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.

Epilepsy in females with mental retardation, is characterized by seizure onset in infancy or early childhood (6–36 months) and cognitive impairment in some cases. Seizures are predominantly generalized, including tonic-clonic, tonic and atonic seizures. The spectrum of phenotypes has been extended to include female patients with early onset epileptic encephalopathies resembling Dravet syndrome, FIRES, Generalized epilepsy with febrile seizures plus (GEFS+) or focal epilepsy with or without mental retardation. EFMR is caused by mutations in PCDH19 (protocadherin 19).

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

- Tonic-clonic seizures present with a contraction of the limbs followed by their extension, along with arching of the back for 10–30 seconds. A cry may be heard due to contraction of the chest muscles. The limbs then begin to shake in unison. After the shaking has stopped it may take 10–30 minutes for the person to return to normal.

- Tonic seizures produce constant contractions of the muscles. The person may turn blue if breathing is impaired.

- Clonic seizures involve shaking of the limbs in unison.

- Myoclonic seizures involve spasms of muscles in either a few areas or generalized through the body.

- Absence seizures can be subtle, with only a slight turn of the head or eye blinking. The person often does not fall over and may return to normal right after the seizure ends, though there may also be a period of post-ictal disorientation.

- Atonic seizures involve the loss of muscle activity for greater than one second. This typically occurs bilaterally (on both sides of the body).

Focal seizures are often preceded by certain experiences, known as an aura. These may include: sensory, visual, psychic, autonomic, olfactory or motor phenomena.

In a complex partial seizure a person may appear confused or dazed and can not respond to questions or direction. Focal seizure may become generalized.

Jerking activity may start in a specific muscle group and spread to surrounding muscle groups—known as a "Jacksonian march". Unusual activities that are not consciously created may occur. These are known as automatisms and include simple activities like smacking of the lips or more complex activities such as attempts to pick something up.

Ohtahara syndrome is rare and the earliest-appearing age-related epileptic encephalopathy, with seizure onset occurring within the first three months of life, and often in the first ten days. Many, but not all, cases of OS evolve into other seizure disorders, namely West syndrome and Lennox-Gastaut syndrome.

The primary outward manifestation of OS is seizures, usually presenting as tonic seizures (a generalized seizure involving a sudden stiffening of the limbs). Other seizure types that may occur include partial seizures, clusters of infantile spasms, and, rarely, myoclonic seizures. In addition to seizures, children with OS exhibit profound mental and physical retardation.

Clinically, OS is characterized by a "burst suppression" pattern on an EEG. This pattern involves high voltage spike wave discharge followed by little brain wave activity.

It is named for the Japanese neurologist Shunsuke Ohtahara (1930–2013), who identified it in 1976.

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.

Generalized epilepsy, also known as primary generalized epilepsy or idiopathic epilepsy, is a form of epilepsy characterised by generalised seizures with no apparent cause. Generalized seizures, as opposed to focal seizures, are a type of seizure that impairs consciousness and distorts the electrical activity of the whole or a larger portion of the brain (which can be seen, for example, on electroencephalography, EEG).

Generalized epilepsy is "primary" because the epilepsy is the originally diagnosed condition itself, as opposed to "secondary" epilepsy, which occurs as a symptom of a diagnosed condition.

The age of onset of seizures is typically between three and five, though onset can occur at an earlier or later age. The syndrome shows clear parallels to West syndrome, enough to suggest a connection.

Daily multiple seizures are typical in LGS. Also typical is the broad range of seizures that can occur, larger than that of any other epileptic syndrome. The most frequently occurring seizure type is tonic seizures, which are often nocturnal (90%); the second most frequent are myoclonic seizures, which often occur when the person is over-tired.

Atonic, atypical absence, tonic, complex partial, focalized and tonic–clonic seizures are also common. Additionally, about half of patients will have status epilepticus, usually the nonconvulsive type, which is characterized by dizziness, apathy, and unresponsiveness. The seizures can cause sudden falling (or spasms in tonic, atonic and myoclonic episodes) and/or loss of balance, which is why patients often wear a helmet to prevent head injury.

In addition to daily multiple seizures of various types, children with LGS frequently have arrested/slowed psycho-motor development and behavior disorders.

The syndrome is also characterized by an (between-seizures) EEG featuring slow spike-wave complexes.

Signs of JME are brief episodes of involuntary muscle twitching occurring early in the morning or shortly before falling asleep. This does not usually result in the person falling, but rather dropping objects. These muscle twitching episodes are more common in the arms than in the legs. Other seizure types such as generalized tonic-clonic and absence seizures can also occur. Patients often report quick jerking movements in the morning that results in knocking over objects such as their morning orange juice. Clusters of myoclonic seizures can lead to absence seizures, and clusters of absence seizures can lead to generalized tonic-clonic seizures. The onset of symptoms is generally around age 10-16 although some patients can present in their 20s or even early 30s. The myoclonic jerks generally precede the generalized tonic-clonic seizures by several months. Some people with the disorder never get generalized tonic-clonic seizures (GTCs). Sleep deprivation is a major factor in triggering GTCs. College students often present with a GTC after "pulling an all-nighter." Patients with JME generally do not have other neurological problems.

Early myoclonic encephalopathy (EME) is an epilepsy syndrome where myoclonic seizures develop in the neonatal period. After several months, the seizure pattern may develop to infantile spasms (West syndrome). Various genetic and metabolic disorders are responsible. The seizures are resistant to treatment. The neurology is very abnormal and patients often do not live beyond one year.

Seizures may occur after traumatic brain injury; these are known as post-traumatic seizures (PTS). However, not everyone who has post-traumatic seizures will continue to have post-traumatic epilepsy, because the latter is a chronic condition. However, the terms PTS and PTE are used interchangeably in medical literature. Seizures due to post-traumatic epilepsy are differentiated from non-epileptic post-traumatic seizures based on their cause and timing after the trauma.

A person with PTE suffers late seizures, those occurring more than a week after the initial trauma. Late seizures are considered to be unprovoked, while early seizures (those occurring within a week of trauma) are thought to result from direct effects of the injury. A provoked seizure is one that results from an exceptional, nonrecurring cause such as the immediate effects of trauma rather than a defect in the brain; it is not an indication of epilepsy. Thus for a diagnosis of PTE, seizures must be unprovoked.

Disagreement exists about whether to define PTE as the occurrence of one or more late, unprovoked seizures, or whether the condition should only be diagnosed in people with two or more. Medical sources usually consider PTE to be present if even one unprovoked seizure occurs, but more recently it has become accepted to restrict the definition of all types of epilepsy to include only conditions in which more than one occur. Requiring more than one seizure for a diagnosis of PTE is more in line with the modern definition of epilepsy, but it eliminates people for whom seizures are controlled by medication after the first seizure.

As with other forms of epilepsy, seizure types in PTE may be partial (affecting only part of one hemisphere of the brain) or generalized (affecting both hemispheres and associated with loss of consciousness). In about a third of cases, people with PTE have partial seizures; these may be simple or complex. In simple partial seizures, level of consciousness is not altered, while in complex partial seizures consciousness is impaired. When generalized seizures occur, they may start out as partial seizures and then spread to become generalized.

Epilepsy is most commonly recognised by involuntary movements of the head and limbs, however other characteristics include salivation, lack of and anxiety. Animals often lose consciousness and are not aware of their surroundings.

The hallmark characteristic of PCDH19 gene-related epilepsy is early-onset cluster seizures that often cause cyanotic spells, which start in infancy or early childhood. The onset of the first cluster of seizures usually coincides with a fever (febrile seizures), however subsequent seizures may be febrile or afebrile. The seizure clusters are generally brief seizures, lasting 1–5 minutes, often accompanied by fearful screaming observed in 63% of girls. These cluster seizures can occur more than 10 times a day over several days, with varying amounts of time between seizure clusters.

Over time, children with PCDH19 gene-related epilepsy tend to exhibit multiple seizure types, including focal, generalized tonic-clonic, tonic, atonic, myclonus, and absence seizures. In a small study of 35 female patients with PCDH19 gene-related epilepsy, rare episodes of status epilepticus occurred in about 30% of patients in the early course of the disorder.

In PCDH19 gene-related epilepsy, the seizures are often refractory to treatment, especially in infancy and childhood. Additionally, seizures are usually characterized by persistence of cluster seizures, with variable frequency. In a study of 35 female patients with PCDH19 gene-related epilepsy, approximately 30% had become seizure free in the girl's childhood (mean age of 12 years), yet some continued into adulthood. In the same study, a few patients still had recurrent cluster seizures that evolved into status epilepticus in childhood or early adolescence.

FIRES seizures are non-focal - there is no specified starting or stopping point - making brain surgery impossible. These seizures damage cognitive abilities of the brain such as memory or sensory abilities. This can result in learning disabilities, behavioral disorders, memory issues, sensory changes, inability to move, and death. Children continue to have seizures throughout their lives.

Ohtahara syndrome (OS), also known as early infantile epileptic encephalopathy with burst-suppression (EIEE), is a progressive epileptic encephalopathy. The syndrome is outwardly characterized by tonic spasms and partial seizures, and receives its more elaborate name from the pattern of burst activity on an electroencephalogram (EEG). It is an extremely debilitating progressive neurological disorder, involving intractable seizures and severe mental retardation. No single cause has been identified, although in many cases structural brain damage is present.

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.

Watching an animal have a seizure can be quite frightening. There is not much that can be done during a seizure except to remain calm and not leave the animal alone. If your pet is having a seizure it is important to make sure they are laying down on the floor away from any water, stairs or other animals. When an animal has a seizure, do not try to grab their tongue or clear their mouth as there is a high chance you will be bitten; contrary to popular myth, neither humans nor animals can "swallow their tongue" during a seizure so it is safest to stay well away from their mouth during one. Timing seizures is also crucial. Take notes of seizures - what time they occur, how often and any other specific information which can be passed onto the vet or emergency animal clinic.

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.

Panayiotopoulos syndrome is now the formally approved nomenclature for this syndrome in the new International League against Epilepsy report on classification, which abandoned a number of previously used descriptive terms such as early onset benign childhood epilepsy with occipital paroxysms, early onset benign childhood occipital epilepsy, nocturnal childhood occipital epilepsy. The reason for this is that these descriptive terms were criticized as incorrect because in Panayiotopoulos syndrome:

“An autonomic seizure is an epileptic seizure characterized by altered autonomic function of any type at seizure onset or in which manifestations consistent with altered autonomic function are prominent (quantitatively dominant or clinically important) even if not present at seizure onset. The altered autonomic function may be objective or subjective or both.”

“Autonomic status epilepticus is an autonomic seizure which lasts for more than 30 minutes, or a series of such seizures over a 30 minute period without full recovery between seizures.”

Beyond early-onset and treatment-resistant cluster seizures, PCDH19 gene-related epilepsy is usually, but not always, associated with cognitive and sensory impairment of varying degrees, and psychiatric and behavioral problems. It is estimated that up to 60 to 75% of the females have cognitive deficits, ranging from mild to severe intellectual disability, which do not appear to be related to frequency or severity of seizures. Development over the course of a female patients’ childhood can follow one of three courses: delays from birth that persist into adulthood, normal development and then regression, or normal intellectual development. It is not yet clear why some people experience delayed intellectual growth and others regress with epilepsy.

From the University of Melbourne study, two-thirds of PCDH19 gene-related epilepsy patients have borderline intellectual functioning or intellectual disability, while one third have normal intelligence. A connection to depression, autism, obsessive and aggressive behaviors and other disorders has been observed in PCDH19 gene-related epilepsy. Approximately 40-60% of girls diagnosed with a PCDH19 mutation are on the autism spectrum.

Many of those with PCDH19 gene mutations also exhibit behavioral and psychological problems – including ADHD, aggression, obsessive-compulsive disorder, and anxiety. Other neurological abnormalities may present, including sleep disturbances, ictal apnea, motor deficits, hypotonia, language delay, sensory integration problems and dysautonomia.

The distinctive clinical features particularly lengthy seizures and ictus emeticus means that the diagnosis of Panayiotopoulos syndrome is easy. However, these are frequently mistaken as nonepileptic conditions such as acute encephalitis, syncope, migraine, cyclic vomiting syndrome, motion sickness, sleep disorder, or gastroenteritis. The consequence is avoidable misdiagnosis, high morbidity, and costly mismanagement.

Autonomic seizures and autonomic status epilepticus as occur in Panayiotopoulos syndrome have not been described in other epileptic syndromes in that sequence though 10–20 per cent of children with the same seizure semiology may have cerebral pathology. The major problem is to recognize emetic and other autonomic manifestations as seizure events and not to dismiss them or erroneously to consider them as unrelated to the ictus and a feature of encephalitis, migraine, syncope or gastro-enteritis.

It is not clear why some patients get PTE while others with very similar injuries do not. However, possible risk factors have been identified, including severity and type of injury, presence of early seizures, and genetic factors.

Lennox–Gastaut syndrome (LGS) is a childhood-onset epilepsy that most often appears between the second and sixth year of life. LGS is characterized by a triad of signs including frequent seizures of multiple types, an abnormal EEG pattern of less than 2.5 Hz slow spike wave activity, and moderate to severe intellectual impairment.

Juvenile myoclonic epilepsy is an inherited genetic syndrome, but the way in which this disorder is inherited is unclear. Frequently (17-49%) those with JME have relatives with a history of epileptic seizures. It is currently unclear if JME is more common in males or females. Almost all cases of JME, however, have an onset in early childhood to puberty.

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.