Tension Headache

The International Headache Society (IHS) began developing a classification system for headaches in 1985. Now in its third edition, this system includes a tension-type headache (TTH) category, further defined as either episodic (frequent and infrequent) or chronic. In infrequent episodic TTH, headache episodes occur less than one day a month, whereas in frequent episodic TTH, headache episodes occur 1 to 14 days a month. In chronic TTH, headaches occur 15 or more days a month.

Headache categories also are defined by whether they are associated with pericranial muscle disorders.[1]

Episodic tension headache usually is associated with a stressful event. This headache type is of moderate intensity, self-limited, and usually responsive to nonprescription drugs.

Chronic tension headache often recurs daily and is associated with contracted muscles of the neck and scalp. This type of headache is bilateral and usually occipitofrontal.

TTH is the most common type of chronic recurring head pain. In the past, pain etiology was presumed to be the muscular contraction of pain-sensitive structures of the cranium, but the IHS intentionally abandoned the terms muscular contraction headache and tension headache because no research supports muscular contraction as the sole pain etiology.

The pathogenesis of tension type headaches is multifactorial. Given the wide variation in frequency and intensity in TTH, not only between individuals but also within individuals over time, it is likely that the underlying pain mechanisms in TTH are dynamic. It is suggested that the mechanisms vary from one individual to another, and potentially from one attack to another in the same individual.[3] These factors include environmental and genetic factors. Environmental factors influence the development of episodic TTH more than chronic TTH, while genetic factors appear to play an important role in the development of chronic TTH.[4, 5, 6]

It is postulated that peripheral activation or sensitization of myofascial nociceptors play a major role in episodic TTH. Extended nociceptive stimuli from pericranial myofascial tissues seems to be responsible for the conversion of episodic to chronic TTH.[3, 7, 8, 9, 10, 11] In chronic THH, stimuli that are normally painless are misinterpreted as pain. This continuous painful input induces central sensitization. The increased nociceptive stimulation of supraspinal structures results in increased facilitation and decreased inhibition of pain transmission at the level of the spinal dorsal horn/trigeminal nucleus, and in increased pericranial muscle activity.[7] This was shown  in a study of women with frequent episodic tension-type headcahces (FETTH). They had  widespread pressure pain hypersensitivity over both nerve trunks and musculoskeletal structures  suggesting this central altered nociceptive processing. This pain was not restrictied to musculoskeletal areas  but also pain evoked from directly provoking the nerve trunks by pressure.[22]

 A study by Kiran et al indicated that patients with chronic tension headaches for longer then 5 years tended to have lower cortisol levels.[2] This was postulated to be due to hippocampus atrophy resulting from chronic stress, a cause of chronic tension headaches. More recently it is believed that there is increased myofascial pain sensitivity caused by central factors such as sensitizatation of neurons in the supraspinal region as well as second order neurons in the spinal dorsal horn/trigeminal nucleus.[3] Another mechanism of pain is decreased antinociception or inability of the body to stop painful stimuli to the supraspinal structures.[4]  

Stress may cause contraction of neck and scalp muscles, although no evidence confirms that the origin of pain is sustained muscle contraction. Other triggers[23, 24] of headache include:

• Stress ( physical or emotional)  and/or anxiety

• Alcohol use

• Caffeine ( toom uch or withdrawal)

• Colds, the ful, sinus infection 

• Dental problems

• Eye strain

• Excessive smaoking

• Poor posture

• Depression

• Fatigue

One study showed that patients with tension-type headache (TTH) have relatively weak neck extension muscles. According to results, these patients are 26% weaker than controls with respect to neck extension muscles, that they have a 12% smaller extension/flexion ratio, and that they have a borderline significant difference in the ability to generate muscle force over the shoulder joint.[5, 6]

Statistics

Headaches account for 1–4% of all emergency department (ED) visits and are in the top most common reasons for a patient to consult a physician. Tension-type headaches (TTH) are common, with a lifetime prevalence in the general population ranging between 30% and 78% in different studies. They affect approximately 1.4 billion people or 20.8% of the population.[7, 8] Of concern is that in 2010, opioids were administered in 35% of ED visits for headache compared to triptans, which were given in only 1.5% of visits.[9]

TTH onset often occurs during the teenage years and affects three women to every two men. Previous studies in the United States had show that tension type headaches peaked in the fourth decade. However, European studies show that these headaches persist occurring even into the 6th decade of life.[10]

Tension-type headaches (TTH) may be painful, but are not harmful. Most cases are intermittent and do not interfere with work or normal life span. However, they may become chronic if life stressors are not changed.

Pain onset in tension-type headache can have a throbbing quality and is usually more gradual than onset in migraines. Compared with migraines, tension-type headaches are more variable in duration, more constant in quality, and less severe.

IHS diagnostic criteria for tension-type headaches states that two of the following characteristics must be present:[1]

• Pressing or tightening (nonpulsatile quality)

• Frontal-occipital location

• Bilateral - Mild/moderate intensity

• Not aggravated by physical activity

Tension-type headache history is as follows:

• Duration of 30 minutes to 7 days

• No nausea or vomiting (anorexia may occur)[11]

• Photophobia and/or phonophobia[11]

• Minimum of 10 previous headache episodes;[11] fewer than 180 days per year with headache to be considered "infrequent"

• Bilateral and occipitonuchal or bifrontal pain

• Pain described as "fullness, tightness/squeezing, pressure," or "bandlike/viselike"

• May occur acutely under emotional distress or intense worry

• Insomnia

• Often present upon rising or shortly thereafter

• Muscular tightness or stiffness in neck, occipital, and frontal regions

• Duration of more than 5 years in 75% of patients with chronic headaches

• Difficulty concentrating

• No prodrome

New headache onset in elderly patients should suggest etiologies other than tension headache.

The physical examination serves mainly to exclude the possibility of other headache causes.

• Vital signs should be normal.

• Normal neurologic examination

• Tenderness may be elicited in the scalp or neck, but no other positive physical exam findings should be noted.

• Pain should not be elicited over temporal arteries or positive trigger zones.

• Some patients with occipital tension headaches may be very tender when upper cervical muscles are palpated.

• Pain associated with neck flexion and stretching of paracervical muscles must be distinguished from nuchal rigidity associated with meningeal irritation.

Complications of headache may include the following:

• Overreliance on nonprescription caffeine-containing analgesics

• Dependence on/addiction to narcotic analgesics

• GI bleed from use of NSAIDs

• Risk of epilepsy 4 times greater than that of the general population

• Medication overuse headache

Laboratory work should be unremarkable in cases of tension-type headache. Specific tests should be obtained if the history or physical examination suggests another diagnostic possibility.

Head CT scan or MRI is necessary only when the headache pattern has changed recently, the headache cannot be clearly defined by the clinician as a common primary headache disorder (that is not a cluster, migraine, or tension-type of headache), or neurologic examination reveals abnormal findings.[11] Such history or physical examination evidence would suggest an alternate cause of headache. Caution should be used in patients with aura in headache that is sensory or motor, or if the aura has changed in character and is not described as typical of their migraine aura. These patients may warrant neuroimaging.

Various modalities are used in the treatment of tension headaches. These include hot or cold packs, ultrasound, electrical stimulation, improvement of posture, trigger point injections, occipital nerve blocks, stretching, and relaxation techniques.

Regular exercise, stretching, balanced meals, and adequate sleep may be part of a headache treatment program.[12]

Non-pharmacological treatments for headache include behavioral treatments such as cognitive-behavioral therapy, relaxation, biofeedback as well as acupuncture and massage. These treatments are options for patients who prefer non-pharmacological treatements or cannot take medications such as pregnant patients.[13] Relaxation techniques such as meditation are effective for chronic headaches as measured by headache parameters. Patients with chronic headaches have been showed to have low levels of cortisol that normalized with the practice of meditation over time.

Acupuncture may be helpful for patients experiencing frequent or chronic TTH. A review of eleven studies involving 2,317 patients found evidence to support acupuncture as a valuable, nonpharmacologic tool for episodic or chronic TTH. Two of the studies reviewed compared acupuncture to treatment of acute headaches or routine care only and found statistically significant and clinically relevant short-term (up to 3 months) benefits of acupuncture over control for response, number of headache days, and pain intensity.[14] According to several studies, massage may also be an effective therapy for individuals suffering from TTH. Massage can relieve tight muscles in the back of the head, neck, and shoulders, which may in turn relieve headache pain.[15, 16]  A combination of therapy with stress reducation and biofeedback may be best for patients. 

There are a variety of medications available to treat the pain of a headache, including pain relievers and combination medications. Patients should be advised to avoid repeated use of OTC pain relievers as these can cause medication overuse headaches. Opioids nor barbituates should be used in TTH when better options (e.g., simple analgesics and combintaion analgesics containing caffeine) are available.[17]

Barbiturates may be used when all other treatment options have failed.

Class Summary

These agents may alleviate headache pain by inhibiting prostaglandin synthesis, reducing serotonin release, and blocking platelet aggregation. Although the effects of NSAIDs in the treatment of headache pain tend to be patient specific, ibuprofen is usually the DOC for initial therapy. Other options include naproxen, ketoprofen, and ketorolac.

Ibuprofen (Ibuprin, Advil, Motrin)

Usually DOC for treatment of mild to moderately severe headache, if no contraindications.

Naproxen (Naprosyn, Naprelan)

For relief of mild to moderately severe pain. Inhibits inflammatory reactions and pain by decreasing enzyme cyclooxygenase activity, thus inhibiting prostaglandin synthesis.

Ketoprofen (Oruvail, Orudis, Actron)

Description For relief of mild to moderately severe pain and inflammation. Small dosages initially indicated in small and elderly patients and in those with renal or liver disease. Doses over 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient for response.

Ketorolac (Toradol)

Inhibits prostaglandin synthesis by decreasing activity of enzyme cyclooxygenase, which results in decreased formation of prostaglandin precursors. PO form offers no advantage over other less expensive PO NSAIDs.

Indomethacin (Indocin, Indochron E-R)

Absorbed rapidly; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation. Useful in diagnosis as it helps other headache syndromes (eg, chronic paroxysmal hemicrania).

Class Summary

These agents alleviate headache, possibly by inhibiting prostaglandin synthesis.

Aspirin (Anacin, Ascriptin, Bayer Aspirin, Bufferin)

Treats mild to moderately severe pain. Inhibits prostaglandin synthesis, which prevents formation of platelet-aggregating thromboxane A2.

Class Summary

These agents are used in combination with aspirin and acetaminophen for pain relief and to induce sleep. Caffeine is used to increase its GI absorption. However, butalbital is associated with rebound headaches. Increasing use of these combination preparations may fail to provide pain relief and worsen headache symptoms.

Butalbital, aspirin, caffeine (Fiorinal)

Drug combination used to relieve tension headaches. Barbiturate component has generalized depressant effect on CNS.

Acetaminophen, butalbital, and caffeine (Fioricet)

Drug combination used to relieve tension headaches. Barbiturate component has generalized depressant effect on CNS.

Class Summary

Patients with infrequent headaches can be treated with simple analgesics initially.

Acetaminophen (Tylenol, Panadol, Aspirin Free Anacin)

DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs or upper GI disease or taking oral anticoagulants.

Acetaminophen with codeine (Tylenol #3)

Indicated for treatment of mild to moderately severe headache.

Acetaminophen and oxycodone (Percocet)

Indicated for relief of moderately severe to severe pain. DOC for aspirin-hypersensitive patients.

Class Summary

These agents are useful in aborting headache and treating emesis that results from acute pain.

Promethazine (Phenergan)

Antidopaminergic agent effective in treating emesis. Blocks postsynaptic mesolimbic dopaminergic receptors in brain and reduces stimuli to brainstem reticular system.

Prochlorperazine (Compazine)

May relieve nausea and vomiting by blocking postsynaptic mesolimbic dopamine-receptors, through anticholinergic effects, and depressing reticular activating system. In addition to antiemetic effects, has advantage of augmenting hypoxic ventilatory response, acting as respiratory stimulant at high altitude.

Metoclopramide (Reglan) can be used as an alternative to prochlorperazine. Studies show prochlorperazine is better.

Metoclopramide (Reglan)

Dopamine antagonist that stimulates acetylcholine release in the myenteric plexus. Acts centrally on chemoreceptor triggers in the floor of the fourth ventricle, which provides important antiemetic activity.

Class Summary

These are direct vasoconstrictors of smooth muscle in cranial blood vessels. Their activity depends on the CNS vascular tone at the time of administration.

Ergotamine tartrate (Cafergot, Cafatine, Cafetrate)

Alpha-adrenergic and serotonin antagonist. Causes constriction of peripheral and cranial blood vessels.

Dihydroergotamine (D.H.E. 45, Migranal Nasal Spray)

Alpha-adrenergic blocking agent with direct stimulating effect on smooth muscle of peripheral and cranial blood vessels; depresses central vasomotor centers. Mechanism of action is similar to ergotamine; nonselective 5HT1 agonist with wide spectrum of receptor affinities outside 5HT1 system; also binds to dopamine. Thus, has alpha-adrenergic antagonist and serotonin antagonist effect. Indicated to abort or prevent vascular headache when rapid control needed or when other routes of administration not feasible.

Available in IV or intranasal preparations, tends to cause less arterial vasoconstriction than ergotamine tartrate.