BPPV
Benign paroxysmal positional vertigo (BPPV)
The main symptom of BPPV is a vertigo lasting seconds precipitated by a change in head position relative to gravity (with the offending ear down, e.g., turning over in bed, looking up to a high shelf, getting out of or into bed), or rarely by linear acceleration (elevator, car). Patients are almost always symptomatic after rolling over in bed. Patients often describe a tumbling, rolling, cartwheeling sensation, with nausea, vomiting and imbalance. They may have persistent dysequilibrium that diminishes as the day goes on. Symptoms are maximum for days to weeks, usually resolves in months, but may recur.
On exam a transient burst of a mixed vertical (upbeat) and torsional (the superior pole of the globe beats toward the side of the dependent ear) nystagmus, usually appearing after a latency of several to 30-45 seconds, and then quickly subsiding, is characteristic of the inappropriate excitation of the posterior semicircullar canals (SCC) that produces typical BPPV. There may also be a small horizontal component with quick phases directed away from the affected ear. Note that if Frenzel lenses are not used during testing for BPPV the torsional component may be more prominent since the vertical (and the small horizontal) component is more easily suppressed by fixation mechanisms. This circumstance, then, is an exception to the rule that pure torsional nystagmus indicates a central lesion. On reassuming the upright position, nystagmus due to BPPV may transiently reappear but it is usually directed oppositely to that in the dependent position. With successive repetitions, the nystagmus of BPPV usually becomes harder to elicit. To summarize the main findings in BBPV
Positional testing may also alter a spontaneous nystagmus. With an acute unilateral loss of labyrinthine function, the horizontal component of the spontaneous nystagmus is increased with the patient lying with the affected ear down and decreased with the affected ear up. In general, patient with an acute unilateral loss of labyrinthine function will lie with the affected ear up.
BPPV is usually due to the posterior SCC becoming gravity sensitive. The usual explanation is that debris, probably otoconia dislodged from the macula of the utricle, is "stuck" in the long arm of the posterior SCC leading to a position-induced, rather than an angular motion-induced flow of endolymph, and hence the inappropriate sense of rotation. This hypothesis is based on the findings at surgery when the posterior SCC is to be plugged, the effectiveness of surgical treatments on the posterior SCC as well as the success of physical therapy maneuvers.
Causes of BPPV include 1)head trauma, which may be mild such as whiplash injuries, 2)prolonged bedrest or assuming unusual postures with the head supine, and 3)as a sequel to a viral or ischemic labyrinthitis involving the structures innervated by the superior division of the vestibular nerve or irrigated by the anterior vestibular artery (anterior and lateral SCC and the utricle). In many patients, especially the elderly in whom BPPV is very common, there is no clear inciting event.
How to treat BPPV. Particularly effective is the Epley maneuver -- slow (abrupt 90deg increments and wait 15-30 secs.) roll of head from offending ear down to offending ear up and then slow rise. Sit up for 48 hr., do not sleep on bad side. In very rare cases a surgical procedure -- now canal plugging, previously a singular nerve section -- is needed. Lateral canal BPPV can be treated with a 270 deg body roll (beginning supine and rolling 270 deg to finish at the bad ear down position) or by simply having the patient lie down for 12 hours, or so, with the bad ear up. Note that a posterior canal BPPV may be converted to a lateral canal BPPV, and vice versa.
Other information can be found at:
Tim Hain's web site
AAN's Guide Lines
The main symptom of BPPV is a vertigo lasting seconds precipitated by a change in head position relative to gravity (with the offending ear down, e.g., turning over in bed, looking up to a high shelf, getting out of or into bed), or rarely by linear acceleration (elevator, car). Patients are almost always symptomatic after rolling over in bed. Patients often describe a tumbling, rolling, cartwheeling sensation, with nausea, vomiting and imbalance. They may have persistent dysequilibrium that diminishes as the day goes on. Symptoms are maximum for days to weeks, usually resolves in months, but may recur.
On exam a transient burst of a mixed vertical (upbeat) and torsional (the superior pole of the globe beats toward the side of the dependent ear) nystagmus, usually appearing after a latency of several to 30-45 seconds, and then quickly subsiding, is characteristic of the inappropriate excitation of the posterior semicircullar canals (SCC) that produces typical BPPV. There may also be a small horizontal component with quick phases directed away from the affected ear. Note that if Frenzel lenses are not used during testing for BPPV the torsional component may be more prominent since the vertical (and the small horizontal) component is more easily suppressed by fixation mechanisms. This circumstance, then, is an exception to the rule that pure torsional nystagmus indicates a central lesion. On reassuming the upright position, nystagmus due to BPPV may transiently reappear but it is usually directed oppositely to that in the dependent position. With successive repetitions, the nystagmus of BPPV usually becomes harder to elicit. To summarize the main findings in BBPV
- Mixed vertical-torsional nystagmus, slow phases downwards and top of eyes roll away from offending (dependent) posterior SCC.
- Nystagmus more vertical when looking toward the up ear, and more torsional when looking toward the down ear.
- Nystagmus more vertical in the up eye; more torsional in the down eye.
- Latency (up to 45 sec), transient (usually less than 15 sec), decreases with repetitive testing.
- Reverses direction on sitting up.
Positional testing may also alter a spontaneous nystagmus. With an acute unilateral loss of labyrinthine function, the horizontal component of the spontaneous nystagmus is increased with the patient lying with the affected ear down and decreased with the affected ear up. In general, patient with an acute unilateral loss of labyrinthine function will lie with the affected ear up.
BPPV is usually due to the posterior SCC becoming gravity sensitive. The usual explanation is that debris, probably otoconia dislodged from the macula of the utricle, is "stuck" in the long arm of the posterior SCC leading to a position-induced, rather than an angular motion-induced flow of endolymph, and hence the inappropriate sense of rotation. This hypothesis is based on the findings at surgery when the posterior SCC is to be plugged, the effectiveness of surgical treatments on the posterior SCC as well as the success of physical therapy maneuvers.
Causes of BPPV include 1)head trauma, which may be mild such as whiplash injuries, 2)prolonged bedrest or assuming unusual postures with the head supine, and 3)as a sequel to a viral or ischemic labyrinthitis involving the structures innervated by the superior division of the vestibular nerve or irrigated by the anterior vestibular artery (anterior and lateral SCC and the utricle). In many patients, especially the elderly in whom BPPV is very common, there is no clear inciting event.
How to treat BPPV. Particularly effective is the Epley maneuver -- slow (abrupt 90deg increments and wait 15-30 secs.) roll of head from offending ear down to offending ear up and then slow rise. Sit up for 48 hr., do not sleep on bad side. In very rare cases a surgical procedure -- now canal plugging, previously a singular nerve section -- is needed. Lateral canal BPPV can be treated with a 270 deg body roll (beginning supine and rolling 270 deg to finish at the bad ear down position) or by simply having the patient lie down for 12 hours, or so, with the bad ear up. Note that a posterior canal BPPV may be converted to a lateral canal BPPV, and vice versa.
Other information can be found at:
Tim Hain's web site
AAN's Guide Lines