Hi All,

Yet another interesting article concerning those of you with BPPV I found on medline in the journal:

Ann Otol Rhinol Laryngol 2003 Jul;112 (7):574-82


Pathology of benign paroxysmal positional vertigo revisited

The pathophysiology of benign paroxysmal positional vertigo (BPPV) is not completely understood. Although the concept of degenerated otoconia transforming the posterior canal (PC) crista into a gravity-sensitive sense organ has gained popular support, several temporal bone (TB) series have revealed similar deposits in normal TBs, suggesting they are a normal change in the aging labyrinth. Furthermore, some TBs from patients with BPPV do not contain particles in the posterior canal. Five TBs from patients with BPPV were studied quantitatively and qualitatively. A small PC cupular deposit was found in 1 TB, while none was seen in the other 4 TBs. The major pathological changes were 1) a 50% loss of ganglion cells in the superior vestibular division of all 5 TBs and 2) a 50% loss of neurons in the inferior division of 3 TBs, and a 30% loss in 2 TBs that contained abnormal saccular ganglion cells. These observations support a concept in the pathophysiology of BPPV that includes loss of the inhibitory effect of otolith organs on canal sense organs.

Not the easiest read but it looks like BPPV may not be as clear cut as we think. It looks like it doesn't always involve ear rocks which is strange considering the Epley seems to work so well.

Cheers...Scott

Interesting. The intricacies of the human body - we just think we understand it and then we find we don't. What is a temporal bone series - didn't understand that bit?

Apart from that, how're you doing Scott? Apart from a slight pre-spin sensation when I lie down/get up and sometimes a v. slight hardly-at-all spin when I turn in bed (usually after waking up, but not before falling asleep - strange) I seem to be 100%. yaay!

Madeleine

Hi Madelaine,

I think "series" in this sense refers to examinations.

I'm pretty good on the lab front (hanging out at about 90% most days) now but managed to come down with a cold on Friday. So the chest is all raw and scratchy. As the virus was approaching (Thursday night) I woke up in the night feeling a bit freaked out with heart palps again. That was a first for weeks. But not unusual to get a lab stir when another virus is around for me. The good news is that it doesn't totally wreck me like it once did when I caught a cold.

Great news about you being 100%.....brilliant..how long did it take you to get there?.....think (hope) I'm not far off too! :bouncing:

Cheers....Scott

Hi,

Well Scott I liked that and I think petty much sums up not only BPPV but Labs as what you have said there about hair cell damage etc is exactly how it was put to me about the damage that is done post labs (scarring from imflammation). Hmmmm am still thinking about it all.

Thanks Ilia xx

Hi Madelaine,

Great news about you being 100%.....brilliant..how long did it take you to get there?.....think (hope) I'm not far off too! :bouncing:

Cheers....Scott

I count my real improvement from the time of my last bout of imbalance, March 14. I only started having treatment last September, and by late october thought I was over it, but it came back within a month, but I didn't go for treatment again till late January as i was in pretty poor shape with my back and didn't feel up to it. I guess overall I've been lucky - never had so many of the awful symptoms most people on these boards suffer from. Mostly I'd have an unsteady day every few weeks, which would hang about, in diminishing severity for anything from 3-7 days. Sometime in February I gave myself a real setback doing a back exercise the wrong way - wow did I suffer, but got over the worst in about 2 weeks. I suppose the whole thing started with me 6-7years ago, but it was like 2-3 weeks a year, and only when lying down or sitting up. Then real nasty vertigo day 2 years ago, that's when I was sent for the audio test, ENG etc., but my doc. didn't prescribe treatment as we both thought it was a one-off day - then a year later, the same thing happened. Only after a third bad day plus some unsteadiness, did he send me for VRT. So I guess I count my real suffering from last summer.

Hope your cold is soon better. You must certainly be on the way to recovery if it didn't freak you out like it used to. I think confidence is a great healer too - it's a whole mind-set. When we panic we just don't have the tools to deal with the dizzies, motion, etc., but once we seem to be even slightly better, we meet the next setback with enough confidence to deal with it positively. At least, that's my view of things from my own experience.

hope you're having a great day - well, I guess it's night down under now.

Cheers
Madeleine

Hi Scott

Only part of that which I have not seen before is:

..."that includes loss of the inhibitory effect of otolith organs on canal sense organs. ".....

Have any insight into what "inhibitory effect" they are talking about?

Never came across any discussions that included an "inhibitory effect" of the otolith organs-----???????????

:cool:

Have any insight into what "inhibitory effect" they are talking about?

Never came across any discussions that included an "inhibitory effect" of the otolith organs-----???????????

Hey Subs,

After reading this article right through I thought it would be better to summarise it for you. It's very interesting indeed. It appears the dreaded herpes virus may play a role in BPPV as well!! Better grab a coffee for this one...


Ann Otol Rhinol Laryngol 2003 Jul;112 (7):574-82
Richard R Gacek

Since a tilted head position is provocative, it (BPPV) was first assumed to be an otolith disorder. Dix and Hallpike supported this interpretation with histopathological evidence of utricular end organ degeneration in the temporal bone (TB) from a patient with BPPV.

Largely because of experimental demonstrations that a nystagmus response is elicited by semicircular canal receptor activation and not by otolith stimulation, the otolith concept for BPPV was not generally embraced.

In one patient the superior vestibular ganglion (SVG) was completely degenerated in this TB, leaving intact the inferior vestibular ganglion (IVG) and sense organs. This observation focused interest on the posterior semicircular canal as the responsible sense organ. The posterior canal sense organ activates the contralateral inferior rectus and ipsilateral superior oblique extraocular muscles (eyes).

Deposits were presumed to represent degenerated otoconia (specific gravity, 2.7) probably derived from the utricular macula. It was hypothesized that these cupular deposits converted the sense organ into a gravity receptor that was activated by the Hallpike maneuver.

Based on these clinical and histopathological observations, a series of head maneuvers were developed to reposition free-floating deposits from the posterior canal ampulla and/or membranous canal, in which they could no longer activate the canal receptor. Although the short-term relief of BPPV by such particle repositioning maneuvers (PRMs) was promising, subsequent reports with longer (>6 months) follow-up, and compared to no treatment, revealed equivalent rates of positional vertigo relief.

The concept of a mechanical alteration in labyrinthine physiology as being responsible for BPPV does not account for several features. These are 1) the latency, limited duration, and fatigability of the rotatory nystagmus despite sustained provocation; 2) the long (sometimes years) periods of remission between episodes of BPPV activity; 3) the absence of nystagmus in the presence of subjective symptoms with provocation in some patients; and 4) the absence of basophilic deposits in the cupula and membranous canal of the posterior canal sense organ in many of the donor TBs with a history of BPPV.

It was suggested that a neural component might be responsible for BPPV and could account for the features not explained by the mechanical concept.

Results of the study based on 5 donors who had BPPV –

The observations in this study indicate that the major pathological change in BPPV is degeneration of vestibular neurons, rather than an alteration in recep-tor sensitivity. Significant loss of SVG and IVG cells was found in all TBs, whereas vestibular sense organs were normal. The assessment of vestibular ganglion cell loss revealed an approximately 50% loss in the SVG of all 5 TBs and in the IVG of 3 TBs with BPPV The IVG of the remaining 2 TBs revealed a 30% loss of neurons, but showed degenerative changes in saccular ganglion cells.

The cause of this ganglionic degeneration is probably the reactivation of latent neurotropic viral infection. Members of the alpha herpes virinae group (herpes simplex I and II, herpes zoster) are the most likely causative agents because of their ubiquity, their affinity for sensory ganglia, and the presence of viral DNA products in patients with vestibular ganglionitis. The common concurrence of BPPV in ears with Meniere's disease, vestibular neuronitis, and idiopathic facial paralysis, as well as other cranial neuropathies (zoster, labialis simplex), represents clinical support for this viral form of vestibular ganglionitis in BPPV. This pattern of neural inflammation and degeneration has been observed in the TBs of patients with Meniere's disease, vestibular neuronitis, BPPV, and idiopathic facial paralysis.

The observation of neural pathological findings rather than deposits in the ampullary or canal segments of the posterior canal is not surprising. The loss of the ionic gradient across cytoplasmic and nuclear membranes disrupted by virus reactivation may be responsible for degeneration of these primary neurons. Such neural degeneration should be reflected in decreased vestibular function. However, in BPPV, the burst of nystagmus and vertigo represents posterior canal receptor activation. This fact is based on anatomic and physiological demonstration of vestibulo-ocular response pathways activated by the posterior canal receptor, as well as the elimination of the response when the nerve to the posterior canal receptor has been transected in patients with BPPV. Therefore, the mechanism responsible for BPPV must include degeneration of neural elements other than those supplying the posterior canal receptor.

The present TB series suggests that degeneration of the saccular ganglion may play a key role in this disorder. The interaction between otolith and canal receptors is pertinent to the pathophysiology of BPPV. There is considerable experimental evidence to support an interactive relationship between otolith and canal sense organs. Convergence of canal and otolith input on neurons in the medial vestibular nucleus has been demonstrated by several investigators. This interaction has usually taken the form of an inhibitory modulation of canal input by otolith activation. Otolith-canal interaction has been explored extensively in cats by Fluur et al. In a large series of experimental conditions involving selective denervation of otolith and canal end organs in the cat, they observed that after denervation of the utricle, a horizontal nystagmus appeared when the lateral canal remained innervated. If lateral canal denervation preceded utricular denervation, nystagmus was absent. When the saccule was denervated in the presence of intact posterior canal innervation, a vertical nystagmus (upbeat-rotatory) appeared. If posterior canal denervation preceded saccular denervation, no nystagmus was observed. These observations indicate that an otolith organ exerts an inhibitory effect on the canal receptors. Without this inhibitory modulation, the response of the canal receptor is released.

When the head is placed in the so-called Hallpike position, the hair cells in the superior part of the saccule and those in the posterior canal crista are depolarized, activating antagonistic extraocular muscles. However, if the saccular macula or its neural input is degenerated, the antagonistic effect on posterior canal input is lost, and the rotatory upbeat nystagmus associated with posterior canal receptor activation is released. If the posterior canal neural input were also degenerated, nystagmus would not appear in the ear with a degenerated saccular nerve. A degenerated or atrophic singular nerve was never encountered in more than 250 surgical exposures of this nerve in patients with chronic BPPV. The nystagmus of posterior canal BPPV, therefore, may result from inadequate inhibition from the saccular macula, especially its superior part. In a similar way, lateral canal BPPV may represent decreased utricular inhibition of lateral canal activation.

The severity (nystagmus and nausea) of the provoked response may depend on the degree to which the saccular input is impaired. It is possible that some patients may have only nausea and imbalance without nystagmus,45 if the saccular deficit is minimal. If the saccular loss is almost total, the vertigo and nausea may be disabling. Most BPPV patients fall somewhere between these two extremes. Alleviation of the response in these patients by PRMs may result from stimulation of remaining functional units in the saccule, which inhibits activation of the posterior canal crista. This form of treatment would succeed in cases in which there is sufficient residual saccular input.

Although this neural concept of BPPV differs radically from the currently held "lithiasis" theory, the treatment of the disorder remains unchanged. Use of the PRM or waiting for spontaneous resolution is still recommended for the initial presentation of BPPV. The PRM may also be effective for symptomatic control of the recurrent form of BPPV. Those patients with a history of chronic (>1 year) disabling BPPV who do not respond to conservative measures may be candidates for surgical ablation of posterior canal function.

Conclusion

Observations in 5 TBs from patients with posterior canal BPPV suggest that the pathophysiological mechanism responsible for a position-induced vestibulo-ocular response in this disorder is neural, rather than mechanical stimulation of the sense organ. Loss of the inhibitory action of otolith organs on canal activation caused by degeneration of otolith neurons (saccular, utricular) is a possible explanation of the brief canal response induced by the positional stimulus.

Hey Subs,

After reading this article right through I thought it would be better to summarise it for you. It's very interesting indeed. It appears the dreaded herpes virus may play a role in BPPV as well!! Better grab a coffee for this one...

Hi Scott

Thanks

Think I got it---now.

Do you know if the quoted study and it's results have undergone any "Peer Review"???

The conclusions---if they hold up---are quite different---from what has been---most of the thinking in this area----however---it(recent medical thinking)--has been inching more towards this type of explanation of BPPV---it will be interesting to see---if the Doc's in at the centers of excellence--in this area---L/L in London, Hain Chicago, Ruckinstien in Phila, etc...---who are researching as well as treating clinically agree

Has a huge impact on medical treatment/rehabilitation if confirmed/true

Thanks again---always a good move to have a up and coming PhD Candidate on the team:cool:

:cool:

Hey Scott and Subs - you two guys have really excelled yourselves! You really do have a wealth of knowledge between you, but I got pretty lost in all that, other than understanding that the cause of BPPV is not what has been hitherto supposed. Can you translate all that into a few simple sentences? What does this mean for the epley manoeuvre? Does it all mean that we're basically all falling apart? Help!

Madeleine

Hey Scott and Subs - you two guys have really excelled yourselves! You really do have a wealth of knowledge between you, but I got pretty lost in all that, other than understanding that the cause of BPPV is not what has been hitherto supposed. Can you translate all that into a few simple sentences? What does this mean for the epley manoeuvre? Does it all mean that we're basically all falling apart? Help!

Madeleine

Hi Madeleine

Not sure where this study---if it holds up to "Peer Review" would lead...

Scott

Here is Northwestern's Univ---Proff Hain's comments on the study(from the Northwestern Univ web site)

..."Gacek RR (2003). "Pathology of benign paroxysmal positional vertigo revisited." Ann Otol Rhinol Laryngol 112(7): 574-82. Gacek reports results of studies of 5 temporal bones from patients with BPPV. Debris was attached to the cupula in one temporal bone. The remainder had reductions in neurons in various divisions of the vestibular nerve. COMMENT: It is difficult to see how neural damage could cause BPPV to remit after a positional maneuver."......

Sounds like---at least---he---is not convinced---interesting!!

:cool:

Hi Subs,

Normally when a manuscript is submitted to a journal for publication, it must go through a review process before it is accepted. For example when I sent a manuscript to The American Journal of Clinical Nutrition, it was first sent out to about 7 other academics in the field. What followed was a critique by all of them. Most of the time the comments are off the mark but there are equally also some very good ones. Information may need to be added or removed from the MS. So this is what happened to me and I was knocked back by that journal in the end (too much criticism). After making the fixes and going back to the data in one case we resubmitted to the J of Nutrition. Again, another review process and this time accepted and then published. Some authors are rejected numerous times and then finally accepted. This is the "peer review" process that goes on for all journals and I assume would have happened for this article as well.

I checked out the page from Prof Hain. He certainly is "the man" when it comes to BPPV. I have to say I wouldn't be totally surprised if there was possibly more to the BPPV story then just debris, particularly when Gacek noted the several features that do not fit the mechanical alteration model. I wonder what Hain would say here? This happenes time and again in science where it appears something is fully understood only to find there's a twist in the story. There's a group, for example, that now have evidence that high cholesterol levels may not be as clear cut in the risk for heart disease as has been the belief for at least 20 years or that having low LDL cholesterol levels is even protective. Go figure!

Madeleine: I think in a nutshell, Gacek is saying that there may be more to the BPPV story than just ear rocks (the result of which is an alteration in receptor sensitivity in the inner ear) and that it may also have something to do with degeneration of vestibular neurons, possibly caused by the reactivation of a virus - like herpes. It may explain the remission periods between BPPV occurences. Perhaps it is just ear rocks in some but not in others or a combination? I wouldn't worry about it though M. From what I can see on this board, almost everyone has benefitted from the Epley when used or the condition has completely sorted itself out with time. But as Subs noted, perhaps new treatments will arise from this info to speed recovery.

Cheers.....Scott

Thanks guys, very interesting. Didn't know that articles submitted to a professional journal had to go through such a process of peer review, all of which makes you think that by the time it does get published, it must have the approval of at least some professionals in that particular field.

Madeleine

Subs,

This is slightly off topic but thought you might be interested in reading this latest bit of info on cholesterol and the risk for heart disease...I thought it was amazing how the data can sometimes be "massaged" as they say.....perhaps the whole thing has been a ploy by companies pushing statins....it really flies in the face of popular belief. Do a search for "doubting hearts debate fat".

Scott

Subs,

This is slightly off topic but thought you might be interested in reading this latest bit of info on cholesterol and the risk for heart disease...I thought it was amazing how the data can sometimes be "massaged" as they say.....perhaps the whole thing has been a ploy by companies pushing statins....it really flies in the face of popular belief. Do a search for "doubting hearts debate fat".

Scott

Hi Scott

Thanks!

Ok found it.

Interesting----can't say---I would try to take any of it to the "bank"!!

Got one of the "GI" books---prob get the other---Friday----looks like good science but---for the avg person---looks kind of "daunting"---may have second thoughts after reading the "life plan"---later!!

:cool:

Hey Subs,

Cool. I'll be interested to hear what you think of it once read. It may seem like a lot to take in at first but I think you'll easily grasp it all once you get through the initial stuff. The cool thing about it, is that it's not meant to be thought of as yet another "diet" but rather eating the way nature intended.

S