Headache
Headache Diagnosis is based on history Classification - IHS (International headache society) – 1988 3rd Edition – ICHD3 - 2017
Headache - classification Part I - Primary headaches Migraine Tension-type headache Trigeminal autonomic cephalalgias Other primary headache disorders
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
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
Migraine Migraine without aura Migraine with aura Chronic migraine Complications of migraine Probable migraine Episodic syndromes that may be associated with migraine
Tension type headache Infrequent episodic tension-type headache Chronic tension-type headache Probable episodic tension-type headache
Trigeminal autonomic cephalalgias (TACs) Cluster headache Paroxysmal hemicrania Short-lasting unilateral neuralgiform headache attacks (SUNCT) Hemicrania continua Probable trigeminal autonomic cephalalgia
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
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
Headache Accompanying signs nauzea, vomitus phonophoby, photophoby aura informations about drugs which are used
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
Pathophysiology of migraine Hypotalamus and limbic system prodroms Neuronal dysfunction and vascular changes aura and headache
Pathophysiology of migraine Spreading depression of CBF from occipital region during aura Spreading depression activate trigeminovascular endings
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.
Pathophysiology of migraine After stimulation of n. V. - production of P substance P and neurokinin A neurogenic inflammation Stimulation of serotoninergic cells
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)
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
Migraine Nauzea Phonophoby Photophoby Pain Unilateral Pulsating Provoke by physical activity Lasts 4 – 72 hodín Haas, D.C., SUNY Upstate Medical University, 2002
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)
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
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
Migraine with aura Aura - visual - sensoric - afasic - motoric IHS – lasts: 4 – 60 min. (70% do 30´)
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
Migraine with aura Visual aura colloured scintilating scotoma Haas, D.C., SUNY Upstate Medical University, 2002
Migraine with aura Positive fenomenons cik-cak Negativ scotoms Haas, D.C., SUNY Upstate Medical University, 2002)
1.6. Compliations of migraine 1.6.1. Status migrenosus headache lasts more than72 hours 1.6.2. brain infarct neurological deficit is not reversible till 7 days and/or infarct on CT or others
Basilar migraine Headache Symptoms from brainstem double vision, NY, tinnitus, dysphonia, dysphagia, desorientation, quadruparesthesia, quadruparesis,
Auxiliary examination Radiological Different headache Daily headache Headache + neurological signs Headache not responding on treatment Posttraumatic headache
Auxiliary examinations Radiological To exclude brain tumor for patient CT-native , with contrast medium MRI, MR angiography, angiography
Auxilliary examinations Elektroencephalography X-ray of skull injury, TU X-ray of cervical spinal column
Auxilliary examinations Duplex ultrasound of carotid arteries, Transkranial Doppler Optic fundus GLAUCOMA
Migraine - therapy Triptans (eletriptan, naratriptan, rizatriptan, sumatriptan, zolmitriptan) – middle or severe attacks of headache ASA Paracetamol + ASA + coffein Ibuprofen Naproxen DHE sc, im, iv
Migraine - therapy Triptany dose max.d. Sumatriptan 25-50-100 mg 300 Zolmitriptan 2,5 – 5 mg 10 Naratriptan 2,5 mg 5 Rizatriptan 5 – 10 mg 30 Eletriptan 40 - 80 mg 160
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
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).
Migraine – therapy Prevention – more than 3 attacks/month betablockers, blockers of calcium, chanels, valproid acid pizotifen
Tension headache The most often chronic headache Prevalence - women – 88% Prevalence – men – 69% the most days outside of work
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
Tension headache Increased muscle tone in the neck Stright cervical lordosis Therapy Analgetics, myorelaxants, nonsteroid antiflogistics, physioteraphy, psychoteraphy, local 1% mesocain
Cluster headache 6 times more frequent in men Pain - periorbital - frontal, temporal - UNILATERAL - burning Haas, D.C., SUNY Upstate Medical University, 2002
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
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
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
Subarachnoid haemorrhage Sudden onset of the strong headache Immediatelly to hospital HOSPITAL
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
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
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
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
Conclusion Headache – one of the most often symptoms Correct differential diagnosis correct therapy shortened headache improving quality of life economical profit, shortened working inability