HUBUNGAN NYERI KEPALA YANG DISERTAI KEJANG

DENGAN DIAGNOSIS MENINGIOMA INTRAKRANIAL

Diajukan oleh :

Johny P.A Kambu

Latar Belakang

MeningiomaMeningioma terjadi pada 13 - 26 % dari tumor intrakranialterjadi pada 13 - 26 % dari tumor intrakranial

usia 40-70 tahunusia 40-70 tahun

Head CT scan Head CT scan

gambaran karakteristik

gambaran karakteristik

Diagnosis akurat & menunjukkan perbedaan

histologis

Diagnosis akurat & menunjukkan perbedaan

histologis

nyeri kepala(66.7%)

nyeri kepala(66.7%)

epilepsi 20–50% - Simptom awal

epilepsi 20–50% - Simptom awal

survival 5 tahunsurvival 5 tahun

• 70% pada pasien tumor benign

• 75% untuk tumor atipikal

• 55% untuk pasien tumor anaplastik

• 70% pada pasien tumor benign

• 75% untuk tumor atipikal

• 55% untuk pasien tumor anaplastik

RS DR. Sardjito Yogya-karta mempunyai re-rata 33,4 kasus per tahun

RS DR. Sardjito Yogya-karta mempunyai re-rata 33,4 kasus per tahun

Latar Belakang(Lanj.)

AstrositomaAstrositoma 80% dari tumor otak primer

80% dari tumor otak primer

• 10% terjadi dibawah umur 20 tahun

• 60% antara umur 20 sampai 45

• sekitar 30% diatas 45 tahun

• 10% terjadi dibawah umur 20 tahun

• 60% antara umur 20 sampai 45

• sekitar 30% diatas 45 tahunSURVIVAL:

• 10 tahun untuk pilocytic astrocytomas (WHO derajat I)

• lebih dari 5 tahun untuk pasien dengan low-grade diffuse astrocytomas (WHO derajat II)

• 2-5 tahun pada penderita anaplastic astrocytomas (WHO derajat III)

• kurang dari 1 tahun untuk pasien dengan glioblastoma (WHO derajat IV)

SURVIVAL: • 10 tahun untuk pilocytic astrocytomas

(WHO derajat I)• lebih dari 5 tahun untuk pasien dengan

low-grade diffuse astrocytomas (WHO derajat II)

• 2-5 tahun pada penderita anaplastic astrocytomas (WHO derajat III)

• kurang dari 1 tahun untuk pasien dengan glioblastoma (WHO derajat IV)

RS DR. Sardjito Yogyakarta mempunyai rerata 16,4 kasus per tahun

RS DR. Sardjito Yogyakarta mempunyai rerata 16,4 kasus per tahun

Latar Belakang(Lanj.)

AstrositomaAstrositomaSetengah sampai dua per tiga pasien dengan glioma derajat

rendah mengalami kejang

Setengah sampai dua per tiga pasien dengan glioma derajat

rendah mengalami kejang

sekitar 50% mengalami

nyeri kepala

sekitar 50% mengalami

nyeri kepala

Pertanyaan Penelitian

• Apakah pasien dengan nyeri kepala yang disertai kejang cenderung mengalami meningioma intrakranial?

Tujuan Penelitian

• Penelitian ini bertujuan untuk melihat kecenderungan nyeri kepala yang disertai kejang dengan kejadian meningioma intrakranial dibandingkan dengan astrositoma

Keaslian Penelitian

Keaslian Penelitian (Lanj.)

Manfaat Penelitian

Penelitian ini diharapkan memberikan tambahan pengetahuan klinisi terhadap kecenderungan nyeri kepala yang disertai kejang dengan kejadian meningioma intrakranial sehingga diharapkan dapat membantu menegakkan diagnosis meningioma.

Kerangka TeoriMENINGIOMA

HiperostosisIritasi Meningens PTBE Iritasi Korteks

TIK

NK Kejang

Efek Massa

ASTROSITOMA

Lokasi

edema difus

hidrosefalus

Metabolic

Demam Stressor

Destruksi Parenkim Kompresi

Kerangka KonsepMENINGIOMA

Hiperostosis (HCTS)

Iritasi Meningens PTBE (HCTS)

Iritasi Korteks

TIK

NK Kejang

Efek Massa (HCTS)

ASTROSITOMA

Lokasi (HCTS)

edema difus

(HCTS)

Hidrosefalus (HCTS)

Metabolic

Demam Stressor

Destruksi Parenkim Kompresi

Hipotesis

• Pasien nyeri kepala yang disertai kejang cenderung menderita meningioma intrakranial.

Rancangan Penelitian

• Penelitian ini menggunakan desain case control restropektif.

• Penelitian case control ini untuk melihat hubungan nyeri kepala yang disertai dengan kejang pada pasien meningioma.

• Penelitian case control restropektif mencakup semua jenis penelitian yang pengukuran variabel-variabelnya dilakukan dari data yang telah diperoleh.

Besar Sampel

• Seluruh pasien meningioma dan astrositoma di RS Dr. Sardjito dari Januari 2006 – Desember 2010 dimasukan dalam penelitian. Metode yang dipakai ini dinamakan metode sensus, dimana seluruh populasi dimasukkan dalam penelitian.

Variabel Penelitian• Variabel yang diteliti dalam penelitian ini adalah

nyeri kepala dan kejang pada pasien meningioma dan astrositoma.

• Karakteristik subyek yang dinilai meliputi umur, jenis kelamin, riwayat trauma kepala, riwayat paparan radiasi, riwayat penyakit tumor pada keluarga, riwayat infeksi serebral.

• Variabel tergantung adalah meningioma dan variabel bebas adalah nyeri kepala dan kejang serta astrositoma sebagai variabel kontrol.

• Gangguan hormonal, metabolik, stressor dan demam menjadi variabel perancu.

Pengolahan dan Analisis Data

• Analisis data dilakukan melalui tiga tahapan yaitu deskripsi variabel penelitian, analisis bivariat dan analisis multivariat.

• Uji statistik yang digunakan tergantung pada besar kecilnya ukuran sampel dan skala pengukuran yang digunakan pada variabel tergantung dan variabel bebas.

Pengolahan dan Analisis Data (lanj.)

• Analisis data bivariat pada penelitian ini menggunakan uji chi square dan analisis multivariat regresi logistik.

• Analisis bivariat dilakukan untuk mengidentifikasi hubungan antara variabel bebas dan variabel tergantung. Hal ini dilakukan dengan tujuan untuk mendapatkan nilai Odss Ratio (OR).

• Nilai untuk ukuran risiko dihitung dengan p value < 0,05 dan tingkat kepercayaan 95% (95% Confidence Interval).

• Analisis multivariat, antara variabel tergantung dan independen diuji secara statistik menggunakan uji regresi.

Alur Penelitian

Waktu Penelitian

Terima Kasih

Low-Grade Astrocytoma, Oligodendroglioma (ODG), Meningioma, Glioblastoma multiforme (GBM), Tumor Metastasis, Abses Serebri, Tuberkuloma

Karakteristik Low-Grade Astrocytoma

ODG MeniNgioma

GBM Tumor metastase

Abses serebri

Tuberkuloma

Pasien

Puncak insiden (tahun)

20-40 35-45 40-50 40-55 60-70 20-40 Anak 45

L : P 3:2 3:2 1:2,8 3:2 Tgt primer 2:1 - P

Progresivitas kronik kronik kronik Subakut Subakut, kronik

Akut kronik kronik

Gejala klinik

Nyeri kepala 50% 22% + 50% 50% 70% + +

Defisit fokal 30-40% + + 30-40% 30-50% 50% +/- -

Papil edema frequent occationally

+/- frequent frequent occatio +/- +

Kejang 15% 87% + 15% 15% + + -

Predileksi Frontal, temporal Frontal, temporal, parietal

Frontal, temporal,

parietal

Temp, parietal, frontal

Parietal, frontal

Front , pariet, tempo, occip

Front,pariet,

tempo, occip,serebelum

Frontal

CT scan kepala

Low densityNo enhance

kalsifikasi Kdg kalsifik,

hiperdens

Ring enhanceNecrosis

Hiepr,hipoisoden

Hipoden, bts

tdk tgs

Hipoden, enhance

enhanceNon

homogen

Edem Prominent Prominen Minimal Prominen Prominen promin Promin Prominen

Lesi soliter soliter soliter soliter Multiple solitermultiple

multiple multiple

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- Contralateral limb weakness- Contralateral sensory loss- Disfasia- Disleksia, disgrafia, diskalkulia- Disorientasi spasial

HemianopsiaHomonim Kontralateral

NistagmusDisartriaAtaksia- Ggn saraf kranial

- Ggn fx vital

- Ggn bahasa- Ggn memori- Ggn mood- Ggn perilaku- Hearing & vision pathways

- Demensia- Ggn mood- Ggn perilaku- Inkontinensia- disfungsi olfaktorius- Disfungsi opticus

(Wilkinson, 1997)

MENINGIOMA

• BENIGNA• ARISE from ARACHNOID CAP CELLS (not DURA)• OUTER LAYER of ARACHNOID• LOCATED ALONG FALX, CONVEXITY, SPHENOID

BONE• ADULT• EPILEPSY >>• MAY BE ASYMTOMATIC• TX –> TOTAL RESECTION• GOOD PROGNOSIS

Meningioma

• SLOW GROWING• CIRCUMCRIBED ( non-Infiltratating)• USSUALLY BENIGNA (1,7% are MALIGNANT)• SOLITAIR (may be MULTIPLE up to 8% of cases)• CAUSED HYPEROSTOSIS OF BONE• USSUALLY CURED IF COMPLETELY

REMOVED

EPIDEMIOLOGY

• 14,3%-19% of Primary Intracranial Tumors

• Peak Incidence: 45 years age

• Female : male ratio= 1,8 : 1

• In childhood & adolescene= 1,5%

A. 3 main categories of ‘classic meningiomas’

• Meningotheliomas / angiomatous• Fibrous or fibroblastic• Transtitional Varian :

microcystic,psammomatous,myxomatous, xanthomatous, lipomatous, granular, secretory, chondroblastic, osteoblastic, melanotic

B. Angioblastic : hemangioblastoma

C. Atypical meningioma

D. Malignant meningiomas : anaplastic,

papilary or sarcomatous

types of meningiomas exist based on malignant behavior (WHO1993):

Benign (grade I) with a recurrence rate of 6.9%: Despite invasion of the adjacent bony structures, grade I meningiomas do not invade the brain parenchyma.

Atypical (grade II) with a recurrence rate of 34.6%: This type of meningioma shows frequent mitosis and an increased nuclear-cytoplasmic ratio.

Malignant (grade III and IV) with a recurrence rate of 72.7%: This type of meningioma shows even greater mitosis, necrosis, and invasion of brain parenchyma.

Acoustic Neurinoma

8%

Other9%

Pituitari adenoma

10%

Meningioma15%

Glioma25%

Metastasis33%

INTRACRANIAL TUMORS

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:

The different types of brain tumors include the following:

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a) Acoustic neuroma rare b) Meningioma 19% c) Pituitary adenoma 10% d) Craniopharyngioma 5%

e) Pineal gland tumor 1%

Primary Benign Tumors of the Brain

•Neurological Dysfunction •May affect speech, memory, vision           •Localized weakness or sensory loss due to invasion or compression of adjacent brain tissue           •The resultant neurologic loss dependant on the location of the tumor

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a) Metastatic carcinomas (60% lung, 30% breast)

b) Meningeal carcinomatosis

a) Low Grade Astrocytoma 25% +

b) High Grade Astrocytoma 10%

c) Ependymoma 6%

d) Oligodendrocytoma 5%

Primary Malignant Tumors of the BrainI.Gliomas (Most common type of primary tumor)

Metastatic Tumors of the Brain

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Tabel 1. Tipe Tumor Jaringan Saraf

Tumor Persentase

Glioma (41%)

Glioblastoma multiforme

Astrocytoma

Ependymoma

Medulloblastoma

Oligodendrocytoma

Meningioma (17%)

Pituitary adenoma (13%)

Neurinoma (Schwannoma) (12%)

Metastatic carcinoma

Craniopharyngioma, dermoid, epidermoid, teratoma

Angioma

Sarcoma

Unclassified (mostly glioma)

Miscellaneous (pinealoma, chordoma, granuloma, lymphoma)

Total

20

10

6

4

5

15

7

7

6

4

4

4

5

3

100Sumber: Victor & Ropper, 2002. Back

ETIOLOGI

• Berhubungan dengan :

• Therapi radiasi

Baik pada dosis tinggi maupun rendah

• Hormone sex

Sekitar 2/3 tumor mengekspresikan reseptor Progesterone

• Genetik

• Genetik:

• Kehilangan kromosom 22

• Mutasi gen NF2

Etiologi dan Faktor Resiko

• Genetik– Familial

• Lingkungan– Radiasi– Trauma kapitis berat– Paparan Kronis bahan petrokimia

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Etilogi tumor

• Perubahan dari protoonkogen menjadi onkogen• Penurunan tumor suppressor gen• Peningkatan gen controlling growth factor• Herediter ( misalnya peningkatan tumor otak

pada neurofibromatosis dan tuberoussklerosis)• Trauma• Infeksi • Radiasi

STRUKTUR SEL NORMAL• Membran sel• Sitoplasma• Inti atau nukleus

SEL TUMOR MALIGNA• Mitosis lebih cepat• Produksi enzim colagenase IV• Kemampuan produksi zat kimia

(angiogenesis factor)Back

In some cancers, it is the body's blood cells which multiply abnormally. These cancers are called leukaemia, myeloma and lymphoma.

                                                                                                                                                              

                                                        

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SIKLUS SELSIKLUS SEL

1.1. G1 : G1 : fase istirahatfase istirahat

2.2. S : S : fase sintesa fase sintesa DNADNA

3.3. G2 : G2 : fase pra fase pra mitosismitosis

4.4. Mitosis : Mitosis : profaseprofase,,anafaseanafase, , telofasetelofase, , metafasemetafase

Fase Fase 3 3 dan dan 4 4 sensitif radiasisensitif radiasi

Fase Fase 1 1 dan dan 2 2 radioresistenradioresisten

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GEJALA KLINIS

TANDA & GEJALA

• Tidak terdapat tanda tunggal atau spesifik untuk meningioma

• Kadang asimptomatis

• Tumor terdeteksi secara tidak sengaja

• Gejala: headache, paresis, seizure, personality change, confusion, visual impairment

TANDA & GEJALA

• Olfactory groove: anosmia, Foster Kenedy symdrome

• Tuberculum sellae: chiasmal syndrome, bitemporal hemianopia

• Cavernous sinus: diplopia, parese n III

• Foramen Magnum: nunchal & suboccipital pain

Symptom and Sign of Brain Tumor Based on Its Location ( Flower, 2000) Back

MEKANISME TANDA KLINIK TUMOR

1. Kompresi pd jaringan neuronal2. Infiltrasi / invasi langsung pd jar

neuronal3. Gangguan pembuluh darah4. Gangguan eksitabilitas5. Penekanan efek massa6. Gangguan sirkulasi aliran LCS

(Spencer, 1989)Back

Gejala Tumor Otak

Ciri utama dari tumor otak ada 4 yaitu:• 1.      defisit neurologis progresif (68%)

– Destruksi-kompresi langsung/tidak langsung

– Akibat masa dan udema

• 2.      motor weakness (45%)• 3.      headache (54%)• 4.      seizure (26%) (Greenberg, 2001)

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Gejala Klinik Tumor Otak (DeAngelis, 2001)

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Def. Neurologis progresif (70%)

Def. Neurologis progresif (70%)

Nyeri kepala (>50%)

Nyeri kepala (>50%)

Kejang (15-20%)

Kejang (15-20%)

-Destruksi atau kompresi langsung-Kompresi akibat massa, edema

-Destruksi atau kompresi langsung-Kompresi akibat massa, edema

Memburuk di pagi hari

Memburuk di pagi hari

-Invasi atau kompresi-TIK tinggi-Sekunder atau psikogenik

-Invasi atau kompresi-TIK tinggi-Sekunder atau psikogenik

Gangguan eksitabilitas neural

Gangguan eksitabilitas neural

Gejala Tumor otak (Crow, 2001)

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NYERI KEPALA PADA TUMOR OTAK

Penyebab kombinasi dari: • 1.  Peningkatan TIK karena:

– a.       Efek massa tumor– b.      Hidrosefalus (obstruktif maupun komunikans)– c.       Efek massa karena edema– d.      Efek masa karena hemorhage

• 2. Invasi/kompresi bangunan peka nyeri : duramater, pembuluh darah, periosteum

• 3. Sekunder gangguan penglihatan:– a.   diplopia, terjadi akibat disfungsi otot ekstraokuler : III,IV,VI, TIK,

inernuklear oftalmoplegi karena ggn brainstem– b.      kesulitan focusing disfungsi nervus optikus

• 4. Ekstrim hipertensi krn kenaikan Tekanan intra kranial • 5. Psikogenik: stress krn kehilangan kemampuan fungsional

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KARAKTERISTIK NYERI KEPALA SOP

1) Tidak terlokalisir dengan baik2) Perjalanan penyakit subakut progresif3) Intensitas sedang sampai berat4) Resisten terhadap analgetik biasa

(Dodick, 1997)

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KARAKTERISTIK NYERI KEPALA SOP

1) memberat pada pagi hari (akibat hipoventilasi selama tidur)

2) memberat dengan batuk, ketegangan3) kepala harus diposisikan tertentu (30% kasus)4) disertai dengan mual dan muntah (40% kasus)

( stl muntah, akibat hiperventilasi)5) Tipe nyeri kepala:

i. 77% menyerupai nyeri kepala tension type headache, ii. 9% menyerupai migraine.iii.8% merupakan nyeri kepala tumor

(Greenberg, 2001)

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Sign and Symptom Tumor Supratentorial

Tumor infratentorial

• Headache + +

• Nausea / vomitus + +

• Papiledema + ++

• Kejang + -

• Gangguan fungsi luhur ++ +

• Ataxia dan gangguan gait - ++

• Vertigo dan nistagmus - ++

• Diplopia + ++

• Ataksia, dismetria, tremor, gangguan koordinasi

- +

• Multicranial nerve palsy - +

• Kelemahan motorik, gangguan endokrin

++ -

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GEJALA DAN TANDA TUMOR SUPRATENTORIAL

• Yang berkaitan dengan TIK : * Dari efek massa tumor dan atau edema * Dari blokade aliran LCS (hidrocefalus) jarang pada terjadi• Defisit fokal : kelemahan, disfasia (37-58% pada

tumor otak di hemisfer kiri. * Destruksi jaringan otak karena infasi tumor * Kompresi jaringan otak oleh massa dan atau edema peritumorald/a perdarahan * Kompresi saraf kranialBack

GEJALA DAN TANDA TUMOR SUPRATENTORIAL

• Nyeri kepala • Kejang• Perubahan status mental: depresi, letargi, apatis,

bingung• Gejala yang menyerupai TIA/stroke: * Oklusi pembuluh darah oleh sel tumor * Perdarahan di dalam tumor• Tumor pituitari : * Gejala yang berhubungan dengan gangguan endokrin * Apopleksi pituitari * Rembesan/bocornya LCS Back

GEJALA DAN TANDA TUMOR INFRATENTORIAL

• Tanda dan gejala efek massa:

* Lesi di hemisfer serebelum : ataksia

ekstremitas, dismetria, tremor

* Lesi di vermis serebelum: ataksia badan

* Batang otak : biasanya melibatkan

multipel saraf kranial dan gangguan

traktus, nistagmus.

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INFRATENTORIAL TUMOR

Peningkatan tek.intrakranial karena hydrosefalus :• Nyeri kepala• Mual / muntah : akibat peningkatan TIK dari

hydrosefalus atau penakanan langsung pada nukleus vagal atau area postrema (pusat muntah)

• Papilledema• Ataxia / ggn berjalan• Vertigo• Diplopia : nervus VI palsy (penekanan langsung pada

nervus VI) (Greenberg, 2001)

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Nyeri kepala

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1. Sinus venosus dan cabang kortikalnya2. Arteria besar di otak3. Duramater yang melingkupi dasar anterior & fossa

posterior4. N. craniales V, IX, X5. Saraf spinal: n. cervical I, II, III

(Gilroy, 2000)

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Gejala dan tanda nyeri kepala yang membutuhkan

kewaspadaan

• Onset nyeri kepala baru pada pasien yang sebelumnya bebas nyeri kepala

• Perubahan pola nyeri kepala ( pola baru dalam intensitas frekuensi dan tipe nyeri kepala)

• Baru saja trauma kepala• Panas yang tidak dijelaskan

(Weinstein, 1999)

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Gejala dan tanda nyeri kepala yang membutuhkan kewaspadaan

• Defisit neurologik fokal dan non fokal ( kelemahan, kesemutan, afasia, gangguan kognitif), perubahan kepribadian, perubahan kesadaran

• Nyeri berat yang belum pernah dirasakan sebelumnya

• Nyeri kepala yang dipicu oleh batuk, bersin dan membungkuk

• Nyeri kepala disertai tanda iritasi meningeal (Weinstein, 1999)

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Red flags pasien nyeri kepala : indikasi klinik untuk

neuroimaging

• Edem papil• Drowsiness, confusion, gangguan

memori, kehilangan kesadaran• Paralisis

(The British Journal of Radiology, 2003)

Red flags nyeri kepala

• Onset baru nyeri kepala pada usia lebih dari 50 tahun

• Onset kejang atau nyeri kepala yang dihubungkan dengan penyakit sistemik termasuk panas

• Perubahan kepribadian• Tanda kenaikan tekanan intrakranial• Nyeri kepala yang memberat dengan batuk, bersin

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(British Medical Journal, 2004)

Red flags Differential diagnosis Possible work-up

Headache beginning after 50 years of age

Temporal arteritis, mass lesion Erythrocyte sedimentation rate, neuroimaging

Sudden onset of headache

Subarachnoid hemorrhage, pituitary apoplexy, hemorrhage into a mass lesion or vascular malformation, mass lesion (especially posterior fossa mass)

Neuroimaging; lumbar puncture if neuroimaging is negative*

Headaches increasing in frequency and severity

Mass lesion, subdural hematoma, medication overuse

Neuroimaging, drug screen

New-onset headache in a patient with risk factors for HIV infection or cancer

Meningitis (chronic or carcinomatous), brain abscess (including toxoplasmosis), metastasis

Neuroimaging; lumbar puncture if neuroimaging is negative*

Headache with signs of systemic illness (fever, stiff neck, rash)

Meningitis, encephalitis, Lyme disease, systemic infection, collagen vascular disease

Neuroimaging, lumbar puncture,¥ serology

Focal neurologic signs or symptoms of disease (other than typical aura)

Mass lesion, vascular malformation, stroke, collagen vascular disease

Neuroimaging, collagen vascular evaluation (including antiphospholipid antibodies)

Papilledema Mass lesion, pseudotumor cerebri, meningitis

Neuroimaging, lumbar puncture¥

Headache subsequent to head trauma

Intracranial hemorrhage, subdural hematoma, epidural hematoma, post-traumatic headache

Neuroimaging of brain, skull and, possibly, cervical spine

Red Flags in the Evaluation of Acute Headaches in Adults

American Family Physician, 2001

Penyebab umum nyeri kepala• Infeksi• Vaskuler Iskemik (trombosis, emboli) Oklusi (arteri, vena) Perdarahan Vaskulitis

• SOP (kompresi,traksi)

Tumor Abses Hematom

• Lain-lain Obstruksi/kebocoran cairan serebrospinal Traumatik Patologi occipito cervical Metabolik Toksik Hipoksik Inflamasi

(Weiner, 1999)

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Acute Primary Headache Disorders More common Migraine with or without aura Tension-type headacheCluster headache

Less commonParoxysmal hemicrania Idiopathic stabbing headache Cold-stimulus headacheBenign cough headache Benign exertional headache Headache associated with sexual activity

American Family Physician, 2001

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Tipe Tempat Karakteristik klinik

Pola Profil

Migren tanpa auraMigren dengan aura

Frontotemporal, uni/bilateral

Berdenyut, berat di belakang mata/telinga, menjadi nyeri tumpul dan menyeluruh

Saat bangun pagi/lebih siang, durasi 4-24 jam

Irreguler, interval minggu sampai bulan

Cluster headache

Orbitotemporal, unilateral

Nyeri hebat, tidak berdenyut

Malam hari, 1-2 jam setelah jatuh tidur

Setiap hari untuk beberapa minggu /bulan, berulang setelah beberapa minggu/tahun

Tension headache

Menyeluruh Menekan, tidak berdenyut

Terus menerusIntensitas berubah dalam hari, minggu, bulan

Satu/lebih periode dari bulan sampai tahun

Iritasi mening

Menyeluruh/bifrontal/bioksipital

Nyeri dalam menetap, hebat

Berulang, berkembang menit sampai jam

Episode tunggal

Tumor otak

Menyeluruh/unilateral

Intensitas berubah, saat bangun, nyeri menetap

Menit sampai jam, memburuk pada pagi

Sekali, minggu sampai bulan

Arteritis temporal

Biasanya temporal

Berdenyut kemudian menetap nyeri dan panas, arteri menebal dan lunak

Berselang kemudian terus menerus

Menetap untuk minggu sampai bulan

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Tipe nyeri kepala (Adams et al, 2001)

Headache associated with head trauma Acute post-traumatic headache

Headache associated with vascular disorders

Subarachnoid hemorrhage Acute ischemic cerebrovascular disorder Unruptured vascular malformation Arteritis (e.g., temporal arteritis) Carotid or vertebral artery pain Venous thrombosis Arterial hypertension

Headache associated with nonvascular intracranial disorder

Benign intracranial hypertension (pseudotumor cerebri) Intracranial infection Low cerebrospinal fluid pressure (e.g., headache subsequent to lumbar puncture)

Headache associated with substance use or withdrawal

Acute use or exposure Chronic use or exposure

Headache associated with noncephalic infection Viral infection Bacterial infection

Headache associated with metabolic disorder Hypoxia Hypercapnia Mixed hypoxia and hypercapnia Hypoglycemia Dialysis Other metabolic abnormality

Headache or facial pain associated with disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cranial structures Cranial neuralgias, nerve trunk pain and deafferentation pain

deafferentation pain

 

Benign intracranial hypertension(pseudotumor cerebri)Intracranial infection Low cerebrospinal fluid pressure (e.g., headache subsequent tolumbar puncture)

American Family Physician, 2001

Acute Secondary Headache Disorders

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Questions to Ask in Obtaining a Headache History Is this your first or worst headache? How bad is your pain on a scale of 1 to 10 (1 means not too bad, and 10 means very bad)? Do you have headaches on a regular basis? Is this headache like the ones you usually have? What symptoms do you have before the headache starts? What symptoms do you have during the headache? What symptoms do you have right now? When did this headache begin? How did it start (gradually, suddenly, other)? Where is your pain? Does the pain seem to spread to any other area? If so, where? What kind of pain do you have (throbbing, stabbing, dull, other)? Do you have other medical problems? If so, what? Do you take any medicines? If so, what? Have you recently hurt your head or had a medical or dental procedure?

 

American Family Physician, 2001 Back

Structural causes of headache

Brain tumor

Traditional features of brain tumor (eg, vomiting, papilledema, and headache that is worse in the morning or worsened by Valsalva's maneuver).

Subacute and progressive in nature New onset in adult life (>40 yr of age) or significant change in established pattern Association with any of the following: •Nausea or vomiting not explained by migraine or systemic illness •Nocturnal occurrence or morning awakening •Precipitation or worsening by changes in posture •Confusion, seizures, or weakness •Any abnormal neurologic sign

Headache features suggestive of a space-occupying lesion

Dodick, 1997 Back

Penyebab nyeri kepala pagi pada tekanan intrakranial meningkat :

• Peninggian pCO 2 selama tidur karena depresi pernapasan, sehingga terjadi vasodilatasi, peninggian volume darah intrakranial serta pembengkakan otak yang berakibat perburukan pada traksi atau pergeseran pembuluh darah.

• Penurunan reabsorpsi cairan serebrospinal.• Posisi berbaring pada malam hari.

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PENINGKATAN TEKANAN INTRAKRANIAL

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Tanda tekanan intrakranial meningkat :

• Trias klasik : nyeri kepala, muntah, edem papil

• Tanda lain : bradikardi, peninggian tekanan darah sistemik, dilatasi pupil, ptosis bilateral, gangguan upgaze, ekstensi terhadap nyeri, pernapasan irreguler dan mengantuk.

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Increase Intracranial Pressure

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CAUSES of RAISED INTRACRANIAL PRESSURE

HYDROCEPHALUS BRAIN ‘BRAIN ‘SWELLINGSWELLING’’

MASSESMASSESTUMOURSTUMOURSABSCESSABSCESS

CYSTSCYSTSHAEMATOMASHAEMATOMAS

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EDEMA SECEBRI

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Cerebral oedema This is an abnormal accumulation of fluid in the cerebral parenchyma.It is usually the result of

breakdown of the blood–brain barrier, and it may occur following damage initiated by several different

causes:Ischaemia, e.g. from infarction.Trauma,e.g.from head injury.Inflammation encephalitis or meningitis.

Oveproduction of CSF by choroid plexus neoplasms

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Edem serebri vasogenik merupakan akibat primer dari meningkatnya permeabilitas blood brain barier

Edem serebri sitotoksik terjadi sekunder dari kerusakan elemen seluler serebri, terlepasnya faktor-faktor toksikdari netrofil dan bakteri. Sehingga terjadi peningkatankandungan air intraseluler, dimana terjadi kebocoran potasium, glukosa digunakan melalui glikolisis anae

robik, produksilaktat.

Edem serebri interstitial terjadi sekunder dari obstruksi aliran LCS akibat inflamasi ruang subarakhnoid, seperti

hidrosefalus.

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Brain Edema

Cytotoxic edema : BBB is closed, no protein extravasation, no enhancement in CT, cell swellVasogenic edema : BBB is disrupted, leaks of protein, enhance inimaging, cell are stable, extracellular space expands, Interstitial : Transudasi

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EDEMA CEREBRI PADA TUMOR

• Vasogenic edema - Increased permeability of the capillary

endotelial cells plasma protein enter the extracellular space

- Defect of the endothelial cell junction - Microvascular transudative factors *protease released by tumor cells weakening BBB

• How is a brain tumor diagnosed?  In addition to a complete medical history and physical examination, diagnostic procedures for brain tumors may include the following:  

1.neurological examination - your physician tests reflexes, muscle strength, eye and mouth movement, coordination, and alertness.

2.CT scans are more detailed than general x-rays , MRI

3.spinal tap (Also called a lumbar puncture.)

On plain head CT scan:1. Usually dural based, isodense - hyperdense

tumors.2. They enhance homogeneously after iodinated

contrast.3. Perilesional edema may be extensive. 4. Hyperostosis and intratumoral calcifications

may be present.5. The tumor compresses the brain without

invading it.6. Multiple meningiomas may be difficult to

differentiate from metastasis

MENINGIOMA: Imaging Studies

• Peningkatan protein: 50 - 2.240mg%• Glukosa normal• Froin’s Syndrome: LCS clotting dan

xantochromia• Queckentedt’s test: kegagalan peningkatan

tekanan LCS pada saat kompresi vena jugular

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THERAPY MENINGIOMA

MeningiomaMeningioma• Treatment : gross total resection. Radiotherapy

debulking & progressivity • Survival after total resection of a benign tumor is

93%, 80%, and 68% at 5, 10, and 15 years • Survival after subtotal resection is 63%, 45%, and 9%

at 5, 10, and 15 years

• Treatment : gross total resection. Radiotherapy debulking & progressivity

• Survival after total resection of a benign tumor is 93%, 80%, and 68% at 5, 10, and 15 years

• Survival after subtotal resection is 63%, 45%, and 9% at 5, 10, and 15 years

Therapy : MENINGIOMA• Chemotherapy : no benefit• Surgery + Radiotherapy : recidif for 10-15 years, radiotx-sclerosing-resection

Radiation TherapyRadiation Therapy

• Valuable in the treatment of benign brain tumor

• Meningioma safe & efficacious

• Management of malignant meningioma remain difficult, but radiation therapy should be considered in all cases

• Valuable in the treatment of benign brain tumor

• Meningioma safe & efficacious

• Management of malignant meningioma remain difficult, but radiation therapy should be considered in all cases

The goals of surgeryThe goals of surgery

• Obtaining an accurate histologic diagnosis• Reducing tumor burden and associated mass

effect• Maintaining or reestablishing pathways for CNF

flow• Achieving potential “cure” by gross total removal

(De Angelis, 2001)

• Obtaining an accurate histologic diagnosis• Reducing tumor burden and associated mass

effect• Maintaining or reestablishing pathways for CNF

flow• Achieving potential “cure” by gross total removal

(De Angelis, 2001)

Radiation Therapy• Radiation is used when the entire primary tumor cannot be surgically removed• External bean irradiation, stereotactic radiosurgery, brachitherap

Therapeutic effects of radiotherapy (Wilson, 2001)

Radiation creates ionized oxygen species that react with cellular DNA.

Tumor cells have less ability than healthy cells for DNA repair.

Thus, between fractionation doses, healthy cells have a greater probability

than tumor cells of repairing themselves. With each subsequent mitosis, the

cumulative effects of unrepaired DNA result in apoptosis (cell death)

of these tumor cells

CHEMOTHERAPYCHEMOTHERAPY

• Ineffective against meningiomas

• Hidroxyurea : arrest meningioma cell growth in the S phase and induce apoptosis

• Ineffective against meningiomas

• Hidroxyurea : arrest meningioma cell growth in the S phase and induce apoptosis

HOW ABOUT CHEMOTHERAPY ?

-Disappointing

- Some chemotherapeutic agents can weaken the blood-

brain barrier (BBB) transiently and allow CNS seeding.

-A number of commonly used chemotherapeutic agents do not

cross the BBB, thus leaving the brain as a safe haven for tumor growth.

(Tse, 2002)

ChemotherapyChemotherapy

• Chemotherapy has limited benefit in treatment of patients with malignant gliomas. It does not significantly lengthen median survival in all patients, but a subgroup seems to have prolonged survival with addition of adjuvant chemotherapy to radiotherapy (De Angelis,2001)

• In a randomized study comparing temozolomide to procarbazine in patients with recurrent glioblastoma, progression-free survival rates at 6 months were 21 % and 8 % ( Yung.A et al,1999)

• Chemotherapy has limited benefit in treatment of patients with malignant gliomas. It does not significantly lengthen median survival in all patients, but a subgroup seems to have prolonged survival with addition of adjuvant chemotherapy to radiotherapy (De Angelis,2001)

• In a randomized study comparing temozolomide to procarbazine in patients with recurrent glioblastoma, progression-free survival rates at 6 months were 21 % and 8 % ( Yung.A et al,1999)

PROGNOSISPROGNOSIS

Prognosis tumor intracranial

Tergantung :- jenis tumor- lokasi tumor- ukuran tumor- pertumbuhan tumor (cepat/lambat)- efek pembedahan / radiotheraphy

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Prognosis greatly depends on all of the following :

•type of tumor

•extent of the disease

•size and location of the tumor

•presence or absence of metastasis

•the tumor’s response to therapy

•your age, overall health, and medical history

•your tolerance of specific medications, procedures, or therapies

•new developments in treatment

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Growth type classification of meningiomas according to cell type: Meningothelial growth is characterized by lobules of cells, marginated chromatin, and pseudoinclusions (ie, invagination of cell and nuclear membrane).

Fibroblastic growth is characterized by spindle-shaped cells in parallel interlacing bundles, intercellular collagen, and reticulin.

Transitional growth shows mixed features of the other 2 categories, and it commonly includes whorls and psammoma bodies usually not present in the other 2 types. Cell type is not indicative of expected behavior of the tumor.

Meningioma Basis Kranii History

Common symptoms include slowly developing unilateral exophthalmos and slight bulging of the bone in the temporal region.

Diffuse tumor infiltration of the orbital area may result in painless proptosis.

Variants of the clinical syndrome include the following:• Anosmia• Oculomotor palsy• Painful ophthalmoplegia (Tolosa-Hunt syndrome)• Blindness and optic atrophy in 1 eye, sometimes with papilledema of the other eye (Foster Kennedy syndrome)• Mental changes• Increased intracranial pressure

Physical: Sphenoid wing meningiomas can be associated with various cranial

nerve dysfunction resulting from foraminal encroachment of cranial nerves located at the skull base. Rarely, a bruit can be heard over a highly vascular tumor.

• Progesteron is a steroid hormone involved in female fertility and in the maintenance of pregnancy.• Meningiomas have attracted attention as possibly being hormone-sensitive tumors due to (1) higher incidence rate in women than in men, (2) the epidemiological association of meningiomas and breast cancer and (3) the reversible aggravation of the symptoms during periods of relative progesterone excess, such as during pregnancy and the luteal fase of menstrual.

HORMONE - MENINGIOMA

Sex hormones stimulate the growth of meningiomas, which may progress more rapidly in the second half of pregnancy. (Gilroy)