All people who present with red flags indicating a dangerous secondary headache should receive neuroimaging. The best form of neuroimaging for these headaches is controversial. Non-contrast computerized tomography (CT) scan is usually the first step in head imaging as it is readily available in Emergency Departments and hospitals and is cheaper than MRI. Non-contrast CT is best for identifying an acute head bleed. Magnetic Resonance Imaging (MRI) is best for brain tumors and problems in the posterior fossa, or back of the brain. MRI is more sensitive for identifying intracranial problems, however it can pick up brain abnormalities that are not relevant to the person's headaches.

The American College of Radiology recommends the following imaging tests for different specific situations:

The US Headache Consortium has guidelines for neuroimaging of non-acute headaches. Most old, chronic headaches do not require neuroimaging. If a person has the characteristic symptoms of a migraine, neuroimaging is not needed as it is very unlikely the person has an intracranial abnormality. If the person has neurological findings, such as weakness, on exam, neuroimaging may be considered.

The diagnosis of a migraine is based on signs and symptoms. Neuroimaging tests are not necessary to diagnose migraine, but may be used to find other causes of headaches in those whose examination and history do not confirm a migraine diagnosis. It is believed that a substantial number of people with the condition remain undiagnosed.

The diagnosis of migraine without aura, according to the International Headache Society, can be made according to the following criteria, the "5, 4, 3, 2, 1 criteria":

- Five or more attacks—for migraine "with" aura, two attacks are sufficient for diagnosis.

- Four hours to three days in duration

- Two or more of the following:

- Unilateral (affecting half the head);

- Pulsating;

- Moderate or severe pain intensity;

- Worsened by or causing avoidance of routine physical activity

- One or more of the following:

- Nausea and/or vomiting;

- Sensitivity to both light (photophobia) and sound (phonophobia)

If someone experiences two of the following: photophobia, nausea, or inability to work or study for a day, the diagnosis is more likely. In those with four out of five of the following: pulsating headache, duration of 4–72 hours, pain on one side of the head, nausea, or symptoms that interfere with the person's life, the probability that this is a migraine is 92%. In those with fewer than three of these symptoms the probability is 17%.

Preventive treatments of migraines include medications, nutritional supplements, lifestyle alterations, and surgery. Prevention is recommended in those who have headaches more than two days a week, cannot tolerate the medications used to treat acute attacks, or those with severe attacks that are not easily controlled.

The goal is to reduce the frequency, painfulness, and/or duration of migraines, and to increase the effectiveness of abortive therapy. Another reason for prevention is to avoid medication overuse headache. This is a common problem and can result in chronic daily headache.

An aura sensation can include some or a combination of the following:

The prevention and treatment of acephalgic migraine is broadly the same as for classical migraine, but the symptoms are usually less severe than those of classic migraine, so treatment is less likely to be required.

Because epileptic seizures may occur with a side effect that resembles migraine aura, it is complicated to diagnose whether a patient is having a normal epileptic episode or if it is a true migraine that is then being followed by a seizure, which would be a true sign of migralepsy. Many neurological symptoms can only be expressed by the patient, who can confuse different feelings, especially when the symptoms of a migraine are extremely similar to that of a seizure. Thus, many physicians are reluctant to consider migralepsy to be a true condition, considering its rarity, and those that do believe in it are prone to over-diagnose it, leading to more problems in terms of finding the truth of the condition.

However, it has been found that EEG scans have been able to differentiate between migraine auras and auras related to epilepsy. It has generally been seen that EEG scans are not as helpful in determining facets of migraines as they are with epilepsy. Though they are able to work in determining the starting and ending points of migraines and the overlap of epileptic episodes during or after them, even if the scans are still lacking in considerable necessary data and confusing results. EEG scans have been able to observe seizures that occur in between the aura and headache phase of migraines and such occurrences have been termed intercalated seizures.

An aura is a perceptual disturbance experienced by some with migraines or seizures before either the headache or seizure begins. It often manifests as the perception of a strange light, an unpleasant smell, or confusing thoughts or experiences. Some people experience aura without a subsequent migraine or seizure (see silent migraine). Auras vary by individual experience; some people experience smells, lights, or hallucinations. Less known symptoms of the eye include disturbances, where the eyes roll in the back of the head caused by photosensitivity. A sufferer of this type of aura may experience tearfulness of the eyes and uncontrollable sensations of light followed by reduced symptoms after approximately 20 minutes; it is the rarest type of aura.

When occurring, auras allow people who have epilepsy time to prevent injury to themselves and/or others. The time between the appearance of the aura and the migraine lasts from a few seconds up to an hour. The aura can stay with a migraine sufferer for the duration of the migraine; depending on the type of aura, it can leave the person disoriented and confused. It is not uncommon for migraine sufferers to experience more than one type of aura during the migraine. Most people who have auras have the same type of aura every time.

Auras can also be confused with sudden onset of panic, panic attacks or anxiety attacks creating difficulties in diagnosis. The differential diagnosis of patients who experience symptoms of paresthesias, derealization, dizziness, chest pain, tremors, and palpitations can be quite challenging.

Treatment depends on identifying behavior that triggers migraine such as stress, sleep deprivation, skipped meals, food sensitivities, or specific activities. Medicines used to treat retinal migraines include aspirin, other NSAIDS, and medicines that reduce high blood pressure.

Acephalgic migraines can occur in individuals of any age. Some individuals, more commonly male, only experience acephalgic migraine, but frequently patients also experience migraine with headache. Generally, the condition is more than twice as likely to occur in females than males. Pediatric acephalgic migraines are listed along with other childhood periodic syndromes by W.A. Al-Twaijri and M.I. Shevell as "migraine equivalents" (although not listed as such in the "International Classification of Headache Disorders"), which can be good predictors of the future development of typical migraines. Individuals who experience acephalgic migraines in childhood are highly likely to develop typical migraines as they grow older. Among women, incidents of acephalgic migraine increase during perimenopause.

Scintillating scotoma is the most common symptom which usually happens concurrently with Expanding Fortification Spectra. Also frequently reported is monocular blindness. Acephalgic migraines typically do not persist more than a few hours and may last for as little as 15 seconds. On rare occasions, they may continue for up to two days.

Acephalgic migraines may resemble transient ischemic attacks or, when longer in duration, stroke. The concurrence of other symptoms such as photophobia and nausea can help in determining the proper diagnosis. Occasionally, patients with acephalgic migraine are misdiagnosed as suffering epilepsy with visual seizures, but the reverse misdiagnosis is more common.

The medical exam should rule out any underlying causes, such as blood clot, stroke, pituitary tumor, or detached retina. A normal retina exam is consistent with retinal migraine.

Since migralepsy is, for all intents and purposes, a combination of migraines and epilepsy, the medication for the conditions supplied individually can be combined jointly in order to lessen the effects of both. It is also helpful that many antiepileptic drugs also work as antimigraines, lessening the number of medications that must be taken. Thus, while neither can be cured, they can be treated so that they occur less frequently and allow a patient to live a relatively normal life.

Scintillating scotomas are most commonly caused by cortical spreading depression, a pattern of changes in the behavior of nerves in the brain during a migraine. Migraines, in turn, may be caused by genetic influences and hormones. People with migraines often self-report triggers for migraines involving stress and a wide variety of foods. While monosodium glutamate (MSG) is frequently reported as a dietary trigger, some scientific studies do not support this claim.

The Framingham Heart Study, published in 1998, surveyed 5,070 people between ages 30–62 and found that scintillating scotomas without other symptoms occurred in 1.23% of the group. The study did not find a link between late-life onset scintillating scotoma and stroke.

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.

EEG testing can diagnose patients with medial temporal lobe epilepsy. Epileptiform abnormalities including spikes and sharp waves in the medial temporal lobe of the brain can diagnose this condition, which can in turn be the cause of an epileptic patient's micropsia.

The Amsler grid test can be used to diagnose macular degeneration. For this test, patients are asked to look at a grid, and distortions or blank spots in the patient's central field of vision can be detected. A positive diagnosis of macular degeneration may account for a patient's micropsia.

A controlled size comparison task can be employed to evaluate objectively whether a person is experiencing hemimicropsia. For each trial, a pair of horizontally aligned circles is presented on a computer screen, and the person being tested is asked to decide which circle is larger. After a set of trials, the overall pattern of responses should display a normal distance effect where the more similar the two circles, the higher the number of errors. This test is able to effectively diagnose micropsia and confirm which hemisphere is being distorted.

Due to the large range of causes that lead to micropsia, diagnosis varies among cases. Computed tomography (CT) and magnetic resonance imaging (MRI) may find lesions and hypodense areas in the temporal and occipital lobes. MRI and CT techniques are able to rule out lesions as the cause for micropsia, but are not sufficient to diagnose the most common causes.

Symptoms typically appear gradually over 5 to 20 minutes and generally last fewer than 60 minutes, leading to the headache in classic migraine with aura, or resolving without consequence in acephalgic migraine. Many migraine sufferers change from scintillating scotoma as a prodrome to migraine to scintillating scotoma without migraine. The scotoma typically spontaneously resolves within the stated time frame, leaving few or no subsequent symptoms, though some report fatigue, nausea, and dizziness as sequelae.

Palinopsia necessitates a full ophthalmologic and neurologic history and physical exam. There are no clear guidelines on the work-up for illusory palinopsia, but it is not unreasonable to order automated visual field testing and neuroimaging since migraine aura can sometimes mimic seizures or cortical lesions. However, in a young patient without risk factors or other worrisome symptoms or signs (vasculopathy, history of cancer, etc.), neuroimaging for illusory palinopsia is low-yield but may grant the patient peace of mind.

The physical exam and work-up are usually non-contributory in illusory palinopsia. Diagnosing the etiology of illusory palinopsia is often based on the clinical history. Palinopsia is attributed to a prescription drug if symptoms begin after drug initiation or dose increase. Palinopsia is attributed to head trauma if symptoms begin shortly after the incident. Continuous illusory palinopsia in a migraineur is usually from persistent visual aura. HPPD can occur any time after hallucinogen ingestion and is a diagnosis of exclusion in patients with previous hallucinogen use. Migraines and HPPD are probably the most common causes of palinopsia. Idiopathic palinopsia may be analogous to the cerebral state in persistent visual aura with non-migraine headache or persistent visual aura without headache.

Due to the subjective nature of the symptoms and the lack of organic findings, clinicians may be dismissive of illusory palinopsia, sometimes causing the patient distress. There is considerable evidence in the literature confirming the symptom legitimacy, so validating the patient’s symptoms can help ease anxiety. Unidirectional visual trails or illusory symptoms confined to part of a visual field suggest cortical pathology and necessitate further work-up.

Palinopsia necessitates a full ophthalmologic and neurologic history and physical exam. Hallucinatory palinopsia warrants automated visual field testing and neuroimaging since the majority of hallucinatory palinopsia is caused by posterior cortical lesions and seizures. It is generally easy to diagnose the underlying cause of hallucinatory palinopsia. The medical history typically includes concerning symptoms, and neuroimaging usually reveals cortical lesions. In patients with hallucinatory palinopsia and unremarkable neuroimaging, blood tests or clinical history often hints at the cause. The practitioner should be considering visual seizures in these cases.

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.

There is limited data on treating the visual disturbances associated with HPPD, persistent visual aura, or post-head trauma visual disturbances, and pharmaceutical treatment is empirically-based. It is not clear if the etiology or type of illusory symptom influences treatment efficacy. Since the symptoms are usually benign, treatment is based on the patient’s zeal and willingness to try many different drugs. There are cases which report successful treatment with clonidine, clonazepam, lamotrigine, nimodipine, topiramate, verapamil, divalproex sodium, gabapentin, furosemide, and acetazolamide, as these drugs have mechanisms that decrease neuronal excitability. However, other patients report treatment failure from the same drugs. Based on the available evidence and side-effect profile, clonidine might be an attractive treatment option. Many patients report improvement from sunglasses. FL-41 tinted lenses may provide additional relief, as they have shown some efficacy in providing relief to visually-sensitive migraineurs.

Diagnosis may be made by noting the correlation between exposure to specific visual stimuli and seizure activity. More precise investigation can be carried out by combining an EEG with a device producing "Intermittent Photic Stimulation" (IPS). The IPS device produces specific types of stimuli that can be controlled and adjusted with precision. The testing physician adjusts the IPS device and looks for characteristic anomalies in the EEG, such as photoparoxysmal response (PPR), that are consistent with PSE and/or may herald the onset of seizure activity. The testing is halted before a seizure actually occurs.

Sometimes diagnostic indicators consistent with PSE can be found through provocative testing with IPS, and yet no seizures may ever occur in real-life situations. Many people will show PSE-like abnormalities in brain activity with sufficiently aggressive stimulation, but they never experience seizures and are not considered to have PSE.

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.

Prenatal screening is not typically done for FHM, however it may be performed if requested. As penetrance is high, individuals found to carry mutations should be expected to develop signs of FHM at some point in life.

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.

Abdominal aura (also known as visceral aura and epigastric aura) is used to denote a type of somatosensory or somaesthetic aura that typically manifests itself as a rising epigastric sensation. The term is indebted to the Latin words abdomen (belly) and aura (wind, smell).

Other presentations of the abdominal aura include viscerosensitive sensations such as abdominal discomfort, visceromotor symptoms presenting in the form of tachycardia, borborygmi or vomiting, and vegetative symptoms such as blushing and sweating.

Pathophysiologically, the abdominal aura is associated with aberrant neuronal discharges in sensory cortical areas representing the abdominal viscera. Etiologically, it is associated primarily with paroxysmal neurological disorders such as migraine and epilepsy. The abdominal aura can be classified as a somatic or coenesthetic hallucination.

The term is used in opposition to various terms denoting other types of somatosensory aura, notably splitting of the body image and paraesthesia.