CASE REPORT

INTRACRANIAL SPACE OCCUPYING LESION

SENIOR CLINICAL CLERKSHIP

By :
Cindy Kesty, S.Ked

04054811416078

Mohammad Areza Bin Boonie, S.Ked

04084811416120

Advisor

dr. H. A. Rachman Toyo, Sp.S(K)

NEUROLOGY DEPARTMENT
MEDICAL FACULTY OF SRIWIJAYA UNIVERSITY
MOHAMMAD HOESIN GENERAL HOSPITAL
PALEMBANG
2015

CERTIFICATION PAGE
Case Report

INTRACRANIAL SPACE OCCUPYING LESION

Presented by:

Cindy Kesty, S.Ked

04054811416078

Mohammad Areza Bin Boonie, S.Ked

04084811416120

Has been accepted as one of requirements in undergoing senior clinical clerkship

period of 7th December 2015 11th January 2016 in Neurology Department
Medical Faculty Sriwijaya University Mohammad Hoesin General Hospital
Palembang.
Palembang, December 2015
Advisor,

Dr. H. A. Rachman Toyo, Sp.S(K)

FOREWORD
The authors offer our praise and gratitude to God for His blessings,
mercy and grace so that this case entitled "Intracranial Space Occupying Lesion"
can be done well. This paper aims as one of the requirements to fulfill the task in
the Neurology Department of

Dr. Mohammad Hoesin General Hospital

Palembang .
The authors would like to thank dr. H. A. Rachman Toyo, Sp.S(K) who
has guided us in finishing this paper.
We realize that this paper still has many shortcomings. Therefore, all
criticism and suggestions for improvement of this paper will be received gladly.
Finally, we hope this paper can provide many advantages to all people especially
health care providers.

Palembang, December 2015

Author

CONTENTS
Cover.................................................................................................................i
Certification Page.............................................................................................ii
Foreword...........................................................................................................iii
Contents............................................................................................................iv
Glossary............................................................................................................v
List of Figures...................................................................................................vi
List of Tables....................................................................................................vii
Chapter I Patients Status..................................................................................1
Chapter II Resume ...........................................................................................11
Chapter III Case Analysis.................................................................................23
Chapter IV Literature Review...........................................................................27
Appendix...........................................................................................................44
References.........................................................................................................46

GLOSSARY
B
CSF
E
ICP
ICHD
L
NCCN
NF-2
SOL

: Babinsky
: Cerebrospinal Fluid
: Enough
: Intracranial Pressure
: International Classification Headache Disorders
: Less
: National Comprehensive Cancer Network
: Neurofibromatosis Type 2
: Space Occupying Lesion

LIST OF TABLES

Table 1. Age-Specific Frequency of Tumor Types with Age............................31

Table 2. Main Categories of The WHO Brain Tumor Classification...............32
Table 3. Symptoms and Signs Associated with Meningiomas.........................40

LIST OF FIGURES
Fig 1. A schematic representation of the astrocytes and endothelial cells
of the capillary wall in the normal state and in vasogenic edema....................36
Fig 2. Common location of meningioma..........................................................38

Fig 3. Histopathology.......................................................................................39
Fig 4. MRI with gadolinium.............................................................................41
Fig 5. Gadolinium-enhanced MRI of meningioma...........................................41
Fig 6. NCCN Guidelines for Meningioma.......................................................42

CHAPTER I
PATIENTS STATUS
IDENTIFICATION
Name

:Mrs. NA

Age

:56 years old

Sex

:Female

Occupation

: Housewife

Address

: Air Putih Air Plakat Tinggi Muba

Religion

: Moslem

Admitted

: 13th December 2015

ANAMNESIS (Autoanamnesis, 19th December 2015)

Patient was admitted to Neurologic Department of Mohammad Hoesin
General Hospital because of severe headache.
Since 3 months before admission, patients experienced headache in the
back of the head and spread to all regions of the head, felt like as being bound
with moderate to severe intensity. Pain is felt increasingly heavier during waking
up, coughing and sneezing, with frequency 3-5 times per day, and duration
approximately 30 minutes. Pain is less felt if patient takes medicine from
paramedics (patient forgets the medicines name) and sleep. Two weeks before
admission, pain is felt increasingly heavier with moderate to severe intensity, with
frequency 4-6 times per day, and duration of approximately 30 minutes. Patient
also has double vision (+), sometimes nausea and vomitting. Three days before
admission, headache is felt very annoying, when waking up, pain is getting worse,
vomitting (+), projectile, the content is what is eaten. Weakness in half of the
body (-), asymmetric mouth (-), seizure (-), loss of consciousness (-). Patient still
understands and can express good thoughts, oral language, writting and gestures.
History of family planning (+), implant for 5 years (from 1989 until 1994)
and injection for approximately 1 year. History of long cough (-), discharge from
the ear (-), cavity in teeth (+), fever (-), hypertension (+) controlled, diabetes (-).
History of falling from motorbike (+) 1 year ago, with the back of the head
crushing asphalt, loss of consciousness (-), headache (+), nausea (-) and vomitting
(-).
This disease occurs for the first time.
PHYSICAL EXAMINATION (19th December 2015)
PRESENT STATE

Internal State
Conciousness

: GCS 15 E4M6V5

Heart

: No abnormality

Nutrition

: Sufficient

Lungs

: No abnormality

Temperature

: 36,7oC

Liver

: No abnormality

Pulse

: 84 beats/min

Spleen

: No abnormality

Respiratory rate

: 22 times/min

Extremities

: See neurological state

Blood pressure

: 170/100 mmHg

Genital

: Normal

Psychiatric state

Facial Expression

Attitude

:Cooperative

Attention

: Yes

: Appropriate

Psychological contact : Yes

Neurological state
Head

Deformity

: No

Shape

: Normocephali

Fracture

: No

Size

: Normal

Fracture pain

: No

Symetric

: Yes

Vessel

: No widening

Hematome

: No

Pulsation

: No

Tumor

: No
Deformity

: No
: No

Neck
Position

: Normal

Tumor

Torticolis

: No

Vessels

Nuchal Rigidity

: No

: No widening

CRANIAL NERVES
N.I: Olfactory nerve

Right

Left

Smelling

Normal

Normal

Anosmia

No

No

Hyposmia

No

No

Parosmia

No

No

Right

Left

Visual acuity

6/6

6/6

Visual Field

V.O.D

V.O.S

N.II: Optical nerve

Anopsia

No

No

Hemianopsia

No

No

Oculi fundus

Papil Edema

No

No

Papil Athropy

No

No

Retinal bleeding

No

No

Right

Left

Yes

Yes

Normal

Normal

No

No

No

No

No

No

No

No

No

No

N.III: Occulomotorius,
N.IV: Trochlearis, and
N.VI: Abducens nerves
Diplopia
Eyes gap
Ptosis
Eyes position

Strabismus

Exophtalmus

Enophtalmus

Deviation conjugae
-1

Eyes movement
Pupil

Round

Round

10

Shape

Size

Isochor/anisochor

Midriasis/miosis

Light reflex

direct

consensuil

accommodation

3mm
Isochor

3mm
Isochor

+/+ Normal

+/+ Normal

Positive

Positive

Positive

Positive

Positive

Positive

No

No

Right

Left

Normal

Normal

No

No

Yes

Yes

Normal

Normal

Normal

Normal

Normal

Normal

Argyl Robertson
N.V: Trigeminus nerve
Motoric

Biting

Trismus

Corneal reflex

Sensory

Forehead

Cheek

Chin
Right

Left

Symmetrical

Symmetrical

Lagophthalmus (-)

Lagophthalmus (-)

Frowning

Normal

Normal

Eyes closing

Normal

Normal

Nasolabial fold

Symmetrical

Symmetrical

Facial shape

Symmetrical

Symmetrical

Normal

Normal

N.VII: Facialis nerve

Motoric

Giggling

Rest

Speaking/whistling

11

Sensory

2/3 anterior tounge

Autonomy

Salivation

Lacrimation

Chvosteks sign

N.VIII: Statoacusticus nerve

Cochlearis nerve
Whispering
Hour ticking

No abnormalities

No abnormalities

No abnormalities

No abnormalities

No

No

Right

Left

Normal

Normal

Normal

Normal

No lateralization

No lateralization

Normal

Normal

No

No

No

No

Right

Left

Symmetrical

Symmetrical

At the center, no disorder

At the center, no disorde

No

No

No

No

Normal

Normal

Yes

Yes

Yes

Yes

Yes

Yes

Yes

Yes

Normal

Normal

Weber test
Rinne test
Vestibularis nerve
Nystagmus
Vertigo
N.IX: Glossopharingeus, and
N.X: Vagus nerves
Pharyngeal arch
Uvula
Swallowing disorder
Hoarsing/nasalising
Heart beat
Reflex

Vomiting

Coughing

Occulocardiac

12

Caroticus sinus

Sensory

1/3 posterior tounge

N.XI: Accessorius Nerve

Right

Left

Shoulder Raising

Normal

Normal

Head Twisting

Normal

Normal

N.XII: Hypoglossus Nerve

Right

Tounge Showing

Left

No deviation

No deviation

Fasciculation

No

No

Papil Athrophy

No

No

Dysarthria

No

No

Right

Left

Motion

Sufficient

Sufficient

Power

Tones

Normal

Normal

MOTORIC
Arms

Physiological Reflex

Biceps

Normal

Normal

Triceps

Normal

Normal

Radius

Normal

Normal

Ulna

Normal

Normal

No

No

No

No

No

No

No

No

Right

Left

Pathological Reflex

Hoffman Tromner

Leri

Meyer

Trofik

13

LEG

Sufficient

Sufficient

Motion

Power

Normal

Normal

Negative

Negative

Negative

Negative

Physiological reflex

Normal

Normal

KPR

Normal

Normal

APR
Negative

Negative

Negative

Negative

Negative

Negative

Negative

Negative

Negative

Negative

Negative

Negative

Negative

Negative

Negative

Negative

Abdominal skin reflex

Negative

Negative

Upper

Negative

Negative

Middle

Negative

Negative

Lower

Tones
Clonus

Thigh

Foot

Pathological reflex

Babinsky

Chaddock

Oppenheim

Gordon

Schaeffer

Rossolimo

Mendel Bechterew

Tropik
SENSORY
No abnormalities
VEGETATIVE FUNCTION
Micturition

: No abnormality

Defecation

: No abnormality

14

VERTEBRAL COLUMN
Kyphosis

: No

Tumor

: No

Lordosis

: No

Meningocele

: No

Gibbus

: No

Hematome

: No

Deformity

: No

Tenderness

: No

MENINGEAL REFLEX
Right

Left

Nuchal Rigidity

No

No

Kerniq

No

No

Lasseque

No

No

Brudzinsky

Neck

No

No

Cheek

No

No

Symphisis

No

No

Leg I

No

No

Leg II

No

No

GAIT AND BALANCE

Gait

Balance and Coordination

Ataxia

: No

Romberg

: No abnormality

Hemiplegic

: No

Dysmetri

: No abnormality

Scissor

: No

finger finger

: No abnormality

Propulsion

: No

finger nose

: No abnormality

Histeric

: No

heel - heel

: No abnormality

Limping

: No

Rebound phenomenon: No abnormality

Steppage

: No

Dysdiadochokinesis : No abnormality

Astasia-Abasia: No

Trunk Ataxia

: No abnormality

Limb Ataxia

: No abnormality

15

ABNORMAL MOVEMENTS
Tremor

: No

Chorea

: No

Athetosis

: No

Ballismus

: No

Dystoni

: No

Myoclonus

: No

LIMBIC FUNCTION
Motoric aphasia

: No

Sensoric aphasia

: No

Apraksia

: No

Agraphia

: No

Alexia

: No

Nominal aphasia

: No

LABORATORY FINDINGS
BLOOD (8th January 2015)
Hematology
-

Hemoglobin 15,2 g/dl

Erythrocyte 5,22 x 106/mm3
Leukocyte 7000/mm3
Hematocrite 45%
Thrombocyte 233,000/microlitre
Diff. Count 0/7/58/27/8

Blood Chemist
- CK-NAC - CK-MB Renal
-

Ureum 18 mg/dl
Creatinin 0,75 mg/dl

Electrolyte
- Ca 9,4 mg/dl

16

- Na 138 mEq/L
- K 3,3 mEq/L
- Cl 111 mmol/L
RADIOLOGY EXAMINATION
Cranium X- Ray

: Not performed

Chest X- Ray

: Performed,

result:

heart

enlargement (inspiration is not

enough)
Vertebralis X-Ray

: Not performed

Electroencephalography

: Not performed

Electroneuromyography

: Not performed

Electrocardiography

: Not performed

Arteriography

: Not performed

Pneumography

: Not performed

Head CT-Scan

: Performed, result: right parietal

SOL

Others

: Not performed

CHAPTER II
RESUME
IDENTIFICATION
Name

:Mrs. NA

Age

:56 years old

17

Sex

:Female

Occupation

: Housewife

Address

: Air Putih Air Plakat Tinggi Muba

Religion

: Moslem

Admitted

: 13th December 2015

ANAMNESIS ((Autoanamnesis, 19th December 2015)

Patient was admitted to Neurologic Department of Mohammad Hoesin
General Hospital because of severe headache.
Since 3 months before admission, patients experienced headache in the
back of the head and spread to all regions of the head, felt like as being bound
with moderate to severe intensity. Pain is felt increasingly heavier during waking
up, coughing and sneezing, with frequency 3-5 times per day, and duration
approximately 30 minutes. Pain is less felt if patient takes medicine from
paramedics (patient forgets the medicines name) and sleep. Two weeks before
admission, pain is felt increasingly heavier with moderate to severe intensity, with
frequency 4-6 times per day, and duration of approximately 30 minutes. Patient
also has double vision (+), sometimes nausea and vomitting. Three days before
admission, headache is felt very annoying, when waking up, pain is getting worse,
vomitting (+), projectile, the content is what is eaten. Weakness in half of the
body (-), asymmetric mouth (-), seizure (-), loss of consciousness (-). Patient still
understands and can express good thoughts, oral language, writting and gestures.
History of family planning (+), implant for 5 years (from 1989 until 1994)
and injection for approximately 1 year. History of long cough (-), discharge from
the ear (-), cavity in teeth (+),fever (-), hypertension (+) controlled, diabetes
(-).History of falling from motorbike (+) 1 year ago, with the back of the head
crushing asphalt, loss of consciousness (-), headache (+), nausea (-) and vomitting
(-).
This disease occurs for the first time.
PHYSICAL EXAMINATION (19th December 2015)

18

General Examination:
Conciousness (GCS score)

: GCS 15 (E4M6V5)

Temperature

: 36,7oC

Pulse

: 84 beats/min

Respiratory rate

: 22 times/min

Blood pressure

: 170/100 mmHg

Neurologic Examination:
N III

: round pupil, isocor, light reflex +/+, diameter 3 mm

N VII : symmetric forehead wrinkles, no lagophthalmus, normal mouth angle,

symmetric nasolabialis fold
N XII : no tongue deviation, no papil atrophy, no fasciculation, no disarthria
Motoric function

Right arm

Left arm

Right leg

Left leg

Sufficient

Sufficient

Motion

Sufficient

Sufficient

Power

Tonus

Normal

Normal

Normal

Normal

Klonus
Physiological reflex Normal
Pathological reflex

Normal

Sensory function

: no abnormality

Limbic function

: no disorder

Vegetative function

: no abnormality

Meningeal signs

: no abnormality

Normal
-

Normal
-

Abnormal movements: no abnormality

Gait and balance

: no abnormality

DIAGNOSIS
Clinical diagnosis

Chronic cephalgia

19

Parese N.VI sinistra

Topical diagnosis :
-

Right temporoparietal lobe

Etiological diagnosis :
-

Intracranial SOL dd/ - tumor intracranial

- abscess cerebri

Additional diagnosis:
-

Tinea cruris et corporis

Hypertension grade II
Gangrene pulpa and radix
Pulpitis

MANAGEMENT
Non-pharmacology

- Head elevation 30o

- Diet: usual rice and low salt 1500 kcal
- Tooth extraction
Pharmacology

IVFD RL gtt xx/minute

Inj. Dexamethason 3 x 5 mg (IV)

Inj. Omeprazole 1 x 40 mg (IV)
Neurobion 1 x 5000 mcg (PO)
Tramadol 3 x 1 amp (IV)
Candesartan 1 x 8 mg (PO)

Therapy from Dermatovenereology Department:

Planning

Ketoconazole cream 2% twice per day

Loratadine 1 x 10 mg (PO)
:

MRI (30th December 2015)

20

PROGNOSIS
Quo ad vitam

: Dubia

Quo ad functionam

: Dubia

FOLLOW UP
Date
20th

Headache felt heavier

Planning
Non-pharmacology :

Dec

General Examination

- Head elevation 30o

Conciousness : GCS 15 (E4M6V5)

- Diet: usual rice and low salt

2015

Blood pressure : 190/120 mmHg

1500 kcal

Pulse

- Tooth extraction

: 84 beats/min

Respiratory rate : 18 times/min

Temperature

: 36,3oC

Pharmacology :

NRS

:5

IVFD RL gtt xx/minute

Inj. Dexamethason 3 x 5 mg

(IV) IV
Inj. Omeprazole 1 x 40 mg

(IV)
Neurobion 1 x 5000mcg (PO)
Tramadol 3 x 1 amp(IV)
Candesartan 1 x 8 mg (PO)

Neurologic Examination: stqa

CD : - Chronic cephalgia
A

- Parese N.VI sinistra

TD : Right temporoparietal lobe
ED : SOL intracranial DD/
-

Tumor intracranial

AD : - Tinea cruris et corporis

- Hypertension grade II
- Gangrene pulpa and radix
- Pulpitis

Therapy

from

Dermatovenereology
Department:
-

Ketoconazole cream 2% twice

21th

Headache felt less

per day
- Loratadine 1 x 10 mg (PO)
Non-pharmacology :

Dec

General Examination

- Head elevation 30o

Conciousness : GCS 15 (E4M6V5)

- Diet: usual rice and low salt

2015

Blood pressure : 170/100 mmHg

Pulse

1500 kcal

: 92 beats/min

Respiratory rate : 18 times/min

Pharmacology :

21

Temperature

: 37,0oC

IVFD RL gtt xx/minute

NRS

:3

Inj. Dexamethason 2 x 5 mg

(IV) I
Inj. Omeprazole 1 x 40 mg

(IV)
Neurobion 1 x 5000mcg (PO)
Tramadol 3 x 1 amp (IV)
Candesartan 1 x 8 mg (PO)
Amlodipine 1 x 10 mg (PO)

Neurologic Examination: stqa

A

CD : - Chronic cephalgia
- Parese N.VI sinistra
TD : Right temporoparietal lobe
ED : SOL intracranial DD/
-

Tumor intracranial

AD : - Tinea cruris et corporis

- Hypertension grade II
- Gangrene pulpa and radix
- Pulpitis

Therapy

from

Dermatovenereology
Department:
-

Ketoconazole cream 2% twice

22th

Headache felt less

per day
- Loratadine 1 x 10 mg (PO)
Non-pharmacology :

Dec

General Examination

- Head elevation 30o

Conciousness : GCS 15 (E4M6V5)

- Diet: usual rice and low salt

2015

Blood pressure : 150/100 mmHg

Pulse

1500 kcal

: 90 beats/min

Respiratory rate : 20 times/min

Pharmacology :

Temperature

: 36,5oC

IVFD RL gtt xx/minute

NRS

:2

Inj. Dexamethason 2 x 5 mg

(IV) II
Inj. Omeprazole 1 x 40 mg

(IV)
Neurobion 1 x 5000mcg (PO)
Tramadol 3 x 1 amp (IV)
Candesartan 1 x 8 mg (PO)
Amlodipine 1 x 10 mg (PO)

Neurologic Examination: stqa

A

CD : - Chronic cephalgia
- Parese N.VI sinistra
TD : Right temporoparietal lobe
ED : SOL intracranial DD/
-

Tumor intracranial

AD : - Tinea cruris et corporis

- Hypertension grade II
- Gangrene pulpa and radix
- Pulpitis

Therapy

from

Dermatovenereology
Department:
-

Ketoconazole cream 2% twice

per day

22

23th

Headache felt less

- Loratadine 1 x 10 mg (PO)
Non-pharmacology :

Dec

General Examination

- Head elevation 30o

Conciousness : GCS 15 (E4M6V5)

- Diet: usual rice and low salt

2015

Blood pressure : 150/100 mmHg

Pulse

1500 kcal

: 82 beats/min

Respiratory rate : 20 times/min

Temperature
NRS

: 36,5oC
:2

Pharmacology :
-

IVFD RL gtt xx/minute

Inj. Dexamethason 2 x 5 mg

(IV) III
Inj. Omeprazole 1 x 40 mg

(IV)
Neurobion 1 x 5000mcg (PO)
Tramadol 3 x 1 amp (IV)
Candesartan 1 x 8 mg (PO)
Amlodipine 1 x 10 mg (PO)

Neurologic Examination: stqa

A

CD : - Chronic cephalgia
- Parese N.VI sinistra
TD : Right temporoparietal lobe
ED : SOL intracranial DD/
-

Tumor intracranial

AD : - Tinea cruris et corporis

- Hypertension grade II
- Gangrene pulpa and radix
- Pulpitis

Therapy

from

Dermatovenereology
Department:
-

Ketoconazole cream 2% twice

24th

Vomit (+), headache felt heavier

per day
- Loratadine 1 x 10 mg (PO)
Non-pharmacology :

Dec

General Examination:

- Head elevation 30o

Conciousness :GCS 15 (E4M6V5)

- Diet: usual rice and low salt

2015

Blood pressure : 150/90 mmHg

Pulse

1500 kcal

: 87 beats/min

Respiratory rate : 24 times/min

Pharmacology :

Temperature

: 37,2oC

IVFD RL gtt xx/minute

NRS

:5

Inj. Dexamethason 2 x 5 mg

(IV) IV
Inj. Omeprazole 1 x 40 mg

(IV)
Neurobion 1 x 5000 mcg (PO)

Neurologic Examination: stqa

A

CD : - Chronic cephalgia

23

- Parese N.VI sinistra

TD : Right temporoparietal lobe

ED : SOL intracranial DD/
-

Therapy

Tumor intracranial

Department:

- Hypertension grade II
- Gangrene pulpa and radix
- Pulpitis
S

Dec
2015

Food

cant

go

from

Dermatovenereology

AD : - Tinea cruris et corporis

25th

Tramadol 3 x 1 amp (IV)

Candesartan 1 x 8 mg (PO)
Amlodipine 1 x 10 mg (PO)

inside,

Ketoconazole cream 2% twice

per day
- Loratadine 1 x 10 mg (PO)
loss Non-pharmacology :

consciousness

- Head elevation 30o

General Examination:

- Liquid diet and low salt 1800

Conciousness :GCS 11 (E3M5V3)

kcal

Blood pressure : 180/100 mmHg

- Applying nasogastric tube

Pulse

: 80 beats/min

Respiratory rate : 24 times/min

Pharmacology :

: 36,9oC

Temperature

Neurologic Examination:

IVFD RL gtt xx/minute

Inj. Dexamethason 3 x 5 mg

(IV) I
Inj. Omeprazole 1 x 40 mg

(IV)
Neurobion 1 x 5000 mcg (PO)
Tramadol 3 x 1 amp (IV)
Candesartan 1 x 8 mg (PO)
Amlodipine 1 x 10 mg (PO)
HCT 1 x 12,5 mg (PO)

morning
Ondansentron 4 mg (if vomit)

N.III: round pupil, isocor, d=3 mm/3

mm, light reflex +/+
N.VII: nasolabial fold symmetrical
N.XII: tongue deviation hard to be
evaluated
Motoric function
R
Motion
Power
Tonus
Clonus
Physiologi
c reflex
Pathologic

A
A L
L
No lateralization
N

N
N

N
N

N
N

N
-

Therapy

from

Dermatovenereology
Department:
-

Ketoconazole cream 2% twice

per day
Loratadine 1 x 10 mg (PO)

reflex

24

Sensoric function: cant be evaluated

Limbic function: cant be evaluated
Vegetative function: no abnormality
Meningeal signs: negative
Abnormal movement: negative
Gait and balance: cant be evaluated
CD : Loss of consciousness
TD : Right temporoparietal lobe
A

ED : SOL intracranial DD/

-

Tumor intracranial

AD : - Tinea cruris et corporis

26th

- Hypertension grade II
- Gangrene pulpa and radix
- Pulpitis
Loss of consciousness

Dec

General Examination

- Head elevation 30o

Conciousness :GCS 11 (E3M5V3)

- Liquid diet and low salt 1800

2015

Blood pressure : 150/100 mmHg

Pulse

Non-pharmacology :

kcal

: 83 beats/min

Respiratory rate : 25 times/min

: 36,8oC

Temperature

Pharmacology :
-

IVFD RL gtt xx/minute

Inj. Dexamethason 3 x 5 mg

(IV) II
Inj. Omeprazole 1 x 40 mg

(IV)
Neurobion 1 x 5000 mcg (PO)
Tramadol 3 x 1 amp (IV)
Candesartan 1 x 8 mg (PO)
Amlodipine 1 x 10 mg (PO)
HCT 1 x 12,5 mg (PO)

morning
Ondansentron 4 mg (if vomit)

Neurologic Examination:
N.III: round pupil, isocor, d=3 mm/3
mm, light reflex +/+
N.VII: nasolabial fold symmetrical
N.XII: tongue deviation hard to be
evaluated
Motoric function
R

Therapy

from

25

Motion
Power
Tonus
Clonus
Physiologi
c reflex
Pathologic

No lateralization
N

N
N

N
N

Dermatovenereology
Department:
-

Ketoconazole cream 2% twice

per day
Loratadine 1 x 10 mg (PO)

reflex
Sensoric function: cant be evaluated
Limbic function: cant be evaluated
Vegetative function: no abnormality
Meningeal signs: negative
Abnormal movement: negative
Gait and balance: cant be evaluated
CD : Loss of consciousness
A

TD : Right temporoparietal lobe

ED : SOL intracranial DD/
-

Tumor intracranial

AD : - Tinea cruris et corporis

27th

- Hypertension grade I
- Gangrene pulpa and radix
- Pulpitis
Loss of consciousness

Dec

General Examination

- Head elevation 30o

Conciousness :GCS 11 (E3M5V3)

- Liquid diet and low salt 1800

2015

Blood pressure : 160/100 mmHg

Pulse

: 37,1oC

Neurologic Examination: stqa

A

kcal

: 92 beats/min

Respiratory rate : 20 times/min

Temperature

Non-pharmacology :

CD : Loss of consciousness
TD : Right temporoparietal lobe

Pharmacology :
-

IVFD RL gtt xx/minute

Inj. Dexamethason 3 x 5 mg

(IV) III
Inj. Omeprazole 1 x 40 mg
(IV)

26

ED : SOL intracranial DD/

-

Tumor intracranial

AD : - Tinea cruris et corporis

- Hypertension grade I
- Gangrene pulpa and radix
- Pulpitis

Neurobion 1 x 5000 mcg (PO)

Tramadol 3 x 1 amp (IV)
Candesartan 1 x 8 mg (PO)
Amlodipine 1 x 10 mg (PO)
HCT 1 x 12,5 mg (PO)

morning
Ondansentron 4 mg (if vomit)

Therapy

from

Dermatovenereology
Department:
-

Ketoconazole cream 2% twice

28th

Loss of consciousness

per day
- Loratadine 1 x 10 mg (PO)
Non-pharmacology :

Dec

General Examination

- Head elevation 30o

Conciousness :GCS 11 (E3M5V3)

- Liquid diet and low salt 1800

2015

Blood pressure : 130/70 mmHg

Pulse

kcal

: 84 beats/min

Respiratory rate : 18 times/min

: 36,8oC

Temperature

Neurologic Examination:

Pharmacology :
-

IVFD RL gtt xx/minute

Inj. Dexamethason 3 x 5 mg

(IV) IV
Inj. Omeprazole 1 x 40 mg

(IV)
Neurobion 1 x 5000 mcg (PO)
Tramadol 3 x 1 amp (IV)
Candesartan 1 x 8 mg (PO)
Amlodipine 1 x 10 mg (PO)
HCT 1 x 12,5 mg (PO)

morning
Ondansentron 4 mg (if vomit)

N.III: round pupil, isocor, d=3 mm/3

mm, light reflex +/+
N.VII: nasolabial fold symmetrical
N.XII: tongue deviation hard to be
evaluated
Motoric function
R
Motion
Power
Tonus
Clonus
Physiologi

A
L
4

A
E
5
N

R
L
L
4

L
L
E
5
N
N

Therapy

from

Dermatovenereology
Department:
-

Ketoconazole cream 2% twice

c reflex

27

Pathologic

reflex
Sensoric function: cant be evaluated

per day
Loratadine 1 x 10 mg (PO)

Limbic function: cant be evaluated

Vegetative function: no abnormality
Meningeal signs: negative
Abnormal movement: negative
Gait and balance: cant be evaluated

CD : -Spastic type right hemiparese

-

Loss of consciousness

TD : Right temporoparietal lobe

ED : SOL intracranial DD/
-

Tumor intracranial

AD : - Tinea cruris et corporis

29th

- Hypertension grade I
- Gangrene pulpa and radix
- Pulpitis
Loss of consciousness

Dec

General Examination

- Head elevation 30o

Conciousness :GCS 12 (E3M5V4)

- Liquid diet and low salt 1800

2015

Blood pressure : 140/90 mmHg

Pulse
Temperature

: 36,8oC

Neurologic Examination: stqa

CD : -Spastic type right hemiparese
-

kcal

: 90 beats/min

Respiratory rate : 20 times/min

Non-pharmacology :

Loss

of

consciousness

observation
TD : Right temporoparietal lobe

Pharmacology :
-

IVFD RL gtt xx/minute

Inj. Dexamethason 3 x 5 mg

(IV) V
Inj. Omeprazole 1 x 40 mg

(IV)
Neurobion 1 x 5000 mcg (PO)
Tramadol 3 x 1 amp (IV)
Candesartan 1 x 8 mg (PO)
Amlodipine 1 x 10 mg (PO)

28

ED : SOL intracranial DD/

-

HCT 1 x 12,5 mg (PO)

morning
Ondansentron 4 mg (if vomit)

Tumor intracranial

AD : - Tinea cruris et corporis

- Hypertension grade I
- Gangrene pulpa and radix
- Pulpitis

Therapy

from

Dermatovenereology
Department:
-

Ketoconazole cream 2% twice

30th

Headache, right side body weakness

per day
- Loratadine 1 x 10 mg (PO)
Non-pharmacology :

Dec

General Examination

- Head elevation 30o

Conciousness :GCS 12 (E3M5V4)

- Liquid diet and low salt 1800

2015

Blood pressure : 140/90 mmHg

Pulse

: 81 beats/min

Respiratory rate : 20 times/min

Temperature

: 36,7oC

Neurologic Examination: stqa

A

CD : -Spastic type right hemiparese

-

Loss

of

consciousness

observation
TD : Right temporoparietal lobe
ED : SOL intracranial DD/
-

kcal
Pharmacology :
-

IVFD RL gtt xx/minute

Inj. Dexamethason 3 x 5 mg

(IV) VI
Inj. Omeprazole 1 x 40 mg

(IV)
Neurobion 1 x 5000 mcg (PO)
Tramadol 3 x 1 amp (IV)
Candesartan 1 x 8 mg (PO)
Amlodipine 1 x 10 mg (PO)
HCT 1 x 12,5 mg (PO)

morning
Ondansentron 4 mg (if vomit)

Tumor intracranial

AD : - Tinea cruris et corporis

- Hypertension grade I
- Gangrene pulpa and radix
- Pulpitis

Therapy

from

Dermatovenereology
Department:
-

Ketoconazole cream 2% twice

per day
Loratadine 1 x 10 mg (PO)

29

CHAPTER III
CASE ANALYSIS
A. Topical Differential Diagnosis

30

Location
Frontal lobe

Temporal
lobe
Parietal
lobe
Occipital
lobe
Ventricular
Cerebellum
Brain stem

Cranial
nerves

Symptoms
Hemiparesis, difficulties in higher-level
functions, personality changes, behavior and
mood changes, fluent speech deficit
Hemiparesis, visual field deficits, memory
deficits, speech and language deficit,
psychomotor seizures
Sensory deficits, neglect, difficulties with
right-leg discrimination
Visual deficits, homonymous hemianopsia
Increased ICP, obstruction
Ataxia, incoordination, nystagmus, nausea
Lower cranial nerve deficits, motor and
sensory deficits, ataxia, incoordination,
nystagmus, nausea, vomitting
Deficits related to the specific cranial nerves

The Patient
-

Hemiparesis dextra
spastic
-

Parese N.VI
sinistra

Based on the anamnesis and physical findings, we suspect that the location of the
SOL is in the temporal lobe. It is also confirmed from CT-Scan that the SOL is
located in the right temporoparietal lobe.
B. Etiological Differential Diagnosis
Cephalgia
Symptoms
Intracranial A. Evidence of causation demonstrated
neoplasm
by at least two of the following:
1. Headache has developed in
temporal relation to development of
the neoplasm, or led to its
discovery
2. Either or both of the following:
a) Headache has significantly
worsened in parallel with
worsening of the neoplasm

The Patient
Headache is felt in
the back of the
head and spread to
all regions of the
head
Headache
is
worsened since 2
weeks ago and the
peak is 3 days ago

b) Headache has significantly Headache

improved in temporal relation improved
to successful treatment of the follow up
neoplasm
3. Headache has at least one of the

is
during

31

following three characteristics:

a) Progressive
b) Worse in the morning or after
daytime napping
c) Aggravated by Valsalva-like
manoeuvres

Progressive
Worse
during
waking up
Worse
during
coughing, sneezing

Because of that, intracranial neoplasm can be included as the differential

diagnosis.
Cephalgia
Symptoms
Traumatic
A. Traumatic injury to the head has
injury of
occurred
the head
B. Headache is reported to have
developed within 7 days after one of
the following:
1.The injury to the head
2.Regaining
of
consciousness
following the injury to the head
3.Discontinuation of medication(s)
that impair ability to sense or report
headache following the injury to
the head
C. Headache persists for >3 months after
the injury to the head

The Patient
Falling
from
motorbike
Headache (+) after
the accident
No
loss
consciousness
(-)

of

Headache is not
felt anymore after
the accident and is
felt again 3 months
ago
Because of that, traumatic injury of head can be excluded from the differential
diagnosis.

Cephalgia
Symptoms
The Patient
Brain
A. A brain abscess has been demonstrated (-)
abscess
B. Evidence of causation demonstrated
by at least two of the following:
1.Headache has developed in
temporal relation to development of Headache is felt in
the abscess, or led to its discovery. the back of the
head and spread to
all regions of the
2.Headache
has
significantly head
worsened
in
parallel
with

32

deterioration of the abscess shown

by any of the following:
a) Worsening
of
other
symptoms and/or clinical signs The
main
arising from the abscess
symptoms of the
patient is only
headache
and
b) Evidence of enlargement of double vision
the abscess
(-)
c) Evidence of rupture of the
abscess
(-)
3.Headache
has
significantly
improved
in
parallel
with Headache
is
improvement in the abscess
improved
with
medicine
and
4.Headache has at least one of the sleeping
following three characteristics:
a) Intensity increasing gradually,
over several hours or days, to Intensity
moderate or severe
increasing
b) Aggravated by straining or gradually
other Valsalva manuvre
Worse
during
c) Accompanied by nausea
coughing, sneezing
Nausea (+)
5.
Other infection signs:
Fever
Focal neurologic deficit
Fever (-)
Present history of disease/injury Parese N.VI
that will cause cerebral abscess Gangrene
pulpa
(OM, rhinosinusitis, head trauma, and radix (+)
brain dissection)
Pulpitis (+)
Based on the anamnesis and physical findings, brain abscess can be included
as differential diagnosis.
Additional
Examination
Laboratorium
Leukocyte
Head CT-Scan

Intracranial

Brain abscess

Patient

neoplasm
Normal

Increasing

Hypodense,
isodense, or
hyperdense, or
they may have

Hypodense center
with a peripheral
uniform
enhancement ring

Normal
(7000/mm3)
There is
hypodense lesion
in right parietal
with perifocal

33

mixed density
(contrast)

(after contrast
injection)

edema (without
contrast)

Based on additional examination, intracranial neoplasm is more possible diagnosis

for this patient. We must still confirm with MRI + contrast which will be done in
30th December 2015.

BAB IV
LITERATURE REVIEW

4.1 Cephalgia
Secondary headache consists of several etiologies. One of them is changes
in intracranial pressure. Both increased and decreased cerebrospinal fluid (CSF)
pressure can lead to headache. Other causes of headache here are non-infectious

34

inflammatory diseases, intracranial neoplasia, seizures, rare conditions such as

intrathecal injections and Chiari malformation type I, and other non-vascular
intracranial disorders. There are several secondary headache which happens
because os Space Occupying Lesion (SOL) namely because of trauma, nonvascular (intracranial neoplasm) and infection (brain abscess).1,2
4.1.1. Headache is attributed to intracranial neoplasm
Description: headache, usually progressive, worse in the morning and
aggravated by Valsalva-like manuvres, caused by one or more space-occupying
intracranial tumours.
Diagnostic criterias are, namely:1,2
B. Headache fulfilling criterion C
C. A space-occupying intracranial neoplasm has been demonstrated
D. Evidence of causation demonstrated by at least two of the following:
4. Headache has developed in temporal relation to development of the
neoplasm, or led to its discovery
5. Either or both of the following:
c) Headache has significantly worsened in parallel with worsening of the
neoplasm
d) Headache has significantly improved in temporal relation to
successful treatment of the neoplasm
6. Headache has at least one of the following three characteristics:
d) Progressive
e) Worse in the morning or after daytime napping
f) Aggravated by Valsalva-like manoeuvres
E. Not better accounted for by another ICHD-3 diagnosis.
4.1.2 Persistent headache attributed to traumatic injury to the head
Traumatic injury to the head is defined as a structural or functional injury
resulting from the action of external forces on the head. These include striking the
head with or the head striking an object, penetration of the head by a foreign body,
forces generated from blasts or explosions, and other forces yet to be defined. Its
diagnostic criterias, are:1,2
D. Any headache fulfilling criteria C and D
E. Traumatic injury to the head has occurred

35

F. Headache is reported to have developed within 7 days after one of the

following:
4.The injury to the head
5.Regaining of consciousness following the injury to the head
6.Discontinuation of medication(s) that impair ability to sense or report
headache following the injury to the head
G. Headache persists for >3 months after the injury to the head
H. Not better accounted for by another ICHD-3 diagnosis.
4.1.3 Headache attributed to brain abscess
The most common organisms causing brain abscess include Streptococcus,
Staphylococcus aureus, Bacteroides species and Enterobacter. Recently, brain
abscesses have also been reported with Aspergillosis and Blastomycosis.
Predisposing factors include infections of the paranasal sinuses, ears, jaws, teeth
or lungs. Direct compression and irritation of the meningeal and/or arterial
structures and increased intracranial pressure are the mechanisms causing
headache attributed to brain abscess.1,2
Description: Headache caused by brain abscess, usually associated with
fever, focal neurological deficit(s) and/or altered mental state (including impaired
vigilance). Its diagnostic criterias consist of:1,2
C. Any headache fulfilling criterion C
D. A brain abscess has been demonstrated
E. Evidence of causation demonstrated by at least two of the following:
6.Headache has developed in temporal relation to development of the
abscess, or led to its discovery.
7.Headache has significantly worsened in parallel with deterioration of the
abscess shown by any of the following:
d) Worsening of other symptoms and/or clinical signs arising from
the abscess
e) Evidence of enlargement of the abscess
f)Evidence of rupture of the abscess
8.Headache has significantly improved in parallel with improvement in the
abscess.
9.Headache has at least one of the following three characteristics:
d) Intensity increasing gradually, over several hours or days, to moderate
or severe b) Aggravated by straining or other Valsalva manuvre

36

e) Accompanied by nausea
F. Not better accounted for by another ICHD-3 diagnosis.
4.2 Tumors of Central Nervous System (CNS)
4.2.1 Definition
Tumors of the central nervous system (CNS) derives from their great
variety; the numerous neurologic symptoms caused by their size, location, and
invasive qualities; the destruction and displacement of tissues in which they are
situated; the elevation of intracranial pressure they cause; and, most of all their
lethality.3

4.2.2 Epidemiology
Currently; in each year there are an estimated 600,000 deaths from cancer
in the United States. Of these, the number of patients who died of primary tumors
of the brain seems comparatively small (approximately 20,000, half of them
malignant gliomas), but in roughly another 130,000 patients the brain is affected
at the time of death by metastases. Viewed from another perspective, in the United
States, the yearly incidence of all tumors that involve the brain is 46 per 100,000,
and of primary brain tumors, 15 per 100,000. Differences are seen between ethnic
groups within the same country, and a 3-fold difference in incidence has been
reported between countries worldwide. Developed countries appear to have the
highest rates, but this may reflect better registration systems.3,4
Most primary brain tumors are of preswned glia cell origin-i.e., gliomas-a
category that includes astrocytomas, oligodendrogliomas, ependymomas, and a
number of rarer types. Other brain tumors arise from ectodermal structures related
to the brain (meningioma), from lymphocytes (CNS lymphoma), or from
precursor neuronal elements (neuroblastoma, medulloblastoma), germ cells
(germinoma, craniopharyngioma, teratoma), or endocrine elements (pituitary
adenoma). Tumors in the posterior fossa predominate in preadolescent children,
with the incidence of supratentorial tumors increasing from adolescence to

37

adulthood. Table 1 provides a detailed tabulation compiled by the Central Brain

Tumor Registry.3,4

Table 1. Age-Specific Frequency of Tumor Types with Age1

4.2.3

Classification

and Grading of

Central

Nervous

System

Table 2
items

and

shows the main

discussion

of

this system can

be found in the

article by Louis

and colleagues

(2007).

The

astrocytic

tumors,

the

forms

of

most
glioma,

common
have

been subdivided into diffuse well-differentiated astrocytoma (grade II), anaplastic

astrocytoma (grade IIl), and glioblastoma (glioblastoma multiforme, or "GBM,"
grade N). The glioblastomas are largely defined by the features of necrosis and
anaplasia of nonneural elements such as vascular proliferation and are set apart
from anaplastic astrocytomas on the basis not only of their histology but also by a
later age of onset than astrocytoma and a more rapid course. The grade I
classification for astrocytomas is reserved for the relatively benign group that
includes pilocytic astrocytomas (well-differentiated tumors mostly of children and

38

young adults); the pleomorphic xanthoastrocytoma (with lipid-filled cells), and

the subependymal giant cell astrocytoma (associated with tuberous sclerosis).
They have been set apart because of their different growth patterns, pathologic
features, and better prognosis.3
The ependymomas are subdivided into cellular, myxopapillary, clear cell,
and mixed types; the anaplastic ependymoma and the subependymoma are given
separate status. They are subdivided into tumors of pure oligodendroglial
composition and those with mixed astrocytes and oligodendroglia. Meningiomas
are classified on the basis of their cytoarchitecture and genetic origin into 4
categories: (1) the common meningothelial or syncytial type, (2) the fibroblastic
and (3) angioblastic variants, and (4) the malignant type.3
Table 2. Main Categories of The WHO Brain Tumor Classification3

39

4.2.4 Pathophysiology
There it was pointed out that the cranial cavity has a restricted volume, and
the three elements contained

there in-the brain (about 1,200 to 1,400 mL),

cerebrospinal fluid (CSF; 70 to 140 mL), and blood (150 mL)-are relatively but
not entirely incompressible, particularly the brain substance, and each is subject to
displacement by a localized mass lesion. According to the MonroKellie doctrine,
the total bulk of the three elements is at all times constant, and any increase in the
volume of one of them must be at the expense of the others. A tumor growing in
one part of the brain therefore compresses the surrounding brain tissue and
displaces CSF and blood; once the limit of this accommodation is reached, the
intracranial pressure (ICP) rises. The elevation of ICP and perioptic pressure
impairs axonal transport in the optic nerve and the venous drainage from the optic
nerve head and retina, manifesting in papilledema.3
The slow growth of most tumors permits accommodation of the brain to
changes in cerebral blood flow and ICP. Only in the advanced stages of tumor
growth do the compensatory mechanisms fail and CSF pressure and ICP rise.
Once pressure is raised in a particular compartment of the cranium, the tumor
begins to displace tissue at first locally and at a distance from the tumor, resulting
in a number of false localizing signs, including coma. Indeed, the transtentorial

herniations, the paradoxical corticospinal signs of Kernahan and Woltman, sixth-

40

and third-nerve palsies, occipital lobe infarcts, midbrain hemorrhages, and

secondary hydrocephalus were all originally described in tumor cases.3
Brain Edema
Brain edema is such a prominent feature of cerebral neoplasm. With tumor
growth, the venules in the cerebral tissue adjacent to the tumor are compressed,
with resulting elevation of capillary pressure, particularly in the cerebral white
matter where edema is most prominent. It has been recognized that conditions
leading to peripheral edema, such as hypoalbuminemia and increased systemic
venous pressure, do not have a similar effect on the brain. By contrast, lesions that
alter the blood-brain barrier cause rapid swelling of brain tissue. Klatzo specified
two categories of edema: vasogenic and cytotoxic. Fishman added a third, which
he called interstitial edema.3
Vasogenic edema is the type seen in the vicinity of tumor growths and
other localized processes as well as in more diffuse injury to the blood vessels.
Presumably, there is increased permeability of the capillary endothelial cells so
that plasma proteins exude into the extracellular spaces (See figure 1). This
heightened permeability has been attributed to a defect in the tight endothelial cell
junctions, but current evidence indicates that active vesicular transport of water
across the endothelial cells is a more important factor.3
Microvascular transudative factors, such as proteases released by tumor
cells, also contribute to vasogenic edema by loosening the blood-brain barrier and
allowing passage of blood proteins. The small protein fragments that are
generated by this protease activity may exert osmotic effects as they spread
through the white matter of the brain. This is the postulated basis of the regional
swelling, or localized cerebral edema that surrounds the tumor. Experimentally,
the increase in permeability has been shown to vary inversely with the molecular
weight of various markers.3
The vulnerability of white matter to vasogenic edema is not well
understood; probably its loose structural organization offers less resistance to fluid
under pressure than the gray matter. There may also be special morphologic
characteristics of white matter capillaries. The accumulation of plasma filtrate,

41

with its high protein content, in the extracellular spaces and between the layers of
myelin sheaths would be expected to alter the ionic balance of nerve fibers,
impairing their function.3
By contrast, in cytotoxic edema, all the cellular elements (neurons, glia,
and endothelial cells) swell with fluid and there is a corresponding reduction in
the extracellular fluid space. Because a shift of water occurs from the extracellular
to the intracellular compartment, there is relatively little mass effect, the opposite
of what occurs with the vascular leak of vasogenic edema. The effect of oxygen

deprivation is the cause of failure of the adenosine triphosphate (ATP)-dependent

sodium pump within cells; sodium accumulates in the cells, and water follows
(See figure 1).3
Figure 1. A schematic representation of the astrocytes and endothelial cells of the
capillary wall in the normal state and in vasogenic edema. Heightened permeability in
vasogenic edema is partly the result of a defect in tight endothelial junctions, but mainly a
result of active vesicular transport across endothelial cells. B. Cellular (cytotoxic) edema,
showing swelling of the endothelial, glial and neuronal cells at the expense of the
extracellular fluid space of the brain.3

Brain Displacement and Herniations

The pressure from a mass within any one dural compartment causes shifts
or herniations of brain tissue to an adjacent compartment where the pressure is
lower. The three wellknown herniations are subfalcial, transtentorial, and
cerebellar-foramen magnum and there are several less familiar ones (upward
cerebellar-tentorial, diencephalic sella turcica, and orbital frontal-middle cranial

42

fossa [transalar]). Herniation of swollen brain through an acquired defect in the

calvarium, in relation to craniocerebral trauma or surgical craniotomy, is yet
another (transcalvarial) type.3
4.3 Meningioma
4.3.1 Description
This is a tumor, first illustrated by Matthew Bailie in his Morbid Anatomy
(1787) and first identified properly by Bright, in 1831, originating from the dura
mater or arachnoid. It was analyzed from every point of view by Harvey Cushing
and was the subject of one of his most important monographs. According to
Rubinstein, meningioma may arise from dural fibroblasts, they are more clearly
derived from arachnoidal (meningothelial) cells, in particular from those forming
the arachnoid villi. Because the clusters of arachnoidal cells penetrate the dura in
largest number in the vicinity of venous sinuses, these are the sites of predilection
for the tumor. Grossly, the tumor is firm, gray, and sharply circumscribed, taking
the shape of the space in which it grows; thus, some tumors are flat and plaquelike, others round and lobulated. They may indent the brain and acquire a piaarachnoid covering as part of their capsule, but they are clearly demarcated from
the brain tissue (extraaxial) except in the unusual circumstance of a malignant
invasive meningioma. Infrequently; they arise from arachnoidal cells within the
choroid plexus, forming an intraventricular meningioma details). 3,5,7
4.3.2

Epidemiology
Meningiomas represent approximately 15 percent of all primary

intracranial tumors; they are more common in women than in men (2: 1) and have
their highest incidence in the sixth and seventh decades of life. Some are
familial.3,5,7
4.3.3

Etiology and Risk Factors

Persons who have undergone radiation therapy to the scalp or cranium are

vulnerable to the development of meningiomas. Besides that, a number of reports

of a meningioma developing at the site of previous trauma, such as a cranial
fracture line. The most frequent acquired genetic defects of meningiomas are

43

truncating (inactivating) mutations in the neurofibromatosis 2 gene (merlin) on

chromosome 22q. In meningiomas of both the sporadic and neurofibromatosis
type 2 (NF2)-associated types, other somatic genetic defects are found, including
deletions on chromosomes 1p, 6q, 9p, 10q, 14q, and 18q. Meningiomas also
elaborate a variety of soluble proteins, some of which (VEGF) are angiogenic and
probably relate to both the highly vascularized nature of these tumors and their
prominent surrounding edema. Some meningiomas contain estrogen and
progesterone receptors. The implications of these findings are not yet clear, but
may relate to the increased incidence of the tumor in women, its tendency to
enlarge during pregnancy, and an association with breast cancer.3,5
Meningiomas occur at sites of dural folds, most commonly the
frontoparietal parasagittal convexities, falx, tentorium cerebelli, sphenoid wings,
olfactory groove, and tuberculum sellae (see Figure 2). Ninety percent of
meningiomas are supratentorial, and the majority of infratentorial meningiomas
occur at the cerebellopontine angle. Some meningiomas-such as those of the
olfactory groove, sphenoid wing, and tuberculum sella express themselves by
highly distinctive syndromes that are almost diagnostic. Rarely, the tumors are
multiple. In as much as the meningioma extends from the dural surface, it
commonly incites hyperostosis of adjacent bone and can, in more malignant cases,
invade and erode the cranial bones or excite an osteoblastic reaction, giving rise to
an exostosis on the external surface of the skull. Most of the following remarks
apply to meningiomas of the parasagittal, sylvian, and other surface areas of the
cerebrum.3,7

44

Figure 2.
location of

Common
meningioma.7

4.3.4

Histopathology
The cells of meningiomas are relatively uniform, with round or elongated
nuclei, visible cytoplasmic membrane, and a characteristic tendency to encircle
one another, forming whorls and psammoma bodies (laminated calcific
concretions). A notable electron microscopic characteristic is the formation of
very complex interdigitations between cells and the presence of desmosomes
(Kepes). Currently neuropathologists recognize a meningothelial (syncytial) form
as being the most common. It is readily distinguished from other similar but
nonmeningothelial tumors such as hemangiopericytomas, fibroblastomas, and
chondrosarcomas.3,8

Figure 3. Histopathology: Typical meningioma specimen malignancy grade I showing an

example of the common transitional meningioma with multiple whorles (a few marked with
arrows).8

4.3.4

Sign and Symptoms

Meningiomas produce their symptoms by several mechanisms. They may

cause symptoms by irritating the underlying cortex, compressing the brain or the

45

cranial nerves, producing hyperostosis and/or invading the overlying soft tissues,
or inducing vascular injuries to the brain. The signs and symptoms secondary to
meningiomas may appear or become exacerbated during pregnancy but usually
abate or improve in the postpartum period.3,5
1. Irritation: By irritating the underlying cortex, meningiomas can cause
seizures. New-onset seizures in adults justify neuroimaging (eg, MRI) to
exclude the possibility of an intracranial neoplasm.
2. Compression: Localized or nonspecific headaches

are

common.

Compression of the underlying brain can give rise to focal or more

generalized cerebral dysfunction, as evinced by focal weakness, dysphasia,
apathy, and/or somnolence.
3. Stereotypic symptoms: Meningiomas in specific locations may give rise to
the stereotyped symptoms listed in the Table 3. These stereotypical
symptoms are not pathognomonic of meningiomas in these locations; they
may occur with other conditions or lesions. Conversely, meningiomas in
these locations may remain asymptomatic or produce other unlisted
symptoms.
4. Vascular: This presentation, although rare, should be considered.
Meningiomas of the skull base may narrow and even occlude important
cerebral arteries, possibly presenting either as transient ischemic attack
(TIA)like episodes or as stroke.
5. Miscellaneous
a. Intraventricular

meningiomas

may

present

with

obstructive

hydrocephalus.
b. Meningiomas in the vicinity of the sella turcica may produce
panhypopituitarism.
c. Meningiomas that compress the visual pathways produce various visual
field defects, depending on their location.
d. Rarely, chordoid

meningiomas

can

present

with

hematologic

disturbances, namely Castleman syndrome.

Table 3. Symptoms and Signs Associated with Meningiomas in Specific Locations 5
Location
Parasagittal

Symptoms
Monoparesis of the contralateral leg

46

Subfrontal
Olfactory groove
Cavernous sinus
Occipital lobe
Cerebellopontine
angle
Spinal cord
Optic nerve

Sphenoid wing
Tentorial
Foramen magnum

4.3.5

Change in mentation, apathy or disinhibited behavior, urinary incontinence

Anosmia with possible ipsilateral optic atrophy and contralateral
papilledema (this triad termed Kennedy-Foster syndrome)
Multiple cranial nerve deficits (II, III, IV, V, VI), leading to decreased
vision and diplopia with associated facial numbness
Contralateral hemianopsia
Decreased hearing with possible facial weakness and facial numbness
Localized spinal pain, Brown-Sequard (hemispinal cord) syndrome
Exophthalmos, monocular loss of vision or blindness, ipsilateral dilated
pupil that does not react to direct light stimulation but might contract on
consensual light stimulation; often, monocular optic nerve swelling with
optociliary shunt vessels
Seizures; multiple cranial nerve palsies if the superior orbital fissure
involved
May protrude within supratentorial and infratentorial compartments,
producing symptoms by compressing specific structures within these 2
compartments[6]
Paraparesis, sphincteric troubles, tongue atrophy associated with
fasciculation

Additional Examination
Even now some tumors reach enormous size, to the point of
causing papilledema, before the patient comes to medical attention. Many
are detected on CT in individuals with unrelated neurologic diseases. The
diagnosis of meningioma is greatly facilitated by their ready visualization
with contrast-enhanced CT and MRl (Figs 4 and 5), which reveal their
tendency to calcify as well as their prominent vascularity. These changes
are reflected by homogeneous contrast enhancement and by "tumor blush"
on angiography. Typically the tumor takes the form of a smoothly
contoured mass sometimes lobulated, with one edge abutting the inner
surface of the skull, along the dura. On CT performed without contrast
they are isointense or slightly hyperintense; calcification at the outer
surface or heterogeneously throughout the mass is common. The amount
of edema surrounding the tumor is highly variable and may relate to the
extent of local brain symptoms. The CSF protein is usually elevated.3

47

Figure 4. A . Parafalcine meningioma; coronal image, MRI with gadolinium. Note the
rightward displacement of an anterior cerebral. artery (hypointense flow void) trapped
between the right lateral margin of the mass and the right medial frontal lobe. B. Small and
asymptomatic left olfactory groove meningioma, MRI with gadolinium. 3

Figure 5. Gadolinium-enhanced MRI of

meningioma. Large subfrontal extraaxial mass
with central calcification and surrounding
vasogenic edema. Homogeneous av:id
enhancement is characteristic of the tumor.3

4.3.6

Treatment

Meningioma

Figure 6. NCCN Guidelines for Meningioma.8

48

Surgical excision should afford long-term or permanent cure in most

symptomatic and accessible tumors. Recurrence is likely if removal is incomplete,
as is often the case, but for some the growth rate is so slow that there may be a
latency of many years or decades. A few tumors show malignant qualities; i.e., a
high mitotic index, nuclear atypia, marked nuclear and cellular pleomorphism and
invasiveness of brain. Their regrowth is then rapid if they are not completely
excised. Tumors that lie beneath the hypothalamus, along the medial part of the
sphenoid bone and parasellar region, or anterior to the brain stem are the most
difficult to remove surgically.3,5
By invading adjacent bone, they may become impossible to remove
totally. Carefully planned radiation therapy, including vanous forms of stereotactic
treatment, is beneficial in cases that are inoperable and when the tumor is
incompletely removed or shows malignant characteristics. Smaller tumors at the
base of the skull can be obliterated or reduced in size by focused radiation,
probably with comparable or less risk than posed by surgery. Conventional
chemotherapy and hormonal therapy are probably ineffective, but the latter has
been a subject of interest. Investigations are being undertaken with antiangiogenic
antibodies for recurrent tumors.3,5
Brain Edema

49

The treatment of brain edema and elevated ICP is governed by the

underlying disease (excision of a tumor, treatment of intracranial infection,
placement of a shunt,etc.). The use of high-potency glucocorticosteroids has a
beneficial effect on the vasogenic edema associated with tumors, both primary
and metastatic, sometimes beginning within hours. Probably these steroids act
directly on the endothelial cells, reducing their permeability. Steroids also shrink
normal brain tissue, thus reducing overall intracranial pressure. Drugs such as
dexamethasone also reduce the vasogenic edema associated with brain abscess
and head injury.3
For patients with brain tumor, it is common practice initially to use doses
of dexamethasone of approximately 4 mg q6h, or the equivalent dose of
methylprednisolone. In patients with large tumors and marked secondary edema,
further benefit is sometimes achieved by the administration of extremely high
doses of dexamethasone, to a total of 100 mg/ d or more for a brief time. An initial
dose may be given intravenously.3

APPENDIX
Rontgen Thorax PA (14th December 2015)
In rontgen thorax PA, it is found
that:
- Bones/soft tissues: no
abnormality
- Cor: seems bigger (inspiration is
not enough)
- Pulmo: no abnormality
- Trachea: position, borders and
diameter normal; no thickenning
of paratracheal line
- Mediastinum: located in the
center and not widened
- Diaphragm: normal position or
shape; right and left
costophrenicus angle are sharp
Result: heart enlargement
(inspiration is not enough)

50

Head CT-Scan (14th December 2015)

In non contrast head CTScan, it is found that:
- There is hipodens lesion in
right parietal with
perifocal edema
- Gray/white matter
differentiation is clear
- No midline structure
deviation
- Ventricle system is
normal, sulci/gyri are
normal
- Pons/cerebellum/CPA are
normal
- Paranasal sinus/cavum
nasi and orbita are normal
- No fracture in the
cranium/bones are good
Result: right
temporoparietal SOL

Raising
Wrinkling
eyebrows
forehead

51
Smiling while showing
teeth tongue
Showing

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52

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53