question: If we don't really have pain receptors on our physical brains, why do headaches hurt our heads?
comment: Because your head isn't just your brain. There are plenty of pain receptors in your scalp, and this is where the effect happens.
passages: 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.
   The tendency to develop head pain when faced with a stressor or strong sensory stimuli can be explained in two ways. First, it may be a side effect of other CNS processes that provide important evolutionary advantages. One example is counteracting the dilation of cranial arteries to counteract dangerous vasoconstriction in the brain. Second, migraine may be an example of how pain has evolved to encourage organisms to avoid potentially harmful situations. Olfactory-induced migraines (migraines stimulated by strong smells) have been explained as an attempt to interrupt the entry of toxins into the brain via the olfactory nerve. Similarly, the low threshold for nausea and vomiting may be a mechanism to enhance elimination of ingested toxins in food. Migraineurs have a lower prevalence of malignant neoplasms in the brain than controls, suggesting that migraines are protective against tumors. However, the mechanism responsible for this difference is unknown.
   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.
   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
   BULLET::::2. The cranial nerves III-XII emerge from the brainstem. These cranial nerves supply the face, head, and viscera. (The first two pairs of cranial nerves arise from the cerebrum).
  
  BULLET::::3. The brainstem has integrative functions being involved in cardiovascular system control, respiratory control, pain sensitivity control, alertness, awareness, and consciousness. Thus, brainstem damage is a very serious and often life-threatening problem.
  
  Section::::Function.:Cranial nerves.
   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.
   Specific neuronal receptors and neurotransmitters thought to be most involved include NMDA and AMPA receptors, glutamate, serotonin (5-HT), β-endorphin, and nitric oxide (NO). Of the neurotransmitters, NO plays a major role in central pain pathways and likely contributes to the process of central sensitization. Briefly, the enzyme nitric oxide synthase (NOS) forms NO which ultimately results in vasodilatation and activation of central nervous system pain pathways. Serotonin may also be of significant importance and involved in malfunctioning pain filter 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. 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 as well as amitriptyline in chronic tension-type headache is not solely due to serotonin reuptake inhibition, and likely other mechanisms are involved.
   Section::::Evolution.:Conflicts with other organisms.
  
  A headache-prone CNS may have resulted from interactions with other organisms in two ways. The first possibility is that migraine offers an advantage to the organism in fighting infection by increasing blood flow to the brain. The second possibility is that certain pathogens evolved to cause headache as a way of speeding their transmission to other organisms. Finally, migraine may benefit neither the host nor the pathogen, but may simply be the result of certain infections. This last explanation is concordant with the apparent negative impact of migraine on human fitness.
  
  Section::::Evolution.:Novel environmental factors.
   There are a number of structures in the cranial cavity that can be effected when you get a traumatic injury to the head. These injuries can be potentially cause major damage to the brain. Moderate injuries can cause a few negative effects while, a severe injury to cranial cavity or any contents, can have very serious results, including death. 
  
  The Cranial Cavity houses the meninges, as well as other necessary organs and these membranes surround the central nervous system. If an infection forms, it can lead to a disease called meningitis which can be potentially fatal.
  
  Section::::External links.
   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.
   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.
   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).
   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.
   Section::::Evolution.:Headache as a design construct.
  
  Finally, migraine may be a component of imperfect central nervous system design. Evidence has suggested a dysfunction of pain-inhibitory pathways in migraine and discordant interaction between the ancient brain stem design and the more evolved neocortex. The brain stem may be unable to suppress excessive input from higher brain centers.
   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.
   Nociceptors are responsible for processing pain and temperature changes. The burning pain and irritation experienced after eating a chili pepper (due to its main ingredient, capsaicin), the cold sensation experienced after ingesting a chemical such as menthol or icillin, as well as the common sensation of pain are all a result of neurons with these receptors.
  
  Problems with mechanoreceptors lead to disorders such as:
  
  BULLET::::- Neuropathic pain - a severe pain condition resulting from a damaged sensory nerve
   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.
   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.
   The cutaneous innervation of the head is as follows:
  
  BULLET::::- Ophthalmic nerve (green)
  
  BULLET::::- Maxillary nerve (pink)
  
  BULLET::::- Mandibular nerve (yellow)
  
  BULLET::::- Cervical plexus (purple)
  
  BULLET::::- Dorsal rami of cervical nerves (blue) and others are in picture which show following in upper column
  
  Section::::Function.
  
  The head contains sensory organs: two eyes, two ears, a nose and tongue inside of the mouth. It also houses the brain. Together, these organs function as a processing center for the body by relaying sensory information to the brain. Humans can process information faster by having this central nerve cluster.
  
  Section::::Society and culture.
   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)
   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.
   “Headaches come from invalidating the self . . . Forgive yourself, let it go, and the headache will dissolve back into the nothingness from where it came . . . Migraine headaches are created by people who want to be perfect and who create a lot of pressure on themselves. A lot of suppressed anger is involved…”
   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.
   BULLET::::- mild or moderate intensity
  
  BULLET::::- not aggravated by routine physical activity such as walking or climbing stairs
  
  BULLET::::- Both of the following:
  
  BULLET::::- no nausea or vomiting
  
  BULLET::::- no more than one of photophobia (sensitivity to bright light) or phonophobia (sensitivity to loud sounds)
  
  Tension-type headaches may be accompanied by tenderness of the scalp on manual pressure during an attack.
  
  Section::::Cause.
  
  Section::::Cause.:Risk Factors.
  
  Various precipitating factors may cause tension-type headaches in susceptible individuals:
  
  BULLET::::- Anxiety
  
  BULLET::::- Stress
  
  BULLET::::- Sleep problems
  
  BULLET::::- Young age
  
  BULLET::::- Poor health
  
  Section::::Mechanism.
  
  Section::::Mechanism.:Overview of Pathophysiology of ETTH and CTTH.
   Injuries to the brain can be life-threatening. Normally the skull protects the brain from damage through its hard unyieldingness; the skull is one of the least deformable structures found in nature with it needing the force of about 1 ton to reduce the diameter of the skull by 1 cm. In some cases, however, of head injury, there can be raised intracranial pressure through mechanisms such as a subdural haematoma. In these cases the raised intracranial pressure can cause herniation of the brain out of the foramen magnum ("coning") because there is no space for the brain to expand; this can result in significant brain damage or death unless an urgent operation is performed to relieve the pressure. This is why patients with concussion must be watched extremely carefully.
  
presuppositions: Our brains do not have brain receptors, therefore we should not experience pain during headaches.  Head pain can only be felt by pain receptors on oour physical brains.
corrections: Pain from headaches does not come from pain receptors in the brain, but from the scalp and other areas on our head.  There are plenty of pain receptors in your scalp.
raw_presuppositions: Our brains do not have brain receptors, therefore we should not experience pain during headaches.  Head pain can only be felt by pain receptors on oour physical brains.
raw_corrections: Pain from headaches does not come from pain receptors in the brain, but from the scalp and other areas on our head.  There are plenty of pain receptors in your scalp.