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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4606_Библиотеки_им_академика_М_И_Перельмана
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E. R. Anson and Y. Gimmon
Vestibular Symptom Quantication
It is essential to use objective and reliable tools to assess vestibular function for
patients with dizziness/vertigo such as the video head impulse test (vHIT) [60, 61],
video nystagmography (VNG) [62], and vestibular-evoked myogenic potentials
(VEMPs) [63, 64]. These physiological assessments are not only important for differential diagnosis, but help in developing a vestibular rehabilitation plan [65]. Of
equal importance, subjective symptoms should also be quantied using valid and
reliable tests [66]. The most common questionnaires characterize subjective dizziness (Dizziness Handicap Inventory [67]) and balance condence (Activity-specic
Balance Condence scale [68]). More specialized questionnaires may only deal
with complaints as specic as oscillopsia severity [21, 57] or the functional impact
of oscillopsia [58]. Other specic symptom scales include the Vertigo Symptom
Scale Short Form [69] and Vertigo Visual Analogue Scale [70, 71]. Here, we
describe some of the more common patient questionnaires used for individuals with
vestibular disease.
The Dizziness Handicap Inventory (DHI
perceived handicap resulting from dizziness symptoms after vestibular disease.
The DHI consists of 25 questions about daily activities and self-care grouped
into three domains representing functional, emotional, and physical aspects of
dizziness. A high DHI score is associated with an increased level of handicap,
range of score is 0–100 (higher scores are worse) [67]. In different populations
the criteria for important change varied between 3 points and 20 points depend-
ing on how meaningful change was determined [67, 72, 73].
The Activities-specic Balance Condence scale (ABC) is a self-report measure-
ment and patient’s rate their balance condence for performing 16 daily living
activities. The score ranges from 0, which indicates no condence, to 100, which
indicates complete condence in the participant’s ability to perform the task
without losing balance. The ABC has excellent test–retest reliability (r=0.92)
and scores of 67% or lower are associated with increased fall risk [68, 74].
The Vertigo Symptom Scale, Short Form (VSS-SF) is a self-report 15-item question-
naire that measures symptoms severity (balance disorders, autonomic arousal,
and somatic anxiety) within the past month. Each item is scored from 0 to 4.
Higher scores indicate more severe symptoms [75].
Vertigo Visual Analogue Scale (VVAS) is based on the pain visual analog scale but
modied for dizzy patients. Participants rate their dizziness level for 16 different
activities on a scale of 0–10 (higher scores are worse). It has excellent reliability
(0.85–0.96) and good validity (r=0.67) [70, 71, 76].
When conducting balance performance assessments for individuals with vestibular disorders it is critical to use an assessment that includes head and body motions
that manipulate sensory availability/reliability. Numerous examples of physical performance tests exist to characterize balance impairments in patients with vestibular
)—This validated scale evaluates the self-
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pathology. Two simple, easy to use, and widespread balance performance-based
measures are:
Timed Up and Go test (TUG): This clinical screening measure examines general
mobility and screens for fall risk. The individual stands up from a standard chair,
walks 3m at a regular pace, turns around, and walks back to the chair and sits
down. The patient can use a walking aid if needed. The average time to complete
two repetitions is the score with shorter performance time indicating better
performance. A performance time longer than 13.5s indicates higher fall risk
[77]. Whitney etal. (2004) showed that the fall risk cut-off score for patients with
vestibular disorders is >11.1s, with a sensitivity of 80% and specicity of 56%
in falls prediction [78].
Dynamic Gait Index (DGI): The DGI is an 8-item scale that was developed initially
to identify fall risk in older adults [79]. The DGI is a sensitive assessment tool to
identify people at risk of falls due to vestibular disorders [80]. Participants are
scored on an ordinal score (0–3) while performing a variety of ambulatory tasks
such as walking with head turns or walking around/over obstacles. Scores of 19
points or less indicates an increased risk of falling [80]. Some patients may score
above the 19 point cut-off, and may benet from a more challenging version of
the test known as the Functional Gait Assessment [81].
A nal category of behavioral tests that are helpful for identifying impairments
for individuals with vestibular disease evaluate behavioral performance of the
VOR.The most common and low tech clinically friendly version of these tests that
quantify gaze stability is the Dynamic Visual Acuity test (DVA) [82]. Computer
aided testing allows for separately evaluating (1) how small a target can be recognized at specied head velocities [83], (2) the fastest velocity that an object of specied size can be recognized [84, 85], and a combined evaluation of the VOR gain and
DVA [86, 87]. Here we briey describe the clinical version of the DVA.
Dynamic Visual Acuity (DVA) test: Vestibular hypofunction leads to impaired gaze
stability due to increased retinal slip during head movement. The DVA test is a
behavioral assessment of gaze stability [82]. The clinical DVA starts with an
evaluation of static visual acuity using a Snellen or EDTRS chart by asking the
patient to read the smallest line that they can see clearly without moving their
head. Then the patient is instructed to read the lines from the top down while the
examiner passively oscillates the patient’s head ±15° to 20° at 2Hz. A difference
of 2 lines or more between the static acuity and the dynamic acuity suggests
uncompensated gaze instability [88, 89]. Computerized versions of the DVA test
were found to be more valid [83].
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E. R. Anson and Y. Gimmon
Vestibular Conditions Manifesting These Symptoms
Unilateral Vestibular Hypofunction
Unilateral vestibular hypofunction (UVH) is the partial or complete loss of function
of one or more of the vestibular organs and/or vestibular nerves on one side [8, 30].
Acute unilateral vestibular hypofunction is most commonly due to vestibular neuritis but other causes include: trauma, surgical nerve transection, ototoxic medication,
vestibular schwannoma, superior canal dehiscence, or Meniere’s disease [8, 30, 90,
91]. Acute asymmetry in resting vestibular tone leads to sudden onset of vertigo,
nausea, and imbalance symptoms and transient spontaneous nystagmus [90, 92].
Although visible nystagmus and vertigo usually subside within hours to 14days,
uncompensated UVH results in imbalance, blurry vision with head movement, dizziness, spatial disorientation, and difculty with path instability when walking [92–
96]. UVH may affect a person’s ability to drive, perform typical daily activities, and
work [97, 98]. Negative changes in quality of life may also lead to secondary problems such as depression and anxiety as well as secondary deconditioning likely due
to reduction in activity participation [99–104]. Importantly, individuals with more
complete hypofunction may take longer to rehabilitate and may continue to report
subjective symptoms after apparent recovery of balance ability [65]. For some people, this may result in a chronic condition called persistent postural-perceptual dizziness (PPPD) [105, 106]. Vestibular rehabilitation is very effective at addressing
the impairments and symptoms related to unilateral vestibular hypofunction [6, 8].
Bilateral Vestibular Hypofunction
BVH is a condition caused by absent or reduced function of the vestibular organs
and/or nerves of both ears. Most instances of BHV are idiopathic [107, 108]. Other
causes of BVH include: trauma, aging, infectious disease, ototoxic medication,
bilateral Meniere’s disease, neurodegenerative disorders, autoimmune disease, and
congenital or genetic abnormalities [107–110]. Common symptoms include oscillopsia with head movement and imbalance, especially in the dark or on unlevel/
uneven surfaces [55, 57–59, 109]. Most individuals with severe BVH do not complain of vertigo. Individuals with BVH often experience difculty walking in the
dark [111]. Herdman and colleagues (2000) reported that about 50% of patient with
BVH had fallen since the onset of the vestibular decit [39]. Quality of life is often
negatively impacted and individuals with BVH report a high socioeconomic burden
due to work-related disabilities [41, 57]. Vestibular rehabilitation is effective at
addressing the impairments and symptoms related to bilateral vestibular hypofunction, although the rehabilitation duration typically takes longer and the level of
recovery may be less complete [6, 8].
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Benign Paroxysmal Positional Vertigo
Benign paroxysmal positional vertigo (BPPV) is one of the most common causes of
vestibular vertigo [112–114]. Loose otoconia dislodged from the utricle that end up
free-oating in the semicircular canals (canalithiasis) or attached to the cupula
(cupulolithiasis) are considered to be the primary cause of BPPV symptoms [115–
120]. BPPV symptoms of vertigo and imbalance are triggered by change in head
orientation to gravity (i.e., bending over, looking up, lying down, rolling in bed)
[121]. Thus, the methods for differential diagnosis depend on changes in head orientation while aligning a set of semicircular canals in the plane of gravity [122,
123]. Many factors including age, acute vestibular loss, and trauma contribute to
otoconia becoming dislodged [124, 125]. Although BPPV has been reported in
some children [126, 127], this is relatively rare and BPPV is much more common in
adulthood with prevalence increasing with age [125, 128, 129].
BPPV occurs in all three semicircular canals, with the posterior canal being most
commonly affected and the anterior canal being the rarest form, and each variant
has many distinct treatment options [130, 131]. It is paramount for clinicians to
accurately identify the affected semicircular canal since the canalith repositioning
treatments are canal specic [123, 131–133]. The Dix–Hallpike test is the clinical
standard for diagnosing posterior canal BPPV (see Fig.14.1) [122, 130, 134].
Some individuals may not be able to tolerate the traditional Dix–Hallpike positions, thus a modied testing position in side-lying was developed that can be used
in those instances (see Fig.14.2) [135–137].
The “Supine-Roll Test” (Fig.14.3) and/or the “Bow and Lean Test” are recommended for differential diagnosis of lateral canal BPPV [123, 138].
Readers are encouraged to reference the most current BPPV clinical practice
guideline for an extensive review of recommended differential diagnostics and
a b
Fig. 14.1 Example of Dix–Hallpike testing for BPPV on the right side, (a) shows the starting
position with the head rotated 45° to the right, (b) shows the testing position maintaining a 45°
rightward head rotation with 20° of neck extension. The testing position should be held for 30–60s
while waiting for symptoms or nystagmus. Infrared goggles can be used to improve visualization
of nystagmus as shown in (b)
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Fig. 14.2 Example of modied side-lying Dix–Hallpike testing for BPPV on the right side, (a)
shows the starting position with the head rotated 45° to the left to place the right posterior canal into
the plane of movement, (b) shows the testing position maintaining a 45° leftward head rotation with
20° of neck extension. The testing position should be held for 30–60s while waiting for symptoms
or nystagmus. Infrared goggles can be used to improve visualization of nystagmus as shown in (b)
E. R. Anson and Y. Gimmon
treatment strategies [130]. In this section we provide a brief overview of the most
commonly used diagnostic tests and the nystagmus characteristics typical for each
subtype of BPPV, see Table14.1. Selected treatment strategies are described later in
this chapter.
Vestibular Migraine
Vestibular migraine is a migraine in the company of vestibular symptoms. In the
past it was described by other terms such as migraine-associated dizziness, migraine
related vestibulopathy and migrainous vertigo. Today, the acceptable term by the
Barany Society and the International Headache Society is “Vestibular Migraine”
[139, 140]. Vestibular migraine is characterized by episodic events of vertigo and/or
dizziness and/or unsteadiness with or without experiencing other symptoms such as
nausea, tinnitus, sound sensitivity, light sensitivity, and visual disturbance [140,
141]. The symptoms can last for minutes to days with occurrences ranges from
every day to twice a year [142, 143]. Vestibular migraines can negatively affect an
individual’s activity and participation, reduce quality of life, lead to work absences,
and interfere with daily activities [142, 144]. Rehabilitation programs for vestibular
migraine are exercise-based. There is some evidence that symptoms and functional
abilities improve with vestibular rehabilitation [145–147]. However, vestibular
rehabilitation is relatively underutilized, and patients should also receive appropriate medical management for optimum results [143].
cd
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a b
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Fig. 14.3 Example of Supine Roll testing for lateral canal BPPV, (a) shows the starting position
with the head in midline and elevated 30°, (b) shows the testing position with the right ear down,
(c) shows the head back in the neutral midline position, (d) shows the head turned with the left ear
down. Each position should be held for 30–60s while waiting for symptoms or nystagmus. Infrared
goggles can be used to improve visualization of nystagmus
Persistent Postural-Perceptual Dizziness
Persistent postural-perceptual dizziness (PPPD) is a functional vestibular disorder,
not a structural or psychiatric vestibular disorder. PPPD is characterized with a persistent dizziness, nonspinning vertigo aggravated by postural challenges with
reported sensitivity to space-motion stimuli [105]. PPPD often develops after
peripheral or central vestibular disorders. However, it might also develop due to
vestibular migraine, panic or anxiety attacks, concussion, whiplash injuries and
even by autonomic disorders [148]. Many patients with PPPD report that upright
posture, standing and walking, worsen their symptoms [149, 150], interfering with
participation in typical daily functions. There is emerging evidence for the importance of vestibular rehabilitation to address the symptoms reported by patients with
PPPD [151–153].
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Table 14.1
Canal Positional test Nystagmus direction
Canalithiasis
Posterior Dix–Hallpike or
Lateral Supine Roll Test or
Anterior Dix–Hallpike
Cupulolithiasis
Posterior Dix–Hallpike or
Lateral Supine Roll Test or
Anterior Dix–Hallpike or
Summary of positional tests and nystagmus characteristics for different types of BPPV
side-lying
Bow & Lean
or
Deep Head Hang
side-lying
Bow & Lean
Deep Head Hang
Up-beating and geotropic
torsional nystagmus
Horizontal geotropic
nystagmus
Down-beating±geotropic
torsional nystagmus
Up-beating and geotropic
torsional nystagmus
Horizontal apogeotropic
nystagmus
Down-beating±geotropic
torsional nystagmus
Nystagmus
duration (s)
<60 5–20s
<60 5–20s
<60 5–20s
>60 Almost none
>60 Almost none
>60 Almost none
Nystagmus
latency
Concussion
Concussion is a mild traumatic brain injury, with a complex pathophysiological
process leading to rapid onset of short lived neurological impairments that typically
resolve spontaneously [154]. Etiology of dizziness postconcussion varies. Patients
might be dizzy due to post traumatic BPPV [155] or peripheral vestibular dysfunction [156]; however, video head impulse testing suggests lateral semicircular canal
function remains intact for many concussed adolescents [157, 158]. Whether from
central or peripheral pathology gaze stability is impaired postconcussion [156, 159,
160]. Oculomotor functions such as smooth pursuit, saccades, convergence motion
of the eyes and accommodation are frequently abnormal after a mild head injury
[161], leading to symptoms of dizziness. In many cases posttraumatic migraine with
aura of dizziness/vestibular migraine might be a result of concussion [160]. Most
patients postconcussion return to their prior level of functional within days to weeks,
yet some patients have prolonged recovery that may be associated with psychiatric
comorbidities such as anxiety, social withdrawal, inter personal sensitivity, and
fearfulness [162–164]. Concussed individuals experiencing dizziness, imbalance,
and oculomotor symptoms benet from symptom management using vestibular
rehabilitation [165–168].
Mal de Debarquement Syndrome (MdDS)
MdDS, sickness of disembarkation, is a subjective perception of an oscillatory sensation of swaying or rocking [169–171]. Possible triggers for MdDS are disembarking from a moving water, air or land-based vessel (boats, airplanes, trains, etc.)
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[169]. History of migraine, stress, medication changes, and sleep deprivation serve
as contributing factors [169]. Symptoms include persistent motion when standing or
lying down, especially with eyes closed. Symptoms often abate slightly during
movement like walking or driving [169]. MdDS patients report reduced condence
during activities of daily living [172]. There are some promising technology driven
treatments for MdDS, but at the moment they remain primarily experimental [173–
176]. Traditional vestibular rehabilitation has been used to address the symptoms of
MdDS; however, reports of effectiveness are inconsistent and additional research is
needed [177, 178].
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Symptom-Based Treatment Approaches
Education
Patient education is a key element in vestibular rehabilitation. Patients are educated
about their symptoms and impairments, the underlying mechanism of their pathology, potential risks, and the importance of symptom provocative treatment strategies improving patient buy-in and participation in home exercises [179]. In addition,
patient education facilitates better self-management of aggravating factors [6].
Hillier and McDonnell reported in their Cochrane review that even a minimal
approach to patient education enhances the effectiveness of vestibular rehabilitation [7].
Positional Vertigo
Benign paroxysmal positional vertigo (BPPV) is one of the most common forms of
vertigo [114], and the primary treatments for BPPV emphasize using gravity to
reposition otoconia debris from the affected semicircular canal [130]. Here we discuss canalith repositioning treatments for the most common subtypes of BPPV followed by a brief discussion on habituation as a less preferred form of treatment
for BPPV.
As we mentioned earlier, the most common type of BPPV involves loose otoconia in the posterior semicircular canal, diagnosed by the Dix–Hallpike test. The two
most common treatment approaches for canalithiasis are the Epley (canalith repositioning) maneuver and the Semont maneuver [133, 180–183]. A description of the
performance for the canalith repositioning maneuver (Epley) and the Semont
maneuver are provided in the captions for Fig.14.4 (Epley) and Fig.14.5 (Semont).
The efcacy (>85%) of the Epley and Semont maneuvers have been shown to be
equivalent when combining the results of two studies [180]. Current evidence supports canalith repositioning treatments as having greater efcacy over other techniques such as the Brandt–Daroff exercises [184].
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E. R. Anson and Y. Gimmon
c
d
e
Fig. 14.4 Example of the Epley treatment for left posterior canal BPPV, (a) shows the starting
position with the head turned 45° to the left, (b) shows the second position with the left ear down
and approximately 20° of neck extension, (c) shows the third position with the right ear down
(head turned 45° to the right) and approximately 20° of neck extension, (d) shows the fourth position in side-lying with the right ear down and approximately 10° of neck exion, (e) shows the nal
position seated at the edge of the mat. Each position should be held for 30–45s after vertigo/nystagmus stops
ab
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c
Fig. 14.5 Example of the Semont treatment for right posterior canal BPPV, (a) shows the starting
position with the head turned 45° to the left, (b) shows the second position with the right ear down
and approximately 20° of neck extension, (c) shows the third position with the nose and left ear
down and approximately 10° of neck exion, (d) shows the nal position seated at the edge of the
mat. Transitions between positions are fast with abrupt stops to dislodge stuck on otoliths. Positions
b and c should be held for 1–2min each after vertigo/nystagmus stops
d
The second most common form of canalithiasis involves the lateral or horizontal
canal. The differential diagnosis is based on horizontal (head referenced) nystagmus
during the Supine Roll Test [123]. The Bow and Lean Test can be helpful in determining the affected ear [138]. Lateral canal canalithiasis can be treated with either
the Supine Roll technique or the Gufoni (Vannucchi) maneuvers [185, 186]. A
description of the performance for the Supine Roll technique and the Gufoni maneuver are provided in the captions for Fig.14.6 (Supine Roll) and Fig.14.7 (Gufoni).
The least common form of canalithiasis involves the anterior canal [187]. There
are two recommended treatment techniques to address canalithiasis involving the
anterior canal. The Epley maneuver has been successfully applied to treat anterior
canalithiasis [188], and more recently a technique developed by Yacovino and colleagues has met with similar success [189]. The overall effectiveness of these techniques for resolving positional vertigo complaints is >75% [187]. A description of
the performance for the deep head hanging maneuver is provided in the captions for
Fig.14.8.
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