Pediatric Annals

CME 

Paroxysmal Nonepileptic Events in Infancy, Childhood, and Adolescence

Aimee F. Luat, MD; Deepak Kamat, MD, PhD; Lalitha Sivaswamy, MD

Abstract

There are a wide variety of paroxysmal nonepileptic events (PNEEs) in children that can mimic seizures. The type of PNEEs that need to be considered in the differential diagnosis depends on the age of symptom onset and the clinical features. In infants and toddlers, conditions that are relatively common in clinical practice such as apnea, jitteriness, shuddering attacks, and breath-holding spells may not present much of a diagnostic conundrum, whereas unusual conditions such as hyperekplexia may cause concern. Similarly, although most types of migraine are easily distinguished from seizures in school-aged children, certain variants such as the “Alice in Wonderland” syndrome or basilar migraine can create diagnostic confusion. Most types of PNEE are exclusive to childhood; therefore, the pediatrician must be familiar with a variety of physiological processes and pathological entities that can raise concern in parents. The pediatrician is in the unique position of being able to reassure families and/or guide further work-up. Many of the PNEEs in young children require no treatment and resolve spontaneously. It is important to distinguish these episodes from true seizures as to avoid unnecessary testing and pharmacological treatment. This review highlights common PNEEs in children, beginning with the neonatal age group and moving upward to adolescence. [Pediatr Ann. 2015;44(2):e18–e23.]

Abstract

There are a wide variety of paroxysmal nonepileptic events (PNEEs) in children that can mimic seizures. The type of PNEEs that need to be considered in the differential diagnosis depends on the age of symptom onset and the clinical features. In infants and toddlers, conditions that are relatively common in clinical practice such as apnea, jitteriness, shuddering attacks, and breath-holding spells may not present much of a diagnostic conundrum, whereas unusual conditions such as hyperekplexia may cause concern. Similarly, although most types of migraine are easily distinguished from seizures in school-aged children, certain variants such as the “Alice in Wonderland” syndrome or basilar migraine can create diagnostic confusion. Most types of PNEE are exclusive to childhood; therefore, the pediatrician must be familiar with a variety of physiological processes and pathological entities that can raise concern in parents. The pediatrician is in the unique position of being able to reassure families and/or guide further work-up. Many of the PNEEs in young children require no treatment and resolve spontaneously. It is important to distinguish these episodes from true seizures as to avoid unnecessary testing and pharmacological treatment. This review highlights common PNEEs in children, beginning with the neonatal age group and moving upward to adolescence. [Pediatr Ann. 2015;44(2):e18–e23.]

Paroxysmal nonepileptic events (PNEEs) in children are conditions that mimic epileptic seizures. Physiologic causes are more common in infants, whereas psychogenic causes tend to predominate in older children and adolescents.1 It is important to differentiate these spells from true seizures to avoid unnecessary testing, allay parental anxiety, and avoid antiepileptic treatment. The diagnosis can reliably be made in most instances by eliciting a careful history and/or observation of the spell. Home-video recording has been proven to be a valuable tool in several circumstances. The purpose of this review is to discuss the differential diagnosis of childhood PNEEs. The PNEEs that mimic seizures are discussed in chronological order of appearance from the neonatal period to adolescence.

Neonates, Infants, and Children Younger than Age 2 Years

Apnea and Acute Life-Threatening Events

Apnea is defined as “unexplained cessation of breathing for at least 20 seconds or a shorter respiratory pause associated with bradycardia, cyanosis, pallor, and/or marked hypotonia.”2 An acute life-threatening event (ALTE) is an episode that often frightens the observer and is characterized by apnea, skin color change (cyanotic or pallid, occasionally erythematous or plethoric), change in muscle tone (usually limpness), and choking/gagging.3 Apnea is very common among premature infants and decreases in frequency with maturity. Most cases of apnea in premature babies resolve by 36 weeks of gestational age.4 Apnea beyond this period can be due to various systemic causes such as sepsis, airway obstruction, gastroesophageal reflux, poor pharyngeal coordination, and rarely seizures.4 Seizures associated with apnea and ALTE are often accompanied by motor symptoms such as jerking and subtle signs such as eye deviation. Pure apneic seizure in full-term infants can be due to intracranial hemorrhage or stroke. Therefore, recurrent apnea and ALTE, especially in full-term infants, without clear etiology always warrants video-electroencephalography monitoring to document any associated seizure activity.4

Tremors

Tremors are involuntary rhythmic movements of equal amplitude around a fixed axis.5 Jitteriness is recurrent tremors. These spells are usually due to immaturity of spinal inhibitory interneurons. They can be classified as fine (high frequency of >6 Hz and low amplitude <3 cm) or coarse (low frequency and higher amplitude).5 Fine tremors are usually benign or due to metabolic causes such as hypoglycemia, whereas coarse tremor can be due to intracranial pathology.5 Both can mimic clonic seizures. Tremors’ “to-and-fro” movements have equal duration whereas clonic seizures have fast and slow phases.6 Tremors can be stopped by gentle restraint of the affected limb. The suckling stimulation test is a bedside test to determine if a tremor is benign: a finger is put into the infant’s mouth and typically benign tremor resolves as the infant sucks the finger.7 Most tremors subside by 6 to 10 weeks postterm.

Hyperekplexia

Hyperekplexia or “startle disease” is a rare disorder with onset in neonatal and early infancy characterized by exaggerated startle reaction to auditory, somatosensory, or visual stimuli leading to tonic rigidity that may lead to a feeding problem and apnea. The triad of congenital generalized stiffness, excessive startling, and rigidity when startled characterize the major form, whereas only excessive startling is seen in the minor form. Generalized rigidity without habituation triggered by tapping the nasal tip or glabella is the clinical hallmark.8 Flexion of the head and limbs toward the trunk (ie, the Vigebano maneuver) may counteract the rigidity and apnea and can be a life-saving procedure.9 Affected infants are at increased risk of sudden infant death syndrome during the first 2 years of life. Hyperekplexia is an autosomal dominant condition most commonly caused by a glycine receptor mutation.10 Electroencephalogram (EEG) is normal between (interictal) episodes but during the episode muscle artifacts are seen followed by EEG slowing, corresponding to the apnea.8 Clonazepam is the medication of choice.

Benign Neonatal Sleep Myoclonus and Benign Myoclonus of Early Infancy

Myoclonus/myocloni are shock-like movements from sudden muscle contractions. Benign neonatal sleep myoclonus (BNSM) typically occurs in newborns, and the spells consist of repetitive myoclonus, usually of the distal extremities. Triggers include sound, rocking, or car travel. Unlike seizures, there are no associated symptoms. They occur only during sleep and stop upon arousal. Conversely, seizures in early-onset epilepsy occur even during wakefulness. However, the jerks in BNSM may not stop (and may even be worsened) by holding the limb, so inability to stop with restraint does not rule out the diagnosis. EEGs between and during the episode are normal. BNSM resolves within 1 year in the majority of children. Neonates with BNSM have normal examination and EEG. It is self-limited and treatment is unnecessary.

Benign myoclonus of early infancy (BMEI) presents during the first year of life and is characterized by nonepileptic myoclonus of the neck, upper limb, and trunk, leading to abrupt head flexion/rotation and limb extension/abductions without changes in consciousness. Episodes may cluster and the spells occur only during wakefulness. EEG is normal. Spells remit within 3 months and stop by age 2 years. BMEI is a popular mimicker of the epileptic spasms in West syndrome,11 an epileptic encephalopathy characterized by intractable epileptic spasms, developmental delay, and hypsarrhythmic EEG. West syndrome can be distinguished from BMEI by its characteristic EEG abnormality and the presence of psychomotor regression/arrest. Epileptic spasms occur in clusters, have stereotyped features, and characteristically occur during awakening, drowsiness, or end of sleep.

Shuddering Attacks

Shuddering attacks are episodes that occur during infancy and early childhood consisting of fine head and bilateral arm tremors. They are sometimes associated with stiffening of the upper extremities, often with posturing and without impairment of consciousness.12 They only last for few seconds but may occur several times per day. Feeding, head movements, and excitement are precipitating factors. EEG is normal.12 Shuddering attacks may be confused with BMEI and benign tremors of childhood.

Breath-Holding Spells

Breath-holding spells (BHS) are common and frightening events that occur between ages 6 months and 4 years. They are classified based on the child’s skin color change (cyanotic, pallid, and mixed). The sequence of events is distinctive: there is a provoking factor (such as frustration, anger, fright, and minor trauma) resulting in crying or an emotionally upset state leading to a noiseless state of expiration (“silent scream”) with color change and ultimately loss of consciousness and tone.13 Tonic, clonic movements and posturing have been described. During the episode, EEG shows diffuse slowing but no seizure activity. BHS can evolve into epileptic seizures, but the initial event is nonepileptic.1 The spells can last for long periods and may be associated with prolonged postictal state. The mechanism involved is poorly understood, but instability of the autonomic system has been speculated. The presence of iron-deficiency anemia should be excluded. Antiepileptic medications are not indicated.

Sandifer Syndrome

Sandifer syndrome is an uncommon, yet well-described syndrome in neonates and infants, characterized by abnormal posturing/spasm-like spells with torticollis and retrocollis secondary to gastroesophageal reflux. It occurs in the context of feeding and may be accompanied by arm jerks/tremors, choking, cyanosis, laryngospasms, and apnea.6 Speculated mechanisms include enhanced acid clearance from the lower esophagus by the posturing, which can relieve the symptom and/or a brainstem phenomenon triggered by pain from esophagitis.6

Paroxysmal Tonic Upgaze

Paroxysmal tonic upgaze is a rare, age-related, infantile ocular syndrome characterized by episodes of sustained conjugate upward eye deviation with downward tilt of the chin. There are incomplete downward saccades on attempted down gaze, but normal horizontal eye movements. The episodes are exacerbated by illness and relieved by sleep.14,15 During the episode, EEG is normal.16 However, it may co-exist with epileptic seizures,17,18 highlighting the importance of capturing the spell on EEG. Differential diagnosis includes tonic and absence seizures, brainstem and pineal lesions, and hydrocephalus. Most cases resolve spontaneously.

Paroxysmal Disorders in School-Age Children and Adolescents

Migraine

The paroxysmal disorder most likely to be confused with seizures in older children is migraine. The two conditions may coexist, especially among those who have migraine with aura.19,20 Specific forms of migraine that mimic seizures are discussed in some detail below.

Basilar-Type Migraine

Basilar-type migraine is characterized by recurrent attacks of brainstem dysfunction, with a predisposition toward affecting adolescent girls.21 Its aura may mimic the aura of a seizure. These symptoms may range from bilateral paresthesia to alteration of consciousness, diplopia, ataxia, visual disturbances, and tinnitus. These symptoms are followed by a migraine headache that often involves the occipital area. Neuroimaging is normal and EEG manifests only slowing during a spell.

Acute Confusional Migraine

Acute confusional migraine (ACM) is a migraine variant peculiar to adolescence characterized by acute confusion or altered sensorium with prominent combativeness. ACM constitutes less than 5% of all childhood migraines.22 During or after the episode, the child may or may not experience migraine headache. The episodes are often short (<24 hours) and may be precipitated by head trauma. The neurological examination shows no deficits. The child often experiences amnesia for the event and the symptoms are characteristically aborted by sleep, although not invariably so. The diagnosis remains one of exclusion and cannot be made with certainty after the first episode. ACM might mimic an episode of nonconvulsive seizures and, therefore, it is recommended that an EEG be performed during the episode. The presence of slow waves on EEG supports the diagnosis of ACM.

“Alice in Wonderland” Syndrome

“Alice in Wonderland” syndrome (AWS) is characterized by the visual and perceptual distortions as experienced by Alice in the children’s book Through the Looking Glass. Objects may appear large (macropsia), small (micropsia), distant (teliopsia), closer than they are (peliopsia), or altered in form (metamorphopsia). Other symptoms include depersonalization and distorted time perception. The sensorium remains unchanged. AWS may occur as a part of a migraine aura or, more frequently, as a predictor of future migraine. In clinical practice, AWS is frequently associated with systemic viral infections such Epstein-Barr virus, varicella, and coxsackie virus, often in the absence of encephalitis.23 The major differential diagnosis is occipital lobe epilepsy. Acute treatment of children with migraine consists of nonsteroidal anti-inflammatory agents, serotonin agonists, and antidopaminergic agents.

Paroxysmal Dyskinesias

Paroxysmal dyskinesias (PD) present with episodic chorea, ballismus, athetosis, or dystonia that may be unilateral, bilateral, or alternating. Some children may experience paresthesias in the affected body part prior to the onset of dyskinesia, which can lead to an erroneous diagnosis of seizure. Facial involvement may lead to dysarthria. PD may be kinesigenic (movement induced), nonkinesigenic, or induced by exercise. Certain forms overlap with epilepsy syndromes, which may complicate the diagnosis. In PD, consciousness is preserved and episodes can last for hours, which is highly unusual for a seizure. Many forms of PD are autosomal dominant. Most children with PD have a normal neurological examination between episodes. Most children respond well to a low dose of carbamazepine, phenytoin, or gabapentin.

Sleep Disorders

Parasomnias

Sleep terrors occur in children between ages 2 and 4 years and consist of abrupt arousal from slow wave sleep with prominent autonomic activity manifest as sweating, tachycardia, pupillary dilatation, and behavioral features such as fear.24

During the episode, the child is inconsolable and disoriented. The spells last for a few minutes and resolve spontaneously. Sleep study can be helpful in establishing the diagnosis. Epilepsy types that classically occur during sleep and their clinical features are discussed in the following section of this article. Most sleep terrors spontaneously resolve with time.

Rapid Eye Movement Sleep Behavior Disorder

Rapid eye movement (REM) sleep behavior disorder (RBD) occurs during REM sleep, which is normally characterized by paralysis of skeletal muscles. However, during RBD the atonia is absent and, therefore, dreams are acted out. Children with RBD exhibit nocturnal behaviors that can mimic a seizure. They have unusual motor behaviors ranging from restlessness to flailing of extremities, and dramatic, semi-purposeful movements that are often aggressive in nature. Loud vocalizations may accompany the episode but true words are rarely uttered. Frontal lobe seizures and RBD have overlapping clinical features, as children with both conditions may have poorly articulated vocalizations and hyperkinetic limb movements.25 Other epilepsy types that typically occur in sleep include benign Rolandic epilepsy of childhood (BREC; see article in this issue by Park and Shahid) and Panayiotopoulos syndrome. Children with autism and developmental delay have a higher incidence of both RBD and epilepsy.26 Furthermore, unrecognized RBD coexists with epilepsy in 12% of otherwise normal individuals with epilepsy, although precise numbers are lacking in the pediatric population.27 Diagnosis of RBD can be established by performing a sleep study. To alleviate this behavior, education and reassurance may be all that is necessary. Clinicians should emphasize good sleeping habits, and in some instances short-term treatment with a low dose of clonazepam can be helpful.

Vasovagal Syncope

Syncope is a transient disorder characterized by loss of consciousness because of a decrease in cerebral blood flow. About 15% of teenagers experience at least one episode of syncope prior to adulthood.28 The majority of patients with syncope do not have an underlying cardiac disease, and the symptoms are due to reflex vasovagal mechanism resulting in bradycardia and hypotension. The most common precipitating factors are prolonged periods of standing and emotional stimuli (ie, sight of blood). Syncope is highly unusual in a child who is sitting or lying down. There is usually a sensation of lightheadedness before the spell, the child appears pale and clammy, experiences fading vision or hearing, and then the child falls to the floor. Recovery is complete within a few minutes without postictal confusion or focal deficits. Rarely, a child with syncope may experience a few convulsive movements but more commonly only trembling of limbs is noted. Recovery is swift after syncope, whereas a convulsive seizure is usually followed by postictal state. Vital aspects of the history can be provided by a witness. Children who fall into a high-risk category may benefit from cardiac evaluation and further testing with an electrocardiogram, echocardiogram, exercise tolerance test, and/or head-up tilt test. First-line treatment for children with no underlying cardiac basis consists of increased fluid and salt intake.

Psychogenic Nonepileptic Attacks

Psychogenic nonepileptic attacks (PNEAs) are commonly misdiagnosed as seizures. PNEAs are equally prevalent in preadolescent boys and girls, with female preponderance occurring in older teens. The term “pseudoseizure” was often used in the literature, but the terms “psychogenic nonepileptic seizure” and PNEA have replaced it in current literature. Most children with PNEA are believed to have a somatoform disorder (ie, they are not voluntarily “faking” the symptoms). The most valuable differentiating information can be obtained from a detailed history. Children with PNEAs tend to have a high frequency of spells that are resistant to multiple antiepileptic drugs, have attacks precipitated by emotional stimuli, provoked by suggestions, and usually occur in the presence of an audience. A history of child abuse, poor academic performance, and a personal history of epilepsy increases the odds of having PNEAs in the adolescent age group.29 The presence of a bite on the side of the tongue, significant injury to other body parts, and fecal incontinence may sway the clinician toward a diagnosis of organic seizure disorder. A diagnosis can be reliably established by performing a video-EEG recording during an attack. Witnessing an episode, even by a physician, is notoriously unreliable in conclusively arriving at a diagnosis. Treatment should start with referral to a psychologist experienced in treating children with PNEA.

Staring Spells

Staring spells are common in children and are often due to either inattention or boredom. Dialeptic seizures can present with motor arrest, but there are usually associated automatisms like eye blinking. Seizures cannot be interrupted by external verbal or physical stimuli, and the spells may interrupt play or daily activities. Dialeptic seizures tend to occur with higher frequency through the day and occur predominantly in younger children than staring spells that are associated with inattention.30 Focal seizures may also present with motor arrest. However, these episodes are relatively easy to diagnose as they may be preceded by an aura and often have associated symptoms such as eye deviation, motor movements, and urinary incontinence. In general, spells with a psychogenic basis tend to be longer and occur in older children. Reassurance is usually all that is required, although children with attention-deficit disorder will benefit from a trial of stimulants.

Conclusion

The clinical features of different seizure-mimickers in infancy, childhood, and adolescence have been presented. A detailed clinical history from the child and witnesses, personal observation of the spell, or video recording of the same plus video-EEG recordings are indispensable tools in arriving at a diagnosis.

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Authors

Aimee F. Luat, MD, is an Assistant Professor of Pediatrics and Neurology, Carman and Ann Adams Department of Pediatrics and the Department of Neurology, Wayne State University School of Medicine, Children’s Hospital of Michigan. Deepak Kamat, MD, PhD, is a Professor of Pediatrics, and the Vice Chair of Education, Department of Pediatrics, Wayne State University School of Medicine; and a Designated Institutional Official, Children’s Hospital of Michigan. Lalitha Sivaswamy, MD, is an Associate Professor of Pediatrics and Neurology, Carman and Ann Adams Department of Pediatrics and the Department of Neurology, Wayne State University School of Medicine, Children’s Hospital of Michigan.

Address correspondence to Lalitha Sivaswamy, MD, Wayne State University School of Medicine, Children’s Hospital of Michigan, 3901 Beaubien Boulevard, Detroit, MI 48201; email: lsivaswamy@med.wayne.edu.

Disclosure: The authors have no relevant financial relationships to disclose.

10.3928/00904481-20150203-07

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