question: what causes the pain in a headache?
comment: OP we **do not know** the answer to this and I regret to inform you some will speak as if they do. There are *many* causes of headache, some more obvious than the other. For instance, some have told you already how it has something to do with the nerves. You do not have sensation in your brain. Local anesthetic is not needed for brain surgeries (ie lobotomies). You can sense pressure inside the head (which is actually distinct from pain), but that is the extent of what we know. Sometimes there are fragments of the skull in serious emergency that break off & cause pain locally, other times there’s well established types of cancers that cause headaches in certain regions, or splitting headaches. For a headache originating from, say, the common cold, we don’t know where they come from or how. There are some theories, but they’re VERY unscientific and some are unfalsifiable (ie making correlation observations) and could be interpreted many ways. TL;DR: We don’t know.
passages: Headaches often result from traction to or irritation of the meninges and blood vessels. The nociceptors may be stimulated by head trauma or tumors and cause headaches. Blood vessel spasms, dilated blood vessels, inflammation or infection of meninges and muscular tension can also stimulate nociceptors and cause pain. Once stimulated, a nociceptor sends a message up the length of the nerve fiber to the nerve cells in the brain, signaling that a part of the body hurts.
   The brain itself is not sensitive to pain, because it lacks pain receptors. However, several areas of the head and neck do have pain receptors and can thus sense pain. These include the extracranial arteries, middle meningeal artery, large veins, venous sinuses, cranial and spinal nerves, head and neck muscles, the meninges, falx cerebri, parts of the brainstem, eyes, ears, teeth and lining of the mouth. Pial arteries, rather than pial veins are responsible for pain production.
   A number of different causes contribute to this class of headache. Several common chemicals may be the culprit. Nitrite compounds dilate blood vessels, causing dull and pounding headaches with repeat exposure. Nitrite is found in dynamite, heart medicine and it is a chemical used to preserve meat (ergo these being known as "nitrite" or "hot dog" headaches). Eating foods prepared with monosodium glutamate (MSG) may thus result in headache. Acetaldehyde from alcohol may also cause a headache either acutely or after a number of hours (hangover).
   Headaches can occur as a result of many conditions whether serious or not. There are a number of different classification systems for headaches. The most well-recognized is that of the International Headache Society. Causes of headaches may include dehydration, fatigue, sleep deprivation, stress, the effects of medications, the effects of recreational drugs, viral infections, loud noises, common colds, head injury, rapid ingestion of a very cold food or beverage, and dental or sinus issues.
   As a final point, throughout TTH literature stress is mentioned as a factor and may be implicated via the adrenal axis. This ultimately results in downstream activation of NMDA receptor activation, NFκB activation, and upregulation of iNOS with subsequent production of NO leading to pain as described above.
  
  Section::::Diagnosis.
  
  With TTH the physical exam is expected to be normal with perhaps the exception of either pericranial tenderness upon palpation of the cranial muscles, or presence of either photophobia or phonophobia.
  
  Section::::Diagnosis.:Differential Diagnosis:.
  
  BULLET::::- Migraine
  
  BULLET::::- Oromandibular dysfunction
  
  BULLET::::- Sinus disease
  
  BULLET::::- Eye disease
  
  BULLET::::- Cervical spine disease
   Cervicogenic headache originates from disorders of the neck, including the anatomical structures innervated by the cervical roots C1–C3. Cervical headache is often precipitated by neck movement and/or sustained awkward head positioning. It is often accompanied by restricted cervical range of motion, ipsilateral neck, shoulder, or arm pain of a rather vague non-radicular nature or, occasionally, arm pain of a radicular nature.
  
  Section::::Traction/inflammatory.
  
  Traction and inflammatory headaches are symptoms of other disorders, ranging from stroke to sinus infection.
  
  Specific types of headaches include:
  
  BULLET::::- Tension headache
  
  BULLET::::- Migraine
  
  BULLET::::- Idiopathic intracranial hypertension (headache with visual symptoms due to raised intracranial pressure)
   Headache attributed to a substance or its withdrawal
  
  Headaches can be attributed to many different substances. Some of these include alcohol, NO, carbon monoxide poisoning, cocaine, caffeine and monosodium glutamate. Chronic use of certain medications used to treat headaches can also start causing headaches, known as medication overuse headaches. Headaches may also be a symptom of medication withdrawal.
  
  Section::::Classification.
  
  These headaches have been further sub classified by the ICHD2 into
  
  BULLET::::- Headaches induced by acute substance use or exposure
  
  BULLET::::- Medication overuse headaches (MOH)
  
  BULLET::::- Headaches attributed to chronic medication use
  
  BULLET::::- Headaches attributed to substance withdrawal
  
  Section::::Causes.
   Headache
  
  Headache is the symptom of pain anywhere in the region of the head or neck. It occurs in migraines (sharp, or throbbing pains), tension-type headaches, and cluster headaches. Frequent headaches can affect relationships and employment. There is also an increased risk of depression in those with severe headaches.
   Section::::Medicinal.:Preventative medications.
  
  The most common medicines used to treat chronic (daily) headaches are called prophylactic medicines, which are used to prevent headaches. Such preventative medication is taken on a daily basis, even when a person may not have a headache. Prophylactic medicines are recommended for chronic headache patients because varied experiments prove that the medications "reduce the frequency, severity, and disability associated with daily headaches". A majority of the prophylactic medications work by inhibiting or increasing neurotransmissions in the brain, often preventing the brain from interpreting pain signals.
   Migraines are currently thought to be caused by dysfunction of the nerves in the brain. Previously, migraines were thought to be caused by a primary problem with the blood vessels in the brain. This vascular theory, which was developed in the 20th century by Wolff, suggested that the aura in migraines is caused by constriction of intracranial vessels (vessels inside the brain), and the headache itself is caused by rebound dilation of extracranial vessels (vessels just outside the brain). Dilation of these extracranial blood vessels activates the pain receptors in the surrounding nerves, causing a headache. The vascular theory is no longer accepted. Studies have shown migraine head pain is not accompanied by extracranial vasodilation, but rather only has some mild intracranial vasodilation.
   Although the musculature of the head and neck and psychological factors such as stress may play a role in the overall pathophysiology of TTH, neither is currently believed to be the sole cause of the development of TTH. The pathologic basis of TTH is most likely derived from a combination of personal factors, environmental factors, and alteration of both peripheral and central pain pathways. Peripheral pain pathways receive pain signals from pericranial (around the head) myofascial tissue (protective tissue of muscles) and alteration of this pathway likely underlies episodic tension-type headache (ETTH). In addition to these myofascial tissue pain signals, pericranial muscle tenderness, inflammation, and muscle ischemia have been postulated in headache literature to be causal factors in the peripheral pathophysiology of TTH. However, multiple studies have failed to illustrate evidence for a pathologic role of either ischemia or inflammation within the muscles. Pericranial tenderness is also not likely a peripheral causal factor for TTH, but may instead act to trigger a chronic pain cycle in which the peripheral pain response is transformed over time into a centralized pain response. It is then these prolonged alterations in the peripheral pain pathways that lead to increased excitability of the central nervous system pain pathways, resulting in the transition of episodic tension-type headache into chronic tension type headache (CTTH). Specifically, the hyperexcitability occurs in central nociceptive neurons (the trigeminal spinal nucleus, thalamus, and cerebral cortex) resulting in central sensitization, which manifests clinically as allodynia and hyperalgesia of CTTH. Additionally, CTTH patients exhibit decreased thermal and pain thresholds which further bolsters support for central sensitization occurring in CTTH.
   People who are more susceptible to experience migraines without headache are those who have a family history of migraines, women, and women who are experiencing hormonal changes or are taking birth control pills or are prescribed hormone replacement therapy.
  
  Tension headaches are thought to be caused by activation of peripheral nerves in the head and neck muscles 
  
  Cluster headaches involve overactivation of the trigeminal nerve and hypothalamus in the brain, but the exact cause is unknown.
  
  Section::::Diagnostic approach.
   Primary headaches are more difficult to understand than secondary headaches. The exact mechanisms which cause migraines, tension headaches and cluster headaches are not known. There have been different hypotheses over time which attempt to explain what happens in the brain to cause these headaches.
   Section::::Diagnostic approach.:Neuroimaging.
  
  Section::::Diagnostic approach.:Neuroimaging.:Old headaches.
  
  The US Headache Consortium has guidelines for neuroimaging of non-acute headaches. Most old, chronic headaches do not require neuroimaging. If a person has the characteristic symptoms of a migraine, neuroimaging is not needed as it is very unlikely the person has an intracranial abnormality. If the person has neurological findings, such as weakness, on exam, neuroimaging may be considered.
  
  Section::::Diagnostic approach.:Neuroimaging.:New headaches.
   MOH is known to occur with frequent use of many different medications, including most commonly: triptans, ergotamines, analgesics, opioids. Dietary and medicinal caffeine consumption appears to be a modest risk factor for chronic daily headache onset, regardless of headache type. 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).
   Section::::Medicinal.
  
  Section::::Medicinal.:Analgesic and abortive medications.
   Old headaches are usually primary headaches and are not dangerous. They are most often caused by migraines or tension headaches. Migraines are often unilateral, pulsing headaches accompanied by nausea or vomiting. There may be an aura (visual symptoms, numbness or tingling) 30–60 minutes before the headache, warning the person of a headache. Migraines may also not have auras. Tension type headaches usually have bilateral "bandlike" pressure on both sides of the head usually without nausea or vomiting. However, some symptoms from both headache groups may overlap. It is important to distinguish between the two because the treatments are different.
   Treatment of a headache depends on the underlying cause, but commonly involves pain medication. A headache is one of the most commonly experienced of all physical discomforts.
  
  About half of adults have a headache in a given year. Tension headaches are the most common, affecting about 1.6 billion people (21.8% of the population) followed by migraine headaches which affect about 848 million (11.7%).
  
  Section::::Cause.
  
  There are more than 200 types of headaches. Some are harmless and some are life-threatening. The description of the headache and findings on neurological examination, determine whether additional tests are needed and what treatment is best.
   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.
   The most common type of vascular headache is "migraine". Migraine headaches are usually characterized by severe pain on one or both sides of the head, an upset stomach, and, for some people, disturbed vision. It is more common in women. While vascular changes are evident during a migraine, the cause of the headache is neurological, not vascular. After migraine, the most common type of vascular headache is the "toxic" headache produced by fever.
   The American Headache Society recommends using "SSNOOP", a mnemonic to remember the red flags for identifying a secondary headache:
  
  BULLET::::- Systemic symptoms (fever or weight loss)
  
  BULLET::::- Systemic disease (HIV infection, malignancy)
  
  BULLET::::- Neurologic symptoms or signs
  
  BULLET::::- Onset sudden (thunderclap headache)
  
  BULLET::::- Onset after age 40 years
  
  BULLET::::- Previous headache history (first, worst, or different headache)
  
  Other red flag symptoms include:
  
  Section::::Diagnostic approach.:Old headaches.
   Section::::Mechanism.:Specific Physiological Changes involved in Central Sensitization and Development of CTTH.
  
  The alterations in physiology that lead to overall process of central sensitization involve changes at the level neural tracts, neurotransmitters and their receptors, the neural synapse, and the post-synaptic membrane. Evidence suggests dysfunction in supraspinal descending inhibitory pain pathways may contribute to the pathogenesis of central sensitization in CTTH.
   BULLET::::- cluster headaches: short episodes (15–180 minutes) of severe pain, usually around one eye, with autonomic symptoms (tearing, red eye, nasal congestion) which occur at the same time every day. Cluster headaches can be treated with triptans and prevented with prednisone, ergotamine or lithium.
  
  BULLET::::- trigeminal neuralgia or occipital neuralgia: shooting face pain
  
  BULLET::::- hemicrania continua: continuous unilateral pain with episodes of severe pain. Hemicrania continua can be relieved by the medication indomethacin.
   BULLET::::- Accidental dural puncture with headache (common, about 1 in 100 insertions). The epidural space in the adult lumbar spine is only 3-5mm thick, which means it is comparatively easy to traverse it and accidentally puncture the dura (and arachnoid) with the needle. This may cause cerebrospinal fluid (CSF) to leak out into the epidural space, which may in turn cause a post dural puncture headache (PDPH). This can be severe and last several days, and in some rare cases weeks or months. It is caused by a reduction in CSF pressure and is characterised by postural exacerbation when the subject raises his/her head above the lying position. Mild PDPH may respond to caffeine and gabapentin administration. If severe it may be successfully treated with an epidural blood patch (a small amount of the subject's own blood given into the epidural space via another epidural needle which clots and seals the leak). Most cases resolve spontaneously with time. A change in headache pattern (e.g., headache worse when the subject lies down) should alert the physician to the possibility of development of rare but dangerous complications, such as subdural hematoma or cerebral venous thrombosis.
   Currently, most specialists think migraines are due to a primary problem with the nerves in the brain. Auras are thought to be caused by a wave of increased activity of neurons in the cerebral cortex (a part of the brain) known as cortical spreading depression followed by a period of depressed activity. Some people think headaches are caused by the activation of sensory nerves which release peptides or serotonin, causing inflammation in arteries, dura and meninges and also cause some vasodilation. Triptans, medications which treat migraines, block serotonin receptors and constrict blood vessels.
  