, and I hope you're not suffering too badly these days.

 

 

[[La...]]

Hi,

I just wanted to share this abstract on the testing for otolith organ function, in case it's of interest. dm123, it might add useful info to your research on this topic. If anyone has had this kind of vestibular testing, I'd be interested to know what the results were. I don't believe it was part of the testing I did.

 

https://www.ncbi.nlm.nih.gov/pubmed/29887827

 

2018 May 25;9:366. doi: 10.3389/fneur.2018.00366. eCollection 2018.

 

Otolithic Receptor Mechanisms for Vestibular-Evoked Myogenic Potentials: A Review.

Curthoys IS1, Grant JW2, Burgess AM1, Pastras CJ3, Brown DJ3, Manzari L4.

 

Author information

 

1

    Vestibular Research Laboratory, School of Psychology, The University of Sydney, Sydney, NSW, Australia.

2

    Department of Biomedical Engineering and Mechanics, VA Tech, Blacksburg, VA, United States.

3

    The Menière's Laboratory, Sydney Medical School, The University of Sydney, Sydney, NSW, Australia.

4

    MSA ENT Academy Center, Cassino, Italy.

 

Abstract

 

Air-conducted sound and bone-conduced vibration activate otolithic receptors and afferent neurons in both the utricular and saccular maculae, and trigger small electromyographic (EMG) responses [called vestibular-evoked myogenic potentials (VEMPs)] in various muscle groups throughout the body. The use of these VEMPs for clinical assessment of human otolithic function is built on the following logical steps: (1) that high-frequency sound and vibration at clinically effective stimulus levels activate otolithic receptors and afferents, rather than semicircular canal afferents, (2) that there is differential anatomical projection of otolith afferents to eye muscles and neck muscles, and (3) that isolated stimulation of the utricular macula induces short latency responses in eye muscles, and that isolated stimulation of the saccular macula induces short latency responses in neck motoneurons. Evidence supports these logical steps, and so VEMPs are increasingly being used for clinical assessment of otolith function, even differential evaluation of utricular and saccular function. The proposal, originally put forward by Curthoys in 2010, is now accepted: that the ocular vestibular-evoked myogenic potential reflects predominantly contralateral utricular function and the cervical vestibular-evoked myogenic potential reflects predominantly ipsilateral saccular function. So VEMPs can provide differential tests of utricular and saccular function, not because of stimulus selectivity for either of the two maculae, but by measuring responses which are predominantly determined by the differential neural projection of utricular as opposed to saccular neural information to various muscle groups. The major question which this review addresses is how the otolithic sensory system, with such a high density otoconial layer, can be activated by individual cycles of sound and vibration and show such tight locking of the timing of action potentials of single primary otolithic afferents to a particular phase angle of the stimulus cycle even at frequencies far above 1,000 Hz. The new explanation is that it is due to the otoliths acting as seismometers at high frequencies and accelerometers at low frequencies. VEMPs are an otolith-dominated response, but in a particular clinical condition, semicircular canal dehiscence, semicircular canal receptors are also activated by sound and vibration, and act to enhance the otolith-dominated VEMP responses.