The vestibular outcomes in non-blast related traumatic brain injury and the role of severity, aetiology and gender: a scoping review

Abstract

Introduction:

Traumatic brain injury (TBI) can lead to various vestibular impairments. This review explored common vestibular outcomes associated with non-blast related TBI and examined possible differences in vestibular outcomes based on TBI severity, aetiology, and gender.

Methods:

A scoping review was conducted using an established methodological framework, which involved electronic and manual searches of databases and journals. Records published in English were included which focused on vestibular outcomes and assessments associated with non-blast related TBI in individuals 18 years and older. Out of a total of 19.200 records, 50 met the inclusion criteria. Data were collated and categorised based on the objectives of the research.

Results:

Benign paroxysmal positional vertigo (BPPV) was found in 38% of 50 studies. Furthermore, despite normal peripheral vestibular function, central processing disorders such as impaired self-motion perception and sensory integration dysfunction were also observed in TBI patients. TBI severity did not have a consistent effect on vestibular outcomes, while in terms of aetiology BPPV was observed to be more common in falls related TBI. Gender differences in vestibular findings were limited and varied across studies.

Conclusion:

The complex nature of TBI, combined with the intricate structure of the vestibular system, makes it difficult to establish a clear framework on the vestibular outcomes following TBI. Additionally, the use of different vestibular assessment methods across studies and the inconsistent reporting of outcomes complicates the holistic analysis of the data. Therefore, in order to better understand and manage the effects of TBI on the vestibular system, it is crucial to develop standardised clinical practices and assessment guidelines.

1 Introduction

Traumatic Brain Injury (TBI) is a widespread cause of death and disability worldwide (1, 2). TBI, with its associated physical, behavioural, cognitive and emotional deterioration (3–5), not only adversely impacts the quality-of-life of individuals but also causes a global burden on states due to the costs it incurs (6). It is estimated that the annual cost of TBI in the United Kingdom (UK) alone is 15 billion pounds (7).

Different methods are used for classifying the severity of TBI. Commonly, the Glasgow Coma Scale (GCS) at the time of injury and the duration of post-traumatic amnesia are employed for classification of TBI as mild (GCS: 13–15; post-traumatic amnesia: <24 h), moderate (9–12; >24 h), or severe (3–8; >7 days) (8). For TBI cases presenting to the hospital, more than 90% are classified as mild TBI (9). The common causes (aetiologies) known to lead to TBI include motor vehicle accidents (MVA), falls, sports-related injuries, assaults (all of these also known as non-blast related) and explosions (blast-related). The mechanisms of brain injury can vary across different aetiologies, particularly between blast-related and non-blast related TBI. In blast-related TBI, damage occurs due to the high-pressure waves generated during the explosion, whereas in non-blast related TBI, damage is typically observed as a result of a blunt force trauma to the head, concussion, or penetration (10). Due to this fundamental distinction and the different damage that would be related to distinct vestibular issues, the focus of this review will be on non-blast related TBI.

Dizziness, vertigo and imbalance stand out as some of the most commonly reported issues associated with TBI. The prevalence of dizziness and/or vertigo post-TBI was found to be between 23.8 and 81% (11, 12). The unpredictable damage caused by TBI to the brain can complicate the detection of the exact source of resulting vertigo and/or dizziness complaints. However, anatomically, TBI can lead to these symptoms by causing damage to the peripheral and central vestibular systems, brainstem pathways, as well as visual, motor, and oculomotor pathways (13). For example, currently, the most commonly reported peripheral vestibular disorder post-TBI is Benign Paroxysmal Positional Vertigo (BPPV) (14–16).

Despite the availability of many studies related to vestibular outcomes associated with TBI, there is a need for a comprehensive review synthesising common vestibular findings related to non-blast related TBI, including the relationship of TBI aetiology, severity and gender with vestibular conditions. A review conducted for this purpose can contribute to the development of diagnostic and treatment methods in this patient group, helping to identify appropriate and effective strategies for addressing vestibular complaints. Thus, a wide range of benefits can be achieved in the long term, from improving individual quality-of-life to alleviating the economic burden on states.

The aim of this study is to map and synthesise the literature on vestibular impairments associated with non-blast related TBI, with specific consideration of the potential influence of injury severity, aetiology, and gender.

In particular, the research questions are:

• i) What are the common vestibular assessments and impairments of TBI,

• ii) Whether vestibular outcomes vary according to severity of TBI,

• iii) Whether vestibular outcomes vary according to aetiology of TBI,

• iv) Whether vestibular outcomes vary by gender following TBI.

To address these broad and diverse research questions, map the literature, summarise the findings, and synthesise evidence from more than one study design, a scoping review was selected as the most appropriate approach (17, 18).

2 Materials and methods

This scoping review followed the 6-stages framework developed by Arksey and O’Malley (18). These stages were conducted in the following order: (1) identifying the research question(s), (2) identifying the relevant studies using appropriate keywords, (3) selecting relevant studies through an iterative scanned title, abstract, and full text, (4) extraction and charting the data, (5) collating, summarising and reporting of the results, (6) clinician review. The review was conducted in accordance with the PRISMA-S guidelines (19) (see Supplementary Appendix Table 1 for PRISMA-ScR Checklist).

2.1 Identifying the research question(s)

The research questions (listed above) were developed collaboratively with team members based on existing knowledge and literature in the field.

2.2 Identifying relevant studies

2.2.1 Eligibility criteria

To be included, records had to report studies involving adults (≥18 years old) with non-blast related TBI, focusing on vestibular outcomes and assessments. This included self-reported vestibular outcomes if vestibular impairment was clinically confirmed. If articles reported both auditory and vestibular outcomes, only the vestibular components were included. Records were eligible if they reported symptoms or assessment pre-treatment and were sourced from cohort studies, randomised control trials, case series, and case studies, as well as from grey literature such as dissertations and theses. In studies where treatments (e.g., Epley or Semont manoeuvre) were applied, the follow-up assessments were not reported in this review. Only initial (pre-treatment) assessments, including any follow-up conducted before treatment were reported. All records included in the study were published in English language and were available in full text. Cases that did not meet our inclusion criteria were removed from the case series studies.

Records were excluded if the studies were reporting adults who may have experienced blast-related TBI, whiplash injuries or non-TBI conditions (e.g., strokes, acoustic neuroma), TBI in childhood or with pre-existing audio-vestibular disorders prior to TBI, or where the aetiology of TBI was unspecified. Records were also excluded if they did not clearly define TBI or did not report structural injury or functional impairment resulting from TBI or only reported auditory condition without any assessment of vestibular outcomes or broadly focused on balance assessments rather than vestibular-specific tests. Records reporting the reliability and validity of tests, animal studies, review articles, including systematic reviews, book chapters, qualitative research studies and any sources presenting protocols, personal/expert opinions or tutorials were excluded.

2.2.2 Search strategy

The research strategy was developed by the research team and was supported by a medical information specialist (Dr Farhad Shokraneh). The search was conducted following Cochrane Handbook (20) and Cochrane’s MECIR (21) and PRESS guideline for peer-reviewing the search strategies (22). Electronic databases were searched, including Embase, MEDLINE, ProQuest Dissertations & Theses A&I, PsycINFO, Science Citation Index Expanded and SPORTDiscus. Initial searches were conducted in May 2022. An additional database search of Cochrane Central Register of Controlled Trials (CENTRAL) was conducted in November 2025. The search strategy included keywords on TBI, auditory and vestibular conditions (a separate review was conducted for auditory outcomes). These were reviewed and revised following a primary search (see Supplementary Appendix Table 2 for search strategy). Specific search term strategies were employed across each search engine, covering article topics, titles, abstracts, and keywords. Filters were implemented to select articles written in English language and involving human participants only, when feasible. No limitations were imposed on the search timeframe. Additionally, manual searches of reference lists and prominent journals, identified using the interquartile rule for outliers, were conducted to identify additional eligible documents. The final database and manual searches were conducted in November 2025.

2.3 Study selection

Records retrieved from electronic searches were transferred to EndNote (version X9), containing citation, title, and abstract, where duplicates were eradicated. Four researchers (KB, KF, LE, OP) independently screened the records via Rayyan (23), initially scrutinizing the title and abstract, followed by a review of the full text. Lead researcher (KB) was responsible for screening all records. The records obtained as a result of the manual search were subjected to full-text screening. In instances of discordance regarding the eligibility of any record, reviewers deliberated on their reasons until an agreement was reached, or a third reviewer (VK) was consulted to achieve a majority decision.

2.4 Extraction and charting of the data

A data extraction form was created and developed in Microsoft Excel and piloted on five included records and was subsequently modified following team discussions. Data from each record was extracted by the lead researcher (KB) and checked by KF. Data were extracted on study characteristics, study population, TBI characteristics, vestibular complaints and assessments/outcomes, and limitations (Box 1).

2.5 Collating, summarising and reporting results

Extracted data were collated and categorised depending on the objectives of our research. Each relevant study was grouped according to categories such as vestibular outcomes, severity of TBI, aetiology, and gender effects. Data were then summarised to highlight common patterns and significant variations in vestibular outcomes.

2.6 Clinician review

Following the identification of categories, categorised findings were reviewed by clinicians (LE & VK).

3 Results

The process of record identification and selection is in the PRISMA flow diagram (Figure 1). Electronic searches were produced in an initial set of 19,188 records. After removing duplicates, 12,561 records remained and of these, 12,024 were excluded during the title and abstract screening due to not meeting the eligibility criteria. Manual searches identified a further 12 potential articles which were subjected to full-text screening. Of the remaining 549 records, a further 499 records were excluded at the full-text screening. Most commonly the studies excluded did not report TBI or clearly define TBI, included participants under 18 years old and did not report TBI aetiology. Full-text records could not be located for 31 records. None of these records could be traced, regardless of support from the University of Nottingham librarian. The electronic and manual searches resulted in a final list of 50 eligible full-text records for data collection.

Figure 1

3.1 Study characteristics

Table 1 summarises the characteristics of the study and participants. Among the 50 included articles, the most commonly reported study design was case report(s)/case series (27/50, 54%) (24–50). The other study designs are shown in Table 1. Articles were published from 1956 to 2024. Studies were mainly conducted in the United States (n = 19), followed by the UK (n = 4) and Australia (n = 4) (Table 1).

3.2 Participant characteristics

Across 50 records, 1,793 participants were included. Of these, 1,218 were in the patient group (all group participants who had TBI, whether they had symptoms or not), whilst 575 were in the control group (either healthy controls or with vestibular symptoms). Pre-TBI status or history of participants are shown in Table 1, however this information was not consistently reported across all studies. Assessment time since injury varied widely across studies, ranging from as early as 2 days (24) to an average of 584.5 days (51) (Table 1). Four sports-related concussions studies included a pre-session baseline assessment (52–55). In 8 studies, follow-up/s’ assessments were performed after the initial time of injury before any treatment was offered (24, 25, 28, 31, 34, 38, 40, 49).

3.3 Overview of vestibular assessments and impairments following non-blast related TBI

Many different symptoms were reported in included studies, from brief dizziness experienced with changes in head position to prolonged dizziness and vertigo accompanied by nausea. These symptoms were assessed using a variety of tests and patient-reported outcome measurements (PROMs). The following sections briefly describe the vestibular assessments, PROMs and findings. A detailed summary of the assessments and PROMs is presented in Supplementary Appendix Table 3, and the results are demonstrated in Table 2. The vestibular impairments reported in the records are presented in Supplementary Appendix Table 4.

3.3.1 Dynamic positional tests

The Dix-Hallpike manoeuvre (56, 57) and the side-lying manoeuvre are used in the differential diagnosis of both peripheral and central types of positional vertigo and posterior and anterior semicircular canals (SCCs) BPPV. The Roll manoeuvre is used to diagnose horizontal SCC BPPV (57). The Dix-Hallpike manoeuvre was reported in 18 studies (25, 30, 38, 40, 43, 46, 49, 50, 52, 58–66) and the side-lying manoeuvre was used in one study (65), whilst both the Dix-Hallpike and Roll manoeuvres (horizontal SCC manoeuvre/supine head turning) were applied in 8 out of the 18 records (25, 46, 52, 59, 63–66). In one study, participants were prospectively audited for the presence or absence of BPPV without any manoeuvres (67), whilst in another study, participants were retrospectively monitored (68).

Positive results in favour of BPPV were observed in 16 out of 18 records in which the Dix-Hallpike and Roll manoeuvres were applied (25, 30, 38, 40, 46, 49, 50, 58–66). Posterior SCC BPPV was reported in 11 of these studies (25, 30, 40, 46, 50, 58–60, 64–66). Horizontal (lateral) SCC BPPV was observed in 6 records (25, 46, 59, 63, 64, 66). Furthermore, the two audit studies, one prospective and one retrospective, Calzolari et al. (67) and Taylor et al. (68) reported the presence of BPPV in participants. Ottaviano et al. (32) reported left post-traumatic benign positional vertigo without specifying the manoeuvre used.

3.3.2 Oculomotor assessment and/or nystagmography (ENG/VNG)

Oculomotor assessment provides a detailed examination of the neurological pathways associated with oculomotor function (69). The Electronystagmography (ENG) and Videonystagmography (VNG) test battery, which provides information about the function of the peripheral and central vestibular system (70), also includes an oculomotor assessment component.

Oculomotor assessment/screening was performed across 4 studies (46, 52, 62, 71). In the 3 studies, Binocular goggles (71), Frenzel goggles (52), or a light bar (62) were utilised; however, there was no detail of using VNG or ENG. Therefore, results from studies utilising VNG/ENG are reported separately from those without such specifications. In 3 studies, oculomotor assessment results were generally found to be normal or did not show significant differences compared to the control group or pre-concussion conditions (46, 52, 62). In one cross-sectional study, although abnormalities were detected in both athlete groups with and without a previous concussion, there was no significant difference in the distribution of normal and abnormal oculomotor findings between the groups (71). The examinations performed within the scope of each oculomotor assessment are provided in detail in Table 2.

In seven studies, eye assessments were presented under various names (e.g., neurological or bedside examination, neurotologic or neuro-vision assessment) (28, 37, 42, 43, 65) or with specific eye assessments such as spontaneous or gaze-evoked nystagmus (39, 49). Although the results were reported differently in each study, visual-vestibular abnormalities were observed in 5 out of 7 studies (28, 37, 39, 42, 65). However, in 1 out of 5 studies, abnormal results were detected in gaze and pursuit tests, whilst spontaneous nystagmus and saccades were normal (65). In remaining 2 studies, the results were normal (43, 49).

Furthermore, ENG (n = 6) (29, 38, 42, 44, 47, 49) and VNG (n = 7) (28, 32, 41, 43, 63, 68, 72) were utilised across a total of 13 studies. In four studies, one using VNG (41) and three using ENG (42, 47, 49), only caloric test results were presented, rather than ENG or VNG. Therefore, these findings are reported in the next section. Normal results were obtained across 3 studies (28, 38, 43), whilst abnormal VNG or ENG results were observed in 8 studies (29, 32, 38, 44, 49, 63, 68, 72) in at least one case. Notably, a normal VNG result was obtained 23 months post-TBI; however, the initial neuro-visual assessment conducted approximately 8 months after the TBI, revealed visuo-vestibular dysfunction in a case study (28). Abnormalities varied across studies, including findings such as spontaneous nystagmus, reduced vestibular responses, gaze-evoked nystagmus and positive optokinetic nystagmus indicating both peripheral and central vestibular dysfunctions (Table 2).

In an observational cohort study, visual vestibulo-ocular reflex assessment (VVOR) and vestibulo-ocular reflex suppression (VORS) were performed. Individuals with TBI showed more positive results in both the VVOR and VORS compared to the controls (63). Similarly, poor VOR suppression was observed in 3.6% of patients following TBI in a retrospective clinical case series study (68).

Vestibular-oculomotor screening (VOMS) tests the ability to complete vestibular and ocular-related performances and measures the level of symptoms provocation caused by them (73). It was used in 6 studies (34, 53–55, 74, 75). In all 6 studies, at least one subtest of VOMS showed impairment, abnormal findings or an increase in symptoms following concussion/TBI (34, 53–55, 74, 75).

3.3.3 Caloric test

The caloric test evaluates the horizontal SCCs and by extension the superior vestibular nerve (76). The caloric test was performed in 18 out of 50 studies (24, 26, 27, 31, 35, 36, 38, 41, 42, 44, 45, 47–49, 62, 67, 68, 72). In caloric testing, bilateral (24, 42, 48, 49), unilateral (27, 36, 41, 42, 44, 45, 49) vestibular dysfunction (e.g., canal paresis, reduced vestibular responses, vestibular areflexia) or abnormal results (68, 72) were reported in 11 out of 18 studies. One study noted central vestibular tonus differences (38), and 8 studies noted normal caloric responses (26, 31, 35, 38, 44, 47, 62, 67). However, one of these, unilateral canal paresis was observed in the follow-up assessment performed 23 months after the injury (31).

3.3.4 Head thrust/head impulse/video head impulse (vHIT) test

The above tests measure VOR and provides physiological information relating to SCC function (77, 78). Head thrust/impulse (n = 5) (33, 46, 49, 58, 71) and vHIT (n = 6) (52, 62, 63, 67, 68, 72) were performed in a total of 11 records. Normal (negative) results were obtained in 5 studies (33, 46, 49, 62, 67), whilst findings such as positive, increased asymmetry, and impairment were observed across 6 studies (52, 58, 63, 68, 71, 72). In two studies, the horizontal SCC was assessed (62, 71), while in two studies, all SCCs were reported to be evaluated (68, 72). In seven studies, there was no indication of which SCCs were assessed (33, 46, 49, 52, 58, 63, 67).

3.3.5 Head shaking test

Head-shaking test enables the determination of vestibular asymmetry by rapid head shaking and abrupt stopping movements (79). Head shaking test was used in three records (49, 58, 71). Abnormal results were observed in 2 studies (e.g., unstable optic disc or impairment in previous concussion group) (58, 71), whilst no nystagmus was observed in one study (49).

3.3.6 Vestibular evoked myogenic potential (VEMP) test

Among VEMPs, cervical VEMP (c-VEMP) evaluates the saccule via the sternocleidomastoid muscle, whilst ocular VEMP (o-VEMP) evaluates the utricle via the inferior oblique muscle (80, 81). VEMP measurement was performed in 8 studies (31, 43, 62, 65, 68, 72, 82, 83). In two studies, both c-VEMP and o-VEMP were applied (62, 68), in 4 studies only c-VEMP was performed (65, 72, 82, 83), and in 2 studies, it was not stated which VEMP method was used (31, 43). VEMP results were normal (31, 43, 62) or showed no significant difference between groups with or without TBI/concussion (62, 83) in four studies. In one study, VEMP was performed only at follow-up assessment (31).

In 4 studies, abnormal findings were observed (65, 68, 72, 82). In the group comparison performed by Felipe and Shelton (82), P13 and N23 latency scores were higher in the concussion group with symptoms and asymptomatic concussion groups than in the control and normative groups. However, there was no difference between the two concussive groups in terms of latency scores. Furthermore, only one study reported that bilateral abnormalities were observed (65).

3.3.7 Rotational testing

Rotational/Rotary chair test allows for the assessment of the VOR through the horizontal SCC (84). Rotary chair testing was utilised in 3 studies (49, 67, 83). Another study published in 1957 (38) used cupulometria evaluation (now not widely used), which is similar to the rotational test, and assesses vestibular responses through rotary chair but uses different stimulus magnitudes and durations (85). The results varied depending on the patients or cases, from normal gain to a severe bilateral vestibular deficit (Table 2). Furthermore, in a study comparing healthy athletes to those with concussions, there was no difference in VOR gain or phase (83). However, the timing of the rotary chair test implementation differs across studies (whether during the initial or follow-up assessments).

Furthermore, VOR thresholds and vestibular motion perceptual thresholds were evaluated using a rotary chair in one study (67). Vestibular motion perceptual thresholds measure the smallest appreciable stimulus or perceiving motion (86). In this assessment, dramatically elevated perceptual thresholds were observed in acute TBI patients with vestibular agnosia compared to controls. The VOR threshold was defined as the lowest acceleration required to elicit appropriately directed both slow and fast phases of vestibular nystagmus (87). Elevated VOR thresholds were observed in acute TBI (67).

3.3.8 Dynamic visual acuity (DVA) test and gaze stabilization test (GST)

Dynamic visual acuity (DVA) measures the ability to maintain visual clarity and focus on a target while the head is in motion, reflecting the function of the VOR (88). DVA test was performed in 2 studies (46, 58). A drop in visual acuity was observed in a participant with BPPV on one side and peripheral vestibular loss on the other side (58), whilst there are cases where positive DVA (≥4 lines difference) indicating reduced VOR or negative DVA results were reported following TBI (46).

Another test that evaluates VOR is the GST, which determines the head velocity that causes significant deterioration in visual acuity (89). In one study in which GST was applied, individuals with a previous concussion were found to have significantly larger GST asymmetry scores (71).

3.3.9 Posturography

Posturography provides information on balance function, interactions and impact of sensory system such as visual, vestibular and proprioceptive systems by evaluating body sway through the measurement of the centre of pressure displacement on a force-measuring platform (90). Posturography is divided into two: static and dynamic. Static posturography evaluates changes in the centre of pressure on a fixed platform (91), whilst dynamic posturography measures postural reactions on a moving platform (92). Posturography was used in 11 out of 50 studies (43, 46, 49, 51, 62, 65, 67, 68, 72, 83, 93). Three studies used static posturography (46, 67, 93) and seven studies used dynamic posturography (43, 49, 51, 62, 65, 68, 83). However, it was not specified in one study which type of posturography was used and observed abnormal results in 38% of participants with concussion (72).

The modified clinical test of sensory integration and balance (mCTSIB), one of the subtests of static posturography, was used in 2 studies (46, 93). Although the results were reported differently, unstability, increased sway or sensory integration dysfunction was observed after TBI in static posturography evaluation in all three studies (46, 67, 93). However, there is also a case where normal results were obtained (46). In addition, acute TBI patients with vestibular agnosia were more unstable on static posturography compared to those without vestibular agnosia (67).

Sensory organization test (SOT), which is one of the subtests of dynamic posturography, was performed in 6 studies (49, 51, 62, 65, 68, 83). In one of these studies, it was not stated that SOT was applied, but it was shown in the figure (49). The results were generally reported differently in each record based on their research aims. However, in general, two studies stated significantly abnormal responses/worse scores in TBI, or concussion groups compared to control groups (62, 83) and increased sway, imbalance or abnormal results on one or more SOT scores were observed in two studies (49, 68). The other two studies reported no significant statistical differences within TBI groups (e.g., symptomatic versus asymptomatic TBI or those with normal versus saccular abnormalities) (51, 65). In one study, the dynamic posturography results were normal following TBI (43).

3.3.10 Other tests

Hennebert’s sign, which is a pressure-induced nystagmus resulting from changes in pressure applied to the external auditory canal, can be a finding that indicates semicircular canal dehiscence, Meniere’s disease or vestibulofibrosis (94, 95). Fistula Test is used to assess the integrity of the bony labyrinth (95). Fistula test was negative in three studies (26, 29, 42). A positive Hennebert’s sign was observed in one study (39). In three of these studies, it was indicated through assessments that the patients had perilymphatic fistula (29, 39, 42).

3.3.11 PROMs

Symptoms, quality-of-life, functional status, experiences or satisfaction can be evaluated via PROMs (96). PROMs related to vestibular disorders were conducted in 14 studies (46, 51, 52, 54, 61–65, 67, 71, 72, 74, 93), of which 4 studies reported using two PROMs (46, 51, 62, 63). The most commonly used PROM was Dizziness Handicap Inventory (DHI) (13/14) (46, 51, 52, 61–65, 67, 71, 72, 74, 93). Two studies used the Neurobehavioural Symptom Inventory (NSI) (51, 62), whilst others used the space and motion discomfort-II (SMD-II) (63), Post-concussion Symptom Scale (PCSS) (54), and Vertigo Symptom Scale Short Form (VSS-SF) (46).

Following TBI/concussion, 11 studies observed impairment based on DHI (46, 51, 52, 61–63, 67, 71, 72, 74, 93). In 2 studies, only reported the mean score of DHI and did not provide any interpretation of the score (64, 65). However, in 5 out of 13 studies, group comparisons (e.g., pre-post, control, with and without vestibular agnosia, positive and negative BPPV, normal and abnormal saccular function) indicated no significant difference in DHI scores (52, 64, 65, 67, 71). In studies using other PROMs in addition to the DHI, impairments were detected, as shown in Table 2 (46, 51, 62, 63).

3.4 Effect of severity of non-blast related TBI on vestibular outcomes

Twenty-three studies have not clearly stated the severity of TBI (23/50) (24–27, 29–33, 36, 38–42, 44, 45, 47–49, 59, 60, 66). Of the remaining 27 studies (7 of which were case studies/series), 9 studies included mild TBI (28, 43, 46, 50, 55, 62, 63, 65, 93), 12 studies reported concussions (i.e., mild TBI) (34, 37, 52–54, 64, 71, 72, 74, 75, 82, 83), one observed moderate/severe TBI (35), one study included severe TBI (58). Two studies included a range from mild to severe TBI (51, 67), whilst two studies involved participants with mild and moderate TBI (61, 68) (see Table 1 for more details on severity).

In four studies that included various TBI severity groups, different assessments were conducted (51, 61, 67, 68), although three studies did not perform any statistical assessment regarding severity (51, 67, 68). In one case comparison interventional study, BPPV was detected significantly more in individuals with moderate TBI (61) and in another study, most individuals with BPPV had moderate to severe TBI (67). In final study, the severity of TBI at which BPPV occurred was not specified (68).

Of the 9 studies in which TBI severity was classified as mild, four were case studies (28, 43, 46, 50). In 2 out of the nine studies, normal peripheral and central vestibular function was observed (43, 46). Although one case study reported a normal result, it was unclear whether normal vestibular function was fully present, as only a VNG test was conducted (28). BPPV was identified in 5 studies following mild TBI (46, 50, 62, 63, 65), whilst in 5 studies, one of the possible diagnoses observed included sensory integration dysfunction (46, 62, 93), persistent sensorimotor impairment (63), or peripheral, central vestibulopathy (55).

Abnormal findings were obtained in at least one test or subtest in 12 studies involving concussion (34, 37, 52–54, 64, 71, 72, 74, 75, 82, 83). Of these 12 studies, two were case studies (34, 37). The most commonly used assessment was VOMS (5/12) (34, 53, 54, 74, 75). Among studies using dynamic positional tests, one identified both posterior and horizontal SCC BPPV (64), whilst the other found no BPPV post-concussion (52). Two studies reported no significant differences in vestibular assessments between pre- and post-concussion or between those with and without a history of concussion (52, 75), whilst three studies observed a significant increase in VOMS scores post-concussion or in patients with a concussion history compared to those without (53, 54, 74). Additionally, throughout concussion-related studies, abnormalities in vestibular function (34, 37, 72), saccular or vestibulocollic function abnormalities (82), vestibulo-oculomotor dysfunction (54), vestibular-vision interaction deficits (71), persistent chronic vestibulo-oculomotor symptom provocation (74), and impairments in the central integration of vestibular function (83) were observed. In the study reporting severe TBI, posterior SCC and bilateral BPPV were observed (58). In moderate/severe TBI, bilateral normal nystagmus was observed on caloric (35).

PROMs were not used in any study in the severe TBI group. In the studies that were used, the results were reported differently from each other and the score severity for DHI, which was the most frequently used in the studies, was not stated consistently in each study. However, both mild TBI and concussion were reported impairments ranging from moderate to severe (46, 74). Furthermore, in studies with various TBI groups from mild to severe, one reported a mild impairment (51) while the other stated a moderate impairment in DHI (67).

In summary, the impact of TBI severity on vestibular outcomes varies across studies. Different outcomes can be observed for each TBI severity, from normal vestibular function to sensory integration dysfunction. In addition, due to differences in the reporting of DHI results and methodological approaches among the studies, a common conclusion could not be reached on the effect of TBI severity on DHI outcome.

3.5 Effect of aetiology of non-blast related TBI on vestibular outcomes

To investigate the impact of different aetiologies associated with TBI, they were categorised into five groups: falls, motor vehicle accidents (MVA), sports-related injuries, assaults, and others. Although penetrating TBI was not explicitly reported as an aetiology in the included studies, cases with potentially penetrating mechanisms may be present within the “other” category (e.g., industrial injuries involving metal impact (45)). The majority of studies (26/50) reported falls as the cause (24, 25, 30, 31, 38–40, 42, 44, 46, 48–51, 58–68, 93), followed by 21 studies reporting MVA (26–29, 32, 35, 36, 38, 43, 46, 49, 58, 59, 61–64, 66–68, 93). Across these aetiologies, a wide range of vestibular impairments were observed; however, BPPV was associated across all aetiologies except those including only sports-related TBI/concussion and was particularly common following falls.

In 15 studies reporting at least one TBI related to falls (26/50), at least one vestibular test showed abnormal results (24, 25, 30, 31, 38–40, 42, 44, 46, 48–50, 60, 65). Posterior, horizontal or anterior SCC BPPV due to fall was observed (25, 30, 40, 46, 50, 60, 65). In 4 studies, BPPV was observed only in the posterior SCC (30, 40, 50, 65); in 2 studies, it was found in both the posterior and horizontal SCCs (25, 46), and in one study, it was identified in both the anterior and posterior SCCs (60). There were 5 studies in which caloric testing showed absent bilateral or unilateral responses (24, 42, 44, 48, 49), while three studies showed normal caloric responses following a fall (31, 38, 44). However, in two studies where normal results were obtained, abnormal caloric results were detected in the follow-up assessment (31, 38).

Across studies reporting MVA (21/50), the most commonly used vestibular assessments were the caloric test (n = 6) (26, 27, 35, 36, 38, 49) or ENG/VNG (n = 5) (28, 29, 32, 38, 43). Similar to findings following falls, a range of results was observed in caloric testing following MVA in the first assessment, from normal (26, 35) responses to unilateral/bilateral abnormalities (27, 36, 49) or central tonus differences (38). Additionally, both normal (28, 43) and abnormal results were recorded in VNG/ENG (29, 32, 38). BPPV (38) or benign positional vertigo (32) was observed in two studies. In one study, it supported normal peripheral and central vestibular function in all tests (43).

In 11 studies reporting sports-related concussion or TBI, various test batteries were used. However, the commonly applied assessment was the VOMS (5/11) (53–55, 74, 75). In all of these studies, abnormal results were obtained in at least one VOMS subtest. Moreover, three studies identified significant differences between groups pre- and post-TBI (53, 54) or between those with and without a concussion history (74). No study reported BPPV in studies that only included sports-related TBI/concussion. However, positional tests were performed in only one study (52). Furthermore, various outcomes were observed across studies, ranging from vestibular dysfunction (72), abnormalities in saccular or vestibulocollic function (82), peripheral vestibular deficits (71), central or peripheral vestibulopathy (55) or impaired central integration of vestibular function despite a normal peripheral vestibular system (83).

Out of 4 studies reporting different types of assaults, normal SCC response (33), unilateral vestibular dysfunction (41, 42), and somatosensory integration dysfunction (46) were detected. Three studies were classified under “other” causes of injury, including striking the back of the head (42), being hit by a volleyball during practice (34), and an object falling from a bookcase (47). Of these three studies, one reported normal vestibular finding (47), whilst the other two reported abnormal vestibular findings (34, 42), including nystagmus on VOMS or spontaneous right-beating nystagmus.

There were 11 studies that included participants with a variety of aetiologies, from falls to assault (51, 58, 59, 61–64, 66–68, 93) (results reported together under all aetiologies). In 5 out of the eleven studies, results of each participant were reported separately, BPPV was observed following TBI due to both MVA and falls (59, 61, 64, 67, 68) (Table 2). Additionally, in one study, BPPV was observed following TBI due to MVA (58), whilst in another study, BPPV was reported but results were not categorised by different aetiologies (e.g., MVA, falls and blow to head) (66). In all studies reporting the affected SCC in cases of BPPV, the posterior SCC was the most impacted following both MVA and falls (59, 64). McCormick and Kolar (64) reported that falls were a statistically significant TBI aetiology for BPPV. In addition, another study reported that falls were a common aetiology among participants with vestibular hypofunction (68).

Although PROMs were utilised in studies examining various TBI aetiologies, the results were not separately reported by aetiology across those studies. Therefore, the effect of aetiology on PROMs could only be assessed in studies focusing on a single aetiology. No PROMs were used in the studies reporting MVA. In studies reporting falls, one study observed moderate and severe impairments (46), whilst studies associated with sports-related injuries identified mild (52) and severe impairments (74) based on DHI scores.

Summarily, while BPPV is commonly observed, particularly due to falls, common or different vestibular findings were detected across various aetiologies, including peripheral and central vestibular dysfunctions, abnormal ocular or postural responses, and impairments in sensory integration.

3.6 Effect of gender on vestibular outcomes following non-blast related TBI

Out of the 50 studies, 21 included both genders (38, 46, 49, 51, 53–55, 58, 59, 61–68, 72, 74, 83, 93), whilst the remaining studies either reported only male participants (n18) (24, 25, 27, 30, 31, 33, 36, 37, 39, 41–45, 48, 60, 71, 75), or only female participants (n10) (26, 28, 29, 32, 34, 35, 40, 47, 50, 82). One study did not specify gender (52).

In 7 out of the 21 studies that included both genders, multiple participants were included, but no results were reported by gender (54, 55, 62, 63, 65, 83, 93). Six out of these 7 studies had more males than females following TBI (54, 55, 63, 65, 83, 93). In the remaining 14 studies, although there were studies with multiple participants, either a statistical analysis was conducted between genders (51, 53, 68, 72, 74), results were presented based on gender in at least one assessment (58, 59, 61, 64, 66, 67), or in case studies, results were reported individually for each patient (38, 46, 49). A statistically significant difference was found for females in smooth pursuit, horizontal, and vertical saccades in the VOMS assessment (53), whilst Smulligan et al. (74) reported no statistically significant relationship between gender and VOMS performance. In two studies with similar vestibular assessments, there was no significant difference between vestibular function abnormalities and gender (68), nor was vestibular dysfunction correlated with gender (72). Moreover, there was no statistically significant relationship between vestibular score and gender in SOT (51). In studies where separate results were obtained, including case studies by gender, BPPV was observed in both males and females (38, 46, 49, 58, 59, 61, 64, 67). However, in 4 out of 8 studies, the number of males with BPPV was higher than the number of females (58, 59, 61, 67). Furthermore, in Ahn et al. (59) study, the number of males with posterior SCC BPPV was higher than females, while in another study, no males were observed with posterior SCC BPPV (64). However, Kim et al. (66) also reported that posterior SCC BPPV was more prevalent in males than females following TBI. Additionally, in all the studies included in this scoping review, the SCCs in which BPPV was observed were not consistently specified (Table 2).

In studies reporting male participants only, in 9 out of 18 studies, the caloric test revealed either a normal response (31, 44) or bilateral (24, 31, 42, 48) and unilateral abnormalities (27, 36, 41, 42, 44, 45). Furthermore, in three studies including only male participants where positional tests were applied, right posterior SCC BPPV was observed (25, 30, 60), while horizontal (25) or anterior SCCs (60) BPPV accompanied posterior SCC in two of these studies. Of the 10 studies including only female participants, normal horizontal SCC function via caloric test was identified in three studies (26, 35, 47). Similarly, in studies involving only females, bilateral or unilateral posterior SCC BPPV (40, 50) and benign positional vertigo (32) were reported. Moreover, following TBI, a range of vestibular outcomes were identified across genders. In males, findings ranged, from normal SCC function (e.g., normal HIT) (33) or overall peripheral and central vestibular functions (43) to perilymphatic fistula (39, 42) or vestibular-visual interaction deficits (37, 71, 75). In females, reported impairments included perilymphatic fistula (29), vestibulo-oculomotor dysfunction (34), and impairments in saccular or vestibulocollic function (e.g., abnormal c-VEMP responses) (82).

None of the studies that included only females used PROMs. In the study with only males, although the previous concussion group had a wider score range, there was no statistically significant difference between the comparison group (71). Among the 12 studies that included both genders, only 3 reported PROMs by gender (46, 72, 74). In two studies, there was no statistically significant association between gender and DHI (74) or that gender was not correlated with DHI score (72). In the case study, severe impairment was reported in male patients, while severe or moderate impairment was observed in females (46).

In summary, a variety of vestibular impairments, including BPPV, perilymphatic fistula, and vestibulo-oculomotor dysfunction, were observed in both male and female participants across different studies.

4 Discussion

This scoping review synthesised the common vestibular impairments associated with non-blast related TBI and investigated the influence of TBI severity, aetiology, and gender on vestibular outcomes. We found large inconsistencies in the reporting of vestibular tests, results and demographics across the studies, which not only highlight methodological and clinical standardisation deficiencies, but also complicate the understanding of the overall impact of TBI on the vestibular system.

In this review, the most commonly detected peripheral vestibular deficit following TBI was BPPV, most frequently involving the posterior SCC (15, 97, 98), which aligns with the anatomical predisposition for otoconia to accumulate in this canal due to gravity (99). In accordance with the existing literature, we also found that TBI can cause damage to other peripheral vestibular structures, including the labyrinth, vestibular nerve, and otolith organs (15, 100). In contrast to the findings reported here, Akin et al. (101) found in their review that otolith organs may be more damaged compared to SSCs following TBI. However, this discrepancy may be due to differences in the inclusion criteria of the reviews, for example, Akin et al. (101) included blast-related TBI. Therefore, a comprehensive assessment of all vestibular components in TBI patients is essential to draw a definitive conclusion regarding the relative susceptibility of otolith organs and SSCs to damage following TBI.

Some studies yielded important findings regarding the central contributions to the vestibular system. For example, Taylor et al. (68) reported that patients with abnormal oculomotor function following chronic TBI had significantly more difficulty in vestibular-dependent conditions on the SOT. Other research highlighted that, despite normal oculomotor and peripheral vestibular function following chronic TBI, a high proportion of abnormal SOT performance was still observed (62). This review also identified that patients with normal peripheral vestibular function who exhibited vestibular agnosia (impaired self-motion perception), and along with acute TBI patients, showed greater posturography instability than those without vestibular agnosia (67). All these findings support the view that balance relies not only on the inner ear and brainstem pathways but also on cortical processing and integration of vestibular signals (102). Moreover, self-motion perception is considered to arise from the integration of multiple brain regions, rather than being localised to a single region (67).

Similar to vestibular tests, the lack of standardisation in the application of PROMs and the reporting of results was observed throughout the records. Although the DHI, which was more commonly used than other PROMs, identified impairments, findings from some studies indicate an inability to differentiate between different groups. This may be an indication that the DHI may not be an appropriate measure of vestibular symptoms and quality-of-life for this specific patient population. To our knowledge, there is no specific study on the validity and reliability of using the DHI for adults with TBI. However, a study investigating the clinical utility of the DHI for Children and Adolescents (DHI-CA) (103) post-concussion reported that its clinical utility was questionable (104). In this context, developing specific PROMs especially for vestibular impairments in adults with TBI or determining which of the existing PROMs is more suitable in this population can be important for evaluating the quality-of-life and monitoring rehabilitation processes.

The observation of both peripheral vestibular impairments and central impairments across different TBI severities, including mild TBI, may suggest that TBI severity does not necessarily influence vestibular outcomes. Similarly, BPPV was reported across all severities, although some studies found BPPV more frequently in moderate (105) or severe TBI (58) than in mild TBI. Remarkably, the finding that even after concussion, central processing of vestibular and visual information may be altered without affecting the peripheral vestibular organs or associated brainstem and cerebellar processes (83) underscores the importance of a comprehensive evaluation in all TBI severities.

The findings suggest that the aetiology of TBI may be associated with the presence of BPPV, influence of aetiology does not follow a clear pattern on other peripheral and central vestibular impairments. Although BPPV was commonly reported following fall in our review, in contrast, MVA was also reported to be one of the most frequent causes of BPPV in the literature (98, 106). Therefore, further studies specifically designed to understand the impact of TBI aetiology on vestibular findings are needed.

The observation of similar peripheral or central vestibular outcomes in both males and females, along with differing statistical results from included studies, made it difficult to draw conclusions about the gender differences. Regarding BPPV, the findings suggest that BPPV may be more common in males, whilst there are studies in the literature that report no gender difference in BPPV following TBI (106, 107). Additionally, in line with the results of Teramoto et al. (53), a few studies were found statistically significant higher impairment in females compared to males in some oculomotor and vestibular assessments (108, 109). However, since these studies were mainly conducted with adolescents and those experiencing sport-related concussions, the generalisability of these results to the entire adult TBI population is limited.

The timing of assessment can have a significant impact on the interpretation of vestibular outcomes following TBI. Although the post-injury assessment times were extracted in the included studies, the results were not analysed according to assessment time. The terms “acute” and “chronic” TBI are commonly used in the literature, whilst there is no consistent agreement regarding the exact time frames for these periods. For example, some of the included studies accepted the acute period to last up to approximately 3 months post-injury (67, 68), whereas other extended this period to 6 months (74). Future research should clearly define different TBI phases such as acute, subacute, chronic, or post-chronic, and stratify vestibular outcomes accordingly. This would allow investigation of whether the effects of certain variables differ over time and contribute to the development of more effective assessment and management strategies. Moreover, future studies should also investigate which vestibular tests and assessment protocols are most appropriate at different post-injury time points to provide guidance for clinical practice.

Our findings provide insights into the common peripheral and central vestibular impairments following non-blast related TBI, while highlighting the complexity of understanding the effects of factors such as severity, aetiology, and gender due to the multifaceted nature of vestibular deficits combined with the intricate nature of TBI. Future research should develop comprehensive vestibular assessment protocols for individuals with TBI and focus on consistent methodology and standardised reporting of results to better understand the effects of variables on vestibular findings.

4.1 Strengths and limitations

This scoping review study provided a comprehensive review of the literature related to the research questions. Through the established inclusion criteria, studies that precisely matched the definition of TBI were carefully selected to ensure the examination of TBI-specific findings. However, the differences across research questions and the heterogeneity in the study designs of the included studies (for example, high proportion of case studies/series) have complicated the synthesis and comparison of the findings. Furthermore, the assessment times reported following TBI (e.g., acute and chronic TBI) were widely variable between records, with some not reporting the assessment time clearly. Moreover, the assessment time for acute TBI is debated in the literature and therefore, it was not possible to group the data into acute and chronic TBI and as such we were unable to investigate the effect of assessment time. Additionally, due to the broad scope of the study, some vestibular findings accompanied by auditory findings in certain studies were addressed in another scoping review. Although including only English-language studies may have limited the results, the inclusion of studies from non-English-speaking countries allowed for the presentation of results from a broader perspective.

5 Conclusion

Our review has demonstrated the diversity of vestibular findings following non-blast related TBI. However, the complexities of the vestibular system and TBI, as well as inconsistencies in vestibular assessment methods and reporting approaches (e.g., lack of clear specification of oculomotor assessment method) and lack of consistent use of PROMs, limit a comprehensive understanding of vestibular findings in individuals with TBI. These limitations hinder the ability to identify which methods should be prioritised for vestibular assessment in individuals with TBI and, consequently, obstruct the development of diagnostic and therapeutic processes. In this context, future research should focus on adopting more consistent methodologies and standardised reporting practices to enhance vestibular assessment and management approaches for individuals with TBI. To achieve this, establishing some level of agreement or consensus on testing protocols can be beneficial. Additionally, investigating the effects of variables such as severity, aetiology, and gender on vestibular findings through large-scale studies is important for developing more effective interventions for this patient group.

References

• 1.

  Dewan MC Rattani A Gupta S Baticulon RE Hung YC Punchak M et al . Estimating the global incidence of traumatic brain injury. J Neurosurg. (2019) 130:1080–97. doi: 10.3171/2017.10.JNS17352,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 2.

  Capizzi A Woo J Verduzco-Gutierrez M . Traumatic brain injury: an overview of epidemiology, pathophysiology, and medical management. Medical Clinics. (2020) 104:213–38. doi: 10.1016/j.mcna.2019.11.001,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 3.

  Benedictus MR Spikman JM Van Der Naalt J . Cognitive and behavioral impairment in traumatic brain injury related to outcome and return to work. Arch Phys Med Rehabil. (2010) 91:1436–41. doi: 10.1016/J.APMR.2010.06.019,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 4.

  Khoury S Benavides R . Pain with traumatic brain injury and psychological disorders. Prog Neuro-Psychopharmacol Biol Psychiatry. (2018) 87:224–33. doi: 10.1016/J.PNPBP.2017.06.007,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 5.

  Kornblith ES Langa KM Yaffe K Gardner RC . Physical and functional impairment among older adults with a history of traumatic brain injury. J. Head Trauma Rehabil. (2020) 35:E320–9. doi: 10.1097/HTR.0000000000000552,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 6.

  Humphreys I Wood RL Phillips CJ Macey S . The costs of traumatic brain injury: a literature review. ClinicoEcon Outcomes Res. (2013) 5:281–7. doi: 10.2147/CEOR.S44625,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 7.

  Ahmed Z . Current clinical trials in traumatic brain injury. Brain Sci. (2022) 12. doi: 10.3390/brainsci12050527,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 8.

  Teasdale G Jennett B . Assessment of coma and impaired consciousness: a practical scale. Lancet. (1974) 304:81–4. doi: 10.1016/S0140-6736(74)91639-0

  • CrossRef
  • Google Scholar

• 9.

  Maas AIR Menon DK Manley GT Abrams M Åkerlund C Andelic N et al . Traumatic brain injury: progress and challenges in prevention, clinical care, and research. Lancet Neurol. (2022) 21:1004–60. doi: 10.1016/S1474-4422(22)00309-X,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 10.

  de Lanerolle Jung H Bandak Faris A . Neuropathology of traumatic brain injury: comparison of penetrating, nonpenetrating direct impact and explosive blast etiologies. Semin Neurol. (2015) 35:12–9. doi: 10.1055/s-0035-1544240,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 11.

  Maskell F Chiarelli P Isles R . Dizziness after traumatic brain injury: overview and measurement in the clinical setting. Brain Inj. (2006) 20:293–305. doi: 10.1080/02699050500488041,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 12.

  Alsalaheen BA Whitney SL Mucha A Morris LO Furman JM Sparto PJ . Exercise prescription patterns in patients treated with vestibular rehabilitation after concussion. Physiother Res Int. (2013) 18:100–8. doi: 10.1002/pri.1532,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 13.

  Wallace B Lifshitz J . Traumatic brain injury and vestibulo-ocular function: current challenges and future prospects. Eye Brain. (2016) 8:153–64. doi: 10.2147/EB.S82670,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 14.

  Kolev O Sergeeva M . Vestibular disorders following different types of head and neck trauma. Funct Neurol. (2015) 31:1–6. doi: 10.11138/FNeur/2016.31.2.075,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 15.

  Šarkić B Douglas JM Simpson A Vasconcelos A Scott BR Melitsis LM et al . Frequency of peripheral vestibular pathology following traumatic brain injury: a systematic review of literature. Int J Audiol. (2021) 60:479–94. doi: 10.1080/14992027.2020.1811905,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 16.

  Smith RM Marroney N Beattie J Newdick A Tahtis V Burgess C et al . A mixed methods randomised feasibility trial investigating the management of benign paroxysmal positional vertigo in acute traumatic brain injury. Pilot Feasibility Stud. (2020) 6:130. doi: 10.1186/s40814-020-00669-z,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 17.

  Peters MDJ Godfrey CM Khalil H McInerney P Parker D Soares CB . Guidance for conducting systematic scoping reviews. Int J Evid Based Healthc. (2015) 13:141–6. doi: 10.1097/XEB.0000000000000050,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 18.

  Arksey H O’Malley L . Scoping studies: towards a methodological framework. Int J Soc Res Methodol Theory Practi. (2005) 8:19–32. doi: 10.1080/1364557032000119616

  • CrossRef
  • Google Scholar

• 19.

  Rethlefsen ML Kirtley S Waffenschmidt S Ayala AP Moher D Page MJ et al . Prisma-s: an extension to the PRISMA statement for reporting literature searches in systematic reviews. Syst Rev. (2021) 10. doi: 10.1186/s13643-020-01542-z,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 20.

  Lefebvre C Glanville J Briscoe S Littlewood A Marshall C Metzendorf M-I et al . Searching for and selecting studies In: HigginsJPTGreenS, editors. Cochrane handbook for systematic reviews of interventions. Version: The Cochrane Collaboration (2025). 6:5, Available online at: cochrane.org/handbook

  • Google Scholar

• 21.

  Higgins JP Lasserson T Chandler J Tovey D Churchill R . Methodological expectations of Cochrane intervention reviews. Cochrane: London. 2019.

  • Google Scholar

• 22.

  McGowan J Sampson M Salzwedel DM Cogo E Foerster V Lefebvre C . PRESS peer review of electronic search strategies: 2015 guideline; statement. J Clin Epidemiol. (2016) 75:40–6. doi: 10.1016/j.jclinepi.2016.01.021,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 23.

  Ouzzani M Hammady H Fedorowicz Z Elmagarmid A . Rayyan—a web and mobile app for systematic reviews. Syst Rev. (2016) 5:210. doi: 10.1186/s13643-016-0384-4,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 24.

  Feneley MR Murthy P . Acute bilateral vestibulo-cochlear dysfunction following occipital fracture. J Laryngol Otol. (1994) 108:54–6. doi: 10.1017/S0022215100125836,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 25.

  Bertholon P Chelikh L Timoshenko AP Tringali S Martin C . Combined horizontal and Posterior Canal benign paroxysmal positional Vertigo in three patients with head trauma. Ann Otol Rhinol Laryngol. (2005) 114:105–10. doi: 10.1177/000348940511400204,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 26.

  Kagoya R Ito K Kashio A Karino S Yamasoba T . Dislocation of stapes with footplate fracture caused by indirect trauma. Ann Otol Rhinol Laryngol. (2010) 119:628–30. doi: 10.1177/000348941011900910,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 27.

  Ylikoski J. Palva T. Sanna M. Dizziness after head trauma: clinical and morphologic findings Am J Otol (1982) 3:343–352.

  • Google Scholar

• 28.

  Roup CM Ross C Whitelaw G . Hearing difficulties as a result of traumatic brain injury. J Am Acad Audiol. (2020) 31:137–46. doi: 10.3766/jaaa.18084,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 29.

  Fitzgerald DC . Persistent dizziness following head trauma and perilymphatic fistula. Arch Phys Med Rehabil. (1995) 76:1017–20. doi: 10.1016/S0003-9993(95)81041-2

  • CrossRef
  • Google Scholar

• 30.

  Ralli G Francesca A Antonio L Giuseppe N . Post-traumatic camel-related benign paroxysmal positional vertigo. Travel Med Infect Dis. (2010) 8:207–9. doi: 10.1016/j.tmaid.2010.07.002,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 31.

  Fujimoto C Ito K Takano S Karino S Iwasaki S . Successful cochlear implantation in a patient with bilateral progressive sensorineural hearing loss after traumatic subarachnoid hemorrhage and brain contusion. Ann Otol Rhinol Laryngol. (2007) 116:897–901. doi: 10.1177/000348940711601205,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 32.

  Ottaviano G Marioni G Marchese-Ragona R Trevisan CP De Filippis C Staffieri A . Anosmia associated with hearing loss and benign positional vertigo after head trauma. Acta Otorhinolaryngol Ital. (2009) 29:270–3.

  • Google Scholar

• 33.

  Kanavati O Salamat AA Tan TY Hellier W . Bilateral temporal bone fractures associated with bilateral profound sensorineural hearing loss. Postgrad Med J. (2016) 92:302–3. doi: 10.1136/postgradmedj-2015-133862,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 34.

  Blackard MF Sawhney V Castillo M Gupta M Pandya AS Patel R . A case report of concussion in female collegiate volleyball player. Sports Orthop Traumatol. (2020) 36:377–83. doi: 10.1016/j.orthtr.2020.08.001

  • CrossRef
  • Google Scholar

• 35.

  Jani NN Laureno R Mark AS Brewer CC . Deafness after bilateral midbrain contusion: a correlation of magnetic resonance imaging with auditory brain stem evoked responses. Neurosurgery (1991) 29:106–9.

  • Google Scholar

• 36.

  Schuknecht HF Davison RC . Deafness and Vertigo from head injury. AMA Arch Otolaryngol. (1956) 63:513–28. doi: 10.1001/archotol.1956.03830110055006,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 37.

  Waninger KN Gloyeske BM Hauth JM Vanic KA Yen DM . Intratympanic hemorrhage and concussion in a football offensive lineman. J Emerg Med. (2014) 46:371–2. doi: 10.1016/j.jemermed.2013.08.043,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 38.

  Preber L Silversklöld BP . Paroxysmal positional Vertigo following head injury: studied by electronystagmography and skin resistance measurements. Acta Otolaryngol. (1957) 48:255–65. doi: 10.3109/00016485709124379,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 39.

  Sousa Menezes A Ribeiro D Miranda DA Martins Pereira S . Perilymphatic fistula and pneumolabyrinth without temporal bone fracture: a rare entity. BMJ Case Rep. (2019) 12:e228457. doi: 10.1136/bcr-2018-228457,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 40.

  Lerut B De Vuyst C Ghekiere J Vanopdenbosch L Kuhweide R . Post-traumatic pulsatile tinnitus: the hallmark of a direct carotico-cavernous fistula. J Laryngol Otol. (2007) 121:1103–7. doi: 10.1017/S0022215107005890,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 41.

  Durbec M Vigier S Brosset R Mottier C Dubreuil C Tringali S . Post-traumatic total deafness with normal CT scan. Eur Ann Otorhinolaryngol Head Neck Dis. (2012) 129:281–3. doi: 10.1016/j.anorl.2011.12.004,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 42.

  Lyos AT Marsh MA Jenkins HA Coker NJ . Progressive hearing loss after transverse temporal bone fracture. Arch Otolaryngol Head Neck Surg. (1995) 121:795–9. doi: 10.1001/archotol.1995.01890070081017,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 43.

  Paxman E Stilling J Mercier L Debert CT . Repetitive transcranial magnetic stimulation (rTMS) as a treatment for chronic dizziness following mild traumatic brain injury. BMJ Case Rep. (2018) 2018:bcr-2018-226698. doi: 10.1136/bcr-2018-226698,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 44.

  Tonkin JP Fagan P . Rupture of the round window membrane. J Laryngol Otol. (1975) 89:733–56. doi: 10.1017/S0022215100080944,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 45.

  Mohd Khairi MD Irfan M Rosdan S . Traumatic head injury with contralateral sensorineural hearing loss. Ann Acad Med Singap. (2009) 38:1017–8. doi: 10.47102/annals-acadmedsg.V38N11p1017,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 46.

  Kleffelgaard I Soberg HL Bruusgaard KA Tamber AL Langhammer B . Vestibular rehabilitation after traumatic brain injury: case series. Phys Ther. (2016) 96:839–49. doi: 10.2522/ptj.20150095,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 47.

  Jacobs GB Lehrer JF Rubin RC Hubbard JH Nalebuff DJ Wille RL . Posttraumatic vertigo: report of three cases. J Neurosurg. (1979) 51:860–1. doi: 10.3171/jns.1979.51.6.0860,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 48.

  Chung JH Shin MC Min HJ Park CW Lee SH . Bilateral cochlear implantation in a patient with bilateral temporal bone fractures. Am J Otolaryngol. (2011) 32:256–8. doi: 10.1016/j.amjoto.2010.03.002,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 49.

  Herdman S. J. Treatment of vestibular disorders in traumatically brain-injured patients. J Head Trauma Rehabil (1990) 5:63–76. doi: 10.1097/00001199-199012000-00008

  • CrossRef
  • Google Scholar

• 50.

  Johnson EG . Clinical Management of a Patient with chronic recurrent Vertigo following a mild traumatic brain injury. Case Rep Med. (2009) 2009:910596. doi: 10.1155/2009/910596,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 51.

  Joseph A-LC Lippa SM Moore B Bagri M Row J Chan L et al . Relating self-reported balance problems to sensory organization and dual-tasking in chronic traumatic brain injury. PM&R. (2021) 13:870–9. doi: 10.1002/pmrj.12478,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 52.

  Hides JA Franettovich Smith MM Mendis MD Smith NA Cooper AJ Treleaven J et al . A prospective investigation of changes in the sensorimotor system following sports concussion. An exploratory study. Musculoskelet Sci Pract. (2017) 29:7–19. doi: 10.1016/j.msksp.2017.02.003,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 53.

  Teramoto M Grover EB Cornwell J Zhang R Boo M Ghajar J et al . Sex differences in common measures of concussion in college athletes. J Head Trauma Rehabil. (2022) 37:E299–309. doi: 10.1097/HTR.0000000000000732,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 54.

  Glendon K Blenkinsop G Belli A Pain M . Does vestibular-ocular-motor (VOM) impairment affect time to return to play, symptom severity, Neurocognition and academic ability in student-athletes following acute concussion?Brain Inj. (2021) 35:788–97. doi: 10.1080/02699052.2021.1911001,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 55.

  Uyeno C Zhang R Cornwell J Teramoto M Boo M Lumba-Brown A . Acute eye-tracking changes correlated with vestibular symptom provocation following mild traumatic brain injury. Clin J Sport Med. (2024) 34:411–6. doi: 10.1097/JSM.0000000000001223,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 56.

  Dix MR Hallpike CS . The pathology, symptomatology and diagnosis of certain common disorders of the vestibular system. Proc R Soc Med. (1952) 45:341–54. doi: 10.1177/003591575204500604,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 57.

  BSA . Recommended Procedure Positioning Tests. (2016). 9–17. Available online at: www.thebsa.org (Accessed October 15, 2024).

  • Google Scholar

• 58.

  Motin M Keren O Groswasser Z Gordon CR . Benign paroxysmal positional vertigo as the cause of dizziness in patients after severe traumatic brain injury: diagnosis and treatment. Brain Inj. (2005) 19:693–7. doi: 10.1080/02699050400013600,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 59.

  Ahn S-K Jeon S-Y Kim J-P Park JJ Hur DG Kim D-W et al . Clinical characteristics and treatment of benign paroxysmal positional vertigo after traumatic brain injury. J Trauma Acute Care Surg. (2011) 70:442–6. doi: 10.1097/TA.0b013e3181d0c3d9,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 60.

  Dlugaiczyk J Siebert S Hecker DJ Brase C Schick B . Involvement of the anterior semicircular canal in posttraumatic benign paroxysmal positioning vertigo. Otol Neurotol. (2011) 32:1285–90. doi: 10.1097/MAO.0b013e31822e94d9,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 61.

  Ouchterlony D Masanic C Michalak A Topolovec-Vranic J Rutka JA . Treating benign paroxysmal positional vertigo in the patient with traumatic brain injury: effectiveness of the canalith repositioning procedure. J Neurosci Nurs. (2016) 48:90–9. doi: 10.1097/JNN.0000000000000186,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 62.

  Campbell KR Parrington L Peterka RJ Martini DN Hullar TE Horak FB et al . Exploring persistent complaints of imbalance after mTBI: oculomotor, peripheral vestibular and central sensory integration function. J Vestib Res. (2021) 31:519–30. doi: 10.3233/VES-201590,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 63.

  Galea O O’Leary S Williams K Treleaven J . Investigation of sensorimotor impairments in individuals 4 weeks to 6 months after mild traumatic brain injury. Arch Phys Med Rehabil. (2022) 103:921–8. doi: 10.1016/j.apmr.2021.10.029,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 64.

  McCormick K Kolar B . Research letter: rate of BPPV in patients diagnosed with concussion. J Head Trauma Rehabil. (2023) 38:434–8. doi: 10.1097/HTR.0000000000000867,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 65.

  Jafarzadeh S Pourbakht A Bahrami E . Vestibular assessment in patients with persistent symptoms of mild traumatic brain injury. Indian J Otolaryngol Head Neck Surg. (2022) 74:272–80. doi: 10.1007/s12070-020-02043-0,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 66.

  Kim C-H Kim H Jung T Lee D-H Shin JE . Clinical characteristics of benign paroxysmal positional vertigo after traumatic brain injury. Brain Inj. (2024) 38:341–6. doi: 10.1080/02699052.2024.2310790,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 67.

  Calzolari E Chepisheva M Smith RM Mahmud M Hellyer PJ Tahtis V et al . Vestibular agnosia in traumatic brain injury and its link to imbalance. Brain. (2021) 144:128–43. doi: 10.1093/brain/awaa386,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 68.

  Taylor RL Wise KJ Taylor D Chaudhary S Thorne PR . Patterns of vestibular dysfunction in chronic traumatic brain injury. Front Neurol. (2022) 13. doi: 10.3389/fneur.2022.942349,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 69.

  Doettl SM McCaslin DL . Oculomotor assessment in children. Semin Hear. (2018) 39:275–87. doi: 10.1055/s-0038-1666818,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 70.

  González JE Kiderman A . ENG/VNG In: KountakisSE, editor. Encyclopedia of otolaryngology, head and neck surgery. Berlin, Heidelberg: Springer Berlin Heidelberg (2013). 785–92.

  • Google Scholar

• 71.

  Honaker JA Criter RE Patterson JN Jones SM . Gaze stabilization test asymmetry score as an indicator of previous concussion in a cohort of collegiate football players. Clin J Sport Med. (2015) 25:361–366. doi: 10.1097/JSM.0000000000000138,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 72.

  Gard A Al-Husseini A Kornaropoulos EN De Maio A Tegner Y Björkman-Burtscher I et al . Post-concussive vestibular dysfunction is related to injury to the inferior vestibular nerve. J Neurotrauma. (2022) 39:829–40. doi: 10.1089/neu.2021.0447,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 73.

  Mucha A Collins MW Elbin RJ Furman JM Troutman-Enseki C DeWolf RM et al . A brief vestibular/ocular motor screening (VOMS) assessment to evaluate concussions: preliminary findings. Am J Sports Med. (2014) 42:2479–86. doi: 10.1177/0363546514543775,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 74.

  Smulligan KL Carry P Smith AC Esopenko C Baugh CM Wilson JC et al . Cervical spine proprioception and vestibular/oculomotor function: an observational study comparing young adults with and without a concussion history. Phys Ther Sport. (2024) 69:33–9. doi: 10.1016/j.ptsp.2024.07.002,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 75.

  Brown DA Grant G Evans K Leung FT Hides JA . Evaluation of the vestibular/ocular motor screening assessment in active combat sport athletes: an exploratory study. Brain Inj. (2022) 36:961–7. doi: 10.1080/02699052.2022.2109741,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 76.

  Hallpike CS . The caloric tests. J Laryngol Otol. (1956) 70:15–28. doi: 10.1017/S0022215100052610,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 77.

  Halmagyi GM Chen L MacDougall HG Weber KP McGarvie LA Curthoys IS . The video head impulse test. Front Neurol. (2017) 8. doi: 10.3389/fneur.2017.00258,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 78.

  Halmagyi GM Curthoys IS . A clinical sign of canal paresis. Arch Neurol. (1988) 45:737–9. doi: 10.1001/archneur.1988.00520310043015,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 79.

  Hall S. F. Laird M. E. Is head-shaking nystagmus a sign of vestibular dysfunction? J Otolaryngol (1992) 21:209–212.

  • Google Scholar

• 80.

  Welgampola MS Colebatch JG . Characteristics and clinical applications of vestibular-evoked myogenic potentials. Neurology. (2005) 64:1682–8. doi: 10.1212/01.WNL.0000161876.20552.AA,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 81.

  Colebatch JG Rosengren SM Welgampola MS . Chapter 10 – Vestibular-evoked myogenic potentials In: FurmanJMLempertT, editors. Handbook of clinical neurology: Elsevier (2016). 133–55.

  • Google Scholar

• 82.

  Felipe L Shelton JA . The clinical utility of the cervical vestibular-evoked myogenic potential (cVEMP) in university-level athletes with concussion. Neurol Sci. (2021) 42:2803–9. doi: 10.1007/s10072-020-04849-w,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 83.

  Christy JB Cochrane GD Almutairi A Busettini C Swanson MW Weise KK . Peripheral vestibular and balance function in athletes with and without concussion. J Neurol Phys Ther. (2019) 43:153–9. doi: 10.1097/NPT.0000000000000280,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 84.

  Zalewski CK McCaslin DL Carlson ML . Rotary chair testing In: BabuSSchuttCABojrabDI, editors. Diagnosis and treatment of vestibular disorders. Cham: Springer International Publishing (2019). 75–98.

  • Google Scholar

• 85.

  Van EAAJ Groen JJ Jongkees LBW . The turning test with small Regulable stimuli. J Laryngol Otol. (1948) 62:63–9. doi: 10.1017/S0022215100008690,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 86.

  Kobel MJ Wagner AR Merfeld DM Mattingly JK . Vestibular thresholds: a review of advances and challenges in clinical applications. Front Neurol. (2021) 12:643634. doi: 10.3389/fneur.2021.643634,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 87.

  Seemungal B Gunaratne IA Fleming I Gresty MA Bronstein A . Perceptual and nystagmic thresholds of vestibular function in yaw. J Vestib Res. (2004) 14:461–6. doi: 10.3233/VES-2004-14604,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 88.

  Herdman SJ Tusa RJ Blatt P Suzuki A Venuto PJ Roberts D . Computerized dynamic visual acuity test in the assessment of vestibular deficits. Am J Otol (1998) 19:790–96. doi: 10.1016/S1567-4231(10)09014-3

  • CrossRef
  • Google Scholar

• 89.

  Goebel JA Tungsiripat N Sinks B Carmody J . Gaze stabilization test: a new clinical test of unilateral vestibular dysfunction. Otol Neurotol. (2007) 28:68–73. doi: 10.1097/01.mao.0000244351.42201.a7,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 90.

  Baloh RW Jacobson KM Beykirch K Honrubia V . Static and dynamic posturography in patients with vestibular and cerebellar lesions. Arch Neurol. (1998) 55:649–54. doi: 10.1001/archneur.55.5.649,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 91.

  Vališ M Dršata J Kalfeřt D Semerák P Kremláček J . Computerised static posturography in neurology. Open Med. (2012) 7:317–22. doi: 10.2478/s11536-011-0152-8

  • CrossRef
  • Google Scholar

• 92.

  Bronstein AM Pavlou M . Chapter 16 – Balance In: BarnesMPGoodDC, editors. Handbook of clinical neurology: Amsterdam Elsevier (2013). 189–208.

  • Google Scholar

• 93.

  Lin L-F Liou T-H Hu C-J Ma H-P Ou J-C Chiang Y-H et al . Balance function and sensory integration after mild traumatic brain injury. Brain Inj. (2015) 29:41–6. doi: 10.3109/02699052.2014.955881,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 94.

  Hennebert C . A new syndrome in her editary syphilis of the labyrinth. Presse Med Belg Brux (1911) 63:467–470. Available online at: https://cir.nii.ac.jp/crid/1573387449164406400.bib?lang=ja (Accessed October 29, 2024)

  • Google Scholar

• 95.

  Pearlman RC . The fistula and Hennebert tests. J Am Audiol Soc. (1976) 2:1–2.

  • Google Scholar

• 96.

  Devlin JN Appleby J . Getting the most out of PROMs: Putting health outcomes at the heart of NHS decision-making. London: King’s Fund (2010). 83 p.

  • Google Scholar

• 97.

  Carr S Rutka J . Post-traumatic dizziness. Curr Otorhinolaryngol Rep. (2017) 5:142–51. doi: 10.1007/s40136-017-0154-4

  • CrossRef
  • Google Scholar

• 98.

  Haripriya GR Mary P Dominic M Goyal R Sahadevan A . Incidence and treatment outcomes of post traumatic BPPV in traumatic brain injury patients. Indian J Otolaryngol Head Neck Surg. (2018) 70:337–41. doi: 10.1007/s12070-018-1329-0,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 99.

  Parnes LS Agrawal SK Atlas J Diagnosis and management of benign paroxysmal positional vertigo (BPPV) Can Med Assoc J (2003) 169:681–93.

  • Google Scholar

• 100.

  Knoll RM Ishai R Trakimas DR Chen JX Nadol J Jb et al . Peripheral vestibular system histopathologic changes following head injury without temporal bone fracture. Otolaryngol Head Neck Surg. (2019) 160:122–30. doi: 10.1177/0194599818795695

  • CrossRef
  • Google Scholar

• 101.

  Akin FW Murnane OD Hall CD Riska KM . Vestibular consequences of mild traumatic brain injury and blast exposure: a review. Brain Inj. (2017) 31:1188–94. doi: 10.1080/02699052.2017.1288928,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 102.

  Hadi Z Mahmud M Seemungal BM . Brain mechanisms explaining postural imbalance in traumatic brain injury: a systematic review. Brain Connect. (2024) 14:144–77. doi: 10.1089/brain.2023.0064,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 103.

  Sousa M da GC de Cruz O Santos AN Ganança C Almeida L Sena EP de Brazilian adaptation of the dizziness handicap inventory for the pediatric population: reliability of the results Audiol. Commun. Res. 2015 20 327–335 doi: 10.1590/2317-6431-2015-1595

  • CrossRef
  • Google Scholar

• 104.

  Tiwari D Gochyyev P . Does the dizziness handicap inventory—children and adolescents (DHI-CA) demonstrate properties to support clinical application in the post-concussion population: a Rasch analysis. Children. (2023) 10:14. doi: 10.3390/children10091428,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 105.

  Andersson H Jablonski GE Nordahl SHG Nordfalk K Helseth E Martens C et al . The risk of benign paroxysmal positional Vertigo after head trauma. Laryngoscope. (2022) 132:443–8. doi: 10.1002/lary.29851,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 106.

  Gordon CR Levite R Joffe V Gadoth N . Is posttraumatic benign paroxysmal positional Vertigo different from the idiopathic form?Arch Neurol. (2004) 61:1590–3. doi: 10.1001/archneur.61.10.1590,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 107.

  Di Cesare T Tricarico L Passali GC Sergi B Paludetti G Galli J et al . Traumatic benign paroxysmal positional vertigo: personal experience and comparison with idiopathic BPPV. Int J Audiol. (2021) 60:393–7. doi: 10.1080/14992027.2020.1821253,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 108.

  Sufrinko AM Mucha A Covassin T Marchetti G Elbin RJ Collins MW et al . Sex differences in vestibular/ocular and neurocognitive outcomes after sport-related concussion. Clin J Sport Med. (2017) 27:133–8. doi: 10.1097/JSM.0000000000000324,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 109.

  Gray M Wilson JC Potter M Provance AJ Howell DR . Female adolescents demonstrate greater oculomotor and vestibular dysfunction than male adolescents following concussion. Phys Ther Sport. (2020) 42:68–74. doi: 10.1016/j.ptsp.2020.01.001,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar

• 110.

  The Management and Rehabilitation of Post-Acute mTBI Work Group . VA/DoD clinical practice guideline for the management and rehabilitation of post-acute mild traumatic brain injury. (2021). Available online at: www.tricare.mil (Accessed October 25, 2024).

  • Google Scholar

• 111.

  McCrory P Meeuwisse W Dvorak J Aubry M Bailes J Broglio S et al . Consensus statement on concussion in sport-the 5th international conference on concussion in sport held in Berlin, October 2016. Br J Sports Med. (2017) 51:838. doi: 10.1136/bjsports-2017-097699

  • CrossRef
  • Google Scholar

• 112.

  Malec JF Brown AW Leibson CL Flaada JT Mandrekar JN Diehl NN et al . The Mayo classification system for traumatic brain injury severity. J Neurotrauma. (2007) 24:1417–24. doi: 10.1089/neu.2006.0245,

  • Pubmed Abstract
  • CrossRef
  • Google Scholar