Benign paroxysma positional vertigo (BPPV) was first introduced by Barany in l921 and subsequently characterized in detail by Dix and Ha1lpike. BPPV~ is the most common form of vestibular peripheral vertigo, with an annual incidence of 64/100,000 J. However, because of the relative lag in its recognition and the fact that vertigo patients often consult different departments such as neurology, pharyngology, orthopedics and emergency medicine according to their own knowledge of the disease, it has not received sufficient clinical attention and therefore has not been correctly diagnosed and managed J. In China, BPPV is often misdiagnosed as vertebrobasilar artery insufficiency of blood supply, Meniere’s disease, cervical spondylosis or other vertigo. As more and more clinicians use Dix.Haalpi~ and other evoked tests to diagnose and Epley, Semont or Barbecue to treat and often obtain dramatic treatment results, the understanding of BPPV is getting deeper and deeper, and the level of treatment of the whole vertigo group has been improved. The concept and properties of BPPV Vertigo is a sudden but non-existent sensation of rotation, floating, tumbling or drifting of oneself and/or external objects in a certain direction, which is a kind of motion hallucination caused by spatial disorientation and balance dysfunction of human body due to the lesion of vestibular semicircular canal system, and it often occurs repeatedly and suddenly, and has a great impact on patients’ daily life, study, work and social activities. True vertigo (once called “true vertigo”) is a condition in which the vestibular system plays a key role in the development of vertigo and is also associated with the cerebellum, vision and deep senses. Depending on the location of the lesion, vertigo can be further divided into peripheral vestibular vertigo (80% of cases, caused by inner ear or auditory nerve lesions) and central vestibular vertigo (20% of cases, caused by lesions in the vestibular nuclei or brain. BPPV is a severe vertigo of less than 30 S duration induced by a certain head position, mostly accompanied by nystagmus, but without deafness, tinnitus and neurological signs and symptoms, which usually subsides within a few weeks, with a few recurrences. Epidemiological studies have shown that BPPV is the most common form of vertigo, with an incidence of about (10.7-64)/100,000 in the population, and that BPPV cases account for 20% to 50% of vertigo cases. In the United States, about half of the elderly over 70 years old have had at least one BPPV_4 J. 2. Pathogenesis and classification BPPV, also known as otolithic vertigo, has not been completely elucidated, but it is believed that the main cause and pathogenesis of the dislodged otolith is the imbalance of the vestibular function on both sides due to the vibration of the endolymph when the head position changes. The majority of patients with otolith dislodgement have an unknown cause (possibly related to vestibular aging) and have idiopathic (primary) BPPV; others have symptomatic (secondary) BPPV secondary to head trauma, viral labyrinthitis, Meniere’s disease, after inner ear surgery, or after the use of ototoxic drugs J. A large German study and studies by other authors have confirmed that advanced age, migraine hypertension, hyperlipidemia, and stroke may be independent risk factors for BPPV . In 1969, Schnknecht found that postmortem pathological examination of temporal bone sections in patients with BPPV during life revealed deposits of basophilic granules in the hemipelvic ridge, probably originating from degenerated ellipsoidal cystic plaques. Since otolith deposition increases the sensitivity of the ridge to weight, vertigo and nystagmus can be induced during head position changes, thus leading to the hypothesis of “crista parietalis”. Hall et al. proposed the theory of “tubular calculi” on this basis. This theory suggested that the otoliths caused by various reasons were dislodged and collected in the proximal part of the semicircular canal, and the free otoliths were moved by gravity in the endolymph, and the density of the otoliths was greater than that of the endolymph, resulting in the “plucking effect”, which caused the displacement of the cristae of the canal and irritation of the vestibular nerve, resulting in symptoms such as vertigo and nystagmus. Epleyl6 further explained that there are some microscopic floaters in the endolymph of the long arm of the posterior semicircular canal, and when the head position is moved to the excitation position (hanging head position), the posterior semicircular canal becomes vertical, the ridge of the potbelly is located above, and the particles are pulled by gravity in the direction of the endolymph away from the potbelly. This time is the latency period of nystagmus, and the fast phase of nystagmus is directed to the lower ear. When the particle moves to a more horizontal position in the semicircular canal, the movement stops and the traction on the endolymph ends, the elasticity causes the crest to return to the intermediate position and the nystagmus disappears, which is the duration of the nystagmus. Repeatedly in the excited position can make the particles dispersed, the endolymphatic pressure drops below the elastic retraction force of the crest, the crest no longer deflects, and the nystagmus disappears. When the upright position is restored, the gravitational effect of the particles is opposite to that of the suspended head position, inducing a reverse rotational nystagmus. This theory is supported by the presence of floating particles in the endolymphatic cavity at the time of posterior hemianoplasty. BPPV is clinically classified into four types according to the involved hemiangium: posterior canal BPPV (PC.BPPV; most common), horizontal canal BPPV (HC-BPPV; more common), superior canal BPPV (SC-BPPV), and posterior canal BPPV (SC-BPPV). HC-BPPV is often further classified into cupulo.1ithiasis and canalithiasis according to the site of stone loss in the hemichannels. A multicenter study of l 692 cases showed that PC-BPPV accounted for 60.9%, HC-BPPV for 31.9%, SC-BPPV for 2.2%, and mixed type for 5.0% E s J. Damman et al. analyzed BPPV in their 10-year consultation and found that PC -BPPV accounted for 72.16%, HC-BPPV accounted for 21.48% (of which 77% were tubular calculi and 23% were crestal calculi), SC.BPPV accounted for 3.33%, and mixed type accounted for 3.03%. 3, clinical manifestations and diagnosis Generally, the older the age, the higher the incidence, the more frequent in women, the right hemiplegic canal is more commonly involved. A study of 3,426 cases of PC-BPPV showed that right:left was 1.41, which may be related to the fact that people are more used to sleep on the right side.10 3. The same results were obtained in a study by Damrnan et al, with 57% on the right side, 38% on the left side, and 5% bilaterally. A large epidemiological survey in Germany showed that BPPV accounts for 8% of the population and has a significant impact on the lives of patients, with only 8% receiving proper treatment, a lifetime prevalence of 2.4% and an annual incidence of 0.6%. The clinical manifestations of BPPV are mainly vertigo, light-headedness, balance disorders, and may be accompanied by nausea and vomiting. These symptoms are almost invariably caused by a change in the position of the head relative to the direction of gravity, most often triggered by waking up, turning over, lifting, washing and lowering the head. Most patients present with recurrent transient vertigo induced by a specific head position (which may have a short latency of a few seconds), usually lasting only a few seconds, with a true vertigo duration of up to 1 min (although some patients may describe the vertigo as longer and should be screened for this). Rotational nystagmus is seen on examination. The patient’s vertigo and nystagmus have the following characteristics: short incubation period (nystagmus appears after a l-5 S change in head position) and short duration.