The exact incidence of dizziness and vertigo during adolescence is not known. For those few adolescents who seek outpatient evaluation for these complaints, the majority are diagnosed with migraine headache. The authors provide a discussion of the differential diagnosis, evaluation, and management of vertigo and dizziness in the adolescence with emphasis on migraine headaches, chronic daily headaches, postural orthostatic tachycardia syndrome, and presentations that may require head imaging.
Key points
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For those few adolescents who seek outpatient evaluation for these complaints, the majority are diagnosed with migraine headaches.
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In addition to migraine headache, the differential diagnosis in this age group includes episodic ataxia type II; chronic daily headaches; postural orthostatic tachycardia; intracranial mass lesions; psychiatric disorders (eg, depression or somatoform disorders); and rarely vestibular disorders, including viral labyrinthitis and Ménière’s disease.
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Evaluation and, in the majority of cases, diagnosis is based on careful history and physical examination with neuroimaging performed for all adolescents with a history of trauma, an abnormal neurologic examination, persistent headaches, or indication of central lesion on vestibular testing.
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M.C. is a 16-year-old girl presenting with a complaint of frequent episodes of dizziness that started when she was 13 years of age. The events are characterized by a feeling that she describes as “losing track of her body in space.” The events are brief and last only 1 to 2 seconds. There is no associated change in vision, palpitations, or sweating. Although she does have a sensation of falling, she has not fallen. The events occur multiple times per week and are more frequent around the time of her menses or just before the onset of a headache, which she describes as a prolonged, severe throbbing pain with associated nausea and vomiting that resolve with sleep. The dizziness can occur both at rest and with activity and in any position. It is not triggered by head position. Her past medical history is otherwise benign. She has not required hospital admission or surgeries. She is not taking any medications. She denies the use of alcohol, tobacco, or illicit drugs; however, she notes that many of her friends have experimented with marijuana. Her review of systems is positive for significant stress regarding grades at school. She is active in several extracurricular activities. She describes much frustration with her parents for not allowing her more freedoms after she was caught attempting to shoplift when she was 13 years old. Her sleep patterns are erratic, and she does not think that she is sleeping well. Her mother has a diagnosis of migraine headaches. There is a maternal aunt who died in her twenties secondary to an astrocytoma and distant paternal cousin who died in his forties of a brain tumor. Her general and neurologic examination is unremarkable. Because of the patient’s and family’s anxiety regarding the family history, an MRI of the brain was obtained, which is unremarkable. Following the appointment, she is started on a low dose of amitriptyline at night, which results in a marked reduction in the frequency of her dizziness and headaches.
The adolescent brain
Adolescence, the developmental transition between the dependency of childhood and the independency of adulthood, encompasses the approximate time period between 12 and 18 years of age. Behavior during this developmental stage is frequently characterized by risk taking, impulsivity, and poor choices. The indestructible attitude of the adolescent, which can be met by negative consequences, promotes experimentation of adult practices, development of self-esteem, and eventually social acceptance.
Although the brain reaches 90% of its adult size by 6 years of age, pruning (resulting in decreasing synaptic density) and cortical thinning occur throughout childhood and adolescence. The volume of white matter increases up to about 20 years of age as the result of ongoing myelination of white matter tracts. One of the last regions to undergo both of these maturational processes is the prefrontal cortex, the region of the brain that participates in executive, attention, and regulatory functions.
Adolescence represents a unique time period of brain development marked by changes in both anatomic connectivity and functional activation. Recently, Casey and colleagues suggested that the differential developmental trajectories of the limbic system and subcortical structures (eg, basal ganglia) as compared with the prefrontal cortex could, in part, explain the impulsivity and risk-taking behavior that occur during adolescence. In their model, earlier maturation of the limbic system and subcortical structures during adolescence drives adolescent behavior. As the connections of the prefrontal cortex mature, the influence of the limbic system and subcortical structures is reduced and the prefrontal cortex dominates, resulting in an improved ability to suppress impulses and greater emphasis on goal-driven choices. Their model is supported by recent demonstrations of an exaggerated response of the nucleus accumbens in the adolescent as compared to the adult and child in a task that manipulated reward values and the correlation of the development of fiber tracts between the prefrontal cortex and basal ganglia with performance on a go/no-go task, a measure of inhibitory control.
Vertigo represents the inappropriate sense or hallucination of motion and is related to dysfunction of the vestibular system. Although morphologic development of the vestibular system is complete by term gestation, studies of the development of postural balance suggest that functional maturation of the vestibular system is ongoing during childhood and adolescence. (See article by O’Reilly and colleagues in this publication.) For example, Steindl and colleagues used the Sensory Organization Test to measure postural stability in 140 children aged 3.5 to 16 years without known peripheral or central vestibular, proprioceptive, or visual disorders or medications that could affect balance. They observed increasing maturation of the vestibular afferent system up to 16 years of age. However, in contrast to a prior study that suggested that vestibular development was not complete by 16 years of age, Steindl and colleagues observed reduced vestibular influence on postural control in adults as compared with the 15- to 16-year-old age groups. Cumberworth and colleagues suggested that the late functional development of the vestibular system as compared with the somatosensory and visual control of balance may explain differential rates of motion sickness in children and adolescents as compared with adults.
The adolescent brain
Adolescence, the developmental transition between the dependency of childhood and the independency of adulthood, encompasses the approximate time period between 12 and 18 years of age. Behavior during this developmental stage is frequently characterized by risk taking, impulsivity, and poor choices. The indestructible attitude of the adolescent, which can be met by negative consequences, promotes experimentation of adult practices, development of self-esteem, and eventually social acceptance.
Although the brain reaches 90% of its adult size by 6 years of age, pruning (resulting in decreasing synaptic density) and cortical thinning occur throughout childhood and adolescence. The volume of white matter increases up to about 20 years of age as the result of ongoing myelination of white matter tracts. One of the last regions to undergo both of these maturational processes is the prefrontal cortex, the region of the brain that participates in executive, attention, and regulatory functions.
Adolescence represents a unique time period of brain development marked by changes in both anatomic connectivity and functional activation. Recently, Casey and colleagues suggested that the differential developmental trajectories of the limbic system and subcortical structures (eg, basal ganglia) as compared with the prefrontal cortex could, in part, explain the impulsivity and risk-taking behavior that occur during adolescence. In their model, earlier maturation of the limbic system and subcortical structures during adolescence drives adolescent behavior. As the connections of the prefrontal cortex mature, the influence of the limbic system and subcortical structures is reduced and the prefrontal cortex dominates, resulting in an improved ability to suppress impulses and greater emphasis on goal-driven choices. Their model is supported by recent demonstrations of an exaggerated response of the nucleus accumbens in the adolescent as compared to the adult and child in a task that manipulated reward values and the correlation of the development of fiber tracts between the prefrontal cortex and basal ganglia with performance on a go/no-go task, a measure of inhibitory control.
Vertigo represents the inappropriate sense or hallucination of motion and is related to dysfunction of the vestibular system. Although morphologic development of the vestibular system is complete by term gestation, studies of the development of postural balance suggest that functional maturation of the vestibular system is ongoing during childhood and adolescence. (See article by O’Reilly and colleagues in this publication.) For example, Steindl and colleagues used the Sensory Organization Test to measure postural stability in 140 children aged 3.5 to 16 years without known peripheral or central vestibular, proprioceptive, or visual disorders or medications that could affect balance. They observed increasing maturation of the vestibular afferent system up to 16 years of age. However, in contrast to a prior study that suggested that vestibular development was not complete by 16 years of age, Steindl and colleagues observed reduced vestibular influence on postural control in adults as compared with the 15- to 16-year-old age groups. Cumberworth and colleagues suggested that the late functional development of the vestibular system as compared with the somatosensory and visual control of balance may explain differential rates of motion sickness in children and adolescents as compared with adults.
Vertigo and Dizziness in the Adolescent
Vertigo and dizziness are not synonymous with each other, although they are often used interchangeably. Individuals with vertigo will often complain of a rotational or room-spinning sensation. They may feel as though they are on a carousel or bobbing in a boat. Nausea and vomiting are often associated complaints. True vertigo implies an equilibrium disturbance associated with the dysfunction of either the central or peripheral vestibular system. In contrast, dizziness may be used by patients to describe a distorted perception of the environment associated with etiologies that range from true vertigo to presyncope to somatoform disorders. The majority of adults who presented to emergency departments (ED) in the United States between 1993 and 2005 with a chief complaint of dizziness did not have a vestibular disorder and were diagnosed with cardiovascular, neurologic, or metabolic/toxic illnesses.
Complaints of dizziness and vertigo are common in the general population, occurring more frequently in women and those older than 60 years. In a review of National Hospital Ambulatory Medical Care Survey data of persons who presented to the ED with a chief complaint that included vertigo/dizziness or the final diagnosis of a vestibular disorder, 16- to 19-year-old patients represented the smallest fraction. In contrast, population-based studies suggest that episodic vertigo and dizziness may be more common during adolescence than suggested by the ED data. Russell and Abu-Arafeh provided a screening questionnaire to 2165 children ranging in age from 5 to 15 years who attended school in the city of Aberdeen, Scotland. Of the children surveyed, 314 (14%) reported at least 1 episode of dizziness in the previous year and 92 children (4%) reported 3 or more episodes of dizziness. Although complaints of dizziness occurred at all ages in this study, it was more common in adolescents, with a peak onset at 12 years of age. More recently, Niemensivu and colleagues, based on prospective polling of children and adolescents ranging in age from 1 to 15 years, found that 8% (75 of 938) experienced an episode of vertigo or dizziness at some point during their life, predominantly between 11 to 15 years of age. These studies and future studies that attempt to define the true prevalence of vertigo and dizziness during childhood and adolescence have multiple potential cofounders including the difficulty young children and adolescents may have in accurately describing their symptoms, the complaint may resolve quickly and thus be disregarded by the adolescent or their family, the family may disregard the complaint, and the vertigo or dizziness may be reported by the adolescent or family as clumsiness.
Vertigo and dizziness during adolescence can be the presenting symptom, or more typically, are part of a complex of symptoms in a wide range of disorders that includes viral illnesses and intracranial tumors ( Box 1 ). In a hospital-based study, Fried reviewed the medical records of all admissions to the Boston City Hospital for the 12-month period that spanned July 1976 to June 1977. The majority of adolescents admitted for dizziness during this time period had experienced a concussion (4 of 9). In contrast, retrospective reviews of outpatient medical records of adolescents evaluated in either neurology or otolaryngology clinics consistently report migraine headaches and benign paroxysmal vertigo of childhood (BPVC) as the most common causes of vertigo and dizziness in adolescents and children. For example, Weisleder and Fife reviewed the charts of 31 children and adolescents ranging in age from 6 to 17 years who were referred for vestibular testing at a tertiary care center over a 6-year period. The majority (n = 11; 35%) were diagnosed with vestibular migraine. Other diagnoses included benign paroxysmal vertigo of childhood (n = 6; 20%), anxiety attacks (n = 3; 10%), Ménière’s disease (n = 2), idiopathic sudden-onset sensorineural hearing loss (n = 1), familial vertigo/ataxia syndrome (episodic ataxia type II, n = 1), and malingering (n = 1).
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Most common
Migraine
Migraine equivalent with benign paroxysmal vertigo of childhood being much more common in children than adolescents
Psychogenic
Viral infections or otitis media
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Common
Chronic daily headache
Trauma
Postural orthostatic tachycardia syndrome
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Less common
Intracranial tumor
Epilepsy
Meniere’s disease
Benign paroxysmal positional vertigo
Vestibular neuritis
Demyelinating disease
In addition to migraine headaches, these clinic-based studies have consistently observed a high incidence of depression and somatoform disorders among children and adolescents evaluated in these specialty clinics for complaints of vertigo or dizziness. For example, Ketola and colleagues reported that psychogenic vertigo accounted for 8% (9 of 119) of children and adolescents with the chief complaint of vertigo who were evaluated at the Otolaryngologic Clinic of Helsinki University Central Hospital between the years of 2000 and 2004. Following psychiatric consultation, 3 children (aged 10 to almost 13 years) were diagnosed with depression; 1 adolescent (age 13.5 years) was diagnosed with a combination of conversion disorder, hyperventilation, and depression; 1 adolescent (age 15.6 years) was diagnosed with psychotic episode and depression; and the other 4 children (aged 9–11 years) were diagnosed with psychogenic headache, obsessive-compulsive disorder, panic disorder, and conversion disorder, respectively. Compared with those children and adolescents who were identified as having an organic cause for the vertigo, this group of children and adolescents had more frequent attacks or a complaint of constant vertigo, were more likely to suffer from school absenteeism, and were more likely to have dysfunctional relationships at school or at home. In addition, Emiroglu and colleagues found that 29 (93.5%) of 31 subjects who presented to a pediatric neurology clinic for complaints of dizziness, headache, or fainting met criteria of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) for a psychiatric comorbidity, even when the primary diagnosis was migraine headache.
Not all cases of vertigo and dizziness in the adolescent are likely to be referred for specialty clinic evaluation. Therefore, multiple causes of dizziness are likely to be underreported in neurology and otolaryngology clinic-based studies of vertigo and dizziness in the adolescent. For example, complaints of vertigo or dizziness in the setting of concussion is likely to be principally managed by the pediatrician ; the child with dizziness in the setting of syncope or presyncope may be managed by the pediatrician or is more likely to be referred to a cardiologist than to a neurologist or to an otolaryngologist for further management, and the child with a brain tumor is most likely to be managed by the oncologist and neurosurgeon.
Diagnosis and Treatment of Specific Causes of Vertigo in the Adolescent
Migraine
Upwards of 30% of adolescent girls experience migraine headaches ; and along with variants, migraines are the most common episodic disorder of childhood with an estimated prevalence of 5% to 10%. Migraine and benign paroxysmal vertigo of childhood, considered by many to be a migraine variant in younger children, account for 50% to 75% of children who present to specialty clinics with vertigo and normal eardrums; migraine frequency increases and BPVC frequency decreases with age (see article by McCaslin and colleagues in this publication).
The vertigo associated with migraine may precede the headache (aura), may be part of the headache itself, or may not be temporally related to the headache in up to 60% of individuals. Furthermore, vertigo is a well-established manifestation of basilar migraines, which also have associated complaints of ataxia, dysarthria, tinnitus, and visual changes. The vertigo associated with these headaches is often brief and frequently accompanied by nausea and vomiting.
The pathophysiology of vertigo in migraines is poorly understood. Unilateral neuronal instability of the peripheral vestibular nerve, idiopathic asymmetric activation of the brainstem vestibular nuclei, and vasospasm causing transient ischemia of the labyrinth or central vestibular pathways have all been suggested. Electronystagmography is often abnormal and demonstrates central findings in adults and children with basilar migraines, even between attacks (see article by Cherchi and Hain in this publication).
Before making the diagnosis of migraine headache in the adolescent who is being evaluated for complaints of headache and vertigo, episodic ataxia type 2 (EA-2; previously known as familial cerebellar ataxia without myokymia, hereditary paroxysmal cerebellar ataxia, periodic vestibulocerebellar ataxia, and acetazolamide-responsive episodic ataxia) should be considered (see article by Cherchi in this publication). This rare autosomal dominant disorder is the result of a spectrum of mutations that affect CACNA1A , the gene that encodes the α1A subunit of P/Q type calcium channels (Ca V 2.1) located on chromosome 19p. Missense mutations of this same gene are linked to familial hemiplegic migraine, and a CAG expansion of exon 47 has been linked to spinocerebellar ataxia type 6. EA-2 is characterized by episodic attacks that last from hours to days and can be precipitated by stress or exercise as well as caffeine and alcohol. Many features of the attack can overlap those of migraine headache: headache, which is typically occipital in location, vertigo, nausea, and vomiting. Indeed, most people with EA-2 also meet the International Headache Society’s diagnostic criteria for migraine. Distinguishing features during the attack are the presence of concurrent ataxia and nystagmus as well as the strong family history consistent with autosomal dominant inheritance. During the attack, dysarthria, diplopia, tinnitus, dystonia, and hemiplegia may also be present. Onset is typically before the 20 years of age with a range from 2 to 61 years. Of interest, a large percentage of individuals with EA-2 develop ataxia and nystagmus in the interictal periods, and atrophy of the cerebellar vermis has been observed on MRI. An important reason to recognize this syndrome early is that acetazolamide has been shown to be effective in reducing the frequency of attacks that are typically rare but have been reported as often as 4 times per week.
Treatment of migraine headaches is divided into abortive and prophylactic therapies. For those with vertigo as the manifestation of their migraine without significant headache, management with antimotion sickness medications, such as scopolamine, has been proposed to provide symptomatic relief. The American Academy of Neurology (AAN) guidelines for acute treatment of migraines in children and adolescents report level A evidence for sumatriptan nasal. Nonsteroidals, triptans, or indomethacin should be used in place of medications with caffeine, barbiturates, or opiates as these are less likely to cause medication overuse. Dihydroergotamine, intravenous valproate, or steroids have also been used for the abortive treatment of severe migraine headaches that have not responded to other outpatient treatments.
If the migraines are frequent or disabling (ie, affecting school performance) then a prophylactic agent should be considered. Calcium channel blockers, beta-blockers, antiepiletpics, such as topirimate and valproate, or tricyclic antidepressants (eg, amitriptyline) have all been shown to be efficacious as migraine prophylaxis, although the AAN guidelines report insufficient evidence to make formal recommendations for the adolescent. One month at a therapeutic dose, if tolerated, should be attempted before altering therapy.