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.

Temporal bone fracture

Diagnosis of temporal bone fracture in a child with a traumatic head injury is typically made on initial presentation, though occasionally it may be missed in the setting of a concussion where a scan was not performed. Most temporal bone fractures are essentially asymptomatic, but if the otic capsule or internal auditory canal is impacted, then resulting symptoms can include hearing loss, vertigo, imbalance, and/or facial nerve weakness. Exam findings are similar to those described for labyrinthine concussion before, though ipsilateral facial muscle weakness may be present. Ear pain and swelling may also be present. Audiologic testing may reveal an SNHL, conductive hearing loss (from ossicular chain disruption, hemotympanum, or tympanic membrane perforation), or a mixed hearing loss. Vestibular test findings may be similar to those described for labyrinthine concussion before, though they may also often be normal. Diagnosis is confirmed by computed tomography (CT) of the temporal bones. Hemotympanum will typically clear spontaneously, and traumatic tympanic membrane perforations may heal without intervention. Acute surgical intervention is rarely necessary, unless a bone fragment is noted to be compressing the cochlear, vestibular, and/or facial nerves, or if a cerebrospinal fluid leak is suspected. Nonurgent surgical management may be warranted for ossicular chain disruption or tympanic membrane perforations that do not heal spontaneously. The primary treatment for persistent vestibular symptoms from a temporal bone fracture is vestibular rehabilitation, if vestibular deficits/symptoms are present. The hearing loss can be managed with amplification, if surgical intervention is not warranted or does not adequately resolve the hearing loss. Classroom accommodations should also be provided when a significant hearing loss is present, as described before in the labyrinthine concussion section.

Superior canal dehiscence

Although not a traumatic peripheral vestibular disorder, per se, superior semicircular canal dehiscence (SSCD) can often become symptomatic after a head injury, so it warrants inclusion in the differential diagnosis of the child or adolescent with posttraumatic vertigo. The etiology of SSCD is thought to be primarily congenital with thinning of the bony roof of the superior semicircular canal that separates it from the dura of the middle cranial fossa; however, many cases may also be due to benign intracranial hypertension, leading to thinning of the bone over time. A traumatic injury may cause a dehiscence of the already thinned bone, leading to the condition becoming symptomatic. The proposed mechanism of the disorder involves the so-called “third-window” effect, where the dehiscence leads to a third entry point into the otic capsule, in addition to the round and oval windows, resulting in conduction of sound pressure through the superior canal and adding an additional route for sound pressure to enter and exit the cochlea. Symptoms may include dysequilibrium, oscillopsia, sound-induced vertigo (Tullio’s phenomenon), hearing loss, autophony, and conductive hyperacusis. Diagnosis is confirmed by a combination of audiometric findings, temporal bone CT (with thin, oblique cuts through the superior semicircular canal plane), and VEMP testing. VEMP results typically demonstrate a reduced threshold and increased amplitude in the affected ear. Treatment is most effectively achieved through surgical resurfacing or occlusion of the affected superior canal via a middle cranial fossa or a transmastoid approach. Transcanal round window occlusion is also sometimes effective at reducing the auditory and vestibular symptoms, though it does not resolve the associated hearing loss, and results with this approach are variable. The overall prevalence of symptomatic SSCD in the pediatric population is unclear but appears to be relatively low. ^{, ,} It is an especially challenging diagnosis to confirm in children, since the roof of the superior canal is already thinner in younger children, in general.

Perilymphatic fistula

A perilymphatic fistula results from a traumatic violation of the round and/or oval window membrane. This will typically cause symptoms that are similar to those of SSCD, including hearing loss, tinnitus, dysequilibrium, sound-induced vertigo, autophony, and conductive hyperacusis. Examination may reveal a positive fistula sign, where tragal pumping of insufflation of the affected ear canal with a pneumatic bulb triggers vertigo and nystagmus; however, this test is not particularly sensitive or specific. Audiometry may reveal a conductive, sensorineural, or mixed hearing loss. Vestibular testing may show unilateral vestibular loss and/or a third window pattern on VEMP testing, though it can also be normal. Temporal bone CT may show pneumolabyrinth, accumulation of fluid in the middle ear, and/or ossicular chain disruption, but also can often be normal. Diagnosis can only be confirmed definitively with surgical exploration of the middle ear, so a high degree of clinical suspicion is paramount. Repair is performed with tissue grafting (e.g., fat, perichondrium, fascia), often along with tissue glue, which is done at the time of middle ear exploration. This can typically be done via a transcanal approach and lends itself particularly well to the use of endoscopic techniques, except in the setting of a particularly brisk leak where a postauricular approach with a microscope may be preferable, particularly in younger children.

Enlarged vestibular aqueduct

Enlarged vestibular aqueduct (EVA) is not a traumatic lesion but can become symptomatic following even very minor head injuries; thus, it warrants discussion in this chapter. EVA is the most common cause of congenital hearing loss that is grossly visible on temporal bone imaging. Children with EVA may have hearing loss at birth, but it can often be delayed in onset and fluctuates over time in many cases. It can be seen in the setting of mutations in the SLC26A4 gene, which is associated with Pendred syndrome when mutations are homozygous, but EVA can also be seen in conjunction with other hearing loss syndromes and often occurs as an isolated anomaly. Patients with EVA are often prone to sudden drops in hearing and/or vestibular function following impacts to the head that may be milder than that required to sustain a concussion or a major traumatic brain injury. Historically, patients with EVA were discouraged from sports activities, though this advice is no longer considered routine. Audiologic testing in children with EVA typically shows a sensorineural or mixed hearing loss that may be unilateral or bilateral. Vestibular testing may show a third window pattern on VEMP testing and a unilateral or bilateral vestibular loss on other vestibular tests. ^, Diagnosis is confirmed by temporal bone CT, though very large vestibular aqueducts can sometimes be seen on MRI. There are multiple different diagnostic criteria for EVA, all of which are based on measurements of the vestibular aqueducts on temporal bone CT. The most commonly used criteria are the Cincinnati criteria, which indicate that EVA is confirmed by the presence of combined measurements of the aqueduct of > 0.9 mm at the midpoint and >1.9 mm at the operculum. EVA is often also associated with an incomplete partition anomaly, type II (IP2), which was formerly known as a Mondini malformation. This anomaly also includes a shortened cochlear of only 1.5 turns, a deficient modiolus, and a deficient interscalar septum. Treatment for EVA-induced vestibular dysfunction may include vestibular PT. Management of EVA-associated hearing loss may include amplification with hearing aids, classroom accommodations, or cochlear implantation. Many providers administer a course of corticosteroids to patients with EVA who have a sudden drop in hearing or vestibular function, particularly after a head injury, but evidence for the benefit of this approach is lacking.

Central vestibulopathy

Imbalance and dizziness have been frequently cited as two of the most common symptoms following head trauma. These symptoms can be seen in both adults and children following head trauma without vestibular end-organ pathology such as impaired VOR or VEMP. ^, Imbalance and dizziness in these children may arise instead from disruption of white matter tracts of central vestibular sensory integration pathways. Disturbances of these tracts impair the inability of the nervous system to properly utilize peripheral vestibular signals, even if those incoming signals are intact.

Central vestibular pathways can be probed clinically through higher-level vestibular testing that requires integration across multiple sensory modalities. The most commonly measured central sensory integration functions in clinic are static balance and gait due to their ease of administration, but other integrative measures such as subjective visual vertical and VOR cancellation tasks may also assess these processes. Both measures of static balance and gait have been associated with DTI MRI changes following pediatric TBI, suggesting that loss of white matter integrity is related to impairments in the central sensory integration process and resulting balance impairments. ^, In addition, static balance and gait step variability—a function believed to be driven heavily by central vestibular processing and not peripheral vestibular functioning—have been correlated in children with TBI, further underscoring central vestibular and sensory integration as a pathophysiological mechanism for balance and gait impairments postinjury. ^, Even in children with severe TBI leading to changes in brain matter gray volume, gait abnormalities have best correlated with loss of volume in regions of the brain crucial for sensory integration like the superior parietal lobe.

Assessment of static balance following TBI in children can be completed several ways and usually takes the form of measurement of postural sway and falls. Stand-alone balance assessments such as the BESS and BOT-2 allow for more standardized grading of balance ability than simple observation by the clinician and appear to be more sensitive to balance dysfunction than subjective self-reported balance status. More comprehensive postinjury tools such as the SCAT include a standardized balance assessment as one of several composite measures. Each of these tools has been validated in children with and without TBI and is sensitive for detecting mild TBI, or concussion. While these tools are most commonly utilized for concussion, some evidence suggests that concussion evaluation tools for balance may not be tolerable in more severe forms of TBI when physical disability impairs ability to perform the task.

Computerized balance assessments of static posturography utilize force plate center-of-gravity sway to quantify balance function, such as the SOT or Wii Balance Board. ^, Wearable inertial sensors and smartphone accelerometer applications are in development and testing stages for more portable, real-life assessment of balance function. ^, These more sophisticated tools are believed to have higher sensitivity for detecting mild alterations in balance function that may persist, though require much more investment by the clinician both financially and in time needed for data processing and interpretation. ^, Even with sophisticated balance data, interpretation in children can be difficult. It has been well established that postural sway decreases as children age, but the exact mechanisms behind this maturation as well as age-specific expectations are unclear. Several studies have suggested adult-like balance strategies are in place by age seven, while other studies still identify differences in preteen to teenage postural sway. Therefore, interpretation of any type of balance data in a child should utilize individualized baseline data whenever possible and take into account normative data of the child’s specific age and preinjury activity level. ^,

Gait function may be assessed through standardized observational grading, computerized walkways, and video analysis. Gait variables frequently included in postTBI analyses include step length, step variability, and sway during gait—sometimes referred to as “dynamic balance.” Current evidence suggests that low-tech measures such as tandem gait speed and stability are reliable measures in children and can be as sensitive as computerized measures of balance function for detection of postconcussion deficits, especially when performed with a concurrent cognitive dual task. Research on gait in children postconcussion has mainly focused on dynamic balance sway, but some studies have additionally identified deficits in gait parameters such as step length and walking speed. ^, Children with more severe TBI have more consistently demonstrated deficits in gait parameters such as step length and variability that also linger beyond resolution of other TBI symptoms. Similar to balance data, gait data in children can be difficult to interpret across age ranges due to variable development and might not correlate well with self-perceived dizziness and imbalance.

Vestibular rehabilitation has emerged as a promising tool for managing central vestibular dysfunction following head injuries in children, though there is a paucity of literature supporting its use. Trials of vestibular rehabilitation in children have mainly focused on those with concussion and not more severe TBI. Protocols for such trials have been developed, and vestibular rehabilitation has been identified as a potential therapy for improving balance following such head injuries; however, these authors are unaware of a study that has specifically focused on vestibular rehabilitation of children following moderate-to-severe TBI. ^, The existing concussion literature does, however, indicate that imbalance improves following rehabilitation in both children and adults, suggesting that rehabilitation works through similar mechanisms to improve symptoms regardless of age.

From the perspective of deficits in central vestibular processing, vestibular rehabilitation techniques such as balance training are hypothesized to work directly on rehabilitating central sensory integration pathways. Vestibular rehabilitation exercises to improve balance and gait focus on training under different sensory conditions to alter the brain’s reliance on specific sensory inputs. This can take the form of practicing balance with eyes closed to reduce the brain’s weight of visual input, which has been shown to be increased following head injury. Sensory reweighting therapies are of particular importance in younger children due to their underdeveloped somatosensory and visual systems for balance so that they do not develop maladaptive sensory processing strategies during critical sensory development periods. Along with improving objective balance function, these exercises also appear to improve symptomatic dizziness in children, further supporting a link between disruption of central sensory processing pathways and dizziness.

Autonomic dysregulation (dysautonomia)

Dizziness due to hemodynamic intolerance (HI) has been identified in children following both concussion and more severe head injury. HI symptoms are driven by alterations in autonomic nervous system functioning such as decreases in cerebral perfusion and/or aberrant sympathetic nervous system responses to changes in position. This autonomic dysregulation is believed to precipitate symptoms such as dizziness, blurred vision, palpitations, lightheadedness, and fatigue. ^, A decrease in cerebral blood flow has been well documented in the TBI literature and associated with worse TBI symptoms and prognosis in both adolescents and young adults. A decrease in cerebral blood flow further exacerbates the increase in neurometabolic demand of the brain following injury and simultaneously reduces blood flow to areas such as the insular cortex responsible for regulating the autonomic response. ^{, ,} Systemic reductions in neurotransmitter release and baroreceptor reflex sensitivity perpetuate this demand further and can result in presyncopal and syncopal symptoms upon changes in positioning.

Two types of HI commonly diagnosed following head injury are orthostatic hypotension and postural orthostatic tachycardia syndrome (POTS). Orthostatic hypotension is defined as a reduction in systolic blood pressure or diastolic blood pressure of >20 mmHg or >10 mmHg, respectively, on standing or during head-up tilt (HUT) testing, whereas POTS is defined as an increase in heart rate of >40 bpm in children within 10 min of standing or during HUT without evidence of orthostatic hypotension. ^, Both of these physiologic responses represent abnormal autonomic responses to hemodynamic changes and may result in symptoms of dizziness know as hemodynamic orthostatic dizziness/vertigo.

Hemodynamic orthostatic dizziness/vertigo is defined by the Bárány Society as episodes of dizziness, unsteadiness, or vertigo that are triggered by postural changes in individuals who also meet the clinical criteria for orthostatic hypotension, postural orthostatic tachycardia syndrome, or syncope. While these authors are unaware of a specific study utilizing this recent Bárány Society definition in children post-TBI, there are a number of studies investigating the incidence and management of both orthostatic hypotension and POTS in children post-TBI with symptoms suspicious for general HI.

Posttraumatic head injury HI has been identified in 8.7% of all children seen in a postconcussion clinic and has been shown to prolong recovery time but is not frequently assessed for properly if at all. ^{, ,} In a study of children with persistent postconcussion symptoms including lightheadedness, 70% demonstrated abnormal HUT results. One retrospective study of new pediatric POTS diagnoses revealed that 11.2% of patients had sustained a head injury within the 3 months prior to their POTS diagnosis. Despite the seemingly high prevalence of HI post-TBI, a major criticism of HI studies in head injury is that no study has prospectively assessed preinjury orthostatic vital signs and HUT responses. As these are not routinely examined and the prevalence of HI symptoms in children is unknown, it is unclear how many children may have qualified for a diagnosis of orthostatic hypotension or POTS prior to their head injury. Prospective studies evaluating the relationship between development of HI and TBI are needed to better understand this complex interaction and better define diagnostic criteria. Nevertheless, there has been an association with normalization of orthostatic vital signs and resolution of orthostatic symptoms in children with TBI. As HI symptoms can play a major role in recovery, are easily assessed, and can potentially be managed through lifestyle changes and medications, they should be managed regardless of their true etiology.

Clinical suspicion of HI in a child with TBI should be raised when the child endorses symptoms of lightheadedness, palpitations, blurred vision, etc. that are associated with changes in position and/or abate upon laying down. The gold standard clinical examination to follow up such symptoms is an HUT; however, as multiple HUT protocols exist and are frequently being modified, specific clinic HUT should be requested to properly interpret results. Furthermore, as HUT likely requires later referral to a specialty clinic, investigation of these symptoms can be completed in an initial clinic visit utilizing supine-to-standing orthostatic vital sign measurements. Like with HUT protocols, different supine-to-standing orthostatic protocols exist with regard to how long patients should remain supine prior to blood pressure and heart rate measurements standing and how long they should remain standing before checking vital signs again. Currently, supine-to-standing measurements are validated for the diagnosis of orthostatic hypotension in children after 3 minutes of standing, though delayed orthostatic hypotension may be missed. ^, A standing time of 10 minutes is required to rule out POTS; some published clinic protocols as long as 17 min, which may be more sensitive for diagnosis but is likely too long to be widely adopted.

In addition to the difficulties in standardization and time requirements of these clinical examinations, there is growing research to suggest that specific orthostatic vital sign cutoffs are not good predictors of symptomatology or responsivity to treatment in children, both with idiopathic HI and post-TBI HI. ^{, ,} Initial treatment strategies for HI symptoms are low risk, consisting of graded exercise plans (already commonly incorporated into a post-TBI treatment plan), compression garments, and increasing fluid and salt intake. Negative HUT or orthostatic vital signs therefore should not preclude attempting conservative management in a child with strong clinical suspicion for hemodynamic orthostatic dizziness based on their reported symptoms. Pharmacological treatment can be initiated if conservative management fails, typically with a very low dose of fludrocortisone or, if not tolerated, midodrine. ^, Beta-blockers, while useful for HI symptoms such as palpitations, are contraindicated in patients with dizziness/lightheadedness-predominant HI due to concerns of exacerbating those symptoms. Future prospective studies should examine the effect these drugs have on HI in children as these treatment recommendations are based on prospective studies completed in adults, with some subjective efficacy reported in children.

Vestibular migraine

Head injury is hypothesized to precipitate migraine-type headaches due to inflammation-mediated hyperexcitability of neuronal pathways and inflammatory vascular responses, most specifically in the trigeminovascular system. ^, Due to significant overlap between trigeminal and vestibular tracts both anatomically and biochemically, migraine-associated dizziness is hypothesized to occur due to simultaneous disruption of vestibular pathways. ^, These inflammatory responses are believed to be driven by axonal damage and the neurometabolic cascade theory described previously. Currently, it is unknown whether chronic post-TBI migraine headaches differ significantly in pathogenesis when compared with idiopathic migraine that is also known to commonly present with vertiginous symptoms. As both types of migraine respond similarly to antimigraine medications, some argue the delineation may not be clinically relevant for proper management. ^{, ,}

Though it has not received the same amount of research focus as post-TBI migraine pain, migraine-associated dizziness has been identified a potential cause of dizziness following TBI in at least two studies that included both adults and children. ^, As official diagnostic criteria for vestibular migraine (VM) were not available prior to one of these studies and not clearly utilized in the other, it is unclear whether these cases of migraine-associated dizziness in children post-TBI met formal criteria for VM. However, as VM has been identified as one of the most common cause of episodic dizziness in both children, even using diagnostic criteria based off adults, it is reasonable to suggest that a portion of migraine-associated dizziness in children post-TBI would meet VM criteria. ^{, ,} Prospective studies evaluating this relationship in children using formalized criteria better suited for children are needed, as children with VM frequently present with few to no objective clinical vestibular deficits and are instead diagnosed based on descriptions of their dizziness and chronicity of migraine attacks. ^,

Management of VM in children has primarily focused on utilization of typical antimigraine medications and lifestyle modifications, based off treatment recommendations for adult VM. Potential medications include either prophylactic or abortive regimens. Based on one retrospective study of VM in children, prophylactic medications such as amitriptyline and nortriptyline, cyproheptadine, and topiramate demonstrated the most efficacy and abortive triptan medications were tolerated with no obvious side effects. Vestibular suppressants such as meclizine were also associated with minor improvements in symptoms, but not resolution. As with diagnostic criteria, more data are needed on medication regimens specifically targeted to children for management of VM.

Medication regimens appear to be easier to adhere to when compared with lifestyle modifications such as dietary restrictions, which can be difficult to maintain in children. Other lifestyle modifications studied in general pediatric migraine that may be easier to adhere to, such as improving sleep hygiene and ensuring adequate hydration, should be examined as supplemental therapies for VM in children. In fact, many of these modifications are recommended for improvement of general postconcussion symptoms and should therefore be encouraged in children with any of the diagnoses described in this chapter.

There is some evidence to suggest that vestibular rehabilitation may be efficacious in improving symptoms of both idiopathic TM and post-TBI VM. ^, Vestibular rehabilitation has been investigated for management of more general post-TBI headache and dizziness and has demonstrated a strong benefit. However, these findings have been seen primarily in children with concurrent balance dysfunction along with their VM symptoms or in combined study samples of both children and adults without a clear diagnosis. Metanalyses suggest the overall data on vestibular rehabilitation in VM is not definitive; therefore, more high-quality, blinded studies need to be done to better characterize this intervention both in general and specifically in children. ^,

Persistent postural–perceptual dizziness

PPPD is a newly recognized unifying diagnosis for a chronic experience of dizziness, unsteadiness, or nonspinning vertigo. These symptoms can be preceded by vestibular diseases described previously in this chapter as well as other neurological, medical, or psychiatric disease. ^, The diagnostic criteria for PPPD were defined by the International Classification of Vestibular Disorders in 2017 ( Tables 17.1 ) and incorporate elements of multiple functional dizziness disorders that were formerly classified by various names, including chronic subjective dizziness, space-motion discomfort, and phobic postural vertigo. These symptoms can be notoriously difficult for patients to describe, especially pediatric patients, making proper diagnosis challenging. It has been hypothesized that PPPD is primarily driven by maladaptive reorganization of vestibular pathways following some insult; unsurprisingly, then, PPPD can present alongside other vestibular diagnoses and is not a diagnosis of exclusion. ^, Comorbid vestibular deficits can further complicate the picture and delay proper treatment.

Table 17.1

Only gold members can continue reading. Log In or Register to continue

Share this:

• Click to share on Twitter (Opens in new window)
• Click to share on Facebook (Opens in new window)

Related

Related posts:

1. Surgical management of auricular trauma
2. Vascular injury following lateral skull base trauma: diagnosis and management
3. Facial nerve injury following temporal bone fracture: diagnosis and management
4. Management of pediatric otologic trauma

Stay updated, free articles. Join our Telegram channel

Join