Headache UPN 04 12

NYERI KEPALA (CEFALGIA / HEADACHE)

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

DEFINISI NYERIDEFINISI NYERI

Pengalaman sensorik dan emosional yang

tidak menyenangkan akibat kerusakan jaringan,

baik aktual maupun potensial, atau yang digambarkan dalam bentuk kerusakan tersebut.

International Association for the Study of Pain (IASP)

KLASIFIKASI NYERIKLASIFIKASI NYERII. Nyeri sederhana / fisiologik Nyeri timbul oleh berbagai stimuli yg

tidak menimbulkan kerusakan jaringan

II. Nyeri patologik / klinis1. Nyeri nosiseptik Nyeri timbul oleh berbagai stimuli yg menimbulkan kerusakan jaringan (somatik,

viseral, nyeri rujuk/referred pain)2. Nyeri neuropatik

3. Nyeri idiopatik / psikogenik

NYERINYERI

N. NEUROPATIKN. NEUROPATIK

N. NOSISEPTIFN. NOSISEPTIF N. PSIKOGENIKN. PSIKOGENIK

PeriferPeriferSentralSentral

N. SomatikN. SomatikN. ViseralN. Viseral

Referred PainReferred Pain

KLASIFIKASI NYERIKLASIFIKASI NYERI

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.

DEFINISI

The Pain Pathway

Pain PerceptionBrain

Dorsal RootGanglion

Dorsal Horn

Nociceptor

Spinal Cord

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 KepalaRasa 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.

(ICHD-II)

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

INTERNATIONAL CLASSI FI CATIONof

HEADACHE DISORDERS2nd edition

(ICHD-II)


Classification

Part 1:Primary headache disorders

Part 2:Secondary headache disorders

Part 3:Cranial neuralgias, central and primary facial pain and other headaches


Primary or secondary headache?

Primary:

• no other causative disorder


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)


Classification

Part 1: The primary headaches1. Migraine2. Tension-type headache3. Cluster headacheand other trigeminal autonomiccephalalgias

4. Other primary headaches


ClassificationPart 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-vascularintracranial disorder

8. Headache attributed to a substance or its withdrawal

9. Headache attributed to infection



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


Classification

Part 3: Cranial neuralgias, central and primary facial pain and other headaches13. Cranial neuralgias and central causes of

facial pain14. Other headache, cranial neuralgia, central

or primary facial pain

MigraineMigraineDescription:Description:Recurrent headache disorder manifesting in attacks Recurrent headache disorder manifesting in attacks

lasting lasting 4-72 hours4-72 hours. Typical characteristics of the . Typical characteristics of the headache are headache are unilateral locationunilateral location, , pulsatingpulsating quality, quality, moderate or severe intensitymoderate or severe intensity, aggravation by , aggravation by routine physical activity and association with routine physical activity and association with nausea and/or photophobia and phonophobia.nausea and/or photophobia and phonophobia.

Status migrainosusStatus migrainosusA debilitating migraine attack lasting for more

than 72 hours.

MigraineMigraineDiagnostic criteria:A. At least 5 attacks1 fulfilling criteria B-DB. Headache attacks lasting 4-72 hours (untreated or

unsuccessfully treated)C. Headache has at least two of the following

characteristics:1. unilateral location2. pulsating quality3. moderate or severe pain intensity4. 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 vomiting2. photophobia and phonophobia

E. Not attributed to another disorder

PatofisiologiPatofisiologi 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 Patofisiologi 22

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 Patofisiologi 33

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 CareModerate Severe Extremely SevereNSAIDs

IsomethepteneErgotamineNaratriptanRizatriptan

SumatriptanZolmitriptanAlmotriptanFrovatriptan

EletriptanDopamine

antagonists

NaratriptanRizatriptan

Sumatriptan (SC,NS)ZolmitriptanAlmotriptanFrovatriptan

EletriptanDHE (NS/IM)ErgotamineDopamine

antagonists

DHE (IV)Opioids

Dopamine antagonists

©International Headache Society 2003/5

Abortive Medication Stratification by Severity

Medical Care


First line High efficacy Beta-blockersTricyclic antidepressantsDivalproexTopiramate

Low efficacy VerapamilNSAIDsSSRIs

Second line High efficacy MethysergideFlunarizineMAOIs

Unproven efficacy CyproheptadineGabapentinLamotrigine

Preventive Drugs

Medical Care


Hypertension Beta-blockersAngina Beta-blockersStress Beta-blockersDepression Tricyclic antidepressants, SSRIsUnderweight Tricyclic antidepressantsEpilepsy Valproic acid, TopiramateMania Valproic acid

Preventive Medication for Comorbid Conditions

2. TENSION-TYPE HEADACHE (TTH)2.1 Infrequent episodic tension-type headache2.1.1 Infrequent episodic tension-type headache associated with pericranial

tenderness2.1.2 Infrequent episodic tension-type headache not associated with pericranial

tenderness2.2 Frequent episodic tension-type headache2.2.1 Frequent episodic tension-type headache associated with pericranial tenderness2.2.2 Frequent episodic tension-type headache not associated with pericranial

tenderness2.3 Chronic tension-type headache2.3.1 Chronic tension-type headache associated with pericranial tenderness2.3.2 Chronic tension-type headache not associated with pericranial tenderness2.4 Probable tension-type headache2.4.1 Probable infrequent episodic tension-type headache2.4.2 Probable frequent episodic tension-type headache2.4.3 Probable chronic tension-type headache

Infrequent episodic tension-type Infrequent episodic tension-type headacheheadacheDescription: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 Infrequent episodic tension-type headacheheadacheDiagnostic criteria:A. At least 10 episodes occurring on <1 day per month on average (<12 days

per year) and fulfilling criteria B-DB. Headache lasting from 30 minutes to 7 daysC. Headache has at least two of the following characteristics:

1. bilateral location2. pressing/tightening (non-pulsating) quality3. mild or moderate intensity4. 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

PathofisiologiStress may cause contraction of neck and

scalp muscles, although no evidence confirms that the origin of pain is sustained muscle contraction. Stress and/or anxietyPoor postureDepressionPsychological or social problems

Pengobatan Sakit Kepala Pengobatan Sakit Kepala Tipe Tegang Tipe Tegang Analgetika Anti ansietas Anti depresan Relaksan otot Terapi relaksasi Nasehat

Olah raga Meditasi Olah seni Rekreasi / hobi Membaca

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.

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


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.


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.


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.


3.1 Cluster headacheDescription: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 headacheDiagnostic criteria:A. At least 5 attacks fulfilling criteria B-DB. Severe or very severe unilateral orbital, supraorbital and/or temporal pain

lasting 15-180 minutes if untreatedC. Headache is accompanied by at least one of the following:

1. ipsilateral conjunctival injection and/or lacrimation2. ipsilateral nasal congestion and/or rhinorrhoea3. ipsilateral eyelid oedema4. ipsilateral forehead and facial sweating5. ipsilateral miosis and/or ptosis6. a sense of restlessness or agitation

D. Attacks have a frequency from one every other day to 8 per dayE. 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.


Drug Category: Abortive agentsThese 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 alkaloidsThese agents are highly effective in relieving acute CH pain.Ergotamine, Sumatriptan, naratriptan

Drug Category: AnestheticsLocal 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 actionIntranasal lidocaine 4%

Drug Category: AnticonvulsantsEfficacy 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 sensitizationDivalproex sodium, Topiramate

Drug Category: Antimigraine agentsThese agents may reduce the inflammation associated with migraine headachesIntranasal zolmitriptan

Other primary headaches4.1 Primary stabbing headache4.2 Primary cough headache4.3 Primary exertional headache4.4 Primary headache associated with

sexual activity4.4.1 Preorgasmic headache4.4.2 Orgasmic headache4.5 Hypnic headache4.6 Primary thunderclap headache4.7 Hemicrania continua4.8 New daily-persistent headache (NDPH)



5. Headache attributed to head and/or neck trauma

6. Headache attributed to cranial or cervical vascular disorder

7. Headache attributed to non-vascularintracranial disorder

8. Headache attributed to a substance or its withdrawal

9. Headache attributed to infection



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

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 headaches13. Cranial neuralgias and central causes of

facial pain14. Other headache, cranial neuralgia, central

or primary facial pain

Classical trigeminal neuralgiaClassical trigeminal neuralgiaDescription:

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 neuralgiaClassical trigeminal neuralgiaDiagnostic 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 SERIUSSakit 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

TTEERRIIMMAAKKAASSIIHH

Headache UPN 04 12

Documents

Transcript of Headache UPN 04 12