Between 12 and 60% of people report foods as triggers. Evidence for such triggers, however, mostly relies on self-reports and is not rigorous enough to prove or disprove any particular triggers. A clear explanation for why food might trigger migraines is also lacking.

There does not appear to be evidence for an effect of tyramine on migraine. Likewise, while monosodium glutamate (MSG) is frequently reported, evidence does not consistently support that it is a dietary trigger.

Common triggers quoted are stress, hunger, and fatigue (these equally contribute to tension headaches). Psychological stress has been reported as a factor by 50 to 80% of people. Migraines have also been associated with post-traumatic stress disorder and abuse. Migraines are more likely to occur around menstruation. Other hormonal influences, such as menarche, oral contraceptive use, pregnancy, perimenopause, and menopause, also play a role. These hormonal influences seem to play a greater role in migraine without aura. Migraines typically do not occur during the second and third trimesters or following menopause.

Approximately 64–77% of people have a headache at some point in their lives. During each year, on average, 46–53% of people have headaches. Most of these headaches are not dangerous. Only approximately 1–5% of people who seek emergency treatment for headaches have a serious underlying cause.

More than 90% of headaches are primary headaches. Most of these primary headaches are tension headaches. Most people with tension headaches have "episodic" tension headaches that come and go. Only 3.3% of adults have chronic tension headaches, with headaches for more than 15 days in a month.

Approximately 12–18% of people in the world have migraines. More women than men experience migraines. In Europe and North America, 5–9% of men experience migraines, while 12–25% of women experience migraines.

Cluster headaches are very rare. They affect only 1–3 per thousand people in the world. Cluster headaches affect approximately three times as many men as women.

In general, children suffer from the same types of headaches as adults do, but their symptoms may be slightly different. The diagnostic approach to headache in children is similar to that of adults. However, young children may not be able to verbalize pain well. If a young child is fussy, they may have a headache.

Approximately 1% of Emergency Department visits for children are for headache. Most of these headaches are not dangerous. The most common type of headache seen in pediatric Emergency Rooms is headache caused by a cold (28.5%). Other headaches diagnosed in the Emergency Department include post-traumatic headache (20%), headache related to a problem with a ventriculoperitoneal shunt (a device put into the brain to remove excess CSF and reduce pressure in the brain) (11.5%) and migraine (8.5%). The most common serious headaches found in children include brain bleeds (subdural hematoma, epidural hematoma), brain abscesses, meningitis and ventriculoperitoneal shunt malfunction. Only 4–6.9% of kids with a headache have a serious cause.

Just as in adults, most headaches are benign, but when head pain is accompanied with other symptoms such as speech problems, muscle weakness, and loss of vision, a more serious underlying cause may exist: hydrocephalus, meningitis, encephalitis, abscess, hemorrhage, tumor, blood clots, or head trauma. In these cases, the headache evaluation may include CT scan or MRI in order to look for possible structural disorders of the central nervous system. If a child with a recurrent headache has a normal physical exam, neuroimaging is not recommended. Guidelines state children with abnormal neurologic exams, confusion, seizures and recent onset of worst headache of life, change in headache type or anything suggesting neurologic problems should receive neuroimaging.

When children complain of headaches, many parents are concerned about a brain tumor. Generally, headaches caused by brain masses are incapacitating and accompanied by vomiting. One study found characteristics associated with brain tumor in children are: headache for greater than 6 months, headache related to sleep, vomiting, confusion, no visual symptoms, no family history of migraine and abnormal neurologic exam.

Some measures can help prevent headaches in children. Drinking plenty of water throughout the day, avoiding caffeine, getting enough and regular sleep, eating balanced meals at the proper times, and reducing stress and excess of activities may prevent headaches. Treatments for children are similar to those for adults, however certain medications such as narcotics should not be given to children.

Children who have headaches will not necessarily have headaches as adults. In one study of 100 children with headache, eight years later 44% of those with tension headache and 28% of those with migraines were headache free. In another study of people with chronic daily headache, 75% did not have chronic daily headaches two years later, and 88% did not have chronic daily headaches eight years later.

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.

The prevalence of migraine and vertigo is 1.6 times higher in 200 dizziness clinic patients than in 200 age- and sex-matched controls from an orthopaedic clinic. Among the patients with unclassified or idiopathic vertigo, the prevalence of migraine was shown to be elevated. In another study, migraine patients reported 2.5 times more vertigo and also 2.5 more dizzy spells during headache-free periods than the controls.

MAV may occur at any age with a female:male ratio of between 1.5 and 5:1. Familial occurrence is not uncommon. In most patients, migraine headaches begin earlier in life than MAV with years of headache-free periods before MAV manifests.

In a diary study, the 1-month prevalence of MAV was 16%, frequency of MAV was higher and duration longer on days with headache, and MAV was a risk factor for co-morbid anxiety.

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.

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.

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.

Benign paroxysmal positional vertigo - Migraine is commonly associated with BPPV, the most common vestibular disorder in patients presenting with dizziness. The two may be linked by genetic factors or by vascular damage to the labyrinth.

Ménière's disease - There is an increased prevalence of migraine in patients with Ménière's disease and migraine leads to a greater susceptibility of developing Ménière’s disease. But they can be distinguished. Ménière's disease may go on for days or even years, while migraines typically do not last longer than 24 hours.

Motion sickness is more prevalent in patients with migraine.

Psychiatric syndromes Dizziness and spinning vertigo are the second most common symptom of panic attacks, and they can also present as a symptom of major depression. Migraine is a risk factor for developing major depression and panic disorder and vice versa.

In general, the prognosis for retinal migraine is similar to that of migraine headache with typical aura. As the true incidence of retinal migraine is unknown, it is uncertain whether there is a higher incidence of permanent neuroretinal injury. The visual field data suggests that there is a higher incidence of end arteriolar distribution infarction and a higher incidence of permanent visual field defects in retinal migraine than in clinically manifest cerebral infarctions in migraine with aura. One study suggests that more than half of reported "recurrent" cases of retinal migraine subsequently experienced permanent visual loss in that eye from infarcts, but more recent studies suggest such loss is a relatively rare side effect.

The pathophysiology of NDPH is poorly understood. Research points to an immune-mediated, inflammatory process. Cervical joint hypermobility and defective internal jugular venous drainage have also been suggested as causes.

In 1987, Vanast first suggested autoimmune disorder with a persistent viral trigger for CDH (now referred to as NDPH). Post-infectious origins have been approximated to make up anywhere between 30–80% of NDPH patients in different studies. Viruses that have been implicated include Epstein-Barr virus, herpes simplex virus and cytomegalovirus.

Non-specific upper respiratory infections including rhinitis and pharyngitis are most often cited by patients. In one study, 46.5% patients recalled a specific trigger with a respiratory tract illness being the most common. In children, almost half report headache onset during an infection.

A study by Rozen and Swindan in 2007 found elevated levels of tumor necrosis factor alpha, a proinflammatory cytokine, in the cerebrospinal fluid but not the blood of patients with NDPH, chronic migraine, and post-traumatic headaches suggesting inflammation as the cause of the headaches.

NDPH as an inflammatory, post-infectious manifestation indicates a potential meningoencephalitis event in NDPH patients. Tissue specificity is a general feature of post-infectious, immune-mediated conditions, and the meninges are a type of connective tissue membrane. Inflammation of the meninges was first proposed as a possible pathophysiology for migraine in the 1960s and has recently been explored again. This hypothesis is based on meningeal mast cell activation. Reactive arthritis (ReA) is a post-infectious disease entity of synovium/joints with connective tissue membrane (synovial membrane of the joints) which provides a corollary.

NDPH has been reported in Hashimoto's encephalopathy, an immune-mediated type of encephalitis. A mean 5-year retrospective analysis of 53 patients with a history of viral meningitis and 17 patients with a history of bacterial meningitis showed an increased onset of subsequent new onset headache and increased severity of those with prior primary headaches.

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.

There are also non-familial cases of hemiplegic migraine, termed sporadic hemiplegic migraine. These cases seem to have the same causes as the familial cases and represent de novo mutations. Sporadic cases are also clinically identical to familial cases with the exception of a lack of family history of attacks.

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.

"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.

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

MOH is known to occur with frequent use of many different medications, including most commonly: triptans, ergotamines, analgesics, opioids. The underlying mechanisms that lead to the development of the condition are still widely unknown and clarification of their role is hampered by a lack of experimental research or suitable animal models. Various pathophysiological abnormalities have been reported and they seem to have an important role in initiating and maintaining chronic headache (genetic disposition, receptor and enzyme physiology and regulation, psychological and behavioural factors, physical dependencies, recent functional imaging results).

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.

Episodes of micropsia or macropsia occur in 9% of adolescents.

10-35% of migraine sufferers experience auras, with 88% of these patients experiencing both visual auras (which include micropsia) and neurological auras.

Micropsia seems to be slightly more common in boys than in girls among children who experience migraines.

Approximately 80% of temporal lobe seizures produce auras that may lead to micropsia or macropsia. They are a common feature of simple partial seizures and usually precede complex partial seizures of temporal lobe origin.

Central Serous Chorioretinopathy (CSCR) which can produce micropsia predominantly affects persons between the ages of 20 and 50. Women appear to be affected more than men by a factor of almost 3 to 1.

Whatever the cause, the bodily related distortions can recur several times a day and may take some time to abate. Understandably, the person can become alarmed, frightened, and panic-stricken throughout the course of the hallucinations—maybe even hurt themselves or others around them. The symptoms of the syndrome themselves are not harmful and are likely to disappear with time.

Micropsia can be caused by swelling of the cornea due to infection by the Epstein-Barr virus (EBV) and can therefore present as an initial symptom of EBV mononucleosis, a disease caused by Epstein-Barr virus infection.

The connection between migraines and epileptic seizures is currently being researched and not much is known. Patients have been shown to have had migraines long before developing epileptic symptoms, creating the possibility of severe cases of migraines creating epilepsy. However, not every migraine may be accompanied by a seizure and sometimes the seizures happen without any migraine involvement. Due to this, finding the origin of migralepsy is difficult and enveloped somewhere in the overlap between both conditions. Some patients have shown that their relatives suffered from migraines as well and even some from migralepsy, forming the possibility that migralepsy is genetic in origin and forms only rarely as both, generally resulting in only one condition or the other.

From 3% to 11% of diagnosed dizziness in neuro-otological clinics are due to Meniere's. The annual incidence rate is estimated to be about 15/100,000 and the prevalence rate is about 218/100,000, and around 15% of people with Meniere's disease are older than 65. In around 9% of cases a relative also had MD, signalling that there may be a genetic predisposition in some cases.

The odds of MD are greater for people of white ethnicity, with severe obesity, and women. Several conditions are often comorbid with MD, including arthritis, psoriasis, gastroesophageal reflux disease, irritable bowel syndrome, and migraine.