Abstract
90% or more of the population is affected by headaches at one time or another. Most of these are mild to moderate in intensity, with vague associated symptoms, and are difficult to classify; they are generally classified under the category of tension-type headache (TTH). Patients who experience headaches with a frequency of 15 days per month or more, over a period of months, are said to have either a chronic tension-type headache (CTTH) or a chronic daily headache (CDH). In addition, patients who have a diagnosis of another, more specific, headache type, such as migraine or cluster, usually have interposed TTH. Overuse of analgesics (in general, the consumption of analgesics 10 or more days per month for at least 3 months) is a frequent contributor to CDH; for prevention strategies to be effective, analgesic use must be discontinued for not less than 2 months. Fibromyalgia, myofascial pain, and cervicogenic disorders are frequently associated with some form of headache. Similarly, sleep disorders, such as snoring, apnea, and restless legs, also may manifest with headache and should be considered and explored in appropriate patients. Mild traumatic brain injury, concussion, and whiplash may trigger chronic headaches that are particularly challenging to treat.
Keywords
chronic daily headache, chronic tension-type headache, posttraumatic headache, tension-type headache
Epidemiology
Tension-type headache (TTH) is the most common headache type and also the most difficult to classify. Many different, and equally vague, terms have been applied to this headache or to what probably are variants of the same syndrome. Headaches in general are thought to affect more than 90% of the population at one time or another, with about 15% of those fitting the description of migrainous or vascular headache. This leaves about 70% of the population with some variant of TTH. Moreover, almost all patients with migraine, cluster headache, trigeminal nerve neuralgias, and other recurring cephalgic syndromes have interposed TTH.
Diagnosis
Tension-Type Headache and Chronic Daily Headache
The pain of a TTH tends to be duller, less intense, and less localized than that of a migraine or a cluster attack. The pain usually lasts several hours to a day, but it may continue for days or weeks. During a severe TTH, patients can experience photophobia, phonophobia, nausea, and occasionally emesis. Pain referred to the neck is common; patients also frequently complain of “a knot in the neck,” but the neurologic examination is normal.
The major variants of TTH are those with disorder of the pericranial muscles, those without disorder of the pericranial muscles, and chronic TTH (CTTH) (with or without disorder of the pericranial muscles). Those with disorder of the pericranial muscles are characterized by tenderness on palpation of those muscles, increased activity on electromyography (EMG), or both. TTH without disorder of the pericranial muscles lacks those characteristics. CTTH, previously called chronic daily headache, is diagnosed in a patient with a headache frequency of 15 days per month or 180 headaches per year averaged over a 6-month period. Fibromyalgia and the myofascial pain syndrome also are associated with frequent or chronic daily headaches.
Analgesic Medication Overuse Headache
A common variety of chronic daily headache occurs in patients with headaches of any sort, particularly, tension-type or episodic migraines, in whom these temporarily exacerbate and become more frequent. Patients begin using analgesic preparations (e.g., nonsteroidal antiinflammatory drugs [NSAIDs], acetaminophen, aspirin, butalbital, narcotics, ergot derivatives, triptans) on a regular basis (generally 10 times or more per month) and eventually develop analgesic overuse, or rebound, headaches. Thus, patients should be advised against using analgesics more than twice per week over a prolonged period. If they require analgesics at least twice per week, they should be offered a prophylactic regimen.
In adolescents (age 12–14 years at the time of diagnosis), the cause and prognosis of chronic daily headache (CDH) might be distinct from that in adults. Many of these children seem to have personal or family history of migraine. When followed for up to 8 years, 40% continue to experience CDH after 1 year, 25% after 2 years, and 12% after 8 years. Without specific medical intervention, the majority of adolescents with CDH seem to evolve into adults who suffer from episodic migraine and episodic TTH.
The mainstay of treatment for medication overuse headache (MOH) is total withdrawal from analgesics for a period not shorter than 2 months. The patients most likely to be headache-free at the end of that time are migraneurs (67% reduction) and those with mixed TTH and migraines (37% reduction); patients diagnosed with TTH alone are less likely to report large reductions in headache frequency but do report large reductions in pain intensity. The initial several days to 2 weeks following analgesic withdrawal might be the most difficult and are frequently punctuated with a severe rebound headache; antiemetics and maintaining hydration, as well as patience, are effective. Using steroids during this period has no effect on outcome. One additional characteristic of patients with MOH is that drugs administered with prophylactic intent tend to not work (or to not work as well) unless analgesics are discontinued. Patients whose MOH is typified by the regular use of narcotics or barbiturates may require a controlled tapering off the drugs and management of potential withdrawal symptoms.
A particularly severe, persistent, or unusual headache should always prompt consideration of alternative explanations, and, when appropriate, these should be investigated thoroughly. For example, temporal arteritis should be considered in an elderly patient with a persistent headache of recent onset whether other typical elements are present in the history and physical examination. In these patients, an erythrocyte sedimentation rate or a sensitive c-reactive protein (s-CRP) should be ordered immediately, and consideration should be given to treatment with a corticosteroid and to a temporal artery biopsy. Likewise, one would not want to miss an infectious meningitis, the sentinel bleed of an aneurysm, an undiagnosed intracranial vascular malformation, a subdural hematoma, acute hydrocephalus, venous thrombosis, or an arterial dissection. Idiopathic intracranial hypertension (previously called pseudotumor cerebri) usually presents in overweight young women with chronic headaches, a normal examination, a normal scan and papilledema, although a subset of these patients do not have papilledema. The diagnosis is made when a lumbar puncture reveals an otherwise normal fluid under high pressure (at least 20–25 cm H 2 O). Therefore, when dictated by clinical judgment, imaging, lumbar puncture, or other tests deemed necessary are indicated.
Pathophysiology of Tension-Type Headache
The pathophysiologic bases for TTH and CTTH are unknown. Some investigators believe that TTH lies at one end of a physiologic spectrum that includes severe migraine and cluster at one end and TTH at the other. Under this assumption, at least to some degree, the underlying mechanism of most chronic, recurring headache syndromes would be shared. The muscle contraction theory of TTH relates pain to prolonged contraction, or spasm, of cervical or pericranial muscles but no objective data support the theory. Most patients with a headache, migrainous or TTH, have pericranial muscle tenderness or sore spots; however, many individuals without headache also have them. During a headache, patients with a more severe headache tend to have more tender pericranial muscles; but the relationship between tenderness of the pericranial muscles and headaches is not straightforward. Increased tenderness during headaches may represent cutaneous allodynia.
The relationship between cervicogenic disorders and headache is similarly unclear, although most painful disorders of the neck are associated with some sort of headache. Cervical pain can be referred to the head from intervertebral discs, interspinous ligaments, zygapophyseal joints, the periosteum, paracervical muscles, carotid and vertebral arteries, and from irritation of the C1, C2, and C3 nerve roots. The dorsal rami of the first three cervical nerve roots supply the sensory innervation to the neck and to the scalp caudal to the innervation of the trigeminal nerve, and to the meninges and arteries of the posterior fossa. Headache also can arise from pathology in the area of the foramen magnum. Some examples include a Chiari I malformation, the Dandy-Walker syndrome, atlantoaxial dislocation (e.g., from rheumatoid arthritis), Paget disease of the bone, and basilar invagination.
Treatment
As with other headache types, both abortive and prophylactic treatment strategies are available for the treatment of TTH and CTTH.
Abortive Treatment Strategies
For the occasional TTH, an over-the-counter (OTC) analgesic preparation is all that is required. The number of OTC preparations continues to increase, and although they are generally safe, the lay population has little basis on which to decide how to choose among them or how to use them properly. Most people decide on a preparation either on a trial-and-error basis or are swayed by the marketing (e.g., “for tension headache,” “for sinus pain,” “multi-symptom relief,” and “PM” preparations). Several OTC analgesic preparations involve combinations of drugs (e.g., aspirin plus acetaminophen) and may contain caffeine. Caffeine combined with analgesics such as aspirin, acetaminophen, and ibuprofen enhances their analgesic effectiveness. Stronger headaches may require an analgesic (aspirin, acetaminophen, or ibuprofen) in combination with either codeine or butalbital with or without caffeine. Used infrequently, the additional analgesic effectiveness obtained by adding codeine or butalbital comes with little increase in adverse effects or risk of dependence.
If aspirin or acetaminophen, with or without codeine, butalbital, or caffeine are ineffective in controlling the headache, the choice of an alternative analgesic should proceed in an orderly fashion by testing in turn members of different NSAID chemical categories at adequate doses. Indomethacin is reported to be more effective than alternative NSAIDs for pain of cephalic origin; it is particularly effective in treating hemicrania—see Chapter 19 . Occasionally, a patient responds well to stress management modalities or acupuncture (anyone considering acupuncture should ascertain the qualifications of the practitioner and insist on new, not sterilized, needles for every session), but it is impossible to predict accurately in whom these modalities are likely to be beneficial. The major chemical categories of NSAIDs include the following:
Carboxylic acids—this group includes aspirin, which is an acetylated acid, and salsalate and choline magnesium trisalicylate, which are nonacetylated.
Propionic acids—ibuprofen, naproxen, ketoprofen, and fenoprofen.
Aryl and heterocyclic acids—indomethacin, diclofenac, sulindac, and tolmetin.
Fenamic acids—mefenamic acid and meclofenamate.
Enolic acids—piroxicam and phenylbutazone.
Pyrrolo-pyrrole—ketorolac.
Cyclooxygenase 2 (COX-2) inhibitors—celecoxib.
Prophylactic Treatment Strategies
Fortunately, CTTH and TTH that are frequent or otherwise annoying respond to many of the agents used in migraine prophylaxis. It is possible that this reflects on the presumed common mechanism that is felt to underlie both disorders.
- A.
Antidepressants, particularly amitriptyline or nortriptylene at a starting dose of 10–25 mg at bedtime, are active prophylactic drugs. Most patients who respond to tricyclic antidepressants (amitriptyline, nortriptyline, imipramine, or desipramine) usually do so at doses of 25–200 mg at bedtime; an occasional patient may require more. Tricyclics help induce sleep, which may constitute one of the mechanisms by which they help. The major side effects from tricyclics relate to their anticholinergic effects and include a dry mouth, excessive daytime sleepiness, dizziness, urinary retention, glaucoma, cardiac arrhythmias, and photosensitization; they can also cause weight gain. The specific serotonin reuptake inhibitors (SSRIs) and specific serotonin-norepinephrine reuptake inhibitors (SNRIs) might be tried in patients who do not respond or who develop intolerable side effects from tricyclic drugs. The major side effects of the SSRIs and SNRIs include jitteriness, tremors, gastrointestinal distress, decreased libido, and occasionally headaches. In addition, these drugs are relatively contraindicated in patients who use triptans, as they may suffer from excessive serotonin stimulation (serotonin syndrome).
- B.
Beta-blockers, such as propranolol, metoprolol, atenolol, timolol, and nadolol, can be tried and sometimes prove effective. In most healthy people, 60–80 mg once per day of a long-acting propranolol preparation can be started and the dosage can be adjusted as necessary. Side effects include dizziness from bradycardia or hypotension, fatigue, depression, worsening of symptoms in patients with asthma or chronic obstructive pulmonary disease, gastrointestinal distress, blunting of hypoglycemic symptoms in patients with diabetes, and vivid dreams.
- C.
Anticonvulsants such as valproic acid (Depakote and Depakote extended release preparation [ER]) are sometimes worth a try to prophylax against frequent TTH. The usual starting dose for Depakote ER is 500 mg per day; the dose should be adjusted as necessary at 2–6-week intervals. The author usually adjusts the dose in 500-mg increments and recommends the ER to maintain once per day dosing. Valproic acid can cause weight gain, hair loss, tremor, and abdominal distress.
- D.
Although still controversial, a botulinum toxin A (Botox) injection into the most tender pericranial muscle(s) or directly into a trigger point has been reported to increase significantly the number of headache-free days in patients with CTTH. This should not be confused with its indication for chronic migraine (see Chapter 19 ), and patients can expect that insurance rarely, if ever, covers the cost.
The drugs used in TTH and CTTH are in Box 20.1 .
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