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Nonepileptic paroxysmal disorders in adolescents and adults

Nonepileptic paroxysmal disorders in adolescents and adults
Authors:
Thien T Nguyen, MD, PhD
Peter W Kaplan, MB, FRCP
Section Editor:
Steven C Schachter, MD
Deputy Editor:
John F Dashe, MD, PhD
Literature review current through: Dec 2022. | This topic last updated: Sep 29, 2021.

INTRODUCTION — The term "epileptic seizure" refers to a transient occurrence of signs and/or symptoms due to abnormally excessive neuronal activity of the brain. Epilepsy is a condition characterized by recurrent seizures.

While it is estimated that 0.5 to 1 percent of the population has epilepsy, nearly 25 percent of patients seen in epilepsy clinic and monitoring units do not have epilepsy [1-4]. It is important for clinicians to recognize these transient nonepileptic events that may resemble seizures in order to avoid unnecessary treatment with antiseizure drugs and to institute the correct treatment when appropriate.

The symptoms of epileptic seizures are diverse. As a result, disorders that might be considered in the differential diagnosis will vary depending on the patient's specific clinical presentation. Clearly, not all of these disorders are considered in any one patient.

Nonepileptic paroxysmal events that can be mistaken for epilepsy also differ significantly by age group (table 1). This topic will review those diagnoses in adolescents and young adults. These diagnoses can be classified into six broad categories:

Syncope

Psychologic disorders

Sleep disorders

Paroxysmal movement disorders

Migraine

Miscellaneous neurologic events

Nonepileptic paroxysmal events in other age groups are reviewed separately. (See "Nonepileptic paroxysmal disorders in infancy" and "Nonepileptic paroxysmal disorders in children" and "Seizures and epilepsy in older adults: Etiology, clinical presentation, and diagnosis", section on 'Differential diagnosis'.)

Psychogenic nonepileptic seizures are discussed in detail elsewhere. (See "Psychogenic nonepileptic seizures: Etiology, clinical features, and diagnosis".)

SYNCOPE — Syncope is an abrupt loss of consciousness due to an interruption of energy sources to the brain, usually because of a sudden reduction of cerebral perfusion (see "Syncope in adults: Clinical manifestations and initial diagnostic evaluation"). It is common to confuse seizure and syncope as the cause of an isolated or episodic loss of consciousness [5-8], especially but not exclusively when the episode is not witnessed.

Clinical features — A careful clinical history is important in distinguishing syncope from epilepsy [9]. Important features are not always volunteered and must be specifically solicited.

Clinical setting – Epileptic seizures and syncope can occur in any setting and are often unprovoked [10,11]. Vasovagal syncope tends to occur in the setting of a strong emotional or painful stimulus, but may also occur with more subtle stimuli, including a hot environment. Reflex syncopes occur with specific stimuli (eg, micturition, cough). Events in the setting of exertion suggest syncope related to structural cardiac disease. Except when caused by a cardiac arrhythmia, it is unusual for syncope to occur when the patient is supine.

Warning symptoms (aura, prodrome) – In vasovagal syncope, a prodrome of presyncope is the rule. These patients may note lightheadedness, warmth, sweating, nausea, and a gradual fading or tunneling of binocular vision. They may reach out to steady themselves. By contrast, symptoms of olfactory hallucinations or déjà vu suggest a seizure aura. However, not all epileptic seizures include a seizure aura. Cardiogenic syncope typically occurs without warning.

Associated symptoms – Pallor and diaphoresis strongly suggest syncope [7]. However, it is unusual for syncope to be associated with lateral tongue biting, head or eye turning to one side, or foaming at the mouth; these suggest epileptic seizure [7,9,12-14]. Urinary incontinence can occur in both seizures and syncope.

Motor activity (convulsive syncope) – While motor activity during an episode of unconsciousness often suggests a seizure diagnosis, brief motor activity, including tonic extension of the trunk and limbs or several clonic jerks, can occur in uncomplicated syncope [11,15]. The severity of convulsive symptoms in syncope varies from subtle signs that are often overlooked to more dramatic symptoms that mimic an epileptic seizure. The combination of seizure-like motor activity in the setting of syncope is sometimes referred to as convulsive syncope. Convulsive syncope is usually brief (<20 seconds).

Relatively few bystanders witnessing syncopal attacks report convulsive symptoms, but clinicians systematically observing attacks (eg, during tilt table testing, invasive cardiac electrophysiologic testing, blood drawing) describe convulsive symptoms in up to half of patients [6,12,16-18]. While these convulsions are common in syncope, a true epileptic seizure ("anoxic seizure") is rare, except in susceptible people or those with prolonged and more severe cerebral ischemia [5,16,19].

Electroencephalography (EEG) recordings during syncopal events usually demonstrate generalized slowing followed by high-voltage frontal delta activity [19,20]. Flattening of the EEG can follow if cerebral hypoperfusion persists. It is at this stage that nonepileptic, seizure-like movements are most often described. It has been suggested that these movements may represent a brainstem-release phenomenon.

Recovery of consciousness – Patients usually wake up quickly after a syncopal event, and may recognize their surroundings within a minute or so. Prolonged confusion or lethargy lasting several minutes or longer favors seizure [7].

Causes

Vasovagal syncope is the most prevalent cause of syncope [20]. This often occurs in response to clinical setting (eg, painful procedures, blood drawing, warm setting). In susceptible individuals, autonomic activation leads to a hyperactive parasympathetic cardioinhibitory response and/or a diminished sympathetic response leading to vasodepression and syncope. (See "Reflex syncope in adults and adolescents: Clinical presentation and diagnostic evaluation".)

Cardiogenic syncope related to either tachy- or bradyarrhythmias is less common but carries a more ominous prognosis. These events are usually unprovoked. Structural heart disease (eg, aortic stenosis) can also lead to syncope by obstructing blood flow. (See "Syncope in adults: Epidemiology, pathogenesis, and etiologies", section on 'Cardiac arrhythmias'.)

In rare cases, epileptic seizures can induce a cardiac arrhythmia. The most commonly described of these phenomena is an ictal bradycardia in the setting of a temporal lobe seizure [21,22]. (See "Sudden unexpected death in epilepsy".)

Hyperventilation with hypocapnia can also lead to syncope [23,24]. In this age group, this is most commonly seen in the setting of a panic attack. The presumed mechanism involves respiratory alkalosis causing cerebral vasoconstriction, which in turn decreases cerebral blood flow, causing syncope. Patients often have prodromal complaints of dyspnea, circumoral or acral paresthesias, and visual phosphenes. Tetany, muscle cramps, carpopedal spasm, and chest pain can also occur. A three-minute trial of hyperventilation may induce similar symptoms and aid in diagnosis [10]. (See 'Panic attacks' below.)

Orthostatic hypotension is more common in older adults than in younger adults, but should be excluded when convulsive syncope is considered in the differential diagnosis [25]. Orthostatic hypotension is defined as a systolic blood pressure decrease of at least 20 mmHg or a diastolic blood pressure decrease of at least 10 mmHg after three minutes of standing. Syncope occurs in the setting of either prolonged standing or a sudden assumption of upright posture. In a first attack, acute blood loss should be excluded. Autonomic neuropathy from diabetes and antihypertensive drugs are some of the more common causes of recurrent episodes. (See "Mechanisms, causes, and evaluation of orthostatic hypotension".)

Reflex syncope (eg, micturition and cough syncope, carotid sinus hypersensitivity) refers to events that are believed to reflect vagal hypersensitivity to specific stimuli [19]. These diagnoses are suggested by the specific provocation under which they occur. (See "Syncope in adults: Epidemiology, pathogenesis, and etiologies".)

Diagnosis — The clinical features described above are helpful in distinguishing syncope from seizure. One study found that, among 539 patients in whom all clinical data could be determined, a point score rating these features correctly classified 94 percent of patients as to syncope versus seizures [7]. However, in many cases, these features are unclear or equivocal, and testing is required.

After a generalized tonic-clonic seizure, creatine kinase (CK) levels are often elevated, and may remain so for several hours or a day. This is unusual in syncope, unless the event was associated with myocardial infarction, in which case the CK elevations are proportionately greater in the MB isoenzyme fraction, rather than the MM fraction, reflecting cardiac rather than skeletal muscle. Serum prolactin levels, however, are not a useful test to distinguish between syncope and seizure, as elevations can occur in either. (See "Evaluation and management of the first seizure in adults", section on 'Initial evaluation'.)

Because the prevalence of syncope in the emergency department is far higher than that of seizures, the positive predictive value of EEG abnormalities is low, rendering EEG testing of questionable use in this setting. Only if the EEG captures an event will it help confirm or refute seizures.

While an interictal EEG has limited utility in differentiating syncope and epileptic seizure, EEG monitoring can be helpful, especially if an ictus is captured. This usually requires recurrent events and prolonged EEG and electrocardiogram (ECG) monitoring.

Other testing that can be helpful in the differentiating syncope from seizures includes:

Tilt table testing can provoke vasovagal syncope and provide support for this diagnosis [6,26]. Confirmation that the induced spell is representative of the episode(s) being evaluated can help avoid a false-positive diagnosis. (See "Reflex syncope in adults and adolescents: Clinical presentation and diagnostic evaluation".)

ECG or Holter monitoring can be helpful in identifying cardiac arrhythmias, which can lead to syncope [6]. In rare patients with epilepsy and arrhythmia, combined EEG and ECG monitoring can be useful to identify the primary event [21]. Long-term cardiac monitoring techniques can be used for patients with infrequent, recurrent attacks. (See "Ambulatory ECG monitoring".)

The diagnostic evaluation of a patient with suspected syncope is discussed in detail separately. (See "Syncope in adults: Risk assessment and additional diagnostic evaluation", section on 'Introduction'.)

PSYCHOLOGICAL DISORDERS

Psychogenic nonepileptic seizures — Among series of patients undergoing video-electroencephalography (EEG) monitoring, the most common disorder mistaken for epilepsy is psychogenic nonepileptic seizures (PNES) [1,27]. While often categorized under somatoform or dissociative disorders, PNES probably have a heterogeneous psychiatric pathogenesis. Patients display episodes that superficially resemble epileptic seizures, but are often atypical in one or more of their features (table 2). Video-EEG monitoring is usually required for diagnosis.

PNES are discussed in detail separately. (See "Psychogenic nonepileptic seizures: Etiology, clinical features, and diagnosis".)

Panic attacks — Panic attacks usually occur in individuals with an underlying anxiety disorder. Attacks are variable in duration (minutes to hours) and can include palpitations, dyspnea, chest pain, presyncope, and a sense of impending doom. Patients often manifest hyperventilation, tachycardia, diaphoresis, and tremulousness during the attack. In rare circumstances, hyperventilation can lead to a brief loss of consciousness [23,24]. (See 'Causes' above.)

When not clearly precipitated by stressful circumstances or when associated with feelings of depersonalization or derealization, panic attacks may be mistaken for seizures. Similarly, seizures can be mistaken for panic attacks because anxiety is a common comorbid condition in individuals with epilepsy, and fear can be an ictal symptom, particularly in temporal lobe epilepsy [28,29]. (See "Focal epilepsy: Causes and clinical features", section on 'Mesial temporal lobe epilepsy'.)

Features that help distinguish epileptic seizures from panic attacks include their short duration (less than two to three minutes), stereotyped nature, abrupt onset, motor automatisms, unresponsiveness, and postictal lethargy, all of which are atypical for panic attacks.

Episodic dyscontrol — Individuals with episodic dyscontrol, also called intermittent explosive disorder (IED), display episodes of rage and violence. This disorder usually presents in teenagers and young adults, although it can occur in younger children as well [30,31]. Behavior exhibited during these episodes can appear as though the individual is "out of control." Other features of the episodes that resemble epileptic seizures include their abrupt onset, often without apparent precipitant, and their short duration, often followed by fatigue and remorse. However, the directed violence of these episodes is rarely a feature of epileptic seizures. (See "Intermittent explosive disorder in adults: Clinical features, assessment, and diagnosis".)

There is a somewhat high prevalence of nonspecific EEG abnormalities in patients with IED, perhaps reflecting an underlying brain pathology; however, a neurobiologic mechanism of this disorder is not defined [32]. (See "Intermittent explosive disorder in adults: Epidemiology and pathogenesis" and "Intermittent explosive disorder in adults: Treatment and prognosis".)

SLEEP DISORDERS — Because of their episodic and often paroxysmal nature, parasomnias and other sleep disorders may be confused with epilepsy [33]. An exclusive nighttime occurrence of events may suggest a sleep disorder, but does not exclude epilepsy, as this is a characteristic of certain epileptic disorders such as nocturnal frontal lobe epilepsy and juvenile myoclonic epilepsy (JME) [12,34]. Epilepsy and sleep disorders can also co-occur (see "Sleep-related epilepsy syndromes"). As an example, disorders of arousal (eg, sleepwalking, confusional arousals) are common in patients with nocturnal frontal lobe epilepsy and their relatives. (See "Disorders of arousal from non-rapid eye movement sleep in adults", section on 'Association with sleep-related hypermotor epilepsy'.)

Specific disorders

Narcolepsy — Narcolepsy is a rare sleep disorder associated with rapid eye movement (REM) sleep invading normal wakefulness. The tetrad of clinical features includes:

Excessive daytime sleep – Irresistible sleepiness can culminate in a "sleep attack," in which sleep onset can occur while talking, driving, or walking.

Cataplexy – This sudden loss of muscle tone with preserved consciousness can be mistaken for an atonic seizure. This can result in falls and brief paralysis, but more often is limited to buckling of the knees and slurring of speech. The attacks are classically precipitated by strong emotion, most commonly laughter, but also anger, fear, surprise, or excitement; this feature helps distinguish these attacks from an epileptic seizure.

Sleep paralysis – An inability to move or speak, sleep paralysis typically occurs upon awakening or falling asleep and lasts less than 10 minutes. Sometimes, the episodes resolve when someone touches the patient. These can be very frightening to the patient who maintains consciousness throughout the event.

Hypnagogic and hypnopompic hallucinations – These are usually visual and less often somatosensory, auditory, vestibular, or olfactory hallucinations that occur while falling asleep (hypnagogic) or on awakening (hypnopompic). The content can be simple (a brief image of a face) or complex (an entire scene occurring in the room). The patient is fully aware during the episode. (See 'Etiologies' below.)

Only 10 to 15 percent of patients with narcolepsy experience all of these symptoms. When daytime sleep attacks, cataplexy, hypnagogic hallucinations, and sleep paralysis occur as isolated features, they may be mistaken for epilepsy and vice versa [35-37]. Polysomnography and a multiple sleep latency test (MSLT) aid in the diagnosis, showing decreased sleep latency and decreased REM latency in patients with narcolepsy. (See "Clinical features and diagnosis of narcolepsy in adults".)

Hypnic jerks — Most people have experienced a sudden jerking movement upon falling asleep, often accompanied by a subjective sensation of falling. This phenomenon, also known as benign hypnic myoclonus or sleep starts, is usually easily recognized. Rarely, hypnic jerks can become unusually violent, very frequent, or repetitive, and confused for myoclonic seizures or even tonic-clonic seizures. The phenomenon is restricted to sleep, and always or virtually always in the transition between sleep and wakefulness, and is not associated with other phenomena. (See "Approach to abnormal movements and behaviors during sleep", section on 'Simple or single movements'.)

Nocturnal paroxysmal dystonia — Nocturnal paroxysmal dystonia or paroxysmal hypnogenic dyskinesia is a name originally given to repeated dystonic or dyskinetic episodes that occurred during or immediately after arousal from non-REM (NREM) sleep, or more rarely, during wakefulness [38-40]. These episodes typically last less than one minute, sometimes up to one hour, and often recur several times per night. The movements are often violent and may result in injury to the patient or bed partner. Patients do not recall the events.

This condition has been reported in children and adults, can be isolated or familial, and is persistent [39,40]. These episodes are often not associated with epileptiform electroencephalography (EEG) activity or other abnormal EEG findings. However, findings of epileptiform activity on zygomatic and sphenoidal leads and response to antiseizure drugs in some patients suggest that this disorder is of epileptic origin, a manifestation of sleep-related hypermotor epilepsy (previously called nocturnal frontal lobe epilepsy) [34,40]. (See "Focal epilepsy: Causes and clinical features", section on 'Frontal lobe epilepsy' and "Sleep-related epilepsy syndromes".)

Periodic limb movements of sleep and restless legs syndrome — Restless legs syndrome (RLS) refers to symptoms of discomfort in the legs that occur at rest and are relieved by movement. RLS is frequently associated with involuntary, jerking movements of the legs during sleep, known as periodic leg movements of sleep (PLMS). The movements are typically characterized by toe extension and flexion at the ankle, knee, and hip and occur at periodic intervals of 20 to 40 seconds, which is unlike an epileptic seizure. PLMS occasionally involve the arms but does not include vocalizations or facial movements. (See "Clinical features and diagnosis of restless legs syndrome and periodic limb movement disorder in adults".)

PLMS usually occur in stage N1 and N2 of NREM sleep, early in the night, in clusters lasting minutes to hours. Patients are usually unaware of the movements, which are often more bothersome to the bed partner. Polysomnography and/or EEG monitoring may aid in the diagnosis. (See "Clinical features and diagnosis of restless legs syndrome and periodic limb movement disorder in adults", section on 'Periodic limb movements of sleep'.)

Sleep-related rhythmic movement disorder — Rhythmic movements such as nocturnal head banging, body rocking, and head rolling typically occur in young children as they try to fall asleep [41]. Episodes usually resolve by five years of age, but can persist into adult life [42,43]. (See "Nonepileptic paroxysmal disorders in children", section on 'Sleep disorders'.)

Sleepwalking and other disorders of arousal — Brief nocturnal arousals occurring during NREM sleep can manifest as confusional arousals, sleepwalking, and night terrors. These conditions are most common in children between 4 and 12 years of age and usually resolve during late adolescence. However, sometimes symptoms persist into adulthood, and up to 15 percent of cases begin in adolescence or adulthood. The emergence of sleepwalking or other disorders of arousal in adults should prompt consideration of common provocative factors, such as sleep deprivation, medications or substances, or a comorbid sleep disorder associated with frequent arousals, such as obstructive sleep apnea. (See "Parasomnias of childhood, including sleepwalking" and "Disorders of arousal from non-rapid eye movement sleep in adults".)

REM sleep behavior disorder — REM sleep behavior disorder (RBD) is characterized by complex movements or behaviors during REM sleep that occur due to a pathologic loss of muscle paralysis (atonia) that normally occurs during REM sleep. The movements often correspond to a dream in which the individual is being chased, threatened, or attacked. Patients typically have partial or complete dream recollection upon awakening.

RBD is most common in older adults in association with alpha-synuclein neurodegenerative disorders including Parkinson disease, multiple system atrophy, and dementia with Lewy bodies. In adolescents and younger adults, RBD is more often associated with a medication (particularly serotonergic antidepressants) or narcolepsy. (See "Rapid eye movement sleep behavior disorder".)

Diagnostic approach — Specific features of the events, including duration, frequency, timing, stereotypy, and vocalizations, can help distinguish nocturnal seizures from sleep disorders (table 3A-C). The Frontal Lobe Epilepsy and Parasomnias (FLEP) Scale is a questionnaire that can help distinguish parasomnias from nocturnal frontal lobe seizures [44]. Recording episodes on video-EEG and polysomnography remains necessary when the diagnosis is unclear [34,39]. (See "Approach to abnormal movements and behaviors during sleep", section on 'Evaluation'.)

MOVEMENT DISORDERS — Hyperkinetic movement disorders or dyskinesias include chorea, dystonia, athetosis, tics, tremors, and ballism. These are described separately. (See "Hyperkinetic movement disorders in children".)

Movement disorders are rarely confused with seizures if the motor activity is classic in appearance and is sustained rather than episodic. Also, impaired consciousness does not occur with movement disorders, and when present, strongly suggests seizures. However, confusion can arise when movement disorders present with episodic symptoms, and when focal epileptic seizures are characterized by isolated dystonic posturing or have continuous symptoms (epilepsia partialis continua). Some patients with dystonia and other movement disorders may obtain symptomatic relief from sensory tricks, such as lightly touching their face to ameliorate cervical dystonia [45]. This phenomenon is known as geste antagoniste and may be a useful feature distinguishing dystonic movements from epilepsy.

Paroxysmal dyskinesia — These paroxysmal movement disorders are rare forms of dystonia that are characterized by episodes of spontaneous or induced dyskinesia with dystonia. (See "Etiology, clinical features, and diagnostic evaluation of dystonia", section on 'Paroxysmal dyskinesia with dystonia'.)

The diagnosis of these disorders is based in large part on history; causes include genetic variants, infections, metabolic derangements, structural brain malformations, and malignancies [46]. A video-electroencephalography (EEG) recording of events is invaluable in difficult cases.

Paroxysmal kinesigenic choreoathetosis, also known as paroxysmal kinesigenic dyskinesia, consists of brief (less than one minute) attacks of choreoathetosis, dystonia, or both, which are precipitated by sudden changes in movement; getting up from a chair and getting out of a car are frequent triggers [47,48]. Movements are often unilateral but may be bilateral. Consciousness is retained. Many individuals may have a brief, nonspecific warning or aura prior to an attack. The interictal examination is normal. The disorder may be a familial, sporadic/idiopathic, or secondary condition (due to multiple sclerosis, stroke, traumatic brain injury). Men are affected more often than women, with an estimated ratio of 3 to 4:1. Carbamazepine or phenytoin is often highly effective [47].

Paroxysmal nonkinesigenic dyskinesia consists of attacks of spontaneous, severe dystonia that may be precipitated by alcohol, caffeine, and stress [49,50]. These episodes last two minutes to several hours, and sometimes two days. Antiseizure medications can be efficacious, but less consistently than in paroxysmal kinesigenic choreoathetosis. Familial, sporadic, and secondary forms have been described.

Paroxysmal exercise-induced dyskinesia consists of brief episodes of dystonia that occur after several minutes of exercise, not at initiation of movement as in paroxysmal kinesigenic choreoathetosis [49,50]. Typically, the part of the body that has been doing the most exercise becomes dystonic. The abnormal movement resolves gradually with cessation of the exercise. This may be a sporadic or hereditary condition. In general, antiseizure drugs are not helpful. Acetazolamide has been effective in some families.

Paroxysmal hypnogenic dyskinesia or nocturnal paroxysmal dystonia consists of dystonic or dyskinetic episodes during or immediately after arousal from non-rapid eye movement (NREM) sleep or, more rarely, during wakefulness. (See 'Nocturnal paroxysmal dystonia' above.)

Tics and stereotypies — Tics are relatively brief, sudden, rapid, and intermittent movements (motor tics) or sounds (vocal tics). They may be repetitive and stereotypic. Tics are usually abrupt in onset and brief (clonic tics) but may be slow and sustained (dystonic tics). Tics are associated with a premonitory feeling that is relieved by performing the tics. Unlike other hyperkinetic dyskinesias and unlike epileptic seizures, tics may be temporarily suppressed. Tics also differ from epilepsy by the variability of the movement and the urge to perform tics. The myoclonic jerks of juvenile myoclonic epilepsy (JME) can be mistaken for tics, but these cannot be suppressed, have no premonitory sensation, and are quicker and more stereotyped [51,52]. (See "Juvenile myoclonic epilepsy", section on 'Seizures'.)

Tics can occur as part of Tourette syndrome, but may also be an isolated phenomenon. More clinical details about the evaluation and treatment of a patient with tics is presented separately. (See "Tourette syndrome: Pathogenesis, clinical features, and diagnosis", section on 'Tics' and "Tourette syndrome: Management", section on 'Approach to management' and "Tourette syndrome: Pathogenesis, clinical features, and diagnosis", section on 'Evaluation and diagnosis'.)

Stereotypies are repetitive, purposeless actions such as head banging, head rolling, body rocking, and hand flapping [53]. Similar to tics, stereotypies may be consciously suppressed and decreased by distraction. Unlike tics, stereotypies are not preceded by a progressive urge or relief following the activities. Often, they manifest as self-stimulating behaviors in response to tension and anxiety and may comfort the patient. Stereotypies may occur alone or may be secondary to trauma, drugs (eg, chronic amphetamine abuse), or toxic-metabolic insult. These movements can be seen in normal individuals, but are more common in those with schizophrenia, mental retardation, and autism. (See "Hyperkinetic movement disorders in children", section on 'Stereotypies'.)

Hemifacial spasm, blepharospasm, and Meige syndrome — Hemifacial spasm is characterized by involuntary synchronous spasms of one side of the face, usually beginning around the eye. They are typically brief, irregular clonic movements but are occasionally tonic. The disorder almost always presents unilaterally, although bilateral involvement may occur in severe cases (less than 5 percent overall) [54]. Brief clonic movements are first noted in the orbicularis oculi and spread over months to years to involve other facial muscles. It never involves muscles other than those innervated by the facial nerve. Patients cannot suppress the movements. Unlike other movement disorders, this can continue during sleep. Onset is most commonly in midlife. Complete remission is rare. Neurovascular compression of the ipsilateral facial nerve is evident in 88 to 93 percent of magnetic resonance imaging studies [55,56]. Botulinum toxin injections are the most effective treatment [57]. (See "Treatment of myoclonus" and "Classification and evaluation of myoclonus", section on 'Anatomic and physiologic classification'.)

Blepharospasm is a focal dystonia characterized by involuntary contractions of the orbicularis oculi muscles, resulting in the bilateral closure of the eyes [58]. This can range from a relatively benign increase in blink frequency to sustained eyelid closure and functional blindness. Onset is gradual and usually occurs in midlife. The etiology of blepharospasm is unknown. (See "Etiology, clinical features, and diagnostic evaluation of dystonia", section on 'Blepharospasm'.)

Meige syndrome or craniocervical dystonia encompasses the dystonic contractions of blepharospasm in addition to spasms of the lower facial muscles, jaw, and neck. Both blepharospasm and Meige syndrome may involve bilateral facial muscle contractions. Most cases have no known etiology. However, these symptoms can be seen as a result of chronic neuroleptic medication.

When unilateral, these conditions can be mistaken for epilepsia partialis continua, and vice versa [59-61]. A routine EEG is usually sufficient for diagnosis.

Stiff-person syndrome — Stiff-person syndrome is characterized by sudden muscle stiffness with superimposed painful cramps. It predominantly affects the axial and proximal limb muscles and is aggravated by emotional, somatosensory, or acoustic stimuli. Startle-induced spasms are common and may be mistaken for stimulus-induced seizures. However, the presence of pain and the sustained spasms with muscle rigidity between spasms are not typical for epilepsy.

Stiff-person syndrome is frequently associated with markedly elevated levels of antibodies against glutamic acid decarboxylase or amphiphysin. Electromyography (EMG) may be helpful in the diagnosis and usually shows continuous low-frequency firing of normal motor action potentials without the ability of voluntary relaxation. EEG is normal.

Stiff person syndrome is reviewed in detail separately. (See "Stiff-person syndrome".)

MIGRAINE — Both migraine and epilepsy are characterized by episodes of neurologic dysfunction that are accompanied by headache, as well as gastrointestinal, autonomic, and psychologic features. Clinical features common to both migraine and epilepsy include:

Headache is a cardinal feature of migraine, but is also a common postictal event, reported in 40 to 45 percent of both pediatric and adult patients with epilepsy [62-70]. This postictal headache often has migrainous features, can last more than a few hours, and occurs after both partial and generalized seizures. At the same time, a third or more of patients with migraine do not have headache with at least some of their migraine events [71]. Sometimes called migraine dissocié, the confidence in making this diagnosis is considerably higher if the patient has previously had similar episodes associated with headaches. (See "Pathophysiology, clinical manifestations, and diagnosis of migraine in adults".)

Visual aura is a feature of classic migraine and occipital epilepsy. In both disorders, simple hallucinations are more common than complex; the images are binocular and often spread or move. Epileptic visual auras tend to include highly colored, circular, or spherical images that move rapidly, are stereotyped, and are relatively brief (a few minutes or less) [63,72,73]. By contrast, migrainous auras are more linear or geometric in appearance, tend to build and spread over several minutes, and last several minutes to an hour. (See "Approach to the patient with visual hallucinations", section on 'Migraine aura' and "Approach to the patient with visual hallucinations", section on 'Seizures'.)

Somatosensory symptoms can occur in both migraine and seizures. As with the visual aura, in migraine, symptoms spread slowly over several minutes to an hour, while in seizures, the symptoms spread quickly and rarely last more than a few minutes. (See "Pathophysiology, clinical manifestations, and diagnosis of migraine in adults", section on 'Migraine aura'.)

Auditory symptoms are a rare manifestation of migraine and epilepsy. In migraine, these are unformed, ringing, clicking, buzzing, humming, hissing, rumbling, or growling noises [74]. In epileptic aura, auditory symptoms range from unformed to complex (eg, voices, music), but again are brief and stereotyped compared with migraine [75]. (See 'Auditory hallucinations' below.)

Motor activity and loss of consciousness during an episode is unusual for migraine and suggests epilepsy. Prolonged confusion or lethargy after an attack favors epilepsy but can occur in some forms of migraine, especially basilar artery migraine. (See "Migraine with brainstem aura".)

HALLUCINATIONS — Hallucinations are the perception of an external sensory stimulus where none exists. These can be somatosensory, visual, auditory, and olfactory. Hallucinations can be part of a seizure aura (see "Focal epilepsy: Causes and clinical features") but can also occur as episodic phenomena in a variety of other conditions. In general, these conditions can be distinguished from each other by the nature of the hallucination and accompanying clinical features.

Somatosensory hallucinations — Somatosensory or haptic hallucinations include external tactile sensations and internal bodily feelings. The former may be described as pain, itching, tingling, and electric shock sensations. Internal feelings include deep pain, nausea and other visceral sensations, and sexual pleasure. Patients may sense that a limb or joint is being moved when it is not.

Visceral hallucinations, such as the feeling of gastric rising, are a common aura in temporal lobe epilepsy. More superficial sensory symptoms of an epileptic aura tend to be lateralized. They may be stationary or they may "march" or spread over several seconds to a few minutes.

Visual hallucinations — Visual hallucinations can be simple (eg, lights, colors, lines, shapes, or geometric designs) or complex (images of people, animals, objects, or a lifelike scene). They may be caused by a wide range of underlying etiologies, including retinal disorders, migraine, epileptic disorders, focal brain lesions, severely impaired vision, neurodegenerative disease, alcohol and drug use, psychiatric illness, and metabolic encephalopathy. These are reviewed in detail separately. (See "Approach to the patient with visual hallucinations", section on 'Etiologies'.)

Visual hallucinations can generally be distinguished by specific clinical features including simple versus complex imagery, monocular versus binocular involvement, triggers, duration, insight, and associated symptoms and signs (table 4). (See "Approach to the patient with visual hallucinations", section on 'Evaluation'.)

Auditory hallucinations — Auditory hallucinations can also arise from injury to any portion of the peripheral and central auditory pathways. As with visual hallucinations, these may be simple and unformed (static, beeping, humming) or may be more complex (voices, music).

Auditory hallucinations are most strongly linked to schizophrenia, for which they are a core symptom, but are also described in patients with Alzheimer disease and patients with epilepsy, as well as in normal individuals [76,77].

Auditory hallucinations are an uncommon manifestation of epilepsy (less than 2 percent of cases) [75,78]. Simple or unformed epileptic auditory auras or auditory distortions (hypacusis or hyperacusis) are often lateralized [79]. Complex, formed auditory hallucinations, such as voices or music, are less common and may be produced by seizures arising from the temporal association or limbic areas. These are often considered psychic rather than auditory, because of associated experiential phenomena (eg, déjà vu) [75,80]. Musical hallucinations most often occur with nondominant hemispheric foci. Prominent auditory hallucinations are a feature of the genetic syndrome, autosomal dominant epilepsy with auditory features (also called familial lateral temporal lobe epilepsy). (See "Focal epilepsy: Causes and clinical features", section on 'Genetic focal epilepsy syndromes'.)

Olfactory hallucinations — Olfactory hallucinations are particularly associated with epilepsy, but can also occur in neurodegenerative disease and in psychiatric conditions. When of epileptic origin, the seizure origin is in the temporal lobe. The hallucination is perceived as intense and foul, but is often otherwise ill described. (See "Focal epilepsy: Causes and clinical features", section on 'Mesial temporal lobe epilepsy'.)

Dysosmia, an altered sense of smell, most often results from a local nasopharyngeal process such as toxin exposure, physical irritant, or medication effect. The abnormal smell perception may occur episodically, when certain airborne aromatic molecules interact with injured receptors. As a result, dysosmia can appear unprovoked, random, and recurrent, and as such, may be reported as an olfactory hallucination [81]. (See "Taste and olfactory disorders in adults: Anatomy and etiology".)

Etiologies

An epileptic aura usually produces hallucinations that involve a single sensory modality or multiple sensory modalities in sequence, rather than simultaneously [80,82]. Olfactory hallucinations may be the best known, but are actually less common than visual, somatosensory, and auditory auras [29,83]. While these hallucinations have some localizing value, they are not reliable in pinpointing the focus of seizure onset. (See "Focal epilepsy: Causes and clinical features".)

In general, epileptic auras are best distinguished from other causes of hallucinations by their paroxysmal onset, brevity (less than two minutes), and stereotyped recurrence. It is also unusual for a hallucination to be the sole manifestation of epilepsy in any given patient; these typically occur as seizure auras, followed by other ictal manifestations [80,82].

Schizophrenia and psychotic depression are usually associated with auditory hallucinations [84]. While other sensory modalities may be involved, auditory hallucinations are usually also present. Distinguishing features of these hallucinations include their personal (often sinister) meaning for the patient, who usually lacks insight as to their unreal nature [85,86]. These hallucinations are less episodic and more prolonged than in other disorders. Patients generally have a clear sensorium (are awake and alert) and manifest other psychotic features (delusions and other abnormal thought content).

Hypnagogic and hypnopompic hallucinations are classically associated with narcolepsy, but are also common in normal individuals who do not manifest other features of this disorder [81]. These are often multimodality hallucinations with congruent visual, auditory, and tactile sensations that are complex and realistic. Insight is usually retained [81,87]. Duration and frequency are variable. The distinguishing feature in these episodes is their invariable occurrence just before falling asleep or just after awakening. (See "Approach to the patient with visual hallucinations", section on 'Narcolepsy'.)

Neurodegenerative disease, particularly dementia with Lewy bodies, but also Parkinson disease, and less often Alzheimer disease, can be associated with hallucinations, usually visual [88]. The visual imagery is typically complex and insight is usually retained. Other manifestations of the disease (eg, parkinsonism, cognitive impairment) are present. Tactile and olfactory hallucinations are less common but have been reported in Parkinson disease [89-91].

Migraine is frequently associated with visual aura. Tactile and, less commonly, auditory hallucinations have also been described in migraine. Characteristic features of migrainous hallucinations include a typical duration of several minutes to an hour or two and that they are usually followed by a headache with typical migrainous features. (See 'Migraine' above.)

Withdrawal states such as delirium tremens and intoxication with amphetamines, cocaine, phencyclidine, chloral hydrate, bupropion, or atropine can be associated with multimodality hallucinations. These states may cause formication, a feeling of ants crawling under the skin, along with complex visual and auditory hallucinations [92]. Patients usually exhibit agitation, confusion, and autonomic activity (tremulousness, tachycardia, diaphoresis). Many other drugs are associated with visual hallucinations (table 5). Isolated auditory hallucinations have been described with salicylates, marijuana, valproate, pentoxifylline, cyproheptadine, beta-blockers, tricyclic antidepressants, and benzodiazepines, usually in the setting of intoxication [74,93]. Sexual hallucinations can occur during or after sedation, especially with newer anesthetic agents such as midazolam and propofol [94].

Delirium may be produced by metabolic abnormalities as well as by drug intoxication or withdrawal and is characterized by a clouded sensorium along with (in order of prevalence) visual, auditory, and tactile hallucinations [95]. (See "Diagnosis of delirium and confusional states" and "Acute toxic-metabolic encephalopathy in adults".)

Focal brain lesions from stroke, multiple sclerosis, and others can produce positive sensory symptoms, usually depending on the represented sensory modality. These are often restricted anatomically. Examples include complex hemifield visual hallucinations with occipital lobe lesions, a pain syndrome with lateral thalamic lesions, and peduncular hallucinosis, a phenomenon characterized by complex visual, tactile, and/or auditory hallucinations with variable retention of insight that is associated with midbrain lesions. (See "Approach to the patient with visual hallucinations", section on 'Peduncular hallucinosis'.)

OTHERS — This topic reviews those imitators of epilepsy that are most common in adolescents and adults. Disorders more prevalent in childhood can occasionally present in this age group as well (table 1). (See "Nonepileptic paroxysmal disorders in children".)

Older adults — In older patients, episodic neurologic symptoms may also represent transient ischemic attack or transient global amnesia, among others. These are discussed separately. (See "Seizures and epilepsy in older adults: Etiology, clinical presentation, and diagnosis".)

SUMMARY

The differential diagnosis of epileptic seizures in adolescents and adults includes a variety of benign, physiologic phenomena as well as pathologic conditions (table 1).

Clinical features of these events help distinguish these from epileptic seizures. In difficult cases, electroencephalography (EEG), particularly video-EEG monitoring, is useful. (See "Video and ambulatory EEG monitoring in the diagnosis of seizures and epilepsy".)

Seizure and syncope are commonly confused as the cause of an isolated or episodic loss of consciousness, especially, but not exclusively, when the episode is not witnessed. A careful history is important in distinguishing syncope from seizure. Key aspects of the history include the clinical setting, warning symptoms, associated symptoms, the quality of motor activity, if present, and the speed of recovery of consciousness. EEG is of limited utility unless an event is captured. (See 'Syncope' above.)

Psychologic disorders that can mimic seizure include psychogenic nonepileptic seizures (PNES), panic attacks, and episodic dyscontrol. (See "Psychogenic nonepileptic seizures: Etiology, clinical features, and diagnosis" and 'Psychological disorders' above.)

Parasomnias, sleep-related movement disorders, and narcolepsy may be confused with epilepsy when events occur at night. Specific features of the events, including duration, frequency, timing, stereotypy, and vocalizations, can help distinguish nocturnal seizures from sleep disorders. (See 'Sleep disorders' above.)

Movement disorders are rarely confused with seizures if the motor activity is classic in appearance and is sustained rather than episodic. Confusion can arise when movement disorders present with episodic symptoms, and when focal epileptic seizures are characterized by isolated dystonic posturing or have continuous symptoms (epilepsia partialis continua). A video-EEG recording of events is invaluable in difficult cases. (See 'Movement disorders' above.)

Migraine and epilepsy share overlapping features. Both are characterized by episodes of neurologic dysfunction that may be accompanied by headache, as well as gastrointestinal, autonomic, and psychologic features. Motor activity and loss of consciousness are unusual for migraine and suggest epilepsy. (See 'Migraine' above.)

Hallucinations can be part of a seizure aura but can also occur as episodic phenomena in a variety of other conditions. In general, these conditions can be distinguished from each other by the nature of the hallucination and accompanying clinical features. (See 'Hallucinations' above.)

  1. Benbadis SR, Allen Hauser W. An estimate of the prevalence of psychogenic non-epileptic seizures. Seizure 2000; 9:280.
  2. Scheepers B, Clough P, Pickles C. The misdiagnosis of epilepsy: findings of a population study. Seizure 1998; 7:403.
  3. Smith D, Defalla BA, Chadwick DW. The misdiagnosis of epilepsy and the management of refractory epilepsy in a specialist clinic. QJM 1999; 92:15.
  4. McDade G, Brown SW. Non-epileptic seizures: management and predictive factors of outcome. Seizure 1992; 1:7.
  5. Gavris MF, Khalighi K, Mascarenhas DA. Idiopathic cardiac asystole presenting as epileptic seizures. J Electrocardiol 2002; 35:279.
  6. Zaidi A, Clough P, Cooper P, et al. Misdiagnosis of epilepsy: many seizure-like attacks have a cardiovascular cause. J Am Coll Cardiol 2000; 36:181.
  7. Sheldon R, Rose S, Ritchie D, et al. Historical criteria that distinguish syncope from seizures. J Am Coll Cardiol 2002; 40:142.
  8. Hoefnagels WA, Padberg GW, Overweg J, Roos RA. Syncope or seizure? A matter of opinion. Clin Neurol Neurosurg 1992; 94:153.
  9. Cooper PN, Westby M, Pitcher DW, Bullock I. Synopsis of the National Institute for Health and Clinical Excellence Guideline for management of transient loss of consciousness. Ann Intern Med 2011; 155:543.
  10. Hadjikoutis S, O'Callaghan P, Smith PE. The investigation of syncope. Seizure 2004; 13:537.
  11. McKeon A, Vaughan C, Delanty N. Seizure versus syncope. Lancet Neurol 2006; 5:171.
  12. Aminoff MJ, Scheinman MM, Griffin JC, Herre JM. Electrocerebral accompaniments of syncope associated with malignant ventricular arrhythmias. Ann Intern Med 1988; 108:791.
  13. Akor F, Liu NM, Besag FM, Ahmed MA. Value of tongue biting in differentiating between epileptic seizures and syncope. Seizure 2013; 22:328.
  14. Brigo F, Bongiovanni LG, Nardone R. Lateral tongue biting versus biting at the tip of the tongue in differentiating between epileptic seizures and syncope. Seizure 2013; 22:801.
  15. Rodrigues Tda R, Sternick EB, Moreira Mda C. Epilepsy or syncope? An analysis of 55 consecutive patients with loss of consciousness, convulsions, falls, and no EEG abnormalities. Pacing Clin Electrophysiol 2010; 33:804.
  16. Passman R, Horvath G, Thomas J, et al. Clinical spectrum and prevalence of neurologic events provoked by tilt table testing. Arch Intern Med 2003; 163:1945.
  17. Lin JT, Ziegler DK, Lai CW, Bayer W. Convulsive syncope in blood donors. Ann Neurol 1982; 11:525.
  18. Lempert T, Bauer M, Schmidt D. Syncope: a videometric analysis of 56 episodes of transient cerebral hypoxia. Ann Neurol 1994; 36:233.
  19. Brenner RP. Electroencephalography in syncope. J Clin Neurophysiol 1997; 14:197.
  20. Britton JW, Benarroch E. Seizures and syncope: anatomic basis and diagnostic considerations. Clin Auton Res 2006; 16:18.
  21. Rossetti AO, Dworetzky BA, Madsen JR, et al. Ictal asystole with convulsive syncope mimicking secondary generalisation: a depth electrode study. J Neurol Neurosurg Psychiatry 2005; 76:885.
  22. Britton JW, Ghearing GR, Benarroch EE, Cascino GD. The ictal bradycardia syndrome: localization and lateralization. Epilepsia 2006; 47:737.
  23. North KN, Ouvrier RA, Nugent M. Pseudoseizures caused by hyperventilation resembling absence epilepsy. J Child Neurol 1990; 5:288.
  24. David JE, Yale SH, Vidaillet HJ. Hyperventilation-induced syncope: no need to panic. Clin Med Res 2003; 1:137.
  25. Saedon NI, Pin Tan M, Frith J. The Prevalence of Orthostatic Hypotension: A Systematic Review and Meta-Analysis. J Gerontol A Biol Sci Med Sci 2020; 75:117.
  26. Eirís-Puñal J, Rodríguez-Núñez A, Fernández-Martínez N, et al. Usefulness of the head-upright tilt test for distinguishing syncope and epilepsy in children. Epilepsia 2001; 42:709.
  27. Benbadis SR, Agrawal V, Tatum WO 4th. How many patients with psychogenic nonepileptic seizures also have epilepsy? Neurology 2001; 57:915.
  28. Chiesa V, Gardella E, Tassi L, et al. Age-related gender differences in reporting ictal fear: analysis of case histories and review of the literature. Epilepsia 2007; 48:2361.
  29. Johanson M, Valli K, Revonsuo A, Wedlund JE. Content analysis of subjective experiences in partial epileptic seizures. Epilepsy Behav 2008; 12:170.
  30. Coccaro EF, Posternak MA, Zimmerman M. Prevalence and features of intermittent explosive disorder in a clinical setting. J Clin Psychiatry 2005; 66:1221.
  31. McTague A, Appleton R. Episodic dyscontrol syndrome. Arch Dis Child 2010; 95:841.
  32. Drake ME Jr, Hietter SA, Pakalnis A. EEG and evoked potentials in episodic-dyscontrol syndrome. Neuropsychobiology 1992; 26:125.
  33. Poceta JS, Mitler MM. Sleep disorders: Diagnosis and treatment, Humana Press, Totowa, New Jersey 1998.
  34. Malow BA. Sleep and epilepsy. Neurol Clin 2005; 23:1127.
  35. Macleod S, Ferrie C, Zuberi SM. Symptoms of narcolepsy in children misinterpreted as epilepsy. Epileptic Disord 2005; 7:13.
  36. Mihaescu M, Malow BA. Sleep disorders: a sometimes forgotten cause of nonepileptic spells. Epilepsy Behav 2003; 4:784.
  37. Galimberti CA, Ossola M, Colnaghi S, Arbasino C. Focal epileptic seizures mimicking sleep paralysis. Epilepsy Behav 2009; 14:562.
  38. Lugaresi E, Cirignotta F. Hypnogenic paroxysmal dystonia: epileptic seizure or a new syndrome? Sleep 1981; 4:129.
  39. Derry CP, Duncan JS, Berkovic SF. Paroxysmal motor disorders of sleep: the clinical spectrum and differentiation from epilepsy. Epilepsia 2006; 47:1775.
  40. Provini F, Plazzi G, Lugaresi E. From nocturnal paroxysmal dystonia to nocturnal frontal lobe epilepsy. Clin Neurophysiol 2000; 111 Suppl 2:S2.
  41. Walters AS. Clinical identification of the simple sleep-related movement disorders. Chest 2007; 131:1260.
  42. Anderson KN, Smith IE, Shneerson JM. Rhythmic movement disorder (head banging) in an adult during rapid eye movement sleep. Mov Disord 2006; 21:866.
  43. Hashizume Y, Yoshijima H, Uchimura N, Maeda H. Case of head banging that continued to adolescence. Psychiatry Clin Neurosci 2002; 56:255.
  44. Derry CP, Davey M, Johns M, et al. Distinguishing sleep disorders from seizures: diagnosing bumps in the night. Arch Neurol 2006; 63:705.
  45. Müller J, Wissel J, Masuhr F, et al. Clinical characteristics of the geste antagoniste in cervical dystonia. J Neurol 2001; 248:478.
  46. McGuire S, Chanchani S, Khurana DS. Paroxysmal Dyskinesias. Semin Pediatr Neurol 2018; 25:75.
  47. Bruno MK, Hallett M, Gwinn-Hardy K, et al. Clinical evaluation of idiopathic paroxysmal kinesigenic dyskinesia: new diagnostic criteria. Neurology 2004; 63:2280.
  48. Lotze T, Jankovic J. Paroxysmal kinesigenic dyskinesias. Semin Pediatr Neurol 2003; 10:68.
  49. Demirkiran M, Jankovic J. Paroxysmal dyskinesias: clinical features and classification. Ann Neurol 1995; 38:571.
  50. Bhatia KP. The paroxysmal dyskinesias. J Neurol 1999; 246:149.
  51. Sethi NK, Labar D, Torgovnick J. Myoclonic epilepsy masquerading as a tic disorder. Clin Neurol Neurosurg 2007; 109:509.
  52. Robakis D. How Much Do We Know about Adult-onset Primary Tics? Prevalence, Epidemiology, and Clinical Features. Tremor Other Hyperkinet Mov (N Y) 2017; 7:441.
  53. Katherine M. Stereotypic Movement Disorders. Semin Pediatr Neurol 2018; 25:19.
  54. Tan NC, Chan LL, Tan EK. Hemifacial spasm and involuntary facial movements. QJM 2002; 95:493.
  55. Port JD. Advanced magnetic resonance imaging techniques for patients with hemifacial spasm. Ophthal Plast Reconstr Surg 2002; 18:72.
  56. Chen SR. Neurological Imaging for Hemifacial Spasm. Int Ophthalmol Clin 2018; 58:97.
  57. Green KE, Rastall D, Eggenberger E. Treatment of Blepharospasm/Hemifacial Spasm. Curr Treat Options Neurol 2017; 19:41.
  58. Hallett M. Blepharospasm: recent advances. Neurology 2002; 59:1306.
  59. Towfigh A, Mostofi N, Motamedi GK. Poststroke partial seizures presenting as hemifacial spasm. Mov Disord 2007; 22:1981.
  60. Arzimanoglou AA, Salefranque F, Goutières F, Aicardi J. Hemifacial spasm or subcortical epilepsy? Epileptic Disord 1999; 1:121.
  61. Espay AJ, Schmithorst VJ, Szaflarski JP. Chronic isolated hemifacial spasm as a manifestation of epilepsia partialis continua. Epilepsy Behav 2008; 12:332.
  62. Syvertsen M, Helde G, Stovner LJ, Brodtkorb E. Headaches add to the burden of epilepsy. J Headache Pain 2007; 8:224.
  63. Menon B. Symptomatic occipital epilepsy misdiagnosed as migraine. Headache 2007; 47:287.
  64. Ito M, Adachi N, Nakamura F, et al. Characteristics of postictal headache in patients with partial epilepsy. Cephalalgia 2004; 24:23.
  65. Leniger T, Isbruch K, von den Driesch S, et al. Seizure-associated headache in epilepsy. Epilepsia 2001; 42:1176.
  66. Yankovsky AE, Andermann F, Bernasconi A. Characteristics of headache associated with intractable partial epilepsy. Epilepsia 2005; 46:1241.
  67. Förderreuther S, Henkel A, Noachtar S, Straube A. Headache associated with epileptic seizures: epidemiology and clinical characteristics. Headache 2002; 42:649.
  68. Cai S, Hamiwka LD, Wirrell EC. Peri-ictal headache in children: prevalence and character. Pediatr Neurol 2008; 39:91.
  69. Fanella M, Fattouch J, Casciato S, et al. Ictal epileptic headache as "subtle" symptom in generalized idiopathic epilepsy. Epilepsia 2012; 53:e67.
  70. Bauer PR, Tolner EA, Keezer MR, et al. Headache in people with epilepsy. Nat Rev Neurol 2021; 17:529.
  71. Russell MB, Olesen J. A nosographic analysis of the migraine aura in a general population. Brain 1996; 119 ( Pt 2):355.
  72. Panayiotopoulos CP. Elementary visual hallucinations, blindness, and headache in idiopathic occipital epilepsy: differentiation from migraine. J Neurol Neurosurg Psychiatry 1999; 66:536.
  73. Panayiotopoulos CP. Visual phenomena and headache in occipital epilepsy: a review, a systematic study and differentiation from migraine. Epileptic Disord 1999; 1:205.
  74. Rubin D, McAbee GN, Feldman-Winter LB. Auditory hallucinations associated with migraine. Headache 2002; 42:646.
  75. Florindo I, Bisulli F, Pittau F, et al. Lateralizing value of the auditory aura in partial seizures. Epilepsia 2006; 47 Suppl 5:68.
  76. Korsnes MS, Hugdahl K, Nygård M, Bjørnaes H. An fMRI study of auditory hallucinations in patients with epilepsy. Epilepsia 2010; 51:610.
  77. Krabbendam L, van Os J. Schizophrenia and urbanicity: a major environmental influence--conditional on genetic risk. Schizophr Bull 2005; 31:795.
  78. Bianchi MT, Dworetzky BA, Bromfield EB. Auditory auras in patients with postencephalitic epilepsy: case series. Epilepsy Behav 2009; 14:250.
  79. Hurst RW, Lee SI. Ictal tinnitus. Epilepsia 1986; 27:769.
  80. Bisulli F, Tinuper P, Avoni P, et al. Idiopathic partial epilepsy with auditory features (IPEAF): a clinical and genetic study of 53 sporadic cases. Brain 2004; 127:1343.
  81. Ohayon MM. Prevalence of hallucinations and their pathological associations in the general population. Psychiatry Res 2000; 97:153.
  82. Widdess-Walsh P, Kotagal P, Jeha L, et al. Multiple auras: clinical significance and pathophysiology. Neurology 2007; 69:755.
  83. Lennox WG, Cobb S. Aura in epilepsy: a statistical review of 1359 cases. Arch Neurol Psychiatry 1933; 30:374.
  84. Shergill SS, Cameron LA, Brammer MJ, et al. Modality specific neural correlates of auditory and somatic hallucinations. J Neurol Neurosurg Psychiatry 2001; 71:688.
  85. Honig A, Romme MA, Ensink BJ, et al. Auditory hallucinations: a comparison between patients and nonpatients. J Nerv Ment Dis 1998; 186:646.
  86. Choong C, Hunter MD, Woodruff PW. Auditory hallucinations in those populations that do not suffer from schizophrenia. Curr Psychiatry Rep 2007; 9:206.
  87. Dauvilliers Y, Billiard M, Montplaisir J. Clinical aspects and pathophysiology of narcolepsy. Clin Neurophysiol 2003; 114:2000.
  88. Assal F, Cummings JL. Neuropsychiatric symptoms in the dementias. Curr Opin Neurol 2002; 15:445.
  89. Fénelon G, Thobois S, Bonnet AM, et al. Tactile hallucinations in Parkinson's disease. J Neurol 2002; 249:1699.
  90. Tousi B, Frankel M. Olfactory and visual hallucinations in Parkinson's disease. Parkinsonism Relat Disord 2004; 10:253.
  91. Bannier S, Berdagué JL, Rieu I, et al. Prevalence and phenomenology of olfactory hallucinations in Parkinson's disease. J Neurol Neurosurg Psychiatry 2012; 83:1019.
  92. Brady KT, Lydiard RB, Malcolm R, Ballenger JC. Cocaine-induced psychosis. J Clin Psychiatry 1991; 52:509.
  93. Evers S, Ellger T. The clinical spectrum of musical hallucinations. J Neurol Sci 2004; 227:55.
  94. Balasubramaniam B, Park GR. Sexual hallucinations during and after sedation and anaesthesia. Anaesthesia 2003; 58:549.
  95. Webster R, Holroyd S. Prevalence of psychotic symptoms in delirium. Psychosomatics 2000; 41:519.
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References