PEMICU 3 SARAF

Angeline Fanardy 10178

LO1. Neuroanatomi

DINDING SSP

SCALP (skin, connective tissue, aponeurosis epicranialis, loose connective tissue , periosteum Oss cranium Endosteum (stratum periostale duramatis) Meningen

Duramater Arachnoid Piamater

Brain

Hemispherium cerebri

Telencephalon Ventrikel lateralis Diencephalon (rostral dari batang otak) Mesencephalon (midbrain) Metencephalon (cerebellum) Myelencephalon (medula oblangata)

Batang otak

Cerebellum

Telencephalon (Hemispherium cerebri)

1.
2.

Tdd dari 2 lapisan: Cortex cerebri- substantia grisea 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 dibagi Frontal Parietal Temporal Oksipital

Bagian otak yg tersembunyi di balik korteks serebri :

Bulbus

olfaktorius Striatum Nukleus accumbens

Sistem limbik menerima informasi dari area asosiasi di korteks serebri & sinyal ini melalui nukleus accumbens. (1) Hipokampus (2)Amigdala

Diensefalon

Terletak di bagian dalam serebrum Struktur utama : Thalamus Hipothalamus 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 peduncles Corpora quadrigemina

Pons Serat 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 mll ganglion akar dorsal. Traktus spinotalamikus lateral Traktus spinotalamikus anterior Traktus lemniscus medialis-kolumna posterior
Akson motorik keluar dari medula spinalis mll akar ventral

JALUR PIRAMIDAL / LANGSUNG (mll piramid medula oblongata ; langsung dari korteks motorik)
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 sensorik dengan saraf motorik REFLEKS

VASKULARISASI OTAK

Vaskularisasi otak - arteri

Vaskularisasi otak - vena

Superior sagittal sinus laid open after remova of the skull cap. The chord Willisii are clearly seen. The venous lacun 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, parietalis bagian 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, korpus genikulatum 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
Duramater: 2 lapisan tidak elastis & kuat

3 lapisan menings:

Araknoid mater: gambaran jaring laba

2 lapisan biasanya melekat erat, dibagian ttt, lapisan terpisah sinus dura, sinus vena
Ruang subaraknoid terisi CSS Ada vilus subaraknoid yg menembus sinus dura tempat CSS direabsorpsi ke vena

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

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 Pada ventrikel 4, CSS keluar mll lubang kecil ruang subaraknoid mengalir rata Ketika mengalir ke bag. Atas otak direabsorpsi mll vilus subaraknoid

Setelah dibentuk, CSS mengalir melalui 4 ventrikel

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

Pertukaran antar sel otak & cairan intersitium diatur o/ sifat membran plasma Cairan Intersitium Otak

Neuron

Transportasi ke dalam otak dari arah sangat dibatasi o/ BBB

Pertukaran bebas

Darah Arteri

Darah Vena

Cairan Serebrospinalis (CSS) Transport selektif dari darah ke CSS melewati plexus koroideus

Sinus dura

PLASMA DARAH

SAWAR DARAH OTAK

Otak dilindungi sawar darah otak

Pertukaran antara zat dalam darah & cairan intersitium sangat terbatas, Hanya dapat terjadi mll kapiler otak
Kapiler otak berbeda dg kapiler lain dd kapiler bersifat taut erat (-) ada pertukaran antara sel, harus melalui sel Zat yg dapat menembus: Zat larut lemak (O2, CO2, alkohol, steroid), atau mol. Air berukuran kecil

Struktur sawar darah otak:

Kapiler otak tsb dikelilingi astrosit dg fungsi:

Memberi sinyal u/ membuat taut erat Diperkirakan berperan dalam transportasi ttt, misalnya K

Daerah 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 abu (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 luar serebrum yg berlekuk Korteks serebrum 6 lap. Tegas dg kolom 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, namun tidak 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 Daerah otak yg lebih tinggi yg mengontrol gerakan terkoordinasi

Daerah otak yg lebih tinggi yg berperan:

Korteks pra motorik & Korteks parietalis posterior

Daerah motorik suplementer

Medial hemisfer, anterior korteks Lateral hemisfer, anterior korteks motorik primer motorik primer Berhub dg korteks parietalis posterior u/ u/ program gerakan kompleks orientasi tubuh ke sasaran
Lesi (-) paralisis

Gerakan dikoordinasikan, tetapi bukan dimulai dari daerah ini

Kenapa Kebanyakan Orang Dominan dg Bagian Kanan?

Hemisfer kiri : tempat daerah bahasa biasanya bag. Ini kontrol motoriknya > halus Namun dalam sisi aktivitas mental, setiap hemisfer ada keunggulan masing
Hemisfer Kiri Tugas logis, analitis, sekuensial & verbal Cth: matematika, filsafat, pembentukan bahasa Bersifat fragmenter & pemikir Hemisfer Kanan Non bahasa, cth: kemampuan artistik & musik

Bersifat holistis & pencipta

KEMAMPUAN BERBAHASA

Daerah Bahasa hanya di hemisfer kiri

ada kerusakan < 2thn 10thn dapat dikompensasi hemisfer kanan Kerusakan > 10thn bersifat permanen, mungkin ada sedikit perbaikan terbatas
Apabila

Bahasa: pemahaman & ekspresi

Wernicke:

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 dari korteks serebrum, sisanya: daerah asosiasi
Daerah asosiasi fungsi tinggi / luhur Pada EEG biasanya silent areas

Kortex asosiasi prafrontalis Anterior kortex motorik primer, bag. Depan frontal Berfungsi untuk: rencana aktivitas volunter konsekuensi kedepan (sosial & fisik) kepribadian

Kortex asosiasi parietalistemporalis-oksipitalis Integrasi sensasi somatik, audiotorik, visual u/ gambaran yg lengkap Membantu wernicke penghubung thd penglihatan & pendengaran

Kortex asosiasi limbik Didalam, antara ke2 lobus temporal Berkaitan 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
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

Penyakit / gangguan pada nukleus basal Parkinson

+ +
Talamus

Kortex serebrum

+
Nukleus Basal

Neuron di Batang Otak Neuron Motorik di Korda Spinalis

Otot rangka

Gerakan

TALAMUS & HIPOTALAMUS

Fungsi 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 Fungsi hipotalamus: Pengaturan langsung lingkungan internal (homeostasis) Kortex serebrum: mengatur tidak langsung lingkungan internal Berperan dalam pola perilaku & emosi

SISTEM LIMBIK

Secara garis besar mencakup: nukleus basal, korteks serebrum, talamus, hipotalamus Sistem limbik: berperan dalam emosi, pola perilaku sosioseksual & 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 homeostasis bergantung pengalaman, belajar, kebiasaan Namun u/ motivasi lain (cth: karir, menang lomba) msh belum dik sempurna

SISTEM LIMBIK

Peran bagian 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 detik kemudian 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
Spino serebelum Informasi perintah motorik

Membuat penyesuaian sesuai keperluan Informasi kinerja sebenarnya

Perintah motorik ke otot

Gerakan

Kontraksi otot rangka

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
Nukleus basal

Serebelum

Memantau & menyesuaikan aktivitas motorik dari kortex motorik; bersifat bawah sadar Memperhalus gerakan cepat Meningkatkan tonus otot Keseimbangan Mengkoordinasi gerakan lambat & menetap Menghambat tonus otot

Walaupun 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, 2cm) keluar dari lubang di dasar tengkorak berjalan didalam kanalis vertebralis Kolumna vertebra 25cm > panjang dari korda spinalis serat saraf tidak sesuai dg lubang vertebra tempat ia keluar Berakhir pada L1 / L2 dibawahnya membentuk kauda ekuina tempat u/ pungsi lumbal
Berbeda dg otak substansi grisea berbentuk kupu2 ditengah, substansi alba dipinggir Substansi alba tr. Kortikospinalis & spinotalamikus

Struktur korda spinalis:

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

Brodmanns Areas
Somatosensory Cortex Central Sulcus

Biological Psychology Ch 2

LO2. Histofisiologi

LO3. CVD

The upper motor neuron

~ pyramidal / corticospinal tracts

fibers that descends from the cerebral cortex

subcortical white matter internal capsule cerebral peduncle basis pontis pyramid of the upper medulla

Decussates the lateral funniculus of the spinal cord Originates entirely from the large motor cells of Betz

Pyramidal tracts contains many fibers from cortical neuron other from Betz:
Broadmann areas 4 & 6 Primary somatosensory cortex (broadmann areas 3,2,1) Superior parietal lobule (area 5 & 7)

Pyramidal tracts also send collaterals to

Striatum Red nucleus Cerebellum Formatio reticularis

converge in corona radiata & descend through posterior limb of internal capsule, basis pedunculi, basis pontis, medulla

Paralysis caused by lesion of the UMN

e/ Interruption of the corticospinal pathways by lesion at any point of it course

Features & characteristics

A group of muscles is always involved

Internal capsule & corona radiata

Corticospinal fibers are intermingled with other tracts Thalamocortical tracts disturbance

The paralysis never involve all the muscles on one side of the body even the severest form

Voluntary drive on spinal motor neuron < slowness of movements Activation of paralyzed muscles as parts of certain automatisms (synkinesia)

Paralyzed arms move suddenly while yawning & stretching

Recovered hemiplegia expression of damage to basal ganglia & thalamic structures

Spasticity

Tremor, athetosis, chorea

The anti gravity muscles predominantly affected Clasp knife phenomena Persistent flaccidity after stroke primary involvement of lentiform nucleus & thalamus
Dorsal ret.spinal tract

At lower levels (cervical cords)

Paralysis of voluntary movements; abolish temporarily spinal reflex below the level of lession; replaced later by spasticity spinal shock Parietal lesion limbs flaccid; reflex retained

Inhibitory effects on stretch reflex

Med ret.spinal & ves.spinal tracts

facilitate extensor tone

Hyperreflexia

Release phenomena of tendon jerks

Interruption of corticobulbar pathways

Result interruption of descending inhibitory pathways

may take form of clonus Spread / irradiation of reflex

Associated with spasticity

Spinal flexion reflexes

Masseter contraction in response to a brisk downward tap of the chin Brisk contraction of orbicularis oris in response to tapping the philtrum Weakness paralysis of tongue, parynx, pharynx, tongue

Babinski sign Part of spasticity e/ disinhibition / release of motor programs in spinal origin Complete form

Lesion of the parietal lobe

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

Unable to maintain stable postures of the outstretched hand when his eyes are closed Cannot exert a steady contraction

Monoplegia without muscular atrophy

Hemiplegia

Lesion on cerebral cortex Usually accompanied by spasticity, reflex >, extensor plantar reflex (babinski)

Involvement of corticospinal pathways Level of lesion

Cortex, corona radiata, internal capsule weakness; paralysis of leg, arm, lower face of the opposite Low pontine lesion Ipsi. Abducens / facial palsy Contralateral paralysis of arm & leg Lateral column of cervical cord ipsilateral hemiplegia Lesion on MO

 Paraplegia
If

Tetraplegia
Lesion

white mater damaged sensoric function may be loss Bilateral damage bowel & bladder sphincters affected

in the cervical Occlusion of the anterior spinal artery Compresion of CI & C2 Repeated strokes affecting both hemispheres

Transient ischemic attacks

brief, reversible episode of focal ischemic brain disturbance without evidence of cerebral infarction

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

Etiology

Warning of impending vascular occlusion (internal carotid artery); often caused by an embolus leaves no lasting clinical effects Excessive viscosity / sludging of blood (polycythemia vera, sickle cell disease, thrombocytosis, leukemia, hyperglobulinemic state) Atherosclerotic vascular disease (23%)

Clinical syndrome

Reflect the involvement of virtually any cerebral arteries Most last 2-15 min Only a few / several hundred attacks

Prolonged, fluctuating TIAs most ominous ABCD systems

Blood pressure Unilateral weakness Speech disturbance Duration of symptoms

no abnormalities between attacks

stroke may occur / the attacks gradually cease & no important paralysis

<1 hour predictive of stroke < >1 hour predictive of stroke >

attacks (carotid artery, anterior circulation involvement ofterritory) 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

Occlusion of small penetrating vessels of the brain Intermittent onset; complete restitution of function Capsular warning syndrome
Escalating

episodes of weakness in the face,

arm, leg

Mechanism of TIA

Blood flow <; embolic particles Related to vascular stenosis (ulceration from atherosclerosis & thrombus) Embolization of fibrin-platelet material from atherosclerotic site States of anemia, polycythemia, thrombocythemia, lipid>, hyperviscocity, sickle cell anemia, hyper/hypoglycemia; antiphospolipid antibodies

DD

Seizure Migraine Transient global amnesia Multiple sclerosis Meningioma & subdural hematoma
Transient

aphasia / speech arrest

Glioblastoma Metastatic brain tumors in cortex

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 earliest possible stage Re-establish perfusion Maintenance of normal blood pressure when start

Antiplatelet drugs
Aspirin

325 mg daily Ticlodipine & clopidogrel

Thrombolytic agents
Recombinant

tPA ~ streptokinase

Anticoagulation
100U/kg continuous drip (1000U/h) Low mol weight heparin (nadroparin)
Heparin
4000U

SC, tid

Warfarin

watch the blood pressure (<220/120)

Atherothrombotic infarction

Hypertension, hyperlypidemia, diabetes atherosclerosis > Most frequent sites

Internal

carotid artery Cervical 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

Whole stroke evolves 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)

side of the head carotid occlusion Forehead & occiput basilar occlusion Behind the ipsilateral ear / above the eyebrow
One

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
slightly > Small number of PMN (3-8/cc) Transient pleocytosis (400-1000 PMN/cc) on the
Protein

Embolic infarction
Most

common cause of stroke

Clinical syndrome
Develop

most

rapidly No warning episodes Neurologic problem unfolds more gradually over many hours 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 a severe neurologic deficit that is only temporary Symptoms abate as the embolus fragments

Laboratory findings

Electrocardiogram & echocardiogram all patients 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

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 stroke symptoms watch our for hemorrhage

Anticoagulants
Warfarin;

Prognosis

Eventual prognosis is determined by the occurence of further emboli & the gravity of underlying illness
Cardiac

failure, myocardial infarction, bacterial endocarditis, malignancy

Primary (hypertensive) intracranial hemorrhage

Result of chronic hypertension & degenerative changes in cerebral arteries Large hemorrhage
Midline

structures displaced to the opposite side of the cranium RAS & respiratory centers compromised coma & death at distance from ventricle no blood in CSF

Small hemorrhage
+

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

Medium/large sized clots hemiplegia from interruption 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
Signs

of upper brainstem compression (coma),

Thalamic hemorrhage

Severe multimodal sensory loss on the entire contralateral 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

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

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

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 in / anterior to the ear, partial hemianopia, fluent aphasia headache, contralateral hemiplegia (arms)

Temporal lobe
Pain

Frontal lobe
Frontal

Laboratory findings

CT scan MRI

brainstem hemorrhage & residual hemorrhage (remain visible long after no longer visible with CT) transiently to 15000/cc

WBC
Rise

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 >;

Spontaneous subarachnoid 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 communicating

artery 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

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

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

Sentinel headache

Vasospasm
delayed hemiplegia & other deficit (3-10days)

Hydrocephalus

Large amount of blood rupture into ventricular system

Grading

Asymptomatic / slight headache & stiff neck

Moderate-severe headache & nuchal rigidity, no focal / lateralizing neurologic signs Drowsiness, confusion, mild focal deficit Persistent stupor, semicoma, early decerebrate rigidity, vegetative disturbance Deep coma & decerebrate rigidity

II

III

IV

Laboratory findings

CT
Detect

blood locally/difussely in the subarachnoid spaces, within the brain, ventricular system blood in the protodensity sequence

MRI
Detect

CSF
Grossly

bloody (30 min or sooner) RBC counts up to 1million/cc or higher

Treatment

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

Rapidly evolving syndrome of severe hypertension 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

CT & MRI

result of an accumulation of fluid

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

CSF

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 Dexamethasone 4-6 mg every 6 hour

Brain edema

LO4. Infeksi

Meningitis
The brain and spinal cord are covered by connective tissue layers collectively called the meninges which form the blood-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, an inflammation 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 nasal secretions,Saliva. Incubation period: 1-10 days. Usually 2-4 days Infectious period: as long as meningococci are present in oral secretions 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. Overcrowding e.g. dormitories and military training camps predispose to spread of infection.

Aseptic Meningitis Definition: A syndrome characterized by acute onset of meningeal symptoms, fever, and cerebrospinal fluid pleocytosis, with bacteriologically sterile cultures. Laboratory criteria for diagnosis: CSF showing 5 WBC/cu mm No evidence of bacterial or fungal meningitis. Case classification Confirmed: a clinically compatible illness diagnosed by a physician as aseptic meningitis, with no laboratory evidence of bacterial or fungal meningitis Comment Aseptic meningitis is a syndrome of multiple etiologies, but most cases are caused by a viral agent

Viral Meningitis 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, and Varicella -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

Klasifikasi 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 virus 6 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 encephalitis virus; tick borne encephalitis virus Bunyaviruses examples: La Crosse strain of California virus Reoviruses example: Colorado tick fever virus

LO5. Tumor

LO6. Trauma

Layers of the Meninges

Epidural Hematoma

Definisi: Accumulation of blood in the potential space 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 force to the calvaria that causes separation of the periosteal 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 the dura at these locations. The temporoparietal region and the middle meningeal artery are involved most commonly (66%)

Epidemiologi: Epidural hematoma complicates 2% of cases of head trauma (approximately 40,000 cases per year) Alcohol and other forms of intoxication have been associated with a higher incidence of epidural hematoma Sex

more frequent in men, with a male-to-female ratio of 4:1 rare in individuals younger than 2 years rare in individuals older than 60 years because the dura is tightly adherent to the calvaria

Age

Gejala Klinis: Head trauma Lucid interval between the initial loss of consciousness at the time of impact and a delayed 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 lenticularshaped mass situated between the brain and the skull, though regions of hypodensity may be seen with serum or fresh blood MRI also demonstrates the evolution of an epidural hematoma, though this imaging modality may not be appropriate for patients in unstable condition

Subdural Hematoma

Definisi : Rapidly clotting blood collection between dura mater and brain Typically, low-pressure venous bleeding of bridging veins (between the cortex and venous sinuses) 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 margins and convex outer margins (crescent shape) Frequency is related directly to the incidence of blunt head trauma Its the most common type of intracranial mass lesion, 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 a mortality rate of about 50% Its associated with age factors related to the risk of blunt head trauma More common in people older than 60 years (bridging veins are more easily damaged/falls are more common) Bilateral SDHs are more common in infants since adhesions existing in the subdural space are absent at birth Interhemispheric SDHs are often associate with child abuse

Age

Gejala Klinis : Usually involves moderately severe to severe blunt head trauma Acute deceleration injury from a fall or motor vehicle accident, 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 Develops after mild head trauma common on elder and those who anticoagulated Neurologic symptoms: hemiparesis,seizures,and behavioral changes

Chronic:

Pemeriksaan Penunjang MRI the size of an acute SDH and its effect on the brain, head CT diagnosis and suffice for immediate management 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 cerebral convexity in the parietal region. The second most common area is above the tentorium cerebelli

Contrast-enhanced CT or MRI is widely recommended for imaging 48-72 hours after head injury because the lesion becomes isodense in the subacute phase In the chronic phase, the lesion becomes hypodense and is easy to appreciate on a noncontrast head CT scan

Epidural Hematoma
Potential space between the dura in the inner table of the skull Cant cross sutures Skull fractures in temporoparietal region Middle meningeal artery Lenticular or biconvex shape

Subdural Hematoma

Between the dura mater and the arachnoid mater Can cross sutures Cortical bridging veins Crescent shape Loss of consciousness Common in elderly

LO7. Degeneratif

Dementia

Dementia is a disease marked by a gradual loss of cognitive functioning which can also incorporate losses of motor, emotional, and social functioning as well It is a permanent and progressive disease that eventually renders people unable to care for themselves.

Dementia - Incidence

Suspected that as many as 50% of people over the age of 80 develop Alzheimers. 5%-8% of all people over 65 have some form of dementia; number doubles every 5 years beyond that age.

Alzheimers causes 50%-70% of all dementia. About 20%-30% of all dementia is believed to be caused by a vascular dysfunction (most common is multi-infarct disease).

Dementia - Causes

50 different causes Neurological disorders such as Alzheimers (est. 5070% of people with dementia have Alzheimers)

Vascular disorders such as multi-infarct disease (multiple strokes) Inherited disorders such as Huntingtons Infections such as HIV

Two types of Dementia

Cortical - Disorder affecting the cortex, the outer portion or layers of the brain. Alzheimers 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.

Subcortical - Dysfunction in parts of the brain that are beneath the cortex. Memory loss & language difficulties not present or less severe than cortical. Huntingtons disease and AIDS dementia complex. Changes in their personality and attention span. Thinking slows down.

Dementia - Early Stage

Begins with forgetfulness isolated incidents of memory loss do not constitute dementia. Forgetfulness progresses to confusion and eventually disorientation.

Problem solving Judgment Decision making Orienting to space and 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 motor function); agnosia (failure to recognize or identify objects despite intact sensory 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

Important to establish the cause of the dementia - Alzheimers and dementia are not the same thing. A differential diagnosis compares the symptoms of two or more diseases. DD is important because some forms of dementia are treatable. Examples of treatable dementias include: chronic drug abuse, Normal Pressure Hydrocephalus, Chronic subdural Hematoma, Benign Brain Tumors, Vitamin Deficiency, and Hypothyroidism.

Dementia - Diagnosis

Medical History - Physician wants to determine the onset of symptoms and how theyve changed over time. Determine risk factors for infection, family history of dementia or other neurological disease, alcohol and drug use, and a patients history of strokes.

Dementia - Diagnosis

Neuropsychological Exam - Evaluates a persons cognitive ability, e.g. orientation in time and space, memory, language skills, reasoning ability, attention, and social appropriateness. Tests involve asking a person to repeat sentences, name objects, etc. Someone with Alzheimers is usually cooperative, attentive, and appropriate but has poor memory. Someone with hydrocephalus is likely to be distracted and less cooperative.

Dementia - Diagnosis

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.

Alzheimers Disease

Progressive disorder in which neurons deteriorate 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

Neuritic Plaques Commonly found in brains of elderly people but appear in excessive numbers in the cortex of AD pt.s Surrounded by deteriorating neurons that produce acetylcholine (neurotransmitter essential for processing memory and learning. Neurofibrillary 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

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 Understanding speech Emotion Memory

Occipital Lobe Understanding visual images Understanding the meaning of the written word.

AD - Neuroanatomy

Hippocampus Plays a crucial role in both the encoding and retrieval of information. Damage to the hippocampus produces global retrograde amnesia, which is the inability to retain newly learned information.

AD - Incidence

About 2 million people in the U.S. suffer from Alzheimers disease. Approx. 5%-8% of people over 65. As many as 50% over the age of 80

AD - Risk Factors

Family History - a clear inherited pattern exists in approximately 10% of cases Downs Syndrome - Nearly 100% of people who live into their 40s Chronic Hypertension - Treatment reduces the risk Head Injuries - Three times more likely to develop AD Gender - inclusive data. Some studies show a greater risk for females while others show an increased risk for males.

AD - Symptoms

Loss of Memory Aphasia Apraxia - (decreased ability to perform physical tasks such as dressing, eating, ADLs 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 with forgetfulness Progresses to disorientation and confusion Personality changes Symptoms of depression/manic behaviors Interventions Medications - Aricept and Cognex (both are commercial names). Both increase acetylcholine (Ach) in the brain by inhibiting the enzyme that breaks it down. Therapy (deal with depression that often accompanies 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-term recall May display anxious, agitated, delusional, or obsessive behavior May be physically or verbally aggressive

Poor personal hygiene Disturbed sleep Inability to carry on a conversation May use word salad (sentence fragments) Posture may be altered Disoriented to time and place May ask questions repeatedly

AD - Middle Stage
Interventions Validation Therapy Structured Areas for Mobility Positive, nurturing, loving environment

Music Therapy Provides avenue for social interaction (Instrumental Improvisation; TGS, Guided Music Listening) Provides a medium for verbal/non-verbal expression (TGS) Can help maintain cognitive and affective 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 are inaccessible

AD - Late Stage

Music Therapy Tape by bedside Gentle singing by therapist ~ one-sided, client will not participate Can provide some connection between patient and family members through singing Use a calm voice Utilize touch: holding hands, hugging, rocking, hand on shoulder, etc.