Pediatric vestibular dysfunction following head injury: Diagnosis and management

Benign paroxysmal positional vertigo

BPPV is a very common and easily treatable cause of posttraumatic vertigo, impacting as much as a third of children and adolescents with posttraumatic dizziness. ^, Unfortunately, it is frequently overlooked and vastly underdiagnosed, which is likely due primarily to the fact that most primary pediatric concussion providers (e.g., sports medicine providers, neurologists, and pediatricians) do not have significant experience in the evaluation and treatment of vestibular disorders. Similarly, most vestibular specialists do not routinely see patients with posttraumatic dizziness until they are several weeks, or even months out from their injury. One study found that the mean delay in diagnosis of BPPV in pediatric patients with postconcussive dizziness was approximately 4 months. Thus, increasing awareness of the evaluation and management of BPPV among primary concussion providers may help to hasten recovery in many cases.

A more detailed discussion of BPPV is covered elsewhere in this book, so the focus of this section is on features of the condition that are specific to the posttraumatic pediatric population. Although BPPV is generally thought to be rare in children, it has actually been demonstrated in multiple recent studies to be much more common than previously supposed, particularly in the setting of concussion. ^, Although the posterior canal is most commonly involved in pediatric BPPV, as in adults, there is a much higher prevalence of horizontal and superior canal involvement in the pediatric age group. This difference is very pertinent to the history and the physical examination. The symptoms of horizontal and superior canal BPPV often differ significantly from those of posterior canal BPPV. Although posterior canal BPPV typically causes episodes of vertigo primarily when turning the head in bed, horizontal canal BPPV can also cause episodic vertigo when upright. Superior canal BPPV can also cause vertigo when supine but is particularly prone to causing symptoms when going from supine to upright, which may cause it to frequently be mistaken for the very common entity of posttraumatic hemodynamic intolerance (described elsewhere in this chapter). Patients with superior canal BPPV may even report symptoms with walking upright and particularly with bending over.

Diagnosis of suspected BPPV is confirmed with diagnostic positional maneuvers. Due to the higher incidence of horizontal and superior canal involvement in pediatric BPPV, it is ideal to use video goggles (VNG or Frenzel lenses) during the assessment and all six semicircular canals should be assessed. The latter is achieved by including not only bilateral Dix-Hallpike maneuvers in the examination (which evaluate both the posterior and superior canals), but also bilateral supine head roll maneuvers (horizontal canals), and a midline head-hang maneuver (superior canals). The presence of characteristic nystagmus and subjective vertigo with a given maneuver is diagnostic of BPPV in the tested canal. Posterior canal BPPV is associated with an upbeating torsional geotropic nystagmus with the Dix-Hallpike maneuver toward the affected side. Horizontal canal BPPV is associated with horizontal nystagmus that can be either geotropic or apogeotropic, with the affected side being that toward which the fast phase of nystagmus beats. Superior canal BPPV is associated with downbeating nystagmus with the Dix-Hallpike maneuver and midline head-hang maneuver, often with an accompanying torsional and/or horizontal component, which typically beats toward the affected ear. It should be noted that some children have difficulty tolerating the Dix-Hallpike maneuver in the presence of posterior or superior canal BPPV, because the movement of going from sitting directly to lying supine along with accompanying vertigo can induce a sense of falling and feel particularly vulnerable. In these children, we have found a partial Semont maneuver to be effective in evaluating for BPPV of the posterior canals. For this maneuver, the child is seating on the side of the examination table or on a parent's lap with their legs hanging of the side in front of them. Their head is turned 45° away from the side being testing, and then they are tipped sideways until they are lying on the shoulder of the side being tested with their head brought down into a hanging position with the head still angled upward. This achieves the same head movement and final head position as the Dix-Hallpike maneuver but can be less frightening and easier to achieve reliably in some younger children.

Treatment of BPPV consists of therapeutic canalith repositioning maneuvers, which are tailored to the affected canal(s). The posterior canal is typically treated with the Epley or Semont therapeutic maneuvers. ^, The horizontal canal is treated with a Lempert or Gufoni maneuver. ^, The superior canal can be treated effectively with a reverse Epley maneuver or with a standing inversion maneuver. In the latter maneuver, the patient is bent over from a standing position until the head is pointed toward the floor and rotated away from the affected side. This position is held for 1 min, and then the patient is rapidly brought back up to the standing position by an assistant. Treatment-resistant cases of BPPV are uncommon, particularly following a head injury, but they may be somewhat more common in children than in adults. Patients with treatment resistant BPPV may benefit from vitamin D supplementation. In truly treatment resistant cases, surgical occlusion of the affected canal may be beneficial.

Labyrinthine concussion

Labyrinthine concussion is a poorly understood entity that causes sudden loss of ipsilateral peripheral vestibular function and/or hearing following a head injury without grossly apparent violation of the labyrinth (e.g., fracture or fistula). The pathophysiology of this phenomenon is unclear, partly due to its overall rarity. However, milder variations of this phenomenon may be more common than previously supposed, as evidenced by an increasing body of literature showing mild peripheral vestibular losses and/or hearing loss in a significant proportion of patients with concussion. ^, Diagnosis of labyrinthine concussion after a head injury should be suspected in the presence of sudden hearing loss, unilateral tinnitus, and/or vertigo exacerbated by rapid head movements. Examination findings that would support this diagnosis include a positive head impulse test on the affected side, contraversive direction-fixed nystagmus that is reduced with fixation, and tuning fork testing that is suggestive of a new sensorineural hearing loss (SNHL) in the affected ear. Diagnosis of labyrinthine concussion is confirmed by demonstrating evidence of a new unilateral SNHL on audiologic testing and/or unilateral vestibular loss on vestibular testing. Temporal bone imaging should be considered when the diagnosis is made, if not already done, to rule out a fracture. Treatment consists of vestibular rehabilitation and hearing amplification, if warranted. The role of steroids in the setting of posttraumatic sudden SNHL remains unclear and is covered elsewhere in this book. Classroom accommodations for children with a persistent hearing loss are important to recommend, ideally consisting of a minimum of preferential seating at the front of the classroom and an FM system, when available.