Benign paroxysmal positional vertigo (BPPV) is a syndrome of vestibular semicircular canal disease in which symptoms are induced by changes in body position and is caused by multiple etiologies. Barany (1921) first reported the disease, Dix and Hallpike established the Dix-Hallpike shift test, and Schuknecht suggested that the symptoms of the disease originated from the abnormal function of the posterior semicircular canal jugular crest. This disease is one of the most common disorders of peripheral vertigo. I. Epidemiology The incidence of benign paroxysmal positional vertigo ranks first among vestibular peripheral disorders. The incidence is roughly estimated to be 10,7-17,3/100,000 in Japan (Mizukoshi et al., 1988) and about 64/100,000 in the United States (Froehling et al., 1991). There is a relationship between the age of onset and the etiology of the disease. The etiology of the disease remains unclear in about half of the patients, and in half of the patients the etiology is related to the following diseases or secondary to the following diseases. 1, head trauma: head trauma, especially in the days and weeks after mild cranial trauma, or sudden acceleration and deceleration movement when riding in a car, resulting in neck “whipping injury”, etc. Viral neuritis Transient ischemic vertigo of the vertebrobasilar artery and impaired blood circulation in the inner ear. Other diseases of the ear, such as middle ear and mastoiditis, post-ear surgery, drug ototoxicity, etc. Pathogenesis 1. Cupulolithiasis theory: Schuknecht (1962, 1969) proposed that the degenerated otoliths are dislodged from the ellipsoidal cystic plaque and such alkaline particles are deposited at the crest of the posterior hemimelia, causing a difference in density between the endolymph and the crest and thus a difference in specific gravity (under normal circumstances, the gravitational effect is the same in both places). This leads to an abnormal perception of gravitational effects. According to the principle of semicircular canal physiology, when the stimulated head position remains unchanged, the crestal apex caused by gravity is also deflected unchanged, so the vertigo and nystagmus caused should persist. However, the actual situation is that the vertigo or nystagmus only lasts for a few seconds and stops, so it is clear that the vertigo and nystagmus are not due to the direct action of gravity on the crista. In addition, according to the anatomical position analysis, when the head is in the draped position, the posterior hemiretinal crest is close to the middle position, so it is impossible to produce the vector of gravity. However, the clinical manifestation of ethanolic positional vertigo supports this theory. 2. Canalithiasis theory: Hall, Ruby and Muclure (1979) proposed that the otoliths are dislodged due to various reasons; or the degenerated otoliths are gathered in the posterior semicircular canal near the pot belly, and when the head position is moved to the excitation position (hanging head position), the semicircular canal becomes vertical, and the otoliths start to move away from the pot belly by the action of gravity. The endolymph is tracted by gravity. In order to overcome the elasticity of the crista and the inertia of the endolymph in the semicircular canal, it takes several seconds before the endolymph and the crista are displaced, which is the latent period for vertigo and nystagmus. The fast phase of nystagmus is directed toward the ear in the lower position. When the canal stone moves to the near horizontal position of the semicircular canal, the traction on the endolymph is reduced or stopped, and the elasticity causes the crest to return to the middle position, so the vertigo and nystagmus stop. When the head position returns to the upright position, the gravitational effect of the canal stone is in the opposite direction to the hanging head position, so the direction of nystagmus is opposite to the hanging head position. When repeatedly performed to excite the head position, the canal stone spreads out and moves back and forth in the canal less frequently, so that the vertigo or nystagmus is diminished or does not occur. Benign paroxysmal positional vertigo with abnormal function of the semicircular canal is mostly seen in the posterior semicircular canal, but the external semicircular canal and anterior semicircular canal can also be involved. Clinical manifestations 1. Symptoms: The onset of vertigo is sudden and the patient has strong rotational vertigo when the head position changes, which often lasts within 60s, accompanied by nystagmus, nausea and vomiting. The symptoms often occur when lying down in a sitting position, or when moving from a lying to a sitting position, or when turning over in bed, and patients can often notice vertigo when turning to a certain head position, and often wake up during sleep due to vertigo attacks. The degree of vertigo varies widely, and in severe cases, it can occur when the head is slightly moved. The entire course of the attack may last from a few hours to a few days, and may last for months or years. The symptoms of the disease may appear to worsen periodically or remit spontaneously. The length of the interval varies, and sometimes it can be 1 year or several years without onset, or even up to 10-20 years without onset. (2) Examination: (1) Dix-Hallpike varus nystagmus test is an important routine examination method for posterior hemianopia BPPV (Figure 5-16-1): (1) the patient sits on the examination bed with the head turned 45o to the right; (2) the examiner is located on the patient’s side, holds the head with both hands, and quickly moves the subject to the supine side hanging head position, the head should be kept at 45o to the sagittal plane. observe for 30s or until the nystagmus stops After 30 s or until the nystagmus has stopped, the head and upper body are returned to the sitting position, and then the lateral suspension head position to the opposite side is performed. Nystagmography should be recorded in both horizontal and vertical duplexes to record the head position in which the nystagmus occurs and to accurately understand the latency and duration, the gradual strength and weakness of the nystagmus, and the decay of the nystagmus after repeated excitation. Rotational nystagmus can be directly observed using Frenzel glasses or infrared visual nystagmography. The nystagmus of posterior semicircular canal BPPV has the following characteristics: (1) the nystagmus is rotational, the direction of the nystagmus at the upper pole of the eye is toward the lower ear, the nystagmus is clockwise when the left ear is in the lower hanging head position, and the rotational nystagmus is counterclockwise when the right ear is lower; (2) there is a latency period, usually 2-10s, mostly 2s; (3) the duration is short, usually 5-10s, not longer than 1min; (4) there is fatigue; ⑤ the nystagmus increases rapidly and then gradually decreases; ⑥ when returning to the sitting position from the suspended head position, a very brief nystagmus with low speed in the reverse direction can occur, which is called typical positional nystagmus. Please refer to the relevant books for the method of BPVV examination of the external and anterior hemiretina. (2) The sinusoidal rotation test is performed to examine patients with BPVV of the external semicircular canal. The patient is seated, head is tilted forward 30o, rotation speed is 0.04Hz~0.5Hz, recorded with ENG closed eyes, positive eye velocity at low frequency is phase shift reduction. (3) Audiological examination generally has no abnormal changes in hearing mechanics, but hemianopsia may appear as abnormal hearing in the affected ear if it occurs in a certain ear disease. (4) Other posturographic examinations may present abnormalities, but are not characteristic. Vestibular function tests, neurological examinations and CT or MRI examinations are mainly used for differential diagnosis or etiological diagnosis. V. Diagnosis and Differentiation The characteristic features of the diagnostic history are extremely important. The diagnosis can be confirmed by combining the history, Hallpike’s dislocation nystagmus test, and audiometry with no abnormal findings in the interval, but the dislocation nystagmus test is best performed during the attack. It should be differentiated from central positional nystagmus, vestibular neuritis, Meniere’s disease, and cerebral blood flow disorders causing vertigo. In some patients, the diagnosis is complicated by the presence of ischemic disease of the vertebrobasilar artery and ischemic changes in the vagus before the onset of the attack. The difference in diagnosis lies in the fact that the duration of the attack does not last longer than 1 min, while the duration of the vertebrobasilar ischemic attack is longer than 1 min, and it should be clarified as much as possible whether it is a posterior or an external hemianopia depending on the excitation head position. Although BPPV is a disease with a tendency to heal itself, it can take months or years to heal itself, and in severe cases, it can lead to loss of working ability, so treatment should be carried out as much as possible. 1.Anti-vertigo drugs Guilizine (Brain Yizine) or Flunarizine, Isoprostanes (Finasteride), etc. have some effect. In recent years, because of the easy operation of head dislocation technique, no special instruments are needed, and the effect is good, it has gained wide attention, and the common method is Epley (1992) canalithparticlerepositioningprocedure. 3, other vestibular rehabilitation therapy training. 4, surgical therapy such as the above treatments are not effective, and affect the quality of life and work, feasible posterior potbelly neurectomy or hemianoplasty obstruction.