question: How come we experience headaches while our brains do not have pain receptors?
comment: It's not a "brain ache." Your brain doesn't hurt; pain-sensitive areas around your brain hurt including the tissue between your brain and skull.
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.
   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
   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.
   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).
   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.
   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::::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.
   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.
   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.
   Neuroimaging is not indicated for patients with stable headaches which are diagnosed as migraine. Studies indicate that presence of migraine does not increase a patient's risk for intracranial disease. A diagnosis of migraine which notes the absence of other problems, such as papilledema, would not indicate a need for neuroimaging. In the course of conducting a careful diagnosis, the physician should consider whether the headache has a cause other than the migraine and might require neuroimaging.
   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.
   Severity of ictal headaches can vary from a slight pressure or "cloud" to an intensity far beyond migraine. Some have called it a "suicide headache" in the worst instances. Temporary blindness may also occur in some cases.
  
  Symptoms besides headache may be either present or absent, and may include unusual thoughts or experiences. In these cases it is especially important to obtain a correct diagnosis. Many people with these experiences are accidentally diagnosed with conditions such as psychosis or schizophrenia and given antipsychotic medications, which may actually increase seizure activity.
  
  Section::::Treatment and diagnosis.
   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).
   Other conditions that can cause similar symptoms to a migraine headache include temporal arteritis, cluster headaches, acute glaucoma, meningitis and subarachnoid hemorrhage. Temporal arteritis typically occurs in people over 50 years old and presents with tenderness over the temple, cluster headaches presents with one-sided nose stuffiness, tears and severe pain around the orbits, acute glaucoma is associated with vision problems, meningitis with fevers, and subarachnoid hemorrhage with a very fast onset. Tension headaches typically occur on both sides, are not pounding, and are less disabling.
   Cranial autonomic nervous symptoms occur with painful exacerbations in 21%, and cutaneous allodynia may be present in 26%.
  
  In 2002, Li and Rozen conducted a study of 56 patients at the Jefferson Headache Center in Philadelphia and published the following results:
  
  BULLET::::- 82% of patients were able to pinpoint the exact day their headache started.
  
  BULLET::::- 30% of the patients, the onset of the headache occurred in correlation with an infection or flu-like illness.
  
  BULLET::::- 38% of the patients had a prior personal history of headache.
  
  BULLET::::- 29% of the patients had a family history of headache.
   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.
   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.
   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.
   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.
   The NIH classification consists of brief definitions of a limited number of headaches.
  
  The NIH system of classification is more succinct and only describes five categories of headaches. In this case, primary headaches are those that do not show organic or structural cause. According to this classification, headaches can only be vascular, myogenic, cervicogenic, traction and inflammatory.
  
  Section::::Management.
  
  Primary headache syndromes have many different possible treatments. In those with chronic headaches the long term use of opioids appears to result in greater harm than benefit.
  
  Section::::Management.:Migraines.
   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.
   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.
   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)
   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.
   The second theory posits that either increased blood flow to the brain or increase in the brain tissue itself may result in the raised pressure. Little evidence has accumulated to support the suggestion that increased blood flow plays a role, but recently Bateman et al. in phase contrast MRA studies have quantified cerebral blood flow (CBF) in vivo and suggests that CBF is abnormally elevated in many people with IIH. Both biopsy samples and various types of brain scans have shown an increased water content of the brain tissue. It remains unclear why this might be the case.
  
presuppositions: Headaches are caused by the brain hurting. Headaches hurt your brain.
corrections: Brains do not hurt. Headaches are caused by areas around your brain hurting. Headaches hurt pain-sensitive areas around your brain.
raw_presuppositions: Headaches are caused by the brain hurting. Headaches hurt your brain.
raw_corrections: Brains do not hurt. Headaches are caused by areas around your brain hurting. Headaches hurt pain-sensitive areas around your brain.