There is a picture and a video: The nystagmus mechanism (V2.0) of the posterior semicircular canal BPPV "Halo" strategizes

BPPV is the most common peripheral vestibular disease in clinical practice.
It was first reported by Bárány in 1921 and officially named "benign paroxysmal positional vertigo" by Dix and Hallpike in 1952
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It is a peripheral vestibular disease that is induced by changes in the head position relative to the direction of gravity, with recurrent transient vertigo and characteristic nystagmus.
It is often self-limiting and easy to relapse (2017 Chinese Standard)
.

Otolithiasis, the lifetime prevalence rate is 2.
4%, accounting for 15-30% of the total number of patients with vestibular vertigo
.

BPPV can be divided into idiopathic and secondary according to the etiology.
The idiopathic etiology is unknown, accounting for more than 50% of all BPPV patients
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It is generally unilateral, and bilateral involvement is rare.
The side and cast of the affected side can be judged by the type of nystagmus induced by the displacement test
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Since the posterior semicircular canal is located behind the entire inner ear capsule and is low in position, otolith particles are easily affected by gravity and fall to this canal.
Therefore, the incidence of PC-BPPV is the highest, accounting for about 80% of all BPPV
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[Horizontal semicircular canal BPPV accounts for 20%
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The true anterior semicircular canal is very rare, less than 1%] The pathogenesis of BPPV There are currently three recognized theories on the pathogenesis of BPPV: (1) Otoliths on the utricle plaque fall off due to various inducements and open from the semicircular canal during head position changes.
(One foot/total foot) slips into the lumen of the semicircular canal (can be on the short arm, forearm, hind arm) to induce positional vertigo and nystagmus during head movement
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That is: the theory of tube calculi
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(2) Otoliths on the utricle plaque fall off due to various causes, and fall from the semicircular canal opening (single foot/total foot) into the semicircular canal during the change of head position.
Crest cap tube side or capsular side), induce positional vertigo and nystagmus during head movement
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That is: the theory of crest calculus
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(3) Light cupula theory (light cupula): Various reasons cause the specific gravity of the crest cap to be lower than the endolymph fluid, which causes the crest cap not to be affected by gravity/buoyancy alone to deviate, and it appears clinically during the Roll test.
Persistent geotropic positional nystagmus
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Not all light crest caps are otolithiasis.
Only when the rare "light otoliths" adhere to the crest caps, causing the crest caps to have a lower specific gravity, the specific postures induced by the persistent geocentric positional nystagmus, And when the reset is valid, it can be merged into BPPV
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 How does BPPV's nystagmus occur? Under normal physiological conditions, when the human body is lying down, getting up, lying on the side, lowering the head and other head positions, the ampullary ridges of the bilateral semicircular canals discharge in concert, causing the extraocular muscles to work together, producing physiological vestibular-eye movement reflexes, and ensuring eyeballs The vision is stable; after the otolith enters the semicircular canal, the otolith will move with the endolymph in the process of the head position of the human body.
When the head position stops, the specific gravity of the otolith is much higher than that of the endolymph, which is affected by inertia , Continue to flow to the lowest point of gravity, agitate the endolymph, impact the crest cap, and form the crest cap deflection, causing the above-mentioned "coordination" disorder.
Although the head position has stopped moving, the brain center mistakenly believes that the head position is still moving and continues to start.
VOR, produces eye movement that alternates between slow phase (otolith stimulation) and fast phase (central correction), which is the formation of nystagmus
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 The nystagmus mechanism of the typical posterior semicircular canal BPPV The arrangement of the apical cilia of the hair cells in the ampullary crest of the posterior semicircular canal is that the static cilia are on the side of the utricle and the dynamic cilia are on the side of the semicircular canal
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According to Ewald's law, the flow of endolymph in the direction of the vertical semicircular canal away from the ampulla, that is, the movement of the static cilia to the moving cilia, can cause the vestibular nerve to excite
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When PC-BPPV patients are sitting in an upright position, the otoliths are generally located at the lowest point of gravity near the end of the posterior semicircular canal near the end of the ampulla.
Dix-Hallpike test is performed.
Deviation to the tube side, generating excitement
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Due to the flow of otoliths, the imbalance of the vestibular tension on both sides leads to slow vertical vestibular eye shift and reflex saccades, resulting in nystagmus with the typical vertical component of PC-BPPV toward the upper pole of the eye and the twist component toward the ground.

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See Figure 1,2
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Figure 1 The cilia arrangement sequence of the posterior semicircular canal in the upright position (the thin red lines are static cilia and the thick red lines are kinesia) and the direction of endolymph flow during excitement (arrows).
Figure 2 PC-BPPV angiolithiasis during the Dix-Hallpike test The otolith flow direction videos 1 and 2: Dix-Hallpike Test technique inspection video 3: Dix-Hallpike Test machine inspection video 4: Typical PC-BPPV nystagmus semicircular canal participates in the mechanism pathway of vertical VOR The posterior semicircular canal mainly participates in vertical eye slowness Fast exercise includes two action pathways: the excitatory pathway and the inhibitory pathway.
The extraocular muscles coordinated by the excitatory pathway include the ipsilateral superior oblique muscle and the contralateral inferior rectus muscle, and the extraocular muscles coordinated by the inhibitory pathway include the ipsilateral inferior muscle.
Oblique and contralateral superior rectus
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When PC-BPPV patients undergo the DH test on the affected side, the posterior semicircular canal of the affected side stimulates excitatory stimulation, and the excitatory pathway causes the superior oblique muscle on the ipsilateral side (mainly internal rotation, followed by downward and external rotation), and the opposite inferior rectus muscle (below The main rotation, external rotation, followed by internal rotation) contraction, resulting in a vertical downward and torsional slow eye movement (slow phase of nystagmus), and then the center initiates a reflex saccade, which produces the opposite direction to the slow eye movement Rapid eye movement (rapid nystagmus) is a nystagmus that moves vertically upwards and twists to the affected side
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At the same time as the excitatory pathway acts, the inhibitory pathway is also activated at the same time, acting on the ipsilateral inferior oblique muscle (mainly external rotation, followed by upturn and external rotation) and the contralateral superior rectus muscle (mainly upturn, internal rotation and internal rotation) Secondly) to relax the muscles and assist the excitement pathway to produce corresponding slow eye movements
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See Figure 3-9 [Take the PC-BPPV on the right as an example]
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Figure 3 Schematic diagram of the nystagmus induced by the movement of the ipsilateral otolith on the right side of the PC-BPPV (excited pathway) Figure 4 Schematic diagram of the nystagmus induced by the movement of the ipsilateral otolith on the right side of the PC-BPPV (inhibition pathway) Figure 5 Three Schematic diagram of the horizontal and vertical VOR pathways involved in the semicircular canals
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   Figure 6 The coupling of the three semicircular canals and the extraocular muscles Figure 7 The innervation of the extraocular muscles Figure 8 Anatomy of the extraocular muscles-1 Figure 9 Anatomy of the extraocular muscles-2 The formation of reverse nystagmus after sitting up with PC-BPPV The mechanism is based on Ewald's law.
When a patient with PC-BPPV sits up, the otoliths in the posterior semicircular canal on the affected side move toward the ampulla, and the crest cap drives the hair cell cilia to swing from the moving cilia to the static cilia.
The lateral anterior semicircular canal is relatively excited
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The anterior semicircular canal participates in the vertical eyeball slow motion, and also includes two action pathways, the excitatory pathway and the inhibitory pathway.
The extraocular muscles that the excitatory pathway is cooperatively coupled include the ipsilateral superior rectus muscle and the contralateral inferior oblique muscle, and the inhibitory pathway is cooperatively coupled The extraocular muscles include the ipsilateral inferior rectus muscle and the contralateral superior oblique muscle
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The action of the excitatory pathway causes the superior rectus on the ipsilateral side (mainly upturned, followed by internal rotation and internal rotation), and the contralateral inferior oblique muscle (mainly external rotation, followed by upturn and external rotation) contraction, resulting in a vertical upward movement, slightly Slow eye movement with torsion (slow nystagmus), and then the center initiates a reflex saccade to produce rapid eye movement (fast nystagmus) in the opposite direction of the slow eye movement, that is, vertical downwards, slightly torsion (torsion) The component is very weak, sometimes difficult to distinguish between left and right) nystagmus
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At the same time, it inhibits the initiation of the pathway, which acts on the ipsilateral inferior rectus muscle (inferior rotation during contraction, followed by internal rotation and external rotation) and the contralateral superior oblique muscle (mainly internal rotation during contraction, followed by downward and external rotation) , Make its muscles relax, and assist the excitatory pathway to produce corresponding slow eye movements (see Figure 10-13)
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Figure 10 When DH test lies down and tilts the head 30°, the otoliths flow away from the ampulla and the affected side is excited
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    Figure 11 When sitting up directly to the upright sitting position without reduction, the otoliths flow to the ampulla, the affected side is inhibited, and the anterior semicircular canal coupled to the contralateral side is excited
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     Figure 12 Schematic diagram of the nystagmus induced by PC-BPPV on the right side (excited pathway) Figure 13 Schematic diagram of the nystagmus induced by PC-BPPV on the right side (inhibitory pathway) Dix-Hallpike of atypical PC-BPPV During the test, the otoliths in the posterior semicircular canal may be located in different positions of the lumen, such as the back arm, forearm, side of the crest cap tube, side of the crest cap capsule, near the total foot, etc.
, as shown in Figure 14
.

Figure 14 The red star indicates the position of otoliths.
When otoliths gather near the total foot due to coagulation, lumen incarceration, body position, etc.
, they may induce flow to the ampullae during the normal Dix-Hallpike Test and produce inhibitory stimuli on the affected side.
The posterior tube is inhibited, and the contralateral anterior tube is relatively excited, which produces jump torsional nystagmus, which is the same as the mechanism of reverse nystagmus after PC-BPPV sits up
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When the otoliths are located on the forearm of the posterior tube, the side of the crest cap tube, the side of the crest cap capsule, and the forearm, perform the Dix-Hallpike Test.
The otoliths drive the crest cap to deviate from the ampulla, forming a jump torsional nystagmus
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When located on the forearm of the posterior tube, the duration of nystagmus is generally less than 1min, and if it is located on the side of the crest cap tube, the side of the crest cap capsule, and the forearm, the duration of nystagmus is generally more than 1min
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 Summary To understand the vestibular anatomy and physiology related to BPPV, and to master its nystagmus formation mechanism on this basis, is to clinically identify the complicated and difficult BPPV affected side, determine whether the reduction is effective or not, analyze whether the otolith is transferred, and infer nystagmus inversion or residual The important prerequisite of the cause, only a deep understanding and proficient application of these basic mechanisms can further improve the overall reduction efficiency of BPPV patients
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 Thinking: 1.
Why does BPPV's nystagmus occur after the head movement stops? 2.
How to distinguish the atypical BPPV of the posterior semicircular canal from the BPPV of the anterior semicircular canal? 3.
What is the nystagmus mechanism of Dix-Hallpike Test induced by the contralateral side? 4.
A small number of PC-BPPV patients have jump torsion nystagmus after sitting up, how to explain? 5.
How to consider when both Dix-Hallpike Tests are down jump nystagmus? If you have any doubts about these questions, please pay attention to the "Dizziness" VIP dizziness advanced course launched by Director Chen on Yimaitong Knowledge Bank
.

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