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Headache.

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Presentation on theme: "Headache."— Presentation transcript:

1 Headache

2 Headache Diagnosis is based on  history Classification - IHS
(International headache society) – 1988 3rd Edition – ICHD

3 Headache - classification
Part I - Primary headaches Migraine Tension-type headache Trigeminal autonomic cephalalgias Other primary headache disorders

4 Headache - classification
Part II - The secondary headaches Headache attributed to trauma or injury to the head and neck Headache attributed to cranial or cervical vascular disorders Headache attributed to non-vascular intracranial disorder Headache attributed o substance or its withdrawal Headache attributed to infection Headache attributed to disorder of homeostasis

5 Headache - classification
Part II - The secondary headaches Headache or facial pain attributed to disorder of the cranium, neck, eyes, ears, nose, sinuses, teeth, mouth, or other facial or cervical structure Headache attributed to psychiatric disorder Part III – Painful cranial neuropathies, other facial pains and other headaches Painful cranial neuropathies and facial pains Other headache disorder

6 Migraine Migraine without aura Migraine with aura Chronic migraine
Complications of migraine Probable migraine Episodic syndromes that may be associated with migraine

7 Tension type headache Infrequent episodic tension-type headache
Chronic tension-type headache Probable episodic tension-type headache

8 Trigeminal autonomic cephalalgias (TACs)
Cluster headache Paroxysmal hemicrania Short-lasting unilateral neuralgiform headache attacks (SUNCT) Hemicrania continua Probable trigeminal autonomic cephalalgia

9 Other primary headaches
Primary stabbing headache Primary cough headache Primary exertonial headache Primary headache associated with sexual activity Hypnic headache Primary tunderclap headache Hemicrania continua New daily-persistent headache

10 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

11 Headache Accompanying signs nauzea, vomitus phonophoby, photophoby
aura informations about drugs which are used

12 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

13 Pathophysiology of migraine
Hypotalamus and limbic system prodroms Neuronal dysfunction and vascular changes aura and headache

14 Pathophysiology of migraine
Spreading depression of CBF from occipital region during aura Spreading depression activate trigeminovascular endings

15 Pathophysiology of migraine
It is unknown mechanism of activation nuclei in brainstem (nc. caudalis trigeminalis) - by spreading depression - by biochemical chnages - both Activation stimulate perifepheral findings of n.V.

16 Pathophysiology of migraine
After stimulation of n. V. - production of P substance P and neurokinin A  neurogenic inflammation Stimulation of serotoninergic cells

17 Pathophysiology of migraine
Receptors of 5-HT: activation of inhibiting 5-HT1B/1D receptores  production of serotonin, P substance, neurokinin  block of neurogenic inflammation agonists of these receptores – treatment of migraine (DH-ergotamín, triptans)

18 Pathophysiology of migraine
The neuropeptide calcitonin gene-related peptide (CGRP) play an integral role in the pathophysiology of migraine. It is a potent peptide vasodilatator

19 Migraine Nauzea Phonophoby Photophoby Pain Unilateral Pulsating
Provoke by physical activity Lasts 4 – 72 hodín              Haas, D.C., SUNY Upstate Medical University, 2002

20 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)

21 Migraine without aura D. During headache ≥1 of the folloving
A. At least 5 atacks fulfilling criteria B-D B. Headache attacks lasting 4-72 hours C. Headache has ≥ of the folloving characteristics Unilateral location Pulsating quality Moderate or severe pain intensity Aggravation by úhysical activity D. During headache ≥1 of the folloving Nausea or vomiting Photoúphobia or phonophobia E. Not better accounted for by another ICH3 diagnosis

22 Migraine with aura A. At least 2 atacks fulfilling criteria B and C
B. ≥ 1of the folloving fully reversible aura symptoms 1. visual, 2. sensory, 3. speech and or llanguage, 4. motor, 5. brainstem, 6. retinal C. ≥ 2 of the folloving 2 characteristics ≥1 aura symptoms preads gradually over ≥ 5 min., and /or ≥ 2 symptoms occur in succession Each individual aura symptom lasts 5-60 min. ≥ 1 aura symptom is unilateral Aura accompanied or followed in < 60 min. by headache D. Not better accounted for by another ICH3 diagnosis and TIA excluded

23 Migraine with aura Aura - visual - sensoric - afasic - motoric
IHS – lasts: 4 – 60 min. (70% do 30´)

24 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

25 Migraine with aura Visual aura colloured scintilating scotoma
Haas, D.C., SUNY Upstate Medical University, 2002

26 Migraine with aura Positive fenomenons cik-cak Negativ scotoms
Haas, D.C., SUNY Upstate Medical University, 2002)

27 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

28 Basilar migraine Headache Symptoms from brainstem
double vision, NY, tinnitus, dysphonia, dysphagia, desorientation, quadruparesthesia, quadruparesis,

29 Auxiliary examination Radiological
Different headache Daily headache Headache + neurological signs Headache not responding on treatment Posttraumatic headache

30 Auxiliary examinations Radiological
To exclude brain tumor for patient CT-native , with contrast medium MRI, MR angiography, angiography

31 Auxilliary examinations
Elektroencephalography X-ray of skull injury, TU X-ray of cervical spinal column

32 Auxilliary examinations
Duplex ultrasound of carotid arteries, Transkranial Doppler Optic fundus  GLAUCOMA

33 Migraine - therapy Triptans (eletriptan, naratriptan, rizatriptan, sumatriptan, zolmitriptan) – middle or severe attacks of headache ASA Paracetamol + ASA + coffein Ibuprofen Naproxen DHE sc, im, iv

34 Migraine - therapy Triptany dose max.d. Sumatriptan 25-50-100 mg 300
Zolmitriptan ,5 – 5 mg Naratriptan ,5 mg Rizatriptan – 10 mg Eletriptan mg

35 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

36 Migraine – New treatment
Calcitonin gene-related peptide (CGRP) plays a crucial role in the pathogenesis of migraine. Monoclonal antibodies against CGRP and CGRP receptors for the treatment of migraine were recently developed Erenumab is a fully human monoclonal antibody developed to block the pathway of calcitonin gene-related peptide (CGRP).

37 Migraine – therapy Prevention – more than 3 attacks/month
betablockers, blockers of calcium, chanels, valproid acid pizotifen

38 Tension headache The most often chronic headache
Prevalence - women – 88% Prevalence – men – 69%  the most days outside of work

39 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

40 Tension headache Increased muscle tone in the neck
Stright cervical lordosis Therapy Analgetics, myorelaxants, nonsteroid antiflogistics, physioteraphy, psychoteraphy, local 1% mesocain

41 Cluster headache 6 times more frequent in men Pain - periorbital
- frontal, temporal - UNILATERAL - burning Haas, D.C., SUNY Upstate Medical University, 2002

42 Cluster headache Pain Alarm-clock pain lasts: 15 – 180 min.
shorter than migraine Congestion Lacrimation Conjuctival inflamation Therapy O2, triptans, DHE Alarm-clock pain -beginning at night

43 Chronic paroxysmal hemicrania
More often in women Pain – unilateral - lasting: 2 – 45 min. - more times during the day - ipsilateral lacrimation, conjuctival inflammation - nasal congescion, rhinorea - ptosis Effect of Indometacin – dg. test

44 Nauzea, phono-, photophoby YES No
Pain Migraine Tensiion headache Cluster headache Localisation Unilateral Bilateral Lasting 4 – 72 hours Hours - days 30 – 180 min Intensity Light - severe Light - middle Severe Nauzea, phono-, photophoby YES (could be) No Lacrimation, nasal congestion It could be

45 Subarachnoid haemorrhage
Sudden onset of the strong headache Immediatelly to hospital HOSPITAL

46 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

47 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

48 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

49 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

50 Conclusion Headache – one of the most often symptoms
Correct differential diagnosis  correct therapy  shortened headache  improving quality of life  economical profit, shortened working inability

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