AJCC Jan 2000 |
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An Adjustment for Dizzy Patientsby Gregg J. Carb, D.C. and Al Ueda, D.C. (Pictures not available online at this time) Vertigo,
or dizziness, is a disturbance in which the patient has a subjective
impression of movement in space (subjective vertigo) or of objects
moving around him (objective vertigo), usually with a loss of
equilibrium.1 Benign Paroxysmal Positional Vertigo, or BPPV, is probably
the most common cause of vertigo, and may be accompanied by nausea,
vomiting, and ataxia, along with the classic presence of nystagmus (a
rhythmic oscillation of the eyes in a horizontal, vertical or rotary
direction). The vertigo and concomitant nystagmus are precipitated by
certain critical positions of the head, usually when the patient lies
flat with the head turned to one or the other side, and most often
begins after a latency averaging 3 to 4 seconds and lasts about 30 to 40
seconds.2
Positional nystagmus may occur with end-organ (vestibulocochlear)
or CNS lesions. The two can generally be differentiated by the latency,
fatigability and limited duration of the response in BPPV vs. that of
CNS lesions. Some of the symptoms experienced in BPPV patients overlap
those of another condition, VertebroBasilar Insufficiency (VBI), which
is of concern to chiropractors considering manipulation of the cervical
spine. VBI is a condition affecting the brainstem, thus the additional
presence of diplopia (double vision), dysarthria (slurred speech) and
paresthesias (abnormal sensations) of the extremities may help to
identify those cases. Nevertheless, learning to recognize and
conservatively treat BPPV will simplify your approach in managing dizzy
patients—especially those also in need of traditional chiropractic
care. Anatomical
Review of the Inner Ear
The internal ear is otherwise referred to as the
vestibulocochlear organ, and is involved with the functions of sound
reception and maintenance of balance. It is buried in the petrous
portion of the temporal bone. The internal ear consists of the
membranous labyrinth, which contains endolymph and the end organs for
hearing and balancing. The membranous labyrinth is surrounded by
perilymph and suspended within the bony labyrinth. The bony labyrinth is
composed of three parts, the cochlea, the vestibule and the semicircular
canals. The cochlea is the part of the internal ear that is concerned
with hearing. The vestibule is an oval bony chamber containing the
utricle and saccule and is continuous anteriorly with the cochlea and
posteriorly with the semi-circular canals. The vestibule and
semi-circular canals are concerned with balance.
In the membranous labyrinth are a series of communicating ducts
and sacs that contain a watery fluid called endolymph. The endolymph
circulates within a closed system of sacs and ducts within the
membranous labyrinth. The semi-circular canals are connected to a
chamber called the utricle, which itself is connected to the saccule.
The utricle and the saccule have a specialized area of sensory
epithelium called a macula. The hair cells in the macula are innervated
by the vestibulocochlear nerve. The maculae are primarily static organs
for signaling the position of the head in space, but also respond to
tilting movements and linear acceleration.
There are three semi-circular canals, anterior, posterior and
lateral, which are set at right angles to each other and occupy the
three planes in space (XYZ). Each semi-circular canal comprises about
two-thirds of a circle and at one end forms an expansion called the
ampulla. In the semi-circular canals, the ampulla contains a sensory
area called a crista. On top of this crista is a gelatinous mass, called
the cupula. The cristae are sensors of movement, recording flow of the
endolymph in the ampulla that result from rotation of the head in the
plane of the canal. Upon motion of the head, endolymph fluid flows from
the semi-circular canal into the ampulla, bending or deflecting the
cupula to one side, depolorizing hair cells and sending the appropriate
signal to the vestibular nerve. The
Cause of BPPV
The pathophysiologic mechanism of BPPV is theoretical. It is
generally agreed that this disease arises from the posterior
semicircular canal and that symptoms are provoked when this structure is
positioned coplanar with gravity (vertical to the ground) with the head
in a dependent position. The leading theory behind BPPV is dubbed the
canalithiasis theory, first offered by Hall.3 It is proposed that dense
particles, presumably dislodged utricular otoconia, are free with the
endolymphatic space of the posterior semicircular canal. When the
Hallpike position (see below) is assumed, particle migration in the
canal leads to a temporary hydrodynamic pull on the cupula (in other
words, a small tidal current is created). The cupula is deflected,
leading to vestibular nerve excitation. Once the particles have reached
the most dependent position of the posterior semicircular canal (bottom
of the “loop”) and have halted their migration, the hydrodynamic
pull is stopped and the elastic restorative force of the cupula returns
it to a normal position. This would explain the short duration of the
nystagmus typically seen with patients. Repeat positioning could lead to
dispersion of the particles throughout the canal such that the resultant
hydrodynamic pull is reduced to a level below that of the elastic
restoring force of the cupula. Thus, cupular deflection would not take
place with repeat Hallpike maneuvers, leading to the clinically observed
phenomenon of response fatigability.
(Dix and Hallpike devised a positioning test to provoke the
classical nystagmus. The test consists of initiation of a critical
position with the affected ear dependent, rotatory nystagmus in the
plane of the ipsilateral posterior semicircular canal, latency of onset
after assumption of the critical position (3-4 seconds), reversal of
rotatory nystagmus with return to the upright position, and habituation
or response decline on repeat testing.)4 Conservative
Treatment for BPPV
Epley5 devised a technique for coaxing the dense particles out of
the posterior semicircular canal, from the cupula at one end around and
into the utricle at the other, by way of adjusting the position of the
patients head through a series of maneuvers. The patient is brought into
the standard Hallpike position, with the affected ear dependent and the
neck slightly extended. The head, still in a dependent position, is
rotated to the contralateral side so that the affected ear is now
superior. The patient is then rolled over onto the hip and shoulder of
the nonaffected side, facing downward 135 degrees from the supine
position. The patient is then brought back to a sitting position, while
the head remains turned contralateral to the affected ear. The head is
then turned forward, with the chin down 20 degrees. The procedure is
repeated until no further nystagmus is seen or until no progress in the
resolution of nystagmus is apparent for two consecutive cycles.
Additionally, a bone-conduction vibrator is applied to the ipsilateral
mastoid during the procedure to mobilize any adherent dense particles.
Harvey et al6 modified Epley’s technique by starting the same,
except the patient is held in the Hallpike position (supine, neck
extended, 45 degrees of rotation to the affected side) for two minutes
after nystagmus subsides. Then the head, remaining dependent in slight
extension, is rotated in 15-20 degree increments, each followed by a
rest period of 30 seconds. After the patient’s head is rotated 135
degrees to the opposite side, the patient is brought onto the hip and
shoulder of the nonaffected side and the head is further rotated to
accomplish a full 180 degree arc from the starting position. Finally,
the patient is slowly brought up to a sitting position and the head
turned back to the primary position. The patient is instructed to avoid
quick head turns and the supine position for 48 hours and to avoid lying
with the affected ear dependent for one week. A
Case History (presented by Dr. Ueda) Patient:
B. Gordon, 69 year old male Chief
complaint: Carpal tunnel pain and dizziness when shaving with the
patient’s neck in extension with right rotation. Chiropractic
manipulation of the spine and hand resolved most of the carpal tunnel
pain and the patient no longer was sleeping with his carpal tunnel
splint. Cervical adjustments had no affect (positive or negative) on the
dizziness. History
of vertigo: Insidious onset but had been constant for at least the last
18 months. Patient would have to sit for about 5 minutes before rising
out of bed to avoid falling down. Treatment:
Hallpike maneuver was performed to locate BPPV side. Left Hallpike
caused slight to moderate vertigo with a latency time of 10 seconds.
Patient demonstrated slight nystagmus on the left side. Canalith
repositioning maneuver was done on the left side repeatedly until
dizziness disappeared. Head rotation was at intervals of 15° per 20
seconds. He was instructed to sleep no lower than a 45° incline angle
for two days. Canalith repositioning was done again the following day.
The patient could not sleep sitting up and finally laid flat. The
patient estimates an 80% reduction in symptoms of vertigo and some
mornings without any vertigo. Total resolution of vertigo while shaving.
No chiropractic adjustments of any kind were done on either of these two
visits. References 1.
Merck Manual, 14th ed. Merck & Co., Rahway, NJ. 1982. 2.
T. Brandt, R. Daroff. Physical Therapy for Benign Paroxysmal Positional
Vertigo. Arch Otolaryngol 106; Aug 80. 3.
S. Hall et al. The Mechanics of Benign Paroxysmal Positional Vertigo. J
Otolaryngol 8; 1979. 4.
R. Dix, C. Hallpike. The Pathology, Symptomatology, and Diagnosis of
Certain Common Disorders of the Vestibular System. Proc R Soc Med 54;
1952. 5.
J. Epley. The Canalith Repositioning Procedure: For Treatment of Benign
Paroxysmal Positional Vertigo. Otolaryngology - Head and Neck Surgery 6.
S. Harvey, T. Haim, L. Adamiec. Modified Liberatory Maneuver: Effective
Treatment for Benign Paroxysmal Positional Vertigo. Laryngoscope 104;
Oct 1994. |