Scientists may have pinpointed a microscopic reason why people suffering from the most common type of vertigo experience a distinct time lag between a rapid head motion and the onset of dizziness. The explanation, the researchers say, could be that it takes five to six seconds for minuscule crystals in the inner ear to sediment after the head moves suddenly, an event that can set a dizzy spell in motion.
The team of engineers and physicians from Harvard University, the California Institute of Technology, and Northwestern University reports in the August issue of the Journal of Biomechanics on a mathematical model they’ve developed to support this theory on the cause of benign paroxysmal positional vertigo (BPPV).
“While BPPV is not life-threatening, it induces disorientation that is severely discomforting and can cause nausea and accidents,” says Howard A. Stone, Harvard College Professor and Gordon McKay Professor of Chemical Engineering and Applied Mechanics in Harvard’s Division of Engineering and Applied Sciences. “We used hydrodynamic models to show that if tiny particles in the inner ear become dislodged, which researchers have previously posited as the trigger for BPPV attacks, the period of time for these particles to fall far enough to adversely impact pressure within the inner ear roughly matches the typical lapse between a head tilt and onset of vertigo.”
BPPV is a mechanical disorder originating in the vestibular system within the inner ear, where three fluid-filled semicircular canals detect head rotation about each of three axes. Many researchers believe BPPV attacks are triggered when calcite particles called otoconia, which normally reside in the inner ear, dislodge and interfere with proper functioning of these semicircular canals. The disorder is characterized by a lag of several seconds between a rapid head movement and the onset of a debilitating spinning sensation.
Along with Harvard undergraduate (now GSAS graduate student) Michael S. Weidman, Todd M. Squires at Caltech, and Timothy C. Hain of Northwestern, Stone examined whether this delay might coincide with movement of otoconia. Their fluid-modeling work showed that the latency characteristic of BPPV nearly matches the amount of time it would take for loose otoconia to detrimentally affect pressure within the semicircular canals of the vestibular system.
“Otoconia are tiny, generally just a minute fraction of a millimeter, but still large enough to cause disruptions in the inner ear,” Stone says. “The otoconia settle over a period of five to six seconds to a point where the semicircular canals undergo a significant reduction in radius, increasing the pressure within the semicircular canals and possibly leading to dizziness.”
BPPV is also known as “top-shelf vertigo,” since attacks are often prompted by a sudden tilting back of the head, as if to look at objects on a high shelf. It is the most commonly diagnosed type of vertigo, with some studies suggesting that it affects 9 percent of older individuals. Treatment for BPPV is purely mechanical, involving a set of head motions (a common version is called the Epley maneuver) that are believed to flush otoconia from the sensitive semicircular canals.
Hain, a medical scientist who studies motor control of the head and neck, originally sought Stone’s assistance in studying the possible role of fluid dynamics in BPPV. Stone says that he, Squires, and Weidman, none of whom are physicians, bring a different perspective to a medical ailment that’s largely mechanical in nature. In addition, Stone and his collaborators are able to provide other quantitative insights useful for characterizing BPPV.
“This is a new way of thinking for the medical community, which tends to look at problems differently than engineers or physicists might,” he says. “Because of its mechanical nature, BPPV may be an illness that requires a degree of cooperation between physicians and engineers.”