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.

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

Criteria for diagnosis of abdominal epilepsy includes frequent periodic abdominal symptoms, an abnormal electroencephalogram (EEG) and significant improvement of gastrointestinal symptoms after taking anti-seizure medication. Medical testing for diagnosis can be completed using MRI scans of the brain, CT scans and ultrasounds of the abdomen, endoscopy of the gastrointestinal tract, and blood tests.

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 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.

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 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)

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.

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.

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.

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.

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.

Occasionally the syndrome is referred to as "idiopathic" West syndrome, when a cause cannot be determined. Important diagnostic criteria are:

- Regular development until the onset of the attacks or before the beginning of the therapy

- no pathological findings in neurological or neuroradiological studies

- no evidence of a trigger for the spasms

Those are becoming rare due to modern medicine.

The lack of generally recognized clinical recommendations available are a reflection of the dearth of data on the effectiveness of any particular clinical strategy, but on the basis of present evidence, the following may be relevant:

- Epileptic seizure control with the appropriate use of medication and lifestyle counseling is the focus of prevention.

- Reduction of stress, participation in physical exercises, and night supervision might minimize the risk of SUDEP.

- Knowledge of how to perform the appropriate first-aid responses to seizure by persons who live with epileptic people may prevent death.

- People associated with arrhythmias during seizures should be submitted to extensive cardiac investigation with a view to determining the indication for on-demand cardiac pacing.

- Successful epilepsy surgery may reduce the risk of SUDEP, but this depends on the outcome in terms of seizure control.

- The use of anti suffocation pillows have been advocated by some practitioners to improve respiration while sleeping, but their effectiveness remain unproven because experimental studies are lacking.

- Providing information to individuals and relatives about SUDEP is beneficial.

The prognosis for epilepsy due to trauma is worse than that for epilepsy of undetermined cause. People with PTE are thought to have shorter life expectancies than people with brain injury who do not suffer from seizures. Compared to people with similar structural brain injuries but without PTE, people with PTE take longer to recover from the injury, have more cognitive and motor problems, and perform worse at everyday tasks. This finding may suggest that PTE is an indicator of a more severe brain injury, rather than a complication that itself worsens outcome. PTE has also been found to be associated with worse social and functional outcomes but not to worsen patients' rehabilitation or ability to return to work. However, people with PTE may have trouble finding employment if they admit to having seizures, especially if their work involves operating heavy machinery.

The period of time between an injury and development of epilepsy varies, and it is not uncommon for an injury to be followed by a latent period with no recurrent seizures. The longer a person goes without developing seizures, the lower the chances are that epilepsy will develop. At least 80–90% of people with PTE have their first seizure within two years of the TBI. People with no seizures within three years of the injury have only a 5% chance of developing epilepsy. However, one study found that head trauma survivors are at an increased risk for PTE as many as 10 years after moderate TBI and over 20 years after severe TBI. Since head trauma is fairly common and epilepsy can occur late after the injury, it can be difficult to determine whether a case of epilepsy resulted from head trauma in the past or whether the trauma was incidental.

The question of how long a person with PTE remains at higher risk for seizures than the general population is controversial. About half of PTE cases go into remission, but cases that occur later may have a smaller chance of doing so.

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.

Like other forms of epilepsy, abdominal epilepsy is treated with anticonvulsant drugs, such as phenytoin. Since no controlled studies exist, however, other drugs may be equally effective.

The presence of porencephalic cysts or cavities can be detected using trans-illumination of the skull of infant patients. Porencephaly is usually diagnosed clinically using the patients and families history, clinical observations, or based on the presence of certain characteristic neurological and physiological features of porencephaly. Advanced medical imaging with computed tomography (CT), magnetic resonance imaging (MRI), or with ultrasonography can be used as a method to exclude other possible neurological disorders. The diagnosis can be made antenatally with ultrasound. Other assessments include memory, speech, or intellect testing to help further determine the exact diagnose of the disorder.

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.

Unfortunately, there is no real way to prevent against vertiginous episodes out of the means of managing the disease. As head trauma is a major cause for vertiginous epilepsy, protecting the head from injury is an easy way to avoid possible onset of these seizures. With recent advances in science it is also possible for an individual to receive genetic screening, but this only tells if the subject is predisposed to developing the condition and will not aid in preventing the disease.

There is a range of ways to manage vertiginous epilepsy depending on the severity of the seizures. For simple partial seizures medical treatment is not always necessary. To the comfort of the patient, someone ailed with this disease may be able to lead a relatively normal life with vertiginous seizures. If, however, the seizures become too much to handle, antiepileptic medication can be administered as the first line of treatment. There are several different types of medication on the market to deter epileptic episodes but there is no support to show that one medication is more effective than another. In fact, research has shown that simple partial seizures do not usually respond well to medication, leaving the patient to self-manage their symptoms. A third option for treatment, used only in extreme cases when seizure symptoms disrupt daily life, is surgery wherein the surgeon will remove the epileptic region.

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 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).

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.