Neurofisiologi Optic Nerve
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Transcript of Neurofisiologi Optic Nerve
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Neurophysiology of Optic Nerve
Dr. Devi Azri Wahyuni, SpM
DEPARTMENT OPHTHALMOLOGY UNIVERSITY OF
SRIWIJAYA / MOHAMMAD HOESIN HOSPITAL
2011
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PREFACE
- The eyes are intimately related to the brain- The eyes give important diagnostic clues to
central nervous system disorders.- Optic nerve is a part of the central nervous
system.
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Anatomy and Topography of Visual Pathway
• Visual pathway consists of:• Retina• Optic nerve• Optic chiasm• Optic tract• Lateral geniculate nucleus (body)• Optic radiation• Visual cortex
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Retina
• The retina is a thin, transparent structure that develops from the inner and outer layers of the optic cup
• It extends almost as far anteriorly as the ciliary boby ending at that point in aragged edge the ora serata
• It has ten layers
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• Ganglion cells fibers coming from the nasal retina can travel uninterrupted directly to the disc
• Fibers from the temporal enter the disc at superior or inferior pole
• Macula fibers enter the disc on its temporal side ( papillomacular bundle )
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Optic Nerve
• Consists of more than 1 million axon that originate in the ganglion cell layer of the retina and extend toward the occipital cortex
• Has varies in length ;35 – 55 mm,usually about 50 mm from eye to optic chiasma
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The optic nerve four parts
• Intraocular ( 1 mm)• Intraorbital ( 25 mm)• Intracanalicular ( 5 mm )• Intra cranial ( 10 mm)
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Intraocular portion
• Optic disk and optic nerve that lies within sclera
• Optic disc 3 mm nasal macula lutea• Nerve fibers exit through the orifices of the
lamina cribrosa
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Intraorbital portion
• 20 mm to 30 mm long,elongated S• diameter 3-4 mm • Bermielin• Between the eyeball and the optic canal• Surrounded orbital fat,embedded the cilliary vessel
and nerve• Posteriorly,nasocilliari nerve and ophthalmic artery
cross above optic n. 25-30 mm• Dikelilingi oleh anulus zinni pada apek orbital• Peradangan pada bagian ini biasanya disertai dengan
nyeri pada pergerakan bolamata
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Intracanalicular potion
• the optic canal lies withinthe lesser ingof the sphenoid bone, 5 mm long
• Passes through the optic canal• Surrounded by duramater, arachnoid and
piamater• Duramater pada bagian ini menyatu dengan
periosteum
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Intracranial portion
• Leaves the canal and pass backward,upward and medially within the subarachnoid space to reach the optic chiasma
• Related above to the olfactory tract, gyrus rectus and anterior cerebrral a.
• Panjang 5 - 16 mm• Sering mengalami kerusakan karena
gangguan dari struktur lain yang berdekatan
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Optic chiasma
• Makes up part of the anterior inferior floor of the third ventricle
• Just antrior to the hypothalamus• Nasal retina fibers cross to the opposite side
to joint the coresponding contralateral fibers
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Optic tract
• Contains ipsilateral temporal and contralateral nasal fibers from the optic nerves
• Just prior to lateral geniculate body• Other fibers exit to the superficial layers of the
superior colliculus via the brachium of the superior colliculus
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Lateral geniculated body
• Is the synaptic zone for the higher visual projection
• Divided into six layers• The four superior levels are the terminus of
parvocellular axons are responsible for mediating maximal spatial resolution and color perception
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CGL
• To inferior layers receive input from the magnocellular fibers, that are more sensitive to detecting motion
• Contralateral eye terminate in layers 1,4,6• Ipsilateral fibers innervate 2,3 and 5
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Optic radiations
• Connect the lateral geniculate body with the cortex of the occipital lobe
• Loop of Meyer
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Visual cortex
• Area 17 Brodmann• Area 18 and 19 Brodmann
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Primary visual area
• Occupies the walls of the deep calcarina sulcus
• Superior retina quadrants (inferior field) pass to the superior wall of the calcarina sulcus
• Inferior retinal quadrants pass to the inferior wall of the calcarina sulcus
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Secondary visual area
• Surround the primary visual area• Relate the visual information
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Blood supply
• Retina :a.ofthalmica,central retina a.• Intraocular :branches anastomose circle
of Zinn post. Cilliary a.• Intraorbital :ophtalmic a.• Intracanalicular : branch pial ophthalmic
a.
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• Intracranial : pial plexus sup. Hypophyseal a. , carotid interna, ophthalmic a.
• Optic chiasma : pial plexus internal carotid, sup hypophyseal, post and ant comunicatting a., cerebral ant a.
• Optic tract s : choroidal ant a.
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• LGB : choroidal ant and post a.• Optic radiation and occipital cortex:middle
and post cerebral a.
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• 1. Papil Atrophy• - primary • -secondary
• 2. Demyelinating optic neuritis• 3. Parainfectious optic neuritis• 4. Infectious optic neuritis• 5. Non Infectious optic neuritis
Disease of optic nerve head
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• 6. Neuroretinitis• 7.neuroretinitis• 8. Non arteritis AION• 9. Arteritik AION• 10. Posterior Ischaemic optic neuropathy• 11. Diabetic papillopathy
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• 12. Leber hereditary optic neuropathy• 13. Hereditary optic atrophy• 14. Nutritional optic neuropathy• 15. Papilloedema
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• Etiologi• 1. Tumor
• Pituitary adenoma, craniopharyngioma dll
• 2. Non neoplastic masses• Aneurysma, arachnoid cysts
• 3. Lain-lain :• Peradangan, demielinisasi, trauma dll
Chiasm lesions
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Optic tract1. incongruous homonimous hemianopia2. wernicke hemianopic pupil3. optic atrophy4 contralateral pyramidal sign
Retrochiasmal Lesions
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Temporal optic radiation1. VF defect : contralateral homonimous, superior quadrant anopia2. Associated feature• Contralateral hemisensory disturbance, mild
hemiparesis, paroxysmal olfactory and gustatory hallucination
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Anterior parietal radiation1. VF defect : incongruous, contralateral, homonimous, inferior quadrantanopia2. Associated feature: • Of dominant parietal lobe disease: agraphia,
left –right disorientation, and finger agnosia• Of non dominan : apraxia and spatial neglect
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Main Radiation1. VF defect : complete homonimous hemianopia2. Optokinetic nystagmus
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Striate cortex1. VF defect : Macular sparing congruous homonimous hemianopia2. Associated feature : visual hallucination, denial of blindness3. causes : vascular disease,migraine, tumor and trauma.
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• Signs of optic nerve dysfunction• I. Reduced visual acuity • 2. Afferent pupillary defect• 3. Dyschromatopsia• 4. Diminished light brightness sensitivity.• 5. Diminished contrast sensitivity,• 6. Visual field defects
Evaluation of optic nerve disease
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• Lesi pada bag retrolamelar dari saraf optik sp badan genikulatum lateral
• Papil pucat, batas tegas, kastembaum sign (+), diffuse atau sektoral
• Etiologi : – neuritis retrobulbar– Tekanan dari tumor atau aneurisma– Neuropati optik herediter– Neuropati optik toksik
Primary optic atrophy
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• Didahului oleh pembengkakan ONH• Papil putih atau keabu-abuan, batas tidak
tegas• Pembuluh darah pada permukaan diskus
berkurang• Etiologi :– Papiledema, papilitis, AION
Secondary optic atrophy
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• Usia 30-50, • Subakut monocular visual impairment• Nyeri pada mata pada saat menggerakkan
bolamata• Papil normal• Papil pucat pada bagian temporal → serangan
berulang• Visus memburuk dalam beberapa hari- 2 mgg,
kemudian mengalami perbaikan dalam 2-4 mgg.
Demyelinating optic neuritis
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• Sindroma klinis ditandai dengan penurunan visus mendadak, nyeri (-), papil edema dan gambaran makular star
• Idiopatik : 25 %• Cat scratch disease : 60%• Penyebab lain : sifilis dan lyme disease
Neuroretinitis
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• Sering pada usia >50 th• Kerusakan saraf optik karena proses iskemik• Painless monocular visual loss• Defek lapang pandang : altitudinal atau
arkuata• Dibagi menjadi arteritik dan non arteritik
AION
Anterior ischemic optic neuropathy
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• Berhub dengan DM tipe 1 dan 2• Penglihatan buram tanpa disertai nyeri• RAPD +/-• VF : perluasan bintik buta• Papil edema, hiperemis dan dilatasi pemb. Darah
pada permukaan disk.
Diabetic papillopathy
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• Defisiensi protein dan vit B komplek• Progresif dan bilateral visual impairment• Diskromatopsia• Papil : normal → atropi (temporal)
Nutritional optic neuropathy
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• Defek lapang pandang :– Sekosentral skotoma
Nutritional optic neuropathy
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Toxic optic neuropathy
• Characterized : gradual, progressive, bilateral and painless
• Central or cecocentral scotoma• Decrease of visual acuity and colour vision• Mild to moderate papil edema• Cause : > methanol medication : INH, ethambutol
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NEUROPATI OPTIK YG PROGRESIF
HILANG LAPANGAN PANDANG
TIO FAKTOR RISIKO
DEFINISI :
TIO KRONIS GLAUKOMA KRONIS
TIO AKUT GLAUKOMA AKUT
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KATARAK 0,78 % GLAUKOMA 0,20 % KELAINAN REFRAKSI 0,14 % PENYAKIT LAIN YG BERHUBUNGAN
DG USIA LANJUT 0,38 %
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GEJALA
AKUT : - GEJALA KHAS : TERLIHAT SAKIT
- ANCAM KEBUTAAN KRONIS : - TANPA GEJALA - DATANG PADA
STADIUM LANJUT
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FAAL AKUOS HUMOR
AKUOS HUMOR MELALUI PUPIL →BILIK MATA DEPAN →TM → KANALIS SCHLEM →
SUB KONJUNGTIVA
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TIO KETIDAKSEIMBANGAN PRODUKSI & SEKRESI
HUMOR AKUOS
PENEKANAN SERABUT SARAF OPTIK
ALIRAN DARAH
ISKEMIK
KEMATIAN SERABUT SARAF
GANGGUAN PENGLIHATAN & LAPANG PANDANG
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TEKANAN INTRAOKULAR
- NORMAL 10 – 20 MMHG - DITENTUKAN :
* KECEPATAN PRODUKSI OLEH KORPUS SILIARIS
* HAMBATAN ALIRAN KELUAR ( PADA TRABEKULUM )
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ALAT UNTUK MENGUKUR TIO
- TONOMETER SCHIOTZ - TONOMETER APLANASI GOLDMANN. - TONOMETER NON KONTAK - KADANG- KADANG CARA DIGITAL
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EKSKAVASI SARAF OPTIK
• DINILAI DENGAN OFTALMOSKOP• UNTUK DIAGNOSTIK DAN EVALUASI TERAPI• LIHAT WARNA PAPIL SARAF OPTIK DAN LEBARNYA EKSKAVASI
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LAPANG PANDANG
• DINILAI MENGGUNAKAN PERIMETER• UNTUK DIAGNOSTIK DAN EVALUASI TERAPI • DOKTER UMUM : BISA CARA KONFRONTASI
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Lapang pandang glaukoma
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Pemeriksaan LP dg alat khusus :Pemeriksaan LP dg alat khusus :
* Perimeter Goldmann* Perimeter Goldmann
LP normal dg GoldmannLP normal dg Goldmann
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Automated perimeter : Humphrey visual field analyzerAutomated perimeter : Humphrey visual field analyzer
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PEMERIKSAAN PADA PENDERITA GLAUKOMA
I. TAJAM PENGLIHATAN ( TP)• BUKAN PEMERIKSAAN KHUSUS TAPI PEMERIKSAAN RUTIN• ALAT : KARTU SNELLEN• TP : 6/6 BELUM TENTU TAK ADA GLAUKOMA
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• PENGLIHATAN SENTRAL BISA MASIH BAIK• “ TUNNEL VISION” – PADA GLAUKOMA KRONIS
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II. TONOMETRI• PEMERIKSAAN PENTING DAN KHUSUS • UNTUK DIAGNOSA DAN EVALUASI TERAPI• MACAM –MACAM TONOMETER :
- TONOMETER SCHIOTZ - TONOMETER APLANASI - TONOMETER NON KONTAK
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Pengukuran dengan Palpasi
• Bersifat kualitatif : N, N+, N-• Tergantung keahlian interpretasi dokter• Dilakukan bila tidak memungkinkan digunakan
alat• Masih memuaskan pada TIO sangat rendah
atau tinggi
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KONTRA INDIKASI TONOMETER - KONTRA INDIKASI RELATIF :
- INFEKSI MATA - LUKA TEMBUS
- KONTRA INDIKASI ABSOLUT : - JARINGAN PARUT KORNEA
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III. FUNDUSKOPI
• PEMERIKSAAN KHUSUS• UNTUK DIAGNOSTIK DAN EVALUASI
TERAPI• ALAT FUNDUSKOPI / OFTALMOSKOP• DILAKUKAN PEMERIKSAAN BERKALA
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IV. LAPANG PANDANG
• ALAT : PERIMETER GOLDMANN • PEMERIKSAAN KHUSUS PADA GLAUKOMA .• UNTUK DIAGNOSTIK DAN EVALUASI TERAPI.
PERLU KETERAMPILAN KHUSUS.
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• KELAINAN LAPANG PANDANG : SKOTOMA - HILANG SELURUHNYA PERIMETER AUTOMATIK - HUMPHREY - OCTOPUS
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GONIOSKOPI
ALAT : LENSA GONIOSKOPI - PEMERIKSAAN : SUDUT BILIK
MATA- LUAS / LEBARNYA SUDUT - PERLEKATAN PADA SUDUT / IRIS
PERIFER
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MERAMALKAN APAKAH SUATU SUDUT MEMPUNYAI KECENDERUNGAN TERTUTUP . - MEMBEDAKAN GLAUKOMA PRIMER SUDUT TERTUTUP DENGAN GLAUKOMA PRIMER SUDUT TERBUKA.
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UNTUK DIAGNOSA, TIDAK UNTUK EVALUASI TERAPI.
KLASIFIKASI GLAUKOMA : 1. GLAUKOMA PRIMER 2. GLAUKOMA SEKUNDER 3. GLAUKOMA KONGENITAL
4. GLAUKOMA ABSOLUT
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I. GLAUKOMA PRIMER
– SEBABNYA TIDAK
DIKETAHUI
– GONOSKOPI :
- SUDUT TERBUKA
- SUDUT TERTUTUP
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II. GLAUKOMA SEKUNDER - SEBABNYA : DIKETAHUI ( PENY. PADA MATA ) 1. KELAINAN PADA LENSA
- LUKSASI - INTUMESEN - FAKOLITIK
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2. KELAINAN UVEA - UVEITIS - TUMOR 3. TRAUMA - HIFEMA - PERFORASI BOLA MATA - TRABEKULITIS
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4. PEMBEDAHAN4. PEMBEDAHAN
- BILIK MATA DEPAN - BILIK MATA DEPAN
DANGKALDANGKAL
5. PENYEBAB LAIN5. PENYEBAB LAIN
- STEROID INDUCED- STEROID INDUCED
- RUBEOSIS IRIDIS - RUBEOSIS IRIDIS
( KELAINAN RETINA )( KELAINAN RETINA )
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III. GLAUKOMA KONGENITAL
» KELAINAN PERKEMBANGAN
SUDUT BMD
» BUFTALMOS
» BISA BERHUBUNGAN
DENGAN SINDROMA LAIN
(KELAINAN KONGENITAL LAIN)
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IV. GLAUKOMA ABSOLUT - STADIUM AKHIR DARI GLAUKOMA - KELUHAN NYERI + | - - TP / LP : HILANG SELURUHNYA
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GLAUKOMA SUDUT TERBUKA - GLAUKOMA KRONIK / SIMPLEK - PENYAKIT BERLANGSUNG LAMA, TANPA GEJALA KHAS - TEKANAN BM TIDAK TERLALU TINGGI
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- - RIWAYAT KELUARGA(+)RIWAYAT KELUARGA(+)
- SERING DATANG SUDAH - SERING DATANG SUDAH TERLAMBAT TERLAMBAT
- DOKTER HARUS AKTIF - DOKTER HARUS AKTIF
MENEMUKAN KASUSMENEMUKAN KASUS
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- TONOMETRI BERKALA PADA POPULASI RESIKO TINGGI - DM - MYOP / HIPERMETROP - USIA > 40 TH - KELUARGA (+)GLAUKOMA
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PENGOBATAN GLAUKOMA SUDUT
TERBUKA
- MEDIKAMENTOSA
- OPERASI PADA KASUS TERTENTU:
- TIO TAK TERKONTROL
DENGAN TERAPI MAKSIMAL
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•
- INTOLERASI DENGAN OBAT - INTOLERASI DENGAN OBAT
ANTI GLUKOMAANTI GLUKOMA
- PROGRESIFITAS PENYAKIT - PROGRESIFITAS PENYAKIT ( LP ( LP
EKSKAVASI MEMBURUK )EKSKAVASI MEMBURUK )
- TAK DISIPLIN DENGAN OBAT- - TAK DISIPLIN DENGAN OBAT-
OBAT. OBAT.
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MEDIKAMENTOSA : - MIOTIKUM : PILOKARPIN 2 % - SIMPATOMIMETIK : EPINEFRIN 0,5– 2% - BETA BLOCKER : TIMOLOL MALEAT 025 – 0,5 % - KARBONIK ANHIDRASE : ASETAZOL AMIDE (4 x 250 MG)
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•
GLAUKOMA SUDUT TERTUTUP :GLAUKOMA SUDUT TERTUTUP :
- GLAUKOMA AKUT / GLAUKOMA- GLAUKOMA AKUT / GLAUKOMA
KONGESTIFKONGESTIF
- GEJALA TANDA KHAS, MUDAH - GEJALA TANDA KHAS, MUDAH
DIKENALIDIKENALI
- HARUS WASPADA,MIRIP PENYA-- HARUS WASPADA,MIRIP PENYA-
KIT SISTEMISKIT SISTEMIS
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- TAJAM PENGLIHATAN MENURUN
MENDADAK, MATA MERAH DAN TIO SANGAT TINGGI - PRODROMAL : - MUAL, MUNTAH - SAKIT KEPALA, SAKIT
PADA SISI MATA YANG
AKUT
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PENANGANAN GLAUKOMA AKUT
GEJALA KLINIS/SUBYEKTIF SAKIT KEPALA, CEKOT-CEKOT
MUNTAH-MUNTAH PENGLIHATAN KABUR MENDADAK MELIHAT SEPERTI HALO
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OBYEKTIF
PALPEBRA BENGKAKKONJUNGTIVA HIPEREMISKORNEA BURAM / EDEMABMD DANGKAL GL. PRIMER & SEKUNDER DALAM GL. SEKUNDERPUPIL MIDRIASIS/MIDDILATASILENSA KERUH BERCAK SPT SUSU / KATARAK IMATUR
KERUH KATARAK HIPERMATURTIO > 50 mmHg
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TANDA GLAUKOMA ACUTE
• Severe corneal oedema • Complete angle closure (Shaffer grade 0)
• Dilated, unreactive, vertically oval pupil
• Shallow anterior chamber
• Ciliary injection
Signs
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PENGOBATAN GLAUKOMA SUDUT
TERTUTUP - TURUNKAN TEKANAN INTRA OKULER SEGERA DENGAN TERAPI MEDIKAMENTOSA - SIAPKAN UNTUK PEMBEDAHAN
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- PENGOBATAN DEFINITIF YAITU PEMBEDAHAN BERUPA :
- IRIDEKTOMI - TRABEKULEKTOMI - IRIDEKTOMI PREFENTIF UNTUK MATA LAINNYA
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INITIAL TREATMENT
PILOKARPIN 2 % 1 TETES/ MENIT SELAMA 5 MENIT TIMOLOL 0,5 % 2 X 1 TETES STEROID + ANTIBIOTIK TETES 6 x 1 tetes ACETAZOLAMID 500 iv 250 mg / 4 JAM KCl 3 x 1 GLICERIN 50 % 3 dd 100 – 150 cc
SEGERA RUJUK KE PELAYANAN KESEHATAN
LEBIH TINGGI !
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DEFINITIF TREATMENT
IRIDEKTOMITRABEKULEKTOMIEKSTRAKSI LENSA
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NON CONTACT TONOMETER
TIO normal
10-21 mmHg
TONOMETRI
TONOMETER SCHIOTZ
CILIARY BODY
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GLAUKOMA PENYEBAB UTAMA KEBUTAAN PERINGKAT KEDUA SETELAH KATARAK
GLAUKOMA TIDAK DAPAT DISEMBUHKAN / DIPERBAIKI
DETEKSI DINI PENANGANAN TEPAT
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DASAR PENGOBATAN GLAUKOMA
TIO PADA LEVEL TERTENTU
MENCEGAH KERUSAKAN SARAF OPTIK LEBIH LANJUT
ADA BUKTI TIO
BISA MEMPERTAHANKAN PENGLIHATAN & LAPANG PANDANGAN