CHAPTER 58 MANAGEMENT OF DIZZINESS IN CHILDREN LYDIA EVIATAR, MD Dizziness is a fairly common complaint in children, who often use the term indiscriminately to describe vertigo, lightheadedness, balance difficulties, anxiety, or even headaches. As it is a nonspecific complaint, it may be caused by a variety of systemic disorders or visual disturbances. The more specific complaint of true vertigo, best described as a spinning sensation (either of self or of the environment), is more likely the result of a true vestibular dysfunction. Obtaining a detailed and accurate history of the patients’ symptoms is essential. The circumstances associated with the occurrence of vertigo and the duration, frequency, and presence of related problems such as dysequilibrium, loss of postural control, confusion, nausea, or vomiting need to be assessed to reach an accurate diagnosis. Precipitating factors may be head trauma, infection, exposure to ototoxic drugs, or abrupt changes in position. In young children, congenital anomalies of the inner ear, such as a Mondini’s malformation or large vestibular aqueduct, may be predisposing factors. A family history of progressive hearing loss suggests a genetically transmitted disorder that may be associated with vestibular dysfunction. Systemic illnesses such as diabetes, endocrine disorders, or severe anemia should be considered. Progressive degenerative neurologic disorders, such as Friedreich’s ataxia, Huntington’s disease, multiple sclerosis, or Refsum’s disease, are associated with vestibular neuropathy and may present with dizziness. Arnold-Chiari malformation and vertebrobasilar insufficiency with or without pontomedullary or cerebellar infarcts are also associated with dizziness or vertigo. Neurovestibular Examination The neurovestibular examination (Table 58-1) should test the integrity of the equilibrium system. Maintenance of equilibrium depends on appropriate information from the visual, proprioceptive, and vestibular systems regarding Current Management in Child Neurology, Third Edition © 2005 Bernard L. Maria, All Rights Reserved BC Decker Inc the position of the body in space and the normal function of the pyramidal and extrapyramidal systems that enable the body to correct its position in response to a change in the center of gravity. The appropriate central integration of sensory input is essential for adequate postural control and, according to more recent investigations, is not fully developed until 15 years of age. An acute visual, vestibular, or proprioceptive disturbance will cause a mismatch to previously stored sensory information and present as dizziness and problems with postural control. The neurologic evaluation should be adapted to the patient’s age and level of maturation. In infants younger than 6 months of age, head tilt, delayed head control, and delayed postural control may be due to vestibular dysfunction. By 6 months, head control should be well established and good symmetric righting reflexes indicate a functional vestibular system. An asymmetric reflex suggests a unilateral lesion when no motor deficit is present. By 4 years, the child’s brain is mature enough to have established equilibrium responses that can be tested clinically or by posturography (Foudriat et al, 1993). The neurologic evaluation should assess the presence of cranial nerve deficits, the integrity of extraocular movements, and the presence of spontaneous, gaze-induced (30° lateral, upward, and downward gaze), or positional nystagmus. The Dix-Hallpike maneuver involves looking for nystagmus induced by abruptly changing the patient’s position from sitting with a lateral head deviation of 45° to reclining with the head hanging off the examining table and maintained in Management of Dizziness in Children Pages 370–376 Management of Dizziness in Children / 371 the same lateral position. This maneuver is repeated with the head to the right, to the left, and hyperextended in the midline position. It will elicit positional-induced nystagmus and is positive in paroxysmal positional nystagmus and other peripheral labyrinthine disorders (ie, labyrinthitis, neuronitis, Meniere’s disease, and perilymphatic fistula). This positionalinduced nystagmus has a brief latency (< 10 s), fatigues with repeated maneuvers, and is most intense when the affected ear is down. The patient will also complain of being most uncomfortable with the affected ear down, which is a typical symptom of a peripheral vestibular lesion (Table 58-2). Nystagmus due to peripheral lesions may be inhibited by fixation. The use of Frenzel goggles (10+ diopters) during this test eliminates fixation and facilitates eye observation by the examiner. It is important to look for latency and duration of response as well as habituation with repeated positioning, as these features help differentiate between central and peripheral lesions (Table 58-3). A central nystagmus is not inhibited by fixation, is not positional, and does not fatigue. Dizziness due to central vestibular disorders, such as cerebellopontine lesions, is usually associated with hearing loss and often with other cranial nerves deficits. With posterior fossa lesions, cerebellar signs and pyramidal signs may be present, affecting gait and coordination. With vestibular disorders, tandem gait with eyes closed may elicit swaying and veering toward the affected side. A reinforced Romberg test is more sensitive than the regular version and helps elicit subtle vestibular findings. The stepping test, introduced by Fukuda, requires the patient to step in place with eyes closed at the intersection of two perpendicular lines while counting to 60. With unilateral vestibular lesions, this maneuver will elicit veering toward the affected side by more than 45°. With bilateral vestibular dysfunction, a significant forward displacement of more than 20 inches may be seen. TABLE 58-2. Peripheral Vestibular Disorder Acute onset vertigo Head tilt or swaying toward affected side Autonomic dysfunction Nystagmus toward unaffected side Positive Dix-Hallpike maneuver Preferred position: supine, affected ear up Improves over time Dizziness may present as part of a preexisting condition or as a seemingly isolated complaint (Figure 58-1). Visual disturbances causing distortion of images often are associated with dizziness. This is especially common when the wrong glasses are prescribed. Systemic disorders, such as diabetes, endocrine disorders, longstanding renal insufficiency with uremia, demyelinating disorders (eg, multiple sclerosis), and degenerative disorders, may be associated with low-grade constant dizziness, fluctuating in intensity, as a result of a chronic vestibular neuropathy. Long-standing use of aminoglycosides, quinine, cisplatin, or diphenylhydantoin may damage the vestibular nerve or the labyrinth and cause unremitting dizziness. Unremitting dizziness may occur in acoustic neuroma, other cerebellopontine (CP) angle lesions, and posterior fossa tumors. There is usually progressive hearing loss and progressive involvement of other cranial nerves, pyramidal tract signs, and cerebellar dysfunction. Magnetic resonance imaging (MRI) of the brain with contrast and thin cuts through the CP angle will obviate the diagnosis. In the absence of neurologic findings, endocrine abnormalities, or exposure to ototoxic drugs, the possibility of anxiety or panic attacks or psychosocial stress needs to be considered. These patients will admit upon questioning to hyperventilation, excessive palm sweating, palpitations, and even chest pressure during the attacks. Many patients complaining of constant dizziness with mild variations in intensity also have frequent headaches. This combination of symptoms may be the manifestation of underlying stress, anxiety, or depression. When headaches are associated with recurrent dizziness, one should consider vertiginous migraines. Autonomic features are often present in vertiginous migraine. The difference between dizziness and vertigo is very important indeed. Whereas dizziness is a less-specific symptom associated with systemic ailments, space-occupying lesions, or psychosocial stresses, vertigo is more likely associated with a true vestibular disorder that can be due to a vascular, inflammatory, or degenerative process. It is helpful to approach the diagnosis of vertigo by separating vertigo with hearing loss from vertigo without TABLE 58-1. Clinical Neurovestibular Testing TABLE 58-3. Central Vestibular Disorder Neurologic examination adapted to child’s age Righting and equilibrium responses Reinforced Romberg test Stepping test Tandem gait, eyes closed Dix-Hallpike maneuver Orthostatic hypotension test Unremitting dizziness or vertigo Nystagmus is constant and not positional; does not habituate and is not inhibited by fixation Dix-Hallpike maneuver noncontributory Cranial nerve deficits may be present Pyramidal or cerebellar deficits may coexist Imaging studies recommended Differential Diagnosis Current Management in Child Neurology, Third Edition © 2005 Bernard L. Maria, All Rights Reserved BC Decker Inc Management of Dizziness in Children Pages 370–376 372 / The Office Visit: Other Neurologic Complaints and Conditions Nature of complaint Chronic dizziness or vertigo Acute paroxysmal vertigo Hearing loss Yes Hearing loss No Yes No Yes Neurologic deficits Yes No Neurologic deficits Yes No Fever No Yes No Age 1–4 CP angle or posterior fossa tumor Cholesteatoma or autoimmune disorder CP angle or posterior fossa tumor Headache Labyrinthitis Any age Trauma BPV Yes No Yes Loss of consciousness No Yes Chronic daily headache Endocrine disorders, anemia, anxiety, or depression Concussion or fistula No Otoxic drugs Yes Syncope or seizure No Nausea or vomiting Yes Otoxicity Nausea or vomiting Yes No No Anxiety or panic Vestibular neuronitis Yes Meniere’s syndrome Vascular event No Vertiginous migraine Psychosomatic Positional Yes PPV or orthostatic hypertension FIGURE 58-1. Dizziness: differential diagnosis. BPV = benign paroxysmal vertigo; CP = cerebellopontine; PPV = paroxysmal positional vertigo. hearing loss and to proceed with a specific line of questioning that will lead to the correct diagnosis. A comprehensive pediatric “dizziness” questionnaire was designed by the author and tested on 62 patients with dizziness. The sensitivity of the questionnaire in reaching the correct diagnosis was calculated at 92%. Acute Paroxysmal Vertigo with Hearing Loss Labyrinthitis The acute onset of vertigo, nausea, and vomiting, aggravated by head motion and associated with fever and hearing loss, is typical of an acute labyrinthitis. The attacks may last several days and are associated with severe equilibrium disturbances and autonomic disturbances. Acute labyrinthitis is probably the most common etiology of vertigo and hearing loss in young children who present with fever and bacterial or viral otitis media. Immediate, aggressive treatment of the otitis is required. Meclizine, diphenhydramine, or a scopolamine patch will alleviate the verCurrent Management in Child Neurology, Third Edition © 2005 Bernard L. Maria, All Rights Reserved BC Decker Inc No Unknown tigo. Intravenous fluids may be required to overcome dehydration resulting from vomiting and antiemetics are helpful in stopping vomiting. Meniere’s Disease Meniere’s disease presents in a similar fashion to labyrinthitis but without fever. It is accompanied by tinnitus, ear pressure, and fluctuating hearing loss. The attacks are recurrent and associated with progressive hearing loss. Fortunately, the condition is very rare in children. Treatment consists of diuretics for the alleged labyrinthine hydrops and symptomatic treatment for vertigo with meclizine, diphenhydramine, or scopolamine patch. Perilymphatic Fistula Head trauma, barotrauma, and exertion may cause a rupture of the round or oval window, leading to a perilymphatic fistula presenting with episodes of vertigo and progressive sensorineural hearing loss (SNHL). As in the previously described peripheral vestibular disorders, the vertigo is usually positional and the attacks may be associated with nystagmus. Nystagmus can often be elicited by Management of Dizziness in Children Pages 370–376 Management of Dizziness in Children / 373 increasing pressure in the ear canal with a pneumatic otoscope. It can be observed with the naked eye or recorded by electronystagmography. Exploratory ear surgery may be required to identify and correct the leak, localized at the oval or the round window. Early corrective surgery may salvage hearing and control the vertigo. Congenital anomalies of the inner ear may be predisposing factors and highresolution computed tomography (CT) of the temporal bone may establish the diagnosis. Head Trauma Head trauma can cause temporal bone fracture resulting in SNHL and vestibular damage, or it may cause a labyrinthine concussion without hearing loss. Auditory brainstem evoked potentials are helpful in detecting brainstem involvement. Steroids have been advocated for reduction of immediate posttraumatic swelling and promoting healing of the cochlear and vestibular nerves. Subsequent vestibular rehabilitation is helpful in promoting adaptation to the acute vestibular trauma. Vascular Occlusion Vascular occlusion of the labyrinthine artery may occur in hypercoagulable states, such as sickle cell disease. Treatment focuses on the underlying condition. Traumatic vertebral artery aneurysmal dissection may cause embolization of brainstem and cerebellum, and acute vertigo. Initial treatment with heparin is indicated to prevent further embolization, followed, in time, by surgical correction of the aneurysm. Autoimmune Disorders Autoimmune disorders, such as Cogan’s syndrome, may cause hearing loss and acute labyrinthine dysfunction. The mechanism is an autoimmune process affecting the cochlea and labyrinth, resulting in elevated anticochlear antibodies. Checking for presence of anticochlear antibodies is recommended. The recommended treatment is intravenous immunoglobulin G or steroids, which are reported to substantially ameliorate the symptoms. Paroxysmal Vertigo without Hearing Loss Paroxysmal vertigo without hearing loss should be evaluated according to the patient’s age. Benign Paroxysmal Vertigo Infants and children younger than the age of 5 years may experience a sudden spinning sensation and loss of equilibrium and hold on to the nearest support, usually their mother, until the vertigo subsides. The attack may last minutes to hours, during which the child appears Current Management in Child Neurology, Third Edition © 2005 Bernard L. Maria, All Rights Reserved BC Decker Inc diaphoretic and pale, with nystagmus often present. Head tilt nausea and vomiting are occasionally present. There is no confusion or automatism during the episode and no confusion or sleepiness after it, as observed with partial complex seizures. Equilibrium is definitely impaired during the attack and the child refuses to move. The neurologic examination between attacks is entirely normal. The condition is called benign paroxysmal vertigo (BPV). There is usually a strong family history of migraine and 50% of these children develop migraine attacks in adolescence. Because the episodes are usually brief, treatment is not indicated, but reassuring the child and the family regarding the benign nature of the condition is very helpful. Children should have a brain MRI and electroencephalogram (EEG) at the time of the first attack to exclude a space-occupying lesion or partial complex seizures. Paroxysmal Torticollis or Tortipelvis Paroxysmal torticollis and paroxysmal tortipelvis also are manifestations of acute vestibular dysfunction in young children. The etiology of these conditions is not fully understood. They are considered migraine equivalents because of the strong association with migraine later in life. Because of the brief duration of the episodes, treatment is usually futile. Children who exhibit poor balance between attacks benefit from physiotherapy. Vestibular Neuronitis In older children and in adolescents, an acute episode of vertigo, often preceded by an upper respiratory infection and associated with nausea, vomiting, and dysequilibrium, is termed vestibular neuronitis. The condition lasts from a few days to several weeks, with decreasing duration and intensity over time. Episodes may recur months and even years later, usually with decreased severity and duration. Acute treatment consists of hydration, bed rest, and symptomatic treatment of the vertigo with meclizine, scopolamine, or diphenhydramine, and antiemetics (Table 58-4). A prospective longitudinal study of 21 children with vestibular neuronitis provides data on the natural history of the condition. It shows progressive decline of symptoms. Complete recovery was documented in all the children studied after 5 years (Taborelli et al, 2000). Symptoms that persist beyond 2 or 3 weeks of treatment with antivertigo medication are helped with physiotherapy aimed at correcting the sensory mismatch and promoting habituation. This is achieved by encouraging the patient to repeatedly assume the most uncomfortable position (affected ear down) while using visual and proprioceptive cues during the procedure. This maneuver helps the patient to compensate for the vestibular loss and promotes central reorganization of postural control, leading to progressive resolution of the dizziness. Management of Dizziness in Children Pages 370–376 374 / The Office Visit: Other Neurologic Complaints and Conditions TABLE 58-4. Treatment of Dizziness Acute vertigo and autonomic symptoms Intravenous hydration Diazepam IV 0.05–0.15 mg/kg/dose or PO 0.12–0.8 mg/kg/dose Meclizine PO 25–100 mg/dose/d Prochlorperazine IM 0.05–0.15 mg/kg/dose or PO 0.4 mg/kg /dose in 3–4 doses Diphenhydramine IV or IM 5 mg/kg/d in 3–4 doses; adolescents: transdermal scopolamine 1.5 mg Hydrops or Meniere’s disease: diuretics (diazides or Diamox®) Bacterial labyrinthitis: antibiotics Autoimmune disorders: steroids Subacute or chronic vertigo Meclizine 25–100 mg/d Treat underlying disorder: Migraine: nonsteroidal antiinflammatory drugs for subacute episode Chronic migraine: amitriptyline 10–75 mg/d, propanolol 10–20 mg bid, or divalproex sodium (Depakote®) 1 or 2 capsules of 125 mg bid or ER 250 mg bid Vertiginous seizures: carbamazepine 25 mg/kg/d or as per EEG CP angle or posterior fossa tumor: surgery Cholesteatoma: surgery Perilymphatic fistula: surgery Orthostatic hypotension: increase fluid and salt intake or mineralcorticoids Paroxysmal positional vertigo: physiotherapy, ie, positioning maneuvers Panic or anxiety attacks: psychiatric counseling; alprazolam 2–4 mg/d or paroxetine 10–40 mg/d bid = twice daily; CP = cerebello-pontine; EEG = electroencephalogram; ER = extended release; IM = intramuscularly; IV = intravenously; PO = orally. Migraine Variants Vertigo may precede or accompany a headache and may be associated with nausea or vomiting. Phonophobia and sonophobia, characteristic of migraine, may or may not be present. This constellation of symptoms is characteristic of the migraine variant known as vertiginous migraine, which respond to the same medications used to treat classic migraine. Basilar Artery Migraine Acute paroxysmal vertigo associated with tinnitus, acroparesthesias, perioral paresthesia, and visual obscuration was initially described by Bickerstaf in prepubescent girls and labeled basilar artery migraine (BAM) because the symptoms are consistent with vasoconstriction in the vertebrobasilar territory. The condition is recognized in all age groups and in both genders and can be a frightening experience for patients and parents alike. It may be associated with loss of consciousness when the decreased perfusion of the reticular activating system in the brainstem is of long duration. Both brain MRI and EEG are indicated to rule out a vascular malformation of the brainstem or a seizure disorder. For suspected vascular malformations, magnetic resonance angiography (MRA) or CT angiography may be necessary to confirm the diagnosis. Treatment of the acute episode is primarily with nonsteroidal antiinflamCurrent Management in Child Neurology, Third Edition © 2005 Bernard L. Maria, All Rights Reserved BC Decker Inc matory agents. Ergot preparations are contraindicated for fear of causing severe vasoconstriction in the vertebrobasilar distribution, causing stroke. Calcium channel blockers may be effective as preventive therapy but should be used with extreme caution. Cyclic Vertigo We described a group of children with cyclic vertigo. The vertigo occurred at very predictable intervals, starting early in the morning with severe photophobia, nausea, and vomiting. After many years of cyclic vertigo, the children developed classic headaches. Three of nine children were subsequently diagnosed with bipolar disorder. This presentation is most likely another migraine variant associated with a functional disturbance of the internal biologic clock. The treatment is symptomatic during the episode. When attacks are frequent, migraine prophylaxis with propranolol, valproate, or topiramate can be effective. Motion Sickness Most children with migraines suffer from motion sickness and are prone to vertigo, nausea, and vomiting during passive locomotion (car rides) or motion in the surrounding environment while they remain still. They may be especially oversensitive to optokinetic stimulation. The explanation for this disorder is not clear but may be due to the patient’s inability to tolerate an abrupt sensory mismatch. Habituation may be achieved by gradually increasing exposure to longer rides and by ensuring a wide-open visual field during rides. The use of meclizine during prolonged trips may be helpful for symptom control. Vertiginous Seizures Loss of consciousness or altered consciousness immediately preceded by vertigo suggests a vertiginous partial complex seizure. Vertiginous seizures are very rare; however, dizziness may be experienced in various seizure types. The diagnosis should rely on EEG abnormalities best elicited after sleep deprivation or, better yet, recorded during the event itself. Treatment should be selected on the basis of the nature of the underlying seizure disorder. Panic Attacks Severe panic attacks, agoraphobias, and claustrophobias have presented as episodic vertigo. A carefully directed line of questioning (as suggested in the “dizziness questionnaire”) will elicit the episodes of hyperventilation, palpitation, and autonomic instability that characterize these conditions and eliminate the need for extensive and costly work-up. Management of the condition preferably should be assigned to a psychiatrist. Antidepressant and antianxiety medication, such as paroxetine or benzodiazepines, can be very helpful in controlling symptoms (see Table 58-4). Management of Dizziness in Children Pages 370–376 Management of Dizziness in Children / 375 Orthostatic Hypotension Vertigo associated with abrupt changes in position from supine to sitting or standing is most likely the result of orthostatic hypotension. This diagnosis can be easily established during the general physical examination by measuring blood pressure in the supine and standing positions and documenting a significant drop of > 20 mm Hg of the systolic pressure during standing. Tilt testing in a neurophysiology laboratory may provide additional confirmatory evidence. Increasing fluid and salt intake may eliminate the orthostatic hypotension; however, corticosteroids (eg, Florinef®) need to be added in severe cases. Paroxysmal Positional Vertigo Paroxysmal positional vertigo occurs during abrupt changes of head position while turning over abruptly in bed or causing other abrupt changes in head position. The sensation of vertigo often is associated with a brief bout of torsional nystagmus elicited when the affected ear is undermost. This can be reproduced in the office by using the Dix-Hallpike maneuver. The etiology is attributed to calcium debris broken off the otololiths and lodging in the posterior semicircular canal. The condition is very rare in children but may occur as the result of head trauma. Treatment consists of head positioning exercises that will induce habituation and may even reposition the debris in some cases. The field of vestibular therapy using multisensory integration modalities is rapidly expanding on the basis of extensive experiments on vestibular compensation in adults and in children. It is a very useful, safe, and effective treatment that is receiving progressively more recognition in clinical practice as an adjunct or a substitute to medication. Laboratory Testing The therapeutic and technology assessment subcommittee of the American Academy of Neurology recently reviewed the vestibular testing techniques used in adults and children (Table 58-5). Most laboratory testing relies on evaluation of the vestibulo-ocular reflex (VOR). This is a short latency reflex that generates compensatory eye movements in response to head movements in order to maintain visual fixation. The VOR can be evaluated during the application of stimuli such as rotation and caloric irrigation. The most common method of testing the VOR is electro-oculography, also referred to as electronystagmography. The technique measures changes in corneoretinal potential using electrodes placed around the inner and outer canthi of the eyes. It permits recording of the direction, amplitude, and velocity of eye movements in different head positions and in response to different types of vestibular stimulation. Infrared video nystagmography uses infrared cameras Current Management in Child Neurology, Third Edition © 2005 Bernard L. Maria, All Rights Reserved BC Decker Inc TABLE 58-5. Laboratory Testing Electronystagmography Hearing test adapted to patient’s age Auditory brainstem potentials in suspected brainstem involvement Brain MRI with contrast in suspected central disorders MRA or CT angiogram in vascular disorders CBC, FBS, TFT, electrolytes, and coagulation studies CBC = complete blood count; CT = computed tomography; FBS = fasting blood sugar; MRA = magnetic resonance angiography; MRI = magnetic resonance imaging; TFT = thyroid function tests. positioned in eye goggles that detect movements of the eyes. Most commercially available techniques record horizontal eye movements. Two methods are used for stimulation of the vestibular apparatus: rotation and caloric irrigation of the ear canals by air or water. Caloric testing should be performed with the head positioned in such manner that the horizontal semicircular canal is vertically placed. The caloric irrigation produces a convection current, causing the endolymph to rise when warmed and sink when cooled. The nystagmus during cool irrigation is away from the ear and during warm irrigation toward the irrigated ear. A pitfall of the technique is that a narrow or an obstructed ear canal may reduce the intensity of the stimulus, causing a reduced response. Using a formula developed by Yonkees, it is possible to determine the presence of a hypoactive labyrinth (less nystagmus generated by hot and cold stimulation in one ear compared with the other ear) or directional preponderance (the nystagmus elicited by the caloric irrigations beats primarily in one direction). The presence of a hypoactive labyrinth suggests damage to the peripheral organ, as in vestibular neuronitis or labyrinthitis. Directional preponderance is more likely associated with a central lesion or an old peripheral lesion. Children older than 3 years of age usually are able to tolerate a bithermal caloric irrigation, even though the procedure requires about half an hour and may cause vertigo, especially when performed after an acute labyrinthine insult. Rotational testing using a sinusoidal stimulation with a computerized rotational chair that delivers frequencies of rotation from 0.01 Hz to 0.16 Hz is more suitable for pediatric testing. Unfortunately, the equipment is expensive and not universally available. Rotational testing allows precise application of multiple frequencies of rotational stimuli, whereas caloric testing is equivalent to a single very low frequency (0.003 Hz). The disadvantage is that it tests both ears simultaneously and is not as reliable in detecting unilateral lesions. The test is suitable for very young children who can be tested while sitting in a parent’s lap. Measurement of the VOR in rotational testing is expressed in terms of gain (eye velocity relative to head velocity) and phase (timing of eye motion relative to head motion). A perfect VOR function will present a gain of 1 and a phase shift of 180°. The VOR is less efficient during very low Management of Dizziness in Children Pages 370–376 376 / The Office Visit: Other Neurologic Complaints and Conditions frequencies of head movement and is best at rotations of 1 to 6 Hz, which closely simulate head motion during locomotion. The VOR may show asymmetry in cases of substantial unilateral labyrinth hypofunction. The rotational test is best suited for assessment of ototoxicity. Posturography uses a computerized moving platform to elicit postural reactions to abrupt changes in the center of gravity with and without visual and proprioceptive clues. The computer analyzes body sway and compensatory postural reactions. The test requires special equipment and has had limited practical use because of its high cost, difficulty administering it in young children, and limited standardization in children. Several studies on posturography from Japan and the United States are available and describe a delay in acquiring mature integrated postural reactions in children younger than 15 years of age. However the studies were performed with equipment designed and used for adults, which may account for some of the alleged delays. The limited number of children studied and the discrepancies between the results published from various centers underlie the difficulty in using these tests for routine diagnostic purposes. Indications for Vestibular Testing Vestibular testing is especially helpful in disorders of the peripheral organ (ie, labyrinthitis, vestibular neuronitis, posttraumatic vertigo, perilymphatic fistula, Meniere’s disease, or vestibular schwannoma). A hypoactive labyrinth will confirm damage to the peripheral organ. Repeated testing may provide a measure of the degree of recovery over time. Drug ototoxicity can be carefully assessed and monitored with rotational testing. Testing also is indicated in balance disorders when it is important to differentiate between poor balance resulting from visual, vestibular, or proprioceptive disorders. Although the history and clinical testing will give a definite clue concerning the disorder’s etiology, vestibular testing helps confirm the diagnosis. Children with acquired or congenital hearing loss also will benefit from testing, as the cochlea and labyrinth are in close proximity and may be affected by the same noxious agents. A child with poor bilateral labyrinthine function may become very disoriented in the dark or while diving into a pool, as visual cues are missing in the dark and proprioceptive clues missing when one is immersed in water. Testing the VOR during smooth pursuit or generation of saccades provides information on cerebellar control of eye motions, and suppression of nystagmus with fixation will indicate that the lesion is peripheral and not central. Hearing testing is essential in all suspected peripheral lesions and suspected posterior fossa lesions, especially vestibular schwannoma. EEG should be performed in cases of vertigo with loss of consciousness or loss of postural control to exclude the Current Management in Child Neurology, Third Edition © 2005 Bernard L. Maria, All Rights Reserved BC Decker Inc possibility of seizures versus basilar artery migraine or vertiginous migraine. MRI of the brain is the method of choice to rule out posterior fossa tumors, including CP angle lesions. When vascular anomalies are suspected, MRA is recommended. CT of the head with thin cuts through the temporal bone is especially helpful to demonstrate congenital anomalies of the inner ear. Determining the etiology for and the management of dizziness and dysequilibrium are very difficult diagnostic dilemmas. Using a comprehensive standardized “dizziness questionnaire” and a step-by-step diagnostic algorithm approach will greatly facilitate finding the etiology and instituting appropriate treatment. Suggested Readings Cutrer FM, Baloh RW. Migraine-associated dizziness. Headache 1992;32:300–4. Eviatar L, Eviatar A. Neurovestibular examination of infants and children. Adv Otorhinolaryngol 1978;23:169–91. Fife TD, Tusa RJ, Furman JM, et al. Assessment: vestibular testing techniques in adults and children: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology 2000;55:1431–41. Foudriat BA, Di Fabbio RP, Anderson JH. Sensory organization of balance responses in children 3–6 years of age: a normative study with diagnostic implications. Int J Pediatr Otorhinolaryngol 1993;27:255–71. Linzer M, Yang EH, Estes NA III, et al. Diagnosing syncope. Part 2: unexplained syncope. Clinical Efficacy Assessment Project of the American College of Physicians. Ann Intern Med 1997;127:76–86. McCabe BF, Ryu JH, Sekitani T. Further experiments on vestibular compensation. Laryngoscope 1972;82:381–96. Taborelli G, Melagrana A, D’Agostino R, et al. Vestibular neuronitis in children: study of medium and long term followup. Int J Pediatr Otorhinolaryngol 2000;54:117–21. Practitioner and Patient Resource Vestibular Disorders Association (VEDA) P.O. Box 4467 Portland, OR 97208-4467 Phone: (503) 229-7705 Fax: (503) 229-8064 E-mail: [email protected] http://www.vestibular.org VEDA is a nonprofit organization that provides information to the public and health professionals about inner-ear balance disorders such as Meniere’s disease, benign paroxysmal positional vertigo, and labyrinthitis. Management of Dizziness in Children Pages 370–376