Benign Paroxysmal Positional Vertigo (BPPV)
The first person to mention a BPPV was ADLER in 1897. BARANY then did it in 1910 and in 1921, tried to provide a first description. In 1952, DIX and HALLPIKE carried out a study of 100 cases and described the positioning manoeuvre to trigger a BPPV. SCHUKNECHT, in 1962 and 1969, provided a physiopathological explanation of cupulolithiasis.
In 1980, SÉMONT found a treatment to this disorder.
It is the most common form of vertigo; it represents around 30% of vertigo disorders in adults. BRANDT and DAROFF, in 1980, and TOUPET, in 1982, indicated that it is more common in women (around 60% of cases).
The ages most affected are those close to retirement; exceptionally, there are sufferers under twenty years of age. Bilateral forms represent 12% to 15% of all BPPV.
The forms that affect the horizontal semi-circular canal appear to represent about 8% of BPPV.
We estimate that 20% of BPPV are post-traumatic. The remaining 80% being idiopathic, even of there is a suspicion that vascular factors might be behind the degeneration of the utricular macula.
It is a veritable kink in the system of rotatory acceleration sensors (posterior or horizontal semi-circular canals) by the system of linear acceleration sensors (utricle). There is a detachment of the otoconiae (otoliths) with a part of the utricular macula attached.
Then, in a second stage, this "amalgam" or "sludge" finds its way to the interior of the offending semi-circular canal and carries out, as a result, a remote pressure or suction canololithiasis of the cupula of the SCC concerned. This well established concept stems from the hypothesis put forward by SCHUKNECHT (1969) explaining that BPPV via canalolithiasis where the otoconia mass pressed against or rather entered into the cupula via the interior or exterior of the canal.
The question and answer session informs us of a sudden onset of a truly violent, rotational vertigo. It often lasts between 10 and 30 seconds. A latency time of several seconds precedes this minor vertiginous crisis. The circumstances are as follows: a sudden change in position, for example rolling over in, or lifting one’s head (careful: the patient often evokes a pathogeny of the cervical rachis that certain practitioners do not hesitate to confirm when in fact it is nothing of the sort).
Also ensure with the triggering of a vertigo that you start from the initial position, which might evoke, for both the patient and the doctor, a contralateral vertigo instead of the real disorder. This vertigo is, on the one hand alarming, but also in certain cases, can provoke a reaction of the neurovegetative system or lead to nausea. The patient must carefully try to avoid any type of movement that will likely trigger their systems. And when they do manage to avoid BPPV, there is a risk of contractures of the pericervical muscles.
BPPV manifests itself through a torsional nystagmus beating towards the lower ear. The nystagmus fades away having reached paroxysm and is reversed upon return to the upright position. Functional explorations show no major anomalies.
The exploratory protocol and the treatment of BPPV are described in the section entitled Vestibular rehabilitation.
Some times, the crises persist but often in some six weeks, evolution is favourable even though relapses are frequent.
If the BPPV manifests itself several times a day over a relatively long period of time, it could result in a neurosensory disruption, the most common of which is scrolling syndrome with visual dependence and the omission of vestibular information.