Approach to Headache a practical approach.pptx

Approach to Headache a practical approach

1. A pproach to Headache

2. C ontents A natomy and Physiology C auses C lassification T ension type headache (TTH) Migraine Trigeminal Autonomic Cephalgia Other primary headache Danger signs Approach to Headache

3. Anatomy and Physiology There is NO pain receptors in the parenchyma Pain sensitive areas of Brain S calp M eningeal arteries D ural sinuses F alx cerebri P roximal segments of the Large pial arteries

4. The key structures involved in primary headache are the following: The large intracranial vessels and dura mater, and the peripheral terminals of the trigeminal nerve that innervate these structures. The caudal portion of the trigeminal nucleus, which extends into the dorsal horns of the upper cervical spinal cord and receives input from the first and second cervical nerve roots (the trigeminocervical complex) Rostral pain-processing regions, such as the ventroposteromedial thalamus and the cortex The pain-modulatory systems in the brain that modulate input from the trigeminal nociceptors at all levels of the pain-processing pathways and influence vegetative functions, such as the hypothalamus and brainstem

5. A classification system developed by the International Headache Society characterizes headache as P rimary S econdary Primary headaches are those in which headache and its associated features are the disorder itself, whereas secondary headaches are those caused by exogenous disorders. 5

6. INTERNATIONAL CLASSIFICATION OF HEADACHE (MODIFIED)

7. T ension type headache (TTH) M ost common type of headache F emale > Male (middle aged female : 30-45 years) O ne third of cases are associated with depression F ullness or tightness or pressure band which doesn’t affect daily activities T here is NO vomiting, photophobia, phonophobia P atient is never disturbed from sleep due to headache No evidence of papilledema during fundal examination Treatment : Acute attack: NSAIDS Chronic: Prophylaxis with Amitryptilline (TCA)

8. MIGRAINE HEADACHE Migraine, the second most common cause of headache , and the most common headache-related, and indeed neurologic, cause of disability in the world, afflicts ~15% of women and 6% of men over a 1-year period It is usually an episodic headache associated with certain features such as sensitivity to light, sound, or movement; nausea and vomiting often accompany the headache. 11

9. A migraine attack has three phases: Premonitory (Prodrome) Headache Phase Postdrome E ach has distinct and sometimes disabling symptoms, which may overlap About 20–25% of migraine patients have a fourth, aura, phase 12

10. Headache Can Be Initiated Or Amplified By Various Triggers Including Glare Bright Lights Sounds Hunger; Let-down From Stress; Physical Exertion Stormy Weather Or Barometric Pressure Changes Hormonal Fluctuations During Menses; Lack Of Or Excess Sleep; And Alcohol Or Other Chemical Stimulation

11. PATHOGENESIS OF MIGRAINE TRIGEMINOVASCULAR SYSTEM Small caliber pseudounipolar sensory neurons that originate from the trigeminal ganglion and upper cervical dorsal roots. These sensory neurons project to innervate large cerebral vessels, pial vessels, dura mater, and large venous sinuses. There is convergence of the projections from the upper cervical nerve roots and the trigeminal nerve at the trigeminal nucleus caudalis . From the trigeminal nucleus caudalis , fibers that are involved in the localization of pain ascend to the thalamus (mostly to the ventroposterior medial nucleus of the thalamus) and to the sensory cortex. 14

12. Other second-order neurons from the trigeminal nucleus caudalis project to numerous subcortical sites including the more rostral segments of the trigeminal complex the reticular formation of the brain stem , the cerebellum , the midbrain and pontine parabrachial nuclei, the ventrobasal thalamus, the posterior thalamus . Stimulation of the trigeminal ganglion results in release of vasoactive neuropeptides, including substance P, calcitonin gene-related peptide (CGRP), and neurokinin A . Release of these neuropeptides is associated with the process of neurogenic inflammation 15

13. DIAGNOSIS AND CLINICAL FEATURES 16

14. Patients with episodes of migraine on 8 or more days per month and with at least 15 total days of headache per month are considered to have chronic migraine Patients with acephalgic migraine experience recurrent neurologic symptoms often with nausea or vomiting, but with little or no headache. 17

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16. MIDAS (MIGRAINE DISABILITY ASSESSMENT SCORE 19

17. TREATMENT NON PHARMALOGICAL: A regulated lifestyle is helpful, including a healthy diet, regular exercise, regular sleep patterns, avoidance of excess caffeine and alcohol, and avoidance of acute changes in stress levels PHARMALOGICAL (ACUTE ATTACKS) Most drugs effective in the treatment of migraine are members of one of five major pharmacologic classes: nonsteroidal anti-inflammatory drugs ; 5-HT1B/1D receptor agonists— triptans ; CGRP receptor antagonists— gepants ; 5-HT1F receptor agonists— ditans ; and dopamine receptor antagonists. 20

18. NSAIDS 21

19. 5-HT 1B/1D RECEPTOR AGNONISTS-TRIPTANS 22

20. CGRP RECEPTOR ANTAGONIST-GEPANTS AND DITANS 23

21. DOPAMINE RECEPTOR ANTAGONISTS 24

22. OTHER TREATMENT 25

23. PREVENTIONS P reventive medication should be considered in patients with four or more attacks a month. Patients are usually started on a low dose of a chosen treatment; the dose is then gradually increased, up to a reasonable maximum, to achieve clinical benefit. Many patients are able to discontinue medication and experience fewer and milder attacks for long periods, suggesting that these drugs may alter the natural history of migraine The advent of CGRP monoclonal antibodies and CGRP receptor antagonists has significantly changed the landscape of preventive treatment 26

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25. Trigeminal Autonomic Cephalgia (TAC) The trigeminal autonomic cephalalgias (TACs) are a group of primary headache disorders that are characterized by strictly unilateral trigeminal distribution pain occurring in association with ipsilateral cranial autonomic symptoms. Unilateral severe headache (sharp stabbing) Restlessness during attack Episodes lasting 15 mins to 3 hours I t includes: Cluster headache Paroxysmal headache SUNCT (Short lasting unilateral neuralgic headache with conjunctival congestion and Tearing) Hemicrania continua

26. TAC- Autonomic Features Cluster headache, congestion and lacrimation N asal congestion a nd rhinorrhoea E yelid edema Forehead or facial swelling F ullness in ear F lushing P tosis / Miosis

27. Cluster Headache Unilateral, short lasting (15 mins to 3 hours, 1-8 attacks/day), Severe A utonomic symptoms Restlessness E pisodic headache (80%), Chronic (20%) P eriorbital region, stabbing or borin pain, Nocturnal pain P recipitated by alcohol Y oung male S ymptoms can last for 8-10 weeks leading to symptom free interval

28. T reatment of C l uster Headache A cute: 100 % Oxygen at 10 L/min for 10-15 mins or 6 mg s/c Sumatriptan Prophylaxis: Short term: Prevention steroids Long term: Verapamil or Lithium

29. P aroxysmal Headache E pisodic ,short lasting, severe, Unilateral headache R estlessness Autonomic symptoms M ale=female (middle aged) S tabbing / boring periorbital pain 5-20 attacks/day, each attack lasting 2-30 mins N o nocturnal preponderance R apid response to indomethacin N ot triggered by alcohol

30. SUNCT (Short lasting unilateral neuralgic headache with conjunctival congestion and Tearing) C onjuctival congestion and tearing Female > Male Each attack lasting for few seconds wi th multiple number of attacks Cutaneous trigger: No refractory periods Acute attacks: IV Lignocaine Prevention: Lamotrigine No migranous features Not triggered by alcohol

31. Hemicrania Continua C ontinuous, unilateral headache Elderly Female > Male A utonomic Symptoms I nvestigation of choice : MRI Responsive to Indomethacin

32. T rigeminal Neuralgia P aroxysms of intense, brief, shock like superficial pain along the distribution of trigeminal nerve lasting few seconds to minutes F emale > Male (50-60 years) U sually V2/V3 involved (ophthalmic division is not involved), objectiv neurological signs absent D iagnosis: 3D MRI Drug of choice: Carbamazepine, Lamotrigine, s/c botox

33. Secondary Headache: C l assification

34. references Harrisons (21st edition) Uptodate