Meniere’s disease is a recurrent acute vertigo and fluctuating hearing loss due to endolymphatic fluid accumulation induced by multiple causes and is the most common cause of recurrent vertigo (Figure 1). Figure 1 Schematic diagram of the inner ear anatomy and endolymphatic fluid accumulation. 1. round window. 2. oval window and stapes. 3. stapedial artery (rat and mouse). 4. cochlea. 5. external semicircular canal. 6. posterior semicircular canal. 7. superior semicircular canal. 8. balloon. 9. ellipsoidal sac. 10. capsular plaque. 11. jugular crest. 12. stapedial circumflex ligament. 13. tympanic order (with ectolymph). 14. vestibular order (with ectolymph). 15. middle order (with endolymph). 16. Caustic apparatus. 17, Basilar membrane. 18, Bone spiral rim. 19, Vestibular membrane (normal position). 20, Spiral ganglion. 21, Medial capillaries. 22, Spiral ligament capillaries. 23, Vascular stripe capillaries. 24, Vestibular membrane (position in effusion). Zou Jing et al. found that the ability to observe experimental endolymphatic hydrops in vivo with magnetic resonance imaging provided the basis for an objective clinical diagnosis of Ménière’s disease.1 The incidence of Ménière’s disease is approximately 50-500/100,000 and severely affects the quality of life and work capacity of patients. Its possible causes are currently considered to be viral infection, immune damage, inflammation, ischemia-reperfusion, etc. Treatment includes pharmacological (glucocorticoids, anti-inflammatory, antiviral, improvement of microcirculation, etc.) therapy, vestibular chemical resection (transbulbar injection of gentamicin), endolymphatic shunt surgery, and vestibular neurectomy. The specificity of endolymphatic shunts for the treatment of Ménière’s disease was questioned by the group at the Danish National Hospital Bretlau, who, through a rigorous double-blind study, designed a sham operation (mastoid corticotomy alone) as a control and found that 70% of patients in both the sham and endolymphatic shunt groups had improved symptoms through 9 years of clinical observation.2 A 2011 study conducted by the Eye and Ear Hospital of Harv University and A joint temporal bone study of patients undergoing endolymphatic shunt at the House Ear Institute in 2011 also strongly supported the non-specific nature of the procedure. 15 temporal bone specimens showed persistent endolymphatic fluid, mostly moderate to severe, and 5 showed failure to expose the endolymphatic sac, while 4 (4/5) of these patients had relief of vertigo; in 8 cases the endolymphatic sac was exposed, but the shunt did not enter the cystic cavity. Therefore, we analyze that endolymphatic shunting interferes with the natural course of the disease by simply applying a strong shear stress response to the inner ear through the violent vibrations generated by drilling and grinding the mastoid, inducing the expression of the corresponding cytokines and changing the original pathological biological environment of the inner ear.4 The treatment of Ménière’s disease by performing this procedure is a clinical operation that has more to gain than to lose and is gradually being abandoned clinically. In 2004, Cohen-Kerem et al. reported the results of a literature study on the treatment of Ménière’s disease with transconjunctival gentamicin by Meta-analysis of randomized effect models, which found that vertigo The rate of complete control (grade A) was 74.7% (95% confidence limit 67.8-81.5%) and the rate of complete or substantial control of vertigo (grade B) was 92.7% (95% confidence limit 89.5-96.0%)5 . There are several explanations for the mechanism of transseptal injection of gentamicin in the treatment of Ménière’s disease, but the accepted mechanism is apoptosis of vestibular type I hair cells and vestibular ganglion cells by inducing the synthesis of nitric oxide (NO) and reactive oxygen species (ROS).6, 7 However, cochlear hair cells and spiral ganglia Therefore, the risk of further hearing loss induced by transseptal injection of gentamicin for Ménière’s disease is certainly present, and the implementation of vestibular selective gentamicin delivery is a practical way to reduce the side effects of hearing damage to date. Jing Zou et al. reported the feasibility of selective, minimally invasive drug delivery in the vestibule via microtubules. In vivo studies found that after injection of magnetic resonance imaging contrast agent (Gd-DTPA) into the upper tympanic chamber, the vestibule first takes up Gd-DTPA and then diffuses it to the vestibular and tympanic steps of the cochlea in turn. We have applied this technique to vestibular selective gentamicin delivery in patients with Meniere’s disease at the University Hospital in Tampere, Finland. The treatment of Ménière’s disease by transseptal injection of gentamicin is not the ultimate goal of otologists, and this treatment provides important clues to the search for safer and more specific treatments for Ménière’s disease. The key pathological process currently recognized as producing the symptoms of Ménière’s disease is endolymphatic hydrops. However, endolymphatic effusion is only a physical manifestation observed morphologically, and the question of whether the symptoms of Ménière’s disease are induced by a simple increase in endolymphatic water pressure or by changes in the composition of the endolymphatic fluid (ionic composition and abnormal protein exudation) is a large question before us. If the rupture of the vestibular membrane (Reissner’s membrane), which is a popular theory today, allows the mixing of internal and external lymphatic fluid, is used as a mechanism to explain the onset of Ménière’s disease, the patient’s vertigo and deafness would not subside in just a few hours because the vestibular membrane could not be repaired in such a short period of time. Moreover, the temporal bone specimens of the 15 patients who underwent endolymphatic shunts reported by Chung et al. showed moderate to severe endolymphatic fluid accumulation, yet 8 of them had relief of vertigo before birth.3 Perhaps the endolymphatic fluid composition returned to normal or near normal in those patients whose vertigo was relieved, and the persistent high hydrostatic pressure of endolymph was not the direct cause of the vertigo. This would explain the lack of specificity of endolymphatic shunts for the treatment of Ménière’s disease. Therefore, endolymphatic treatment is the mainstay of the treatment of Ménière’s disease. Transcranial vibration may be an alternative to endolymphatic sac surgery for the treatment of Ménière’s disease, at low cost and without any risk of surgery.