Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4606_Библиотеки_им_академика_М_И_Перельмана

A few years later in 1956, Drs. John Lindsay and Garth Hemenway at the University of Chicago studied patients with acute unilateral vestibular losses fol­lowed by positional vertigo, and noted that the utricle was not the source of posi­tional vertigo spells following those losses, because their cases had a total loss of utricular function. They correctly surmised that the problem lay in the posterior semicircular canal or saccule, since these were the only structures undamaged in the ears they studied [4].

Dr. Harold Schuknecht, Chief of Otolaryngology at the Massachusetts Eye and Ear Inrmary, published a 1962 paper that identied the posterior semicircular canal as the site of the problem and provided a mechanism for the disorder [5]. He posited correctly that particles within the inner ear, probably otoconia, moved into the canal and affected the cupula. He proposed that cupulolithiasis, particles adher­ent to the cupula in the affected canal, cause the attacks. This is may be true for a small subset of patients with BPPV but did not explain the more typical attacks.

The fact that particles could be moved by gravity and were in an open-ended canal suggested the possibility that they could be removed without surgery. A year later, Dr. John Epley devised a clever maneuver to remove these particles from the posterior canal, and over time demonstrated its efcacy [7]. A series of other maneu­vers have since been devised.

Velocity storage affects the responses to BPPV.Natural horizontal head rotations are larger and more prolonged than vertical head rotations and velocity storage is thus greatly enhanced for the horizontal canals compared to the vertical canals [14]. These differences tend to enhance the vertigo and nystagmus of H-BPPV compared to the anterior and posterior canal forms.

Horizontal canal BPPV (H-BPPV) caused by free-oating particles is often more violent than the posterior canal variety and more likely to cause vomiting. Onset is usually while performing maneuvers for P-BPPV [15]. After a successful P-BPPV maneuver that has displaced particles back into the utricle, repeating the Dix– Hallpike maneuver places the horizontal canal immediately below the removed par­ticles. They can then easily reux into the utricular arm of the horizontal canal. Since this canal has its greatest response to ampullopetal uid motion, reux causes intense stimulation. The patient sees the room spin horizontally, exhibits consider­able distress, and may vomit within as little as 30s. Rotating the head while supine will set off additional spells with reversals in nystagmus direction. Nystagmus in H-BPPV is usually characterized as either geotropic (beating toward the oor), or apogeotropic (beating away from the oor/toward the ceiling). The nystagmus tends to last longer than P-BPPV, sometimes exceeding 1min.

Canalith jam can result in a prolonged blockage of the canal with a spontaneous nystagmus and canal paresis on caloric testing, or can be reversible [17, 19, 21]. It can result in an apogeotropic positional nystagmus, and thus can mimic cupuloli­thiasis [17]. Free-oating particles trapped in the ampullary arm by a narrowed area in the canal could alternately lodge in the narrowing to form a jam, then dislodge and move into the ampulla and directly impact the cupula. This type of reversible jamming results in an apogeotropic positional nystagmus and so may not be easily distinguished from cupulolithiasis.

Once placed in the head hanging position, there is a brief latency of a few to several seconds, followed by the onset of a torsional up beating nystagmus follow­ing a crescendo-decrescendo pattern that peaks and declines over 10–60s [22]. The velocity of the nystagmus is very brisk. The upward most eye is easiest to view and is best used to analyze the nystagmus. The axis of rotation of this eye is located in the upper medial quadrant of the upward eye near the iris edge if the pupil is cen­tered, resulting in a mixed torsional and upbeating nystagmus (Fig.7.5(1)), but the position of the rotational axis in the upper quadrant of the globe does not change with pupil movement [23]. If the pupil of the upward eye is moved toward the rota­tional axis nearer the medial canthus, the nystagmus becomes more purely torsional, and as it is moved away from the rotational axis toward the lateral canthus, it tran­scribes a wider arc and thus the nystagmus becomes more vertical. During success­ful maneuvers, the torsional and upbeating nystagmus continues as particles are rotated ampullofugally and out of the canal. On repeated Dix–Hallpike, a torsional upbeating nystagmus will be seen if some particles remain in the canal. The appear­ance of a new, ne downbeating nystagmus on Dix–Hallpike after a successful maneuver indicates that removed particles are reuxing back into the posterior canal through the common crus. This can also occur if particles are not completely removed during a maneuver, allowing them to reux back toward the ampulla when the patient sits up. Particles trapped within the ampulla will result in a persistent positional nystagmus that resembles classic torsional upbeating nystagmus when supine or in head hanging, but milder and prolonged greater than 1min. When the patient is raised to the upright seated position and then bent forward with the face down, the nystagmus reverses to a ne downbeating nystagmus [24].