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.

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.

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.

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.

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.

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.

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).

A review on potential triggers in the indoor and outdoor environment concluded that there is insufficient evidence to confirm environmental factors as causing migraines. They nevertheless suggested that people with migraines take some preventive measures related to indoor air quality and lighting.

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.

Chronic headache, or chronic daily headache (CDH), is classified as experiencing fifteen or more days with a headache per month. It is estimated that chronic headaches affect "4% to 5% of the general population". Chronic headaches consist of different sub-groups, primarily categorized as chronic tension-type headaches and chronic migraine headaches. The treatments for chronic headache are vast and varied. Medicinal and non-medicinal methods exist to help patients cope with chronic headache, because chronic headaches cannot be cured. Whether pharmacological or not, treatment plans are often created on an individual basis. Multiple sources recommend "multimodal treatment", which is a combination of medicinal and non-medicinal remedies. Some treatments are controversial and are still being tested for effectiveness. Suggested treatments for chronic headaches include medication, physical therapy, acupuncture, relaxation training, and biofeedback. In addition, dietary alteration and behavioral therapy or psychological therapy are other possible treatments for chronic headaches.

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).

The pathophysiology of SUNCT is incompletely understood. Recent studies suggest the existence of a relationship between the hypothalamus and the condition.

Functional MRI and deep brain stimulation of a large patient pool showed activation of the posterior hypothalamus during attacks of primary SUNCT, on both sides and contralaterally (on the opposite side). Functional MRI studies suggest brain stem activation during attacks as well. Activation of the trigeminocervical complex and other related structures results from innervation from branches of trigeminal and upper cervical nerves.

There exists a direct connection between trigeminal nucleus caudalis, which is located in the brain stem, and the posterior hypothalamus. Therefore, it is possible that stimulation of the peripheral trigeminal nerve activates the hypothalamus and the hypothalamus in turn communicates with the trigeminal nucleus caudalis via neurotransmitters such as orexin.

Elevated levels of prolactin, secretion of which is regulated by the hypothalamus, seem to be associated with SUNCT attacks. Some patients with a pituitary tumor only experience attacks at night. These patients only exhibit higher levels of prolactin at night, even where hormone levels, including prolactin, were normal throughout the day.

SUNCT is considered a primary headache (or condition), but can also occur as a secondary symptom of other conditions. However, a patient can only be diagnosed with SUNCT as a primary condition.

A pituitary tumor causes SUNCT as a secondary headache. Some patients with a pituitary tumor complain of short-lasting heachaches. Upon removal of the tumor, the symptoms of SUNCT may disappear permanently.

Although it occurs very rarely, paranasal sinusitis can also cause secondary SUNCT. The symptoms of SUNCT in such cases can be removed permanently with endoscopic sinus surgery.

Short-lasting unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT syndrome), is a rare headache disorder that belongs to the group of headaches called trigeminal autonomic cephalalgia (TACs). Symptoms include excruciating burning, stabbing, or electrical headaches mainly near the eye and typically these sensations are only on one side of the body. The headache attacks are typically accompanied by cranial autonomic signs that are unique to SUNCT. Each attack can last from five seconds to six minutes and may occur up to 200 times daily.

TACs are caused by activation of the autonomic nervous system of the trigeminal nerve in the face.

As of 2015 about 50 cases have been described in the medical literature. Onset of the symptoms usually come later in life, at an average age of about 50. Although the majority of patients are men over the age of 50, it is not uncommon to find SUNCT present among other age groups, including children and infants.

These headaches are estimated to appear in roughly 1% of the population. They can occur with sexual activity at any age. It is more common in men than women, with studies putting the gender ratio between 1.2:1 and 3:1.

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.

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.

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."

Although CPH is often compared to cluster headaches, it is much less prevalent, occurring in only 1–3% of those who experience cluster headaches. CPH occurs roughly in 1 in 50,000 people, while cluster headaches are comparatively more common and are found in 1 in 1000 people.

Cluster headaches occur primarily in men, while CPH is more commonly diagnosed in women. The female to male ratio of diagnosed patients can range anywhere from 1.6:1 to 2.36:1. Symptoms may begin to appear at any age, but onset usually occurs in adulthood with a mean starting age within the thirties.

The most common chronic treatment method is the use of medicine. Many people try to seek pain relief from analgesic medicines (commonly termed pain killers), such as aspirin, acetaminophen, aspirin compounds, ibuprofen, and opioids. The long term use of opioids; however, appears to result in greater harm than benefit. Also, abortive medications can be used to "stop a headache once it has begun"; such drugs include ergotamine (Cafergot), triptans (Imitrex), and prednisone (Deltasone). However, medical professionals advise that abuse of analgesics and abortive medications can actually lead to an increase in headaches. The painkiller medicines help headaches temporarily, but as the "quick fix" wears off, headaches become more re-current and grow in intensity. These "rebound headaches" can actually make the body less responsive to preventive medication. The conditions keep worsening if one takes paracetamol, aspirin and non-steroidal anti-inflammatory drugs (NSAIDs) for 15 days a month or more. Therefore, analgesic and abortive medications are often advised for headaches that are not chronic in nature.

A ten-patient study conducted by Pareja et al. found that all patients diagnosed with CPH were responsive to indomethacin and were able to completely control their symptoms. Doses of the drug ranged from 25 mg per day to 150 mg per day with a median dose of 75 mg per 24-hour period.

Almost all cases of CPH respond positively and effectively to indometacin, but as much as 25 percent of patients discontinued use of the drug due to adverse side effects, namely complications in the gastrointestinal tract.

According to a case study by Milanlioglu et al., 100mg of lamotrigine, an antiepileptic drug, administered twice daily alleviated all painful symptoms. No side effects were noted after two months of treatment. Dosage of lamotrigine was decreased to 50mg a day after the first two months, and no symptoms or side-effects were recorded after a three-month followup.

Use of topiramate has also been found to be an effective treatment for CPH, but cluster headache medications have been found to have little effect.

The International Headache Society's International Classification of Headache Disorders classifies hemicrania continua as a primary headache disorder.

Hemicrania was mentioned in 1881 in The Therapeutic Gazette Vol. 2, by G.S.Davis, and the incident has been cited in King's American Dispensatory (1898 and later editions) in the description of the strong analgesic Jamaican Dogwood, a relatively low dose of which reportedly produced convulsions and prolonged respiratory depression over six hours in an elderly woman with this condition.

In newer times, Hemicrania continua was described in 1981; at that time around 130 cases were described in the literature. However, rising awareness of the condition has led to increasingly frequent diagnosis in headache clinics, and it seems that it is not as rare as these figures would imply. The condition occurs more often in women than men and tends to present first in adulthood, although it has also been reported in children as young as 5 years old.

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.

Hypnic headaches are benign primary headaches that affect the elderly, with the average age of onset being 63 ± 11 years. They are moderate, throbbing, bilateral or unilateral headaches that wake the sufferer from sleep once or multiple times a night. They typically begin a few hours after sleep begins and can last from 15–180 min. There is normally no nausea, photophobia, phonophobia or autonomic symptoms associated with the headache. They commonly occur at the same time every night possibly linking the headaches with circadian rhythm, but polysomnography has recently revealed that the onset of hypnic headaches may be associated with REM sleep.

Lithium carbonate 200–600 mg at bedtime is an effective treatment for most patients but for those that can not tolerate Lithium, Verapamil, indomethacin or methylsergilide may be tried. Two patients have also responded to flunarizine 5 mg. It has also been shown that 1–2 cups of coffee or 100–200 mg of caffeine before bed can prevent hypnic headaches.

For diagnosis of hypnic headache syndrome, headaches should occur at least 15 times per month for at least one month. Included in the differential diagnosis of a new onset nighttime headaches in the elderly is drug withdrawal, temporal arteritis, Sleep apnea, oxygen desaturated, Pheochromocytoma, intracranial causes, primary and secondary neoplasms, communicating hydrocephalus, subdural hematoma, vascular lesions, migraines, cluster headaches, chronic paroxysmal hemicrania and hypnic headache. All other causes must be ruled out before the diagnosis of hypnic headache can be made.