關於國小數學

大叔碎碎念 關於國小數學

最近不知道為什麼常常想到一個老話題，事情是這樣的，一個媽媽在某社團分享了一張圖片是關於他小學的孩子在學校考卷上答了一個問題，明明答的方式正確，但被老師打叉。這個問題印象中是這樣：

"小明跟發哥的雜貨店買了5顆光碟機IC，一顆IC價錢是2塊錢，請問小明花了多少錢？"

結果小孩的答案是 5 X 2 = 10 元  (然後上面被畫了一個大紅叉)
然後老師的答案是 2 X 5 = 10 元

OK，我想你應該猜的到底下的留言應該是幹聲連連，說什麼老師莫名其妙什麼的，然後就有老師出來解釋說：這是在建立孩子解讀題目以及乘數/被乘數的觀念，要告訴孩子 "單位量×單位數＝總量"
所以
2 X 5 =10元 代表你用2塊之單價買了5顆IC

但我想，難道我們的數學教育不能引導孩子解釋成 "買了5顆2塊錢的IC"嗎？我的意思是說，為什麼一定要遵守"單位量×單位數＝總量"這個沒有科學概念的說明式，如果硬要照這樣教，那麼比較妥善的說明式是
5[顆] X 2 [元/每顆] = 10 元
2 [元/每顆] X 5[顆] = 10 元
兩者都對

也就是要求直接把單位寫上來，這樣一來純量交換率不會被破壞，也同時讓孩子知道單位的重要性，更重要的是當孩子學到除法與分式的時候他會知道[顆]是可以跟著算式一起被相消的，學校該教的是這樣的真理，不會因為時間的過去才發現今是昨非，更不需要在那邊咬文嚼字然後沒事找事做

純量的乘法有交換性，我相信每個數學老師都有大學數學系或是相關學歷，難道這些老師在說服自己接受"單位量×單位數＝總量"這個說明式的時候，心裡沒有痛苦的矛盾感嗎？難道這種教育方式不是間接的告訴孩子：即使是真理 也可以今是昨非，而且現在又不是在教孩子向量或是張量，有必要讓孩子的數學表達跟生活經驗充滿了矛盾嗎？當你用這種尺度去作為數學教育的度量衡，那麼你期待教出來的孩子要怎麼用正確的數學態度去解釋所有的生活行為？

OK這只是一個問題，其他不少留言才更讓我傻眼了，有家長說:"數學這麼計較幹嘛啦，我以前數學很爛，現在還不是月入X萬，而且離開學校以後根本就用不到數學，數學又不能拿來賺錢，現在手機這麼發達拿出來按一下就知道答案了啦，學什麼數學"。這種"數學無用論"留言讓我覺得很心裡很憂鬱

我憂鬱的並不是 "對啊數學真的沒有用 我還花這麼多時間學 ，根本浪費時間"，而是憂鬱: 在台灣，基礎學問的重要性被忽視與踐踏的程度，事實上這些忽視與踐踏的人都是曾經在學校學過這些學科然後靠著這些分數畢業拿到文憑的人，為什麼這些人會這麼輕視數學？

首先 台灣的教育並沒有好好的區分 "算術 與 數學"，讓很多人在畢業若干年後只記得"算術"，而根本忘記數學，很多人會說"學算術就夠用了啊，學什麼一元二次方程式, 二元一次方程式啊？會這些真的用不到又不能賺錢啊"

其實生活在現代，數學真真實實的存在你生活裡的每一處
你每天乘坐的各種交通工具如果沒有數學，你每天出門根本都是在自殺；你每天用的GPS如果沒有數學，不會看地圖的你根本永遠到不了目的地；隨便把一根USB裝置插上電腦這過程有數學；你家會有電也是數學；引擎內燃機有數學；潮潮最愛的唉鳳溝溝肉裏面是滿到多出來的數學。

不要再告訴你的孩子學數學不能賺錢了，會這樣想的人你一定永遠都想不到用數學賺錢的人到底從你身上賺了多少錢

#小弟數學沒有很好不要噹我啦

Stephen Spring Protocol 進度報告 (持續更新中)

Stephen Spring Protocol 進度報告 2017/07/02 - update to 2017/07/26

之前我的梅尼爾氏症(MD)病況已經在下列這篇文章的前言中有敘述到
https://allenmeniere.blogspot.tw/2017/01/43441810-reviewent-currently-there-is.html
簡單來說我的MD發作程度已經讓我沒辦法工作賺錢，現在已經留停在家休養，家裡經濟也呈現斷炊的狀態，為了拯救全家的命運，後來努力在網路上找尋國外資訊，輾轉得知關於Stephen Spring這個人的資訊(也看到了一些關於他的爭議)，他有一個網站，有興趣可以點進去看看。總之，在死馬當活馬醫的狀況下，後來我決定跟他合作看看。

因為必須要跟Stephen Spring簽一張NDA才能正式進行SSP treatment，所以我不能在部落格上寫出SSP進行的細節，這篇文主要只是紀錄我在開始與進行SSP過程中的一些大事紀時間點與病情變化。

2017/01/01, 決定開始用email跟Stephen諮詢他對MD研究的看法,主要是我提問關於與他合作的模式, 付費方式, 需要做什麼樣的檢查才能確認我是他的target, 以及SSP treatment的副作用, 這個過程差不多花了兩個禮拜，在這之前眩暈的發作頻率大約是一周2~3次

2017/01/13, 我根據在網路上蒐集到的資訊判斷思考後，決定告知SS我要嘗試SSP並且開始進行一連串的檢查(想當然爾健保不給付, 前前後後跑醫院和醫檢所大約花了一萬五)

2017/02/14, SS認為我的狀況屬於他的防守範圍，答應會寄MeniVac給我，這期間我已經開始使用抗HSV病毒藥物Valtrex進一個半月了(依照國外研究建議的劑量)，但沒什麼進展，眩暈發作頻率仍然是一週兩到三次

2017/04/10, 收到第1批MeniVac, 這段期間仍然持續吃Valtrex，但眩暈一樣一週兩到三次

2017/04/12, 開始第1次服用MeniVac

2017/05/08, 服用大約1個月(用量約2罐)，眩暈一樣一週兩到三次，有時候似乎變嚴重了，嚴重到每天1次，因為手上只剩下1罐，所以下訂單請SS再寄一批給我

2017/05/24, 第1批買的3罐已經用完了，但遲遲不見新的一批寄來, 此時眩暈大約減緩到一周一次 (似乎是有好轉的預兆？)，發作的強度似乎有降低，天旋地轉的程度似乎沒有之前嚴重了, 此時因為反正MeniVac沒得吃，所以我把之前買了沒用的左旋離胺酸+B12來搭配Valtrex一起用

2017/05/30, 端午節連假回高雄，回程在高鐵上發作，一路吐回家，此時眩暈大約一周一次

2017/06/10, 眩暈發作，與上次眩暈發作大約10天了，似乎眩暈發作間隔又拉長了，且眩暈強度又再降低，服用Diazepam與Meclizine後不至於到吐的程度，但這次發作完，左耳的低頻一直處於聽不到的狀態，低頻耳鳴也持續嗡嗡作響

2017/06/13, 終於第2批MeniVac寄來了，左旋離胺酸+B12仍然沒有中斷，持續搭著服用

2017/07/02, 一直到做紀錄的今天，這接近三周的時間都沒有眩暈發作，且低頻聽力與低頻耳鳴用一種非常緩慢的速度在緩解，漸漸的低頻耳鳴不見了，低頻聽力也慢慢聽的到了，剩下高頻的eeeee耳鳴，但還在可以接受的範圍，這應該是從去年發病以來，維持不發作的時間最長的一次，希望可以保持下去

=====================2017/07/26 update

2017/07/07 話真的不能說太早，07/02開始發燒，07/07我就也被傳染到也開始發燒，燒了四天以後看醫生說是流感，直接投克流感，這四天過程中又開始覺得耳悶 低頻聽不到了，

2017/07/15 眩暈又發作，之後又開始維持三四天一次的頻率到 07/26 ，不過暈的程度沒有之前嚴重，有時候三四個小時就過了，也不至於天旋地轉

2017/07/19 開始去大林慈濟看李醫師，當天就打了有名的慢點滴 (類固醇 + Diazepam + 心率調節藥物當作自律神經調節用) 口服藥物則是領了flunarizine  + 舒安得(輕微的BZD藥物) ，感覺這個口服藥的組合跟楊怡和醫師開的 flunarizine  + fludiazepam(中度的BZD藥物) 作用差不多，希望可以跟李醫師溝通不要打類固醇，因為類固醇有免疫抑制的作用，擔心會跟SSP起衝突。

Immulox與梅尼爾氏症的關聯

Immulox與梅尼爾氏症的關聯

從網路上可以找到梅尼爾的免疫治療 與 Immulox之間的有趣關聯

相關連結

http://baike.baidu.com/item/%E5%AF%8C%E8%84%AF%E6%B0%A8%E9%85%B8%E5%A4%9A%E8%82%BD

http://www.bio2u.us.com/%E7%B4%A0%E6%9D%90%E4%BB%8B%E7%B4%B9/item/aps-biogroup-immulox-%E7%9B%8A%E6%95%8F%E8%82%BD.html

http://www.choicesunlimited.ca/when-t1-t2-are-out-of-balance/

https://www.kingnet.com.tw/knNew/news/single-article.html?newId=7990

還是有點懶，細節之後有空再補上好了 @@

*首先兩者都是從牛乳製品中製造而來 (Immulox是從初乳的過慮製程而來)

*再者Immulox中的PRPs (富脯氨酸多肽)也同樣具備有特定的Th1/Th2平衡效果,

" In particular PRP are thought to modulate thymus function, specifically the T helper 1 / T helper 2 (Th1 / Th2) balance. "

from

http://calostart.com/app/docs/ALZHEIMER/CALOSTART-ALZHEIMER/CaloStart%20-%20THE%20EFFECT%20OF%20A%20COLOSTRUM%20EXTRACT%20OF%20PROLINE%20RICH%20POLYPEPTIDES.pdf

這跟某個梅尼爾氏症的免疫治療其假設為需要改變 T1/T2 balance的精神很類似

過敏與梅尼爾的關係?

Is Allergy Related to Meniere’s Disease?

原文：  https://www.researchgate.net/publication/223136937_Is_Allergy_Related_to_Meniere's_Disease

過敏與梅尼爾氏病的關係之前有跟大家分享國外許多研究對梅尼爾氏病的不同面向，有自體免疫, 過敏, 病毒, 壓力, 等等, 這篇論文則是review過敏這個因素，其中提到幾個重點跟大家分享

*在一個大型的研究中，從734個MD病人當中survey，發現過敏在MD病人中的盛行率約為41%

*有過敏性鼻炎的人，可能會有氣喘,鼻瘜肉,中耳炎,或慢性鼻竇炎。而有氣喘與過敏性鼻炎的人則會有較高的食物過敏盛行率。在2000年的一份研究中指出在MD病人中，小麥是最常見的食物過敏原68%。麥膠蛋白被認為是造成小麥過敏的人們對"IgE誘導產生的過敏"(第1型過敏)最主要的原因

*Derebery等人認為有三種過敏機制可能造成梅尼爾症狀，第1種是IgE誘導的過敏反應在內淋巴囊造成局部發炎, 第2種是免疫複合物在內耳淋巴囊附近的微血管堆積造成局部發炎，有研究顯示MD病人的循環免疫複合物的檢驗結果比控制組高了21~96%, 第3種是病毒侵入造成內淋巴囊的輕微發炎反應

*Derebery等人建議病人使用過敏免疫治療(allergen immunotherapy)並且/或是移除過敏源，在113個接受治療的病人中，所有人都回報症狀有所改善

摘錄一些重點如下


• In a large study, Derebery and Berliner investigated the prevalence of allergy in MD. In a survey of 734 patients with MD, concurrent allergic disease was found in 41 %.

在一個大型的研究中，從734個MD病人當中survey，發現過敏在MD病人中的盛行率約為41%

•  Likewise, in allergy-susceptible patients, an allergic response can evoke responses in distal sites.

在疑似過敏的患者身上，過敏反應可能會觸發末梢的反應

• This likely occurs via an integration of neurological, immunologic, and allergic responses involved in inflammation.

這可能會經由神經性,免疫性, 與有發炎之過敏反應的結合而發生

• People with ARmay have asthma, nasal polyposis, otitis media, or chronicrhinosinusitis [36]. People with asthma and AR have a higherprevalence of food allergies, the estimated prevalence ofwhich in America is 3.5 % to 6 % 

有過敏性鼻炎的人，可能會有氣喘,鼻瘜肉,中耳炎,或慢性鼻竇炎。而有氣喘與過敏性鼻炎的人則會有較高的食物過敏盛行率

• Derebery and Berliner [18] in 2000 reported wheat as the most common food allergen found in patients with MD(68.2 %).

2000年的一份研究中指出在MD病人中，小麥是最常見的過敏原68%

• Gliadin is considered the major cause of IgE-mediated hypersensitivity in people with wheat allergy.

麥膠蛋白被認為是造成小麥過敏的人們對"IgE誘導產生的過敏"(第1型過敏)最主要的原因

• Allergic reactions are considered to be one of the many causes of migraines. Numerous studies have reported an association between migraines and allergies. They found that the incidences of both allergy and migraine were significantly higher in the Meniere’s group and that the incidence of allergy in the MD migraine group was significantly higher than that in the group with MD alone.
• 
  
• Derebery and Berliner [21] outlined three proposed mechanisms by which allergy can produce MD symptoms.
• 
  
• The first mechanism, the endolymphatic sac, could be atarget organ of the allergic reaction. The antigen enters the endolymphatic sac andcauses an IgE-mediated degranulation of mast cells. Thisproduces a local inflammatory response that impairs theendolymphatic sac’s filtering function, and a buildup oftoxic metabolic products results, interfering with hair cell function. Histamine and other vasoactive mediators releasedin an allergic response elsewhere may also exert an effecton the well-vascularized fenestrated blood vessels of the endolymphatic sac, thereby affecting reabsorption. 
• 
  
• The second mechanism proposed is deposition of circu-lating immune complexes (CICs). These CICs are depositedand accumulate in the fenestrated blood vessels of the en-dolymphatic sac and stria vascularis. This results in inflam-mation and an increased permeability of the leaky capillariesthat surround the endolymphatic sac. The inflammationinterferes with the capability of the endolymphatic sac’shomeostasis function. Several studies demonstrated an in-crease in circulating immune complexes: 21 % to 96 % ofpatients with MD compared with controls 
• 
  
• The third mechanism is the viral antigen–allergic inter-action. This mechanism suggests that a viral insult canantigenically stimulate Waldeyer’s ring, with T-cell homingto the endolymphatic sac, causing a low-grade inflammatoryresponse. This impairs absorption of the endolymphatic sacbut does not produce symptoms. Then, later in life, anunknown trigger in the system stimulates excessive fluidproduction. Then, later in life, anunknown trigger in the system stimulates excessive fluidproduction.  Derebery and Berliner [21] referenced howviruses are capable of exacerbating allergic symptoms by avariety of means, including causing histamine release,thought to be mediated by interferon. They can also damageepithelial surfaces, enhancing antigen entry and increasingresponsiveness of target organs to histamine. Derebery[22••]noted heat shock protein 70 (HSP70), an antibodyfrequently seen increased in both MD and autoimmuneinner ear disease, is often upregulated in viral infections. They concluded that patients with clinically “certain” MD do not have a significantly raised incidence of HSP70 antibodies.
• 
  
• Derebery [19] (2000): 113 patients accepted treatment;all 113 reported improvementof symptoms after treatmentof allergy
• In Derebery’s clinicalexperience, patients who have both MD and allergybenefit from immunotherapy and/or dietary avoidanceof reactive food allergens. The symptoms of MD aregenerally better controlled, with fewer vertigo attacksand more stable hearing
• 
  
• The association of allergy andMD is well-documented. At the present time, it is generallyaccepted that the cause of MD is likely to be multifactorial,consisting of an underlying genetic predisposition, com-bined with an extrinsic insult. Allergy may well be involvedin the final common inflammatory pathway in a selectsubpopulation of patients with MD 
• 有點懶，之後再繼續讀這篇論文

關於第一二三型過敏反應的解釋 可參照這裡
https://smallcollation.blogspot.tw/2013/10/hypersensitivity.html#gsc.tab=0
"1.第Ⅰ型過敏反應－IgE誘導發生的過敏反應
造成第I型過敏反應的機制為：當過敏原第一次進入人體在與特定B細胞上的抗體結合後，會引起特定IgE的大量製造，分泌出的IgE與過敏原結合後，會附著在肥大細胞(Mast cell)表面的Fcε受體。當相同的過敏原再度入侵人體，過敏原和肥大細胞表面上的IgE結合，會誘發肥大細胞釋出發炎物質，如組織胺、介白素、細胞激素，造成紅腫發癢等症狀"

"3.第Ⅲ型過敏反應－免疫複合體(immune complex)引發的過敏反應
...複合物如果沒有被清除，且在腎、血管壁、心臟瓣膜等處沉積，進而引發過度的免疫反應，如吞噬細胞企圖吞噬複合物，但複合物太大無法吞噬，於是釋放出酵素，導致發炎並造成該部位的傷害...複合物沉積的位置可以是全身性或局部性...造成的原因有可能是病患自己產生自體抗體與自體抗原形成免疫複合體而引發，如全身紅斑性狼瘡(systemic lupus erythematosus) 、類風濕關節炎的患者；或者是持續性感染，其抗原的量雖然不多，但一直存在，使得免疫複合物持續產生，並堆積在各個器官，如麻瘋病、瘧疾、B型肝炎"

前庭神經炎 最新的治療方法

前庭神經炎 最新的治療方法

耳科主治醫師 廖文輝

原文出處

前庭神經炎又稱流行性眩暈症，此病好發於氣候轉換的季節如晚秋、初春時節，臨床上為第二常見的末稍性前庭障礙疾患，僅次於最常見的良性陣發位置性眩暈；後者發病後，其前庭功能一般可完全恢復至正常，但前庭神經炎的預後很不同，本病症眩暈發作後，其前庭功能恢復情況並不樂觀，僅有少數患者可完全恢復至先前正常的前庭（溫差測試）功能，即使經過一年後，仍有半數的患者其前庭功能未能恢復至發病前正常的情形；甚至多數的患者會有殘存非典型的眩暈症狀及身體姿勢不平衡的後遺症；同時本病眩暈發作的期間會較其他眩暈
症長，短則數小時甚至到數天之久；部分病患也會有再復發的眩暈發作情況，可能持續有數個月之久，此種殘留的暈眩發作情形和身體姿勢不平衡的後遺症，時常造成病患夜夜無法安眠，隨時擔心有眩暈不定時的發作，如此心靈受到的煎熬與痛苦，除非真正有過此種可怕經
歷的患者，是無法用筆墨形容的！前庭神經炎對於病患的影響如同惡魔的靈魂附身般痛苦，這種情形是患者真正難以忍受的情況。前庭神經炎的臨床典型症狀為急性、持續性、旋轉式的眩暈發作，身體姿勢常無法保持平衡，有自發性眼振出現，會有噁心甚至嘔吐的情
形。臨床上診斷前庭神經炎的標準是依眩暈發作的病史和前庭功能檢查的異常為依據，必需先排除其他中樞性與周邊性前庭疾患，並且要符合以下四個診斷條件：1.急性、持續性的眩暈發作，發作後無法立即恢復到發作前的前庭功能狀況。2.不伴隨有聽力損失的情形。3.患
側的前庭功能檢查溫差測試有明顯的低下。4.為急性單側末稍性前庭的病變。眩暈發作是前庭神經炎最主要的症狀，許多中樞性與末稍性前庭的疾患也有類似的症狀，因此需要仔細做鑑別診斷，所以許多眩暈患者常需要耳鼻喉科與神經內科兩科的共同會診，才能做出正確診
斷。前庭神經炎常是選擇性侵犯前庭神經的上半支（影響到水平和前側三半規管及橢圓囊），而下半支（影響到後側三半規管及橢圓囊）的部位一般不會侵犯到。前庭神經炎真正的病因目前仍不明，以病毒感染的病因較為醫界所接受。因為許多患者發病前皆有病毒感染的一些症狀；例如上呼吸道感染，至於真正病因仍是眾說紛紜，此病症常好發於氣候轉變的時候，如初春、晚秋的季節，也正是流行性感冒盛行的季節，治療的目標是使用抗病毒藥物來阻斷其發炎的情況，期能有效地改善前庭神經炎患者發病後前庭功能恢復的情形。

臨床上對於前庭神經炎有三種基本標準治療的原則：第一種為使用抗眩暈藥物，以控制其急性眩暈發作和嘔吐的症狀，但是眩暈發作時常常無法口服給予，多數採用靜脈或肌肉注射，以減輕急性期發作的症狀，主要的目的是幫助患者度過眩暈發作的急性期，待依患者本身的
免疫功能逐漸地恢復，當患者已產生中樞性代償的現象，即不會有嚴重的眩暈感覺，但如果其前庭功能有嚴重受損的情形，仍會有不定時姿勢不平衡的後遺症。第二種為給予靜脈注射點滴補充體液，以控制患者急性暈眩發作及嘔吐所導致的脫水症狀。第三種為眩暈復健運動
治療，至於眩暈復健運動治療的情形，儘早進行眩暈復健運動，其前庭功能恢復的情形會較好，而病患的眩暈症狀和身體姿勢不平衡的改善情況也會較明顯。

目前針對於此病症的治療方法，除了以上傳統標準抗眩暈藥物治療方法外，本科於 2005 年開始嘗試使用抗病毒藥物來治療，其治療劑量為每天兩次，每次兩顆（Valtrex 500mg），治療期約為 10-14 天（此為日本北海道七戶醫師依其治療約三千位病患的實際臨床經驗調整後的
建議劑量），本人使用的臨床經驗為：急性發作期仍是以類固醇（Decadron）為首選（要排除糖尿病、胃潰瘍、高血壓等患者），因其效果較為快速，而此抗病毒藥物的療效，約於 7-10 天後才會明顯的看到效果，但是對於復發性前庭神經炎或不明原因的眩暈症，此抗病
毒藥物的療效卻相當不錯，尤其對於反覆性前庭病變的病患，因其慢性且長期的眩暈症狀，故療效常要 10-14 天才會明顯看到效果，希望各位要耐心等待。也不知是否是病患已經用盡所有抗眩暈藥物，腦部循環改善劑、止嘔吐藥等？或而且此藥物的價錢較高（健保不給
付），目前病患們反映其療效是很滿意！因此特別於順風耳這裡告知各位前輩及先進們，以提供另一種前庭神經炎治療方法。

VIRAL THEORY FOR MENIERE’S DISEASE

VIRAL THEORY FOR MENIERE’S DISEASE
很有趣的一篇文章 原文網址是:

http://www.whirledfoundation.org/wp-content/uploads/2015/10/0212_Viral-Theory-For-Menieres-Disease.pdf
裡面提到了一些內容關於傳統認定的眩暈發生機制與病毒致病的可能性，我摘錄一些重點如下

• 最早認為梅尼爾氏症的致病機制為血管痙攣收縮，因此有了betahistine這種藥物的治療，用意為擴張血管，也因為這個中心思想，醫生多囑咐病人少食用咖啡因與避免尼古丁，但這個觀念現在多半已經被捨棄
• 有研究指出過分的攝取鹽分會引發眩暈，但因為沒辦法進行有效的雙盲試驗去證明，不過一些傳聞的確指出鹽攝取量是一個重要的因素
• 1960年提出的薄膜破裂理論，是過去50年最受歡迎的理論，其主張為過多的內淋巴液造成薄膜破裂而造成鉀離子對前庭神經產生中毒，過多的淋巴液堆積是由於淋巴液無法流進內淋巴囊，此理論認為內淋巴液會持續的流入內淋巴囊，因此如果發生阻塞則會造成淋巴液堆積進而壓迫薄膜破裂，這個概念引導出了內淋巴囊引流手術，藉由於內淋巴囊置入小管或是矽膠片去吸收淋巴液，這個手術觀念目前已經被大幅捨去，有研究顯示內淋巴囊並不是被動的吸入淋巴液，而是一種類似海綿組織的構造，且只有在它分泌醣蛋白並且重新吸收時才會引入內淋巴液，也有研究顯示內淋巴液不會持續的流入內淋巴囊，而是只有在內淋巴液體積突然增加時才會產生流動，甚至還有研究指出眩暈發作期間患者的耳蝸功能並沒有喪失
• 新的研究提出眩暈的產生是因為淋巴液突然變多以後，拉扯或是壓垮了半規管皺摺內的前庭毛細胞
• 一位研究人員提出的排水理論假設前庭部的橢圓囊裡的內淋巴液會突然增加是因為在縱向排水期間從內耳耳蝸來的內淋巴液逆流而產生
• 這個排水理論提出一開始淋巴液會增加的原因為內耳內部的發炎反應，一旦多餘的淋巴液產生，淋巴液輕微的波動就會造成發作，經過一連串的發作後，多餘的體積減少，則會進入一段緩解期，等到下一次的發炎狀況產生就又會產生一連串的發作
• 由皰疹病毒造成初始發炎反應的說法十分令人信服，病毒在發作後會進入休眠期潛藏在內耳神經附近，等待下一次的活躍又會產生發炎反應，進而產生過多淋巴液造成一連串的發作

VIRAL THEORY FOR MENIERE’S DISEASE

By Professor William Gibson AM M.D., F.R.A.C.S. F.R.C.S.
Professor of Otolaryngology, University of Sydney

Meniere’s disease was first described by Prosper Ménière in 1861. His idea that vertigo was caused by an inner ear disorder was not accepted by the scientific community who supported the concept that vertigo was a brain disorder.

Ménière accurately described the condition but his original paper was not published because of the adverse scientific opinions. Fortunately several of his subsequent papers were published. Prosper Ménière died in 1862 after contracting pneumonia. It was ten years later that Ménière’s ideas became accepted so he never received any acknowledgement during his lifetime.

Meniere’s disease causes four major symptoms; attacks of vertigo which tend to occur in clusters, a fluctuating and usually progressive hearing loss in the affected ear, tinnitus and a sensation of aural fullness. Other symptoms such as tiredness, ‘brain fog’, and poor memory are less commonly mentioned.

It is estimated that approximately 50,000 people in Australia suffer from Meniere’s disease. Meniere’s disease tends to occur initially in mid adult life with a median age of 50 years. The attacks of vertigo tend to occur in clusters lasting a few months followed by variable periods of remission. Eventually the attacks of vertigo peter out when the hearing becomes poor, which is known as ‘burn out’ or stage 3 of the condition.

The attacks of vertigo cause great distress. The sensation of spinning can last for several hours associated with nausea and vomiting. The attacks are unpredictable and often the bread winner cannot continue work or a parent is unable to cope with the family. Often the sufferer hopes for ‘burn out’ even though they become very deaf in the affected ear and may continue to be plagued by tinnitus. Discovering the cause of the attacks of vertigo must be the first step towards finding the cure for this terribly disabling condition.

Discovering the cause of the attacks of vertigo

The initial concept was that the vertigo was due to vascular spasms within the inner ear. In the period after WW2, this belief led to the use of medications which dilate the blood vessels such as nicotinic acid and an operation called cervical sympathectomy [1]. To avoid the skin of the face reddening, Betahistine (Serc®) was developed and this still remains a popular treatment. The concept that constriction of the blood vessels in the inner ear caused the attacks was the reason why doctors told their patients to avoid coffee, caffeine drinks and nicotine. As Meniere’s disease occurs in a younger age group than vascular disease and there is no increased prevalence of Meniere’s disease amongst people with vascular problems, the concept that Meniere’s is due to vascular spasm has been mostly abandoned.

In the 1930’s, Swedish doctors noticed that many people noticed that salty foods could precipitate attacks of vertigo [2]. In the 1950’s two English researchers (Harrison and Naftalin) gave Meniere’s disease sufferers salt loads and demonstrated that vertigo attacks occurred when increased salt was excreted in the urine [3]. It is not possible to do a proper ‘double blinded trial’ of salt but the anecdotal evidence does suggest that salt loading is a significant factor.

In 1960, Schucknect at Boston showed small ruptures had occurred in the membranes in the inner ear which had healed up but left some tell-tale scarring. He proposed a rupture theory [4]. This theory suggested that an increase in the inner ear fluid called endolymph bulged the membrane causing ruptures which allowed potassium from the endolymph to poison the balance nerve endings leaving the ear. This caused a temporary loss of function resulting in vertigo until the rupture was closed off and the ionic balance restored. This theory has been favoured for the past 50 years.

The cause of the increased endolymph volume was attributed to a failure of the flow of endolymph to the endolymphatic sac. It was thought that there was a constant ‘longitudinal’ flow of endolymph toward the sac, and if a blockage occurred there was a build up of endolymph in the inner ear until the membranes ruptured. This led to the concept of endolymphatic shunt surgery, where a tube or sialastic sheeting was placed in the endolymphatic sac to facilitate its ability to absorb the fluid. This concept has now been largely discounted. Swedish workers have shown that the endolymphatic sac
is a sponge like structure and not a sac which passively accepts endolymph [5]. Endolymph is only attracted into the sac when it secretes and reabsorbs glycoproteins. Salt and his co-workers have demonstrated that there is no constant flow of endolymph to the endolymphatic sac but longitudinal flow only occurs when there is a sudden increase in endolymph volume [6]. Furthermore, audiological studies and electrophysiological studies undertaken by the author and others have shown no loss of cochlear function during the attacks of vertigo [7]. In a controversial study the author has shown that removal of the endolymphatic sac rather than shunt surgery provides a better outcome as it hastens the ‘burn out’ stage of MD [8].

The search is now on to find the real cause of the attacks of vertigo. The Meniere’s Research Laboratory has been established in Sydney under the care of Dr Daniel Brown. Here work has been undertaken to increase the volume of endolymph in the inner ear while observing the changes in the firing of the vestibular and cochlear nerves. Studies suggest that sudden changes in endolymph volume cause a stretching or collapse of the vestibular hair cells within the cristae of the semicircular canals. The author proposed a ‘drainage theory’ which postulates that the increased volume of endolymph inside the utricle (vestibular portion) is due to reflux of endolymph from the cochlear part of the inner ear during periods of longitudinal drainage [9]. Further studies are presently occurring.

Gibson’s drainage theory proposes that there is an initial increase in endolymph volume due to an inflammatory reaction inside the inner ear. Once this extra volume of fluid is present minor fluctuations in the level of excess endolymph could be the trigger for each attack: for example, after ingestion of salt or when stress causes a hormone (vasopressin) to be released. After a series of attacks the excess volume decreases and a period of remission from attacks occurs until another inflammatory event occurs causing another cluster of attacks.

What causes the initial increase in endolymph volume and the recurrent attacks of vertigo?

Many researchers consider that Meniere’s Disease is multifactorial and there are many different causes which lead to the situation which results in Meniere’s disease.

It is known that the bony vestibular duct which contains the membranous duct leading to the endolymphatic sac is narrow in Meniere’s disease sufferers although it is also narrow in some people who do not suffer with Meniere’s disease. Furthermore, there is a genetic abnormality associated with Meniere’s disease.

Possible causes include congenital disorders such as viral illness during the pregnancy including rubella (German measles) and toxoplasmosis. Diseases of the bone surrounding the ear such as otosclerosis or Padgets disease, tumours of the endolymphatic sac or vestibular nerve, allergies especially to food substances, various infections caused by syphilis, yaws or viruses, autoimmune problems and failure of the immunodefence mechanism.

If the cause of the increased endolymph is due to an inflammatory reaction inside the inner ear, then steroids should limit this inflammation. There has been a vogue towards using oral or intratympanic steroids to stop clusters of attacks of vertigo. The validity of this approach has yet to be clearly shown although clinical evidence does seem to suggest it is an effective treatment.

Is a virus the most common cause of Meniere’s disease?

Over fifty years ago Lempert and his co-workers suggested that Meniere’s disease was caused in the majority of ears by a herpes virus [10]. The herpes family of viruses consist of at least 8 members including HSV1 (causes cold sores), HSV2 (causes genital herpes), VCV (causes chicken pox and shingles), EBV (causes glandular fever) and CMV (causes birth defects).

The herpes virus has been found in autopsy specimens obtained from Meniere’s disease sufferers in both the endolymphatic sac and in the ganglion of the vestibular and cochlear nerves. However ears from non Meniere’s disease sufferers often also contain the virus.

The idea of a herpes virus causing the initial inflammatory response in the inner ear is compelling. For example, herpes simplex virus causes cold sores which erupt on the lip and then the virus lies latent or hides in the nerve for a while and then can erupt again causing more cold sores. It is postulated that a similar virus causes an initial inflammatory response in the ear and results in inflammation which causes excess endolymphatic fluid (endolymphatic hydrops). As the virus lies latent within the ear, it can erupt again causing another cluster of attacks.

Unfortunately there is no medical treatment which can kill the virus when it goes into its latent state. Anti-virals may be effective in stopping eruptions of the virus but would have to be taken continually.

The need for research into a viral cause

The first step in the research will be to find out which Meniere’s disease sufferers have a viral cause for their condition. A prolonged, double blind trial needs to be undertaken to determine if antiviral drugs can prevent clusters of attacks occurring. A double blind trial means that a placebo which looks exactly like the antiviral agent is used in some subjects and the actual antiviral medication is used in others. Neither the doctor nor the patient will know which is being used. If a subject has
another cluster of attacks, the secret is revealed and if that person is on the placebo, they will be offered the active medication.

Why do some ears have the virus present but do not develop Meniere’s disease?

While the virus lies latent (hidden) within the inner ear structures, the function of the ear is unaffected. When the virus erupts it causes the inflammatory response resulting in the production of excess endolymph. If the ear can mount an adequate defence mechanism, the virus can be destroyed before it causes an excessive inflammatory reaction. Some ears can mount this defence mechanism, whereas ears affected by Meniere’s disease cannot.

The immune system clears viruses and other pathogens from the body using special cells called lymphocytes. Lymphocytes are developed in the bone marrow (B lymphocytes) and in the thymus (T lymphocytes or T cells). Viruses are cleared by a specific lymphocyte known as Th1 and the ear needs lots of these Th1 lymphocytes to prevent the virus from causing the inflammatory reaction.
T cells are made specifically for certain tasks. T cells develop from immature T cells in the thymus and these can differentiate into specific types with highly specialised tasks. Some may develop into T1 cells and these can be measured with a blood test using a special marker called CD8+. Other immature T cells develop into Th2 cells which communicate with B lymphocytes (which produce anti-bodies to combat bacterial infections and parasites). Th2 cells have a CD4+ marker. Furthermore, other T cells are produced that limit the immune system so the body does not attack its own tissues, a process known as autoimmunity.
Perhaps if a person with Meniere’s disease has insufficient or inefficient specialised immune cells, they may be unable to prevent the virus erupting and causing inflammation in the inner ear. This may be the reason why some ears which contain the virus do not suffer from Meniere’s disease.
Stephen Spring, himself a Meniere’s disease sufferer, has discovered a possible means of altering the T1/T2 balance which may provide long term relief and we hope to be able to properly evaluate his ideas at the University, but such is the fickle nature of Meniere’s disease that isolated cures cannot be taken as definite proof of efficacy.

Our hopes for the future
It is our aim at the University of Sydney to be able to explain the mechanism which causes Meniere’s and to find an eventual cure. We feel that some definite strides towards this goal have already been made. We are desperately keen to be able to complete the tasks and hope that there will be sufficient funding to make this possible. The Meniere’s Research Fund under the superb leadership of Bruce Kirkpatrick has been the lifeline and we urge all Meniere’s disease sufferers and their families to continue to support this cause.

We need to recruit Meniere’s disease sufferers who are willing to become part of our research programme. Specifically we need sufferers who are experiencing clusters of attacks of vertigo so that we can discover if antiviral medication can be effective.
If a reader wishes to help us, please contact me (Professor Gibson at 02 9844 6801).

References
1. Passe ERG, Seymour JS (1948) Meniere’s syndrome: successful treatment by surgery on the sympathetic. Brit Med J, 2,
812-816
2. Furstenberg AC, Lashmet FH, Lathrop F (1934) Ann ORL, 43, 1035-1046
3. Harrison MS, Naftalin L (1968) Meniere’s disease: Mechanism and management, Springfield: Charles C Thomas
4. Schuknecht H. Correlation of pathology with symptoms of Meniere’s disease. Otolaryngol Clin N Amer 1968; 1:433-438
5. Bagger-Sjöbäck, Friberg U, Rask-Andersen H: The human endolymphatic sac: an ultrastructural study. Arch Otoalryngol Head Neck Surg 112: 398-409 1986
6. Salt AN: Fluid homeostasis in the inner ear. In Harris JP (ed) Meniere’s Disease. The Hague, Kugler Publications 93-101 1999
7. McNeil C, Cohen M, Gibson WPR (2009) Changes in audiometric thresholds before, during and after attacks of vertigo associated with Meniere’s syndrome Acta Otolaryngol. 129, 1404-1409.
8. Gibson WPR (2005) The effect of removal of the extra-osseous portion of the endolymphatic sac in ears affected by Meniere’s disease. In ‘Meniere’s Disease & Inner ear homeostasis disorders’ Ed Lim DJ. Pages 239-240. House Ear Institute publication, Los Angeles (ISBN 0-9776204-0-9)
9. Gibson WPR (2010) Hypothetical mechanism for vertigo in Meniere’s Disease. Otolaryngol Clin N Am 43: 1019-1027
10. Lempert J, Wolff D, Rambo JHT, Wever EG, Lawrence M. (1952) New theory for the correlation of the pathology and the symptomatology of Meniere’s disease; a research study of the vestibular endolymphatic labyrinth. Anna ORL.61,717–746

梅尼爾氏症的病毒假說與免疫理論

梅尼爾氏症的病毒假說與免疫理論

翻譯自
http://www.sciencedirect.com/science/article/pii/S1568997212000092

Endolymphatic hydrops of the membranous labyrinth has been recognised as the pathological correlate of Meniere's disease for over 70 years
迷路薄膜的內耳水腫已經被公認為與MD致病機轉超過70年了

Significant questions to this proposed pathophysiological mechanism persist.
但這個提出的致病機轉仍然有許多重要問題存在

First, although endolymphatic hydrops is readily produced by surgical obliteration of the endolymphatic sac in lower organisms
首先，在低等動物的實驗中可以輕易藉由手術閉合內淋巴囊使內淋巴產生水腫，但是在高等哺乳類動物卻沒以這個反應。

Second, imbalance (vertigo) has not been observed in these animal models. Third, the temporal bones of animal models with experimentally induced endolymphatic hydrops do not contain fibrous tissue adjacent to the stapes footplate with attachment to the saccular wall.
其次，平衡問題與眩暈在這些動物實驗上並沒有發生。第三，這些被刻意產生內淋巴水腫的動物顱骨在緊貼球囊壁的鐙骨足板鄰近並沒有產生組織纖維化的現象

Viral infection has been advocated as a possible cause of Meniere's disease by many authors
許多作者提出MD的可能原因是病毒感染

It has also been postulated that certain viruses have more affinity than others for affecting the inner ear. 
猜測特定病毒相較於其他病毒更容易感染內耳

For this reason, many studies have been carried out to verify whether viruses such as the neurotropic viruses, herpes simplex virus (HSV) types 1 and 2 [32], varicella zoster virus (VZV), and cytomegalovirus (CMV) [33], can cause Meniere's disease by invading the endolymphatic sac. 
因此，須多研究提出驗證到底是哪些病毒入侵內淋巴囊造成MD，例如嗜神經病毒，人類簡單泡疹病毒 HSV I & II型, 水痘泡疹病毒VZV，巨型細胞病毒CMV

The endolymphatic sac is known to be the site of immune reaction due to the existence of lymphocytes and immunoglobulins in addition to the resorption of endolymphatic fluid
內淋巴囊被認為是免疫反應站因其具有淋巴球與免疫球蛋白，除此之外還可以吸收內淋巴液

有研究發現MD病人的外淋巴內存有高IgG抗體。這個結果支持了HSV病毒在MD致病機轉中扮演重要角色的假說。且有研究發現相對於對照組病人，在MD病人的血清中發現有對腺病毒與VZV病毒的高IgG(?)。這些發現支持了腺病毒與VZV病毒可能在MD發病過程也很重要

各種病毒感染造成MD的機制不同，這是因為病毒與宿主抗原之間存在的變化性。首先病毒必須要是容易感染內爾的結構。其次在一般正常狀況下，病毒的入侵球囊會被免疫機制給阻擋。抗原可能會長時間存在但躲在宿主的免疫系統中直到有活化病毒感染。在病毒感染的期間，病毒的釋放或暴露會以造成細胞損壞的方式出現。如此一來先前休眠的抗原會被宿主認為是外來物，並且使得免疫反映去產生抗體且可能透過自體免疫進入組織破壞的下一個循環

一個可能在迷路上的化學性損害源頭是從前庭神經端釋放的傳染性核酸連帶著前庭神經節上的病毒再次活化。不像其他病毒的核酸，這種核酸有某程度的感染力是被血液成分中的核酸脢釋放來中和。比較MD患者與正常人的顱骨，前者前庭神經細胞有明顯損失，這支持了病毒造成MD的這個假說。病毒的再度活化與病毒量有關，當病毒量達到某個臨界水準，病毒的活性會克服宿主免疫反應並且是放病毒核酸。這些有毒物質在迷路的釋放會早成迷路炎，其為中會造成前庭槽纖維化與內淋巴水腫。

近來，MD的病毒神經病理學的直接證據已經被提出(經由電子顯微鏡觀察MD病人的前庭神經節細胞病毒結構)。抗病毒藥物的臨床反應指出MD的眩暈可以有85~90%的舒緩率。沒有超過九成的這個結果並不令人驚訝，因為HSV的突變株會對 acyclovir的抗病毒藥物產生抗藥性。在更新的抗病毒藥物發展出來前，有將近10%的MD患者的眩暈將沒辦法被控制。相較之下，抗病毒藥物對聽力症狀的改善則較無效，原因是毛細胞的損失是不可逆的。

服用acyclovir的副作用很小，通常是消化道機能亢進，在停藥後可以舒緩。其他的副作用有皮膚癢、頭痛、顫抖。這些狀況發生後，病人需要其他方式來控制眩暈，像是中耳鼓室注射抗病毒藥物Ganciclovir，一些研究指出長期(超過十年)服用acyclovir並不會讓負作用增加或是產生抗藥性。


免疫理論
將近有1/3的MD患者有其他的自體免疫疾病，雖然牽涉的免疫機制還不清楚，但有許多理論提出AIED如何引起的

交叉反應: 抗體或是T細胞造成意外的內耳受損，原因是內耳與一些具有潛在有害物(例如細菌病毒)共用共同的抗原，這是目前最受歡迎的AIED理論 (免疫系統經由辨識抗原去攻擊外來物時會誤傷到內耳)

旁觀者損害: 內耳的損傷會造成細胞激素釋放，這會在一段時間以後刺激一些額外的免疫反應，這個理論可以解釋MD的週期性反覆發作

無容忍性: 人體不能辨認人體所有的內耳抗原，當抗原釋放的時候(也許是在手術或是感染後)，人體可能會錯誤的對"外來"抗原發出攻擊，在一耳受影響的狀況下，另一耳也可能會受影響，此現象在動物實驗中可以複製出來。

基因因素: 看不懂

自體免疫似乎在單耳MD病人中造成6%的影響，在雙耳MD中大約有16%的影響，

TNF-alpha is a cytokine that induces the infiltration of immunocompetent cells into the tissues and amplifies the immune response.

TNF-alpha 是一種可以造成免疫功能正常細胞浸潤到組織且加劇免疫反應的一種細胞激素

 the TNF-alpha blocker, Etanercept, was shown to reduce the amount of inflammation in guinea pigs 
在天竺鼠動物實驗上，TNF-alpha blocker, Etanercept (腫瘤壞死因子抑制劑)可以減緩發炎

Encouraging results in a clinical study have shown that the administration of Etanercept to patients with immune-mediated inner ear diseases, including MD patients, improved or stabilised symptoms in 50% of treated patients
投入Etanercept 給予自我免疫內耳疾病(包含MD患者)在臨床上顯示有50%的症狀改善率 (眩暈耳鳴耳悶改善)

A statistically significant elevation in the levels of antiphospholipid antibodies has been demonstrated in patients with Meniere's disease
有研究提出數據顯示MD患者體內抗磷脂質抗體有顯著的統計上的提升

These data support the hypothesis that antiphospholipid antibodies are involved in the pathogenesis of some forms of inner ear dysfunction, presumably by causing microthrombus formation in the labyrinthine vasculature. 
這些數據支持抗磷脂質抗體與部分內耳功能失調患者的致病原因有關，可能是造成迷路血管微血栓的形成

Clinical studies to evaluate the efficacy of anticoagulation in Meniere's disease patients are also required
需要臨床研究來評估抗凝血藥物對MD患者的效用

On the contrary, antibodies to ubiquitous antigens, which are commonly recognised by systemic autoimmune disease sera, are not present in Meniere's disease patients. At the same time, signs and symptoms of autoimmune disorders are not present in these patients, and significant associations with connective tissue disorders have not been found. 
在自體免疫疾病中扮演重要角色的抗體在MD患者中並沒有被發現，且這些病人也沒有出現自我免疫失調也沒有發現跟結締組織失調有明顯相關

The results obtained in many studies suggest that the immune response in Meniere's disease is focused on inner ear antigens.
許多研究的結果將MD的免疫反應聚焦在內耳抗原上

It remains unclear whether the antibodies to these antigens play a role in the pathogenesis of Meniere's disease or if they represent the result of inflammation and tissue destruction. 
還不能釐清的是 對這些抗體的抗原是MD的致病因素還是組織遭到破壞發炎的結果

While specific tests for autoimmunity to the inner ear would be desirable, there are currently none that are both commercially available and proven to be useful. 
目前還沒有商業化且被證明有效的測試以供內耳自體免疫檢測用

 At the same time, steroid responsiveness is high, and with prompt treatment, inner ear damage may be reversible. Currently, the diagnosis of autoimmune inner ear disease is based either on clinical criteria or on a positive response to steroids.
如果對類固醇反應為陽性，如果接受適當治療，內耳損傷可能是可逆的。目前AIED的診斷在臨床上是基於對類固醇的臨床反應為陽性。

 Conclusion

The treatment of Meniere's disease is still based on incomplete knowledge about the underlying pathophysiology.
MD的治療方式仍然是基於不完整的基礎病理學的知識而來


The fact that so many patients with recurrent vertigo are referred because of the ineffectiveness of diuretics, low salt diets, and vestibular suppressants (Meclizine, Diazepam) indicates that the currently employed medical management of recurrent dizziness needs to be changed.

因為利尿劑、低鈉飲食、前庭抑制劑使用無效，許多有反覆眩暈的病人指出現有針對反覆眩暈的治療方式必須要改變

The antiviral approach to the very common disabling balance symptoms experienced by patients with Meniere's disease has virtually eliminated the use of various surgical methods used in the past. 
使用抗病毒藥物在MD患者常見的平衡症狀上已經實質上的消除了使用過去使用各種破壞性手術的必要

These include labyrinthectomy, endolymphatic sac decompression and vestibular nerve transection. The high (90%) rate of vertigo control with orally administered antivirals should be considered as a frontline treatment for vertigo.
這些手術包含迷路切除術，內耳淋巴囊減壓術，前庭神經切除術。以口服的抗病毒藥物有近九成的眩暈控制率，應該要被考慮當作眩暈的前線治療藥物

TNF-alpha blockers (Etanercept) could play a role in the treatment of Meniere's disease in the future 

TNF-alpha blockers將來也許會伴也MD治療的重要角色

 At the same time, steroid responsiveness is high, and with prompt treatment, inner ear damage may be reversible.
如果對類固醇反應為陽性，如果接受適當治療，內耳損傷可能是可逆的。

 If patients do not respond to the oral steroids, intratympanic injection can be given.
如果病人對口服類固醇沒有反應，則可給予中耳鼓室類固醇注射

Diagnosis of autoimmune inner ear disorders is still based on the response to steroid therapy. 
目前AIED的診斷在臨床上仍然是基於對類固醇的臨床反應為陽性

The cure for this disease is yet to be discovered, but it could lie in genetic re-engineering that might require a functioning labyrinth for an effective outcome.
MD的治療還需要再探索，但它可能要依靠基因重建工程，而基因工程可能需要完整功能的迷路以產生有意義的治療結果。

Therefore, destructive procedures like transtympanic perfusion of Gentamicin, which might preclude a possible cure for patients in the future, should be avoided. 
因此，破壞性的手段例如ITG，可能會排除未來痊癒的可能性，應該盡量避免

Gene therapy has been characterised over the last decade and can be used to transfer genetic material into inner ear cells using viral vectors.
基因治療在過去這十年已經提及可以運用病毒載具將基因物質送到內耳

Theoretically, and now experimentally, gene therapy can be used to alter the cellular microenvironment of the inner ear as well as change the cellular phenotype to protect, preserve, rescue, and even regenerate hair cells
理論上(且目前正在進行實驗)，基因治療可以刺激內耳的細胞微環境也可以改變細胞表型來保護、保存、拯救、甚至重建內耳毛細胞

Take-home messages

•

Meniere's disease is an autoimmune disorder. Its etiopathogenesis includes viral infection. The histopathological correlate of Meniere's disease is endolymphatic hydrops and vestibular endorgans demonstrates variable degrees of neuroepithelial degeneration

MD是一種自體免疫失調，其致病機轉包含病毒感染。與MD相關的組織病理表現為內淋巴水腫，且前庭感覺器官顯示不同程度的神經上皮退化

•

Due to the possible autoimmune pathogenesis of the disease, pharmacotherapy for Meniere's disease may include corticosteroids, etanercept and warfarin. The use of antiviral agents corresponds to the viral hypothesis and has eliminated the various surgical methods of the past.

根據可能的自體免疫致病機轉，MD的藥物治療可能包含類固醇 etanercept (TNF抑制劑) and warfarin (口服抗凝血藥物)。對應病毒感染的假設加以使用抗病毒藥物，已經可以免除過去各種破壞性手術的實施。

•

Gene therapy could be used in the future to transfer genetic material into inner ear cells using viral vectors and to protect, rescue, and even regenerate hair cells of the inner ear

在未來基因治療可以用來藉由病毒載體轉移基因物質到內耳細胞內並且保護、拯救、甚至重建內耳毛細胞