I've written before about how important meditation has been to me in coping with Meniere's and all the fun stuff that goes along with it. But I'm sure I've never said it as well as this blogger does. Just insert vertigo or your symptom du jour if, or where, he says anxiety or depression. Although, most of us have those, too! I can relate to every word he writes and have worked through each of these mistakes along the way. I'm not perfect in avoiding them all, but at least I usually recognize them more quickly for what they are: thoughts and nothing more.
6 Mistakes We Make When Depressed or Having a Panic Attack
By Nikolay Perov
“You are today where your thoughts have brought you; you will be tomorrow where your thoughts take you.” ~James Allen
When I was eighteen I went through a very stressful period, which led to the onset of panic attacks. I often remember how in bed one night I was suddenly overwhelmed by a feeling of terror. I’d never experienced such fear before. Sure, I was scared of lots of things, but this new feeling was unique.
The most accurate way I can describe it is a kind of animal-like horror. It seemed to have come from the deepest, darkest recesses of my subconscious mind, caused by primeval, bestial mechanisms.
The feeling was so deep and all encompassing that it was as if nothing else existed, just this fear coursing through my body as I writhed about, sweaty and tense.
The most unfamiliar and therefore terrifying aspect of the fear was that it didn't have an object: it wasn't clear what I was actually afraid of. From the very start, it was simply fear—unconnected to any tangible thing.
That night marked the beginning of my period of panic attacks. Over time, depression, anxiety, sleep problems, and general health issues augmented these.
At the age of twenty-four, I started to fight back; with the help of meditation I managed to get over my depression and panic, and now they no longer torment me.
During my struggle I came to realize that I was hindering myself with mistakes I was making, and it was only when I overcame these that I started to make real progress.
I often talk with people who have been or are going through the same kinds of problems, and I notice just how many of them also come up against these mistakes. So what are they?
1. Resisting.
When we feel a bad mood, depression, or panic coming on, our first wish is to get rid of it as quickly as possible, to change the “bad” mood into a “good” one. This is natural; it’s how we’re made. But all too often our attempts just make everything worse.
Resistance forces us to think constantly about our condition, to focus all of our attention on it, to feel bad because it won’t go away, to wait tensely for relief.
But the simple truth is that you can’t control everything. Attempting to get your condition “under control” often leads to extra stress and unwanted bad feelings. It’s sometimes best just to relinquish control and cease resistance.
If we relax and let our depression or panic come without trying to control anything, accepting that they’re only temporary feelings which will pass in due course, things become much easier.
2. Feeling bad about feeling bad.
We start to have thoughts such as “I’m going to die or go crazy,” “This’ll never end,” and “I hate that I can’t enjoy life like other people; I feel utterly miserable.”
Our mind starts to add new fears and negative emotions to the depression we already have. And, as I saw for myself, these fears and feelings end up constituting the main part of our condition.
It’s actually your mind, not the depression and panic themselves, which makes each episode so unbearable.
If you don’t believe me, try this experiment: The next time you’re overwhelmed by an attack, try to simply observe it without getting caught up in or assessing it in any way. Just watch it in its pure form, without any thoughts. Try to notice which parts of your body you feel it in and how it comes and goes.
In this way, you’ll remove your mind from the formula of your distress. You’ll notice how much weaker the attacks become when they’re no longer supported by your thought processes. Give it a try, making notes of the results if you like. Would it be true to say that it’s not all as terrifying and dreadful as it seemed at first?
When you stop feeding your depression with fears and thoughts it becomes much easier to shake off.
3. Comparing.
“Everything was so good when I wasn’t depressed! What an amazing time it was, and how awful it is now. Why can’t I go back?!” These are the kinds of things many people think, me included, but such thoughts bring nothing but harm.
If you want to beat depression or panic, you have to stop comparing. Forget that there’s a past and future. What’s happened has happened. Don’t dwell on it, and instead live in the here and now.
Start with what you have, and don’t think about how it all was before. Learning how to live in the present moment will make your depression or panic much more bearable.
4. Asking pointless questions.
Many people spend hours asking themselves all kinds of questions: “When will this end?” “Why me?” and “What have I done to deserve this?”
To make use of a well-known Buddhist parable, these questions are as much use as trying to figure out the source of the arrow which blinded you: it’s just not that important. What you need to know is how to pull the arrow out.
Questions of the “Why me?” ilk just make your condition worse, forcing you as they do to complain and be upset about something that’s already happened. Focus on what will help you get past your depression and don’t bother with questions which don’t serve this purpose.
5. Believing your fears.
We think that because we experience such fear at the idea of going outside, meeting people, or going on the underground, it means that something bad is going to happen. There’s nothing surprising in this, because nature has made fear in order to warn us of danger. We’re made in such a way that we instinctively believe this fear and respond to it.
But our fear hardly ever arises due to a real threat. For example, the fear of losing your mind or suffocating during a panic attack is simply fallacious. Stop believing this fear. Whatever it is you’re afraid of at these times isn’t going to happen.
Fear is nothing more than a feeling, a chemical reaction in your head. If you’re overcome with terror when you go down into the underground, it doesn’t mean that something horrific is laying in wait there. It’s like a malfunctioning fire alarm—just because it’s going off doesn’t mean there’s actually a fire.
So stop listening to your “inner alarm” every time it goes off. Don’t pay it any heed: go out, meet your friends, get on a plane, and let the alarm keep ringing. Nor should you try to “switch it off,” as this doesn’t always work. Just ignore it. In other words, stop taking your fear as something real.
6. Seeking reasons for your depression in the outside world.
This is another mistake I made myself. I thought that my malaise was linked solely to the way my life and work were going. I believed that if I could just change that, I’d be happy.
But then, with meditation, I realized that everything I needed to be happy was inside me, and likewise what was causing me to suffer!
I was so edgy, anxious, feeble, caught up in bad habits, undisciplined, and irresponsible that even if I’d succeeded in changing the external circumstances of my life, the traits that had given rise to my depression would still be there.
In order to get rid of my depression, I had to get rid of the internal reasons that had caused it.
So don’t keep telling yourself, “If I get a new job, everything’ll be smooth sailing,” or “If I get rid of everything I’m scared of, there won’t be anything to be afraid of any more.” Your depression and fears reside inside you, so wherever you are, they will be too, projected onto the outside world.
Of course, this doesn’t mean that you shouldn’t strive to improve your life. First of all, though, you need to direct your efforts inwards.
Conclusion: Acting Against What Feels Like Common Sense
Now, when I look at these mistakes and remember making them myself, I can see the one thing that unites them.
The reason we make them is that when depression or panic pounces on us, we start to think and act in the way our instincts and gut feelings tell to us. “Be afraid, run away, resist, danger awaits you everywhere, you’re trapped,” they whisper.
Tuning in to this during a bout of depression aggravates our situation. This is because our mind, emotions, and instincts are strongly conditioned by depression, so listening to them is like listening to the voice of a malicious, invisible demon intent on leading you to ruin.
To free yourself from depression once and for all you have to drop all your notions of common sense; abandoning your sense of reason, you must act against them.
Don’t resist your depression, accept your fears and allow them to simply pass; don’t get caught up in them and don’t believe them; don’t compare your current situation to how it was before—all things that feel illogical when you’re in a state of terror or intense depression.
What I’m advising may seem to be the polar opposite of what your gut encourages you to do. But it’s precisely because people continue to give credence to and obey these feelings that depression is such a widespread complaint. You need to act somewhat paradoxically to get rid of it.
My own experience has convinced me of this. The understanding I reached allowed me to come through my difficult situation and continues to help me cope with challenges I encounter on my journey.
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About Nikolay Perov
Nikolay Perov formerly suffered from depression, panic attacks, addictions, laziness and communication problems. He coped with the help of meditation. His blog (also available in English) became popular in Russia, his native country. It has helped a lot of people get rid of depression, nervousness and alcohol problems and discover the new meaning of life. Read him on nperov.com!
Thursday, October 9, 2014
Saturday, September 20, 2014
Thursday, September 18, 2014
Assessment of Meniere's disease from a radiological aspect – saccular otoconia as a cause of Meniere's disease?
I found this to be a very interesting study out of the Osaka City University Graduate School of Medicine. Even better, it's a full-text article!
First of all, I think it is very exciting that the use of 3D cone beam CT is being used to visualize the inner ear because, up until now, the ability to see the structures of the cochlea and membranous labyrinth have only been possible using postmortem specimens. In other words, after the poor person has died. But another exciting aspect of this relatively short report is that it not only nicely summarizes the variety of potential etiologies, or causes, of Meniere's symptoms, but it also suggests hope for future treatments which might be able to return patency of the blocked ducts and hopefully eliminate, or at least greatly reduce, symptoms. Finally, the findings of this study seem to suggest to me that perhaps the varying degrees and types of hearing loss and vestibular symptoms those of us with Meniere's disease suffer might be dependent on the varying degree of occlusion and which or how many ducts are affected.
P.S. Go straight to the article to see the cool color images produced by the 3D cone beam CT.
Assessment of Meniere's disease from a radiological aspect – saccular otoconia as a cause of Meniere's disease?
Hideo Yamane,corresponding author 1 Kishiko Sunami, 1 Hiroyoshi Iguchi, 1 Hiramori Sakamoto, 1 Toshio Imoto, 1 and Helge Rask-Andersen 2
Author information ► Article notes ► Copyright and License information ►
This article has been cited by other articles in PMC.
Abstract
Significant reduced visualization of the reuniting duct (ductus reuniens; RD), saccular duct (SD) and endolymphatic sinus (ES) in Meniere's disease (MD) compared with normal control ears on three-dimensional (3D) CT imaging suggests the blockage of endolymphatic flow there with radiodense substances, which may be explained by dislodged otoconia from the saccule. These structures could be involved in the pathogenesis of MD.
Objective
This study was designed to visualize and assess the RD, SD and ES in patients with MD using 3D CT.
Methods
Sixty-two patients with a definite diagnose of unilateral MD, based on criteria proposed by the Committee on Hearing and Equilibrium of the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS), were compared with contralateral ears and normal controls (26 ears) using 3D CT. The RD, SD and ES were scrutinized for patency on 3D CT images.
Results
MD ears showed loss of continuity of the RD, SD and ES based on evaluation of 3D CT images, and differed significantly from normal healthy control ears (p < 0.01).
Keywords: Saccular duct, saccule, endolymphatic hydrops, endolymphatic duct, CT image, bilaterality
Introduction
The etiology of Meniere's disease (MD) remains a riddle in spite of many studies. Most such studies are based on the idea of endolympatic hydrops [1,2]. Even though the existence of a ‘longitudinal flow’ has been challenged experimentally by some researchers in recent years, a disturbance of endolymph circulation within the duct system is generally agreed to be an important factor for generation of endolymphatic hydrops in MD [3,4].
We previously reported on the visualization of the reuniting duct (RD) and saccular duct (SD) and endolymphatic sinus (ES) of the human inner ear by analysing their bony grooves using three-dimensional (3D) cone beam CT images [5,6]. As the RD, SD and ES each lodge onto these bony grooves, analysis of the grooves can yield information on the condition of the RD, SD and ES. Using this strategy, we reported that MD patients, defined as grade 3 by the criteria of MD from the Committee on Hearing and Equilibrium of the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS), showed significant discontinuity of the bony groove of the RD in comparison with normal ears. This discontinuity suggests that the RD may be blocked by a radiodense substance [7], and this substance could represent dislodged saccular otoconia.
The saccule contains two ducts, the RD and the SD. They are believed to convey endolymph or pressure release between the endolymphatic compartments. Investigating these two ducts may be crucial when analysing MD patients from the viewpoint of patent ‘longitudinal flow’. In the present study we report on the incidence of patency of these two ducts and the ES in MD patients compared to controls.
Material and methods
Subjects
We studied 62 patients (29 males and 33 females; mean age 55.5 years, range 25–86 years) with diagnosed unilateral MD as defined by the criteria of the Committee on Hearing and Equilibrium of the AAO-HNS. The affected ears of patients with MD were compared with the non-affected contralateral ears and the bilateral healthy ears in 13 volunteers (6 males and 7 females, mean age 57.9 years, range 35–79 years). Four frequencies at 0.5, 1, 2 and 4 kHz were used to calculate pure tone averages. Although a 3 kHz threshold is included in the four pure tone averages used for definition of MD by AAO-HNS, 3 kHz is not commonly used in Japan, and 4 kHz was substituted for 3 kHz in this study.
Approval for this study was obtained from the ethics committee of Osaka City University Graduate School of Medicine.
Analysis of CT image
The temporal bones were examined using 3D cone beam CT (3D Accuitomo; J. Morita Mfg Corp., Kyoto, Japan) using the same conditions as reported previously [5,6]: 80 kV; 6 mA; voxel, 0.125 mm × 0.125 mm × 0.125 mm; slice thickness, 0.5 mm. The CT images were taken in a region of interest of diameter 6 cm and height 6 cm. Reconstructed 3D images of the inner ear were obtained by rendering software (IVIEW) in perspective view with a viewing angle of 15° and 0.25 mm voxel size (0.25 mm × 0.25 mm × 0.25 mm).
We previously reported how to reduce artefacts due to rendering effects [5,6] by comparing the findings of a cadaver temporal bone and its 3D CT image using several landmarks. In the present investigation of the image patterns of the RD, SD and ES, we adopted an additional image in which the common crus formed a horizontal line, so rotation would not change the view from directly above.
We evaluated the patency of the grooves of the RD, SD and ES (Figure 1). The patency of the RD was assessed on the orifice of the saccule to the RD based on our previous report [7]. The patencies of the SD and ES were analysed in the same manner by assessing the continuity of their bony grooves [6]. In this study the appearances of the grooves of the RD, SD and ES as not fully recognized was defined as closed and any other state was defined as open to avoid the weak point of the subjective visual evaluation of 3D CT images (Figure 2).
Figure 1.
Figure 1.
3D CT image of the reuniting duct (RD), saccular duct (SD) and endolymphatic sinus (ES) of a healthy volunteer's ear (left), cadaver's ear (upper right), and schematic view (lower right). All these views are left ears. Red arrows show the RD and yellow ...
Figure 2.
Figure 2.
Drawings demonstrating the patency of the reuniting duct (RD), saccular duct (SD) and endolymphatic sinus (ES) on 3D CT images. When otoconia are dislodged into the RD, SD or ES, they lose continuity of the surface of their bony grooves and become vague ...
Additionally, we examined CT images of a cadaver with a small piece of muscle or small amount of calcium carbonate on the bony grooves of SD and ES to assess changes in the CT images, as in our previous report [7].
Statistical analysis
The 62 patients were analyzed in comparison with the normal subjects. The incidence of abnormal images of the bony grooves of those portions in affected ears in MD patients was compared with the non-affected contralateral ears and control volunteer ears and analysed by Yates 2 × 2 chi-squared test.
Results
Findings of RD aspects
Figures 3 and and44 show representative views of different patencies of the RD, SD and ES. Of the ears on the affected side of MD patients (Figures 3A and and4A),4A), 37% (23/62)) had closed RD compared with 9.7% (6/62) of the ears on the non-affected side (Table I). None (0/26) were closed in the normal group (Figures 3B and and4B).4B). There were significant differences between the ears on the affected side of MD patients and normal ears, and between the affected ears and the non-affected ears (p < 0.01) (Figure 5). There was no significant difference between non-affected ears of MD patients and normal ears (p = 0.078).
Figure 3.
Figure 3.
Representative views of the left ear of a patient with Meniere's disease (MD) (A) and a volunteer's healthy ear (B). (A) Although the outline of the bony groove of the reuniting duct (RD) (arrows), saccular duct (SD) and endolymphatic sinus (ES) can be ...
Figure 4.
Figure 4.
Representative views of the right ear of a patient with Meniere's disease (MD) (A) and a volunteer's healthy ear (B). (A) Both the bony grooves of the reuniting duct (RD) and the endolymphatic sinus (ES) are fully occupied by a dense, bony substance and ...
Table I.
Table I.
Status of the reuniting duct (RD), saccular duct (SD) and endolymphatic sinus (ES) in 62 patients with Meniere's disease (MD) and 13 healthy volunteers.
Figure 5.
Figure 5.
Distribution pattern of the reuniting duct (RD) in affected and non-affected ears of patients with Meniere's disease (MD) and healthy ears of volunteers.
Findings of SD aspects
The patencies of the affected and non-affected ears of MD were 51.6% (32/62) and 16.1% (12/62), respectively (Table I). In contrast, all the SDs (26/26) were patent in the healthy ears (Figures 3B and and4B).4B). There were significant differences between the affected ears and healthy ears and between the affected ears and the non-affected ears (p < 0.01). There was a slight but significant difference between the non-affected ears and healthy ears (p = 0.015) (Figure 6).
Figure 6.
Figure 6.
Distribution pattern of the saccular duct (SD) in affected and non-affected ears of patients with Meniere's disease (MD) and healthy ears of volunteers.
Findings of ES aspects
The distribution pattern of the ES resembled that of the SD. The patencies of the affected ears and non-affected ears of MD patients were 64.5% (40/62) and 17.7% (11/62), respectively (Table I). All the ESs (26/26) were patent in the healthy ears (Figures 3B and and4B).4B). There were significant differences between the affected ears and healthy ears and between the affected ears and the non-affected ears (p < 0.01). There was a slight difference between the non-affected ears and healthy ears (p = 0.030) (Figure 7).
Figure 7.
Figure 7.
Distribution pattern of the endolymphatic sinus (ES) in affected and non-affected ears of patients with Meniere's disease (MD) and healthy ears of volunteers.
Findings in the SD and ES of a cadaver treated with CaCO3 and soft tissue fragments
The bony grooves of the SD and ES treated with CaCO3 appeared vague (Figure 8A), but those with muscle fragments were not affected (Figure 8B).
Figure 8.
Figure 8.
3D CT views of a cadaver temporal bone. The bony grooves underlining the saccular duct (SD) and the endolymphatic sinus (ES) treated with CaCO3 (A) appear vague compared with those treated with muscle fragments (B). Note the difference in continuity of ...
Discussion
We could demonstrate differences in visualization or patency of the RD, SD and ES between the affected ears of MD patients and normal ears, suggesting that the RD, SD or ES in MD ears may be partly or entirely occluded compared with healthy ears. The reduced visualization of the RD, SD and ES suggests that these ducts were involved as lesions of MD.
Debris, pathogens or unusual substances in the inner ear can be transported in these narrow ducts and become obstacles to the pathway of longitudinal flow of endolymph resulting in endolymphatic hydrops.
We speculate that a reasonable explanation for this reduced visualization may be an occlusion caused by dislodged otoconia from the saccule. This is based on experimental findings from cadavers showing that the bony groove appears vague when covered with CaCO3 but not when covered with muscle fragments. The data from the present and previous studies [7] suggest that the occlusion may be situated between the saccule and the RD or the SD and the ES.
Saccular otoconia could be dislodged by various causes such as aging as the natural fate, infection, disturbance of blood circulation, trauma, etc., and the dislodged otoconia from the saccule can disperse into the surrounding membranous labyrinth [8,9].
If otoconia fall into such a narrow pathway, the RD to the cochlea or the SD and ES to the endolymphatic duct, they could disturb the endolymphatic flow.
Although saccular otoconia are more susceptible than those of the utricle [10], the incidence of MD patients is not so high in comparison with benign paroxysmal positional vertigo (BPPV) possibly caused by dislodged utricular otoconia [11]. We do not have conclusive data proving this. However, some speculation from our present results may answer this question. The risk of saccular otoconia falling into the RD may not be so high because of its narrowness, even if it is near the saccular otolithic membrane.
The longitudinal endolymph may work to oppose saccular otoconia falling into the RD. On the other hand, the SD and ES are in the path of the anterograde endolymph system. Therefore, the SD (51.6%) and ES (64.5%) may be more occluded than the RD (37%). The character of MD may be due to the rate of occlusion of these narrow ducts.
Histological studies reported that the endolympatic duct (ED) was obstructed with fibrous tissue, basophilic substance or bone in MD [12] and a radiological study also showed narrow and poor development of the ED in MD [13]. The lesions of the ED may have a similar pathology to those of the SD and ES because all these regions are connected as successive membranous pathways, which could support our hypothesis that dislodged saccular otoconia could be a cause of MD. However, more precise investigation of these areas of the human temporal bone in MD is necessary.
Although the non-affected ears in patients with MD showed a similar RD pattern to the affected ears, the similarity was not statistically supported. On the other hand, there were slight differences in the patency of the SD and ES between the non-affected ears and healthy ears. This tendency of occlusion in the SD and ES of the non-affected ears of MD patients suggests that the contralateral non-affected ears may also be challenged but functionally compensated. Earlier acoustic biasing experiments have shown that incipient endolymphatic hydrops may exist in the healthy contralateral ear in MD.
Bilateral engagement of MD varies according to different authors. The longer the duration of the disease the more frequent is the incidence of bilateral disease [14]. In a recent German study where the long-term course of MD was revisited, as many as 35% of subjects suffered from MD in both ears after 10 years and 47% after 20 years [15]. Some studies show a low bilateral incidence (5%) while audiometric low-tone changes occur more frequently (16%) [16]. Also, the modulation depth was found to be significantly reduced in the contralateral non-symptomatic ears of MD patients using low-frequency masking to diagnose endolymphatic hydrops [17]. This has led to the conception that MD is basically a bilateral disease with differing expression in the two ears. In addition, histopathological changes have been described to a large extent in the contralateral temporal bone in patients with unilateral MD [18]. Genetic alterations such as single nucelotide polymorphisms have been described in patients with bilateral MD [19]. The onset of MD has also been found to be earlier when both ears are affected [20]. Although we could not verify signs of bilateralism in our patients with MD in the present unilateral cases, the unilateral group may have included some bilateral cases. This is supported by our 3D CT findings. However, bilaterality of MD must be fully investigated in a future study.
We hypothesize that MD is a pathological condition brought about by saccular dislodged otoconia due to several causes, obstructing the narrow paths of the endolymph, based on the etiology of BPPV caused by dislodged otoconia from the utricle (Figure 9). Although we must investigate many factors of MD and the mechanism of MD attack in the future, the opening of these narrow paths could be one effective therapy for MD.
Figure 9.
Figure 9.
Hypothetical view of blockage of the reuniting duct (RD), saccular duct (SD) and endolymphatic sinus (ES) by dislodged otoconia from the saccule in patients with Meniere's disease (MD). ED, endolymphatic duct; EnS, endolymphatic sac; L, lateral semicircular ...
We evaluated the patency of the RD, SD and ES by 3D CT imaging, reflected by their bony grooves and not the actual ducts and ES. We thus obtained no definitive data on the degree of obstruction using the present 3D CT images.
In addition, the differences on 3D CT images among the various stages of MD that are categorized by degree of hearing deterioration must be investigated in the future.
Acknowledgements
We are indebted to Dr Hiroshi Aradate of J. Morita Corp. for valuable technical assistance.
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References
[1] Yamakawa K. Über die pathologishe Veränderung bei einem Meniere-Kranken. J Otorhinolarngol Soc (Jpn) 1938;44:2310–2.
[2] Hallpike CS, Cairns H. Observation on the pathology of Meniere's syndrome. J Laryngol Otol. 1938;53:625–55.
[3] Kimura RS, Schuknecht HF. Membranous hydrops in the inner ear of the guinea pig after obliteration of the endolymphatic sac. Pract Otorhinolaryngol. 1965;27:343–54.
[4] Schuknecht HF, Rüther A. Blockage of longitudinal flow in the endolymphatic hydrops. Eur Arch Otorhinolaryngol. 1991;248:209–17. [PubMed]
[5] Yamane H, Takayama M, Sunami K, Sakamoto H, Anniko M. Assessment of the reuniting duct by three-dimensional CT rendering. Acta Otolaryngol. 2009;129:1166–8. [PubMed]
[6] Yamane H, Takayama M, Sunami K, Sakamoto H, Imoto T, Anniko M. Visualization and assessment of saccular duct and endolymphatic sinus. Acta Otolaryngol. 2011;131:469–73. [PMC free article] [PubMed]
[7] Yamane H, Takayama M, Sunami K, Sakamoto H, Imoto T, Anniko M. Blockage of reuniting duct in Meniere's disease. Acta Otolaryngol. 2010;130:233–9. [PubMed]
[8] Yamane H, Imoto T, Nakai Y, Igarashi M, Rask-Andersen H. Otoconia degradation. Acta Otolaryngol Suppl. 1984;406:263–70. [PubMed]
[9] Gussen R, Adkins WY., Jr Saccule degeneration and ductus reunions obstruction. Arch Otolaryngol. 1974;99:132–5. [PubMed]
[10] Johnsson L-G. Degenerative changes and anomalies of the vestibular system in man. Laryngoscope. 1971;81:1682–94. [PubMed]
[11] Schuknecht HF. Cupulolithiasis. Arch Otolaryngol. 1969;90:765–78. [PubMed]
[12] Schuknecht HF. Pathology of the ear. 2nd edition. Pennsylvania: Lea & Febiger; 1993. Disorders of unknown or multiple causes; pp. 449–553. p.
[13] Yamamoto E, Mizukaimi C, Isono M, Ohmura M, Hirono Y. Observation of the external aperture of the vestibular duct using three-dimensional surface reconstruction imaging. Laryngoscope. 1991;101:480–3. [PubMed]
[14] Friberg U, Stahle J, Svedberg A. The natural course of Meniere's disease. Acta Otolaryngol Suppl. 1984;406:72–7. [PubMed]
[15] Huppert D, Strupp M, Brandt T. Long-term course of Meniere's disease revisited. Acta Otolaryngol. 2010;130:644–51. [PubMed]
[16] Perez R, Chen JM, Nedzelski JM. The status of the contralateral ear in established unilateral Meniere's disease. Laryngoscope. 2004;114:1373–6. [PubMed]
[17] Mrowinski D, Scholz G, Krompass S, Nubel K. Diagnosis of endolymphatic hydrops by low-frequency masking. Audiol Neurootol. 1997;1:125–34. [PubMed]
[18] Kariya S, Cureoglu S, Fukushima H, Kusunoki T, Schachern PA, Nishizaki K, et al. Histopathologic changes of contralateral human temporal bone in unilateral Meniere's disease. Otol Neurotol. 2007;28:1063–8. [PubMed]
[19] Lopez-Escamez JA, Saenz-Lopez P, Acosta L, Moreno A, Gazquez I, Perez-Garrigues H, et al. Association of a functional polymorphism of PTPN22 encoding a lymphoid protein phosphatase in bilateral Meniere's disease. Laryngoscope. 2010;120:103–7. [PubMed]
[20] Chaves AG, Boari L, Lei Munhoz MS. The outcome of patients with Meniere's disease. Braz J Otorhinolaryngol. 2007;73:346–50. [PubMed]
First of all, I think it is very exciting that the use of 3D cone beam CT is being used to visualize the inner ear because, up until now, the ability to see the structures of the cochlea and membranous labyrinth have only been possible using postmortem specimens. In other words, after the poor person has died. But another exciting aspect of this relatively short report is that it not only nicely summarizes the variety of potential etiologies, or causes, of Meniere's symptoms, but it also suggests hope for future treatments which might be able to return patency of the blocked ducts and hopefully eliminate, or at least greatly reduce, symptoms. Finally, the findings of this study seem to suggest to me that perhaps the varying degrees and types of hearing loss and vestibular symptoms those of us with Meniere's disease suffer might be dependent on the varying degree of occlusion and which or how many ducts are affected.
P.S. Go straight to the article to see the cool color images produced by the 3D cone beam CT.
Assessment of Meniere's disease from a radiological aspect – saccular otoconia as a cause of Meniere's disease?
Hideo Yamane,corresponding author 1 Kishiko Sunami, 1 Hiroyoshi Iguchi, 1 Hiramori Sakamoto, 1 Toshio Imoto, 1 and Helge Rask-Andersen 2
Author information ► Article notes ► Copyright and License information ►
This article has been cited by other articles in PMC.
Abstract
Significant reduced visualization of the reuniting duct (ductus reuniens; RD), saccular duct (SD) and endolymphatic sinus (ES) in Meniere's disease (MD) compared with normal control ears on three-dimensional (3D) CT imaging suggests the blockage of endolymphatic flow there with radiodense substances, which may be explained by dislodged otoconia from the saccule. These structures could be involved in the pathogenesis of MD.
Objective
This study was designed to visualize and assess the RD, SD and ES in patients with MD using 3D CT.
Methods
Sixty-two patients with a definite diagnose of unilateral MD, based on criteria proposed by the Committee on Hearing and Equilibrium of the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS), were compared with contralateral ears and normal controls (26 ears) using 3D CT. The RD, SD and ES were scrutinized for patency on 3D CT images.
Results
MD ears showed loss of continuity of the RD, SD and ES based on evaluation of 3D CT images, and differed significantly from normal healthy control ears (p < 0.01).
Keywords: Saccular duct, saccule, endolymphatic hydrops, endolymphatic duct, CT image, bilaterality
Introduction
The etiology of Meniere's disease (MD) remains a riddle in spite of many studies. Most such studies are based on the idea of endolympatic hydrops [1,2]. Even though the existence of a ‘longitudinal flow’ has been challenged experimentally by some researchers in recent years, a disturbance of endolymph circulation within the duct system is generally agreed to be an important factor for generation of endolymphatic hydrops in MD [3,4].
We previously reported on the visualization of the reuniting duct (RD) and saccular duct (SD) and endolymphatic sinus (ES) of the human inner ear by analysing their bony grooves using three-dimensional (3D) cone beam CT images [5,6]. As the RD, SD and ES each lodge onto these bony grooves, analysis of the grooves can yield information on the condition of the RD, SD and ES. Using this strategy, we reported that MD patients, defined as grade 3 by the criteria of MD from the Committee on Hearing and Equilibrium of the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS), showed significant discontinuity of the bony groove of the RD in comparison with normal ears. This discontinuity suggests that the RD may be blocked by a radiodense substance [7], and this substance could represent dislodged saccular otoconia.
The saccule contains two ducts, the RD and the SD. They are believed to convey endolymph or pressure release between the endolymphatic compartments. Investigating these two ducts may be crucial when analysing MD patients from the viewpoint of patent ‘longitudinal flow’. In the present study we report on the incidence of patency of these two ducts and the ES in MD patients compared to controls.
Material and methods
Subjects
We studied 62 patients (29 males and 33 females; mean age 55.5 years, range 25–86 years) with diagnosed unilateral MD as defined by the criteria of the Committee on Hearing and Equilibrium of the AAO-HNS. The affected ears of patients with MD were compared with the non-affected contralateral ears and the bilateral healthy ears in 13 volunteers (6 males and 7 females, mean age 57.9 years, range 35–79 years). Four frequencies at 0.5, 1, 2 and 4 kHz were used to calculate pure tone averages. Although a 3 kHz threshold is included in the four pure tone averages used for definition of MD by AAO-HNS, 3 kHz is not commonly used in Japan, and 4 kHz was substituted for 3 kHz in this study.
Approval for this study was obtained from the ethics committee of Osaka City University Graduate School of Medicine.
Analysis of CT image
The temporal bones were examined using 3D cone beam CT (3D Accuitomo; J. Morita Mfg Corp., Kyoto, Japan) using the same conditions as reported previously [5,6]: 80 kV; 6 mA; voxel, 0.125 mm × 0.125 mm × 0.125 mm; slice thickness, 0.5 mm. The CT images were taken in a region of interest of diameter 6 cm and height 6 cm. Reconstructed 3D images of the inner ear were obtained by rendering software (IVIEW) in perspective view with a viewing angle of 15° and 0.25 mm voxel size (0.25 mm × 0.25 mm × 0.25 mm).
We previously reported how to reduce artefacts due to rendering effects [5,6] by comparing the findings of a cadaver temporal bone and its 3D CT image using several landmarks. In the present investigation of the image patterns of the RD, SD and ES, we adopted an additional image in which the common crus formed a horizontal line, so rotation would not change the view from directly above.
We evaluated the patency of the grooves of the RD, SD and ES (Figure 1). The patency of the RD was assessed on the orifice of the saccule to the RD based on our previous report [7]. The patencies of the SD and ES were analysed in the same manner by assessing the continuity of their bony grooves [6]. In this study the appearances of the grooves of the RD, SD and ES as not fully recognized was defined as closed and any other state was defined as open to avoid the weak point of the subjective visual evaluation of 3D CT images (Figure 2).
Figure 1.
Figure 1.
3D CT image of the reuniting duct (RD), saccular duct (SD) and endolymphatic sinus (ES) of a healthy volunteer's ear (left), cadaver's ear (upper right), and schematic view (lower right). All these views are left ears. Red arrows show the RD and yellow ...
Figure 2.
Figure 2.
Drawings demonstrating the patency of the reuniting duct (RD), saccular duct (SD) and endolymphatic sinus (ES) on 3D CT images. When otoconia are dislodged into the RD, SD or ES, they lose continuity of the surface of their bony grooves and become vague ...
Additionally, we examined CT images of a cadaver with a small piece of muscle or small amount of calcium carbonate on the bony grooves of SD and ES to assess changes in the CT images, as in our previous report [7].
Statistical analysis
The 62 patients were analyzed in comparison with the normal subjects. The incidence of abnormal images of the bony grooves of those portions in affected ears in MD patients was compared with the non-affected contralateral ears and control volunteer ears and analysed by Yates 2 × 2 chi-squared test.
Results
Findings of RD aspects
Figures 3 and and44 show representative views of different patencies of the RD, SD and ES. Of the ears on the affected side of MD patients (Figures 3A and and4A),4A), 37% (23/62)) had closed RD compared with 9.7% (6/62) of the ears on the non-affected side (Table I). None (0/26) were closed in the normal group (Figures 3B and and4B).4B). There were significant differences between the ears on the affected side of MD patients and normal ears, and between the affected ears and the non-affected ears (p < 0.01) (Figure 5). There was no significant difference between non-affected ears of MD patients and normal ears (p = 0.078).
Figure 3.
Figure 3.
Representative views of the left ear of a patient with Meniere's disease (MD) (A) and a volunteer's healthy ear (B). (A) Although the outline of the bony groove of the reuniting duct (RD) (arrows), saccular duct (SD) and endolymphatic sinus (ES) can be ...
Figure 4.
Figure 4.
Representative views of the right ear of a patient with Meniere's disease (MD) (A) and a volunteer's healthy ear (B). (A) Both the bony grooves of the reuniting duct (RD) and the endolymphatic sinus (ES) are fully occupied by a dense, bony substance and ...
Table I.
Table I.
Status of the reuniting duct (RD), saccular duct (SD) and endolymphatic sinus (ES) in 62 patients with Meniere's disease (MD) and 13 healthy volunteers.
Figure 5.
Figure 5.
Distribution pattern of the reuniting duct (RD) in affected and non-affected ears of patients with Meniere's disease (MD) and healthy ears of volunteers.
Findings of SD aspects
The patencies of the affected and non-affected ears of MD were 51.6% (32/62) and 16.1% (12/62), respectively (Table I). In contrast, all the SDs (26/26) were patent in the healthy ears (Figures 3B and and4B).4B). There were significant differences between the affected ears and healthy ears and between the affected ears and the non-affected ears (p < 0.01). There was a slight but significant difference between the non-affected ears and healthy ears (p = 0.015) (Figure 6).
Figure 6.
Figure 6.
Distribution pattern of the saccular duct (SD) in affected and non-affected ears of patients with Meniere's disease (MD) and healthy ears of volunteers.
Findings of ES aspects
The distribution pattern of the ES resembled that of the SD. The patencies of the affected ears and non-affected ears of MD patients were 64.5% (40/62) and 17.7% (11/62), respectively (Table I). All the ESs (26/26) were patent in the healthy ears (Figures 3B and and4B).4B). There were significant differences between the affected ears and healthy ears and between the affected ears and the non-affected ears (p < 0.01). There was a slight difference between the non-affected ears and healthy ears (p = 0.030) (Figure 7).
Figure 7.
Figure 7.
Distribution pattern of the endolymphatic sinus (ES) in affected and non-affected ears of patients with Meniere's disease (MD) and healthy ears of volunteers.
Findings in the SD and ES of a cadaver treated with CaCO3 and soft tissue fragments
The bony grooves of the SD and ES treated with CaCO3 appeared vague (Figure 8A), but those with muscle fragments were not affected (Figure 8B).
Figure 8.
Figure 8.
3D CT views of a cadaver temporal bone. The bony grooves underlining the saccular duct (SD) and the endolymphatic sinus (ES) treated with CaCO3 (A) appear vague compared with those treated with muscle fragments (B). Note the difference in continuity of ...
Discussion
We could demonstrate differences in visualization or patency of the RD, SD and ES between the affected ears of MD patients and normal ears, suggesting that the RD, SD or ES in MD ears may be partly or entirely occluded compared with healthy ears. The reduced visualization of the RD, SD and ES suggests that these ducts were involved as lesions of MD.
Debris, pathogens or unusual substances in the inner ear can be transported in these narrow ducts and become obstacles to the pathway of longitudinal flow of endolymph resulting in endolymphatic hydrops.
We speculate that a reasonable explanation for this reduced visualization may be an occlusion caused by dislodged otoconia from the saccule. This is based on experimental findings from cadavers showing that the bony groove appears vague when covered with CaCO3 but not when covered with muscle fragments. The data from the present and previous studies [7] suggest that the occlusion may be situated between the saccule and the RD or the SD and the ES.
Saccular otoconia could be dislodged by various causes such as aging as the natural fate, infection, disturbance of blood circulation, trauma, etc., and the dislodged otoconia from the saccule can disperse into the surrounding membranous labyrinth [8,9].
If otoconia fall into such a narrow pathway, the RD to the cochlea or the SD and ES to the endolymphatic duct, they could disturb the endolymphatic flow.
Although saccular otoconia are more susceptible than those of the utricle [10], the incidence of MD patients is not so high in comparison with benign paroxysmal positional vertigo (BPPV) possibly caused by dislodged utricular otoconia [11]. We do not have conclusive data proving this. However, some speculation from our present results may answer this question. The risk of saccular otoconia falling into the RD may not be so high because of its narrowness, even if it is near the saccular otolithic membrane.
The longitudinal endolymph may work to oppose saccular otoconia falling into the RD. On the other hand, the SD and ES are in the path of the anterograde endolymph system. Therefore, the SD (51.6%) and ES (64.5%) may be more occluded than the RD (37%). The character of MD may be due to the rate of occlusion of these narrow ducts.
Histological studies reported that the endolympatic duct (ED) was obstructed with fibrous tissue, basophilic substance or bone in MD [12] and a radiological study also showed narrow and poor development of the ED in MD [13]. The lesions of the ED may have a similar pathology to those of the SD and ES because all these regions are connected as successive membranous pathways, which could support our hypothesis that dislodged saccular otoconia could be a cause of MD. However, more precise investigation of these areas of the human temporal bone in MD is necessary.
Although the non-affected ears in patients with MD showed a similar RD pattern to the affected ears, the similarity was not statistically supported. On the other hand, there were slight differences in the patency of the SD and ES between the non-affected ears and healthy ears. This tendency of occlusion in the SD and ES of the non-affected ears of MD patients suggests that the contralateral non-affected ears may also be challenged but functionally compensated. Earlier acoustic biasing experiments have shown that incipient endolymphatic hydrops may exist in the healthy contralateral ear in MD.
Bilateral engagement of MD varies according to different authors. The longer the duration of the disease the more frequent is the incidence of bilateral disease [14]. In a recent German study where the long-term course of MD was revisited, as many as 35% of subjects suffered from MD in both ears after 10 years and 47% after 20 years [15]. Some studies show a low bilateral incidence (5%) while audiometric low-tone changes occur more frequently (16%) [16]. Also, the modulation depth was found to be significantly reduced in the contralateral non-symptomatic ears of MD patients using low-frequency masking to diagnose endolymphatic hydrops [17]. This has led to the conception that MD is basically a bilateral disease with differing expression in the two ears. In addition, histopathological changes have been described to a large extent in the contralateral temporal bone in patients with unilateral MD [18]. Genetic alterations such as single nucelotide polymorphisms have been described in patients with bilateral MD [19]. The onset of MD has also been found to be earlier when both ears are affected [20]. Although we could not verify signs of bilateralism in our patients with MD in the present unilateral cases, the unilateral group may have included some bilateral cases. This is supported by our 3D CT findings. However, bilaterality of MD must be fully investigated in a future study.
We hypothesize that MD is a pathological condition brought about by saccular dislodged otoconia due to several causes, obstructing the narrow paths of the endolymph, based on the etiology of BPPV caused by dislodged otoconia from the utricle (Figure 9). Although we must investigate many factors of MD and the mechanism of MD attack in the future, the opening of these narrow paths could be one effective therapy for MD.
Figure 9.
Figure 9.
Hypothetical view of blockage of the reuniting duct (RD), saccular duct (SD) and endolymphatic sinus (ES) by dislodged otoconia from the saccule in patients with Meniere's disease (MD). ED, endolymphatic duct; EnS, endolymphatic sac; L, lateral semicircular ...
We evaluated the patency of the RD, SD and ES by 3D CT imaging, reflected by their bony grooves and not the actual ducts and ES. We thus obtained no definitive data on the degree of obstruction using the present 3D CT images.
In addition, the differences on 3D CT images among the various stages of MD that are categorized by degree of hearing deterioration must be investigated in the future.
Acknowledgements
We are indebted to Dr Hiroshi Aradate of J. Morita Corp. for valuable technical assistance.
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
References
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Thursday, September 11, 2014
Bilateral Vestibular Hypofunction
I know I have experienced many of these symptoms over the years. I always find some reassurance in knowing I'm not completely crazy, so I thought others might appreciate this article I read at Hearing Health Matters . Org.
Bilateral vestibular hypofunction: An interesting problem
By Pathways On September 3, 2014 · Add Comment
Although Pathways primarily focuses on neuroaudiology and CAPD, we will occasionally have articles on closely related issues such as the one below reviewing bilateral vestibular hypofunction, which is not only a peripheral, but also a central vestibular problem.
Bilateral vestibular hypofunction: An interesting problem
Stephanie A. Waryasz, B.S.
University of Connecticut
Bilateral vestibular hypofunction (BVH) is a disorder that creates reduced or absent function on both sides of the vestibular system, as its name implies. The disorder is characterized by general imbalance, especially during movement, movement-induced dizziness and movement-induced vision instability, also known as oscillopsia. Such symptoms are usually debilitating and greatly affects one’s ability to participate in activities daily living such as walking, driving, and reading, which can consequently impact a person’s employability, social life, and emotional well-being (Braswell & Rine, 2006; Herdman, Hall, Schubert, Das, & Tusa, 2007; Guinand, Pijnenburg, Janssen, & Kingma, 2012; Ward, Agrawal, Hoffman, Carey, & Della Santina, 2013).
BVH has also been associated with certain cognitive deficits such as spatial learning and spatial memory deficits due to a 17% reduction in hippocampal volume and decreased metabolic activity within the anterior hippocampus (McCall & Yates, 2011). From data analysis of the 2008 US National Health Interview Survey, it is believed that severe to profound BVH affects upwards of 28 in 100,000 adults in the United States or 64,046 Americans (Ward et al., 2013). These prevalence estimates are considered to be conservative, as people with confounding neurological and visual conditions, which could comorbidly exist with BVH, were excluded from the criteria used by Ward et al. (2013). Furthermore, Ward et al. (2013) used strict criteria to estimate the prevalence of BVH based on affirmations to case history questions that are known symptoms of severe to profound BVH. By extrapolating United States estimates, Ward et al. (2013) suggest that 1.8 million people worldwide could be affected by BVH, with the caveat that prevalence of BVH may vary geographically based on medical treatments such as the use of vestibulotoxic drugs.
Etiology
The most common etiology of BVH is systemic vestibulotoxicity from aminoglycoside antibiotics, specifically gentamicin and streptomycin (Schubert & Minor, 2004; Ward et al., 2013). These types of antibiotics are known for more selectively damaging vestibular hair cells while oftentimes leaving auditory hair cells unharmed, depending on the medication dosage administered (Schubert & Minor, 2004). The incidence of BVH ranges between 3%-4% when a patient is treated with gentamicin (Schubert & Minor, 2004). The incidence of BVH increases to between 12.5% and 30% for patients treated with both gentamicin and renal dialysis simultaneously (Schubert & Minor, 2004). These figures further emphasize the vulnerability and susceptibility of vestibular hair cells to drug-induced toxicity effects.
Less common etiologies of BVH include meningitis, head trauma, transient ischemic episodes of vessels supplying the vestibular system, bilateral tumors on cranial nerve VIII including vestibular schwannoma tumors, and sequential cases of unilateral vestibular neuronitis (Schubert & Minor, 2004). Ménière’s disease, encephalitis, labyrinthitis, autoimmune disease, and iatrogenic damage due to surgical procedures such as cochlear implantation have also been cited as potential etiologies of BVH (McCall & Yates, 2011; Ward et al., 2013;).
Pathological Process
The pathological process of BVH suggests a deficit in the vestibular system that results in inadequate compensatory eye movements during head movement that creates a slip of visual targets across the retina (McCall & Yates, 2011; Schubert & Minor, 2004), which consequently yields oscillopsia, one of the critical symptoms of BVH for differential diagnosis (Ward et al., 2013). This deficit makes it impossible for the vestibulo-ocular reflex (VOR) to respond appropriately. The VOR is responsible for generating compensatory eye movements that correspond to opposite head movements, ultimately stabilizing vision and gaze (Guinand et al., 2012; Vital et al., 2010). VOR deficits contribute to issues with gait, postural instability, and disequilibrium upon movement (Schubert & Minor, 2004). Such deficits are enhanced with an increase the velocity of head movements (Guinand et al., 2012; Vital et al., 2010).
Clinical Assessment
Clinical tests often used to diagnose BVH include the head thrust test to examine the VOR (Minor, 1998; McCall & Yates, 2011), various Romberg stances and tandem walks to view static imbalance (Minor, 1998; McCall & Yates, 2011), rapid full-body turns or external perturbations such as light shoves can help to assess dynamic imbalance (Minor, 1998; McCall & Yates, 2011), optokinetic testing presents with a severe reduction in nystagmus or no nystagmus with BVH (McCall & Yates, 2011), and caloric testing, which can identify reduced gaze stabilization of the VOR in the low frequency range (Vital et al., 2010). Due to the symptomology of BVH indicating severe deficits in gaze stabilization especially with movement, perhaps one of the best tests to assess BVH is the dynamic visual acuity test (Guinand et al., 2012; Herdman et al., 2007; Herdman et al., 1998; Schubert & Minor, 2004; Vital et al., 2010).
The dynamic visual acuity test assesses visual acuity while the head is in motion, which is typically self-generated (Schubert & Minor, 2004). Additionally, it examines the capacity of the VOR to maintain gaze stability during such head movement (Minor, 1998). Many different versions of this test exist, ranging from bedside to computerized to using scleral search coils to performing functional assessment on a treadmill (Guinand et al., 2012; Herdman et al., 2007; Herdman et al., 1998; Minor, 1998; Schubert & Minor, 2004; Vital et al., 2010). The bedside test can be performed informally by having the patient read a newspaper with the head remaining still, then having the patient try to continue reading while moving their head from side to side at a rate of about 2 cycles per second (Minor, 1998).
A more formal option would be to utilize computerized dynamic visual acuity testing. Herdman and colleagues (1998 & 2007) researched a method of calculating dynamic visual acuity by counting the total number of errors in identifying the orientation of the computerized optotype “E” while the subject’s head was moved predictability to the right or to the left. This quantity was then subtracted from the subject’s static visual acuity score to yield their dynamic visual acuity score. Herdman et al. (1998) reported 96.2% sensitivity, 100% specificity, and 97.5% overall accuracy in using this test to identify subjects with BVH in comparison to normal control subjects. The capacity of this test to distinguish between unilateral vestibular hypofunction (UVH) and BVH was also noted.
Dynamic Visual Acuity Testing Research
Vital et al. (2010) created a different computerized dynamic visual acuity test to assess peripheral vestibular function. This study assessed the subject’s ability to compute differences between visual acuity in static and dynamic conditions during active and passive horizontal head rotations at velocities exceeding 100°/sec and exceeding 150°/sec, respectively. Velocities were measured with a Sparkfun velocity sensory fixed to a headset worn by each subject. An active head rotation was generated by the subject’s participation in active movements. The passive head rotations were delivered by the examiner at random intervals by holding the head laterally on both sides outside of the subject’s visual field. To obtain the visual acuity level for each condition, the subject needed to identify the orientation of Landolt rings, a common optotype used for vision tests that looks like the letter “C”. Landolt rings were presented in sets of five for each visual acuity level.
The test terminated after the subject was unable to correctly identify at least three Landolt ring orientations at a given visual acuity level. To help with fixation during head rotation, a small dot was placed on the center of the monitor, which was only extinguished immediately before a Landolt ring was presented.
Vital and colleagues (2010) also verified their computerized results with quantitative horizontal head impulse testing (qHIT) with scleral search coils around the cornea of the right eye. The researchers noted that this test was clinically useful in identifying semicircular canal function in the high frequency range, which was reported to be more important in the assessment of gaze stabilization of the VOR.
The benefit of this test is that it can be easily administered within the office excluding the scleral search coil verification. However, the researchers warn that the examiner should be experienced with this test before utilizing it and the patient should be trained to minimize learning curve effects. The sensitivity of this test for identifying BVH was reported to be 100% and the specificity was reported to be 94% when performing passive rotation with the head velocity exceeding 150°/sec.
Guinand et al. (2012) created a unique type of dynamic visual acuity test that assessed functional dynamic visual acuity while on a treadmill. The difference between static and dynamic visual acuity was computed to determine the subject’s total dynamic visual acuity. Subjects were asked to read Sloan letters placed 2.8 meters away starting at the 20/25 visual acuity line. The visual acuity value of the most finite visual acuity with at least three correct responses was recorded as the acuity level for that test. Dynamic visual acuity testing was performed at three different velocities on a treadmill: 2 km/hr, 4 km/hr, and 6 km/hr. Researchers reported 97% sensitivity to identifying BVH when the visual acuity was measured at all three velocities. The sensitivity decreased to 76% if only 2 km/hr was recorded in the dynamic condition and 84% sensitivity if only 4 km/hr was recorded. If the dynamic testing was conducted at both 2 and 4 km/hr the sensitivity increased to 95%. Specificity was not reported by Guinand and colleagues (2012).
The benefits of this type of testing include its simple and cost-effective procedure that could be performed in less than 10 minutes without prior training for the patient or the test administrator. The main drawback to this test is that it requires a treadmill, which may not be accessible to all clinicians who would like to assess dynamic visual acuity. The researchers also noted that this test may be clinically useful in assessing functional outcomes of a vestibular training protocol. Additionally, this test could be used to assess candidacy for treatment options such as vestibular prosthesis implantation and post-surgical functional assessment. A summary of the three previously reviewed types of dynamic visual assessment tests (Guinand et al., 2012; Herdman et al., 2007; Herdman et al., 1998; Vital et al., 2010) can be seen in the Table below.
Table: A review of different dynamic visual acuity (DVA) assessment measures to identify bilateral vestibular hypofunction (BVH) with reported benefits, drawbacks, and clinical utility of each protocol from supporting research.
Table: A review of different dynamic visual acuity (DVA) assessment measures to identify bilateral vestibular hypofunction (BVH) with reported benefits, drawbacks, and clinical utility of each protocol from supporting research.
Due to the disease process of BVH, spontaneous recovery is rare (McCall & Yates, 2011). Therefore, techniques are necessary to provide relief to patients dealing with the debilitating effects of this disorder. There is currently no standardized treatment for BVH; however, research has shown potential for therapies and procedures to help manage BVH.
A review by McCall and Yates (2011) discusses vestibular physical therapy as a treatment option for BVH that has been shown to improve dynamic gait stability in addition to dynamic visual acuity in approximately 50% of patients. This figure suggests that half of the BVH patient population may already have innate compensatory processes that render such treatment fruitless. Sensory substitution has been highlighted as an alternative treatment method for BVH. This technique offers information typically processed by the vestibular system in an alternate modality such as visual, auditory, or tactile. The use of visual cues, auditory cues, head-mounted vibrotactile devices, or electrotactile feedback to the tongue are examples of alternate means of providing sensory feedback for the patient. Current research shows promise of a vestibular prosthesis in humans, which will function similarly to a cochlear implant in that an electrode array will be inserted into the semicircular canal. Conversely, the electrical stimulation for the vestibular prosthesis would be controlled by an accelerometer to detect head motion. It is believed that this stimulation will elicit appropriate eye movement compensation.
In summation, BVH is a debilitating disorder affecting both peripheral and central vestibular systems that most commonly yields postural instability, gait deficits, and oscillopsia due to a slip of the visual target across the retina interfering with the VOR (Herdman et al., 2007; Guinand et al., 2012; Ward et al., 2013). Central basis for BVH would likely also have central auditory findings, as these pathways are very close in proximity to each other, especially in the brainstem. The most commonly reported etiology of BVH is vestibulotoxicity due to use of aminoglycoside antibiotics (Schubert & Minor, 2004; Ward et al., 2013). This disorder can be identified through numerous tests, with dynamic visual acuity testing being one of the most clinically useful (Guinand et al., 2012; Herdman et al., 2007; Herdman et al., 1998; Schubert & Minor, 2004; Vital et al., 2010). Treatment options are widely varied for this disorder and should be individualized to meet the specific needs of the patient.
Stephanie Waryasz is a third year doctoral student of Audiology at the University of Connecticut. She completed her undergraduate Bachelor of Science degree in Communication Disorders at Southern Connecticut State University graduating with departmental honors. At Southern Connecticut State University, she completed an undergraduate thesis on the topic of mild traumatic brain injury and the treatment of blast victims in VA facilities returning from the Iraq and Afghanistan wars. Currently, Stephanie is examining the effects of sports-related concussion on auditory processing in university athletes for her Au.D. capstone research project at U Conn. Stephanie also enjoys volunteering for the Healthy Hearing Initiative at the Special Olympics in New Haven, CT and for Hear Here Hartford in Wethersfield, CT – an organization that helps to empower teens and young adults with hearing loss.
References
Braswell, J., & Rine, R. M. (2006). Evidence that vestibular hypofunction affects reading acuity in children. International Journal of Pediatric Otorhinolaryngology, 70, 1957–1965.
Guinand, N., Pijnenburg, M., Janssen, M., & Kingma, H. (2012). Visual acuity while walking and oscillopsia severity in healthy subjects and patients with unilateral and bilateral vestibular function loss. Arch Otolaryngol Head Neck Surg, 138(3), 301–306.
Herdman, S. J., Hall, C. D., Schubert, M. C., Das, V. E., & Tusa, R. J. (2007). Recovery of dynamic visual acuity in bilateral vestibular hypofunction. Arch Otolaryngol Head Neck Surg, 133, 383–389.
Herdman, S. J., Tusa, R. J., Blatt, P., Suzuki, A., Venuto, P., & Roberts, D. (1998). Computerized dynamic visual acuity test in the assessment of vestibular deficits. Am J Otol, 19, 790–796.
McCall, A. A., & Yates, B. J. (2011). Compensation following bilateral vestibular damage. Frontiers in Neurology, 2, 1–13.
Minor, L. B. (1998). Gentamicin-induced bilateral vestibular hypofunction. JAMA, 279(7), 541–544.
Schubert, M. C., & Minor, L. B. (2004). Vestibulo-ocular physiology underlying vestibular hypofunction. Physical Therapy, 84(4), 373–385.
Vital, D., Hegemann, S. C. A., Straumann, D., Bergamin, O., Bockisch, C. J., Angehrn, D., … Probst, R. (2010). A new dynamic visual acuity test to assess peripheral vestibular hypofunction. Arch Otolaryngol Head Neck Surg, 136(7), 686–691.
Ward, B. K., Agrawal, Y., Hoffman, H. J., Carey, J. P., & Della Santina, C. C. (2013).
Prevalence and impact of bilateral vestibular hypofunction: Results from the 2008 US National Health Interview Survey. JAMA Otolaryngology-Head & Neck Surgery, 139(8), 803–810.
This article is a publication of the Pathways Society. Copyright Hearing Health & Technology Matters. All rights reserved, 2014. For permission to republish this article, please contact Dr. Frank Musiek.
Bilateral vestibular hypofunction: An interesting problem
By Pathways On September 3, 2014 · Add Comment
Although Pathways primarily focuses on neuroaudiology and CAPD, we will occasionally have articles on closely related issues such as the one below reviewing bilateral vestibular hypofunction, which is not only a peripheral, but also a central vestibular problem.
Bilateral vestibular hypofunction: An interesting problem
Stephanie A. Waryasz, B.S.
University of Connecticut
Bilateral vestibular hypofunction (BVH) is a disorder that creates reduced or absent function on both sides of the vestibular system, as its name implies. The disorder is characterized by general imbalance, especially during movement, movement-induced dizziness and movement-induced vision instability, also known as oscillopsia. Such symptoms are usually debilitating and greatly affects one’s ability to participate in activities daily living such as walking, driving, and reading, which can consequently impact a person’s employability, social life, and emotional well-being (Braswell & Rine, 2006; Herdman, Hall, Schubert, Das, & Tusa, 2007; Guinand, Pijnenburg, Janssen, & Kingma, 2012; Ward, Agrawal, Hoffman, Carey, & Della Santina, 2013).
BVH has also been associated with certain cognitive deficits such as spatial learning and spatial memory deficits due to a 17% reduction in hippocampal volume and decreased metabolic activity within the anterior hippocampus (McCall & Yates, 2011). From data analysis of the 2008 US National Health Interview Survey, it is believed that severe to profound BVH affects upwards of 28 in 100,000 adults in the United States or 64,046 Americans (Ward et al., 2013). These prevalence estimates are considered to be conservative, as people with confounding neurological and visual conditions, which could comorbidly exist with BVH, were excluded from the criteria used by Ward et al. (2013). Furthermore, Ward et al. (2013) used strict criteria to estimate the prevalence of BVH based on affirmations to case history questions that are known symptoms of severe to profound BVH. By extrapolating United States estimates, Ward et al. (2013) suggest that 1.8 million people worldwide could be affected by BVH, with the caveat that prevalence of BVH may vary geographically based on medical treatments such as the use of vestibulotoxic drugs.
Etiology
The most common etiology of BVH is systemic vestibulotoxicity from aminoglycoside antibiotics, specifically gentamicin and streptomycin (Schubert & Minor, 2004; Ward et al., 2013). These types of antibiotics are known for more selectively damaging vestibular hair cells while oftentimes leaving auditory hair cells unharmed, depending on the medication dosage administered (Schubert & Minor, 2004). The incidence of BVH ranges between 3%-4% when a patient is treated with gentamicin (Schubert & Minor, 2004). The incidence of BVH increases to between 12.5% and 30% for patients treated with both gentamicin and renal dialysis simultaneously (Schubert & Minor, 2004). These figures further emphasize the vulnerability and susceptibility of vestibular hair cells to drug-induced toxicity effects.
Less common etiologies of BVH include meningitis, head trauma, transient ischemic episodes of vessels supplying the vestibular system, bilateral tumors on cranial nerve VIII including vestibular schwannoma tumors, and sequential cases of unilateral vestibular neuronitis (Schubert & Minor, 2004). Ménière’s disease, encephalitis, labyrinthitis, autoimmune disease, and iatrogenic damage due to surgical procedures such as cochlear implantation have also been cited as potential etiologies of BVH (McCall & Yates, 2011; Ward et al., 2013;).
Pathological Process
The pathological process of BVH suggests a deficit in the vestibular system that results in inadequate compensatory eye movements during head movement that creates a slip of visual targets across the retina (McCall & Yates, 2011; Schubert & Minor, 2004), which consequently yields oscillopsia, one of the critical symptoms of BVH for differential diagnosis (Ward et al., 2013). This deficit makes it impossible for the vestibulo-ocular reflex (VOR) to respond appropriately. The VOR is responsible for generating compensatory eye movements that correspond to opposite head movements, ultimately stabilizing vision and gaze (Guinand et al., 2012; Vital et al., 2010). VOR deficits contribute to issues with gait, postural instability, and disequilibrium upon movement (Schubert & Minor, 2004). Such deficits are enhanced with an increase the velocity of head movements (Guinand et al., 2012; Vital et al., 2010).
Clinical Assessment
Clinical tests often used to diagnose BVH include the head thrust test to examine the VOR (Minor, 1998; McCall & Yates, 2011), various Romberg stances and tandem walks to view static imbalance (Minor, 1998; McCall & Yates, 2011), rapid full-body turns or external perturbations such as light shoves can help to assess dynamic imbalance (Minor, 1998; McCall & Yates, 2011), optokinetic testing presents with a severe reduction in nystagmus or no nystagmus with BVH (McCall & Yates, 2011), and caloric testing, which can identify reduced gaze stabilization of the VOR in the low frequency range (Vital et al., 2010). Due to the symptomology of BVH indicating severe deficits in gaze stabilization especially with movement, perhaps one of the best tests to assess BVH is the dynamic visual acuity test (Guinand et al., 2012; Herdman et al., 2007; Herdman et al., 1998; Schubert & Minor, 2004; Vital et al., 2010).
The dynamic visual acuity test assesses visual acuity while the head is in motion, which is typically self-generated (Schubert & Minor, 2004). Additionally, it examines the capacity of the VOR to maintain gaze stability during such head movement (Minor, 1998). Many different versions of this test exist, ranging from bedside to computerized to using scleral search coils to performing functional assessment on a treadmill (Guinand et al., 2012; Herdman et al., 2007; Herdman et al., 1998; Minor, 1998; Schubert & Minor, 2004; Vital et al., 2010). The bedside test can be performed informally by having the patient read a newspaper with the head remaining still, then having the patient try to continue reading while moving their head from side to side at a rate of about 2 cycles per second (Minor, 1998).
A more formal option would be to utilize computerized dynamic visual acuity testing. Herdman and colleagues (1998 & 2007) researched a method of calculating dynamic visual acuity by counting the total number of errors in identifying the orientation of the computerized optotype “E” while the subject’s head was moved predictability to the right or to the left. This quantity was then subtracted from the subject’s static visual acuity score to yield their dynamic visual acuity score. Herdman et al. (1998) reported 96.2% sensitivity, 100% specificity, and 97.5% overall accuracy in using this test to identify subjects with BVH in comparison to normal control subjects. The capacity of this test to distinguish between unilateral vestibular hypofunction (UVH) and BVH was also noted.
Dynamic Visual Acuity Testing Research
Vital et al. (2010) created a different computerized dynamic visual acuity test to assess peripheral vestibular function. This study assessed the subject’s ability to compute differences between visual acuity in static and dynamic conditions during active and passive horizontal head rotations at velocities exceeding 100°/sec and exceeding 150°/sec, respectively. Velocities were measured with a Sparkfun velocity sensory fixed to a headset worn by each subject. An active head rotation was generated by the subject’s participation in active movements. The passive head rotations were delivered by the examiner at random intervals by holding the head laterally on both sides outside of the subject’s visual field. To obtain the visual acuity level for each condition, the subject needed to identify the orientation of Landolt rings, a common optotype used for vision tests that looks like the letter “C”. Landolt rings were presented in sets of five for each visual acuity level.
The test terminated after the subject was unable to correctly identify at least three Landolt ring orientations at a given visual acuity level. To help with fixation during head rotation, a small dot was placed on the center of the monitor, which was only extinguished immediately before a Landolt ring was presented.
Vital and colleagues (2010) also verified their computerized results with quantitative horizontal head impulse testing (qHIT) with scleral search coils around the cornea of the right eye. The researchers noted that this test was clinically useful in identifying semicircular canal function in the high frequency range, which was reported to be more important in the assessment of gaze stabilization of the VOR.
The benefit of this test is that it can be easily administered within the office excluding the scleral search coil verification. However, the researchers warn that the examiner should be experienced with this test before utilizing it and the patient should be trained to minimize learning curve effects. The sensitivity of this test for identifying BVH was reported to be 100% and the specificity was reported to be 94% when performing passive rotation with the head velocity exceeding 150°/sec.
Guinand et al. (2012) created a unique type of dynamic visual acuity test that assessed functional dynamic visual acuity while on a treadmill. The difference between static and dynamic visual acuity was computed to determine the subject’s total dynamic visual acuity. Subjects were asked to read Sloan letters placed 2.8 meters away starting at the 20/25 visual acuity line. The visual acuity value of the most finite visual acuity with at least three correct responses was recorded as the acuity level for that test. Dynamic visual acuity testing was performed at three different velocities on a treadmill: 2 km/hr, 4 km/hr, and 6 km/hr. Researchers reported 97% sensitivity to identifying BVH when the visual acuity was measured at all three velocities. The sensitivity decreased to 76% if only 2 km/hr was recorded in the dynamic condition and 84% sensitivity if only 4 km/hr was recorded. If the dynamic testing was conducted at both 2 and 4 km/hr the sensitivity increased to 95%. Specificity was not reported by Guinand and colleagues (2012).
The benefits of this type of testing include its simple and cost-effective procedure that could be performed in less than 10 minutes without prior training for the patient or the test administrator. The main drawback to this test is that it requires a treadmill, which may not be accessible to all clinicians who would like to assess dynamic visual acuity. The researchers also noted that this test may be clinically useful in assessing functional outcomes of a vestibular training protocol. Additionally, this test could be used to assess candidacy for treatment options such as vestibular prosthesis implantation and post-surgical functional assessment. A summary of the three previously reviewed types of dynamic visual assessment tests (Guinand et al., 2012; Herdman et al., 2007; Herdman et al., 1998; Vital et al., 2010) can be seen in the Table below.
Table: A review of different dynamic visual acuity (DVA) assessment measures to identify bilateral vestibular hypofunction (BVH) with reported benefits, drawbacks, and clinical utility of each protocol from supporting research.
Table: A review of different dynamic visual acuity (DVA) assessment measures to identify bilateral vestibular hypofunction (BVH) with reported benefits, drawbacks, and clinical utility of each protocol from supporting research.
Due to the disease process of BVH, spontaneous recovery is rare (McCall & Yates, 2011). Therefore, techniques are necessary to provide relief to patients dealing with the debilitating effects of this disorder. There is currently no standardized treatment for BVH; however, research has shown potential for therapies and procedures to help manage BVH.
A review by McCall and Yates (2011) discusses vestibular physical therapy as a treatment option for BVH that has been shown to improve dynamic gait stability in addition to dynamic visual acuity in approximately 50% of patients. This figure suggests that half of the BVH patient population may already have innate compensatory processes that render such treatment fruitless. Sensory substitution has been highlighted as an alternative treatment method for BVH. This technique offers information typically processed by the vestibular system in an alternate modality such as visual, auditory, or tactile. The use of visual cues, auditory cues, head-mounted vibrotactile devices, or electrotactile feedback to the tongue are examples of alternate means of providing sensory feedback for the patient. Current research shows promise of a vestibular prosthesis in humans, which will function similarly to a cochlear implant in that an electrode array will be inserted into the semicircular canal. Conversely, the electrical stimulation for the vestibular prosthesis would be controlled by an accelerometer to detect head motion. It is believed that this stimulation will elicit appropriate eye movement compensation.
In summation, BVH is a debilitating disorder affecting both peripheral and central vestibular systems that most commonly yields postural instability, gait deficits, and oscillopsia due to a slip of the visual target across the retina interfering with the VOR (Herdman et al., 2007; Guinand et al., 2012; Ward et al., 2013). Central basis for BVH would likely also have central auditory findings, as these pathways are very close in proximity to each other, especially in the brainstem. The most commonly reported etiology of BVH is vestibulotoxicity due to use of aminoglycoside antibiotics (Schubert & Minor, 2004; Ward et al., 2013). This disorder can be identified through numerous tests, with dynamic visual acuity testing being one of the most clinically useful (Guinand et al., 2012; Herdman et al., 2007; Herdman et al., 1998; Schubert & Minor, 2004; Vital et al., 2010). Treatment options are widely varied for this disorder and should be individualized to meet the specific needs of the patient.
Stephanie Waryasz is a third year doctoral student of Audiology at the University of Connecticut. She completed her undergraduate Bachelor of Science degree in Communication Disorders at Southern Connecticut State University graduating with departmental honors. At Southern Connecticut State University, she completed an undergraduate thesis on the topic of mild traumatic brain injury and the treatment of blast victims in VA facilities returning from the Iraq and Afghanistan wars. Currently, Stephanie is examining the effects of sports-related concussion on auditory processing in university athletes for her Au.D. capstone research project at U Conn. Stephanie also enjoys volunteering for the Healthy Hearing Initiative at the Special Olympics in New Haven, CT and for Hear Here Hartford in Wethersfield, CT – an organization that helps to empower teens and young adults with hearing loss.
References
Braswell, J., & Rine, R. M. (2006). Evidence that vestibular hypofunction affects reading acuity in children. International Journal of Pediatric Otorhinolaryngology, 70, 1957–1965.
Guinand, N., Pijnenburg, M., Janssen, M., & Kingma, H. (2012). Visual acuity while walking and oscillopsia severity in healthy subjects and patients with unilateral and bilateral vestibular function loss. Arch Otolaryngol Head Neck Surg, 138(3), 301–306.
Herdman, S. J., Hall, C. D., Schubert, M. C., Das, V. E., & Tusa, R. J. (2007). Recovery of dynamic visual acuity in bilateral vestibular hypofunction. Arch Otolaryngol Head Neck Surg, 133, 383–389.
Herdman, S. J., Tusa, R. J., Blatt, P., Suzuki, A., Venuto, P., & Roberts, D. (1998). Computerized dynamic visual acuity test in the assessment of vestibular deficits. Am J Otol, 19, 790–796.
McCall, A. A., & Yates, B. J. (2011). Compensation following bilateral vestibular damage. Frontiers in Neurology, 2, 1–13.
Minor, L. B. (1998). Gentamicin-induced bilateral vestibular hypofunction. JAMA, 279(7), 541–544.
Schubert, M. C., & Minor, L. B. (2004). Vestibulo-ocular physiology underlying vestibular hypofunction. Physical Therapy, 84(4), 373–385.
Vital, D., Hegemann, S. C. A., Straumann, D., Bergamin, O., Bockisch, C. J., Angehrn, D., … Probst, R. (2010). A new dynamic visual acuity test to assess peripheral vestibular hypofunction. Arch Otolaryngol Head Neck Surg, 136(7), 686–691.
Ward, B. K., Agrawal, Y., Hoffman, H. J., Carey, J. P., & Della Santina, C. C. (2013).
Prevalence and impact of bilateral vestibular hypofunction: Results from the 2008 US National Health Interview Survey. JAMA Otolaryngology-Head & Neck Surgery, 139(8), 803–810.
This article is a publication of the Pathways Society. Copyright Hearing Health & Technology Matters. All rights reserved, 2014. For permission to republish this article, please contact Dr. Frank Musiek.
Monday, August 25, 2014
Lessons from the Front Lines
We all view life through a unique lens. How we respond to our circumstances is relative and probably depends on a combination of our innate temperament and our life experiences, among other things. In general, my own temperament is such that I tend to over analyze things. When faced with a dilemma, I want to classify my options into nice little black and white boxes and then, as my husband says, I ruminate. When coping with a chronic disease, this is not a particularly helpful approach to take.
My life experiences, fortunately, have afforded me some unique insights into how others cope with chronic illness, most of the time it's not just a nuisance disease, but something of the life-threatening variety. It is a humbling experience to sit with someone as they work through the details of how they are going to adapt to their "new normal". As we all know, a chronic disease can affect every aspect of one's life and lifestyle.
While I am simply a resource to help my patients learn to meet their nutrition needs, this alone is often an overwhelming and emotional task for them - and me! Their disease state, treatment, and/or surgical interventions can have a profound effect on what they can and cannot eat. While not insurmountable to change, it cannot be overestimated just how much what, when, and how we eat is a part of who we are. So while my focus is always on the science and practice of nutrition, there is quite a bit of psychology that goes into applying this knowledge. Oh, and marriage counseling, too! By that I mean, Mr. Smith will say, "I'm eating just fine." While his wife begs to differ. And so we must all come to an agreement of what the problem is or if there even is one. But I digress...
As we (meaning me, the patient and their family or caregivers, as well as the rest of the medical team) work together through the patient's nutrition options, I often learn more about who this person is, who they used to be, and who they hope to become, sometimes as they are just beginning to see the light at the end of the proverbial tunnel. You know what light I mean.
I had a bit of an epiphany at work recently. I realized that many of the patients I meet with are currently, or have been at some point in their lives, quite successful, powerful, and in control. Just like those of us with Meniere's. I'm sure they used to exude confidence and strength. But usually when I meet them for the first or tenth time, they nearly always have furrowed brow lines, fear in their voices, and a palpable aura of anxiety surrounding them. At least a few tears are not uncommon. This is the average person I come across with a cancer, or other life-changing, diagnosis.
Once in a while, though, people take it to a whole new level. Please keep in mind, I am not judging anyone's response to a clearly very stressful situation. Whether it be cancer, advanced diabetes, dementia or Alzheimer's diseases, multiple sclerosis, Crohn's disease, or Parkinson's disease to name a few, these are all life-altering conditions with few options for treatment. But, for a few people, this really knocks them off the rails. It can really be quite frightening for them and everyone around them. The level of angst can often get in the way of the patient's treatment and result in a very poor quality of life. Some people are able to pull themselves together with the support of their family, friends, and professional counseling, but others sadly do not.
It's observing the people on the other end of the spectrum that softens my heart and inspires me, for they have an important lesson to impart. As I have explored with them how they are coping with their disease, as I always do since this can certainly affect appetite and compliance to nutrition recommendations, this person usually says something to the effect, "Well, this is it. I will do what I need to do to manage my symptoms as best as we can, but I am not afraid. This is just how life goes, isn't it?" Yes. Yes, it is.
My life experiences, fortunately, have afforded me some unique insights into how others cope with chronic illness, most of the time it's not just a nuisance disease, but something of the life-threatening variety. It is a humbling experience to sit with someone as they work through the details of how they are going to adapt to their "new normal". As we all know, a chronic disease can affect every aspect of one's life and lifestyle.
While I am simply a resource to help my patients learn to meet their nutrition needs, this alone is often an overwhelming and emotional task for them - and me! Their disease state, treatment, and/or surgical interventions can have a profound effect on what they can and cannot eat. While not insurmountable to change, it cannot be overestimated just how much what, when, and how we eat is a part of who we are. So while my focus is always on the science and practice of nutrition, there is quite a bit of psychology that goes into applying this knowledge. Oh, and marriage counseling, too! By that I mean, Mr. Smith will say, "I'm eating just fine." While his wife begs to differ. And so we must all come to an agreement of what the problem is or if there even is one. But I digress...
As we (meaning me, the patient and their family or caregivers, as well as the rest of the medical team) work together through the patient's nutrition options, I often learn more about who this person is, who they used to be, and who they hope to become, sometimes as they are just beginning to see the light at the end of the proverbial tunnel. You know what light I mean.
I had a bit of an epiphany at work recently. I realized that many of the patients I meet with are currently, or have been at some point in their lives, quite successful, powerful, and in control. Just like those of us with Meniere's. I'm sure they used to exude confidence and strength. But usually when I meet them for the first or tenth time, they nearly always have furrowed brow lines, fear in their voices, and a palpable aura of anxiety surrounding them. At least a few tears are not uncommon. This is the average person I come across with a cancer, or other life-changing, diagnosis.
Once in a while, though, people take it to a whole new level. Please keep in mind, I am not judging anyone's response to a clearly very stressful situation. Whether it be cancer, advanced diabetes, dementia or Alzheimer's diseases, multiple sclerosis, Crohn's disease, or Parkinson's disease to name a few, these are all life-altering conditions with few options for treatment. But, for a few people, this really knocks them off the rails. It can really be quite frightening for them and everyone around them. The level of angst can often get in the way of the patient's treatment and result in a very poor quality of life. Some people are able to pull themselves together with the support of their family, friends, and professional counseling, but others sadly do not.
It's observing the people on the other end of the spectrum that softens my heart and inspires me, for they have an important lesson to impart. As I have explored with them how they are coping with their disease, as I always do since this can certainly affect appetite and compliance to nutrition recommendations, this person usually says something to the effect, "Well, this is it. I will do what I need to do to manage my symptoms as best as we can, but I am not afraid. This is just how life goes, isn't it?" Yes. Yes, it is.
Monday, August 11, 2014
The Art and Science of Treating Meniere's Disease
Note: I know this needs some editing, but I'm short on time so I'll try to come back to clean it up later. Here's my B-student mentality coming through.
Most people would consider art to be something solely based on subjective preferences and emotion, while the practice of medicine as based wholly on scientific objectivity. While there is truth in both of these assumptions, the reality is that the two overlap more than they might appear on the surface.
In an effort to produce a desired look, a good artist understands the physical and chemical properties of their medium. They learn how and why they must use oil or acrylic paints on canvas, while watercolors must be used on a specific type of paper. Or that there are different types of clay to be used for sculpting and that one must choose the right one depending on what the final product is to be. Even in understanding and using the right tools and media to produce specific types of art, not everyone will agree on the beauty of the artist's final rendering.
The practice of medicine is actually quite similar. While the practice of medicine has evolved rapidly over the last 100 years and can now treat many previously-deadly diseases quite effectively with modern medical interventions, there are still many, many conditions for which modern science has yet to understand with enough detail as to be able to manage or cure them. You know where, I'm going with this, right?
I have spent my entire 15-year career as a dietitian working with the sickest of the sick. The patients I have worked with have almost exclusively been dependent on tube- or IV-nutrition or have advanced-stage cancer. In this population, I see a lot of very malnourished patients. Severe malnutrition creates a lot of anxiety not only for patients and their families, but also for their physicians. Many times, a doctor will ask me what "one test" can they order to track their patient's nutrition progress. While there are many tests that are indicators of nutrition status, there is as-yet no one reliable indicator of nutrition status. It's safe to say that the same could be said of any other measure of health. With most chronic diseases, it is the assessment of blood tests, physical assessment, and functional status which inform the clinician of the effectiveness of their intervention(s). And oftentimes, it is the subjective measures which are most important to patients. Ultimately, I tell physicians and patients alike that the assessment of nutrition status is as much an art as it is a science and that the goal is really to prevent poor nutrition from interfering with treatment of the disease at hand and/or to promote optimal quality of life within the limitations of the disease's symptoms as they relate to nutrition status. I wish there was a better understanding of nutrition and diet and how they are related to optimal health outcomes, but the science just isn't there yet. And sadly I don't think it ever will be. There are just too many factors and moving targets.
If we compare the current understanding and treatments for Meniere's disease to art, I think it's safe to say we're stuck square in the Middle Ages. The scientific understanding, at least as portrayed to us by the experts, feels entirely two-dimensional. There are some interesting nuances that appear from time-to-time, but as a whole, if compared to art, we are long way from the 4-dimensional, Technicolor experience we all hope and wish for.
Accepting the reality of the current limitations in understanding this disease, I think many of us would appreciate a little more honest discourse from our physicians. I am tired of the words "idiopathic" and "symptom management." I can read all of that on-line. I want to hear their personal and professional assessment of the latest research. Where do they think it is heading? What should be following in the literature? Which scientists are doing the most interesting work?
My belief is that, just like the emergence of the Renaissance after the Middle Ages, the understanding of the cause(s) and treatment of Meniere's disease will eventually take a giant leap forward, moving us closer to that 4-dimensional, Technicolor rendering of Meniere's disease interventions and outcomes.
Most people would consider art to be something solely based on subjective preferences and emotion, while the practice of medicine as based wholly on scientific objectivity. While there is truth in both of these assumptions, the reality is that the two overlap more than they might appear on the surface.
In an effort to produce a desired look, a good artist understands the physical and chemical properties of their medium. They learn how and why they must use oil or acrylic paints on canvas, while watercolors must be used on a specific type of paper. Or that there are different types of clay to be used for sculpting and that one must choose the right one depending on what the final product is to be. Even in understanding and using the right tools and media to produce specific types of art, not everyone will agree on the beauty of the artist's final rendering.
The practice of medicine is actually quite similar. While the practice of medicine has evolved rapidly over the last 100 years and can now treat many previously-deadly diseases quite effectively with modern medical interventions, there are still many, many conditions for which modern science has yet to understand with enough detail as to be able to manage or cure them. You know where, I'm going with this, right?
I have spent my entire 15-year career as a dietitian working with the sickest of the sick. The patients I have worked with have almost exclusively been dependent on tube- or IV-nutrition or have advanced-stage cancer. In this population, I see a lot of very malnourished patients. Severe malnutrition creates a lot of anxiety not only for patients and their families, but also for their physicians. Many times, a doctor will ask me what "one test" can they order to track their patient's nutrition progress. While there are many tests that are indicators of nutrition status, there is as-yet no one reliable indicator of nutrition status. It's safe to say that the same could be said of any other measure of health. With most chronic diseases, it is the assessment of blood tests, physical assessment, and functional status which inform the clinician of the effectiveness of their intervention(s). And oftentimes, it is the subjective measures which are most important to patients. Ultimately, I tell physicians and patients alike that the assessment of nutrition status is as much an art as it is a science and that the goal is really to prevent poor nutrition from interfering with treatment of the disease at hand and/or to promote optimal quality of life within the limitations of the disease's symptoms as they relate to nutrition status. I wish there was a better understanding of nutrition and diet and how they are related to optimal health outcomes, but the science just isn't there yet. And sadly I don't think it ever will be. There are just too many factors and moving targets.
If we compare the current understanding and treatments for Meniere's disease to art, I think it's safe to say we're stuck square in the Middle Ages. The scientific understanding, at least as portrayed to us by the experts, feels entirely two-dimensional. There are some interesting nuances that appear from time-to-time, but as a whole, if compared to art, we are long way from the 4-dimensional, Technicolor experience we all hope and wish for.
Accepting the reality of the current limitations in understanding this disease, I think many of us would appreciate a little more honest discourse from our physicians. I am tired of the words "idiopathic" and "symptom management." I can read all of that on-line. I want to hear their personal and professional assessment of the latest research. Where do they think it is heading? What should be following in the literature? Which scientists are doing the most interesting work?
My belief is that, just like the emergence of the Renaissance after the Middle Ages, the understanding of the cause(s) and treatment of Meniere's disease will eventually take a giant leap forward, moving us closer to that 4-dimensional, Technicolor rendering of Meniere's disease interventions and outcomes.
Thursday, August 7, 2014
The Weird and Seemingly Secret Symptoms of Meniere's
I have weird symptoms that I am convinced are absolutely related to my Meniere's disease. Over the years, I have asked all of my doctors about them and in almost every case, I get no more than a weird look and a shrug of the shoulders from them. I have also asked fellow sufferers the same questions and, in many cases, I get a yeah-me-too, response.
Let's start by reviewing the standard definition of Meniere's disease. In a nutshell, once all other causes, such as a brain tumor, have been ruled out, there are four "official" symptoms which will put you in the Meniere's disease camp: episodic hearing loss, usually in the lower frequencies, aural pressure, tinnitus, and vertigo. When I go back and read about Meniere's disease on just about any medically-valid website, the description and prognosis are so sterile and practically benign that it's almost laughable. For me, Meniere's has been so much more than these four symptoms. Things have come and gone, but over the years I have also experienced the following:
Frequent Urination
I don't seem to get this anymore, but I used to get it every time the aural pressure would build up in the hours leading up to a vertigo attack. After doing some research, I concluded that a possible explanations is that as the endolymphatic sac (ES) becomes swollen with fluid, the aquaporins on its surface will send signals to the brain to decrease the production of antidiuretic hormone. This causes diuresis and I guess is the body's way of responding to the SOS being sent out by the ear that it's fluid overloaded. This would often persist through most of a vertigo attack, as well. As if it's not bad enough to be spinning so violently that I cannot possibly stand up, much less walk to the bathroom, I now had to pee like a racehorse every 30 minutes!
Sinus Pressure and Inflammation
There is some validating evidence in the literature that people with Meniere's disease are more likely to experience environmental and food allergies. The leading expert on this phenomenon happens to be one of my doctors, M. Jennifer Derebery at House Ear Clinic in Los Angeles. She is adamant that she doesn't believe that allergies cause Meniere's disease, only that there is a correlation. Now she didn't personally tell me this, but if you've read my previous post, you know that there is some evidence to suggest that Meniere's disease is in fact one of immune dysfunction. So, could it be that this dysfunctional immune response lends itself to the development of allergies or allergy-like symptoms? Anyway, for the first few years, I kept telling any doctor who would listen that my sinuses often felt swollen and inflamed, at times even tingling, the sensation extending into my ears. Each doctor agreed that they could visualize this inflammation when they looked in my nose and they threw different drugs at it, namely nasal steroids and a host of allergy medications. The nasal steroids often temporarily helped and Claritin seemed to take the edge off, but nothing really made much of a difference until I started allergy shots. The weird thing is that the first allergist I saw tested me for well over 30 allergens and could not find one thing I would react to. He was as frustrated as I was because, like all the others, he could see that my nasal membranes were really inflamed. Ultimately he named it 'nonallergic rhinitis' and sent me on my way. It was shortly after this that I was referred to Dr. Derebery. Rather than the standard scratch tests most allergists use, she injects small amounts of allergen solution under the skin, just like a TB test, in varying concentrations in an effort to elicit a reaction. Testing in this way, she was able to identify 5 or 6 things that I seemed to react to, including mold, and from there I began allergy shots. With time, they significantly alleviated my sinus inflammation. I mention the mold specifically because I believe all of my problems began with a persistent exposure to mold about six years ago. Other sufferers have reported a similar experience with a large mold exposure in the months leading up to the onset of their Meniere's.
The Absence of Infectious Illnesses
The literature has shown that people with Meniere's disease have an increased incidence of having one or more autoimmune diseases, such as rheumatoid arthritis, lupus, multiple sclerosis, Hashimoto's disease, Sjogren's, and others. Meniere's disease itself is not an autoimmune disease. While, knock on wood, I don't seem to have any other chronic conditions, I have made an odd observation in the past five years: I have not had one single cold, flu, or other known viral infection! This is amazing because during this time, all three of my kids were in elementary school and constantly passing around the germ du jour. Most recently it was hand, food, and mouth disease. Ugh. Even my husband catches a cold once or twice a year. But not me. I might feel like I'm fighting something off for a day, but it has never developed into full-blown illness. Before Meniere's, I got the usual number of colds, tummy bugs, and even a couple of sinus infections, but that all seems to have changed. My theory is that the type and degree of immune dysfunction causing my Meniere's symptoms has somehow protected me from viral infections.
GI Issues
Since the very beginning, I have felt like my body is fighting off a chronic infection. This is evidenced by the chronic episodes of exhaustion and fatigue, but also the fact that I often have "unusual" bowel movements. Sorry for the grossness factor. I happen to talk about poop in great detail on a daily basis with my patients at work, but I appreciate that it's a sensitive subject for many. I don't have diarrhea, per se, but it's not normal like it used to be either. Most days it's just once first thing in the morning, but when my ear is acting up, it is rather urgent in nature and really just not anywhere near normal. Like so many other things, this symptom lends itself to the theory of a disrupted immune system, specifically at the level of the mucous-associated lymph tissue (MALT) which lines everything between our ears and rectum.
Ear, Jaw, Neck, and Tooth Pain and Swollen Lymph Nodes
To me, this seems to be a huge oversight on the part of doctors and researchers and no one seems to have anything to say about it. I know I am not alone in experiencing these symptoms. I have had so many dental exams, going so far as to have my crowns replaced and having antibiotics injected under my gum line, because at times my teeth on the right side of my jaw ache and become sensitive to hot and cold. It comes and goes, but always correlates with an earache such that if I even touch the aural area in front of the ear, I will feel almost-excruciating pain. During these episodes, my ear canal also narrows, indicating some kind of inflammation, which I suspect is caused by swelling of the aural lymph node. These episodes also coincide with a sore throat and a sensation of a swollen node in my throat, along with aches and pains down the side of my neck correlating with other lymph nodes. Sometimes I can feel them by palpating them with my fingers, sometimes I can't. I knew my ear canal was swollen and painful when I used to wear my hearing aid as during these episodes it would be very difficult to put in my ear. Now I can tell simply by inserting a cotton swab in my ear. Some days there is plenty of room and it's painless, other times I can barely get the swab in there and it's quite painful.
Facial Tingling
I really get weird looks from doctors when I mention this one. This may, or may not, be related to the Meniere's. But I get these weird, very brief tingling sensations across one or the other of my cheekbones or across the bridge of my nose. It feels like a spiderweb or feather brushing the skin and lasts for just a second or two. It never happens all at once, just in one of the three locations. I think it's been quite some time since I have felt this one, though, and I don't recall that it would correlate with any other symptoms.
Balance Problems other than Vertigo
In the summers of 2012 and 2013, we took road trips. After each, trip I developed Mal de Barquement syndrome, with the symptoms lasting about six months! What that meant for me was that after any time spent driving or in the car, even 5 minutes, I would feel like I was moving for anywhere from 30 minutes to a couple of hours. At times, driving was very difficult because my eyes couldn't track all the motion around me. And, as everyone with Meniere's disease knows, we experience a very wide range of vestibular disturbances aside from vertigo. Some wax and wane and others persist. I don't think doctors like to bring it up because there's not much to be done about it. There is vestibular therapy or rehabilitation, but as far as I can tell, it works best for people with a static and permanent loss. For those of us with fluctuating symptoms, I'm not sure how much vestibular exercises can help to retrain the brain. Just as soon as our brain adapts to a change, something else gives and we're back to square one. Many of us also experience a kind of slow nystagmus, or eye darting, another really annoying and distracting symptom. Fun stuff!
Cognitive Dysfunction and Fatigue
In my experience, doctors and researchers like to pin brain fog and exhaustion on the brain working so hard to keep us balanced. But I think it's far more complex than that. I've again come to the conclusion that it is somehow related to some kind of chronic infection and underlying immune response. I also believe it is complicated by hearing loss and tinnitus. Despite these symptoms having a huge impact on our quality of life, no one likes to talk about them - maybe because they are poorly understood and there is no known treatment.
I hope this post validates some of the symptoms you've been having , too. Did I forget anything? Let me know what weird symptoms you have that no one talks about being related to Meniere's disease.
Let's start by reviewing the standard definition of Meniere's disease. In a nutshell, once all other causes, such as a brain tumor, have been ruled out, there are four "official" symptoms which will put you in the Meniere's disease camp: episodic hearing loss, usually in the lower frequencies, aural pressure, tinnitus, and vertigo. When I go back and read about Meniere's disease on just about any medically-valid website, the description and prognosis are so sterile and practically benign that it's almost laughable. For me, Meniere's has been so much more than these four symptoms. Things have come and gone, but over the years I have also experienced the following:
Frequent Urination
I don't seem to get this anymore, but I used to get it every time the aural pressure would build up in the hours leading up to a vertigo attack. After doing some research, I concluded that a possible explanations is that as the endolymphatic sac (ES) becomes swollen with fluid, the aquaporins on its surface will send signals to the brain to decrease the production of antidiuretic hormone. This causes diuresis and I guess is the body's way of responding to the SOS being sent out by the ear that it's fluid overloaded. This would often persist through most of a vertigo attack, as well. As if it's not bad enough to be spinning so violently that I cannot possibly stand up, much less walk to the bathroom, I now had to pee like a racehorse every 30 minutes!
Sinus Pressure and Inflammation
There is some validating evidence in the literature that people with Meniere's disease are more likely to experience environmental and food allergies. The leading expert on this phenomenon happens to be one of my doctors, M. Jennifer Derebery at House Ear Clinic in Los Angeles. She is adamant that she doesn't believe that allergies cause Meniere's disease, only that there is a correlation. Now she didn't personally tell me this, but if you've read my previous post, you know that there is some evidence to suggest that Meniere's disease is in fact one of immune dysfunction. So, could it be that this dysfunctional immune response lends itself to the development of allergies or allergy-like symptoms? Anyway, for the first few years, I kept telling any doctor who would listen that my sinuses often felt swollen and inflamed, at times even tingling, the sensation extending into my ears. Each doctor agreed that they could visualize this inflammation when they looked in my nose and they threw different drugs at it, namely nasal steroids and a host of allergy medications. The nasal steroids often temporarily helped and Claritin seemed to take the edge off, but nothing really made much of a difference until I started allergy shots. The weird thing is that the first allergist I saw tested me for well over 30 allergens and could not find one thing I would react to. He was as frustrated as I was because, like all the others, he could see that my nasal membranes were really inflamed. Ultimately he named it 'nonallergic rhinitis' and sent me on my way. It was shortly after this that I was referred to Dr. Derebery. Rather than the standard scratch tests most allergists use, she injects small amounts of allergen solution under the skin, just like a TB test, in varying concentrations in an effort to elicit a reaction. Testing in this way, she was able to identify 5 or 6 things that I seemed to react to, including mold, and from there I began allergy shots. With time, they significantly alleviated my sinus inflammation. I mention the mold specifically because I believe all of my problems began with a persistent exposure to mold about six years ago. Other sufferers have reported a similar experience with a large mold exposure in the months leading up to the onset of their Meniere's.
The Absence of Infectious Illnesses
The literature has shown that people with Meniere's disease have an increased incidence of having one or more autoimmune diseases, such as rheumatoid arthritis, lupus, multiple sclerosis, Hashimoto's disease, Sjogren's, and others. Meniere's disease itself is not an autoimmune disease. While, knock on wood, I don't seem to have any other chronic conditions, I have made an odd observation in the past five years: I have not had one single cold, flu, or other known viral infection! This is amazing because during this time, all three of my kids were in elementary school and constantly passing around the germ du jour. Most recently it was hand, food, and mouth disease. Ugh. Even my husband catches a cold once or twice a year. But not me. I might feel like I'm fighting something off for a day, but it has never developed into full-blown illness. Before Meniere's, I got the usual number of colds, tummy bugs, and even a couple of sinus infections, but that all seems to have changed. My theory is that the type and degree of immune dysfunction causing my Meniere's symptoms has somehow protected me from viral infections.
GI Issues
Since the very beginning, I have felt like my body is fighting off a chronic infection. This is evidenced by the chronic episodes of exhaustion and fatigue, but also the fact that I often have "unusual" bowel movements. Sorry for the grossness factor. I happen to talk about poop in great detail on a daily basis with my patients at work, but I appreciate that it's a sensitive subject for many. I don't have diarrhea, per se, but it's not normal like it used to be either. Most days it's just once first thing in the morning, but when my ear is acting up, it is rather urgent in nature and really just not anywhere near normal. Like so many other things, this symptom lends itself to the theory of a disrupted immune system, specifically at the level of the mucous-associated lymph tissue (MALT) which lines everything between our ears and rectum.
Ear, Jaw, Neck, and Tooth Pain and Swollen Lymph Nodes
To me, this seems to be a huge oversight on the part of doctors and researchers and no one seems to have anything to say about it. I know I am not alone in experiencing these symptoms. I have had so many dental exams, going so far as to have my crowns replaced and having antibiotics injected under my gum line, because at times my teeth on the right side of my jaw ache and become sensitive to hot and cold. It comes and goes, but always correlates with an earache such that if I even touch the aural area in front of the ear, I will feel almost-excruciating pain. During these episodes, my ear canal also narrows, indicating some kind of inflammation, which I suspect is caused by swelling of the aural lymph node. These episodes also coincide with a sore throat and a sensation of a swollen node in my throat, along with aches and pains down the side of my neck correlating with other lymph nodes. Sometimes I can feel them by palpating them with my fingers, sometimes I can't. I knew my ear canal was swollen and painful when I used to wear my hearing aid as during these episodes it would be very difficult to put in my ear. Now I can tell simply by inserting a cotton swab in my ear. Some days there is plenty of room and it's painless, other times I can barely get the swab in there and it's quite painful.
Facial Tingling
I really get weird looks from doctors when I mention this one. This may, or may not, be related to the Meniere's. But I get these weird, very brief tingling sensations across one or the other of my cheekbones or across the bridge of my nose. It feels like a spiderweb or feather brushing the skin and lasts for just a second or two. It never happens all at once, just in one of the three locations. I think it's been quite some time since I have felt this one, though, and I don't recall that it would correlate with any other symptoms.
Balance Problems other than Vertigo
In the summers of 2012 and 2013, we took road trips. After each, trip I developed Mal de Barquement syndrome, with the symptoms lasting about six months! What that meant for me was that after any time spent driving or in the car, even 5 minutes, I would feel like I was moving for anywhere from 30 minutes to a couple of hours. At times, driving was very difficult because my eyes couldn't track all the motion around me. And, as everyone with Meniere's disease knows, we experience a very wide range of vestibular disturbances aside from vertigo. Some wax and wane and others persist. I don't think doctors like to bring it up because there's not much to be done about it. There is vestibular therapy or rehabilitation, but as far as I can tell, it works best for people with a static and permanent loss. For those of us with fluctuating symptoms, I'm not sure how much vestibular exercises can help to retrain the brain. Just as soon as our brain adapts to a change, something else gives and we're back to square one. Many of us also experience a kind of slow nystagmus, or eye darting, another really annoying and distracting symptom. Fun stuff!
Cognitive Dysfunction and Fatigue
In my experience, doctors and researchers like to pin brain fog and exhaustion on the brain working so hard to keep us balanced. But I think it's far more complex than that. I've again come to the conclusion that it is somehow related to some kind of chronic infection and underlying immune response. I also believe it is complicated by hearing loss and tinnitus. Despite these symptoms having a huge impact on our quality of life, no one likes to talk about them - maybe because they are poorly understood and there is no known treatment.
I hope this post validates some of the symptoms you've been having , too. Did I forget anything? Let me know what weird symptoms you have that no one talks about being related to Meniere's disease.
My Symptoms Pre-Stephen Spring Treatment
To understand how far I've come in the past 11 months on the Stephen Spring Treatment Program, one needs to know where I started. There were lots of ups and downs in the 4-plus years leading up to my decision to try this treatment. I had several temporary responses to various treatments, namely intratympanic (IT) dexamethasone, IT gentamicin, antiviral medications, and allergy shots. With the exception of the gent shots, each of the above treatments gave me no more than three months of relief from the worst of my symptoms.
I thought that when the vertigo stopped after my 3rd gent injection, I was finally home free, at least in my bad ear. The spinning stopped for well-over a year, maybe two. But I continued to have frequent and persistent episodes of brain fog, fluctuating tinnitus with a really annoying and loud buzzing sensation, hyperacusis, and of course my hearing was so bad that I finally relented and invested $1800 into a hearing aid (which was a great success in alleviating my hyperacusis and minimizing the tinnitus - and helping my hearing). Most insidious was the brain-numbing fatigue. I needed 9-10 hours of sleep most nights. I would wake up in the morning exhausted and struggle to make it through dinnertime with my family. Staying awake until 10 pm took Herculean effort, so most nights I was asleep by 8:30 or 9 pm.
A good day still included some noticeable degree of whole-body fatigue and brain exhaustion from struggling to make sense of the sound in my environment.
During this time following that last gent injection, I started allergy shots with the hope that they would help control some or all of the non-vertigo symptoms. But, again, I had a meaningful response around the 3-month mark in that my energy level improved significantly, as did my brain fog. But gradually over the next 9-12 months, the positive effect began to wear off and 18-months into allergy treatment I was right back where I started - minus the sinus inflammation and weird tingling sensations in my sinus cavities that I had before treatment.
Then in June, 2013, the vertigo returned! It was less intense and much shorter in duration, lasting maybe an hour or two instead of the usual eight- to twelve-hour spinfests I had pre-gent, but it was no less life-altering. I was at the point of having a labyrinthectomy. I had gone so far as to be evaluated for the surgery. But I was also experiencing ringing and pressure in my good ear by this time. I fully understood the risk I would be taking by having a laby in my bad ear in that I couldn't count on my good ear to provide hearing and balance indefinitely.
It was my husband who urged me, really convinced me, to give the Stephen Spring treatment a try for at least six months before electing to have surgery. Even though I had been communicating regularly with Stephen for nearly two years and was certainly convinced that he was on to something important, I felt guilty and unworthy to some degree, I guess. I felt guilty that my debility had already been such a burden to my family and then the thought of spending a significant amount of money on me that we could use on so many other things - well, it just didn't seem fair. There were (are) no guarantees and, of course, the risks are unknown. That being said, there were already many, many risks and potential financial burdens associated with doing nothing and even with pursuing surgery. The decision wasn't an easy one since no option was a slamdunk.
But Phil insisted and I had to relent. Except for the money, and I suppose the fear of the unknown potential side effects of the treatment, I had to agree that I had nothing to lose. As for the money, I had become so disabled that I could rarely drive and was truly beginning to believe that I was on the way to becoming declared permanently disabled. I concluded that if the SS treatment worked, then we would come out ahead financially since I'd be able to continue working. If it didn't work, well then we'd recover from the financial hit.
As for any potential side effects, I had been discussing the general contents of the vaccine with Stephen for a long time, doing my own research, and eventually coming to the conclusion that the risk for short- and long-term side effects is likely to be very small. I had long ago realized that with Meniere's disease that there are no guarantees in life, so anything I could do to get more good days, the better. Ultimately, I took my first dose of the vaccine* on September 11, 2013.
I and others have shared the experience of undergoing the Stephen Spring treatment, that it's two steps forward and one step back. But today I can say with certainty that my ratio of good days to bad days has done a 180-degree turn. I now have mostly good days, tons of energy, and I've had reversal of my hearing loss. The latter providing objective data that this treatment has in fact done something for me that no one usually thinks is even possible. I don't know how long my good fortune will last, but I am eternally grateful for every good day I have in this life!
----------------------------------------------------------------------------------------------------------------------------------------
*For those unfamiliar with Stephen Spring or the treatment he has developed, he is an Australian attorney who himself suffered from Meniere's disease for several years in the early 2000's. Having failed conventional treatments and watching as life as he knew it was unraveling due to the effects of the disease, he began doing his own research. He scoured hundreds, if not thousands, of medical and research journal articles, became intimately involved with the Meniere's Disease Research Fund affiliated with the University of Sydney, and eventually began travelling around the world to attend Meniere's disease conferences and to meet with researchers who have dedicated their careers to studying the differing aspects of the potential underlying causes and treatments for Meniere's disease. Stephen eventually came to the conclusion that, in many cases, Meniere's symptoms are caused by an underlying immune dysfunction as a result of infection. There is quite a bit of substantiating evidence published in the literature to support this conclusion, however not all of it will be found in Meniere's disease-specific work. There is also a tremendous amount of money and time being spent by Meniere's experts on the study and use of treatments aimed at symptom management, as opposed to underlying cause and cure. Hopefully, with time this will change as more evidence becomes available and circulated through the appropriate channels.
The vaccine Stephen developed to correct the underlying immune dysfunction is a proprietary powder and is part of the overall process of testing and retesting to correct the immune function and identify infection. This is done in partnership with one's physician and cannot be undertaken without medical supervision. Stephen's product is manufactured in the United States by an independent laboratory and is approved for use in humans due to its manufacturing classification and delivery method.
The hope is that some day in the not too distant future, doctors and researchers within the conventional medical establishment will invest the necessary time and money needed to study and validate Stephen's conclusions and treatment. In order for this to be possible, Stephen has applied certain legal protections to his intellectual property. Due to a legally-binding non-disclosure agreement, I cannot speak in any more detail regarding the contents of the vaccine.
I thought that when the vertigo stopped after my 3rd gent injection, I was finally home free, at least in my bad ear. The spinning stopped for well-over a year, maybe two. But I continued to have frequent and persistent episodes of brain fog, fluctuating tinnitus with a really annoying and loud buzzing sensation, hyperacusis, and of course my hearing was so bad that I finally relented and invested $1800 into a hearing aid (which was a great success in alleviating my hyperacusis and minimizing the tinnitus - and helping my hearing). Most insidious was the brain-numbing fatigue. I needed 9-10 hours of sleep most nights. I would wake up in the morning exhausted and struggle to make it through dinnertime with my family. Staying awake until 10 pm took Herculean effort, so most nights I was asleep by 8:30 or 9 pm.
A good day still included some noticeable degree of whole-body fatigue and brain exhaustion from struggling to make sense of the sound in my environment.
During this time following that last gent injection, I started allergy shots with the hope that they would help control some or all of the non-vertigo symptoms. But, again, I had a meaningful response around the 3-month mark in that my energy level improved significantly, as did my brain fog. But gradually over the next 9-12 months, the positive effect began to wear off and 18-months into allergy treatment I was right back where I started - minus the sinus inflammation and weird tingling sensations in my sinus cavities that I had before treatment.
Then in June, 2013, the vertigo returned! It was less intense and much shorter in duration, lasting maybe an hour or two instead of the usual eight- to twelve-hour spinfests I had pre-gent, but it was no less life-altering. I was at the point of having a labyrinthectomy. I had gone so far as to be evaluated for the surgery. But I was also experiencing ringing and pressure in my good ear by this time. I fully understood the risk I would be taking by having a laby in my bad ear in that I couldn't count on my good ear to provide hearing and balance indefinitely.
It was my husband who urged me, really convinced me, to give the Stephen Spring treatment a try for at least six months before electing to have surgery. Even though I had been communicating regularly with Stephen for nearly two years and was certainly convinced that he was on to something important, I felt guilty and unworthy to some degree, I guess. I felt guilty that my debility had already been such a burden to my family and then the thought of spending a significant amount of money on me that we could use on so many other things - well, it just didn't seem fair. There were (are) no guarantees and, of course, the risks are unknown. That being said, there were already many, many risks and potential financial burdens associated with doing nothing and even with pursuing surgery. The decision wasn't an easy one since no option was a slamdunk.
But Phil insisted and I had to relent. Except for the money, and I suppose the fear of the unknown potential side effects of the treatment, I had to agree that I had nothing to lose. As for the money, I had become so disabled that I could rarely drive and was truly beginning to believe that I was on the way to becoming declared permanently disabled. I concluded that if the SS treatment worked, then we would come out ahead financially since I'd be able to continue working. If it didn't work, well then we'd recover from the financial hit.
As for any potential side effects, I had been discussing the general contents of the vaccine with Stephen for a long time, doing my own research, and eventually coming to the conclusion that the risk for short- and long-term side effects is likely to be very small. I had long ago realized that with Meniere's disease that there are no guarantees in life, so anything I could do to get more good days, the better. Ultimately, I took my first dose of the vaccine* on September 11, 2013.
I and others have shared the experience of undergoing the Stephen Spring treatment, that it's two steps forward and one step back. But today I can say with certainty that my ratio of good days to bad days has done a 180-degree turn. I now have mostly good days, tons of energy, and I've had reversal of my hearing loss. The latter providing objective data that this treatment has in fact done something for me that no one usually thinks is even possible. I don't know how long my good fortune will last, but I am eternally grateful for every good day I have in this life!
----------------------------------------------------------------------------------------------------------------------------------------
*For those unfamiliar with Stephen Spring or the treatment he has developed, he is an Australian attorney who himself suffered from Meniere's disease for several years in the early 2000's. Having failed conventional treatments and watching as life as he knew it was unraveling due to the effects of the disease, he began doing his own research. He scoured hundreds, if not thousands, of medical and research journal articles, became intimately involved with the Meniere's Disease Research Fund affiliated with the University of Sydney, and eventually began travelling around the world to attend Meniere's disease conferences and to meet with researchers who have dedicated their careers to studying the differing aspects of the potential underlying causes and treatments for Meniere's disease. Stephen eventually came to the conclusion that, in many cases, Meniere's symptoms are caused by an underlying immune dysfunction as a result of infection. There is quite a bit of substantiating evidence published in the literature to support this conclusion, however not all of it will be found in Meniere's disease-specific work. There is also a tremendous amount of money and time being spent by Meniere's experts on the study and use of treatments aimed at symptom management, as opposed to underlying cause and cure. Hopefully, with time this will change as more evidence becomes available and circulated through the appropriate channels.
The vaccine Stephen developed to correct the underlying immune dysfunction is a proprietary powder and is part of the overall process of testing and retesting to correct the immune function and identify infection. This is done in partnership with one's physician and cannot be undertaken without medical supervision. Stephen's product is manufactured in the United States by an independent laboratory and is approved for use in humans due to its manufacturing classification and delivery method.
The hope is that some day in the not too distant future, doctors and researchers within the conventional medical establishment will invest the necessary time and money needed to study and validate Stephen's conclusions and treatment. In order for this to be possible, Stephen has applied certain legal protections to his intellectual property. Due to a legally-binding non-disclosure agreement, I cannot speak in any more detail regarding the contents of the vaccine.
Saturday, July 19, 2014
Quick Up-Date on My Status
I've been meaning to post an up-date on my status as it has been just over 10 months since I started the Stephen Spring treatment. As I close in on the one-year mark, I can say without a doubt that it has been an effective treatment for me thus far.
As others warned, Stephen included, improvement does not happen in a straight line. At the 10-month mark, however, I am feeling well 95% of the time. I still have tinnitus, but most of the time it is nothing more than a soft hum. My energy level is through the roof. I now need only 6-7 hours of sleep each night and no naps.
My bad days now consist of moderate brain fog and some mild disequilibrium, perhaps from having had three gent shots a few years back. From start to finish an "attack" might last anywhere from 6 to 48 hours and then I go back to feeling well again. This is a one-eighty from where I started! Rarely, I might have an uptick in tinnitus and buzzing in my ear, but that happens very infrequently now.
From about the 7th month until a few weeks ago, I had an annoying symptom where I was getting frequent, but short, episodes of "mini spins". These tended to be a bit positional, coming on if I tilted my head a certain way or turned too quickly. Sometimes they seemed to happen for no reason at all. Some days I'd have 2 or 3 and other days I might feel them 12 or more times throughout the day. But they occurred in the absence of any changes in hearing, tinnitus, pressure, or cognitive dysfunction (aka brain fog). It didn't take me long to realize they wouldn't turn into full-blown vertigo and that they dissipated within a minute or two at most, so I just rolled with them. With time, they have become less intense and less frequent. As of the past couple of weeks, I'm only getting them a couple of times a week. I've come to see them as a sign of change which seems to be in the direction of "good" versus "evil."
Today, I continue to take just the vaccine each day. I have no side effects from it, no new symptoms, no headaches, no congestion or drainage. I do get an earache in my bad ear from time to time, as if the lymph node in there is inflamed a bit. In fact, the diameter of my ear canal reflects some kind of inflammation during that time as I can feel it if I attempt to clean it with a cotton swab.
I am not posting much because I am too busy living life again. I don't know how long it will last, but I hope forever! But even if someday my symptoms return, today I am utterly grateful for this reprieve.
Below are screenshots of hearing tests I did using an app. The first one I did today and the second one is one I took in August, 2013, one month before starting the vaccine. I no longer wear my hearing aid.
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As others warned, Stephen included, improvement does not happen in a straight line. At the 10-month mark, however, I am feeling well 95% of the time. I still have tinnitus, but most of the time it is nothing more than a soft hum. My energy level is through the roof. I now need only 6-7 hours of sleep each night and no naps.
My bad days now consist of moderate brain fog and some mild disequilibrium, perhaps from having had three gent shots a few years back. From start to finish an "attack" might last anywhere from 6 to 48 hours and then I go back to feeling well again. This is a one-eighty from where I started! Rarely, I might have an uptick in tinnitus and buzzing in my ear, but that happens very infrequently now.
From about the 7th month until a few weeks ago, I had an annoying symptom where I was getting frequent, but short, episodes of "mini spins". These tended to be a bit positional, coming on if I tilted my head a certain way or turned too quickly. Sometimes they seemed to happen for no reason at all. Some days I'd have 2 or 3 and other days I might feel them 12 or more times throughout the day. But they occurred in the absence of any changes in hearing, tinnitus, pressure, or cognitive dysfunction (aka brain fog). It didn't take me long to realize they wouldn't turn into full-blown vertigo and that they dissipated within a minute or two at most, so I just rolled with them. With time, they have become less intense and less frequent. As of the past couple of weeks, I'm only getting them a couple of times a week. I've come to see them as a sign of change which seems to be in the direction of "good" versus "evil."
Today, I continue to take just the vaccine each day. I have no side effects from it, no new symptoms, no headaches, no congestion or drainage. I do get an earache in my bad ear from time to time, as if the lymph node in there is inflamed a bit. In fact, the diameter of my ear canal reflects some kind of inflammation during that time as I can feel it if I attempt to clean it with a cotton swab.
I am not posting much because I am too busy living life again. I don't know how long it will last, but I hope forever! But even if someday my symptoms return, today I am utterly grateful for this reprieve.
Below are screenshots of hearing tests I did using an app. The first one I did today and the second one is one I took in August, 2013, one month before starting the vaccine. I no longer wear my hearing aid.
July 19, 2014
August 17, 2013
Saturday, June 14, 2014
New Hearing App
While there are many types of hearing loss, that caused by Meniere's disease is unique in that it fluctuates for most of us. And hearing is one of the only objective measures many of us have to measure the success or failure of a new treatment or intervention. It's just not feasible to run in to see our audiologist on a moment's notice when we feel there has been a sudden change in our hearing, so many of us rely on hearing test apps to measure changes in our hearing. Those that I've found are fairly limited and often awkward to use and interpret.
But a new company, called Mimi, plans to launch an iPhone app to not only allow users to test their hearing but to, among other things, enhance it much in the way hearing aids can. It sounds like there are some regulatory hoops to jump through to implement the latter, but it's a step in the right direction IMO, given the exorbitant cost of hearing aids.
Read more about this exciting technology here.
But a new company, called Mimi, plans to launch an iPhone app to not only allow users to test their hearing but to, among other things, enhance it much in the way hearing aids can. It sounds like there are some regulatory hoops to jump through to implement the latter, but it's a step in the right direction IMO, given the exorbitant cost of hearing aids.
Read more about this exciting technology here.
Wednesday, June 4, 2014
Wednesday, May 28, 2014
We Are Not Alone
We started re-watching The X-Files series the other night on Netflix. The show harkens back to those peaceful pre-parenthood years of watching whatever we liked, whenever we liked. Now that the kids are in middle school, we've been pushing the envelope a bit by introducing them to our own TV and movie nostalgia. Airplane!? A little sketchy. Ferris Bueller's Day Off? The kids told us that was not appropriate. The X-Files? We have one believer and two hiding under the covers. Phil and I are enjoying the trip down memory lane nevertheless. But I digress.
What I meant by We Are Not Alone, is that misery loves company and I came across a fellow-sufferer of Meniere's-like fun who writes rather eloquently about what it's like to have a condition that no one can seem to diagnose, much less treat effectively. From time to time I post "borrowed" articles here on the blog. This one I found while lurking over at www.menieres.org (which I still refuse to re-join). Anyway, seemed share-worthy here. Note the mention of Regenokine and Dana White for those who've been following that as a treatment option for Meniere's. I do agree with the author regarding taking on the attitude of equanimity and practicing as much meditation as one can muster. Enjoy!
P.S. Sam Harris, the author, is quite nice to look at, if you don't mind me saying.
What I meant by We Are Not Alone, is that misery loves company and I came across a fellow-sufferer of Meniere's-like fun who writes rather eloquently about what it's like to have a condition that no one can seem to diagnose, much less treat effectively. From time to time I post "borrowed" articles here on the blog. This one I found while lurking over at www.menieres.org (which I still refuse to re-join). Anyway, seemed share-worthy here. Note the mention of Regenokine and Dana White for those who've been following that as a treatment option for Meniere's. I do agree with the author regarding taking on the attitude of equanimity and practicing as much meditation as one can muster. Enjoy!
P.S. Sam Harris, the author, is quite nice to look at, if you don't mind me saying.
Monday, May 26, 2014
Book Review and Recovery
I have been taking it easy since my surgery three days ago which has allowed me to catch up on some reading. As a dietitian, I am often asked about the "best" diet, especially with regard to weight loss, so I was eager to read The Diet Fix, by Yoni Freedhoff, MD.
I've been following the pragmatic rantings of Dr. Freedhoff on his blog, Weighty Matters, for over a year now. As a physician who specializes in bariatric medicine, he offers unique insight into the causes and treatment of obesity in North America. He is not opposed to bariatric surgery in some cases, but his practice focuses on behavior change and education as the primary intervention for weight management. Most importantly, he recognizes the dysfunctional food environment we all live in and has developed a program to help his patients manage their weight and live happily everafter in doing so.
Dr. Freedhoff acknowledges that there is no one perfect diet. In fact, he concedes that there is more than one way to lose weight and keep it off. The key, he argues, is setting realistic weight and health goals within a framework of compromises that an individual can live with without feeling hungry or deprived of their favorite foods. He also readily admits that you cannot "outrun your fork". Exercise is emphasized, but in whatever form you can stick with and incorporate into your daily routine, what he calls your "toothbrush level." In other words, equating the importance of daily exercise with that of brushing your teeth.
The book is designed to be a 10-day plan to reset your habits into ones which you will hopefully carry with you to help you overcome what he calls post-traumatic dieting disorder. While I'm not a fan of people making up new diagnoses willy-nilly, I think he hits this one right on the head! I've seen so many people over the years who have such a dysfunctional and confused approach to eating that they no longer know what is normal and what is disordered. Dr. Freedhoff outlines the steps necessary to undo years of dysfunctional dieting and recommends implementing each one day at a time. They are as follows:
Day One: Gear Up
To learn to about appropriate serving sizes and calorie-content of your favorite foods, Freedhoff recommends you have some basic tools on-hand, such as a food scale, measuring cups and spoons, and some on-line reference tools. He also asks that you have some shoes and comfortable clothes to wear to perform your choice of exercise.
Day Two: Diarize
Several studies have shown that this one habit alone can be responsible for promoting as much as three times more weight loss compared to dieters who do not keep a food diary. With today's on-line tools and apps, we have a fantastic tool to better assess where extra calories are sneaking into our diet, giving us valuable information in which to make choices.
Day Three: Banish Hunger
I love this chapter! Here, Dr. Freedhoff tells readers to eat and eat often. Many-a-binge has been the result of under-eating until we can't take it anymore. The psychology and physiology of dieting are explored in this chapter and strategies to undo years of disordered eating habits are addressed.
Day Four: Cook
This chapter offers basic organizational skills, teaching the reader how to plan and prepare simple meals. He points out that to control our calorie intake, we really have to have control over the food we are eating. Every time we eat out, we relinquish that control to a degree because in most cases we cannot be sure that the food we are served does not contain hidden calories we wouldn't even imagine are there.
Day Five: Think
Today, Dr. Freedhoff asks the reader to challenge their beliefs and identity as they relate to food and weight. He offers a new perspective to many, one that revolves around setting realistic expectations. He states, "If we're talking about weight and food, it means eating the smallest number of calories you need to honestly enjoy your day." Regarding exercise, "it also means exercising only as much as you can honestly enjoy." "Weight-wise, it means that rather than talking about your ideal weight, or some body mass index, or your body fat percentage, instead you're talking about your 'best' weight, where your best weight is whatever weight you reach when you're living the healthiest life that you can honestly and realistically enjoy." Love this!
Day Six: Exercise
Here Dr. Freedhoff again focuses on reality and evidence. The evidence is that exercise plays a relatively small role in losing weight, but is definitely correlated with keeping weight off. An important point to consider when losing weight is that, as one loses pounds, the body requires fewer calories. Eventually, if someone loses enough weight, they'd be forced to eat virtually nothing to keep losing. Exercise helps to offset this phenomenon by building metabolically active lean body mass and burning a few extra calories, as well. Exercise also offers a host of non-weight related benefits, such as stress management, cardiac health, and reducing the risk for developing certain types of cancer - all independent of body weight.
Day Seven: Indulge
Here is where Dr. Freedhoff's pragmatism takes off. He has learned over the years that food indulgences are a normal part of life and to ban them sets people up for feelings of failure and loss of control. Like the author, I am not a fan of saying any food should never cross your lips. It's what you do most of the time that counts and incorporating indulgences in the normal course of life is, well, normal.
Day Eight: Eat Out
See Day Seven. Ok, there are strategies offered in this chapter to help the reader avoid overeating and how to make choices that are healthier without leaving you feeling deprived.
Day Nine: Set Goals
I've never been a big setter of goals. Maybe that's a problem that I should work on. I did find this chapter thoughtful and filled with some good tips on learning to set realistic goals.
Day Ten: Troubleshoot and Move Forward
Again, more thinking and reworking what is realistic for you and the lifestyle you want and can live with.
The final chapters of the book, Reset Any Diet, Live, Eat, Move, Think, Weigh, Heal, and Parent, delve deeper into the 10-day strategies and offer case studies based on patients Dr. Freedhoff has worked with over the years.
Ultimately, I really, really liked this book. Not only will I be applying these strategies with some of my cancer patients, many who have a history of dysfunctional dieting now fueled on by fear of recurrence of their disease, but I will be experimenting on myself, as well.
Most of us with Meniere's have found that the disease has had an impact on how, or even if, we exercise, what we eat, and how we feel about certain foods. While for most of us, dietary triggers are hit and miss, it certainly can't hurt to eat better and not use food as a comfort or to fear food unnecessarily. I think this book offers some very easy, clear guidelines for just about anyone wanting to get away from strict diets and learn to enjoy food again in a way that promotes good health - whatever that might mean to you.
I've been following the pragmatic rantings of Dr. Freedhoff on his blog, Weighty Matters, for over a year now. As a physician who specializes in bariatric medicine, he offers unique insight into the causes and treatment of obesity in North America. He is not opposed to bariatric surgery in some cases, but his practice focuses on behavior change and education as the primary intervention for weight management. Most importantly, he recognizes the dysfunctional food environment we all live in and has developed a program to help his patients manage their weight and live happily everafter in doing so.
Dr. Freedhoff acknowledges that there is no one perfect diet. In fact, he concedes that there is more than one way to lose weight and keep it off. The key, he argues, is setting realistic weight and health goals within a framework of compromises that an individual can live with without feeling hungry or deprived of their favorite foods. He also readily admits that you cannot "outrun your fork". Exercise is emphasized, but in whatever form you can stick with and incorporate into your daily routine, what he calls your "toothbrush level." In other words, equating the importance of daily exercise with that of brushing your teeth.
The book is designed to be a 10-day plan to reset your habits into ones which you will hopefully carry with you to help you overcome what he calls post-traumatic dieting disorder. While I'm not a fan of people making up new diagnoses willy-nilly, I think he hits this one right on the head! I've seen so many people over the years who have such a dysfunctional and confused approach to eating that they no longer know what is normal and what is disordered. Dr. Freedhoff outlines the steps necessary to undo years of dysfunctional dieting and recommends implementing each one day at a time. They are as follows:
Day One: Gear Up
To learn to about appropriate serving sizes and calorie-content of your favorite foods, Freedhoff recommends you have some basic tools on-hand, such as a food scale, measuring cups and spoons, and some on-line reference tools. He also asks that you have some shoes and comfortable clothes to wear to perform your choice of exercise.
Day Two: Diarize
Several studies have shown that this one habit alone can be responsible for promoting as much as three times more weight loss compared to dieters who do not keep a food diary. With today's on-line tools and apps, we have a fantastic tool to better assess where extra calories are sneaking into our diet, giving us valuable information in which to make choices.
Day Three: Banish Hunger
I love this chapter! Here, Dr. Freedhoff tells readers to eat and eat often. Many-a-binge has been the result of under-eating until we can't take it anymore. The psychology and physiology of dieting are explored in this chapter and strategies to undo years of disordered eating habits are addressed.
Day Four: Cook
This chapter offers basic organizational skills, teaching the reader how to plan and prepare simple meals. He points out that to control our calorie intake, we really have to have control over the food we are eating. Every time we eat out, we relinquish that control to a degree because in most cases we cannot be sure that the food we are served does not contain hidden calories we wouldn't even imagine are there.
Day Five: Think
Today, Dr. Freedhoff asks the reader to challenge their beliefs and identity as they relate to food and weight. He offers a new perspective to many, one that revolves around setting realistic expectations. He states, "If we're talking about weight and food, it means eating the smallest number of calories you need to honestly enjoy your day." Regarding exercise, "it also means exercising only as much as you can honestly enjoy." "Weight-wise, it means that rather than talking about your ideal weight, or some body mass index, or your body fat percentage, instead you're talking about your 'best' weight, where your best weight is whatever weight you reach when you're living the healthiest life that you can honestly and realistically enjoy." Love this!
Day Six: Exercise
Here Dr. Freedhoff again focuses on reality and evidence. The evidence is that exercise plays a relatively small role in losing weight, but is definitely correlated with keeping weight off. An important point to consider when losing weight is that, as one loses pounds, the body requires fewer calories. Eventually, if someone loses enough weight, they'd be forced to eat virtually nothing to keep losing. Exercise helps to offset this phenomenon by building metabolically active lean body mass and burning a few extra calories, as well. Exercise also offers a host of non-weight related benefits, such as stress management, cardiac health, and reducing the risk for developing certain types of cancer - all independent of body weight.
Day Seven: Indulge
Here is where Dr. Freedhoff's pragmatism takes off. He has learned over the years that food indulgences are a normal part of life and to ban them sets people up for feelings of failure and loss of control. Like the author, I am not a fan of saying any food should never cross your lips. It's what you do most of the time that counts and incorporating indulgences in the normal course of life is, well, normal.
Day Eight: Eat Out
See Day Seven. Ok, there are strategies offered in this chapter to help the reader avoid overeating and how to make choices that are healthier without leaving you feeling deprived.
Day Nine: Set Goals
I've never been a big setter of goals. Maybe that's a problem that I should work on. I did find this chapter thoughtful and filled with some good tips on learning to set realistic goals.
Day Ten: Troubleshoot and Move Forward
Again, more thinking and reworking what is realistic for you and the lifestyle you want and can live with.
The final chapters of the book, Reset Any Diet, Live, Eat, Move, Think, Weigh, Heal, and Parent, delve deeper into the 10-day strategies and offer case studies based on patients Dr. Freedhoff has worked with over the years.
Ultimately, I really, really liked this book. Not only will I be applying these strategies with some of my cancer patients, many who have a history of dysfunctional dieting now fueled on by fear of recurrence of their disease, but I will be experimenting on myself, as well.
Most of us with Meniere's have found that the disease has had an impact on how, or even if, we exercise, what we eat, and how we feel about certain foods. While for most of us, dietary triggers are hit and miss, it certainly can't hurt to eat better and not use food as a comfort or to fear food unnecessarily. I think this book offers some very easy, clear guidelines for just about anyone wanting to get away from strict diets and learn to enjoy food again in a way that promotes good health - whatever that might mean to you.
Saturday, May 24, 2014
Surgery! NOT on My Ear
Back in December, I went to the ER with symptoms resembling appendicitis. While that was ruled out, several weeks and more tests later, an ovarian cyst was discovered. Since it was causing me quite a bit of pain and discomfort, it had to come out. So yesterday was the day. I am happy to report that everything went smoothly and I am home, recovering.
The anesthesiologist was very kind. He astutely noticed my history of Meniere's disease and introduced himself with a Scopolamine patch in-hand - just in case, he said, as he slapped it behind my ear. While he meant well, when I got home I remembered how that drug made me feel: extremely dry mouth and double vision. Since I have big plans to read a lot while recovering, the patch had to go. Plus I didn't have any indications that my ear was acting up or that I would be dizzy.
Physically, I feel better today than I did yesterday - but this evening my ear is buzzing more than usual. I hate that feeling! I'm sure it must be from all the drugs I was given yesterday, not to mention the physical stress and inflammatory response of surgery. So I'll just hope for the best that I wake up tomorrow back to my new-normal, soft hum.
Ironically, Phil and I both observed today that we were experiencing some PTSD flashbacks of me being confined to bed and him anxiously checking on me every 30 minutes or so to see if I needed anything. I definitely hate lying in bed all day and I know it worries him when I have to be here. At least this time around, I can get up and walk around any time I feel like it. Even though I feel like someone literally kicked me in the gut, it's a million times better than even one of my mildest vertigo attacks.
I am just so glad this week is over. In addition to the surgery, I also had two crowns replaced last week. I am ready to put all of this behind me and continue enjoying life without vertigo, abdominal pain, and old crowns on my teeth.
The anesthesiologist was very kind. He astutely noticed my history of Meniere's disease and introduced himself with a Scopolamine patch in-hand - just in case, he said, as he slapped it behind my ear. While he meant well, when I got home I remembered how that drug made me feel: extremely dry mouth and double vision. Since I have big plans to read a lot while recovering, the patch had to go. Plus I didn't have any indications that my ear was acting up or that I would be dizzy.
Physically, I feel better today than I did yesterday - but this evening my ear is buzzing more than usual. I hate that feeling! I'm sure it must be from all the drugs I was given yesterday, not to mention the physical stress and inflammatory response of surgery. So I'll just hope for the best that I wake up tomorrow back to my new-normal, soft hum.
Ironically, Phil and I both observed today that we were experiencing some PTSD flashbacks of me being confined to bed and him anxiously checking on me every 30 minutes or so to see if I needed anything. I definitely hate lying in bed all day and I know it worries him when I have to be here. At least this time around, I can get up and walk around any time I feel like it. Even though I feel like someone literally kicked me in the gut, it's a million times better than even one of my mildest vertigo attacks.
I am just so glad this week is over. In addition to the surgery, I also had two crowns replaced last week. I am ready to put all of this behind me and continue enjoying life without vertigo, abdominal pain, and old crowns on my teeth.
Wednesday, May 21, 2014
The Tides are Changing
If the idea that Meniere's disease could be caused through a pathogenic process which goes on to produce immune dysfunction is new to you, you might find this article about the practice of rheumatology very interesting. Wouldn't it be great if the mystery surrounding these diseases of unknown origin could finally be solved and each of us went on to be treated by the appropriate medical specialist?
Is this the end of rheumatology as we know it?
JONATHAN S. HAUSMANN, MD | CONDITIONS | MAY 21, 2014
Recently, an international research team led by Xavier Rodó published a fascinating study in PNAS suggesting that Kawasaki disease is caused by an agent transported by wind from farms in Northeast China. This agent, possibly a fungal toxin, is responsible for triggering an exuberant immune response in children, causing the typical manifestation of the disease: fevers, rash, conjunctivitis, “strawberry tongue,” enlarged lymph nodes, and swelling of the extremities. Untreated, Kawasaki disease can cause aneurysms of the coronary arteries, premature heart disease, and even death.
What I find so fascinating about this article is that it sheds light on the possible etiology of a rheumatic illness. As rheumatologists, one of the biggest challenges we face is not knowing the causes of most of the diseases we treat (that’s our dirty little secret!). Even though we use state-of-the-art medicines, our understanding of disease is still in the Dark Ages.
Fortunately, we’ve had some progress. Rheumatic fever, for example, was found to be caused by Streptococcus, the same bug that causes Strep throat. We learned that treating Strep throat with antibiotics prevents rheumatic fever, likely the reason why rheumatic fever is now extremely rare in the United States.
In the 1970′s, an epidemic of arthritis struck Connecticut, affecting many children. Detailed research showed that it was due to a bacteria, Borrelia burgdorferi, carried by a tick. To prevent disease, we advise people to use repellents and avoid tick-infested areas. If they develop Lyme, we offer effective treatments with antibiotics.
We have also made progress in understanding of some types of vasculitis (diseases that cause inflammation of blood vessels). Polyarteritis nodosa is often caused by hepatitis B virus, and cryoglobulinemic vasculitis is due to hepatitis C virus. Cures for these types of vasculitides can be achieved by eradicating the virus.
Is it a coincidence that several diseases that we considered to be “rheumatic” are now known to be caused by bacterial, viral (and perhaps) fungal elements? Not really, especially if we understand evolutionary medicine. This often-overlooked field of study helps explain why humans, despite millions of years of evolution, are still vulnerable to disease. Two common reasons include pathogens (which are able to evolve faster than we can), and the mismatch between our bodies and our new environment (likely responsible for the obesity epidemic).
Unfortunately, most rheumatology research is conducted without an awareness of evolution. It seeks to find abnormalities of the immune system that cause disease, without first asking why any abnormality would exist in the first place. It tries to identify genes that make people susceptible for a disease, without asking how deleterious genes could be passed down through generations.
Fortunately, the winds of change may be near. Interest in P. gingivalis as a cause for rheumatoid arthritis continues to grow, and the role of the microbiome in the development of rheumatic diseases shows promise. With a better understanding of why we get sick, we may uncover other environmental triggers responsible for the rest of the rheumatic diseases that we treat.
Gary Hoffman, a rheumatologist who studies vasculitis at the Cleveland Clinic, has said that understanding the cause of a disease is the “most crucial element.” He writes: “How empowering that knowledge is, especially when the etiological agent persists and perpetuates the process. In that setting, given adequate therapeutic interventions, we can even affect cures.”
Scientific progress is said to occur through “paradigm shifts,” or radical changes in our way of thinking, which abruptly transforms the field. Will a fungal toxin mark this change for rheumatology?
Jonathan S. Hausmann is a rheumatology fellow who blogs at Autoinflammatory diseases.
Is this the end of rheumatology as we know it?
JONATHAN S. HAUSMANN, MD | CONDITIONS | MAY 21, 2014
Recently, an international research team led by Xavier Rodó published a fascinating study in PNAS suggesting that Kawasaki disease is caused by an agent transported by wind from farms in Northeast China. This agent, possibly a fungal toxin, is responsible for triggering an exuberant immune response in children, causing the typical manifestation of the disease: fevers, rash, conjunctivitis, “strawberry tongue,” enlarged lymph nodes, and swelling of the extremities. Untreated, Kawasaki disease can cause aneurysms of the coronary arteries, premature heart disease, and even death.
What I find so fascinating about this article is that it sheds light on the possible etiology of a rheumatic illness. As rheumatologists, one of the biggest challenges we face is not knowing the causes of most of the diseases we treat (that’s our dirty little secret!). Even though we use state-of-the-art medicines, our understanding of disease is still in the Dark Ages.
Fortunately, we’ve had some progress. Rheumatic fever, for example, was found to be caused by Streptococcus, the same bug that causes Strep throat. We learned that treating Strep throat with antibiotics prevents rheumatic fever, likely the reason why rheumatic fever is now extremely rare in the United States.
In the 1970′s, an epidemic of arthritis struck Connecticut, affecting many children. Detailed research showed that it was due to a bacteria, Borrelia burgdorferi, carried by a tick. To prevent disease, we advise people to use repellents and avoid tick-infested areas. If they develop Lyme, we offer effective treatments with antibiotics.
We have also made progress in understanding of some types of vasculitis (diseases that cause inflammation of blood vessels). Polyarteritis nodosa is often caused by hepatitis B virus, and cryoglobulinemic vasculitis is due to hepatitis C virus. Cures for these types of vasculitides can be achieved by eradicating the virus.
Is it a coincidence that several diseases that we considered to be “rheumatic” are now known to be caused by bacterial, viral (and perhaps) fungal elements? Not really, especially if we understand evolutionary medicine. This often-overlooked field of study helps explain why humans, despite millions of years of evolution, are still vulnerable to disease. Two common reasons include pathogens (which are able to evolve faster than we can), and the mismatch between our bodies and our new environment (likely responsible for the obesity epidemic).
Unfortunately, most rheumatology research is conducted without an awareness of evolution. It seeks to find abnormalities of the immune system that cause disease, without first asking why any abnormality would exist in the first place. It tries to identify genes that make people susceptible for a disease, without asking how deleterious genes could be passed down through generations.
Fortunately, the winds of change may be near. Interest in P. gingivalis as a cause for rheumatoid arthritis continues to grow, and the role of the microbiome in the development of rheumatic diseases shows promise. With a better understanding of why we get sick, we may uncover other environmental triggers responsible for the rest of the rheumatic diseases that we treat.
Gary Hoffman, a rheumatologist who studies vasculitis at the Cleveland Clinic, has said that understanding the cause of a disease is the “most crucial element.” He writes: “How empowering that knowledge is, especially when the etiological agent persists and perpetuates the process. In that setting, given adequate therapeutic interventions, we can even affect cures.”
Scientific progress is said to occur through “paradigm shifts,” or radical changes in our way of thinking, which abruptly transforms the field. Will a fungal toxin mark this change for rheumatology?
Jonathan S. Hausmann is a rheumatology fellow who blogs at Autoinflammatory diseases.
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