Objectives To assess the efficacy of the particle repositioning maneuver (PRM) in patients presenting with idiopathic benign paroxysmal positional vertigo (BPPV) compared with those with evidence of additional peripheral vestibulopathies.
Methods Retrospective administration of the Dizziness Handicap Inventory (DHI) to 41 patients with primary BPPV and 31 patients with secondary BPPV to subjectively evaluate their symptoms before and after the PRM.
Results Both groups indicated a marked improvement in symptoms after the PRM. Only two patients reported an increase in their symptoms after the PRM and both had secondary BPPV.
Conclusions The PRM was found to be highly effective in all forms of BPPV, but careful history and judicious testing may identify patients requiring additional intervention to relieve their symptoms.
Benign paroxysmal positional vertigo (BPPV) is a disorder of the semicircular canals characterized by free-floating debris thought to be displaced otoconia. It is the most frequently encountered disease among patients with balance complaints. 1–3 The diagnosis rests on the appropriate history and demonstration of compatible nystagmus with the Dix-Hallpike test. 4,5 The posterior semicircular canal is most commonly involved. 1,6
Many authors have noted that BPPV can be found in isolation, termed idiopathic BPPV, or in combination with, and possibly a consequence of, other vestibular disorders. 4,7–10 The expression of BPPV as a consequence of the vestibular insult has temporally varied from 1 week to 20 years after the initial injury. 7,8 The most frequent association is with significant head trauma, but several progressive degenerative vestibular disorders have been found to result in the clinical syndrome of BPPV. It has been speculated that otolith infarction resulting from various vestibular pathologies liberates free-floating particles into the endolymphatic space. 11 The clinical findings suggest that the posterior semicircular canal has been spared by the initial vestibular insult or has recovered function. 8 We prefer to term isolated, idiopathic BPPV “primary” BPPV and BPPV associated with other vestibular disorders “secondary” BPPV.
The excellent response of patients with BPPV to various liberatory maneuvers has been well documented. 8,9,12–14 Cure rates of approximately 90% can be expected with a single treatment session. 1,2,11 Few data exist regarding the utility of these maneuvers in patients with other concurrent vestibular derangements. 15 Most series have grouped patients with isolated BPPV together with subjects displaying other abnormalities on history, clinical examination, or vestibular testing. The profound effect of other vestibulopathies on balance function is well known. 2
The goal of our study was to evaluate the efficacy of the particle repositioning maneuver (PRM) on the balance function of patients with primary and secondary BPPV using the Dizziness Handicap Inventory to assess their subjective response. 16,17 The concurrent vestibulopathies found among these patients as well as the specifics of patients who did not meet with success will be reviewed.
MATERIALS AND METHODS
A retrospective chart review was conducted for patients presenting to the Mercy Hearing and Balance Center between October 1996 and March 1999 with a final diagnosis of BPPV. Only patients with documented BPPV on physical examination or objective testing were included. Subjects were restricted to those with unilateral disease displaying the characteristic delayed onset, fatigable torsional-vertical nystagmus characteristic of posterior semicircular canalithiasis. 2 A minimum of 1 month follow-up was required. All patients underwent the PRM as described by Parnes and McClure 18 on the initial visit and underwent repeat PRM on subsequent follow-up visits only if they continued to have objective evidence of BPPV on Dix-Hallpike testing. 4 No other neurotologic therapeutic interventions were carried out before the conclusion of the study (vestibular rehabilitation, medications, surgical intervention, etc.). On the conclusion of therapy, patients were asked to complete a pretreatment and posttreatment Dizziness Handicap Inventory (DHI) 16 to subjectively assess their response to treatment.
Patients were divided into two groups by history, physical examination, and objective testing. Those individuals who displayed positive unilateral Dix-Hallpike test results, without other abnormalities on complete neurotologic examination, historical evidence of peripheral vestibulopathy, or recent (<3 mo) head trauma were categorized as having primary BPPV. Patients were considered to have secondary BPPV if, in addition to the described positive Dix-Hallpike test results, they showed evidence of unilateral peripheral vestibular weakness on neurotologic examination (abnormal head thrust, head-shake with Frenzel lenses, strong rotation on Fukuda stepping test, spontaneous or gaze-evoked nystagmus, abnormalities on neurologic examination), strong history of peripheral vestibular disturbance (prolonged or nonpositional vertigo, with or without auditory symptoms, severe, recent head trauma, symptoms of progressive neurologic disease or cerebrovascular insufficiency), or objective evidence of unilateral or bilateral abnormalities on cochleovestibular testing (electronystagmography, rotational chair testing, computerized dynamic posturography, or fluctuating or unilateral sensorineural hearing loss).
The data were analyzed using the InStat software (GraphPad Software, San Diego, CA.). The Kolmogorov-Smirnov test for normality was used on each data set to determine whether parametric or nonparametric comparisons could be employed. Box and whisker plots were developed to display the results.
Of 121 patients identified, 72 met the inclusion criteria. Forty-one patients were categorized with primary BPPV, and 31 with secondary BPPV. Table I lists associated vestibular disorders found in patients categorized as having secondary BPPV. The majority had historic evidence of a viral vestibular insult, reporting a single distinct episode of the acute onset of vertigo, nausea, and emesis lasting days to weeks. Those with a demonstrable sensorineural hearing loss in the involved ear received a diagnosis of labyrinthitis (19%) and those without a loss received a diagnosis of vestibular neuritis (26%). Patients without a clear history of an acute vestibular insult but with objective evidence of a unilateral auditory deficit or vestibular weakness in the ear displaying BPPV were categorized as having progressive idiopathic vestibulopathy (13%). Patients with significant recent head trauma (skull fracture, concussion, loss of consciousness) accounted for 13% of the group.
Table Table 1.. Other Vestibular Disorders in Secondary Benign Paroxysmal Positional Vertigo (BPPV).
Table II shows the demographics and response to treatment in each group. The average age for both groups was 61 years. A female preponderance was found in both groups. With an average of 10.6 and 9.2 months' follow-up, both groups had an equivalent number of PRMs. All data sets had a normal distribution except for the posttreatment scores in the primary BPPPV group. The pretreatment and posttreatment DHI was slightly higher among patients with secondary BPPV, but both groups reported a large improvement in their DHI, averaging 28 points in patients with primary BPPV and 34.3 points in those with secondary BPPV.
Table Table 2.. Patient Demographics and Treatment Outcome.
Statistical analysis revealed a highly significant difference in the pretreatment and posttreatment DHI in primary BPPV (P < .0001, Wilcoxon matched-pairs signed-ranks test) and secondary BPPV (P < .0001, paired t test). The pretreatment DHI was statistically different between the primary and secondary BPPV groups (P = .03, unpaired t test), but the posttreatment scores were not (P = .3, Mann-Whitney test). There was no significant difference in the improvement in DHI between the groups (P = .2, unpaired t test).
There were a few patients in both groups who did not follow this trend. One patient with primary BPPV failed to show an improvement in the DHI. This was a 74-year-old woman with a history of hypertension, hyperlipidemia, coronary artery disease, and anemia who was found to be normal on neurotologic examination except for left BPPV. The PRM was performed successfully on the first visit with complete resolution of the positional nystagmus on post-PRM Dix-Hallpike testing. The patient reported no change in her DHI. Further neurotologic evaluations were negative for other vestibular disorders. No patients with primary BPPV reported an increase in their DHI.
Two patients with secondary BPPV had an increase in their DHI. One patient reported control of positional symptoms but continued dysequilibrium. This was an 88-year-old man with cardiac and cerebrovascular disease with several abnormalities on neurotologic work-up (falling gain and failure of fixation suppression on rotational chair testing, surface-dependent pattern on computerized dynamic posturography, small vessel ischemic changes on contrast head computed tomography). A 57-year-old woman with abnormal caloric tests on electronystagmography and panic disorder reported no improvement after PRM despite resolution of nystagmus on follow-up Dix-Hallpike testing.
Two patients with secondary BPPV reported no change in their DHI. A 74- year-old woman with a history of otosclerosis in the involved ear and abnormalities on neurotologic testing (asymmetric sensorineural hearing loss, abnormal phase and gain on rotational chair testing) required PRM on two separate visits because her Dix-Hallpike test results were positive. She failed to note improvement on DHI despite clinical evidence of resolution of the positional nystagmus. A 73-year-old woman reported 1 week of relief of positional symptoms after left PRM. She had a history of whiplash injury and head trauma from a motor vehicle accident in 1989. Prior neurotologic examination had shown a positive contralateral right Dix-Hallpike test in 1990. Past medical history included breast cancer, insulin-dependent diabetes, and hypertension. Physical examination showed severe cervical spine arthritic degeneration, positive Romberg and cerebellar abnormalities. Results of post-PRM Dix-Hallpike tests were negative.
Summary parameters (Table III) and graphic representation of the results in box and whisker format 19 are shown in Figure 1. A significant benefit from the PRM can be clearly seen in both groups with a sharp decline in the median DHI in both primary and secondary BPPV. Although the pretreatment and posttreatment DHI was higher in the secondary BPPV group, the relative gain (improvement) in this group was larger, with a median gain of 34 points as opposed to 26 points in the primary BPPV group. There is less dispersion of the results in posttreatment DHI in both groups.
Table Table 3.. Summary Parameters.
The effectiveness of PRM in relieving the vertigo associated with BPPV has been repeatedly demonstrated. It is a simple therapeutic maneuver and is contraindicated only in patients with high-grade carotid stenosis, unstable heart disease, or severe neck disease. 2 A 15% per year recurrence rate has been noted by Furman and Cass. 2 The end-point for success in most studies has been the elimination of nystagmus during repeat Dix-Hallpike testing and the subjective relief of positional vertigo. 1,7,12,20 Our study demonstrates the impact of the PRM on the patients' subjective sense of improvement in the context of their overall balance disorder utilizing the DHI and evaluates its comparative utility in subjects with concurrent vestibular disorders.
The results of this study substantiate the excellent control of positional vertigo obtained with the PRM and also demonstrate a more global improvement in perceived balance function. This is demonstrated by the predictable improvement in the DHI in both forms of BPPV and suggests that patients not only suffer from acute episodes of vertigo but also have more persistent disruption of their sense of balance. The motion sensitivity of patients with active BPPV has been documented and thought to be secondary to either cupulolithiasis or the free movement of otoliths in the endolymphatic space with head movement. 2 In patients with secondary BPPV, uncompensated vestibular imbalance, fluctuations in vestibular function, and central disorders augment the sense of imbalance.
Unlike other investigators, we found the most common associated vestibular disorder in patients with secondary BPPV to be viral inner ear infection as opposed to head trauma. 2,7,21 However, this may reflect the fact that we restricted the diagnosis of secondary BPPV to patients with proximate and severe head trauma to reflect the impact of vestibular concussion on their syndrome. It should be noted that Katsarkas and Kirkham 22 found no association between the severity of head injury and the development of BPPV.
The average age in our study (61 years) is comparable to other studies 7,23 and may reflect the degenerative nature of this disorder, particularly in primary BPPV. A female preponderance was also found, although the significance of this is not clear.
The higher pretreatment DHI scores in patients with secondary BPPV reflect the additive impact of concurrent vestibular disorders on this population and quantitate this effect relative to the subgroup with primary BPPV. The slightly higher posttreatment scores in patients with secondary BPPV illustrate the residual impact of these vestibular disorders, because no treatments beyond the PRM had been instituted at the time of data collection. It is likely, however, that the few cases reporting an elevation in posttreatment DHI reflect fluctuations in their underlying vestibular disorders, rather than representing a negative effect of the PRM on their status. Atypical forms of BPPV have been found to have a more prolonged clinical course and less favorable prognosis. 15 The findings suggest that an excellent response to the PRM can be anticipated in all forms of BPPV.
The PRM is effective in improving the subjective assessment of balance function in patients with both primary and secondary BPPV. Patients with secondary BPPV may require additional testing and treatment for optimal outcome.