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VESTIBULAR DISORDERS

Posttraumatic Dizziness: Navigating the Maze Towards Accurate Vestibular Diagnosis and Treatment

Grzesiak, Melissa∗,†; Carender, Wendy∗,†; Basura, Gregory J.

Author Information
doi: 10.1097/MAO.0000000000003035

Abstract

Traumatic brain injury (TBI) often causes dizziness or balance problems (1,2). The etiology of posttraumatic balance dysfunction is frequently multifactorial and may be central (brain) and/or peripheral (ear or 8th cranial nerve) (3,4). Following TBI, patients with either central or peripheral etiology may describe vertigo, imbalance, nausea, and hearing loss (5,6). Benign paroxysmal positional vertigo (BPPV) is common after TBI resulting from displacement of inner ear otoconia into the semi-circular canals (SCCs) and can involve multiple SCCs simultaneously or sequentially (7). Temporal bone fractures can lead to perilymphatic fistula at the oval or round windows (6) and vestibulocochlear nerve injury (4) that may lead to permanent hearing loss and tinnitus. Peripheral vestibular hypofunction may cause difficulties with gaze stabilization, motion provoked dizziness, and chronic disequilibrium.

Incorrect or delayed diagnosis of central and/or peripheral vestibular dysfunction following TBI may lead to prolonged physical, emotional, or neurological problems and poor quality of life (1,8,9). This clinical capsule highlights the importance of a comprehensive differential diagnosis and correct identification of nystagmus patterns when evaluating a patient following TBI. Here we emphasize clinical objective measures to differentiate peripheral from central causes of dizziness. We present videos of nystagmus that highlight the complexity of multiple canal BPPV and peripheral vestibular involvement.

MATERIALS AND METHODS

Subject

A 73-year-old active man presented following a 6-foot fall onto a concrete driveway, striking the right side of his head. He lost consciousness for 2 to 3 minutes. Before this injury, he worked full-time and maintained regular physical activity. A head computed tomography (CT) revealed a subdural hematoma and right mastoid and middle ear opacification. An otic capsule sparing, transverse temporal bone fracture involving the mastoid and squamosal portions of the temporal bone was found on the right side. The fracture line extended to the temporomandibular joint and external auditory canal (EAC). Physical examination revealed a positive Battle's sign, middle ear hemotympanum, without cerebrospinal fluid leak or facial nerve weakness.

Audiology

Before the fall, the patient's audiometric testing was consistent with age-related hearing loss or presbyacusis. Following the fall, his hearing remained unchanged as evidenced by a persistent, symmetric bilateral high frequency sensorineural hearing loss (SNHL) with intact word discrimination.

Otolaryngology

Outpatient otolaryngology examination was performed 8 days later. The patient's complaints included hearing loss and fullness in the right ear, left-sided headache, chronic imbalance, positional vertigo, and right shoulder pain. Binocular microscopy revealed patent EACs and normal tympanic membranes. There were no step-offs or abnormalities within the bony EAC. Right Dix-Hallpike testing (10) revealed a delayed-onset right torsional (directed toward the downward ear) up-beating nystagmus, lasting seconds, consistent with right posterior semi-circular canal (PSCC) BPPV, canalithiasis variant (11,12). Supine roll test (13,14) revealed geotropic (toward the earth) horizontal nystagmus, lasting less than a minute, more robust with the head/body turned to the right, consistent with right geotropic horizontal semi-circular canal (HSCC) BPPV (11,12). Overall impression: TBI with possible labyrinthine concussion including posttraumatic multiple canal (PSCC and HSCC) BPPV and stable SNHL. Recommendations included a same day referral to vestibular physical therapy (VPT) for evaluation and treatment.

Vestibular Physical Therapy

Functional limitations included inability to safely participate in activities of daily living (ADLs), work, driving, or exercise. Dizziness Handicap Inventory (DHI) (15) score was 54/100, consistent with moderate perceived disability. VPT positional testing with visual fixation removed using video-oculography goggles (RealEyes xDVR, Micromedical Technologies Chicago, IL) confirmed right PSCC (see video, supplemental digital content 1, http://links.lww.com/MAO/B187) and HSCC (both geotropic-toward the earth and apogeotropic-away from the earth) BPPV (12,13). In addition, a 3rd degree left-beating spontaneous nystagmus, following Alexander Law (16) was appreciated, suggestive of unilateral vestibular hypofunction. Treatment began with the right canalith repositioning maneuver (CRM) (12,17,18) for the most symptomatic right PSCC. The right Epley CRM was performed twice and treatment appeared successful as evidenced by resolution of the right torsional up-beating nystagmus throughout the second maneuver (12,17,18). However, multi-directional positional nystagmus was present throughout, consistent with active bilateral, multicanal (PSCC and HSCC) BPPV.

He was seen for six VPT visits over the course of 7 weeks. Specific patterns of nystagmus observed during positional testing, interpretation of findings, and interventions from each visit are outlined in Table 1. During visits 2–4, positional testing with visual fixation removed using video-oculography goggles revealed active left PSCC (see video, Supplemental Digital Content 3, http://links.lww.com/MAO/B189) and both right and left HSCC BPPV (see video, Supplemental Digital Content 2, http://links.lww.com/MAO/B188 and 4, http://links.lww.com/MAO/B190). Intervention was aimed at treating one canal per visit, beginning with the most symptomatic canal, using the appropriate CRM. At his fifth visit, positional testing was negative for BPPV, however ocular-motor examination with visual fixation removed, revealed a 2nd degree right-beating spontaneous nystagmus. Ongoing functional deficits included a two-line difference in dynamic visual acuity (DVA) (19), a mild vestibular dysfunction balance pattern on the modified Clinical Test of Sensory Interaction (mCTSIB) (20), and motion sensitivity (21). Findings were suggestive of an uncompensated unilateral vestibular hypofunction. Treatment was adjusted to include gaze stabilization, habituation, balance exercises, and daily walking (22,23). Before VPT discharge, he was instructed in common causes of central vestibular decompensation such as poor sleep, physical inactivity, central vestibular suppressants, and/or stress. Additional education focused on recurrent BPPV (7,24), including how to determine the involved side and how to treat PSCC BPPV by utilizing home CRM (25). At his sixth and final visit, he reported full resolution of dizziness and disequilibrium. He had returned to driving, work, and his regular exercise.

TABLE 1
TABLE 1:
Vestibular physical therapy interventions and outcomes

One week following discharge, he returned reporting reoccurring motion provoked disequilibrium following air travel with poor sleep and limited physical exercise. VPT examination was negative for BPPV, however ocular-motor examination with visual fixation removed, revealed a 2nd degree right-beating spontaneous nystagmus. In addition, a three-line DVA difference, a vestibular dysfunction balance pattern on mCTSIB, and motion sensitivity, were all consistent with a unilateral vestibular hypofunction (23). Findings were accordant with central decompensation (23) and he was instructed in gaze stabilization, habituation, balance exercises, and walking.

Five weeks later, he noted re-occurring positional vertigo. Due to the severity of his symptoms, he was not comfortable attempting a CRM independently. VPT examination revealed active bilateral PSCC BPPV, canalithiasis variant. He was treated for PSCC BPPV on three separate visits utilizing appropriate CRM in addition to performing self-CRM at home. He cancelled his last VPT appointment, reporting that he was no longer symptomatic following successful completion of self-CRMs.

RESULTS

The patient was seen for a total of 10 VPT visits over a 3-month time period and successfully treated for BPPV involving four different SCCs and a suspected unilateral vestibular hypofunction. His DHI score improved 48 points (54/100 initially to 6/100 before discharge), thus meeting the minimal clinically important difference (15). Video goggle examination upon discharge was negative for spontaneous, gaze, and post head shake nystagmus suggesting that the peripheral vestibular hypofunction was well compensated (26). He demonstrated independence in identifying and treating PSCC BPPV (27). He implemented life-style modifications to prevent future decompensation and returned to his pre-injury activities.

DISCUSSION

Successful treatment of dizziness following TBI is contingent upon an accurate diagnosis of central and/or peripheral etiologies. A thorough history and physical examination, identifying the mechanism of injury, and specific symptoms including provoking and mitigating factors is paramount in making a diagnosis. Central origins of dizziness are typically constant and often slow to improve (28). Peripheral etiologies often manifest symptoms that are provoked by quick head or body movements. BPPV (PSCC most common), symptoms are commonly triggered when looking up, bending over, or getting into or out of bed and rolling over (29).

To delineate peripheral from central causes of dizziness, eye movements must be evaluated both in room light (with fixation) and with video goggles (without fixation). Video goggles provide enhanced viewing and recording of nystagmus patterns (30). Typically, nystagmus associated with peripheral vestibulopathies can be suppressed in room light with gaze fixation and stays unidirectional during right and left gaze; per Alexander's Law (16). Named for the fast phase of the nystagmus, horizontal post head shaking beats away from the side of the peripheral lesion. These fast beats will be present in patients with uncompensated unilateral peripheral vestibular hypofunction (31). Table 2 summarizes the clinical bedside examination to differentiate peripheral versus central vestibular etiologies. Table 3 summarizes common patterns of peripheral (including BPPV) and central related nystagmus.

TABLE 2 - Clinical examination to differentiate peripheral from central involvement
Examination Examination Condition How to Perform the Examination Peripheral Central
Spontaneous nystagmus Both in room light (with fixation) and with videogoggles (without fixation) Observe for nystagmus with eyes in center position in room light (with fixation) and while wearing video goggles (without fixation/dark) 1st, 2nd, or 3rd degree, horizontal nystagmusthat suppresses in room light. Pure vertical or torsional nystagmus. Horizontal nystagmuspresent in room light
Gaze nystagmus Both in room light (with fixation) and with video goggles (without fixation) Observe for nystagmus while eyes gaze 20 degrees to the right, then left, for 5–10 seconds with and without visual fixation Remains the same direction with both left and right gaze The pattern of nystagmus changes direction when in left and right gaze
Post head shake nystagmus With video goggles (without fixation) Head position is tipped down 20 degrees with eyes closed. The clinician oscillates the patient's head at 2 Hz, 20 times horizontally. Patient instructed to open eyes and clinician observes for nystagmus immediately upon stopping the head movement. Increases in intensity, same direction as spontaneous Not present
Head impulse test In room light (with fixation) Clinician rotates patient's head horizontally in a small range, high velocity while patient is instructed to keep eyes fixed on a target. Clinician observes for a refixation/corrective saccade Positive for refixation saccade to the deficit side(s) Negative
Pursuits In room light (with fixation) Patient head is stationary: clinician observe patient's eyes following a moving target (clinicians finger) horizontally and vertically Smooth Saccadic, disconjugate
Saccades In room light (with fixation) Patient head is stationary, clinician observes patient's eyes jumping quickly between two targets, horizontally and vertically Accurate, fast, without latency Hypometric, hypermetric, slow
Vertical skew deviation In room light (with fixation) Cover/Uncover test (32) Usually not present Typically present in posterior fossa CVA
Based on examination, the below findings including direction of nystagmus indicates either peripheral or central involvement.

TABLE 3 - Common patterns of nystagmus differentiating peripheral versus central vertigo and BPPV
Feature Peripheral Vertigo Central Vertigo
Spontaneous nystagmus 1st, 2nd, or 3rd degree horizontal spontaneous nystagmus Pure UB or DBPure TORPure horizontal (see below)(spontaneous or positional)
Positional nystagmus Negative for BPPV Posterior SCC BPPV Anterior SCC BPPV Horizontal SCC BPPV
No change from spontaneous nystagmus UB and TOR (towards the affected ear) DB and TOR (towards the affected ear) HorizontalGEO/APO
Direction of nystagmus or effect of gaze Unidirectional/ stays same direction with gaze Negative for spontaneous or gaze nystagmus Negative for spontaneous or gaze nystagmus Horizontal (pseudo) spontaneous (11) nystagmus may be present Direction changing: RB in right gaze, LB in left gazeDirection of nystagmus switches within the same head or body position
Effect of fixation (light) Suppresses with fixation No change or increases with fixation
Duration Persists without fixation (video goggles) <60 seconds = canalithaisis>60 seconds = cupulolithiasis Nystagmus persists
Nystagmus findings indicate whether vertigo is related to peripheral or central origin. Based on clinical examination including positional testing, the clinician can determine whether nystagmus findings suggest a peripheral cause including a vestibulopathy or BPPV or central involvement.APO indicates Apogeotropic (away from the earth); DB, downbeating; GEO, geotropic (towards the earth); LB, left beating; RB, rightbeating; SCC, semicircular Canal; TOR, torsional; UB, upbeating.

Posttraumatic BPPV exhibits several distinctive features, including a high incidence of bilateral, and multiple SCC involvement, equal sex occurrence, peak onset among young people, more difficulties in treating, and frequent reoccurrences (33,34). Diagnosis of multiple SCC BPPV is complex, as changes in nystagmus patterns caused by the simultaneous stimulation of more than one SCC can make it challenging to correctly identify (7). A summary of clinical tests to diagnose and treat BPPV is listed in Table 4.

TABLE 4 - Diagnosis and treatment of BPPV
Semicircular Canal Posterior (PSCC) Horizontal (HSCC) Anterior (ASCC)
Diagnostic test Dix-HallpikeSide lying test (32) Supine Roll test Dix-HallpikeDeep Center Head Hang test (35)
Nystagmus UB, Ipsilateral TOR (torsion toward the downward ear) Horizontal on both right and left sides DB, Ipsilateral TOR (torsion toward downward ear)
Duration <60 seconds; delayed onset; extinguishes >60 seconds; immediate onset; persistent Most commonly <60 seconds (If >60 seconds, may be light cupula) (36) Can be <60 seconds (short arm canalithiasis) OR >60 seconds (Cupulolithiasis) <60 seconds; delayed onset; extinguishes >60 seconds; immediate onset; persistent
Variant Canalithiasis (otoconia free floating in endolymph) Cupulolithiasis (ototoconia adhered to cupula) GEO (towards the earth) APO (away from the earth) Canalithiasis Cupulolithiasis
Treatment maneuvers  Canalith repositioning maneuver (12) Half-somersault (37) Liberatory maneuver (12)  Liberatory (12)∗Consider mastoid vibration  BBQ Roll (12) Gufoni/ Appiani (12) Forced prolonged positioning (12)∗No known treatment for light cupula  Gufoni/Casani (12) Kim manuever (38)∗Consider mastoid vibration  Canalith repositioning maneuver (39) Deep head hang (40) Modified liberatory (39)  Modified liberatory (39)∗Consider mastoid vibration
This table demonstrates positional testing and clinical findings including patterns of nystagmus for each of the three SCCs. Based on the direction and duration of nystagmus, the clinician is able to make an accurate diagnosis of SCC involvement. Once BPPV is accurately diagnosed, the clinician can perform the appropriate CRM specific to the active canal.APO indicates apogeotropic (away from the earth); DB, downbeating; GEO, geotropic (towards the earth); TOR, torsional; UB, upbeating.

CONCLUSION

This case highlights that early identification and treatment of dizziness after TBI are critical for optimal patient outcomes (41,42). Differentiating between multiple SSC BPPV in addition to other peripheral and central vestibular etiologies is complex. It is imperative to have a clear understanding of nystagmus patterns. Patient education regarding symptom presentation associated with BPPV and central decompensation, as well as self-management of symptoms, can improve overall long-term outcome and quality of life for this population.

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        Keywords:

        Benign paroxysmal positional vertigo; Canalith repositioning maneuver; Vestibular therapy

        Supplemental Digital Content

        Copyright © 2020 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of Otology & Neurotology, Inc.