My own slim attempt at covering the extremely complex and ever evolving field of migraine pathophysiology. Not intended by any means to be exhaustive but more like a unique take and beginner's guide.
Calcium channel blocking drugs (CCBs) bind to different calcium channel sites and have varying effects on cardiac and vascular tissue. Nifedipine is the most selective vasodilator while verapamil and diltiazem are more equipotent between cardiac tissue and vasculature. CCBs reduce afterload through peripheral vasodilation but have little effect on preload or contractility. Nifedipine is most likely to cause hypotension and reflex tachycardia due to its strong vasodilatory effects, while verapamil may worsen heart failure or cause heart block.
Pharmacotherapy, Management of Hypertension, JNC 8 guidelinesankitamishra1402
This document discusses the pharmacotherapy of hypertension. It begins by defining hypertension and discussing its physiological regulation. It then covers the principles of antihypertensive therapy, classifying drugs by their primary mechanisms of action. The main drug classes discussed are diuretics, sympatholytics, calcium channel blockers, ACE inhibitors, angiotensin receptor blockers, direct renin inhibitors, and vasodilators. For each class, it describes the pharmacological effects, therapeutic uses, dosing, and adverse drug reactions. It concludes by discussing lifestyle modifications and strategies for dosing antihypertensive drugs according to JNC8 guidelines.
This document discusses neuropathic pain, including its classification, signs and symptoms, diagnosis, and management. Some key points:
- Neuropathic pain arises from lesions or diseases affecting the somatosensory system and is often chronic in nature. Common causes include low back pain, diabetes, herpes zoster infections, and postsurgical pain.
- Both nociceptive and neuropathic pain components may co-exist in conditions like low back pain. Neuropathic pain is often described as burning, electric shock-like, or tingling and may occur in areas distant from the site of injury.
- Diagnosis involves listening to the patient's descriptions of their pain, locating areas of abnormal sensation, and looking for signs
This document discusses psychosis, antipsychotics, and the brain. It begins with definitions of psychosis and descriptions of biological markers and FDA-approved antipsychotics of the past decade. It then discusses computational models of psychosis and the relationship between psychosis, antipsychotics, and brain tissue loss. The document also discusses patient-specific cultured neurons and summarizes key points about conventional versus atypical antipsychotics. The rest of the document details various antipsychotics approved in the past decade, events shaping antipsychotic development, advances in neuroimaging and connectomics in schizophrenia research. It discusses causes and substances related to psychosis and default mode networks in the brain. The document concludes by discussing brain changes associated with antip
My own slim attempt at covering the extremely complex and ever evolving field of migraine pathophysiology. Not intended by any means to be exhaustive but more like a unique take and beginner's guide.
Calcium channel blocking drugs (CCBs) bind to different calcium channel sites and have varying effects on cardiac and vascular tissue. Nifedipine is the most selective vasodilator while verapamil and diltiazem are more equipotent between cardiac tissue and vasculature. CCBs reduce afterload through peripheral vasodilation but have little effect on preload or contractility. Nifedipine is most likely to cause hypotension and reflex tachycardia due to its strong vasodilatory effects, while verapamil may worsen heart failure or cause heart block.
Pharmacotherapy, Management of Hypertension, JNC 8 guidelinesankitamishra1402
This document discusses the pharmacotherapy of hypertension. It begins by defining hypertension and discussing its physiological regulation. It then covers the principles of antihypertensive therapy, classifying drugs by their primary mechanisms of action. The main drug classes discussed are diuretics, sympatholytics, calcium channel blockers, ACE inhibitors, angiotensin receptor blockers, direct renin inhibitors, and vasodilators. For each class, it describes the pharmacological effects, therapeutic uses, dosing, and adverse drug reactions. It concludes by discussing lifestyle modifications and strategies for dosing antihypertensive drugs according to JNC8 guidelines.
This document discusses neuropathic pain, including its classification, signs and symptoms, diagnosis, and management. Some key points:
- Neuropathic pain arises from lesions or diseases affecting the somatosensory system and is often chronic in nature. Common causes include low back pain, diabetes, herpes zoster infections, and postsurgical pain.
- Both nociceptive and neuropathic pain components may co-exist in conditions like low back pain. Neuropathic pain is often described as burning, electric shock-like, or tingling and may occur in areas distant from the site of injury.
- Diagnosis involves listening to the patient's descriptions of their pain, locating areas of abnormal sensation, and looking for signs
This document discusses psychosis, antipsychotics, and the brain. It begins with definitions of psychosis and descriptions of biological markers and FDA-approved antipsychotics of the past decade. It then discusses computational models of psychosis and the relationship between psychosis, antipsychotics, and brain tissue loss. The document also discusses patient-specific cultured neurons and summarizes key points about conventional versus atypical antipsychotics. The rest of the document details various antipsychotics approved in the past decade, events shaping antipsychotic development, advances in neuroimaging and connectomics in schizophrenia research. It discusses causes and substances related to psychosis and default mode networks in the brain. The document concludes by discussing brain changes associated with antip
This document discusses the use of antidepressants in treating neuropathic pain disorders. It notes that tricyclic antidepressants like amitriptyline, desipramine, and nortriptyline as well as SNRIs like duloxetine and venlafaxine can be effective for peripheral diabetic neuropathy and postherpetic neuralgia by inhibiting the reuptake of norepinephrine and serotonin. Duloxetine is specifically approved for peripheral diabetic neuropathy. While not FDA-approved for pain, TCAs and SNRIs provide analgesic effects independent of their antidepressant effects through improvements in insomnia, anxiety, and depression. Bupropion may also help neuropathic pain. The document recommends TCAs, SNRIs
Proton pump inhibitors (PPIs) like omeprazole irreversibly inhibit the gastric H+/K+-ATPase enzyme to reduce acid secretion. They are effective for treating acid-related disorders like GERD and peptic ulcers. PPIs have high bioavailability but require acidic conditions for activation. Common side effects include diarrhea and headache, while long term use may increase risks of infections, fractures, and nutrient deficiencies. Drug interactions are rare due to short half-lives, but some PPIs inhibit CYP2C19 and decrease clopidogrel effectiveness.
This document discusses beta blockers (ß blockers), which competitively inhibit ß1 and ß2 adrenergic receptors. It covers the mechanism of action, classification, pharmacological properties, individual drugs, therapeutic uses, adverse effects, contraindications, and more. Beta blockers are classified based on generation and properties like selectivity, intrinsic sympathomimetic activity, and membrane stabilization. They are used for cardiovascular conditions like hypertension, angina, heart failure as well as non-cardiovascular uses including migraine prophylaxis, anxiety, glaucoma, and others. Adverse effects are related to ß1 and ß2 blockade.
This document provides information about psychotic disorders and their treatment. It discusses:
- Types of psychotic disorders like schizophrenia, brief psychotic disorder, and others.
- Causes of psychosis including genetic, environmental, and psychosocial factors.
- Signs and symptoms of psychosis such as delusions, hallucinations, and behavioral changes.
- Types of antipsychotic medications including first-generation ("typical") and second-generation ("atypical") drugs. It provides examples of drugs from each class and their mechanisms of action and side effects.
Antiepileptic drugs work to treat epilepsy by modifying ion conductance to increase inhibitory GABAergic transmission and decrease excitatory glutamatergic activity. Common antiepileptic drugs include phenobarbital, phenytoin, carbamazepine, oxcarbazepine, valproic acid, diazepam, lamotrigine, gabapentin, topiramate, and newer drugs. Most antiepileptics have the potential for drug interactions due to enzyme inducing effects and require monitoring of drug levels and side effects.
This document provides an overview of the pharmacology of antidepressants. It discusses the history of antidepressant development beginning in the 1950s. It then classifies antidepressants and describes the mechanisms of action, pharmacokinetics, pharmacological actions, adverse effects and recent advances for various classes including tricyclic antidepressants, SSRIs, SNRIs, atypical antidepressants. It provides details on specific drugs within each class.
Current concept for management of neuropathic painNeurologyKota
The document discusses pain classification and mechanisms. It defines pain and different types including nociceptive, neuropathic, and chronic pain. It describes peripheral and central sensitization mechanisms. It discusses evaluation and management of neuropathic pain including first-line options like gabapentin, pregabalin, amitriptyline and second-line options like duloxetine, tramadol, opioids. Adverse effects and considerations with long term use are also summarized.
Second generation atypical anti-psychotic used for mental disorders more extensively for bipolar disorder. have very low side effects than other SGA Medications
Methadone is an opioid analgesic that is used to treat severe pain and prevent withdrawal symptoms in opioid addicts. It works by binding to the same receptors in the brain as opioids like heroin and preventing cravings. While methadone is itself addictive, it blocks the euphoric effects of other opioids when taken as prescribed, allowing addicts to break the cycle of addiction and seek further treatment without withdrawal symptoms. There is an ongoing debate around replacing one addiction for another with methadone maintenance treatment, but proponents argue it provides a medically-supervised and safer alternative while the person seeks additional help for their underlying addiction.
This document summarizes pharmacological treatments for obesity. Candidates for treatment have a BMI over 30 or over 27 with comorbidities. Approved drugs include anorexiants like phentermine and diethylpropion which increase norepinephrine; the lipase inhibitor orlistat which decreases fat absorption; and the serotonin agonist lorcaserin. Combination therapy with phentermine and topiramate is also approved. All treatments carry risk of side effects and should only be used with lifestyle modifications and medical supervision.
This document discusses bisoprolol, a beta-1 selective adrenoceptor blocking agent used to treat hypertension and angina. It provides details on bisoprolol's history, pharmacological properties, therapeutic indications, contraindications, adverse reactions, and toxicological studies. Bisoprolol is a highly selective beta-1 blocker that is well-absorbed orally and has a half-life of 10-12 hours. It is used to treat hypertension, angina, and heart failure by reducing heart rate and contractility. Adverse effects include fatigue, dizziness, and bronchospasm. Toxicology studies found it to be non-cytotoxic, non-mutagenic, and
This document summarizes different types of anxiety disorders and their pharmacological treatments. It discusses generalized anxiety disorder, obsessive-compulsive disorder, panic disorder, phobic disorders, and stress disorders. For each disorder, it provides details on symptoms and recommended drug classes for treatment, including benzodiazepines, azapirone drugs like buspirone, selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants, and monoamine oxidase inhibitors. It also discusses future prospects for new anxiolytic drugs that target cholecystokinin, alpiderm, corticotropin-releasing factor, and neuroactive steroids.
Diabetes mellitus (DM) is a metabolic disease characterized by hyperglycemia. DM prevalence in Saudi Arabia is high at 23.7%. DM is diagnosed based on classic symptoms and elevated blood glucose levels. Prediabetes conditions like impaired fasting glucose and impaired glucose tolerance are risk factors for future diabetes and cardiovascular disease. Glycemic goals aim for an A1C below 7% and treatment involves medical nutrition therapy, oral medications, insulin, and preventing complications. Management of DM focuses on controlling blood glucose, blood pressure, lipids, and screening for and treating common complications.
BASIC PHARMACOLOGY REVISION NOTES BASED ON HIGH YEILD TOPIC AND LECTURE NOTES
ANTIPARKINSONIAN DRUGS
LEVODOPA DRUGS
PERIPHERAL DECARBOXYLASE INHIBITOR
COMT INHIBITOR
ENTACAPONE
TOLCAPONE
MAO B INHIBITORS
This document discusses various cognition enhancers or cerebroactive drugs, grouping them into cholinergic activators, glutamate antagonists, and miscellaneous drugs. Cholinergic activators like donepezil and rivastigmine are anti-cholinesterases that improve cognitive symptoms in Alzheimer's disease but with mild side effects. Memantine is a NMDA receptor antagonist that has been shown to slow functional decline in moderate to severe Alzheimer's. Other drugs mentioned include piracetam, pyritinol, dihydroergotoxine, citicoline, piribedil, and Ginkgo biloba extracts, which are claimed to improve cerebral blood flow, metabolism, or memory but also have potential
This document summarizes the pharmacokinetics of various classes of antidepressants. It discusses their absorption, metabolism, protein binding, and elimination profiles. The main classes covered are SSRIs, SNRIs, TCAs, 5-HT2 antagonists, tetracyclic/unicyclic agents, and MAOIs. Key points include that most are well absorbed orally, undergo hepatic metabolism primarily through the CYP system, and have half-lives ranging from a few hours to over 24 hours, necessitating different dosing schedules.
This document summarizes information about the anti-seizure medications gabapentin and pregabalin. It discusses gabapentin's mechanism of action, approved uses, dosing, pharmacokinetics, interactions, adverse effects and overdose treatment. It then summarizes a clinical study comparing the dose-response relationship of pregabalin and gabapentin in patients with partial seizures, finding that pregabalin was more potent and effective at reducing seizure frequency.
Migraine and Tension Headache Diagnosis and Treatment GuidelineUtai Sukviwatsirikul
This document provides guidelines for diagnosing and treating migraines and tension headaches. It begins with criteria for differentiating migraine, tension, and cluster headaches based on location, intensity, duration, and associated symptoms. Potential alternative diagnoses are outlined if warning signs are present. Treatment guidelines recommend lifestyle modifications and avoiding medication overuse. Acute migraine treatment options include over-the-counter or prescription analgesics, triptans, dihydroergotamine, or ketorolac. Preventive medication options and follow-up monitoring are also discussed.
A talk covering epidemiology, diagnosis and management of primary headache disorders, common cases of secondary headache disorders and when to order brain imaging, lumbar puncture in headaches.
This document discusses the use of antidepressants in treating neuropathic pain disorders. It notes that tricyclic antidepressants like amitriptyline, desipramine, and nortriptyline as well as SNRIs like duloxetine and venlafaxine can be effective for peripheral diabetic neuropathy and postherpetic neuralgia by inhibiting the reuptake of norepinephrine and serotonin. Duloxetine is specifically approved for peripheral diabetic neuropathy. While not FDA-approved for pain, TCAs and SNRIs provide analgesic effects independent of their antidepressant effects through improvements in insomnia, anxiety, and depression. Bupropion may also help neuropathic pain. The document recommends TCAs, SNRIs
Proton pump inhibitors (PPIs) like omeprazole irreversibly inhibit the gastric H+/K+-ATPase enzyme to reduce acid secretion. They are effective for treating acid-related disorders like GERD and peptic ulcers. PPIs have high bioavailability but require acidic conditions for activation. Common side effects include diarrhea and headache, while long term use may increase risks of infections, fractures, and nutrient deficiencies. Drug interactions are rare due to short half-lives, but some PPIs inhibit CYP2C19 and decrease clopidogrel effectiveness.
This document discusses beta blockers (ß blockers), which competitively inhibit ß1 and ß2 adrenergic receptors. It covers the mechanism of action, classification, pharmacological properties, individual drugs, therapeutic uses, adverse effects, contraindications, and more. Beta blockers are classified based on generation and properties like selectivity, intrinsic sympathomimetic activity, and membrane stabilization. They are used for cardiovascular conditions like hypertension, angina, heart failure as well as non-cardiovascular uses including migraine prophylaxis, anxiety, glaucoma, and others. Adverse effects are related to ß1 and ß2 blockade.
This document provides information about psychotic disorders and their treatment. It discusses:
- Types of psychotic disorders like schizophrenia, brief psychotic disorder, and others.
- Causes of psychosis including genetic, environmental, and psychosocial factors.
- Signs and symptoms of psychosis such as delusions, hallucinations, and behavioral changes.
- Types of antipsychotic medications including first-generation ("typical") and second-generation ("atypical") drugs. It provides examples of drugs from each class and their mechanisms of action and side effects.
Antiepileptic drugs work to treat epilepsy by modifying ion conductance to increase inhibitory GABAergic transmission and decrease excitatory glutamatergic activity. Common antiepileptic drugs include phenobarbital, phenytoin, carbamazepine, oxcarbazepine, valproic acid, diazepam, lamotrigine, gabapentin, topiramate, and newer drugs. Most antiepileptics have the potential for drug interactions due to enzyme inducing effects and require monitoring of drug levels and side effects.
This document provides an overview of the pharmacology of antidepressants. It discusses the history of antidepressant development beginning in the 1950s. It then classifies antidepressants and describes the mechanisms of action, pharmacokinetics, pharmacological actions, adverse effects and recent advances for various classes including tricyclic antidepressants, SSRIs, SNRIs, atypical antidepressants. It provides details on specific drugs within each class.
Current concept for management of neuropathic painNeurologyKota
The document discusses pain classification and mechanisms. It defines pain and different types including nociceptive, neuropathic, and chronic pain. It describes peripheral and central sensitization mechanisms. It discusses evaluation and management of neuropathic pain including first-line options like gabapentin, pregabalin, amitriptyline and second-line options like duloxetine, tramadol, opioids. Adverse effects and considerations with long term use are also summarized.
Second generation atypical anti-psychotic used for mental disorders more extensively for bipolar disorder. have very low side effects than other SGA Medications
Methadone is an opioid analgesic that is used to treat severe pain and prevent withdrawal symptoms in opioid addicts. It works by binding to the same receptors in the brain as opioids like heroin and preventing cravings. While methadone is itself addictive, it blocks the euphoric effects of other opioids when taken as prescribed, allowing addicts to break the cycle of addiction and seek further treatment without withdrawal symptoms. There is an ongoing debate around replacing one addiction for another with methadone maintenance treatment, but proponents argue it provides a medically-supervised and safer alternative while the person seeks additional help for their underlying addiction.
This document summarizes pharmacological treatments for obesity. Candidates for treatment have a BMI over 30 or over 27 with comorbidities. Approved drugs include anorexiants like phentermine and diethylpropion which increase norepinephrine; the lipase inhibitor orlistat which decreases fat absorption; and the serotonin agonist lorcaserin. Combination therapy with phentermine and topiramate is also approved. All treatments carry risk of side effects and should only be used with lifestyle modifications and medical supervision.
This document discusses bisoprolol, a beta-1 selective adrenoceptor blocking agent used to treat hypertension and angina. It provides details on bisoprolol's history, pharmacological properties, therapeutic indications, contraindications, adverse reactions, and toxicological studies. Bisoprolol is a highly selective beta-1 blocker that is well-absorbed orally and has a half-life of 10-12 hours. It is used to treat hypertension, angina, and heart failure by reducing heart rate and contractility. Adverse effects include fatigue, dizziness, and bronchospasm. Toxicology studies found it to be non-cytotoxic, non-mutagenic, and
This document summarizes different types of anxiety disorders and their pharmacological treatments. It discusses generalized anxiety disorder, obsessive-compulsive disorder, panic disorder, phobic disorders, and stress disorders. For each disorder, it provides details on symptoms and recommended drug classes for treatment, including benzodiazepines, azapirone drugs like buspirone, selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants, and monoamine oxidase inhibitors. It also discusses future prospects for new anxiolytic drugs that target cholecystokinin, alpiderm, corticotropin-releasing factor, and neuroactive steroids.
Diabetes mellitus (DM) is a metabolic disease characterized by hyperglycemia. DM prevalence in Saudi Arabia is high at 23.7%. DM is diagnosed based on classic symptoms and elevated blood glucose levels. Prediabetes conditions like impaired fasting glucose and impaired glucose tolerance are risk factors for future diabetes and cardiovascular disease. Glycemic goals aim for an A1C below 7% and treatment involves medical nutrition therapy, oral medications, insulin, and preventing complications. Management of DM focuses on controlling blood glucose, blood pressure, lipids, and screening for and treating common complications.
BASIC PHARMACOLOGY REVISION NOTES BASED ON HIGH YEILD TOPIC AND LECTURE NOTES
ANTIPARKINSONIAN DRUGS
LEVODOPA DRUGS
PERIPHERAL DECARBOXYLASE INHIBITOR
COMT INHIBITOR
ENTACAPONE
TOLCAPONE
MAO B INHIBITORS
This document discusses various cognition enhancers or cerebroactive drugs, grouping them into cholinergic activators, glutamate antagonists, and miscellaneous drugs. Cholinergic activators like donepezil and rivastigmine are anti-cholinesterases that improve cognitive symptoms in Alzheimer's disease but with mild side effects. Memantine is a NMDA receptor antagonist that has been shown to slow functional decline in moderate to severe Alzheimer's. Other drugs mentioned include piracetam, pyritinol, dihydroergotoxine, citicoline, piribedil, and Ginkgo biloba extracts, which are claimed to improve cerebral blood flow, metabolism, or memory but also have potential
This document summarizes the pharmacokinetics of various classes of antidepressants. It discusses their absorption, metabolism, protein binding, and elimination profiles. The main classes covered are SSRIs, SNRIs, TCAs, 5-HT2 antagonists, tetracyclic/unicyclic agents, and MAOIs. Key points include that most are well absorbed orally, undergo hepatic metabolism primarily through the CYP system, and have half-lives ranging from a few hours to over 24 hours, necessitating different dosing schedules.
This document summarizes information about the anti-seizure medications gabapentin and pregabalin. It discusses gabapentin's mechanism of action, approved uses, dosing, pharmacokinetics, interactions, adverse effects and overdose treatment. It then summarizes a clinical study comparing the dose-response relationship of pregabalin and gabapentin in patients with partial seizures, finding that pregabalin was more potent and effective at reducing seizure frequency.
Migraine and Tension Headache Diagnosis and Treatment GuidelineUtai Sukviwatsirikul
This document provides guidelines for diagnosing and treating migraines and tension headaches. It begins with criteria for differentiating migraine, tension, and cluster headaches based on location, intensity, duration, and associated symptoms. Potential alternative diagnoses are outlined if warning signs are present. Treatment guidelines recommend lifestyle modifications and avoiding medication overuse. Acute migraine treatment options include over-the-counter or prescription analgesics, triptans, dihydroergotamine, or ketorolac. Preventive medication options and follow-up monitoring are also discussed.
A talk covering epidemiology, diagnosis and management of primary headache disorders, common cases of secondary headache disorders and when to order brain imaging, lumbar puncture in headaches.
This document provides information on primary headache disorders, with a focus on migraine. It discusses the structures in the head that are sensitive to pain, and classifies headaches as either primary (having no underlying cause) or secondary (having an identifiable structural or metabolic cause). The primary headaches are further classified, with detailed descriptions and diagnostic criteria provided for migraine without aura, migraine with aura, and tension-type headache. Pathophysiology, epidemiology, triggers, management approaches including acute and preventive therapies are summarized for migraine. Botulinum toxin, triptans, ergot alkaloids, and other medication options are outlined for migraine treatment.
This document summarizes several primary headache syndromes:
Tension type headache is the most common and involves gradual onset of bilateral dull pain that increases throughout the day. Migraine is the second most common and involves severe unilateral throbbing pain along with nausea, vomiting, and sensitivity to light and sound. Trigeminal neuralgia causes brief, severe facial pain triggered by activities like eating or shaving. Cluster headache is characterized by severe unilateral pain around the eye accompanied by redness, tearing and nasal congestion. These primary headache syndromes are differentiated based on their symptoms and pathophysiology.
Classification and pathophysiology of headacheAbino David
The document discusses the International Classification of Headache Disorders (ICHD) and provides information on primary and secondary headaches. It outlines the main types of primary headaches like tension-type headache, migraine, and cluster headache. It also discusses some specific secondary headache types and their potential underlying causes like intracranial bleeding or infection. Key anatomical structures involved in headache pain are identified as the large intracranial vessels, dura mater, trigeminal nerve, and pain modulatory brain systems.
This PowerPoint presentation discusses various types of headaches, their causes, symptoms, and treatments. It covers common headaches like tension headaches as well as more complex migraine types such as classic migraine, common migraine, basilar migraine, and cluster headaches. For migraines, it describes genetic and vascular theories of causation as well as the roles of serotonin and nitric oxide. Treatment approaches covered include acute medications for migraine attacks as well as various prophylactic drugs.
Headache is a common reason patients seek medical attention and can be primary or secondary. Primary headaches include tension-type headaches, which cause bilateral tight band-like pain, and migraines, which often cause severe one-sided throbbing pain accompanied by sensitivity to light, sound, and nausea. Migraines are thought to involve neurovascular and serotonergic mechanisms. Cluster headaches are rare but cause excruciating unilateral orbital or temporal pain and may be associated with autonomic symptoms. Treatment involves acute abortive medications as well as preventive medications depending on headache type and frequency. Secondary headaches require evaluation for underlying causes such as infection, trauma, or vascular abnormalities.
- Migraine is a recurrent headache disorder that is one of the most common complaints in medicine. It is classified into migraine with aura and without aura.
- The pathophysiology involves complex vascular and neural mechanisms including cortical spreading depression, trigeminal nerve activation, and release of vasoactive substances. Genetic and environmental factors can also play a role in migraine triggers and risk.
- Diagnosis is based on criteria involving recurrent attacks of moderate to severe pulsating headache, photophobia, phonophobia, and possibly nausea. Physical exam is typically normal but may reveal associated neurological symptoms.
This document provides an overview of different types of headaches including their classification, epidemiology, clinical presentation, diagnosis, pathophysiology and treatment. It discusses primary headaches such as migraines, tension headaches and cluster headaches. It also covers secondary headaches which are symptomatic of underlying conditions. Key points include migraines affecting 10-15% of the population, being more common in women, and the importance of differentiating between primary and secondary headaches to guide treatment.
1. Migraines can be classified as either primary or secondary headaches. Primary migraines include migraine without aura, migraine with aura, and tension-type headaches. Secondary migraines are caused by underlying structural or metabolic abnormalities.
2. Migraines can originate from extracranial or intracranial pain-sensitive structures. Common extracranial structures include the sinuses, eyes, ears, teeth, and blood vessels. Intracranial structures include arteries, dural veins and sinuses, and the meninges.
3. Migraines are treated either acutely to stop an attack or preventively to reduce frequency and severity. Acute treatments aim to rapidly relieve pain and associated
Dr Gina Kennedy provides an overview of headache diagnosis and management. Primary headaches include migraine, tension-type headache, and trigeminal autonomic cephalalgias. It is important to identify red flags and consider secondary causes. Treatment involves lifestyle modifications, acute medications, and preventive medications. Medication overuse headache is common and requires addressing overuse before initiating preventive treatment. Referral is indicated for atypical presentations or lack of response to treatment.
Headache for post basic neuroscience course 2015Ahmad Shahir
This document provides information on different types of headaches, including migraine, tension-type headache, cluster headache, and medication overuse headache. It discusses the classification, symptoms, diagnosis, and management of various headaches. For diagnosis, it emphasizes taking a thorough history and physical exam. It outlines red flags that warrant further investigation. Treatment involves acute and preventative medications. The focus is on a personalized approach and lifestyle modifications like keeping a headache diary.
This talk summarizes the definition, diagnosis and management strategies of migraine. It will be useful for general public as well as healthcare professionals.
This is more of a summary of recent evidence available on migraine management. It is easy to read and understand. Please post your queries and comments.
Migraine is a common neurological disorder characterized by severe headaches. Common triggers include diet, hormones, environment, and stress. Migraine attacks involve a headache phase with throbbing pain that worsens with activity along with symptoms like nausea and sensitivity to light/sound. Some people experience an aura phase before the headache with visual or sensory disturbances.
Treatment involves managing triggers, acute treatments like triptans to stop headaches, and preventive medications for those with frequent attacks. Preventive options include beta blockers, anti-seizure medications, and antidepressants, with the goal of reducing attack frequency and severity. Proper acute and preventive treatment along with lifestyle modifications can help manage migraine.
Pharmacological and non pharmacological treatment of primary headacheswael ezzat
This document discusses various treatment strategies and medications for acute and preventive migraine treatment. It describes three approaches to treating acute migraines - step care across attacks, step care within attacks, and stratified care. For preventive treatment, it outlines common medication classes used, including beta-blockers, antidepressants, anticonvulsants, calcium channel blockers, and botulinum toxin. It stresses the importance of lifestyle changes, behavioral therapy, and addressing comorbidities for chronic migraine treatment.
Quick Fire Top Neurology Tips discusses several topics in neurology:
1) TIA risk stratification now uses the ABCD2 score.
2) Guidelines recommend individual decisions on anticoagulation for atrial fibrillation patients with multiple falls and subdural hematomas based on risk versus benefit.
3) MS can generally be excluded with a normal MRI even with significant symptoms, though spinal MRI and evoked potentials may also be used in diagnostic workup for MS.
This document provides an overview of common types of headaches, including migraine, tension-type headache, cluster headache, and medication overuse headache. It discusses the signs, symptoms, diagnostic approach, and management strategies for each type. The diagnostic approach involves taking a thorough history, performing a physical examination, and ordering imaging tests only if indicated. Management involves both acute and preventative treatment depending on the headache type. The document emphasizes the importance of making an accurate diagnosis and reassuring patients that other pathology has been excluded.
This document discusses pain and its classification into nociceptive and neuropathic pain. It also discusses acute and chronic pain and different types of pain such as cancer and non-cancer pain. Pain is assessed using a pain scale and choice of drug depends on patient's self-reported pain severity. Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used for mild pain and can be combined with opioids. Acetaminophen is also discussed along with its dosing, mechanisms of action, and toxicity. Side effects and risks of various NSAIDs like ibuprofen, indomethacin, and naproxen are summarized.
This document provides an overview of headache diagnosis and management. It discusses that headache is a common reason for seeking medical care, with over 50% of adults experiencing headaches. Primary headaches include migraine, tension-type headache, and cluster headache. Migraine is further classified and diagnostic criteria are provided. Chronic migraine occurs on 15 or more days per month. Management involves non-pharmacological approaches as well as acute and preventative pharmacological treatment. Tension-type headache is also classified and diagnostic criteria outlined.
This document provides information on neurology for GPs, focusing on different types of headaches. It discusses the GP liaison role, common headache types like migraine, tension headache, and cluster headache. Guidelines are provided on evaluation, diagnosis, acute and preventive treatment. Referral criteria include atypical features, treatment failure, or uncertain diagnoses. The goal is to appropriately manage most headache cases in primary care while recognizing red flags that warrant specialty referral.
The document is a disclosure statement from Dr. Ahmad Saladdin Sultan stating that he does not have any financial conflicts of interest in relation to the program or presentation being given. It provides background on Dr. Sultan's qualifications and specialty in emergency medicine. The document then covers three parts: headaches including types like migraine, tension, and cluster headaches; Bell's palsy including symptoms, causes, and treatment; and seizures including types, evaluation, and management.
This document discusses different types of headaches and their treatment. It begins by defining primary and secondary headaches. Primary headaches include tension headaches, migraines, and cluster headaches. Migraines can be triggered by various factors and cause nausea. Secondary headaches have an underlying cause like head trauma. Treatment discussed includes acetaminophen, NSAIDs, and lifestyle changes. Medication overuse headaches are also addressed. The document provides guidance on treating specific headache types and exclusions for self-treatment.
This document provides an overview of treatment options for various headache conditions. It begins with disclosures and objectives from the speaker. It then outlines treatments for migraine (including during pregnancy/lactation), chronic migraine, medication overuse headache, tension-type headache, and cluster headache. Specific acute and preventive migraine treatment options are discussed in detail, along with principles, evidence, formulations, and troubleshooting. Other topics covered include chronic daily headache classification and secondary causes.
Right therapeutic approach for migraine Sudhir Kumar
Migraine is a common disease and about 15-20% of population suffers from it. Every physician needs to know the principles of migraine management. The current article describes the diagnostic criteria and treatment of migraine.
This document provides an overview of common medications used to treat migraines, including both preventative and rescue medications. It discusses lifestyle modifications that should be implemented alongside medications. For rescue medications, it emphasizes treating early in the migraine attack to improve effectiveness. Common over-the-counter options like NSAIDs, acetaminophen, and combination products are reviewed, alongside prescription medications including triptans, anti-nausea drugs, and opioids. The document cautions against medication overuse headache and stresses individualizing treatment based on a patient's needs and triggers.
This document provides information on evaluating and managing different types of headaches. It discusses taking a thorough history including red flags. Red flags for headaches include new onset headaches, worsening headaches, headaches associated with seizures, meningismus, or neurological deficits. It also summarizes migraine headaches, including diagnostic criteria, triggers, and acute and preventive treatment options. Additional headache types covered include tension headaches, cluster headaches, trigeminal neuralgia, glaucoma, medication overuse headaches, increased intracranial pressure, and acute sinusitis.
This document provides information on Dr. Ganta Rajasekhar's academic qualifications and areas of interest in neurology. It then discusses approaches to evaluating headache, classifications of primary and secondary headache disorders, migraine pathogenesis and management, tension-type headache, and trigeminal autonomic cephalalgias. Evaluation and treatment strategies for acute migraine, preventive migraine therapy, medication overuse headache, and special headache conditions are covered. Common questions in headache management are also addressed.
แนวทางการจัดการความเสี่ยงที่ส่งผลต่อต้นทุนการจัดการสินค้าคงคลัง
ของร้านขายยา CDE ในจังหวัดขอนแก่น
The Approach of Risk Management that Affecting the
Inventory Management Cost of CDE Drugstore in Khonkaen Province
Best Practice in Communication
ราชวิทยาลัยกุมารแพทย์แห่งประเทศไทย สมาคมกุมารแพทย์แห่งประเทศไทย
บรรณาธิการ วินัดดา ปิยะศิลป์ วันดี นิงสานนท์
ISBN 978-616-91972-1-8
Saccharomyces boulardii in the prevention of antibiotic-associated diarrhoeaUtai Sukviwatsirikul
This systematic review and meta-analysis evaluated the effectiveness of Saccharomyces boulardii in preventing antibiotic-associated diarrhea in children and adults based on 21 randomized controlled trials involving 4780 participants. The administration of S. boulardii compared to placebo or no treatment reduced the risk of antibiotic-associated diarrhea from 18.7% to 8.5%. S. boulardii was effective in reducing the risk of antibiotic-associated diarrhea in both children and adults. It also reduced the risk of Clostridium difficile-associated diarrhea in children but not adults. Overall, the results confirm that S. boulardii is effective for preventing antibiotic-associated diarrhea in children and adults.
This document provides information on drugs used to treat acute diarrhea. It begins with definitions of diarrhea from WHO. It then discusses estimates of child mortality due to diarrhea in Thailand from 2010 to 2012. It presents data on the age distribution of diarrhea cases and hospital admissions. It lists common bacterial, viral, and parasitic pathogens that cause childhood diarrhea. It discusses the pathogenesis of acute diarrhea and describes fluid and electrolyte losses and consequences of dehydration and nutritional deficits. It provides details on fluid and electrolyte composition of diarrheal stool from different pathogens. It outlines the objectives of diarrhea treatment and causes of death. It then discusses use of oral rehydration therapy and solutions. It recommends probiotics, continued feeding, and zinc supplementation. It
Systematic review with meta-analysis: Saccharomyces boulardii in the preventi...Utai Sukviwatsirikul
This systematic review and meta-analysis evaluated the effectiveness of Saccharomyces boulardii in preventing antibiotic-associated diarrhea in children and adults based on 21 randomized controlled trials involving 4780 participants. The administration of S. boulardii compared to placebo or no treatment reduced the risk of antibiotic-associated diarrhea from 18.7% to 8.5%. S. boulardii was effective in reducing the risk of antibiotic-associated diarrhea in both children and adults. It also reduced the risk of Clostridium difficile-associated diarrhea in children. The quality of evidence was rated as moderate to low based on limitations in the design and reporting of the included studies. This meta-analysis confirms the effectiveness of
Saccharomyces boulardii in the prevention of antibiotic-associated diarrhoea ...Utai Sukviwatsirikul
Saccharomyces boulardii in the prevention of antibiotic-associated
diarrhoea in children: a randomized double-blind placebo-controlled
trial
M. KOTOWSKA, P. ALBRECHT & H. SZAJEWSKA
Department of Pediatric Gastroenterology and Nutrition, The Medical University of Warsaw, Warsaw, Poland
Accepted for publication 24 November 2004
DECLARATION OF HELSINKI - History and principlesanaghabharat01
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The droplets have a tendency to conglomerate to one big mass, but on being shaken they fall apart into countless little droplets again. It is used to ignite explosives, like mercury fulminate, the explosive character is one of its general themes.
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share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
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2. Migraine and Tension Headache Diagnosis and Treatment Guideline 2
Diagnosis: Headache Classification
Table 1. Identification of headache type: migraine, tension, or cluster
Migraine Tension Cluster
Location Unilateral Bilateral Supraorbital/temporal
Pain intensity 1
Moderate to severe Mild to moderate Severe
Duration 4–72 hours 30 minutes to 7 days 15–180 minutes
Characterization of pain Pulsing Pressure/squeezing Boring/stabbing
Sensitivity to light/sound One or both may be
present.
Both are absent or
only one is present.
No
Nausea/vomiting One or both may be
present.
No One or both may be
present.
Aggravated by routine
activity
Yes No No
Aura May be present No No
Associated symptoms None None Miosis, ptosis, rhinorrhea
1
Pain intensity
• Mild—Patient is aware of a headache, but is able to continue daily routine with minimum alterations.
• Moderate—The headache inhibits daily activities, but is not incapacitating.
• Severe—The headache is incapacitating.
3. Migraine and Tension Headache Diagnosis and Treatment Guideline 3
Alternative Diagnoses to Consider
For patients with a rapidly accelerating course, a recent history of head injury, or focal neurologic findings,
consult with a neurologist or neurosurgeon.
Table 2. Warning signs for possible disorders other than primary headache
Signs/symptoms Alternative diagnoses Testing/investigation
Subacute and/or progressive
headaches that worsen over time
(weeks to months)
Intracranial head lesion
• Tumor
• Subdural hematoma
• Hydrocephalus (acute or obstructive)
• MRI with or without contrast
Vasculopathy
• Subarachnoid hemorrhage
• Venous sinus thrombosis
• Carotid dissection
Infection
• Bacterial meningitis
• A new or different headache in
patients with established
headache disorders
• Statement by the patient that
“This is the worst headache of
my life.”
• Headache of sudden onset
(e.g., like a thunder clap) Structural defect
•Spontaneous cerebral spinal fluid leak
• CT scan without contrast
• If there is no evidence of
subarachnoid hemorrhage, a
lumbar puncture should be
performed.
• If both tests are normal and
suspicion is still high, order an
MRI with or without contrast (i.e.,
gadolinium).
• Discuss next steps with
Neurology.
• Red eye
• Halos
• Unilateral visual symptoms
Angle closure glaucoma Acute angle closure glaucoma is an
ophthalmological emergency.
Age 50 or older and symptoms
including:
• Polymyalgia rheumatica
• Jaw claudication
• Scalp tenderness
• Fever
• Firm, nodular temporal arteries
• Decreased temporal pulses
Giant cell arteritis • Elevated sedimentation rate
• C-reactive protein
• Consider brain imaging if
associated with focal neurologic
findings.
1
• Discuss next steps with
rheumatology
Rhinosinusitis symptoms lasting
7 days or longer and any of the
following:
• Yellow-green or blood-tinged
nasal discharge
• Pain, pressure, and fullness in
cheeks, brow, or forehead,
especially unilateral
• Unilateral maxillary sinus
tenderness
• Worsening symptoms after initial
improvement
• Fever
• Sore throat
• Cough
• Fatigue
• Achy feeling in upper teeth
Acute bacterial rhinosinusitis • Non-contrast CT is indicated in
patients with clinical signs or
symptoms of complicated acute
bacterial rhinosinusitis, including:
diminished visual acuity,
diplopia, periorbital edema,
severe headache, or altered
mental status.
• Non-contrast CT may also be
helpful in recurrent or treatment-
resistant sinusitis to help identify
anatomic blockage of the
ostiomeatal complex.
• Jaw soreness
• Pain radiating from the jaw
• Waking with headache
• Ear pain
• Hyperacusis
• Tinnitus
• Palpable or audible joint click as
the jaw is opened and closed
Temporomandibular joint (TMJ)
disorder
• History
• Exam
• Consider dental referral.
• Consider bite splint/night guard.
1
In most cases a non-contrast CT is the best initial test. Contrast-enhanced CT or MRI might be appropriate in
persons with a rapidly accelerating course, a recent history of head injury, or focal neurologic findings.
4. Migraine and Tension Headache Diagnosis and Treatment Guideline 4
Treatment: Migraine Headaches
Goals
Develop a written headache treatment plan for prevention and management of acute migraine to:
• Decrease headache frequency. (Aim for fewer than 5 headache days per month.)
• Decrease headache severity. (Headaches will respond quickly to an abortive therapy.)
• Avoid medication/caffeine overuse headache. (See Treatment: Medication Overuse Headaches.)
• Within Group Health, consider using the .pidxmigraine SmartPhrase in Epic to document the
headache treatment plan for the After Visit Summary.
Lifestyle Modifications/Non-Pharmacologic Options
Provide self-management education. Teach and encourage patients to:
• Maintain a healthy lifestyle. Develop an action plan to address:
- Proper nutrition
- Regular physical activity
- Adequate sleep
- Stress reduction strategies
• Identify and avoid triggers (e.g., tobacco smoke, strong odors, or sprays).
• Address workplace ergonomics. (Attention to workplace ergonomics and instruction in self-care of
neck tension can have a dramatic effect on headache frequency.)
Pharmacologic Options
• The choice of acute migraine treatments should be dictated by the rapidity of onset, headache
severity, associated symptoms (e.g., nausea/vomiting), and patient preference.
• Rule out rebound syndrome prior to initiating therapy. If rebound is present, prevention and acute
migraine medications may not be effective.
• Before considering a patient to have failed treatment with a given migraine prevention medication,
advance to the maximum recommended dose.
• If a patient doesn’t respond to 1–2 adequate doses of a given medication during a migraine
episode, it is appropriate to try another medication.
• Individuals may respond differently to different triptans. If patient does not respond to one triptan,
offer an alternative triptan.
For information on side effects, contraindications, formulary status (e.g., prior authorization), and other
pharmacy-related issues, see the Group Health Formulary online:
5. Migraine and Tension Headache Diagnosis and Treatment Guideline 5
Table 3. Pharmacologic options for acute treatment of headache
Eligible population Medication 1
Initial dose Maximum dose
Aspirin 1000 mg PO once. Give an
additional 1000 mg if needed.
4000 mg daily.
Do not exceed 3 days of use per
week.
Ibuprofen 400 mg PO once.
Give an additional 200–
400 mg if needed.
1200 mg daily.
Do not exceed 3 days of use per
week.
Acetaminophen/
aspirin/caffeine
500 mg (aspirin component)
PO once.
Give an additional 500 mg if
needed.
4000 mg daily.
Do not exceed 3 days of use per
week.
Patients with mild to
moderate headache
Naproxen 500–750 mg PO once.
Give an additional 250–
500 mg if needed.
1250 mg daily.
Do not exceed 3 days of use per
week.
Oral tablet
25–100 mg PO once.
May repeat after 2 hours.
Oral tablet
200 mg daily
Nasal [PA]
5–20 mg spray in one nostril
once. May repeat after
2 hours.
Nasal
40 mg daily
Sumatriptan
2,3
SQ [PA]
6 mg SQ once. May
repeat after 1 hour.
SQ
12 mg daily
Rizatriptan
2,3,4
5–10 mg PO once. May
repeat after 2 hours.
30 mg daily
Naratriptan
2,3,5
1–2.5 mg PO once. May
repeat after 4 hours.
5 mg daily
Nasal
1 spray (0.5 mg) each nostril.
May repeat after 15 minutes.
Nasal
2 mg daily (4 sprays); 4 mg/week
(8 sprays)
Dihydroergotamine
mesylate (DHE)
3,6
SQ/IM
1 mg (1 mL) SQ/IM once.
May repeat after 1 hour.
SQ/IM
3 mg daily;
6 mg/week
IM
60 mg
IM
120 mg daily
Patients with:
Moderate to severe
headache
or
Mild to severe
headache with nausea
or vomiting
or
Rapid progression to
severe headache
or
Mild to moderate
headache that
responds poorly to
first-line treatment
Ketorolac
7
IV
30 mg
IV
120 mg daily
1
If the patient is experiencing nausea, consider adding an antiemetic such as metoclopramide or
prochlorperazine.
2
If using two different formulations of a triptan, use no more than two doses combined in 24 hours. Do not
exceed 3 days of use per week.
3
Do not take triptans within 24 hours of any ergotamine or vice versa.
4
Use a 5 mg dose of rizatriptan in patients receiving propranolol with a maximum of 15 mg daily.
5
Naratriptan has a longer half-life than other triptans and therefore may be better for those patients with
headaches of long duration.
6
Some patients may benefit from DHE IV. This treatment option may be offered to patients in urgent care
settings. See Appendix 1, DHE Raskin Protocol (Urgent Care).
7
For patients under 110 lbs or aged 65 years or over: IM dose = 30 mg, IV dose = 15 mg.
6. Migraine and Tension Headache Diagnosis and Treatment Guideline 6
Additional pharmacologic acute treatment options: There is insufficient evidence pertaining to safety
and effectiveness to support a recommendation for or against the use of the following medications. When
the options above have failed to provide relief, local expert opinion favors consideration of the following
agents:
• Corticosteroids (60 mg PO initially, then 5 mg less per day over 12 days).
• IV valproic acid (500 mg IV x 1). FDA safety alert: Valproic acid is pregnancy category X when
used for headaches (category D for more serious conditions such as seizures and bipolar disorder).
It is therefore contraindicated in women who are pregnant or may become pregnant. It should be
used in women of childbearing age only after shared decision making of the potential risks, and
only if contraception is used regularly.
Not recommended: The following pharmacologic options are not recommended/not on the Group
Health formulary due to the high potential for the development of medication overuse headaches.
Consider virtual or phone consultation with a neurologist to discuss next steps.
• Opioid medications
• Fiorinal (butalbital, caffeine, and aspirin)
7. Migraine and Tension Headache Diagnosis and Treatment Guideline 7
Treatment: Medication Overuse Headaches
• Medication overuse headache is a state of daily or near-daily refractory headaches resulting from
overuse of acute pain medicines by a patient with migraine.
• Potential triggers include over-the-counter or prescribed symptomatic medications (all narcotics,
analgesics, triptans, DHE, benzodiazepines, or decongestants) and caffeine in more than moderate
amounts.
• It is imperative that this condition be eliminated in order to allow prevention and acute migraine
treatments to work.
Treatment Overview
1. Provide patient education.
2. Stop overused medication. (Tapering may be required—see the Chronic Opioid Therapy for
Chronic Non-Cancer Pain Guideline or the Adult Drug Misuse & Withdrawal Guideline.)
3. Treat symptoms during withdrawal of overused medication. (See Table 4.)
4. Develop a written headache treatment plan that includes acute and prophylactic treatment. Within
Group Health, consider using the .pidxheadachemedoveruse SmartPhrase in Epic to document
the treatment plan for the After Visit Summary.
5. Develop a follow-up and relapse prevention plan. (See Monitoring/Follow-up section.)
Table 4. Symptomatic outpatient treatment for medication overuse headache 1
Eligible population Line Medication Initial dose Maximum dose
1st
Stop overused medication. Advise patient that rebound headache may
take 2–6 weeks to resolve after elimination of medication overuse.
2nd
Prednisone 60 mg on days 1 and 2
40 mg on days 3 and 4
20 mg on days 5 and 6
or
60 mg PO with a 5 mg
per day taper over
12 days
—
Patients with:
Headache 15 or more
days/month
Regular overuse for
more than 3 months of
one or more
acute/symptomatic
treatments:
• Ergotamine, triptan,
opioids, or
combination analgesic
medications on
10 or more
days/month
• Simple analgesic or
any combination of
ergotamine, triptans,
or analgesic opioids
on 15 or more
days/month
Headache developed or
markedly worsened
during medication
overuse
3rd
Dihydroergotamine
mesylate (DHE) SQ/IM
1 mg SQ/IM at the first
sign of headache, then
repeat hourly up to total
of 3 mg
3 mg daily;
6 mg/week
8. Migraine and Tension Headache Diagnosis and Treatment Guideline 8
Treatment: Migraine Prophylaxis
Overview
There are no clear evidence-based recommendations for when to start preventive therapy for migraine.
The choice of migraine prevention medication should be made based on comorbid conditions (e.g.,
tricyclics for patients with depression and/or neuropathic pain syndromes, valproic acid/divalproex for
persons with seizure disorders) and the relative value the patient places on efficacy versus avoidance of
side effects.
Pharmacologic Options
Guiding principles of prophylaxis
• Each medication dose change may take 2–4 weeks to reach maximal effectiveness.
• Using 4 headache days per month as a goal, the initial dose of each medication should be fairly
low, and gradually increased to the maximal tolerated or maximal safe dose. Keep medication at
that dose for 1 month before making modifications to therapy.
• If there is no relief after 4 weeks at the maximal recommended or tolerated dose of the initial
medication, add a second prophylactic medication.
• When headache days remain fewer than 4 per month for 1 to 2 months, start tapering therapy of
the least well-tolerated medication to find the lowest effective dose.
• Patients not responding to combinations of two or three prophylactic medications should be
reassessed for an alternate diagnosis, analgesic or acute migraine drug rebound, or confounding
psychiatric or social stresses. Drug therapy alone may not be sufficient.
9. Migraine and Tension Headache Diagnosis and Treatment Guideline 9
Table 5a. Pharmacologic options for migraine prophylaxis 1
Eligible population Line Medication Initial dose Maximum
daily dose
Patients with:
Four or more days with
migraine headaches per
month
Fewer than four migraine
headaches per month but
with severe pain refractory
to all migraine-specific
acute therapies
Complicated migraines
(e.g., migraine associated
with focal neurologic signs
such as nystagmus or
hemiplegia)
1
st
Propranolol
2
40 mg b.i.d.; increase by
40 mg every week (in 3
divided doses).
240 mg
2nd
Nortriptyline 3
10–25 mg daily at bedtime;
increase by 10–25 mg every
week.
150 mg
3rd
Venlafaxine IR 37.5 mg daily; increase by
75 mg every week (in 2
divided doses).
150 mg
Topiramate 4,5
25 mg daily in the evening;
increase by 25 mg every
week (in 2 divided doses).
100 mg
Divalproex DR 6
125 mg twice daily; increase
by 125 mg every week (in
2 divided doses).
2,000 mg
FDA safety alert: Divalproex is pregnancy category X when used
for headaches (category D for more serious conditions such as
seizures and bipolar disorder). It is therefore contraindicated in
women who are pregnant or may become pregnant. It should be
used in women of childbearing age only after shared decision
making of the potential risks, and only if contraception is used
regularly.
1
Gabapentin is not FDA-approved for the prophylaxis of migraine headache. There is insufficient evidence to
determine the safety and efficacy of gabapentin for the prophylaxis of migraines.
2
The best evidence favors propranolol. Efficacy is less certain with other beta-blockers.
3
Other tricyclics may be as effective (e.g., amitryptiline).
4
Check serum bicarbonate after 2 weeks of therapy and every 3 months.
5
Within Group Health, see Anticonvulsant/Contraceptive Drug-Drug Interactions information for patients on
oral contraceptives, at http://incontext.ghc.org/rx/med/documents/anticonvulsant_contraceptive_ddi.pdf.
6
Check trough level, CBC, platelets, and SGOT at 500 mg twice daily. Don't exceed trough level of
100 mcg/dL. Divalproex XR is non-formulary.
Note: Consider Neurology consultation for patients with migraine headache who have not responded to
the recommended options for migraine prophylaxis. OnabotulinumtoxinA (Botox) may be an option for
patients who meet all the following criteria:
• Meet diagnostic criteria for migraine or migraine with muscle tension headache.
• Patients will do what is necessary to eliminate rebound headache prior to authorization for Botox.
• Patient has tried and failed at least four prophylactic agents and three abortive drugs listed in the
Headache Guideline.
• Patient has been seen by a neurologist who recommends the trial of Botox.
Botox is administered as a trial; if the treatment is found unhelpful after two injection sessions, then it is
discontinued. Botox is approved by the FDA for chronic migraine (defined as 15 or more headache days
per month with a headache lasting 4 hours or longer each day).
There is insufficient evidence pertaining to safety and effectiveness to support a recommendation for or
against the use of the following medications for migraine prophylaxis:
• Lisinopril
• Verapamil
10. Migraine and Tension Headache Diagnosis and Treatment Guideline 10
Special Population: Women With Menstruation-related Migraines
Advise a woman with suspected menstrual migraine to keep a headache diary for at least 2 months to
determine if she is having regular and predictable menses and if these correlate with headache onset.
Some women experience migraines during ovulation (either alone or in addition to menses).
Consider a short course of prophylaxis with naproxen or a triptan taken twice a day starting 2–3 days
before the anticipated onset of the headache and continued for 5 days through the at-risk period (ICSI
2011, SIGN 2008).
Table 5b. Pharmacologic options for the prevention of menstrual migraine
Eligible
population
Line Medication Daily dose Timing
1st
Naproxen 500–750 mg
Sumatriptan Oral tablet
25–100 mg
Rizatriptan 1
5–10 mg
Women with
regular and
predictable
menses that
correlate with
headache
onset
2nd
Naratriptan 1–2.5 mg
2–3 days before the anticipated onset of the
headache and continuing through the at-risk period
Women with
irregular,
unpredictable
menses that
correlate with
headache
onset
or
Women for
whom
NSAIDs and
triptans are
ineffective for
prophylaxis
of menstrual
migraines
1
st
Oral
contraceptives 2
Within Group Health, see Think Preferred OCP, at
http://incontext.ghc.org/rx/med/documents/oralcontraceptive_pocketcard.pdf
CAUTION: Women with migraines with aura should avoid taking combined
oral contraceptive pills because of increased risk for stroke. Among women
with migraine, women who also had aura had a higher risk for stroke than
did those without aura. Women with a history of migraine who use
combined oral contraceptive pills are about 2–4 times as likely to have an
ischemic stroke as nonusers with a history of migraine (CDC MMWR).
1
Use a 5 mg dose of rizatriptan in patients receiving propranolol, with a maximum of 15 mg daily.
2
Combined oral contraceptive pills may be offered for prophylaxis, although the evidence for this option is limited. In a
contraceptive-containing drosperinone, an extended 168-day placebo-free oral contraceptive regimen showed a significant
decrease in duration and severity of headaches and in loss of function due to headache compared with a standard 21/7
oral contraceptive cycle (Sulak 2007).
11. Migraine and Tension Headache Diagnosis and Treatment Guideline 11
Non-prescription Options for Migraine Prophylaxis and Treatment
While there is some evidence supporting their use for the prevention of migraine headaches, there is
insufficient evidence to determine the long-term safety and effectiveness of the following therapies:
Table 6. Complementary and alternative therapies for migraine prophylaxis
Eligible population Medication Initial dose
Riboflavin 1
400 mg daily
Coenzyme Q10 1
100 mg t.i.d.
Patients with:
• Four or more days of headache per month
• Four or more episodes of headache per month
• Fewer than 4 headache days per month but with severe
pain refractory to all migraine-specific acute therapies Butterbur 2
75 mg daily
1
Weak evidence from a small, placebo-controlled trial.
2
Placebo-controlled RCTs suggest that a 75 mg dose of butterbur may be effective at reducing headache
frequency; however, there is insufficient evidence pertaining to the long-term safety and efficacy of butterbur.
There is insufficient evidence to make a recommendation on the safety or efficacy of the following non-
prescription therapies for migraine prophylaxis:
• Magnesium
There is insufficient evidence to make a recommendation on the safety or efficacy of the following non-
pharmacologic therapies for the treatment of migraine:
• Transcutaneous electrical stimulation (TENS)
• Massage
• Acupuncture
Monitoring/Follow-up
Advise the patient to keep and review a headache diary to monitor the effects of treatment on severity,
frequency, and disability. Diary entries should include:
• Day/time
• Headache severity
• Other symptoms (nausea, vomiting, photophobia)
• Impact on usual activities
• Duration of attack
• Prescribed medication
• OTC medication
• Menstrual cycle day
12. Migraine and Tension Headache Diagnosis and Treatment Guideline 12
Evidence Summary
This guideline was adapted from the following:
Scottish Intercollegiate Guideline Network (SIGN). Diagnosis and management of headache in adults.
Edinburgh: SIGN 2008 (SIGN publication no.107, cited May 2011). Available online at:
www.sign.ac.uk/pdf/sign107.pdf [PDF].
Institute for Clinical Systems Improvement (ICSI). Diagnosis and treatment of headache. ICSI 2011
(Tenth edition, cited May 2011). Available online at:
http://www.icsi.org/headache/headache__diagnosis_and_treatment_of_2609.html [PDF].
Medication overuse headache
The evidence base for the treatment of medication overuse headache is limited.
Prednisone
Two randomized controlled trials (RCTs) evaluated the efficacy of prednisone for treatment of
medication overuse headache. Results from these trials were mixed. Results from the first trial, which
included 102 patients, suggest that compared to placebo, 60 mg of prednisone tapered down over
6 days does not reduce withdrawal headaches in patients with medication overuse headache (Bøe
2007). Results from the second trial suggest that 100 mg of prednisone given once daily for the first
5 days of withdrawal may be more effective than placebo for reducing headache severity. These
results should be interpreted with caution, as the study included only 20 patients and an ITT analysis
was not performed (Pageler 2008).
Migraine prophylaxis
Gabapentin
The Group Health Pharmacy and Therapeutics (P&T) committee recently reviewed the evidence on
the safety and efficacy of gabapentin for migraine prophylaxis and concluded that the evidence does
not support the use of gabapentin for migraine prophylaxis. The published evidence on the use of
gabapentin for migraine prophylaxis mostly revolves around one study with major flaws in study
design (e.g., unblinding) and publication bias (Mathew 2001). Additionally, other unpublished studies
found negative results.
Botulinum toxin type A
Two double-blind, placebo-controlled randomized trials evaluated the safety and efficacy of
onabotulinumtoxinA (botox) for the prevention of migraine headache in adults with chronic migraines.
In both trials, participants were given two injections of onabotulinumtoxinA 12 weeks apart. The first
trial followed 679 participants for 24 weeks. There was no significant difference in the primary
outcome frequency of headache episodes after 24 weeks. However, patients who received
onabotulinumtoxinA had significantly fewer headache days and migraine days compared to patients
who received placebo. Additionally, the mean Headache Impact Test (HIT)-6 score was significantly
lower for patients who received onabotulinumtoxinA (Aurora 2010).
The second trial followed 705 participants for 24 weeks. The primary outcome was changed during
the study. Results from this study suggest that patients who received onabotulinumtoxinA had
significantly fewer headache days (new primary outcome), migraine days, moderate to severe
headache days, headache episodes, and HIT-6 scores compared to patients who received placebo
(Diener 2010). It should be noted that both of these trials received industry funding and the treatment
was compared to placebo and not to another active prophylactic treatment. The most common
adverse events with onabotulinumtoxinA were neck pain, muscle weakness, eyelid ptosis, myalgia,
worsening migraine, and musculoskeletal stiffness (Aurora 2010, Diener 2010).
13. Migraine and Tension Headache Diagnosis and Treatment Guideline 13
Complementary and alternative medicine
Riboflavin
There is weak evidence from one small trial with 55 patients that riboflavin has more than a placebo
effect in migraine prophylaxis and minimal adverse effects. The study showed that patients receiving
oral riboflavin (400 mg daily for 3 months) had a significantly reduced attack frequency and had fewer
migraine days compared with those in the placebo group. The trial had a valid methodology but a
very small sample size (Schoenen 1998). Larger trials are needed to provide more evidence on the
efficacy of riboflavin in migraine prophylaxis and to compare riboflavin with other standard
prophylactic agents.
Coenzyme Q10
There is weak evidence from one recent, small (N = 43) RCT that coenzyme Q10 may be effective in
migraine prophylaxis (Sandor 2005). Larger trials with longer follow-up are needed to determine the
efficacy and safety of CoQ10 in migraine prophylaxis.
Butterbur
The best evidence on the safety and efficacy of butterbur for the prevention of migraines comes from
a placebo-controlled RCT that followed 233 subjects for 16 weeks. Results from this trial suggest that
compared to placebo, a 75 mg dose of butterbur may reduce the frequency of migraine attacks. The
long-term safety and efficacy of this medication is unknown. Additionally, the efficacy of butterbur
compared with other prophylactic medications is unknown (Lipton 2004).
Magnesium
The available literature does not provide sufficient evidence to determine the efficacy of magnesium
in migraine prophylaxis.
Acupuncture
Results from a meta-analysis of RCTs suggest that compared to acute treatment only or
pharmacological prophylaxis, acupuncture may reduce headache frequency; however, there was no
significant difference when acupuncture was compared with a sham intervention (Linde 2009).
Transcutaneous electrical stimulation (TENS)
The available literature does not provide sufficient evidence to determine the efficacy of
transcutaneous electrical stimulation for the treatment of migraine.
Massage
The available literature does not provide sufficient evidence to determine the efficacy of massage for
the treatment of migraine.
References
Aurora SK, Dodick DW, Turkel CC, et al. OnabotulinumtoxinA for treatment of chronic migraine: results
from the double-blind, randomized, placebo-controlled phase of the PREEMPT 1 trial. Cephalalgia. Jul
2010;30(7):793–803.
Bøe MG, Mygland A, and Salvesen R. Prednisolone does not reduce withdrawal headache: a
randomized, double-blind study. Neurology. 2007;69:26-31.
Centers for Disease Control and Prevention. U.S. Medical Eligibility Criteria for Contraceptive Use.
MMWR Early Release. 2010;59:1–86.
Diener HC, Dodick DW, Aurora SK, et al. OnabotulinumtoxinA for treatment of chronic migraine: results
from the double-blind, randomized, placebo-controlled phase of the PREEMPT 2 trial. Cephalalgia. Jul
2010;30(7):804–814.
14. Migraine and Tension Headache Diagnosis and Treatment Guideline 14
Institute for Clinical Systems Improvement (ICSI). Diagnosis and treatment of headache (10th
edition).
January 2011. Available online at:
http://www.icsi.org/headache/headache__diagnosis_and_treatment_of_2609.html.
Linde K, Allais G, Brinkhaus B, Manheimer E, Vickers A, and White AR. Acupuncture for migraine
prophylaxis. Cochrane Database of Systematic Reviews 2009, Issue 1. Art. No.: CD001218. DOI:
10.1002/14651858.CD001218.pub2.
Lipton RB, Gobel H, Einhaupl KM, Wilks K, and Mauskop A. Petasites hybridus root (butterbur) is an
effective preventive treatment for migraine. Neurology. 2004;63:2240-2244.
Mathew NT, Rapoport A, Saper J, et al. Efficacy of gabapentin in migraine prophylaxis. Headache. Feb
2001;41(2):119-128.
Pageler L, Katsarava Z, Diener HC, Limmroth V. Prednisone vs. placebo in withdrawal therapy following
medication overuse headache. Cephalalgia. 2008;28:152-156.
Sandor PS, Di Clemente L, Coppola G, et al. Efficacy of coenzyme Q10 in migraine prophylaxis: a
randomized controlled trial. Neurology. Feb 22 2005;64(4):713–715.
Schoenen J, Jacquy J, Lenaerts M. Effectiveness of high-dose riboflavin in migraine prophylaxis. A
randomized controlled trial. Neurology. Feb 1998;50(2):466–470.
Scottish Intercollegiate Guideline Network (SIGN). Diagnosis and management of headache in adults.
Edinburg: SIGN 2008; (SIGN publication no. 107) Available online at:
http://www.sign.ac.uk/pdf/sign107.pdf.
Sulak P, Willis S, Kuehl T, Coffee A, and Clark J. Headaches and oral contraceptives:impact of
eliminating the standard 7-day placebo interval. Headache. 2007;47:27–37.
15. Migraine and Tension Headache Diagnosis and Treatment Guideline 15
Guideline Development Process and Team
Development Process
To develop the Migraine & Tension Headache Guideline, Group Health adapted recommendations from
externally developed evidence-based guidelines. The Group Health guideline team reviewed additional
evidence in the areas of medication overuse headache, migraine prophylaxis, and complementary and
alternative medicine. For details, see Evidence Summary and References.
This edition of the guideline was approved for publication by the Guideline Oversight Group in June 2011.
Team
The Migraine & Tension Headache Guideline development team included representatives from the
following specialties: emergency medicine, family medicine, internal medicine, neurology, nursing,
pharmacy.
Content expert: Tim Scearce, MD, Neurology
Clinician lead: David K. McCulloch, MD, Medical Director, Clinical Improvement, mcculloch.d@ghc.org
Guideline coordinator: Avra Cohen, MN, Clinical Improvement & Prevention, cohen.al@ghc.org
Beth Arnold, PharmD, Pharmacy
Patricia Auerbach, MD, Emergency Medicine
Rebecca Doheny, MPH, Epidemiologist, Clinical Improvement & Prevention
Denise Hastings, MD, Internal Medicine
Jennifer Macuiba, Clinical Improvement & Prevention
Robyn Mayfield, Health Education Specialist, Clinical Improvement & Prevention
Michelle Seelig, MD, Family Medicine
Kathy Sobon, RN, Nursing Operations
Ann Stedronsky, Clinical Publications, Clinical Improvement & Prevention
16. Migraine and Tension Headache Diagnosis and Treatment Guideline 16
Appendix 1. Dihydroergotamine Mesylate (DHE) Raskin Protocol (Urgent Care)
This protocol is for use with patients being treated in urgent care settings. When headache relief is
achieved, patients may be discharged and directed to follow up with primary care or return to urgent care
as needed.
Table 7. Dihydroergotamine mesylate (DHE) 1
Raskin protocol for refractory migraine headache
(urgent care settings)
Step Medication Dose
Anti-emetic
premediation 2
1 Metoclopramide 10 mg IV over 30 minutes
2 DHE test dose 0.5 mg IV over 2–3 minutesAnalgesic test
dose
Monitor/assess patient for 1 hour post–test dose.
If blood pressure is greater than 165/95 mm Hg or patient develops chest pain or
severe nausea, discontinue DHE.
If not, go to Step 3.
Metoclopramide 10 mg IV every 8 hours as needed3a
Headache persists
WITH side effects 3 DHE NO DHE for 8 hours, then repeat DHE 0.3–
0.4 mg IV every 8 hours as needed, if
tolerated, for up to 3 days.
Metoclopramide 10 mg IV every 8 hours as needed3b
Headache relief, no
side effects DHE 0.5 mg IV given if/ when headache recurs
and repeated every 8 hours as needed for
2–5 days
HOLD when administering DHE 1 hour
post–test dose
Metoclopramide
10 mg IV every 8 hours as needed, with
subsequent doses of DHE
0.5 mg IV administered 1 hour post–test
dose WITHOUT metoclopramide
THEN
If patient is nauseated: 0.75 mg IV
administered WITH metaclopramide if/
when headache recurs and repeated every
8 hours as needed for 2–5 days
Analgesic
3c
Headache persists,
no side effects
DHE
If patient is NOT nauseated: 1.0 mg IV
administered WITH metaclopramide if/
when headache recurs and repeated every
8 hours as needed for 2–5 days
1
DHE should not be given within 24 hours of a triptan.
2
Consider IV hydration if needed.
3
Common side effects include: nausea, vomiting, diarrhea, abdominal cramps, dizziness, paresthesia, and leg
pain. By reducing the dose and co-administering metoclopramide as an antiemetic, these side effects can
usually be resolved.