(07Mei) Nyeri Kepala - Sefalgia - Headache (1)

NYERI KEPALA (CEFALGIA / HEADACHE)dr. Sholihul Muhibbi, Sp.S, M.Si.Med.

DEFINISI NYERIPengalaman 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 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

NYERIN. NEUROPATIKN. NOSISEPTIFN. PSIKOGENIKPeriferSentralN. SomatikN. ViseralReferred PainKLASIFIKASI 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 PathwayPain PerceptionBrainDorsal RootGanglionDorsal HornNociceptorSpinal CordGottschalk A et al. Am Fam Physician. 2001;63:1979-84.Fields HL et al. Harrisons 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)

MigraineDescription: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 migrainosusA debilitating migraine attack lasting for more than 72 hours.

MigraineDiagnostic 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 phonophobiaE.Not attributed to another disorder

PatofisiologiThe 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 alIn 1944, Leao proposed the theory of Cortikal Spreading Depression (CSD) to explain the mechanism of migraine with aura.

Patofisiologi 2Positron 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 3Another 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 CareInternational Headache Society 2003/5Abortive Medication Stratification by Severity

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

International Headache Society 2003/5

Medical CareInternational Headache Society 2003/5Preventive Drugs

First lineHigh efficacyBeta-blockers Tricyclic antidepressants Divalproex TopiramateLow efficacyVerapamil NSAIDs SSRIsSecond lineHigh efficacyMethysergide Flunarizine MAOIsUnproven efficacyCyproheptadine Gabapentin Lamotrigine


Medical CareInternational Headache Society 2003/5Preventive Medication for Comorbid Conditions

HypertensionBeta-blockersAnginaBeta-blockersStressBeta-blockersDepressionTricyclic antidepressants, SSRIsUnderweightTricyclic antidepressantsEpilepsyValproic acid, TopiramateManiaValproic acid


2. TENSION-TYPE HEADACHE (TTH)2.1Infrequent 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 tenderness2.3Chronic tension-type headache2.3.1 Chronic tension-type headache associated with pericranial tenderness2.3.2 Chronic tension-type headache not associated with pericranial tenderness2.4Probable tension-type headache2.4.1Probable infrequent episodic tension-type headache2.4.2Probable frequent episodic tension-type headache2.4.3Probable chronic tension-type headache

Infrequent episodic tension-type headacheDescription: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 headacheDiagnostic criteria:A.At least 10 episodes occurring on

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

PathophysiologyPathogenesis 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


PathophysiologySeveral 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 CTTHInternational Headache Society 2003/5


TreatmentManagement 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 2Consider 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 3Psychophysiologic 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.



Pengobatan Sakit Kepala Tipe Tegang AnalgetikaAnti ansietasAnti depresanRelaksan ototTerapi relaksasiNasehat Olah raga Meditasi Olah seni Rekreasi / hobi Membaca

3.1Cluster 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.

3.1Cluster 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 agitationD. 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 triptanII. Terapi preventif Flunarizine Pizatifen CyproheptadinIII.Nasehat : Hindari 5K es, coklat, keju

PathophysiologyThe 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 minDrug 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, TopiramateDrug Category: Antimigraine agentsThese agents may reduce the inflammation associated with migraine headachesIntranasal zolmitriptan

Other primary headaches4.1Primary stabbing headache4.2Primary cough headache4.3Primary exertional headache4.4Primary headache associated with sexual activity4.4.1Preorgasmic headache4.4.2Orgasmic headache4.5Hypnic headache4.6Primary thunderclap headache4.7Hemicrania continua4.8New daily-persistent headache (NDPH)

Diagnostic criteria for secondary headaches: A.Headache with one (or more) of the following [listed] characteristics1;2 and fulfilling criteria C and DB.Another disorder known to be able to cause headache has been demonstratedC.Headache occurs in close temporal relation to the other disorder and/or there is other evidence of a causal relationshipD.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

Classical 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 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 CB. Pain has at least one of the following characteristics:1.intense, sharp, superficial or stabbing2.precipitated from trigger areas or by trigger factorsC. Attacks are stereotyped in the individual patientD. There is no clinically evident neurological deficitE. Not attributed to another disorder

PathophysiologyUsually 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 KarbamazepinSuntikan lokalOperasi

Sakit kepala yang SERIUSSakit kepala yang hebatSakit kepala yang progresifSakit kepala yang disertai kesadaran menurun kebingungan demam tinggi gangguan pengelihatan gangguan keseimbangan kelemahan

TERIMAKASIH

*Nyeri adalah pengalaman sensorik dan emosional yang tidak menyenangkan akibat kerusakan jaringan,baik aktual maupun potensial, atau yang digambarkan dalam bentuk kerusakan tersebut.Dari definisi nyeri, tersurat selain pengalaman sensoris terdapat pula pengalaman emosional. Kedua hal tersebut perlu diperhatikan dalam penanganan. *Nyeri dapat berupa nyeri sederhana/fisiologik, nyeri inflamasi ( nyeri nosiseptik ), nyeri neuropatik, dan nyeri idiopatik, termasuk nyeri psikogenik. Nyeri neuropatik adalah nyeri yang didahului atau disebabkan oleh lesi atau disfungsi primer pada sistem saraf. Bila pada sistem saraf perifer disebut nyeri neuropatik perifer dan bila pada sistem saraf sentral disebut nyeri sentral.Pada nyeri psikogenik tidak ada kerusakan jaringan atau patafisiologik sebagai penyebab. **Activation of peripheral pain receptors, also called nociceptors, by noxious stimuli generates signals that travel to the dorsal horn of the spinal cord via the dorsal root ganglion. From the dorsal horn, the signals are carried along the ascending pain pathway or the spinothalamic tract to the thalamus and the cortex. Pain can be controlled by pain-inhibiting and pain-facilitating neurons. Descending signals originating in supraspinal centers can modulate activity in the dorsal horn by controlling spinal pain transmission.1,2

Gottschalk A, Smith DS. New concepts in acute pain therapy: preemptive analgesia. Am Fam Physician. 2001;63:1979-1984. Fields HL, Martin JB. Pain: pathophysiology and management. In: Fauci AS, Braunwald E, Isselbacher KF, et al, eds. Harrisons Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998:53-58.

2:19793:552:19813:55

(07Mei) Nyeri Kepala - Sefalgia - Headache (1)

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