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.

As of 2013 tension headaches affect about 1.6 billion people (20.8% of the population) and are more common in women than men (23% to 18% respectively). Despite its benign character, tension-type headache, especially in its chronic form, can impart significant disability on patients as well as burden on society at large.

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.

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.

About 65% of persons with CH are, or have been, tobacco smokers. Stopping smoking does not lead to improvement of the condition and CH also occurs in those who have never smoked (e.g. children); it is thought unlikely that smoking is a cause. People with CH may be predisposed to certain traits, including smoking or other lifestyle habits.

Cluster headache may, but rarely, run in some families in an autosomal dominant inheritance pattern. People with a first degree relative with the condition are about 14–48 times more likely to develop it themselves, and between 1.9 and 20% of persons with CH have a positive family history. Possible genetic factors warrant further research, current evidence for genetic inheritance is limited.

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.

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 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.

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 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.

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.

"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.

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.

Various precipitating factors may cause tension-type headaches in susceptible individuals:

- Stress: usually occurs in the afternoon after long stressful work hours or after an exam

- Sleep deprivation

- Uncomfortable stressful position and/or bad posture

- Irregular meal time (hunger)

- Eyestrain

Tension-type headaches may be caused by muscle tension around the head and neck.

Another theory is that the pain may be caused by a malfunctioning pain filter which is located in the brain stem. The view is that the brain misinterprets information—for example from the temporal muscle or other muscles—and interprets this signal as pain. One of the main neurotransmitters that is probably involved is serotonin. Evidence for this theory comes from the fact that chronic tension-type headaches may be successfully treated with certain antidepressants such as nortriptyline. However, the analgesic effect of nortriptyline in chronic tension-type headache is not solely due to serotonin reuptake inhibition, and likely other mechanisms are involved. Recent studies of nitric oxide (NO) mechanisms suggest that NO may play a key role in the pathophysiology of CTTH. The sensitization of pain pathways may be caused by or associated with activation of nitric oxide synthase (NOS) and the generation of NO. Patients with chronic tension-type headache have increased muscle and skin pain sensitivity, demonstrated by low mechanical, thermal and electrical pain thresholds. Hyperexcitability of central nociceptive neurons (in trigeminal spinal nucleus, thalamus, and cerebral cortex) is believed to be involved in the pathophysiology of chronic tension-type headache. Recent evidence for generalized increased pain sensitivity or hyperalgesia in CTTH strongly suggests that pain processing in the central nervous system is abnormal in this primary headache disorder. Moreover, a dysfunction in pain inhibitory systems may also play a role in the pathophysiology of chronic tension-type headache.

If other treatment is not working, a health care provider may use an MRI to confirm a more complicated diagnosis (i.e. New daily persistent headache).

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.

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.

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.

A vascular headache is an outdated term to describe certain types of headache which were thought to be related to blood vessel swelling and hyperemia as cause of pain.

There is no doubt that "some" headaches are caused by vascular effects. However, it is no longer a recognized term and not mentioned in the Headache classification of the International Headache society (IHS), although it is still used by some physicians and still mentioned in some medical classification systems. There are many types of vascular headaches. Other types of vascular headaches include headaches produced by fever, cluster headaches, and headaches from a rise in blood pressure (OSU Wexner Medical Center, 2012).

Headaches that were described as being vascular headaches include:

- Cluster headache

- Migraine

- Toxic headache

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.

Ophthalmodynia periodica does not have a confirmed cause, being a primary headache, but can be identified with other primary conditions. "As many as 40% of all individuals with ice pick headaches have also been diagnosed as suffering with some form of migraine headache."

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).

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.

Benign paroxysmal vertigo of childhood is an uncommon neurological disorder which presents with recurrent episodes of dizziness. The presentation is usually between the ages of 2 years and 7 years of age and is characterised by short episodes of vertigo of sudden onset when the child appears distressed and unwell. The child may cling to something or someone for support. The episode lasts only minutes and resolves suddenly and completely. It is a self-limiting condition and usually resolves after about eighteen months, although many go on to experience migrainous vertigo (or vertiginous migraine) when older.

Benign paroxysmal vertigo of childhood is a migrainous phenomenon with more than 50% of those affected having a family history of migraines affecting a first-degree relative. It has no relationship to benign paroxysmal positional vertigo which is a different condition entirely.