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Dr.Muktasim Billah, Sp.

S
Department of Neurology
Universitas Islam Sultan Agung
Semarang
Hematoma epidural :
1. Rambut arteri meningea media
2. Kulit/kutisEpidermis
Hematoma subdural :
Dermis vena
3. Gallea Aponeurotica (tendo m. Occipitofrontalis)
4. Calvaria Lamina Externa
Diploe
Lamina interna
5. Cavum Epidural
6. Duramater Lamina Externa (Endosteal)sinus
venosus
Lamina Interna (Meningeal)
7. Cavum Subdural
8. Arachnoideamater
9. Cavum subarachnoid
10. Piamater menempel langsung di otak 2
Duramater (Pachymeninx) Paling luar
Arachnoideamater
Leptomeninx
Piamater Paling Dalam
Duramater
Arachnoidea Mater
A.Meningea
Media

Granulationes
Arachnoidea
e

3
4
Perlekatan paling erat di linea mediana di
atas sinus sagittalis superior + sutura +
percabangan a. meningea media
Basis cranii sangat erat terutama di crista
galli, lamina cribrosa, foramen opticum,
fissura orbitalis superior, foramen rotundum,
foramen ovale, foramen lacerum os.
Sphenoid, foramen magnum, foramen
jugulare, meatus acusticus internus
Perlekatan kurang erat di sinus venosus
5
Falx cerebri
di fissura longitudinalis cerebri
Anterior : melekat di crista galli
Posterior : menyatu dg tentorium cerebelli
Pertemuan dg tentorium sinus rectus
Tentorium cerebelli
Antara bagian posterior hemispherium cerebri dg cerebellum
Dr proc.clinoideus posterior sulcus sinus transversi ossis occipitalis :
memisahkan fossa cranii media dr fossa cranii posterior
Falx cerebelli
Memisahkan hemispherium cerebelli
Diaphragma sellae
Atap fossa hipofisis, berlubang u/ ditembus infundibulum
Dr tuberculum sellae ke proc. Clinoideus posterior
Cavum trigeminale Meckeli
Evaginasi duramater fossa posterior ke fossa media
Membungkus ganglion trigeminale

6
Posterosuperior Anteroinferior
1. Sinus sagittalis superior 1. Sinus Cavernosus
2. Sinus sagittalis inferior 2. Sinus Sphenopalatinus
3. Sinus Rectus 3. Sinus intercavernosus
4. Sinus Occipitalis 4. Sinus Petrosus superior
5. Sinus transversus 5. Sinus Petrosus inferior
6. Sinus sigmoideus 6. Plexus Basilaris

7
LCS dibentuk dlm plexus choroideus dan
beredar dlm ventrikel-ventrikel & cavum
subarachnoid, kmdn LCS direabsorbsi oleh
vili arachnoidalis ke dalam sinus-sinus
duramater
Merupakan cairan yang jernih, tidak
berwarna.
Berada dalam ruang subarachnoid
Volume: 120 - 150 cc
Kecepatan produksi 3cc/menit
Fungsi:
Merupakan bantalan bagi otak yang
melindunginya dari pukulan atau goncangan
Merupakan media untuk pembuangan
komponen2 yang berlebihan atau bahan2
sisa dari cairan ekstraseluler ke dalam sistem
sirkulasi darah.
Tekanan normal LCS pada
posisi berbaring berkisar
50 180 mm H20, yang
dapat dipengaruhi oleh
tekanan vena, obat-obatan,
dan lesi massa desak ruang
(SOL)
Diresorbsi oleh vili arachnoid
yang terletak di bagian atas
otak (dalam sinus sagitalis)
Mengandung beberapa
komponen:
Protein : 15 45 mg%
Glukosa: 45 80 mg%
Sel : sel mononukleus/wbc 1 5
/mm3
Terdapat 4 buah ventrikel yang saling
berhubungan satu sama lainnya
2 ventrikel lateral (kanan dan kiri) pada hemisfer
serebri
Ventrikel III diensefalon
Ventrikel IV pons dan medula oblongata
Dindingnya dibatasi oleh sel epitel kuboid
disebut sel ependim tempat-tempat
tertentu melebar disebut pleksus khoroideus
yang berfungsi memproduksi LCS
Masing-masing ventrikel
lateral dihubungkan
dengan ventrikel III melalui
foramen interventrikulare
(monro)

Ventrikel III berhubungan


dengan ventrikel IV
aquaductus serebri (sylvius)

Ventrikel IV berhubungan
dengan rongga
subarachnoid melalui
foramen luscka (di sebelah
lateral) dan foramen
magendi (di sebelah
medial)
Arah sirkulasi :
ventrikel lateral foramen interventrikulare
(Foramen Monro) ventrikel tertius
aqueductus mesencephali (sylvii)
ventrikel quartus 1 foramen Magendie
(medial) & 2 foramen luscha (lateral) cavum
subarachnoid vili arachnoidalis /
granulationes arachnoidea
Adalah volume LCS yang berlebihan di
dalam ventrikel.
Terjadi akibat ketidakseimbangan antara
sekresi dan absorpsi (menyebabkan
peningkatan tekanan intraventrikel)
melalui 3 mekanisme:
1. Produksi likuor yang berlebihan
2. Peningkatan resistensi aliran likuor
3. Peningkatan tekanan sinus venosa
Penyebabnya:
Kelainan bawaan/congenital
Didapat : infeksi otak,tumor otak,
perdarahan otak, cedera kepala
1. Non-communicating: obstruction of the csf
outflow within the ventricles such as
congenital malformation, neoplasm, or
hematoma; blockage of CSF flow within
the ventricular system, with dilatation
proximal to the obstruction
2. Communicating hydrocephalus (non-
obstructive): results from faulty absorption or
inadequate absorption of cerebrospinal fluid
(CSF) resulting from infection, trauma, or
obstruction by thick arachnoid membrane or
meninges; blockage of CSF flow beyond
the outlet of the 4th ventricle
is the situation where there is
communication between the ventricular
system and the subarachnoid space
Blockage of CSF flow over the cerebral
convexities/absorption at the arachnoid
granulations secondary to:
SAH, meningeal metastasis,
granulomatous meningitis
Rapid CSF production
eg. choroid plexus papilloma
is no communication between the ventricular system
and the subarachnoid space
Location of obstruction/causes:
Lateral ventricles ependymoma,
meningioma
Foramen of Monro third ventricular colloid
cyst
Aqueduct of Sylvius congenital
aqueductal stenosis, IVH
Fourth ventricle/foramen of Luschka and
Magendie congenital, tumour, extrinsic
compression
1. Increasing head size in the infant because of
open sutures and bulging fontanels
2. Prominent scalp veins and taut, shiny skin
3. "Sunset" eyes
4. Increased intracranial pressure: projectile
vomiting not associated with feeding,
irritability, anorexia, high shrill cry, seizures,
cracked pot sign, conciousness
5. Damage to the brain because increased
pressure decreases blood flow to the cells,
causing necrosis
Cracked pot
Tense anterior sounds on skull
fontanelle percussion

Lid retraction

Impaired
upward gaze

Thin scalp
with dilated
viens
a condition that Etiologi:
rarely occurs in 50% cases NPH secondary
to other illnesses
patients younger Subarachnoid hemorrhage
than 60 years Meningitis
Cranial trauma
50% cases idiopathic

Diagnostic Triad:
Gait Disturbance
Urinary Incontinence
Dementia
Skull x-ray
Ventriculography
MRI
C T scan
Enlarged Ventricles
Enlarged
Ventricles
EnlargedVentricles
1. Shunting
Immediate effect
~ 100% reliability (although 50%
of current shunts are replaced
within 5 years)
~75% of patients are treated by
3. Ventriculostomy this methodology 2. Drug treatment
(intracranial procedure) Initially, it was shown that
Immediate effect Acetazolamide reduced CSF
When first developed the production by the choroid
procedure had high mortality plexus
and morbidity rates. Today it is In a series of Hydrocephalus in
Shunting is the
a very safe procedure immature infants the drug was
preferred
~25% of patients are treated used and success was claimed
treatment
by this methodology as shunts was avoided in 50%
of the cases
0% of patients are treated by
this methodology
PATHOPHYSIOLOGI OF
INTRACRANIAL PRESSURE
Brain Blood

V darah (150) + V LCS (150) + V otak (1200) CSF Mas


Bones
ICP

DAYS WEEKS HOURS DEATH

CONING
FOCAL VENTRICULAR HYDROCEPHALUS
DISPLACEMENTS DISTORTION CENTRAL HERNIA
HYDROCEPHALUS BRAIN SWELLING

MASSES

TUMOUR
ABSCESS
CYST
HAEMATOMA
Cephalgia
Proyectile
nausea
Papil oedema
Vasogenic :
kerusakan vaskuler endotel kapiler,
gangguan tight junction, permeabilitas
meningkat
Cytotoxic :
gangguan pompa Na, K, ATP ase, Na intrasel
meningkat
Interstisial :
Transudasi

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