Journal of the Neurological Sciences, 111 (1992) 229-230 © 1992 Elsevier Science Publishers B.V. All rights reserved 0022-510X/92/$05.00
L e t t e r t o t h e Editor
Benign paroxysmal positional vertigo (BPPV) or bubble provoked positional vertigo? A.G. Gordon London, UK (Received 9 December, 1991) (Accepted 6 April, 1992)
Sir, Brandt (1990) gives a very useful discussion of the mechanism of BPPV and a provides a thoughtful critique of Schulmecht's cupulolithiasis theory, which involves particles falling from the utricle onto the cupula of the posterior semicircular canal, thereby increasing its specific gravity. It has seemed intuitively to me that the phenomenon of BPPV is best explained mechanically by the movement of air bubbles inside the cochlea and labyrinth, and I was disappointed to see that Brandt did not consider this mechanism. This idea derived from the realisation that perilymph fistulas must be a very common cause of many otological, psychiatric and neurological syndromes (Gordon 1976). A mild head injury could easily cause a labyrinthine window rupture and air bubbles to enter the cochlea, leading to various auditory, vestibular or "post-concussional" symptoms (Gordon 1989). This idea is not in fact new: Meurman (1929) suspected that air bubbles were a cause of positional n~tagmus in experiments on rabbits° Epidemiological evidence in favor of this idea includes: (i) BPPV is common after mild head injury or ear surgery. (ii) It is associated with homolateral otitis media. I have proposed that many cases of otitis, especially if unilateral, are caused by leaks of perilymph or CSF into the middle ear (Gordon 1976). This provides a retrograde route for air bubbles. (iii) Prolonged bedrest or sleep predisposes to BPPV. This could allow air to build up in tissues around the labyrinth, especially if there is also hypotension or low labyrinthine pressure. (iv) Labyrinthine air bubbles have been found in humans complaining of vertigo a n d / o r
Correspondence to: A.G. Gordon, 32 Love Walk, London SE5 gAD, UK.
deafness after head injury or ear surgery (Bordure et al. 1990). Air could be easily missed, especially if there was a low index of suspicion. Previously, no one had reported air in the glenoid fossa after temporal bone fracture, yet Betz and Wiener (1991) found some there in 20% of cases. Also, pneumocephalus occurred in 19%. As for the actual mechanism of BPPV, the air bubble theory has many apparent advantages over competing theories: (1) The vertigo is positioning rather than positional. Slow head movement gives bubbles time to disperse or squeeze past obstacles, or they may simply lack the momentum to deflect the cupula, or they can creep round comers into a different trouble-free tract. (2) Vertigo is of delayed onset and builds in intensity. This is consistent with a slowly moving bubble (or string of bubbles) moving in a restricted channel. (3) Vertigo is of limited duration. Perhaps the bubbles have now squeezed past the cupula. (4) Vertigo reverses when the patient reverts to a seated position. The bubble(s) reverse(s) in direction. (5) Vertigo fatigues with repetition or provocative exercises. Constant movements will cause the bubbles to disperse to innocuous parts of the cochlea or labyrinth, or to be absorbed. (6) Vertigo occurs when the damaged ear is undermost. This allows the air an opportunity to rise upwards to deflect the cupula. (7) Vertigo derives from the posterior semicircular canal. In Barany's or Dix and Hallpike's manoeuvre of lateral head tilt, the anatomy and geometry dictate that the air bubble would traverse and rise in the posterior and not in the superior or horizontal canals. Air will only collect in restricted areas or pockets, and will only travel in circumscribed directions. Debris is found all over the labyrinth, so vertigo from this cause would be
230 expected in many head directions and from all canals. (8) Vertigo derives from an ampullofugal and not an ampullopetal stimulation of the posterior canal. Brandt points out this fatal flaw in Schuknecht's theory, which relies on heavy debris falling on the cupola. Air bubbles, however, approach the cupula from below, avoiding this problem. (9) BPPV is an intricate but stereotyped phenomenon. The movement of bubbles inside the membranous labyrinth will be more lawful and predictable than the dislodgement and adhesion of solid particles. The mechanism of BPPV is a complex problem of 3-D geometry and dynamics. The air bubble theory is simple and "feels" right, but I have not studied the problem in as much detail as Brandt. I would therefore be grateful if he could explain, preferably with detailed perspective diagrams, why he thinks the bubble theory is wrong, as I cannot see why myself. It is easy to make mistakes, as there are so many degrees of freedom that if one gets one parameter wrong or reversed, the whole explanation collapses like a stack of cards. This, p~surnably, is how Brandt would characterise Schuknecht's influential theory. Brandt (1991) still rejects gravity as the main cause of BPPV. The bubble theory
is simple and elegant and implicates the obvious causal canditate, i.e. gravity. It also dispenses with the ad hoc unexplained phenomenon of pos'trotatory overexcitability of a "heavy cupula".
References Betz, B.W. and M.D. Wiener (1991) Air in the temporomandibular joint fossa: CT sign of temporal bone fracture. Radiology,180: 463-466. Bordure, P., F. Legent, C. Calais, D. Loheac and C. Beauvillain (1990) Pneumolabyrinthe et fistule p~rilymphatique apr~:s stap~dectomie.Ann. Oto-Laryngol.,107, 359-362. Brandt, T. (1990) Positional and positioningvertigo and nystagmus. J. NeuroL Sci., 95: 1-28. Brandt, T. (1991) Man in motion. Historical and clinical aspects of vestibular function.Brain, 114: 2159-2174. Gordon, A.G. (1976) Perilymphfistula: a cause of auditory,vestibular, neurologicaland psychiatricdisorder. IVied.Hypoth.,2: 125134. Gordon, A.G. (1989) Post-concussionsyndrome(PCS). Aust. N.Z.J. Psych., 23: 154-155. Meurman, Y. (1929) Observations on some pressure phenomena accompanying artificial labyrinthine fistula. Acta Otolaryngol., 13: 552-571.