Posttraumatic Vertigo and Dizziness
Benign paroxysmal positional vertigo (BPPV) is among the most common causes of vertigo resulting from head trauma. The forces applied to the skull during trauma cause traumatic dislodgement of otoconia from the macula of the utricle. Like idiopathic BPPV, episodes of vertigo lasting 10 to 30 seconds are evoked by turning in bed or vertical head movements. Benign paroxysmal positional vertigo should always be considered in patients with head trauma with complaints of positional vertigo. Paroxysmal positional nystagmus is seen with Dix-Hallpike positioning and treatment with canalith-repositioning maneuvers or Semont's liberatory maneuver is highly effective. Recurrence rates are similar to idiopathic BPPV, but it may take more positioning maneuvers to achieve success. In addition, traumatic BPPV is more likely to be bilateral, occurring in 25% compared with only 2% in idiopathic BPPV.
Labyrinthine concussion is a term that presumes a nonspecified injury to the membranous labyrinthine resulting from acceleration-deceleration forces on the bony labyrinth from trauma. Hearing loss, dizziness, and tinnitus are the typical features and often these improve. Thus, this term is given to define a syndrome and presumed cause rather than a specific well-defined injury. The injury may include ruptures of portions of the membranous labyrinth or bleeding or traumatic ischemia. Labyrinthine concussion may also occur on the side opposite a temporal bone fracture.
Ménière's disease is thought to be caused by dysfunctional regulation endolymphatic fluid homeostasis that leads to periodic endolymphatic hydrops. This influx of fluid to the endolymph space causes attacks of vertigo, muffled hearing, and ear pressure with tinnitus all in the affected ear. Attacks may last as little as 20 minutes, but usually last 2 to 4 hours. Diagnostic criteria have been developed for the diagnosis. Low-frequency pure-tone hearing loss is a characteristic feature; over time, hearing loss becomes permanent as does vestibular loss. The relationship between endolymphatic hydrops and trauma can be difficult to determine because the condition may come on de novo without trauma. In one series of 120 patients with Ménière's disease, less than 3% were found to have the condition due to trauma. Nevertheless, there seems to be support for the idea of microstructural changes in the labyrinthine membranes, which render them prone to producing endolymphatic hydrops. There does not seem to be good evidence supporting noise exposure or other acoustic trauma as a cause, however. Initial treatment consists of sodium restriction to < 1500 mg per day and the addition of a diuretic, but if this fails to control vertigo attacks, additional interventions are available and discussed elsewhere.
Until recently, patients with posttraumatic dizziness and normal testing of horizontal vestibular function by caloric or rotational chair testing were considered to have no vestibular dysfunction. However, recent studies have found that this assumption is sometimes erroneous. Isolated dysfunction of the otolith organs (utricle and saccule) may occur even when caloric responses are normal; this can be measured by vestibular evoked myogenic potentials (VEMPS). Patients with acute loss of the otolith sensory organ function may acutely have severe postural imbalance or a sense of tilting. Otolith sensory dysfunction may also affect quick head position changes and may account for some cases of positional dizziness on Dix-Hallpike positioning with no visible nystagmus. The time necessary to achieve functional adaptation to unilateral utricular or saccular loss is unclear. The asymmetric standing posture may recover much sooner as a result of central nervous system plasticity, but postural regulation during locomotion and dynamic movements may take longer, perhaps months, to recover.
Head trauma can sometimes result in a rupture or other abnormal opening of the fluid filled membranous labyrinth. These membrane ruptures usually occur at the round or oval window due to increased membrane elasticity between the middle ear and inner ear. Barotrauma as from scuba diving, blasts, large pressure fluctuations, or head trauma, particularly when associated with temporal bone fracture, can lead to a traumatic fistula. The findings may include unilateral deafness or sensorineural hearing loss, fluid or blood from the ear, a perforated tympanic membrane, tinnitus, vertigo, or unsteadiness. The diagnosis is notoriously difficult as evidenced by the small number of documented fistulas seen at the time of surgery even among those in whom it has been suspected. Some fistulas heal spontaneously, but surgical repair is needed in cases that do not improve with time.
Labyrinthine Traumatic Injury
Benign Paroxysmal Positional Vertigo
Benign paroxysmal positional vertigo (BPPV) is among the most common causes of vertigo resulting from head trauma. The forces applied to the skull during trauma cause traumatic dislodgement of otoconia from the macula of the utricle. Like idiopathic BPPV, episodes of vertigo lasting 10 to 30 seconds are evoked by turning in bed or vertical head movements. Benign paroxysmal positional vertigo should always be considered in patients with head trauma with complaints of positional vertigo. Paroxysmal positional nystagmus is seen with Dix-Hallpike positioning and treatment with canalith-repositioning maneuvers or Semont's liberatory maneuver is highly effective. Recurrence rates are similar to idiopathic BPPV, but it may take more positioning maneuvers to achieve success. In addition, traumatic BPPV is more likely to be bilateral, occurring in 25% compared with only 2% in idiopathic BPPV.
Labyrinthine Concussion
Labyrinthine concussion is a term that presumes a nonspecified injury to the membranous labyrinthine resulting from acceleration-deceleration forces on the bony labyrinth from trauma. Hearing loss, dizziness, and tinnitus are the typical features and often these improve. Thus, this term is given to define a syndrome and presumed cause rather than a specific well-defined injury. The injury may include ruptures of portions of the membranous labyrinth or bleeding or traumatic ischemia. Labyrinthine concussion may also occur on the side opposite a temporal bone fracture.
Posttraumatic Ménière's Disease
Ménière's disease is thought to be caused by dysfunctional regulation endolymphatic fluid homeostasis that leads to periodic endolymphatic hydrops. This influx of fluid to the endolymph space causes attacks of vertigo, muffled hearing, and ear pressure with tinnitus all in the affected ear. Attacks may last as little as 20 minutes, but usually last 2 to 4 hours. Diagnostic criteria have been developed for the diagnosis. Low-frequency pure-tone hearing loss is a characteristic feature; over time, hearing loss becomes permanent as does vestibular loss. The relationship between endolymphatic hydrops and trauma can be difficult to determine because the condition may come on de novo without trauma. In one series of 120 patients with Ménière's disease, less than 3% were found to have the condition due to trauma. Nevertheless, there seems to be support for the idea of microstructural changes in the labyrinthine membranes, which render them prone to producing endolymphatic hydrops. There does not seem to be good evidence supporting noise exposure or other acoustic trauma as a cause, however. Initial treatment consists of sodium restriction to < 1500 mg per day and the addition of a diuretic, but if this fails to control vertigo attacks, additional interventions are available and discussed elsewhere.
Utriculosaccular Injuries
Until recently, patients with posttraumatic dizziness and normal testing of horizontal vestibular function by caloric or rotational chair testing were considered to have no vestibular dysfunction. However, recent studies have found that this assumption is sometimes erroneous. Isolated dysfunction of the otolith organs (utricle and saccule) may occur even when caloric responses are normal; this can be measured by vestibular evoked myogenic potentials (VEMPS). Patients with acute loss of the otolith sensory organ function may acutely have severe postural imbalance or a sense of tilting. Otolith sensory dysfunction may also affect quick head position changes and may account for some cases of positional dizziness on Dix-Hallpike positioning with no visible nystagmus. The time necessary to achieve functional adaptation to unilateral utricular or saccular loss is unclear. The asymmetric standing posture may recover much sooner as a result of central nervous system plasticity, but postural regulation during locomotion and dynamic movements may take longer, perhaps months, to recover.
Perilymphatic Fistulas
Head trauma can sometimes result in a rupture or other abnormal opening of the fluid filled membranous labyrinth. These membrane ruptures usually occur at the round or oval window due to increased membrane elasticity between the middle ear and inner ear. Barotrauma as from scuba diving, blasts, large pressure fluctuations, or head trauma, particularly when associated with temporal bone fracture, can lead to a traumatic fistula. The findings may include unilateral deafness or sensorineural hearing loss, fluid or blood from the ear, a perforated tympanic membrane, tinnitus, vertigo, or unsteadiness. The diagnosis is notoriously difficult as evidenced by the small number of documented fistulas seen at the time of surgery even among those in whom it has been suspected. Some fistulas heal spontaneously, but surgical repair is needed in cases that do not improve with time.
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