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NEUROPATOLOGI
dr. DevyAriany, M.Biomed
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Menerima& integrasi informasi dari
sensorik
Mengolahnya
Koordinasi motorik
Prosesberpikir
Pengaturanemosi
Penyimpananmemori
Sel neuron =pelaksana
Sel glia =menyediakanlingkunganyang adekuat
Pembuluhdarah=suplai nutrisi
Meningen, CSF =proteksi
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Neuropatologi
Kongenital
Kelainan
vaskular
Trauma
Infeksi
Degenerasi
Neoplasma
Metabolik
Kerusakansel saraf : neuron, sel glia
Kerusakansawar darahotak
Edema, herniasi, hidrosefalus
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Kerusakanneuron :
1. Nekrosis
Terjadi cepat
Nukleuspiknotik
Sitoplasmamengerut
2. Atrofi
Terjadi perlahan
Ukuransel mengecil ataumembesar dengan
metabolikabnormal
Kerusakansel glia:
1. Astrosit gliosis
2. Oligodendrosit satelitosis
3. Mikroglia lipophage
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Expanding lesion :
Intracerebral
Meningen
TIK
Tahapkompensasi
volumeCSF
volume darahintrakranial
Tahapdekompensasi
herniasi dandistorsi
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Gyrusmendatar, melebar
Sulkusmenyempit
Ventrikel lateral sempit
EDEMA SEREBRI
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Subfalcine(cingulate) herniation
Ekspansi unilateral hemisfer
serebri kearahgirussinguli,
dibawahfalksserebri
Seringterjadi penekanan
a.serebri anterior
HERNIASI
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Transtentorial uncal-hippocampal herniation
Area medial lobustemporal tertekantepi tentoriumserebelum
Saat lobustemporal bergeser N.kranial III tertekan
dilatasi pupil dangangguanpergerakanmatapadasisi lesi
Arteri serebri posterior dapat tertekan iskemikkorteks
visual primer
Jikaherniasi cukupbesar pedunculusserebri kontralateral ikut
tertekan Kernohansnotch hemiparesisipsilateral padasisi
herniasi
gejalahemiparesisipsilateral ini dapat mengecohpemeriksa
bahwapasienmempunyai lesi padaarea yang berlawanan
(hemisfer yang sehat)
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Tahaplanjut dapat disertai denganlesi hemoragikpada
mesencephalondanpons(Duret hemorrhages)
Didugaakibat sobeknyavena danarteri yang mensuplai batang
otakatas
AdanyaDuret hemorrhage menandakanprognosis buruk
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Tonsillar herniation
Pergeserantonsillar serebelumkearahforamen magnum.
Tekananbatangotak gangguanpusat respirasi dankardio
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Obstruksi dapat terjadi di ventrikel ataudi ruangsubarachnoid
Di ventrikel (noncommunicatinghydrocephalus) hubungan(-) antara
ventrikel ruangsubarachnoid
Di ruangsubarachnoid (communicating hydrocephalus)
Bilasuturakranial belumtertutup terjadi
pembesarankepala
Bilasesudahsuturakranial tertutup
ventrikel membesardanpeningkatanTIK tanpa
adanyaperubahandalamlingkar kepala
Kepala>>, mukatampak
kecil
Hemisferserebri
kolaps, tipis,
mengembang,
ventrikel dilatasi
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DEFEK TABUNG SARAF
Faktor resiko: defisiensi folat padaminggu-mingguawal kehamilan
Dapat dideteksi denganUSG danmaternal screening (peningkatan
!-fetoprotein )
Padaumumnyadefektabungsaraf melibatkanMS
Dapat asimptomatik(spinabifida occulta) sampai
menimbulkanmalformasi yang berat seperti
disorganisasi segmenMS ygdisertai dengan
penonjolanmeningeal
Meningomyelocele
(saraf, meninges,
MS)
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Meningomyelocele
Keluarnyajaringansaraf melalui defek
padakolumnavertebralis
terutamadaerahlumbosakral
timbul defisit motorikdansensorik
padaekstremitasbawahdanmasalah
defekasi danmiksi
Anencephaly
Padaakhir perkembanganotak
Malformasi tabungsaraf anterior
Tidakadaotakdankraniumbagian
atas
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Encephalocele
Divertikulumjaringansaraf melalui defekpadakranium
Paling seringterjadi di regiooccipital ataufossaposterior
Bilaterjadi di anterior dapat meluaskesinus
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TRAUMA
Coup injury
Contrecoupinjury
Contusio
Traumatic parenchymal injury
Perdarahanintraparenkimal
Edema
diffuse axonal injury
Traumatic vascular injury
Hematomepidural
Hematomsubdural
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Ruptur a. meningeamedia
Pada ruang antara cranium duramater
Interval lucid
Operasi cito
CT scan : efek massa yg
mendorongventrikel lateral dan
midline kearahkiri
HEMATOMA EPIDURAL
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Ruptur bridging veins
Duramatercerebrum
Self-limited
Chronic subdural
hematoma
Kiri : hematom
menekanotakke
kanan
Kanan: hematom
bilateral, ireguler
(mulai terbentukjar
granulasi)
HEMATOMA SUBDURAL
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CEREBROVASCULAR DISEASE
Perubahanalirandarahotak
Alirandarah
Perdarahan
Iskemik
Infark
Hematomintraserebral
Perdarahansubarachnoid
Defisitneurologik(STROKE)
Aterosklerosis
Hipertensi, malformasi PD
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MENINGITIS
Prosesinflamasi padameninges
Meningoencephalitis
Klasifikasi : acute pyogenic(bacterial), aseptic(viral), dan
chronic(tuberculous, spirochetal, cryptococcal) eksudat
(pemCSF)
Eksudatkuningtebal di ruang
subarachnoid
Sebukansel PMN yang padat
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MENINGITIS acute pyogenic aseptic chronic
Agent Neonatus: E.coli,
Streptococcus
Remaja: Neisseria
meningitides
Dewasa:
Pneumococcus,
Meningicoccus
Enterovirus Mycobacterium
tuberculosis
CSF Keruh(pus)
Netrofil >>
Protein
Glukosa
Limfosit>>
Protein
Glukosanormal
Gelatinous-fibrinous
Monosit
Protein
Glukosa /normal
Gejalaklinis Sakit kepala, fotofobia, iritabilitas, gangguan
kesadaran, kejang, defisitneurologik
Demam
Sakit kepala,
fotofobia, iritabilitas,
gangguankesadaran,
kejang, defisit
neurologik
Demam
Malaise
Mual - muntah
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ABSES OTAK
Infeksi bakteri : Staphylococcus, Streptococcus
Penyebaran: hematogen(fokusprimer di jantung, paru-paru, cabut gigi);
perkontinuitatum(mastoiditis, sinusitis paranasal); langsung(trauma)
Lesi destruktir defisit neurologikprogresif, gejalapeningkatanTIK
CSF : lekositosis, protein , glukosanormal
Absesruptur ventrikulitis, meningitis, trombosissinus venosus
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Lesi denganarea nekrosisliquefactiveberisi
pus, dindingkapsul fibrosa
Pewarnaantrichrome:
fibrosis (biru), abses(kiri)
CT-scan : lobusoccipital sinistra
terdptring enhancement
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Viral encephalitis
Infeksi parenkimotak biasanyajugaterjadi inflamasi meningeal
meningoencephalitis
Gejalaklinisberagam gambaranhistopatologik : infiltratsel
mononuklearperivascular danparenchymal, microglial nodules, dan
neuronophagia virus tertentumembentuk inclusion bodies
Rabies : badaninklusi
Negri
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DIFFUSES CORTICAL DEMENTIA (Alzheimers disease)
Memory impairment, defisit kognitif, gejalapsikiatrik
Prosesberjalanterussecaralambat
Etiologi beragam: neurodegeneratifprimer, infeksi, trauma, defisiensi gizi
Bukanprosesmenuanormal prosespatologik
Akumulasi peptida( amiloid) di otak toksikthdneuron dansinapstuarea
frontal, temporal danparietal
Atrofi otak dikompensasi denganpembesaranventrikel (hidrosefalusex
vacuo)
Ketebalankorteksberkurang, atrofi, ventrikel dilatasi
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Neuriticplaque (Lesi ekstraseluler
amyloidplaque : A )
Neurofibrillarytangles
(Lesi intraseluler
protein Tau)
Plaque di area frontal korteksserebri
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PARKINSONISM
Sindromklinis ekspresi wajah (masked
facies), postur kaku, pergerakanvolunter
melambat, festinating gait (progressively
shortened, accelerated steps), rigidity dan"pill-
rolling" tremor
Gangguanmotorik: kerusakanneuron
dopaminergikpadasubstansianigra
Akinetic-rigid form (extrapyramidal disease)
Substansianigradanlocus cereleuspucat Normal
Lewybodies : single
/multiple, intracytoplasmic,
eosinophilic, round to
elongated inclusions , dense
core ( -synuclein)
surrounded by a pale halo.
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TUMOR OTAK
Polapertumbuhan: low-grade lesions (low mitotic
rate, cellular uniformity, and slow growth)
Walaumikroskopikjinak(meningiomabenigna)
menekanmedula cardiorespiratoryarrest
Operasi terbatasakibat lokasinya
Sangat jarangmetastasis
Gejalaklinis: kejang, defisit neurologik, gejala
psikiatrik, tandapeningkatanTIK
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Glioblastoma
80% tumor otakpd dewasa
Massa tumor dgnarea nekrosis,
batasireguler, meluas
Hiperkromatik,
pleomorfism,
vaskularisasi
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Astrositoma
Lobusfrontal sinistra:
massaabu-abuhomogen&
lunak
Sel astrosit protoplasmik
denganhiperkromatik
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Meningioma
Massa tumor, batastegas,
di bawah
dura, dari sel arachnoid,
menekan
hemisfer cerebri
sel-sel meningotelial
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Whorled pattern, psammoma
bodies (deposit kalsium)
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Schwannoma
Neuromaakustik
Asal n. cranial VIII
Pendengaran/- atau
tinnitus
Kiri : polaAntoni A (
nucleus tsusunpalisade)
dikell area pink verocay
bodies
Kanan: polaAntoni B (sel
kecil, stromalonggar
Neurofibromatosis
Multiple nodul
Kulit diatasnya
hiperpigmentasi
Dermis : elongated
spindle cells,
struktur bergelombang,
kolagen
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