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Headache types & management

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definition - types of headaches
symptoms & signs
Pathophysiology
-diagnosis and treatment of primary headache syndromes

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Headache types & management

  1. 1. HEADACHE Dr. Sameh Ahmad Muhamad abdelghany Lecturer Of Clinical Pharmacology Mansura Faculty of medicine
  2. 2. 2 CONTENTS 1 4 5 3 2 Diagnosis PREVENTION &TREATMENT INTRODUCTION TYPES PRIMARY HEADACHE SYNDROMES
  3. 3. 3 1 INTRODUCTION
  4. 4. 4 Introduction  Definition : A headache is a pain or discomfort in the head , scalp , or neck  One of the most common of all human physical complaints.  Headache is actually a symptom rather than a disease a stress response, vasodilation (migraine),skeletal muscle tension (tension headache), or a combination of factors.
  5. 5. 5 Worldwide problem  Up to 25% of adults have a severe headache each year  Up to 4% have daily or near-daily headache  Lifetime prevalence: 90% or more  Significant suffering and economic loss
  6. 6. 6 2 TYPES
  7. 7. 7 Classification I. PRIMARY HEADCHE  A headache that is not caused by another underlying disease, trauma or medical condition.  Accounts for about ninety percent of all headaches.
  8. 8. 8  Intrinsic dysfunction of the nervous system  Most patients presenting with headache have primary headache syndromes  Episodic headache: more common  Chronic headache: attacks occurring more frequently than 15 days/month for more than 6 months Cont.
  9. 9. 9  <2% of headaches in primary care offices  Caused by exogenous disorders: o Head trauma o Vascular disease o Neoplasms o Substance abuse or withdrawal o Infection/Inflammation o Metabolic disorders o others II. SECONDARY HEADCHE
  10. 10. 10 3 PRIMARY HEADACHE SYNDROMES
  11. 11. 11  PRIMARY HEADACHE SYNDROMES  Tension type headache  Migraine  Trigeminal Neuralgia  Cluster headache  Others
  12. 12. 12 I- TENSION TYPE  Most common-69%  Episodic or chronic  Primary disorder of CNS pain modulation  seen equally in both sexes
  13. 13. 13  Precipitating factors  Stress: usually occurs in the afternoon after long stressful work hours or after an exam  Sleep deprivation  Uncomfortable stressful position and/or bad posture  Irregular meal time (hunger)  Eyestrain  Caffeine withdrawal  Dehydration
  14. 14. 14 Symptoms & Signs  Gradual onset , radiate forward from occiput  Bilateral, dull, tight, band like pain  Less in morning, pain increase as day goes on  No accompanying N,V, throbbing, sensitivity to light, sound or movement
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  16. 16. 16  Management  Paracetamol,Aspirin,NSAIDs  Behavioral approach-relaxation  Chronic-amitriptyline
  17. 17. 17 II- MIGRAINE  2nd most common-16%  15% women and 6% men  Severe, episodic, unilateral,throbbing pain  Nausea,Vomiting  Sensitivity to light ,sound, movement  Genetic predisposition
  18. 18. 18 Pathophysiology  Different theories suggest different causes I. Vascular theory :  vasoconstriction followed by vasodilation with resulting in changes in blood flow causes the throbbing pain . II. Second theory :  pain results from muscular tension III. Biochemical changes:  changes in serotonin level
  19. 19. 19 Triggers  Flashing lights , Loud sounds , Strong odors  Stress  Hunger  Fatigue  Smoking  Menstruation , Pregnancy , Menopause , Oral Contraceptives  Sleep changes  Caffeine ,Chocolate ,Tyramine
  20. 20. 20 Classical Migraine or Migraine with AURA  Symptom Triad  Paroxysmal headache  nausea &/or vomiting  aura of focal neurological events(visual) 20-25%
  21. 21. 21  AURA:  Flashing lights, silvery zigzag lines moving across visual field over a period of 20 minutes  Sometimes leaving a trail of temporary visual field loss  Sometimes-Auditory ,Olfactory, gustatory hallucinations  Sensory aura-spreading front of tingling and numbness, from one body part to another
  22. 22. 22 Common Migraine or Migraine without AURA  Paroxysmal headache  Vomiting +/-  NO AURA
  23. 23. 23 Diagnosis  Simplified Diagnostic Criteria for MIGRAINE At least 2 of the following + At least 1 of the following: o Unilateral pain o Throbbing pain o Aggravation by movement o Moderate or severe intensity o Nausea/vomitting o Photophobia and phonophobia
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  25. 25. 25 Management  Non drug treatmenr  Preventive therapy  Abortive therapy
  26. 26. 26 Management  Non drug treatment  Avoid headache triggers: foods, drugs, activities  Avoid frequent abortive treatment  Stop smoking  Normalize sleeping and eating  Exercise  Relaxation and biofeedback  Psychotherapy
  27. 27. 27 Management  Preventive Treatment  Tricyclic antidepressants (first-line) o Amitriptyline  Beta-blockers (first-line) o Atenolol, nadolol  Ca++ channel blockers – less effective o Verapamil most commonly used
  28. 28. 28 Management  Preventive Treatment  Anticonvulsants (second-line; valuable)  Valproate and topiramate are quite effective  Gabapentin  Lamotrigine, levetiracetam  Pregabalin
  29. 29. 29 Management  Preventive Treatment  Ergots: Rarely used for prevention o Side effects may be problematic o Methysergide: fibrosis (use 6 months max)  MAOIs: Can be very effective o Tyramine-free diet a must o Numerous drug interactions
  30. 30. 30 Management  Abortive Treatment  Simple and combined analgesics e.g NSAIDs.  Mixed analgesics (barbiturate plus simple analgesics)  Ergot derivatives  Triptans  Opioids
  31. 31. 31 Management  Triptans:  Serotonin 5-HT1 agonists  Reduce neurogenic inflammation  Most effective if used at onset of headache or aura, though may be helpful at other phases  Used specifically for migraine  For nonresponders, try ergots (also act on NE, DA, other receptors)
  32. 32. 32 Management  Other Agents  Antiemetics/Neuroleptics: o often combined with abortive agents o Prochlorperazine, hydroxyzine, promethazine, metoclopramide
  33. 33. 33  Drugs To Avoid  Butorphanol nasal spray  Meperidine  Overuse of any short-acting analgesic (opioids, triptans)
  34. 34. 34 III- Trigeminal Neuralgia  Lancinating pain in 2nd and 3rd divisions of trigeminal nerve  >50yrs  Severe, brief ,repetitive pain causing patient to flinch  Precipitated by touching trigger zones: washing, shaving, eating, cold wind
  35. 35. 35 Pathophysiology  Compression of trigeminal N by aberrant loop of cerebellar arteries as nerve enters brainstem  Other benign compressive lesions  Multiple sclerosis: occurs due to plaque of demyelination in trigeminal root entry zone
  36. 36. 36
  37. 37. 37 Management  Carbamazepine  Intolerant-Gabapentin/Pregabalin  Injection of alcohol into peripheral branch of nerve  Posterior craniotomy to relieve vascular compression of trigeminal nerve
  38. 38. 38 IV- CLUSTER HEADACHE  Headaches occur during a short time span.  The cluster then recurs periodically.  A typical cluster of headaches may last 4- 8weeks with 1-2 headaches/day during the cluster.  Patient may be free 6months to 1year before another cluster of headache occurs.  Male to Female ratio 5:1
  39. 39. 39 Symptoms & Signs  Abrupt onset of headache originating in the eye and spreading over the temporal area.  Pain extremely severe and last 20-60minutes  The headache associated with  Nasal stuffiness  Rhinorrhoea  Redness of the Eye  Flush and edema of the cheek
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  41. 41. 41 Management  Acute:  Oxygen inhalation 100%  Triptans/ergots  Indomethacin
  42. 42. 42 Management  Chronic/Preventive:  Verapamil, lithium  Valproate, topiramate  Prednisone burst  Melatonin  Ergots
  43. 43. 43 Medication Overuse Headache  Persistent, recurring headache in the setting of regular analgesic use  Continues until medication is stopped  Often responsible for “transformation” of episodic into chronic headache
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  46. 46. Thanks for Coming

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