Childhood vestibular disorders: a tutorial.
Disorders affecting the human vestibular or balance system typically are perceived as problems affecting only adults. A growing body of evidence, however, suggests that childhood vestibular disorders, although rare, do exist (Bower & Cotton, 1995, Eviatar, 1994; Hausler, Toupet, Guidetti, Basseres, & Montandon, 1987; Tusa, 2000a). The incidence of vestibular symptoms associated with childhood disorders reported in the literature ranges from 0.5% (Eviatar & Eviatar, 1974) to 6% (Fried, 1980), depending on the type of population (pediatric, otolaryngology, or neurology clinic patients) under investigation (Bower & Cotton).
Few vestibular studies focus on children. Information regarding vestibular problems in children, therefore, is lacking, as is awareness of the problems. Although disorders affecting the vestibular mechanism are typically not life threatening, they can affect a person's quality of life and future earning potential. Furthermore, there is a high prevalence of psychological disorders, particularly anxiety disorders, associated with patients with vestibular problems (Jacob, 1988; Tusa, 2000b). Timely diagnosis and intervention are crucial for the health and well-being of these children. The purpose of this tutorial is to broaden the knowledge base and promote increased awareness of childhood disorders associated with vestibular symptoms among speech-language pathologists, audiologists, and educators of children who are deaf or hard-of-hearing. The tutorial addresses the pathophysiology, symptoms, and management options of some of the more common childhood disorders that can affect the vestibular system. Differential diagnosis of these disorders is discussed when appropriate because many of these conditions have similar signs and symptoms but quite different implications for treatment and intervention.
ANATOMY AND PHYSIOLOGY OF THE VESTIBULAR SYSTEM
A brief overview of the anatomy and physiology of the human vestibular system will provide a better understanding of various disorders that may disrupt the system. No single system or structure constitutes the vestibular system. It is made up of three primary components: (a) a peripheral sensory apparatus, (b) a central vestibular system, and (c) motor output (Hain, Ramaswamy, & Hillman, 2000).
The peripheral sensory apparatus (also called the vestibular labyrinth), housed in the inner ear, consists of two types of motion sensors: three semicircular canals and the otolith organs. The semicircular canals are sensors for angular motion; for example, when the head is turned from left to right or up and down. The otolith organs include the utricle and saccule, which are sensors for linear acceleration with respect to gravity. Acceleration is sensed by the utricle in the horizontal plane and the saccule in the vertical plane. The utricle and the saccule also sense changes in head motion related to gravity, such as putting the chin on the chest (pitch) or touching the ear to the shoulder (roll). The information regarding head movement is relayed from the peripheral to the central vestibular system by the vestibular portion of the vestibulocochlear nerve (cranial nerve VIII). Because the cochlea and the vestibular labyrinth are in close proximity in the inner ear and share a blood supply, disorders affecting the vestibular labyrinth often affect the cochlea. Vestibular symptoms, such as dizziness and disequilibrium, are often accompanied by hearing loss, tinnitus, or both (Furman & Cass, 2003).
The central vestibular system receives input from the peripheral vestibular mechanism. This input is channeled primarily to parts of the cerebellum and four vestibular nuclei located in the pons. Input from the vestibular labyrinth is processed in association with somatosensory and visual sensory input. As a result, output from the vestibular nuclei influences eye movement, truncal stability, and spatial orientation (Furman & Cass, 2003). Most responses to peripheral vestibular stimulation are reflexive in nature. Some input from the periphery, however, reaches the cerebral cortex, resulting in voluntary responses. This input to the cortex is responsible for conscious perception of motion, providing some of the information necessary for orientation of the head and body in space (Ganong, 1985).
The motor output of the vestibular system is primarily integrated into vestibular reflexes: (a) the vestibulo-ocular reflex (VOR), (b) the vestibulospinal reflex (VSR), and (c) the vestibulocollic reflex (VCR). The VOR ensures that eye movements are equal and opposite to head movements to stabilize gaze. The clinical manifestation of disparity between eye and head movement is unstable gaze during head movement. The VSR is a collection of reflexes that stabilize the head and control erect stance relative to gravity while a person is standing and walking. Input is from the semicircular canals and otolith organs. Output is to the antigravity muscles (i.e., muscles of the neck, trunk, extremities). The VCR acts on the neck muscles to stabilize the head. For a detailed description of vestibular reflexes, see Hain et al. (2000).
All three components of the vestibular system--the peripheral apparatus, the central mechanism, and motor output--work together to maintain balance by orienting a person's body position and motion in space (Drachman, 1998). As shown in Figure 1, the peripheral apparatus sends information regarding the head's speed of movement, direction, and orientation with respect to gravity to the central vestibular system. The vestibular nuclear complex processes these signals and combines them with extravestibular sensory information (e.g., proprioceptive, auditory, visual) to estimate head orientation. The output of the central vestibular system goes to the ocular muscles to serve the VOR, which stabilizes gaze during head motion, and to the spinal cord (VSR) to prevent falls. The performance of the VOR and the VSR are monitored by the central vestibular system and are calibrated and recalibrated as necessary by the cerebellum (Hain et al., 2000). Lesions of the cerebellum are, therefore, associated with nystagmus (involuntary eye movements) and gait ataxia.
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SIGNS AND SYMPTOMS ASSOCIATED WITH DISORDERS OF THE VESTIBULAR SYSTEM
Whenever the vestibular mechanism is damaged or diseased, common clinical manifestations that can result are dizziness, vertigo, and nystagmus. Dizziness is a nonspecific complaint that can occur in association with vestibular lesions, as well as other causes. Different terms have been used to describe dizziness, such as spinning, light-headedness, giddiness, and unsteady gait. Typically, dizzy spells associated with vestibular disorders are abrupt in onset and short in duration. Symptoms such as nausea and vomiting are commonly associated with dizziness that is due to vestibular disorders. Dizziness due to other causes is rarely accompanied by nausea and vomiting (LaRouere, Seidman, & Kartush, 1997).
Vertigo is a type of dizziness specific to vestibular system disease (Baloh & Honrubia, 1990; Drachman, 1998). True vertigo is a frightening and distressing condition because it is associated with an illusory sense of motion or rotation of either self (subjective vertigo) or the environment (objective vertigo) over which the individual has no control. Vertigo occurs in distinct episodes with sudden onset. True vertigo is almost always caused by deficits within the peripheral labyrinth or its connections to the central vestibular system (Drachman). Vertigo of peripheral origin is usually severe and rotatory; it is often associated with such other symptoms as hearing loss, nausea, vomiting, and a staggering gait (Drachman). Vertigo of central origin has a gradual onset, is moderately severe, and is persistent. It may be associated with general weakness of the extremities, a tendency to fall, and seizures (Honrubia, 2000). According to some researchers (e.g., Bower & Cotton, 1995), peripheral vertigo is more common in children than is central vertigo.
The term nystagmus refers to a disturbance of ocular movement characterized by nonvoluntary rhythmic oscillations or rapid jerky movements of one or both eyes. Nystagmus is a reflex not initiated by visual impulses; therefore, it is also present in persons who are blind (Ganong, 1985). Although nystagmus may not always be easily visualized, it almost always accompanies true vertigo and is not seen in other types of dizziness (Schwaber, 1997). Nystagmus can occur spontaneously in response to a vestibular upset, or it may be evoked by head and eye movements. The detection and nature of the nystagmus in response to eye gaze, positional changes, and vestibular stimulation by rotation and temperature variations (caloric irrigation) form the primary basis for electronystagmography (ENG) and videonystagmography (VNG) tests (Eviatar, 1994).
Describing the sensations of a vestibular disorder can be difficult for most adults and may not be possible for children, particularly young children. The difficulty in describing vestibular symptoms is probably due to the relatively few neural projections from the peripheral vestibular system to the cortex. In addition, vestibular information at the cerebral level is mixed with somatic sensations, further reducing the specificity of the vestibular sensations and making it difficult to describe vestibular symptoms (Furman & Cass, 2003). For children, these problems are compounded by the lack of basic communication skills necessary to relay an accurate account of vestibular symptoms and distinguish among vertigo, dizziness, and disequilibrium, making the diagnosis more difficult (Bower & Cotton, 1995). Furthermore, children's responses to these sensations may vary greatly from adult responses. Because children are unable to describe what they are feeling, they may appear anxious, angry, or fearful; clutch onto stationary objects; or appear unable to understand what was said (Haybach, 2004). Some experts suggest that children's responses may be misinterpreted as a behavioral problem or considered insignificant, leading to misdiagnosis or under-diagnosis (Haybach). In the presence of a vestibular deficit, a child may present with any of the signs and symptoms included in Figure 2. It is important to remember, however, that many of these signs and symptoms also may occur in the absence of a vestibular disorder (Haybach, 2002).
FIGURE 2. Signs and symptoms associated with vestibular disorders in children. Anxious or angry behavior Blurred vision Balance difficulties in the dark Clutching or holding on to stationary objects Difficulty concentrating and/or distractibility Difficulty understanding spoken words Fullness in the ear Faintness, lightheadedness, or a heavy head Fatigue Fear, fright, alarm, terror Groping for words Headache and/or neck ache Hearing loss or deafness Increased sensitivity to sound Motion intolerance or sickness Nausea and/or vomiting Nystagmus Rapid pulse Slurred speech Staggering and/or sudden falls Tinnitus Vertigo
Signs and symptoms associated with acute peripheral vestibular injury typically occur because of an asymmetry of input between the right and left central vestibular nuclei, such as when there is a unilateral deficit of the peripheral vestibular mechanism. These symptoms may gradually abate through compensatory mechanisms. The process of vestibular compensation involves changes in the central vestibular nuclei that lead to partial restoration of lost neural activity within the affected nuclei, which reduces the asymmetry and rebalances vestibular neural activity (Furman & Cass, 2003). Vestibular compensation restores function of the VOR and VSR reflexes when the individual is stationary and improves the VOR function during head movement. The ability of the vestibular system to repair and adapt, particularly following unilateral peripheral deficit, can make finding clinical evidence of vestibular dysfunction difficult (Hain et al., 2000). Patients with compensated chronic unilateral peripheral vestibular deficits, however, may continue to demonstrate VOR-related abnormalities on ENG tests (Furman & Cass).
EVALUATION FOR VESTIBULAR DISORDERS
An evaluation of a patient with a balance disorder may include the following: (a) case history; (b) general physical examination; (c) neurological examination adapted to the patient's age; (d) ear, nose, and throat examination; (e) blood tests; (f) ENG or VNG tests; (g) rotational tests; (h) electroencephalography (EEG) to rule out seizures; and (i) computerized tomography (CT) scanning or magnetic resonance imaging (MRI). Children may not be good candidates for vestibular testing because it requires an alert, awake, and cooperative child. Parental support and encouragement is crucial during test procedures. Younger or uncooperative children may receive sedation during a CT scan or an MRI procedure because sedatives do not affect the validity of the results of these two tests (Haybach, 2002).
Vestibular system maturation can affect the successful evaluation of this system in children. Although the human vestibular system is developed and functional at birth, vestibular responses in neonates and young children can vary (Melagrana, D'Agositino, Pasquale, & Taborelli, 1996). VOR responses are poor in neonates, significantly improve in function by 2 months of age (Weissman, DiScenna, & Leigh, 1989), and continue to mature to adult levels during the first 2 years of life (Ornitz, Atwell, Walter, Hartmann, & Kaplan, 1979). Absence of VOR responses by 10 months of age is considered abnormal (Melagrana et al.; Ornitz et al.). Caloric responses can be successfully obtained by 1 year of age in children who are developing normally (Levens, 1988). Vestibular responses to caloric and rotational tests may not always be obtained in premature neonates and infants younger than 6 months of age (Eviatar & Eviatar, 1979).
CHILDHOOD DISORDERS AFFECTING THE VESTIBULAR SYSTEM
The most common childhood disorders that affect the vestibular system are discussed in the following section. Other disorders that are rare during childhood but are associated with vestibular symptoms are reported in Table 1.
Otitis Media With Effusion
Otitis media is one of the most common causes of vestibular symptoms in children (Bower & Cotton, 1995; Busis, 1990). Otitis media with effusion (OME) is a worldwide health problem, particularly among infants and children under 6 years of age (Klein, 1994; Stool et al., 1994). Nearly 50% of children in the United States experience an episode of OME by 1 year of age (Hoffman, MacTurk, Gravel, Chiu, & Cosgrove, 1999). Although the majority of children with OME will experience spontaneous resorption of middle ear fluid within 3 months, about 5% to 10% will develop persistent or chronic OME (Tos, 1980). A family history of otitis media is commonly reported (e.g., Goycoolea, Goycoolea, & Farfan, 1988; Stenstrom, & Ingvarsson, 1997).
A large body of literature has established links between chronic OME, hearing loss, speech and language deficits, and learning disabilities (e.g., Bess, Dodd-Murphy, & Parker, 1998; Brown, 1994; Bryant, 1990; Gravel & Wallace, 2000; Shriberg, Friel-Patti, Flipsen, & Brown, 2000). A smaller but significant body of literature has documented the effect of chronic OME on coordination difficulties; motor abilities, including delayed walking; and balance problems (e.g., Brookhouser & Goldgar, 1987; Casselbrandt, Furman, Rubenstein, & Mandel, 1995; Jones, Radomskij, Prichard, & Snashall, 1990; Orlin, Effgen, & Handler, 1997).
Bower and Cotton (1995) studied 34 pediatric patients in an otolaryngology clinic who presented with vertigo and dizziness. OME was the most commonly identified etiology (23%). In a more recent study, Engel-Yeger, Golz, and Parush (2004), examined the impact of OME on balance and muscle strength of affected children ranging in age from 4 to 7 years. They concluded that OME significantly affected balance, whereas muscle strength was less affected. A significant correlation also was found between parents' responses to their child's performance on balance abilities in daily living activities and results of the child's performance on actual tests of balance function. Casselbrant, Furman, Mandell, Kurs-Lasky, and Rockette (2000) reported that a history of recurrent or chronic OME affected the vestibular function of children when tested in the absence of a concurrent episode of OME. The researchers suggested that the possible sequelae of vestibular involvement should be weighed in future considerations of early intervention for OME. In nonverbal children, vestibular deficits associated with OME may manifest as delay in walking and poor coordination (Bower & Cotton; Engel-Yeger et al.).
One mechanism by which chronic OME can cause vertigo or dizziness is the invasion of bacterial toxins in the inner ear. The round window membrane changes as a result of the OME infection, allowing toxins and inflammatory cells to reach the inner ear. This process, referred to as serous labyrinthitis, can result in permanent high-frequency sensorineural hearing loss (SNHL) because the basal turn of the cochlea is most affected (Hunter et al., 1996; Margolis, Saly, & Hunter, 2000). A second mechanism is the formation of a cholesteatoma (pseudotumor), which is a rare but serious complication of chronic OME. A cholesteatoma is a skin cyst that behaves like a localized tumor. It can destroy bone and other tissue (Furman & Cass, 2003). A common complication of cholesteatoma is perilymphatic fistula, which can lead to severe balance problems and vertigo. Chronic OME and cholesteatoma can both lead to labyrinthitis, resulting in vestibular symptoms (Furman & Cass; Shepard & Telian, 1996).
For children who present with OME-related balance problems, the OME should be treated prior to further evaluation (Bower & Cotton, 1995). Treatment of OME includes a combination of observation, control of environmental risk factors, and oral or local antibiotics (Stool et al., 1994). If local care fails, surgical options, such as myringotomy with or without placement of pressure equalization (PE) tubes and adenoidectomy, may be considered. Surgery also may be required if the infection spreads to the mastoid bone or if cholesteatoma is present (Furman & Cass, 2003; Handler, 1994). Differential diagnosis includes benign paroxysmal vertigo of childhood (BPVC), migraine, and labyrinthitis (Hughes, 1997), all of which are discussed later.
Labyrinthitis and Vestibular Neuronitis/Neuritis
Labyrinthitis and vestibular neuronitis/neuritis cause an inflammation of the labyrinth. History of infection, such as cold, influenza, otitis media, measles, mumps, meningitis, or infectious mononucleosis, often precedes the onset of symptoms (Baloh & Honrubia, 1990). Both disorders present with similar symptoms. The difference is that cochlear symptoms are present in labyrinthitis but absent in neuronitis/neuritis. Cochlear symptoms include high-frequency SNHL and tinnitus. The hearing loss resolves completely or partially in about 50% of cases (Baloh & Honrubia; Shepard & Telian, 1996). Vestibular neuronitis/neuritis and labyrinthitis may be responsible for about 5% of dizziness and about 15% of vertigo reported in all age groups, but they are rare in children (Hain, 2002b). Reliable incidence and prevalence figures for children are not available. Serous labyrinthitis, however, is known to be the single most common complication of acute or chronic OME (Baloh & Honrubia). Symptoms common to labyrinthitis and neuronitis/neuritis include acute vertigo, nausea and vomiting, and nystagmus. An attack can last from a few days to a week. ENG results indicate peripheral vestibular anomalies.
Treatment includes antibiotic or antiviral drugs and symptomatic treatment with vestibular suppressant drugs for acute symptoms. Steroids also have been used for their anti-inflammatory effects to reverse hearing loss, but results have been mixed (Baloh & Honrubia, 1990). Differential diagnosis includes OME, perilymphatic fistula, and BPVC (Baloh & Honrubia).
According to the International Headache Society (IHS; 2004), migraine is a common disabling primary headache disorder with high prevalence; the socioeconomic and personal impacts are well documented by epidemiologic studies. According to the World Health Organization (as cited in IHS), migraine is now ranked 19th worldwide among all diseases causing disability. According to some estimates (Stewart, Lipton, & Celentano, 1992), migraine affects approximately 4% of children. Abu-Arefeh and Russell (1994) reported the prevalence of migraine at 10.6% in children between the ages of 5 to 15 years. The prevalence increased with age, with male preponderance before 12 years of age and female preponderance after 12 years of age. In childhood migraine, however, a headache is not always evident (IHS; Watson & Steele, 1974). The risk of a child developing migraine is 70% when both parents are affected and 45% when one parent is affected (Evans & Mathew, 2000).
Migraine is a vascular disorder affecting the blood supply to the brain. Migraine attacks are caused by initial vasodilation of blood vessels followed by vasoconstriction, which gives rise to headache and other symptoms (Fried, 1980; IHS, 2004). The severity and length of each attack vary. Migraine probably has a biochemical basis in both children and adults. Migraine attacks can be triggered by hormonal adjustments, certain foods or chemicals (e.g., alcohol, caffeine, chocolate, dairy products, nitrites, as in hot dogs), mood changes, and stressful situations (IHS; Tusa, 2000a). The discovery of a genetic cause for some types of migraine offers a breakthrough in treating this disorder (Tusa, 2000a).
Vestibular symptoms frequently occur in migraine patients of all ages. In children, migraine attacks are associated with episodic vertigo and disequilibrium (Fried, 1980; Gans, 2002a; Tusa, 2000a). Watson and Steele (1974) evaluated 286 children diagnosed with migraine. About 23% (66 children) reported true vertigo. In addition, 45% to 50% of children with diagnosed migraine reported a history of motion sickness (Barabas, Matthews, & Ferrari, 1983; Kayan & Hood, 1984). The epidemiologic link between migraine and vestibular symptoms suggests a shared pathogenic mechanism. The basis of a pathophysiological model for migraine-related vertigo may be explained by the physiologic link between the vestibular nuclei, trigeminal nerve system, and thalamocortical processing centers (Furman, Marcus, & Balaban, 2003).
The Headache Classification Committee of the IHS (2004) classified migraine into two major subtypes: (a) migraine without aura and (b) migraine with aura. Childhood periodic syndromes that are common precursors of migraine are included in the latter subtype.
Migraine Without Aura. Migraine without aura--previously known as common migraine--is described as a recurrent headache disorder with attacks lasting 4 to 72 hours (IHS, 2004). It is a throbbing, unilateral headache of moderate to severe intensity associated with nausea and vomiting, photophobia, and phonophobia. The headache can be aggravated by routine physical activity. A strong family history of migraine is common. Migraine without aura generally occurs more frequently and is more disabling than migraine with aura (IHS). Abu-Arefeh and Russell (1994) reported a prevalence of 7.8% of migraine without aura in children.
According to the IHS (2004), migraine without aura in children can present differently than it does in adults. In children, the attacks are shorter in duration, lasting 1 to 72 hours. In addition, the headache is usually bilateral, with the adult unilateral pattern emerging in late adolescence or early adulthood. A migraine headache typically occurs in the frontotemporal region. An occipital headache in children, either unilateral or bilateral, therefore, may be an indication of a structural lesion rather than migraine. Young children may not be able to describe the symptoms of photophobia or phonophobia, but the presence of phobia may be inferred from their behavior. Migraine without aura often has a strict menstrual relationship, which may aid diagnosis in young girls (IHS).
Migraine With Aura. Migraine with aura--previously known as classic or classical migraine--is associated with headache and neurological symptoms and is less common than migraine without aura (IHS, 2004). An aura is a focal neurological disorder generally associated with abnormal sensory perception, such as visions of jagged lines and bright lights shortly before the onset of pain (Gans, 2002a). Abu-Arefeh and Russell (1994) reported a prevalence of 2.8% of migraine with aura in children.
Basilar-type migraine--formerly known as basilar artery migraine or basilar migraine--is included in this subtype. Bickerstaff (1961) evaluated 300 patients and found that 11% (34) had basilar-type migraine, the majority of which were adolescent girls. There was a 3:1 female preponderance postpuberty. The onset peaked during adolescence (Evans & Mathew, 2000), with the majority of initial attacks occurring prior to 20 years of age (Tusa, 2000a). The migraine presents with symptoms clearly originating from the brain stem but without associated motor weakness (IHS, 2004). The onset occurs with visual symptoms, such as flashing lights and bilateral visual loss, causing fear and anxiety for the child (Bickerstaff, 1961). Visual symptoms are followed by vertigo, tinnitus, hearing loss, dysarthria, gait ataxia, occasional drop attacks with or without loss of consciousness, and vertigo as an aura to generalized seizures (vertiginous seizures; Bickerstaff; Eviatar, 1994; Tusa, 2000a). Sensory symptoms include bilateral paresthesia of hands, feet, and tongue (Bickerstaff). A pounding headache generally follows (Eviatar, 1994, Tusa, 2000a). The typical attack lasts from 5 minutes to 1 hour (Tusa, 2000a).
These symptoms are probably due to impaired blood flow within the vertebral basilar artery distribution, causing ischemia of occipital lobes and brain stem (IHS, 2004; Eviatar, 1994). Children with basilar-type migraine develop the more typical migraine headache with aura later in life. This type of migraine is associated with a family history of migraine (IHS; Tusa, 2000a). An EEG should be performed in the sleep-deprived state to rule out vertiginous epilepsy; EEG abnormalities are reported in less than 20% of cases (Evans & Mathew, 2000). An MRI should be performed to rule out tumors and vascular malformations. The ENG test results vary and may demonstrate directional or labyrinthine preponderance on caloric irrigation (Eviatar, 1981).
Childhood Periodic Syndromes Associated With Migraine. Several neuro-otologic disorders may be precursors of migraine in children. They include cyclical vomiting, abdominal migraine, and benign paroxysmal vertigo of childhood (BPVC; IHS, 2004; Tusa, 2000a).
Cyclical Vomiting. According to the IHS (2004), children with cyclical vomiting experience recurrent episodic attacks of intense nausea and vomiting lasting from 1 hour to 5 days; pallor and lethargy are common. Complete resolution of symptoms occurs between attacks. Physical examination indicates no gastrointestinal symptoms, and the symptoms are not attributable to any other disorder.
Abdominal Migraine. According to the IHS (2004), abdominal migraine is an idiopathic recurrent disorder of moderate to severe episodic midline abdominal pain occurring in children. The attacks can last from 1 to 72 hours with no symptoms between attacks. There is associated nausea, vomiting, anorexia, and pallor. As in cyclical vomiting, symptoms are not attributable to any other disorder.
According to the IHS (2004), cyclical vomiting and abdominal migraine are considered precursors of migraine in children because the clinical features of these two conditions resemble migraine symptoms. In addition, multiple research threads have indicated that they are related to migraine. Furthermore, most children presenting with these symptoms develop migraine in later life.
Benign Paroxysmal Vertigo of Childhood. BPVC is the most common cause of acute vertigo in young children after otitis media and labyrinthitis (Eviatar, 1981). It is believed to account for up to 35% of migraine occurrences in children (Bower & Cotton, 1995). The cause appears to be an interruption in the blood supply to the brain (Gans, 2002b; Haybach, 2004). The pathophsyiology is unclear, but vasoconstriction may occur within the posterior cerebral circulation, which, in turn, affects the vestibular nuclei (Gans, 2002b). The attacks typically first appear between 1 and 4 years of age but can occur before 1 year of age (Evans & Mathew, 2000) or any time during the first decade of life (Tusa, 2000a). The condition can manifest as unprovoked, recurrent, spontaneous episodes of true vertigo and disequilibrium without hearing loss or tinnitus in otherwise healthy children (Gans, 2002b; IHS, 2004; Watson & Steele, 1974). Other symptoms may include visual disturbances, pallor, extreme unsteadiness, ataxia, inability to maintain an upright posture, nausea, and vomiting (Gans, 2002b; Tusa, 2000a). The attacks can last from seconds to hours but average 1 to 5 minutes (Evans & Mathew). During an attack, the child may be alert but fearful. The episode may mimic night terror because often the child will act as though nothing has happened following an attack (Gans, 2002b). Initially, headache is not a major symptom, but a significant proportion of these children (30% to 50%) develop typical migraine later in life (Evans & Mathew; IHS). Fortunately, most children grow out of this condition by about 7 to 8 years of age with no permanent vestibular involvement (Gans, 2002b). In most cases of BPVC, a normal audiogram, ENG, and MRI are reported. Treatment is generally symptomatic. An EEG may be required to rule out seizure disorders.
Paroxysmal torticollis of infancy is a disorder of unknown etiology that may be an early variant of BPVC (Fried, 1980; Tusa 2000a). Torticollis may be caused by vasoconstriction of the vestibular nuclear blood vessels, which, in turn, affects the otolith organs in the inner ear. The otolithic involvement through the VCR causes contraction of the sternocleidomastoid muscle, resulting in abnormal twisting of the neck (Gans, 2002b). The most characteristic feature is a head tilt to one side, which may be accompanied by nausea, vomiting, pallor, ataxia, and agitation (Tusa, 2000a). In the majority of cases, the attacks begin during infancy and cease spontaneously by 1 to 2 years of age. Many who experienced attacks as infants, especially those with a family history of migraine, report symptoms of typical migraine headache by early childhood (Tusa, 2000a).
Migraine treatment can be divided into three categories: (a) symptomatic, (b) abortive, and (c) prophylactic. Symptomatic treatment includes analgesics and anti-inflammatory medication, which are generally available without prescription (Koch, 2004; Tusa, 2000a). Abortive medical therapy is used to reduce the severity of an existing attack (Tusa, 2000a). Ergotamines used for abortive therapy are generally not prescribed for children younger than 6 years of age because they can cause gastrointestinal problems (Koch). In addition, because younger children may not be able to communicate adequately about early migraine symptoms, administering timely abortive therapies may be difficult (Koch). If migraine attacks occur several times a month, a schedule of prophylactic daily medication should be used to prevent or decrease the frequency of attacks. Beta-blockers are used commonly as prophylactic therapy for childhood migraine. Efficacy of calcium channel blockers as prophylactic therapy in children is variable (Koch). Avoidance of triggering factors, if known, can be helpful in preventing the onset of attacks. It also is highly recommended that parents ensure children eat breakfast daily, including weekends, and obtain adequate sleep at night (Tusa, 2000a). Vertigo and disequilibrium secondary to migraine will usually respond to the same treatment as migraine headache (Tusa, 2000a). Tricyclic antidepressants are prescribed when depression and migraine occur together (Prensky, 1976).
Differential diagnosis of migraine includes BPVC, recurrent vestibular neuronitis, and headache due to other causes (Gans, 2002a). Repetitive headache of emotional origin also may be confused with common migraine. Unlike migraine, however, headache of emotional origin is not throbbing or unilateral, and there is no family history of migraine (IHS, 2004; Prensky, 1976).
Vertigo Secondary to Trauma
Closed head trauma and whiplash injury can cause dizziness and vertigo (Fried, 1980). The incidence of posttraumatic vestibular signs and symptoms is between 50% and 60% (Rowe & Carlson, 1980; Toglia, 1976; Toglia, Rosenberg, & Ronis, 1970). Perilymphatic fistula also can occur following trauma. In children, fistulas are commonly seen following meningitis or chronic ear infections (Bluestone, 1988). Rarely, fistulas can occur spontaneously (Haybach, 2004; Mattox, 2000). A fistula can result in sudden onset hearing loss, tinnitus, sudden or episodic vertigo or mild unsteadiness, nausea, and vomiting (Furman & Cass, 2003). A perilymphatic fistula may be far more common in children than initially suspected because it can be caused by minor trauma that may have been overlooked or forgotten (Eviatar, 1994).
Labyrinthine concussion due to head trauma can occur with or without temporal bone fractures (Eviatar, Bergtraum, & Randel, 1986). Symptoms include disequilibrium, vertigo or dizziness, a tendency to fall toward the affected side, and seizures (Eviatar, 1994).
Treatment is usually symptomatic, but in some cases surgical intervention may be required. Differential diagnosis is from vertiginous seizures and migraine. A history of head trauma may be the most significant clue for differential diagnosis. If symptoms persist, the condition may be functional (Eviatar et al., 1986), which is extremely rare in children.
Certain therapeutic drugs and chemical substances are toxic to the inner ear, causing functional impairment and cellular degeneration of inner ear tissue, especially the end organs (cochlear and vestibular hair cells) and neurons of cranial nerve VIII. Some drugs affecting the inner ear may be more toxic to the cochlea (ototoxic), whereas others may be more toxic to the vestibular system (vestibulotoxic). There is a long list of therapeutic drugs associated with ototoxicity and vestibulotoxicity. Certain drugs have received greater scrutiny because of frequency of use. These include (a) the aminoglycoside antibiotics (gentamicin and streptomycin are more vestibulotoxic), (b) loop diuretics such as furosemide (Lasix), (c) salicylates (aspirin), and (d) chemotherapeutic agents such as cis-platinum, which are more vestibulotoxic (Baloh & Honrubia, 1990; Monsell, Teixido, Wilson, & Hughes, 1997). The exact incidence and prevalence rates of vestibulotoxicity in humans, especially in children, are not currently available because very few prospective studies assessing these rates have been performed. In the aminoglycoside group, overall prevalence rates range from 2% to 15% (Kahlmeter & Kahlager, 1984; Martz, 1993), although the rates differ for individual antibiotics within the group.
A major risk factor associated with drug toxicity includes impaired renal function because most of these drugs are excreted out of the body via the kidneys. Impaired renal function prolongs drug elimination, increasing the concentration of these drugs in the inner ear fluid and increasing their toxic potential (Monsell et al., 1997). Premature infants are particularly vulnerable because of compromised renal function (Gallagher & Jones, 1979). Other risk factors include duration of drug use, concomitant use of vestibulotoxic and ototoxic drugs (e.g., gentamicin and furosemide), and prior use of these drugs (Baloh & Honrubia, 1990). A genetic susceptibility to aminoglycoside ototoxicity (aminoglycoside-induced deafness) also has been identified and linked to mutation of mitochondrial DNA (Higashi, 1989).
Symptoms generally include bilateral SNHL with a flat or high-frequency configuration, which may or may not be reversible; tinnitus; and dizziness. Gentamicin is the single most common cause of bilateral vestibulopathy, accounting for 15% to 50% of all cases (Hain, 2002a). Bilateral vestibulopathy is characterized by damage to peripheral vestibular structures in both ears, resulting in visual problems, especially during walking, and disequilibrium, which is worse in the dark. Vestibular compensation is rare, resulting in permanent disability (Marais & Rutka, 1998).
In the ambulatory patient, rotational tests can identify early vestibular ototoxicity. ENG tests may indicate abnormal caloric irrigation and functional impairment of the VOR. Spontaneous and positional nystagmus also may be present (Baloh & Honrubia, 1990; Black, Pesznecker, Homer, & Stallings, 2004). The key to management of ototoxicity and vestibulotoxicity is prevention. If toxic drug effects are identified, adjustment of dosage or use of different, less toxic drugs may be possible (Baloh & Honrubia). Depending on duration and dosage, the effects of certain drugs (e.g., salicylates) may be completely or partially reversible.
Fetal Alcohol Syndrome
Maternal alcohol abuse during pregnancy is associated with fetal alcohol syndrome (FAS) or fetal alcohol abuse syndrome. Alcohol is a physical and behavioral teratogen and one of the leading causes of mental deficiency in the world (Canadian Pediatric Society, 2002). The incidence of FAS in the general population in the United States is about 2 cases per 1,000, and the incidence among children born to heavy drinkers is about 4% (Abel, 1995). Although FAS does not discriminate on the basis of race, the incidence is disproportionately higher among Native Americans and Canadian Aboriginal people (Aase, 1981; Williams, Odaibo, & McGee, 1990).
The hallmark of in utero alcohol exposure is delayed maturation of the central nervous system (Abel, 1997). This syndrome is associated with abnormal balance; ataxia (Claren, 1981); mental retardation;, craniofacial anomalies; growth retardation; hearing loss of varying severity; and delayed language acquisition, primarily due to hearing loss and impaired cognitive function (Becker, Warr-Leeper, & Leeper, 1990; Church & Abel, 1998). Animal studies have demonstrated alcohol-related damage to the precursors of the inner ear, cranial nerve VIII, and the brain stem during embryonic development (e.g., Kaneko, Riley, & Ehlers 1993). Peripheral vestibular disorders in children with FAS, therefore, might be expected. Clinical evidence for peripheral vestibular dysfunction in FAS, however, is ambiguous (Church & Kaltenbach, 1997). Furthermore, vestibular studies in humans demonstrate no compelling evidence of peripheral vestibular damage. For these reasons, FAS-related balance problems are considered more likely to be of cerebellar, rather than vestibular, origin (Church & Abel). Histologic evaluation of human and animal brain tissue and imaging studies of children with FAS have demonstrated corpus callosum abnormalities (Riley et al., 1995) and cerebellum hypoplasia (Mattson et al., 1992; Mattson et al., 1994), particularly loss of Purkinjee cells in the anterior cerebellar vermis (Sowell et al., 1996). There also is considerable variability of lesions in the brains of children with FAS. This variability is probably a result of differences in the amount of maternal alcohol ingested, pattern and timing of drinking, or the mother's genetic abilities to metabolize alcohol (Canadian Pediatric Society, 2002).
Children with FAS should be evaluated thoroughly and undergo intervention for balance, hearing, and speech and language disorders. Conversely, children with craniofacial anomalies, balance problems, hearing loss, or speech and language disorders should be evaluated for FAS, ensuring better patient care and outcome (Church & Abel, 1998). Early diagnosis of FAS is crucial because delayed intervention can lead to behavioral and cognitive problems, loss of self-esteem, frustration, and acting out. Although the abnormalities associated with FAS are permanent, some can be modified with early intervention (Canadian Pediatric Society, 2002).
Vestibular Deficits in Children Who Are Deaf
The embryologic and anatomic relationship between the cochlea and the peripheral vestibular system logically raises the question of how congenital and acquired deafness affect the vestibular systems (Selz, Girardi, Konrad, & Hughes, 1996). There are limited data regarding the status of the vestibular system of children who are deaf. A few studies have examined results of rotational and caloric tests in children with congenital and acquired hearing loss. In these studies, vestibular deficits identified in children who are deaf range widely, from 49% to 95% (Horak, Shumway-Cook, Crowe, & Black, 1988; Rosenblut, Goldstein, & Landau, 1960; Sandberg & Terkildsen, 1965; Teng, Liu, & Hsu, 1962).
Most children who are deaf, however, demonstrate no outward abnormalities of gait or motor coordination (Horak et al., 1988; Selz et al., 1996). Vestibular compensation may be the reason that balance problems are rarely demonstrated by children who are deaf. Another reason may be that these children have experienced vestibular dysfunction most or all of their lives and, therefore, may not perceive impaired vestibular sensations as abnormal (Selz et al.). Children who are deaf, however, demonstrate abnormalities on positional and ENG tests, including eye gaze abnormalities (Horak et al.; Sandberg & Terkildsen, 1965; Selz et al.; Teng et al., 1962), indicating that although there may be no outward signs of vestibular deficit, the vestibular system, both peripheral and central, may be affected by the same etiology that led to the hearing loss. These anomalies are more pronounced in children with acquired hearing loss, especially loss due to meningitis. The meningeal infection may cause damage both at the level of the peripheral structures and along the central vestibular pathways responsible for eye movements (Selz et al.). Children who contract meningitis should be identified because as the children age and the proprioceptive and visual senses fail, the children may demonstrate vestibular deficits and their associated negative effects, such as frequent falls (Selz et al.).
Childhood vestibular disorders are more common than traditionally believed; thus, speech-language pathologists, audiologists, and educators of children who are deaf and hard-of-hearing may encounter children with these disorders. Management of most childhood disorders affecting the vestibular system requires medical intervention, so it is important for professionals working with children to recognize these disorders, bring them to the attention of caregivers, and recommend appropriate medical referral. Young children's inability to describe vestibular symptoms combined with lack of awareness of these disorders by professionals may lead to misdiagnosis or underdiagnosis of these conditions. A case in point is migraine. The general perception is that migraine is an adult-onset headache disorder. Migraine, however, does occur in children and can present with vestibular disturbances and other symptoms without headache.
Children may be alarmed and anxious when experiencing vestibular symptoms because they are not sure what is happening to them or how to express their anxiety and fear. It is important to involve the child in understanding the disease to provide him or her with a feeling of control over the condition (Haybach, 2002). Furthermore, it is important that school officials, caregivers, and others who come into contact with the child are informed of the diagnosis and limitations, if any, the condition may place on the child. According to Haybach (2002), children with vestibular disorders may require extra help with learning because the disorder may impair their ability to learn new concepts, especially spatial concepts. They also may need extra time with tasks requiring memorization. Vestibular disorders may result in lost school days, adding further stress on the child to make up missed work. Abu-Arefeh and Russell (1994) found that children with migraine lost an average of 7.8 school days (range 0-80) per school year due to illness as compared to an average of 3.7 days lost by children without migraine.
A vestibular disorder can be an ongoing and disruptive influence on family life, especially if it is a chronic condition. Family support groups may be available at the local level, or caregivers can access information through the Vestibular Disorders Association (VEDA; http://www.vestibular.org/children.html). Other resources for professionals and families include the American Institute of Balance (www.dizzy.com), the Balance and Mobility information site (www.balanceandmobility.com), the Family Village educational site (www.familyvillage.wisc.edu), DizzyMates (http://health.groups.yahoo.com/group /steadymates/), the American Headache Society (http://www.ahsnet.org/), and the American Council for Headache Education (http://www.achenet.org/kids/).
Zarin Mehta and Daria B. Stakiw
Wichita State University
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Zarin Mehta, PhD, CCC-A, FAAA, is a clinical associate at Arizona State University, where she participates in the clinic and teaches graduate courses in the AuD program. Her current research interests include assessment and management of auditory disorders across the age spectrum. Daria B. Stakiw, AuD, CCC-A, FAAA, is a consulting audiologist for Advanced Audiology in Vail, Colorado, and the Mountain BOCES school district. She also is an NIHS regional consultant for the State of Colorado's universal newborn hearing and research development program and project coordinator for Project ECHO. Her clinical and research interests include diagnosis and management of vestibular disorders and pediatric assessment. Address: Zarin Mehta, Arizona State University, Department of Speech and Hearing Science, Main Campus, PO Box 870102, Tempe, AZ 85287-0102; e-mail: Zarin.Mehta@asu.edu
Table 1. Rare Childhood Disorders Presenting With Vestibular Symptoms Disorder Description Resources Juvenile Characterized by the Hausler, Toupet, Meniere's triad of vertigo, Guidetti, Basseres, disease tinnitus, and & Montandon, 1987; fluctuating Stahle, Stahle, sensorineural & Arenberg, 1978 hearing loss. Vestibular Tumor arising from Mahaley, Mettlin, schwannoma cranial nerve Natarajan, Laws, VIII. Hearing & Peace, 1990; loss is common, but Selesnick, Jackler, vestibular symptoms & Pitts, 1993 are rare. Neurofibromatosis, Genetic disorder Evans, 2004 Type 2 (NF-2) presenting with multiple tumors of the peripheral and central nervous system. Symptoms include hearing loss, tinnitus, disequilibrium, headache, and visual problems. Psychological Includes anxiety, Fried, 1980; disorders depression conversion Tusa, 2000b disorder, panic attacks, phobias, and mal de debarquement syndrome.
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|Author:||Mehta, Zarin; Stakiw, Daria B.|
|Publication:||Communication Disorders Quarterly|
|Date:||Sep 22, 2004|
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