Headache

Headache

• Diagnosis is based on history

• Classification - IHS

(International headache society) – 1988

• 3rd Edition – ICHD3 - 2018

Headache - classification

Part I - Primary headaches

1. Migraine

2. Tension-type headache

3. Trigeminal autonomic cephalalgias

4. Other primary headache disorders

Headache - classification

Part II - The secondary headaches5. Headache attributed to trauma or injury to the head and

neck

6. Headache attributed to cranial or cervical vascular

disorders

7. Headache attributed to non-vascular intracranial disorder

8. Headache attributed o substance or its withdrawal

9. Headache attributed to infection

10. Headache attributed to disorder of homeostasis

Headache - classification

Part II - The secondary headaches11. Headache or facial pain attributed to disorder of the

cranium, neck, eyes, ears, nose, sinuses, teeth, mouth, or

other facial or cervical structure

12. Headache attributed to psychiatric disorder

Part III – Painful cranial neuropathies, other facial pains and

other headaches

13. Painful cranial neuropathies and facial pains

14. Other headache disorder

Migraine

1. Migraine without aura

2. Migraine with aura

3. Chronic migraine

4. Complications of migraine

5. Probable migraine

6. Episodic syndromes that may be associated with

migraine

Tension type headache

1. Infrequent episodic tension-type headache

2. Frequent episodic tension-type headache

3. Chronic tension-type headache

4. Probable episodic tension-type headache

Trigeminal autonomic cephalalgias

(TACs)

1. Cluster headache

2. Paroxysmal hemicrania

3. Short-lasting unilateral neuralgiform headache

attacks (SUNCT)

4. Hemicrania continua

5. Probable trigeminal autonomic cephalalgia

Other primary headaches

1. Primary stabbing headache

2. Primary cough headache

3. Primary exertonial headache

4. Primary headache associated with sexual activity

5. Hypnic headache

6. Primary tunderclap headache

7. Hemicrania continua

8. New daily-persistent headache

Secondary headaches

5. Headache attributed to trauma or injury to the head and/or neck

6. Headache attributed to cranial or cervical vascular disorder

stroke, brain haemorrhage, AVM, aneurysm, cerebral venous

thrombosis

7. Headache attributed to non-vascular intracranial disorder

CSF hypotension, CSF hypertension, brain tumors, epileptic seizures,

etc.

8. Headache attributed to a substance or its withdrawal

acute intoxication, using of drugs, etc.

9. Headache attributed to infection

meningitis, encephalitis, etc.

Secondary headaches

10. Headache attributed to disorder of homoeostasis

brain hypoxy, arterial hypertension, hypotyreosis, hunger,

etc.

11. Headache or facial pain attributed to disorder of the

cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or

other facial or cervical structure

12. Headache attributed to psychiatric disorder

Part three: painful cranial neuropathies,

other facial pains and other headaches

13. Painful lesions of the cranial nerves and other facial pain

trigeminal neuralgia, glossopharyngeal neuralgia

14. Other headache disorders

Headache

diagnosis - based on history

• characteristics

• quality (sharp, blunt

pulsing)

• intensity

• localisation

• response on the physical

• activity

• accompanying signs

Haas, D.C., SUNY Upstate Medical University, 2002

Headache

diagnosis - based on history

• Accompanying signs

nauzea, vomitus

phonophoby, photophoby

aura

informations about drugs which are used

Migraine

•Nauzea

•Fonofóbia

•Fotofóbia

•Bolesť

Unilaterálna

Pulzujúca

Provokovaná

fyzickou aktivitou

• prevalence – 10%

• prevalence in

women

17,5 %

• prevalence in men

5,7 %

• positive familial

history

58 %

Haas, D.C., SUNY Upstate Medical University, 2002

Migraine is a common disabling

primary headache disorder.

1.1 Migraine without aura – 80%

• Diagnostic criteria:

A. At least five attacks1 fulfilling criteria B-D

B. Headache attacks lasting 4-72 hr (untreated or unsuccessfully treated)2;3

C. Headache has at least two of the following four characteristics:

1. unilateral location

2. pulsating quality

3. moderate or severe pain intensity

4. aggravation by or causing avoidance of routine physical activity (eg,

walking or climbing stairs)

D. During headache at least one of the following:

1. nausea and/or vomiting

2. photophobia and phonophobi

E. Not better accounted for by another ICHD-3 diagnosis.

1.2 Migraine with aura – 18%

• Diagnostic criteria:

A. At least two attacks fulfilling criteria B and C

B. One or more of the following fully reversible aura symptoms:

1. visual

2. sensory

3. speech and/or language

4. motor

5. brainstem

6. retinal

1.2 Migraine with aura – 18%

C. At least three of the following six characteristics:

1. at least one aura symptom spreads gradually over ≥5 minutes

2. two or more aura symptoms occur in succession

3. each individual aura symptom lasts 5-60 minutes1

4. at least one aura symptom is unilateral2

5. at least one aura symptom is positive3

6. the aura is accompanied, or followed within 60 minutes, by headache

D. Not better accounted for by another ICHD-3 diagnosis.

1.4 Complications of migraine

• Status migrainosus

• Persistent aura without infarction

• Migrainous infarction

• Migraine aura-trigerred seizure

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

• Stimulation of n. V. lead to release of substance P

and neurokinin A

neurogenic inflammation

Pathophysiology of migraine• Stimulation of serotoninergic cells – increased blood flow

and vasodilatation

• Sleeping – reduce releasing of 5-HT

- Sleeping treat migraine

Pathophysiology of migraine

• Receptors 5-HT are different

activation of inhibting 5-HT1B/1D receptors

release of serotonin, substance P, neurokinin

block neurogenic inflammation

• receptors agonists – triptans – treatment of

migraine

(triptans)

CGRP - neuropeptid involved in

pathophysiology of migraine

Potent vasodilatator

Increased level during headache

CGRP = calcitonino gene related peptid

Goadsby PJ, et al. Ann Neurol. 1990;28:183-187.. 5. Cernuda-Morollón E, et al. Neurology. 2013;81:1191-1196.

Figure adapted from Pellesi L, et al. Clin Pharmacol Drug Dev. 2017.216

Binding of mAbs determines their therapeutic effects

CLR = calcitonin receptor-like receptor; RAMP1 = receptor activity-modifying protein; mAbs = monoclonal antibodies;

RCP = receptor component protein.

216. Pellesi L, et al. Clin Pharmacol Drug Dev. 2017. doi: 10.1002/cpdd.345.

Ligand-receptor interaction mAbs blocking ligand

(CGRP)mAbs blocking receptor

CGRP primarily binds its

receptor under normal

conditions

CGRP is neutralized

Other ligands may

interact with the CGRP

receptor

Receptor interaction

is impeded

CGRP and other ligands

may bind other receptors

Ligand (other than CGRP)

CGRP

CLRRAMP1

CGRP

CLRRAMP1

CGRP

CLRRAMP1

RCP RCP RCP

CGRP

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 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

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

• ASA

• Paracetamol + ASA + coffein

• Ibuprofen

• Naproxen

• Triptans (eletriptan, naratriptan, rizatriptan,

sumatriptan, zolmitriptan) – middle or severe attacks of headache

Migraine - therapy

• Triptans 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 – therapymechanism 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 – therapy

• Prevention – more than 3 attacks/month

betablockers, blockers of calcium,

chanels, antiepileptics – topiramat,

valproid acid

pizotifen

Monoclonal antibodies against CGRP

receptor

Mechanism of erenumab action

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

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

Pain Migraine Tensiion

headache

Cluster

headache

Localisation Unilateral

Bilateral

Bilateral Unilateral

Lasting 4 – 72 hours Hours -

days

30 – 180 min

Intensity Light -

severe

Light -

middle

Severe

Nauzea, phono-,

photophoby

YES

(could be)

No No

Lacrimation, nasal

congestion

It could be No YES

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