I. Basic definition
Benign episodic positional vertigo (BPPV) is a common mechanical disorder of the inner ear, accounting for about 20% of all vertigo and the cause of about half of all benign episodic positional vertigo pathogenic vertigo of the ear. Although it is an otologic disorder, it is often first diagnosed in neurology and is often misdiagnosed as vertebrobasilar artery insufficiency and cervical vertigo, which delays treatment. Now, we would like to summarize the etiology, pathogenesis and treatment of this disease in order to increase the understanding of this disease and reduce the misdiagnosis rate.
BPPV was first reported by Barany in 1921, and there have been many similar reports since then. years), and is more common in women than men.
II. Etiology and pathogenesis
The etiology of BPPV was thought to be crestal cap sinkhole or canal sinkhole in early studies. Later ear surgery on patients and autopsies on individual patients revealed free calcium carbonate crystals in the semicircular canal, confirming the canal sedimentation theory [7,8]. This theory postulates that otoliths on the ellipsoidal saccule patch are dislodged by infection, trauma or degeneration and are mostly deposited in the horizontal semicircular canal due to the anatomical location. The change in head position (head down or head up) puts the horizontal semicircular canal in a horizontal position, and turning the head causes the otolith fragments to move by gravity in the canal. Because of its greater lymphatic ratio than the internal vagus, it produces an “unplugging effect”, which displaces the potbelly crest and stimulates the vestibular nerve, producing vertigo [1–5]. This theory can well explain the various clinical features of BPPV: the otolith fragments have an inertia before the latency period; soon after the cessation of the head position change, the otolith fragments also stop moving and the vertigo is transient; when the head position returns to the original position, the otolith fragments move again in the opposite direction, producing another vertigo; after several movements, the “plucking effect” decreases After several movements, the “unplugging effect” decreases and fatigue appears. However, most patients do not have a clear cause, 17% of them have a history of head trauma, 15% have a history of vestibular neuronitis (which can occur within 2 weeks to 8 years after inflammation), and a few may have a history of insufficient blood supply to the basilar artery. It is still believed that canal sedimentation is the main etiology.
III. Clinical manifestations
The clinical manifestations of BPPV are characterized by 5 features.
(1) Latency: vertigo appears only after 1 – 4 seconds after the change of head position.
(2) Rotational: vertigo has a distinct sense of rotation, and the patient sees objects rotating or closes his eyes with a sense of his own rotation.
(3) Transient: vertigo stops on its own in less than 1 minute.
(4) Transition: Returning the head to the original position can induce vertigo again.
(5) Fatigue: The symptoms of vertigo gradually decrease after several changes of head position.
IV. Diagnosis
The diagnosis of BPPV is based entirely on the typical clinical manifestations and positive Dix–Hallpike test results.
Dix–Hallpike test.
The patient sits on the examination table and quickly takes a supine suspended head position with the help of the examiner and deviates 45 degrees to one side. In PC-BPPV, transient vertigo and vertical rotational nystagmus appear after a few seconds of latency when the head is turned to the affected side, and there is fatigue on repeated tests.
In addition, there is the supine lateral head position test, in which the patient sits on the examination table and quickly takes a flat position, followed by a 90-degree head turn to the side, and those with HC-BPPV immediately develop intense rotational vertigo and horizontal nystagmus.
Since the above tests can induce vertigo, patients will be fearful, shout or uncooperative, so the purpose should be explained clearly before the examination to obtain cooperation and ensure that the eyes are not closed. It should be used with caution or contraindicated in patients with severe heart disease, cervical spondylosis, or carotid stenosis. Since the prognosis of BPPV is good and various neurological and otologic examinations are normal, Dix-Hallpike test should be performed on all patients with outpatient vertigo, and those who are positive can be diagnosed immediately to avoid unnecessary examinations and ineffective “symptomatic treatment”.
V. Differential diagnosis
BPPV needs to be differentiated from many kinds of peripheral and central vertigo. It is not difficult to differentiate BPPV by mastering the clinical features of BPPV and Dix-Hallpike test, and paying attention to the corresponding medical history. About 1/3 of patients do not actively complain of postural triggers, so the absence of an attack does not exclude the possibility of BPPV.
Commonly misdiagnosed disorders include cervical vertigo, vertebrobasilar system insufficiency, nonspecific dizziness, cardiogenic dizziness, and neurological disorders.
1. Cervical vertigo.
It is also called vertebral artery compression syndrome. The cause may be degenerative changes of the cervical spine, lesions of the cervical muscles and soft tissues of the neck, tumors of the neck and malformations of the skull base that cause compression of the vertebral artery and lead to ischemia and vertigo; lesions of the vertebral artery itself, such as atherosclerotic stenosis and malformations, are more likely to develop. Direct or indirect stimulation of the cervical sympathetic plexus can cause spasm of the vertebral artery or reflex impairment of inner ear circulation and lead to the onset of vertigo. Abnormal reflexes can also cause, for example, various stimuli to the cervical reflex receptors in the circumoccipital joint and the upper three cervical joint capsules, whose impulses can be transmitted to the cerebellum or vestibular nuclei to produce vertigo and balance disorders. The main clinical manifestations are various forms of vertigo, the occurrence of which is obviously related to sudden head rotation, often accompanied by nausea, vomiting, ataxia, etc. Sometimes there can be black haze, diplopia, amblyopia, etc. The symptoms last for a short time. Treatment may include neck traction, physical therapy, massage, etc.; appropriate application of vasodilators, microcirculatory improvement drugs and vitamins, etc.
2. Inadequate blood supply of the vertebrobasilar system.
The vertebral-basilar artery has three important features in anatomy and pathology: first, the two sides of the vertebral artery tube diameter is unequal in normal people accounted for 2 / 3, and even unilateral vertebral artery is small or missing; second, the vertebral artery through the 6th – 1 cervical transverse foramen after the occipital bone The vertebral artery enters the skull through the foramen ovale of the 6th and 1st cervical vertebrae, which means that it is walking in a bony tunnel with great mobility, and after the age of 50, the cervical vertebrae are prone to degenerative changes and formation of bone redundancy, and low blood pressure is more likely to promote blood supply insufficiency. The main clinical manifestations are acute vertigo, which is often the first symptom, accompanied by nausea, vomiting, impaired balance, unsteadiness and weakness of both lower limbs.
VI. Treatment
The treatment of BPPV is based on the repositioning treatment of the tubular stone. The efficiency of this treatment is 71% – 92%. A randomized controlled trial demonstrated that the efficiency of canalolith repositioning therapy was 89% [11]. There are two types of repositioning methods for the different hallux valgus involved.
Epley maneuver (for posterior hallux valgus otoliths).
(1) The patient is seated on the treatment table and quickly placed in a supine suspended head position with the help of the therapist and twisted 45° to the affected side.
(2) The head is gradually turned upright and then continues to deviate 45° to the healthy side.
(3) Turning the patient’s head and body to the healthy side so that he or she is lying on the treatment table on his or her side, with the head deviated from the supine position up to 135°.
(4) Sit up with the head tilted forward by 20 degrees.
The above 4 steps are completed in 1 treatment cycle, and each position is held for 1 min after the nystagmus disappears.
Barbecue tumbling method (for horizontal hemianopsia).
(1) The patient sits on the treatment table and quickly lies flat with the help of the therapist, with the head twisted 90° to the healthy side.
(2) The body is turned toward the healthy side so that the face is facing downward.
(3) Continue to turn toward the healthy side so that the side lies on the affected side.
(4) Sit up.
The above four steps were completed in one treatment cycle, and each position was held for 1 min after the nystagmus disappeared.
The experience of most researchers is that a large rotation angle, fast speed and induced nystagmus are effective. If the initial treatment is ineffective, it can be repeated more often with good results. Traditional repositioning of the canal requires that the patient not lie down for 2 days after treatment to avoid the flow of otolith fragments back into the semicircular canal. Recently, however, it has been reported that lying down after treatment can have the same effect as the traditional method. Slow rotation using a special swivel chair can avoid vertigo during treatment. Vibrating the mastoid with a vibrator can dislodge or disintegrate the otolith fragment from the membrane or canal wall, which helps the fragment to be transferred out of the semicircular canal. The Semont method of exercise has been reported for those who have failed to be treated by canal stone repositioning [12], and the efficacy is comparable to that of canal stone repositioning, but this method is often difficult for patients to accept. In cases where various treatments have failed, semicircular canal block treatment can be considered.