Headache Presentation PDF

HEADACH E I VA N E D U KU M O Z U , P H A R M D. , P H D. D E PA RT M E N T O F P H A R M A C O T H E RA P E U T I C S A N D P H A R M A C Y P RA C T I C E SCHOOL OF PHARMACY AND PHARMACEUTICAL SCIENCES U N I V E R S I T Y O F C A P E C O A S T. HEADAC...

HEADACH E I VA N E D U KU M O Z U , P H A R M D. , P H D. D E PA RT M E N T O F P H A R M A C O T H E RA P E U T I C S A N D P H A R M A C Y P RA C T I C E SCHOOL OF PHARMACY AND PHARMACEUTICAL SCIENCES U N I V E R S I T Y O F C A P E C O A S T. HEADACHE 1 INTRODUCTION Headache is characterized by pain or discomfort in the head, scalp, or neck. It can be symptomatic of a distinct pathologic process or can occur without an underlying cause. Headache is one of the most common complaints encountered by healthcare practitioners. Headache disorders are a worldwide problem, affecting people of all races, income levels and geographical areas. Headaches are more common in females than males. HEADACHE 2  Classification International Classification of Headache Disorders ◦ Primary Headache Disorders ◦ Secondary Headache Disorders - ◦ These are not caused by another these are caused by an underlying medical condition. condition, such as: ◦ 1. Migraine trauma or injury to the head ◦ 2. Tension type headache and/or neck ◦ 3. Trigeminal autonomic cranial or cervical (non)vascular cephalalgias ….(Cluster disorder headache) substance or its withdrawal ◦ 4. Other primary headache infection disorders disorder of homoeostasis disorder of the cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cervical HEADACHE structure. 3 MIGRAINE Migraine attack can have up to 4 phases: 1. Prodromal Phase ◦ Occurs in 60% of patients ◦ Occurs hours or days before onset of Headache. ◦ Symptoms ◦ Phonophobia, photophobia, difficult concentration, anxiety, depression, irritability, fatigue, constipation, food craving, increased yawning, polyuria. HEADACHE 4 Migraine 2. Aura Phase ◦ Auras are focal neurologic symptoms precede or accompany migraine. ◦ Found in about 20% of patients. ◦ Last 5-20 mins about 60 mins before Headache. ◦ They can be visual or neurologic. ◦ Visual auras - scintillations (sparks/flashes) Photopsia (see light without a source) or scotoma (blindspots) ◦ Neurologic symptoms - hemiparesis, parethesias. HEADACHE 5 HEADACHE 6 Migraine 3. Headache ◦ Gradual onset with variable length of 4-72h ◦ Unilateral throbbing pain in frontotemporal region ◦ Nausea/vomiting **Chronic Migraine: This type usually occurs in 15 or more days per month for more than three(3) months, where in at least 8 days per month there are features of migraine headache. HEADACHE 7 Migraine 4. Post-drome: After the migraine, a person may feel drained or confused for up to a day, known as the “migraine hangover.” HEADACHE 8 HEADACHE 9 Migraine -triggers Stress: Stress is one of the most common migraine triggers. Sleep Disturbances: Too much or too little sleep, Irregular sleep patterns (e.g., jet lag or shift work). Diet: Skipping meals or fasting, dehydration or excessive caffeine consumption. Physical Exertion: Intense physical activity or exercise. Sensory Stimuli: Bright lights, loud noises, or strong smells. Hormonal Triggers: Menstrual cycle, Pregnancy, Hormonal contraceptives or hormone replacement therapy. Weather/Altitude Changes: Sudden shifts in temperature, humidity, flying in airplanes. Allergens: Seasonal allergies. Medications and Substance: Overuse of painkillers (rebound headaches), Vasodilators etc. Emotional Triggers :Anxiety and depression, excitement, grief. HEADACHE 10 Pathophysiology Vascular Theory ◦ Intracerebral arterial vasoconstriction ◦ Followed by reactive extracranial vasodilation Neurovascular Dysfunction Theory ◦ Trigeminovascular system Historically, the vascular theory was central to explaining migraines, but current understanding emphasizes neurovascular dysfunction involving both vascular and neuronal components. HEADACHE 11  Vascular Theory  Intracerebral arterial vasoconstriction: o Thought to cause the aura phase of migraines. o Decreased blood flow to certain areas of the brain (spreading oligemia) leads to aura symptoms like visual disturbances or sensory changes.  Reactive extracranial vasodilation: o Believed to occur during the headache phase. o Vasodilation (widening) of blood vessels outside the brain was thought to increase pain through activation of pain-sensitive receptors in the meninges and blood vessels. HEADACHE 12  Neurovascular Dysfunction Theory This theory integrates both vascular and neuronal components, emphasizing the role of the trigeminovascular system in migraines. Trigeminovascular System - The trigeminal nerve innervates blood vessels and the meninges.  Activation of the trigeminal nerve causes the release of neuropeptides such as: Calcitonin gene-related peptide (CGRP), Substance P and neurokinin A. These neuropeptides lead to vasodilation of meningeal blood vessels, inflammation and sensitization of pain pathways. Serotonin, a vasoactive neurotransmitter released by brainstem nuclei of the trigeminovascular system, also plays a role in migraine pathogenesis. Auras (Neuronal Dysfunction) - Auras are linked to cortical spreading depression: A wave of neuronal excitation followed by inhibition that moves across the brain cortex. Leads to aura symptoms (e.g., visual disturbances, sensory changes). Triggers the activation of the trigeminovascular system, initiating the headache. Headache Phase - Pain arises from sensitization of Peripheral pathways: Trigeminal nerve endings in blood vessels and meninges. Central pathways: Thalamus and HEADACHE 13 Neurovascular Dysfunction Theory HEADACHE 14 HEADACHE 15 Diagnosis Detailed history: Origin - either it is related to a diseased condition eg HTN, depression, previous head trauma Frequency and duration of attack- sudden onset, lasting for hrs/days Location of pain- frontal, unilateral, occipital Severity Presence or otherwise of aura Triggering factors Family history Medication history- both orthodox and herbal Imaging-sometime in hospitals but typically not used unless further investigations are to be made. HEADACHE 16 Management of Migraine Goals of therapy Reduce the pain and duration of the attack Reduce recurrence Identify underlying cause Identify triggering factors Improve functionality Provide effective agents for proper management HEADACHE 17  Pharmacologic Agents for Treatment of Migraines Migraine therapy is separated into abortive therapies and Prophylactic therapies. Abortive therapies try to halt the progression of the HA and are best taken at the onset of the HA. Prophylactic therapies Abortive therapies ◦ Beta blockers ◦ Ergot alkaloids ◦ Antidepressants ◦ Serotonin agonists ◦ NSAIDS ◦ NSAIDS ◦ Valproic Acid ◦ Combination analgesics ◦ Calcium Channel Blockers ◦ Antiemetics ◦ Botulinum Toxin ◦ CGRP (Calcitonin Gene-Related Peptide) Inhibitors ◦ Lisinopril (Off-label) HEADACHE 18 Ergot alkaloids Derived from a fungus that infects grain ◦ Ergotism/ St. Anthony’s fire - fiery pain, gangrene, hallucinations, confusion, and abortion ◦ Binds to 5-HT, - and -adrenergic, and dopamine receptors HEADACHE 19 Ergotamine/dihydroergotamine Ergotamine and dihydroergotamine are not as commonly used as before due to the availability of newer agents. 5-HT1 receptor agonists - cause vasoconstriction, inhibition of neuroinflammation, and pain signal transmission Ergotamine tartrate ◦ PO, SL, Rectal routes ◦ Products contain caffeine to increase absorption Dihydroergotamine (DHE) ◦ IM, SQ, Nasal Spray ◦ faster onset compared to orally and rectal routes HEADACHE 20 Ergotamine/DHE Side effects ◦ Nausea/vomiting ◦ Chest tightness Separate from triptans by >24 hours Contraindications ◦ Renal and/or hepatic failure ◦ Coronary, cerebral, peripheral vascular disease HEADACHE 21 Serotonin Receptor Agonists - Triptans Triptans are considered first-line treatment for moderate to severe acute migraines due to their ability to provide rapid relief of symptoms. They have been shown to significantly reduce headache severity, as well as alleviate nausea, photophobia, and phonophobia. HEADACHE 22 Serotonin Receptor Agonists - Triptans Selective agonists of 5-HT1b/5-HT1d (Triptans) ◦ Vasoconstriction of pain producing intracranial blood vessels ◦ Inhibition of vasoactive peptides release ◦ Interruption of pain signal transmission Eg. Sumatriptan ◦ Tablets, SC injection, Nasal Spray ◦ Acute migraine – Oral, 50-100mg initially followed by the 50 -100mg after at least 2hrs if migraine reoccurs (Patient not responding to initial dose should not take second dose for same attack) , Maximum 300mg per day. HEADACHE 23 Serotonin Receptor Agonists- Triptans Other examples Zolmitriptan 2.5mg then rpt after 2 hours Rizatriptan 10mg (equiv sumatriptan 100mg) Almotritan 12.5mg Limit use to 2-3 days per week Patients who fail on one triptan often respond to another Do not use one triptan within 24 hours of another HEADACHE 24 Serotonin Receptor Agonists Adverse effects Contraindications ◦Fatigue ◦Ischemic heart disease ◦Dizziness ◦Uncontrolled ◦Flushing/warm sensation hypertension ◦Chest symptoms ◦Cerebrovascular ◦Cardiac events disease ◦Peripheral Vascular ◦Stroke disease ◦Increased blood pressure HEADACHE 25 NSAIDs & Other Analgesics NSAIDS are used to treat mild to moderate migraines Prevent neurogenically-mediated inflammation ◦ Inhibition of prostaglandin synthesis ◦ Short-acting>Long-acting ◦ Short acting eg. Ibuprofen, Naproxen, Diclofenac Combination products ◦ Para/Aspirin/Caffeine HEADACHE 26 Opiates Opiate analgesics are commonly used in the Emergency treatment of migraines. They should not be used as standard abortive therapy. Opiates are mainly agonists at opiate receptors to produce analgesia. They can be addicting and if over used can exacerbate headache. The also upset the stomach and can cause constipation Examples ◦ Pethidine ◦ Butorphanol (Nasal Spray) ◦ Oxycodone Adverse Effects ◦ Addiction ◦ Rebound Headache ◦ Nausea /Vomiting ◦ Constipation HEADACHE 27 Antiemetics Adjunctive therapy ◦ Prevent/treatment migraine-induced nausea/vomiting ◦ Improve GI motility ◦ Enhance absorption of other anti-migraine medications Common Agents ◦ Metoclopramide ◦ Chlorpromazine Adverse Effects ◦ Extrapyramidal side effects ◦ Drowsiness HEADACHE 28 Migraine prophylaxis May take 2-3 months before benefits are seen. Ineffective for medication overuse headaches. Use for 4-6 months-taper off over 2-3 weeks. Non drug therapies ?? HEADACHE 29 Prophylaxis Therapy Prevent Migraine occurrence ◦Reduce frequency/severity/duration Consider for the following patients ◦Significant disability ◦Attacks >2/week ◦Attacks >2 a month that last > 3 days of disability ◦Acute therapy ineffective/contraindicated HEADACHE 30 Beta-Blockers Often prescribed as a first-line option for migraine prophylaxis They are effective because they help reduce the sympathetic nervous system activity, which can lower migraine frequency. Raise migraine threshold ◦ Modulate serotonergic neurotransmission Adverse Effects ◦ Fatigue ◦ Sleep Disturbances ◦ Bradycardia ◦ Hypotension ◦ Impotence HEADACHE 31 Beta-Blockers Propranolol – Adult, Initial; Oral, 40 mg 12 hourly, maintenance; 80-240 mg in divided doses, the dose may be adjusted based on the patient's response. Atenolol - Often started at 50 mg daily, with potential dose adjustments based on patient response to 200mg in divided doses. Nadolol - Initially 40 mg once daily, then increased in steps of 40 mg every week, adjusted according to response; maintenance 80-160 mg once daily. Metoprolol - Administered in extended-release formulations, starting at 25-50 mg daily and adjusted as needed. Maintenance; 100-200 mg in divided doses HEADACHE 32 Antidepressants Tricyclic antidepressants (TCAs) eg. Amitriptyline, Imipramine, Doxepine ◦ Antagonism of 5-HT2 receptors on cerebral vessels ◦ Suppression of serotonergic neuronal activity in brain stem Selective Serotonin Reuptake Inhibitors (SSRIs) - Fluoxetine ◦ Less effective than TCAs Side effects (TCAs) – Anticholinergic, Weight gain, Orthostatic hypotension,Cardiac toxicity Precautions Benign prostatic hyperplasia Glaucoma Suicide risk HEADACHE 33 Valproic acid Inhibition of serotonergic neurons ◦ Facilitate GABA neurotransmission ◦ reducing excitability, ◦ prevents the cortical spreading depression that triggers migraines. Other anticonvulsants –Topiramate, Gabapentin Adverse Effects ◦ Nausea/ vomiting ◦ Tremor ◦ Weight gain ◦ Blood dyscrasias ◦ Hepatotoxicity HEADACHE 34 Calcium Channel Blockers CCBs may also help stabilize neuronal excitability and reduce the cortical spreading depression believed to be a key event in migraine aura and pain. Verapamil ◦ Inhibition of 5-HT release (by inhibiting calcium influx into neurons- influence the release of various neurotransmitters) Adverse effects ◦ Constipation ◦ Hypotension ◦ Bradycardia ◦ AV block HEADACHE 35 CGRP (Calcitonin Gene-Related Peptide) Inhibitors CGRP is involved in migraine pathophysiology, particularly in the dilation of blood vessels and neurogenic inflammation. CGRP Inhibitors block CGRP receptors or its ligand, effectively preventing migraine attacks. These drugs are highly effective in reducing the frequency of migraines and are used for patients with frequent or severe migraines. Examples - Erenumab, Fremanezumab, Galcanezumab, Eptinezumab HEADACHE 36 NSAIDs Typically, not used for long-term migraine prophylaxis. Reasons NSAIDs Are Not Commonly Used for Prophylaxis: Short Duration of Action Chronic Use and Side Effects More Effective Prophylactic Treatment Short-Term Prophylaxis Use: NSAIDs might be prescribed as a short- term prophylactic option to prevent migraines during a period of increased risk, such as during menstrual migraines. For example, naproxen may be used to reduce migraine risk during a woman’s menstrual cycle, starting a few days before menstruation and continuing through the period. HEADACHE 37 CLUSTER HEADACHE (Trigeminal autonomic cephalalgias) Cluster headaches are rare, affecting less than 1% of the population. They are more common in men than women and typically start between the ages of 20 and 40. The diagnosis of cluster headaches is usually straightforward because the symptoms are distinctive. Sudden, severe, unilateral pain often around the eye or temple. Accompanied by autonomic symptoms. Each headache attack typically lasts 15 minutes to 3 hours and occurs in "clusters" (several times a day for weeks or months, followed by remission periods). HEADACHE 38 Cluster Headache Short (< 3 hours), Unilateral, Severe with autonomic symptoms ◦ ptosis, ◦ miosis, ◦ Redness and/or lacrimation, ◦ conjunctival injection, ◦ rhinorrhea, ◦ nasal congestion ◦ sweating on the affected side of the face HEADACHE 39 Treatment Acute Treatments - Used to abort attacks quickly when they occur: 1.Oxygen: High-flow 100% oxygen via a mask is very effective in aborting an attack within minutes for many patients. 2.Triptans: Injectable sumatriptan or intranasal zolmitriptan are commonly used. 3.Octreotide: A less common option, used for patients who cannot tolerate triptans. 4.Lidocaine (Intranasal): A local anesthetic applied intranasally to relieve pain. 5.Ergot derivatives (ergotamine or dihydroergotamine): Less commonly used due to side effects. 6.Prednisolone: Sometimes used in the short term to break the cycle of attacks during a cluster period. HEADACHE 40 Preventive Treatments Used to reduce the frequency and severity of attacks during cluster periods: 1.Calcium Channel Blockers (CCBs): Verapamil is the first- line preventive treatment and is highly effective for most patients. ◦ Short-term prednisolone may be used to prevent attacks while other preventives (like verapamil) take effect. 2.Lithium: Effective for chronic cluster headaches or when verapamil is contraindicated. 3.Topiramate: May also be used. HEADACHE 41 Less Commonly Used Preventives Pizotifen: An anti-serotonergic drug, less commonly used but can reduce attack frequency. Valproic Acid: Another anticonvulsant that may help in some patients. Capsaicin: Applied intranasally, can desensitize pain pathways. Ergot: Preventive use of ergotamine derivatives is limited due to side effects. Melatonin: A natural hormone sometimes used for its role in circadian rhythm regulation, as cluster headaches often follow a strict diurnal pattern. Prednisolone: Though more commonly used acutely, it may be used preventively in specific cases. HEADACHE 42 TENSION TYPE HEADACHE (TTH) Most common – Occurs in up to 80% of the population, pain is usually mild to moderate. Most patients treat with OTCs and do not seek medical attention Triggers - Often stress/lifestyle related Types – infrequent episodic (< 1 /month), freq episodic (1-14/month), and chronic (> 15 days a month) Pathophysiology – multifactorial. Normally innocuous stimuli are interpreted as pain in the dorsal horn neurons. Women slightly more affected than men. Blacks less than whites. Pain Characteristics Bandlike, Bilateral Extends from forehead to sides of temples Involves posterior neck in cape-like distribution HEADACHE 43 Tension Type Headache A person experiencing a tension-type headache, with pain extending from the back of the head and neck and spreading over the shoulders in a cape-like distribution. HEADACHE 44 Diagnosis TTH TTH is characterized by having at least two of the following four features: The location of the pain is bilateral in either the head or neck The quality of the pain is steady /dull (eg, pressing or tightening) and non-throbbing The intensity of the pain is mild to moderate There is no aggravation of the headache by normal physical activity HEADACHE 45 Acute Treatment - TTH First line – OTC analgesics (Paracetamol, NSAIDS) Second line – Aspirin + Paracetamol + Caffeine, butalbital (barbiturate) containing products High risk of rebound headache Limit acute treatment to 2-3 days per week. HEADACHE 46 Preventive Treatment - Chronic Consider for patients with > 15 headaches per month. Non-Pharmacologic Pharmacologic Proper sleep hygiene TCAS (best efficacy) Stress management SSRIs (better tolerated) Acupuncture Physical therapy Reassurance Avoidance of precipitating causes Massage & ice bags HEADACHE 47 The Headache Diary Keep a headache diary of related activities and triggers. Pain Score Characteristics of pain Associated Symptoms Acute treatment used and response Triggers HEADACHE 48  TENSION TYPE CLUSTER MIGRAINE A B C HEADACHE 49 HEADACHE 50 THANK YOU HEADACHE 51