An electroencephalography is only recommended in those who likely had an epileptic seizure and may help determine the type of seizure or syndrome present. In children it is typically only needed after a second seizure. It cannot be used to rule out the diagnosis and may be falsely positive in those without the disease. In certain situations it may be useful to prefer the EEG while sleeping or sleep deprived.

Diagnostic imaging by CT scan and MRI is recommended after a first non-febrile seizure to detect structural problems inside the brain. MRI is generally a better imaging test except when intracranial bleeding is suspected. Imaging may be done at a later point in time in those who return to their normal selves while in the emergency room. If a person has a previous diagnosis of epilepsy with previous imaging repeat imaging is not usually needed with subsequent seizures.

In adults, testing electrolytes, blood glucose and calcium levels is important to rule these out as causes, as is an electrocardiogram. A lumbar puncture may be useful to diagnose a central nervous system infection but is not routinely needed. Routine antiseizure medical levels in the blood are not required in adults or children. In children additional tests may be required.

A high blood prolactin level within the first 20 minutes following a seizure may be useful to confirm an epileptic seizure as opposed to psychogenic non-epileptic seizure. Serum prolactin level is less useful for detecting partial seizures. If it is normal an epileptic seizure is still possible and a serum prolactin does not separate epileptic seizures from syncope. It is not recommended as a routine part of diagnosis epilepsy.

Differentiating an epileptic seizure from other conditions such as syncope can be difficult. Other possible conditions that can mimic a seizure include: decerebrate posturing, psychogenic seizures, tetanus, dystonia, migraine headaches, and strychnine poisoning. In addition, 5% of people with a positive tilt table test may have seizure-like activity that seems to be due to cerebral hypoxia. Convulsions may occur due to psychological reasons and this is known as a psychogenic non-epileptic seizure. Non-epileptic seizures may also occur due to a number of other reasons.

The diagnosis or suspicion of LGS is often a question of probability rather than certainty. This is because the varied presentations of LGS share features with other disorders, many of which may be said to have overlapping characteristics.

The diagnosis is more obvious when the epilepsy has frequent and manifold attacks, with the classic pattern on the electro-encephalogram (EEG); the latter is a slowed rhythm with Spike-wave-pattern, or with a multifocal and generalizing Sharp-slow-wave-discharges at 1.5–2.5 Hz. During sleep, frequently, tonic patterns can be seen. But variations of these patterns are known in patients with no diagnosis other than LGS, and they can differ bilaterally, and from time to time, within the same patient.

General medical investigation usually reveals developmental delay and cognitive deficiencies in children with true LGS. These may precede development of seizures, or require up to two years after the seizures begin, in order to become apparent.

Exclusion of organic or structural brain lesions is also important in establishing a correct diagnosis of LGS; this may require magnetic resonance imaging (MRI) or computerized tomography (CT). An important differential diagnosis is 'Pseudo-Lennox-Syndrome', which differs from LGS, in that there are no tonic seizures; sleeping EEG provides the best basis for distinguishing between the two.

Intravenous immunoglobulin therapy has been used in Lennox–Gastaut syndrome as early as 1986, when van Rijckevorsel-Harmant and colleagues used it in seven patients with ostensibly idiopathic LGS and saw EEG improvement and decreased seizure frequency in six of them.

Diagnosis can be made by EEG. In case of epileptic spasms, EEG shows typical patterns.

The test is particularly indicated in children who have had cluster seizures in series. It is also recommended for patients who are diagnosed GEFS+ and when the seizures are associated with fever, infection, experienced regression, delayed cognitive growth or behavioral problems. The test is typically ordered by neurologists. The diagnostic test can be done by drawing blood or saliva of the patient and their immediate family. It is analyzed in laboratories that specialize in genetic testing. Genetic testing can aid in a firmer diagnosis and understanding of the disorder, may aid in identifying the optimal treatment plan and if positive, testing of the parents can determine if they are carriers. (See Genetic Counseling)

PCDH19 gene-related epilepsy is clinically based on patient and family seizure history, cognitive and behavioral neuropsychological evaluation, neurological examination, electroencephalogram (EEG) studies, and long term observation. Diagnosis is confirmed using molecular testing for PCDH19 mutations.

Continuous prophylactic antiepileptic drug (AED) treatment may not be needed particularly for children with only 1-2 or brief seizures. This is probably best reserved for children whose seizures are unusually frequent, prolonged, distressing, or otherwise significantly interfering with the child’s life. There is no evidence of superiority of monotherapy with any particular common AED.

Autonomic status epilepticus in the acute stage needs thorough evaluation for proper diagnosis and assessment of the neurologic/autonomic state of the child. "Rescue" benzodiazepines are commonly used to terminate it. Aggressive treatment should be avoided because of the risk of iatrogenic complications, including cardiovascular arrest. There is some concern that intravenous lorazepam and/or diazepam may precipitate cardiovascular arrest. Early parental treatment is more effective than late emergency treatment. Buccal midazolam is probably the first choice medication for out of hospital termination of autonomic status epilepticus which should be administered as soon as the child shows evidence of onset of its habitual autonomic seizures.

Parental education about Panayiotopoulos syndrome is the cornerstone of correct management. The traumatizing, sometimes long-lasting effect on parents is significant particularly because autonomic seizures may last for many hours compounded by physicians’ uncertainty regarding diagnosis, management, and prognosis.

Panayiotopoulos syndrome is remarkably benign in terms of its evolution. The risk of developing epilepsy in adult life is probably no more than of the general population. Most patients have one or 2-5 seizures. Only a third of patients may have more than 5 seizures, and these may be frequent, but outcome is again favorable. However, one fifth of patients may develop other types of infrequent, usually rolandic seizures during childhood and early teens. These are also age-related and remit before the age of 16 years. Atypical evolutions with absences and drop attacks are exceptional. Children with pre-existing neurobehavioral disorders tend to be pharmacoresistant and have frequent seizures though these also remit with age.

Formal neuropsychological assessment of children with Panayiotopoulos syndrome showed that these children have normal IQ and they are not on any significant risk of developing cognitive and behavioural aberrations, which when they occur they are usually mild and reversible. Prognosis of cognitive function is good even for patients with atypical evolutions.

However, though Panayiotopoulos syndrome is benign in terms of its evolution, autonomic seizures are potentially life-threatening in the rare context of cardiorespiratory arrest.

The differential diagnosis of PNES firstly involves ruling out epilepsy as the cause of the seizure episodes, along with other organic causes of non-epileptic seizures, including syncope, migraine, vertigo, anoxia, hypoglycemia, and stroke. However, between 5-20% of patients with PNES also have epilepsy. Frontal lobe seizures can be mistaken for PNES, though these tend to have shorter duration, stereotyped patterns of movements and occurrence during sleep. Next, an exclusion of factitious disorder (a subconscious somatic symptom disorder, where seizures are caused by psychological reasons) and malingering (simulating seizures intentionally for conscious personal gain – such as monetary compensation or avoidance of criminal punishment) is conducted. Finally other psychiatric conditions that may superficially resemble seizures are eliminated, including panic disorder, schizophrenia, and depersonalisation disorder.

The most conclusive test to distinguish epilepsy from PNES is long term video-EEG monitoring, with the aim of capturing one or two episodes on both videotape and EEG simultaneously (some clinicians may use suggestion to attempt to trigger an episode). Conventional EEG may not be particularly helpful because of a high false-positive rate for abnormal findings in the general population, but also of abnormal findings in patients with some of the psychiatric disorders that can mimic PNES. Additional diagnostic criteria are usually considered when diagnosing PNES from long term video-EEG monitoring because frontal lobe epilepsy may be undetectable with surface EEGs.

Following most tonic-clonic or complex partial epileptic seizures, blood levels of serum prolactin rise, which can be detected by laboratory testing if a sample is taken in the right time window. However, due to false positives and variability in results this test is relied upon less frequently.

It is not possible to make a generalised prognosis for development due to the variability of causes, as mentioned above, the differing types of symptoms and cause. Each case must be considered individually.

The prognosis for children with idiopathic West syndrome are mostly more positive than for those with the cryptogenic or symptomatic forms. Idiopathic cases are less likely to show signs of developmental problems before the attacks begin, the attacks can often be treated more easily and effectively and there is a lower relapse rate. Children with this form of the syndrome are less likely to go on to develop other forms of epilepsy; around two in every five children develop at the same rate as healthy children.

In other cases, however, treatment of West syndrome is relatively difficult and the results of therapy often dissatisfying; for children with symptomatic and cryptogenic West syndrome, the prognosis is generally not positive, especially when they prove resistant to therapy.

Statistically, 5 out of every 100 children with West syndrome do not survive beyond five years of age, in some cases due to the cause of the syndrome, in others for reasons related to their medication. Only less than half of all children can become entirely free from attacks with the help of medication. Statistics show that treatment produces a satisfactory result in around three out of ten cases, with only one in every 25 children's cognitive and motoric development developing more or less normally.

A large proportion (up to 90%) of children suffer severe physical and cognitive impairments, even when treatment for the attacks is successful. This is not usually because of the epileptic fits, but rather because of the causes behind them (cerebral anomalies or their location or degree of severity). Severe, frequent attacks can (further) damage the brain.

Permanent damage often associated with West syndrome in the literature include cognitive disabilities, learning difficulties and behavioural problems, cerebral palsy (up to 5 out of 10 children), psychological disorders and often autism (in around 3 out of 10 children). Once more, the cause of each individual case of West syndrome must be considered when debating cause and effect.

As many as 6 out of 10 children with West syndrome suffer from epilepsy later in life. Sometimes West syndrome turns into a focal or other generalised epilepsy. Around half of all children develop Lennox-Gastaut syndrome.

Seven anti-epileptic drugs are approved for use in cases of suspected primary generalized epilepsy:

- Felbamate

- Levetiracetam

- Zonisamide

- Topiramate

- Valproate

- Lamotrigine

- Perampanel

Valproate, a relatively old drug, is often considered the first-line treatment. It is highly effective, but its association with fetal malformations when taken in pregnancy limits its use in young women.

All anti-epileptic drugs (including the above) can be used in cases of partial seizures.

Blood tests, cerebrospinal fluid examination by lumbar puncture (also known as spinal tap), brain imaging studies, electroencephalography (EEG), and similar diagnostic studies may be used to differentiate the various causes of encephalopathy.

Diagnosis is frequently clinical. That is, no set of tests give the diagnosis, but the entire presentation of the illness with nonspecific test results informs the experienced clinician of the diagnosis.

Many antiepileptic drugs are used for the management of canine epilepsy. Oral phenobarbital, in particular, and imepitoin are considered to be the most effective antiepileptic drugs and usually used as ‘first line’ treatment. Other anti-epileptics such as zonisamide, primidone, gabapentin, pregabalin, sodium valproate, felbamate and topiramate may also be effective and used in various combinations. A crucial part of the treatment of pets with epilepsy is owner education to ensure compliance and successful management.

There are three types of epilepsy in dogs: reactive, secondary, and primary. Reactive epileptic seizures are caused by metabolic issues, such as low blood sugar or kidney or liver failure. Epilepsy attributed to brain tumor, stroke or other trauma is known as secondary or symptomatic epilepsy.

There is no known cause for primary or idiopathic epilepsy, which is only diagnosed by eliminating other possible causes for the seizures. Dogs with idiopathic epilepsy experience their first seizure between the ages of one and three. However, the age at diagnosis is only one factor in diagnosing canine epilepsy, as one study found cause for seizures in one-third of dogs between the ages of one and three, indicating secondary or reactive rather than primary epilepsy.

A veterinarian's initial work-up for a dog presenting with a history of seizures may include a physical and neurological exam, a complete blood count, serum chemistry profile, urinalysis, bile tests, and thyroid function tests. These tests verify seizures and may determine cause for reactive or secondary epilepsy. Veterinarians may also request that dog owners keep a "seizure log" documenting the timing, length, severity, and recovery of each seizure, as well as dietary or environmental changes.

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.

Most generalized epilepsy starts during childhood. While some patients outgrow their epilepsy during adolescence and no longer need medication, in others, the condition remains for life, thereby requiring lifelong medication and monitoring.

The table below demonstrates the extensive and differential diagnosis of acquired epileptic aphasia along with Cognitive and Behavioral Regression:

Note: EEG = electroencephalographic; ESES = electrical status epilepticus of sleep; RL = receptive language; S = sociability

- Continuous spike and wave of slow-wave sleep (>85% of slow-wave sleep).

Most children who develop epilepsy are treated conventionally with anticonvulsants. In about 70% of cases of childhood epilepsy, medication can completely control seizures. Unfortunately, medications come with an extensive list of side effects that range from mild discomfort to major cognitive impairment. Usually, the adverse cognitive effects are ablated following dose reduction or cessation of the drug.

Medicating a child is not always easy. Many pills are made only to be swallowed, which can be difficult for a child. For some medications, chewable versions do exist.

The ketogenic diet is used to treat children who have not responded successfully to other treatments. This diet is low in carbohydrates, adequate in protein and high in fat. It has proven successful in two thirds of epilepsy cases.

In some cases, severe epilepsy is treated with the hemispherectomy, a drastic surgical procedure in which part or all of one of the hemispheres of the brain is removed.

No single cause of OS has been identified. In most cases, there is severe atrophy of both hemispheres of the brain. Less often, the root of the disorder is an underlying metabolic syndrome. Although it was initially published that no genetic connection had been established, several genes have since associated with Ohtahara syndrome. It can be associated with mutations in "ARX", "CDKL5", "SLC25A22", "STXBP1", "SPTAN1", "KCNQ2", "ARHGEF9", "PCDH19", "PNKP", "SCN2A", "PLCB1", "SCN8A", and likely others.

Treatment outlook is poor. Anticonvulsant drugs and glucocorticoid steroids may be used to try to control the seizures, but their effectiveness is limited. Most therapies are related to symptoms and day-to-day living.

The syndrome can be difficult to diagnose and may be misdiagnosed as autism, pervasive developmental disorder, hearing impairment, learning disability, auditory/verbal processing disorder, attention deficit hyperactivity disorder, intellectual disability, childhood schizophrenia, or emotional/behavioral problems. An EEG (electroencephalogram) test is imperative to a diagnosis. Many cases of patients exhibiting LKS will show abnormal electrical brain activity in both the right and left hemispheres of the brain; this is exhibited frequently during sleep. Even though an abnormal EEG reading is common in LKS patients, a relationship has not been identified between EEG abnormalities and the presence and intensity of language problems. In many cases however, abnormalities in the EEG test has preceded language deterioration and improvement in the EEG tracing has preceded language improvement (this occurs in about half of all affected children). Many factors inhibit the reliability of the EEG data: neurologic deficits do not closely follow the maximal EEG changes in time.

The most effective way of confirming LKS is by obtaining overnight sleep EEGs, including EEGs in all stages of sleep. Many conditions like demyelination and brain tumors can be ruled out by using magnetic resonance imaging (MRI). In LKS, fluorodeoxyglucose (FDG) and positron emission tomography (PET) scanning can show decreased metabolism in one or both temporal lobes - hypermetabolism has been seen in patients with acquired epileptic aphasia.

Most cases of LKS do not have a known cause. Occasionally, the condition may be induced secondary to other diagnoses such as low-grade brain tumors, closed-head injury, neurocysticercosis, and demyelinating disease. Central Nervous System vasculitis may be associated with this condition as well.

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.

The cause of FIRES is not known. It does not happen twice in the same family, but the medical community does not know if it is genetic. It happens in boys more than girls. After the initial status, life expectancy is not affected directly. Issues such as overdose of medications or infections at a food tube site are examples of things that would be secondary to the status.

The causes of epilepsy in childhood vary. In about ⅔ of cases, it is unknown.

- Unknown 67.6%

- Congenital 20%

- Trauma 4.7%

- Infection 4%

- Stroke 1.5%

- Tumor 1.5%

- Degenerative .7%

West syndrome is a triad of developmental delay, seizures termed infantile spasms, and EEG demonstrating a pattern termed hypsarrhythmia. Onset occurs between three months and two years, with peak onset between eight and 9 months. West syndrome may arise from idiopathic, symptomatic, or cryptogenic causes. The most common cause is tuberous sclerosis. The prognosis varies with the underlying cause. In general, most surviving patients remain with significant cognitive impairment and continuing seizures and may evolve to another eponymic syndrome, Lennox-Gastaut syndrome. It can be classified as idiopathic, syndromic, or cryptogenic depending on cause and can arise from both focal or generalized epileptic lesions.