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Headache Very common; Very common; Sensitive people; highly competitive; perfectionistic; Sensitive people; highly competitive; perfectionistic; rigid.

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Presentation on theme: "Headache Very common; Very common; Sensitive people; highly competitive; perfectionistic; Sensitive people; highly competitive; perfectionistic; rigid."— Presentation transcript:

1 Headache Very common; Very common; Sensitive people; highly competitive; perfectionistic; Sensitive people; highly competitive; perfectionistic; rigid control in dealing with life situatn rigid control in dealing with life situatn over respond to stress producing situations; over respond to stress producing situations; difficulty in adjusting to stress of life difficulty in adjusting to stress of life probably the most common human complaint - most prevalent neurologic symptom associated with any dx probably the most common human complaint - most prevalent neurologic symptom associated with any dx

2 Headache Headache DEFINITION DEFINITION CLASSIFICATION AND CAUSES CLASSIFICATION AND CAUSES PATHO PHYSIOLOGY PATHO PHYSIOLOGY INVESTIGATIONS INVESTIGATIONS MANAGEMENT MANAGEMENT

3 Definition Head ache / Pain Head ache / Pain cephalalgia cephalalgia

4 CLASSIFICATION Diagnosis Diagnosis good clinical management good clinical management Research Research epidemiologic studies epidemiologic studies clinical trials clinical trials IHS classification in 1988 IHS classification in 1988 Revised in 2004 (ICHD-2) Revised in 2004 (ICHD-2) On-going revision.. On-going revision.. 4

5 5 The International Classification of Headache Disorders - II Part one: The primary headaches Part one: The primary headaches Part two: The secondary headaches Part two: The secondary headaches Part three: Cranial neuralgias, central and primary facial pain, and other headaches Part three: Cranial neuralgias, central and primary facial pain, and other headaches

6 6 The primary headaches 1. Migraine 2. Tension-type headache (TTH) 3. Cluster headache and other trigeminal autonomic cephalalgias 4. Other primary headaches

7 7 The secondary headaches 5. Headache attributed to head and/or neck trauma 6. Headache attributed to cranial or cervical vascular disorder 7. Headache attributed to non-vascular intracranial disorder 8. Headache attributed to a substance or its withdrawal 9. Headache attributed to infection 10. Headache attributed to disorder of homoeostasis 11. Headache or facial pain attributed to disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth, or other facial or cranial structures 12. Headache attributed to psychiatric disorder

8 8 Cranial neuralgias, central and primary facial pain, and other headaches 13. Cranial neuralgias and central causes of facial pain 14. Other headache, cranial neuralgia, central or primary facial pain

9 9 4. Other primary headaches 4.1 Primary stabbing headache 4.2 Primary cough headache 4.3 Primary exertional headache 4.4 Primary headache associated with sexual activity Preorgasmic headache Orgasmic headache 4.5 Hypnic headache 4.6 Primary thunderclap headache 4.7 Hemicrania continua 4.8 New daily-persistent headache

10 Classification Headache classification committee of Headache classification committee of I.H.S. I.H.S. (International Headache society) 1988 (International Headache society) 1988 MIGRAINE HEADACHE MIGRAINE HEADACHE TENSION HEADACHE TENSION HEADACHE CLUSTER (M. Neuralgia) SYNDROME CLUSTER (M. Neuralgia) SYNDROME

11 Headache Classification Headache Classification H. assoc with non-haemorrhagic arterial / arteriolar disorder. Temporal/Giant arteritis) H. assoc with non-haemorrhagic arterial / arteriolar disorder. Temporal/Giant arteritis) H. assoc with abuse/withdrawal of substances H. assoc with abuse/withdrawal of substances.> 45g Aspirin; 300mg of valium monthly; Alcohol.> 45g Aspirin; 300mg of valium monthly; Alcohol H. assoc with systemic infection or focal infection outside Head H. assoc with systemic infection or focal infection outside Head H. assoc with metabolic abnormality H. assoc with metabolic abnormality H or facial pain from cranium; eye; ENT. H or facial pain from cranium; eye; ENT. CRANIAL NEURALGIA & Other types of Headache. CRANIAL NEURALGIA & Other types of Headache. Post traumatic ; S.O.L; H in depression. Post traumatic ; S.O.L; H in depression. Referred pain ; Benign coital headache. Referred pain ; Benign coital headache. Cervico-genic H ;Traction H; Cough H. Cervico-genic H ;Traction H; Cough H. Post-lumbar puncture H. (starts > 48hrs; worse on standing up Post-lumbar puncture H. (starts > 48hrs; worse on standing up

12 Migraine 10% adult; > in females; 10% adult; > in females; autosomal dominant + incomplete penetrance autosomal dominant + incomplete penetrance defn: episodic disorder manifest. by H. defn: episodic disorder manifest. by H. accompanied by anorexia; N&V; photo / phonophobia. accompanied by anorexia; N&V; photo / phonophobia. lasts 4-72 hrs; < 2 ce a week. lasts 4-72 hrs; < 2 ce a week. ATTRIBUTES TO ESTABLISH Diagnosis ATTRIBUTES TO ESTABLISH Diagnosis ≥ 2 of the ff ≥ 2 of the ff.Unilateral location.Unilateral location.Pulsatile quality.Pulsatile quality.Moderate to severe intensity.Moderate to severe intensity.exacerbation by physical activity.exacerbation by physical activity > 1 of ff must accompany > 1 of ff must accompany. N/V; Photo / phonophobia. N/V; Photo / phonophobia

13 Subdivisions of M.H (modified by OLSER & GOADSBY 1996) M with AURA 10% [CLASSIC M] M without AURA 85% [COMMON] M with prolonged unilateral sensory/motor deficit sensory/motor deficit Familial Hemiplegic M. 60% family hx. Opthalmoplegic M. (?Post comm-artery). BASILAR M [aura:vertigo;dysarthria/tinnitus/diplopia/at axia [aura:vertigo;dysarthria/tinnitus/diplopia/at axia M. Equivalents (acephalic M) : No Headache / No vomiting No vomiting ABDOMINAL M./episodic transient disturbance CARDIAC M. responds to prophylatic treatment for M.

14 Aura Consists of well defined transient focal neurologic dysfunction in clear consciousness Consists of well defined transient focal neurologic dysfunction in clear consciousness devs over the course of > 4 mins & lasts 4 mins & lasts < hr. Visual disorder Visual disorder see stripes/spots/lines; fortification spectra/scotoma see stripes/spots/lines; fortification spectra/scotoma unilateral paraesthesia / numbness unilateral paraesthesia / numbness Unilateral weakness Unilateral weakness Aphasia or other speech disorder Aphasia or other speech disorder precede /appear or recur at height of H. precede /appear or recur at height of H.

15 Prodromal symptoms.Begins insidiously Lasts several hours  days Lasts several hours  days characteristically involves characteristically involves Changes in mood / behaviour ; cognitive disturbance ; fatigue ; depression; elation; insomnia; somnolence ; hunger ; thirst ; oliguria ; altered libido ; > urinary frequency. Changes in mood / behaviour ; cognitive disturbance ; fatigue ; depression; elation; insomnia; somnolence ; hunger ; thirst ; oliguria ; altered libido ; > urinary frequency. Depression + lassitude  most common Depression + lassitude  most common Feeling of well being; augmented energy and clarity of thought ; > appetite especially for sweet. Feeling of well being; augmented energy and clarity of thought ; > appetite especially for sweet.

16 Tension Headache (Muscle Tension H) HATBAND distribution; HATBAND distribution; pp ; tightness sensation of wearing tight cap, pressing; pp ; tightness sensation of wearing tight cap, pressing; non pulsatile ; non pulsatile ; bilateral bilateral Tender spots / in neck scalp - accentuate H Tender spots / in neck scalp - accentuate H worse in the evening. worse in the evening. Not worsen with routine physical activity Not worsen with routine physical activity Not prevent sleep Not prevent sleep Does not awaken patient Does not awaken patient No nausea / vomiting No nausea / vomiting Photphobia / Sonophobia may be present Photphobia / Sonophobia may be present H > 2 ce/wk  T.H. not migraine H > 2 ce/wk  T.H. not migraine Episodic T.H. / Chronic T.H. Episodic T.H. / Chronic T.H.

17 Cluster Headache (Migraneous Neuralgia) Lasts 8-12/52; with remission of M Lasts 8-12/52; with remission of M Periodicity Periodicity lasts 45mins  3 hours lasts 45mins  3 hours Common in males; middle aged 30 – 50 yrs Common in males; middle aged 30 – 50 yrs Alcohol Provokes Alcohol Provokes unilateral; orbital area / supra-orbital / peri-orbital, temporal area unilateral; orbital area / supra-orbital / peri-orbital, temporal area conjuctival injection / flushing of face conjuctival injection / flushing of face nasal stuffiness; Rhinnorhea; nasal stuffiness; Rhinnorhea; lacrimation / tearing lacrimation / tearing Fore-head / Facial sweating; eyelid oedema Fore-head / Facial sweating; eyelid oedema ptosis + ; Miosis + (Horner’s syndrome) ptosis + ; Miosis + (Horner’s syndrome) Most patients are restless or agitated during an attack. Most patients are restless or agitated during an attack.

18 18 3. Cluster headache and other trigeminal autonomic cephalalgias 3.1 Cluster headache 3.2 Paroxysmal hemicrania 3.3 Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) 3.4 Probable trigeminal autonomic cephalalgia

19 Pathophysiology PAIN inducing structures: PAIN inducing structures: Skin, subcutaneous tissue; muscle Skin, subcutaneous tissue; muscle (pericranium / periosteum of skull (pericranium / periosteum of skull tissue of eye, ENT & nasal sinuses; tissue of eye, ENT & nasal sinuses; vessels vessels V - > tentorium = ant cranium V - > tentorium = ant cranium IX / X – Ear / Throat. IX / X – Ear / Throat. 1 st 3 cervical  Post fossae 1 st 3 cervical  Post fossae

20 Serotonin - 5 HT plays role centrally in pain perception & CBF regulation plays role centrally in pain perception & CBF regulation Serotonin receptors in Serotonin receptors in 1) Cranial blood vessel (large – constrict; small – dilate). 1) Cranial blood vessel (large – constrict; small – dilate). 2) Central Neurons 2) Central Neurons 3) Dorsal raphe Nucleus and trigeminal Nuclei in brainstem - 3) Dorsal raphe Nucleus and trigeminal Nuclei in brainstem - (high concentration) (high concentration) ( Low central serotonin syndrome) ( Low central serotonin syndrome) < Platelet Serotonin content reflects change in central serotonergic activity < Platelet Serotonin content reflects change in central serotonergic activity at onset of headache  at onset of headache  < 5HT and < urinary excretion of its metabolites – < 5HT and < urinary excretion of its metabolites – > 5HIAA > 5HIAA

21 Serotonin All in all  14 HT receptors 1-7 All in all  14 HT receptors 1-7 Serotonin receptors  7 Serotonin receptors  7  5 sub class  5 sub class 1DB  vascular - involved in Migraine 1DB  vascular - involved in Migraine ID&  Neuronal ID&  Neuronal 1A: ID&; IDB; IE; IF; 1A: ID&; IDB; IE; IF; 2A: 2B; 2C (HT2 – Prophylactic anti-migraine) 2A: 2B; 2C (HT2 – Prophylactic anti-migraine) 5A: 5B 5A: 5B Others 1 each. 3,4,6,7 Others 1 each. 3,4,6,7 (HT3 - analgesic) (HT3 - analgesic)

22 5/5/ Pain Neurotransmitters Sub P+ / 5HT- / NR+ Sub-P : Neurohormone/transmitter/modulator Sub-P : Neurohormone/transmitter/modulator released by central process of DRG at the synapse in S. gelatinosa. released by central process of DRG at the synapse in S. gelatinosa. Vasodilatator Vasodilatator Degranulates mast cells Degranulates mast cells Chemoattractants for leukocytes Chemoattractants for leukocytes >production and release of inflammatory mediators >production and release of inflammatory mediators (Pro-inflamatory substances) (Pro-inflamatory substances) Neurogenic inflammation Neurogenic inflammation

23 5/5/ HT 5-HT 3 : inhibitory from PMP 5-HT 3 : inhibitory from PMP (Pain Modulation Pathway)descending (Pain Modulation Pathway)descending cf PTP (Pain Transmission Pathway) - ascending cf PTP (Pain Transmission Pathway) - ascending NR – inhibitory from PMP NR – inhibitory from PMP but activates / sensitizes nociceptors but activates / sensitizes nociceptors Bradykinin enhances stimulatn of C-fib Bradykinin enhances stimulatn of C-fib PMP inhibits S.C.P.N by PMP inhibits S.C.P.N by inhibitory transmitters from PMP (5HT) or excitation of inhibitory enkephalinergic interneurons. inhibitory transmitters from PMP (5HT) or excitation of inhibitory enkephalinergic interneurons.

24 Theories of Migraine (1. Cerebrovascular) AV shunts (opening) AV shunts (opening) instability of vessel vasoconstriction/dilatation instability of vessel vasoconstriction/dilatation excessive dilatation of arteries in Meninges excessive dilatation of arteries in Meninges

25 Theoriesof Migraine ( 2. Neurogenic - Cerebroparnchymal) 2. NEUROGENIC THEORY (Moskowitz) (Cerebroparenchymal) 2. NEUROGENIC THEORY (Moskowitz) (Cerebroparenchymal) PRODROME:- Hypothalamic PRODROME:- Hypothalamic AURA – LEAO’S spreading cortical depression and vascular changes AURA – LEAO’S spreading cortical depression and vascular changes Does not ff a vascular territory - spreading oligaemia 3ml/min or 2mm/min Does not ff a vascular territory - spreading oligaemia 3ml/min or 2mm/min

26 26 Initiating Mechanisms of Headache Pain: Cortical Spreading Depression  Wave of intense cortical neuron activity –↑ rCBF  Followed by neuronal suppression –↓ rCBF  Velocity: 2–3 mm/min  Underlies visual aura rCBF = regional cerebral blood flow. Adapted with permission from Hadjikhani N, Sanchez del-Rio M, et al. Mechanisms of migraine aura revealed by functional MRI in human visual cortex. Proc Natl Acad Sci U S A. 2001;98: Copyright 2001 National Academy of Sciences, U.S.A. Pietrobon D. Neuroscientist. 2005;11:373–386; Goadsby PJ et al. N Engl J Med. 2002;346:257–270. Time(s) Occipital cortex

27 Theories of Migraine ( 3. Trigemino-vascular) Theories of Migraine ( 3. Trigemino-vascular) Headache  Neurogenic inflammation antidromic stimulation of Trigeminal Nucleus antidromic stimulation of Trigeminal Nucleus Neuropeptides – substance P; Neurokinin A and Calcitonin – G- Related Protein. Neuropeptides – substance P; Neurokinin A and Calcitonin – G- Related Protein. Nitric oxide; Glutamate Nitric oxide; Glutamate M.H. AND T.H.  Same pathogenesis M.H. AND T.H.  Same pathogenesis Sudden drop level of 5HT  Migraine in BS. Sudden drop level of 5HT  Migraine in BS. Chronic Low Level of 5HT in T.H (v. low) Chronic Low Level of 5HT in T.H (v. low) not due to muscle contraction- also fd in M. not due to muscle contraction- also fd in M.

28 TRIGEMINO VASCULAR HYPOTHESIS. Release of Neuropeptides (CGRP; Sub P & Neurokinin A; NO ; Glutamate) Release of Neuropeptides (CGRP; Sub P & Neurokinin A; NO ; Glutamate) which act as neurotrammiters of Trigeminal N branches which act as neurotrammiters of Trigeminal N branches leads to inflammatory process leads to inflammatory process (Neurogenic inflammation) (Neurogenic inflammation) plasma extravasation and vasodilatation plasma extravasation and vasodilatation Increased permeability Increased permeability IDb receptor IDb receptor Agents acting on ID (stimulator)  prevent release of peptides (not histamine) Agents acting on ID (stimulator)  prevent release of peptides (not histamine)

29

30 Approach to Treatment > 5HT receptor agonist > 5HT receptor agonist Non- 5HT receptor agonist Non- 5HT receptor agonist e.g Rά - methyl histamine (e.g somatostatin) e.g Rά - methyl histamine (e.g somatostatin) Neurokinin receptor antagonist Neurokinin receptor antagonist CGRP receptor antagonist CGRP receptor antagonist

31 31 Dura Migraine Pathophysiology: Central Role of the Trigeminovascular System Trigeminal nerves TNC CSD = cortical spreading depression; TNC = trigeminal nucleus caudalis. Pietrobon D et al. Nat Rev Neuro. 2003;4:386–398. PAIN CSD TGVS activated

32 32 Initiating Mechanisms of Migraine: Brainstem Dysfunction Dysfunction in areas involved in central control of nociception - PAG Dysfunction in areas involved in central control of nociception - PAG Induces migraine? Induces migraine? –Brainstem generator Facilitates activation and sensitization of TNC neurons? Facilitates activation and sensitization of TNC neurons? –Decreased descending inhibition during a migraine attack PAG = periaqueductal gray region Adapted with permission from Pietrobon D. Nat Rev Neurosci. 2003;4:386–398. PAG TGVS activation HEADACHE Substance P

33 33 Low threshold to abnormal cortical activity Cortical Spreading Depression The Primary Cause of Migraine Headache Lies in the Brain Cortical neuronal hyperexcitability and/or brainstem dysfunction Activation & sensitization of the TGVS Prolonged headache pain of migraine Genetic predisposition in some patients Trigger

34 34 Migraine Pathophysiology: Proposed Mechanisms AuraCSD Cortical neuronal hyperexcitability Activation and peripheral sensitization of TGVS Neurogenic inflammation Central sensitization HEADACHE ? + + Genetic predisposition Migraine initiation Pain generation/ perpetuation Abnormal brainstem function

35 Cluster Headache Hypothalamic dysfn Hypothalamic dysfn Post. Hypothalamic  Autonomic Post. Hypothalamic  Autonomic Ant. Hypothalamic  biologic clock Ant. Hypothalamic  biologic clock Hypoxaemia – Carotid body chemo receptor dysfn Hypoxaemia – Carotid body chemo receptor dysfn Periodic discharge by TVS Periodic discharge by TVS Changes in level of cortisol; melantonin; prolactin ; B- endorphin. Changes in level of cortisol; melantonin; prolactin ; B- endorphin.

36 Diagnosis - Investigations a clinical problem: a clinical problem: Solved by taking a careful medical history. Solved by taking a careful medical history. Not need Not need.EEG / SKULL X-ray.EEG / SKULL X-ray.Isotope Brain scan.Isotope Brain scan.CAT.CAT except if suspect Brain T or Surgery. except if suspect Brain T or Surgery.

37 Diagnosis - History psychological and environmental background. psychological and environmental background. family history, age of onset; head injury behavioural changes, environmental stress. family history, age of onset; head injury behavioural changes, environmental stress. Time, duration. Time, duration. Chracteristics Chracteristics.Visual/sensory somatic syndrome.Visual/sensory somatic syndrome.Location  ? vascular malformation if.Location  ? vascular malformation if same side same side Throbbing/Stabbing/Steady ache Throbbing/Stabbing/Steady ache Assoc symptoms  N/V/photo/Phonophobia; Assoc symptoms  N/V/photo/Phonophobia; conjuctival injection; lacrimation; flushing of face. conjuctival injection; lacrimation; flushing of face.

38 History - predisposing factors familial; pills; menses familial; pills; menses and other ppt factors / provocative and other ppt factors / provocative Alcohol Alcohol Food  cheese, chocolate, orange/tomatoes Food  cheese, chocolate, orange/tomatoes Physical & mental stress Physical & mental stress Relaxation after stress Relaxation after stress Absence of food; Hormonal variation Absence of food; Hormonal variation Red wine; Bright light; insomnia Red wine; Bright light; insomnia

39 Treatment – mild attack Treat underlying problem ACUTE ATTACK (ABORTIVE) ACUTE ATTACK (ABORTIVE) Simple Measures Simple Measures Darkened room Darkened room ANALGESICS ANALGESICS ASPIRIN / PROPOXYPHENE HCL ASPIRIN / PROPOXYPHENE HCL NAPROXEN/ IBUPROFEN/PARACETAMOL NAPROXEN/ IBUPROFEN/PARACETAMOL ISOMETHAPTENE (MIDRIN) ISOMETHAPTENE (MIDRIN)

40 Treatment – abortive / prophylaxis Acute treatment Acute treatment  HTIDb  presynaptic  HTIDb  presynaptic prophylactic prophylactic  HT2  post synaptic  HT2  post synaptic

41 Treatment - more severe attack 1928: ERGOTAMINE – 5HT1 receptor 1928: ERGOTAMINE – 5HT1 receptor Inhibit 5HT2 ; Stimulate 5HT1 Inhibit 5HT2 ; Stimulate 5HT1.Sublingual.Sublingual.Oral.Oral.Rectal.Rectal.Inhalation.Inhalation 1-2mg taken early in attack preferably at onset of prodromal symptoms. 1-2mg taken early in attack preferably at onset of prodromal symptoms. Repeat > 30mins Repeat > 30mins Repeated doses thereafter useless / harmful. Repeated doses thereafter useless / harmful. Max dose 10-12mg/wk Max dose 10-12mg/wk

42 Ergotamine – adverse effects vomiting - use as suppository vomiting - use as suppository Muscle cramps: peripheral tingling and gangrene Muscle cramps: peripheral tingling and gangrene C.I.  Peripheral Vascular Disease. C.I.  Peripheral Vascular Disease. added caffeine (Cafegot) added caffeine (Cafegot) Raynauds Phenomenon Raynauds Phenomenon Dihydro ergotamine -- HT1D agonist Dihydro ergotamine -- HT1D agonist.S.C./I.V/I.M.S.C./I.V/I.M.

43 Sumatriptan Has antiemetic effect Has antiemetic effect Rapid absorbtion Rapid absorbtion 5HTID receptor agonist 5HTID receptor agonist Orally / parenterally Orally / parenterally

44 Prophylaxis.AVOID TRIGGER FACTORS.AVOID TRIGGER FACTORS Food ; stress Food ; stress.Life style changes..Life style changes. Physical / occupation Rx Physical / occupation Rx.Drug treatment if > 3 attacks / mth.Drug treatment if > 3 attacks / mth

45 Prophylaxis 5HT2 receptors antagonist PROMETHAZINE 25mg PROMETHAZINE 25mg B- BLOCKERS B- BLOCKERS PROPRANOLOL 20mg bd – 80mg tds; PROPRANOLOL 20mg bd – 80mg tds; ATENOLOL; NADOLOL; TIMOLOL ATENOLOL; NADOLOL; TIMOLOL TRICYCLIC ANTIDEPRESSANTS TRICYCLIC ANTIDEPRESSANTS. Amitryptilline. Amitryptilline. Low dose: > 1/12 for effect. Low dose: > 1/12 for effect.Nortriptyline; b-Blockers.Nortriptyline; b-Blockers Prevents reuptake – 5HT1 Prevents reuptake – 5HT1 Blocks 5HT2 Blocks 5HT2

46 Prophylaxis PIZOTIFEN (SANDO MIGRAINE) mg t.d.s. – 5HT 2 receptor blockade PIZOTIFEN (SANDO MIGRAINE) mg t.d.s. – 5HT 2 receptor blockade CLONIDINE 25 ug bd – 50ug tds CLONIDINE 25 ug bd – 50ug tds Site of action  uncertain - ? central vasomotor blockade or direct action on vessel wall Site of action  uncertain - ? central vasomotor blockade or direct action on vessel wall CALCIUM – CHANNEL BLOCKERS CALCIUM – CHANNEL BLOCKERS Prevent Ca influx induced by 5HT. Prevent Ca influx induced by 5HT. Verapamil Verapamil Nifedipine Nifedipine Diltiazem Diltiazem Flunarizine Flunarizine

47 Prophylaxis – serotonin antagonists Cyproheptadine Cyproheptadine MAO Inhibitor (phenelzine) 15mg tds MAO Inhibitor (phenelzine) 15mg tds Aspirin Aspirin Methysergide 1mg/d  2mg/d Methysergide 1mg/d  2mg/d (Retro peritoneal fibrosis) (Retro peritoneal fibrosis)

48 Other treatment short course steroid short course steroid Neuroleptics Neuroleptics Occipital Nerve block Occipital Nerve block

49 Fig 1 Midbrain / brain stem Midbrain / brain stem forebrain forebrain Low 5HT  Excitatory Low 5HT  Excitatory Excess 5HT – inhibitory at synapse Excess 5HT – inhibitory at synapse

50 Treatment – Tension H Same Treatment Same Treatment No place for No place for Anxiolytic Anxiolytic muscle relaxant muscle relaxant

51 Treatment - CLUSTER H abortive.O %.O %.ERGOTAMINE.ERGOTAMINE.Dihydroergotamine.Dihydroergotamine.Sumatriptan.Sumatriptan.Corticosteroids.Corticosteroids.Local anaesthetic.Local anaesthetic.4% xylocaine -instil in Nostril.4% xylocaine -instil in Nostril.Sphenopalatine ganglian block.Sphenopalatine ganglian block

52 Treatment – Cluster H prophylaxis Ca 2+ channel blocker - Verapami Lithium carbonate Methysergide Steroids - Predinsolone 40 – 80mg/d

53 NEWER TREATMENT – Cluster H Valproate Valproate Nerve blockers Nerve blockers Light treatment Light treatment expose patient to light change expose patient to light change circadian rhythm circadian rhythm

54 Prognosis Good Good except if symptomatic migraine except if symptomatic migraine due to due to cerebrovascular malformation cerebrovascular malformation Cererovascular angioma. Cererovascular angioma. Cerebrovascular aneurysm Cerebrovascular aneurysm

55 55 1. Migraine 1.1 Migraine without aura 1.2 Migraine with aura 1.3 Childhood periodic syndromes that are commonly precursors of migraine commonly precursors of migraine 1.4 Retinal migraine 1.5 Complications of migraine 1.6 Probable migraine

56 Migraine without aura A recurrent headache disorder manifesting in attacks lasting 4-72 hours. A recurrent headache disorder manifesting in attacks lasting 4-72 hours. Typical characteristics of the headache are unilateral location, pulsating quality, moderate or severe intensity, aggravation by routine physical activity and association with nausea and/or photophobia and phonophobia. Typical characteristics of the headache are unilateral location, pulsating quality, moderate or severe intensity, aggravation by routine physical activity and association with nausea and/or photophobia and phonophobia.

57 57 IHS Diagnostic Criteria for Migraine without aura A. At least 5 attacks fulfilling criteria B through D B. Headache attacks lasting 4-72 hrs (untreated or unsuccessfully treated) C. Headache has at least two of the following characteristics: 1. Unilateral location 2. Pulsating quality 3. Moderate or severe pain intensity 4. Aggravation by or causing avoidance of routine physical activity (eg, climbing stairs) D. During headache at least 1 of the following: 1. Nausea and/or vomiting 2. Photophobia and phonophobia E. Not attributed to another disorder

58 Migraine with aura A recurrent disorder manifesting in attacks of reversible focal neurological symptoms that usually develop gradually over 5-20 minutes and last for less than 60 minutes. A recurrent disorder manifesting in attacks of reversible focal neurological symptoms that usually develop gradually over 5-20 minutes and last for less than 60 minutes. Headache with the features of migraine without aura usually follows the aura symptoms. Headache with the features of migraine without aura usually follows the aura symptoms. Headache may be absent. Headache may be absent.

59 Migraine with aura Typical aura with migraine headache Typical aura with non-migraine headache Typical aura without headache Familial hemiplegic migraine Sporadic hemiplegic migraine Basilar-type migraine

60 60 IHS Diagnostic Criteria for Migraine with aura A. At least 2 attacks fulfilling criteria B through D B. Aura consisting of at least one of the following but no motor weakness: 1. fully reversible visual symptoms including positive features (eg, flickering lights, spots or lines) and/or negative features (ie,loss of vision) 1. fully reversible visual symptoms including positive features (eg, flickering lights, spots or lines) and/or negative features (ie,loss of vision) 2. fully reversible sensory symptoms including positive features (ie, pins and needles) and/or negative features (ie, numbness) 2. fully reversible sensory symptoms including positive features (ie, pins and needles) and/or negative features (ie, numbness) 3. fully reversible dysphasic speech disturbance 3. fully reversible dysphasic speech disturbance C. At least two of the following: 1. homonymous visual symptoms and/or unilateral sensory symptoms 1. homonymous visual symptoms and/or unilateral sensory symptoms 2. at least one aura symptom develops gradually over ≥5 minutes and/or different aura symptoms occur in succession over ≥5 minutes 2. at least one aura symptom develops gradually over ≥5 minutes and/or different aura symptoms occur in succession over ≥5 minutes 3. each symptom lasts ≥5 and ≤60 minutes 3. each symptom lasts ≥5 and ≤60 minutes D. Headache fulfilling criteria B-D for Migraine without aura begins during the aura or follows aura within 60 minutes E. Not attributable to another disorder

61 61 2. Tension-type headache (TTH) 2.1 Infrequent episodic TTH 2.2 Frequent episodic TTH 2.3 Chronic TTH 2.4 Probable TTH

62 Infrequent episodic TTH Infrequent episodes of headache lasting minutes to days. Infrequent episodes of headache lasting minutes to days. The pain is typically bilateral, pressing or tightening in quality and of mild to moderate intensity, and does not worsen with routine physical activity. The pain is typically bilateral, pressing or tightening in quality and of mild to moderate intensity, and does not worsen with routine physical activity. There is no nausea but photophobia or phonophobia may be present. There is no nausea but photophobia or phonophobia may be present.

63 63 IHS Diagnostic Criteria for Infrequent Episodic TTH A.At least 10 episodes occurring on <1 day per month on average (<12 days per year) and fulfilling criteria B through D B. Headache lasting from 30 mins to 7 days C. Headache has at least two of the following characteristics: 1. bilateral location 2. pressing/tightening (non-pulsating) quality 3. mild or moderate intensity 4. not aggravated by routine physical activity such as walking or climbing stairs D. Both of the following: 1. no nausea or vomiting (anorexia may occur) 2. no more than one of photophobia or phonophobia E. Not attributed to another disorder

64 Frequent episodic TTH Frequent episodes of headache lasting minutes to days. Frequent episodes of headache lasting minutes to days. The pain is typically bilateral, pressing or tightening in quality and of mild to moderate intensity, and does not worsen with routine physical activity. The pain is typically bilateral, pressing or tightening in quality and of mild to moderate intensity, and does not worsen with routine physical activity. There is no nausea but photophobia or phonophobia may be present. There is no nausea but photophobia or phonophobia may be present.

65 65 IHS Diagnostic Criteria for frequent Episodic TTH A.At least 10 episodes occurring on ≥1 but <15 days per month for at least 3 months (≥12 and <180 days per year) and fulfilling criteria B through D B. Headache lasting from 30 mins to 7 days C. Headache has at least two of the following characteristics: 1. bilateral location 2. pressing/tightening (non-pulsating) quality 3. mild or moderate intensity 4. not aggravated by routine physical activity such as walking or climbing stairs D. Both of the following: 1. no nausea or vomiting (anorexia may occur) 2. no more than one of photophobia or phonophobia E. Not attributed to another disorder

66 Chronic TTH A disorder evolving from episodic tension-type headache, with daily or very frequent episodes of headache lasting minutes to days. A disorder evolving from episodic tension-type headache, with daily or very frequent episodes of headache lasting minutes to days. The pain is typically bilateral, pressing or tightening in quality and of mild to moderate intensity, and it does not worsen with routine physical activity. The pain is typically bilateral, pressing or tightening in quality and of mild to moderate intensity, and it does not worsen with routine physical activity. There may be mild nausea, photophobia or phonophobia. There may be mild nausea, photophobia or phonophobia.

67 67 IHS Diagnostic Criteria for chronic TTH A.Headache occurring on ≥15 days per month on average for >3 months (≥180 days per year) and fulfilling criteria B through D B.Headache lasts hours or may be continuous C.Headache has at least two of the following characteristics: 1. bilateral location 2. pressing/tightening (non-pulsating) quality 3. mild or moderate intensity 4. not aggravated by routine physical activity such as walking or climbing stairs D.Both of the following: 1. no more than one of photophobia, phonophobia or mild nausea 2. neither moderate or severe nausea nor vomiting E.Not attributed to another disorder

68 Cluster headache This is a disorder with attacks of severe, strictly unilateral pain which is orbital, supraorbital, temporal or in any combination of these sites, lasting minutes and occurring from once every other day to 8 times a day. This is a disorder with attacks of severe, strictly unilateral pain which is orbital, supraorbital, temporal or in any combination of these sites, lasting minutes and occurring from once every other day to 8 times a day. The attacks are associated with one or more of the following, all of which are ipsilateral: conjunctival injection, lacrimation, nasal congestion, rhinorrhoea, forehead and facial sweating, miosis, ptosis, eyelid oedema. The attacks are associated with one or more of the following, all of which are ipsilateral: conjunctival injection, lacrimation, nasal congestion, rhinorrhoea, forehead and facial sweating, miosis, ptosis, eyelid oedema. Most patients are restless or agitated during an attack. Most patients are restless or agitated during an attack.

69 Cluster headache Episodic cluster headache Chronic cluster headache

70 70 IHS Diagnostic Criteria for Cluster Headache A.At least 5 attacks fulfilling criteria B through D B.Severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting mins if untreated C.Headache is accompanied by at least one of the following: 1. ipsilateral conjunctival injection and/or lacrimation 2. ipsilateral nasal congestion and/or rhinorrhoea 3. ipsilateral eyelid oedema 4. ipsilateral forehead and facial swelling 5. ipsilateral miosis and/or ptosis 6. a sense of restlessness or agitation D.Attacks have a frequency from one every other day to 8 per day E.Not attributed to another disorder

71 Episodic cluster headache Cluster headache attacks occurring in periods lasting 7 days to 1 year separated by pain-free periods lasting 1 month or longer Cluster headache attacks occurring in periods lasting 7 days to 1 year separated by pain-free periods lasting 1 month or longer

72 Chronic cluster headache Cluster headache attacks occurring for more than 1 year without remission or with remissions lasting less than 1 month. Cluster headache attacks occurring for more than 1 year without remission or with remissions lasting less than 1 month.


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