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.

The diagnosis can be confirmed when the characteristic centrotemporal spikes are seen on electroencephalography (EEG). Typically, high-voltage spikes followed by slow waves are seen. Given the nocturnal activity, a sleep EEG can often be helpful. Technically, the label "benign" can only be confirmed if the child's development continues to be normal during follow-up. Neuroimaging, usually with an MRI scan, is only advised for cases with atypical presentation or atypical findings on clinical examination or EEG.

The disorder should be differentiated from several other conditions, especially centrotemporal spikes without seizures, centrotemporal spikes with local brain pathology, central spikes in Rett syndrome and fragile X syndrome, malignant Rolandic epilepsy, temporal lobe epilepsy and Landau-Kleffner syndrome.

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.

An electroencephalogram (EEG) can assist in showing brain activity suggestive of an increased risk of seizures. It is only recommended for those who are likely to have had an epileptic seizure on the basis of symptoms. In the diagnosis of epilepsy, electroencephalography may help distinguish 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 perform the EEG while the affected individual is sleeping or sleep deprived.

Diagnostic imaging by CT scan and MRI is recommended after a first non-febrile seizure to detect structural problems in and around the brain. MRI is generally a better imaging test except when bleeding is suspected, for which CT is more sensitive and more easily available. If someone attends the emergency room with a seizure but returns to normal quickly, imaging tests may be done at a later point. If a person has a previous diagnosis of epilepsy with previous imaging, repeating the imaging is usually not needed even if there are subsequent seizures.

For adults, the testing of electrolyte, blood glucose and calcium levels is important to rule out problems with these as causes. An electrocardiogram can rule out problems with the rhythm of the heart. A lumbar puncture may be useful to diagnose a central nervous system infection but is not routinely needed. In children additional tests may be required such as urine biochemistry and blood testing looking for metabolic disorders.

A high blood prolactin level within the first 20 minutes following a seizure may be useful to help confirm an epileptic seizure as opposed to psychogenic non-epileptic seizure. Serum prolactin level is less useful for detecting focal 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 the diagnosis of epilepsy.

A diagnosis is difficult, especially in children, due to the difficulty in differentiating between actual laughing or crying, versus a seizure that involves laughing and crying. In pre-verbal infants, a diagnosis may be impossible. A long history must be taken with a description of all the signs leading to and during the seizure. The episodes can also be confused with behavioral and emotional disorders. Some doctors ask parents to videotape the children's outbursts. The tapes may be difficult to obtain, but can be very helpful in speeding up the difficult diagnosis process. Diagnosis is also complicated due to the many possible causes of the seizures. Imaging is always helpful in an attempt to diagnose seizures caused by hypothalamic hamartoma. If there is evidence of this, the diagnosis takes much less time.

Diagnosis of epilepsy can be difficult. A number of other conditions may present very similar signs and symptoms to seizures, including syncope, hyperventilation, migraines, narcolepsy, panic attacks and psychogenic non-epileptic seizures (PNES). In particular a syncope can be accompanied by a short episode of convulsions. Nocturnal frontal lobe epilepsy, often misdiagnosed as nightmares, was considered to be a parasomnia but later identified to be an epilepsy syndrome. Attacks of the movement disorder paroxysmal dyskinesia may be taken for epileptic seizures. The cause of a drop attack can be, among many others, an atonic seizure.

Children may have behaviors that are easily mistaken for epileptic seizures but are not. These include breath-holding spells, bed wetting, night terrors, tics and shudder attacks. Gastroesophageal reflux may cause arching of the back and twisting of the head to the side in infants, which may be mistaken for tonic-clonic seizures.

Misdiagnosis is frequent (occurring in about 5 to 30% of cases). Different studies showed that in many cases seizure-like attacks in apparent treatment-resistant epilepsy have a cardiovascular cause. Approximately 20% of the people seen at epilepsy clinics have PNES and of those who have PNES about 10% also have epilepsy; separating the two based on the seizure episode alone without further testing is often difficult.

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.

The most important factor in diagnosing a patient with vertiginous epilepsy is the subject’s detailed description of the episode. However, due to the associated symptoms of the syndrome a subject may have difficulty remembering the specifics of the experience. This makes it difficult for a physician to confirm the diagnosis with absolute certainty. A questionnaire may be used to help patients, especially children, describe their symptoms. Clinicians may also consult family members for assistance in diagnosis, relying on their observations to help understand the episodes. In addition to the description of the event, neurological, physical and hematologic examinations are completed to assist in diagnosis. For proper diagnosis, an otological exam (examination of the ear) should also be completed to rule out disorders of the inner ear, which could also be responsible for manifestations of vertigo. This may include an audiological assessment and vestibular function test. During diagnosis, history-taking is essential in determining possible causes of vertiginous epilepsy as well as tracking the progress of the disorder over time.

Other means used in diagnosis of vertiginous epilepsy include:

- Electroencephalography (EEG)

- Magnetic resonance imaging (MRI)

- Positron emission tomography (PET)

- Neuropsychological testing

The EEG measures electrical activity in the brain, allowing a physician to identify any unusual patterns. While EEGs are good for identifying abnormal brain activity is it not helpful in localizing where the seizure originates because they spread so quickly across the brain. MRIs are used to look for masses or lesions in the temporal lobe of the brain, indicating possible tumors or cancer as the cause of the seizures. When using a PET scan, a physician is looking to detect abnormal blood flow and glucose metabolism in the brain, which is visible between seizures, to indicate the region of origin.

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.

The prognosis for Rolandic seizures is invariably excellent, with probably less than 2% risk of developing absence seizures and less often GTCS in adult life.

Remission usually occurs within 2–4 years from onset and before the age of 16 years. The total number of seizures is low, the majority of patients having fewer than 10 seizures; 10–20% have just a single seizure. About 10–20% may have frequent seizures, but these also remit with age.

Children with Rolandic seizures may develop usually mild and reversible linguistic, cognitive and behavioural abnormalities during the active phase of the disease. These may be worse in children with onset of seizures before 8 years of age, high rate of occurrence and multifocal EEG spikes.

The development, social adaptation and occupations of adults with a previous history of Rolandic seizures were found normal.

Like many other types of seizures, gelastic seizures are hard to control for an extended period of time. The best outlook is for children suffering the seizures due to a benign tumor in their hypothalamus. The removal of these tumors can be effective not only for the frequency of the seizures, but also the behavioral and cognitive symptoms that come along with the syndrome. Cases have also been described where that antiepileptic drugs have stopped seizures fully.

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.

Some features are more or less likely to suggest PNES but they are not conclusive and should be considered within the broader clinical picture. Features that are common in PNES but rarer in epilepsy include: biting the tip of the tongue, seizures lasting more than 2 minutes (easiest factor to distinguish), seizures having a gradual onset, a fluctuating course of disease severity, the eyes being closed during a seizure, and side to side head movements. Features that are uncommon in PNES include automatisms (automatic complex movements during the seizure), severe tongue biting, biting the inside of the mouth, and incontinence.

If a patient with suspected PNES has an episode during a clinical examination, there are a number of signs that can be elicited to help support or refute the diagnosis of PNES. Compared to patients with epilepsy, patients with PNES will tend to resist having their eyes forced open (if they are closed during the seizure), will stop their hands from hitting their own face if the hand is dropped over the head, and will fixate their eyes in a way suggesting an absence of neurological interference. Mellers et al. warn that such tests are neither conclusive nor impossible for a determined patient with factitious disorder to "pass" through faking convincingly.

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.

There is no general treatment for patients with a seizure disorder. Each treatment plan is specifically tailored to the individual patient based on their diagnosis and symptoms. Treatment options may include medical therapy, nerve stimulation, dietary therapy, or surgery, as appropriate. Clinical trials may also be a valuable treatment alternative.

Usually, anticonvulsants are given based on other symptoms and / or associated problems.

Because the areas of the cerebellum which determine increases and decreases in muscular tonus are close together, people experiencing atonic seizures are most likely experiencing myoclonic ones too, at some point. This may play a role in therapy and diagnostic.

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.

Diagnosis is typically made upon patient history, although EEG recordings can be confirmatory if they occur during attacks.

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

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.

To be diagnosed with PTE, a person must have a history of head trauma and no history of seizures prior to the injury. Witnessing a seizure is the most effective way to diagnose PTE. Electroencephalography (EEG) is a tool used to diagnose a seizure disorder, but a large portion of people with PTE may not have the abnormal "epileptiform" EEG findings indicative of epilepsy. In one study, about a fifth of people who had normal EEGs three months after an injury later developed PTE. However, while EEG is not useful for predicting who will develop PTE, it can be useful to localize the epileptic focus, to determine severity, and to predict whether a person will suffer more seizures if they stop taking antiepileptic medications.

Magnetic resonance imaging (MRI) is performed in people with PTE, and CT scanning can be used to detect brain lesions if MRI is unavailable. However, it is frequently not possible to detect the epileptic focus using neuroimaging.

For a diagnosis of PTE, seizures must not be attributable to another obvious cause. Seizures that occur after head injury are not necessarily due to epilepsy or even to the head trauma. Like anyone else, TBI survivors may suffer seizures due to factors including imbalances of fluid or electrolytes, epilepsy from other causes, hypoxia (insufficient oxygen), and ischemia (insufficient blood flow to the brain). Withdrawal from alcohol is another potential cause of seizures. Thus these factors must be ruled out as causes of seizures in people with head injury before a diagnosis of PTE can be made.

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.

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 have been early and consistent strategies for measurement to better understand vertiginous epilepsy including caloric reflex test, posture and gait, or rotational experimentation.

In Japan, Kaga et al prepared a longitudinal study of rotation tests comparing congenital deafness and children with delayed acquisition of motor system skills. They were able to demonstrate the development of post-rotation nystagmus response from the frequency of beat and duration period from birth to six years to compare to adult values. Overall, the study demonstrated that some infants from the deaf population had impaired vestibular responses related to head control and walking age. A side interpretation included the evaluation of the vestibular system in reference to matching data with age.

Research in this area of medicine is limited due to its lacking need for urgent attention. But, the American Hearing Research Foundation (AHRF) conducts studies in which they hope to make new discoveries to help advance treatment of the disease and possibly one day prevent vertiginous seizures altogether.

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.