Drugs for headache

CHAPTER 30


Drugs for headache


Headache is a common symptom that can be triggered by a variety of stimuli, including stress, fatigue, acute illness, and sensitivity to alcohol. Many people experience mild, episodic headaches that can be relieved with over-the-counter medications, such as aspirin, acetaminophen [Tylenol, others], and ibuprofen [Motrin, Advil, others]. For these individuals, medical intervention is unnecessary. In contrast, some people experience severe, recurrent, debilitating headaches that are frequently unresponsive to aspirin-like drugs. For these individuals, medical attention is merited. In this chapter, we focus on severe forms of headache—specifically, migraine, cluster, and tension-type headaches. Defining characteristics of these headaches are summarized in Table 30–1.



When attempting to treat headache, we must differentiate between headaches that have an identifiable underlying cause (eg, severe hypertension; hyperthyroidism; tumors; infection; disorders of the eye, ear, nose, sinuses, and throat) and headaches that have no identifiable cause (eg, migraine and cluster headaches). Obviously, if there is a clear cause, it should be treated directly.


As we consider drugs for headache, keep three basic principles in mind. First, antiheadache drugs may be used in two ways: to abort an ongoing attack or to prevent an attack from occurring. Second, not all patients with a particular type of headache respond to the same drugs. Hence, therapy must be individualized. Third, several of the drugs employed to treat severe headaches (eg, ergotamine, opioids) can cause physical dependence. Accordingly, every effort should be made to keep dependence from developing. If dependence does develop, a withdrawal procedure is needed.



Migraine headache


Characteristics, pathophysiology, and overview of treatment




Characteristics

Migraine headache is characterized by throbbing head pain of moderate to severe intensity that may be unilateral (60%) or bilateral (40%). Most patients also experience nausea and vomiting, along with neck pain and sensitivity to light and sound. Physical activity intensifies the pain. During a prolonged attack, patients develop hyperalgesia (augmented responses to painful stimuli) and allodynia (painful responses to normally innocuous stimuli). Migraines usually develop in the morning after arising. Pain increases gradually and lasts 4 to 72 hours (median duration 24 hours). On average, attacks occur 1.5 times a month. Precipitating factors include anxiety, fatigue, stress, menstruation, alcohol, weather changes, and tyramine-containing foods (Table 30–2).



Migraine has two primary forms: migraine with aura and migraine without aura. In migraine with aura, the headache is preceded by visual symptoms (flashes of light, a blank area in the field of vision, zigzag patterns). Of the two forms, migraine without aura is more common, affecting about 70% of migraineurs.


Migraine afflicts 29.5 million people in the United States and 324 million worldwide. The headaches are more common and more severe in females, with a lifetime incidence of 43%, compared with 18% in males. About 65% of migraineurs are women in their late teens, 20s, or 30s. With some women, migraine attacks are worse during menstruation but subside during pregnancy and cease after menopause, indicating a hormonal component to the attacks. A family history of the disease is typical.


Migraine is highly debilitating. An attack can prevent participation in social and leisure activities, and can result in lost productivity at home, school, and work. According to the World Health Organization, disability caused by a severe migraine attack equals that caused by quadriplegia, psychosis, or dementia.



Pathophysiology

Migraine headache is a neurovascular disorder that involves dilation and inflammation of intracranial blood vessels. Headache generation begins with neural events that trigger vasodilation. Vasodilation then leads to pain, which leads to further neural activation, thereby amplifying pain-generating signals. Neurons of the trigeminal vascular system, which innervate intracranial blood vessels, are key components.


The exact cause of migraine pain is not completely understood—although vasodilation and inflammation are clearly involved. Available data suggest that two compounds—calcitonin gene–related peptide (CGRP) and serotonin (5-hydroxytryptamine [5-HT])—play important roles. The role of CGRP is to promote migraine, and the role of 5-HT is to suppress migraine. Data that implicate CGRP as a cause of migraine include the following:



Data that support a protective role for 5-HT include the following:




Overview of treatment

Drugs for migraine are employed in two ways: to abort an ongoing attack and to prevent attacks from occurring. Drugs used to abort an attack fall into two groups: nonspecific analgesics (aspirin-like drugs and opioid analgesics) and migraine-specific drugs (ergot alkaloids and serotonin1B/1D receptor agonists [triptans]). Drugs employed for prophylaxis include beta blockers (eg, propranolol), tricyclic antidepressants (eg, amitriptyline), and antiepileptic drugs (eg, divalproex).


Nondrug measures can help. Patients should try to control or eliminate triggers (see Table 30–2) and should maintain a regular pattern of eating, sleeping, and exercise. Why? Because, in people with migraine, the brain seems to have a low tolerance for the ups and downs of life. Once an attack has begun, the migraineur should retire to a dark, quiet room. Placing an ice pack on the neck and scalp can help.



Abortive therapy


The objective of abortive therapy is to eliminate headache pain and suppress associated nausea and vomiting. Treatment should commence at the earliest sign of an attack. Because migraine causes GI disturbances (nausea, vomiting, and gastric stasis), oral therapy may be ineffective once an attack has begun. Hence, for treatment of an established attack, a drug that can be administered by injection, nasal spray, or rectal suppository may be best. As noted, two types of drugs are used: nonspecific analgesics and migraine-specific agents. Representative drugs are listed in Table 30–3.



Drug selection depends on the intensity of the attack. For mild to moderate symptoms, an aspirin-like drug (eg, aspirin, naproxen, acetaminophen) may be sufficient. For moderate to severe symptoms, patients should take a migraine-specific drug—either an ergot alkaloid (ergotamine or dihydroergotamine) or a serotonin1B/1D agonist. If these agents fail to relieve pain, an opioid analgesic (eg, butorphanol, meperidine) may be needed.


Use of abortive medications (both nonspecific and migraine specific) should be limited to 1 or 2 days a week. Why? Because more frequent use can lead to medication overuse headache (MOH), also known as drug-induced headache or drug-rebound headache (Box 30–1).



imageBOX 30–1    SPECIAL INTEREST TOPIC


MEDICATION OVERUSE HEADACHE: TOO MUCH OF A GOOD THING


People who take headache medicine every day often develop medication overuse headaches (MOHs), also known as drug-rebound headaches or drug-induced headaches. What’s a MOH? A chronic headache that develops in response to frequent use of headache medicines, and that resolves days to weeks after the overused drug is withdrawn. The stage for MOH is set when headache drugs are taken too often—especially if the dosage is high. Once the stage has been set, discontinuing the medication brings on the MOH, which causes the patient to resume taking medicine—thereby setting up a repeating cycle of MOH, followed by medication use and discontinuation, followed by another MOH, and so on. One reason the cycle gets established is that patients don’t realize that the drugs they’re taking to treat headache can, if taken too often, become the cause of headache. Failing to recognize MOH for what it is, patients take more and more medicine to make their headaches go away—but only succeed in making MOH worse.


Which drugs can cause MOH? Almost all of the medicines used for abortive headache therapy. Hence, MOH can be caused by overuse of analgesics (aspirin-like drugs, opioids), ergotamine (but not dihydroergotamine), triptans, and caffeine.


How can MOH be treated? The only hope is to stop taking all headache medicines. Unfortunately, when medication is withdrawn, headaches will increase for a while. Their duration and intensity depend on the drug that was overused. With triptans, withdrawal headaches are relatively mild and often resolve in a few days. In contrast, with analgesics or ergots, withdrawal headaches are more intense and may persist for 2 weeks or more.


Is there a way to make withdrawal more comfortable? Yes. In 2010, Italian researchers published a new protocol, consisting of abrupt discontinuation of the overused drug, plus 7 to 15 days of the following treatment:



If a severe withdrawal headache occurred during the procedure, patients were allowed a single rescue medication, but always a drug different from the one they had overused. Not only did this procedure reduce the discomfort of medication withdrawal, it produced a sustained reduction in medication use.


Several measures can decrease the risk of developing MOH. The most important is to limit the use of abortive medicines. If possible, patients should take these drugs no more than 2 or 3 times a week—and doses should be no higher than actually needed. Alternating headache medicines may help too, since this would limit exposure to any one drug. If headaches begin to occur more than 2 or 3 times a month, prophylactic therapy should be tried. Implementing nondrug measures—stress reduction, avoidance of triggers, getting sufficient sleep, relaxation techniques, and biofeedback—can reduce the need for headache medicines, and can thereby decrease exposure to the drugs that cause MOH.


Antiemetics are important adjuncts to migraine therapy. By reducing nausea and vomiting, these drugs can (1) make the patient more comfortable and (2) permit therapy with oral antimigraine drugs. Two antiemetics—metoclopramide [Reglan] and prochlorperazine (formerly available as Compazine)—are used most often. Of the two, metoclopramide is preferred. Why? Because, in addition to suppressing nausea and vomiting, metoclopramide can reverse gastric stasis caused by the attack, and can thereby facilitate absorption of oral antimigraine drugs. Like metoclopramide, prochlorperazine suppresses nausea and vomiting. However, because of its anticholinergic actions, prochlorperazine can make gastric stasis even worse.



Analgesics





Ergot alkaloids



Ergotamine







Drug interactions. 





Contraindications.

Ergotamine is contraindicated for patients with hepatic or renal impairment, sepsis (gangrene has resulted), coronary artery disease (CAD), and peripheral vascular disease, and for those taking potent inhibitors of CYP3A4. In addition, the drug should not be taken during pregnancy. Why? Ergotamine can promote uterine contractions, and hence might cause fetal harm or abortion. In fact, because of its effects on the uterus, ergotamine is classified in Food and Drug Administration (FDA) Pregnancy Risk Category X: The risk of use by pregnant women clearly outweighs any possible benefits. Warn women of child-bearing age to avoid pregnancy while using this drug.








Preparations, dosage, and administration.


Ergotamine by itself is available in tablets for sublingual use. In addition, ergotamine is available in combination with caffeine for oral and rectal dosing.







Dihydroergotamine






Contraindications.

Like ergotamine, dihydroergotamine is contraindicated for patients with CAD, peripheral vascular disease, sepsis, pregnancy, and hepatic or renal impairment, and for patients taking triptans or potent inhibitors of CYP3A4.








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Jul 24, 2016 | Posted by in NURSING | Comments Off on Drugs for headache

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