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 The leading web portal for pharmacy resources, news, education and careers February 4, 2012
Pharmacy Choice - Headache Disease State Management - February 4, 2012

Headache Disease State Management

Pharmacist Focus on Tension Headaches
by Darrell Hulisz, RPh, PharmD
Associate Professor of Family Medicine
Case Western Reserve University, School of Medicine
University Hospitals, Case Medical Center
Lubna E. Kousa, MS
Pharmacy Intern, University of Findlay

Headache disorders are among the most common complaints encountered by healthcare professionals. Headaches are classified as primary, occurring without an underlying cause, or secondary, attributed to a discrete pathologic process. Diagnosis and management of headache syndromes are based on a careful clinical approach that relies on an understanding of the anatomy, physiology, and pharmacology of the nervous system pathways that mediate the various headache disorders.

Tension headache is the most common type of primary headache as classified according to the International Headache Society (HIS), with an estimated 1-year prevalence of 63% in men and 86% in women. Tension headache is more common than other primary headaches such as migraines and cluster headaches. The first onset of tension headache appears early in life; younger than 20 years of age in more than 40% of patients, while prevalence peaks between the ages of 20 and 50 years. The mean frequency of attacks is approximated to 3 days per month, with most sufferers experiencing less than one attack per month. When tension headache occurs more than 180 days per year it is classified as chronic. The majority of patients who experience tension-type headache suffer a degree of functional impairments during an attack; nevertheless, only 15% seek medical attention.

The pathophysiology of tension headache is poorly and incompletely understood. The name tension headache implies that pain is a product of the nervous system. Unlike migraine, which involves a generalized disturbance of sensory modulation, tension headache appears to be a primary disorder of CNS pain modulation alone. Muscle contraction has been considered to be a feature that distinguishes tension headache from migraine. In episodic tension headache the pain is thought to originate from the myofascial factors and peripheral sensitization of nociceptors, as well as central mechanisms being involved. Other factors thought to initiate the stimulus include non-physiologic motor stress, mental stress, and local myofascial release of irritants. Once the suprapinal pain perception structures get activated, a self-limiting headache is initiated in response to the central modulation of the incoming peripheral stimuli. On the other hand, chronic tension headache may evolve from episodic tension headache in predisposed patients due to the disturbance of central nociceptive processing and subsequent sensitization of the CNS.

Tension headache is generally characterized by bilateral tight, band-like discomfort. The pain builds slowly, fluctuates in severity, and may persist for several days in chronic cases. Tension-type pain is often described as dull, nonpulsatile tightness or pressure without premonitory symptoms or aura. Tension headaches are not usually accompanied by an aura, or migraine-associated symptoms, such as nausea, vomiting, throbbing, and aggravation with movement. However, photophobia or phonophobia may be reported. Difficulty in diagnosis and treatment are common in patients who fit the tension –type criteria but have migraines at times or typical migraine triggers along with family history of migraine. These patients are considered biologically different and may experience tension headache with none of the clinical features. It is worth noting that the disability associated with tension-type headache is typically minor when compared with migraine and routine physical activity does not affect headache severity.

The vast majority of patients with tension-type headache seek over the counter medications for relief without consulting healthcare professionals. Although several non-pharmacologic and pharmacologic approaches have been used; simple analgesics such as acetaminophen or NSAIDs are considered the mainstay of acute attacks. Moreover, clinical studies have demonstrated a relative lack of efficacy with triptans in treatment of pure tension headache.

Non-pharmacologic interventions include counseling, stress management, relaxation training and biofeedback. These techniques result in a ~50% reduction in headache activity. Some patients may experience tension headaches die to poor posture or because of cervical strain. These patients may be referred to a physical therapist. Inconsistent evidence exists to support physical therapeutic options such as heat or cold packs, electrical nerve stimulation, stretching, exercise, massage, acupuncture, manipulations, ergonomic instruction, and trigger point injections or occipital nerve blocks. However, these many interventions may benefit some patients.

Pharmacologic treatment is effective in acute treatment of mild to moderate episodes. Analgesics; alone or in combination with caffeine, and NSAIDS are first line in therapy. Acetaminophen, aspirin, ibuprofen, naproxen, ketoprofen, indomethacin and ketorolac have shown efficacy in clinical trials and comparative studies. Moreover, high dose NSAIDs in combination with butalbital or codeine are considered effective options. Nevertheless, these combinations should be last line and avoided when possible due to their high potential of abuse and dependency. Medications for acute episodes should not be used for more than two days per week to prevent the development of chronic headache. Prophylactic treatment may only be used if headaches occur more than two times per week and last over three to four hours, or if the severity of the headache is interfering with activities of daily living and causing substantial disability. Tricyclic antidepressants, such as amitriptyline are sometimes used for prophylaxis, however, side effects as well as other comorbidities need to be considered. Selective serotonin reuptake inhibitors, and benzodiazapines have not shown to be effective for chronic treatment.

Although tension headache appears to be a result of neuronal dysfunction, the exact etiology and mechanism of the dysfunction remain unknown. Pharmacists can play an important role in indentifying this patient population; determine appropriate candidates for self care, or refer patient to a primary care physician when needed. Management of tension type headache is directed towards pain management and prevention of future attacks. A better understanding of the pathophysiologic mechanism will lead to the development and use of more efficacious pharmacologic treatments.

References:
  1. Lipton RB, Stewart WF, Diamond S, et al. Prevalence and burden of migraine in the United States: Data from the American Migraine Study II. Headache 2001;41:646–657.
  2. Mueller L. Tension-type, the forgotten headache. Postgrad Med 2002;111:25–50.
  3. Mueller L. Tension-type, the forgotten headache. Postgrad Med 2002;111:25–50.
  4. Jensen R. Mechanisms of tension-type headache. Cephalalgia 2001:21:786–789.
  5. Kaniecki RG. Migraine and tension-type headache: An assessment of challenges in diagnosis. Neurology 2002;58(Suppl 6):S15–20.
  6. Jensen R, Olesen J. Tension-type headache: An update on mechanisms and treatment. Curr Opin Neurol 2000;13:285–289.

Resources
American Migraine Foundation

American Academy of Neurology

American Headache Society

National Headache Foundation

National Institute of Neurological Disorders & Stroke

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