![HEADACHE
MODERATOR:-Dr.ARUN JOSHI MD [HOD]
GENERAL MEDICINE
PRESENTED BY:-Dr.SUBEG SINGH PGJR2](https://image.slidesharecdn.com/headace-180116044704/85/Headace-1-320.jpg)
![Pathophysiology Of Headache
* Two Suggested Theories For The
Pathophysiology Of Headaches / Migraines :
[1]Old : The Vascular Theory :
Intracranial vasoconstriction is responsible for
the aura of the migraine.
Headache is results from the subsequent rebound
dilatation which leads to the activation of the
perivascular nociceptive nerves.](https://image.slidesharecdn.com/headace-180116044704/85/Headace-9-320.jpg)
![Pathophysiology Of Headache
- [2]New : The Neurological Theory :
- Headaches/ Migraines are triggered by a
complex series of neural and vascular events ,
due to Neuronal hyper-excitability in
the cerebral cortex, especially in the occipital
cortex.](https://image.slidesharecdn.com/headace-180116044704/85/Headace-10-320.jpg)
![TREATMENT
• 1. abortive
• 2.prophylactic
• [1]ABORTIVE
• Oxygen
The standard acute treatment of cluster headache
is inhalation of 100% oxygen by at a rate of 7 to 10
L/min for 15 to 25 minutes](https://image.slidesharecdn.com/headace-180116044704/85/Headace-45-320.jpg)
Headace
- 1. HEADACHE MODERATOR:-Dr.ARUN JOSHI MD [HOD] GENERAL MEDICINE PRESENTED BY:-Dr.SUBEG SINGH PGJR2
- 2. INTRODUCTION • Headache is among the most common reasons patients seek medical attention. • Primary headaches ▫ Recurrent ▫ Benign ▫ No organic disease as their cause • Secondary headaches ▫ Underlying organic disease
- 3. TYPES OF HEADACHE • Primary headache disorders are characterized by the lack of an identifiable and treatable underlying cause. • Migraine, tension-type, and cluster headaches are examples • Secondary headache disorders are those associated with a variety of organic causes such as trauma, cerebrovascular malformations, and brain tumors.
- 4. International Headache Society(IHS) • Migraine • Tension-Type • Cluster • Miscellaneous Headaches Unassociated with Structural Lesion (e.g., cold stimulus headache, benign exertional headache) • Headache Associated with Head Trauma • Headache Associated with Vascular Disorders • Headache Associated with Nonvascular Intracranial Disorder (e.g., high or low CSF pressure, intracranial infection, or neoplasm)
- 5. • Headache Associated with Substances or their Withdrawal (e.g., withdrawal from alcohol, caffeine,ergotamine, narcotics) • Headache Associated with Noncephalic Infection (e.g., viral or bacterial infection) • Headache Associated with Metabolic Disorder(e.g., hypoxia, hypercapnia, hypoglycemia, dialysis) • Headache or Facial Pain Associated with Disorder of Cranium, Neck, Eyes, Ears, Nose, Sinuses, Teeth,Mouth, or Other Facial or Cranial Structures • Cranial Neuralgias, Nerve Trunk Pain and Deafferentation Pain (e.g., compression, demyelination, infarction, or inflammation.
- 6. Common Causes of Headache • Primary Headache • Type % • Tension-type 69 • Migraine 16 • Idiopathic stabbing 2 • Exertional 1 • Cluster 0.1
- 7. Common Causes of Headache • Secondary Headache • Type % • Systemic infection 63 • Head injury 4 • Vascular disorders 1 • Subarachnoid hemorrhage <1 • Brain tumor 0.1
- 8. Anatomy and Physiology of Headache • Relatively few cranial structures are pain-producing; • the scalp, • middle meningeal artery, • dural sinuses, • falx cerebri, and • proximal segments of the large pial arteries. • The ventricular ependyma, choroid plexus, pial veins, and much of the brain parenchyma are not pain- producing.
- 9. Pathophysiology Of Headache * Two Suggested Theories For The Pathophysiology Of Headaches / Migraines : [1]Old : The Vascular Theory : Intracranial vasoconstriction is responsible for the aura of the migraine. Headache is results from the subsequent rebound dilatation which leads to the activation of the perivascular nociceptive nerves.
- 10. Pathophysiology Of Headache - [2]New : The Neurological Theory : - Headaches/ Migraines are triggered by a complex series of neural and vascular events , due to Neuronal hyper-excitability in the cerebral cortex, especially in the occipital cortex.
- 11. HISTORY IN HEADACHE • Character & Pattern. • Onset • Duration & Frequency. • Location & Radiation. • Severity / Intensity / Impact. • Relieving/ Aggravation Factors. • Relation To Actions Or Events. • Response To Treatment. • Associated Symptoms. • Previous Experience
- 12. PRIMARY HEADACHE SYNDROMES • Tension type headache • Migraine • Trigeminal Neuralgia • Atypical facial pain • Cluster headache • Benign paroxysmal headaches
- 13. TENSION TYPE • Most common-69% • Episodic or chronic • Gradual onset , radiate forward from occiput • Bilateral, dull, tight, band like pain • Less in morning, pain increase as day goes on • No accompanying Nausea & Vomiting, throbbing, sensitivity to light, sound or movement
- 14. Pathophysiology • Primary disorder of CNS pain modulation alone, unlike migraine, which involves a more generalized disturbance of sensory modulation. . • The name tension-type headache implies that pain is a product of nervous tension, but there is no clear evidence for tension as an etiology. • Muscle contraction has been considered to be a feature that distinguishes TTH from migraine, but there appear to be no differences in contraction between the two headache types.
- 15. • Primary disorder of CNS pain modulation • 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
- 16. 2 Theories Muscle tension around head and neck Malfunctioning pain filter located in brain stem, brain misinterprets information and interprets this signal as pain. One of the main neurotransmitters which is probably involved is serotonin
- 17. Management • Paracetamol,Aspirin,NSAIDs • Behavioral approach-relaxation • Amitriptyline
- 18. Treatment: Tension-Type Headache • The pain of TTH can generally be managed with simple analgesics such as acetaminophen, aspirin, or NSAIDs. • Behavioral approaches including relaxation can also be effective. • TRIPTANS in pure TTH are NOT HELPFUL, although triptans are effective in TTH when the patient also has migraine.
- 19. MIGRAINE • 2nd most common-16% • 15% women and 6% men • Severe, episodic, unilateral,throbbing pain • Nausea,Vomiting • Sensitivity to light ,sound, movement • Genetic predisposition
- 20. ©International Headache Society 2003/4ICHD-II. Cephalalgia 2004; 24 (Suppl 1) 1. Migraine 1.1 Migraine without aura 1.2 Migraine with aura 1.3 Childhood periodic syndromes that are commonly precursors of migraine 1.4 Retinal migraine 1.5 Complications of migraine 1.6 Probable migraine ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4 1. Migraine 1.1 Migraine without aura 1.2 Migraine with aura 1.3 Childhood periodic syndromes that are commonly precursors of migraine 1.4 Retinal migraine 1.5 Complications of migraine 1.6 Probable migraine
- 21. Classical Migraine or Migraine with AURA Symptom Triad Paroxysmal headache nausea &/or vomiting aura of focal neurological events(visual) 20-25%
- 22. 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
- 23. Rare aura: • Vertigo • Aphasia • Hemiparesis • Delirium Migraine with limb weakness-Hemiplegic migraine Symptoms of aura do not resolve leaving permanent neurological damage-Complicated migraine
- 24. Common Migraine or Migraine without AURA • Paroxysmal headache • Vomiting +/- • NO AURA
- 25. Simplified Diagnostic Criteria for MIGRAINE At least 2 of the following: + At least 1 of the following: • Unilateral pain • Throbbing pain • Aggravation by movement • Moderate or severe intensity • Nausea/vomitting • Photophobia and phonophobia
- 26. Clinical phases of a migraine attack Vulnerability Prodrome Aura Pain Postdrome Attack Initiation
- 27. Triggers • Flashing lights • Loud sounds • Strong odors • Stress • Hunger • Fatigue • Alcohol • Smoking • Menstruation • Pregnancy • Menopause • Oral Contraceptives • Sleep changes • Caffeine • Chocolate • Tyramine • MSG
- 28. Pathophysiology of Migraine • Cortical spreading depression • Vascular • Low Serotonin • Melanopsin receptor
- 29. Cortical spreading depression • Dysfunction of ion channels-Quick depolarization(activation) followed by long- lasting depression over an area of cortex • Release of inflammatory mediators • Irritation of cranial nerve roots-trigeminal
- 30. Vascular Vasoconstriction of blood vessels in brain-Aura (begins in occipital lobe) Vasodilatation of scalp blood vessels Inflammation Pain
- 31. Migraine Pain-Trigeminovascular • Key pathway for pain is trigeminovascular input from meningeal vessels • Modulation of trigeminovascular input comes from dorsal raphe nucleus, locus coeruleus and nucleus raphe magnus
- 32. Presymptomatic hyperexcitabilty increases brain stem response to triggers Release of Neurotransmitters (5-HT, NE, DA, GABA, Glutamate, NO, CGRP, Substance P, Estrogen) Neurotransmitters activate the Trigeminal Nucleus Dilation of Meningeal blood vessels (Throbbing) Activation of Area Postrema NAUSEA & VOMITING Activation of Cortex and Thalamus (Head pain) Activation of Hypothalamus (Hypersensitivity) Activation of cervical trigeminal system (Muscle spasm)
- 36. Management • Acute attack- aspirin/paracetamol+metoclopromide/ domperidone • Severe attack-Sumatriptan • Frequent attacks- Propranolol,Amitriptyline,Sodium valproate or Topiramate
- 37. MIGRAINE MANAGMENT Non pharmacological treatment • Identification of triggers • Meditation • Relax techniques • Psychotherapy Pharmacological treatment • Abortive treatment • Preventive treatment
- 38. INDICATION OF PROPHYLAXIS • Patients who have very frequent headaches (more than 2-3/week) • Attack duration> 48hrs • Headache severity is extreme • Migraine attacks are accompanied by severe aura • Contraindication to acute treatment • Unacceptable adverse effects occur with acute migraine treatment • Patients preference
- 40. CLUSTER HEADACHES • Cluster headaches derive their name from a characteristic pattern of recurrent headaches that are separated by periods of remission that last from months to even years. • During those periods when clusters of headaches are experienced, the headaches usually occur at least once daily. • The headache generally is unilateral, occurs behind the eye, reaches maximal intensity over several minutes, and lasts for <3 hours.
- 41. • Unilateral lacrimation, rhinorrhea, and facial flushing may accompany the cluster headache. • by alcohol, naps, and vasodilating drugs. • common in males than females.
- 43. Pathophysiology • Not commonly undestood. • The cyclic nature of attack implicates a pathogenesis of hypothalamic dysfunction with resulting alterations in circadian rhythms. • During a cluster headache, thermography shows increased peri-orbital heat emission ipsilateral to the head pain. • Also, patients commonly report flushing in the same area, and these observations suggest that extracranial vasodilation occurs. • Abnormal plasma levels of melatonin, growth hormone,testosterone, and prolactin have been reported
- 44. • occur commonly at night • Attacks occur suddenly, with pain peaking quickly after onset and generally lasting 15 to 180 minutes. • Auras are not present with cluster headaches. • The pain is excruciating, penetrating,and of a boring intensity in orbital, supraorbital, and temporal unilateral locations. • The headache can be accompanied by conjunctival injection, lacrimation, nasal stuffiness, rhinorrhea, eyelid edema, facial sweating, miosis/ptosis, and restlessness or agitation. • During the cluster period, attacks occur from once every other day to eight times per day
- 45. TREATMENT • 1. abortive • 2.prophylactic • [1]ABORTIVE • Oxygen The standard acute treatment of cluster headache is inhalation of 100% oxygen by at a rate of 7 to 10 L/min for 15 to 25 minutes
- 46. • Ergotamine Derivatives • All forms of ergotamine have been used • Intravenous dihydroergotamine results in the quickest response and repeated administration for 3 to 7 days can break the cycle of frequent cluster headache attacks. • Ergotamine tartrate also has provided effective relief sublingually or rectally
- 47. • TRIPTANS • The quick onset of subcutaneous and intranasal triptans make them safe and effective abortive agents for cluster headaches. • Subcutaneous sumatriptan (6 mg) is the most effective agent. • oral zolmitriptan(10 mg) also used
- 48. PROPHYLACTIC • Verapamil, the preferred calcium channel blocker for the preventionof cluster headaches, is effective in approximately 70% of patients. • The beneficial effects of verapamil often appear after 1week of therapy
- 49. • LITHIUM • Lithium carbonate is effective for episodic and chronic cluster headache attacks and can be used in combination with verapamil. • The usual dose is 600mg to 1.2g/day, • starting dose of 300 mg twice daily. • Initial side effects are mild and include tremor, lethargy, nausea,diarrhea, and abdominal discomfort
- 50. • ERGOTAMINE • an efficacious agent for prophylactic as well as abortive therapy of cluster headaches. • A 2mg bedtime dose is beneficial for the prevention of nocturnal headache attacks. • Daily use of 1 to 2 mg ergotamine alone or in combination with verapamil or lithium can provide effective prophylaxis in patients refractory to other agents
- 51. • MRTHYSERGIDE In patients unresponsive to other therapies, methysergide 4 to 8 mg/day in divided doses is usually effective in shortening the course of cluster headache. • CORTICOSTEROIDS • Corticosteroids are useful for inducing remission. • Therapy is initiated with 40 to 60 mg/day prednisone and tapered over approximately 3 weeks. • Relief appears within 1 to 2 days of initiating therapy ster headaches
- 52. 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
- 53. Pathophysiology • Compression of trigeminal N by aberrant loop of cerebellar arteries as nerve enters brainstem • Other benign compressive lesions • Multiple sclerosis- TN occurs due to plaque of demyelination in trigeminal root entry zone
- 54. Management • Carbamazepine-DOC • Intolerant-Gabapentin/Pregabalin • Injection of alcohol into peripheral branch of nerve • Posterior craniotomy to relieve vascular compression of trigeminal nerve
- 55. Atypical facial pain • Persistent idiopathic facial pain • Continuous, burning/crushing,unremittent, centred over maxilla usually left side • Middle aged women • Early form of trigeminal neuralgia • Rx-Amitriptyline, Gabapentin
- 56. Other causes of facial pain Sinusitis • Frontal-pain more in morning, decreases as day progresses, stooping and blowing nose increase pain • Ethmoid and Sphenoid-pain over vertex, less in morning and increase gradually
- 58. Post herpetic neuralgia-continuous, burning pain sensitive to light touch, shingles
- 59. REREFERENCES ERENCES • ADAMS & VICTOR’S Principles of Neurology 9th edition chapter 10 headache page no 162. • DAVIDSON’S Principles & Practice of Medicine 22nd edition chapter 26 page no 1156. • HARRISON’S Principles of Internal Medicine 19th edition chapter 21 page no 107 volume 1. • API TEXT BOOK OF MEDICINE 10th edition part 2 volume 1 page no 25.
- 60. THANK YOU