Benign centrotemporal lobe epilepsy of childhood or benign Rolandic epilepsy is an idiopathic localization-related epilepsy that occurs in children between the ages of 3 and 13 years, with peak onset in prepubertal late childhood. Apart from their seizure disorder, these patients are otherwise normal. This syndrome features simple focal seizures that involve facial muscles and frequently cause drooling. Although most episodes are brief, seizures sometimes spread and generalize. Seizures are typically nocturnal and confined to sleep. The EEG may demonstrate spike discharges that occur over the centrotemporal scalp over the central sulcus of the brain (the Rolandic sulcus) that are predisposed to occur during drowsiness or light sleep. Seizures cease near puberty. Seizures may require anticonvulsant treatment, but sometimes are infrequent enough to allow physicians to defer treatment.

Benign occipital epilepsy of childhood (BOEC) is an idiopathic localization-related epilepsy and consists of an evolving group of syndromes. Most authorities include two subtypes, an early subtype with onset between three and five years, and a late onset between seven and 10 years. Seizures in BOEC usually feature visual symptoms such as scotoma or fortifications (brightly colored spots or lines) or amaurosis (blindness or impairment of vision). Convulsions involving one half the body, hemiconvulsions, or forced eye deviation or head turning are common. Younger patients typically experience symptoms similar to migraine with nausea and headache, and older patients typically complain of more visual symptoms. The EEG in BOEC shows spikes recorded from the occipital (back of head) regions. The EEG and genetic pattern suggest an autosomal dominant transmission as described by Ruben Kuzniecky, et al. Lately, a group of epilepsies termed Panayiotopoulos syndrome that share some clinical features of BOEC but have a wider variety of EEG findings are classified by some as BOEC.

Seizures are purely occipital and primarily manifest with elementary visual hallucinations, blindness or both.

They are usually frequent and diurnal, develop rapidly within seconds and are brief, lasting from a few seconds to 1–3 min, and, rarely, longer.

Elementary visual hallucinations are the most common and characteristic ictal symptoms, and are most likely to be the first and often the only clinical manifestation. They consist mainly of small multicoloured circular patterns that often appear in the periphery of a visual field, becoming larger and multiplying during the course of the seizure, frequently moving horizontally towards the other side.

Other occipital symptoms, such as sensory illusions of ocular movements and ocular pain, tonic deviation of the eyes, eyelid fluttering or repetitive eye closures, may occur at the onset of the seizures or appear after the elementary visual hallucinations. "Deviation of the eyes", often associated with ipsilateral turning of the head, is the most common (in about 70% of cases) nonvisual ictal symptom. It is often associated with ipsilateral turning of the head and usually starts after visual hallucinations, although it may also occur while the hallucinations still persist. It may be mild, but more often it is severe and progresses to hemiconvulsions and secondarily generalised tonic clonic seizures (GTCS). Some children may have seizures of eye deviation from the start without visual hallucinations.

"Forced eyelid closure and eyelid blinking" occur in about 10% of patients, usually at a stage at which consciousness is impaired. They signal an impending secondarily GTCS.

"Ictal blindness", appearing from the start or, less commonly, after other manifestations of occipital seizures, usually lasts for 3–5 min. It can occur alone and be the only ictal event in patients who could, at other times, have visual hallucinations without blindness.

Complex visual hallucinations, visual illusions and other symptoms resulting from more anterior ictal spreading rarely occur from the start. They may terminate in hemiconvulsions or generalised convulsions.

Ictal headache, or mainly orbital pain, may occur and often precedes visual or other ictal occipital symptoms in a small number of patients.

Consciousness is not impaired during the visual symptoms (simple focal seizures), but may be disturbed or lost in the course of the seizure, usually before eye deviation or convulsions.

Occipital seizures of ICOE-G may rarely progress to extra-occipital manifestations, such as hemiparaesthesia. Spread to produce symptoms of temporal lobe involvement is exceptional and may indicate a symptomatic cause.

Post-ictal headache, mainly diffuse, but also severe, unilateral and pulsating, or indistinguishable from migraine headache, occurs in half the patients, in 10% of whom it may be associated with nausea and vomiting.

Circadian distribution: Visual seizures are predominantly diurnal and can occur at any time of the day. Longer seizures, with or without hemi or generalised convulsions, tend to occur either during sleep, causing the patient to wake up, or after awakening. Thus, some children may have numerous diurnal visual seizures and only a few seizures that are exclusively nocturnal or occur on awakening.

Frequency of seizures: If untreated, patients experience frequent and brief visual seizures (often several every day or weekly). However, propagation to other seizure manifestations, such as focal or generalised convulsions, is much less frequent.

The cardinal features of Rolandic epilepsy are infrequent, often single, focal seizures consisting of:

Hemifacial sensorimotor seizures are often entirely localised in the lower lip or spread to the ipsilateral hand. Motor manifestations are sudden, continuous or bursts of clonic contractions, usually lasting from a few seconds to a minute. Ipsilateral tonic deviation of the mouth is also common. Hemifacial sensory symptoms consist of unilateral numbness mainly in the corner of the mouth.

Hemifacial seizures are often associated with an inability to speak and hypersalivation:

"The left side of my mouth felt numb and started jerking and pulling to the left, and I could not speak to say what was happening to me."

Negative myoclonus can be observed in some cases, as an interruption of tonic muscular activity

Oropharyngolaryngeal ictal manifestations are unilateral sensorimotor symptoms inside the mouth. Numbness, and more commonly paraesthesias (tingling, prickling, freezing), are usually diffuse on one side or, exceptionally, may be highly localised even to one tooth. Motor oropharyngolaryngeal symptoms produce strange sounds, such as death rattle, gargling, grunting and guttural sounds, and combinations:

"In his sleep, he was making guttural noises, with his mouth pulled to the right, ‘as if he was chewing his tongue’". "We heard her making strange noises ‘like roaring’ and found her unresponsive, head raised from the pillow, eyes wide open, rivers of saliva coming out of her mouth, rigid."

Arrest of speech is a form of anarthria. The child is unable to utter a single intelligible word and attempts to communicate with gestures.

"My mouth opened and I could not speak. I wanted to say I cannot speak. At the same time, it was as if somebody was strangling me."

Hypersalivation , a prominent autonomic manifestation, is often associated with hemifacial seizures, oro-pharyngo-laryngeal symptoms and speech arrest. Hypersalivation is not just frothing:

"Suddenly my mouth is full of saliva, it runs out like a river and I cannot speak."

Syncope-like epileptic seizures may occur, probably as a concurrent symptom of Panayiotopoulos syndrome:

"She lies there, unconscious with no movements, no convulsions, like a wax work, no life."

Consciousness and recollection are fully retained in more than half (58%) of Rolandic seizures.

"I felt that air was forced into my mouth, I could not speak and I could not close my mouth. I could understand well everything said to me. Other times I feel that there is food in my mouth and there is also a lot of salivation. I cannot speak."

In the remainder (42%), consciousness becomes impaired during the ictal progress and in one third there is no recollection of ictal events.

Progression to hemiconvulsions or generalised tonic–clonic seizures occurs in around half of children and hemiconvulsions may be followed by postictal Todd’s hemiparesis .

Duration and circadian distribution: Rolandic seizures are usually brief, lasting for 1–3 min. Three quarters of seizures occur during nonrapid eye movement sleep, mainly at sleep onset or just before awakening.

Status epilepticus: Although rare, focal motor status or hemiconvulsive status epilepticus is more likely to occur than secondarily generalised convulsive status epilepticus, which is exceptional. Opercular status epilepticus usually occurs in children with atypical evolution or may be induced by carbamazepine or lamotrigine. This state lasts for hours to months and consists of ongoing unilateral or bilateral contractions of the mouth, tongue or eyelids, positive or negative subtle perioral or other myoclonus, dysarthria, speech arrest, difficulties in swallowing, buccofacial apraxia and hypersalivation. These are often associated with continuous spikes and waves on an EEG during NREM sleep.

Other seizure types: Despite prominent hypersalivation, focal seizures with primarily autonomic manifestations (autonomic seizures) are not considered part of the core clinical syndrome of Rolandic epilepsy. However, some children may present with independent autonomic seizures or seizures with mixed Rolandic-autonomic manifestations including emesis as in Panayiotopoulos syndrome.

Atypical forms: Rolandic epilepsy may present with atypical manifestations such early age at onset, developmental delay or learning difficulties at inclusion, other seizure types, atypical EEG abnormalities.

These children usually have normal intelligence and development. Learning can remain unimpaired while a child is afflicted with Rolandic epilepsy.

"Focal aware" means that the level of consciousness is not altered during the seizure. In temporal lobe epilepsy, a focal seizure usually causes abnormal sensations only.

These may be:

- Sensations such as déjà vu (a feeling of familiarity), jamais vu (a feeling of unfamiliarity)

- Amnesia; or a single memory or set of memories

- A sudden sense of unprovoked fear and anxiety

- Nausea

- Auditory, visual, olfactory, gustatory, or tactile hallucinations.

- Visual distortions such as macropsia and micropsia

- Dissociation or derealisation

- Synesthesia (stimulation of one sense experienced in a second sense) may transpire.

- Dysphoric or euphoric feelings, fear, anger, and other emotions may also occur. Often, the patient cannot describe the sensations.

Olfactory hallucinations often seem indescribable to patients beyond "pleasant" or "unpleasant".

Focal aware seizures are often called "auras" when they serve as a warning sign of a subsequent seizure. Regardless an "aura" is actually a seizure itself, and such a focal seizure may or may not progress to a focal impaired awareness seizure. People who only experience focal aware seizures may not recognize what they are, nor seek medical care.

The most common symptom of abdominal epilepsy is abdominal pain followed by uncontrollable vomiting, usually preceded by lethargy. Symptoms also include generalized tonic-clonic seizures followed by sleep, confusion, and unresponsiveness.

Other medical conditions with similar symptoms include panic attacks, psychosis spectrum disorders, tardive dyskinesia, and occipital lobe epilepsy.

Epileptic symptoms are frequently the product of the spread of overactivation occurring within one central foci that travels to lateral brain regions thereby causing an array of symptoms. Due to the massive amount of diversity in both the cognitive and motor functions that occur within the frontal lobes, there is an immense variety in the types of symptoms that can arise from epileptic seizures based on the side and topography of the focal origin. In general these symptoms can range anywhere from asymmetric and abnormal body positioning to repetitive vocal outbursts and repetitive jerking movements. The symptoms typically come in short bursts that last less than a minute and often occur while a patient is sleeping. In most cases, a patient will experience a physical or emotional Aura of tingling, numbness or tension prior to a seizure occurring. Fear is associated with temporal and frontal lobe epilepsies, but in FLE the fear is predominantly expressed on the person's face whereas in TLE the fear is subjective and internal, not perceptible to the observer.

Tonic posture and clonic movements are common symptoms among most of the areas of the frontal lobe, therefore the type of seizures associated with frontal lobe epilepsy are commonly called tonic-clonic seizures. Dystonic motor movements are common to both TLE and FLE, but are usually the first symptom in FLE episodes where they are quite brief and do not affect consciousness. The seizures are complex partial, simple partial, secondarily generalized or a combination of the three. These partial seizures are often misdiagnosed as psychogenic seizures. A wide range of more specific symptoms arise when different parts of the frontal cortex are affected.

- Supplementary motor area (SMA)

- The onset and relief of the seizure are quite abrupt.

- The tonic posturing in this area is unilateral or asymmetric between the left and right hemispheres. A somatosensory aura frequently precedes many large motor and vocal symptoms and most often the afflicted person is responsive.

- "Motor symptoms": Facial grimacing and complex automatisms like kicking and pelvic thrusting

- "Vocal symptoms": Laughing, yelling, or speech arrest.

- Primary motor cortex

- The primary motor cortex has jacksonian seizures that spread to adjacent areas of the lobe which often trigger a second round of seizures originating in another cortical area. The seizures are much simpler than those that originate in the SMA and are usually clonic or myoclonic movements with speech arrest. Some dystonic or contralateral adversive posturing may also be present.

- Medial frontal, cingulate gyrus, orbitofrontal, or frontopolar regions

- Motor symptoms of seizures in this area are accompanied by emotional feelings and viscerosensory symptoms. Motor and vocal agitation are similar to that of the SMA with short repetitive thrashing, pedaling, thrusting, laughing, screaming and/or crying.

- This is some of what can cause the misdiagnosis of a psychological disorder.

- Dorsolateral cortex

- This area does not seem to have many motor symptoms beyond tonic posturing or clonic movements. Contralateral or less commonly ipsilateral head turn and eye deviation are commonly associated with this area as well.

- Operculum

- Many of the symptoms associated with this area involve the head and digestive tract: swallowing, salivation, mastication and possibly gustatory hallucinations. Preceding the seizure the person is fearful and often has an epigastric aura. There is not much physical movement except clonic facial movements. Speech is often arrested.

The signs of vertiginous epilepsy often occur without a change in the subject’s consciousness so that they are still aware while experiencing the symptoms. It is often described as a sudden onset of feeling like one is turning in one direction, typically lasting several seconds. Although subjects are aware during an episode, they often cannot remember specific details due to disorientation, discomfort, and/or partial cognitive impairment. This sensation of rotational movement in the visual and auditory planes is also known as a vertiginous aura (symptom), which can precede a seizure or may constitute a seizure itself. Auras are a “portion of the seizure that occur before consciousness is lost and for which memory is retained afterwards.” Auras can be focused in different regions of the brain and can thus affect different functions. Some such symptoms that may accompany vertiginous epilepsy include:

- Auditory hallucination

- Cognitive impairment

- Motor activity

- Ictal behavior

- Limbic auras

Many people tend to mistake dizziness as vertigo, and although they sound similar, dizziness is not considered a symptom of vertiginous epilepsy. Dizziness is the sensation of imbalance or floating, impending loss of consciousness, and/or confusion. This is different from vertigo which is characterized by the illusion of rotational movement caused by the “conflict between the signals sent to the brain by balance- and position-sensing systems of the body”.

Northern Epilepsy Syndrome causes recurrent seizures between the ages of five to ten. These seizures, that may last up to 15 minutes, can be classified mostly as tonic-clonic, but partial seizures could also occur. The seizures commonly involve muscle rigidity, convulsions, and loss of consciousness. Generally, the recurrence is one to two times per month.

In the years following the onset of seizures, a noticeable decrease in intellectual capacity is observed.

Prognosis is generally good, and seizures usually respond to classic antiepileptics Resection of pathological tissue has been used successfully to treat occipital lobe epilepsy.

During puberty, seizure frequency increases to one to two times per week. Mental function has a rapid decline, as observed by a lack of coordination, failure to complete education, and fine motor activities. In rare cases, some suffered from loss of vision.

There may be an increased family history of epilepsies (37% of cases) or migraine (16% of cases) but a family history of similar seizures is exceptional.

Episodes that include complex hyperactivity of the proximal portions of the limbs that lead to increased overall motor activity are called hypermotor seizures. When associated with bizarre movements and vocalizations these seizures are often misdiagnosed as pseudoseizures or other episodic movement disorders such as psychogenic movement disorders, familial paroxysmal dystonic choreoathetosis, paroxysmal kinesogenic choreoathetosis, or episodic ataxia type 1. Hypermotor seizure in children are often confused with pavor nocturnus (night terrors). Paroxysmal nocturnal dystonia or hypnogenic paroxysmal dystonia are other names given to describe FLE symptoms but are simply just FLE.

Autosomal Dominant Nocturnal Frontal Lobe Epilepsy (ADNFLE) is the best understood form of frontal lobe epilepsy but is often misdiagnosed as sleep apnea. Both disorders are characterized by awakening during the night which leads to daytime sleepiness. Some symptoms of sleep apnea overlap with those of ADNFLE, such as sudden awakening accompanied by a feeling of choking and on occasion motor activity which makes diagnosis difficult based on symptoms alone. Video surveillance as well as EEG is occasionally needed to differentiate between the two disorders. It has been reported that sleep apnea might be associated with epilepsy which would account for some of the misdiagnoses.

Focal aware seizures are seizures which affect only a small region of the brain, often the temporal lobes or structures found there such as the hippocampi. People who have focal aware seizures remain conscious. Focal aware seizures often precede larger focal impaired awareness seizures, where the abnormal electrical activity spreads to a larger area of the brain. This can result in a tonic-clonic seizure.

- Presentation

Focal onset aware seizures are a very subjective experience, and the symptoms vary greatly between people. This is due to the varying locations of the brain the seizures originate in e.g.: Rolandic. A focal aware seizure may go unnoticed by others or shrugged off by the sufferer as merely a "funny turn." Focal aware seizures usually start suddenly and are very brief, typically lasting 60 to 120 seconds.

Some common symptoms of a focal onset aware seizure, when the person is awake, are:

- preserved consciousness

- sudden and inexplicable feelings of fear, anger, sadness, happiness or nausea

- sensations of falling or movement

- experiencing of unusual feelings or sensations

- altered sense of hearing, smelling, tasting, seeing, and tactile perception (sensory illusions or hallucinations), or feeling as though the environment is not real (derealization) or dissociation from the environment or self (depersonalization)

- a sense of spatial distortion—things close by may appear to be at a distance

- déjà vu (familiarity) or jamais vu (unfamiliarity)

- laboured speech or inability to speak at all

- usually the event is remembered in detail

When the seizure occurs during sleep, the person will often become semi-conscious and act out a dream they were having while engaging with the real environment as normal. Objects and people usually appear normal or only slightly distorted to them, and will be able to communicate with them on an otherwise normal level.

However, since the person is still acting in the dream-like state from which they woke, they will assimilate any hallucinations or delusions into their communication, often speaking to a hallucinatory person or speaking of events or thoughts normally pertaining to the dream they were having or other hallucination.

While asleep symptoms include:

- onset usually in REM sleep

- dream like state

- appearance of full consciousness

- hallucinations or delusions

- behavior or visions typical in dreams

- ability to engage with the environment and other people as in full consciousness, though often behaving abnormally, erratically, or failing to be coherent

- complete amnesia or assimilating the memory as though it was a normal dream on regaining full consciousness

Although hallucinations may occur during focal aware seizures they are differentiated from psychotic symptoms by the fact that the person is usually aware that the hallucinations are not real.

- Jacksonian march

Jacksonian march or Jacksonian seizure is a phenomenon where a focal aware seizure spreads from the distal part of the limb toward the face (on same side of body). They involve a progression of the location of the seizure in the brain, which leads to a "march" of the motor presentation of symptoms.

Jacksonian seizures are initiated with abnormal electrical activity within the primary motor cortex. They are unique in that they travel through the primary motor cortex in succession, affecting the corresponding muscles, often beginning with the fingers. This is felt as a tingling sensation, or a feeling of waves through the fingers when touched together. It then affects the hand and moves on to more proximal areas on the same side of body. Symptoms often associated with a Jacksonian seizure are sudden head and eye movements, tingling, numbness, smacking of the lips, and sudden muscle contractions. Most of the time any one of these actions can be seen as normal movements, without being associated with the seizure occurring. They occur at no particular moment and last only briefly. They may result in secondary generalized seizure involving both hemispheres. They can also start at the feet, manifesting as tingling or pins and needles, and there are painful cramps in the foot muscles, due to the signals from the brain. Because it is a partial seizure, the postictal state is of normal consciousness .

A focal impaired awareness seizure is a seizure that is associated with unilateral cerebral hemisphere involvement and causes impairment of awareness or responsiveness, i.e. alteration of consciousness.

- Presentation

Focal impaired awareness seizures are often preceded by an aura. The seizure aura is a focal aware seizure. The aura may manifest itself as a feeling of déjà vu, jamais vu, fear, euphoria or depersonalization. The aura might also occur as a visual disturbance, such as tunnel vision or a change in the perceived size of objects. Once consciousness is impaired, the person may display automatisms such as lip smacking, chewing or swallowing. There may also be loss of memory (amnesia) surrounding the seizural event. The person may still be able to perform routine tasks such as walking, although such movements are not purposeful or planned. Witnesses may not recognize that anything is wrong.

Focal impaired awareness seizures might arise from any lobe of the brain. They most commonly arise from the temporal lobe, particularly the amygdala, hippocampus, and neocortical regions. A common associated brain abnormality is mesial temporal sclerosis. Mesial temporal sclerosis is a specific pattern of hippocampal neuronal loss accompanied by hippocampal gliosis and atrophy. Focal onset impaired awareness seizures occur when excessive and synchronous electrical brain activity causes the impaired awareness and responsiveness. The abnormal electrical activity might spread to the rest of the brain and cause a "focal to bilateral seizure" or a generalized tonic–clonic seizure. The newer classification of 2017 groups only focal and generalized seizures, and generalised seizures are those that involve both sides of the brain from the onset.

Benign Rolandic epilepsy or benign childhood epilepsy with centrotemporal spikes (BCECTS) is the most common epilepsy syndrome in childhood. Most children will outgrow the syndrome (it starts around the age of 3-13 with a peak around 8–9 years and stops around age 14-18), hence the label benign. The seizures, sometimes referred to as "sylvian seizures", start around the central sulcus of the brain (also called the centrotemporal area, located around the Rolandic fissure, after Luigi Rolando).

The most frequently reported symptoms are elementary "visual hallucinations" characterized by basic irritations to perception of sight. Scotomas and aumarosis also occur and are predictors of poor medication response Hallucinations may be described as flashing small circular patterns or zigzags. Vomiting or temporary blindness may occur and visual seizures may be followed by a headache leading to a frequent misdiagnosis as migraine. Seizures may become generalized.

Abdominal epilepsy, also known as autonomic epilepsy, is a rare condition most frequently found in children, consisting of gastrointestinal (GI) disturbances caused by epileptiform seizure activity.

It has been described as a type of temporal lobe epilepsy. Responsiveness to anticonvulsants can aid in the diagnosis.

Most published medical literature dealing with abdominal epilepsy is in the form of individual case reports. A 2005 review article found a total of 36 cases described in the medical literature.

Benign familial infantile epilepsy (BFIE), also known as benign familial infantile seizures (BFIS) or benign familial infantile convulsions (BFIC) is an epilepsy syndrome. Affected children, who have no other health or developmental problems, develop seizures during infancy. These seizures have focal origin within the brain but may then spread to become generalised seizures. The seizures may occur several times a day, often grouped in clusters over one to three days followed by a gap of one to three months. Treatment with anticonvulsant drugs is not necessary but they are often prescribed and are effective at controlling the seizures. This form of epilepsy resolves after one or two years, and appears to be completely benign. The EEG of these children, between seizures, is normal. The brain appears normal on MRI scan.

A family history of epilepsy in infancy distinguishes this syndrome from the non-familial classification (see benign infantile epilepsy), though the latter may be simply sporadic cases of the same genetic mutations. The condition is inherited with an autosomal dominant transmission. There are several genes responsible for this syndrome, on chromosomes 2, 16 and 19. It is generally described as idiopathic, meaning that no other neurological condition is associated with it or causes it. However, there are some forms that are linked to neurological conditions. One variant known as infantile convulsions and choreoathetosis (ICCA) forms an association between BFIE and paroxysmal kinesigenic choreoathetosis and has been linked to the PRRT2 gene on chromosome 16. An association with some forms of familial hemiplegic migraine (FHM) has also been found. Benign familial infantile epilepsy is not genetically related to benign familial neonatal epilepsy (BFNE), which occurs in neonates. However, a variation with seizure onset between two days and seven months called "benign familial neonatal–infantile seizures" (BFNIS) has been described, which is due to a mutation in the SCN2A gene.

The condition may be difficult to diagnose. The subject may be unaware they have a seizure disorder. To others, the involuntary movements made during sleep may appear no different from those typical of normal sleep.People who have nocturnal seizures may notice unusual conditions upon awakening in the morning, such as a headache, having wet the bed, having bitten the tongue, a bone or joint injury, muscle strains or weakness, fatigue, or lightheadedness. Others may notice unusual mental behaviors consistent with the aftermath of a seizure. Objects near the bed may have been knocked to the floor, or the subject may be surprised to find themselves on the floor.

There are many risks associated with nocturnal seizures including concussion, suffocation and sudden unexpected death (SUDEP).

Most people with PNES (75%) are women, with onset in the late teens to early twenties being typical.

Some studies have reported an elevated frequency of childhood abuse in people with PNES. However, others that have controlled for other demographic factors have failed to find a higher rate of reported childhood abuse than in a comparable groups with organic disease (usually epilepsy).

A number of studies have also reported a high incidence of abnormal personality traits or personality disorders in people with PNES such as borderline personality. However, again, when an appropriate control group is used, the incidence of such characteristics it not always higher in PNES than in similar illnesses arising due to organic disease (e.g., epilepsy).

Other risk factors for PNES include having a diagnosis of epilepsy, having recently had a head injury or recently undergone neurosurgery.

Generalized seizures can be either absence seizures, myoclonic seizures, clonic seizures, tonic-clonic seizures or atonic seizures.

Generalized seizures occur in various seizure syndromes, including myoclonic epilepsy, familial neonatal convulsions, childhood absence epilepsy, absence epilepsy, infantile spasms (West's syndrome), Juvenile Myoclonic Epilepsy and Lennox-Gastaut syndrome.

The use of older terms including pseudoseizures and hysterical seizures are discouraged. While it is correct that PNES may resemble epileptic seizures, pseudo can also connote "false, fraudulent, or pretending to be something that it is not."

PNES may also be referred to as non-epileptic attack disorder or functional seizures. Within DSM IV the attacks are classified as a somatoform disorder, whilst in ICD 10 the term dissociative convulsions is used, classed as a conversion disorder.

Musicogenic epilepsy is a form of reflex epilepsy with seizures elicited by special stimuli.

It has probably been described for the first time in 1605 by the French philosopher and scholar Joseph Justus Scaliger (1540-1609). Later publications were, in the eighteenth century, among others, by the German physician Samuel Schaarschmidt, in the nineteenth century 1823 by the British physician John C. Cooke, 1881 by the British neurologist and epileptologist William Richard Gowers, as well as in 1913 by the Russian neurologist, clinical neurophysiologist and psychiatrist Vladimir Mikhailovich Bekhterev. In 1937 the British neurologist Macdonald Critchley coined the term for the first time and classified it as a form of reflex epilepsy.

Most patients have temporal lobe epilepsy. Listening, probably also thinking or playing, of usually very specific music with an emotional content triggers focal seizures with or without loss of awareness, occasionally also evolving to bilateral tonic-clonic seizures.

Although musicality is at least in non-musicians predominantly located in the right temporal lobe, the seizure onset may also be left-hemispherical. Of the approximately 100 patients reported in the literature so far, about 75% had temporal lobe epilepsy, women were slightly more affected, and the mean age of onset was about 28 years. Ictal EEG and SPECT findings as well as functional MRI studies localized the epileptogenic area predominantly in the right temporal lobe. Treatment with epilepsy surgery leading to complete seizure freedom has been reported.