PEMICU 4

Saraf & Kejiwaan

Cindy Claudia
405140139
MM Anatomi SSP
(Telencephalon,Diencephalon,Mesencephalon,Metmecenphalon ,P.D
OTAK,12 Nervus Cranialis,LCS
The cranial meninges:
• Protect the brain.
• Form the supporting framework for
arteries, veins, and venous sinuses.
• Enclose a fluid-filled cavity, the
subarachnoid space, which is vital to
the normal function of the brain.
The meninges are composed of three membranous connective tissue layers (Fig. 7.28A, B & D):
1. Dura mater (dura): tough, thick external fibrous layer.
2. Arachnoid mater (arachnoid): thin intermediate layer.
3. Pia mater (pia): delicate internal vasculated layer.
The intermediate and internal layers (arachnoid and pia) are continuous membranes that collectively
make up the leptomeninx (G. slender membrane) .

The arachnoid is separated from the pia by the subarachnoid (leptomeningeal) space, which
contains cerebrospinal fluid (CSF).

This fluid-filled space helps maintain the balance of extracellular fluid in the brain. CSF is a clear
liquid similar to blood in constitution; it provides nutrients but has less protein and a different ion
concentration.

CSF is formed by the choroid plexuses of the four ventricles of the brain This fluid leaves
the ventricular system and enters the subarachnoid space between the arachnoid and pia mater, where it
cushions and nourishes the brain.
 BRAIN
• The brain (contained by the neurocranium) is composed of the cerebrum,
cerebellum, and brainstem .
• When the calvaria and dura are removed, gyri (folds), sulci (grooves), and fissures
(clefts) of the cerebral cortex are visible through the delicate arachnoid–pia layer

• The cerebrum (L. brain) includes the cerebral hemispheres and basal ganglia.

• The cerebral hemispheres, separated by the falx cerebri within the longitudinal
cerebral fissure, are the dominant features of the brain .

• Each cerebral hemisphere is divided four lobes, each of which is related to, but
the boundaries of which do not correspond to, the overlying bones of the same
name.

• From a superior view, the cerebrum is essentially divided into quarters by the
median longitudinal cerebral fissure and the coronal central sulcus.
• The central sulcus separates the frontal lobes (anteriorly) from
the parietal lobes (posteriorly).

• The posteriorly placed occipital lobes are separated from the

parietal and temporal lobes by the plane of the parieto-occipital
sulcus, visible on the medial surface of the cerebrum in a
hemisected brain
•

• The hemispheres occupy the entire supratentorial cranial cavity

• The frontal lobes occupy the anterior cranial fossae, the temporal
lobes occupy the lateral parts of the middle cranial fossae, and the
occipital lobes extend posteriorly over the tentorium cerebell
Ventricular System of Brain
• The ventricular system of the brain consists  two lateral ventricles and the midline 3rd and 4th
ventricles connected by the cerebral aqueduct.

• CSF, largely secreted by the choroid plexuses of the ventricles, fills these brain cavities and the
subarachnoid space of the brain and spinal cord.

VENTRICLES OF BRAIN

• The lateral ventricles the 1st and 2nd ventricles, are the largest cavities of the ventricular system and
occupy large areas of the cerebral hemispheres.

• Each lateral ventricle opens through an interventricular foramen into the 3rd ventricle.

• The 3rd ventricle, a slit-like cavity between the right and the left halves of the diencephalon, is continuous
postero-inferiorly with the cerebral aqueduct, a narrow channel in the midbrain connecting the 3rd and
4th ventricles

• The pyramid-shaped 4th ventricle in the posterior part of the pons and medulla extends inferoposteriorly.

• Inferiorly, it tapers to a narrow channel that continues into the cervical region of the spinal cord as the
central canal.

• CSF drains into the subarachnoid space from the 4th ventricle through a single median aperture and paired
lateral apertures. These apertures are the only means by which CSF enters the subarachnoid space. If
they are blocked, CSF accumulates and the ventricles distend, producing compression of the substance of
the cerebral hemispheres.
 SUBARACHNOID CISTERNS
• SUBARACHNOID CISTERNS

At certain areas on the base of the brain, the arachnoid and pia are widely separated by subarachnoid cisterns
which contain CSF, and soft tissue structures that “anchor” the brain, such as the arachnoid
trabeculae, vasculature, and in some cases, cranial nerve roots.

The cisterns are usually named according to the structures related to them.
Major intracranial subarachnoid cisterns include the:

• Cerebellomedullary cistern: the largest of the subarachnoid cisterns, located between the cerebellum and
the medulla; receives CSF from the apertures of the 4th ventricle. It is divided into the posterior
cerebellomedullary cistern (cisterna magna) and the lateral cerebellomedullary cistern.
•
Pontocerebellar cistern (pontine cistern): an extensive space ventral to the pons, continuous inferiorly
with the spinal subarachnoid space.
• Interpeduncular cistern (basal cistern): located in the interpeduncular fossa between the cerebral
peduncles of the midbrain.
•
Chiasmatic cistern (cistern of optic chiasma): inferior and anterior to the optic chiasm, the point of
crossing or decussation of optic nerve fibers.

• Quadrigeminal cistern (cistern of great cerebral vein): located between the posterior part of the corpus
callosum and the superior surface of the cerebellum; contains parts of the great cerebral vein.

• Cisterna ambiens (ambient cistern): located on the lateral aspect of the midbrain and continuous
posteriorly with the quadrigeminal cistern (not illustrated).
SECRETION OF CEREBROSPINAL
FLUID
• Cerebrospinal fluid (CSF) is secreted (at the rate of 400–500
mL/day) mainly by choroidal epithelial cells (modified
ependymal cells) of the choroid plexuses in the lateral, 3rd,
and 4th ventricles (Figs. 7.36C, 7.37, and 7.38).

• The choroid plexuses consist of fringes of vascular pia mater

(tela choroidea) covered by cuboidal epithelial cells.

• They are invaginated into the roofs of the 3rd and 4th
ventricles and on the floors of the bodies and inferior horns of
the lateral ventricles.
CIRCULATION OF CEREBROSPINAL
FLUID
• CSF leaves the lateral ventricles through the interventricular foramina and enters
the 3rd ventricle (Fig. 7.37A)CSF passes through the cerebral aqueduct into the
4th ventricle. Some CSF leaves this ventricle through its median and lateral
apertures and enters the subarachnoid space, which is continuous around the spinal
cord and posterosuperiorly over the cerebellum.

• However, most CSF flows into the interpeduncular and quadrigeminal cisterns.

• CSF from the various subarachnoid cisterns flows superiorly through the sulci and
fissures on the medial and superolateral surfaces of the cerebral hemispheres.

• CSF also passes into the extensions of the subarachnoid space around the cranial
nerves, the most important of which are the subarachnoid space extensions
surrounding the optic nerves (CN II).
ABSORPTION OF CEREBROSPINAL FLUID
• The main site of CSF absorption into the venous system is through the
arachnoid granulations (Figs. 7.35 and 7.37A), especially those that
protrude into the superior sagittal sinus and its lateral lacunae (Fig.
7.28D).

• The subarachnoid space containing CSF extends into the cores of the
arachnoid granulations.

• CSF enters the venous system through two routes:

(1) most CSF enters the venous system by transport through the cells of the
arachnoid granulations into the dural venous sinuses
(2) some CSF moves between the cells making up the arachnoid granulations
Arterial Blood Supply to Brain
• The blood supply to the brain is
derived from the internal
carotid and vertebral arteries
,the terminal branches of which
lie in the subarachnoid space.

• Venous drainage from the brain

occurs via cerebral and
cerebellar veins that drain to the
adjacent dural venous sinuses
VERTEBRAL ARTERIES
• VERTEBRAL ARTERIES
• The vertebral arteries begin in the root of the neck (the prevertebral parts of the
vertebral arteries) as the first branches of the first part of the subclavian arteries

• The two vertebral arteries are usually unequal in size, the left being larger than the
right.

▫ The atlantic parts of the vertebral arteries (parts related to the atlas, vertebra C1)
perforate the dura and arachnoid and pass through the foramen magnum.
▫ The intracranial parts of the vertebral arteries unite at the caudal border of the pons to
form the basilar artery.
▫ The vertebrobasilar arterial system and its branches are often referred to clinically as the
posterior circulation of the brain.

• The basilar artery, so-named because of its close relationship to the cranial base,
ascends the clivus, the sloping surface from the dorsum sellae to the foramen
magnum, through the pontocerebellar cistern to the superior border of the pons. It ends
by dividing into the two posterior cerebral arteries.
Moore Clinically Oriented Anatomy
• Figure 13-2.
• Major cerebral arteries. The
anterior and posterior cerebral
circulations comprise arteries
that arise anterior and posterior to
the posterior communicating
arteries, respectively.

• The circle of Willis is formed by

the anterior communicating
artery and the anterior cerebral,
internal carotid, posterior
communicating, and posterior
cerebral arteries. (Reproduced,
with permission, from Waxman S.
Clinical Neuroanatomy. 26th ed.
New York, NY: McGraw-Hill;
2010.)
Clincal Neurology
Mm Histologi SSP
Struktur mikroskopik : korteks serebrum ,batang otak, medulla
spinalis yg berkaitan dgn UMN
Kortek serebri
• Jaringan yg bertanggung jawab untuk fungsi
pembelajaran,memori,integrasi ,sensoris ,analisis
informasi & permulaan respon motorik.

• Substansia grisea pd bag tepi hemisfer serebri berlipat2

mbntuk bnyak tonjolan girus & sulcus

• Korteks serebri dibagi mnjadi 6 lapisan dibentuk oleh

sel saraf
• Lap paling luar trletak dibawah piamater
• Lapisan terdalam ( korteks serebri berbatasan dengan
substansia alba otak besar)
 KORTEKS Serebri

Difiore –Atlas of
The most superficial is the molecular layer (I).
• Overlying and covering the molecular cell layer (I) is the delicate
connective tissue of the brain, the pia mater (1).

• The peripheral portion of molecular layer (I) is composed

predominantly of neuroglial cells (2) and horizontal cells of Cajal.

• Their axons contribute to the horizontal fibers that are seen in the
molecular layer (I).

The external granular layer (II) contains mainly different

• types of neuroglial cells and small pyramidal cells (3)Note that
the pyramidal cells get progressively larger in successively deeper
layers of the cortex.
• In the external pyramidal layer (III), medium-
sized pyramidal cells (5) predominate.

• The internal granular layer (IV) is a thin layer and

contains mainly small granule cells (6), some
pyramidal cells, and different neuroglia that form
numerous complex connections with the pyramidal
cells.
• The internal pyramidal layer (V) contains numerous
neuroglial cells and the largest pyramidal cells (8),
especially in the motor area of the cerebral cortex.

• The deepest layer is the multiform layer (VI). This layer is

adjacent to the white matter (10) of the cerebral cortex.

• The multiform layer (VI) contains intermixed cells of varying

shapes and sizes, such as the fusiform cells, granule cells,
stellate cells, and cells of Martinotti.

• Bundles of axons (9) enter and leave the white matter (10).
MM Fisiologi SSP
No. Tanda Kelumpuhan UMN
1. Hipertonia (tonus meninggi) •Khas pada disfungsi komponen ekstrapiramidal UMN.
•Hilangnya pengaruh inhibisi korteks motorik tambahan
terhadap inti-inti intrinsik medula spinalis.
•Otot-otot fleksor seluruh lengan, serta otot aduktor
bahu, dan pada tungkai : otot-otot ekstensor dan otot-
otot plantarfleksi kaki.

2. Hiperefleksia •Keadaan setelah impuls inhibisi dari susunan piramidal

dan ekstrapiramidal tidak dapat disampaikan ke
motorneuron  Reflek tendon >> peka dari normal.

3. Klonus •Diiringi hiperefleksia

•Gerak otot reflektorik yang bangkit secara berulang-
ulang selama perangsangan masih berlangsung.

4. Reflek patologik (+) •Refleks babinski, reflek tomner Hoffmann, dll

5. ≠ atrofi pada otot lumpuh •Motoneuron tidak rusak  tidak atrofi
6. Refleks automatisme spinal
•TIA (Transient Ischemic Attack)
•Infark Serebral
•Hematom Intraserebral
•Perdarahan Subarachnoid
•Ensefalopati Hipertensi
•Complete Spinal Transaction
•Acute Medulla Compression
•CVD : stroke
 ACUTE MEDULLA COMPRESSION
Definisi
• Kompresi med spin  ada lesi struktural di kolumna vertebra yg mendesak
canalis spinalis  gejala mielopati
Etiologi
• Trauma, neoplasma, abses epidural, herniasi diskus, kelainan vertebra
• Abses : Staphylococcus aureus; gram-negative bacilli, Streptococcus,
anaerobes, and fungi, Tuberculosis from an adjacent vertebral source (Pott’s
disease)

• Lesi plg sering : segmen thoracal (70%), lumbosacral (20%), cervical (10%)
• Mrpk komplikasi neurologik dri neoplasma sistemik
• Penyebaran kanker paru, mammae, prostat, ginjal, limfoma ke vertebra 
tekan med spin
• Imunodef (DM, gagal ginjal, alkoholisme, keganasan), penya;ahgunaan obat
IV, inf  resiko kompresi akibat abses

Harrison’s Principles of Internal Medicine. 19ed. 2015.

 Patogenesis
• Neoplasma ke vertebra mll PD / ekstensi lgsg (limfoma)
• Sel tumor  bntuk massa / kerapuhan columna vertebra  tekan med spin 
edema, inflamasi, trauma pd saraf & vaskuler, gang oksigenasi
• Massa membesar  vertebra lemah, tdk stabil, hancur
• Abses membesar  kongesti vena & trombosis
Manifestasi klinis
• Nyeri : lokal / radikular, bertahan 2-4 bulan sblm timbul gejala lain
• Lesi C5 ke atas : gang napas
• Lesi setinggi vertebra cervical : tetraparesis
• Lesi daerah thoracal – lumbal : paraparesis
• Gang sensorik (baal, kesemutan) sesuai dermatom yg terkena
• Gang otonom (inkontinensia, retensi urin / alvi, hipohidrosis) sesuai dermatom
yg terkena
Harrison’s Principles of Internal Medicine. 19ed. 2015.
 • Penyebab abses :
▫ Nyeri dorsal di midline
▫ Demam
▫ Kelemahan tungkai progresif
▫ Bs nyeri tumpul di daerah tulang belakang / pola radikuler, biasa nyeri ≤ 2 minggu tpi bs berbulan”
Anamnesis
• Nyeri : lokal / menjalar, spt ditusuk / terbakar, tdk hilang / tmbh parah saat
batuk/bersin/bergerak, bs menyebabkan pasien bangun pd malam hari
• Nyeri radikuler sesuai dg letak lesi : daerah cervical  dri leher ke bahu / lengan, thoracal 
spt terikat (tight band) pd dada / perut, lumbal  menjalar ke paha / tungkai bawah
• Gang motorik : kaku otot, kaki / tangan terasa berat, sulit naik tangga, gang koordinasi
• Gang sendorik : baal, kesemutan, dingin pd ekstremitas
• Gang otonom : inkontinensia urin / alvi, baal pd daerah perianal (sindrom kauda ekuina)
• Riw keganasan, gejala umum keganasan (BB, anoreksia)

Harrison’s Principles of Internal Medicine. 19ed. 2015.

 PF
• ABC & TTV
• P. area nyeri : deformitas daerah punggung, nyeri tekan pd segmen vertebra ttt
• P. status neurologis : sensorik, motorik, otonom
PP
• Foto polos cervical, thoracal, lumbosacral : AP & lateral (sesuai segmen yg dicurigai)
• MRI spinal (+ kontras u/ keganasan)  metastasis : hipointense pd sequens T1, stlh
diberi gadolinum : contrast enhancement bs meningkatkan intensitas shg mirip ke
sumtul N; infeksi (osteomielitis) : melewati disk space ke vertebral body
• Elektromiografi : lihat iritasi / kompresi pd radiks ttt
• Bone scan : lihat metastasis di slrh spinal & tulang lain
• LP : jk ada ensefalopati / tanda lain yg mengarah ke meningitis
• Lab : WBC, LED, CRP =  (abses)
• Kultur darah, aspirasi lgsg dri abses dg op
• High cervical tap : kdg” plg aman
• CSF : pelositosis dg PMN, protein,glukosa
Harrison’s Principles of Internal Medicine. 19ed. 2015.
Harrison’s Principles of Internal Medicine. 19ed. 2015.
 Tatalaksana
• u/ nyeri :
▫ Gabapentin 600-1200 mg/ hari : sbg adjuvan opiat
▫ Kortiko : u/ kurangi edema & nyeri, diberi sblm p. imaging, dosis diturunkan sp radioTh/
selesai (curiga keganasan)  Dexa IV 10 mg, dilanjutkan 16 mg/hari
• Keganasan :
▫ RadioTh/ : pd lesi yg simptomatik & Th/ spesifik u/ etiologi tumor yg mendasari
▫ Biopsi massa epidural
▫ Pembedahan dg laminektomi dekompresi / reseksi corpus vertebra
• Abses :
▫ Laminektomi dekompresi dg debridement + Th/ AB jangka pjg
▫ Evakuasi bedah : cegah paralisis
▫ AB : mulai scr empirik sblm op, diganti sesuai hasil kultur & dilanjutkan min 4 minggu

Harrison’s Principles of Internal Medicine. 19ed. 2015.

 Prognosis
• Defisit motorik tetap (paraplegia / quadriplegia), jk menetap >12 jam 
tdk membaik, >48 jam  pemulihan fs motorik buruk
• RadioTh/ cepat dilakukan : 50% pemulihan parsial fs motorik
• Survival : 3-6 bulan (lbh tinggi dri pasien rawat jalan & jk tumor b’sifat
radiosensitif)
• 10% relaps

Harrison’s Principles of Internal Medicine. 19ed. 2015.

 Diagnosis
• Bdsrkn gejala klinis, statis (tdk progresif)
• DD : distonia, ataxia, spastisitas yg progresif  gang metabolik,
metachromatic leukodystrophy, movement disorders such as levodopa-
responsive dystonia
• MRI : eksklusi penyebab struktural (tumor, stroke, AVM)
Tatalaksana
• multidisciplinary approach is necessary
• early infant stimulation
• physical and occupational therapy
• orthopedic and psychological evaluation
• speech therapy.

Blueprints Neurologyy – Lippincott Wlliams & Wilkins. 2009.

 Stroke
• Sindrom yg terdiri dari tanda & / gejala hilangnya fungsi SSP fokal yg
berkembang cpt (dlm dtk /mnt)

• Gejalabrlangsung lbh dari 24 jam

• Mekanisme vaskular yg menyebabkan stroke :
▫ Infark (emboli /trombosis )
▫ Hemoragik
• Infark pd SSP
▫ Etiologi & Patogenesis
 Trombosis arteri (atau vena) pd SSP dpt disebabkan 1 /lbh dri trias Virchow:
a) Abnormalitas dinding P.D (umumnya krn pnyakit degeneratif) ,dpt jg inflammasi
(vaskulitis),trauma
b) Abnormalitas darah (ms polisitemia )
c) Gg aliran darah
• Embolisme dpt merupakan komplikasi dari pnyakit degeneratif arteri SSP
/dpt jg berasal dari jantung :
▫ Pnyakit katup jantung
▫ Fibrilasi atrium
▫ Infark miokard yg baru terjadi
• Pnyebab tersering stroke  pnyakit degeneratif arterial (aterosklerosis p.d )/p.d
kecil
Stroke

Clinical Neurology
PATOFISIOLOGI
Mekanisme terjadinya cedera
• Energy Failure
• Gradien Ion
• Disregulasi Kalsium
• Eksitotoxicity
• Oxidative & Nitrosative injury
• Cell death Cascade
• Inflammation
Patofisiologi
• Ketika arteri tersumbat scara akut o/trombus /embolus area SSP
yg diperdarahi akan mengalamiinfark (jika tdk ada perdarahan
kolateral yg adekuat).

• Disekitar zona nekrotik sentral terdapt “penumbra iskemik” (yg

ttp viabel suatu wktu ,artinya fungsi dpt pulih jika aliran darah baik
kembali).
• Iskemia krn SSP dpt disertai o/ pembengkakan krn?
▫ Edema sitotoksi akumulasi air pd sel glia & neuron yg rusak.
▫ Edema vasogenikakumulasi cairan ekstraselular akibat perombakan
sawar darah otak
Gambaran klinis & klasifikasi
• Infark total sirkulasi anterior (karotis)
▫ Hemiplegia (krusakan bag atas traktus kortikospinal)
▫ Hemianopia (kerusakan pd radiasio optikus)
▫ Defisit kortikal ( disfasia (hemisfer dominan),hilangnya visuospasial (
• Hemplegia dan hemianopia /hnya defisit kortikal saja
• Infark lakunar
▫ Pnyakit intrinsik (lipohialinosis )pd arteri kecil profunda
▫ Infark lakunar multipel dpt menyebabkan dpt mnyebabkan defisit
neurolgois multipel (trmsk gg kognitif (demensia multinfark
• Infark sirkulasi posterior (vertebro-basilar)
▫ Tanda lesi batang otak ( ms: vertigo,diplopia,perubahan kesadaran)
▫ Hemianopia homonim
• Infark medula spinalis
Stroke Iskemik
• Faktor resiko stroke :
▫ Faktor yg dpt dimodifikasi /dilakukan tatalaksana
(hipertensi,diabetes melitus,merokok,obesitas ,asam
urat & hiperkolesterol
▫ Faktor resiko yg tdk dpt dimodifikasi usia,jenis
kelamin & etnis
Patofisiologi Stroke Iskemik Akut
• Proses terjadinya stroke iskemia diawali oleh adanya
sumbatan p.darah o/ trombus /emboli sel otak gg
metabolisme (krn tdk mendapat suplai darah,o2 & energi
)
▫ Trombus trbntuk oleh adanya proses aterosklerosis pd
arkus aorta ,arteri karotis /p.darah serebral.
 Proses ini diawali o/ cedera endotel & inflammasi trbentuk
plak pd dinding p.d plak makin tebal dan sklerotik
 Trombosit melekat pd plak melepaskan faktor2 yg
menginisiasi kaskade koagulasi & p’tukan trombus dpt lepas
& mnjdi embolus iskemia jaringan otak infark
• Disekeliling area sel otak yg
mngalami infarkmengalami gg
metabolisme & gg perfusi bersifat
smentara (daerah penumbra)
▫ Daerah ini akan bs diselamatkan
jika dilakukan p’rbaikan aliran
darah kmbali (reperfusi
segera)mencegah kerusakan sel
yg lbh luas
Aliran darah jaringan otak normal :
40-50 cc/100 g otak/menit
Ttp pd daerah infark,tdk ada aliran
sama skali ( CBF(cerebral blood
flow) 0 mL/100 g otak/mnt)
Daerah dekat infark CBF : 10cc/100
g otak/menit threshold of neuronal
death (o/ krn sel otak tdk hidup bila
CBF <5cc/100 g/mnt )

▫ Jika tdk infark (bs jg

disebabtkan o/ proses
inflammasi,gg sawar darah ,zat
neurotoksik akibat hipoksia,
mnurunnya aliran darah
mikrosirkulasi
• Daerah iskemikATP turun kegagalan pompa K+ &
Na+ ,pningkatan kadar laktat intraseluler depolarisasi
& pningkatan pelepasan neurotransmiter glutamat
mningkatkan kadar kalsium intrasel

• Glutamat dari synapse terminalikatan dgn reseptor

glutamat (NMDA),AMPA masuk Ca+ intraseluler
mmicu trbentuk radikal bebas,NO,inflamasi &
kerusakan DNA (mlalui jalur Ca2+ -ATPase ,calcium
dependent phospholipase ,protease ,endonuklease &
kaspase )kematian sel
Harrison”s neurology in Clinical Medicine
Faktor yg mempengaruhi
• Kondisi stress oksidatif
• Asidosis: pningkatan metabolisme anerob memicu
p’tukan asam laktat shingga terjadi
asidosismasuknya Na+ & Cl- ke dlm sel (melalui
ikatan Na+/H+ dgn Cl- /HCO3-)edema intrasel &
pningkatan t.kanan intrakranial
• Depolarisasi
• Inflamasi
Etiologi
Mechanisms that have been proposed to explain these events include drug-
induced vasospasm, vasculitis,
and the rupture of preexisting aneurysms or vascular malformation.
1. Cocaine hydrochloride is most often associated with intracerebral
hemorrhage but can also cause subarachnoid hemorrhage or ischemic stroke.
2. Alkaloidal (crack) cocaine use can lead to stroke that is usually ischemic in
origin, but intracerebral or subarachnoid hemorrhage also occurs.
3. Amphetamines can produce vasculitis, with necrosis of the vessel wall
leading to intracerebral hemorrhage; ischemic stroke and subarachnoid
hemorrhage are less frequent.

4. Other sympathomimetic amines, including phenylpropanolamine and

ephedrine, are also associated with an increased risk of stroke.
5. Heroin is associated primarily with embolic stroke related to endocarditis.
GEJALA & Tanda
• Gejala gg fungsi otak pd stroke sangat tergantung pd daerah
otak yg terkena.
• Defisit neurologis yg ditimbulkanny dpt bersifat fokal /global:
▫ Kelumpuhan sesisi/ke2 sisi,kelumpuhan 1 extremitas
,kelumpuhan otot penggerak bola mata ,kelumpuhan otot2 untuk
proses menelan,bicara & sbgnya
• Gg fungsi keseimbangan
• Gg fungsi penghidu
• Gg fungsi penglihatan
• Gg fungsi pendengaran
• Gg fungsi sensoris
• Gg fungsi kognitif
• Gg global
• Px sderhana untuk mengenali gejala & tanda stroke
mnggunakan singkatan FAST
• F:facial droop
• A: arm weakness
• S: speech difficulties
• T: time to seek medical help
• Tnda klinis stroke jg dpt dilakukan dgn cara pf
neurologi untuk mngkonfirmasi kembali tanda & gejala
▫ Px fisik utama: pnurunan kesadaran berdasar GCS
,kelumpuhan saraf kranial,kelemahan motorik ,defisit
sensorik,gg otonom ,gg fungsi kognitif
Diagnosis
• Kriteria diagnosis: trdpt gejala defisit neurologis global
/slh 1 bbrp defisit neurologis fokal yg terjd mendadak dgn
bukti gmbaran pncitraan otak (CT scan/MRI)
• Diperlukan px penunjang untuk memastikan diagnosis
serta untuk mengeksplorasi faktor resiko & etiologis
troke iskemik:
▫ EKG
▫ Pncitraan otak:Ctscan kepala non kontras & difusi serta
MRA
▫ Doppler karotis & vertebralis
▫ Doppler transkranial
▫ PX lab
Komplikasi
• Pneumonia
• ISK
• Trombosis vena dalam
• Dekubitus
• Spastisitas & nyeri
• Depresi
• Gg fungsi kognitif
• Komplikasi metab gg elektrolit
Tatalaksana
• Stabilisasi Jalan Napas & Pernapasan
• Stabilisasi Hemodinamik
• Pengendalian Peningkatan Tekanan Intrakranial
▫ Pmantauan ketat pd kasus dgn resiko edema serebri dgn
mmprthatikan perburukan gejala & tanda neurologis
▫ Sasaran terapi : TiK krg dari 20 mmHg & tekanan
perfusi otak : >70mmHg
• Pengendalian suhu tubuh
Nutrisi
• Nutrisi enteral pling lambat sudah harus diberikan dlm 48
jam ,nutrisi oral hanya bole diberikan stlh hasil fungsi
menelan baik
• Jika ada gg menelan/kesadaran turundiberi melalui
pipa nasogastrik
• Pd keadaan akut kebutuhan kalori 25-30kkcal/kg/hari dgn
kompoisis:
▫ Karbohidrat 30-40% dari total kalori
▫ Lemak 20-35% (pd gg nafas dpt lbh tinggi 35-55%)
▫ Protein 20-30% ( pd keadaan stress kebutuhan protein 1,4-
2,0 g/kg/hari )(pd ps gg ginjal: <0,8 /kgbb/hari
Drugs used in the prevention or treatment of
cerebrovascular disease are listed in Table 13-
6. Treatment
related to specific underlying vascular, cardiac,
and hematologic causes of stroke (eg, anti-
inflammatory,
antibiotic or anti-arrhythmic drugs)
Pemberian antikoagulan sbg
pncegahan sekunder
• Tujuan: untuk mmprbaiki keluaran/sbg pencegahan
dini terjadinya stroke ulang
• Pengobatan antikoagulan dlm 24 jam trhdp ps yg
mndapat Rtpa IV TDK DIREKOMENDASI
• Warfarinlini prtama untuk pencegahan sekunder
strok iskemik
▫ Dpt mningkatkan resiko perdarahan
▫ Dpt mnecegah terjdi nya strok emboli kardiogenik &
mncegah emboli ulang
 Dosis : 2 mg perhari dgn target INR 2,0-3,0
PREVENTION
• Pencegahan primer dari stroke hrus berdasarkan
penyebabnya apa
(hipertensi,merokok,dyslipidemia,diabetes,obesitas &
inaktivitas)
• Pnggunaan aspirindiduga dpt mnurunkan insiden KV
(biasanya pd ps hipertensi)
▫ Pd laki2 65 thn & wnita 71 thn dgn t.d 140 mmhg & tdk ada
faktor resiko lain (dm,merokok dll)
• Sumber kardioembolik prevensi pd ps dgn kelainan jantung
cth : fibrilasi atrial,infark miokard,kelainan katup jantung
▫ Pemberian warfarin dgn target INR 2,0-3,0 dpt mnurunkan
kejadian stroke 50-70%
▫ Rivaroxaban (20 mg orally daily )inhibitor faktor Xa
Stroke Hemoragik
• Perdarahan intraserebral pecahnya p.darah
intaserebral
• Dpt mnimbulkan gejala neurologis yg terjadi scara
tiba2 & seringkali diikuti pningkatan tekanan
intrakranial
Patofisiologi
• Kerusakan dinding P.D di otak akibat hipertensi
• Hipertensi kronikdpt mnyebabkan terbentuknya
aneurisma
• Terjadi proses turbulensi aliran darah nekrosis
fibrinoid ,nekrosis sel /jaringan dgn akumulasi
matriks fibrin
• herniasi dinding arterior & ruptur tunika
intimamikroaneurisma yg disebut Charcot
Bouchard dpt pecah mndadak saat t.d mningkat
• Hipertensi tkanan darah tinggi terus2terjadinya
proses hialinisasi pd dinding p.dp.darah kehilangan
elastisitasnya
▫ Berbahya krn p/d serebral tdk lagi bsa menyesuaikan diri
dgn fluaktuasi t.darah sistemik ,kenaikan t.d mendadak
pecah p.darah
▫ Darah yg keluar akan terakumulasi & mmbntk bekuan
darah di parenkim otak
▫ Vol hematom akan ber+ mmberikan desak
ruangmenekan parenkim otakmningkatkan TIK
▫ Mmprburuk kondisi ps (umumnya brlgsg dlm 24-48 jam
akibat perdarahan terus dgn edema diskitarnya)
• Trjdi efek desak ruang pergeseran garis tengah
(midline shift) & herniasi otak iskemia & perdarahan
sekunder
• Pergeseran jg dpt menekan sistem ventrikel otak &
mngakibatkan hidrosefalus sekunder

• Kompensasai untuk mmpertahankan perfusi

otaktekanan arteri jg akan mningkat

• Stroke hemoragik yg dikaitkan dgn hipertensi struktur

otak bag dalam yg diperdarahi oleh penetrating arteri (spt
pd area talamus,pons,dserebelum
DEEP CEREBRAL HEMORRHAGE
 Gejala & Tanda Klinis
• Perjalanan klinis ps stroke dpt
berkembang dari defisit neurologis
fokal  gejala pningkatan TIK berupa
nyeri kepala,pnurunan kesadaran &
muntah
▫ Perburukan klinis def neuroligis 
perluasan lesi perdarahan yg mberikan
efek desak ruang

▫ CT SCAN mnunjukan hematom akan

mmbesar dalam 6 jam prtama
 Tik dapat berkurang seiring dgn
berkrgnya vol hematom akibat
perdarahan yg terhenti /hematom msk ke
ruang ventrikel
• Nyeri kepala berkaitan dgn lokasi & luasnya lesi perdarahan
(yaitu stroke hemoragik didaerah lobaris,serebelum & lokasi yg
berdekatan dgn meningen),jika perdarahan kecil di parenkim otak
yg tdk pnya serabut nyeri tdk terdapat nyeri saat fase awal
perdarahan
• Pnurunan kesadarankrn efek desak ruang & pningkatan TIK serta
keterlibatan RAS dibatan otak
• Muntahakibat pningkatan TIK /krusakan lokal di ventrikel ke 4
biasanya perdarahan sirkulasi posterior
• Kejang (biasanya lokasi yg bersifat epileptogenik :perdarahan
lobar ,gray white matter junction di korteks serebri
• Kaku kudukdpt terjadi perdarahan di talamus,serebelum
• Aritmia jantung & edema paru
DIAGNOSIS
• Anamnesa apakah keluhan terjadi scara tiba2 ,saat
pasien beraktivitas /saat ps baru bgn tidur (pd stroke
hemoragik ,pasien umumnya berada dlm kondisi sedang
berada dlm aktivitas /emosi tdk terkontrol )

• Ps dgn keluhan skit kepala disertai muntah (tnpa mual )

& pnurunan kesadaranumumnya kcurigaan kpd stroke
hemoragik dgn pningkatan TIK akibat efek desak ruang.
• Ps stroke hemoragik:kesadaran umum lbh buruk dr stroke
iskemik
• Px neurolgois pnilaian tingkat kesadaran kmudian
refleks batang otak
Pemeriksaan pnunjang
• Ctscan mrupakan gold standart dlm diagnosis stroke
hemoragik
• CT scan unggul dlm mendeteksi perdarahan lgsg
berdasarakna gmbaran hiperdensitas diparenkim otak
dibanding MRI
Medical
• Initial medical management includes airway support with ventilatory
assistance if required.

• The use of antihypertensive drugs is controversial because reducing

systemic blood pressure may compromise cerebral blood flow and lead to
infarction surrounding the hematoma, whereas continued hypertension
may increase hematoma size.

• One recommendation is to lower systolic blood pressure to approximately

180 mm Hg, using intravenous vasodilator drugs with short half-lives.

▫ Another approach involves the use of nitroglycerin paste (½-1 inch topically),
which can be wiped off the skin to quickly terminate its effect if needed.

▫ If volume overload contributes to hypertension, judicious use of a diuretic (eg,

furosemide, from 10 mg intravenously in patients new to the drug to 40 mg
intravenously in patients accustomed to receiving it) can be helpful.

• Corticosteroids are sometimes prescribed to reduce vasogenic edema in

patients with intracerebral hemorrhage, but the evidence of their benefit is
poor. Antiedema agents provide only temporary benefit.

• Hemostatic treatment with activated recombinant factor VII does not

improve outcome.
Surgical
1. Cerebellar hemorrhage—The most important
therapeutic intervention in hypertensive
hemorrhage is decompressive posterior fossa surgery
or endoscopic removal of cerebellar hematomas.

 This may reverse the neurologic deficit and, if

undertaken promptly, may avert a fatal outcome or
unexpected deterioration.

 Indications include neurologic deterioration, brainstem

compression, and hydrocephalus, but results are best in
conscious patients.
2. Lobar hemorrhage—Surgical evacuation can also be
useful for lobar hematomas, especially those located
within approximately 1 cm of the brain surface and
operated on within approximately 12 hours.

• Stereotactic or endoscopic evacuation, if available, is

associated with fewer complications than open
craniotomy.
• The prognosis is directly related to the level of
consciousness before the operation, and surgery is usually
fruitless in an already comatose patient.
3. Deep hemorrhage—Surgery is not indicated for
pontine or deep cerebral hypertensive
hemorrhages, because in most cases spontaneous
decompression occurs with rupture into the
ventricles—and the areas in question are accessible
only at the expense of normal overlying brain.
4. Intraventricular hemorrhage and hydrocephalus—
Each of these complications is a poor prognostic
indicator.

• Ventricular drainage and ventriculoperitoneal shunting

may help to remove intraventricular clots and relieve
obstruction of the CSF pathways.

• Endoscopic removal of intraventricular blood and

intraventricular administration of thrombolytic agents are
under study.
• PREVENTION Hypertension is the leading cause
of primary intracerebral hemorrhage. Prevention is
aimed at reducing hypertension, excessive alcohol
use, and use of illicit drugs such as cocaine and
amphetamines.
TATALAKSANA
• Stabilisasi Napas & pernapasan
• Stabilisasi Hemodinamik
• Tatalaksana pningkatan TIK
• Pngendalian suhu tubuh
• Tatalaksana Cairan
• Nutrisi dpt enteral ,ttp jika terjdi komplikasi perdarahan lambung
dpt ditunda smpai terjdi perbaikan & sisa cairan lambung dlm 2 jam
pertama < 150 cc
▫ Keadaan akut kebutuhan kalori: 20-25 kkal/kg/hari dgn komposisi:
 Karbohidrat 50-60% dari total kalori
 Lemak 25-30%
 Protein 10-20%
 Pd keadaan adanya stressor pd tubuh 1,4-2,0 kgbb/hari
 Kebutuhan protein disesuaikan pd gg fungsi ginjal 0,6-0,8 kg/bb /hari
• Mmprtahankan CPP
▫ Usahakan t.d sistolik <160 mmgHg & CPP dijaga >60-
70 mmgHg
▫ Hal ini dpt dicapai dgn mnurunkan TIK ke nilai normal
dgn pmberian manitol/op
▫ Jika perlu diberi :
 Phenlyephrine 2-10 ug/kg /mnt
 Dopamin 2-10 ug/kg /mnt atau
 Norepinefrin dimulai dgn dosis 0,05 -0,2 um/kg/mnt &
dititrasi smpai efek yg diinginkan
•Demensia
•Parkinson
•Amnesia pasca trauma
DEMENSIA Alzheimer Disease
Vascular Dementia
Penyebab : • Infeksi Dementia with Lewy Bodies
• Degeneratif • Neoplasma
Progressive Supranuclear Palsy
• Metabolic • Vaskuler
• Ggn • Hidrosefalus Huntington Disease
penyimpanan • Trauma
lemak & • Idiopatik Parkinson Disease
leukodistrofi • Campuran FTD
• Toxic
Demensia karena Infeksi
Demensia karena
penyebab metabolik
Gejala :
• Gangguan Terapi :
mengingat Diagnosis : • AD (Donepezil, Rivastigmine,
• Anamnesa Tacrine, Ibuprofen, Vitamin E,
• Pe↓an fungsi • Pemeriksaan Estrogen)
kognitif fisik • Vascular dementia
• Perubahan • Pemeriksaan (Antihipertensi, Warfarin, Aspirin,
tingkah laku penunjang/lab Clopidogrel, Dipyridamole &
• Emosi labil Aspirin, Vit E)

Characterized by a gradual, progressive
decline in intellectual function, coupled
with impairment of memory, judgment and
problem solving, language, and perception.
The symptoms can be divided into
cognitive and noncognitive.
Stages:
Mild, moderate, severe
*based on review of performance in six
categories (memory, orientation, judgment
and problem solving, community affairs,
home and hobbies, and personal care)
Diagnostic criteria:
Definite AD: meets the criteria for probable
Alzheimer's disease and has histopathologic
evidence of AD
Probable AD: Dementia has been established by
clinical and neuropsychological examination.
Absence of conditions that can cause cognitive
impairment and mimic AD.
Possible AD: A dementia syndrome with an
atypical onset, presentation or progression; and
without a known etiology; but no co-morbid
diseases capable of producing dementia are
believed to be in the origin of it.
Treatment:
Cholinesterase inhibitors
NMDA Receptor Antagonists
Vit/supplements
•Lesi batang otak
•Cerebral palsy
•Alzheimer
•Hematom Epidural
•Hematom Subdural
•Trauma medulla spinalis
•Siringomelia
•Mielopati
•Neoplasma
 Cerebral Palsy
Definisi
• Gang statis yg disebabkan o/ kerusakan cerebromotor pathway saat pre /
perinatal
Etiologi
• Genetik, didapat
FR
• Hypoxic ischemic insult to the brain in perinatal period, prematur, BBLR,
korioamnionitis, inf virus prenatal, perinatal stroke

Blueprints Neurologyy – Lippincott Wlliams & Wilkins. 2009.

 Klasifikasi bdsrkn ekstremitas yg terkena :
• Hemiparesis : kelemahan & spastisitas pd 1 sisi tubuh
▫ fisting on the affected side, early hand preference, and increased reflexes with upgoing
toes on the affected side
• Diaparesis : spastisitas di ke4 ekstremitas, lbh mempengaruhi kaki drpd
tangan
▫ normal intelligence and are less likely to have seizures than children with other forms of
CP.
• Spastic quadriplegia : ke4 ekstremitas terpengaruh
▫ Seizures usually occur within the first 48 hours of life. The infant may show signs of
cerebral hypo- tonia
Manifestasi klinis
• Bis didiagnosis pd minggu 1 kehidupan
• Infant : flaccid weakness, asymmetric limb movements, or seizures
• Older children : spasticity, dystonia, developmental delay, and drooling
Blueprints Neurologyy – Lippincott Wlliams & Wilkins. 2009.
 Diagnosis
• Bdsrkn gejala klinis, statis (tdk progresif)
• DD : distonia, ataxia, spastisitas yg progresif  gang metabolik,
metachromatic leukodystrophy, movement disorders such as levodopa-
responsive dystonia
• MRI : eksklusi penyebab struktural (tumor, stroke, AVM)
Tatalaksana
• multidisciplinary approach is necessary
• early infant stimulation
• physical and occupational therapy
• orthopedic and psychological evaluation
• speech therapy.

Blueprints Neurologyy – Lippincott Wlliams & Wilkins. 2009.

COMPRESSIVE MYELOPATHIES
Neoplastic Spinal Cord Compression
• In adults, most neoplasms are epidural in origin,
resulting from metastases to the adjacent spinal
bones.

• Almost any malignant tumor can metastasize to the

spinal column, with breast, lung, prostate, kidney,
lymphoma, and plasma cell dyscrasia being
particularly frequent.
Clinical Finding
• Pain is usually the initial symptom; it may be aching and
localized or sharp and radiating in quality.

• This spinal ache typically worsens with movement,

coughing, or sneezing and characteristically awakens
patients at night.

• A recent onset of persistent back pain, particularly if in

the thoracic spine (which is uncommonly involved by
spondylosis), should prompt consideration of vertebral
metastasis
• Vertebral metastases are usually
hypointense relative to a normal bone
marrow signal on T1-weighted MRI
scans; after the administration of
gadolinium, contrast enhancement may
deceptively “normalize” the appearance
of the tumor by increasing its intensity to
that of normal bone marrow.
Treatment:
NEOPLASTIC SPINAL CORD
COMPRESSION
• Management of cord compression includes
▫ Glucocorticoids to reduce cord edema, local
radiotherapy (initiated as early as possible) to the
symptomatic lesion, and specific therapy for the
underlying tumor type.

▫ Glucocorticoids (dexamethasone, up to 40 mg daily)

can be administered before the imaging study if the
clinical suspicion is strong and continued at a lower
dose until radiotherapy (generally 3000 cGy
administered in 15 daily fractions) is completed
• Radiotherapy appears to be as effective as surgery, even
for most classically radioresistant metastases.

• Biopsy of the epidural mass is unnecessary in patients

with known preexisting cancer but is indicated if a history
of underlying cancer is lacking.

• Surgery, either decompression by laminectomy or

vertebral body resection, should be considered when
signs of cord compression worsen despite radiotherapy
 NONCOMPRESSIVE
MYELOPATHIES

• The most frequent causes

of noncompressive acute
transverse myelopathy
(ATM) are spinal cord
infarction; systemic
inflammatory disorders.
SPINAL CORD INFARCTION
• Spinal cord infarction results from
▫ aortic atherosclerosis,
▫ dissecting aortic aneurysm (manifest as chest or back
pain with diminished pulses in legs)
▫ vertebral artery occlusion or dissection in the neck, or
profound hypotension from any cause.
▫ Cardiogenic emboli, vasculitis related to collagen
vascular disease [particularly SLE and the
antiphospholipid antibody syndrome
▫ surgical interruption of aorticaneurysms are other
causative condition
SPINAL CORD INFARCTION
• The cord is supplied by three arteries that course
vertically over its surface: a single anterior spinal
artery and paired posterior spinal arteries.

• the anterior spinal artery is fed by radicular vessels that

arise at C6, at an upper thoracic level, and, most
consistently, at T11-L2 (artery of Adamkiewicz).

• With systemic hypotension, cord infarction occurs at the

level of greatest ischemic risk, usually T3- T4, and also at
boundary zones between the anterior and posterior spinal
artery territories.
 Acute infarction in the territory of the anterior
spinal artery produces paraplegia or quadriplegia,
dissociated sensory loss affecting pain and
temperature sense but sparing vibration and position
sense, and loss of sphincter control (“anterior cord
syndrome”).

 Onset may be sudden and dramatic but more

typically is progressive over minutes or a few hours,
quite unlike stroke in the cerebral hemispheres.
• In cord infarction due to presumed thromboembolism,
acute anticoagulation is probably not indicated, with the
exception of the unusual transient ischemic attack or
incomplete infarction with a stuttering or progressive
course.

• The antiphospholipid antibody syndrome is treated with

anticoagulation.

• Drainage of spinal fluid has reportedly been successful in

some cases of cord infarction but has not been studied
systematically.
MIELOPATI
Definisi / Etiologi
• Merupakan suatu gangguan fungsi atau struktur dari
medulla spinalis oleh adanya lesi komplit atau
inkomplit.
Etiologi
- Vaskuler - Tumor
- Obat-obatan - Demielinisasi
- Radiasi - Trauma
- Infeksi - Tidak diketahui
- Degenerasi
KRITERIA DIAGNOSIS
• Anamnesis: Lemah / lumpuh anggota gerak, gangguan buang air kecil dan buang air
besar,
gangguan sensibilitas.
• Fisis : parese / plegi tipe UMN (tergantung lokalisasi lesi, dapat dijumpai gejala UMN
atau campuran UMN dan LMN), hipestesi / anestesi segmental, gangguan fungsi
otonom.
• Kejadiannya dapat akut, subakut, kronik progresif.
• Tidak ditemui tanda-tanda radang atau penyebabnya tidak diketahui.
• Pemeriksaan Penunjang
• Pemeriksaan Laboratorium:
• Darah rutin, kimia darah, urin lengkap, dan bila perlu tes kadar obat : kokain, heroin
• Likuor serebrospinalis

• Pemeriksaan Radiologik :
• Foto polos vertebra AP / Lateral / Oblik
• Mielografi
• CT mielografi

• Pemeriksaan penunjang lain :

• EMNGelectromyoneurography ( penggabungan dari electromyography &
electroneurography)
TATALAKSANA
• Kausal
• Simptomatik
• Suportif
• Rehabilitatif : Fisioterapi ekstremitas dan latihan buli-
buli
PENYULIT
• Bronkopneumoni, dekubitus, kontraktur sendi, atrofi
otot, infeksi saluran kemih