Tension-type headache (TTH) represents one of the most costly diseases because of its very high prevalence. TTH is the most common type of headache, and it is classified as episodic (ETTH) or chronic (CTTH). It had various ill-defined names in the past including tension headache, stress headache, muscle contraction headache, psychomyogenic headache, ordinary headache, and psychogenic headache. See Medscape's Headache Resource Center for more information.
The International Headache Society (IHS) defines TTH more precisely and differentiates between the episodic and the chronic types.
Episodic tension-type headache
The following is a modified outline of the IHS diagnostic criteria:
At least 10 previous headaches fulfilling the following criteria; number of days with such headache fewer than 15 per month
Headaches lasting from 30 minutes to 7 days
At least 2 of the following pain characteristics:
Pressing/tightening (nonpulsating) quality
Mild or moderate intensity (may inhibit but does not prohibit activities)
Bilateral location
No aggravation from climbing stairs or similar routine physical activity
Both of the following:
No nausea or vomiting
Photophobia and phonophobia absent or only one present
Secondary headache types not suggested or confirmed
Chronic tension-type headache
See the list below:
Average headache frequency of more than 15 days per month for more than 6 months fulfilling the following criteria
At least 2 of the following pain characteristics:
Pressing/tightening (nonpulsating) quality
Mild or moderate intensity (may inhibit but does not prohibit activities)
Bilateral location
No aggravation from climbing stairs or similar routine physical activity
Both of the following:
No vomiting
No more than one of the following: nausea, photophobia, or phonophobia
Secondary headache types not suggested or confirmed
Pathogenesis of TTH is complex and multifactorial, with contributions from both central and peripheral factors. In the past, various mechanisms including vascular, muscular (ie, constant overcontraction of scalp muscles), and psychogenic factors were suggested. The more likely cause of these headaches is believed now to be abnormal neuronal sensitivity and pain facilitation, not abnormal muscle contraction.
Various evidence suggests that, like migraine, TTH is associated with exteroceptive suppression (ES2), abnormal platelet serotonin, and decreased cerebrospinal fluid beta-endorphin. In one study, plasma levels of substance P, neuropeptide Y, and vasoactive intestinal peptide were found to be normal in patients with CTTH and unrelated to the headache state.
Several concurrent pathophysiologic mechanisms may be responsible for TTH; according to Jensen, extracranial myofascial nociception is one of them. Headache is not related directly to muscle contraction, and possible hypersensitivity of neurons in the trigeminal nucleus caudalis has been suggested.
Bendtsen described central sensitization at the level of the spinal dorsal horn/trigeminal nucleus due to prolonged nociceptive inputs from pericranial myofascial tissues.[1] The central neuroplastic changes may affect regulation of peripheral mechanisms and can lead to increased pericranial muscle activity or release of neurotransmitters in myofascial tissues. This central sensitization may be maintained even after the initial eliciting factors have been normalized, resulting in conversion of ETTH into CTTH.
Further research is necessary to understand and clarify the mechanisms of TTH. Research may lead to the development of more specific and effective management in the future.
Rasmussen et al reported a lifetime prevalence of TTH of 69% in men and 88% in women in the Danish population.[2] The patient may experience more than one primary headache syndrome. In one study by Ulrich et al, the 1-year prevalence of TTH was the same among individuals with and without migraine.[3]
Sex
Women are slightly more likely to be affected than men.
The female-to-male ratio for TTH is approximately 1.4:1.
In CTTH, female preponderance is 1.9:1.
Age
TTH can occur at any age, but onset during adolescence or young adulthood is common. It can begin in childhood.
Tension-type headaches (TTHs) are characterized by pain that is usually mild or moderate in severity and bilateral in distribution. Unilateral pain may be experienced by 10-20% of patients. Headache is a constant, tight, pressing, or bandlike sensation in the frontal, temporal, occipital, or parietal area (with frontal and temporal regions most common).
Ulrich et al reported that 82% of TTHs last less than 24 hours.[3]
The deep steady ache differs from the typical throbbing quality of migraine headache.
Prodrome and aura are absent.
Occasionally, the headache may be throbbing or unilateral, but most patients do not report photophobia, sonophobia, or nausea, which commonly are associated with migraine.
Some patients may have neck, jaw, or temporomandibular joint discomfort.
Various precipitating factors may cause TTH in susceptible individuals. One half of patients with TTH identify stress or hunger as a precipitating factor.
Stress - Usually occurs in the afternoon after long stressful work hours
Sleep deprivation
Uncomfortable stressful position and/or bad posture
Management of TTH consists of pharmacotherapy, psychophysiologic therapy, and physical therapy.
Treatment of headache must be tailored for individual patients.
Recognition of comorbid illness is essential. Migraine may be associated with TTH, and management overlaps. Other associated conditions may include depression, anxiety, and emotional or adjustment disorders.
Management of CTTH with a combination of tricyclic antidepressant medication and stress management therapy may result in a better outcome than monotherapy.[4]
Pharmacotherapy consists of abortive therapy (to stop or reduce severity of the individual attack) and long-term preventive therapy. Preventive drugs are the main therapy for CTTH, but they seldom are needed for ETTH.
These headaches (especially ETTH) generally respond to simple over-the-counter (OTC) analgesics such as paracetamol (ie, acetaminophen), ibuprofen, aspirin, or naproxen.
If treatment is unsatisfactory, the addition of caffeine or use of prescription drugs is recommended. If possible, avoid use of barbiturates or opiate agonists.
Also discourage overuse of all symptomatic analgesics because of the risk of dependence, abuse, and development of chronic daily headache.
Fiorinal with codeine is generally significantly more effective than placebo or Fiorinal alone. The combination is also significantly better than codeine alone in relieving pain and maintaining ability to perform daily activities. However, Fiorinal with codeine is not first-line therapy and carries a significant risk of abuse.
Consider preventive medications if the headaches are frequent (>2 attacks per wk), of long duration (>3-4 h), or severe enough to cause significant disability or overuse of abortive medication.
Amitriptyline (Elavil) and nortriptyline (Pamelor) are the most frequently used tricyclic antidepressants.
The selective serotonin reuptake inhibitors (SSRIs) fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft) also are used commonly by many physicians. In a double-blind placebo-controlled trial conducted by Saper et al of fluoxetine in patients with chronic daily headache and migraine, it was reported to be helpful.[5]
Other antidepressants such as doxepin, desipramine, protriptyline, and buspirone also can be used. According to Cohen, protriptyline may be comparable in effectiveness to amitriptyline in CTTH without producing drowsiness and weight gain.
As reported by Bendtsen et al, in one double-blind trial that compared citalopram to amitriptyline and a placebo, patients on citalopram demonstrated lower headache scores than those on placebo, but amitriptyline was significantly more effective.[6]
Tizanidine may improve inhibitory function in the central nervous system and can provide pain relief. One recent study by Saper et al provides support for the efficacy of tizanidine in the prophylaxis of chronic daily headache.[7] Currently the use of tizanidine remains investigational in the treatment of this disorder.
Physical therapy techniques include hot or cold applications, positioning, stretching exercises, traction, massage, ultrasound therapy, transcutaneous electrical nerve stimulation (TENS), and manipulations.
Heat, massage, and stretching can be used to alleviate excess muscle contraction and pain.
Cranial electrotherapy stimulation is different from TENS, is safe, and may be effective in alleviating the pain intensity of TTH. It may be considered as an alternative to long-term analgesic use.
Psychophysiologic therapy includes reassurance, counseling, relaxation therapy, stress management programs, and biofeedback techniques. With these modalities of treatment, both frequency and severity of chronic headache may be reduced.
In a few studies, such as that by Holroyd et al, benefits from cognitive-behavioral therapy and biofeedback therapy have been reported.[4]
Biofeedback may be helpful in some patients when combined with medications.
One prospective study of TTH in an elderly population suggested that relaxation therapy may be an effective intervention.
The following various minimally invasive techniques may provide pain relief:
Trigger point injections
Greater or lesser occipital nerve blocks
Auriculotemporal nerve block
Supraorbital nerve block
Botulinum toxin injection in the pericranial muscle
Other alternative treatments: In one study, Biondi and Portuesi suggested that acupuncture results are difficult to assess and that acupuncture should be reserved for selected patients.[8]
These agents inhibit inflammatory reactions and pain by decreasing activity of cyclooxygenase, which is responsible for prostaglandin synthesis. They generally are used in mild to moderately severe headaches; however, they also may be effective for severe headaches.
These drugs increase the synaptic concentration of serotonin and/or norepinephrine in CNS by inhibiting their reuptake by the presynaptic neuronal membrane.
Cymbalta can also be helpful for patients who have coexisting depression.
Clinical Context:
Atypical nontricyclic antidepressant with potent specific 5-HT uptake inhibition and fewer anticholinergic and cardiovascular adverse effects than TCAs.
Clinical Context:
Atypical nontricyclic antidepressant with potent specific 5-HT uptake inhibition and fewer anticholinergic and cardiovascular adverse effects than TCAs.
Advise the patient with tension-type headaches (TTHs) to take the following actions:
Avoid stressful situations if possible
Maintain a regular sleep schedule
Exercise regularly
Eat balanced meals and remain well hydrated
Avoid uncomfortable stressful positions and bad posture
Avoid eyestrain
Try biofeedback and relaxation techniques including meditation
Discuss with dentist regarding a mouth if bruxsim contributing to headache
For excellent patient education resources, visit eMedicineHealth's Headache Center. Also, see eMedicineHealth's patient education articles Causes and Treatments of Migraine and Related Headaches, Tension Headache, and Chronic Pain.
What is tension-type headache (TTH)?What are the HIS diagnostic criteria for episodic tension-type headache (TTH)?What are the HIS diagnostic criteria for chronic tension-type headache (TTH)?What is the pathophysiology of tension-type headache (TTH)?What is the prevalence of tension-type headache (TTH)?What are the sexual predilections of tension-type headache (TTH)?Which age groups have the highest prevalence of tension-type headache (TTH)?Which clinical history findings are characteristic of tension-type headache (TTH)?Which physical findings are characteristic of tension-type headache (TTH)?What causes tension-type headache (TTH)?What are the differential diagnoses for Muscle Contraction Tension Headache?What is the role of lab tests in the workup of tension-type headache (TTH)?What is the role of imaging studies in the workup of tension-type headache (TTH)?What is the role of lumbar puncture in the workup of tension-type headache (TTH)?What is the role of minimally invasive therapies in the treatment of tension-type headache (TTH)?How is tension-type headache (TTH) treated?What is the role of medications in the treatment of tension-type headache (TTH)?What is the role of physical therapy (PT) in the treatment of tension-type headache (TTH)?What is the role of behavioral therapies in the treatment of tension-type headache (TTH)?Which specialist consultations are beneficial to patients with tension-type headache (TTH)?Which activity modifications are used in the treatment of tension-type headache (TTH)?What is the role of medications in the treatment tension-type headache (TTH)?Which medications in the drug class Electrolyte supplements are used in the treatment of Muscle Contraction Tension Headache?Which medications in the drug class Serotonin reuptake inhibitors are used in the treatment of Muscle Contraction Tension Headache?Which medications in the drug class Antidepressants are used in the treatment of Muscle Contraction Tension Headache?Which medications in the drug class Nonsteroidal anti-inflammatory drugs (NSAIDs) are used in the treatment of Muscle Contraction Tension Headache?Which medications in the drug class Analgesics are used in the treatment of Muscle Contraction Tension Headache?What is included in patient education about tension-type headache (TTH)?
Syed M S Ahmed, MD, Neurologist and Sleep Specialist, Capital Neurology and Sleep Medicine; Staff Attending in Neurology and Sleep Medicine, Montgomery General Hospital; Staff Attending in Neurology and Sleep Medicine, Suburban Hospital
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Chief Editor
Tarakad S Ramachandran, MBBS, MBA, MPH, FAAN, FACP, FAHA, FRCP, FRCPC, FRS, LRCP, MRCP, MRCS, Professor Emeritus of Neurology and Psychiatry, Clinical Professor of Medicine, Clinical Professor of Family Medicine, Clinical Professor of Neurosurgery, State University of New York Upstate Medical University; Neuroscience Director, Department of Neurology, Crouse Irving Memorial Hospital
Disclosure: Nothing to disclose.
Additional Contributors
Joseph Carcione, Jr, DO, MBA, Consultant in Neurology and Medical Acupuncture, Medical Management and Organizational Consulting, Central Westchester Neuromuscular Care, PC; Medical Director, Oxford Health Plans
Disclosure: Nothing to disclose.
Manish K Singh, MD, Assistant Professor, Department of Neurology, Teaching Faculty for Pain Management and Neurology Residency Program, Hahnemann University Hospital, Drexel College of Medicine; Medical Director, Neurology and Pain Management, Jersey Institute of Neuroscience
