Keywords
balance diseases - BPPV - Dizziness Handicap Inventory - video-oculography
Introduction
Vertigo and dizziness cover several multisensory and sensorimotor syndromes of various
etiologies and pathogenesis. It may be central or peripheral in origin.[1] Benign paroxysmal positional vertigo (BPPV) is a commonly recognized vestibular
disorder, accounting for approximately one-third of the cases. It is characterized
by brief periods of vertigo triggered by a changing head position relative to gravity.[2] The first clinical description of positional vertigo is attributed to Barany in
1921 and in 1952, Dix and Hallpike were the first to clearly describe the provoking
maneuvers.[3]
BPPV have an estimated lifetime prevalence of 2.4%. In studies of both young adults
and the elderly, a prevalence of 9% has been described.[3] The incidence of BPPV increases with age. BPPV is often unrecognized in older adults.
Epidemiologically, fourth and fifth decades of life are the most commonly afflicted
age groups but may also affect the younger population. There has been reported to
be higher incidence in females.[4]
BPPV affects the calcium carbonate crystals, otoconia, in the sensory organs of inner
ear, macula of utricle and saccule. They have a greater density than the surrounding
endolymph, thus making the macula sensitive to changes in linear acceleration and,
importantly, gravity. The semi-circular canals, in contrast, are sensitive to changes
in angular acceleration. In BPPV, otoconia from the utricle is thought to collect
in the semi-circular canals, making them abnormally gravity sensitive. The net result
is that changes in the head position with respect to gravity result in an abnormal
displacement of the cupula and stimulation of the corresponding vestibular afferents.
This results in the characteristically abnormal eye movements and vertigo.[3]
Most cases of BPPV are idiopathic in origin and probably result from the degeneration
of the macula. Some risk factors can increase its incidence such as old age, osteoporosis,
vitamin D deficiency, and vertebro-basilar insufficiency.[5] Several studies indicated the association between BPPV with osteoporosis and vitamin
D deficiency, implying that abnormal calcium metabolism may underlie BPPV.[6] Secondary causes of BPPV refer to identifiable causes of otoconial dislodgement.
These include otologic and non-otologic surgery, head trauma, vestibular neuritis,
and Meniere’s disease and sudden sensorineural hearing loss.[7]
Any of the semi-circular canals can be affected by BPPV, but in the great majority
of cases, only the posterior canal (80–90%) is involved although occasionally the
lateral (5–10%) and the anterior semi-circular canal (1–2%) is affected. Unilateral
BPPV is much more common than bilateral involvement. BPPV that simultaneously involves
multiple canals is rare and usually affects canals in the same labyrinth. The elicitation
of more than one pattern of nystagmus by the positional and positioning maneuvers
suggests a combined lesion that affects more than one semi-circular canal at the same
time.[8]
The definite diagnosis of BPPV requires diagnostic positional maneuvers that lead
to the observation of a canal specific positional nystagmus. Positional testing involves
the provocation of vertigo and nystagmus, and different maneuvers test different semi-circular
canals, e.g., DixHall Pike maneuver for posterior semi-circular canal, supine head
roll test for lateral semi-circular canal, supine head extension maneuver for anterior
semi-circular canal. A canal specific response is diagnosed when a rotation of the
head in the plane of a semicircular canal evokes positional nystagmus of maximal intensity
(in terms of slow phase velocity).
Frenzel goggles or video-oculography can be helpful, particularly when the nystagmus
is weak or momentary[9] The VNG examination provides a unique opportunity for the simultaneous quantitative
and qualitative assessment of both horizontal and vertical components of nystagmus.[10] It also assesses the function of the vestibular end organs, central vestibulo-ocular
pathway, and oculomotor processes.[11] The nystagmus in BPPV has a crescendo-decrescendo characteristic, and the fine ocular
responses, most of the time, are difficult to be seen through Frenzel glasses. Using
video-oculography, we can also record the characteristic of nystagmus. The ocular
responses on record can be repeatedly examined and analyzed, which ensures reliable
evaluation.[12]
An objective way to assess the impact of vertigo on the quality of life. The 25-item
Dizziness Handicap Inventory (DHI) was developed by Gary Jacobson and Craig Newman
to evaluate the self-perceived handicapping effects imposed by vestibular system disease.
The items were sub-grouped into three content domains representing functional, emotional,
and physical aspects of dizziness and unsteadiness.[13] Total scores range from 0 to 100 with increasing scores signifying greater perception
of handicap because of dizziness. The scoring for the dizziness handicap is done as
follows: 16 to 34 points (mild handicap), 36 to 52 points (moderate handicap), 54+
points (severe handicap)[14] ([►Fig. 1]).
Fig. 1 Dizziness Handicap Inventory Score.
Our study here aims at diagnosing more and more patients with complaints of vertigo
associated with head and neck movements suggestive of BPPV and managing it with repositioning
maneuver. This study also aims at measuring the Dizziness Handicap Inventory pre and
post repositioning maneuver and reducing handicap with directed management.
Methods and Materials
The patients presented to OPD or admitted in the Department of Otorhinolaryngology
and Head & Neck Surgery, Choithram Hospital & Research Center (CH &RC), Indore, Madhya
Pradesh, were included in the study after obtaining a written informed consent. History
was documented and clinical evaluation was performed to differentiate peripheral from
central causes of vertigo. Positional tests were undertaken to provoke BPPV. In those
subjects with a strong history suggestive of BPPV and the absence of nystagmus on
clinical positioning tests were further studied with video-oculography. Similarly,
those patients showing a classical single canal involvement but with atypical accessory
nystagmus (suspected of multi-canal involvement) were further evaluated with video-oculography.
With video Frenzel glasses, we documented the characteristic of nystagmus to isolate
the semi-circular canal/s that were involved in the causation of vertigo. Serum Vitamin
D levels were checked. The repositioning maneuver were performed subsequently for
respective canals. The Dizziness Handicap Inventory was documented pre and post repositioning
maneuvers.
As per the statistical calculations, 126 samples were included in the study.
Results
Majority of the patients were in the age group 51 to 60 (44 patients) years and 61
to 70 years (37 patients) and mean age of 53.07 ± 12.24 with female predilection (69
females and 57 males). In 81 (64.3%) patients, the posterior canal was involved and
Epley’s maneuver was performed for them; in 39 (30.9%) patients, the lateral canal
was involved, Barbecue roll maneuver was performed; in 26 (20.6%) patients, the anterior
canal was involved for which Yacovino maneuver was performed ([►Fig. 2]). Multi canal involvement was seen in 20 patients. Canal with more intense nystagmus
was reposited first.
Fig. 2 Distribution of BPPV according to canal involvement.
In 106 (84.1%) patients, only one canal was involved, while in 20 patients (15.8%),
multiple canals were involved. Left side was more common in lateral canal BPPV, whereas
the right side was found more common in posterior canal BPPV.
The mean pre-intervention Dizziness Handicap Inventory Score was 41.29 ± 15.90 and
the mean post-intervention Dizziness Handicap Inventory score was 14.84 ± 11.52. The
difference was found to be statistically significant (p = 0.001), showing a significantly lower post-intervention score ([►Figs. 3] and [4]). In the post-intervention period, at the end of 14 days, 84 (66.7%) patients were
totally asymptomatic, 31 patients (24.6%) had mild DHI score, while 11 patients (8.7%)
had moderate DHI score. In total, 95 patients (75.4%) required single repositioning
maneuver, 23 patients (18.3%) required two maneuvers, while 8 (6.3%) patients required
three maneuvers for relief. Theses maneuvers were repeated at an interval of 3 days.
Fig. 3 Comparison of pre- and post-intervention DHI severity score.
Fig. 4 Comparison of mean pre- and post-intervention DHI score.
Forty-five patients were taken for video-oculography. Twenty-five patients, who were
undiagnosed on clinical evaluation could be correctly diagnosed with video-oculography.
Rest 20 cases, the patients who showed a classical single canal involvement but with
atypical accessory nystagmus (suspected of multi-canal involvement) on clinical positional
testing were diagnosed as multi-canal involvement on VOG.
In our study, 117 patients had vitamin D levels below the normal range, 56 (44.4%)
patients had deficient levels (< 25 nmol/L), while 61 (48.4%) patients had insufficient
levels of vitamin D (25–75 nmol/L). Only nine (7.1%) patients had sufficient levels
(> 75 nmol/L) ([►Fig. 5]). None of the patients had vitamin D levels in the potentially toxic range. The
association between the vitamin D status and the number of maneuvers required was
found to be statistically not significant.
Fig. 5 Distribution as per vitamin D levels.
Discussion
BPPV is a subset of vertigo that is triggered with the stimulation of the vestibular
system. Most commonly, it is a disease of elderly women. The dizziness due to BPPV
causes moderate handicap in most cases and can be very easily treated with repositioning
maneuvers.
The diagnosis and the treatment of BPPV have been assisted with the invent of video-oculography.
The video Frenzel goggles help to pick up the weak nystagmus, which is not appreciated
by the naked eyes. The video Frenzel goggles allow us to record eye movements and
nystagmus both with and without fixation.
The studies by von Breveren et al, Furman et al, Swain et al, Shim et al found mean
ages of 49.4 (SD 13.8),[4] 54 years,[15] 41.4 years,[2] and 54.4 ± 14.8[16] respectively. These findings were consistent with our findings of mean age of 53.07
± 12.24 years. All these studies had shown female preponderance similar to our study.
Korres et al[17] and Balatsouras et al[18] had shown involvement of anterior canal BPPV in 1 to 2% cases, while Jackson et
al[19] and Lopez-Escamez et al[20] reported anterior canal BPPV in 21.2% cases and 17.14% respectively. The later findings
were consistent with findings of our study (20.6%).
Shim et al,[16] Tomaz et al,[8] Balatsouras’[18] and Lopez-Escamez et al[20] had reported multi-canal involvement in 4.6%, 1.5%, 9.3%, and 20% of cases, respectively.
In our study, multiple canals were involved in 20 out of 126 cases. Jackson et al,[19] Lopez-Escamez et al,[20],[21] and Maslovara et al[22] had shown importance of video-oculography in their studies for precise and accurate
diagnosis of anterior canal BPPV and multiple canal involvement. The use of video-oculography
has proven beneficial in our study too, where 45 cases out of 126 were diagnosed correctly.
Whitney et al and Martens et al,[23]
[24] van der Zaag-Loonen et al,[25] Nishino et al,[26] and Amrish et al,[27] have reported higher Dizziness Handicap Inventory score in cases of BPPV. This was
similar to the findings of our study with mean pre-intervention score of 41.29 ± 15.90
and the mean post-intervention score of 14.84 ± 11.52. Eighty-four patients were asymptomatic,
31 patients had mild DHI score, while 11 patients had moderate DHI score after repositioning
maneuver ([►Figs. 3] and [4]). The maximum pre-intervention DHI was found in cases of anterior canal involvement,
which was 44.31 ± 15.37.
Buki et al,[28] Jeong et al,[29]
[30] and Sheikhzade et al[31] had shown correlation between vitamin D deficiency and BPPV. These studies had also
reported to be higher recurrence rate of BPPV in vitamin D deficiency. In our study
also, 117 patients had vitamin D levels below the normal range. Fifty-six (44.4%)
patients had deficient levels (< 25 nmol/L), while 61 (48.4%) patients had insufficient
levels of vitamin D (25–75nmol/L) ([►Fig. 5]).
Conclusion
Video-oculography is a helpful tool in the diagnosis and treatment of benign paroxysmal
positional vertigo. It not only helps us to detect the weakest of nystagmus but also
correctly diagnose the involvement of canals. Dizziness Handicap Inventory is an objective
way to assess functional performance in patients having vestibular disease. The higher
number of asymptomatic patients in the post-intervention period in our study lead
us to conclude that repositioning maneuvers form the main stay treatment for BPPV.
Correction of vitamin D levels may help to reduce the occurrence of BPPV.
