Lap PBL I Neuro Kel.15

1 MODULE
REPORT
ST
HEMIPARESE
GROUP 15
NEUROPSYCHIATRY SYSTEM
MEDICAL FACULTY
MOSLEM UNIVERSITY OF INDONESIA
2015
PERSONALIA
TUTOR :
dr. Marlianty, Sp. M
MEMBERS
:
Andi Fikrah Muliani 110 213 086
Lesthary Kadir
110 213 114
Khaerunnisa A.Y. 110 213 094
Siti Shahrina T.A. 110 213 099
A. Nur Qalby T.S.M 110 213 117
Andi Azizah Noor 110 213 120
Erza Alifianda 110 213 129
Andy Billa Vini F.A. 110 213 123
Ikram Hanafi 110 213 131
Andi Nurul Fasty Batari
110 213 136
SCENARIO
A woman 56 years old experienced
suddenly the weakness of left body and
right facial droop since 2 days ago,
headache and vomiting. One moment
after experiencing weakness of left
body, the patient is difficult to
communicate and looked sleepy.
DIFFICULT WORDS
Facial droop : stiffness/ parese of half
face.
Weakness : reduction of normal power
of muscle.
Looked sleepy : Samnolent, low
consciousness
KEYWORDS
Woman, 56 years old
Sudden weakness of left body
Right facial droop
Headache
Vomiting
Difficult to communicate
Looked sleepy
QUESTIONS:
1. What is the anatomy and physiology of the related
system by case?
2. Why did the patient get a sudden weakness in left
than the facial droop in right?
3. How did the patient get a headache and vomiting
related by this case?
4. Why did the patient looked sleepy and difficult to
communicate?
5. What are the diagnostic procedures?
6. What are the differencial diagnoses and the
complications of each differential diagnoses?
7. What are the treatments given to the patient?
8. How to prevent this disease?
9. What are the risc factors related by this case?
10.What is the Islamic perspective related to this case?
1. What is the anatomy

and physiology of the
related system by case?
The Central
Nerve
System
Enchepalo
n
Cerebrum
Medulla Spinalis
(Spinal Cord)
The
Nerve
System
Cerebellum
Truncus Cerebri
Mesenchepalon
The
Peripheral
Nerve
System
Nn. Cranialis (12

pair)
N. Spinalis (31 pair)
Otonom (Involunter)
Symphatis
Parasymphatis
1. Sehati, Nouzhan.Brain and Spine Surgery. University of California, Los Angeles (UCLA) Medical Center.
2. http://www.le.ac.uk/pa/teach/va/anatomy/case3/frmst3.html
The Anatomy of Nerve

System
Cranial Nerve
Cranial nerve I (Olfactory nerve): Smell
Cranial nerve II (Optic nerve): Vision
Cranial nerve III (Oculomotor nerve): Eye
movements and opening of the eyelid
Cranial nerve IV (Trochlear nerve): Eye
movements
Cranial nerve V (Trigeminal nerve): Facial
sensation and jaw movement
Cranial nerve VI (Abducens nerve): Eye
movements
Cranial nerve VII (Facial nerve): Eyelid
closing, facial expression and taste sensation
Cranial nerve VIII (Vestibulocochlear nerve):
Hearing and sense of balance
Cranial nerve IX (Glossopharyngeal nerve):
Taste sensation and swallowing
Cranial nerve X (Vagus nerve): Heart rate,
swallowing, and taste sensation
Cranial nerve XI (Spinal accessory nerve):
Control of neck and shoulder muscles
Cranial nerve XII (Hypoglossal nerve): Tongue
movement
The Physiology of Nerve

System
The Nerve Impulse
2. Why did the patient get a

sudden weakness in left
than the facial droop in
right?
PATOMECANISM
LESI IN THE BRAIN
BLOOD SUPPLIES
REDUCED
THE DISTURBANCE OF
NERVE MOTOR IN BRAIN
LACK HALF OF BODY
CLINICAL MANIFESTATION
HEADACHE
THE EYES AWAY
NAUSEA AND VOMITING
SLEEPY
3. How did the patient get a

headache and vomiting
related by this case?
Headache
Stimulation of pain receptors in the
cerebral vault above the tentorium
Initiates pain impulses in the cerebral

portion of the 5th nerve
Headache
Guyton and Hall. 2006. Textbook of Medical Psycology 11th Edition. Philadelphia: Elsevier
Vomitting
The sensory signals that initiate
vomiting originate mainly form
the pharynx, esophagus,
stomach, and upper portions of
the small intestines.
From here, motor impulse that
cause the actual vomiting are
transmitted from the vomiting
center to the way of the 5th, 7th,
9th, 10th, and 12th cranial nerves
to the lower tract, and through
spinall nerves to the diaphragm
and abdominal muscles
Guyton and Hall. 2006. Textbook of Medical Psycology 11 th Edition. Philadelphia: Elsevier
4. Why did the patient

looked sleepy and
difficult to
communicate?
Looked sleepy and difficult to

communicate
loss of blood flow to one or
more regions of the brain
Loss of consciousness and

aphasia (brocas aphasia/
wernickes aphasia/ global
aphasia)
Low of oxygen and

important nutrients
Brain cell death
5. What are the

diagnostic
procedures?
1. ANAMNESIS / HISTORY TAKING

2. PHYSICAL EXAMINATION
3. SUPPORTING EXAMINATION
Glass, Alan, M.D. and Allyson R. Zazulia, M.D. 2011. Lecture Notes of Clinical Skills:
Neurological Examination. Accessed from
http://neuro.wustl.edu/files/3913/4461/1673/Neurological_Exam_Lecture_Notes.pdf June
1st 2015
I. Mental Status.
A. Level of consciousness
B. Attentiveness.
C. Orientation.
D. Speech and language.
Listen to patients verbal output: motor ability to produce
words, quantity of
E. Memory.
F. Higher intellectual function.
II. Cranial Nerves.

A. CN I Olfactory.
B. CN II Optic.
C. CN III, IV, VI Oculomotor, Trochlear, Abducens
D. CN V Trigeminal.
E. CN VII Facial.
F. CN VIII Acoustic.
G. CN IX & X Glossopharyngeal & Vagus.
H. CN XI Spinal Accessory.
I. CN XII Hypoglossal.
Neurological
Examination. Accessed from
III. Motoric System

IV. Reflexes.
A. Muscle stretch reflexes.
a. Biceps (C5, C6; musculocutaneous nerve).
b. Triceps (C6, C7; radial nerve) .
c. Knee (L2, L3, L4; femoral nerve).
d. Ankle (S1, S2; tibial nerve).
B. Test for clonus

C. Assign grade on scale of 0-4.
0
1
2
3
4
Absent
Hypoactive
Normal
Brisk/hyperactive
Markedly hyperactive with clonus and/or spreading
D. Plantar response (L4-S2, especially

S1; tibial
nerve).
Neurological
Examination.
Accessed from
V. Sensory System.
A. General points.
B. Vibration.
C. Joint position sense.
D. Pain.
E. Temperature.
F. Light touch.
G. Double simultaneous stimulation (test for
extinction/tactile neglect).
H. Graphesthesia (integrative sensation).
I. Stereognosis (integrative sensation).
J. Romberg.
1st 2015
VI. Coordination.
A. Truncal stability.
B. Fine finger movements (finger tapping).
C. Toe tapping.
D. Finger-nose-finger.
E. Heel-knee-shin.
F. Rapid Alternating Movements.
VII. Station and Gait.
A. Observe the patient do the following:
1. Rise from a seated position.
2. Walk across room, turn, and come back.
3. Walk on toes.
4. Walk on heels.
5. Walk heel to toe (tandem gait) in a straight line.
(Many otherwise normal elderly people cannot perform
this task.)
B. Be prepared to catch the patient if necessary

C. Pay attention to the following:
1.
2.
3.
4.
5.
6.
Posture of body and extremities

Length, speed, and rhythm of steps.
Base of gait (how far apart are the legs).
Arm swing
Steadiness.
Turning
VIII. Meningeal Signs.

A. Ask patient to flex and extend neck.
B. Passively flex and extend patients neck.
C. Observe for palpable stiffness on either active
or passive movement.
1st 2015
6. What are the

differencial diagnoses
and the complications
of each differential
diagnoses?
NON HEMORRAGIC
STROKE
Stroke non
hemorrhagic
Etiology :
-Embolism (the clot is from other part of the body,
usually cardiogenic embolism)
-Thrombosis (Obstruction of blood vessel by a clot
that formed locally)
Wade S. Smith, S. Claiborne

Johnston, J Donald Easton.
Cerebrovascular Disease.
Harrison : The Principles of
Internal Medicine vol.4.
Definition :
Neurological deficit of cerebrovascular cause that
persists beyond 24 hours or is interrupted by death
within 24 hours (WHO)
Occlusion (partial or complete) decreasing of

PO2 and increasing of PCO2
Lactic acid
increased (oxidative process is replaced by the
anaerob process causing toxicity environment
Vasoparalysis Nerve cells damaging
Swelling of nerve fibers and myelin
Irreversible damage (necrosis)
Brain tissue
edema
Increasing intracranial pressure
If its only transient ischemic attack, the plaque

may disintegrated into small piece, and the
obstructed blood vessel will be recirculated.

Patogenesis
The symptoms only occured in one side of the face and one
side of the body. The side of the face that is being affected
is ipsilateral with the location of the lesion, while the side
of the body that is being affected contralateral with the
side of the lesion (due to the decussatio pyramidalis)
If the area of the brain affected contains one of the three
prominent central nervous system pathways the
spinothalamic tract, corticospinal tract, and dorsal column (
medial lemniscus), symptoms may include:
hemiplegia and muscle weakness of the face
numbness
reduction in sensory or vibratory sensation
initial flaccidity (reduced muscle tone), replaced by
spasticity (increased muscle tone), excessive reflexes,
and obligatory synergies.

Symptoms
If the location is in the brainstem, it will affect the twelve

cranial nerves. Therefore it can produce symptoms relating
to deficits in these cranial nerves:
altered smell, taste, hearing, or vision (total or partial)
drooping of eyelid (ptosis) and weakness of
ocular muscles
decreased reflexes: gag, swallow, pupil reactivity to light
decreased sensation and muscle weakness of the face
balance problems and nystagmus
altered breathing and heart rate
weakness in sternocleidomastoid muscle with inability
to turn head to one side
weakness in tongue (inability to stick out the tongue
and/or move it from side to side)

Symptoms
If the cerebral cortex is involved, the CNS pathways can again

be affected, but also can produce the following symptoms:
aphasia (difficulty with verbal expression, auditory
comprehension, reading and/or writing; Broca's or
Wernicke's area typically involved)
dysarthria (motor speech disorder resulting from
neurological injury)
apraxia (altered voluntary movements)
visual field defect
memory deficits (involvement of temporal lobe)
hemineglect (involvement of parietal lobe)
disorganized thinking, confusion, hypersexual gestures (with
involvement of frontal lobe)
lack of insight of his or her, usually stroke-related, disability

Symptoms
If the cerebellum is involved, the patient may have

the following:
altered walking gait
altered movement coordination
vertigo and or disequilibrium
The symptoms of nausea and vomiting usually more

typicall in the hemorrhagic stroke due to the sudden
increase of intracranial pressure.

Symptoms
Diagnostic procedure

CT Scan and MRI will provide the best imaging of

the exact location of the lesion and the blood
vessels that involved in the stroke attack.

Management of Therapy
-Anti coagulan : Heparin and Warfarin natrium
-Anti trombosit : Aspirin
-Anti edema : Mannitol
Disability affects 75% of stroke survivors enough to decrease their

employability. Stroke can affect people physically, mentally,
emotionally, or a combination of the three. The results of stroke vary
widely depending on size and location of the lesion. Dysfunctions
correspond to areas in the brain that have been damaged.
Some of the physical disabilities that can result from stroke include
muscle weakness, numbness, pressure sores, pneumonia,
incontinence, apraxia (inability to perform learned movements),
difficulties carrying out daily activities, appetite loss, speech loss,
vision loss and pain. If the stroke is severe enough, or in a certain
location such as parts of the brainstem, coma or death can result.
Emotional problems following a stroke can be due to direct damage
to emotional centers in the brain or from frustration and difficulty
adapting to new limitations. Post-stroke emotional difficulties include
anxiety, panic attacks, flat affect (failure to express emotions),
mania, apathy and psychosis. Other difficulties may include a
decreased ability to communicate emotions through facial
expression, body language and voice.

Prognosis
-Body weight management

-Lipid fraction management
-Healthy lifestyle and exercise
-Diet management
Preventions
HEMORRAGIC STROKE
DD
STROKE HEMORAGIC
Definition
Stroke or injure the cerebrovaskuler is brain function loss

resulted by desisting it blood supply to brain shares
often this iskulminasi of disease serebrovaskuler for a
number of years
Etiology
Thrombosis ( dilution clot in brain vein )

Cerebral embolism ( clot of other;dissimilar material or
blood )
Iskemia ( Degradation of blood stream to brain area)
Patomekanisme
Brain embolism result the blood stream to brain decrease

or desisted is at all to area of distal brain so that brain of
insuffiency of source of calorie of berpa of other;dissimilar
mineral and glucose and also oxygen
Clinical
symptom
Paralisis at adversative side foot/feet, balance trouble,

cognate trouble, trouble sensori, afasia, memory damage,
dll
Therapy
control of Sugar of blood and blood pressure, diuretik,

antokoaulan, antitrombosit, Endosteroktomi Karotis,
Revaskularisasi, konseling psikososial
TUMOR INTRACRANIAL
Definition
Brain tumours are among the most devastating of
all malignant disease, frequently producing
profound and progressive disability leading to
death. Simplified classification of brain tumours:
1. Primary tumours: gliomas, astrocytoma,
glioblastoma multiforme, ependyoma,
oligodendrodlioma, etc.
2. Secondary tumours: common sites of origin,
lung, breast, melanoma, etc.
Etiology
Very little is known of the etiology:
1. Several familial syndromes
2. Cranial radiation
Epidemiology
Brain tumours are slightly more common in males
(1,2:1), with the exception of meningiomas, which
are commoner in women.
Clinical Features
Symptoms can be divided into the following groups:
1. The tumour can exert a mass affect and lead to raised
intracranial pressure, with headache, drowsiness,
nausea and vomiting as the cardinal symptoms
2. There is a large group of focal symptoms caused by
damage to local structures
3. The third group of symptoms results from remote
endocrine effects, occurring with tumours of the
pituitary and hypothalamus
4. Tumours of the CNS occasionally metastasize
5. Childhood brain tumours may present with other
symptoms including weight loss, precocious puberty,
growth failure and macrocephaly in addition to the
classical symptoms noted in tumours of adults
Supporting Examination
CT and MRI
Management
Surgical removal or biopsy is desirable both for
histological diagnosis and sometimes for definitive
treatment
Prognosis
Malignant gliomas, the prognosis is heavily dependent on tumour
grade and on other well-established prognostic factors. Patients with
malignant glioma fall chiefly into two prognostic groups since those
with grade I and II tumours have a relatively good prognosis and 5
and 10 year survival rates of approximately 65 and 35%, whereas
those with grade III and IV tumours have a 5 year survival rate of
under 10%, with a much worse prognosis in the grade IV category.
Medulloblastoma, age at diagnosis and completeness of excision are
both important; children over 15 years of age have a better
prognosis.
Ependyoma, prognosis depends on tumour grade. The median
survival following surgery in low-grade ependyoma is approximately
10 years. Recurrences are frequently of a higher histological grade,
and median overall survival in high-grade ependyoma is no better
than 2-3 years.
Pituitary tumours and meningiomas, have an excellent prognosis
following surgical removal and, where appropriate, postoperative
radiotherapy
7. What are the

treatments given to
the patient?
Acute Stroke in Emergency Unit

1. Stabilize the airway, breathing, and circulation.
2. Give an intubation if the patient have a stupor or breath
failure.
3. Stabilize patients fluid with NaCl 0,9% IV 20 ml/ hour,
dont give a hypotonic fluid (Dextrose 0,9%, NaCl 0,45%,
etc) because it can make a meaningful progress for their
brain edem.
4. Oxygenation for 2 4 l/ minute
5. Give a NGT action.
6. Ask to get an ECG test and thorax rontgen
7. Get a Blood examination
8. Get an alcohol examination, hepar function test, Blood
gas, toxicology screening if theres some indications.
9. Continue by history taking and physical examination.
10. And for gold standard: CT Scan or Magnetic Resonantion.
Manshoer, Arif. 2001. Kapita Selekta Kedokteran edisi 3 jilid 2. Jakarta.
Non Hemorragic Stroke

1. Trombolizes with rtPA (Recombinant TissuePlasminogen Activator) within 3 hours if the
result of CT Scan is normal.
2. Do the therapy in therapy windows for 27
hours to decrease the risk progression or
neurology deterioration.
3. Neurology deterioration includes to:
1. For the edem cause of infarc, we give a hypertonic or
isotonic fluid.
2. For Infarc territorial extension, we optamilize a volume
status and blood tension.
3. For the hemorragic conversion, we give an anti
coagulanodepend on the risk of patient.
4. Prevent an early repeating stroke ( at least

more than 30 days after the first onset).
Hemorragic Stroke
1. If the protrombin result is longer, give FFP and Vitamin
K till get a normal numbers.
2. Control the blood tension.
3. Get an angiography.
4. Consule to The Spesialist of Nerve Surgery.
5. Give a mannitol 20% for patient in comateus.
6. Give Fenitoin if theres a wide bleeding and low
consciousness.
7. Give a hipervolemic fluid and nifodipin to prevent a
vasospasme.
8. How to prevent this

disease?
Primary:
National campaign
Free and Health life style withour stroke
Secondary:
Modifice a risk life style.
Family support
Medica mentosa
Invasif action: flebotomi for polysutemia,
enarterectomy, etc
9. What are the risc

factors related by this
case?
STROKE RISK FACTOR

1. Stroke risk factors can not be modified
- Age
- Gender
- Ethnic
- Family History
(Reference
: http://eprints.undip.ac.id/33923/3/Bab_2.pdf )
2. Stroke risk factors can be modified

- Risk factors (have been proven) :
a. Hypertension
b. General fibrillation
c. Smoking
d. Diabetes
(Reference
Cont..
e. Hyperlipidemia
f. Carotid stenosis
g. A cursory history of ischemic attacks
h. Obesity
i. Sickle cells disease
(Reference
- Risk factors (have not been proven)

a. Heart disease
Myocard infarction
Left ventrivuly dysfunction
Heart valve disease
Left ventrivuly hypertrophy
Septurm atrium aneurysm
Mitral anuler calsification
(Reference
Cont..
b. Mitral valve rupture
c. Ateroma arcus aorta
d. Poor diet style
e. Lipoprotein
f. Alcohol consumption
g. Oral contraception
h. Druge abuse
i. Hyperfibrinogemia
j. Migrain
(Reference
3. Infection / chronic
inflammation
(Reference
10. What is the Islamic

perspective related to
this case?
ISLAMIC PERSPECTIVE
Prophet said
:
We are type of person that eat before
hungry, and if
we eat, we dont eat too
much
Sujoods benefit :
If we do the sujood in the right way, we will
get many
benefits
When our heart position on upper side of our
brain, it will cause our blood that full of
oxygen will flow more to our brain.
SUMMARY
Our group takes a summary of this case
is suspect Non Hemorragic Stroke. It
looks from the sudden symtomps and
patients history. But we still need to do
some gold standard for this patient such
as CT Scan, MRI, etc.
DAFTAR PUSTAKA
1. Greenstein, Ben. Dkk. 2010. At a Glance Sistem Endokrin. Edisi
Kedua.Jakarta: Erlangga Medical Series. Halaman 8-9.
2. Price, Sylvia. Patofisiologi jilid 2. EGC. Jakarta
3. Buku Ajar IlmuPenyakitDalam. Jilid 3 Edisi 5.Halaman 1998]
4. McPhee SJ, Lingappa V, Ganong WF. Pathophysiology of Disease.
An introduction to clinical medicine. 4th ed, New York: Lange
Medical Books/McGraw Hill, 2003 p 556-76.
5. Weetman AP. Graves Disease. N Engl J Med 2000; 343: 1236-41.
6. Royani, Ida. Penuntun CSL Sistem Endokrin 2015. FK UMI
7. McGlynn, Burnside. Adams Diagnosis Fisis edisi 17. EGC. Jakarta
8. Tandra, Hans. Mencegah dan Mengatasi Penyakit Tiroid. EGC.
Jakarta
9. Buku Ajar Ilmu Penyakit Dalam, halaman 2003-2005
10.Panduan Praktik Klinis Bagi Dokter di Fasilitas Pelayanan
Kesehatan Primer. Menteri Kesehatan RI no.5 tahun 2014. Jakarta
11.Ilmu Penyakit Dalam. Edisi v. Jilid III. Hal 2720
Thank you..^^

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1 MODULE

1. What is the anatomy

Nn. Cranialis (12

The Anatomy of Nerve

The Physiology of Nerve

2. Why did the patient get a

LACK HALF OF BODY

3. How did the patient get a

Initiates pain impulses in the cerebral

4. Why did the patient

Looked sleepy and difficult to

Loss of consciousness and

Low of oxygen and

Brain cell death

5. What are the

1. ANAMNESIS / HISTORY TAKING

II. Cranial Nerves.

III. Motoric System

B. Test for clonus

D. Plantar response (L4-S2, especially

B. Be prepared to catch the patient if necessary

Posture of body and extremities

VIII. Meningeal Signs.

6. What are the

Wade S. Smith, S. Claiborne

Occlusion (partial or complete) decreasing of

If its only transient ischemic attack, the plaque

Wade S. Smith, S. Claiborne

Wade S. Smith, S. Claiborne

If the location is in the brainstem, it will affect the twelve

Wade S. Smith, S. Claiborne

If the cerebral cortex is involved, the CNS pathways can again

Wade S. Smith, S. Claiborne

If the cerebellum is involved, the patient may have

The symptoms of nausea and vomiting usually more

Wade S. Smith, S. Claiborne

Wade S. Smith, S. Claiborne

CT Scan and MRI will provide the best imaging of

Wade S. Smith, S. Claiborne

Disability affects 75% of stroke survivors enough to decrease their

Wade S. Smith, S. Claiborne

-Body weight management

Stroke or injure the cerebrovaskuler is brain function loss

Thrombosis ( dilution clot in brain vein )

Brain embolism result the blood stream to brain decrease

Paralisis at adversative side foot/feet, balance trouble,

control of Sugar of blood and blood pressure, diuretik,

7. What are the

Acute Stroke in Emergency Unit

Non Hemorragic Stroke

4. Prevent an early repeating stroke ( at least

Manshoer, Arif. 2001. Kapita Selekta Kedokteran edisi 3 jilid 2. Jakarta.

Manshoer, Arif. 2001. Kapita Selekta Kedokteran edisi 3 jilid 2. Jakarta.

8. How to prevent this

Manshoer, Arif. 2001. Kapita Selekta Kedokteran edisi 3 jilid 2. Jakarta.

9. What are the risc

STROKE RISK FACTOR

2. Stroke risk factors can be modified

- Risk factors (have not been proven)

10. What is the Islamic

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