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Headache
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2nd Edition of The International Headache Classification (ICHD-2)
published by International Headache Society in Cephalalgia 2004 electronic version –
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Primary headaches 1. MIGRAINE 2. TENSION-TYPE HEADACHE (TTH)
3. CLUSTER HEADACHE AND OTHER TRIGEMINAL AUTONOMIC CEPHALALGIAS 4. OTHER PRIMARY HEADACHES
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1. Migraine 1.1. Migraine without aura 1.2. Migraine with aura
1.3. Childhood periodic syndromes that are commonly precusors of migraine 1.4. Retinal migraine 1.5. Complications of migraine 1.6. Probable migraine
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2. Tension-type headache
2.1. Infrequent episodic tension-type headache 2.2. Frequent episodic tension-type headache 2.3. Chronic tension-type headache 2.4. Probable tension-type headache
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3. Cluster headache and other trigeminal autonomic cephalalgias
3.2. Paroxysmal hemicrania 3.3. Short-lasting unilateral neuralgiform headache attacks with conjuctival injection and tearing (SUNCT) 3.4. Probable trigeminal autonomic cephalalgia
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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 4.5. Hypnic headache 4.6. Primary tunderclap headache 4.7. Hemicrania continua 4.8. New daily-persistent headache (NDPH)
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Secondary headaches 5. Headache attributed to head and/or neck trauma
6. Headache attributed to cranial or cervical vascular disorders 7. Headache attributed to non-vascular intracranial disorders 8. Headache attributed to a substance or its withdrawal 9. Headache attributed to infection
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Secondary headaches 10. Headache attributed to disorders of homeostasis 11. Headache attributed to facial pain attributed to disorder of cranial, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial cranial structures 12. Headache attributed to psychiatric disorder
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Cranial neuralgias and central causes of facial pain
13.1. – 13.19 13.1. Trigeminal neuralgia 14. Other headache, cranial neuralgia, central or primary facial pain
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Headache quality intensity localisation response on the physical
characteristics quality intensity localisation response on the physical activity accompanying signs Haas, D.C., SUNY Upstate Medical University, 2002
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Headache Accompanying signs nauzea, vomitus phonophoby, photophoby
aura informations about drugs which are used
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Migraine prevalence – 10% prevalence in women Nauzea 17,5 % Fonofóbia
prevalence in men 5,7 % positive familial history 58 % Nauzea Fonofóbia Fotofóbia Bolesť Unilaterálna Pulzujúca Provokovaná fyzickou aktivitou Haas, D.C., SUNY Upstate Medical University, 2002
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Pathophysiology of migraine
Hypotalamus and limbic system prodroms Neuronal dysfunction and vascular changes aura and headache
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Pathophysiology of migraine
Spreading depression of CBF from occipital region during aura Spreading depression activate trigeminovascular endings
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Pathophysiology of migraine
There is unknown mechanism of activation nuclei in brainstem (nc. caudalis trigeminalis) - by spreading depression - by biochemical changes - both Activation stimulate peripheral findings of n.V.
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Pathophysiology of migraine
After stimulation of n. V. - production of P substance P and neurokinin A neurogenic inflammation Stimulation of serotoninergic cells
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Pathophysiology of migraine
Receptors of 5-HT (serotonin): activation of inhibiting 5-HT1B/1D receptores production of serotonin, P substance, neurokinin block of neurogenic inflammation agonists of these receptores (triptans) – treatment of migraine
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Factors provoke atack of migraine
Hormonal (menstruation, kontraceptives) Dietetical (alcohol, Na glutamat, chocolate, cheese) Psychological (stress, anxieta, depression) From environment (odors, changes of weather, high above sea-level) Drugs ( NTG, histamin, reserpin, estrogens) Others (head injury, physical activity)
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1. Migraine 1.1. Migraine without aura („common“, hemicrania simplex)
1.2. Migraine with aura
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Migraine with aura Aura - visual - sensoric - afasic - motoric
IHS – lasts: 4 – 60 min. (70% do 30´)
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Migraine with aura Visual aura scintilating scotoma
small point is enlarging to cik-cak border (scintilation), in the middle is dark scotoma Haas, D.C., SUNY Upstate Medical University, 2002
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Migraine with aura Visual aura colloured scintilating scotoma
Haas, D.C., SUNY Upstate Medical University, 2002
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Migraine with aura Positive fenomenons cik-cak Negativ scotoms
Haas, D.C., SUNY Upstate Medical University, 2002)
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Migraine Nauzea Phonophoby Photophoby Pain Unilateral Pulsating
Provoke by physical activity Lasts 4 – 72 hodín Haas, D.C., SUNY Upstate Medical University, 2002
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1.6. Compliations of migraine
Status migrenosus headache lasts more than72 hours brain infarct neurological deficit is not reversible till 7 days and/or infarct on CT or others
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Migraine - therapy Triptans (eletriptan, naratriptan, rizatriptan, sumatriptan, zolmitriptan) – middle or severe attacks of headache ASA Paracetamol + ASA + coffein Ibuprofen Naproxen DHE sc, im, iv
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Migraine – therapy mechanism of triptans
Vasoconstriction of meningeal, cerebral, pial vessels activation 5-HT1B receptores in smooth muscles of vessels Inhibition of neurogenic inflamation stimulation 5-HT1D receptores at the endings of trigeminal C and A fibers (subst. P, neurokinín A, CGRP) Central inhibition of pain activation 5-HT1D, 1F receptores in brainstem decrease excitability of neurones ncl. trig. caudalis
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Migraine – therapy Prevention – more than 3 attacks/month
betablockers, blockers of calcium, chanels, antiepileptics
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Tension headache The most often chronic headache
Prevalence - women – 88% Prevalence – men – 69% the most days outside of work
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Tension headache Pain - around the head - nonpulsating - bilateral
- 30 min. – 7 days - not increased by physical activity Haas, D.C., SUNY Upstate Medical University, 2002
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Cluster headache 6 times more frequent in men Pain - periorbital
- frontal, temporal - UNILATERAL - burning Haas, D.C., SUNY Upstate Medical University, 2002
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Cluster headache Pain Alarm-clock pain lasts: 15 – 180 min.
shorter than migraine Congestion Lacrimation Conjuctival inflamation Alarm-clock pain -beginning at night
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Cluster headache 02, triptans, DHE,
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Tension headache Increased muscle tone in the neck
Stright cervical lordosis Therapy Analgetics, myorelaxants, nonsteroid antiflogistics, physioteraphy, psychoteraphy, local 1% mesocain
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Trigeminal neuralgia Etiology – focal demyelinisation of n.V. or of ganglion Idiopatic – pulsations of arteries near n.V. Symptomatic – tumors Prevalence – 6/100000,more women, and older people
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Trigeminal neuralgy Clinical feature
shooting pain in area of n.V., increasing after chawing, in symptomatic - trigger area, loose of weight Therapy anticonvulsants – Gabapentin, alcoholisation of ganglion, surgery
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Temporal arteriitis Inflammation of a. temporalis superficialis
Age – risc factor Headache in temporal region, thick, painful temporal superficial artery, chawing claudications, stronger pain polymyalgia reumatica – spasm and pain of masticatory muscles
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Temporal arteriitis Late diagnosis– risc of blindness and stroke
Dg. – laboratory – FW, CRP, AG, biopsy Therapy – Prednison – 60 (100) mg/day long time, after decreasing – control of FW, FW – back to former dose
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