Introduction

Vertigo in children may escape recognition because of the child’s inability to describe the symptoms, the short duration of most vertiginous episodes, the presence of overwhelming autonomic symptoms, or the mistaken idea that an episode of vertigo may be a manifestation of a behavioral disorder.

Vertigo is defined in clinical practice as a subjective sensation of movement, such as spinning, turning, or whirling, of the patient or the surroundings. Dizziness is a nonspecific term used by patients to describe sensations of altered orientation to the environment that may or may not include vertigo.

While vertigo may be a symptom of a vestibular disorder in the pediatric population, patients react to and describe dizziness in different ways in relation to their age. For instance, young children cannot accurately relate symptoms of dizziness. Preschool children rarely complain of vertigo or dizziness but may feel clumsy or be perceived as such by family or teachers. Older children and adolescents are usually able to explain their symptoms well, with their explanations differing little from the explanations of adults.

In any case, a vestibular abnormality should be suspected in a child who is observed to be clumsy, displays unprovoked fright, or who spontaneously clings to a parent. Sudden and recurrent bouts of unexplained nausea and vomiting also are suggestive of a vestibular abnormality.

In children, as well as in adults, a careful history, physical examination, and laboratory testing can establish the cause of dizziness in most patients.

Physiologic Basis of Balance

When a hair cell is stimulated by rotation, translation, or change in orientation with respect to gravity, the firing rate in the eighth nerve fiber innervating that particular hair cell either increases or decreases. Movements that cause the stereocilia to bend toward the kinocilium result in a depolarization of the hair cell and cause the eighth nerve fiber to increase its firing rate, while movements that bend the stereocilia away from the kinocilium decrease the neural firing in the eighth nerve. The eighth nerve synapses in the vestibular nuclei, which consist of superior, medial, lateral, and inferior divisions. In addition to the input from the labyrinth, the vestibular nuclei receive input from other sensory systems, such as vision, somatic sensation, and audition. The sensory information is integrated and the output from the vestibular nuclei influence eye movements, truncal stability, and spatial orientation.

The oculovestibular reflex is a mechanism by which a head movement automatically results in an eye movement that is equal and opposite to the head movement so that the visual axis of the eye stays on target: that is, a leftward head movement is associated with a rightward eye movement and vice versa. Another feature of the oculovestibular reflex is that the two vestibular nuclear complexes on either side of the brainstem cooperate with one another in such a way that, for the horizontal system, when one nucleus is excited, the other is inhibited. The central nervous system responds to differences in neural activity between the two vestibular complexes. When there is no head movement, the neural activity, i.e., the resting discharge, is symmetrical in the two vestibular nuclei. The brain detects no differences in neural activity and concludes that the head is not moving (Figure 8-1A). When the head moves, e.g., to the left, endolymph flow produces an excitatory response in the labyrinth on the side toward which the head moves, e.g., on the left, and an inhibitory response on the opposite side, e.g., on the right. Thus, neural activity in the vestibular nerve and nuclei, e.g., on the left and right, increases and decreases, respectively (Figure 8-1B). The brain interprets this difference in neural activity between the two vestibular complexes as a head movement and generates appropriate oculovestibular and postural responses. This reciprocal push-pull balance between the two labyrinths is disrupted following labyrinthine injury.

Fig. 8-1 Schematic illustrations of the “push-pull” effect of the oculovestibular reflex.

A, No head movement in healthy subject. B, Head movement to the left in healthy subject. C, Right acute peripheral vestibular injury.

An acute loss of peripheral vestibular function unilaterally, e.g., on the right, causes a loss of resting neural discharge activity in that vestibular nerve and the ipsilateral nucleus (Figure 8-1C). Since the brain responds to differences between the two labyrinths, this will be interpreted by the brain as a rapid head movement toward the healthy labyrinth, i.e. vertigo. “Corrective” eye movements are produced toward the opposite side, resulting in nystagmus, with the slow component moving toward the abnormal side, e.g., the right, and the quick components of nystagmus moving toward the healthy labyrinth, e.g., the left.

Evaluation of Patients with Dizziness

At the initial visit, in addition to the chief complaint, a complete medical history that includes associated symptoms, past medical history, family history, and medication use is mandatory.

After the interview, a complete physical examination should be performed, with particular emphasis on the cranial nerves, including an examination of eye movements.

History

Chief Complaint

It is important that the child explain the symptoms in his or her own vocabulary and describe associated sensations, such as headache, nausea, vomiting, or motion sickness. It might be helpful to relate the patient’s symptoms to experiences, such as being on a merry-go-round. It is important to establish the onset, duration, and frequency of dizziness episodes and to associate the episodes with certain activities.

The clinician should inquire about the presence of hearing loss, its onset, evolution or progression, fluctuation and worsening, and improving or stable status. Does the patient have tinnitus or a feeling of fullness? Is the hearing loss bilateral or unilateral? To establish the presence of neurologic symptoms, the clinician should determine whether there have been instances of convulsions, altered mental status, weakness, numbness, disturbances of swallowing or taste, coughing, facial paralysis, or blurring and loss of vision.

Physical Examination

In addition to a complete neurologic examination, the child should also be observed when walking or running for incoordination of movements, i.e., ataxia. Also, an assessment of nystagmus is especially important. Spontaneous nystagmus is an involuntary, rhythmic movement of the eyes not induced by any external stimulation. Spontaneous nystagmus has two components: slow and fast. Nystagmus is named by the fast component, which is easily identified. Spontaneous nystagmus is tested by having the patient look straight ahead with and without fixation. Gaze-evoked nystagmus is assessed by having the patient deviate the eyes laterally (no greater than 30 degrees) with fixation. Positional testing is performed with the use of maneuvers that may produce nystagmus or vertigo. Static positional nystagmus is assessed by placing the patient in each of the following six positions: sitting, supine, supine with the head turned to the right, supine with the head turned to the left, and right and left lateral positions. Positional nystagmus presents as soon as the patient assumes the position and persists for as long as the patient remains in the provocative position. Assessment of vestibulospinal function with a foam pad (Figure 8-2) should be performed with or without a visual conflict dome.

Fig. 8-2 The Pediatric Clinical Test of Sensory Organization and Balance.

A, A child standing on the medium-density foam with her eyes open. B, The same child standing on the foam with the visual conflict dome.

In addition to a history and physical examination, an assessment may include vestibular testing. Vestibular laboratory testing is recommended in any child with a history of vertigo in whom a thorough history and physical examination have not established a diagnosis, in order to differentiate between a peripheral or central vestibular lesion, and to identify the side of the lesion in a peripheral abnormality. In addition, vestibular laboratory testing provides permanent documentation, and changes can be followed by repeat testing. Vestibular laboratory testing includes oculovestibular and vestibulospinal tests. Both types of tests provide only an indirect measure of the function of the vestibular end organs, in that they rely on measures of motor response, e.g., eye movements or postural sway, resulting from vestibular sensory input.

Videonystagmography

Videonystagmography (VNG) is currently the most widely used method of recording eye movements; it uses infrared light. Ocular motor testing, positional testing, and caloric testing constitute a common test battery that requires about 1 hour. Sedatives and vestibular suppressant medications should be discontinued for 2 days prior to testing. Ocular motor testing evaluates neural motor output independent of the vestibular system (Figure 8-3). Abnormalities in the ocular motor system may cause misleading conclusions from vestibular testing that relies on eye movements. Testing saccades uses a computer-controlled sequence of target jumps. Saccade abnormalities are defined as overshooting the target (hypermetric saccades) and undershooting the target (hypometric saccades). Disorders in the saccadic system suggest a central nervous system abnormality. Spontaneous nystagmus and gaze-evoked nystagmus are recorded with and without fixation (closing the eyes or darkness) (Figure 8-4), and by asking the patient to look 30 degrees to the right and left. Spontaneous nystagmus present in darkness without fixation, which decreases or resolves with visual fixation, suggests a peripheral vestibular disorder. However, spontaneous nystagmus that is present with fixation and does not significantly decrease with loss of fixation is most likely a central nervous system abnormality. Ocular pursuit involves asking the patient to follow a moving target back and forth along a slow pendular path. Normal subjects can follow a target smoothly without interruption. Abnormalities of pursuit tracking are caused by lesions in the central nervous system. Laboratory testing of optokinetic nystagmus uses black-and-white stripes moving left and right. Abnormalities include asymmetries or absence of responses, which suggest a central nervous system abnormality.

Fig. 8-3 Examples of normal responses and abnormalities of the saccadic eye movement system, the pursuit system, and optokinetic nystagmus.

(From Baloh RW. The Essentials of Neurotology. Philadelphia: Oxford University Press, Inc, 1984.)

Fig. 8-4 Recording of spontaneous nystagmus.

Note that during eyes open (with fixation) the patient had almost no nystagmus, but during eyes open in the dark (without fixation) a latent vestibular nystagmus became manifest. Upward deflections denote rightward movement.

(From Furman JM, Cass SP. Evaluation of dizzy patients. Slide lecture series. American Academy of Otolaryngology-Head and Neck Surgery Inc., Alexandria, VA 1994.)

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