KEPANITERAAN KLINIK ILMU PENYAKIT SARAF

PERIODE 8 JANUARI-10 FEBUARI 2018

Pembimbing : dr. RR. Josephine Retno, Sp.S

Presentan :
Jessica Filbertine (2015-061-205)
Nadia Sylvano (2016-061-)
 Name :N
 Age : 22 years old
 Sex : men
 Address : Pluit
 Agama : Moslem
 Date of admission : 27th January 2018
 Chief complain
 Loss of consciousness since 7 days prior

 Additional complains
 Didn’t speak since 2 days
 Decreasing oral intake since 7 days prior
 7 days prior 5 days prior 2 days prior Admission

Not responsive

• Good
response Decreasing speech 1-2 words No words
• Good oral
intake
• Speaks
Decreasing food and water intake
(-) food and water intake
(5 tablespoons)

No complains of headache, nausea, vomit, blurred vision

Trauma (-), fever (-), common cold (-),

Patient has no difficulty to speech.

 7 days prior

Patient spoke less words than usual  only 1-2 words.

 2 days prior

Patient spoke no word

No complaints nor difficulties in eating and drinking water. Patient
usually finish a plate of food.

 7 days prior
Patient ate only 5 tablespoons of food.
Drank less water.

 2 days prior
Patient didn’t eat or drink water
Patient usually speak fluently with the parent. Answers when asked.
He can walk, sit, watch TV at home.

 2 days prior
The patient didn’t response well like he used to. He just lay on the bed, didn’t
answer to question.
 Patient had experienced similarly in 2015 and 2016. He then
diagnosed as having non-communicant hydrocephalus and underwent
VP-shunt operation.
 No trauma history
 No food and medication allergy known.
 No seizure history.
 No lung tuberculosis history.
 No brain infection history.
 2015
• Diagnosis: non communicants hydrocephalus
• Operation type: right VP shunt installation

• The patient feels stiffness when walking since 1 week and the limbs move
unintentionally since 1 week. The patient also feels headache since 3
months ago, unable to either stand nor walk. Patient also unable to talk
properly, no fever and seizure.
• Then the patient take CT-Scan, and seen Hidrosephalus e.c susp.
Obstructive e.c. cerebropontin angle mass DD/ infection. Then the patient
got VP shunt operation.
 Sistem ventrikel melebar, sistem sisterna
menyempit. Kortikal sulci dan fissura silvii
menyempit dengan penyangatan pasca
pemberian kontras.
 Kesan : sugestif gambaran
meningoencephalitis.
 Post pemasangan VP shunt tampak
ventrikulomegali berkurang dan
edema cerebri berkurang (perbaikan)
• Diagnosis: non communicants hydrocephalus
• Operation type: VP shunt installation
• Patient become unconscious suddenly , without any trauma, fever, headache. The
GCS E2M4V1. The patient then taken to CT scan and seen broad verticulitis,
cerebritis corpus calosum, the hydrocephalus become harder than the CT taken
before
• After VP shunt operation, the cerebrospinal fluid also got checked and the results are
: leucocyte = 4 /uL, diff count= only mononuclear, protein = 25mg/dL, brain glucose
=74mg/dL. BTA= negative, The CSF also got cultured and got no bacterial growth.
• After the VP shunt operation, 4 days later the patient brought back to have CT scan
without contrast
 hasil satuan Nilai normal
Mikroskopik
Jumlah leukosit 24 /uL <5
Hitung jenis
MN Hanya MN %
Kimia
Nonne + Negatif
Pandy + Negatif
Protein 12.6 mg/dL 0-70
Glukosa Cairan Otak 62 mg/dL 50-75
Glukosa serum 105 mg/dL
 hasil satuan Nilai normal
Mikroskopik
Jumlah leukosit 36 /uL <5
Hitung jenis
MN Hanya MN %
Kimia
Nonne + Negatif
Pandy + Negatif
Glukosa Cairan Otak 93 mg/dL 50-75
 Dibandingkan CT scan kepala tanggal
11/10/2016 saat ini kondisi ventriculitis
dan cerebritis relatif stqa.
 Hidrocephalus stqa
 Posisi tip VP shunt di medial ventrikel
lateral kanan, stqa
 Dibandingkan CT scan kepala tanggal
29/10/2016, saat ini kondisi ventriculitis dan
cerebritis tampak berkurang (ada
perbaikan) dengan derajat hidrocephalus
lebih ringan.
 Diagnosa pra-operatif: hidrosefalus non communicans
 Diagnosa pasca-operatif: hidrosefalus non communicans
 hasil satuan Nilai normal
Mikroskopik
Jumlah leukosit 12 /uL <5
Hitung jenis
MN Hanya MN %
Kimia
Protein 2.5 mg/dL 0-70
Glukosa Cairan Otak 33 mg/dL 50-75
 No similar complaint in family.
 No family history of lung tuberculosis living in the same house.
 No seizure or brain infection history.
 General condition: severly ill
 consciousness : E2M5V2, stupor
 Cooperation : not cooperative
 Body type : athletics
 Body height, weight : 180 cm, 70 kg  BMI= 21.6 km/m2
 Vital sign:
 Blood pressure : 130/70 mmHg
 Pulse rate : 64 times/ min. (regular, adequate ,full).
 Respiration rate : 20 times/ min.
 temperature : 36,30C (Normal = 36,50C – 37,50C)
 O2 saturation : 98%
 Head  Nose
 palpable shunt a/r bilateral  Septum deviation (-), secret (-)
temporal  Mouth
 Face  Wet oral mucosa, cyanosis (-)
 symmetrical  Ear
 Eye  Hiperemic external acoustic meatus
 Anemic conjungtiva-/- -/-
 Icteric sclera -/-  Intact timpanic membrane +/+
 Pupil : isochoric, 3 mm / 3 mm  Serumen +/+, secret (-)
 Direct and indirect light reflex -  Neck
/-  Trachea in midline
 Funduscopic: bilateral papil  Lymph node enlargement (-)
atrophy
 Thyroid enlargement (-)
Thorax
1. Lung

 Inspection : symmetrical movement

 Palpation : symmetrical tactile fremitus
 Auscultation : vesicular +/+,Wheezing -/-.

2. Jantung
 Inspection : ictus cordis not visible
 Palpation : ictus cordis not palpable
 Auscultation : regular 1st and 2nd heart sound , murmur (-), gallop (-).
 Abdomen

 Inspection : flat, vein dilatation (-), striae (-), Abdominal aorta

pulsation (-),

 Auscultation : bowel sound (+) 5x / minute

 Percussion : tympanic in all region

 Palpation : supple , pain (-) in all region

 Extremity

 Cold akral, CRT < 2 seconds.

 Genital, Anus and Rectum

 Not examined
 Meningeal sign
- Neck stiff :+ - Brudzinski I : -/-
- Kernig : -/- - (Brudzinski II) : -/-

 Increased intracranial pressure sign

- headache: difficult to asses
- Blurred vision: difficult to asses
- Bradycardia : -
- Papil oedema : -
N. I (right/left) : difficult to assess
N. II (right/left) :
Acies visus : difficult to assess
Color blindness : difficult to assess
Campus visus : difficult to assess
Funduscopy : bilateral papilla atrophy
N.III-IV-VI (right/left) : Pupil : round, diameter
Eyebals position : central 3mm/3mm, isochoric
 Ptosis : +/+
 Exo/endoftalmus: -/- Light relfex :
 Diplopia : difficult to -Direct : -/ -
assess -Indirect : - / -
 Eye movements : -Acomodation: difficult to
difficult to assess assess
N. V (right/left) N.VII (right/left)
Motor  Facial expression : simetris
 Open mouth : difficult to  Frowning : difficult to
assess assess
 Closing eye : difficult to
 Jaw movement: difficult to assess assess
 Chewing : difficult to assess  Inflate cheek : difficult to
Sensoric assess
 Opthalmic : difficult to  Showing teeth : difficult to
assess assess
 Pouting lips : difficult to
 Maxilar : difficult to assess
assess
 Taste of 2/3 tongue: difficult to
 Mandibula : difficult to assess
assess
• Corneal reflex : +/+
• Maseter reflex : difficult to
N. VIII (right/left) N. IX-X (right/left)
N. Vestibular  Sound (aphony/dysphony/normal):
 Nystagmus : -/- difficult to assess
 Swallow : difficult to assess
 Vertigo : difficult to assess
 Cough : difficult to assess
 Balance : difficult to assess
 Pharyngeal reflex: difficult to assess
 N. Cochlear
 Arch of pharyng
 Tinitus : difficult to assess
 Rest : symmetric, center
 Finger movement: difficult to assess uvula
 Schwabach test: difficult to assess  Phonation : symmetric, center
 Rinne test : difficult to assess uvula
 Weber test : difficult to assess
N. XI (right/left) N. XII (right/left)
 Turning head (M.  Dysarthria : difficult to
assess
Sternokleidomastoideus):
difficult to assess  Tongue position
Inside mouth : center
Out of mouth : difficult to
 Elevate shoulder (M. Trapezius) assess
: difficult to assess
 Tongue movement
To the right : difficult to
assess
To the left : difficult to
assess
 Fasiculation : difficult to
assess
 Athrophy :-
 Muscle strength (right/left) :
 Left spastic lateralization
Hands:
Upper arms • Flexion : difficult to assess
 Ante flexion : difficult to assess • Extension : difficult to assess
 Retro flexion : difficult to assess
 Abduction : difficult to assess
Finger
 Adduction : difficult to assess
• Flexion : difficult to assess
• Extension : difficult to assess
Lower arms
• Abduction: difficult to assess
 Flexion : difficult to assess
 Extention : difficult to assess • Adduction: difficult to assess
Upper limbs
 Ante flexion : difficult to Foot:
assess
• Flexion : difficult to assess
 Retro flexion : difficult to
assess • Extension : difficult to assess
 Abduction : difficult to Finger
assess • Flexion : difficult to assess
 Adduction : difficult to • Extension : difficult to assess
assess
• Abduction: difficult to assess
Lower limbs
• Adduction : difficult to assess
 Flexion : difficult to
assess
 Extention : difficult to Walking: difficult to assess
assess
 Biceps : +++/+++
 Triceps : +++/+++
 Knee : +++/+++
 Ankle : +++/+++

 Abdomen skin :
 Upper : +/+
 Middle : +/+
 Lower : +/+

 Muscle of abdomen: +
 Hoffman Trommer : -/-
 Babinski : -/-
 Chaddock : -/-
 Oppenheim : -/-
 Gordon : -/-
 Schaeffer : -/-
 Clonus • Trophic :
 Knee : -/- • Arms: normotrophy
 Heel : +/+ • Legs: normotrophy

 Tonus : normotonus
Arms:
 At rest : normo/normo
 passive : spastic +/+, rigids -

Legs :
 At rest : normo/normo
 Passive : spastic - , rigid -
Static:
 Sit : difficult to assess
 Stand up : difficult to assess
 Intention tremor : difficult to assess
 Disdiadokokinesia : difficult to assess
 Rebound Phenomenon : difficult to assess

Dynamic :
 Finger-finger : difficult to assess
 Finger-nose : difficult to assess
 Ankle-knee : difficult to assess
Exteroceptive[tactile, temperature, pain]: Autonomic system
 Arms : difficult to assess • Micturition : (+) on catheter
 Legs : difficult to assess • Defecation :-
 Body : difficult to assess • Sweat :+
Propioceptive:
 positional : difficult to assess
 vibration : difficult to assess
 2 point discrimination : difficult to assess
Cognitive function • Regretion sign

 Afasia motor : difficult to assess • Glabelar reflex :-

 Afasia sensor : difficult to assess • Snout reflex :-
 Memory function : difficult to assess • Grasp reflex :-
 Apraksia : difficult to assess
 Male, 22 years, with loss of consciousness since 7 days prior. Patient also had
decreasing oral intake since 7 days prior which worsening since 2 days that he
took no oral intake (food and water). The patient normally speak before 7 days
prior, but speak less (1-2 words) since 7 days, and didn’t speak since 2 days.
 Patient had experienced similarly in 2015 and 2016. He then diagnosed as having
non-communicant hydrocephalus and underwent VP-shunt operation in 2015, 2016.
 No family history having similar complaints.
 General condition : severly ill
 consciousness : E2M5V2,
stupor
 Cooperation : not cooperative  Neurological exam :
 Neck stiff
 Body type : athletics
 N. III lesion impression
 Body height, weight : 180 cm, 70 kg   Physiological reflex
BMI= 21.6 km/m2
+++/+++/+++/+++
 Vital sign:  Clonus: Heel: +/+
 Blood pressure : 130/70 mmHg
 Pulse rate : 64 times/ min.  Tonus : normotonus
(regular, adequate ,full) • Arms:
 Respiration rate : 20 times/ min.  At rest : hyper/hyper
 temperature : 36,30C (Normal =  passive : spastic +/+, rigids -
36,50C – 37,50C)
 O2 saturation : 98% • Legs :
 General examination : cold akral  At rest : normo/normo
 Passive : spastic - , rigid -
 Clinical : neck stiff, N. III lesion impression, physiological reflex
+++/+++/+++/+++, clonus of heel +/+, hypertonic +/+/-/-, spastic +/+/-/-
 Topic : medulla oblongata, mesencephalon
 Etiology : SOL
 Pathology : pendesakkan, edema

 Working Diagnosis
 Male, 22 years old, with N. III lesion impression, physiological reflex
+++/+++/+++/+++, clonus of heel +/+, hypertonic +/+/-/-, spastic +/+/-/- e.c
suspect cerebral SOL e.c suspect posterior fossa tumor e.c germinoma
 Tuberculoma, suspect immunocompromised
 Meningitis, suspect immunocompromised
 Contrast brain MRI (if not possible : contrast brain CT scan)
 Routine blood test
 Electrolyte
 Blood glucose test
 LED
 Intensive care unit
 Bed rest + head up 30⁰
 IVFD NaCl 0.9% 500 ml/12 jam
 Install nasogastric tube
 Ceftriaxone 2x2 gram IV
 Dexamethasone 4x10 mg IV
 Paracetamol 3x 1000 gram IV
 Pantoprazole 2x40 mg IV
 Consult to neurosurgery specialist
 Quo Ad Vitam: dubia ad malam
 Quo Ad Functionam : malam
 Quo Ad Sanationam : malam
DARAH RUTIN
Hemoglobin 14.5 12,5 – 16,1 g/dL
Hematokrit 41 36 – 47 %
Leukosit 7,1 4.0 – 10,5 ribu/uL
Eritrosit 4,94 4,0 – 5,2 Juta/ uL
Trombosit 397 150 – 400 ribu/uL
Diff Count
Basofil 0 0-2 %
Eosinofil 2 0-6 %
Batang 4 0-5 %
Segmen 76 40-70 %
Limfosit 12 20-50 %
Monosit 6 4-8 %
MCV 81,6 79-93,3 fL
MCH 29,4 26,7-31,9 Pg
MCHC 336,0 32,3-35,9 g/dL
KIMIA KLINIK
Gula Darah Sewaktu 86 60 – 140 mg/dL

FUNGSI GINJAL
Ureum 35 7,0 – 18,0 mg/dL
Kreatinin 1,0 0,5 – 1,0 mg/dL
eGFR 98,42 >60 ml/menit
FUNGSI HEPAR
SGOT 16 0-31 U/l
SGPT 9 0-31 U/l
ELEKTROLIT
Natrium 133 134-146 mmoL/L
Kalium 4,80 3.3-4.6 mmoL/L
Kalsium 1,2 1.09-1.3 mmoL/L
Klorida 98 96-108 mmoL/L
CAIRAN TUBUH
Uribolinogen Positif 2 Negatif mmoL/L
Keton Positif 1 Negatif mmoL/L
 LED = 11 mm/jam
 CT scan kepala tanpa kontras tampak
massa solid luas, sebagian berkalsifikasi
yang meliputi vermis cerebellum, pons,
mesencephalon, periventrikel 4-3-lateralis
bilateral dan corpus callosum dengan
pendesakan ventrikel lateralis kanan dan
slight midline shift ke kiri serta herniasi
peg cerebellum
 Infark pada thallamus kiri dengan suspek
edema/lesi ischemia periventrikel lateralis
bilateral-cerebellum
 Terpasang VP shunt insitu bi-ventrikel,tak
tampak hidrocephalus
25/6/2017
 Tampak enhanced mass luas, sebagian
berkalsifikasi yang meliputi vermis
cerebellum, pons, mesencephalon,
periventrikel 4-3-lateralis bilateral dan corpus
callosum dengan pendesakan ventrikel
lateralis kanan dan slight midline shift ke kiri
serta herniasi peg cerebellum
 Infark pada thalamus kiri dengan suspek
edema/ lesi ischemia periventrikel lateralis
bilateral-cerebellum
 Terpasang VP shunt insitu bi-ventrikel, tak
tampak hydrocephalus

25/6/2017
Hitung jenis satuan
PMN 30 %
MN 70 %
 Objectives
• Definition
• Types
• Clinical Presentations
• Diagnosis
• Treatment
 Definition
These are lesions which expand in volume to displace normal
neural structures & may lead to increase in intra – cranial
pressure.
 Intracranial Mass Lesions – Differential Considerations
1. Primary Brain Tumor/Lesion (non-neoplastic cysts, congenital, etc.)
2. Metastatic Lesion
3. Trauma (subdural, extra-dural haematomas)

Metastatic
Lesions
Intracranial
Bleed
Primary BrainTumor
4. Parasitic (Cysticercosis, Hydratid cyst, Amebicabscess)
5. Vascular (aneurysms, AVMs, stroke, etc.)
6. Inflammatory (Abscess, Tuberculoma, Syphilitic gumma,
fungal Granulomas)

Angiogram:AVM Tuberculoma
 Tumors
• Gliomas
• Meningiomas
• Schwannoma
Primary • PNET
• Pituitary
• Pineal

• Metastatic
Secondary • Lung
• Kidney
• Breast
 Clinical Presentations
Headache

Increased ICP Seizures

Papilledema Personality
Changes

Focal Deficits
 GLIOMAS Meningiomas Schwannomas

• Site • Middle age • Hearing

• Seizures • Slow growing Problems
• Language • Headache • Vertigo
Difficulty • Seizures • Headache
• Headache • Facial weakness/numb
• Behavioral
Changes
• Hemiparesis
Pituitary Adenoma
Penial Region

• Headache • Headache
• Visual Effects • Hydrochephalus
• Endocrine • Perinaud’s
Syndrome
 Diagnosis
• Physical Examination Findings
• CTScan Brain
• MRI Brain
• MRAngiography
• Laboratory Studies ( CBC,ESR,LFTS,Tumor Makers, etc)
• Biopsy
 Gliomas
• Most common Primary BrainTumors
Grade III
Astrocytoma
Meningioma
Acoustic Schwannoma
Pineal Gland Tumor
Pituitary Adenomas
 Treatment
Varies on histology of various tumors
Craniotomy+ Craniotomy +
Biopsy Excision

Radiotherapy
Chemotherapy

Palliative
 • Benign: Surgical Excision
Gliomas • Malignant: Surgical Excision + Radiotherapy

• Surgical Resection +/- Radiotherapy

Meningiomas

• Surgical resection >3cm

Schwannoma
 • Surgical: (Trans-shenoidal Transcranial)
• Pharmacological Rx (Dopamine agonist
Pituitary Somatostatin analogs)
• Radiotherapy

• Depends on histology
Pineal • Resection and Radiotherapy

• For solitary lesion or less than 4 lesions all < 3 cm. – biopsy if
undiagnosed, plus GammaKnife

Mets • For > 3 cm. tumor, surgery followed by WBRT

• For > 4 lesions, biopsy for diagnosis, plus whole
brain radiation therapy
 Trauma
Intracranial haematomas
I. Extra dural haematomas :-
– between the dura &the skull
– middle meningeal artery
– Common site is temporal fossa.

• Progressive deterioration of level of

Clinical Features consciousness
• Lucid Interval
EDH • Pupillary changes :- called
Hutchinson’s pupillary reaction.
INVESTIGATIONS:
CT Biconvex hyperdense lesion
MRICEREBRALANGIOGRAPHY

Treatment:
Surgical evacuation followed by
Craniotomy
• II. Subdural haematomas:-
– between the dura and the arachnoid.
– Common causes are bleeding from superficial
veins or venoussinuses.
– Anticoagulant treatment predispose to intracranial
bleeding and subdural haematoma.
• Clinical features:
– Acute : Clinical features are similar to extradural hematoma.
– Chronic : Dementia, altered behaviour, psychiatric manifestations or
focal neurological deficits may develop.
– In middle aged headache, contralateral hemiplegia,
papilledema
– children: vomiting, restlessness. Irritability, refusal to feed, anaemia,
seizures and failure to thrive.
 DIAGNOSIS:
•Acute-concave hyperdense lesion on CT
•Chronic- 0-10days(hyperdense)
10days-2wks(isodense)
>2wks(hypodense) lesions on CT.

Treatment:
•Craniotomy for Acute Subdural Hematoma
•Surgical evacuation by Burr hole for chronic
subdural hematoma.
 BrainAbcess

• Mostly single may be multiple

• Majority Supratentorial, 10%infratentorial
• Metastatic:
• – hematogenesis,direct spread from adjacent structures or
penetrating brain injury.
 Clinical presentation
• Neurologic:
– Raised ICP(nausea,vomiting)
– Focal neurologic deficits(hemi-pariasis)
– Epileptic seizures
• Systemic toxicity(Fever,malaise)
• Symptoms of primary focus
infection(Otitis,sinusitis etc)
 Diagnosis
• Method of Choice- CTscan of Brain
– Ring enhancing Lesion
• Peripheral Blood smear
– Leukocytosis
– Raised ESR
 Treatment
• SPECIFICTREATMENT
– Anti-microbial therapy
• MEASURESTOREDUCEICP
– Drainage of abscess
– Mannitol
– corticosteroids
• ANTI-EPILEPTICTREATMENT
– Phenytoin
– Carbamazapine
 Surgical Treatment
• GOALS:
– Obtain pus for culture & sensitivity
– Decrease ICP
• TECHNIQUES:
– Burr hole & aspiration
– Excision & craniotomy for recurrent,thickwalled brain abscess.
 Intracranial Tuberculoma
• Mostly in developing countries causedby Micro-
bacterium tuberculus.
• Nodular or irregular avascular massesof variable sizes
surrounded by edema.
• Frequently multiple
• Common location: sub-cortical in cerebral hemisphere.
 Clinical Presentation
Symptoms & signs of progressiveintracranial SOL:
– Raised ICP
– Focal neurologic deficits
– Seizures etc
– General malaise,fever in 50%patients.
 Investigation
• Lab work-up
– Leukocytosis
– ESR-raised or normal
– Mantox test- often+ve
• Chest X-ray
• Plain skull X-ray
• CT& MRI- Investigation of choice
Hyper-dense masses with ring andsurroundind edema,
often”Target sign”
 TREATMENT
• Anti-tubercular therapy
• Measures to reduceICP
• Control seizure
 SURGICALTREATMENT

INDICATIONS:
Intracranial lesions could not bespecified Progressive neurological detoriation

ALTERNATIVES:
Excision:
CSF-shunting: mandatory in complicating obstructive hydrocephalus
DAFTAR PUSTAKA
1. Intracranial Space Occupying Lesions - Review of 386 Cases [Internet]. Available
from:http://www.jpma.org.pk/full_article_text.php?article_id=4690
2. Irfan A, Qureshi A. Intracranial space occupying lesions--review of 386 cases. J Pak Med
Assoc. 1995 Dec;45(12):319–20.
3. Analytic study of clinical presentation of intracranial space-occupying lesions in adult
patients - viewcontent.cgi [Internet]. Available from:
https://ecommons.aku.edu/cgi/viewcontent.cgi?referer=https://www.google.com/&https
redir=1&article=1070&context=pjns
4. Kamble RB, Jayakumar PN, Shivashankar R. Role of dynamic CT perfusion study in
evaluating various intracranial space-occupying lesions. Indian Journal of Radiology and
Imaging. 2015 Apr 1;25(2):162.
5. Dawoud. Intracranial space occupying lesions: could differentiation be reached without
biopsy? [Internet]. Available from: http://www.tdj.eg.net/article.asp?issn=1110-
1415;year=2016;volume=44;issue=1;spage=23;epage=32;aulast=Dawoud
6. Epelman M, Daneman A, Blaser SI, Ortiz-Neira C, Konen O, Jarrín J, et al. Differential
Diagnosis of Intracranial Cystic Lesions at Head US: Correlation with CT and MR Imaging.
RadioGraphics. 2006 Jan 1;26(1):173–96.