Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
TUTOR :
dr. Marlianty, Sp. M.
GROUP 15:
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
NEUROPSYCHIATRY SYSTEM
MEDICAL FACULTY
MOSLEM UNIVERSITY OF INDONESIA
MAKASSAR
2015
OPENING
Assalamualaikum warahmatullahi wabarakatuh
Mercy and blessing to Allah SWT for all His Rahmat to us till we can
do all our activities and reach our dream until this time.
Shalawat and salam to Our Prophet Muhammad SAW, who has a
great influence to this world to be so much brightness as now and we
can get out from last Jahiliyahs century.
So, we thanks gratefuly to our teacher, a tutor that had guided us to
finish this report till the end.
And thus how our report had to be done as we composed as well
with all their shortages. Than, we hope some critics and suggestions to
be our next learnings and educations for the future. May Allah bless us,
thank you.
Wassalamualaikum warahmatullahi wabarakatuh
Group 15
A. 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.
B. DIFFICULT WORDS
1. Facial droop
: stiffness/ parese of half face.
2. Weakness
: reduction of normal power of muscle.
3. Looked sleepy : Samnolent, low consciousness.
C. KEY WORD
1. Woman, 56 years old
2. Sudden weakness of left body
3. Right facial droop
4. Headache
5. Vomiting
6. Difficult to communicate
7. Looked sleepy
D. 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?
E. ANSWERS
1. What is the anatomy and physiology of the related system by case?
Anatomy of the Central Nervous System
The frontal lobe is concerned with higher intellectual functions, such as abstract
thought and reason, speech (Broca's area in the left hemisphere only), olfaction,
and emotion. Voluntary movement is controlled in the precentral gyrus (the
primary motor area).
The parietal lobe is dedicated to sensory awareness, particularly in the postcentral
gyrus (the primary sensory area). It is also concernes with abstract reasoning,
language interpretation and formation of a mental egocentric map of the
surrounding area.
The occipital lobe is responsible for interpretation and processing of visual stimuli
from the optic nerves, and association of these stimuli with other nervous imputs
and memories.
The temporal lobe is concerned with emotional development and formation, and also
contains the auditory area responsible for processing and discrimination of sound.
It is also the area thought to be responsible for the formation and processing of
memories.
Cranial nerve
There are 12 pairs of nerves that originate from the brain itself, as compared to spinal
nerves that initiate in the spinal cord. These nerves are responsible for specific
activities and are named and numbered as follows:
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
Pineal Gland
The pineal gland is an outgrowth from the back portion of the third ventricle, and has
some role in sexual maturation, although the exact function of the pineal gland in
humans is unclear.
Spinal Cord
The spinal cord is a long,
thin, tubular bundle of
neurons and support cells
that extends from the bottom of the brain down to the space between the first and
second lumbar vertebrae, and is housed and protected by the bony vertebral column.
The spinal cord functions primarily in the transmission of signals between the brain
and the rest of the body, allowing movement and sensation, but it also contains
neural circuits that can control numerous reflexes independent of the brain.
General Structure: The length of the spinal cord is much shorter than the length of
the bony spinal column, extending about 45 cm (18 inches). It is ovoid in shape and
is enlarged in the cervical (neck) and lumbar (lower back) regions. Similar to the
brain, the spinal cord is protected by three layers of tissue, called spinal meninges.
The dura mater is the outermost layer, and it forms a tough protective coating.
Between the dura mater and the surrounding bone of the vertebrae is a space called
the epidural space, which is filled with fatty tissue and a network of blood vessels.
The arachnoid mater is the middle protective layer. The space between the
arachnoid and the underlyng pia mater is called the subarachnoid space which
contains cerebrospinal fluid (CSF). The medical procedure known as a lumbar
puncture (or spinal tap) involves use of a needle to withdraw cerebrospinal fluid
from the subarachnoid space, usually from the lumbar (lower back) region of the
spine. The pia mater is the innermost protective layer. It is very delicate and it is
tightly associated with the surface of the spinal cord.
In the upper part of the vertebral column, spinal nerves exit directly from the spinal
cord, whereas in the lower part of the vertebral column nerves pass further down the
column before exiting. The terminal portion of the spinal cord is called the conus
medullaris. A collection of nerves, called the cauda equina, continues to travel in the
spinal column below the level of the conus medullaris. The cauda equina forms as a
result of the fact that the spinal cord stops growing in length at about age four, even
though the vertebral column continues to lengthen until adulthood.
Three arteries provide blood supply to the spinal cord by running along its length.
These are the two Posterior Spinal Arteries and the one Anterior Spinal Artery.
These travel in the subarachnoid space and send branches into the spinal cord that
communicate with branches from arteries on the other side.
Function: The spinal cord is divided into 33 different segments. At every segment, a
pair of spinal nerves (right and left) exit the spinal cord and carry motor
(movement) and sensory information. There are 8 pairs of cervical (neck) nerves
named C1 through C8, 12 pairs of thoracic (upper back) nerves termed T1 through
T12, 5 pairs of lumbar (lower back) nerves named L1 through L5, 5 pairs of sacral
(pelvis) nerves numbered S1 through S5, and 3-4 pairs of coccygeal (tailbone)
nerves. These nerves combine to supply strength to various muscles throughout the
body as follows:
C1-C6: Neck flexion
C1-T1: Neck extension
C3-C5: Diaphragm
C5-C6: Shoulder movement and elbow flexion
C6-C8: Elbow and wrist extension
C7-T1: Wrist flexion
C8-T1: Hand movement
T1-T6: Trunk muscles above the waiste
T7-L1: Abdominal muscles
L1-L4: Thigh flexion
L2-L4: Thigh adduction (movement toward the body)
to open. The rapid change in polarity that moves along the nerve fiber is called the
"action potential." This moving change in polarity has several stages:
Depolarization
The upswing is caused when positively charged sodium
ions (Na+) suddenly rush through open sodium gates
into a nerve cell. The membrane potential of the
stimulated cell undergoes a localized change from
-65 millivolts to 0 in a limited area.
As additional sodium rushes in, the
membrane potential actually reverses its
polarity so that the outside of the
membrane is
the membrane actually develops a positive value for a moment(+40 millivolts). The
change in voltage stimulates the opening of additional sodium channels (called a
voltage-gated ion channel). This is an example of a positive feedback loop.
Repolarization
The downswing is caused by the closing of sodium ion channels and the opening of
potassium ion channels. Release of positively charged potassium ions (K+) from the
nerve cell when potassium gates open. Again, these are opened in response to the
positive voltage--they are voltage gated. This expulsion acts to restore the localized
negative membrane potential of the cell (about -65 or -70 mV is typical for nerves).
Refractory phase
The refractory period is a short period of time after the depolarization stage. Shortly
after the sodium gates open, they close and go into an inactive conformation. The
sodium gates cannot be opened again until the membrane is repolarized to its
normal resting potential. The sodium-potassium pump returns sodium ions to the
outside and potassium ions to the inside. During the refractory phase this particular
area of the nerve cell membrane cannot be depolarized. This refractory area explains
why action potentials can only move forward from the point of stimulation.1,2
2. Why did the patient get a sudden weakness in left than the facial droop in right?
surface areas supplied by this somatosensory portion of the fifth cranial nerve, as shown
in figure 48-9,
Conversely, pain impulses from beneath the tentorium enter the central nervous
system mainly through the glossopharyngeal, vagal, and second cervical nerves, which
also supply the scalp above, behind, and slightly below the ear. Subtentorial pain stimuli
cause occipital headache referred to the posterior part of the head.
Types of intracranial Headache
Headache of meningitis. one of the most severe headaches of all is that resulting from
meningitis, which causes inflammation of all the meninges, including the sensitive areas
of the dura and the sensitive areas around the venous sinuses. such intense damage can
cause extreme headache pain referred over the entire head.
Headache caused by low cerebrospinal fluid pressure. Removing as little as 20 milliliters
of fluid from the spinal canal, particularly if the person remains in an upright position,
often causes intense intractranial headache.
Migraine Headache. Migraine headache is a special type of headache that is thought to
result from abnormal vascular phenomena, although the exact mechanism is unknown.
Migraine headaches often begin with various prodromal sensations, such as nausea, loss
of vision in part of the field of vision, visual aura,and other types of sensory
hallucinations. Ordinarily, the prodromal symptomps .
One of the theories of the cause of migraine headaches is that prolonged emotion or
tension causes reflex vasospasm of some of the artiries of the head, incluiding arteries
that supply the brain. The vasospasm theorecally produces ischemia of portions of the
brain, and this is responsible for the prodromal symptoms. Then, as a result of the
intense ischemia, something happens to the vascular walls, perhaps exhaustion of
smooth muscle contraction, to allow the blood vessels to become flaccid and incapable
of maintaining vascular tone for 24 to 48 hours. The blood pressure in the vessels causes
them to dilate and pulsate intensely, and it is postulated that the excessive stretching of
the walls of the arteries-incluiding some extracranial arteries, such as the temporal
artery-causes the actualpain of migraine headachesinslude spreading cortical depression,
psychological abnormalities, and vasospasm caused by excess local potassium in the
cerebral extracellular fluid
There may be genetic predisposition to migraine headaches, beause a positive family
history for migraine has been reported in 65 to 90 percent of cases. Migraine headaches
also occur about twice as frequently in women than in men.
speech,
rate
of
speech
production,
sentence
structure,
4. Naming.
Point to objects around room, asking what they are: watch, pen, telephone.
If done well, ask more difficult ones: (watch) band, (pen) cap, (telephone) receiver.
5. Reading.
Have patient read and follow a written command: Close Your Eyes.
6. Writing.
Have patient write a complete sentence of their choosing.
E. Memory.
1. Registration: Repeat these words after me: apple, table, penny. Do not proceed to
memory testing until patient says them all correctly.
2. Immediate Recall: 1-3 minutes later, What were those 3 words I asked you to
remember?
3. Recent memory: What did you have for breakfast this morning?
4. Remote memory: Where did you grow up/go to school? When was your
wedding/child born/military service?
F. Higher intellectual function.
1. General knowledge: Who is the Indonesia president/South Sulawesi governor?
What is the capital of East Java?
2. Abstraction: What does People in glass houses shouldnt throw stones mean?
3. Judgment: What would you do if you found a sealed, stamped, addressed envelope
lying on the ground?
4. Insight: Why did your daughter bring you to the hospital?
5. Reasoning: How do a lie and a mistake differ? Note: the examples of commands
and questions used in assessing mental status that are provided in the preceding
section are merely examples, not specific instructions you are expected to follow.
ii. Move a finger or penlight into the periphery of each visual quadrant (upper and
lower temporal and nasal), asking patient to indicate when movement is detected. It
should be seen by you and patient at the same time.
3. Fundoscopy.
a. Have patient focus on distant wall.
b. Be sure your head is not obstructing patients view of that target.
c. View optic disc using ophthalmoscope.
d. Note disc color and presence of venous pulsations, papilledema (disc hyperemia,
blurred margins, absent venous pulsation), or hemorrhages.
4. Pupillary function (CN II and CN III).
a. Test pupillary reaction to light.
i. Dim room lights as necessary.
ii. Ask patient to look into distance to avoid effect of accommodation.
iii. Shine bright light obliquely into each pupil.
iv. Look for both direct (same eye) and consensual (other eye) constriction.
v. Record pupil size in mm (normal is about 2-5 mm) and any asymmetry or
irregularity.
b. If light reflex is abnormal, test pupillary reaction to accommodation.
i. Hold finger 10 cm from patients nose.
ii. Have patient alternate looking into distance and at finger.
iii. Observe pupillary response.
C. CN III, IV, VI Oculomotor, Trochlear, Abducens.
1. Visual inspection.
a. Look at ocular alignment at rest (primary gaze). Does the reflection of light hit at
same location in each eye? Is one eye deviated in, down and out, or up?
b. Observe for ptosis (lid droopiness).
2. 6 cardinal directions of gaze.
a. Stand 3-6 feet in front of patient.
b. Ask patient to follow your finger with the eyes without moving the head. Place
your hand on top of head to keep it still if necessary.
c. Move your finger in the six cardinal directions and observe whether movements are
full in each eye.
3. Convergence.
a. Ask patient to follow your finger with the eyes without moving the head. Hold lids
up if necessary.
b. Move your finger toward bridge of patient's nose and observe eye movements.
4. Smooth pursuits (smooth following movements).
a. Steadily move your finger horizontally and then vertically as in testing individual
extraocular muscles, but this time, look at smoothness of following movements.
5. Saccades (discrete, rapid movements from one object to another).
a. Hold up your hands in front of patient (with each hand held a few inches lateral to
the eye).
b. Have patient alternate looking from one hand to the other.
c. Observe accuracy with which eyes reach target. Do they consistently undershoot or
overshoot the target? Is there oscillation before hitting the target?
6. Nystagmus.
a. Observe for involuntary horizontal, vertical, or rotary oscillation of the eyeballs at
primary gaze (looking straight ahead) and on sustained horizontal and vertical
gaze.
a. Smile.
b. Puff out cheeks.
c. Close both lips and resist your attempt to open them.
d. Close both eyes and resist your attempt to open them.
e. Raise eyebrows.
3. Corneal reflex (see CN V).
F. CN VIII Acoustic.
1. Screen hearing.
a. Face patient and hold out your arms with your fingers near each ear.
b. Rub your fingers together on one side.
c. Ask patient to tell you when and on which side the rubbing is.
d. Increase intensity as needed.
e. Note any asymmetry.
G. CN IX & X Glossopharyngeal & Vagus.
1. Listen to patients voice. Note any hoarseness, nasal, or breathy quality.
2. Ask patient to say Ah and watch movement of soft palate and pharynx. (Do not
pay attention to uvula, which can deviate to one side or another in the normal
person.)
a. Note any asymmetry of palate elevation.
3. Ask patient to swallow and to cough.
4. In the unconscious or uncooperative patient, test gag reflex.
a. Stimulate back of throat with a cotton swab on each side.
b. Look for gagging after each stimulus.
H. CN XI Spinal Accessory.
1. Trapezius.
a. From behind patient, look for atrophy or asymmetry of trapezii.
b. Ask patient to shrug shoulders against resistance and note strength.
c. Ask patient to push head back against resistance and note strength.
2. Sternocleidomastoid.
a. Place hand on lower face and ask patient to turn head towards that side against
resistance.
b. Observe contraction of opposite sternocleidomastoid.
I. CN XII Hypoglossal.
1. Note tongue position at rest in the mouth and on protrusion. Does tongue deviate in
either position?
2. Ask patient to stick out tongue and move it from side to side. Note strength and
rapidity of movements.
3. Have patient push tongue into each cheek while you push from the outside. Note
strength.
III. Motor System.
A. Visual inspection.
1. Note muscle bulk. Look for generalized or focal muscle wasting or hypertrophy.
2. Look for extraneous movements, e.g., tremor (At rest? With action?), fasciculation
(muscle twitching).
3. Note speed of movement, e.g., slow to initiate (bradykinesia).
B. Tone (muscle tension at rest).
1. Ask patient to relax.
6. Assign score of 0-5 for each muscle based on Medical Research Council scale.
Grade Description
0/5 No muscular contraction
1/5 Visible muscle contraction, but no movement at the joint
2/5 Movement at the joint, but not against gravity
3/5 Movement against gravity, but not against added resistance
4/5 Movement against resistance, but less than full
5/5 Movement against full resistance; normal strength
7. Note if strength fatigues after sustained muscle contraction.
IV. Reflexes.
A. Muscle stretch reflexes.
1. Position limb and place muscle in slight tension.
2. Quickly tap the tendon/periosteum to which muscle is attached.
3. Observe vigor and briskness of response and compare side-to-side.
4. If reflexes are diminished or absent, try reinforcing the reflex by distraction or via
isometric contraction of other muscles (clenched teeth).
5. Test at least the following reflexes: (spinal nerve root in bold is the predominant
contributor).
a. Biceps (C5, C6; musculocutaneous nerve).
i. Patient's arm should be partially flexed at the elbow with palm down.
ii. Place your thumb or finger firmly on biceps tendon.
iii. Strike your finger with reflex hammer.
iv. You should feel the response even if you can't see it.
5. Repeat on other side, being sure to strike the fork with about equal force, and compare
duration vibration is felt.
6. If vibration sense is impaired, move proximally one joint at a time until it is felt.
7. Test the fingers in a similar fashion.
C. Joint position sense.
1. Grasp patient's great toe on sides of distal phalanx and hold it away from other toes to
avoid friction.
2. Demonstrate to patient what "up" and "down" feel like and tell patient you will move
the toe in one of these two directions only.
3. Move toe a few degrees and ask patient to identify direction in which toe was moved.
4. If position sense is impaired, increase stimulus intensity (move toe a greater distance);
if still impaired, test at more proximal joint (ankle-->knee-->hip).
5. Test fingers in a similar fashion.
D. Pain.
1. Use a safety pin or sharp end of a broken cotton swab.
2. Test for a distal gradient of sensory loss in leg by applying stimulus at toes and
marching your way up to knee.
a. Ask patient if the sensation is about the same or if it changes as you move up the
leg.
3. Test for sensory loss in most commonly affected nerve and nerve root distributions.
a. Test the following areas:
i. Palmar aspect of index finger (median nerve).
ii. Palmar aspect of 5th finger (ulnar nerve).
iii. Web space between thumb and index finger on dorsal surface of hand (radial nerve).
iv. Web space between great toe and 2nd toe on dorsal surface of foot (L5).
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. If there is any doubt in your mind as to
whether the patient may fall, get assistance (nurse, patient care technician, resident)
before testing gait. Do not use this doubt as a reason not to test gait, however.
C. Pay attention to the following:
1. Posture of body and extremities (e.g., leaning or pulling towards one side or
backwards, twisting or holding back one arm).
2. Length, speed, and rhythm of steps.
3. Base of gait (how far apart are the legs).
4. Arm swing (is it reduced unilaterally or bilaterally).
5. Steadiness.
6. Turning (steadiness of turns and number of steps required to complete the turn).
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. 7
6. What are the differencial diagnoses and the complications of each differential diagnoses?
a. Non Hemorragic Stroke
Definition :
Neurological deficit of cerebrovascular cause that persists beyond 24 hours or is
interrupted by death within 24 hours (WHO)
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)
Patogenesis :
Occlusion (partial or complete)
Lactic acid increased (oxidative process is replaced by the anaerob process causing
toxicity environment
Vasoparalysis
Swelling of
Brain tissue
If its only transient ischemic attack, the plaque may disintegrated into small piece, and
the obstructed blood vessel will be recirculated.
Symptoms :
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 pathwaysthe spinothalamic tract, corticospinal tract, and dorsal column
(medial lemniscus), symptoms may include:
numbness
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:
weakness in tongue (inability to stick out the tongue and/or move it from side
to side)
If the cerebral cortex is involved, the CNS pathways can again be affected, but also
can produce the following symptoms:
The symptoms of nausea and vomiting usually more typicall in the hemorrhagic
stroke due to the sudden increase of intracranial pressure.
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
Prognosis :
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
Hemorragic Stroke
Hemorrhagic stroke is approximately 20% of all types of stroke, caused by the rupture
of an aneurysm of the micro charcotatauetatcrible in the brain. Distinguished between
intracerebral hemorrhage, subdural and subarachnoid.
Age
Gender, pre-menopausal women is lower than men (1: 2). After the incident
hiperfibrinogenimia, etc.
Genetic
Hypovolemia and shock, especially in the elderly, where the reflex circulation
is not good anymore.
Lesions in capsule
More broadly, the area opposed to the lesion
Primary Sensation missing
Talk and eyesight may be affected
3. Heart problems
As a cause or as a complication of this situation requires special attention.
4.Respiratory disorders
Due to infection or due to an emphasis on the respiratory center
5. Infeksidan sepsis
Stroke is a serious complication. Kidney and liver disorders
Stress ulcer
Often causing hematemesis and melena
Chronic complications: chronic stroke due to frequent and need to be considered. Is:
Due to the long bed rest can happen pneumonia, decubitus, incontinence.
Recurrence of stroke
Impaired social-economic
psychological disorders
Management
Diagnosis to attain information among others:
Is the patient suffering from stroke or not
If it is a stroke, the location, type, and extent of the lesion. Gold standard is a CTscan and MRI
The status of patients overall, including TD, sugar, kardiorespi state, the state of
hydration, elektorlit,
Common treatments
To provide optimal care in the over lying to patients decreased consciousness, giving
it enough hydration treatments are also quite important. Besides assessment
swallowing disorders should also be considered.
Blood preassure
In early studies of stroke will increase the TD as compensation and returned to
normal within 2-3 days. Therefore high TD beginning pelu not corrected, except
reach very high values (systolic> 220 mmHg / diastolic> 130 mmHg) or the
emergency TD and TD is also slowly decline. To fall in BP is distinguished whether
a patient with chronic hypertension should be reduced to 180 / 100-105mmHg, if no
target hypertension 160-180 / 90-100mmHg, if planned thrombolysis systolic BP
should not exceed 180mmHg. In order to decrease the blood can be carried out
titration recommended drug labetalol / urapidil / nitoprusid or IV nitroglycerin or
oral katopril. Nefedipin or drugs that lowering BP too drastic needs to be avoided.
Blood Sugar
In the study an increase in blood sugar will aggravate brain damage, so that the
elevation of blood sugar levels in the first days of stroke should be lowered as
normal as possible, if necessary, by administering insulin syringe.
Kardiorespi circumstances.
It takes a good monitoring and given drugs if necessary, as this will cause death.
Stress ulcers, infections
Kidney or liver disorders is also noteworthy because it usually will determine the
survival of patients.
Pulmonary embolism and / or deep vein thrombosis
It is often a complication of stroke, how to avoid the provision of adequate hydration
Ischemic lesions
Repair tissue around the infarct (tissue penumbra) effort is intended that the area
does not become infarction, this area will be a chain of metabolic reactions, among
others influx of calcium ions and intracellular lactate, causing edema and necrosis
finally, here's some therapeutic action:
Fix the general status (TD, blood sugar, hydration, acid-base balance, kardiorespi
etc.)
Provision of anticoagulants (heparin, warfarin), thrombolysis is only done with
tissue plasminogen activator (rtPA), despite the use of heparin streptokinase showed
the results but will be complications hemorrhagic infarct area or other areas.
Giving antiagregasi platelets (aspirin) 100-300mg to reduce mortality and prevent
re meaningful stroke, aspirin should not be given if it will be done thrombolysis
Improved metabolic around the lesion, give a vasoconstrictor expected
vasodilation in lesion area
Early Rehabilitassi
Performed when the patient is stable, passive physiotherapy can be done while in the
intense and active physiotherapy proceed whenever possible, speech therapy, and
swallowing disorders can be granted if there is an interruption.
Primary tumours
Gliomas
Astrocytoma
Glioblastoma multiforme
Ependymoma
Oligodendroglioma
(including medulloblastoma)
Pituitary tumours
Pituitary adenoma
Craniopharyngioma
Pituitary carcinoma
Meningiomas
Benign
Malignant (meningiosarcoma)
Pineal tumours
Pinealoblastoma
Pinealocytoma
Grminoma
Teratoma
Intracranial lymphoma
Histiocytic lymphoma
Microglioma
Acoustic
Chordoma
Neuronal tumours
Ganglioneuroma
Ganglioglioma
Colloid cyst
2.
Secondary tumours
Common sites of origin
Lung
Breast
Melanoma
Less common sites of origin
Ovary
Testis
Gut
Bladder
Kidney
Pancreas
Liver
Leukemia and lymphoma
Miscellaneous
Langerhans cell histiocytosis
3.
Etiology
4.
Epidemiology
6.
Clinical features
42
8.
1.
The tumour can exert a mass affect and lead to raised intracranial
in
thyroid-stimulating
hormone
(TSH)
production,
only see a new case of a childhood cancer every six years, of which
about a quarter will be brain tumours.
10.
11.
Supporting Examination
12.
Management
14.
Prognosis
17.
46
prognosis
following
surgical
removal
and,
where
appropriate,
normal numbers.
Control the blood tension.
Get an angiography.
Consule to The Spesialist of Nerve Surgery.
Give a mannitol 20% for patient in comateus.
Give Fenitoin if theres a wide bleeding and low consciousness. 10
Give a hipervolemic fluid and nifodipin to prevent a vasospasme.10
27.
8. How to prevent this disease?
1) Primary
a. National campaign
b. Free and Health life style withour stroke
2) Secondary
a. Modifice a risk life style.
b. Family support
c. Medica mentosa
d. Invasif action: flebotomi for polysutemia, enarterectomy, etc.10
28.
9. What are the risc factors related by this case?
29.
30.
- Age
31.
- Gender
32.
- Ethnic
33.
- Family History
48
34.
35.
36.
a. Hypertension
37.
b. General fibrillation
38.
c. Smoking
39.
d. Diabetes
40.
e. Hyperlipidemia
41.
f. Carotid stenosis
42.
43.
h. Obesity
44.
45.
46.
a. Heart disease
1)
2)
3)
4)
5)
6)
Myocard infarction
Left ventrivuly dysfunction
Heart valve disease
Left ventrivuly hypertrophy
Septurm atrium aneurysm
Mitral anuler calsification
47.
48.
49.
50.
e. Lipoprotein
51.
f. Alcohol consumption
52.
g. Oral contraception
49
56.
53.
h. Druge abuse
54.
i. Hyperfibrinogemia
55.
j. Migrain
57.
58.
59.
10. What is the Islamic perspective related to this case?
Prophet said
:
60.
Sujoods benefit
61.
benefits
62.
cause our blood that full of oxygen will flow more to our brain.12
F. SUMMARY
63. 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.
64.
65.
66.
67.
68.
69.
70.
71.
72.
73.
74.
50
75.
76.
77.
78.
79.
80.
81.
82.
G. DAFTAR PUSTAKA
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
3. Manshoer, Arif. 2001. Kapita Selekta Kedokteran edisi 3 jilid 2. Jakarta.
4. Guyton and Hall. 2006. Textbook of Medical Psycology 11 th Edition.
Philadelphia: Elsevier
1
Grote E, Hassler W. The critical first minutes after subarachnoid
5.
of
Neurology
and
Neurotherapeutics.
http://www.strokecenter.org/patients/caregiver-and-patientresources/aphasia-information/
7. 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_Lectur
e_Notes.pdf June 1st 2015
8. Wade S. Smith, S. Claiborne Johnston, J Donald Easton. Cerebrovascular
Disease. Harrison : The Principles of Internal Medicine vol.4. Chapter
370.
9. Tobias J. and D. Hochhauser. 2010. Cancer and its Management ed. 7th.
USA: Wiley Blackwell.
10. Manshoer, Arif. 2001. Kapita Selekta Kedokteran edisi 3 jilid 2. Jakarta.
11. http://eprints.undip.ac.id/33923/3/Bab_2.pdf )
12. Hizbut Tahrir Journal. 12/11/2014
83.
84.
51