- Email: [email protected]
Management of posttraumatic vertigo
Management of posttraumatic vertigo ARNE ERNST, MD, PHD, DIETMAR BASTA, ANDREW CLARKE, PHD, Berlin, Germany
PHD,
RAINER O. SEIDL,
OBJECTIVE: To evaluate patients after blunt trauma of the head, neck, and craniocervical junction (without fractures) with vertigo and to report the results of treatment after extensive diagnostics. STUDY DESIGN: Prospective study of consecutive new cases with vertigo after trauma at different periods of onset. During 2000-2002, 63 patients were examined and treated. SETTING: Regional trauma medical center for the greater Berlin Area, tertiary referral unit. RESULTS: The primary disorders included labyrinthine concussion (18), rupture of the round window membrane (6), and cervicogenic vertigo (12). The secondary disorders included otolith disorders (5), delayed endolymphatic hydrops (12), and canalolithiasis (9). The patients were free of vertigo symptoms (except cervicogenic and otolith disorder) after treatment, which consisted of habituation training, medical and surgical therapy options. The follow-up was 1 year. CONCLUSION: Posttraumatic vertigo can be treated with a high success rate once the underlying disorder has been identified. The extent of the neurotological test battery determines the precision and quality of diagnostics. Surgical measures should be an integral part of treatment modalities if conservative treatment is not effective. SIGNIFICANCE: Minor trauma of the head, neck, and craniocervical junction can have major impact on the vestibular system at different sites. Patients need to be carefully diagnosed, even if the onset of vertigo occurs a few weeks or months after the initial trauma. (Otolaryngol Head Neck Surg 2005;132:554-558.)
From the Department of Otolaryngology at ukb Medical Center (Drs Ernst, Basta, Seidl, and Todt) and the Department of Otolaryngology, Vestibular Research Labs at University Hospital Berlin (Charité), Benjamin Franklin Medical Center, (Drs Scherer and Clarke) Berlin, Germany. Supported by a grant from the Sonnenfeld Foundation, Berlin, Germany. Presented at the Annual Meeting of the American Academy of Otolaryngology–Head and Neck Surgery, Orlando, FL, September 21-24, 2003. Reprint requests: Prof. Arne Ernst, Department of Otolaryngology at ukb, Warener Str. 7, D-12683 Berlin, Germany; e-mail, [email protected]. 0194-5998/$30.00 Copyright © 2005 by the American Academy of Otolaryngology–Head and Neck Surgery Foundation, Inc. doi:10.1016/j.otohns.2004.09.034
554
MD,
INGO TODT,
MD,
HANS SCHERER,
MD,
and
B
lunt trauma of the head, neck, and craniocervical junction can result from injuries such as falls, whiplashtype injuries, contact injuries after impact with a solid object, among others. The trauma mechanisms can vary as well as the impact forces. The vestibular system can be impaired at different sites despite the fact that scanning (by MRI, CT) usually reveals no evident intracranial pathological changes, skull base fractures, or changes of the craniocervical junction. There are several reports in the literature about neurotological sequelae of a blunt trauma of the head, neck, and craniocervical junction.1-5 One of the most common pathologies described is benign paroxysmal positional vertigo (BPPV), which can be treated by repositioning maneuvers with a high success rate.6 It is, therefore, the aim of the present paper to summarize the vestibular findings of a larger sample of trauma patients who complained of dizziness and to outline management strategies. MATERIALS AND METHODS In a prospective study, 63 consecutive patients who complained of vertigo (52 female, 11 male; age range 17-59 years with a mean of 27.5 years) after blunt trauma of the head, neck, and craniocervical junction were included (from 2000 through 2002). The patients gave their informed consent to participate in the study. The pathomechanisms of the trauma, the related diagnoses, and the gender ratio are summarized in Table 1. In all cases, primary care and further diagnostics were performed by the Departments of Trauma Surgery, Neurology, and Radiology. After clinical examination, MRI or CT scanning was performed of the neurocranium, the skull base, and the craniocervical junction. When no evident pathology (e.g., fractures, wounds, intracranial pathology, or neurological deficits) was found, the patients were asked to describe any additional symptoms or health problems. If they complained of vertigo (“dizziness”, “unsteadiness”, “slipping away”, “rotational or positional vertigo”), they were transferred to our department. This is denoted here as “primary disorder”, i.e., occurrence within the first 24 hours after the trauma. In the other cases in which any such symptoms were reported during a later consultation, they were referred to “secondary disorder” (3 weeks to 3 months after the trauma). Auditory or other sensory deficits (e.g., blurred vision or anosmia) are not dealt with in the present study, although a
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Table 1. Pathomechanisms involved in blunt trauma of the head, neck, and craniocervical junction and neurotological disorders involved in the 63 patients. Note that in some patients 2 or more disorders could be observed simultaneously or successively. Number of patients Trauma mechanisms Brain concussion (i.e. falling from different heights on the ground) Brain concussion with cervical compression (i.e. falling from a horse on the head) Anteretroflexion of the cervical spine (classical “whiplash” mechanism) Anteretroflexion of the cervical spine with contact trauma the head hits interior parts of the car, in addition to the head restraint) Other mechanisms (i.e. the head is hit by another solid item, e.g., a door, a blunt instrument, a soccer ball) Neurotological disorders Perilymphatic fistula (round-window rupture) Benign paroxysmal positional vertigo Labyrinthine concussion Central vestibular disorder Delayed endolymphatic hydrops (posttraumatic) Otolith disorder(saccular or utricular dysfunction) Cervicogenic vertigo (vestibulospinal postural instability)
n n n n
⫽ ⫽ ⫽ ⫽
12 (9 f, 3 m) 8 (3 f, 5 m) 23 (22 f, 1 m) 16 (16 f)
n ⫽ 4 (2 f, 2 m) n n n n n n n
⫽3 (1 f, 2 m) ⫽ 36 (33 f, 3 m) ⫽ 12 (11 f, 1 m) ⫽ 3 (3 f) ⫽ 12 (10 f, 2 m) ⫽ 16 (10 f, 6 m) ⫽ 17 (16 f, 1 m)
n, number of patients in each subgroup; f, female; m, male.
pure-tone audiogram (PTA) was obtained from all patients. On referral, the case history of each patient was taken (trauma mechanism, date, initial complaints, subjective typing of vertigo); an otoscopic examination was carried out and the following neurotological tests were performed: vestibulospinal tests (Romberg, Unterberger test); videooculographic testing of spontaneous, positional nystagmus, random horizontal or fixed horizontal saccades; caloric irrigation (VOR testing); rotational chair testing (sinusoidal harmonic acceleration testing of low-frequency VOR gain and phase; GN Otometrics, Neckartenzlingen, Germany); dynamic posturography testing [sensory organization test (SOT), motor control test (MCT); Neurocom, Clakamas, OR7]; otolith testing [saccular testing by VEMP recordings and utricular testing using subjective visual vertical (SVV) and/or otolith-ocular response (OOR) during eccentric rotation; VIKING V, Nicolet Biomedical, Kornwestheim, Germany; for methodology see Refs. 8 and 9]; electrocochleography (optional, only performed in cases of suspected delayed, posttraumatic, endolymphatic hydrops10; trunk sway measures of postural stability by Sway Star (optional, only performed in cases of suspected cervicogenic vertigo; Balance Int Innovations, Basle, Switzerland11,12). After diagnosing the different neurotological disease entities (Table 1), they were subject to a management scheme according to the underlying disease (Table 2). The follow-up period of the patients was 1 year. The patients’ test results were compared to age- and gender-related control subjects without a history of head and neck trauma. A statistically significant correlation between the trauma mechanisms and the type of neurotological disorder could not be found.
RESULTS The different trauma mechanisms led to a variety of neurotological disorders (Table 1) although no significant correlation was found between mechanism and types of disorder. The primary disorders that affected the patients within the first 24 hours after trauma included: ● BPPV (n ⫽ 36), which reoccurred in 9 patients. Primary treatment consisted of repositioning maneuver6,13 repeated up to 3 times if required. After reoccurrence, 2 patients were surgically treated by occlusion of the posterior semicircular canal.14 A positional, torsional nystagmus upon Dix-Hallpike’s maneuver was taken as confirmation of the diagnosis. ● Labyrinthine concussion (n ⫽ 12) had normalized over the first 5 days with drug treatment (sedatives, antemetics) on average. The occurrence of spontaneous nystagmus, initial unilateral hyporesponsiveness upon caloric irrigation, pathological rotational chair test result (peripheral lesion), and deviation upon vestibulospinal testing was taken as confirmation of the diagnosis. ● Perilymphatic fistulae (n ⫽ 3) led to a sudden onset of dizziness in combination with sensorineural hearing loss (SNHL) of varying degree. These patients were treated surgically by patching the round and oval window niches with connective tissue and fibrin glue. The occurrence of spontaneous nystagmus, initial unilateral hyporesponsiveness upon caloric irrigation, pathological rotational chair test result (periph-
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556 ERNST et al
Table 2. Neurotological disorders, their leading clinical symptoms, time-of-onset (i.e. primary, within 24 hours after the trauma, or secondary, with a certain time-lag, and the management schemes applied in each disorder (for details see “Results”) Neurotological disorder
Clinical symptoms/time-of-onset
Perilymphatic fistula BPPV Labyrinthine concussion Central vestibular disorder Delayed endolymphatic hydrops
Dizziness, hearing loss (primary) Positional vertigo (primary, but reoccurring) Dizziness, lateropulsion vomiting (primary) Mixed, “tumbling” (primary) Attacks of rotational vertigo (Ménière-like) (secondary) Unsteadiness, stumbling (secondary) “Tumbling”, “feeling drunk” (correlated to pain) (secondary)
Otolith disorder Cervicogenic vertigo
eral lesion), deviation upon vestibulospinal testing, a sensorineural hearing loss of different extent (in 50 % more than 40 dB over all frequencies) with/without tinnitus was taken as confirmation of the diagnosis. ● Central vestibular disorder (n ⫽ 3) had a mixed pathology with the leading symptom of “tumbling”. The patients were instructed to rest, they were treated by drugs (sedatives, antemetics) and 2 of them had fully recovered within the first 5 days. One patient was additionally given an individualized home training. Different types of nystagmus (vertical nystagmus, skew deviation, ocular torsion), horizontal body rotations upon vestibulospinal tests, pathological SOT over all conditions (I-VI) was taken as confirmation of the diagnosis. The following secondary disorders were diagnosed at a later date (3 weeks to 3 months, 6 weeks on average after the trauma): ● Delayed endolymphatic hydrops (n ⫽ 12). The patients reported classical Mènière-like type of vertigo with attacks, but without hearing loss or tinnitus. EcoG was used to confirm the presence of hydrops. 8 patients were free of vertigo under (betahistine) drug treatment, 4 patients were operated on by endolymphatic sac surgery (saccus exposure) and were free of vertigo after the operation. ● Cervicogenic vertigo (n ⫽ 17) occurred widely, but not only after a “whiplash-type” of injury. The diagnosis was confirmed by Sway Star testing (pathological), by exclusion of other disorders and by pathological SOT (conditions 5 and 6, visual preference with unilateral stance imbalance7,12). These patients gave mixed symptoms that were reinforced when the neck pain and the limitation of cervical spine mobility was maximal. In general, the extent and expression of
Therapeutic management Tympanoscopy (patching the RW) Repositioning maneuver, posterior canal occlusion Drugs (sedatives, antemetics) Drugs (sedatives, antemetics) habituation training Drugs (betahistidine), surgery (endolymphatic sac exposure) Habituation training (platform training) Physiotherapy, analgesics, habituation training
vertigo varied in dependence of the physical condition of the patient. The patients were primarily treated by physiotherapy (e.g., osteopathy, exercises), analgesics and antirheumatics and by platform training on the BalanceMaster (Neurocom, Clakamas, OR) to give them better control of their increase in sway in the roll and pitch plane. These patients produced widely scattered results; only 12 patients were definitely free of vertigo after 1 year. 5 patients complained, to varying degrees, but continuously, about vertiginous episodes after 1 year. ● Otolith disorders (n ⫽ 16) were determined by VEMP testing (saccular) or eccentric rotation (utricular). A combination of saccular and and utricular dysfunction was usually found, whereas in 2 cases an isolated utricular dysfunction was found. The patients with otolith disorders generally presented after a longer period of time (usually after approximately 10 weeks) because 85 % did not consider their “unsteadiness” as a specific symptom, but rather as common sequelae of the trauma. These patients were provided with individualized training routines on a tilting platform. The success of such a habituation training can only be determined after a 12- to 24-month period. After 12 months, 35% of the patients reported partial improvement of their symptoms. The remaining patients had not yet found the habituation training to be effective. Of the 63 patients, 29 (46%) manifested a combination of 2 different types of neurotological disorders (e.g., initially BPPV, followed by a delayed endolymphatic hydrops); whereas 7 patients (11 %) had more than 2 neurotological disorders (e.g., labyrinthine concussion, followed by otolith disorder and cervicogenic vertigo; Table 3).
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TABLE 3. Parallel or subsequent occurrence of different neurotological disorders Type of disorders Labyrinthine concussion, BPPV (parallel) Labyrinthine concussion, central vestibular disorder (parallel) Labyrinthine concussion, cervicogenic vertigo (subsequent) BPPV, delayed el hydrops (subsequent) Otolith disorder, cervicogenic vertigo (subsequent) Perilymphatic fistula, otolith disorder (subsequent) Labyrinthine concussion, otolith disorder, cervicogenic vertigo (subsequent) BPPV, otolith disorder, cervicogenic vertigo (subsequent) BPPV, delayed el hydrops, cervicogenic vertigo (subsequent)
Number of patients 8 1 1 9 7 3 1 4 2
BPPV, benign paroxysmal positional vertigo; el hydrops, endolymphatic hydrops.
DISCUSSION The present study is intended to evaluate the impact of acceleration or forces applied to the head, neck region, and to the craniocervical junction (blunt trauma). The 2 most interesting findings are the lack of correlation between the trauma mechanism and a particular neurotological disorder; and the variety of disorders found concomitantly or successively in some of the patients. We did not systematically work up the patients’ subjective complaints or the impact of vertigo on the quality of life (e.g., by the Dizziness Handicap Inventory15) in this study; this requires the long-term perspective and is therefore still in progress. A majority of the patients (76%) also reported temporary subjective hearing loss, although we only found substantial hearing losses in the subpopulation with perilymphatic fistula (a SNHL could be evidenced in all cases by PTA). However, we could report recently on the impact of blunt head trauma on the central auditory processing that can be significantly impaired.16 There is a longstanding controversy in the literature as to whether blunt trauma to the head and neck, “whiplash” type of injury, or other types of injury can affect the vestibular system (see Refs. 1-3, 5 and the comments on this article). In our series, the patients with cervicogenic vertigo had undergone various trauma mechanisms (including brain concussion with cervical compression, having the head and craniocervical junction hit by another solid item, apart from “whiplash”) and were frequently affected by another or even 2 other types of neurotological disorders (Table 3). The majority of our patients were female, which is due to the fact that the prevailing trauma mechanisms (ante/retroflexion of the
cervical spine, Table 1) affected young women without trained musculoskeletal system (frequently on diet, contraceptive intake, in smaller cars) with no adequate muscular resistance against a sudden impact (e.g. rearend collision) (see below). This female prevalence is in line with the literature, the Quebec Task Force in particular17 and our recent paper on auditory symptoms after blunt head trauma.16 When considering the medium-term prognosis (1 year) of each type of neurotological disorder, the primary disorders had the best outcome. This is in line with other reports (13, 14, 18). The poorest outcome was observed in the (largely female) subpopulation of patients with cervicogenic vertigo and otolith disorder. The first is presumed to be the result of the interindividual variation in the musculoskeletal system (and the ability to develop coping strategies by habituation/training7,12,19) and the highly variable conditions of the cervical spine and the soft tissue (muscles, ligaments, joints) in the largely female patients (pain episodes, pre-trauma conditions, contraceptive intake, etc.). Otolithic vertigo could likewise only be treated with very limited success in the mediumterm perspective. This seems to be based on the specific nature (gravity sensor) of this type of receptor20and its ancient phylogenetic origin, which makes it and the central vestibular correlates quite resistant to external influences, including training and habituation. Vestibular (inferior branch) neurectomy could be an alternative treatment option in the long-term perspective.21 In essence, posttraumatic vertigo can become a challenge for the otolaryngologist because of the variability and the late onset of symptoms. An extended neurotological test battery is required to reliably assess those patients. REFERENCES 1. Fitzgerald DC. Head trauma: hearing loss and dizziness. J Trauma 1996;40:488-96. 2. Guyot JP, Liard P, Thielen K, et al. Isolated vestibular areflexia after blunt head trauma. Ann Otol Rhinol Laryngol 2001;110: 562-5. 3. Vibert D, Hausler R. Acute vestibular deficits after whiplash injuries. Ann Otol Rhinol Laryngol 2003;112:246-51. 4. Basford JR, Chou LS, Kaufmann KR, et al. An assessment of gait and balance deficits after traumatic brain injury. Arch Phys Med Rehabil 2003;84:343-9. 5. Rubin AM, Wooley SM, Dailey DV, et al. Postural stability following mild head or whiplash injury. Am J Otol 1995;16: 216-21. 6. Parnes LS, Price-Jones RG. Particle repositioning manoeuver for BPPV. Ann Otol Rhinol Otol 1993;102:325-31. 7. Allum JHJ, Shepard NT. An overview of the clinical use of dynamic posturography in the differential diagnosis of balance disorders. J Vest Res 1999;9:223-52. 8. Colebatch JG, Halmagyi GM, Skuse NF. Myogenic potentials generated by a click-evoked vestibulocollic reflex. J Neurol Neurosurg Psychiatry 1994;57:190-7. 9. Clarke AH, Engelhorn A. Unilateral testing of utricular function. Exp Brain Res 1998;121:457-64.
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10. Ge X, Shea JJ. Transtympanic electrocochleography: a 10-year experience. Otol Neurotol 2001;22:465-70. 11. Allum JHJ, Aitkin AL, Ernst A. Differences between trunk sway characteristics on a foam support surface and on the Equitest ankle-sway-referenced support surface. Gait Posture 2002;16: 264-70. 12. Sjostrom H, Allum JHJ, Carpenter MG, et al. Trunk sway measures of postural stability during clinical balance tests in patients with chronic whiplash injury symptoms. Spine 2003; 28:1725-34. 13. Epley JM. Particle repositioning for BPPV. Otolaryngol Clin North Am 1996;29:323-31. 14. Parnes LS, McClure JA. Posterior semicircular canal occlusion in the normal hearing ear. Otolaryngol Head Neck Surg 1991; 104:52-7. 15. Jacobson GP, Newman CW. The development of the Dizziness Handicap Inventory. Arch Otolaryngol Head Neck Surg 1990; 116:424-7.
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16. Nölle C, Todt I, Ernst A. Pathophysiological changes of the central auditory pathway after blunt trauma of the head. J Neurotrauma 2004;21:251-8. 17. Spitzer WO, Skovron ML, Salmi LR, et al. Scientific monograph of the Quebec Task Force on Whiplash-Associated Disorders: redefining whiplash and ist management. Spine 1995;20(Suppl 8):1S-73S. 18. Shea JJ, Xianxi G, Orchik DJ. Traumatic endolymphatic hydrops. Am J Otol 1995;16:235-40. 19. Allum JHJ, Bloem BR, Carpenter MG, et al. Differential diagnosis of proprioceptive and vestibular deficits using dynamic support-surface posturography. Gait Posture 2001;14: 217-26. 20. Clarke A, Schonfeld U, Helling K. Unilateral examination of utricle and saccule function. J Vest Res 2003;13:215-25. 21. Sanna M, Ylikoski J. Vestibular neurectomy for dizziness after head trauma. ORL J Otorhinolaryngol Relat Spec 1983; 45:216-25.
PHD,
RAINER O. SEIDL,
OBJECTIVE: To evaluate patients after blunt trauma of the head, neck, and craniocervical junction (without fractures) with vertigo and to report the results of treatment after extensive diagnostics. STUDY DESIGN: Prospective study of consecutive new cases with vertigo after trauma at different periods of onset. During 2000-2002, 63 patients were examined and treated. SETTING: Regional trauma medical center for the greater Berlin Area, tertiary referral unit. RESULTS: The primary disorders included labyrinthine concussion (18), rupture of the round window membrane (6), and cervicogenic vertigo (12). The secondary disorders included otolith disorders (5), delayed endolymphatic hydrops (12), and canalolithiasis (9). The patients were free of vertigo symptoms (except cervicogenic and otolith disorder) after treatment, which consisted of habituation training, medical and surgical therapy options. The follow-up was 1 year. CONCLUSION: Posttraumatic vertigo can be treated with a high success rate once the underlying disorder has been identified. The extent of the neurotological test battery determines the precision and quality of diagnostics. Surgical measures should be an integral part of treatment modalities if conservative treatment is not effective. SIGNIFICANCE: Minor trauma of the head, neck, and craniocervical junction can have major impact on the vestibular system at different sites. Patients need to be carefully diagnosed, even if the onset of vertigo occurs a few weeks or months after the initial trauma. (Otolaryngol Head Neck Surg 2005;132:554-558.)
From the Department of Otolaryngology at ukb Medical Center (Drs Ernst, Basta, Seidl, and Todt) and the Department of Otolaryngology, Vestibular Research Labs at University Hospital Berlin (Charité), Benjamin Franklin Medical Center, (Drs Scherer and Clarke) Berlin, Germany. Supported by a grant from the Sonnenfeld Foundation, Berlin, Germany. Presented at the Annual Meeting of the American Academy of Otolaryngology–Head and Neck Surgery, Orlando, FL, September 21-24, 2003. Reprint requests: Prof. Arne Ernst, Department of Otolaryngology at ukb, Warener Str. 7, D-12683 Berlin, Germany; e-mail, [email protected]. 0194-5998/$30.00 Copyright © 2005 by the American Academy of Otolaryngology–Head and Neck Surgery Foundation, Inc. doi:10.1016/j.otohns.2004.09.034
554
MD,
INGO TODT,
MD,
HANS SCHERER,
MD,
and
B
lunt trauma of the head, neck, and craniocervical junction can result from injuries such as falls, whiplashtype injuries, contact injuries after impact with a solid object, among others. The trauma mechanisms can vary as well as the impact forces. The vestibular system can be impaired at different sites despite the fact that scanning (by MRI, CT) usually reveals no evident intracranial pathological changes, skull base fractures, or changes of the craniocervical junction. There are several reports in the literature about neurotological sequelae of a blunt trauma of the head, neck, and craniocervical junction.1-5 One of the most common pathologies described is benign paroxysmal positional vertigo (BPPV), which can be treated by repositioning maneuvers with a high success rate.6 It is, therefore, the aim of the present paper to summarize the vestibular findings of a larger sample of trauma patients who complained of dizziness and to outline management strategies. MATERIALS AND METHODS In a prospective study, 63 consecutive patients who complained of vertigo (52 female, 11 male; age range 17-59 years with a mean of 27.5 years) after blunt trauma of the head, neck, and craniocervical junction were included (from 2000 through 2002). The patients gave their informed consent to participate in the study. The pathomechanisms of the trauma, the related diagnoses, and the gender ratio are summarized in Table 1. In all cases, primary care and further diagnostics were performed by the Departments of Trauma Surgery, Neurology, and Radiology. After clinical examination, MRI or CT scanning was performed of the neurocranium, the skull base, and the craniocervical junction. When no evident pathology (e.g., fractures, wounds, intracranial pathology, or neurological deficits) was found, the patients were asked to describe any additional symptoms or health problems. If they complained of vertigo (“dizziness”, “unsteadiness”, “slipping away”, “rotational or positional vertigo”), they were transferred to our department. This is denoted here as “primary disorder”, i.e., occurrence within the first 24 hours after the trauma. In the other cases in which any such symptoms were reported during a later consultation, they were referred to “secondary disorder” (3 weeks to 3 months after the trauma). Auditory or other sensory deficits (e.g., blurred vision or anosmia) are not dealt with in the present study, although a
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Table 1. Pathomechanisms involved in blunt trauma of the head, neck, and craniocervical junction and neurotological disorders involved in the 63 patients. Note that in some patients 2 or more disorders could be observed simultaneously or successively. Number of patients Trauma mechanisms Brain concussion (i.e. falling from different heights on the ground) Brain concussion with cervical compression (i.e. falling from a horse on the head) Anteretroflexion of the cervical spine (classical “whiplash” mechanism) Anteretroflexion of the cervical spine with contact trauma the head hits interior parts of the car, in addition to the head restraint) Other mechanisms (i.e. the head is hit by another solid item, e.g., a door, a blunt instrument, a soccer ball) Neurotological disorders Perilymphatic fistula (round-window rupture) Benign paroxysmal positional vertigo Labyrinthine concussion Central vestibular disorder Delayed endolymphatic hydrops (posttraumatic) Otolith disorder(saccular or utricular dysfunction) Cervicogenic vertigo (vestibulospinal postural instability)
n n n n
⫽ ⫽ ⫽ ⫽
12 (9 f, 3 m) 8 (3 f, 5 m) 23 (22 f, 1 m) 16 (16 f)
n ⫽ 4 (2 f, 2 m) n n n n n n n
⫽3 (1 f, 2 m) ⫽ 36 (33 f, 3 m) ⫽ 12 (11 f, 1 m) ⫽ 3 (3 f) ⫽ 12 (10 f, 2 m) ⫽ 16 (10 f, 6 m) ⫽ 17 (16 f, 1 m)
n, number of patients in each subgroup; f, female; m, male.
pure-tone audiogram (PTA) was obtained from all patients. On referral, the case history of each patient was taken (trauma mechanism, date, initial complaints, subjective typing of vertigo); an otoscopic examination was carried out and the following neurotological tests were performed: vestibulospinal tests (Romberg, Unterberger test); videooculographic testing of spontaneous, positional nystagmus, random horizontal or fixed horizontal saccades; caloric irrigation (VOR testing); rotational chair testing (sinusoidal harmonic acceleration testing of low-frequency VOR gain and phase; GN Otometrics, Neckartenzlingen, Germany); dynamic posturography testing [sensory organization test (SOT), motor control test (MCT); Neurocom, Clakamas, OR7]; otolith testing [saccular testing by VEMP recordings and utricular testing using subjective visual vertical (SVV) and/or otolith-ocular response (OOR) during eccentric rotation; VIKING V, Nicolet Biomedical, Kornwestheim, Germany; for methodology see Refs. 8 and 9]; electrocochleography (optional, only performed in cases of suspected delayed, posttraumatic, endolymphatic hydrops10; trunk sway measures of postural stability by Sway Star (optional, only performed in cases of suspected cervicogenic vertigo; Balance Int Innovations, Basle, Switzerland11,12). After diagnosing the different neurotological disease entities (Table 1), they were subject to a management scheme according to the underlying disease (Table 2). The follow-up period of the patients was 1 year. The patients’ test results were compared to age- and gender-related control subjects without a history of head and neck trauma. A statistically significant correlation between the trauma mechanisms and the type of neurotological disorder could not be found.
RESULTS The different trauma mechanisms led to a variety of neurotological disorders (Table 1) although no significant correlation was found between mechanism and types of disorder. The primary disorders that affected the patients within the first 24 hours after trauma included: ● BPPV (n ⫽ 36), which reoccurred in 9 patients. Primary treatment consisted of repositioning maneuver6,13 repeated up to 3 times if required. After reoccurrence, 2 patients were surgically treated by occlusion of the posterior semicircular canal.14 A positional, torsional nystagmus upon Dix-Hallpike’s maneuver was taken as confirmation of the diagnosis. ● Labyrinthine concussion (n ⫽ 12) had normalized over the first 5 days with drug treatment (sedatives, antemetics) on average. The occurrence of spontaneous nystagmus, initial unilateral hyporesponsiveness upon caloric irrigation, pathological rotational chair test result (peripheral lesion), and deviation upon vestibulospinal testing was taken as confirmation of the diagnosis. ● Perilymphatic fistulae (n ⫽ 3) led to a sudden onset of dizziness in combination with sensorineural hearing loss (SNHL) of varying degree. These patients were treated surgically by patching the round and oval window niches with connective tissue and fibrin glue. The occurrence of spontaneous nystagmus, initial unilateral hyporesponsiveness upon caloric irrigation, pathological rotational chair test result (periph-
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556 ERNST et al
Table 2. Neurotological disorders, their leading clinical symptoms, time-of-onset (i.e. primary, within 24 hours after the trauma, or secondary, with a certain time-lag, and the management schemes applied in each disorder (for details see “Results”) Neurotological disorder
Clinical symptoms/time-of-onset
Perilymphatic fistula BPPV Labyrinthine concussion Central vestibular disorder Delayed endolymphatic hydrops
Dizziness, hearing loss (primary) Positional vertigo (primary, but reoccurring) Dizziness, lateropulsion vomiting (primary) Mixed, “tumbling” (primary) Attacks of rotational vertigo (Ménière-like) (secondary) Unsteadiness, stumbling (secondary) “Tumbling”, “feeling drunk” (correlated to pain) (secondary)
Otolith disorder Cervicogenic vertigo
eral lesion), deviation upon vestibulospinal testing, a sensorineural hearing loss of different extent (in 50 % more than 40 dB over all frequencies) with/without tinnitus was taken as confirmation of the diagnosis. ● Central vestibular disorder (n ⫽ 3) had a mixed pathology with the leading symptom of “tumbling”. The patients were instructed to rest, they were treated by drugs (sedatives, antemetics) and 2 of them had fully recovered within the first 5 days. One patient was additionally given an individualized home training. Different types of nystagmus (vertical nystagmus, skew deviation, ocular torsion), horizontal body rotations upon vestibulospinal tests, pathological SOT over all conditions (I-VI) was taken as confirmation of the diagnosis. The following secondary disorders were diagnosed at a later date (3 weeks to 3 months, 6 weeks on average after the trauma): ● Delayed endolymphatic hydrops (n ⫽ 12). The patients reported classical Mènière-like type of vertigo with attacks, but without hearing loss or tinnitus. EcoG was used to confirm the presence of hydrops. 8 patients were free of vertigo under (betahistine) drug treatment, 4 patients were operated on by endolymphatic sac surgery (saccus exposure) and were free of vertigo after the operation. ● Cervicogenic vertigo (n ⫽ 17) occurred widely, but not only after a “whiplash-type” of injury. The diagnosis was confirmed by Sway Star testing (pathological), by exclusion of other disorders and by pathological SOT (conditions 5 and 6, visual preference with unilateral stance imbalance7,12). These patients gave mixed symptoms that were reinforced when the neck pain and the limitation of cervical spine mobility was maximal. In general, the extent and expression of
Therapeutic management Tympanoscopy (patching the RW) Repositioning maneuver, posterior canal occlusion Drugs (sedatives, antemetics) Drugs (sedatives, antemetics) habituation training Drugs (betahistidine), surgery (endolymphatic sac exposure) Habituation training (platform training) Physiotherapy, analgesics, habituation training
vertigo varied in dependence of the physical condition of the patient. The patients were primarily treated by physiotherapy (e.g., osteopathy, exercises), analgesics and antirheumatics and by platform training on the BalanceMaster (Neurocom, Clakamas, OR) to give them better control of their increase in sway in the roll and pitch plane. These patients produced widely scattered results; only 12 patients were definitely free of vertigo after 1 year. 5 patients complained, to varying degrees, but continuously, about vertiginous episodes after 1 year. ● Otolith disorders (n ⫽ 16) were determined by VEMP testing (saccular) or eccentric rotation (utricular). A combination of saccular and and utricular dysfunction was usually found, whereas in 2 cases an isolated utricular dysfunction was found. The patients with otolith disorders generally presented after a longer period of time (usually after approximately 10 weeks) because 85 % did not consider their “unsteadiness” as a specific symptom, but rather as common sequelae of the trauma. These patients were provided with individualized training routines on a tilting platform. The success of such a habituation training can only be determined after a 12- to 24-month period. After 12 months, 35% of the patients reported partial improvement of their symptoms. The remaining patients had not yet found the habituation training to be effective. Of the 63 patients, 29 (46%) manifested a combination of 2 different types of neurotological disorders (e.g., initially BPPV, followed by a delayed endolymphatic hydrops); whereas 7 patients (11 %) had more than 2 neurotological disorders (e.g., labyrinthine concussion, followed by otolith disorder and cervicogenic vertigo; Table 3).
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TABLE 3. Parallel or subsequent occurrence of different neurotological disorders Type of disorders Labyrinthine concussion, BPPV (parallel) Labyrinthine concussion, central vestibular disorder (parallel) Labyrinthine concussion, cervicogenic vertigo (subsequent) BPPV, delayed el hydrops (subsequent) Otolith disorder, cervicogenic vertigo (subsequent) Perilymphatic fistula, otolith disorder (subsequent) Labyrinthine concussion, otolith disorder, cervicogenic vertigo (subsequent) BPPV, otolith disorder, cervicogenic vertigo (subsequent) BPPV, delayed el hydrops, cervicogenic vertigo (subsequent)
Number of patients 8 1 1 9 7 3 1 4 2
BPPV, benign paroxysmal positional vertigo; el hydrops, endolymphatic hydrops.
DISCUSSION The present study is intended to evaluate the impact of acceleration or forces applied to the head, neck region, and to the craniocervical junction (blunt trauma). The 2 most interesting findings are the lack of correlation between the trauma mechanism and a particular neurotological disorder; and the variety of disorders found concomitantly or successively in some of the patients. We did not systematically work up the patients’ subjective complaints or the impact of vertigo on the quality of life (e.g., by the Dizziness Handicap Inventory15) in this study; this requires the long-term perspective and is therefore still in progress. A majority of the patients (76%) also reported temporary subjective hearing loss, although we only found substantial hearing losses in the subpopulation with perilymphatic fistula (a SNHL could be evidenced in all cases by PTA). However, we could report recently on the impact of blunt head trauma on the central auditory processing that can be significantly impaired.16 There is a longstanding controversy in the literature as to whether blunt trauma to the head and neck, “whiplash” type of injury, or other types of injury can affect the vestibular system (see Refs. 1-3, 5 and the comments on this article). In our series, the patients with cervicogenic vertigo had undergone various trauma mechanisms (including brain concussion with cervical compression, having the head and craniocervical junction hit by another solid item, apart from “whiplash”) and were frequently affected by another or even 2 other types of neurotological disorders (Table 3). The majority of our patients were female, which is due to the fact that the prevailing trauma mechanisms (ante/retroflexion of the
cervical spine, Table 1) affected young women without trained musculoskeletal system (frequently on diet, contraceptive intake, in smaller cars) with no adequate muscular resistance against a sudden impact (e.g. rearend collision) (see below). This female prevalence is in line with the literature, the Quebec Task Force in particular17 and our recent paper on auditory symptoms after blunt head trauma.16 When considering the medium-term prognosis (1 year) of each type of neurotological disorder, the primary disorders had the best outcome. This is in line with other reports (13, 14, 18). The poorest outcome was observed in the (largely female) subpopulation of patients with cervicogenic vertigo and otolith disorder. The first is presumed to be the result of the interindividual variation in the musculoskeletal system (and the ability to develop coping strategies by habituation/training7,12,19) and the highly variable conditions of the cervical spine and the soft tissue (muscles, ligaments, joints) in the largely female patients (pain episodes, pre-trauma conditions, contraceptive intake, etc.). Otolithic vertigo could likewise only be treated with very limited success in the mediumterm perspective. This seems to be based on the specific nature (gravity sensor) of this type of receptor20and its ancient phylogenetic origin, which makes it and the central vestibular correlates quite resistant to external influences, including training and habituation. Vestibular (inferior branch) neurectomy could be an alternative treatment option in the long-term perspective.21 In essence, posttraumatic vertigo can become a challenge for the otolaryngologist because of the variability and the late onset of symptoms. An extended neurotological test battery is required to reliably assess those patients. REFERENCES 1. Fitzgerald DC. Head trauma: hearing loss and dizziness. J Trauma 1996;40:488-96. 2. Guyot JP, Liard P, Thielen K, et al. Isolated vestibular areflexia after blunt head trauma. Ann Otol Rhinol Laryngol 2001;110: 562-5. 3. Vibert D, Hausler R. Acute vestibular deficits after whiplash injuries. Ann Otol Rhinol Laryngol 2003;112:246-51. 4. Basford JR, Chou LS, Kaufmann KR, et al. An assessment of gait and balance deficits after traumatic brain injury. Arch Phys Med Rehabil 2003;84:343-9. 5. Rubin AM, Wooley SM, Dailey DV, et al. Postural stability following mild head or whiplash injury. Am J Otol 1995;16: 216-21. 6. Parnes LS, Price-Jones RG. Particle repositioning manoeuver for BPPV. Ann Otol Rhinol Otol 1993;102:325-31. 7. Allum JHJ, Shepard NT. An overview of the clinical use of dynamic posturography in the differential diagnosis of balance disorders. J Vest Res 1999;9:223-52. 8. Colebatch JG, Halmagyi GM, Skuse NF. Myogenic potentials generated by a click-evoked vestibulocollic reflex. J Neurol Neurosurg Psychiatry 1994;57:190-7. 9. Clarke AH, Engelhorn A. Unilateral testing of utricular function. Exp Brain Res 1998;121:457-64.
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10. Ge X, Shea JJ. Transtympanic electrocochleography: a 10-year experience. Otol Neurotol 2001;22:465-70. 11. Allum JHJ, Aitkin AL, Ernst A. Differences between trunk sway characteristics on a foam support surface and on the Equitest ankle-sway-referenced support surface. Gait Posture 2002;16: 264-70. 12. Sjostrom H, Allum JHJ, Carpenter MG, et al. Trunk sway measures of postural stability during clinical balance tests in patients with chronic whiplash injury symptoms. Spine 2003; 28:1725-34. 13. Epley JM. Particle repositioning for BPPV. Otolaryngol Clin North Am 1996;29:323-31. 14. Parnes LS, McClure JA. Posterior semicircular canal occlusion in the normal hearing ear. Otolaryngol Head Neck Surg 1991; 104:52-7. 15. Jacobson GP, Newman CW. The development of the Dizziness Handicap Inventory. Arch Otolaryngol Head Neck Surg 1990; 116:424-7.
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16. Nölle C, Todt I, Ernst A. Pathophysiological changes of the central auditory pathway after blunt trauma of the head. J Neurotrauma 2004;21:251-8. 17. Spitzer WO, Skovron ML, Salmi LR, et al. Scientific monograph of the Quebec Task Force on Whiplash-Associated Disorders: redefining whiplash and ist management. Spine 1995;20(Suppl 8):1S-73S. 18. Shea JJ, Xianxi G, Orchik DJ. Traumatic endolymphatic hydrops. Am J Otol 1995;16:235-40. 19. Allum JHJ, Bloem BR, Carpenter MG, et al. Differential diagnosis of proprioceptive and vestibular deficits using dynamic support-surface posturography. Gait Posture 2001;14: 217-26. 20. Clarke A, Schonfeld U, Helling K. Unilateral examination of utricle and saccule function. J Vest Res 2003;13:215-25. 21. Sanna M, Ylikoski J. Vestibular neurectomy for dizziness after head trauma. ORL J Otorhinolaryngol Relat Spec 1983; 45:216-25.