What are Headaches?

Headaches explained by Denver, Golden, Aurora, Boulder, Broomfield, Jefferson, and Littleton Colorado’s top pain doctors

Headaches are a widespread condition, thought to affect approximately 16% of adults in the US. Painful sensations within the skull or upper neck area, or those felt in discrete parts of the face, head, or base of the skull are all regarded as types of headache.

Bad headacheHeadaches may be either consistent in nature (i.e. chronic) or occur as abrupt attacks of pain (acute). Acute headaches tend to take the form of pains that feel as though they are being caused by needles or other sharp objects. This type of headache is diagnosed if very rapid-onset discomfort or pain is felt in the head or neck and subsequently intensifies.

In contrast, episodic or recurrent headaches take place regularly, and often at the same approximate time of day. Recent studies suggest that 45 million U.S. adults are subject to this type of headache.Headaches are often perceived as throbbing or stabbing pains deep within the brain or just around it. This is misleading as the brain does not in fact possess the receptors (i.e. the biological sensors) necessary to feel pain.

Certain major nerves that transmit painful stimuli into the brain give rise to this impression. Headaches are a result of damage or irritation of the nerves and other tissues just outside the brain. These include the face and its musculature, major facial or cranial nerves, and the inner linings of the skull. Pain in these structures is mostly associated with injury, inflammation, or other damage. Headaches may be relatively mild and irritating, or a source of considerable functional deterioration. Severe headaches are a source of significant economic and healthcare burden.

Classification Of Headaches

There are a number of headache types that are classified as singular conditions based on their symptoms. These are known as primary headaches. Primary conditions are diagnosed if there are no known underlying conditions that may be associated with the type of headache pain concerned. Headaches caused by another illness or injury are known as secondary conditions. The following are some conditions with a very high prevalence (i.e. rate of development or number of cases per year).

Migraine Headaches

Research indicates that migraines are the most widespread primary headache condition. According to recent studies, up to 12% of people in the U.S. report the development of migraine symptoms per year. Women appear to be at higher risk of migraine pain than men. Some researchers associate the onset of migraine symptoms with the menstrual cycle of female patients. This type of headache is a recurrent condition, diagnosed in many cases by complaints of episodic, intense, pulsating pain in the front of the skull. Migraine pain is often perceived as located above or behind an eye (often the same eye per episode). This may eventually spread further outwards to other areas of the face, particularly without treatment. Migraines may have other, concomitant symptoms, such as nausea, vomiting, photophobia (i.e. light sensitivity), and strong adverse reactions to smells or noises.

The duration of these symptoms ranges from a number of hours to a number of days. Migraine episodes are commonly understood to go through some or all of the following stages:

  • Prodromal phase: This takes place at about 24 hours before an actual attack of migraine pain. It may be seen as a warning sign of an oncoming migraine episode. Migraine patients may experience prodromal symptoms such as deteriorations in mood, feelings of fatigue, compulsive yawning, and frequent urges to urinate.
  • Aura phase: Some patients may develop neurological effects prior to an attack of migraine pain. This is known as an aura phase. These effects may concern motor control, sensory perception, or vision. They can take the form of jagged lines or flashes in the field of vision or temporary blurring or sight loss in one eye. Aura phase may also include problems with proprioception before a migraine attack. Motion problems and weakness can also occur. Sensory complications such as the feeling of pins and needles or numbness are also symptoms of the aura phase.
  • Attack phase: This is the phase in which patients typically experience the pain and other symptoms of an acute migraine episode. The attack phase can last from four hours to three days. This can however be reduced by effective treatment.
  • Postdromal phase: This is a period of time after the attack phase has abated in which patients may feel weak and tired. In some cases, a wave of euphoria may be experienced in this phase.

Most episodes and phases are related to the primary condition and are not indicative of a more serious illness. However, if migraine pain or other symptoms are unusually severe, have a sudden and unprecedented onset, or worsen abruptly, seeking medical attention should be considered.

Cluster-Type Headaches

Cluster headaches are similar to migraine episodes in intensity and location. They are normally felt just above one eye, in a temple, or both. Cluster headaches are associated with sleep disturbances, i.e. they tend to occur at night, with sufficient severity to wake a patient. The pain associated with this type of headache may last as long as two hours. They are known as cluster headaches as they can occur as a succession of pain episodes. Patients can suffer as many as eight in a row per day. Cluster headaches are also associated with symptoms such as eye-watering, nasal congestion, and photophobia. Men of ages between 20 and 40 years are at a higher risk of developing this type of headache. Cluster headaches are reported to affect approximately 0.01% of the global population. They are regarded as one of the worst pains known to mankind.

Tension-Type Headaches

Tension-type headaches are perceived as located on or within the forehead, or in the back of the skull. Patients often experience them in a consistent pattern; e.g. they may have an onset every afternoon, abate in the evening, and then resume later at night. This type of headache may also last all day or for days on end (i.e. chronic tension headache). These must occur on 15 days or more per month to be diagnosed as a chronic condition. They are often described as a band of pressure around the head or forehead. Tension headaches may be associated with additional symptoms such as photophobia, sound sensitivity (sonophobia), or facial pains. Tension headaches are the most common headache type. There are roughly 210 million tension headache patients worldwide. They are not strongly associated with severe pain as are migraines or cluster headaches. They are associated with irritability, concentration detriments, and increased sensitivity to “headache triggers” such as lights, sounds, or smells.

Secondary Headaches

A secondary headache involves symptoms of the primary disorders as above, but is in fact a consequence of a pre-existing illness. It may also be an adverse reaction to drug therapy. Secondary headaches are associated with conditions such as fibromyalgia and meningitis. Most illnesses that cause secondary headaches are not fatal, however. A history of headache is not necessarily indicative of an underlying condition. The sudden onset, or exacerbation of, headache symptoms, or an otherwise atypical headache, may be cause to consult a physician however.

If the headache is accompanied by aura symptoms that are not explained by a migraine diagnosis, this may indicate a serious condition. If this is triggered by exertions involving involuntary muscle contraction, such as coughing, this may be associated with a stroke or an embolism. If the headache is accompanied by unusual mood shifts or personality changes this may also indicate a serious disorder. A headache in conjunction with loss of consciousness should be treated as a reason to seek emergency medical treatment. Headache pain may indicate meningitis, if neck stiffness, a rash, or fever is also present. Tenderness around or in the temples with headache pain may be a symptom of a disorder such as an aneurysm. These symptoms in conjunction with a headache may be no cause for concern, but are valid reasons to consult a doctor to eliminate the possibility of serious illness nonetheless.

Headaches, even alone, are associated with significant healthcare burden in any case. They are a leading source of over-the-counter analgesic (i.e. painkillers such as aspirin and ibuprofen) use. Patients with chronic or episodic cases of headache often find this type of treatment ineffective, however. Headaches can cause a significant reduction in concentration levels, cognitive function, and functional status in general.

Causes And Pathophysiology Of Headaches

Migrain Headache DiagramThe pain felt as a headache is conducted to the brain by major cranial or facial nerves or those serving the meninges (the inner linings of the skull). This may be associated with injury or inflammation to these nerves. The etiologies of chronic and episodic headaches in particular are thought to be linked to nerve damage. The main headache categories are also defined according to these theories. As discussed above, secondary headaches are linked to nerve damage in many areas of the body caused by an underlying disorder or condition. Primary headache conditions are associated with damage or inflammation of the major cranial nerves. Some headache cases (idiopathic headaches) have no discernible link to either of these explanations, however.

Pain that is perceived as emanating from the upper neck or base of the skull is associated with inflammation or injury to the occipital nerve. Migraine headaches are linked to a group of major nerves belonging to the trigemino-cervical complex, an important “nexus point” in the upper spine. The attack phase, and also some other symptoms, such as photophobia, are also associated with disorders of this network. Some cases of migraine pain can be attributed to trigeminal nerve damage. Some cluster headaches are also associated with this major cranial nerve, though some researchers believe they are caused by a different type of damage to that associated with migraines. Other cluster headaches are associated with an important cluster of nerve endings in the skull known as the sphenopalatine ganglion (SPG).

Tension headaches are thought not to be strongly associated with nerve damage. Many studies suggest they are attributed rather to specific stressors such as psychological conditions such as anxiety, eye strain, and nutrient deficiencies. This type of headache is also associated with sleep deprivation. Tension headaches are also linked to mandibular (jaw) stress, such as tooth-grinding and jaw-clenching. Unlike other types of primary headache, tension headaches have not been found to have a convincing link to a particular nerve, ganglion, or network. It may rather be caused by strain in some main groups of facial muscles, such as those in the jaw or temples, which is relayed by several nerves. These include all of the major nerves and clusters mentioned above.

Risk Factors For Headaches

HeadacheHeadaches have a wide variety of factors that may increase the probability of their onset. Tension-type headaches have many common triggers, as outlined above. Headaches are associated with nerve inflammation that is associated with many disorders, including stress, arthritis, and cancer. Certain tumors may also cause headaches, by direct damage to or pressure on specific nerves due to their location. Treatments intended to eradicate cancer may also cause nerve damage as a side-effect. These may be radiation- or chemically-based, and may cause injury to healthy tissue, including neural tissue, around a tumor. This can result in damage that may be long-lasting and thus cause chronic pain conditions as a consequence.

Other factors may also be associated with the onset of headache, including hunger or dehydration. A headache may also be an adverse reaction to many conventional drugs, including caffeine. Medication overuse headache, the result of long-term use or abuse of many drugs, is also common. Depression is also increasingly linked to headache development. However, it is not clear if this is a causative or coincidental relationship; i.e. if headaches are a symptom of depression, or if chronic, treatment-resistant headaches contribute to a depressive episode due to the psychological deterioration they may cause.

Diagnostic Methods For Headaches

Primary conditions can be diagnosed by a doctor or pain specialist by analyzing a patient’s self-report of their headache pain. This can be achieved by using one of many standard scoring systems designed to distinguish headache conditions. Another method is to visualize the source of a headache, i.e. damaged nerve tissue, using techniques such as magnetic resonance imaging (MRI).

If a particular nerve group may be linked to a case of headache pain, its ability to conduct pain “signals” may be pharmacologically inhibited. This may be done by the administration of local anesthetics (e.g. lidocaine) by needle, directly to the nerve. For example, inhibition of the trigeminal nerve may result in relief from a migraine episode. This technique is known as a nerve block.

Treatments For Headaches

The first-line headache treatment is conventional analgesics, most often in tablet form. Drugs that reduce or inhibit inflammation are often recommended to treat primary headache conditions.

Over-The-Counter Medications

Examples of these are non-steroidal anti-inflammatory drugs (NSAIDs, e.g. aspirin). These are regarded as most effective for patients who suffer episodic migraines for ten days or less per month. High-dose acetominaphen (paracetamol) is associated with significant reduction of mild episodic migraines only. Opioids (e.g. morphine, oxycodone) are prescribed to patients with very severe migraine pain. Anticonvulsants, such as carbamezapine and gabapentin, are associated with episodic migraine treatment.

Nerve Blocks

NeuromodulationNerve blocks are also used as treatments for chronic or recurrent headaches that do not respond to conventional oral analgesics. In addition to local anesthetics, corticosteroids may also be included in the injected formulation in order to reduce inflammation, if present. Blocking injections administered to the trigeminal or occipital nerves, or to the SPG, are effective in relieving chronic migraine and cluster headaches. They can provide medium-term (i.e. several weeks to a number of months) inhibition of pain. Trigemino-cervical blocks are injected into the top of the neck. SPG blocks are administered with thin catheters or needles extended into its location deep within the skull, through the oral or nasal passages.

Other Direct Nerve Treatments

There are cases of severe headaches that do not respond to nerve blocks, however. The next line of treatment here may be radiofrequency ablation (RFA) of the nerve or nerve group in question. Here, thin probes are passed through the skin (under local anesthetic) until they reach the nerve or nerve group. These emit radiofrequency or electrothermal impulses to the nerve. This will create a lesion on the nerve, which is a selective type of damage directed at only the specific parts of the nerve responsible for conducting pain signals. Ablation of the SPG is associated with effective inhibition of chronic headache pain. Occipital nerve RFA is associated with pain relief comparable to that of occipital nerve blocks.

Spinal cord stimulation (SCS) is a similarly invasive method of pain treatment. In this technique, thin, flexible devices are implanted adjacent to the spinal cord, near nerves associated with headache, e.g. the trigemino-cervical complex. These are attached to external leads that are attached to a controlling device the patient can operate themselves. When the implants are thus activated, the implants deliver a mild electrical impulse that interferes with the pain signals being transmitted by the nearby nerve. Spinal cord stimulation is associated with relief from migraine episodes.

Alternative Or Complementary Treatments

Alternative treatments such as acupuncture and biofeedback are associated with effective treatment of tension-type headaches. Biofeedback is a technique in which the patient is made familiar with biological measures taken during headache onset. These can include readings of brain activity (i.e. electroencephalogram recordings), muscle tension, (electromyographic measurements), and galvanic skin response. These vital signs are known to be impacted by stress and other headache triggers. By studying these measurements, patients may understand the physiological effects linked to their headaches and apply them to a system of enhanced conscious control involving relaxation techniques. Biofeedback may initially require learning and practice at a setting such as a pain clinic, but patients can eventually apply the technique alone at home, with or without access to the visual aids. Biofeedback may help a patient recognize the triggers associated with tension-type headaches and apply conscious control techniques when they are encountered, or avoid them altogether.

Chiropractic or other physical therapies may also have a positive effect on the severity of tension headaches. Massage or manipulation of the strained facial muscle groups may contribute to relief from headache pain associated with this. Manipulation may correct this strain or tension, thus reducing pain. Massage is associated with reduction of stress levels, and may thus reduce headache if triggered by this, in addition to easing muscle strain.

Side Effects And Risk Factors Of Treatment

Severe HeadacheNSAID intake is associated with organ damage, particularly if they are taken at a high dose or at a constant rate over time. This risk may be magnified in migraine sufferers, as doctors often advise them to increase their dose in response to an attack of pain. Acetaminophen is also associated with serious liver damage, particularly if taken in very large doses. Opioids are linked to high rates of addiction, abuse, and tolerance. In addition, withdrawal from these drugs by migraine patients may result in significant increases in pain intensity. The anticonvulsant carbamezapine is also associated with severe adverse reactions. These include irritation or even necrolysis of the skin and other immune responses. These can cause damage to the skin. Patients of Asian ancestry may be more susceptible to these side-effects.

Nerve blocks are also associated with some adverse effects. These include side-effects of the anesthetics used, nausea, transient neurological complications, breathing problems, discomfort, and numbness in the injected area. Steroids, if included in a nerve block, are associated with side effects such as fluctuations in body weight, the increased risk of arthritis development, and immune system dysfunctions. Other risks of these procedures are needle placement or injection into the wrong area when targeting a nerve. This can result in discomfort or desensitization of the area injected, paralysis, and respiratory problems. The probability of any of these effects occurring is reduced significantly however through the use of imaging technology (such as fluoroscopy) to precisely locate the nerve(s) to be injected and the skill of a competent and well-regarded physician and pain specialist. Temporary complications such as a headache are more common.

RFA carries similar risks arising from the inaccurate insertion or extension of the probe(s) used. Again, these are avoidable through adequate imaging, skill, and training. The more common after-effects of this procedure are discomfort, infection, or bleeding around the probe insertion site. SCS implants in the vicinity of the trigeminocervical complex may result in infections of the tissues around the insertion site. Failed SCS procedures may cause magnification of the pain. The implants may move away from their desired location, resulting in nerve or tissue damage as they do so. This may cause pain, numbness, or even paralysis. The incidences of SCS failure or migration are very low, however.

New And Upcoming Developments In Headache Treatment

There are other pharmacological options available, or at the trial stage, for the treatment of headache conditions.

Alternative And Emerging Pharmacological Treatments

Botulinum toxin type-A, also known as BOTOX™, is used in the cosmetic medicine industry to reduce wrinkles through muscular inhibition. This is a neurotoxin that can cause respiratory suppression in concentrations found in nature. At lower doses, it causes milder muscle paralysis in the areas injected.

Recently, formulations of this concentration have demonstrated an effect on headache pain when injected near the associated damaged nerves or into strained facial muscles. Therefore, the toxin may have a pain-blocking effect, and also acts through its ability to disrupt signaling between nerve and muscle cells. BOTOX for chronic tension-type and migraine headache has gone through a series of clinical trials sponsored by Allergan and will soon be widely available for this application. Despite this, independent studies have found that the analgesic properties of the formulation are in fact moderate. BOTOX is however associated with significant effects on migraines accompanied by facial pain and on medication-overuse headaches.

More examples of alternative pharmacological treatments include triptan—a classic headache drug—in a new formulation designed to be delivered by either nasal sprays or inhalers. These target headache pain linked to SPG dysfunction, that is cluster-type headaches. Chronic migraine pain, cluster headaches, and some tension-type headaches can be treated by verapamil, which is normally associated with vascular problems such as hypertension. However, it is associated with side-effects, which include other types of headache. Valproate is an anticonvulsant that is not normally associated with headache, but may have potential in treating migraine.

An emerging theory in the search of alternative drugs concerns the effects of antidepressants on these conditions. Venlafaxine and amitryptyline have shown potential in trials in patients with tension-type and migraine headaches. It is not clear, however, if these effects are limited to headache cases associated with depression alone or not. Lithium, a nearly first-generation (and defunct) depression medication, has also shown potential in relieving sleep disturbance-associated headaches.


There are other novel and emerging options for headaches that are either currently available or in development. Some of these employ the same science leading to the invention of spinal cord stimulation, as they interfere (electrically or otherwise) with the painful signaling conducted by the nerve or nerves involved in a case of headache. This technique is known as neuromodulation and there are a number of variations that can be applied to the treatment of headache.

One of these is a procedure known as deep brain stimulation (DBS). This involves the implantation of electrode devices into areas of the brain that can either override pain signals or promote more “non-pain” signals to compensate. Trials of DBS in treatment of cluster- and tension-type headaches have been conducted. The hypothalamus, an important brain region concerned with the regulation of many activities in or of the body including sleeping and waking, is often the target of DBS implants in headache cases. If more of these trials yield positive results it may indicate more evidence for the theories of the associations of these headache types with sleep disturbances. This research is still ongoing, and may result in another option for intractable headache relief. DBS may be associated with serious risks, however, involving as it does major invasive brain surgery.

A similar technique, involving microstimulator device implantation into the SPG, may be effective in treating headache pain associated with this nerve cluster. One trial on this type of device showed significant pain reduction in 68% of the subjects included. Microstimulators can be operated by patients, in a similar way to SCS implants. Research into SPG implants has yielded some positive results, though there are doubts about the time-frames of pain relief and the longevity of the devices used. The operations to implant these may also be associated with risks of numbness in the area served by the ganglion and changes in sensory perception. SPG implantation would also be relatively invasive and may result in infections and damage in the relevant areas. Microstimulators, or SCS-like devices, may also be implanted to treat occipital nerve-related pain. Trials studying these options have resulted in effective relief from tension- type, cluster, or migraine headaches.

Transcranial Stimulation

There are also non-invasive methods of neuromodulation available. One of the best-researched of these is transcranial stimulation. This process uses pads or a cap attached or fitted onto the scalp, containing wires or circuits that deliver impulses or waves that permeate the skull to stimulate the nerve or nerve groups associated with headache pain. There are a number of types of transcranial stimulation. The vagus nerve is a major cranial nerve that regulates pain signals from a number of other nerves and also conducts “analgesic” signals. Transcutaneous electrical nerve stimulation (TENS) of this nerve may be a new treatment option for severe headache. This is known as tVNS, and has demonstrated positive effects on cluster-type and migraine headache pain in some studies. tVNS is associated with relatively mild and temporary side-effects, including pain and muscle cramps around the skull.

Transcranial direct current stimulation (tDCS) has shown potential in treating chronic migraine, particularly when applied at the attack phase. One study (of 42 patients) administered either tDCS or a seemingly identical dummy procedure. The results showed significant relief for the patients who received active tDCS. In another trial, 13 chronic migraine patients underwent a tDCS procedure, and then a placebo treatment. Only the active tDCS produced significant results on pain intensity and durations of migraine episodes. tDCS is associated with some adverse reactions, such as burning, stinging , or itching sensations in the scalp where electrodes are placed. In addition, transient neurological events such as flashes in the field of vision, skin redness, and nausea may occur. Certain medications, including carbamezapine, may inhibit the effects of tDCS and as such is not suitable for patients taking these.

Episodic migraine may also be treated by transcranial magnetic stimulation (TMS). One study on TMS demonstrated significant results on the severity and frequency of pain attacks. The procedure also resulted in a decrease in analgesic medication intake and in the functional decline of the patients caused by migraine. Therefore, transcranial stimulation and its variations may have a positive impact as a treatment option. The procedures are relatively non-invasive, are not time-consuming, and should be relatively straightforward as pain-management techniques. There are existing medical devices available that deliver TENS, TMS, and tDCS. These can be applied or adapted to headache treatment. However, transcranial stimulation for headache still requires further research and clinical trials to confirm their potential and to develop these techniques for use in this industry.

Alternative Theories Of Pathophysiology And Treatment

Developments in research on headache also include new theories of their etiology and underlying causes.

Altered Pain Perception

The conventional wisdom of headache causes, an association with nerve or tissue damage, are still consistent with evidence published. Novel theories on headache development may also be valid, though, and are necessary to further the understanding of this common source of pain. For example, further study of tension-type headaches, to crystallize the more than slightly vague current explanation for them, is needed. These mainly concern the emerging “pain processing” theory that defines tension headaches as a result of abnormally high activity in the pain-sensing regions of the brain in affected people. There is some evidence to support this, such as published research with the conclusions that tension-headache patients are more sensitive to pain in comparison to non-sufferers. Tension-type headaches are reported to respond well to some types of transcranial stimulation, which may also contribute to this alternative hypothesis.

The Neck Pain Hypothesis

There is another novel explanation of headache development emerging within the research community. This theory associates many types of primary headache with neck damage or inflammation (i.e. cervicogenic pain). The trigemino-cervical complex and occipital nerve are located in the upper neck, which may lend credence to this hypothesis. As treatments that either block or modulate occipital activity are associated with headache relief, as discussed above, this may add to the basis for the theory. Verification of the cervicogenic hypothesis may result in the relegation of conditions currently regarded as primary headaches as symptoms of, or secondary to, neck injury or inflammation.

Currently, headaches in the elderly and other groups commonly linked to neck damage or injury (as a result of posture defects, accidents, or illnesses), are increasingly diagnosed as cervicogenic. Headaches in office workers, who are often subject to neck pain resulting from poor posture related to long periods of sitting or reading a screen, may also be explained by this theory. The possibility of cervicogenic headache may be addressed by nerve blocks, RFA, or physical therapies.

Another condition recently correlated with headache is post-traumatic stress disorder. Patients who develop PTSD (e.g. army personnel) may be at higher risk of head or neck injury, which is one of many possible explanations for this association.


Headache is a widespread source of pain, functional decline, and healthcare burden. There are many types of headache (i.e. pain in the skull or top of the neck) that can be chronic, recurrent, or acute in nature. Headache conditions are often classified according to the area affected and to damage in certain nerves or nerve groups. This damage can be physical (e.g. injury or other mechanical damage) or chemical (e.g. inflammation). Headaches are either caused by nerve damage alone or by damage and inflammation caused by an underlying disorder or illness. Alternative hypotheses of headache state that the pain is in fact associated with neck damage or with increased sensitivity of pain-processing regions of the brain.

Some headaches can be treated by conventional oral medications. More severe headaches may require slightly more invasive therapies such as nerve blocks or radiofrequency ablation. More severe cases may be treated with spinal cord stimulation. Alternative or emerging treatments include Botox (which inhibits muscle contraction), venlaflaxine, and lithium. Other novel techniques such as transcranial nerve stimulation are currently being investigated as potential therapies for severe cluster or migraine headaches.

There are other novel and emerging options for these conditions, however, that are either currently available or in development, such as neuromodulation, deep brain stimulation, and transcranial direct current. These techniques have the advantages of being convenient and non-invasive, but require more clinical testing and development before they are approved as headache treatments. Adequate diagnosis and consultation with a pain specialist or physician has an important role in devising an effective and appropriate form of treatment for effective headache relief.

At Pain Doctor our goal is to relieve your headache pain and improve function to increase your quality of life.
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  1. Clinch CR. Evaluation of acute headaches in adults. Am Fam Physician. 2001;63(4):685-92.
  2. Hainer BL, Matheson EM. Approach to acute headache in adults. Am Fam Physician. 2013;87(10):682-7.
  3. Mathew NT. The prophylactic treatment of chronic daily headache. Headache. 2006;46(10):1552-64.
  4. Rabbie R, Derry S, Moore RA. Ibuprofen with our without an antiemetic for acute migraine headaches in adults. Cochrane Database Syst Rev. 2013;4.
  5. Rapoport AM. Acute treatment of migraine: Established and emerging therapies. Headache. 2012;52(Suppl2):60-4.
  6. Rapoport AM. The therapeutic future in headache. Neurol Sci. 2012;33(Suppl 1):S119-25.
  7. Cooper RJ. Over-the-counter medicine abuse – a review of the literature. Journal of substance use. 2013;18(2):82-107.
  8. Rodman R, Dutton J. Endoscopic neural blockade for rhinogenic headache and facial pain: 2011 update. International forum of allergy & rhinology. 2012;2(4):325-330.
  9. Martelletti P, Jensen RH, Antal A, et al. Neuromodulation of chronic headaches: position statement from the European Headache Federation. The journal of headache and pain. 2013;14(1):86.
  10. Gabrhelik T, Michalek P, Adamus M. Pulsed radiofrequency therapy versus greater occipital nerve block in the management of refractory cervicogenic headache – a pilot study. Prague medical report. 2011;112(4):279-287.
  11. Levin M. Nerve blocks in the treatment of headache. Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics. 2010;7(2):197-203.
  12. Bayer E, Racz GB, Miles D, Heavner J. Sphenopalatine ganglion pulsed radiofrequency treatment in 30 patients suffering from chronic face and head pain. Pain practice : the official journal of World Institute of Pain. 2005;5(3):223-227.
  13. Oomen KP, van Wijck AJ, Hordijk GJ, de Ru JA. Effects of radiofrequency thermocoagulation of the sphenopalatine ganglion on headache and facial pain: correlation with diagnosis. Journal of orofacial pain. 2012;26(1):59-64.
  14. Sacco S, Ricci S, Carolei A. Migraine and vascular diseases: A review of the evidence and potential implications for management. Cephalalgia. 2012;32(10):785-95.
  15. Shapiro RE. Preventive Treatment of Migraine. Headache. 2012;52(Suppl 2):65-9.
  16. Silberstein SD. Treatment recommendations for migraine. Nat Clin Pract Neurol. 2008;4(9):482-9.
  17. Silberstein SD, Holland S, Freitag F, Dodick DW, Argoff C, Ashman E, Quality Standards Subcommittee of the American Academy of Neurology and the American Headache Society. Evidence-based guideline update: Pharmacologic treatment for episodic migraine prevention in adults: Report of the Quality Standards Subcommittee of the American Academy of Neurology and the American Headache Society. Neurology. 2012;78(17):1337-45.
  18. McMurtray AM, Saito EK, Diaz N, Mehta B, Nakamoto B. Greater frequency of depression associated with chronic primary headaches than chronic post-traumatic headaches. International journal of psychiatry in medicine. 2013;45(3):227-236.
  19. Holle D, Obermann M. The role of neuroimaging in the diagnosis of headache disorders. Therapeutic advances in neurological disorders. 2013;6(6):369-374.
  20. Tfelt-Hansen PC, Jensen RH. Management of cluster headache. CNS drugs. 2012;26(7):571-580.
  21. Shimazu T. The recent pathophysiology of cluster headache (trigeminal autonomic cephalalgias; TACs). Rinsho shinkeigaku = Clinical neurology. 2013;53(11):1125-1127.
  22. Shimizu T. New treatments for cluster headache. Rinsho shinkeigaku = Clinical neurology. 2013;53(11):1131-1133.
  23. Lambru G, Abu Bakar N, Stahlhut L, et al. Greater occipital nerve blocks in chronic cluster headache: a prospective open-label study. European journal of neurology : the official journal of the European Federation of Neurological Societies. Dec 7 2013.
  24. Goyal A, Panchani R, Varma T, Bhalla S, Tripathi S. Adrenal incidentaloma: A case of pheochromocytoma with sub-clinical Cushing’s syndrome. Indian journal of endocrinology and metabolism. Oct 2013;17(Suppl 1):S246-248.
  25. Martelletti P, Jensen RH, Antal A, et al. Neuromodulation of chronic headaches: position statement from the European Headache Federation. The journal of headache and pain. 2013;14(1):86.
  26. Singh NN, Sahota P. Sleep-related headache and its management. Current treatment options in neurology. 2013;15(6):704-722.
  27. Clelland CD, Zheng Z, Kim W, Bari A, Pouratian N. Common cerebral networks associated with distinct deep brain stimulation targets for cluster headache. Cephalalgia : an international journal of headache. Oct 16 2013.
  28. Lin KH, Chen SP, Fuh JL, Wang YF, Wang SJ. Efficacy, safety, and predictors of response to botulinum toxin type A in refractory chronic migraine: A retrospective study. Journal of the Chinese Medical Association : JCMA. Oct 23 2013.
  29. Gady J, Ferneini EM. Botulinum toxin A and headache treatment. Connecticut medicine. 2013;77(3):165-166.
  30. Hu Y, Guan X, Fan L, et al. Therapeutic efficacy and safety of botulinum toxin type A in trigeminal neuralgia: a systematic review. The journal of headache and pain. 2013;14(1):72.
  31. Watanabe Y, Takashima R, Iwanami H, Suzuki S, Igarashi H, Hirata K. Management of chronic migraine in Japan. Rinsho shinkeigaku = Clinical neurology. 2013;53(11):1228-1230.
  32. Linde M, Mulleners WM, Chronicle EP, McCrory DC. Antiepileptics other than gabapentin, pregabalin, topiramate, and valproate for the prophylaxis of episodic migraine in adults. The Cochrane database of systematic reviews. 2013;6:Cd010608.
  33. Smitherman TA, Walters AB, Maizels M, Penzien DB. The use of antidepressants for headache prophylaxis. CNS neuroscience & therapeutics. 2011;17(5):462-469.
  34. Bezov D, Ashina S, Jensen R, Bendtsen L. Pain perception studies in tension-type headache. Headache. 2011;51(2):262-271.
  35. Chua NH, Suijlekom HV, Wilder-Smith OH, Vissers KC. Understanding cervicogenic headache. Anesthesiology and pain medicine. 2012;2(1):3-4.
  36. De Hertogh W, Vaes P, Versijpt J. Diagnostic work-up of an elderly patient with unilateral head and neck pain. A case report. Manual therapy. 2013;18(6):598-601.
  37. Huber J, Lisinski P, Polowczyk A. Reinvestigation of the dysfunction in neck and shoulder girdle muscles as the reason of cervicogenic headache among office workers. Disability and rehabilitation. 2013;35(10):793-802.
  38. Chaibi A, Russell MB. Manual therapies for cervicogenic headache: a systematic review. The journal of headache and pain. 2012;13(5):351-359.
  39. Carlson KF, Taylor BC, Hagel EM, Cutting A, Kerns R, Sayer NA. Headache Diagnoses Among Iraq and Afghanistan War Veterans Enrolled in VA: A Gender Comparison. Headache. 2013;53(10):1573-1582.
  40. Runnals JJ, Van Voorhees E, Robbins AT, et al. Self-Reported Pain Complaints among Afghanistan/Iraq Era Men and Women Veterans with Comorbid Posttraumatic Stress Disorder and Major Depressive Disorder. Pain medicine (Malden, Mass.). Aug 7 2013.
  41. Moeller DR. Evaluation of a Removable Intraoral Soft Stabilization Splint for the Reduction of Headaches and Nightmares in Military PTSD Patients: A Large Case Series. Journal of special operations medicine : a peer reviewed journal for SOF medical professionals. 2013;13(1):49-54.
  42. Freitag F. Managing and treating tension-type headache. The Medical clinics of North America. 2013;97(2):281-292.
  43. Krusz JC. Tension-type headaches: what they are and how to treat them. Primary care. 2004;31(2):293-311, vi.
  44. Alves AC, Alchieri JC, Barbosa GA. Bruxism. Masticatory implications and anxiety. Acta odontologica latinoamericana : AOL. 2013;26(1):15-22.
  45. Castien R, Blankenstein A, van der Windt D, Heymans MW, Dekker J. The working mechanism of manual therapy in participants with chronic tension-type headache. The Journal of orthopaedic and sports physical therapy. 2013;43(10):693-699.
  46. Singh NN, Sahota P. Sleep-related headache and its management. Current treatment options in neurology. 2013;15(6):704-722.
  47. Manaka S. [Application of acupuncture as a headache management tool]. Rinsho shinkeigaku = Clinical neurology. 2012;52(11):1299-1302.
  48. Bendtsen L, Evers S, Linde M, Mitsikostas DD, Sandrini G, Schoenen J. EFNS guideline on the treatment of tension-type headache – report of an EFNS task force. European journal of neurology : the official journal of the European Federation of Neurological Societies. 2010;17(11):1318-1325.
  49. Bendtsen L, Jensen R. Treating tension-type headache — an expert opinion. Expert opinion on pharmacotherapy. 2011;12(7):1099-1109.
  50. Smitherman TA, Burch R, Sheikh H, Loder E. The prevalence, impact, and treatment of migraine and severe headaches in the United States: a review of statistics from national surveillance studies. Headache. Mar 2013;53(3):427-436.
  51. Ilik F, Ilik K. Alice in Wonderland syndrome as aura of migraine. Neurocase. Aug 2014;20(4):474-475.