View
153
Download
2
Category
Preview:
Citation preview
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
Back
- 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
Back
:
The different types of brain tumors include the following:
Back
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
Back
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
Back
Back
Back
Back
Back
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
Back
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.
Back
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
Back
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)
Back
Gejala Klinik Tumor Otak (DeAngelis, 2001)
Back
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)
Back
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
Back
KARAKTERISTIK NYERI KEPALA SOP
1) Tidak terlokalisir dengan baik2) Perjalanan penyakit subakut progresif3) Intensitas sedang sampai berat4) Resisten terhadap analgetik biasa
(Dodick, 1997)
Back
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)
Back
Back
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
++ -
Back
Back
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.
Back
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)
Back
Nyeri kepala
Back
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)
Back
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)
Back
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)
Back
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
Back
(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)
Back
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
Back
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
Back
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
Back
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.
Back
PENINGKATAN TEKANAN INTRAKRANIAL
Back
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.
Back
Increase Intracranial Pressure
Back
CAUSES of RAISED INTRACRANIAL PRESSURE
HYDROCEPHALUS BRAIN ‘BRAIN ‘SWELLINGSWELLING’’
MASSESMASSESTUMOURSTUMOURSABSCESSABSCESS
CYSTSCYSTSHAEMATOMASHAEMATOMAS
Back
Back
EDEMA SECEBRI
Back
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
Back
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.
Back
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
Back
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
Back
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
Back
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
Back
Back
Back
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)
Recommended