Discussion
This is the first report of a prospective, randomised trial investigating therapist-led management of post-traumatic BPPV in acute settings. One of our feasibility aims was to determine the safety of undertaking therapy-led BPPV assessment and treatment in patients with acute TBI. We believe the results show that assessment and treatment procedures are safe in this population as (1) no serious adverse events were reported, (2) the frequency of adverse events is in line with previous rigorously conducted BPPV trials21 and (3) intervention monitoring criteria noted procedures were undertaken consistently and accurately between sites and therapists. This is an important finding given previous research has highlighted clinicians’ concerns regarding the safety of managing post-traumatic BPPV.10 Patient and therapist acceptability of assessment and treatment procedures, important for future implementation, will be reported separately.
In this study, BPPV was present in just over a third of acute TBI patients who were identified, eligible and agreeable to positional testing, a slightly lower figure than previously cited.13 This may be due to different recruitment criteria and a lower proportion of moderate-severe TBI in the present trial compared with other research.13 Based on previously published data, a higher rate of BPPV would be expected in a sample with a higher, overall TBI severity.7 Data from this study noted repositioning manoeuvres seemingly provided greater BPPV resolution. Interestingly, Brandt–Daroff exercises did not provide superior resolution compared with advice, perhaps due to the higher numbers of patients with more complex BPPV in the Brandt–Daroff group compared with the advice group. A larger, more definitive trial would be required to confirm the superior effectiveness of repositioning manoeuvres versus advice and Brandt–Daroff exercises.
We noted some interesting features of post-traumatic BPPV. Skull fracture and, in particular, temporal bone fracture, were significantly associated with the presence of BPPV, replicating findings from a previous single-centre study in TBI.7 The rate of bilateral BPPV in the present study is somewhat higher in comparison to previous subacute studies,35 36 a factor, alongside skull fracture, which was also linked to BPPV recurrence. The overall recurrence rate of BPPV in the present study is not dissimilar to previous research.14 36 However, recurrences noted in our data occurred during a much shorter follow-up period. Therefore, the optimal timing of treatment for patients at risk of recurrence remains unclear. Until this is established, we propose that the best clinical practice would be to closely monitor patients with bilateral or more complex BPPV and consider the provision of earlier follow-up. The mechanisms of BPPV recurrence are intriguing. An animal model of TBI showed persistent otoconial shedding over 12 weeks post-injury,15 while histopathological evidence noted degeneration of the utricle and semi-circular canals.37 If there are ongoing processes inimical for recovery of inner ear structure and function via inner ear hair cell regeneration or degeneration, then a single, acute repositioning treatment for patients with post-TBI BPPV may well be insufficient. We speculate the link noted between bilateral BPPV and/or skull fracture and recurrence is mediated by the amount of force sustained to the head at the time of injury. Higher forces may worsen inner ear ultrastructural damage and/or brain injury and, thus, lead to more protracted or less complete recovery.
Lastly, the lack of symptom reporting before and during diagnostic BPPV testing (ie, vestibular agnosia) in this study supports the need for objective, examination-based screening and treatment of post-traumatic BPPV, rather than traditional symptom-based screening. Indeed, symptomatic screening for BPPV found 6% BPPV rates38 versus 58% obtained by examination in moderate-to-severe TBI survivors in a rehabilitation setting, of whom less than 10% had vertigo symptoms.39 We previously showed that vestibular agnosia is linked to disrupted central brain circuits,13 40 which in turn is linked to TBI severity. Thus, differences in cohort TBI severity affect vestibular agnosia rates.
Our findings reveal that patients with acute post-traumatic BPPV had reduced gait speed compared with community-dwelling patients with idiopathic BPPV.8 There is currently little data on gait speed in patients with acute moderate-severe TBI, but it is likely there is a deleterious effect of BPPV on gait function that depends in part on the degree of brain injury. Gait speed is a known risk factor for falls in patients with8 and without BPPV.41 Compared with patients with idiopathic BPPV, post-traumatic BPPV patients are more likely to be at increased risk of falls, yet have less vertigo symptoms due to TBI-linked vestibular agnosia.13 In our study, almost 20% of TBI patients had a fall during the 12-week follow-up period, with 64% of fallers having active BPPV. The feasibility nature of the study did not allow us to investigate the underlying mechanisms of these falls; however, this would be a key aim of a future, larger trial. A recent systematic review and meta-analysis of community-dwelling patients with idiopathic BPPV noted repositioning manoeuvres reduced falls and improved gait speed.8 Similarly, data from the present study demonstrated repositioning manoeuvres were associated with BPPV resolution, increased gait speed and improved balance confidence. Given that secondary falls in TBI survivors carry significant morbidity and mortality,6 modifying fall risk, for example, by treating BPPV, could be considered critical.
The 2023 UK NICE acute head injury guidelines11 do not mention the need for BPPV assessment. However, in light of the findings that post-traumatic BPPV is highly prevalent,2 7 linked to falls (and thus morbidity and mortality) and not always associated with vertigo,13 we recommend a screening approach for BPPV in all those with acute TBI, but particularly patients with skull fracture or those with moderate-severe TBI. Previous studies have noted that trauma ward therapists23 and doctors working in emergency areas42 can be trained and mentored to manage BPPV. However, much implementation work remains to be undertaken in both trauma and accident and emergency settings for such skills to be embedded in practice. Given the link between post-traumatic BPPV and skull fracture noted in this, and a previous study,7 one approach could involve healthcare professionals who work in an accident and emergency setting assessing acute TBI patients for positional nystagmus and, if positive (regardless of cause), referring patients for a CT head scan and for a more complete vestibular neurology assessment. Further, specific work conducted in emergency areas is needed to validate this theory. A gold-standard approach might be for hospitalised acute traumatic brain injury patients to be assessed by a ward vestibular team (eg, comprising neurologist, therapist and vestibular scientist and other specialists with relevant expertise), since the complex balance problems affecting TBI patients typically combine peripheral and vestibular dysfunction, and are complicated by other neurological injury (brain, spine, muscle, peripheral nerve) and interactions with medication, including anti-epileptics43 and opiates.44
Limitations
We recognise several limitations of our study. Despite the multi-centre design, the catchment population of our London (UK) trauma units limits generalisability. The self-reported dizziness measures used were predominantly designed for community-dwelling patients. An appropriate acute vestibular questionnaire is currently lacking and would be necessary for a future trial. Videonystagmography was not used to verify acute BPPV diagnosis; however, this is not mandatory as per the Barany Society criteria.22 It is possible that the overall BPPV frequency was underestimated as we did not routinely obtain videonystagmography; however, the therapists were trained by the research team, and videos were recorded of the therapists performing diagnostic and therapeutic manoeuvres, which confirmed diagnostic and treatment fidelity (see video). Despite this, some variation in the overall frequency of BPPV is expected given its link to TBI severity.7 Small variations in BPPV frequency between cohorts would not have affected the feasibility study’s aims and objectives. It is possible that some of our cohort who suffered a fall had undiagnosed pre-morbid idiopathic BPPV and, thus, may have been wrongly classified as having post-traumatic BPPV. A large proportion of patients who denied pre-morbid dizziness reduces this likelihood, although previous BPPV cannot be fully discounted due to the cognitive impact of TBI, for example, retrograde amnesia.