Angel-Pemicu 3 Saraf

7/28/2019 Angel-Pemicu 3 Saraf

http://slidepdf.com/reader/full/angel-pemicu-3-saraf 1/170

PEMICU 3 SARAF

Angeline Fanardy 10’178



LO1. Neuroanatomi



DINDING SSP

• SCALP (skin, connective tissue, aponeurosisepicranialis, loose connective tissue ,periosteum

• Oss cranium• Endosteum (stratum periostale duramatis)

• Meningen

– Duramater

– Arachnoid

– Piamater







Brain

• Hemispherium cerebri

– Telencephalon

– Ventrikel lateralis

• Batang otak

– Diencephalon (rostral dari batang otak)

– Mesencephalon (midbrain)

– Metencephalon (cerebellum) – Myelencephalon (medula oblangata)

• Cerebellum



Telencephalon

(Hemispherium cerebri)

Tdd dari 2 lapisan:

1. Cortex cerebri- substantia grisea

2. Medulla cerebri- substantia alba

1)Lobus frontalis : di fossa cranii anterior

2)Lobus temporalis : fossa cranii media

3)

Lobus parietalis : di superior 4)Lobus occipitalis : di posterior







Serebrum

Bagian terbesar otak manusia.

Ada 2 hemisfer hemisfer kanan

hemisfer kiri

Tiap hemisfer dibagiFrontalParietalTemporalOksipital



Bagian otak yg tersembunyi di balik korteksserebri :

Bulbus olfaktorius

Striatum

Nukleus accumbens



• Sistem limbik menerima informasi dariarea asosiasi di korteks serebri & sinyal inimelalui nukleus accumbens.

(1) Hipokampus

(2) Amigdala



Diensefalon

Terletak di bagian dalam serebrum

Struktur utama :

ThalamusHipothalamus

Thalamus :

(1) epithalamus(2) thalamus ventral(3) thalamus dorsal



Hypothalamus

Area pengaturan lingkungan internal tubuh

Pusat pengaturan : Suhu

Lapar

Haus

Bau Respons takut & berani

Perilaku seksual

Fungsi endokrin

Sekresi hipofisis posterior Sekresi hipofisis anterior



Serebelum

Cerebellar peduncles Hemisfer

Korteks serebelar

Nukleus serebelum Vermis

Duramater



Batang Otak (Brain Stem)

Midbrain (Mesensefalon),Cerebral aqueduct Cerebral pedunclesCorpora quadrigemina

PonsSerat transversal Serat longitudinal

Pusat pernapasan Nukleus dari saraf kranial Formasio Retikular



Medula oblongata

Pyramid

Decussation Pusat pernapasan

Pusat pengaturan jantung

Pusat vasomotor

Pusat refleks nonvital

Nukleus dari saraf kranial



MEDULA SPINALIS

Ada 31 pasang saraf spinal

Akson sensorik masuk ke medula spinalis mllganglion akar dorsal.

Traktus spinotalamikus lateralTraktus spinotalamikus anterior Traktus lemniscus medialis-kolumna

posterior

Akson motorik keluar dari medula spinalis mllakar ventral



JALUR PIRAMIDAL / LANGSUNG (mll piramid

medula oblongata ; langsung dari korteksmotorik)

Traktus kortikospinal lateral Traktus kortikospinal anterior Traktus kortikobulbar



EKSTRAPIRAMIDAL / TAK LANGSUNG

(sirkuit polisinaps di ganglia basal, thalamus, &serebelum)

Traktus vestibulospinal Traktus tektospinal

Interneuron menghubungkan saraf sensorikdengan saraf motorik → REFLEKS





VASKULARISASI OTAK





Vaskularisasi

otak - arteri









Vaskularisasi otak - vena



Superior sagittal sinus laid open after remova of the skull cap. The chordæ

Willisii are clearly seen. The venous lacunæ are also well shown; from two

of them probes are passed into the superior sagittal sinus





Vaskularisasi Otak

• Arteri karotis interna regio sentral dan lateral hemisfer.

• Arteri serebri anterior korteks orbitalis, frontalis, parietalisbagian tengah, korpus kalosum dan nukleus kaudatus.

• Arteri serebri media korteks orbitalis, lobus frontalis,parietalis dan temporalis.

• Arteri vertebralis batang otak dan medula spinalis atas.

• Arteri basilaris pons.

• Arteri serebri posterior lobus temporalis, oksipitalis,sebagian kapsula interna, talamus, hipokampus, korpusgenikulatum dan mamilaria, pleksus koroid dan batang otak

bagian atas.• Arteri koroidal pleksus koroid temporal lateral ventrikel.









PELINDUNG SSP

• Pelindung SSP: – Kranium otak; kolumna vertebralis spinal cord, 3

membran menings,CSS, Sawar darah otak

• 3 lapisan menings: – Duramater: 2 lapisan tidak elastis & kuat

• 2 lapisan biasanya melekat erat, dibagian² ttt, lapisan terpisah sinus dura, sinus vena

– Araknoid mater: gambaran “jaring laba²” • Ruang subaraknoid terisi CSS

• Ada vilus subaraknoid yg menembus sinus dura tempatCSS direabsorpsi ke vena

– Pia mater: melekat erat ke permukaan otak & kordaspinalis & memasok PD pada bag. Otak dalam





PEMBENTUKAN & ALIRAN



PEMBENTUKAN & ALIRAN

CSS CSS dibentuk t.u oleh plexus koroideus pada rongga

ventrikel Plexus koroideus: jar. Piamater seperti kembang kol, kaya

p.darah yg masuk ke dalam rongga ventrikel

Setelah dibentuk, CSS mengalir melalui 4 ventrikel Pada ventrikel 4, CSS keluar mll lubang kecil ruang

subaraknoid mengalir rata

Ketika mengalir ke bag. Atas otak direabsorpsi mll vilussubaraknoid

CSS 125-150 ml & mempunyai 2 fungsi: Shock-absorbent / bantalan & pertukaran bahan antara

cairan tubuh & otak

Pertukaran zat antara cairan intersitium & CSS relatif bebas



Neuroglia NeuronPertukaran antar sel otak &

cairan intersitium diatur o/ sifat

membran plasma

Cairan IntersitiumOtak

Pertukaran

bebas

Transportasi ke

dalam otak dari

arah sangat dibatasi

o/ BBB

Cairan

Serebrospinalis

(CSS)Darah Vena Darah Arteri

PLASMA DARAH

Transport selektif daridarah ke CSS melewati

plexus koroideus

Sinus

dura



SAWAR DARAH OTAK

Otak dilindungi sawar darah otak Pertukaran antara zat dalam darah & cairan intersitium

sangat terbatas, Hanya dapat terjadi mll kapiler otak

Struktur sawar darah otak:

Kapiler otak berbeda dg kapiler lain

dd kapiler bersifattaut erat

(-) ada pertukaran antara sel, harus melalui sel

Zat² yg dapat menembus: Zat larut lemak (O2, CO2,alkohol, steroid), atau mol. Air berukuran kecil

Kapiler otak tsb dikelilingi astrosit dg fungsi: Memberi “sinyal” u/ membuat taut erat

Diperkirakan berperan dalam transportasi ttt, misalnya K

Daerah² ttt yg tidak dilindungi BBB cth: hipotalamus





Serebrum hemisfer kiri & kanan

Dihub o/ korpus kalosum pita tebal

dengan 300 juta akson

Setiap hemisfer terdiri dari:

• lap. Luar tipis berwarna abu²

(substansia grisea) kortex serebrum

• lap. Tengah tebal berwarna putih

(substansia alba)

• didalam s. alba, ada s. grisea lain

s. Grisea badan sel + dendrit

s. Alba akson dg lemak mielin

Korteks serebrum: lapisan luarserebrum yg berlekuk²

Korteks serebrum 6 lap. Tegas dg

kolom² vertikal yg mengurus fs berbeda



Lobus occipital & temporal (POSTERIOR)

• occipital masukan penglihatan ;

• temporal masukan sensasi suara

Lobus Frontalis:

• aktivitas motorik volunter, kemampuan

bicara, elaborasi pikiran

• korteks motorik primer (depan sulkus)

daerah utama

• motorik: mengolah sisi” berlawanan !

Lobur parietalis

• sensorik (sentuhan, tekanan, panas, dingin, nyeri (sensasi somestetik) &

proprioseptif • korteks somatosensorik tempat u/ pengolahan awal (dibelakang sulkus

sentralis)

• masukan sensorik diterima terbalik !

• talamus bisa merasakan sentuhan, tekanan, suhu sederhana, namuntidak

bisa menentukan lokasi & intensitas





KONTROL MOTORIK

Korteks motorik primer pencetus sinyal eferen ke

organ efektor, namun banyak organ lain yg terlibat

dalam proses motorik:

Daerah otak yg lebih rendah & spinal cord kontrol aktivitas

otok involunter c/ postur Daerah² otak yg lebih tinggi yg mengontrol gerakan terkoordinasi

Daerah² otak yg lebih tinggi yg berperan:

Daerah motorik

suplementer

Korteks pra motorik & Korteks parietalis

posterior • Medial hemisfer, anterior korteks

motorik primer

• u/ program gerakan kompleks

• Lesi (-) paralisis

• Lateral hemisfer, anterior korteks motorik primer

• Berhub dg korteks parietalis posterior u/

orientasi tubuh ke sasaran

Gerakan dikoordinasikan, tetapi bukan dimulai dari daerah² ini



Hemisfer Kiri Hemisfer KananTugas logis, analitis, sekuensial &

verbal

Cth: matematika, filsafat,

pembentukan bahasa

Non bahasa, cth: kemampuan artistik

& musik

Bersifat fragmenter & “pemikir” Bersifat holistis & “pencipta”

Hemisfer kiri :

• tempat daerah bahasa

• biasanya bag. Ini kontrol motoriknya > halus

Namun dalam sisi aktivitas mental, setiap hemisfer ada

keunggulan masing²

Kenapa Kebanyakan Orang

Dominan dg Bagian Kanan?



KEMAMPUAN BERBAHASA

Daerah Bahasa hanya di hemisfer kiri Apabila ada kerusakan < 2thn – 10thn dapat

dikompensasi hemisfer kanan

Kerusakan > 10thn bersifat permanen,

mungkin ada sedikit perbaikan terbatas Bahasa: pemahaman & ekspresiWernicke: di pertemuan lobus parietalis,

temporalis & oksipitalis u/ pemahaman baik

lisan & tertulis

diteruskan ke Broca Broca: u/ ekspresi bicara, berkaitan dg area

motorik u/ kemampuan artikulasi

Gangguan berbahasa afasia





DAERAH ASOSIASI

Daerah motorik, sensorik, bahasa ½ dari

korteks serebrum, sisanya: daerah asosiasi

Daerah asosiasi fungsi tinggi / luhur

Pada EEG biasanya silent areas

Kortex asosiasi

prafrontalis

Kortex asosiasi parietalis-

temporalis-oksipitalis

Kortex asosiasi

limbik

Anterior kortex motorik

primer, bag. Depan frontalBerfungsi untuk:

• rencana aktivitas

volunter

• konsekuensi kedepan

(sosial & fisik)

• kepribadian

Integrasi sensasi somatik,

audiotorik, visual u/gambaran yg lengkap

Membantu wernicke

penghubung thd penglihatan

& pendengaran

Didalam, antara ke2

lobus temporalBerkaitan dengan:

• emosi

• Motivasi

• Ingatan



DAERAH SUBKORTEKS

Nukleus basal

Hipotalamus

Talamus



NUKLEUS / GANGLIA BASAL

Fungsi nukleus basal:

Menghambat tonus otot diseluruh tubuh

Memilih & mempertahankan pola gerakan / aktivitas motorik ttt

(& membuang yg tidak berguna)

Memantau & u/ koordinasi kontraksi menetap & lambat cth:kontraksi yg berkaitan dg postur

Penyakit / gangguan pada nukleus basal Parkinson

Peningkatan tonus otot / rigiditas (kekakuan)

Gerakan involunter yg tidak berguna & tidak diinginkan tremor istirahat

Perlambatan perilaku motorik cth: lagi duduk, cenderung duduk,

mau berdiri, dilakukan sangat lambat

+



Kortex

serebrum

Talamus Nukleus Basal

Neuron

Motorik di

Korda

Spinalis

Neuron di

Batang Otak

Otot rangka

Gerakan

+

+ +

+

+

-

-



TALAMUS & HIPOTALAMUS

Fungsi² talamus:

Pengolahan awal semua masukan sensorik menyaring

& mengarahkan ke kortex somatosensorik

Talamus – batang otak – daerah asosiasi kemampuan

mengarahkan perhatian ke rangsangan menarik Fs lain: u/ sensorik kasar & memperkuat motorik volunter

Fungsi² hipotalamus:

Pengaturan langsung lingkungan internal (homeostasis)

Kortex serebrum: mengatur tidak langsung lingkunganinternal

Berperan dalam pola perilaku & emosi



SISTEM LIMBIK

Secara garis besar mencakup: nukleus basal,korteks serebrum, talamus, hipotalamus

Sistem limbik: berperan dalam emosi, pola perilakusosioseksual & kelangsungan hidup, motivasi,belajar

Adanya pusat “penghargaan” & “hukuman”

Mekanisme rasa “motivasi”: Sebagian motivasi / perilaku berkaitan dg homeostasis,

cth: haus ok defisit air motivasi u/ minum

Namun jenis minuman yg dipilih (-) berkait dg homeostasisbergantung pengalaman, belajar, kebiasaan

Namun u/ motivasi lain (cth: karir, menang lomba) mshbelum dik sempurna



SISTEM LIMBIK

Peran bagian² dalam sistem limbik:

Hipotalamus persiapan lingkungan internal sesuai

dg keadaan emosi c/ HR, TD, pernafasan ↑ saat

marah

Korteks serebri u/ ekspresi emosi/perasaan,

dibutuhkan koordinasi otot c/ utk menyerang, senyum

Urutan gerakan yg diatur korteks, tampaknya dapat

“diprogram” dan “dipanggil” sewaktu-waktu o/ sistem limbik

volunter & involunter Kortex memperkuat / menekan respons emosi

secara sadar



SEREBELUM

Belakang-atas batang otak, dibawah oksipital 3 bagian: Vestibuloserebelum: keseimbangan & kontrol mata

Spinoserebelum Mengatur tonus otot & gerakan terkoordinasi

Dapat memperkirakan posisi sepersekian detikkemudian

Melakukan penyesuaian t.u pada aktivitas cepat cth:

main piano, mengetik, berlari Serebroserebelum: Inisiasi aktivitas volunter dg mengirim sinyal ke korteks

motorik berhub dg ingatan prosedural





Korteks

motorik

Spinoserebelum

Perintah

motorik ke otot

Kontraksi

otot rangka

Informasiperintah motorik

Membuat

penyesuaian sesuai

keperluan

Gerakan

Informasi kinerja

sebenarnya



SEREBELUM

Manifestasi Gangguan2 pada serebelum:

Gangguan keseimbangan, nistagmus

Penurunan tonus otot tanpa paralisis

Ketidakmampuan melakukan gerakan cepat dengan mulus

Tremor intensional

Gerakan maju mundur sewaktu mendekati tujuan yg dikehendaki

berbeda dg tremor istirahat pada gg nukleus basal

Serebelum Nukleus basal

Memantau & menyesuaikan aktivitas motorik dari kortex motorik; bersifat bawahsadar

• Memperhalus gerakan cepat

• Meningkatkan tonus otot

• Keseimbangan

• Mengkoordinasi gerakan lambat &

menetap

• Menghambat tonus ototWalaupun gerakan motorik diperintah o/ kortex motorik secara volunter, namun rangkaian

aktivitas nya dilaksanakan & dikoordinasikan secara tidak sadar



BATANG OTAK

Medula, pons, midbrain

Fungsi batang otak:

Sebagian besar 12 pasang saraf kranialis berasal dari batang

otak

Tempat pusat sirkulasi, respirasi, pencernaan

Berperan dalam modulasi nyeri, & reflex otot yg berhub dg

keseimbangan & postur

Di batang otak ~ talamus jar. Neuron (formasio retikularis)

mengintegrasikan semua masukan / info asenden

menyebarkan ke serebrum dalam bentuk sinyal. (Reticular

Activating System / RAS)

Bertanggung jawab dalam proses tidur





KORDA SPINALIS

Korda spinalis:

Silinder jar. Saraf yg panjang & ramping (45cm, Ф 2cm) keluar

dari lubang di dasar tengkorak berjalan didalam kanalis

vertebralis

Kolumna vertebra 25cm > panjang dari korda spinalis

seratsaraf tidak sesuai dg lubang vertebra tempat ia keluar

Berakhir pada L1 / L2 dibawahnya membentuk kauda ekuina

tempat u/ pungsi lumbal

Struktur korda spinalis:

Berbeda dg otak substansi grisea berbentuk kupu2 ditengah,

substansi alba dipinggir

Substansi alba tr. Kortikospinalis & spinotalamikus



Serat aferen akar dorsal (ganglion akar dorsal)

Serat eferen

akar ventral (berpangkal substansia grisea) Akar dorsal & akar ventral bersatu 1 saraf spinalis

1 kolom 1 pasang saraf spinalis

31 pasang saraf spinalis + 12 pasang saraf kranialis sistem saraf perifer















Brodmann’s Areas

Central Sulcus

Somatosensory

Cortex

Biological Psychology Ch 2

LO2 Hi t fi i l i



LO2. Histofisiologi

LO3 CVD



LO3. CVD

Th t



The upper motor neuron

~ pyramidal / corticospinaltracts fibers that descends from

the cerebral cortex subcortical white matter internal capsule

cerebral peduncle basispontis pyramid of theupper medulla

Decussates the lateralfunniculus of the spinalcord

Originates entirely from thelarge motor cells of Betz



Paralysis caused by lesion of the



y y

UMN

e/ Interruption of thecorticospinal pathways bylesion at any point of itcourse Internal capsule & corona

radiata Corticospinal fibers are

intermingled with other tracts

Thalamocortical tractsdisturbance

Features & characteristics A group of muscles is

always involved The paralysis never involve

all the muscles on one sideof the body even the

severest form Voluntary drive on spinal

motor neuron < slowness of movements

Activation of paralyzedmuscles as parts of certain

automatisms (synkinesia) Paralyzed arms move

suddenly while yawning &stretching



Recovered hemiplegia expression of damage to basal ganglia& thalamic structures Tremor, athetosis,

chorea

At lower levels (cervicalcords) Paralysis of voluntary

movements; abolish

temporarily spinal reflexbelow the level of lession; replaced later by spasticity spinalshock

Parietal lesion limbsflaccid; reflex retained

Spasticity The anti gravity muscles predominantlyaffected

Clasp knife phenomena

Persistent flaccidity after stroke primaryinvolvement of lentiformnucleus & thalamus

Dorsal ret.spinal tract Inhibitory effects on

stretch reflex

Med ret.spinal &ves.spinal tracts facilitate extensor

tone



Hyperreflexia Release phenomena of tendon

jerks Result interruption of

descending inhibitorypathways

may take form of clonus

Spread / irradiation of reflex Associated with spasticity

Spinal flexion reflexes Babinski sign

Part of spasticity

e/ disinhibition / release of motor programs in spinal

origin Complete form

Nocifensive flexor synergy(knee, hip, foot, big toe) triple flexion response

Interruption of corticobulbar pathways Masseter contraction in

response to a brisk downwardtap of the chin

Brisk contraction of orbicularisoris in response to tapping the

philtrum Weakness paralysis of tongue,

parynx, pharynx, tongue

Lesion of the parietal lobe Unable to maintain stable

postures of the outstretched

hand when his eyes are closed Cannot exert a steady

contraction



Monoplegia withoutmuscular atrophy Lesion on cerebral cortex

Usually accompanied byspasticity, reflex >,extensor plantar reflex(babinski)

Hemiplegia Involvement of

corticospinal pathways

Level of lesion Cortex, corona radiata,

internal capsule

weakness; paralysisof leg, arm, lower face of the opposite

Low pontine lesion

Ipsi. Abducens /facial palsy

Contralateralparalysis of arm &

leg Lateral column of cervical

cord ipsilateralhemiplegia

Lesion on MO



Paraplegia If white mater

damaged sensoric

function may be loss

Bilateral damage bowel & bladder

sphincters affected

Tetraplegia Lesion in the cervical

Occlusion of the

anterior spinal artery

Compresion of CI &C2

Repeated strokes

affecting both

hemispheres

Transient ischemic attacks



Transient ischemic attacks

brief, reversible episode of focal ischemic braindisturbance without evidence of cerebral infarction

Underlying process (atherothrombotic involving large &small blood vessel) that precede a stroke

Etiology

Warning of impending vascular occlusion (internal carotidartery); often caused by an embolus leaves no lastingclinical effects

Excessive viscosity / sludging of blood (polycythemia vera,sickle cell disease, thrombocytosis, leukemia,hyperglobulinemic state)

Atherosclerotic vascular disease (23%)

Clinical syndrome



Clinical syndrome

Reflect theinvolvement of virtually any cerebralarteries

Most last 2-15 min

Only a few / severalhundred attacks no abnormalities

between attacks

stroke may occur / theattacks graduallycease & no importantparalysis

Prolonged, fluctuatingTIAs most ominous

ABCD systems

Blood pressure Unilateral weakness

Speech disturbance

Duration of symptoms <1 hour

predictive of stroke < >1 hour

predictive of stroke >

attacks



(carotid artery, anterior

circulation territory) involvement of 1 cerebral hemisphere/eye

Visual disturbance is ipsilateral

Sensorimotor disturbance is contralateral

Ischemia of the distal territory of the MCA

weakness / numbness of the opposite hand &

arm

Shake irregularly (limb shaking TIA)Other transient movement disorders

Confusion, aphasia, difficulty in calculation,

apractagnosia (less common)

Occular attacks transient monocular

attacks



(vertebrobasilar, posterior

circulation territory) Less stereotyped; more prolonged

Vertigo, diplopia, dysarthria, bifacial

numbness, ataxia, weakness / numbness of

part / all of one or both side of body Staggering, veering to one side, feeling of

cross-eyedness, dark vision, blurred vision,

tunnel vision, partial / complete blindness,

pupilary change, ptosis, paralysis of gaze,

dysphagia

May be identical to one episode to another

Involved parts affected simultaneously

Lacunar TIA



Lacunar TIA

Occlusion of small penetrating vessels of thebrain

Intermittent onset; complete restitution of

function

Capsular warning syndrome

Escalating episodes of weakness in the face,arm, leg

Mechanism of TIA



Mechanism of TIA

Blood flow <; embolic particles

Related to vascular stenosis (ulceration from

atherosclerosis & thrombus)

Embolization of fibrin-platelet material fromatherosclerotic site

States of anemia, polycythemia,

thrombocythemia, lipid>, hyperviscocity, sicklecell anemia, hyper/hypoglycemia;

antiphospolipid antibodies

>

DD



DD

Seizure

Migraine

Transient global amnesia

Multiple sclerosis

Meningioma & subdural hematoma

Transient aphasia / speech arrest

Glioblastoma Metastatic brain tumors in cortex

Treatment



Treatment

Acute phase

Protocols to prevent excessive hypertension after

thrombolytic agents

Prevention of DVT, pulmonary embolism,coronary syndromes

Measures to restore the circulation & arrest the

pathologic process

Diagnosis of thrombotic stroke at the earliestpossible stage

Re-establish perfusion

Maintenance of normal blood pressure when start



Antiplatelet drugs

Aspirin 325 mg daily

Ticlodipine & clopidogrel

Thrombolytic agentsRecombinant tPA ~ streptokinase

Anticoagulation

Heparin 100U/kg

continuous drip (1000U/h) Low mol weight heparin (nadroparin)

4000U SC, tid

Warfarin

watch the blood ressure <220/120

Atherothrombotic infarction



Atherothrombotic infarction

Hypertension, hyperlypidemia, diabetes atherosclerosis >

Most frequent sites

Internal carotid arteryCervical part of vertebral arteries; junction to

basilar artery

Stem/main bifurcation of MCA

Proximal posterior cerebral arteries

Proximal anterior cerebral arteries

nearly complete occlusion later

Clinical pictures



Clinical pictures

Whole strokeevolves over a few

hours/less

stuttering/intermitten

t progression of

neurologic deficits

extending over several hours / day /

longer

Partial stroke may

occur rapid



Stroke in the sleep (awakens paralyzed, either during the night / in the morning)

Artery to artery embolus

evolution of atherothrombotic stroke Embolus passing to branch of ipsilateral

middle/anterior cerebral artery blockage of vertebral

/ lower basilar artery transient pontine ischemia

Cranial pain (some cases)One side of the head carotid occlusion

Forehead & occiput basilar occlusion

Behind the ipsilateral ear / above the eyebrow

Laboratory findings



Laboratory findings

USG luminal diameter of cervical vessels

MRI ischemic damage (few hours in both

white & gray matter)

MRA / CTA major cervical & intracranial arteries

Detect the irregular lumen / occlusion of

atherosclerosis

CSF

Protein slightly >

Small number of PMN (3-8/cc)

Transient leoc tosis 400-1000 PMN/cc on the

Embolic infarction



Embolic infarction

Most common causeof stroke

Clinical syndromeDevelop most

rapidly

No warningepisodes

Neurologic problem

unfolds more

gradually over manyhours with some

fluctuation

Depend on the

artery that involved



Upper basilar bifurcation abrupt

onset of coma,

unilateral / bilateral

homonymous

hemianopsia

Temporal branch

thalamus sub

thalamus complex

disorders of memory,sensation, movement

Undersurface of

cerebellum ataxia,

subtle sign of lateral

May produce asevere neurologic

deficit that is only

temporary

Symptoms abate asthe embolus

fragments

Laboratory findings



Laboratory findings

Electrocardiogram & echocardiogram allpatients with stroke of uncertain origin

USG & MRA image the aortic arch

CT scan & MRI CSF

Minority of ischemic stroke do red cells enter the

CSF (10000/cc); slight xanthochromia after a few

days

Subacute bacterial endocarditis WBC 200/cc

or higher

Treatment & prevention



Treatment & prevention

Measures directed to restoring the circulation

Measures instituted to prevent reccurent

embolus

Physical therapy & rehabilitation

Thrombolysis

Injection of tPA; 4,5 hours of the 1st strokesymptoms

Anticoagulants

Warfarin; watch our for hemorrhage

Prognosis



Prognosis

Eventual prognosis is determined by theoccurence of further emboli & the gravity of

underlying illness

Cardiac failure, myocardial infarction, bacterialendocarditis, malignancy

Primary (hypertensive)



intracranial hemorrhage

Result of chronic hypertension & degenerativechanges in cerebral arteries

Large hemorrhageMidline structures displaced to the opposite side

of the cranium RAS & respiratory centers

compromised coma & death

Small hemorrhage

+ at distance from ventricle no blood in CSF

Clinical pictures



Clinical pictures

Acute reactive hypertension

Vomitting

Severe headache

Seizures

Small hemorrhages in silent regions of the

brain may escape clinical detection Hemorrhages have been described in relation

with phenylpropanolamine consumption

Putaminal hemorrhage



Putaminal hemorrhage

Medium/large sized clots hemiplegia frominterruption of the capsule

Vomitting (50%)

Headache; other abnormal cephalic sensation Large hemorrhage stupor

Few minutes/less

Face sags on one side, aphasic/slurred speech,weaken arm & leg, eyes tend to deviate away

from the side of paretic limbs

Advanced stages

Si ns of u er brainstem com ression coma

Thalamic hemorrhage



Thalamic hemorrhage

Severe multimodal sensory loss on the entirecontralateral body

Compression of the capsule

hemiplegia/paresis Extension into the subthalamus & high

midbrain ocular disturbance

Pseudoabducens palsies

Palsies of vertical & lateral gaze

Forced deviation of the eye downward

Inequality of pupils

Ipsilateral ptosis & miosis

Pontine hemorrhage



Pontine hemorrhage

Deep coma in few minutes

Total paralysis with bilateral babinski sign,

decerebrate rigidity, small pupil that react to

light Death in few hours

Smaller lesion in tegmentum

Disturbances of lateral ocular movements,crossed sensory, or motor disturbances, small

pupils, cranial nerve palsies

Cerebellar hemorrhage



Cerebellar hemorrhage

Develops over a period of 1 or more hours

Repeated vomitting, occipital headache,

vertigo, inability to sit/walk

Nystagmus & cerebellar ataxia (minority of cases)

Mild ipsilateral facial weakness

Paresis of conjugate lateral gaze to the side of the hemorrhage, forced deviation of the eyes

to the opposite side, ipsilateral CN VI

weakness

Lobar hemorrhage



Lobar hemorrhage

Bleeding in subcortical white matter of one of the lobes of the cerebral hemisphere; not

associated strictly with hypertension

Occipital lobe Pain around ipsilateral eye, dense homonymous

hemianopia

Temporal lobe

Pain in / anterior to the ear, partial hemianopia,

fluent aphasia

Frontal lobe

Frontal headache, contralateral hemiplegia (arms)

Laboratory findings



Laboratory findings

CT scan

MRI

brainstem hemorrhage & residual hemorrhage

(remain visible long after no longer visible withCT)

WBC

Rise transiently to 15000/cc

Treatment



Treatment

Coma maintenance of adequate ventilation,selective acute use of controlled

hyperventilation to a PCO2 of 25 – 30 mmHg,

monitoring ICP

Limitting IV infusions to normal saline

Rapid reduction of moderately elevated blood

pressure (140-160mmHg) NOT

recommended

Sustained mean blood pressure >110 mmHg

(160 mmHg systolic) cerebral edema >;

pon aneous su arac nohemorrhage



hemorrhage

(ruptured saccular aneurysm) Saccular aneurysm ~ Berry aneurysm Aneurysms most often occur in persons with

normal blood pressure

The most common sites

Proximal portions of the anterior communicatingartery

Origin of the posterior communicating artery 1st major bifurcation of the middle cerebral artery

Bifurcation of the internal carotid into the middle &anterior cerebral arteries

Clinical syndrome



Clinical syndrome

Patient is stricken with an excruciating generalized headache & vomitting;falls unconscious almost immediately

Severe generalized headache develops in the same instantaneous manner but the patient remains relatively lucid with varying degrees of stiff neck

Consciousness is lost so quickly that there is no preceeding complaint

Convulsive seizures Brief & generalized

Sentinel headache

Refer to both a headache that preceed subarachnoid hemorrhage & smallleakage prior to a major rupture

Vasospasm

delayed hemiplegia & other deficit (3-10days)

Hydrocephalus

Large amount of blood rupture into ventricular system

Grading



Grading

I Asymptomatic / slight headache & stiff neck

II Moderate-severe headache & nuchal rigidity, no focal /

lateralizing neurologic signs

III Drowsiness, confusion, mild focal deficit

IV Persistent stupor, semicoma, early decerebrate rigidity,

vegetative disturbance V

Deep coma & decerebrate rigidity

Laboratory findings



Laboratory findings

CTDetect blood locally/difussely in the subarachnoid

spaces, within the brain, ventricular system

MRIDetect blood in the protodensity sequence

CSF

Grossly bloody (30 min or sooner) RBC counts

up to 1million/cc or higher

Treatment



ea e

Acute stage Bed rest, fluid administration

Administration of CCB reduce infarction from

vasospasm

Nimodipine 60 mg PO every 4 hours

Beta adrenergic blockers reduce greatly elevated

blood pressure (maintain at 150 mmHg/<)

Nitroprusside

Pain releaving medication for headache

Surgical

Hypertensive encephalopathy



yp p p y

Rapidly evolving syndrome of severehypertension in association with headache,nausea, vomitting, visual disturbances, confusion,advanced case stupor & coma

Clinical features

Multiple seizures

Diffuse cerebral disturbance + focal/laterallizing

neurologic signs Clustering of multiple microinfarcts & petechial

hemorrhage mild hemiparesis, aphasic disorder,rapid failure of vision

Laboratory features & treatment



y

CT & MRI result of an accumulation of fluid

CSF Pressure >, protein > (>100 mg/cc)

Treatments Lowering the blood pressure (safe target 150/100

mmHg) Sodium nitroprusside IV 0,5-0,8 mg/kg/min

Nifedipine 10-20mg SL Beta blocker IV (labetalol 20-40 mg IV infusion 2 mg/min)

ACE-I

Brain edema Dexamethasone 4-6 mg every 6 hour

LO4. Infeksi



Meningitis



g

The brain and spinal cord are covered byconnective tissue layers collectivelycalled the meninges which form theblood-brain barrier.

1. the pia mater (closest to the CNS)

2. the arachnoid mater 3. the dura mater (farthest from the

CNS).

The meninges contain cerebrospinal fluid

(CSF).Definition : Meningitis is an inflammation

of the meninges, which, if severe,may become encephalitis, aninflammation of the brain.



Etiologi: Bacterial Infections Pneumococcal, Streptococcus pneumoniae (38%)

Meningococcal, Neisseria meningitidis (14%)

Haemophilus influenzae (4%) Staphylococcal, Staphylococcus aureus (5%)

Tuberculous, Mycobacterium tuberculosis

Viral Infections

Fungal Infections Cryptococcus neoformans

Coccidiodes immitus



Meningococcal e/ : Neisseria meningitidis

Reservoir: Humans only. 5-15% healthy carriers

Mode of transmission: direct contact with patients oral or nasalsecretions,Saliva.

Incubation period: 1-10 days. Usually 2-4 days

Infectious period: as long as meningococci are present in oralsecretions or until 24 hrs of effective antibiotic therapy

Epidemiology:

Sporadic cases worldwide.

“Meningitis belt” –sub-Saharan Africa into India/Nepal.

In US most cases seen during late winter and early spring.

Children under five and adolescent most susceptible. Overcrowdinge.g. dormitories and military training camps predispose to spread of infection.



Asept ic Mening i t is Definition: A syndrome characterized by acute onset of meningeal

symptoms, fever, and cerebrospinal fluid pleocytosis, withbacteriologically sterile cultures.

Laboratory criteria for diagnosis:

CSF showing ≥ 5 WBC/cu mm

No evidence of bacterial or fungal meningitis.Case classification

Conf i rmed : a clinically compatible illness diagnosed by a physicianas aseptic meningitis, with no laboratory evidence of bacterial or fungal meningitis

Comment

Aseptic meningitis is a syndrome of multiple etiologies, but mostcases are caused by a viral agent



Viral Menin git is

Etiological Agents: Enteroviruses (Coxsackie's and echovirus): most common.

-Adenovirus-Arbovirus-Measles virus

-Herpes Simplex Virus-Varicella

Reservoirs:

-Humans for Enteroviruses, Adenovirus, Measles, Herpes Simplex, andVaricella

-Natural reservoir for arbovirus birds, rodents etc.

Modes of transmission:-Primarily person to person and arthopod vectors for Arboviruses

Incubation Period:-Variable. For enteroviruses 3-6 days, for arboviruses 2-15 days

Treatment: No specific treatment available.Most patients recover completely on their own.





Ensefalitis



adalah suatu proses peradangan pada susunan saraf pusat yang disebabkan mikroorganisme seperti bakteri, spiroseta,

jamur, cacing, dan virus

Permulaan: tiba-tiba atau bertahap Kasus berat

Malaise

Demam

Sakit kepala

Pusing

Lesu

Letargi Kaku kuduk

Mual dan muntah

Ataksia

Tremor

Hiperaktivitas

Susah berbicara

Gangguan status mental

Demam tinggi

Stupor

Seizure

Disorientasi

Spasticity

Koma (sampai kematian) Kelumpuhan okular

Paralysis



Klasi f ikasi

Ensefalitis supuratif akut Bakteri Staphylococcus aureus,

streptokokus, E.Coli. Ketiga bakteri ini menimbulkan penanahan pada

korteks serebri sehingga terbentuk abses serebri

Ensefalitis Sifilis Kuman Treponema Pallidum.

Ensefalitis Virus Virus RNA (virus parotitis, virus morbili, virus rabies,

virus rubela, virus ensefalitis jepang B, virus dengue, virus polio,

cocksakie A, cocksakie B, echovirus, dan virus koriomeningitis limfositari)dan virus DNA (virus herpes zostevarisela, herpes simpleks,

cytomegalovirus, variola, vaksinia, dan AIDS).



Diagnosa:

1. Nyeri berhubungan dengan adanya proses infeksi ditandai dengan

anak menangis, gelisah

2. Gangguan rasa nyaman berhubungan dengan sakit kepala mual.3. Resiko tinggi infeksi berhubungan dengan daya tahan terhadap

infeksi turun.

4. Resiko tinggi perubahan perfusi jaringan berhubungan dengan

Hepofalemia, anemia.5. Gangguan asupan nutrisi kurang dari kebutuhan tubuh

berhubungan dengan mual muntah



6. Gangguan mobilitas berhubungan dengan penurunan kekuatan

otot yang ditandai dengan ROM terbatas.

7. Resiko tinggi terhadap trauma berhubungan dengan aktivitas

kejang umum

8. Resiko gangguan integritas kulit berhubungan dengan daya

pertahanan tubuh terhadap infeksi turun.

9. Resiko terjadi kontraktur berhubungan dengan spastik berulang

10. Gangguan sensorik motorik (penglihatan, pendengaran, gaya

bicara) berhubungan dengan kerusakan susunan saraf pusat.

Causes of Viral Encephalitis



Herpes viruses – HSV-1, HSV-2, varicella zoster virus,cytomegalovirus, Epstein-Barr virus, human herpes virus6

Adenoviruses

Influenza A

Enteroviruses, poliovirus Measles, mumps, and rubella viruses

Rabies

Arboviruses – examples: Japanese encephalitis; St.

Louis encephalitis virus; West Nile encephalitis virus;Eastern, Western and Venzuelan equine encephalitisvirus; tick borne encephalitis virus

Bunyaviruses – examples: La Crosse strain of Californiavirus

Reoviruses – example: Colorado tick fever virus

LO5. Tumor



LO6. Trauma



Layers of the Meninges



Layers of the Meninges

Epidural Hematoma



Definisi : Accumulation of blood in the potentialspace between duramater and bone

EDH is considered to be the most serious

complication of head injury, requiring

immediate diagnosis and surgical intervention

(mortality rate associated with epidural

hematoma has been estimated to be 5-50%)



Patofisiologi

Usually results from a brief linear contact forceto the calvaria that causes separation of theperiosteal dura from bone and disruption of

interposed vessels due to shearing stress Skull fractures occur in 85-95% of adult cases Extension of the hematoma usually is limited by

suture lines owing to the tight attachment of thedura at these locations.

The temporoparietal region and the middlemeningeal artery are involved most commonly(66%)



Epidemiologi:

Epidural hematoma complicates 2% of cases of headtrauma (approximately 40,000 cases per year)

Alcohol and other forms of intoxication have beenassociated with a higher incidence of epiduralhematoma

Sex

more frequent in men, with a male-to-female ratio of 4:1

Age

rare in individuals younger than 2 years

rare in individuals older than 60 years because the dura is tightlyadherent to the calvaria



Gejala Klinis:

Head trauma

Lucid interval between the initial loss of

consciousness at the time of impact and adelayed decline in mental status (10-33% of cases)

Headache

Nausea/vomiting Seizures

Focal neurological deficits (eg, visual field cuts,aphasia, weakness, numbness)



Pemeriksaan Penunjang:

Head CT-scan (imaging study of choice for intracranial EDH) not only visualizes skull fractures,but also directly images an epidural hematoma

It appears as a hyperdense biconvex or lenticular-shaped mass situated between the brain and theskull, though regions of hypodensity may be seenwith serum or fresh blood

MRI also demonstrates the evolution of an epiduralhematoma, though this imaging modality may not be appropriate for patients in unstable condition





Subdural Hematoma



Definisi : Rapidly clotting blood collectionbetween dura mater and brain

Typically, low-pressure venous bleeding of bridging veins (between the cortex and venoussinuses) dissects the arachnoid away from the

dura and layers out along the cerebral convexity It conforms to the shape of the brain and the

cranial vault, exhibiting concave inner marginsand convex outer margins (crescent shape)

Frequency is related directly to the incidence of blunt head trauma

It’s the most common type of intracranial masslesion, occurring in about a third of those with

severe head injuries



Epidemiologi

Mortality Simple SDH (no parenchymal injury) is associated with a

mortality rate of about 20%

Complicated SDH (parenchymal injury) is associated with amortality rate of about 50%

Age It’s associated with age factors related to the risk of blunt head

trauma

More common in people older than 60 years (bridging veins aremore easily damaged/falls are more common)

Bilateral SDHs are more common in infants since adhesionsexisting in the subdural space are absent at birth

Interhemispheric SDHs are often associate with child abuse



Gejala Klinis :

Usually involves moderately severe to severe blunt head trauma

Acute deceleration injury from a fall or motor vehicleaccident, but rarely associated with skull fracture

Generally loss of consciousness Acute:

After head trauma and can be life threatening Headache with contralateral hemiparesis,seizures and cortical

dysfunction

↑TIK alteration level of consciousness Chronic:

Develops after mild head trauma common on elder andthose who anticoagulated

Neurologic symptoms: hemiparesis,seizures,and behavioralchanges



Pemeriksaan Penunjang

MRI the size of an acute SDH and its effect on thebrain, head CT diagnosis and suffice for immediatemanagement purposes

Noncontrast head CT scan (imaging study of choice for acute SDH) The SDH appears as a hyperdense (white) crescentic mass along

the inner table of the skull, most commonly over the cerebralconvexity in the parietal region. The second most common area isabove the tentorium cerebelli

Contrast-enhanced CT or MRI is widely recommendedfor imaging 48-72 hours after head injury because thelesion becomes isodense in the subacute phase

In the chronic phase, the lesion becomes hypodense andis easy to appreciate on a noncontrast head CT scan







Epidural Hematoma Potential spacebetween the dura inthe inner table of theskull

Can’t cross sutures

Skull fractures intemporoparietal region Middle meningeal

artery Lenticular or biconvex

shape

SubduralHematoma Between the dura

mater and thearachnoid mater

Can cross sutures Cortical bridging veins Crescent shape Loss of

consciousness

Common in elderly

LO7. Degeneratif



Dementia



Dementia is a diseasemarked by a gradualloss of cognitivefunctioning which can

also incorporate lossesof motor, emotional,and social functioningas well

It is a permanent and

progressive diseasethat eventually renderspeople unable to carefor themselves.

Dementia - Incidence



Suspected that asmany as 50% of people over the ageof 80 develop

Alzheimer’s. 5%-8% of all people

over 65 have someform of dementia;

number doublesevery 5 yearsbeyond that age.

Alzheimer’s causes50%-70% of alldementia.

About 20%-30% of

all dementia isbelieved to becaused by avascular dysfunction

(most common ismulti-infarctdisease).

Dementia - Causes



50 different causes Neurological

disorders such as

Alzheimer’s (est. 50-

70% of people with

dementia have

Alzheimer’s)

Vascular disorderssuch as multi-infarct

disease (multiple

strokes)

Inherited disorders

such as

Huntington’s

Infections such asHIV

Two types of Dementia



Cort ical - Disorder affecting the cortex, theouter portion or layers of the brain.

Alzheimer’s and Creutzfeldt-Jakob are two

forms of cortical dementia

Memory and language difficulties(Aphasia)

most pronounced symptoms.

Aphasia is the inability to recall words and

understand common language.



Subco rt ical - Dysfunction in parts of the brainthat are beneath the cortex.

Memory loss & language difficulties not

present or less severe than cortical.

Huntington’s disease and AIDS dementia

complex.

Changes in their personality and attention

span.

Thinking slows down.

Dementia - Early Stage



Begins withforgetfulness -

isolated incidents of

memory loss do not

constitute dementia.

Forgetfulness

progresses to

confusion andeventually

disorientation.

Problem solving Judgment

Decision making

Orienting to spaceand time

Personality changes

- irritable, agitated,

sadness

(depression), manic

episodes

Table 8. Diagnostic Criteria for Dementia (DSM-IV)

♠ Memory impairment: impaired ability to learn new information or to



recall old information

♠ One or more of the following: aphasia (language disturbance); apraxia(impaired ability to carry out motor activities despite intact motorfunction); agnosia (failure to recognize or identify objects despite intactsensory function); disturbance in executive functioning-impaired ability to plan, organize, sequence, abstract

♠ The cognitive deficits result in functional impairment(social/occupational)

♠ The cognitive deficits do not occur exclusively solely during a delirium

♠ NOT due to other medical or psychiatric conditions



Dementia - Diagnosis



Medical History - Physician wants to determinethe onset of symptoms and how they’ve

changed over time.

Determine risk factors for infection, family

history of dementia or other neurological

disease, alcohol and drug use, and a patient’s

history of strokes.




Neuropsychological Exam - Evaluates aperson’s cognitive ability, e.g. orientation intime and space, memory, language skills,reasoning ability, attention, and social

appropriateness. Tests involve asking a person to repeat

sentences, name objects, etc.

Someone with Alzheimer’s is usually

cooperative, attentive, and appropriate but haspoor memory.

Someone with hydrocephalus is likely to bedistracted and less cooperative.




Brain Imaging/Lab Tests - CT or MRI,cerebrospinal fluid (all used to confirm a

diagnosis or eliminate various possibilities)

Blood tests - used to diagnosis neurosyphilis.

Metabolic tests - determine treatable disorders

such as a vitamin B12 deficiency

EEG (electroencephalography) is used to

diagnose Creutzfeldt-Jakob disease.

Alzheimer’s Disease



Progressive disorder in which neuronsdeteriorate resulting in the loss of cognitive

functions (memory), judgment and reasoning,

movement coordination, and pattern

recognition.

Predominantly affects the cerebral cortex and

hippocampus which atrophy as the disease

progresses.

AD - Plaques and Tangles



Neuri t ic Plaques Commonly found in

brains of elderlypeople but appear inexcessive numbers in

the cortex of AD pt.’s Surrounded by

deteriorating neuronsthat produceacetylcholine(neurotransmitter essential for processing memoryand learning.

Neurof ibr i l lary Tangles

Twisted remains of a

protein which is

essential for maintaining proper

cell structure.

It is not known

whether the plaques

and tangles are the

cause of AD or part of

the results of the

AD - Plaques and Tangles

http://www.alzheimers.org/rmedia/mediaroom.htm

http://www.alzheimers.org/rmedia/mediaroom.htm



AD - Neuroanatomy



Frontal lobe Controlling responses

to input from the rest of the CNS

Voluntary movement

Emotion Planning and execution

of behavior

Intellect

Memory Speech

Writing

Parietal Lobe Interprets

sensations of tactile

stimulation, e.g.

pain, temperature,

touch, size, shape,

and body part

awareness.

AD - Neuroanatomy



Temporal Lobe Understanding

sounds

Understandingspeech

Emotion

Memory

Occipital Lobe Understanding

visual images

Understanding themeaning of the

written word.

AD - Neuroanatomy



Hippocampus Plays a crucial role in both the encoding and

retrieval of information.

Damage to the hippocampus produces globalretrograde amnesia, which is the inability to

retain newly learned information.



AD - Risk Factors



Family History - a clear inherited pattern existsin approximately 10% of cases

Down’s Syndrome - Nearly 100% of peoplewho live into their 40’s

Chronic Hypertension - Treatment reduces therisk

Head Injuries - Three times more likely todevelop AD

Gender - inclusive data. Some studies show agreater risk for females while others show anincreased risk for males.

AD - Symptoms



Loss of Memory Aphasia

Apraxia - (decreased ability to perform physical taskssuch as dressing, eating, ADL’s

Delusions

Easily lost and confused

Inability to learn new tasks

Loss of judgment and reason

Loss of inhibitions and belligerence

Social Withdrawal Visual hallucinations

AD Early Stage



Characteristics

Begins withforgetfulness

Progresses todisorientation and

confusion Personality changes

Symptoms of depression/manicbehaviors

Interventions

Medications - Ariceptand Cognex (both arecommercial names).

Both increase

acetylcholine (Ach) inthe brain by inhibitingthe enzyme that breaksit down.

Therapy (deal with

depression that oftenaccompanies diagnosis

Counseling with family

AD - Early Stage



Music Therapy Used to relieve depression

Coupled with exercise and relaxation

techniques Increase or maintain social relationships

(dancing, improvisation)

Maintain positive activities (church choir,

Handbell choir, Senior social dances, etc.)

AD - Middle Stage



Characteristics Need assistance with

ADLs

Unable to remember names

Loss of short-termrecall

May display anxious,agitated, delusional,

or obsessive behavior May be physically or

verbally aggressive

Poor personalhygiene

Disturbed sleep

Inability to carry on aconversation

May use “word salad”(sentence fragments)

Posture may bealtered

Disoriented to timeand place

May ask questionsrepeatedly

AD - Middle Stage



Interventions Validation Therapy

Structured Areas for Mobility

Positive, nurturing,loving environment

Music Therapy Provides avenue for

social interaction(InstrumentalImprovisation; TGS,

Guided MusicListening)

Provides a mediumfor verbal/non-verbalexpression (TGS)

Can help maintaincognitive andaffective functioning

AD - Late Stage



Characteristics Loss of verbal

articulation

Loss of ambulation

Bowel and bladder incontinence

Extended sleep

patterns Unresponsive to

most stimuli

Interventions Caring for physical

needs

Maintain integrity of

the skin Medical

interventions

Most activities areinaccessible

AD - Late Stage



Music Therapy Tape by bedside

Gentle singing by therapist ~ one-sided, clientwill not participate

Can provide some connection between patientand family members through singing

Use a calm voice

Utilize touch: holding hands hugging rockingh d h ld t

Documents

Angel-Pemicu 3 Saraf