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GANGGUAN N II DAN KESEIMBANGAN PADA KELAINAN INTRASEREBRAL

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Optic Nerve (II)

Sensory nerve of vision
Filaments of olfactory nerve (I) Olfactory bulb Olfactory tract

Optic nerve (II)

Optic chiasma Optic tract Oculomotor nerve (III) Trochlear nerve (IV) Trigeminal nerve (V) Abducens nerve (VI) Cerebellum Medulla

Table 14.3 (2 of 12)

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N. Optikus (N II)
Tajam penglihatan
Normal: 6/6 Melihat jari: 6/60 Lambaian tangan: 1/300 Melihat sinar: 1/~

Lapang pandang
Tes konfrontasi dgn tangan Tes kampimeter Tes perimeter

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N. Optikus (N.II) contd

Tes warna
Stilling-Ishihara

Funduskopi
Pemeriksaan papil N. II

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N. Optikus (N.II) contd

Gangguan N. II
Mata kabur = visus turun Melihat dobel (diplopia) = aksis visual terganggu Lapang penglihatan menurun Mata buta Mata menjadi gelap Papiledema

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Cerebrovascular Disease

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General consideration
Cerebrovascular disease: any abnormality of the brain resulting from a pathologic process of the blood vessels. Cerebrovascular accident or stroke may be defined as a sudden interruption of blood supply or hemorrhage into apart of the brain. the third commonest cause of death

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Classification
Ischemic transient ischemic attack (TIA) cerebral thrombosis cerebral embolism cerebral infarction lacunar infarct Hemorrhagic cerebral hemorrhage subarachnoid hemorrhage (SAH)

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Blood supply of brain

1. Internal carotid system Branchiocephalic trunkright common carotid artery left common carotid artery internal carotid artery carotid foramen Ophthalmic artery Anterior choroidal artery Posterior communicating artery Anterior cerebral artery Middle cerebral artery

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Supply eyes and anterior 3/5 of the brain: frontal, parietal, part of temporal lobe, basal ganglia.

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Blood supply of brain

2. Vertebral-basilar system Subclavian artery vertebral artery C6-C1
transverse foramen great occipital foramen basilar artery posterior spinal arteries, anterior spinal artery posterior inferior cerebellar artery auditory artery posterior cerebral arteries

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supply cerebellum, brain stem, posterior 2/5 of brain (occipital, part of tempral lobe)

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3. Circle of Willis

Blood supply of brain

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Risk factors of CVD

Age, family history, race Hypertension Heart disease Diabetes Hyperlipemia Smoking, excessive drinking Obesity, diet, contraceptive drugs

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TIA
A transient ischemic attack is a focal disturbance of the cerebral circulation, frequently repetitive, resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours). Attacks can occur in the carotid and/or vertebral artery territories.

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Etiology
Micro embolism Spasm of cerebral blood vessel Hemodynamic change Compression of vertebral artery, steal syndrome

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Clinical feature
1. 50-70, M>F characteristics: Abrupt onset Transient Complete recovery Repetitive

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Clinical feature
2. Transient carotid ischemic attacks (1)Common symptoms: Weakness of the contralateral arm and/or leg. (2) Characteristic symptoms: Transient loss of vision in the eye contralateral to the paresis (amaurosis fugax). Horner sign (3) Symptoms may present: Dysphasia Paraesthesia or numbness in the contralateral limbs. hemianopia

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Clinical feature
3. Transient vertebral basilar ischemic attack (1) Common symptoms Vertigo, nausea, vomiting (2) Characteristic symptoms: Drop attack Transient global amnesia, TGA Cortical blindness Crossed paralysis or sensory disturbance

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Clinical feature
(3) Symptoms may present: Dysphagia, dysarthria Ataxia Disturbance of consciousness diplopia

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Diagnosis
Clinical features No signs between attack

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Differential diagnosis
Partial epilepsy Meniere disease

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Cerebral Thrombosis
Infarction of an area of the brain secondary to arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation.

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Etiology
Atherosclerosis Arteritis: such as leptospirosis, rheumatic fever Rare cause: congenital vascular malformation, polycythemia blood hypercoagulability

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Pathology
Vessel: carotid > middle > posterior > anterior > vertebral-basilar Super-early stage: 1-6 hour Necrosis cyst
White infarct Red infarct: hemorrhagic infarct

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Pathophysiology
Neurons are sensitive to ischemia Central necrosis Ischemic penumbra Super early stage: < 6 hours

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Clinical feature
Onset is rapid Usually occur in the rest and sleep Premonitory symptoms such as weakness of a limb, transient ischemic attack The headache, vomit, and loss of consciousness may be absent or slight. Focal signs develop in several days

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Clinical type
Complete stroke Progressive stroke Reversible ischemic neurological deficit (RIND)

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Clinical syndrome
1. Internal carotid artery may have no signs (if the collateral supply, from the other side, is good ) amaurosis fugax, uniocular blindness Horner's syndrome may present in the side of the occlusion. contralateral hemiplegia and hemianesthesia.

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Clinical syndrome
2. Middle cerebral artery contralateral hemiplegia, hemianesthesia, hemianopia aphasia (if the dominant hemisphere is affected) disturbance of body image (non-dominant hemisphere)

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Clinical syndrome
3. Anterior cerebral artery contralateral hemiplegia, the leg frequently being more affected than the arm. paracentral lobule: regulation of sphincter function, retention or incontinence mental symptoms: apathy, euphoria

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Clinical syndrome
4. Posterior cerebral artery contralateral hemianopia or quadrantanopia thalamic syndrome: contralateral hemianesthesia, thalamic pain, ataxia, tremor, athetosis

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Clinical syndrome
5. Vertebro-basilar artery (1) Main trunk nausea, vomiting, tetraplegia, coma, death (2) Weber syndrome Unilateral lesion of midbrain Ipsilateral oculomotor nerve paralysis, contra lateral hemiplegia

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Clinical syndrome
(3) locked-in syndrome Bilateral infarction in the basis pontis Tetraplegia, can not speak, can not swallow Conscious Can only respond by vertical gaze and blinking

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Clinical syndrome
6. posterior inferior cerebellar artery Wallenberg's syndrome, Lateral medullary syndrome Vertigo, vomiting, nystagmus Crossed sensory disturbance Ipsilateral Horner sign Dysphagia, dysarthria Ipsilateral ataxia

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Investigation
1. CT Low density focus after 2448 hours

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Investigation
2. MRI
A right carotid artery occlusion, low signal of T1, and high signal of T2 weighted image.

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Investigation
3. Lumbar puncture Normal. Large infarct: pressure Hemorrhagic infarction: RBC 4. DSA 5. TCD

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Diagnosis
after middle or old age. rapid onset focal cerebral symptoms premonitory symptoms occurs in rest or sleep CT/MRI find cerebral infarction focus

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Differential diagnosis
Cerebral hemorrhage Cerebral embolism Intracranial tumor

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Lacunar infarct

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Pathology
3-4mm, <15-20mm Small liquid cavity Basal ganglia, thalamus, brain stem Small artery: 100-200m Atherosclerosis

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Clinical feature
40-60 years of age Always combined with hypertension Lacunar syndrome: 1. Pure motor hemiparesis 2. Pure sensory stroke 3. Ataxic-hemiparesis 4. Dysarthric-clumsy hand syndrome 5. Sensorimotor stroke 6. Lacunar state

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Cerebral embolism
Occlusion of a major cerebral artery by an embolus, with resultant infarction of part of the brain.

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Etiology
Cardiac cause: Atrial fibrillation, rheumatic valve disease, endocarditis, atrial myxoma, myocardial infarction Non-cardiac: Atherosclerosis plaque, pus embolus, fat embolus, tumor embolus Embolus of unknown origin

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Clinical feature
Left middle cerebral artery abrupt onset, maximum disability occurring at once In some cases, there is rapid improvement The primary disease, such as rheumatic heart disease

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Vertebrobasilar Ischemia
Symptoms: Commonly manifested as vertigo, visual

disturbances, progressive neuro deficit Mechanisms:

Microembolization: from heart or more proximal arteries. Less

common.
innominate, prox subclavian, and vertebrals

Low-flow: lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid.
More frequent Stenosis/occlusion of vert, also extrinsic compression Orthostatic hypotension, antihypertensive meds, arrythmias, CHF, pacemaker malfunction, anemia

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Evaluation of Patients
Dizziness, vertebral artery stenosis are common complaints/findings Imaging brain to r/o tumor, investigate for infarctions Check bilateral arm BPs to r/o subclavian steal syndrome
Document reversal of flow by duplex

Extrinsic compression by osteophytes

Turning head side to side, slowly, then briskly to differentiate from BPV Confirm with angiogram

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Global ischemia
Drop attacks comprise roughly 30% of presentations One or both internal carotid arteries occluded or with severe siphon stenosis. Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded.
Minimal anatomic req to justify vert reconstruction is >60% stenosis in dominant if contra is hypoplastic, or >60% in both.

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Head Injury
Epidemiology
1.5 million Non-fatal TBIs 370,000 Hospitalizations 80,000 cases of neurological sequela 52,000 Die from TBIs 4 billion annually for cost of treatment Peak incidence:
Males age 15-24 years

Causes of TBI
Young: GSW Old: Falls

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Head Injury-Anatomy
Scalp Blood supply Calvaria Brain
Occupies 80% of calvarium

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Head Injury-Pathophysiology
Primary injury
Irreversible cellular injury as a direct result of the injury Prevent the event

Secondary injury
Damage to cells that are not initially injured Occurs hours to weeks after injury Prevent hypoxia and ischemia

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Head Injury-Normal Physiology

Brain consumes 20% of total O2 Receives 15% of Cardiac Output Brain tissue perfusion CPP versus CBF
CPP=MAP-ICP
MAP=(SBP-DBP/3) + DBP
ICP=IVM

Autoregulation
50-150 mm Hg

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ICP

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Spectrum of Traumatic Brain Injury

Mild TBI
GCS 14-15 80% of all TBI Low Risk
GCS 15 and no LOC, amnesia, vomiting or diffuse HA Less than 0.1% risk of hematoma requiring evacuation

Medium Risk
GCS 15 and LOC, amnesia, vomiting or Diffuse HA 1-3% risk of hematoma requiring evacuation CT should be done in medium risk mild TBI

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Spectrum of Traumatic Brain Injury

Mild TBI
High Risk
GCS 14-15 Neurologic deficits Up to 10% risk of hematoma requiring evacuation Anyone with coagulopathy, drug/alcohol consumption, epilepsy, age >60 and previous neurosurgery

Disposition
No CT indicated or negative CT with GCS 15-Home GCS 14 and negative CT-Observation admit

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Spectrum of Traumatic Brain Injury

Moderate TBI
GCS 9-13 10% of all TBI <20% mortality 50% morbidity 40% positive CT 8% NS intervention <10 make moderate recovery

Severe TBI
GCS <9 10% of all TBI 40% mortality

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Intracerebral Pressure
Normal <15 mm Hg ICP >20-25 mm Hg
Increases morbidity and mortality

ICP monitoring rarely available in the ED Must use physical findings

Neurologic deterioration Unilaterally dilated pupil

Hemiparesis Posturing

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Specific Head Injuries

Scalp Lacerations
May lead to massive blood loss Small galeal lacerations may be left alone

Skull Fracture
Linear and simple comminuted skull fractures
Exploration of wound Prophylactic antibiotics are controversial Occipital fractures have a high incidence of other injury If depressed beyond outer table-requires NS repair

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Specific Head Injuries

Skull Fractures
Basilar Fracture
Most common-petrous portion of temporal bone, the EAC and TM Dural tear
CSF otorrhea CSF rhinorrhea Battle Sign Raccoon Sign Hemotympanum Vertigo Hearing loss Seventh nerve palsy

CSF testing
Ring sign, glucose or CSF transferrin

Should be started on prophylactic antibiotics

Ceftriaxone 1-2 gm

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The Ring Sign

Ann Emerg Med. 1993 Apr;22(4):718-20. The 'ring sign': is it a reliable indicator for cerebral spinal fluid? Dula DJ, Fales W. Department of Emergency Medicine, Geisinger Medical Center, Danville, Pennsylvania. STUDY OBJECTIVE: To study the development of a ring sign when blood is mixed with various fluids. METHODS: One drop of blood and one drop of either spinal fluid, saline, tap water, or rhinorrhea fluid were placed simultaneously on filter paper, and the specimens were examined after ten minutes for the development of a ring. A variety of filter paper agents were used, including standard laboratory filter paper, paper towels, coffee filters, and bed linens. RESULTS: All fluids, when mixed with blood, gave rise to a ring sign; blood alone did not. The type of filter paper did not affect the development of a ring. CONCLUSION: In this experimental setting, the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid.

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Specific Head Injuries

Brain Herniation
Four Types
Uncal Transtentorial Central Transtentorial Cerebellotonsillar Upward Posterior Fossa

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Specific Head Injuries

Traumatic Subarachnoid Hemorrhage
Most common CT finding in moderate to severe TBI If isolated head injury, may present with headache, photophobia and meningismus Early tSAH development triples mortality Size of bleed and outcome Timing of CT Nimodipine reduces death and disability by 55%

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Specific Head Injuries

Epidural Hematoma
Occurs in 0.5% of all head injuries Blunt trauma to temporoparietal region Eighty percent with associated skull fracture May occur with venous sinus tears Classic presentation only 30% of the time

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Specific Head Injuries

Subdural Hematoma
Sudden acceleration-deceleration injury with tearing of bridging veins Common in elderly and alcoholics Classified as acute, subacute or chronic
Acute <2 weeks Chronic >2 weeks

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Specific Head Injuries

Diffuse Axonal Injury
Disruption of axons in white matter and brainstem Injury occurs immediately and is irreversible Seen after MVC or shaken baby syndrome Usually have persistent vegetative state CT usually normal MRI with multiple, diffuse abnormalities

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Specific Head Injuries

Penetrating Injury
Gunshot Wounds
Injury due to direct brain injury and cavitary effects GCS predicts prognosis
GCS >8 and reactive pupils = 25% mortality GCS <5 = nears 100% mortality

Stab wounds

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Complications-Long Term Sequela

Seizure Disorder
2% Early post-traumatic incidence Increased to 30% in children, alcoholics and with intracranial hematoma
Prophylactic antiepileptics reduce early occurrence Use not supported by the literature

Concussion
- Brief LOC
- Vertigo - Nausea - Dizziness - Headache - Vomiting - Photophobia - Cognitive/Memory dysfunction

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Complications-Long Term Sequela

Concussion
Up to 80% may have symptoms at 3 months 15% may have symptoms at 1 year Persistence of these symptoms is termed Postconcussive Syndrome 85-90% recover after 1 year Risk factors:
- Female - Litigation - Low socioeconomic status

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BRAIN TUMOR

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INSIDEN
1. 2. 3. Tumor otak memp. 2 puncak, pertama usia anak-anak 3-12 tahun, puncak kedua 50-70 tahun. Dua pertiga, terjadi pd anak-anak, terletak infra tentorial, berasal dari : serebellum, batang otak, dan mesensefalon. Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak. Insiden pd pria hampir sama dg wanita, astrositoma > pd pria, sedang meningioma > pd wanita. Di USA, 1998 tumor otak primer 34.000, 170.000 tumor otak metastasis. Tahun 2003, 18.300 kasus baru dg kematian 13.100 orang.

4.
5.

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DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak/ selaputnya, yang menyebabkan proses desak ruang, dan menyebabkan perubahan patologis. Tumor primer (50%) dari seluruh tumor otak t.d : glioma 50%, meningioma (20%), adenoma (15%), neurinoma (7%) Tumor sekunder (50 %) t.d : tumor metastasis Letak tumor, pada dewasa : (60%) supratentorial, pada anak : (70%) infratentorial

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ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui.

1. Bawaan :Dijumpai pada anggota keluarga mis : meningioma, astrositoma, neurofibroma. 2. Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik, mis: kraniofaringioma, teratoma intra kranium, kordoma (berasal dari: kantung rathke, mesenkim-ektoderma embrional, korda dorsalis)

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ETIOLOGI TUMOR OTAK (2)

3. Radiasi : Dosis subterapi dapat merang sang pertumb. sel mesenkim mjd tumor. 4. Virus : Telah terbukti oleh Burkitt, bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus. 5. Zat karsinogenik : Methylcholantrone, nitroseethyl-urea, dpt menyebabkan tumor otak pada percobaan binatang.
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ISI KRANIUM (1)

1. Isi kranium : selalu konstan, yaitu : otak, cairan serebrospinal, pembuluh darah dg isinya 2. Otak mikroskopis t.d : NEURON, NEUROGLIA (Astrosit fibosa & protoplasmatis, mikroglia, oligodendroglia, dan sel ependim) MENING, PEMBULUH DARAH.
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ISI KRANIUM (2)

Volume otak : 1400 ml, cairan LCS : 150 ml, darah : 150 ml Hukum Monro Kellie : total volume dr ketiga komponen selalu konstan Bila ada kenaikan volume salah satu komponen, akan terjadi kompresi komponen lainnya.

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NEOPLASMA OTAK
NEOPLASMA INTRA AKSIAL, GLIAL, GLIOM Asal : parenkim otak, neuron, neuroglia
Sifat : infiltratif Contoh : Astrositoma, Ependimoma, Meduloblastoma, Oligodendroglioma

NEOPLASMA EKSTRA AKSIAL, NON GLIAL Asal : luar otak, meningen, Hipofisis, embrional, metas Sifat : ekspansif Contoh : Meningioma, neurinoma akus tikus, adenoma hipofise, kranio paringioma , tumor epider moid.

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I. SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE THREE MAJOR SIGNS : HEADACHE VOMITING CHOKED DISK

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1.HEADACHE
1. 2. 3. 4. 5. 6. A QUARTER OF PATIENTS WITH INCREASED ICP NOT SO SEVERE, GENERALLY OCCURS IN THE MORNING : EARLY MORNING HEDACHE. MAY BE PULSATILE, N BECOME WORSE WITH VOLUNTARY STRAINING. MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF SUCH PAIN SENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE) GENERALLY, THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR. SUPRATENTORIAL TUMOR : FOREHEAD PARASELLAR TUMOR : PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR : PAIN SPREADING OVER NUCHAL AREA.

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2.VOMITING
1. OCCURS AT THE END OF INTRACRAN. HYPERTENSION 2. NOT RELATED TO INGESTION, PROJECTILE TYPE. 3. AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN 4. PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE.

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3.CHOKED DISC (CD) N VISUAL DITURBANCE.

1. 2. 3. 4. 5. NOT ALL BT CAUSE CD IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L), SUCH AS BT. CD IS SELDOM SEEN IN INFANTS. WHEN ICP INCREASE GRADUALLY, THE EDEMA OF THE DISC MAY NOT BE OBSERVED, AND IT WILL BE CONVERTED INTO ATROPHIC STAGE. BESIDES, DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)

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4.ENLARGEMENT OF THE HEAD

WHEN ICP INCREASES, THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE, WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET.

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5.NUCHAL RIGIDITY
WHEN THE CEREBELLAR TONSIL HERNIATES, RIGIDITY WILL BE OBSERVED, N THEREFORE , IS A DANGEROUS SIGN , IN PATIENT WITH INCREASED ICP.

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6.INTELLECTUAL DETERIORATION( ID)

1. 2. 3. 4. 5. ID, MAY BE PRESENT WITH INTRACRAN. HYPERTENSION. INDIFFERENCE N APATHY ARE OBSERVED. NEXT, MENTAL N PHYSICAL FATIQUE. FOLLOWED BY ,MEMORY DISTURBANCE . FINALLY, AROUSAL DIORDER, RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE

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7.SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)

1. FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM & POSNERS CENTRAL SYNDROME). 2. COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)

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7.SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)

1. FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM & POSNERS CENTRAL SYNDROME). 2. COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)

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MANIFESTASI KLINIK TUMOR OTAK (1)

1. Tanda & gejala lokalisatorik yg benar. Dasar : Bagian otak ttt punya fungsi ttt Bila ada ggnfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan/ luput dihargai, setelah ada proses desak ruang baru disadari. 2. Gejala ini timbul sebelum ada manifestasi TIK meninggi, mis : monoparesis,hemiparesis, hemianopsia, anosmia.

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MANIFESTASI KLINIK TUMOR OTAK (2)

3. Gejala dan tanda lokalisatorik yang menyesatkan. Tak sesuai dengan ggnfs bagian otak di mana tumor berada. Misal : - kelumpuhan N III, IV, VI - refleks pathologis ke-2 sisi - gangguan mental - gangguan endokrin - encephalomalasia

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MANIFESTASI KLINIK TUMOR OTAK (3)

4. Tanda dan gejala akibat TIK meninggi. Misal : gangguan kesadaran, sefalgia, muntah, kejang, gangguan mental, rasa abnormal, papiledema, pembesaran kepala anak, bradikardi-tensi meninggi, gangguan irama napas dll. Gejala umum ini terjadi akibat langsung dari masa tumor, edema otak atau obstruksi LCS.

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MANIFESTASI KLINIK TUMOR OTAK (4)

Tanda tanda fisik diagnostik : Papil edema. Pembesaran kepala anak dgn pelebaran sutura Hipertensi yang progresif, sbg mekanisme kompensasi, bradikardi. Irama & frekuensi pernapasan yg berubah.

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MANIFESTASI KLINIK TUMOR OTAK (5)

GANGGUAN KESADARAN : Akibat tekanan intrakranial meninggi, timbul ancaman herniasi otak, dgn akibat penurunan kesadaran. Misalnya : Sindroma unkus atau kompresi diensephalon ke lateral, sindroma kompresi sentro rostrokaodal thd BO, herniasi otak kecil ke foramen magnum. Keadaan ini menyebabkan kegawatdaruratan medik.

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DIAGNOSIS TUMOR OTAK (1)

ANAMNESIS ; Keluhan yang sifatnya kronis-progresif. Misalnya : Nyeri kepala m.l.m hebat dlm bbrp minggu / bulan. Atau nyeri kepala, kemudian diikuti defisit neurologik yang lain. Misal : gangguan motorik, sensorik, sensibel.

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DIAGNOSIS TUMOR OTAK (2)

INGAT GEJALA UMUM: 1. Sefalgia:berdenyut, terasa pagi hari, meningkat bila mengejan, batuk atau angkat berat. 2. Muntah :pagi hari, tak bhb dg makanan, sifatnya proyektil. 3. Kejang :fokal/ umum, tumor dekat girus pre sentralis. 4. Perubahan mental : demensia, apatis, gangg. berpikir dan daya ingat. 5. Papiledema dgn pem funduskopi. 6. Pembesaran kepala anak. 7. Bradikardi dan hipertensi.

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DIAGNOSIS TUMOR OTAK (3)

INGAT SINDROM FOKAL/ LOKALISATORIK : Lobus Frontalis : sefalgia & gangguan mental Lobus Temporalis : tinitus, halusinasi auditorik,afasi sensorik. Daerah Pre Sentralis: kejang dan hemiparesis, kontralateral. Lobus Parietalis : gangg. sensibilitas, asteriognosia (tak mampu mengenal barang yang dipegang).

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DIAGNOSIS TUMOR OTAK (4)

INGAT SINDROM FOKAL: Lobus Oksipitalis : sefalgia, gangguan medan penglihatan, agnosia visual. Serebelum : ataksia, disdiadokokinesis, dismetri, rebound phenomen, disartri. Batang Otak : gangguan kesadaran & gangguan saraf spinal.

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DIAGNOSIS TUMOR OTAK (5)

INGAT TANDA2 LOKALISATORIK YG MENYESATKAN : Kelumpuhan N III , IV , VI Refleks patologis positif. Gangguan mental < demensia dll. Gangguan endokrin.

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