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    Nyeri Kepala IAFKU, DR Betty, SPS

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    Muhammad Asrizal
    The document discusses various types of primary and secondary headaches. It describes migraines, tension-type headaches, cluster headaches and other trigeminal autonomic cephalalgias. For each type, it covers characteristics, pathophysiology and treatment options including both pharmacological and non-pharmacological approaches. Physical examination factors are also outlined to help in diagnosis.

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    Nyeri Kepala IAFKU, DR Betty, SPS

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    Muhammad Asrizal
    58 views43 pages
    The document discusses various types of primary and secondary headaches. It describes migraines, tension-type headaches, cluster headaches and other trigeminal autonomic cephalalgias. For each type, it covers characteristics, pathophysiology and treatment options including both pharmacological and non-pharmacological approaches. Physical examination factors are also outlined to help in diagnosis.

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    The document discusses various types of primary and secondary headaches. It describes migraines, tension-type headaches, cluster headaches and other trigeminal autonomic cephalalgias. For each type, it covers characteristics, pathophysiology and treatment options including both pharmacological and non-pharmacological approaches. Physical examination factors are also outlined to help in diagnosis.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    58 views43 pages

    Nyeri Kepala IAFKU, DR Betty, SPS

    Uploaded by

    Muhammad Asrizal
    The document discusses various types of primary and secondary headaches. It describes migraines, tension-type headaches, cluster headaches and other trigeminal autonomic cephalalgias. For each type, it covers characteristics, pathophysiology and treatment options including both pharmacological and non-pharmacological approaches. Physical examination factors are also outlined to help in diagnosis.

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    HEADACHE

    Dr. Betty Soedaly Sp. S


    HEADACHE
    ALL ACHES AND PAINS LOCATED IN THE HEAD.
    ORBITA  OCCIPUT

    Migraine treatment in 1200 BC


    THE ROLE OF NEUROTRANSMITTER :
    SEROTONIN (5 HT)
    THE ENDOGENOUS PAIN CONTROL MECHANISM -> OPIOID
    GABA
    The International Classification of Headache Disorders
    ICHD 2 ( IHS 2004 )
    The Primary Headaches
    Migraine
    Tension-type headache (TTH)
    Cluster headache
    Other primary headaches

    The Secondary Headaches


    Headache attributed to head and/or neck trauma
    Headache attributed to cranial or cervical vascular disorders
    Headache attributed to non-vascular intracranial disorders
    Headache attributed to a substance or its withdrawal
    Headache attributed to infection
    Headache attributed to disorder of homoeostasis
    Headache or facial pain attributed disorder of cranial, neck, eyes, ears,
    nose, sinuses, teeth, mouth or other facial or cranial structures
    Headache attributed to psychiatric disorders

    Cranial Neuralgias, central & primary facial pain & other headaches
    Cranial neuralgias & central causes of facial pain
    Others headache, cranial neuralgias & central or primary facial pain
    PAIN SENSITIVE STRUCTURES OF THE HEAD

     SKIN, SUBCUTANEUS TISSUE


     MUSCLES
     EXTRACRANIAL ARTERIES
     PERIOSTEUM OF THE SKULL
     EYE, EAR, NASAL CAVITIES, SINUSES, TEETH,
    OROPHARYNX
     VENOUS SINUSES
     DURA AT THE BASE OF THE BRAIN
     ARTERIES within DURA & PIA ARACHNOID
     MIDDLE MENINGEAL &SUPERFICIAL TEMPORAL
    ARTERIES
     N II, N III, N V, N IX, N X
     C 1, 2, 3
     SENSORY NUCLEI OF THE THALAMUS
     BRAIN STEM PERIAQUEDUCTAL GRAY MATTER
     SUPRATENTORIAL STRUCTURES
    ANT / MED FOSSAE N V - N V 1-2

     INFRATENTORIAL STRUCTURES C 1, 2, 3
    POST FOSSAE N IX, N X

     ANT, 2/3 OF THE HEAD NV


    BACK OF THE HEAD, NECK C 1, 2, 3
    INSENSITIVE TO PAIN

     BONY SKULL
     PIA
    - ARACHNOID & DURA OVER THE
    CONVEXITY OF THE BRAIN
     BRAIN PARENCHYMA
     EPENDYMA, CHOROID PLEXUS
    HISTORY :
     AGE AT ONSET
     ATTACK ONSET
     QUALITY
     SEVERITY
     LOCATION, RADITION OF PAIN
     MODE OF ONSET :early warning symtom, aura
     TIME, INTENSITY, CURVE, DURATION
     CONDITION WHICH EXACERBATE / RELIEVE THE PAIN
     ASSOCIATED FEATURES
     PREVIOUS TREATMENT
     GENERAL HEALTH
     SOCIAL HISTORY, FAMILY HISTORY
     PAST HEADACHE&HEALTH HISTORY
     HEADACHE IMPACT
     EMOTIONAL STATE
    Catatan Harian Nyeri Kepala
    nama : …………………………………

    Hari/Tgl Mulai Akhir Berat Gejala Disabilitas Obat Pencetus


    NK NK NK penyerta NK NK
    (jam) (jam) (nilai 0-3) (nilai 0-4) (nilai 0-3)
    _______________________________________________________________________

    Berat nyeri kepala : 0:tak ada 1:ringan 2:sedang 3:berat


    Gejala Penyerta : 0:tak ada 1:mual 2:muntah 3:peka cahaya 4:peka suara
    Disabilitas : 0:tak ada 1:ringan 2:sedang 3:berat
    Faktor Pencetus Nyeri Kepala

    Stres, relaksasi setelah stres


    Kurang/kebanyakan tidur
    Ubah jadwal
    Tidak/telat makan
    Bau menyengat : parfum,rokok
    Lingkungan: cahaya silau/berkedip,gaduh
    ketinggian,panas,lembab
    ruang berasap
    Makanan/minuman
    Obat
    Hormonal
    Trauma kapitis
    PHYSICAL EXAMINATION :

    INSPECTION

    PALPATION

    AUSCULTATION

     head, neck and nervous system

    Is the examination abnormal ?


    CLUSTER HEADACHE
    MIGRAINE
     Migraine without aura
     Migraine with aura (typical aura with/wo
    non/migraine headache, Fam/sporadic HM,
    basilar-type M)
     Childhood periodic syndrome (cyclical vomiting,
    abdominal M,BPV of childhood)
     Retinal Migraine
     Complications of migraine (chronic M,Status M,
    persistent aura wo infarction, migranous
    infarction), M triggered seizure)
     Probable migraine
    MIGRAINE PATHOPHYSIOLOGY
     GENETIC FACTORS
     VASOCONTRICTION (AURA) & VASODILATATION (HEADACHE)
     CORTICAL SPREADING DEPRESSION
     OLIGAEMIA PROPAGATING ACROSS THE CORTEX POSTERIOR TO
    FRONTAL
     ACTIVATION OF THE TRIGEMINO-VASCULAR SYSTEM
     SEROTONIN (5-HT) : VESSELS, PLATELET, NEURON
     AMINERGIC BRAINSTEM NUCLEI
    - MIGRAINE GENERATOR
    - CORTICAL HYPEREXITABILITY
     N. O.
     Mg , DA DEFICIENCY
     EAA : GLU
     DEFECTIVE ENDOGENOUS PAIN CONTROL SYSTEM
     MIGRAINE TRIGGERS, i.e. : HORMONAL FLUCTUATION, EMOTION,
    FATIGUE, FASTING, METEOROLOGIGAL CHANGES, DIETARY FACTORS
    Phases of Migraine

    HAS/NEURO
    HAS/Neuro S1/Bdg/04 ( Evans, 2000 )
    Migrainous Vertigo
     Childhood : Benign Paroxysmal Vertigo :
    Vertigo, nystagmus, maybe cyclic. vomit.,paroxys. Torticollis
    Migraine equivalent?
    Ceased spontaneously ( mo-yr)
     Adult : 7% pts in dizziness clinic, 9% pts in migraine clinic
    Basilar-type M
    Benign recurrent vertigo : Spontan.vertigo, young/middle-aged
    no cochlear/neuro.
    Symtoms : female>,fam.hystory, precipitat.fact(+)
    Tx: pizotifen, propranolol

    Abnormality of the vestibular system


    Circulation disturbances of internal auditory artery
    Hormonal Fluctuation Migraine-triggered seizures
    ( Evans, 2000 )
    Terapi Farmaka

    Pengobatan Abortif/ Akut :


    Reda / hilangkan nyeri kepala
    Cegah nyeri kepala berlanjut

    Pengobatan Preventif/Pencegahan :
    Kurangi frekwensi
    Kurangi beratnya nyeri kepala
    TREATMENT :
    Pre-emptive : domperidone, ergot
    a. ABORTIVE : 2-3 d/w
    - ANALGESICS :
    ACETAMINOPHEN, ASA, NSAID, combination tx
    SPECIFIC DRUGS : - ERGOT ALKALOIDS
    ( ERGOTAMINE T, DHE ) max 10mg/w
    - ANTIEMETICS : - TRIPTAN (C.I! )
    METOCLOPRAMIDE, DOMPERIDONE

    b. PREVENTIVE : episodic, short-term,chronic(3-6mo)


    >2-4attacks/mo& disability >2d
    CI , overused
    - ANTICONVULSANTS (valproate,topiramate,gabapentin)
    - ADRENOCEPTOR BLOCKERS (propranolol,nadolol,timolol,atenolol,metoprolol )
    - ANTIDEPRESSANTS (amitriptyline)
    - Ca-CHANNEL BLOCKERS (flunarizine,verapamil)
    Cortex
    PAIN
    Phonophobia
    Photophobia 5-HT1B
    Thalamus receptor
    Trigeminal
    ganglion
    Intracranial
    Vasoconstriction

    Autonomic activation
    Nausea, Emesis
    Trigeminal 5-HT1D Receptor
    nucleus caudalis Trigeminal
    Decreased pain Inhibition
    signal transmission

    Adapted from Hargreaves et al. Can J Neurol Sci 1999 Nov;26 Suppl 3:S12-9
    Penanganan nonfarmaka
    Edukasi
    Mengenal & menghindari faktor pencetus

    Modifikasi perilaku
    Latihan
    Relaksasi
    Biofeedback
    Terapi perilaku kognisi

    Terapi fisik
    TENS (transcutaneus electric
    nerves stimulation)
    TENSION-TYPE HEADACHE
    • Infrequent Episodic TTH-iFETTH (<1d/mo or <12 d/yr)
    • Frequent Episodic TTH - FTTH (>12d and < 180d/yr)
    • Chronic TTH- CTTH
    assosiated with disorder of pericranial muscles
    not associated with disorder of pericranial muscles

    • Probable TTH

    ICHD-2
    TENSION-TYPE HEADACHE
     PRESSING, TIGHTENING, FULLNESS
     MILD TO MODERATE INTENSITY
     BILATERAL
     NO NAUSEA OR VOMITTING
     PHOTOPHOBIA OR PHONOPHOBIA
    MAY BE PRESENT

     WOMEN > MEN, MIDDLEAGE


     COINCIDE WITH ANXIETY &
    DEPRESSION
    HYPERVENTILATION SYNDROME
    Tension Type Headache
     Psychologic factors
     Muscle contraction and myofacial

    tenderness
     Vascular factorsn : NO
     Humoral factors : 5HT
     Central factors : central pain control system
    TTH TREATMENT
    ABORTIVE :

     ANALGESICS :

    ACETAMINOPHEN, ASA, NSAID

    PREVENTIVE :

     ANTIDEPRESSANTS : AMITRIPTYLINE (6MO, / 2-3MO)

    NONPHARMACOLOGIC :

     RELAXATION, BIOFEEDBACK

     PSYCHOTHERAPY

     ACCUPUNCTURE ?

     BOTULINUM TOXIN A ?
    CLUSTER HEADACHE &
    other trigeminal autonomic cephalalgias

     Cluster headache ( episodic, chronic CH)


     Paroxismal hemicrania (episodic, chronic PH)
     SUNCT ( short-lasting unilateral neuralgiform
    headache attacks with conjunctival injection and
    tearing)
     Probable trigeminal autonomic cephalalgias
    CLUSTER HEADACHE
    YOUNG ADULT MEN ( M : F = 5 : 1 )
    UNILATERAL PAIN
    PATHOPHYSIOLOGY OF THE CLUSTER
    HEADACHE

     PAROXYSMAL PARASYMPATHETIC DISCHARGE


    OF THE GREATER SUPERFICIAL PETROSAL
    NERVE & SPHENOPALATINE GANGLION
     SWELLING OF THE ARTERIAL WALL OF THE

    INTERNAL CAROTID ARTERY


     HISTAMINE RELEASE

     HYPOTHALAMIC MECHANISM
    TREATMENT OF THE CLUSTER HA
     ABORTIVE :
    ◦ 100% O2 INHALATION
    ◦ TRIPTANS SC
    ◦ ERGOT ALKALOIDS
    ◦ TOPICAL LA : LIDOCAINE 4-6%NASAL DROPS
    ◦ ANALGESICS?
    ◦ OTHERS : OCREOTIDE, OLANZAPINE

     PREVENTIVE : SHORT/LONG-TERM
    Short-term : triptan, ergot, corticosteroid
    Long-term :
    ◦ VERAPAMIL
    ◦ LITHIUM
    ◦ CHLORPROMAZINE
    ◦ ERGOT ALKALOIDS
    ◦ TOPIRAMATE
    ◦ CORTICOSTEROID
    ◦ OCCIP NERVE BLOCKADE

    NO ALCOHOL
    PAROXYSMAL HEMICRANIA

      CLUSTER HEADACHE
     SHORTER LASTING ( 2 - 45’), MORE FREQUENT
     MOSTLY FEMALES
     ABSOLUTE EFFECTIVENESS OF INDOMETHACIN

    SUNCT :~ TGN
    LAMOTRIGINE
    GABAPENTIN
    TOPIRAMATE
    OTHERS PRIMARY HEADACHES
     Primary stabbing headache
     Primary cough headache
     Primary exertional headache
     Headache associated with sexual activity
     Hypnic headache
     Thunderlap headache
     Hemicrania Continua
     NDPH ( new daily persistent headache )
    Beberapa Analgesik Terapi Abortif Nyeri Kepala
    (Rowbotham MC, Petersen KL, 2001)

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