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

[[La...]]

Well, I gotta say, BB has helped. Plus keeping my mind busy -- reading, listening to the radio, watching things online, staying connected with people, trying to move around to the best of my ability, etc. I have also done my fair share of crying and whining and carrying on. It's a really tough symptom to deal with. Thankfully, I have some less dizzy days, and those are the days that keep me hopeful.

 

It's just a one-day-at-a-time thing for me. I really can't think of any other way to do it. Just get through it.....

[[Aj...]]

So, you're pretty sure this feeling is from the benzo, then? It sounds like it to me, but I always think it's good to get it checked out, if you're unsure. Dizziness can be caused by so many things, but it can be hard to diagnose.

 

Do you mean me?

 

It has got much worse since withdrawal. So the exacerbation is due to withdrawal.

[Guest [Le...]]

Hi Lapis and Everyone!

 

Just thought I’d check in at two years off.

 

Dizziness is finally way down and, weirdly, if I get up in the middle of the night, it is sometimes completely gone.

 

Even though it’s around during the day, it’s no longer debilitating. Once I walk it dissipates, and I can turn without losing my balance as long as I don’t do it suddenly. It’s most pronounced when I get up from lying down, but I can actually stand up and walk immediately without having to sit up slowly, wait, stand slowly, wait, walk a few steps . . . well, you know the drill.

 

Amazing it took two years to stop completely spinning, and maybe one day it will stop completely, but I’m grateful that it’s at a level that I can live with now, because it was really frightening trying to navigate the subways like this, yikes. For a long time I could only manage taxis and some buses.

 

Hoping everyone else is making steady progress, and please take good care of your foot, Lapis!

 

[[La...]]

Hi LeslieAsh,

Congrats! That's fantastic news! Thanks so much for updating us on how it's going for you. It's proof positive that this symptom fades away. I'm sure you're not taking any of those good times for granted. I know I'd be over the moon to feel what you're feeling. Enjoy it all, and please stay in touch!

 

[[Fi...]]

Well, I gotta say, BB has helped. Plus keeping my mind busy -- reading, listening to the radio, watching things online, staying connected with people, trying to move around to the best of my ability, etc. I have also done my fair share of crying and whining and carrying on. It's a really tough symptom to deal with. Thankfully, I have some less dizzy days, and those are the days that keep me hopeful.

 

It's just a one-day-at-a-time thing for me. I really can't think of any other way to do it. Just get through it.....

 

Lapis,

 

I just got back from my neurologist, so far tests are not showing anything with regards to the Floaty Boaty feeling.  Blood work is showing only vitamin D is low.    Personally I’m Shocked that this could actually be Benzo WD.  Shows my ignorance. 

 

How are you doing?  Things going ok? 

F4M

[[La...]]

Hi F4M,

Well, that's good news, then! I know it seems unbelievable that benzos can create such intense disequilibrium, but I think the hundreds of posts here on BB on this exact topic attest to the fact that it's true. As well, the medical literature's reference to benzodiazepines as "vestibular suppressants" is quite descriptive in and of itself. According to an Ear, Nose and Throat textbook excerpt that I came across a few years ago, these medications interfere with the process of vestibular compensation, which is the body's way of normalizing balance. So, the longer one takes them, the more s/he is holding up that process.

 

Anyway, it's good that the neurologist didn't find any other worrying signs with your testing. You can correct that vitamin D issue with some supplementation. I take a supplement for that daily, since I'm housebound. Also, here in Canada, we just don't get enough sunshine for about half of the year, so supplementation is recommended.

 

By the way, when doing research on this topic a few years ago, I also came across a paper that was able to pinpoint the way that the benzo (in the paper, it was lorazepam) selectively suppressed a certain part of the vestibular system. After finding that paper, things made better sense to me. What didn't make sense was the fact that the doctors I consulted weren't familiar with the effects of long-term benzo use, and basically suggested that the "small dose" I was on couldn't possibly cause me any trouble.

 

Right.

 

Uh-huh.

 

Ah, well, we just have to keep going.

 

Are you having whole days of dizziness? Or just partial days? I really hope it's a short-lived thing for you. Fingers crossed!

 

 

[[Fi...]]

Hi F4M,

Well, that's good news, then! I know it seems unbelievable that benzos can create such intense disequilibrium, but I think the hundreds of posts here on BB on this exact topic attest to the fact that it's true. As well, the medical literature's reference to benzodiazepines as "vestibular suppressants" is quite descriptive in and of itself. According to an Ear, Nose and Throat textbook excerpt that I came across a few years ago, these medications interfere with the process of vestibular compensation, which is the body's way of normalizing balance. So, the longer one takes them, the more s/he is holding up that process.

 

Anyway, it's good that the neurologist didn't find any other worrying signs with your testing. You can correct that vitamin D issue with some supplementation. I take a supplement for that daily, since I'm housebound. Also, here in Canada, we just don't get enough sunshine for about half of the year, so supplementation is recommended.

 

By the way, when doing research on this topic a few years ago, I also came across a paper that was able to pinpoint the way that the benzo (in the paper, it was lorazepam) selectively suppressed a certain part of the vestibular system. After finding that paper, things made better sense to me. What didn't make sense was the fact that the doctors I consulted weren't familiar with the effects of long-term benzo use, and basically suggested that the "small dose" I was on couldn't possibly cause me any trouble.

 

Right.

 

Uh-huh.

 

Ah, well, we just have to keep going.

 

Are you having whole days of dizziness? Or just partial days? I really hope it's a short-lived thing for you. Fingers crossed!

 

Lapis,

 

I think it varies in intensity.  I did get a walker that has a seat on it so I can sit when needed.  I walked outside for a little while earlier today.  My vision is blurry so that with the Floaty Boaty is really challenging me. 

 

If you don’t mind me asking, how long have you been housebound?

 

Thank you for sharing that information from that article with me.  I really appreciate it. 

 

Have a good night. 

[[La...]]

Hi F4M,

Good idea to get the walker, I think. You do what you have to do under such circumstances.

 

As for me, my inability to walk and get out is complicated by ongoing foot issues (slow-healing fracture in one foot, chronic issue with other foot), which have been made much worse by the dizziness. If I weren't dizzy, these things could heal in a much more normal timeline. Suffice to say, it's been way too long.

 

Which meds did you take and for how long? What dose? What kind of taper did you do/are you doing? Perhaps you could put a signature in so that the rest of us can understand your story.

[[La...]]

Hi Dizzy Buds,

I just wanted to share a recent study on Mal de Debarquement, which is a topic that seems to come up around here fairly regularly. There's an abstract, plus the full study, so if you're interested, do take the time to read the whole thing. It's based on questionnaires and interviews with those suffering the symptoms, so it's not one of those randomized controlled trials or anything.

 

Some interesting points: Where a woman is in her menstrual cycle seemed to affect a number of the women in the study. Also, some of them were taking either benzos or SSRIs, both of which, as we all know, are associated with dizziness. A number of people reported feeling worse when lying down. Some felt better when in motion, and some felt worse.

 

Anyway, there's lots more to consider, so do have a look! And if you do read it, please share your thoughts here.

 

"Comprehensive Clinical Profile of Mal De Debarquement Syndrome"

 

Abstract:

 

https://www.ncbi.nlm.nih.gov/pubmed/29867709 

 

Full Study:

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5950831/ 

 

 

[[cs...]]

Hi Dizzy Buds,

I just wanted to share a recent study on Mal de Debarquement, which is a topic that seems to come up around here fairly regularly. There's an abstract, plus the full study, so if you're interested, do take the time to read the whole thing. It's based on questionnaires and interviews with those suffering the symptoms, so it's not one of those randomized controlled trials or anything.

 

Some interesting points: Where a woman is in her menstrual cycle seemed to affect a number of the women in the study. Also, some of them were taking either benzos or SSRIs, both of which, as we all know, are associated with dizziness. A number of people reported feeling worse when lying down. Some felt better when in motion, and some felt worse.

 

Anyway, there's lots more to consider, so do have a look! And if you do read it, please share your thoughts here.

 

"Comprehensive Clinical Profile of Mal De Debarquement Syndrome"

 

Abstract:

 

https://www.ncbi.nlm.nih.gov/pubmed/29867709 

 

Full Study:

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5950831/

 

Hi Lapis, thanks for posting this

 

“Where a woman is in her menstrual cycle seemed to affect a number of the women in the study. ”

 

As you know Neurosteroids are very potent PAMs of the GABAaRs.  There’s much research in this area. 

 

In your opinion, anecdotally, are women more susceptible to vestibular disturbances following new benzdiazaphine withdrawal than men?

[[La...]]

Anecdotally, yes! I would have to say so. Maybe some other dizzy gals around here can chime in, but I think our cycles do play a role.

[[cs...]]

Anecdotally, yes! I would have to say so. Maybe some other dizzy gals around here can chime in, but I think our cycles do play a role.

 

I found it in table 1. For the MT and non-MT its a resounding yes.  Approximately 80/20% F/m

 

“There was a similar distribution of women vs. men in the MT vs. non-MT groups with a strong skew toward women (81% women vs. 19% men)”

 

 

 

Quote

 

Since the majority of affected individuals with MdDS were women, the relationship between MdDS and the effect of hormone transitions was queried (Table 6). Ages of onset of menarche, menopause, and MdDS showed no statistically significant differences between the MT and non-MT groups. Peri-menstrual worsening of symptoms was typical (71%) in both groups. Of MdDS occurring during hormonal transitions, only contraception change was significantly more common in the non-MT group.

 

End quote

 

Table 6.

 

 

So it’s definitely related to the Neurosteroid  GABAERGIC system, at least in part.

 

 

Table 8

I hadn’t realized benzdiazaphines were so effective for this type of thing.

[[La...]]

Well, the use of benzos and SSRIs created a huge question mark for me, because they can both CAUSE dizziness. I wouldn't touch either one, and I have to wonder if those people were making things worse overall by taking them. Since this is a questionnaire, rather than a study, it's difficult to know certain things, but I just don't understand the use of a "vestibular suppressant" for an ongoing dizziness problem. They are sometimes prescribed short-term (a day or two) for some types of dizziness, but as we all know, they aren't meant for long-term use. SSRIs, too, have dizziness as a side effect.

 

As far as menstrual issues go, I wouldn't want to take anything to try to counteract what's going on. There are probably quite a few threads on this topic here on BB, but personally, I wouldn't want to take any hormonal medications of any kind. I just think it would be too fraught.

 

 

[[cs...]]

 

Hi Lapis,

 

I agree.  Medicating based on theory can be risky business.  I did not like the fact that they indicated Benzodiazaphines were effective and non habit forming at low doses.  This simply isn’t true.

 

 

I’m posting a long dissection of an article on stress, stress hormones, and vestibular compensation.  I’m posting it as an FYI and as a possible explanation as to why and how vestibular symptoms perpetuate long after benzdiazaphine washout.  It aligns well with the layman’s benzdiazaphine model, but I suspect it’s only part of the full story.

 

 

Well, the use of benzos and SSRIs created a huge question mark for me, because they can both CAUSE dizziness. I wouldn't touch either one, and I have to wonder if those people were making things worse overall by taking them. Since this is a questionnaire, rather than a study, it's difficult to know certain things, but I just don't understand the use of a "vestibular suppressant" for an ongoing dizziness problem. They are sometimes prescribed short-term (a day or two) for some types of dizziness, but as we all know, they aren't meant for long-term use. SSRIs, too, have dizziness as a side effect.

 

As far as menstrual issues go, I wouldn't want to take anything to try to counteract what's going on. There are probably quite a few threads on this topic here on BB, but personally, I wouldn't want to take any hormonal medications of any kind. I just think it would be too fraught.

[[cs...]]

https://www.frontiersin.org/articles/10.3389/fneur.2012.00116/full

 

Quote

 

Stress may influence central vestibular function in health and disease either directly through the actions of glucocorticoids (cortisol and corticosterone) on ion channels and neurotransmission in the brain, or indirectly through the effects of stress-related neuroactive substances (e.g., histamine, neurosteroids) on these structures. In the periphery stress hormones also regulate the function of ion transporters and ionic homeostasis in the inner ear, while in some conditions the anti-inflammatory actions of glucocorticoids may also come into play (Hamid et al., 2009). Stress hormones may thus modulate peripheral vestibular end-organ and cochlear function through similar mechanisms of ionic homeostasis (Canlon et al., 2007; Hamid et al., 2009), and modulate central processing in the vestibular and auditory pathways (Seemungal et al., 2001; Paterson et al., 2004; Straka et al., 2005; Mazurek et al., 2010).

 

 

………

 

In relation to vestibular lesions and central vestibular compensation, evidence from animal studies has demonstrated neural pathways linking the vestibular nuclei with the limbic system including the hypothalamus and that stress responses evoked by vestibular symptoms promote synaptic and neuronal plasticity in the vestibular system. However in man conclusive evidence relating to the interactions between stress and vestibular system plasticity is lacking. In patients who remain poorly compensated following vestibular damage, clinical evidence implicates stress both as a causative agent and as a compounding factor that impedes compensation. In parallel the use of steroids in the treatment of acute vestibular symptoms also indicates a role for the acute stress response in facilitating vestibular compensation. Factors that tend to constrain a fuller understanding of the effects of stress in human vestibular disease include sometimes nebulous clinical definitions, difficult to measure endpoints whether clinical or physiological, and variations in the stress response between individuals and within the same individual over time. Nevertheless, the effects of stress on vestibular function and compensation are significant and increasingly recognized as important in the management of vestibular dysfunction in man.

 

…..

 

Excessive Stress Can Impair Compensation

An optimal level of stress and GR activation seems necessary to facilitate vestibular compensation because additional stress, in the form of restraint applied to a compensating animal after UVD, impedes behavioral recovery and causes de-compensation (the re-appearance of vestibular deafferentation symptoms; Yamamoto et al., 2000). Anecdotally it has been reported that just handling animals after UVD would cause nystagmus to re-appear, perhaps due to stress (Curthoys and Halmagyi, 1995). In addition to the acute de-compensating effects of stress, it should also be noted that neurogenesis and the survival of newly born neurons in the hippocampus is sensitive to stress (Gould et al., 2000; Snyder et al., 2009). Lacour and co-workers have recently provided evidence to suggest that neurogenesis occurs in the cat MVN over a period of time after UVN, and have proposed that this may be involved in vestibular compensation (Tighilet et al., 2007;Dutheil et al., 2009, 2011). Stress may therefore also interact with vestibular compensation by affecting the survival of new neurons in the MVN after vestibular deafferentation, though this remains to be investigated experimentally.

 

…….

 

Stress Hormones and Neurosteroids Affect MVN Neuron Excitation

Animal studies suggest glucocorticoids facilitate behavioral recovery during vestibular compensation by actions on the medial vestibular nucleus (MVN) and the cerebellum (Seemungal et al., 2001; Paterson et al., 2004; Straka et al., 2005). Prednisone has been shown to excite neurons in the MVN of the cat (Yamanaka et al., 1995a). In addition, neurosteroids can significantly modulate GABAergic and glutamatergic neurotransmission in the MVN. Pregnanolone sulfate and DHEAS reduce GABA receptor efficacy and thus enhance neuronal activity (Yamamoto et al., 1998a,b), while 20-hydroxyecdysone increases GABA activity thus inhibiting neuronal excitability (Okada et al., 1998). Pregnanolone sulfate modulates glutamate receptors and increases MVN neuron activity (Yamamoto et al., 1998b). Tetrahydrodeoxycorticosterone and allopregnanolone also modulate MVN neuronal activity by their actions on GABA and AMPA/kainate receptors (Grassi et al., 2007), while 17 β-estradiol modulates MVN activity by increasing excitatory glutamatergic transmission and reducing GABAergic transmission (Grassi et al., 2009a,b, 2010). These various effects represent a potent and hitherto largely uncharacterized mechanism that regulates the function of the vestibular neural networks. These modulatory effects are likely to be important both in the normal state with basal levels of circulating stress hormones, and the stressed state with elevated levels of stress hormones. In addition, such endocrine modulatory control may mediate the effects of estrogens in menstruating women and potentially explain the increasingly apparent links between the menstrual cycle and the susceptibility to motion sickness, dizziness, and migrainous vertigo (Grassi et al., 2009a)

 

 

End quote

 

Here’s the Grassi reference.  I will read it when I have more time…..I’m sure there are many in this area.

 

Grassi, S., Frondaroli, A., Dieni, C., and Scarduzio, M. (2009a). Effects of 17beta-estradiol on synaptic plasticity in the rat medial vestibular nuclei. Acta Otolaryngol. 129, 390–394.

 

 

 

And this, below. In the laymans thread the central thesis is the perpetuation of symptoms (PWS) via a dysfunctional stress system that affects Neuroplasticity, Action potential dynamics of the neurons, and aberrant neurogenesis.(and oxidative and mitochondrial stress also feed back into the stress system)

 

Negative stress is deconstructive, and positive stress can be constructive. With vestibular disturbances, the actual symptoms of the disturbance provoke additional negative stressors and the cycle perpetuates.  From the other quote above, we know that Neurosteroids and stress hormones profoundly affect the excitability of neurons and thus their plasticity, and in vestibular nuclei would exasperate vestibular dysfunction.

 

More From this article::

 

Quote

 

Dimensions of the Stress Response in Humans

While the above focuses on the physiological activation of the HPA axis as an indicator of stress, a more holistic view in recent literature defines stress as “experiences that are challenging emotionally and physiologically” (McEwen, 2007), which normally produce protective and adaptive effects but can also produce deleterious outcomes in certain situations. Stress is regarded as a mechanism of “allostasis,” the process of maintaining homeostatic stability by active means through the production of stress hormones, while “allostatic load or overload” results in wear and tear on the body and brain when this system is dysfunctional (McEwen, 2007). Colloquially this has been termed “good stress and bad stress,” with the former leading to a beneficial outcome while the latter is associated with a failure of homeostatic recovery and the development of abnormal physiological or psychological states

 

The effects of stress axis activation on vestibular compensation demonstrated in animal studies, where recovery is facilitated by acute stress but impeded by inappropriate stress as discussed above, can be viewed as an example of such an interaction.

 

 

End quote

 

 

And the authors go on to state the role of decompensated stress response on chronic dizziness, ie poorly compensated patients….

 

Quote

 

If the process of vestibular compensation is inadequate, the underlying dysfunction may persist and eventually present as chronic dizziness (Bronstein et al., 2010). Thus the nature of the stress response in individual patients is likely to vary according to the underlying dysfunction, with an acute episode of vertigo in vestibular neuritis that gradually subsides having a different stress response profile compared with the unpredictable episodes in patients with Meniere’s disease or migrainous vertigo, or the chronic dizziness of the poorly compensated patient.

 

While animal studies (e.g., in Figure 2) indicate that vestibular imbalance is stressful in itself, the nature of additional stressors that may interact to influence compensation in the human clinical context remain to be determined.

 

As discussed by Joels et al. (2006), a normal stress response within the context of a learning situation focuses attention and improves learning and memory, and this may be a significant role for the vestibular-evoked stress response in facilitating compensation. However for optimal learning to occur the stressor must occur at the same time and act on the same neural circuits (Joels et al., 2006), so that if for example the vestibular stress response competes with an additional stressor such as anxiety, this may prevent vestibular compensation from occurring optimally.

 

End quote

 

The author goes on to state how the hippocampus is involved in vestibular disturbances.  We know the hippocampus is profoundly affect by benzdiazaphine used because it’s highly plastic and neurogenic.

 

 

And this

 

Quote

 

Increased physical activity has been shown in animals to affect brain morphology by promoting neurogenesis in the hippocampus (van Praag et al., 2005) and vestibular exercises and the promotion of physical activity in general may have similar effects in humans. Social support also seems important to alleviate the effects of increased allostatic load by helping humans to cope with acute and chronic stressors (McEwen and Gianaros, 2011). While these are the basic components of any vestibular rehabilitation strategy, further research is needed to clarify the interactions between these interventions and the stress response in relation to compensation.

 

Consequently, a significant problem in the study of the interactions between stress and vestibular compensation in humans is the potentially idiosyncratic variation in stress responsiveness between patients, and also in the same patient over time. While animal models offer the potential to isolate and control many of these factors, the application of findings from animal studies to the human clinical context, and the design of effective research paradigms to understand these interactions and their effect on brain plasticity, remains a significant challenge for the foreseeable future. Understanding the factors that optimize a “good” stress response during vestibular rehabilitation to promote compensation, and the extent to which this is altered in anxious patients, deserves further investigation.

 

End quote

 

 

And it’s clear that chronic disequilibrium induces more negative stress

 

Quote

 

This suggests a chronic stress response in patients with persistent vestibular dysfunction (Horner and Cazals, 2005). In a prospective longitudinal study of the relationship between stress and the symptoms of Meniere’s disease over a period averaging 7 months, Andersson et al. (1997) found that dizziness was the symptom most associated with stress. However there was no evidence that stress on preceding days was responsible for the symptoms, suggesting that chronic stress could be the result of symptoms rather than the cause (Andersson et al., 1997).

 

It is well established that patients with chronic stress undergo hippocampal remodeling and display hippocampal atrophy with deficits in spatial memory (McEwen, 2001; Kim and Diamond, 2002). However, vestibular inputs are also known to be very important in the dynamic spatial tuning of hippocampal place cells (Stackman et al., 2002; Russell et al., 2006). Thus the loss of vestibular input, as well as chronic stress, may synergize in causing the deleterious effects on hippocampal function and total volume in patients.

 

End quote

 

 

 

A cycle ensues.  It’s not just anxiety, because the stress alters Neurosteroid and stress hormone homeostasis, which exasperates the disequilibrium physiologically from a neuroplastic, neurogenic and action potential perspective.  And neuroatonomically the vestibular neural system is tied to the hypothalamic and limbic system (emotional processing).  There’s a figure early  in the source document.

 

https://www.frontiersin.org/files/Articles/21102/fneur-03-00116-HTML/image_m/fneur-03-00116-g001.jpg

 

Ultimately stress resiliency partially determines outcome.  ( chronic vs. recoverable).  And we know that in benzdiazaphine PWS,  stress resiliency is greatly compromised, and this perpetuates the symptomatic loop.

 

Quote

 

It was postulated that autonomic symptoms initially associated with a vertiginous attack cause anxiety and further arousal, which worsens the vertigo in a vicious cycle (Yardley et al., 1994).

 

…..

In particular the nucleus tractus solitarii have extensive relationships with the vestibular nuclei both via direct projections and indirectly through the parabrachial nucleus, which provides a major input into the limbic system including the extended central amygdaloid nucleus, the infralimbic cortex, and the hypothalamus (Balaban and Thayer, 2001; Balaban, 2002).

 

End quote

 

 

Quote

 

However repeated exposure to stressful stimuli or chronic stress can lead to an inhibition of brain plasticity and lasting detrimental changes in the hippocampus, amygdala, and prefrontal cortex (de Kloet et al., 2005; McEwen, 2007; Roozendaal et al., 2009). A range of factors influence the responsiveness of an individual

 

 

End quote

 

 

Quote

 

An aberrant acute stress response elicited by vestibular symptoms may, in susceptible individuals, affect the process of central compensation, possibly leading to lasting deficits.

 

End quote

 

[[La...]]

Thanks so much for sharing this info, dm123. I'll have a closer look today, if I can. I appreciate your saying that you think the above issue is only part of the full story. In my case, I've had numerous stressful experiences where my dizziness does NOT increase. Yesterday, for instance. Fire alarm. No increase in dizziness in what was, largely, a less dizzy day for me. Another time I got stuck in an elevator. You can bet I was extremely stressed, as I was with yesterday's alarm, but those stress responses did NOT bring on increased dizziness. To me, there are other things at play, in my case. I usually get whole day of intense dizziness, followed by another day with less intense dizziness. There's no rhyme or reason. The only change is that I went to sleep. My dizziness has never been event-related.

 

The fact that dizziness is stressful to the body in and of itself makes this even more of a brutal situation for many of us. Feeling as if one is going to fall at any moment is unnerving. Having broken a bone in one of my feet attests to the fact that we have to react to the sudden internal sensations in what may be awkward ways. Muscles react to dizziness in order to prevent us from falling. It's inevitable and, of course, lifesaving. At least, I didn't hit the ground with my head!

 

One other fact for me: I'm perimenopausal at this point, and I suspect that might be playing a role in my situation. I'd love to hear from the other women regarding their own situations.

[[La...]]

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.

 

 

 

 

[[...]]

Hey Lapsy, I did read it and my very short take on it was overall disappointment.  I really don't know I gleaned anything of any value from it or even food for thought.  Total sampling of 40 people, questions and reportings too scanty (including ADD, seriously?), no detail on medication history (except med "changes"), no detail on past injuries (concussions, etc) etc, etc. 

 

Also, this.  Huh?  Since when?  What/how/why?

"Since women and men could experience MdDS symptoms differently, scores were analyzed separately for women and men as well as for all MT and all non-MT respondents".

 

My eyes did bulge over the duration though, sheesh. 

 

So, yeah, seems like it just raised more questions than anything else.  Fail.

 

What did you think?

[[La...]]

Hey abcd,

It's a questionnaire, rather than a study, so, of course, it has limitations. If the gathering of such info helps researchers understand the clinical profile of those suffering and, eventually, find appropriate treatments, then it's certainly useful. I believe the total number of participants was 112 (80 + 42), by the way.

 

I was interested in the info about the effect of women's cycles on their symptoms, as well as the effect of travel, which we've discussed a bit around here. The fact that some of the people were taking medications which we know can cause dizziness (benzos, SSRIs) made me wonder if they were getting appropriate info. I don't think so, but then again, I, too, was told to try an SSRI to see if it would help. For me, it clouds the picture as to what people are suffering from (motion-induced? medication-induced?), but from the reading I've done, it just seems that dizziness is hard to diagnose and treat. The pictures are always muddied by a number of other factors.

 

In my case, I've never thought I have Mal de Debarquement Syndrome, just a similar sensation of motion. One of the first ENTs I saw stated that, before he sent me for other tests and investigations.

 

Clearly, much more study is required. I do wish there was a bigger push to improve the vestibular testing so that there was a better sense of what is actually going on in the brain. It's a complicated system, though.

 

 

[[cs...]]

Thanks so much for sharing this info, dm123. I'll have a closer look today, if I can. I appreciate your saying that you think the above issue is only part of the full story. In my case, I've had numerous stressful experiences where my dizziness does NOT increase. Yesterday, for instance. Fire alarm. No increase in dizziness in what was, largely, a less dizzy day for me. Another time I got stuck in an elevator. You can bet I was extremely stressed, as I was with yesterday's alarm, but those stress responses did NOT bring on increased dizziness. To me, there are other things at play, in my case. I usually get whole day of intense dizziness, followed by another day with less intense dizziness. There's no rhyme or reason. The only change is that I went to sleep. My dizziness has never been event-related.

 

The fact that dizziness is stressful to the body in and of itself makes this even more of a brutal situation for many of us. Feeling as if one is going to fall at any moment is unnerving. Having broken a bone in one of my feet attests to the fact that we have to react to the sudden internal sensations in what may be awkward ways. Muscles react to dizziness in order to prevent us from falling. It's inevitable and, of course, lifesaving. At least, I didn't hit the ground with my head!

 

One other fact for me: I'm perimenopausal at this point, and I suspect that might be playing a role in my situation. I'd love to hear from the other women regarding their own situations.

 

Hi Lapis,

 

I asked the same questions myself prior to posting this.  I do get into differentiating types of stress in the layman’s thread, but in short, we are referring to negative and prolonged stressors, which are very different from positive or acute stressors.

 

Negative stressors have some very common attributes

-unpredictable

-prlolonged and relentless (this refers to psychologically, and physiologically.  By psychologically, if one does not see any end in sight to the stress, example)

-uncontrollable

-repeated

 

Certainly the fire alarm is an acute stressor, especially on the vestibular neurons and auditory neurons, and it is uncontrollable, but it’s not persistently unpredictable.  In fact we physiologically acclimate to such stressors very well due to their predictable nature.  Acute stressors actually help us recover.

 

Getting stuck on an elevator is a very acute stressor, and more closely fits the definition of negative stressors, and had you been trapped in there for many many hours physiologically things would have been different.  I don’t know if your dizziness would have gotten worse, but I do know that a set of physiological changes would have started (including hormonal and Neurosteroid changes) that would have affected your nervous system.  These changes that occur over days and weeks are very different than those that occur over hours or minutes.  The article alludes to these neuroplastic and neurogenic changes.

 

Regarding negative stressors, and allosteric load I’ve repasted the quote below.  It’s a very complex but worthwhile area of study because it affects all aspects of our physiology and recovery.

 

Quote

Dimensions of the Stress Response in Humans

While the above focuses on the physiological activation of the HPA axis as an indicator of stress, a more holistic view in recent literature defines stress as “experiences that are challenging emotionally and physiologically” (McEwen, 2007), which normally produce protective and adaptive effects but can also produce deleterious outcomes in certain situations. Stress is regarded as a mechanism of “allostasis,” the process of maintaining homeostatic stability by active means through the production of stress hormones, while “allostatic load or overload” results in wear and tear on the body and brain when this system is dysfunctional (McEwen, 2007). Colloquially this has been termed “good stress and bad stress,” with the former leading to a beneficial outcome while the latter is associated with a failure of homeostatic recovery and the development of abnormal physiological or psychological states

 

The effects of stress axis activation on vestibular compensation demonstrated in animal studies, where recovery is facilitated by acute stress but impeded by inappropriate stress as discussed above, can be viewed as an example of such an interaction.

 

End quote

 

 

Regarding the perimenapausal aspect, it is related to the Neurosteroids fluctuations, and the bolded text in my original post explains how this ties into vestibular compensation.

 

Also Please note, the article is on compensation, so it attempts to address how the compensation itself is affected by the stress system.  The traumas in the article are clearly not benzdiazaphine induced, but to raise questions on a theory we have to extrapolate what we have and work from there.    The traumas incite compensation, but if that compensation is hampered or inefficient, recovery will be long.  Benzdiazaphines, inflict damage (trauma) on a wide variety of neurons as you know.  In the end, the trauma inflicts dysfunction in how the neurons communicate with each other and how each individual neuron responds to neurotransmitters. 

 

I’ve written a lot about Neurosteroids and Benzodiazaphines and GABAARs , and Neurosteroids are considered part of the greater stress system.  The vestibular nuclei are directly affected by the hypothalamic stress system and the hypothalamic stress system is directly affected by the vestibular nuclei.  And we also know the vestibular nuclei also effect the limbic system.

 

It’s not a complete theory to explain the horrendous symptoms that you have, but the tie in to the Neurosteroid system is telling.    I’ve had my own set of horrendous symtoms during taper and I know how hideous the benzdiazaphine is.  It affects each of us in a unique fashion, because our neurons are  all very very different from a genetic perspective.

[[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

 

[[...]]

Hey abcd,

It's a questionnaire, rather than a study, so, of course, it has limitations. If the gathering of such info helps researchers understand the clinical profile of those suffering and, eventually, find appropriate treatments, then it's certainly useful. I believe the total number of participants was 112 (80 + 42), by the way.

 

I was interested in the info about the effect of women's cycles on their symptoms, as well as the effect of travel, which we've discussed a bit around here. The fact that some of the people were taking medications which we know can cause dizziness (benzos, SSRIs) made me wonder if they were getting appropriate info. I don't think so, but then again, I, too, was told to try an SSRI to see if it would help. For me, it clouds the picture as to what people are suffering from (motion-induced? medication-induced?), but from the reading I've done, it just seems that dizziness is hard to diagnose and treat. The pictures are always muddied by a number of other factors.

 

In my case, I've never thought I have Mal de Debarquement Syndrome, just a similar sensation of motion. One of the first ENTs I saw stated that, before he sent me for other tests and investigations.

 

Clearly, much more study is required. I do wish there was a bigger push to improve the vestibular testing so that there was a better sense of what is actually going on in the brain. It's a complicated system, though.

 

Heya Lap, sorry for the choppy post ...one of those mucho pain days so I tried to spit something out quickly.

 

So anyway, yes, 42 non-MT, okay I rounded it off to 40 ...  I discounted the MT participants as we've agreed it's not applicable in our case ... I did check out their results too though. 

 

As far as you or any other BB having MdDS?  I think - considering it's merely a catch-all label for unexplained "motion triggered" symptoms which they later expanded to include those without the motion component - there's no reason why we couldn't be diagnosed with it.  We fit the bill in that sense, right?  And that's where I was going with my critique of this article because the medication component is such important information to gather.  How many non-MT folk could be diagnosed with the "Spontaneous MdDS" label and are completely unaware that their medication might in fact be the culprit.  Whether it's benzo and/or SSRI or xyz or a combo.  Such a crucial piece of the puzzle and one they apparently totally ignored. 

 

Here's their description of physical stressors:

 

"Examples of physical stressors were concurrent medical illness or recent surgery. Mental health stressors included situations such as increased job or family stress or financial problems. Sleep deprivation was generally over a period of several weeks. Medication changes were of any variety, but the most important was rapid tapering of antidepressants. Hormone changes were typically abrupt switching of oral contraception. P-values reflect differences between the MT and non-MT group totals. There were no significant differences in past medical history or context of trigger between the MT and non-MT groups, but there was a trend toward a higher rater of baseline migraine in the non-MT group".

 

That's very telling that they added the AD tapering although, as we well know, it doesn't have to be rapid tapering either.  But then they totally missed the boat (see what I did there, hah, sorry, couldn't resist ) and didn't delve any deeper.  A missed opportunity for sure.  I think it would've also added a heck of a lot more value had they incorporated a very comprehensive screening for other possible physical causes, e.g. past head/neck injuries, ear infections, epilepsy, and so on.  Wouldn't you think?  Um, more valuable than ADD if they have no interest in quizzing their stimulant use. 

 

I'm not sure what to think about the worsening of sxs around the women's cycles because, if we're hypothesizing about the effect of hormones, how would we explain the fact that over 55% of the women were post-menopausal at time of onset? 

 

Anyhow, I'll stop there, I still give it a big fat thumbs down.  My humble opinion, of course.

 

So, hey, did you see this one on the side bar?  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5834551/  I haven't read it yet, but could be some more fun reading for us.

 

Hi dm!    I'll leave you and Lapis to wax scientific, I'm from a completely different school of thought in that regard, i.e. the blind men and the elephant, the more I read and read, the more I realize we know nuthin' about nuthin'. 

 

[[La...]]

Hi abcd,

You made some good points regarding this survey and what other information would be useful to have in order to provide a true "comprehensive" clinical profile. Thanks for sharing that other study from the sidebar. I noticed that one of the participating doctors is Dr. M. Dai, from NYC -- one of the docs who did the study we looked at awhile back. In that study, they made a great effort to understand the underlying mechanism by which people's balance was affected during a motion-triggered event. Once again, this doesn't apply to those of us who have these symptoms as a result of taking medication. For me, the common factor is likely the actual part of the vestibular system that's affected, but that's just a guess.

 

I keep thinking of a study I read ages ago in which they pinpointed the part of the vestibular system that lorazepam suppressed. I always wish to find a follow-up article to that one. It was done on astronauts, who, inevitably, come back from space and are unable to walk properly due to balance issues.

[[La...]]

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.

[[cs...]]

Hey abcd,

It's a questionnaire, rather than a study, so, of course, it has limitations. If the gathering of such info helps researchers understand the clinical profile of those suffering and, eventually, find appropriate treatments, then it's certainly useful. I believe the total number of participants was 112 (80 + 42), by the way.

 

I was interested in the info about the effect of women's cycles on their symptoms, as well as the effect of travel, which we've discussed a bit around here. The fact that some of the people were taking medications which we know can cause dizziness (benzos, SSRIs) made me wonder if they were getting appropriate info. I don't think so, but then again, I, too, was told to try an SSRI to see if it would help. For me, it clouds the picture as to what people are suffering from (motion-induced? medication-induced?), but from the reading I've done, it just seems that dizziness is hard to diagnose and treat. The pictures are always muddied by a number of other factors.

 

In my case, I've never thought I have Mal de Debarquement Syndrome, just a similar sensation of motion. One of the first ENTs I saw stated that, before he sent me for other tests and investigations.

 

Clearly, much more study is required. I do wish there was a bigger push to improve the vestibular testing so that there was a better sense of what is actually going on in the brain. It's a complicated system, though.

 

Heya Lap, sorry for the choppy post ...one of those mucho pain days so I tried to spit something out quickly.

 

So anyway, yes, 42 non-MT, okay I rounded it off to 40 ...  I discounted the MT participants as we've agreed it's not applicable in our case ... I did check out their results too though. 

 

As far as you or any other BB having MdDS?  I think - considering it's merely a catch-all label for unexplained "motion triggered" symptoms which they later expanded to include those without the motion component - there's no reason why we couldn't be diagnosed with it.  We fit the bill in that sense, right?  And that's where I was going with my critique of this article because the medication component is such important information to gather.  How many non-MT folk could be diagnosed with the "Spontaneous MdDS" label and are completely unaware that their medication might in fact be the culprit.  Whether it's benzo and/or SSRI or xyz or a combo.  Such a crucial piece of the puzzle and one they apparently totally ignored. 

 

Here's their description of physical stressors:

 

"Examples of physical stressors were concurrent medical illness or recent surgery. Mental health stressors included situations such as increased job or family stress or financial problems. Sleep deprivation was generally over a period of several weeks. Medication changes were of any variety, but the most important was rapid tapering of antidepressants. Hormone changes were typically abrupt switching of oral contraception. P-values reflect differences between the MT and non-MT group totals. There were no significant differences in past medical history or context of trigger between the MT and non-MT groups, but there was a trend toward a higher rater of baseline migraine in the non-MT group".

 

That's very telling that they added the AD tapering although, as we well know, it doesn't have to be rapid tapering either.  But then they totally missed the boat (see what I did there, hah, sorry, couldn't resist ) and didn't delve any deeper.  A missed opportunity for sure.  I think it would've also added a heck of a lot more value had they incorporated a very comprehensive screening for other possible physical causes, e.g. past head/neck injuries, ear infections, epilepsy, and so on.  Wouldn't you think?  Um, more valuable than ADD if they have no interest in quizzing their stimulant use. 

 

I'm not sure what to think about the worsening of sxs around the women's cycles because, if we're hypothesizing about the effect of hormones, how would we explain the fact that over 55% of the women were post-menopausal at time of onset? 

 

Anyhow, I'll stop there, I still give it a big fat thumbs down.  My humble opinion, of course.

 

So, hey, did you see this one on the side bar?  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5834551/  I haven't read it yet, but could be some more fun reading for us.

 

Hi dm!    I'll leave you and Lapis to wax scientific, I'm from a completely different school of thought in that regard, i.e. the blind men and the elephant, the more I read and read, the more I realize we know nuthin' about nuthin'. 

 

Hi abcd

 

The more I learn the less I know.  And this is the truth.

 

I’ve just started on this    I wish I had more time to dig into this area.  It’s very interesting.  I’m going to start with Soto’s work.

 

Regarding the table 6, hormone status, that is the Neurosteroid fluctuations at work on the dysfunctional vestibular neural circuits.

 

Regarding table 8, the stress reduction on nonMT@42% is more effective than I would have thought, under clinical testing scenario.  Does the article indicate how long they instituted stress reduction therapy, and what type of therapy it was.  You not only have to reduce negative stressors, but you must introduce a strict regimen of positive stressors.  Otherwise it is not fully effective in restoring homeostasis.