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.

"See the equivalent section in the main migraine article."

People with FHM are encouraged to avoid activities that may trigger their attacks. Minor head trauma is a common attack precipitant, so FHM sufferers should avoid contact sports. Acetazolamide or standard drugs are often used to treat attacks, though those leading to vasoconstriction should be avoided due to the risk of stroke.

MAV is not recognized as a distinct diagnostic entity. Lembert and Neuhauser propose criteria for definite and probable migraine-associated vertigo.

A diagnosis of "definite migraine-associated vertigo" includes a case history of:

- episodic vestibular symptoms of at least moderate severity;

- current or previous history of migraine according to the 2004 "International Classification of Headache Disorders";

- one of the following migrainous symptoms during two or more attacks of vertigo: migrainous headache, photophobia, phonophobia, visual or other auras; and

- other causes ruled out by appropriate investigations.

A diagnosis of "probable migraine-associated vertigo" includes a case history of episodic vestibular symptoms of at least moderate severity and one of the following:

- current or previous history of migraine according to the 2004 "International Classification of Headache Disorders";

- migrainous symptoms during vestibular symptoms;

- migraine precipitants of vertigo in more than 50% of attacks, such as food triggers, sleep irregularities, or hormonal change;

- response to migraine medications in more than 50% of attacks; and

- other causes ruled out by appropriate investigations.

Note that, in both of the above criteria, headache is not required to make the diagnosis of migraine-associated vertigo.

They add that, in patients with a clear-cut history, no vestibular tests are required. Other historical criteria which are helpful in making the diagnosis of migraine-associated vertigo are vertiginous symptoms throughout the patient’s entire life, a long history of motion intolerance, sensitivity to environmental stimuli, illusions of motion of the environment, and vertigo that awakens the patient.

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:

A lumbar puncture is a procedure in which cerebral spinal fluid is removed from the spine with a needle. A lumbar puncture is necessary to look for infection or blood in the spinal fluid. A lumbar puncture can also evaluate the pressure in the spinal column, which can be useful for people with idiopathic intracranial hypertension (usually young, obese women who have increased intracranial pressure), or other causes of increased intracranial pressure. In most cases, a CT scan should be done first.

Treatment of migraine-associated vertigo is the same as the treatment for migraine in general.

Long term prognosis in people with migraines is variable. Most people with migraines have periods of lost productivity due to their disease; however typically the condition is fairly benign and is not associated with an increased risk of death. There are four main patterns to the disease: symptoms can resolve completely, symptoms can continue but become gradually less with time, symptoms may continue at the same frequency and severity, or attacks may become worse and more frequent.

Migraines with aura appear to be a risk factor for ischemic stroke doubling the risk. Being a young adult, being female, using hormonal birth control, and smoking further increases this risk. There also appears to be an association with cervical artery dissection. Migraines without aura do not appear to be a factor. The relationship with heart problems is inconclusive with a single study supporting an association. Overall however migraines do not appear to increase the risk of death from stroke or heart disease. Preventative therapy of migraines in those with migraines with auras may prevent associated strokes. People with migraines, particularly women, may develop higher than average numbers of white matter brain lesions of unclear significance.

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.

Although the original Silberstein–Lipton criteria and the original description by Vanast make no suggestion for the exclusion of migrainous features in NDPH, the current ICHD criteria exclude patients with migrainous features. When migraine features are present, classification thus becomes problematic.

It has been reported that migraine symptoms may be present in over 50% of NDPH patients. The current criteria definition thus excludes more than half of patients with new onset of daily headache. This exclusion due to migrainous features could have adverse scientific, diagnostic, and treatment consequences.

One proposal for reclassification of the criteria is from a study conducted on retrospective analysis of the records of 1348 patients regularly treated at the headache clinic of the Department of Neurology of Santa Casa de São Paulo, Brazil, and would be the following subdivision: NDPH with migraine features and without migraine features that would allow the inclusion of all individuals present who has a daily and persistent headache from the beginning.

Another proposed reclassification of the criteria is from a study conducted as a retrospective chart review of patients seen at the Headache Center at Montefiore Medical Center in Bronx, New York, from September 2005 to April 2009. The revised criteria for NDPH definition does not exclude migraine features (NDPH-R), and three subdivisions were created and described based on prognosis: Persisting, remitting, and relapsing–remitting. Additionally, this revised criteria would not include parts C or D currently required by the ICHD diagnostic criteria for NDPH.

Most patients have persistent headaches, although about 15% will remit, and 8% will have a relapsing-remitting type. It is not infrequent for NDPH to be an intractable headache disorder that is unresponsive to standard headache therapies.

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.

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.

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.

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.

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.

Diagnosis of FHM is made according to the following criteria:

- Two attacks of each of the following:

- At least one close (first or second degree) relative with FHM

- No other likely cause

Sporadic forms follow the same diagnostic criteria, with the exception of family history.

In all cases, family and patient history is used for diagnosis. Brain imaging techniques, such as MRI, CAT scans and SPECT, are used to look for signs of other familial conditions such as CADASIL or mitochondrial disease, and for evidence of cerebellar degeneration. With the discovery of causative genes, genetic sequencing can also be used to verify diagnosis (though not all genetic loci are known).

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.

MRI features can be suggestive of cortical hyper intensity and edema.

MOH is common and can be treated. The overused medications must be stopped for the patient's headache to resolve. Clinical data shows that the treatment of election is abrupt drugs withdrawal, followed by starting prophylactic therapy. However, the discontinuation of overused drugs usually leads to the worsening of headache and the appearance of drug withdrawal symptoms (that greatly depend on the previously overused drugs and typically last from two to ten days and that are relieved by the further intake of the overused medication), which might reinforce the continuation of overuse. Where physical dependence or a rebound effect such as rebound headache is possible, gradual reduction of medication may be necessary. It is important that the patient's physician be consulted before abruptly discontinuing certain medications as such a course of action has the potential to induce medically significant physical withdrawal symptoms. Abruptly discontinuing butalbital, for example, can actually induce seizures in some patients, although simple over the counter analgesics can safely be stopped by the patient without medical supervision. A long-acting analgesic/anti-inflammatory, such as naproxen (500 mg twice a day), can be used to ease headache during the withdrawal period. Two months after the completion of a medication withdrawal, patients suffering from MOH typically notice a marked reduction in headache frequency and intensity.

Drug withdrawal is performed very differently within and across countries. Most physicians prefer inpatients programmes, however effective drug withdrawal may also be achieved in an outpatient setting in uncomplicated MOH patients (i.e. subjects without important co-morbidities, not overusing opioids or ergotaminics and who are at their first detoxification attempt). In the absence of evidence-based indications, in MOH patients the choice of preventive agent should be based on the primary headache type (migraine or TTH), on the drug side-effect profile, on the presence of co-morbid and co-existent conditions, on patient’s preferences, and on previous therapeutic experiences.

Following an initial improvement of headache with the return to an episodic pattern, a relevant proportion (up to 45%) of patients relapse, reverting to the overuse of symptomatic drugs.

Predictors of the relapse, and that could influence treatment strategies, are considered the type of primary headache, from which MOH has evolved, and the type of drug abused (analgesics, and mostly combination of analgesics, but also drugs containing barbiturates or tranquillisers cause significantly higher relapse rates), while gender, age, duration of disease and previous intake of preventative treatment do not seem to predict relapse rate.

MOH is clearly a cause of disability and, if not adequately treated, it represents a condition of risk of possible co-morbidities associated to the excessive intake of drugs that are not devoid of side-effect. MOH can be treated through withdrawal of the overused drug(s) and by means of specific approaches that focus on the development of a close doctor-patient relationship in the post-withdrawal period.

In general, any patient who has frequent headaches or migraine attacks should be considered as a potential candidate for preventive medications instead of being encouraged to take more and more painkillers or other rebound-causing medications. Preventive medications are taken on a daily basis. Some patients may require preventive medications for many years; others may require them for only a relatively short period of time such as six months. Effective preventive medications have been found to come from many classes of medications including neuronal stabilizing agents (aka anticonvulsants), antidepressants, antihypertensives, and antihistamines. Some effective preventive medications include Elavil (amitriptyline), Depakote (valproate), Topamax (topiramate), and Inderal (propranolol).

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

Prevalence is estimated to be 0.005%. The age of onset has been found to be under 15 years in 40% of cases while it is between 10 and 14 years in one third of the cases. Females outnumber males, 4 to 1. Only 3% have attacks after age 52.

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.

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.