NYERI KEPALA

(CEFALGIA / HEADACHE)

dr. Sholihul Muhibbi, Sp.S, M.Si.Med.

 DEFINISI NYERI
International Association for the Study of Pain (IASP)

Pengalaman sensorik dan emosional yang

tidak menyenangkan akibat kerusakan jaringan,
baik aktual maupun potensial, atau yang
digambarkan dalam bentuk kerusakan tersebut.
KLASIFIKASI NYERI
I. Nyeri sederhana / fisiologik
Nyeri timbul oleh berbagai stimuli yg
tidak menimbulkan kerusakan jaringan

II. Nyeri patologik / klinis

1. Nyeri nosiseptik
Nyeri timbul oleh berbagai stimuli yg
menimbulkan kerusakan jaringan (somatik,
viseral, nyeri rujuk/referred pain)
2. Nyeri neuropatik
3. Nyeri idiopatik / psikogenik
 KLASIFIKASI NYERI

NYERI

N. NOSISEPTIF N. PSIKOGENIK

N. Somatik N. NEUROPATIK
N. Viseral
Referred Pain Perifer
Sentral
DEFINISI
NYERI NOSISEPTIF:
Nyeri yang timbul bila reseptor nyeri (nosiseptor)
teraktivasi.

NYERI NEUROPATIK:
Nyeri yang timbul akibat lesi atau disfungsi pada susunan
saraf

NYERI PSIKOGENIK:
Nyeri dengan faktor psikogen tanpa sebab organik.
 The Pain Pathway

Pain Perception
Brain

Dorsal Root Dorsal Horn

Ganglion

Spinal Cord
Nociceptor Gottschalk A et al. Am Fam Physician. 2001;63:1979-84.
Fields HL et al. Harrison’s Principles of Internal Medicine. 1998:53-8.
 Definisi Nyeri Kepala
Rasa nyeri atau rasa tidak mengenakkan pada
daerah atas kepala memanjang dari orbita
sampai kedaerah belakang kepala (area
oksipital dan sebagian daerah tengkuk)
Patofisiologi :
a. Rangsang nyeri bisa disebabkan oleh adanya
tekanan, traksi displacement maupun proses
kimiawi & inflamasi thd nosiseptor2 pd struktur yg
pain sensitive di kepala. Jk struktur2 pain sensitive
yg terletak pd ataupun diatas tentorium serebelli
dirangsang mk rasa nyeri akan timbul terasa
menjalar pd daerah didpn batas garis vertikal yg
ditarik dari kedua telinga kiri dan kanan
melewati puncak kepala (daerah frontotemporal
dan parietal anterior). Rasa nyeri ini ditransmisi
oleh N. V (Trigeminus)
b. Sedangkan rangsangan thd struktur yg peka thd
nyeri dibwh tentorium (yi yg terletak pada fosa
kranii posterior) radix servikalis bag atas dg cab2
saraf perifernya akan menimbulkan nyeri pd
daerah diblk garis tsb diatas, yaitu pd daerah
oksipital, sub oksipital area dan servikal bag
atas. Rasa nyeri ini ditransmisi oleh saraf kranial
IX, X dan saraf spinal C-1, C-2 dan C3.
c. Ada 3 pembagian besar dr struktur yg pain sensitive di
kepala :
1. Struktur Intra Kranial :
- Sinus kranialis dan vena aferen (sinus
venosus, dan vena2 yg mensuplay sinus2 tsb)
- Arteri dr duramater (a. meningea media)
- Arteri di basis kranii yg membentuk sirkulus
Willisi dan cab2 besarnya.
- Sebagian dr duramater yg berdekatan dg
pembuluh darah besar terutama yg terletak
dibasis fossa kranii anterior dan posterior dan
meningens
2. Struktur Ekstra kranial
- Kulit, Scalp, otot, tendon & fascia daerah kepala
dan leher
- Mukosa sinus paranasalis & cavum nasi.
- Gigi geligi,
- Telinga luar dan tengah,
- Tlg tengkorak tu. daerah supra orbita, temporal
dan oksipital bwh, rongga orbita beserta isinya.
- Arteri ekstra kranial.
3. Saraf
- N. Trigeminus, N. Fasialis, N. Glossofaringeus,
N. Vagus.
- Saraf spinal servikalis 1,2,3.
d. Sedangkan struktur parenkim otak , sebagian
duramater tengkorak adalah relatif tidak sensitif
thd nyeri.
INTERNATIONAL CLASSIFICATION
of
HEADACHE DISORDERS (ICHD-II)

2nd edition

(ICHD-II)

ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4

 Classification

Part 1:
Primary headache disorders
Part 2:
Secondary headache disorders
Part 3:
Cranial neuralgias, central and primary
facial pain and other headaches

ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4

 Primary or secondary
headache?

Primary:

• no other causative disorder

ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4

 Primary or secondary
headache?

Secondary
(ie, caused by another disorder):
• new headache occurring in close temporal
relation to another disorder that is a known
cause of headache
• coded as attributed to that disorder
(in place of previously used term associated
with)

ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4

 Classification

Part 1: The primary headaches

1. Migraine
2. Tension-type headache
3. Cluster headache
and other trigeminal autonomic cephalalgias
4. Other primary headaches

ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4

 Classification
Part 2: The secondary headaches
5. Headache attributed to head and/or neck
trauma
6. Headache attributed to cranial or cervical
vascular disorder
7. Headache attributed to non-vascular
intracranial disorder
8. Headache attributed to a substance or its
withdrawal
9. Headache attributed to infection
ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
 Classification
Part 2: The secondary headaches
10.Headache attributed to disorder of
homoeostasis
11. Headache or facial pain attributed to
disorder of cranium, neck, eyes, ears, nose,
sinuses, teeth, mouth or other facial or
cranial structures
12. Headache attributed to psychiatric
disorder

ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4

 Classification

Part 3: Cranial neuralgias, central

and primary facial pain and other
headaches
13. Cranial neuralgias and central causes of
facial pain
14. Other headache, cranial neuralgia, central
or primary facial pain

ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4

Migraine
Description:
Recurrent headache disorder manifesting in
attacks lasting 4-72 hours. Typical characteristics
of the headache are unilateral location, pulsating
quality, moderate or severe intensity, aggravation
by routine physical activity and association with
nausea and/or photophobia and phonophobia.
Status migrainosus
A debilitating migraine attack lasting for more
than 72 hours.
Migraine
Diagnostic criteria:
A. At least 5 attacks1 fulfilling criteria B-D
B. Headache attacks lasting 4-72 hours (untreated or
unsuccessfully treated)
C. Headache has at least two of the following
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 phonophobia
E. Not attributed to another disorder
Patofisiologi
 The neurovascular (trigeminovascular) theory,
one of the oldest, states that intracranial
vasoconstriction is responsible for migraine
aura, and the subsequent rebound
vasodilatation and activation of perivascular
nociceptive nerves results in headache. Wolff et
al
 In 1944, Leao proposed the theory of Cortikal
Spreading Depression (CSD) to explain the
mechanism of migraine with aura.
Patofisiologi 2
 Positron emission tomography (PET) scanning
demonstrates that blood flow is reduced
moderately during a migraine attack.
 In 1977, Sicuteri : a state of dopaminergic
hypersensitivity is present in patients with
migraine. Interest in this theory has been
renewed recently. A variety of prodromal
symptoms (eg, yawning, irritability, nausea,
vomiting) can be attributed to relative
dopaminergic stimulation.
Patofisiologi 3
 Another theory proposes that deficiency of
magnesium in the brain triggers a chain of
events, starting with platelet aggregation and
glutamate release and, finally, resulting in the
release of 5-HT, which is a vasoconstrictor.
Medical Care
Abortive Medication Stratification by Severity

Moderate Severe Extremely Severe

NSAIDs Naratriptan DHE (IV)
Isometheptene Rizatriptan Opioids
Ergotamine Sumatriptan (SC,NS) Dopamine antagonists
Naratriptan Zolmitriptan
Rizatriptan Almotriptan
Sumatriptan Frovatriptan
Zolmitriptan Eletriptan
Almotriptan DHE (NS/IM)
Frovatriptan Ergotamine
Eletriptan Dopamine
Dopamine antagonists
antagonists

©International Headache Society

2003/5
Medical Care
Preventive Drugs

First line High efficacy Beta-blockers

Tricyclic antidepressants
Divalproex
Topiramate
Low efficacy Verapamil
NSAIDs
SSRIs
Second line High efficacy Methysergide
Flunarizine
MAOIs
Unproven efficacy Cyproheptadine
Gabapentin
Lamotrigine

©International Headache Society

2003/5
Medical Care
Preventive Medication for Comorbid Conditions

Hypertension Beta-blockers
Angina Beta-blockers
Stress Beta-blockers
Depression Tricyclic antidepressants, SSRIs
Underweight Tricyclic antidepressants
Epilepsy Valproic acid, Topiramate
Mania Valproic acid

©International Headache Society

2003/5
2. TENSION-TYPE HEADACHE (TTH)
2.1 Infrequent episodic tension-type headache
2.1.1 Infrequent episodic tension-type headache associated with pericranial
tenderness
2.1.2 Infrequent episodic tension-type headache not associated with
pericranial tenderness
2.2 Frequent episodic tension-type headache
2.2.1 Frequent episodic tension-type headache associated with pericranial
tenderness
2.2.2 Frequent episodic tension-type headache not associated with pericranial
tenderness
2.3 Chronic tension-type headache
2.3.1 Chronic tension-type headache associated with pericranial tenderness
2.3.2 Chronic tension-type headache not associated with pericranial
tenderness
2.4 Probable tension-type headache
2.4.1 Probable infrequent episodic tension-type headache
2.4.2 Probable frequent episodic tension-type headache
2.4.3 Probable chronic tension-type headache
Infrequent episodic tension-type headache

Description:
Infrequent episodes of headache lasting minutes
to days. The pain is typically bilateral, pressing
or tightening in quality and of mild to moderate
intensity, and it does not worsen with routine
physical activity. There is no nausea but
photophobia or phonophobia may be present.
Infrequent episodic tension-type headache
Diagnostic criteria:
A. At least 10 episodes occurring on <1 day per month on
average (<12 days per year) and fulfilling criteria B-D
B. Headache lasting from 30 minutes to 7 days
C. Headache has at least two of the following characteristics:
1. bilateral location
2. pressing/tightening (non-pulsating) quality
3. mild or moderate intensity
4. not aggravated by routine physical activity such as
walking or climbing stairs
D. Both of the following:
1. no nausea or vomiting (anorexia may occur)
2. no more than one of photophobia or phonophobia
E. Not attributed to another disorder1
Pathofisiologi
Stress may cause contraction of neck and
scalp muscles, although no evidence
confirms that the origin of pain is
sustained muscle contraction.
 Stress and/or anxiety
 Poor posture
 Depression
 Psychological or social problems
Pathophysiology
 Pathogenesis of TTH is complex and multifactorial, with
contributions from both central and peripheral factors. In the
past, various mechanisms including vascular, muscular (ie,
constant overcontraction of scalp muscles), and psychogenic
factors were suggested. The more likely cause of these
headaches is believed now to be abnormal neuronal sensitivity
and pain facilitation, not abnormal muscle contraction.
 Various evidence suggests that, like migraine, TTH is associated
with exteroceptive suppression (ES2), abnormal platelet
serotonin, and decreased cerebrospinal fluid beta-endorphin. In
one study, plasma levels of substance P, neuropeptide Y, and
vasoactive intestinal peptide were found to be normal in patients
with CTTH and unrelated to the headache state.

©International Headache Society

2003/5
Pathophysiology
 Several concurrent pathophysiologic mechanisms may be
responsible for TTH; according to Jensen, extracranial
myofascial nociception is one of them. Headache is not related
directly to muscle contraction, and possible hypersensitivity of
neurons in the trigeminal nucleus caudalis has been suggested.
 Bendtsen described central sensitization at the level of the spinal
dorsal horn/trigeminal nucleus due to prolonged nociceptive
inputs from pericranial myofascial tissues. The central
neuroplastic changes may affect regulation of peripheral
mechanisms and can lead to increased pericranial muscle
activity or release of neurotransmitters in myofascial tissues.
This central sensitization may be maintained even after the initial
eliciting factors have been normalized, resulting in conversion of
ETTH into CTTH
©International Headache Society
2003/5
Treatment
 Management of TTH consists of pharmacotherapy, psychophysiologic therapy, and
physical therapy.
 Treatment of headache must be tailored for individual patients.
 Recognition of comorbid illness is essential. Migraine may be associated with TTH, and
management overlaps. Other associated conditions may include depression, anxiety, and
emotional or adjustment disorders.
 Management of CTTH with a combination of tricyclic antidepressant medication and stress
management therapy may result in a better outcome than monotherapy (Holroyd et al, 2001).
 Pharmacotherapy consists of abortive therapy (to stop or reduce severity of the
individual attack) and long-term preventive therapy. Preventive drugs are the main
therapy for CTTH, but they seldom are needed for ETTH.
 These headaches (especially ETTH) generally respond to simple over-the-counter (OTC)
analgesics such as paracetamol (ie, acetaminophen), ibuprofen, aspirin, or naproxen.
 If treatment is unsatisfactory, the addition of caffeine or use of prescription drugs is
recommended. If possible, avoid use of barbiturates or opiate agonists.
 Also discourage overuse of all symptomatic analgesics because of the risk of dependence,
abuse, and development of chronic daily headache.
 Fiorinal with codeine is generally significantly more effective than placebo or Fiorinal alone. The
combination is also significantly better than codeine alone in relieving pain and maintaining
ability to perform daily activities. However, Fiorinal with codeine is not first-line therapy and
carries a significant risk of abuse.
©International Headache Society
2003/5
 Treatment 2
 Consider preventive medications if the headaches are frequent (>2 attacks per wk), of long duration (>3-4
h), or severe enough to cause significant disability or overuse of abortive medication.
 Amitriptyline (Elavil) and nortriptyline (Pamelor) are the most frequently used tricyclic antidepressants.
 The selective serotonin reuptake inhibitors (SSRIs) fluoxetine (Prozac), paroxetine (Paxil), and
sertraline (Zoloft) also are used commonly by many physicians. In a double-blind placebo-controlled
trial conducted by Saper et al of fluoxetine in patients with chronic daily headache and migraine, it
was reported to be helpful.
 Other antidepressants such as doxepin, desipramine, protriptyline, and buspirone also can be used.
According to Cohen, protriptyline may be comparable in effectiveness to amitriptyline in CTTH without
producing drowsiness and weight gain.
 As reported by Bendtsen et al, in one double-blind trial that compared citalopram to amitriptyline and
a placebo, patients on citalopram demonstrated lower headache scores than those on placebo, but
amitriptyline was significantly more effective.
 Tizanidine may improve inhibitory function in the central nervous system and can provide pain relief.
One recent study by Saper et al provides support for the efficacy of tizanidine in the prophylaxis of
chronic daily headache. Currently the use of tizanidine remains investigational in the treatment of this
disorder.
 Physical therapy techniques include hot or cold applications, positioning, stretching exercises, traction,
massage, ultrasound therapy, transcutaneous electrical nerve stimulation (TENS), and manipulations.
 Heat, massage, and stretching can be used to alleviate excess muscle contraction and pain.
 Cranial electrotherapy stimulation is different from TENS, is safe, and may be effective in alleviating
the pain intensity of TTH. It may be considered as an alternative to long-term analgesic use.

©International Headache Society

2003/5
Treatment 3
 Psychophysiologic therapy includes reassurance, counseling, relaxation
therapy, stress management programs, and biofeedback techniques. With
these modalities of treatment, both frequency and severity of chronic
headache may be reduced.
 In a few studies, such as that by Holroyd et al, benefits from cognitive-behavioral
therapy and biofeedback therapy have been reported.
 Biofeedback may be helpful in some patients when combined with medications.
 One prospective study of TTH in an elderly population suggested that relaxation
therapy may be an effective intervention.
 The following various minimally invasive techniques may provide pain
relief:
 Trigger point injections
 Greater or lesser occipital nerve blocks
 Auriculotemporal nerve block
 Supraorbital nerve block
 Botulinum toxin injection in the pericranial muscle
 Other alternative treatments: In one study, Biondi and Portuesi suggested that
acupuncture results are difficult to assess and that acupuncture should be
reserved for selected patients.
©International Headache Society
2003/5
Pengobatan Sakit Kepala Tipe
Tegang
 Analgetika
 Anti ansietas
 Anti depresan
 Relaksan otot
 Terapi relaksasi
 Nasehat
 Olah raga  Meditasi
 Olah seni  Rekreasi / hobi
 Membaca
3.1 Cluster headache
Description:
Attacks of severe, strictly unilateral pain which is orbital,
supraorbital, temporal or in any combination of these
sites, lasting 15-180 minutes and occurring from once
every other day to 8 times a day. The attacks are
associated with one or more of the following, all of which
are ipsilateral: conjunctival injection, lacrimation, nasal
congestion, rhinorrhoea, forehead and facial sweating,
miosis, ptosis, eyelid oedema. Most patients are restless
or agitated during an attack.
3.1 Cluster headache
Diagnostic criteria:
A. At least 5 attacks fulfilling criteria B-D
B. Severe or very severe unilateral orbital, supraorbital and/or
temporal pain lasting 15-180 minutes if untreated
C. Headache is accompanied by at least one of the following:
1. ipsilateral conjunctival injection and/or lacrimation
2. ipsilateral nasal congestion and/or rhinorrhoea
3. ipsilateral eyelid oedema
4. ipsilateral forehead and facial sweating
5. ipsilateral miosis and/or ptosis
6. a sense of restlessness or agitation
D. Attacks have a frequency from one every other day to 8 per day
E. Not attributed to another disorder
Pengobatan Migren / Klaster
I. Migren akut
 Analgetika
 NSAID
 Ergotamin
 Gol triptan
II. Terapi preventif
 Flunarizine
 Pizatifen
 Cyproheptadin
III. Nasehat : Hindari “5K” es, coklat, keju
Pathophysiology
 The pathophysiology of CH is not entirely understood. Its typical
periodicity has been attributed to hypothalamic (particularly
suprachiasmatic nuclei) hormonal influences. More recently, functional
neuroimaging with positron emission tomography (PET) and
anatomical imaging with voxel-based morphometry have identified the
posterior hypothalamic grey matter as the key area for the basic
defect in CH. Hypothalamic dysfunction has recently been confirmed
by abnormal metabolism based on the N-acetylaspartate neuronal
marker in magnetic resonance spectroscopy.
 CH pain is thought to be generated at the level of the
pericarotid/cavernous sinus complex. This region receives
sympathetic and parasympathetic input from the brain stem, possibly
mediating occurrence of autonomic phenomena during an attack. The
exact roles of immunologic and vasoregulatory factors, as well as the
influence of hypoxemia and hypocapnia, in CH are still controversial.

©International Headache Society

2003/5
Drug Category: Abortive agents
These agents are administered to abort an attack of CH. Because of the duration
of the attacks, they must provide immediate relief.
High-flow oxygen 6-8 L/min concentrated (100%) oxygen by face mask for no
longer than 15 min

Drug Category: Ergot alkaloids

These agents are highly effective in relieving acute CH pain.
Ergotamine, Sumatriptan, naratriptan

Drug Category: Anesthetics

Local anesthetics stabilize the neuronal membrane so the neuron is less
permeable to ions. This prevents initiation and transmission of nerve impulses,
thereby producing the local anesthetic action
Intranasal lidocaine 4%
Drug Category: Anticonvulsants
Efficacy in the prophylaxis of CH has been demonstrated in a few relatively small
controlled studies. Unclear mechanism of action for the prevention of CH. May
act by regulating central sensitization
Divalproex sodium, Topiramate
Drug Category: Antimigraine agents
These agents may reduce the inflammation associated with migraine headaches
Intranasal zolmitriptan
Other primary headaches
4.1 Primary stabbing headache
4.2 Primary cough headache
4.3 Primary exertional headache
4.4 Primary headache associated with sexual
activity
4.4.1 Preorgasmic headache
4.4.2 Orgasmic headache
4.5 Hypnic headache
4.6 Primary thunderclap headache
4.7 Hemicrania continua
4.8 New daily-persistent headache (NDPH)
 Classification
Part 2: The secondary headaches
5. Headache attributed to head and/or neck
trauma
6. Headache attributed to cranial or cervical
vascular disorder
7. Headache attributed to non-vascular
intracranial disorder
8. Headache attributed to a substance or its
withdrawal
9. Headache attributed to infection
ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
 Classification
Part 2: The secondary headaches
10.Headache attributed to disorder of
homoeostasis
11. Headache or facial pain attributed to
disorder of cranium, neck, eyes, ears, nose,
sinuses, teeth, mouth or other facial or
cranial structures
12. Headache attributed to psychiatric
disorder

ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4

Diagnostic criteria for secondary
headaches:
A. Headache with one (or more) of the following
[listed] characteristics1;2 and fulfilling criteria C and
D
B. Another disorder known to be able to cause
headache has been demonstrated
C. Headache occurs in close temporal relation to the
other disorder and/or there is other evidence of a
causal relationship
D. Headache is greatly reduced or resolves within 3
months (this may be shorter for some disorders)
after successful treatment or spontaneous
remission of the causative disorder3
 Classification

Part 3: Cranial neuralgias, central

and primary facial pain and other
headaches
13. Cranial neuralgias and central causes of
facial pain
14. Other headache, cranial neuralgia, central
or primary facial pain

ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4

Classical trigeminal neuralgia
Description:

Trigeminal neuralgia is a unilateral disorder characterised

by brief electric shock-like pains, abrupt in onset and
termination, limited to the distribution of one or more
divisions of the trigeminal nerve. Pain is commonly
evoked by trivial stimuli including washing, shaving,
smoking, talking and/or brushing the teeth (trigger
factors) and frequently occurs spontaneously.
Classical trigeminal neuralgia
Diagnostic criteria:
A. Paroxysmal attacks of pain lasting from a fraction of a
second to 2 minutes, affecting one or more divisions of
the trigeminal nerve and fulfilling criteria B and C
B. Pain has at least one of the following characteristics:
1. intense, sharp, superficial or stabbing
2. precipitated from trigger areas or by trigger factors
C. Attacks are stereotyped in the individual patient
D. There is no clinically evident neurological deficit
E. Not attributed to another disorder
Pathophysiology
 Usually no structural lesion is present, although
many investigators agree that vascular
compression, typically venous or arterial loops
at the trigeminal nerve entry into the pons, is
critical to the pathogenesis of the idiopathic
variety. This compression results in focal
trigeminal nerve demyelination.
 Since the exact pathophysiology remains
controversial, TN may have either a central
and/or peripheral etiology
Pengobatan Neuralgia Trigeminus

 Karbamazepin
 Suntikan lokal
 Operasi
Sakit kepala yang SERIUS
 Sakit kepala yang hebat
 Sakit kepala yang progresif
 Sakit kepala yang disertai
 kesadaran menurun
 kebingungan
 demam tinggi
 gangguan pengelihatan
 gangguan keseimbangan
 kelemahan
TERIMAKASIH