1. WESTERN ETIOLOGY AND PATHOGENESIS

    The factors and pathogenesis of Ménière’s syndrome are still unclear. In 1938, Hallpike and Cairns reported that the main pathological ifactor of this disease is endolymphatic hydrops, and this finding has been demonstrated by many scholars. However, the generation of endolymphatic hydrops can hardly be clearly explained. Inducing causes known at present are as follows: various infection factors (bacteria, viruses, etc.), injuries (mechanical injury or noiseinduced injury), otosclerosis, syphilis, genetic factors, allergy, tumors, leukemia, autoimmune diseases, etc. DeSousa (2002) named the vestibular symptoms induced by endolymphatic hydrops with known causes as Ménière’s syndrome, while Ménière’s disease involves idiopathic endolymphatic hydrops.

2. CLINICAL MANIFESTATIONS

    Four typical symptoms of Ménière’s syndrome are as follows: vertigo, hearing loss, tinnitus and aural fullness.

     2.1. Vertigo

     The vertigo in question is mostly sudden rotatory vertigo. Patients often feel that surrounding objects are rotating in a direction around themselves, which can be relieved after eye closure. The vertigo is often accompanied by autonomic reflex symptoms such as nausea, vomiting, pallor, cold sweat and hypotension. Any head movements can aggravate this vertigo. Patients are conscious throughout episodes, and some patients are conscious even when they suddenly fall down. The duration of the vertigo is usually tens of minutes to several hours, with the longest duration less than 24 hours. After continuing for a period, the vertigo will abate, and the symptoms will disappear. The duration of intermission varies from several days to several years among individuals. The vertigo may involve repeated attacks, with the duration and severity of each attack varying among patients. More attacks of vertigo are associated with each attack having a longer duration and shorter intermission.

      2.2. Hearing Loss

      In early stage, the deafness is usually sensorineural hearing loss with low frequency hearing loss (125– 500 Hz), which may be paroxysmal or fluctuating. Hearing decreases during the attack, but recovers partially or completely during intermission. With the progression of the disease, the hearing loss may aggravate gradually, and high frequency hearing loss (2–8 kHz) will gradually present. A special hearing change phenomenon may occur in this disease: diplacusis, namely a single auditory stimulus can be perceived by the affected ear and healthy ear as two sounds which may differ in pitch and timbre, or the patient may describe that they can hear an end sound.

      2.3. Tinnitus

      Tinnitus may be the earliest symptom of this disease, manifested as a persistent low-pitched blowing sound, whereas noises with various tones, such as the sound of a bell, song of cicada or aeolian tone, can present in an advanced stage. The tinnitus can suddenly occur or be aggravated before a vertigo attack. It disappears during intermission, but some patients with a long illness can have persistent tinnitus. A few patients may have bilateral tinnitus.

      2.4. Aural Fullness

      During the vertigo attack, the affected ear may have aural fullness, compression and heaviness. A few patients describe mild pain and itching of the affected ear.

            3. Key Points of Diagnosis

(1) The disease usually occurs in middle aged people after fatigue, emotional changes and a lack of sleep.

(2) The patient has paroxysmal vertigo, which is rotatory or up and down, accompanied by spontaneous nystagmus, nausea, vomiting, pale face, cold sweat, etc. The vertigo attack can last for several minutes or several hours, and the patient is conscious during the attack.

(3) The patient has persistent tinnitus, which is aggravated before the attack.

(4) The patient has sensorineural hearing loss, which fluctuates before and after the attack, and there is a phenomenon of “hypersensitivity” to high pitch.

(5) Head and aural fullness.

(6) Examination: Tympanic membrane is normal. Horizontal or slightly rotatory nystagmus can be observed during the attack. Hearing test shows sensorineural hearing loss, with recruitment. Vestibular function test shows decreased function during attack.

(7) Glycerol test is positive, which is mainly used to judge whether there is endolymphatic hydrops. Glycerol has high osmotic pressure, and its molecular diameter is smaller than that of poles on cell membrane, so that it can diffuse to the border cells of inner ear and increase the intracellular osmotic pressure, allowing the water in endolymph to enter the blood vessels of striavascularis via cellular channel to achieve decompression.

(8) Vestibular function test.

(8.1) Caloric test shows that the vestibular function of the affected side in the early stage may be normal or mildly decreased. After multiple attacks, directional preponderance of healthy side can be observed. In the advanced stage, canal paresis or loss of function can occur.

(8.2) Vestibular evoked myogenic potential can present abnormal amplitude and threshold.

(8.3)When there is adhesion between the stapes footplate and distent saccule, the increase or decrease of air pressure in the external auditory canal can induce vertigo and nystagmus. Henenbert sign can be positive in patients with Ménière’s disease.

(9) Imaging examination. Temporal CT can reveal stenosis of vestibular aqueduct. With special contrast, an MRI of the inner ear membranous labyrinth can reveal that the endolymphatic duct of some patients is narrow.

(10) Immunological examination Some patients have HSP70 antibody and 68 kD antigen antibody.

4. DIFFERENTIAL DIAGNOSIS

Before Ménière’s syndrome is confirmed, various diseases that may cause vertigo should be excluded, such as central nervous system diseases, vestibular system diseases and diseases of other systems.

4.1. Central Nervous System Diseases

Acoustic neuroma, multiple sclerosis, aneurysm, cerebellar or brain stem tumors, cervical vertigo, Amolk-Chiat malformation, transient ischemic attack, cerebrovascular accident, insufficient cerebrovascular supply, etc. Particularly for an acute vertigo attack, acute diseases of neurology should be excluded first, such as Wallenberg syndrome, posterior circulation ischemia and cerebrovascular diseases.

4.2. Peripheral Diseases

Benign paroxysmal positional vertigo, vestibular neuritis, vestibular drug poisoning, labyrinthitis, sudden deafness, Hunt syndrome, otosclerosis, autoimmune inner ear disease, perilymphatic fistula, etc.

4.3. Metabolic Diseases

Diabetes, hyperthyroidism or hypothyroidism, Cogan syndrome, blood diseases, autoimmune diseases, etc.

4.4. Diseases of Other Systems

Heart disease, primary hypertension, etc.

5. WESTERN MEDICAL TREATMENT

5.1. Surgery can be used for treatment of Ménière’s syndrome. Surgery has not been used for the treatment of Ménière’s syndrome in the global medical field for a very long time. In 1957, labyrinthectomy and cochlear vestibular neurectomy were performed. In 1966, surgeries were summarized as three types: destructive type, semi-destructive type and conservative type. Briefly, there are many conservative surgeries, such as endolymphatic sac incision, saccule decompression, sympathectomy, chorda tympanectomy, endolymphatic subarachnoid shunt operation, stapes footplate fenestration, and endolymphatic mastoid shunt. Comprehensively, the most common surgery is fenestration decompression. Recently, the international vertigo conference summarized that the efficacy of surgery is unsatisfactory, but short time fenestration decompression may have some effects.

5.2. Infusion can be used for treatment of Ménière’s syndrome. Currently, infusion is generally used during attack of Ménière’s syndrome. Infusion has been demonstrated by clinical evidence to be able to relieve most types of vertigo. Adding diuretics into the liquid can achieve better efficacy, because it can temporarily reduce the endolymphatic pressure in the organ of equilibration and thus relieve the symptom of vertigo. Therefore, infusion is a symptomatic treatment but not curative treatment. 

5.3. Drugs can be used for treatment of Ménière’s syndrome. At the beginning of his research on vertigo, Doctor Ménière identified the position of vertigo and its pathogenic mechanism through anatomy. His work made a great contribution to vertigo research, leading many countries and doctors to be devoted to treatment research of Ménière’s syndrome, with drug therapy as the focus. With Ménière’s syndrome as the focus, many drugs have been studied, but no ideal drugs have been identified from ancient times to the present. Two reasons have been confirmed through extensive data to explain why the therapeutic efficacy on Ménière’s syndrome is unsatisfactory.

First, the important part involved in this disease is millimeter-grade in size, which exists in temporal bone and is close to the inner ear. Around the world, no drug can penetrate to this part at present.

Second, the drug is distributed across the whole body, but little can reach the labyrinth. The important component of vertigo is millimeter-grade in size, so even if the drug can penetrate into this part, it will have very little effect. Therefore, the therapeutic efficacy of treatments on Ménière’s syndrome is always unsatisfactory. This is why Ménière’s syndrome is recognized as problem worldwide.

To be continued......

Written by Guanhu Yang, Ji Zhang, Jasmine Ma, Xuejiao Xie, and Decheng Chen

Contact the authors:

Guanhu Yang

Acupuncture Wellness Center of Cincinnati, 5887 unit 4, Cornell Rd, Cincinnati, Ohio 45242 e-mail: guanhuyang@gmail.com

Ji Zhang

JI Acupuncture & Herbs, 2035 Westwood Blvd. Suite 209, Los Angeles, CA 90025, USA

Jasmine Ma

Whole Health & Wellness Center, 7635-A Leesburg Pike, Falls Church, VA 22043, USA

Xuejiao Xie

Zhongjing Theory Section, Hunan University of Chinese Medicine, Yuelu Area, Changsha,hunan Province, China

Decheng Chen

Natural Acupuncture & Wellness P.C., 161 Madison Ave, Suite 2N, New York, NY 10016, USA