|Year : 2014 | Volume
| Issue : 3 | Page : 95-98
MK Taneja1, Vivek Taneja2, Himanshu Varshney3
1 Editor-in-Chief IJO, Indian Institute of Ear Diseases, Muzaffarnagar, New Delhi, India
2 Department of Otorthinolaryngology, Subharti Medical College, Meerut, India
3 Department of ENT and Head Neck Surgery, Sri Sai Hospital, Moradabad, Uttar Pradesh, India
|Date of Web Publication||16-Jul-2014|
M K Taneja
Editor-in-Chief IJO, Indian Institute of Ear Diseases, Muzaffarnagar, New Delhi
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Taneja M K, Taneja V, Varshney H. Post-traumatic vertigo. Indian J Otol 2014;20:95-8
| Introduction|| |
Vertigo, dizziness and imbalance are the frequent symptoms in patients who suffer trauma to the head, neck or craniovertebral junction and can result in peripheral or central vestibular dysfunction. The trauma may be by injuries due to fall, motor vehicle accident, assault, contact sport and blast injury. The initial descriptions of vestibular symptoms after injuries were given by Robert Barany during World War I.  The incidence of posttraumatic dizziness or imbalance ranges from 24% to 83%, respectively.  It can be classified into peripheral and central depending on the structures affected. The great variability of trauma mechanisms and impact forces results in multiple possible anatomic sites of injury to the vestibular system. The vulnerability of the inner ear and brain to impact may even lead to symptoms in the absence of substantial injury (as in posttraumatic benign paroxysmal positioning vertigo [BPPV]) and fractures of skull bones. Peripheral vertigo is more frequent than central, and can be divided as early versus late. Early peripheral vestibular syndromes occurring within 24 h include BPPV, labyrinthine concussion, traumatic labyrinthine dysfunction and perilymph fistulae. The very rare posttraumatic Meniere's disease tends to occur months after trauma. Early central vertigo is caused by ischemia of the brainstem or the cerebellum. Secondary somatoform vertigo also develops after weeks to months of injury.
| Pathophysiology|| |
The function of the vestibular system is to sense the head movements in relation to body position and gravity, especially involuntary movements and reflexly counter them with body and eyes movements to prevent the body from falling. The signals from the vestibular labyrinth by inertial sensor detect rotatory, linear and gravitational acceleration. Three pairs of semicircular canals (SCCs) of two sides are arranged orthogonally, complimentary to each other and as coplanar pairs where one canal is stimulated, and another side canal is inhibited. The SCCs perceive angular accelerations of the head; impairment of which leads to rotatory vertigo. Otolith organs (utricle and saccule) senses gravitational and linear acceleration. Signals are transmitted by secondary vestibular neurons through vestibular nuclei in the brain stem to (1) occulomotor nuclei to extra-ocular muscles (vestibulo-ocular reflex, [VOR]) (2) cervico-spinal motor nuclei to generate cervico-ocular reflex (COR) (3) lower motor spinal nuclei to generate the vestibulo-spinal reflex. The somato-sensory information from proprioceptive sensors in the limbs contributes to a sense of vertical body position. Postural information is also provided from major blood vessels and abdominal viscera by gravity receptors. It also imparts sensation to autonomic center, which controls the cerebral perfusion. Finally, the vestibular input to the cerebellum is necessary for coordination and adaptation of reflexes. 
| Diagnosis|| |
- Clinical examination with Frenzel's goggles, the head-impulse test and positioning maneuvers are mandatory
- Caloric test is the "gold standard" for identifying peripheral unilateral vestibular hypofunction 
- Dynamic visual acuity measures visual acuity during self-generated horizontal motion of the head. Patients with vestibular hypofunction show decrease in visual acuity during head motion compared with the head still 
- Cervical vestibular evoked myogenic potential (cVEMP) test for saccular function 
- Ocular vestibular evoked myogenic potential (oVEMP) test for the utricular function 
- Subjective visual vertical test for acute unilateral vestibular dysfunction due to otolith-organ dysfunction. 
| Early Posttraumatic Peripheral Vertigo|| |
Benign paroxysmal positional vertigo
It is diagnosed by violent vertigo associated with nystagmus, ataxia and nausea or vomiting. The posture is characteristic as vertigo is induced by turning the head in a particular position. If the head is maintained in the same position, a few moments later the vertigo or symptoms become diminished or absent. Vertigo usually lasts for less than a minute. Most of the time precipitating posture corresponds to one of the following three positions (a) Lying down with the cheek on the pillow and the head turned to the right or left (b) turning over while lying down in bed (c) Sudden inclination of the head laterally when in a seated posture. The vertigo can be reproduced by asking the patient to mimic the precipitating posture or by Dix-Hallpike maneuver as follows: The patient being seated on a hard bed is made to lie down abruptly on his back with his head extended and turned laterally on one ear. Nonfatigable positional vertigo may be due to midline cerebellar lesion.  BPPV occurs in 18-20% of patients as posttraumatic positioning vertigo. In canalolithiasis, free floating calcium crystals residing in the canal portion of the SCC cause vertigo by exerting a force of heavier otolith debris leading to abnormal fluid endolymph displacement depending upon head position. In contrast, cupulolithiasis refers to densities adhered to the cupula of the crista ampullaris. Posttraumatic BPPV occurs bilaterally in 10% cases, thus prolonging the therapy and requiring repeated sessions of libratory maneuvers.
Pathology of labyrinth mostly affects more than one canal and by observing the axis of the nystagmus, examiner can interpret what combination of SCCs are stimulated or diminished. When one labyrinth is irritated as after stapes surgery, slow phase of nystagmus is towards the contralateral side and torsional component moving the superior pole towards the contralateral side and after destructive surgery like labyrinthectomy nystagmus will be ipsilateral and counter-clockwise and slow phase will be rightward and clockwise beating. Always remember that magnitude of vestibular nystagmus is influenced by the gaze will be ipsilateral.
Utricle senses linear acceleration, which is tangential to its curved surface and in a horizontal plane. Ipsilateral loss of utricular nerve activity results in ocular tilt reaction that is, head tilts towards the side of the lesion and disconjugate deviation as pupil of the side of the lesion is depressed, and intact side pupil is elevated.
Saccule lies in the parasagittal plane, excited by displacement away from striola, mostly senses up and down motion, but some afferents can sense to and fro movements also. Afferents in the upper half are excited by upward acceleration as in sudden fall and compensatory reflex activates the extensor of trunk and body, while flexor are relaxed to restore the tone and posture of the body, the otoconia are stimulated by gravity (9.8 m/s 2 ) constantly pulling it toward the earth.
Head injury can cause an acute episode of vertigo by abruptly affecting the vestibular end-organ directly that is, a labyrinthine concussion. The mechanism of injury is poorly understood. Several theories have been proposed such as transmission of pressure waves directly to the labyrinth through the skull or intracranially via the cochlear aqueduct, which may cause rupture of the membranous labyrinth or damage to hair cells, hair bundles or specialized structures in the ampulla or macula.
It should be suspected when there is the history of direct trauma of the petrous bone and associated symptoms of vertigo (elicited by rapid changes in head position from upright to head hanging), postural imbalance, lateropulsion, nausea, vomiting and/or tinnitus or hearing loss after other diagnoses have been excluded.  The occurrence of spontaneous nystagmus, initial unilateral decreased response upon caloric irrigation, abnormal rotational chair test result and deviation upon vestibule-spinal testing support the diagnosis. Vestibular rehabilitation therapy and short-term therapy with sedatives and antiemetics help in the treatment and should lead to an improvement of symptoms within a few weeks.
Head trauma causing petrous bone fracture can lead to direct injury of the vestibular nerve and/or the labyrinth. Transverse petrous bone fracture leads to vestibular and cochlear symptoms much more frequently than the longitudinal fracture, resulting in rotatory vertigo and hearing loss. Clinically it presents like an acute unilateral vestibular loss as in vestibular neuritis, with patients complaining of severe, persistent rotatory vertigo, peripheral vestibular spontaneous nystagmus, tendency to fall and nausea and vomiting lasting for days. Bed rest and labyrinthine sedatives are given during initial few days of severe nausea and vomiting, as drugs delay central compensation. Corticosteroids are indicated for several days, in case of trauma-induced edema. Role of vestibular training program is important. It should be initiated at an early date to accelerate central compensation.
Otolith organs dysfunction
It occurs commonly in concussion injuries. Patients complain of prolonged mild to moderate imbalance after trauma. Usually, this instability lasts from months to years. cVEMP and oVEMP tests are useful in the diagnosis. Vestibular rehabilitation therapy gives some relief in these patients.
It is a condition in which an abnormal communication is present either because of a third window due to a superior canal dehiscence syndrome or between the perilymphatic space of the inner ear and the middle ear or mastoid via oval window or round window. The oval window is believed to be the most common site of communication. Blunt or penetrating trauma may cause temporal bone fracture resulting in disruption of the otic capsule and subsequent leakage of perilymph into the middle ear. Goodhill proposed mechanisms of "implosive" and "explosive" barotraumas in its etiology.  Implosive etiologies (nose-blowing, flying and scuba diving) introduce positive pressure into the middle ear, which is then transmitted to the inner ear via the oval or round windows. Explosive etiologies (valsalva maneuver, cough, weight-lifting or other straining) can result from forces that increase intracranial pressure, which is then transmitted to perilymph via the internal auditory canal or cochlear aqueduct.
When a fistula is present, changes in middle-ear pressure will directly affect the inner ear, stimulating the balance and/or hearing structures and causing symptoms such as rotatory vertigo, tinnitus, fluctuating hearing loss, imbalance, nausea or vomiting. Sensorineural hearing loss of different extent (in 50% >40 dB over all frequencies) with/without tinnitus is a prominent feature. Symptoms often depend on the position of the head, on movement or on air pressure (valsalva maneuver). Sounds can also trigger dizziness and oscillopsia (Tullio's phenomenon). In many cases, a fistula will heal itself with strict bed rest. If symptoms are severe and have not responded to bed rest, or if progressive hearing loss has occurred, surgical repair of the fistula after exploratory tympanotomy may be required.  At the time of surgery, fluid from the middle ear should be collected and sent for β-2 transferrin testing, which is considered to be an objective test for the diagnosis of a perilymphatic fistula.
| Delayed Posttraumatic Peripheral Vertigo|| |
They usually occur 3 weeks to 3 months after trauma. The causes are:
It is characterized by a syndrome of endolymphatic hydrops and the sudden, episodic attack of vertigo associated with fullness of ear, tinnitus and unilateral fluctuating hearing loss.  It accounts for ~20% of delayed posttraumatic vertigos.  The main mechanism is the disruption of the endolymphatic duct secondary to a temporal bone fracture. Displaced epithelia of the sensory end-organs and other cellular elements including the otoconia of the saccule and utricle could result from the shock of trauma. This cellular debris could mechanically or chemically cause decreased endolymphatic absorption through the endolymphatic duct, leading to endolymphatic hydrops.
It is also thought to be caused by bleeding into the inner ear followed by a disturbance of fluid transport in some cases. It may be due to dilatation (stretching or widening) of the endolymphatic spaces (hydrops) with evidence of ruptures and healing of the membranous labyrinth.  The diagnosis is made by history of trauma, such as barotraumas, a blow to the head, or perhaps a previous ear operation, such as the stapedectomy; the presence of typical symptoms of endolymphatic hydrops, including ear fullness, tinnitus, fluctuating hearing loss, and episodic vertigo. Electrocochleography is diagnostic and demonstrates elevated negative summating potential and an increased summating-potential/action-potential ratio. 
Cervical vertigo results from para vertebral stretch receptors in the neck. Physiologically, there are various causes of cervical vertigo, the most important cause being vascular compression of the vertebral artery. Vertebral artery, which arises from the first branch of the subclavian artery, is closely associated in the neck in its cervical course as it passes through the foramina in the transverse canal of all cervical vertebrae except seventh. Transverse process of the seventh cervical vertebrae lies posterior to it, it is medial to rectus capitis lateralis, and covered by semispinalis capitis in the suboccipital triangle, hence involvement of muscles and ligaments may also results in vascular compression. Another important cause is dissection of the vertebral artery which can be damaged at points where it is anchored in the neck. 
Conditions like pain, whiplash injury, anxiety, or ergonomics may produce hyperlordosis in lower cervical spine and kyphosis in upper cervical spine, resulting in overactivity of the extensor group of the muscles and underactivity of the flexor group of muscles of the neck. Neck trauma, even minor, neck manipulation, or spontaneous cervical spondylosis may result in transient ischemia by reduced flow via vertebral artery, basilar artery, and finally posterior inferior cerebellar artery supplying the dorsolateral medulla, inferior cerebellar penduncle, and posterior inferior cerebellar peduncle of the ipsilateral side.
There is no need to emphasize that proprioception has its own place in the balance. In the cervical region, short muscles of the neck are rich in spindle, specifically rectus capitis lateralis and semispinalis capitis. Proprioception is also maintained by the pacini receptors and golgi tendon organ of periarticular tissue of cervical vertebrae.
The COR works in conjunction with VOR and optokinetic reflex, to prevent visual slip over the retina during head movement. Hence, COR induces eye movement in response to afferent proprioceptive signals from the neck which shows significantly lower equilibrium scores in the patients with vertigo than in controls and much lower scales in a particular position to provoke unsteadiness.
Cervical vertigo is associated with neck tenderness and limitation of movement which is attributed to inflammatory mediator of sensitive muscles spindle and myofascial trigger points. This may result in a mismatch between vestibular and proprioceptive system input, hence resulting in cervical vertigo. 
The cervical vertigo is usually characterized by ataxia, unsteadiness and sense of floating while walking and not by rotational or linear vertigo. Neurological, vestibular, and psychosomatic disorder must first be excluded with the available investigations before the dizziness of unsteadiness in cervical pain syndrome can be attributed as cervical vertigo. 
| Posttraumatic Central Vertigo|| |
In most cases central-type vertigo is caused by vascular diseases (i.e. brainstem ischemia, cerebellar infarction, intracranial hemorrhage, vertebrobasilar insufficiency). They can be caused by a direct concussion of these structures or secondary due to ischemia caused by a traumatic dissection of the vertebral artery. Diagnosis is based on clinical signs of impaired central vestibular, ocular motor or cerebellar dysfunction as well as imaging, preferably with cranial magnetic resonance imaging. Trauma such as concussion or hemorrhage along the vestibular pathways, extending from the vestibular nuclei in the medulla oblongata to the occulomotor nuclei and integration centers in the midbrain, and to the vestibulocerebellum, the thalamus, and multisensory vestibular cortex areas in the temporo-parietal cortex can lead to the symptom of vertigo. 
Brainstem dysfunctions resulting from vascular disease of the posterior circulation often begin with severe vertigo. These are usually associated with other brainstem signs. The vertigo can be persistent in some patients with brainstem infarcts. Arterial dissections particularly vertebral artery dissections secondary to neck manipulation, torsion, or minor trauma present with headache, vertigo and signs and symptoms of brainstem dysfunction. These are uncommon, the incidence of carotid and vertebral dissection being 1.7/100,000/year versus 1/100,000 respectively. Nevertheless, in every patient with clinical signs of central posttraumatic vertigo one should carefully look for a vertebral artery dissection either by digital subtraction angiography or magnetic resonance angiography. In the latter, a dissection is characterized by signal voids surrounded by concentric signal hyper intensity. Treatment includes aspirin or warfarin for 3-6 months.
| Conclusion|| |
Traumatic injury may lead to the gross morbidity apart from brain injury. It may be due to the involvement of the vestibular system, which includes labyrinth and proprioceptive system of the cervical region. Hence when evaluating a case of posttraumatic vertigo or dizziness, BPPV, cervical injury, labyrinthine injury, perilymph fistula and Meniere's disease should be kept in mind and excluded before labeling a patient dizziness of idiopathic or psychogenic in origin. Accurate diagnosis and timely management helps a lot in posttraumatic vertigo. Vestibular rehabilitation therapy plays an important role in the management.
| References|| |
|1.||Ba′ra′ny R. Nobel Lectures, Physiology or Medicine 1901-1921. Amsterdam: Elsevier Publishing Company; 1967. |
|2.||Griffiths MV. The incidence of auditory and vestibular concussion following minor head injury. J Laryngol Otol 1979;93:253-65. |
|3.||Taneja MK. Particle repositioning maneuver. Indian J Otol 2007;13:3-7. |
|4.||Grossman GE, Leigh RJ, Abel LA, Lanska DJ, Thurston SE. Frequency and velocity of rotational head perturbations during locomotion. Exp Brain Res 1988;70:470-6. |
|5.||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;19:790-6. |
|6.||Curthoys IS, Dai MJ, Halmagyi GM. Human ocular torsional position before and after unilateral vestibular neurectomy. Exp Brain Res 1991;85:218-25. |
|7.||Taneja MK. Some aspects of vertigo. Indian J Otol 1996;2:30-5. |
|8.||Marzo SJ, Leonetti JP, Raffin MJ, Letarte P. Diagnosis and management of post-traumatic vertigo. Laryngoscope 2004;114:1720-3. |
|9.||Goodhill V. Sudden deafness and round window rupture. Laryngoscope 1971;81:1462-74. |
|10.||Minor LB. Labyrinthine fistulae: Pathobiology and management. Curr Opin Otolaryngol Head Neck Surg 2003;11:340-6. |
|11.||Taneja MK. Meniere′s disease and allergy. Indian J Otol 2001;7:95-6. |
|12.||Ernst A, Basta D, Seidl RO, Todt I, Scherer H, Clarke A. Management of posttraumatic vertigo. Otolaryngol Head Neck Surg 2005;132:554-8. |
|13.||Taneja MK. Meniere′s disease: Diagnosis and current treatment options. Indian J Otol 2008;14:16-9. |
|14.||Shea JJ Jr, Ge X, Orchik DJ. Traumatic endolymphatic hydrops. Am J Otol 1995;16:235-40. |
|15.||Taneja MK. Cervico-ocular reflux in cervical vertigo. Indian J Otol 2011;17:51-3. |
|16.||Brandt T, Dieterich M. Central vestibular syndromes in roll, pitch, and yaw planes. Topographic diagnosis from brainstem to cortex. Neuroophthalmology 1995;15:291-303. |