Focal impaired awareness seizures are seizures which impair consciousness to some extent: they alter the person's ability to interact normally with their environment. They usually begin with a focal aware seizure, then spread to a larger portion of the temporal lobe, resulting in impaired consciousness. They may include autonomic and psychic features present in focal aware seizures.

Signs may include:

- Motionless staring

- Automatic movements of the hands or mouth

- Confusion and disorientation

- Altered ability to respond to others, unusual speech

- Transient aphasia (losing ability to speak, read, or comprehend spoken word)

These seizures tend to have a warning or aura before they occur, and when they occur they generally tend to last only 1–2 minutes. It is not uncommon for an individual to be tired or confused for up to 15 minutes after a seizure has occurred, although postictal confusion can last for hours or even days. Though they may not seem harmful, due to the fact that the individual does not normally seize, they can be extremely harmful if the individual is left alone around dangerous objects. For example, if a person with complex partial seizures is driving alone, this can cause them to run into the ditch, or worse, cause an accident involving multiple people. With this type, some people do not even realize they are having a seizure and most of the time their memory from right before or after the seizure is wiped. First-aid is only required if there has been an injury or if this is the first time a person has had a seizure.

"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.

As of 2017, focal seizures are split into two main categories, "focal onset aware", and "focal onset impaired awareness". What was previously termed a "secondary generalised seizure" is now termed a "focal to bilateral seizure".

In focal onset aware seizures, a small part of one of the lobes may be affected and the person remains conscious. This can often be a precursor to a larger focal onset impaired awareness seizure. When this is the case, the focal aware seizure is usually called an aura.

A focal impaired awareness seizure affects a larger part of the hemisphere and the person may lose consciousness.

If a focal seizure spreads from one hemisphere to the other side of the brain, this will give rise to a "focal to bilateral seizure". The person will become unconscious and may well have a tonic clonic seizure. When people have multiple focal seizures they generally have a condition known as temporal lobe epilepsy. (A generalized seizure is one that involves both sides of the brain from the onset).

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 .

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 most common type (60%) of seizures are convulsive. Of these, one-third begin as generalized seizures from the start, affecting both hemispheres of the brain. Two-thirds begin as focal seizures (which affect one hemisphere of the brain) which may then progress to generalized seizures. The remaining 40% of seizures are non-convulsive. An example of this type is the absence seizure, which presents as a decreased level of consciousness and usually lasts about 10 seconds.

Focal seizures are often preceded by certain experiences, known as auras. They include sensory (visual, hearing, or smell), psychic, autonomic, and motor phenomena. Jerking activity may start in a specific muscle group and spread to surrounding muscle groups in which case it is known as a Jacksonian march. Automatisms may occur, which are non-consciously-generated activities and mostly simple repetitive movements like smacking of the lips or more complex activities such as attempts to pick up something.

There are six main types of generalized seizures: tonic-clonic, tonic, clonic, myoclonic, absence, and atonic seizures. They all involve loss of consciousness and typically happen without warning.

Tonic-clonic seizures occur with a contraction of the limbs followed by their extension along with arching of the back which lasts 10–30 seconds (the tonic phase). A cry may be heard due to contraction of the chest muscles, followed by a shaking of the limbs in unison (clonic phase). Tonic seizures produce constant contractions of the muscles. A person often turns blue as breathing is stopped. In clonic seizures there is shaking of the limbs in unison. After the shaking has stopped it may take 10–30 minutes for the person to return to normal; this period is called the "postictal state" or "postictal phase." Loss of bowel or bladder control may occur during a seizure. The tongue may be bitten at either the tip or on the sides during a seizure. In tonic-clonic seizure, bites to the sides are more common. Tongue bites are also relatively common in psychogenic non-epileptic seizures.

Myoclonic seizures involve spasms of muscles in either a few areas or all over. Absence seizures can be subtle with only a slight turn of the head or eye blinking. The person does not fall over and returns to normal right after it ends. Atonic seizures involve the loss of muscle activity for greater than one second. This typically occurs on both sides of the body.

About 6% of those with epilepsy have seizures that are often triggered by specific events and are known as reflex seizures. Those with reflex epilepsy have seizures that are only triggered by specific stimuli. Common triggers include flashing lights and sudden noises. In certain types of epilepsy, seizures happen more often during sleep, and in other types they occur almost only when sleeping.

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.

Juvenile myoclonic epilepsy (JME) is an idiopathic generalized epilepsy that occurs in patients aged 8 to 20 years. Patients have normal cognition and are otherwise neurologically intact. The most common seizure is myoclonic jerks, although generalized tonic-clonic seizures and absence seizures may occur as well. Myoclonic jerks usually cluster in the early morning after awakening. The EEG reveals generalized 4–6 Hz spike wave discharges or multiple spike discharges. These patients are often first diagnosed when they have their first generalized tonic-clonic seizure later in life, when they experience sleep deprivation (e.g., freshman year in college after staying up late to study for exams). Alcohol withdrawal can also be a major contributing factor in breakthrough seizures, as well. The risk of the tendency to have seizures is lifelong; however, the majority have well-controlled seizures with anticonvulsant medication and avoidance of seizure precipitants.

Frontal lobe epilepsy, usually a symptomatic or cryptogenic localization-related epilepsy, arises from lesions causing seizures that occur in the frontal lobes of the brain. These epilepsies can be difficult to diagnose because the symptoms of seizures can easily be confused with nonepileptic spells and, because of limitations of the EEG, be difficult to "see" with standard scalp EEG.

Juvenile absence epilepsy is an idiopathic generalized epilepsy with later onset than CAE, typically in prepubertal adolescence, with the most frequent seizure type being absence seizures. Generalized tonic-clonic seizures can occur. Often, 3 Hz spike-wave or multiple spike discharges can be seen on EEG. The prognosis is mixed, with some patients going on to a syndrome that is poorly distinguishable from JME.

After the active portion of a seizure (the ictal state) there is typically a period of recovery during which there is confusion, referred to as the postictal period before a normal level of consciousness returns. It usually lasts 3 to 15 minutes but may last for hours. Other common symptoms include feeling tired, headache, difficulty speaking, and abnormal behavior. Psychosis after a seizure is relatively common, occurring in 6–10% of people. Often people do not remember what happened during this time. Localized weakness, known as Todd's paralysis, may also occur after a focal seizure. When it occurs it typically lasts for seconds to minutes but may rarely last for a day or two.

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.

The inter-ictal EEG shows occipital paroxysms, often demonstrating fixation-off sensitivity. However, some patients may only have random occipital spikes, whereas others may have occipital spikes only in the sleep EEG, and a few may have a consistently normal EEG. Photoparoxysmal abnormalities occur in patients whose seizures are triggered by lights.

Ictal EEG, preceded by regression of occipital paroxysms, is characterised by the sudden appearance of an occipital discharge that consists of fast rhythms, fast spikes or both. Ictal EEG during blindness show pseudo-periodic slow waves and spikes, which differ from those seen in ictal visual hallucinations. There are usually no postictal abnormalities.

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.

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

Myoclonus can be described as brief jerks of the body; it can involve any part of the body, but it is mostly seen in limbs or facial muscles. The jerks are usually involuntary and can lead to falls. EEG is used to read brain wave activity. Spike activity produced from the brain is usually correlated with brief jerks seen on EMG or excessive muscle artifact. They usually occur without detectable loss of consciousness and may be generalized, regional or focal on the EEG tracing. Myclonus jerks can be epileptic or not epileptic. Epileptic myoclonus is an elementary electroclinical manifestation of epilepsy involving descending neurons, whose spatial (spread) or temporal (self-sustained repetition) amplification can trigger overt epileptic activity.

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).

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”.

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.

Myoclonic jerks that are not epileptic may be due to a nervous system disorder or other metabolic abnormalities that may arise in renal (e.g. hyperuraemia) and liver failure (e.g. high ammonia states).

A person who suffers from epilepsy regardless of whether it is nocturnal or not, can be categorized into two different types of epilepsy either being generalized, or partial. A generalized epilepsy syndrome is associated with an overall hyperactivity in the brain, where electrical discharges occur all over the brain at once; this syndrome often has a genetic basis. While generalized epilepsy occurs all over the brain, partial epilepsy consists of a regional or localized hyperactivity, which means that the seizures occur conversely in one part of the brain or several parts at once.

A differential diagnosis should include:

- Thrombosis of the basilar artery

- Cardioembolic stroke

- Complex partial seizures

- Frontal lobe epilepsy

- Lacunar syndromes

- Migraine variants

- Posterior cerebral artery stroke

- Syncope and related paroxysmal spells

- Temporal lobe epilepsy

If the event lasts less than one hour, transient epileptic amnesia (TEA) might be implicated.

If the condition lasts longer than 24 hours, it is not considered TGA by definition. A diagnostic investigation would then probably focus on some form of undetected ischemic attack or cranial bleed.

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.

The underlying cause of TGA remains enigmatic.

The leading hypotheses are some form of epileptic event, a problem with blood circulation around, to or from the brain, or some kind of migraine-like phenomenon.

The differences are sufficiently meaningful that transient amnesia may be considered a heterogeneous clinical syndrome with multiple etiologies, corresponding mechanisms, and differing prognoses.

The main sign of a gelastic seizure is a sudden outburst of laughter or crying with no apparent cause. The laughter may sound unpleasant and sardonic rather than joyful. The outburst usually lasts for less than a minute. During or shortly after a seizure, an individual might display some twitching, strange eye movements, lip smacking, fidgeting or mumbling. If a person who suffers from the seizures is hooked up to an electroencephalogram it will reveal interictal epileptic discharges. This syndrome usually manifests itself before the individual reaches the age of three or four. The temporal lobes, and the hypothalamus are the areas of the brain with the most involvement with these seizures. This may cause learning disabilities, and faulted cognitive function as well. It is not uncommon for children to have tonic-clonic seizures, and atonic seizures directly following the seizure. Those that are associated with hypothalamic hamartomas may occur as often as several times hourly and typically begin during infancy. Seizures that occur in infancy may include bursts of cooing, respirations, giggling, and smiling. Due to early hypothalamic-pituitary-gonadal axis activation in girls who suffer from the seizures, it is not uncommon for them to display secondary sex characteristics before the age of eight.

A gelastic seizure is typically caused by a hypothalamic hamartoma, or a brain tumor. A hypothalamic hamartoma is defined as a benign mass of glial tissue on or near the hypothalamus. The size of the hamartoma can vary from one centimeter to larger than three centimeters. They can cause several different types of seizures including a Gelastic Seizure. These structures can be detected with different imaging modalities such as computed tomography and magnetic resonance imaging. A computed tomography scan of an individual with a hypothalamic hamartoma would reveal an suprasellar mass with the same density as brain tissue. Images of these masses are not enhanced with the use of contrast. However, although a computed tomography scan may be useful in diagnosing the cause of a seizure, in the case of a hypothalamic hamartoma, magnetic resonance imaging is the tool of choice due to the cerebrospinal fluid which defines these masses. Photon emission computed tomography may also be used. This involves the use of a radiotracer which is taken up by the ictal region of the brain which is typically where the tumor lies. Gelastic seizures have been observed after taking a birth control pill (Maxim (R)).

Optic nerve hypoplasia is the only reported condition with gelastic seizures without hypothalamic hamartomas, suggesting that hypothalamic disorganization alone can cause gelastic seizures.