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4.1 Introduction

After head and neck pain, dizziness is the most frequent chronic complication of a mild head trauma (Friedman 2004; Kashluba et al. 2006; Schütze et al. 2008) or of a whiplash injury. If radiological methods do not reveal a petrous bone fracture with hemotympanum or the presence of air in the labyrinth (pneumolabyrinth) or a brainstem contusion cannot be clinically confirmed, the first questions to ask are the following:

  • Is this dizziness organic or psychogenic (Staab 2012)?

  • What is the underlying mechanism of the dizziness (peripheral or central vestibular)?

The following posttraumatic forms of vertigo are well known:

  • BPPV

  • Posttraumatic otolithic vertigo

  • Unilateral or bilateral peripheral vestibular disorder culminating in labyrinthine failure (e.g., due to a labyrinth contusion or a petrous bone fracture)

  • Perilymph fistula (that leads to a pathological transfer of pressure)

  • A barotrauma-induced vertigo.

Frequently a false diagnosis of “cervicogenic vertigo” is made to explain the attacks of dizziness following a whiplash injury. It is still a subject of controversy whether this form of vertigo exists at all and if so, what its pathomechanism could be (see below). However, it is probable that in many cases of a whiplash injury or head trauma, a loosening of otoconia (even without BPPV) takes place, resulting in a posttraumatic otolithic vertigo in the form of a transient gait and postural instability.

4.2 Traumatic Peripheral Vestibular Forms of Vertigo

4.2.1 Posttraumatic BPPV

The most frequent peripheral labyrinthine form of vertigo is BPPV (Sect. 2.2) (http://extra.springer.com).

It is characterized by short attacks of rotatory vertigo and typical rotatory crescendo–decrescendo nystagmus, which is triggered by positioning the head toward the affected ear or tilting it backward and resolves within seconds. Rotatory vertigo and nystagmus occur after positioning with a short latency of seconds and cease temporarily after repeated positioning maneuvers. BPPV occurs in approximately 10 % of patients as posttraumatic positioning vertigo (Gordon et al. 2004; Motin et al. 2005). It is frequently bilateral and asymmetrical (ca. 20 %) and is occasionally also found in children. In two-thirds of the cases, the posterior canal is affected, in one-third, the horizontal canal (Ahn et al. 2011). In our experience the interval between the actual head trauma or whiplash injury and its manifestation as positioning vertigo can last from days up to several weeks. It is possible that the otoconia become detached from the macula bed in two steps or in the first phase remain in the endolymphatic space of the utricle and only reach the canal later, at which time they induce the typical positioning vertigo. This delay can be important in situations requiring expert witness evidence. Immediately after the trauma the patients occasionally complain of unsteadiness of gait (like walking on a mattress), probably due to an “otolithic vertigo.” Only subsequently do the typical symptoms of BPPV appear. Traumatic BPPV has been frequently reported after neurosurgical, maxillary, as well as ENT operations of the skull (Chiarella et al. 2007).

The pathophysiology and treatment of posttraumatic BPPV correspond to that of idiopathic BPPV (Sect. 2.2). The therapy phase is occasionally longer, in part because it frequently occurs bilaterally, and liberatory maneuvers have to be repeated, beginning with the treatment of the more-affected ear until the patient is symptom-free (Ahn et al. 2011). The recurrence rate of traumatic BPPV is evidently not higher than that of idiopathic BPPV (Ahn et al. 2011; Brandt et al. 2006, 2010). The different types of liberatory maneuvers (Semont, Epley) are successfully used for a canalolithiasis of the posterior canal (Herdman 1990; Fife et al. 2008). Generally more than 90 % of patients are asymptomatic after 1 week of treatment (von Brevern et al. 2006; Mandala et al. 2012). Cases of the more rarely affected horizontal canal are treated with a “barbecue” maneuver, a 12-h period of lying on the healthy ear (Fife et al. 2008) or by the Gufoni maneuver (Kim et al. 2012). Therapy failures are very rare (<1 %).

4.2.2 Traumatic Labyrinthine Failure

A unilateral hemorrhage or a petrous bone fracture (vestibulocochlear disorders occur more frequently with transverse than with longitudinal fractures) can lead to direct injury of the vestibular nerve or the labyrinth (Sect. 2.2). This causes:

  • Violent rotatory vertigo, which continues for days

  • Horizontal rotatory nystagmus to the unaffected side

  • Posture and gait instability with deviation to the affected side

  • Nausea and vomiting.

The clinical symptoms are similar to those of vestibular neuritis (http://extra.springer.com) (Sect. 2.2). Three forms of petrous bone fractures can be differentiated as the following: mixed, longitudinal, and transverse (Rafferty et al. 2006; Gladwell and Viozzi 2008).

  • Longitudinal petrous bone fractures (Fig. 4.1) are more frequent; they cause injury to the middle ear and bleeding from the ear.

    Fig. 4.1
    figure 00041

    Longitudinal petrous bone fracture: CT of base of skull in bone kernel, two consecutive slices (a, b). Short arrow: fracture line through the right petrous bone with multiple mastoid cell opacity. Dashed arrow: additional fracture of the squamous portion of the right temporal bone (Figure was kindly provided by PD Dr. Jenny Linn, Department of Neuroradiology, University of Munich, Grosshadern)

    Full size image

  • The transverse petrous bone fracture with labyrinthine lesion and resulting rotatory vertigo and hearing loss, as well as possible injury to the facial nerve, occur more seldom.

If there is a direct trauma of the petrous bone and corresponding symptoms of rotatory vertigo and hearing loss, but the injury cannot be confirmed either macroscopically or by X-ray, one speaks of a labyrinthine contusion.

The first phase of manifest dysfunction is characterized by a strong feeling of ­illness with continuous rotatory vertigo, nausea, and vomiting. These ­symptoms slowly dissipate over 2–3 weeks. Bed rest and antivertiginous drugs (e.g., dimenhydrinate) should be prescribed only within the first days for severe nausea and vomiting. The same limited therapy is recommended for vestibular ­neuritis, as these drugs delay central compensation. The patient should begin a ­vestibular training program as soon as possible to accelerate and improve central compensation (Strupp et al. 1998). Similarly, treatment with corticosteroids ­(methylprednisolone) is also indicated for a few days, in most cases because of trauma-induced edema.

Vertigo, oscillopsia, and hearing loss are also frequent complications of traumas due to military or terrorist blasts (Scherer et al. 2007). They can take a progressive course (Hoffer et al. 2010).

4.2.3 Traumatic Perilymph Fistula

Usually the air in the middle ear is of normal atmospheric pressure, since air supply via the nasopharynx passes through the Eustachian tube. In disorders of air supply to the Eustachian tube, painful pressure gradients occur on the eardrum and in the middle ear. During head trauma, extreme increases in pressure can occur in the middle ear and cause a defect at the round and oval windows or more seldom a ­luxation of the stapes footplate in the direction of the inner ear with pathological transfer of pressure to the perilymphatic space or with a pneumolabyrinth (Sarac et al. 2006; Hatano et al. 2009). The changes in pressure can also lead to a dehiscence of the anterior semicircular canal (superior canal dehiscence syndrome, Sect. 2.7). The consequences are:

  • Attacks of dizziness, in part with oscillopsia (generally due to pressure changes from coughing, pressing, sneezing, lifting heavy weights, or loud sounds)

  • Fluctuating hearing loss, seldom autophonia

  • Ear pressure

  • Tinnitus.

The complaints can depend on the position of the head or on movement as in perilymph fistulas of other etiologies (Maitland 2001; Bourgeois et al. 2005) (Sect. 2.7) (http://extra.springer.com). Generally a high-resolution CT of the inner ear can prove the etiology, e.g., a bony defect of the superior canal. The presence of air in the labyrinth (pneumolabyrinth) following a trauma indicates a traumatic perilymph fistula (Tsubota et al. 2009).

Clinically, dizziness can be classified as either a canal type with rotatory vertigo and nystagmus or an otolithic type (in cases of fistulas of the oval window) with postural vertigo, unsteadiness, and stance and gait ataxia, especially during linear head acceleration (when standing up or walking). The otolithic type of dizziness can also be caused by luxation of the stapes footplate without resulting in continuous perilymph leakage; this happens when the luxated stapes footplate via the peri/endolymph fluid pressure stimulates the otoliths during the acoustically induced stapedial reflex (otolithic Tullio phenomenon). At the same time, loud sounds of certain frequencies induce paroxysmal excitations of the anterior canal in cases of bony dehiscence or otolithic symptoms (head tilt and postural instability).

An initially conservative therapy of several days of bed rest with the head elevated, perhaps mild sedation, and the administration of laxatives results in recovery in the majority of cases. If such conservative therapy fails, and hearing loss or vestibular symptoms increase, then an exploratory tympanotomy or in cases of a dehiscence of the superior canal, surgical canal plugging is indicated.

4.2.4 Alternobaric Vertigo

Rapid changes of pressure in the middle ear—primarily during the decompression experienced by divers (Klingmann et al. 2006) or by pilots and aircrews during flights (Subtil et al. 2007)—can cause a transient rotatory vertigo that is called alternobaric vertigo. At the very beginning of the rotatory vertigo and nystagmus, which spontaneously resolves after seconds or hours, there is a feeling of fullness in the ear. Acute rotatory vertigo indicates an inadequate stimulation of a semicircular canal, which is triggered by an asymmetrical, excessive acute pressure on the round and oval windows in the middle ear (Molvaer and Albrektsen 1988). The same mechanism underlies perilymph fistulas.

Dysfunctions of the Eustachian tube are a special risk factor for developing an alternobaric vertigo (Uzun 2005). Women appear to be at a higher risk of developing alternobaric vertigo during scuba diving than men (Klingmann et al. 2006), but retrospective studies do not show that this vertigo leads to life-threatening situations underwater.

4.2.5 Otolithic Vertigo

Traumatic otolithic vertigo probably occurs more often than is generally assumed (Brandt and Daroff 1980; Ernst et al. 2005). Immediately after a head trauma or after a latency, patients often report having experienced:

  • Postural imbalance that is exacerbated by head movements

  • Oscillopsia during head movements

  • Gait instability that is like walking on a water pillow.

These are typical disorders of otolithic function. As shown in animal studies, the traumatic accelerations probably cause loosening of the otoconia, which leads to unequal otolithic masses on the two sides. The different otolithic weights on the two sides can result in a temporary disturbance of spatial orientation. Within days or weeks, however, central compensation corrects for the otolithic imbalance, and the postural instability during head movements and gait ataxia abates. If complaints persist, a differential diagnosis must be made which takes into account the possibility of a secondary somatoform vertigo.

4.3 Traumatic Central Vestibular Forms of Vertigo

The various central vestibular syndromes are triggered by disorders of brainstem or cerebellar function in connection with a contusion or hemorrhage or, indirectly, due to a traumatic vertebral dissection. In principle, parts of the brainstem and cerebellum, the midbrain and thalamus, the pons to the medulla oblongata and cerebellum, can be affected; the mesencephalon is affected relatively often.

The individual syndromes are described in Sect. 3.1.

4.4 Traumatic Cervicogenic Vertigo

The question of whether there is a medical entity “cervicogenic vertigo” is still a subject of controversy (see Sect. 6.3). The neck afferents not only take part in coordinating eyes, head, and body but they are also involved in the orientation of the body in space and the control of posture. This means that in principle, a stimulation or lesion of these structures could trigger vertigo. It has been shown in animal experiments in primates (Macaca) that a unilateral local anesthesia or section of the superior cervical roots induces a tendency to fall due to a temporary increase of tonus of the extensor muscles on the ipsilateral side and a decrease on the contralateral side, as well as ipsiversive past-pointing. Positional nystagmus, however, is elicited only in certain species and to different degrees (most pronounced in rabbits, less in cats) but not at all in Rhesus monkeys (De Jong et al. 1977). This type of positional nystagmus that derives from an imbalance in tonus of the superior cervical roots has not been proven to exist in humans. Patients with C2 root blockades (for cervicogenic headache) exhibit a slight instability of gait with minor ipsilateral deviation of gait and past-pointing without ocular motor disorders (Dieterich et al. 1993); this corresponds to findings in the animal experiments with Macaca. One would expect similar symptoms such as instability of gait in “cervicogenic vertigo” always in connection with cervico-vertebrogenic pain and movement restriction of the cervical vertebrae but not with rotatory vertigo or spontaneous, positional, or provocation-induced nystagmus.

Unfortunately, there are still no useful tests to confirm “cervicogenic vertigo” (gait instability), as the tests available use passive head turns while the trunk is fixed and trigger the same amount of nystagmus with the same frequency in healthy subjects (Holtmann et al. 1993). These tests are still in use in some places nowadays, but they fail to give meaningful results. For this reason the differential diagnosis must always include careful otoneurological diagnostics (Ernst et al. 2005), especially if complaints are not initially present but appear only in the course of the disorder. In such a case, a secondary (psychogenic) somatoform vertigo must be considered, since it can appear in up to ca. 50 % of patients with a primarily organic vertigo syndrome, depending on the comorbidity ­(Eckhardt-Henn et al. 2008).

4.5 Posttraumatic Psychogenic Vertigo

If vertigo persists for a long time after a head trauma or a whiplash injury and otoneurological or ocular motor deficits cannot be determined, this can indicate a psychogenic or somatoform vertigo (Sect. 5).

The most frequent psychosomatic form of vertigo and the second most frequent cause of vertigo in neurological patients is the somatoform phobic postural vertigo (Sect. 5.2). It often occurs secondary to organic forms of vertigo (Huppert et al. 1995; Eckhardt-Henn et al. 2008). A clear increase in the cases of somatoform ­phobic postural vertigo was observed in Georgia after a strong earthquake (Tevzadze and Shakarishvili 2007). In cases of chronic, long-term complaints, the desire to retire must also be considered in the differential diagnosis.