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.

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.

Migraine itself is a very common disorder, occurring in 15–20% of the population. Hemiplegic migraine, be it familial or spontaneous, is less prevalent, 0.01% prevalence according to one report. Women are three times more likely to be affected than males.

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.

Sporadic hemiplegic migraine (SHM) has clinical symptoms identical to familial hemiplegic migraine (FHM) and distinct from migraine with aura. By definition the neurodeficits are supposed to be reversible. However, some cases with permanent neurological deficits have also been noted.

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.

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.

Migraine itself is a very common disorder, occurring in 15–20% of the population. Hemiplegic migraine, be it familial or spontaneous, is less prevalent, 0.01% prevalence according to one report. Women are three times more likely to be affected than males.

Familial hemiplegic migraine (FHM) is an autosomal dominant type of hemiplegic migraine that typically includes weakness of half the body which can last for hours, days or weeks. It can be accompanied by other symptoms, such as ataxia, coma and paralysis. There is clinical overlap in some FHM patients with episodic ataxia type 2 and spinocerebellar ataxia type 6, benign familial infantile epilepsy, and alternating hemiplegia of childhood. There are 3 known loci for FHM. FHM1, which accounts for approximately 50% of FHM patients, is caused by mutations in a gene coding for the P/Q-type calcium channel α subunit, CACNA1A. FHM1 is also associated with cerebellar degeneration. FHM2, which accounts for <25% of FHM cases, is caused by mutations in the /-ATPase gene ATP1A2. FHM3 is a rare subtype of FHM and is caused by mutations in a sodium channel α-subunit coding gene, SCN1A. These three subtypes do not account for all cases of FHM, suggesting the existence of at least one other locus (FHM4). Many of the non-familial cases of hemiplegic migraine (sporadic hemiplegic migraine) are also caused by mutations at these loci. A fourth gene that has been associated with this condition is the proline rich transmembrane protein 2 (PRRT2) - an axonal protein associated with the exocytosis complex. A fifth gene associated with this condition is SLC4A4 which encodes the electrogenic NaHCO3cotransporter NBCe1.

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.

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.

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.

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.

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 pathophysiology of MAV is not completely understood; both central and peripheral defects have been observed.

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 cause of benign paroxysmal torticollis in infants is thought to be migrainous. More than 50% of infants have a family history of migraine in first degree relatives. The cause is likely to be genetic.

The mechanism of action of benign paroxysmal torticollis is not yet understood. It has been suggested that unilateral vestibular dysfunction or vascular disturbance in the brain stem may be responsible for the condition.

Acephalgic migraine (also called acephalalgic migraine, migraine aura without headache, amigrainous migraine, isolated visual migraine, and optical migraine) is a neurological syndrome. It is a relatively uncommon variant of migraine in which the patient may experience aura, nausea, photophobia, hemiparesis, and other migraine symptoms, but does not experience headache. It is generally classified as an event fulfilling the conditions of migraine with aura with no (or minimal) headache. It is sometimes distinguished from visual-only migraine aura without headache, also called ocular migraine.

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 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.

The cause of AHC is unknown. It was initially thought to be a form of complicated migraine because of strong family histories of migraine reported in AHC cases. AHC has also been considered to be a movement disorder or a form of epilepsy. Suggested causes have included channelopathy, mitochondrial dysfunction, and cerebrovascular dysfunction. The disorder most closely related to AHC is familial hemiplegic migraine, and this was recently discovered to be caused by a mutation in a gene for calcium channel receptors. It is suspected that AHC may be caused by a similar channelopathy, and this is a current area of investigation into the cause of AHC. An association with "ATP1A2" mutation has been found in some patients, but other studies have found no mutations and thus a lack of evidence that mutations which cause AHC are in the same genes as mutations which cause familial hemiplegic migraine.

Because alternating hemiplegia of childhood is so rare, there is no increased risk of AHC for the children of siblings of someone with AHC, but it is believed to be autosomal dominant, by which a person with AHC has a 50% change of passing the disorder on to their children. AHC is questionably a progressive disease, because cognitive abilities do appear to decline over time. This cannot be completely determined however, because the mechanism of AHC's progression is unknown. It is likely that it is caused by a generalized cellular dysfunction caused by a mitochondrial disorder. However, studies involving mechanisms of AHC have been inconclusive. Experts currently researching this disorder believe that the cause of AHC is a mutated ion channel. This would make the cause difficult to find because one disrupted channel may be represented differently in different tissues. This mutation is suspected because the most closely related disease, FHM, is also caused by a mutated ion channel. A small number of genes which were suspected to carry a mutation for AHC have been screened for sodium channel protein mutations, ATP pump mutations, and excitatory amino acid transmitter mutations. None of these have yet been successful in determining the underlying cause of AHC.

One large study has identified the gene ATP1A3 as the likely genetic cause of this disorder. This gene is located on the long arm of chromosome 19 (19q13.31).

Persistent aura without infarction (PAWOI) is a little-known condition, first described under the designation prolonged migraine aura status, that is not yet fully understood. PAWOI is said to be a possible cause of a variety of neurological symptoms, including visual snow, loss of vision, increased afterimages, tinnitus, and others. However, the pathogenesis of PAWOI is unknown; in other words, it is not known exactly what causes these symptoms. Furthermore, it is not clear which medical examinations are useful in diagnosing PAWOI. At present, PAWOI is usually diagnosed solely based on the patient's present and past symptoms. It may be possible that an overactive brain or a chemical imbalance is partly to blame for the disorder.

Different medication has been tried as treatment, notably acetazolamide, valproate, lamotrigine, topiramate, and furosemide.

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.

The prevalence of SCA6 varies by culture. In Germany, SCA6 accounts for 10-25% of all autosomal dominant cases of SCA (SCA itself having a prevalence of 1 in 100,000). This prevalence in lower in Japan, however, where SCA6 accounts for only ~6% of spinocerebellar ataxias. In Australia, SCA6 accounts for 30% of spinocerebellar ataxia cases while 11% in the Dutch.

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.