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.

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 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.

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.

The prognosis of ICOE-G is unclear, although available data indicate that remission occurs in 50–60% of patients within 2–4 years of onset. Seizures show a dramatically good response to carbamazepine in more than 90% of patients. However, 40–50% of patients may continue to have visual seizures and infrequent secondarily generalized convulsions, particularly if they have not been appropriately treated with antiepileptic drugs.

The differential diagnosis of ICOE-G is mainly from symptomatic occipital epilepsy and migraine where misdiagnosis is high. The differential diagnosis from migraine should be easy because elementary visual hallucinations of occipital seizures develop rapidly within seconds, are brief in duration (2–3 minutes) are usually colored and circular. These are fundamentally different from the visual aura of migraine which develops slowly in minutes, is longer lasting ≥5 minutes and mainly achromatic with linear patterns.

Symptomatic occipital epilepsy often imitates ICOE-G; neuroophthalmological examination and brain imaging may be normal. Thus, high resolution MRI is required to detect subtle lesions.

The differentiation of ICOE-G from Panayiotopoulos syndrome is straightforward. The seizures of ICOE-G are purely occipital, brief, frequent and diurnal. Conversely seizures in Panayiotopoulos syndrome manifest with autonomic manifestations, they are lengthy and infrequent; visual symptoms are rare and not the sole manifestation of a seizure.

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.

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 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.

In epilepsy surgery a distinction can be made between resective and disconnective procedures. In a resective procedure the area of the brain that causes the seizures is removed. In a disconnective procedure the neural connections in the brain that allow the seizures to spread are disconnected. In most cases epilepsy surgery is only an option when the area of the brain that causes the seizures - the so-called epileptic focus can be clearly identified and is not responsible for critical functions such as language. Several imaging techniques such as magnetic resonance tomography and functional techniques like electrocorticography are used to demarcate the epileptic focus clearly.

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 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.

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.

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.

The ring 20 abnormality may be limited to as few as 5% of cells, so a screen for chromosomal mosaicism is critical. Newer array technology will not detect the ring chromosome and the standard metaphase chromosome analysis has been recommended. A karyotype analysis examining at least 50 cells should be requested to properly detect mosaicism.

if the source of seizures is a lesion for example a scar tissue from a brain injury a tumor or malformed blood vessels this lesion can be removed surgically in a lesionectomy.

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.

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 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.

Epilepsy surgery has been performed since the 1860s and doctors have observed that it is highly effective in producing freedom from seizures. However, it was not until 2001 that a scientifically sound study was carried out to examine the effectiveness of temporal lobectomy.

Temporal lobe surgery can be complicated by decreased cognitive function. However, after temporal lobectomy, memory function is supported by the opposite temporal lobe; and recruitment of the frontal lobe. Cognitive rehabilitation may also help.

Where surgery is not recommended, further management options include new (including experimental) anticonvulsants, and vagus nerve stimulation. The ketogenic diet is also recommended for children, and some adults. Other options include brain cortex responsive neural stimulators, deep brain stimulation, stereotactic radiosurgery, such as the gamma knife, and laser ablation.

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%

There have been assertions of a possible link between TGA and the use of statins (a class of drug used in treating cholesterol).

En bloc memory loss which is total, permanent, and irrecoverable can occur as an alcoholic "black out," usually lasting longer than an hour and up to 2–5 days.

Marijuana intoxication, Halogenated hydroxyquinolines such as Clioquinol, PDE inhibitors such as sildenafil, Digitalis and scopolamine intoxication, and general anaesthesia have been reported with TGA.

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.