Adolescent Health Care: A Practical Guide

Chapter 23

Syncope and Vertigo

Amy D. DiVasta

Wendy G. Mitchell

Mark E. Alexander

Cardiac symptoms in the adolescent are very common; true cardiac disease is not. Syncope is a frequent complaint, accounting for 1% to 6% of hospitalizations and 3% of emergency room visits annually. These episodes often raise concerns that they could be predecessors to future sudden cardiac death (SCD). The clinician's critical task is to distinguish between presyncopal episodes, vertigo, the benign forms of syncope, and syncope associated with an increased risk of SCD. Each has separate implications for evaluation and therapy. This differentiation is made initially by detailed history, careful physical examination, and, in almost all cases, an electrocardiogram (ECG). Specialized testing may be needed in a minority of patients to confirm these initial conclusions.



Syncope is a sudden, transient loss of consciousness and postural tone, usually lasting several seconds to a minute, followed by spontaneous recovery. Syncope is common, with a female predominance and a peak incidence between ages 15 to 19 years. Although most episodes are benign, any condition that leads to decreased cerebral perfusion may cause syncope.


There are three major categories of syncope:

  1. Neurocardiogenic
  2. Vasovagal/reflex
  3. Postural orthostatic tachycardia
  4. Cardiovascular
  5. Structural
  6. Arrhythmogenic
  7. Noncardiovascular
  8. Epileptic
  9. Psychogenic

Both population-based data and pediatric cardiology clinic experience have demonstrated that syncope of unknown origin (often termed simple syncope) and neurocardiogenic syncope account for more than 85% to 90% of events (Driscoll et al., 1997; Ritter et al., 2000; Steinberg et al., 2005). The final common pathway of any true syncopal event is ineffective cerebral blood flow, resulting from inadequate cardiac output. Between 1% and 5% of patients will have significant cardiac disease. Another small minority will have seizures and psychiatric diagnoses including anxiety disorders and pseudoseizures.

History and Physical Examination

The most important step to an accurate diagnosis is a detailed history (including family history) and thorough physical examination.


Key elements of the history should include the following:

  1. Onset and frequency of episodes.
  2. Circumstances: Relation to exercise, posture, and precipitating factors (such as stress, recent infection [labyrinthitis], exercise, position, and environmental factors). Descriptions of the episode help define the nature of the event. If the teen cannot describe the attack, it is helpful to get a description from another witness. Symptoms in others, particularly peers, may be useful in suspected group hysteria.
  3. Prodromal symptoms: Dizziness, diaphoresis, nausea, pallor, palpitations, chest pain, and dyspnea. Description of color changes (initial pallor versus cyanosis or flushing) and prodromal sensations is critical and may help distinguish syncope from seizure.
  4. Complete or incomplete loss of consciousness, duration, and time to recovery.
  5. Abnormal movements, incontinence, or injury. Convulsive activity during the attack, incontinence, or tongue biting suggests epilepsy, although syncope may induce a brief seizure. The order of events is extremely helpful in making this determination. See Table 23.1 for distinguishing features of common fainting versus seizure.
  6. Past medical history and medications (including complementary and alternative medications).
  7. Family history: Sudden death (particularly if age less than 40 years), similar episodes, early onset heart disease.

The physician should be alert for warning signs that suggest a more serious etiology. These include syncope


during exercise, syncope while in a supine position, family history of sudden death in a person younger than 30 to 40 years, personal history of cardiac disease, or an event precipitated by a loud noise, intense emotion, or fright.

TABLE 23.1
Neurocardiogenic Syncope versus Seizure


Neurocardiogenic syncope



Usually prodromal symptoms

Aura common




Position at onset

Usually erect

Any position

Color change

Pallor frequent

Flushing or cyanosis


Rare, opisthotonic/myoclonic

Common, may be focal

Urinary incontinence



Postictal state

Residual symptoms common

Disorientation, headaches

Physical Examination

The physical examination should include orthostatic vital signs, a careful neurological assessment, and a dynamic cardiac examination performed with the patient in multiple positions to evaluate for a pathological murmur (see Chapter 14).

Neurocardiogenic Syncope

With synonyms including vasovagal syncope, neurocardiac syncope, and reflex syncope, this is the most common form of syncope. The history and physical examination findings should be normal, without any of the warning signs suggestive of a more serious etiology. The physiological basis of the syncopal event represents a temporary derangement of cardiac and vascular regulation.

  1. Duration: May last for a few seconds to a few minutes.
  2. Onset: Gradual; the patient is generally aware that something is wrong.
  3. Etiology: Precipitating factors are usually identifiable. Fear, anxiety, pain, hunger, overcrowding, fatigue, injections, and the sight of blood are common precipitants. Alcohol and exposure to cold or heat can also precipitate an attack. Prolonged upright posture, particularly without movement, may contribute. Group hysteria may precipitate syncopal “epidemics,” particularly in schools or other closed populations.
  4. Prodromal symptoms: Typical prodromal symptoms include nausea, dizziness, visual spots or dimming, feelings of apprehension, pallor, yawning, diaphoresis, and feelings of warmth.
  5. Syncopal event: The loss of consciousness is usually brief, with gradual loss of muscle tone.
  6. Syncopal seizures: Rarely, a brief tonic or clonic seizure will be precipitated by syncope. It always follows the preceding syncopal symptoms. A seizure is more likely to happen if the patient faints while sitting or is kept from assuming the recumbent position upon loss of consciousness. Convulsive syncope is also commonly triggered by the sight of blood.
  7. Recovery: Consciousness generally returns in <1 minute, often with a brief period of perceived inability to respond despite awareness of the environment. The patient may report residual symptoms of fatigue, malaise, weakness, nausea, and headache for up to an hour after fainting.
  8. Pathophysiology: The exact pathophysiology is still not completely understood. With standing position there is significant venous pooling, between 400 to 800 m This volume shift leads to decreased ventricular filling and pulse pressure, and activates many homeostatic reflexes (including baroreceptors, carotid body receptors, and C fibers). If the vagal and sympathetic cardiovascular responses are adequate, cerebral perfusion is maintained. However, if responses are exaggerated or ineffective, there can be a paradoxical vagal activation and inappropriate decrease in sympathetic activity. This induces bradycardia and hypotension, further impairs cerebral blood flow, and can lead to syncope.

Diagnostic Evaluation of Neurocardiogenic Syncope

In addition to the history and physical examination, adolescents suffering a true syncopal event should have an ECG performed. The ECG is the ideal screening test for more serious disease in syncopal patients. It allows evaluation of the intervals, rhythm, and ventricular size. Additionally, it is noninvasive, readily available, and inexpensive. A normal diagnostic screen (reassuring history, benign physical examination, and normal ECG) is generally sufficient to exclude the possibility of cardiac disease. Further investigation is warranted only if there are lingering concerns or suspicions of cardiac disease.

  1. No laboratory investigations, electroencephalogram (EEG), or intracranial imaging are needed.
  2. Echocardiogram: Routine echocardiography has very low yield and is not part of the routine evaluation of a typical syncopal event.
  3. Ambulatory ECG monitoring is not generally indicated. If episodes are relatively frequent, temporary memory looping event monitors, which can store 3 to 5 minutes of rhythm during an episode, may be useful.
  4. Exercise testing: Required if syncopal episodes occur during exercise.
  5. Tilt table testing: Tilt table testing should be reserved for challenging patients with recurrent symptoms, or for patients needing further reassurance. The patient's pulse, blood pressure, and symptoms are monitored first in the supine position, and then in a head-up tilt to 60 to 70 degrees for 12 minutes or more, depending on local protocol. In a positive test, the patient is symptomatic with hypotension ± pulse change. However, tilt testing is not a gold standard; as many as 40% of normal


adolescents will have a positive tilt test. Specificity is poor (35%–100%) and sensitivity is variable (75%–85%).

  1. Implantable loop recorder: A subcutaneous device that allows for up to 18 months of monitoring. No patient adherence is required. Can establish a symptom-rhythm correlation in most patients. However, these are invasive and therefore reserved for patients who experience severe, recurrent episodes.

Management of Neurocardiogenic Syncope

The mainstay of treatment is reassurance, and educating patients and parents regarding the benign nature of the condition as well as ways to prevent further episodes. Adolescents should take adequate oral fluids to prevent volume depletion, and avoid caffeine. Postural techniques (including isometric contractions of the extremities, folding the arms, or crossing the legs) help increase systemic blood pressure and venous return to the heart, and can help abort a syncopal episode. If patients begin to experience prodromal symptoms, they should ideally assume a supine position. Upright, weight-bearing exercise may also be helpful in decreasing the frequency of events. Most adolescents outgrow their episodes over time, even if they are highly symptomatic. Drug therapy may be needed for refractory cases that do not respond to supportive therapy. Options are summarized in Table 23.2. Pharmacological therapy is largely driven by tradition, rather than data, in the adolescent population. Pediatric experience suggests that fludrocortisone and β-blockers are comparable in efficacy. Generally, a 12-month symptom-free interval is considered a reasonable duration of treatment; subsequently, a trial off medication is warranted.

TABLE 23.2
Pharmacological Treatment Options for Neurocardiogenic Syncope



Proposed Mechanism of Action

Side Effects

Quality of Data

SSRIs, serotonin reuptake inhibitors; GI, gastrointestinal.
+, moderate data to support efficacy; ++: strong data to support efficacy; ± mixed data to support efficacy.


0.1–0.2 mg/d

↑ Renal Na+ absorption

Bloating or edema


↑ Circulating blood volume







5–10 mg q4h




Maximum four doses/d

↑ Peripheral vascular resistance

Scalp pruritus





Urinary retention


Difficult adherence to treatment




Blocks excess sympathetic response (paradoxical effect)




25–50 mg daily





25–50 mg b.i.d.




↑ Extracellular serotonin leads to down-regulation of receptor density




20 mg daily





50 mg daily


GI effects


Postural Orthostatic Tachycardia Syndrome

Postural orthostatic tachycardia syndrome (POTS) is a heterogeneous disorder of autonomic regulation. POTS is well described in adolescence, and has a female predominance. Patients commonly complain of fatigue, dizziness, and exercise intolerance with upright position.

  1. POTS is characterized by a marked pulse change (>30 bpm) or excessive tachycardia (>120 bpm) in response to being upright during a 6-minute stand test.
  2. There is little or no blood pressure change.
  3. Mechanisms of abnormal autonomic regulation, both acquired and genetic, are as follows:
  4. Enhanced noradrenergic tone at rest, but blunted sympathetic response to standing
  5. Partial sympathetic denervation
  6. Impaired synaptic norepinephrine clearance
  7. Decreased cardiac vagal baroreflex sensitivity
  8. Impaired regulation of cerebrovascular tone
  9. There is significant overlap between chronic fatigue syndrome and POTS. In one study by Stewart et al., 25 of 26 chronic fatigue patients had severe orthostatic symptoms on tilt test, compared with only 4 of 13 age-matched controls.
  10. Treatment: Fluids and vasoconstrictors relieve symptoms in most patients. β-Blockers are also commonly used for treatment.

Orthostatic Hypotension

Orthostatic hypotension is uncommon in adolescents. It is defined as a drop in systolic blood pressure >20 mm Hg and a drop in diastolic pressure >10 mm Hg with assumption of upright posture. Etiologies of orthostatic hypotension include the following:

  1. Inadequate homeostatic mechanisms: Prolonged bed rest, exhaustion after intense exercise, pregnancy, anorexia nervosa, heat exposure, fever, and marijuana use.



  1. Reduced effective blood volume: Hemorrhage, dehydration, burns, diabetes insipidus, hemodialysis, adrenal insufficiency, and varicose veins.
  2. Medications and illicit drugs: Antihypertensives, phenothiazines, antidepressants, narcotics, sedatives, calcium channel blockers, and alcohol.
  3. Autonomic neuropathies: Pure autonomic neuropathies may be autoimmune or familial (familial dysautonomia). Mixed motor and sensory neuropathies may be genetic or acquired due to autoimmune phenomena (e.g., Guillain-Barré syndrome and chronic immune demyelinating polyneuropathy), diabetes, nutritional deficiencies, uremia, metabolic causes, heavy metal poisoning, porphyria, pernicious anemia, vincristine toxicity, or chronic hydrocarbon toxicity (secondary to inhalant abuse).
  4. Central Nervous System: Spinal cord injury, transverse myelitis, spinal cord tumor, or syringomyelia may cause autonomic dysfunction. Orthostatic hypotension (and positional hypertension) is particularly common with acute paraplegia due to spinal injury from any cause. Hydrocephalus and posterior fossa tumors may occasionally cause orthostatic hypotension.
  5. Miscellaneous: Syndromes of neurotransmitter excess including carcinoid syndrome, systemic mastocytosis, and pheochromocytoma.

Cardiovascular Syncope

Cardiac syncope is characterized by an acute collapse with few premonitory symptoms, often in association with exercise or exertion. Occurs secondary to either arrhythmia or hemodynamic events, including obstructed left ventricular (LV) filling, obstructed LV outflow, or ineffective myocardial contraction. Cardiac syncope should be suspected when any of the “warning signs” are present (see preceding text). The physical examination or ECG may be abnormal. See Table 23.3 for a listing of the more common electrical and structural cardiac conditions that can lead to syncope. A few key conditions are summarized in the subsequent text.

TABLE 23.3
Differential Diagnosis of Cardiac Syncope



LV, left ventricle.

Heart block

Inadequate LV filling


 Pulmonary hypertension


 Pulmonic stenosis

Wolff-Parkinson-White syndrome

Inadequate LV output


 Aortic stenosis

Long QT syndrome

 Hypertrophic cardiomyopathy


Dilated cardiomyopathy


Coronary artery anomalies

Brugada syndrome


Postoperative congenital heart disease


Arrhythmogenic right ventricular dysplasia

Marfan syndrome

Hypertrophic Cardiomyopathy

  1. Definition: An inherited cardiac muscle disorder leading to myocardial hypertrophy. Prevalence estimated at 1 in 500.
  2. Natural history and prognosis: Symptoms generally begin during periods of rapid somatic growth, such as adolescence. Genetically and phenotypically heterogeneous, with wide variation in terms of symptom status, LV wall thickness, and arrhythmia risk. Most patients are asymptomatic. If symptoms develop, usual complaints include exertional chest pain, exercise intolerance, shortness of breath, and syncope.
  3. Diagnostic findings in hypertrophic cardiomyopathy (HCM):
  4. Physical examination findings include a systolic ejection murmur at the left lower sternal border (with increasing intensity in standing position and decreasing intensity with squatting) and a prominent LV lift.
  5. ECG may reveal signs of LV hypertrophy, ST-T wave changes, or atrial enlargement. However, ECGs are problematic, as there are many false negatives and false positives. The ECG may be abnormal in up to 25% of patients with HCM.
  6. The echocardiogram is close to the “gold standard” for identifying affected individuals. Key findings include thickened interventricular septum and LV free wall, asymmetric septal hypertrophy, systolic anterior motion of the mitral valve, and dynamic LV outflow tract obstruction. A small number of competitive male athletes may have ECG findings suggestive of HCM; they may require 1 to 3 months of deconditioning to prove they have “athletic heart syndrome,” which is a benign adaptation to systematic athletic training with no adverse cardiovascular consequences.
  7. Sudden death: HCM is the most common cause of SCD for the 15- to 35-year old age group, but is still rare. SCD due to previously undiagnosed cardiomyopathy accounts for <1 death per 1,000,000/year. Patients develop myocardial ischemia from increased myocardial oxygen demand and reduced myocardial perfusion.


Mechanism of cardiac arrest is ventricular fibrillation. Risk factors for sudden death are as follows:

  1. Previous cardiac arrest
  2. Positive family history of sudden death
  3. Exertion-related syncope
  4. Severe (≥3 cm) hypertrophy
  5. Nonsustained ventricular tachycardia during Holter monitoring
  6. Abnormal blood pressure response to upright exercise testing
  7. Treatment: May be inherited in autosomal dominant manner, so all family members should be screened. Course is variable, but even asymptomatic patients should avoid athletic participation. Symptomatic relief is difficult, and may be treated with medications such as B-blockers, calcium channel antagonists, and disopyramide. Surgical options include catheter ethanol ablation of the hypertrophic septum and surgical septectomy. These may not change the risk of SCD, but can achieve long-term symptom relief in up to 70% of patients. For patients at high risk of SCD, implantable defibrillator therapy is recommended; some patients choose implantable cardioverter-defibrillator (ICD) therapy simply based on combinations of family history and LV wall thickness.

Long QT Syndrome

  1. Definition: Disorder of delayed ventricular repolarization. Patients are at risk for development of arrhythmias (such as torsades de pointes or ventricular fibrillation), syncope, seizure, and SCD. Patients may be asymptomatic, or present with recurrent syncopal episodes, palpitations, dizziness, or even sudden death.
  2. Hereditary long QT syndrome (LQTS): Both autosomal recessive and autosomal dominant patterns of inheritance have been described. Currently, seven genes and >150 mutations have been described. LQT1, LQT2, and LQT3 account for >95% of identified mutations. Genetic testing is available commercially with approximately 70% sensitivity. The tests cost approximately $5,000; insurance coverage is variable.
  3. Acquired LQTS: May be related to underlying disease state, or secondary to drug effect. See Table 23.4 for a list of the more common conditions and medications associated with acquired LQTS. Current recommendations are to monitor ECG before starting select psychotropic agents.
  4. Diagnosis: ECG is the diagnostic tool of choice.
  5. Long QT interval ≥0.46 second (has a positive and negative predictive value of 95%) is most accurate in identifying gene carriers
  6. Notched/bifid T wave in V2to V4
  7. May present with syncope, seizure, or sudden death
  8. May be asymptomatic
  9. ECG should be obtained on all primary relatives of those patients diagnosed with LQTS
  10. Holter monitors, exercise testing, and drug challenges are of limited utility. Electrophysiologic (EP) testing is not useful.
  11. Treatment of LQTS: Although no treatment is perfect, all patients who carry the diagnosis should be referred to a cardiologist and treated, even if asymptomatic. Mortality rate has been estimated to be 1% to 20% annually in patients not receiving treatment; this rate decreases to 1% to 2% per year if therapy is initiated. Therapy for LQTS includes the following:
  12. Restriction from competitive athletics, and prudent changes in recreational activities
  13. Avoidance of drugs/medications known to prolong the QT interval (for frequently updated information, see
  14. Avoidance of loud noises, emotional stressors, or vigorous activity which may precipitate a syncopal episode
  15. ECG evaluation of all family members
  16. β-Blockers: The initial treatment of choice, B-blockers decrease adrenergic triggers. β-Blocker treatment significantly decreases cardiac events, but does not change the QT interval nor provide absolute protection against sudden death. No absolute reduction in deaths is proven. Medication compliance is essential to prevent rebound receptor catecholamine hyper-sensitivity, which can precipitate a life-threatening arrhythmia if the medication is suddenly discontinued. There is increasing use of long-acting agents to improve adherence to therapy, for example, using nadolol rather than atenolol.
  17. Left cervicothoracic sympathetic ganglionectomy
  18. ICDs
  19. Gene-specific LQTS therapy: not yet available

TABLE 23.4
Conditions/Medications Associated with QT Interval Prolongation



CVA, cerebrovascular accident.
a Limited availability.
b Off the market.

Coronary artery disease






Eating disorders


Electrolyte abnormality


Liquid protein diets








Traumatic brain injury


Subarachnoid hemorrhage


Other Ion Channel Defect Disorders

Although LQTS is the most common genetic ion channel disorder, defects in other channels can also lead to syncope. Brugada syndrome is a distinctive mutation of the cardiac sodium channel gene (SCN5A) located on chromosome 3. The mutation leads to dynamic right ventricular conduction delays. Patients often present with syncope or cardiac arrest. Other ion channel defects include catecholaminergic ventricular tachycardia, and a newly described short QT syndrome. Although not an ion channel defect, a similar range of genotype–phenotype variation is seen in hereditary cardiomyopathies, such as arrhythmogenic right ventricular dysplasia, in which syncope may be the sentinel symptom.



Management of Suspected Cardiac Syncope

If cardiac disease is suspected as the etiology of a syncopal episode, referral to a pediatric cardiologist is in order. Patients with high-risk presentations should be restricted from competitive athletics until evaluated by the cardiologist. Adolescents should avoid driving a motor vehicle until their evaluation is complete. In many states an episode of cardiac syncope, like a seizure, invalidates the individual's driver's license for a period of several months.

Noncardiovascular Syncopes

  1. Hyperventilation: Hyperventilation is a frequent cause of dizziness in the adolescent, although a true syncopal episode occurs only rarely. Attacks often occur during stressful situations, and the adolescent may be unaware of the hyperventilation. Symptoms of hyperventilation include the following:
  2. Respiratory: Subjective shortness of breath secondary to increased thoracic respiratory efforts; chest pain either secondary to pressure on the diaphragm from gastric distension or related to thoracic muscle strain; and increased thoracic breathing, sighing, and yawning.
  3. Cardiovascular: Palpitations, tachycardia, and precordial chest pain.
  4. Neurological: Perioral or peripheral paresthesias, lightheadedness, dizziness, disorientation, impaired thinking, tetany, seizures, syncope, and headaches.
  5. Gastrointestinal: Epigastric pain (usually related to aerophagia), dry mouth, belching, bloating, and flatulence.
  6. Musculoskeletal: Muscle pains and cramps, tremors, stiffness, and muscle spasm.
  7. Psychiatric: Anxiety, depression, phobias, insomnia, sensations of unreality, and nightmares.
  8. General: Fatigue, weakness, and exhaustion, particularly as attack subsides.
  9. Pathophysiology: The alkalosis from hyperventilation leads to cerebral vasoconstriction and decreased cerebral perfusion. It is estimated that cerebral blood flow is decreased by 2% for each 1 mm Hg decrease in PaCo2. The alkalosis also leads to a decrease in peripheral release of oxygen (secondary to the Bohr effect on oxyhemoglobin), decreased ionized calcium level, hypophosphatemia, and possible coronary vasospasm.
  10. Treatment of hyperventilation includes reassurance, education about the physiology of hyperventilation, and teaching of strategies to deal with any identifiable precipitating stressors and to manage the hyperventilation itself. Interventions can include having the patient breathe into a paper bag or teaching diaphragmatic breathing. For example, the teenager should be instructed to place one hand on the abdomen and the other on the chest and to practice breathing so that the lower hand moves while the upper hand is held still.
  11. Metabolic disturbances: Hypokalemia and hypomagnesemia can lead to syncope. Hypoglycemia is characterized by a gradual onset of anxiety, weakness, sweating, palpitations, and tremor. Recovery is prompt with carbohydrate intake, but no relief is obtained on recumbency. Symptomatic hypoglycemia other than in the context of insulin-dependent diabetes is very rare in adolescents and is over-diagnosed by patients and families.
  12. Psychogenic syncope: “Hysterical syncope” is typically characterized by a patient who, almost always in the presence of others, gracefully slumps or swoons to the floor, usually without injury. The patient is not anxious. There are generally no blood pressure or pulse alterations or associated physiological changes. Other psychiatric causes include pseudoseizure and panic disorder. Many of these patients may have had an episode of typical syncope that is embellished so that those symptoms dominate the pseudofits, similar to epileptic patients who present with pseudoseizure.
  13. Subclavian steal syndrome: An uncommon cause of syncope related to occlusion in the proximal subclavian artery. This can lead to reversal of blood flow in the adjacent vertebral artery if vascular resistance in the arm decreases (during exercise), causing blood to flow away from the brain.
  14. Micturition syncope: Reported in older adolescents and young adults, but more common in older populations. Usually not associated with any serious illnesses when it occurs in this age-group. Episodes most frequently occur after the patient rises at night for urination. Rapid emptying of the bladder leads to a reflex vasodilation and a resultant decrease in cerebral blood flow, with a sudden loss of consciousness.
  15. Cough syncope: Uncommon in the adolescent, except in patients with chronic lung disease (cystic fibrosis or severe asthma). Episodes are caused by a prolonged bout of severe coughing, leading to increased intrathoracic pressure and a secondary decrease in cardiac output.
  16. Cerebroocclusive disease: Extremely rare in the adolescent, unless some predisposing factor such as sickle cell anemia, vasculitis, or vascular anomaly exists.
  17. Migraine: Adolescents with migraines can have syncope, vertigo, or dizziness, either preceding or accompanying the headaches. These symptoms may be the presenting complaint, and more prominent than the headache itself (see Chapter 22). Migraines characterized by vertigo, dizziness, or ataxia are generally classified as basilar artery migraines.


Vertigo is a sensation of rotary movement. The world seems to revolve around the patient or the patient senses that he or she is spinning. In contrast, dizziness is generally a sensation of movement or instability without a directional rotary component. Vertigo is much less common in the adolescent than nonspecific dizziness, lightheadedness, or syncope. Causes of true vertigo may be either peripheral or central. Occasionally, vertigo may be the primary or initial symptom of a complex partial seizure (see Chapter 21).

Peripheral Etiologies

Most peripheral vertigo is accompanied by tinnitus and/or hearing loss.

  1. Vestibular neuritis (acute labyrinthitis): Usually a result of an acute viral or bacterial infection or local trauma. This usually resolves over several days. Vertigo is


generally intense, position sensitive, and accompanied by nausea and vomiting.

  1. Benign positional vertigo: Characterized by a spinning sensation after quick movements of the head or body. The attacks last seconds to minutes, occur abruptly, and are generally not associated with nausea or vomiting. The cause is unknown in most patients. In older patients, canaliths (small accretions in the semicircular canals) may cause positional vertigo and may respond to maneuvers to alter their position.
  2. Ototoxic drugs: Aminoglycosides, diuretics (furosemide), aspirin, caffeine, phenytoin (Dilantin), and alcohol may cause transient or permanent vertigo.
  3. Acoustic neuromas: Vertigo with or without tinnitus and hearing loss in the affected ear. Bilateral acoustic neuromas are associated with neurofibromatosis type 2, often with onset in adolescence.
  4. Méniére disease: Rare in adolescents. This is characterized by vertigo, tinnitus, and hearing loss secondary to an increase in endolymph. Symptoms are generally intermittent.
  5. Perilymphatic fistulas: Are commonly associated with sudden onset of vertigo and hearing loss.
  6. Otitis media: Occasionally associated with true vertigo in adolescents.
  7. Motion sickness.
  8. Ear obstruction (i.e., cerumen compacted against the tympanic membrane).

Central Etiologies

Central lesions of the brain stem or cerebellar tracts involving vestibular input or vestibuloocular pathways may cause vertigo. Central lesions causing true vertigo are often accompanied by ataxia or other motor signs due to involvement of adjacent structures. Cerebellar or brain stem lesions may be caused by the following:

  1. Tumors, including lesions of the brain stem and cerebellum.
  2. Demyelinating diseases (e.g., multiple sclerosis).
  3. Vasculitis (lupus, isolated central nervous system [CNS] angiitis).
  4. Cerebral infarctions (stroke).
  5. Infections of the nervous system (encephalitis) or postinfectious inflammatory demyelination.
  6. Migraine: Basilar migraine may include symptoms of vertigo, although nonspecific dizziness is more common.
  7. Brain injury due to head trauma.


History is crucial to the evaluation of vertigo, because it allows differentiation of vertigo from syncope and seizures. The history may also be helpful in identifying the specific etiology for the vertigo. In most cases, the diagnosis is established by history and negative physical and neurological examination findings.

  1. Descriptions of the episode and any previous attacks help define the nature of the attack.
  2. Circumstances preceding the attack.
  3. Precipitating factors.
  4. Alleviating factors: Recumbency; food, fresh air, and sudden movements.
  5. The history may also be helpful in differentiating peripheral from central vertigo (Table 23.5).

TABLE 23.5
Peripheral versus Central Vertigo


Peripheral Vertigo

Central Vertigo


Usually paroxysmal

Seldom paroxysmal



Seldom severe


Usually short


Influence of head position



Autonomic nervous system symptoms


Less intense or absent



Seldom present

Hearing loss

Frequently present

Seldom present

Disturbances of consciousness

Seldom present

More frequently present

Focal neurological deficits



Associated symptoms

Nausea, vomiting

Visual, headaches

Physical Examination

General physical examination with special emphasis on the following:

  1. Neurological examination:
  2. Evidence of cranial nerve deficits, particularly III, IV, VI, VII, and VIII; funduscopic examination
  3. Focal motor deficits
  4. Tendon reflexes: Loss, asymmetry, and hyperreflexia
  5. Cerebellar function: Truncal or appendicular ataxia
  6. Nystagmus with straight gaze: Horizontal suggests peripheral etiology, whereas a vertical and diagonal nystagmus is more suggestive of central etiology
  7. Sensory abnormalities: Peripheral sensory loss suggests neuropathy
  8. Skin color, temperature, response to “scratch” to check for evidence of autonomic neuropathy
  9. Special examination procedures for vertigo:
  10. Quick head turn
  11. The Valsalva maneuver
  12. Sudden turn while walking



  1. Nylen-Bárány test: Have the adolescent sit at the edge of a table. Holding on to the adolescent's head, have the adolescent abruptly lie back as you place his or her head 45 degrees below the table and at a 45-degree angle to one side. Repeat the test with his head at a 45-degree angle to the opposite side. Elicitation of nystagmus indicates a “positive” test result, suggesting benign positional vertigo.

Further Evaluation

For sustained vertigo unassociated with an acute infection or vertigo that seems positional in origin, referral to a neurologist or otolaryngologist is advisable for further evaluation and testing. Patients with abrupt onset of vertigo and hearing loss should be promptly evaluated by an otolaryngologist.


Dizziness and vertigo associated with migraine should be treated as migraine (see Chapter 22). Treatment of vertigo is difficult. For the short-term treatment of vertigo and vomiting associated with acute labyrinthitis, antiemetics or mild sedatives may be useful, but they all cause drowsiness.

Benign positional vertigo may respond to deconditioning maneuvers (e.g., repeatedly provoking the vertigo with position changes to gradually suppress the response). Benign positional vertigo due to canaliths may respond to maneuvers for repositioning the canalith.

Vertigo associated with significant CNS disease is problematic, because long-term treatment with sedating medication is generally unacceptable, and nonsedating medications are usually ineffective. Central vertigo due to acute CNS lesions such as strokes generally decreases or abates entirely, but this process may take months or years. Epileptic vertigo is rare but generally responds to anticonvulsant drugs (see Chapter 21).

Sudden Death in Adolescents and Young Adults

Accidents, suicide, and homicide are the most frequent causes of sudden death in adolescents. After these traumatic events, exacerbations of chronic medical conditions—notably asthma and epilepsy—are significant, with SCD representing only approximately 10% of the overall sudden death rate (Driscoll and Edwards, 1985). The incidence of SCD is approximately 1/100,000 patient-years in the pediatric and young adult population, whereas the overall U.S. mortality rate is 17/100,000 patient-years for 15- to 19-year olds (Wren et al., 2000) ( HCM is the most common cause of SCD in the 15- to 35-year old age group, yet it is still rare, with an incidence of <1 death per 1,000,000/year (Wren, 2002). Despite the rarity of SCD, sudden death due to HCM, LQTS, and other potentially occult cardiac conditions occurs in several hundred adolescents in the United States each year.

Etiologies of Sudden Unexpected Cardiac Death in Children and Adolescents

  1. Structural or functional abnormalities: Many of these conditions may have a familial component
  2. HCM (described in the preceding text)
  3. Arrhythmogenic right ventricular dysplasia
  4. Coronary artery abnormalities, including aberrant left and right coronary arteries, hypoplastic coronary artery syndrome, Kawasaki syndrome, and Williams syndrome with coronary ostial stenosis
  5. Primary pulmonary hypertension
  6. Myocarditis/dilated cardiomyopathy
  7. Restrictive cardiomyopathy
  8. Marfan syndrome with aortic dissection
  9. Aortic valve stenosis
  10. Primary electrical abnormalities
  11. LQTSs, acquired or congenital (described in the preceding text)
  12. Brugada syndrome
  13. Wolff-Parkinson-White syndrome
  14. Primary or idiopathic ventricular tachycardia/fibrillation
  15. Catecholamine-exercise ventricular tachycardia
  16. Heart block, congenital or acquired
  17. Acquired conditions
  18. Commotio cordis
  19. Drug abuse: Cocaine, stimulants, inhalants (“sudden sniffing death syndrome”)
  20. Secondary pulmonary artery hypertension (Eisenmenger syndrome)
  21. Atherosclerotic coronary artery disease (CAD)
  22. Postoperative congenital heart disease
  23. Tetralogy of Fallot
  24. Transposition of the great arteries (after Mustard/Senning repair or after the arterial switch operation)
  25. Fontan surgery
  26. Hypoplastic left heart syndrome
  27. Coarctation of the aorta (after patch angioplasty, aneurysm at repair site)
  28. Cardiac transplantation

Each of these cardiac abnormalities carries differing levels of risk for SCD or other morbidity. Any patient with a suspected cardiac condition should be referred to a cardiologist for a full evaluation, and determination of appropriate athletic and recreational activities.


Important historical details include a history of syncopal episodes, significant exercise intolerance, exertional chest discomfort, and a family history of premature CAD, sudden death in a person younger than 40 years, syncope, or hypertension.

Physical Examination

Clues to cardiac disease include hypertension, abnormal cardiac rhythm, heart murmur, or a body habitus suggestive of Marfan syndrome. However, most patients at risk of sudden death will have a completely normal physical examination.



Laboratory Tests

The ECG is a convenient screening tool, but is often normal. Exercise electrocardiography is useful in an adolescent with symptoms of exertional chest discomfort, syncope, exercise intolerance, or worrisome palpitations. Routine screening with echocardiography or chest x-ray offers little additional value, and is not recommended. For further recommendations on athletic limitations associated with these conditions, see Chapter 18.


SCD in children, adolescents, and young adults may be prevented by both primary and secondary prevention programs. The accuracy of presymptomatic diagnostic testing and cost-effectiveness of a widespread preparticipation screening program are controversial issues. Current opinion in the United States is that existing data do not demonstrate that screening with ECGs, echocardiograms, or exercise testing prevents sudden death. In 1996, the American Heart Association concluded that the best screening for cardiovascular disease in athletes is a complete personal history, with thorough evaluation of cardiac or exercise-associated symptoms, a thorough family history, and a careful physical examination (Maron, 2003). Pilot studies continue with the use of screening echocardiography. Secondary prevention programs include chest protectors, maintenance of adequate hydration, the use of automatic electrical defibrillators, emergency response plans for schools, and training of personnel in basic cardiopulmonary resuscitation (CPR).

Web Sites

For Teenagers and Parents A comprehensive clinical center for patients who have fainted, who are recurrently lightheaded, or who have related cardiovascular disease. Much information on syncope. American Heart Association site. Search for syncope.

For Health Professionals Links to July 1997 Annals of Internal Medicine position paper with informed, adult-oriented but relevant clinical guidelines for diagnosing syncope. A comprehensive, and frequently updated, list of drugs affecting the QT interval.

References and Additional Readings

Abu-Arafeh I, Russell G. Paroxysmal vertigo as a migraine equivalent in children: a population-based study. Cephalalgia 1995;15:22.

Aysun S, Apak A. Syncope as a first sign of seizure disorder. J Child Neurol 2000;15:59.

Benditt DL, Fahy GJ, Lurie KG, et al. Pharmacotherapy of neurally mediated syncope. Circulation 1999;100:1242.

Boehm KE, Morris EJ, Kip KT, et al. Diagnosis and management of neurally mediated syncope and related conditions in adolescents. J Adolesc Health 2001;28:2.

Bower CM, Cotton RT. The spectrum of vertigo in children. Arch Otolaryngol Head Neck Surg 1995;121:911.

Cadman CS. Medical therapy of neurocardiogenic syncope. Cardiol Clin 2001;19:203.

D'Agostino R, Tarantino V, Melagrana A, et al. Otoneurologic evaluation of child vertigo. Int J Pediatr Otorhinolaryngol 1997;40:133.

DiVasta AD, Alexander ME. Fainting freshmen and sinking sophomores: cardiovascular issues of the adolescent. Curr Opin Pediatr 2004;16:350.

Driscoll DJ, Edwards WD. Sudden unexpected death in children and adolescents. J Am Coll Cardiol 1985;5:118B.

Driscoll DJ, Jacobsen SJ, Porter CJ, et al. Syncope in children and adolescents. J Am Coll Cardiol 1997;29:1039.

Goroll AH, May LA, Mulley AG. Evaluation of dizziness. In: Goroll AH, May LA, Mulley AG, eds. Primary care medicine. Philadelphia: JB Lippincott Co, 1995.

Grubb BP. Clinical practice. Neurocardiogenic syncope. N Engl J Med 2005;352:1004.

Hanna DE, Hodgens JB, Daniel WA Jr. Hyperventilation syndrome. Pediatr Ann 1986;15:708.

Heaton JM, Barton J, Ranalli P, et al. Evaluation of the dizzy patient: experience from a multidisciplinary neurology clinic. J Laryngol Otol 1999;113:19.

Ishiyama A, Jacobson KM, Baloh RW. Migraine and benign positional vertigo. Ann Otol Rhinol Laryngol 2000;109:377.

Kentala E. Characteristics of six otologic diseases involving vertigo. Am J Otol 1996;17:883.

Lanzi G, Balottin U, Fazzi E, et al. Benign paroxysmal vertigo of childhood: a long-term follow-up. Cephalalgia 1994;14:458.

Lee PW, Leung PW, Fung AS, et al. An episode of syncope attacks in adolescent schoolgirls: investigations, intervention, and outcome. Br J Med Psychol 1996;69(Pt 3):247.

Lewis DA, Dhala A. Syncope in the pediatric patient. The cardiologist's perspective. Pediatr Clin North Am 1999;46:205.

Linzer M, Varia I, Pontinen M, et al. Medically unexplained syncope: relationship to psychiatric illness. Am J Med 1992;92:185.

Mathias CJ, Kimber JR. Postural hypotension: causes, clinical features, investigation, and management [Review]. Annu Rev Med 1999;50:317.

McLeod KA. Syncope in childhood. Arch Dis Child 2003;88:350.

Moss AJ. Long QT syndrome. JAMA 2003;289:2041.

Nishimura RA, Holmes DR Jr. Clinical practice. Hypertrophic obstructive cardiomyopathy. N Engl J Med 2004;350:1320.

Ritter S, Tani LY, Etheridge SP, et al. What is the yield of screening echocardiography in pediatric syncope? Pediatrics 2000;105:E58.

Russell G, Abu-Arafeh I. Paroxysmal vertigo in children—an epidemiological study. Int J Pediatr Otorhinolaryngol 1999;49 (Suppl 1):S105.

Salim MA, Di Sessa TG. Effectiveness of fludrocortisone and salt in preventing syncope recurrence in children: a double-blind, placebo-controlled, randomized trial. J Am Coll Cardiol 2005;45:484.

Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med 2002;347:878.



Steinberg LA, Knilans TK. Syncope in children: diagnostic tests have a high cost and low yield. J Pediatr 2005;146: 355.

Stewart JM. Transient orthostatic hypotension is common in adolescents. J Pediatr 2002;140:418.

Stewart JM, Gewitz MH, Weldon A, et al. Orthostatic intolerance in adolescent chronic fatigue syndrome. Pediatrics 1999;102:116.

Sung RY, Du ZD, Yu CW, et al. Cerebral blood flow during vasovagal syncope induced by active standing or head up tilt. Arch Dis Child 2000;82:154.

Willis J. Syncope. Pediatr Rev 2000;21:201.

Wren C. Sudden death in children and adolescents. Heart 2002;88:426.

Wren C, O'Sullivan JJ, Wright C. Sudden death in children and adolescents. Heart 2000;83:410.