Tension headache


Tension headache, stress headache, or tension-type headache, is the most common type of primary headache. The pain usually radiates from the lower back of the head, the neck, the eyes, or other muscle groups in the body typically affecting both sides of the head. Tension-type headaches account for nearly 90% of all headaches.
Pain medications, such as paracetamol and ibuprofen, are effective for the treatment of tension headache. Tricyclic antidepressants appear to be useful for prevention. Evidence is poor for SSRIs, propranolol and muscle relaxants.
The 2016 Global Burden of Disease study revealed that TTHs affect about 1.89 billion people and are more common in women than men. TTH was most prevalent between ages 35 and 39. Despite its benign character, tension-type headache, especially in its chronic form, can impart significant disability on patients as well as burden on society at large. In 2016, the global burden of TTH was reported to be 7.2 million years of life lived with disability. The YLD was calculated using TTH prevalence and average time spent with TTH multiplied by percentage health loss caused by TTH.

Signs and symptoms

According to the third edition of the International Classification of Headache Disorders, the attacks must meet the following criteria:
  • A duration of between 30 minutes and 7 days.
  • At least two of the following four characteristics:
  • * bilateral location
  • * pressing or tightening quality
  • * mild or moderate intensity
  • * not aggravated by routine physical activity such as walking or climbing stairs
  • Both of the following:
  • * no nausea or vomiting
  • * no more than one of photophobia or phonophobia
Tension-type headaches may be accompanied by tenderness of the scalp on manual pressure during an attack.

Risk factors

Various precipitating factors may cause tension-type headaches in susceptible individuals:
  • Anxiety
  • Stress
  • Sleep problems
  • Young age
  • Poor health

    Mechanism

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 myofascial tissue and alteration of this pathway likely underlies episodic tension-type headache. In addition, 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. This is when the peripheral pain response is transformed over time into a centralized pain response. These prolonged alterations in the peripheral pain pathways can lead to increased excitability of the central nervous system pain pathways, resulting in the transition of ETTH into chronic tension-type headache. Specifically, the hyperexcitability occurs in central nociceptive neurons 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.
The alterations in physiology that leads to the overall process of central sensitization, involves changes at the level of neural tracts, neurotransmitters and their receptors, the neural synapse, and the post-synaptic membrane. Evidence also suggests that dysfunction in supraspinal descending inhibitory pain pathways may contribute to the pathogenesis of central sensitization in CTTH.

Neurotransmitters

Specific neuronal receptors and neurotransmitters thought to be most involved include NMDA and AMPA receptors, glutamate, serotonin, β-endorphin, and nitric oxide. 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 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.

Synapses

Regarding synaptic level changes, homosynaptic facilitation and heterosynaptic facilitation are both likely to be involved in central sensitization. Homosynaptic facilitation occurs when synapses normally involved in pain pathways undergo changes involving receptors on the post-synaptic membrane as well as the molecular pathways activated upon synaptic transmission. Lower pain thresholds of CTTH result from this homosynaptic facilitation. In contrast, heterosynaptic facilitation occurs when synapses not normally involved in pain pathways become involved. Once this occurs innocuous signals are interpreted as painful signals. Allodynia and hyperalgesia of CTTH represent this heterosynaptic facilitation clinically.

Stress

In the 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.

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.

Classification

The International Headache Society's most current classification system for headache disorders is the International Classification of Headache Disorders 3rd edition as of 2018. This classification system separates tension-type headache into two main groups: episodic and chronic. CTTH is defined as fifteen days or more per month with headache for greater than three months, or one-hundred eighty days or more, with headache per year. ETTH is less than fifteen days per month with headache or less than one-hundred eighty days with headache per year. However, ETTH is further sub-divided into frequent and infrequent TTH. Frequent TTH is defined as ten or more episodes of headache over the course of one to fourteen days per month for greater than three months, or at least twelve days per year, but less than one-hundred eighty days per year. Infrequent TTH is defined as ten or more episodes of headache for less than one day per month or less than twelve days per year. Furthermore, all sub-classes of TTH can be classified as having presence or absence of pericranial tenderness, which is tenderness of the muscles of the head. Probable TTH is utilized for patients with some characteristics, but not all characteristics of a given sub-type of TTH.

Differential diagnosis

Extensive testing is not needed as TTH is diagnosed by history and physical examination. However, if symptoms indicative of a more serious diagnosis are present, a contrast enhanced MRI may be utilized. Furthermore, giant cell arteritis should be considered in those 50 years of age and beyond. Screening for giant cell arteritis involves the blood tests of erythrocyte sedimentation rate and c-reactive protein.
  • Migraine
  • Oromandibular dysfunction
  • Sinus disease
  • Eye disease
  • Cervical spine disease
  • Infection in immunocompromised
  • Intracranial mass
  • Idiopathic intracranial hypertension
  • Medication overuse headache
  • Secondary headache
  • Giant cell arteritis
  • Dermatochalasis

    Prevention

Lifestyle

Good posture might prevent headaches if there is neck pain.
Drinking alcohol can make headaches more likely or severe.
Drinking water and avoiding dehydration helps in preventing tension headache.
People who have jaw clenching might develop headaches, and getting treatment from a dentist might prevent those headaches.
Using stress management and relaxing often makes headaches less likely.
Biofeedback techniques may also help.

Medications

People who have 15 or more headaches in a month may be treated with certain types of daily antidepressants which act to prevent continued tension headaches from occurring. In those who are predisposed to tension type headaches the first-line preventative treatment is amitriptyline, whereas mirtazapine and venlafaxine are second-line treatment options. Tricyclic antidepressants appear to be useful for prevention. Tricyclic antidepressants have been found to be more effective than SSRIs but have greater side effects. Evidence is poor for the use of SSRIs, propranolol, and muscle relaxants for prevention of tension headaches.

Treatment

Treatment for a current tension headache is to drink water and confirm that there is no dehydration. If symptoms do not resolve within an hour for a person who has had water, then stress reduction might resolve the issue.

Exercise

Evidence supports simple neck and shoulder exercises in managing ETTH and CTTH for headaches associated with neck pain. Exercises include stretching, strengthening and range of motion exercises. CTTH can also benefit from combined therapy from stress therapy, exercises and postural correction.