Post on 26-Oct-2020
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