07- Headache danya new (1).pdf

Headache Prof. Ibrahim AL-Adham Dr. Dania Alhyari Taken from Handbook of Nonprescription Drugs > Chapter 5. Headache 1  Classification of headache Headaches a...

Headache Prof. Ibrahim AL-Adham Dr. Dania Alhyari Taken from Handbook of Nonprescription Drugs > Chapter 5. Headache 1  Classification of headache Headaches are generally classified as primary or secondary. Primary headaches (approximately 90% of headaches) are not associated with an underlying illness. Examples include episodic and chronic tension type headaches, migraine headache with and without aura, cluster headaches, and medication overuse headaches. Secondary headaches are symptoms of an underlying condition, such as head trauma, stroke, substance abuse or withdrawal, bacterial and viral diseases, and disorders of craniofacial structures. 2  Types of headache We will focus on the most common headaches that are amenable to self treatment: 1. Tension type, 2. Diagnosed migraine, 3. Sinus headaches. 3 Tension headaches Tension type headaches, also called stress headaches, can be episodic or chronic. Chronic tension type headaches occurring at least 15 days per month for at least 6 months may be a manifestation of psychological conflict, depression, or anxiety. These headaches may be associated with sleep disturbances, shortness of breath, constipation, weight loss, fatigue, decreased sexual drive, palpitations, and menstrual changes.. 4 Tension headaches The prevalence of tension type headache is greatest in the age range 40-49 years, occurs in a ratio of 5:4 of women to men, and increases with higher levels of education. Among children, boys and girls are affected equally, but attacks usually greatly decrease in boys after puberty. Migraine without aura (i.e.,neurologic symptoms that precede the head pain) occurs almost twice as frequently as migraine with aura, and many individuals may have both types of headaches 5 6 Tension type headaches- cont. Tension type headaches often manifest in response to stress, anxiety, depression, emotional conflicts, and other stimuli. The episodic tension type headache subtype is thought to have a peripheral pain source, whereas the chronic tension type headache has a central mechanism. (Sensitization of second-order neurons at the level of the spinal dorsal horn sensitization of supraspinal neurons, and decreased descending inhibition from supraspinal structures play a major role in the pathophysiology of chronic tension-type headache.) 7 Migraine Migraine headaches are classified as migraine with or without aura. headaches Migraine auras are the sensory symptoms (neurologic, gastrointestinal, and autonomic) that can occur before or during a migraine episode. Aura manifests as a series of neurologic symptoms: shimmering or flashing areas, blind spots, visual and auditory hallucinations, muscle weakness that is usually one sided, and difficulty speaking (rarely). These symptoms may last up to 30 minutes, and the throbbing headache pain that follows may last from several hours to 2 days. Migraines without aura begin immediately with throbbing headache pain. 8 9  Migraine headaches – cont. Migraine headaches probably arise from a complex interaction of neuronal and vascular factors. Stress, fatigue, irregular sleep patterns, fasting or a missed meal, vasoactive substances in food, caffeine, alcohol, changes in female hormones, changes in barometric pressure and altitude, lights, odor, neck pain, exercise, and sexual activity may trigger migraine. Medications (e.g., reserpine, nitrates, oral contraceptives, and postmenopausal hormones) can also trigger migraine. Premonitary (prodrome) symptoms in migraine can be: Neuropsychiatric (e.g., anxiety, irritability,yawning, unhappiness, and insomnia), Sensory (e.g., phonophobia, photophobia, focusing difficulties, and speech difficulties), digestive (e.g., food craving, nausea, vomiting, diarrhea, and constipation), general (e.g., asthenia,tiredness, fluid retention, and urinary frequency). 10 Sinus headache Sinus headache occurs when infection or blockage of the paranasal sinuses causes inflammation or distension of the sensitive sinus walls. Sinus headache is usually localized to facial areas over the sinuses and is difficult to differentiate from migraine without aura. The pain quality of a sinus headache is typically a dull and pressure like sensation. Stooping or blowing the nose often intensifies the pain of sinus headache, but the headache is not accompanied by nausea, vomiting, or visual disturbances. Persistent sinus pain and/or discharge suggests possible infection and requires referral for medical evaluation. 11  Medication overuse headache Medication overuse headache results from a rebound effect after the withdrawal of an analgesic. This type of headache differs from a headache related to a medication side effect. Some patients who suffer from migraine or tension headaches receive some relief from nonprescription medication, and over time may increase their use of the nonprescription treatment, which can lead to medication overuse headaches. These headaches are usually associated with frequent use (more than twice weekly) for 3 months or longer and occur within hours of stopping the agent; re administration of the agent provides relief. Agents associated with medication over use headaches are acetaminophen, some nonsteroidal anti-inflammatory drugs (NSAIDs), aspirin, caffeine, triptans, opioids, butalbital, and ergotamine formulations. 12 Characteristics of Tension Type, Migraine, and Sinus Headaches Tension Type Migraine Sinus Headaches Bilateral Location Face, forehead, or periorbital Over the top of the head, Usually unilateral area extending to base of skull Pressure behind eyes or face; Nature Varies from diffuse ache to tight, Throbbing; may be dull, bilateral pain; worse in pressing, constricting pain preceded by an aura the morning Simultaneous with sinus Onset Gradual Sudden symptoms, including purulent nasal discharge Days (resolves with sinus Duration Minutes to days Hours to 2 days symptoms) Non-headache symptoms Scalp tenderness Nausea Nasal congestion 13 Treatment of Headache The goals of treating headache are (1) to alleviate acute pain, (2) to restore normal functioning, (3) to prevent relapse, (4) to minimize side effects. For chronic headache, an additional goal is to reduce the frequency of headaches. General Treatment Approach Most patients with episodic headaches respond adequately to self-treatment with nonpharmacologic interventions, nonprescription medications, or both. 14  Episodic tension type headaches often respond well to Treatment of nonprescription analgesics, including acetaminophen, Headache – cont NSAIDs, and salicylates, especially when taken at onset of the headache. If nonprescription analgesics are used to treat chronic headache, frequency of use should be limited to less than 3 days per week to prevent medication overuse headache. 15  Treatment of Headache – cont A medical diagnosis of migraine headache is required before self treatment can be recommended. Taking an NSAID or salicylate at the onset of symptoms can abort mild or moderate migraine headache. Once a migraine has evolved, analgesics are less effective. Patients with migraines who can predict the occurrence of the headache (e.g., during menstruation) should take an analgesic (usually an NSAID) before occurrence of the event known to trigger the headache, as well as throughout the duration of the event. For patients with coexisting tension and migraine headaches, treatment of the initiating headache type can abort the mixed headache. Sinus headaches respond well to decongestants (e.g., pseudoephedrine or phenylephrine), which are useful for sinus drainage. Concomitant use of decongestants and nonprescription analgesics can relieve sinus headache pain. 16 Nonpharmacologic Therapy Chronic tension type headaches may respond to relaxation exercises and physical therapy that emphasizes stretching and strengthening of head and neck muscles. 17 Nonpharmacologic Therapy General treatment measures for migraine include maintaining regular sleeping, eating, and exercise schedules, stress management, biofeedback, and cognitive therapy. Applying ice or cold packs combined with pressure to the forehead or temple areas to reduce pain associated with acute migraine attacks. 18  Nutritional strategies Nutritional strategies are intended to prevent migraine and are based on: (1) dietary restriction of foods that contain triggers, (2) avoidance of hunger and low blood glucose (a trigger of migraine), (3) magnesium supplementation. Advocates of nutritional therapy recommend avoiding known food allergies and foods with vasoactive substances, such as nitrites; Tyramine (found in red wine and aged cheese); Phenylalanine (found in the artificial sweetener aspartame); Monosodium glutamate (often found in asian food); Caffeine; 19 Theobromines (found in chocolate). Pharmacologic Therapy - Acetaminophen Acetaminophen is an effective analgesic and antipyretic. Acetaminophen produces analgesia through central inhibition of prostaglandin synthesis. Acetaminophen is rapidly absorbed from the gastrointestinal (GI) tract and extensively metabolized in the liver to inactive glucuronic and sulfuric acid conjugates. Duration of activity is about 4 hours and is increased to 6-8 hours with an extended release formulation. 20  Acetaminophen – cont It is effective in relieving mild-moderate pain of non- visceral origin (i.e., pain that is not organ related). Recent changes implemented to decrease pediatric dosing errors with liquid acetaminophen formulations include having only one concentration (160 mL/5 mL) available for all children younger than 12 years. Acetaminophen is potentially hepatotoxic in doses exceeding 4 g/day, especially with chronic use. Patients with glucose-6-phosphate dehydrogenase deficiency, a hereditary disease that causes premature breakdown of red blood cells, should use caution when taking acetaminophen. 21 Nonsteroidal Anti-Inflammatory Drugs NSAIDs relieve pain through central and peripheral inhibition of cyclooxygenase (COX) and subsequent inhibition of prostaglandin synthesis. All nonprescription NSAIDs are rapidly absorbed from the GI tract with consistently high bioavailability. They are extensively metabolized, mainly by glucuronidation, to inactive compounds in the liver. Elimination occurs primarily through the kidneys. Onset of activity for naproxen sodium and standard ibuprofen is about 30 minutes. Duration of activity for naproxen sodium is up to 12 hours and 6-8 hours for ibuprofen. NSAIDs have analgesic, antipyretic, and anti-inflammatory activity, and they are useful in managing mild moderate pain of non-visceral origin. 22  NSAIDs – cont The most frequent adverse effects of NSAIDs involve the GI tract and include dyspepsia, heartburn, nausea, anorexia, and epigastric pain, even among children using pediatric formulations. NSAIDs may be taken with food, milk, or antacids if upset stomach occurs. Tablets should be taken with a full glass of water, suspensions should be shaken thoroughly, and enteric coated or sustained release preparations should be neither crushed nor chewed. This product contains an NSAID, which may cause severe stomach bleeding. The chance is higher if you: Are age 60 or older. Have had stomach ulcers or bleeding problems. Take a blood thinning (anticoagulant) or steroid drug. Take other drugs containing prescription or nonprescription NSAIDs (aspirin, ibuprofen, naproxen, or others). Have 3 or more alcoholic drinks every day while using this product. Take more or for a longer time than directed. 23 NSAIDs –cont NSAIDs are associated with increased risk for myocardial infarction, heart failure, hypertension, and stroke. The cardiovascular risk of nonselective NSAIDs is depend on dose and duration. However, ibuprofen has been associated with a significant increase in cardiovascular risk, whereas naproxen has not; thus, naproxen is considered the preferred, safer option. 24 Salicylates Salicylates inhibit prostaglandin synthesis from arachidonic acid by inhibiting both isoforms of the COX enzyme (COX1 and COX2). The resulting decrease in prostaglandins reduces the sensitivity of pain receptors to the initiation of pain impulses at sites of inflammation and trauma. Salicylates are absorbed by passive diffusion of the non-ionized drug in the stomach and small intestine. Factors affecting absorption include dosage form, gastric pH, gastric emptying time, dissolution rate, and the presence of antacids or food. 25 Salicylates – cont Protein binding is concentration dependent. At concentrations lower than 100 mg/mL, approximately 90% of salicylic acid is bound to albumin, whereas at concentrations greater than 400 mg/mL, approximately 75% is bound. Salicylic acid is largely eliminated through the kidney. Urine pH determines the amount of unchanged drug that is eliminated, with urinary concentrations increasing substantially in more alkaline urine (pH ~8). Salicylates also are effective in treating mild moderate pain from musculoskeletal conditions and fever. Because of its inhibitory effects on platelet function, aspirin is also indicated for prevention of thromboembolic events (e.g., myocardial infarction and stroke) in high risk patients. 26 Salicylates – cont The maximum analgesic dosage for self medication with aspirin is 4 g/day; therefore, anti-inflammatory activity often will not occur unless the drug is used at the high end of the acceptable dosage range. Symptoms of salicylates over dose include headache, dizziness, tinnitus, difficulty hearing, dimness of vision, mental confusion, lassitude, drowsiness, sweating, thirst, hyperventilation, nausea, vomiting, and occasional diarrhea. Conditions that predispose patients to salicylate toxicity include (1) marked renal or hepatic impairment (e.g., uremia, cirrhosis, or hepatitis); (2) metabolic disorders (e.g., hypoxia or hypothyroidism); (3) unstable disease (e.g., cardiac arrhythmias, intractable epilepsy, or poorly controlled diabetes); (4) status asthmaticus; 27  Salicylates – cont Risk factors of taking salicylates include (1) history of uncomplicated or bleeding peptic ulcer; (2) age older than 60 years; (3) concomitant use of aspirin or other NSAIDs, anticoagulants, antiplatelet agents, bisphosphonates, selective serotonin reuptake inhibitors, or systemic corticosteroids; (4) infection with Helicobacter pylori; (5) rheumatoid arthritis; (6) NSAID related dyspepsia; (7) concomitant use of alcohol. Ten percent of people diagnosed with asthma have aspirin sensitivity Aspirin should be discontinued 2-7 days before surgery and should not be used to relieve pain after tonsillectomy, dental extraction, or other surgical procedures, except under the close supervision of a health care provider. 28 Salicylates – cont Reye’s syndrome is an acute illness occurring almost exclusively in children 15 years of age or younger. The cause is unknown, but viral and toxic agents, especially salicylates, have been associated with the syndrome. Onset usually follows a viral infection with influenza (type A or B) or varicella zoster (chickenpox). 29 Clinically Important Drug-Drug Interactions with Nonprescription Analgesic Agents Drug Management/Preventive Analgesic/Antipyretic Interaction Potential Measures Acetaminophen Increased risk of hepatotoxicity Avoid concurrent use if possible; minimize Alcohol alcohol intake when using acetaminophen. Limit acetaminophen to occasional use; Increased risk of bleeding Acetaminophen monitor INR for several weeks when Warfarin (elevations in INR) acetaminophen 2-4 grams daily is added or discontinued in patients on warfarin. Displacement from Protein binding Aspirin Valproic Avoid concurrent use; use naproxen instead of sites and inhibition of valproic acid acid aspirin (no interaction). metabolism Including COX2 inhibitors Aspirin, Avoid concurrent use if possible; consider use NSAIDs Increased risk of gastroduodenal of gastroprotective agents (e.g., PPIs). ulcers and bleeding 30 Clinically Important Drug-Drug Interactions with Nonprescription Analgesic Agents Management/Preventive Analgesic/Antipyretic Drug Potential Interaction Measures Aspirin should be taken at least 30 Ibuprofen Decreased antiplatelet effect of minutes before or 8 hours after Aspirin aspirin ibuprofen. Use acetaminophen (or other analgesic) instead of ibuprofen. Displacement from protein Monitor free phenytoin levels; adjust Ibuprofen Phenytoin binding sites dose as indicated. Increased risk of GI or esophageal NSAIDs (several) Bisphosphonates Use caution with concomitant use. ulceration NSAIDs (several) Renal clearance of digoxin Monitor digoxin levels; adjust dose as Digoxin inhibited indicated. Antihypertensive Antihypertensive effect inhibited; Salicylates and agents, betablockers, possible hyperkalemia with Monitor blood pressure, cardiac NSAIDs (several) ACE inhibitors, potassium sparing diuretics and function, and potassium levels vasodilators, diuretics ACE inhibitors 31  Clinically Important Drug-Drug Interactions with Nonprescription Analgesic Agents Management/Preventive Analgesic/Antipyretic Drug Potential Interaction Measures Salicylates and Avoid concurrent use, if possible; risk is lowest Increased risk of bleeding, NSAIDs Anticoagulants with salsalate and choline magnesium especially GI trisalicylate. Salicylates and Increased risk of GI Avoid concurrent use, if possible; minimize NSAIDs Alcohol bleeding alcohol intake when using salicylates and NSAIDs. Salicylates and Decreased methotrexate Avoid salicylates and NSAIDs with highdose NSAIDs (several) Methotrexate clearance methotrexate therapy; monitor levels with concurrent treatment. Salicylates Avoid concurrent use, if possible; monitor (moderate-high Increased risk of Sulfonylureas blood glucose levels when changing salicylate doses) hypoglycemia dose. 32 Combination Products Many nonprescription analgesics are available in combination products. Caffeine is used as an adjunct to analgesics for tension type and migraine headaches. It also may have its own analgesic properties and is known to cause withdrawal headache when taken regularly. Combination dosage forms containing a decongestant and either acetaminophen or an NSAID are also available. These combinations appear logical for use in sinus headaches or other indications for which both analgesia and decongestion are needed. 33 Patient Factors For pediatric it was recommended: (1) a single concentration for solid dose, single ingredient acetaminophen products for children, (2) the addition of weight-based dosing for children ages 2-12, (3) the addition of new label directions for children ages 6 months to 2 years that would include the indication for fever reduction. Patients with significant alcohol ingestion (three or more drinks per day) should avoid selftreatment with nonprescription analgesics. 34  Patient Factors – cont Patients who are intolerant to aspirin also may cross-react with other chemicals or drugs. Up to 15% of patients who are intolerant to aspirin may cross-react when exposed to tartrazine which can be found in many drugs and foods. Among those with the respiratory type of aspirin sensitivity, the rate of cross reaction between aspirin and acetaminophen, ibuprofen, and naproxen in documented aspirin intolerant patients is 7%, 98%, and 100%, respectively. Patients with a history of aspirin intolerance should be advised to avoid all aspirin and NSAID containing products. 35