A.

Scenario

A 56 years old woman suddenly experience weakness of left body and right facial drop
since 2 days ago, headache and vomiting. Patient also difficult to communicate and look
sleepy.

B. Keywords
 A 56 years old woman suddenly experience weakness of left body and right
facial drop since 2 days ago
Patient also having headache and vomiting
Patient difficult to communicate and look sleepy

C. Questions
1. What is neuroanatomy and neurophysiology according to scenario?
2. What is the pathomechanism of hemiperese and the etiology?
3. What is pathomechanism of vomiting and headache?
4. Why patient look sleepy and difficult to communicate?
5. What is the pathomechanism of facial drop?
6. How to diagnose?
7. What is the differential diagnosis?
A. Hemorrhagic stroke
B. Non-hemorrhagic stroke
C. Meningioma
8. What is the first managemen
9. How the Islamic perspective?

D. Answers
1. What is neuroanatomy and neurophysiology according to scenario?
Jawab :

2. What is the pathomechanism of hemiperese and the etiology?

Jawab :
Primary motor cortex
The primary motor cortex (girus presentralis) is a set of tissues cortically located
on the side that is flanked by the central sulcus of primary somatosensory cortex (in
postsentralis gene). And extends upward and passing through the superomedial edge
of the cerebral hemisphere to its medial surface. Area which presents the throat and
larynx located at the inferior end. Primary motor cortex; on top of it, on an ongoing
basis, is the area which represents the face, upper limb, body, and lower extremities.
This structure is "homunculus motoric".

Corticospinal tract
This tract is derived from the motoric cortex and runs through substantia alba
Cerebri (corona radiate), posterius crucial internal capsule (fibers located very
Adjacent here), the central part of the cerebral peduncle, the pons, and Basal medulla
(anterior portion), where the tract is seen as a small protrusion Called pyramid. At
the lower end of the medulla, 80-85% fibers. Pyramidal crosses to the other side of
the decuscation pyramidum. No fibers Crosses here running down the spinal cord in
the anterior funiculus Ipsilateral as an anterior corticospinal tract; these fibers cross
more Down (usually at the level of the segment it supplies) through the anterior
commissure Spinal cord. At the cervical and thoracic levels, there is also a possibility
some fibers that remain intangible and supply the motor neurons Ipsilateral in the
anterior horn, so muscleot Neck and body gain Bilateral cortical innervation.
The majority of pyramidal tract fibers crosses the decuses of the pyramidium,
Then down the spinal cord in the contralateral lateral funiculus Lateral corticospinal
tract. This tract decreases in the area of its intersection When walking down the spinal
cord, because of some fibers Ends in each Segment along the way. About 90% of All
 fibers of the pyramidal tract end up forming a synapse with an interneuron,Which
then imparts the motoric impulse to the large motor neurons on Horn anterius, as
well as to smaller motoric neurons.

UMN
Generally, Upper Motoric Neuron (UMN) paralysis strikes next door ody so
called hemiparesis, hemiplegia, or hemiparalisis, because The lesion occupies a
pyramidal composition area. The three terms are Meaning paralysis of the body is
used freely, though. Hemiparesis actually means mild and mild limb paralysis
Hemiplegia or hemiparalysis means severe paralysis of the body.
Hemiplegia alternans due to lesions in the pons are forever UMN paralysis
Which involves the contralateral side hemisphere, which is below the level Lesions,
which combine with LMN paralysis of the muscles Which is innervated By nervus
abdusens (n VI) or facial nerve (n.VII) Alternative hemiplegia syndrome in the
medulla oblongata Regional area Vascularization in the medulla oblongata
corresponds to the lesilesi area The underlying hemiplegia alternans syndrome in the
medulla oblongata. Part Paramedian medulla oblongata is elevated by a.vertebralis
branch. Part Laterally obtaining vascularization of the posterior inferior a.serebelli,
whereas The dorsal portion is fixed by a. The posterior spinal and inferior a.serebelli
Posterior. Unilateral lesions that produce hemiplegia alternans are obvious Occupy
the pyramid region of the sides and must be crossed by the root of the nerve
Hypoglossus, then from the paralysis of the UMN paralysis that occurred struck The
contralateral hemisphere that is below the level of the neck and accompanied by LMN
paralysis of the ipsilateral side of the tongue. That's the hemiplegia syndrome
Alternans of the hypoglossal nerve or medial medial syndrome.

a. Hemiplagia due to hemillitis in the primary motor cortex

Damage to the entire pyramidal cortex may result in paralysis UMN on
the contralateral side of the body. The condition is known as Hemiparalysis
or hemiplegia. Complete damage, but not yet Tearing down all cortical
 parrots of the pyramidal cortex, causing paralysis In the mild to moderate
contralateral hemispheres. In this case Used the term hemiparesis.
Although the right or left hemisphere is paralyzed, it is generally present
Different degrees of paralysis between the affected arm and limb. Difference
More pronounced if hemiplegia is caused by vascular lesions at the cortical
level and There is almost no difference if the lesion is vascular in the capsule
Interna.

b. Hemiplagia due to hemillitis in the internal capsule

The internal capsule region is bypassed by the fibers The order of
extrapyramidal. Hence, the paralysis of lesions in the internal capsule is
almost always With typical hypertonia. Signs UMN can arise clearly.
Hypertonia due to lesions in the region of pyramidal arrangement, called
spasticity, Can only be found in a group of certain muscles that are paralyzed,
so Causing an abnormal movement

c. Hemiplegia alternans due to hemillitis in the brain stem

Alternative hemiplegia syndrome in mesensefalon
Hemiplegia alternans in which the ipsilateral oculomotor nerve is
involved are known As hemiplegia alternans n. Okulomotorius or Weber
syndrome. As for Manifestations of n.III paralysis are (a) paralysis m.
Rectus internus (medial), M. Superior rectus, m. The inferior rectus m.
The inferior oblique and m. Palpebral levator Superior so that there is:
strabismus divergens. Diplopia if looked over Majors and ptosis, (b)
paralysis m. Sphincter pupilae, so that there are pupils Widen (=
midriasis)

Alternans hemiplegia syndrome in the pons

Hemiplegia alternans in the pons are caused by unilateral vascular
lesions. Aligned With arteriarotic branching pattern, Then the vascular
 lesions in the pons can be divided In: (1) a peramedian lesion due to
blockage of one branch of hemp Perforantes medialis a. Basilar, (2)
lateral lesions, corresponding to the region Short circular bleeding, (3)
lesions in the section tegmentum Rostral punch due to blockage a.
Superior serebelli, and (4) tegmental lesions The caudal part of the
punch, which corresponds to the circumferential region of the
circumferential branch the long one.

LMN
LMN paralysis arises from damage to the 'final common path', 'motor end Plate
'and muscle. The term 'common common path' of Sherrington is sufficient 'lower'
Motorneuron and axon. Below this LMN paralysis will be described According to its
components LMN.
1. LMN paralysis due to lesions in the motorneuron
2. LMN paralysis due to lesion in ventralist root
3. Paralysis from damage to the brachial plexus
4. Paralysis from lesions in the lumbosacral plexus
5. Paralysis due to lesions in the fascia
6. Paralysis due to lesions in peripheral nerves

Etiology of hemiperese
o Stroke
Often referred to as cerebro vascular accident (CVA), Cerebrovescular
insult (CVI), or in layman's language is called an attack on the brain Caused
by loss of brain function due to disruption of blood supply to the brain. This
disorder can be caused by ischemia (lack of blood flow) or bleeding. As a
result, the affected part of the brain is not biased in functioning Normal, which
may result in an inability to move one or More limbs on one side of the body,
failure to understand or Formulate sentences, or disturbances of vision from
one side of the field of view
 o Infection: a brain abscess
A brain abscess (or cerebral abscess) is an abscess caused by
inflammation And the collection of infected materials, originating from an
infection source, either Local (ear infection, dental abscess) or remote (lung,
Heart, kidneys etc) Occurs in brain tissue. Infections can also occur due to
skull fractures After head trauma or surgical procedure.

o Neoplastic: Meningioma
Meningioma is a tumor arising from the meninges, the membrane layer
Which surrounds the system of arachnoid cells in the arachnoid villi in the
meninges. Is a benign tumor, but there is a small part of the malignant. Most
meningiomas do not give symptoms, and do not require Treatment other than
periodic observers. Symptomatic meningioma is usually treated Using radio
surgery or conventional surgery.

o Demyelination: multiple sclerosis

Multiple sclerosis (MS), also referred to as disseminated sclerosis or
Ecephelomyelitis disseminate is an inflammatory disease that attacks The
wrapping layer of blood cells in the brain and the spinal cord. This damage
Can impair the ability of the nervous system part to communicate, Causing
various signs and symptoms including physical, mental, or physical
symptoms One's psychic problem. Multiple sclerosis has some form of
clinical and symptomatic manifestations, both Which occurs in isolated
attacks (relapse) or increases from time to time Time (progressive). Among
the attacks, symptoms can disappear completely. However, Permanent
neurological problems are common, mainly due to development disease.

Compston A, Coles A (October 2008). Multiple sclerosis. Lancet 372 (9648): 150217.
 Duus, Peter. Diagnosis Topik Neurologi : anatomi, fisiologi, tanda, gejala, Jakarta :
EGC. 2010
Mahardjono, Mahar & Priguna Shidarta. 2003. Neurologi Klinis Dasar. Jakarta : EGC .
Hal 2027

3. What is pathomechanism of vomiting and headache?

Jawab :
Vomiting
The ability to regurgitate is an advantage because it allows the release of toxins
from the stomach. Vomiting occurs when there is stimulation of the vomiting center,
a control center in the medulla adjacent to the respiratory center or the Chemoreceptor
Trigger Zone (CTZ) in the postrema area on the fourth ventricular floor of the
Nervous System. Coordination of the vomiting center can be trans- ferred through
various pathways. Vomiting can occur due to psychological distress through the
pathway of the cerebral cortex and limbic system to the vomiting center (VC).
Prevention of vomiting may be via this mechanism. Vomiting occurs when the
vomiting center is aroused through the vestibular or vestibuloserebella system from
the labyrinth in the ear. Chemical stimulation through blood or cerebrospinal fluid
(LCS) will be detected by CTZ. This mechanism is the target of many anti-emetic
drugs. Vagal and visceral nerves are the fourth pathway that can stimulate vomiting
through gastrointestinal irritation with slow digestive tract and gastric emptying.
Once the vomiting center is aroused then this cascade will run and will cause
vomiting. Vomiting is a complex behavior, in which vomiting consists of three
related activities, nausea (nausea), retching and gastric contents. There are two
regions of the anatomy in the medulla that control vomiting, 1) chemoreceptor trigger
zone (CTZ) and 2) central vomiting center (CVC).
CTZ is located in the postrema area at the base of the ventricular IV caudal end
outside the blood brain barrier. Receptors in this area are activated by proemetic
materials in the blood circulation or in the cerebrospinal fluid (CSF). The efferent
 from CTZ is sent to the CVC and then a series of events begun through vagal eferan
spanchnic. The CVC is located dinukleus tractus solitarius and adjacent to the
medulla reticulular formation just below the CTZ.
CTZ contains receptor receptors for a variety of neuroactive signals that can
cause vomiting. Receptors for dopamine are the working points of apomorphine
acethylcholine, vasopressine, enkephalin, angiotensin, insulin, endhorphine,
substance P, and other mediators. The 3 ', 5' cyclic monophosphate (cyclic AMP)
mediator may be involved in the excitation response for all peptides. Stimulators by
theophyline may inhibit the proemetic activity of the neuropeptic material. Emesis in
response to irritant gastrointestinal eg sopper, abdominal radiation, gastrointestinal
dilatation is as a result of vagal aferan signals to a central patter generator induced by
the release of local mediator of inflammation, from damaged mucosa, with secondary
exclusion of the most important excitation neurotransmitters is serotonin from the
cell Mucosal entrochromaffin. In motion sickness, afferent signals to the central
patter generator come from the higher vestibular organ, visual cortex, and cortical
center as integrated sensory inputs are more important than the afferents of the
gastrointestinal 4. Vomiting stimulation comes from gastrointestinal, ocular
vestibule, The higher cortical afferent, which leads to the CVC and then begins
nausea, retching, gastric contents of the contents. Gastrointestinal symptoms include
peristaltic, salvias, takhipnea, tachycardia.
Referensi: dr. deddy satriya putra. Sp.A. patofisiologi muntah . arifin achmad
general hospital faculty of medicine. University of riau.2009.

Headache
Some theories that cause headache continue to develop until now. Like, cranial
vasodilation theory, peripheral trigeminal activation, localization and second order
physiology trigeminovascular neurons, cortical spreading depression, activation of
rostral brainstem.
Stimulation of pain can be caused by pressure, traction, displacement and
chemical processes and inflammation of nociceptors-nociceptors in pain-sensitive
structures in the head. If such structures are located on or above the tentacles of the
cerebelli stimulated, the pain will arise in the region of the vertical line drawn from
both left and right ears across the top of the head (frontotemporal and parietal regions
anterior). The pain is transmitted by the trigeminal nerve. While stimulation of pain
sensitive structures below tentorium (on the posterior cranial fossa) the upper cervical
spine with peripheral nerve branches will cause pain in the area behind the line, ie
the upper occipital, suboxipital and cervical regions. The pain is transmitted by the
cranial nerves IX, X and the spinal nerves C-1, C-2, and C-3. However, sometimes
the upper cervical spine and the major occipital nerve will spread the pain to the
frontal and the eye on the ipsilateral side. It has been shown that there is a close
relationship between the trigeminal nucleus and the dorsal root of the upper cervical
segment. Trigemino cervical reflex can be proven by stimulation of n.supraorbitalis
and recorded by electrode installation on sternokleidomastoideus muscle. The
exteroceptive and nocictive input of the trigemino-cervical reflex is transmitted via a
polysynaptic route, including the trigeminal spinal nuclei and achieves the cervical
motorneuron. With this relationship it is clear that pain in the neck area can be felt or
forwarded to the head and vice versa. One of the most popular theories about the
cause of headache is the contraction of facial, neck, and shoulder muscles. The
muscles that are usually involved include m. Splenius capitis, m. Temporalis, m.
Masseter, m. Sternocleidomastoideus, m. Trapezius, m. Posterior cervicalis, and m.
Levator scapulae. The study says that these headache sufferers may have greater
facial and head muscle tension than others who make them more susceptible to
headaches after muscle contraction. This contraction can be triggered by long-held
body positions causing tension in the muscles or the wrong sleeping position. There
is also a saying that patients with chronic headaches can be very sensitive to pain in
general or an increase in pain against muscle contraction.
A theory also says the tension or stress that produces muscle contraction around
the skull causes vasoconstriction of blood vessels resulting in reduced blood flow that
causes oxygen inhibition and accumulation of metabolic outcomes that will
eventually cause pain.
 Researchers are now beginning to believe that these headaches can arise from
changes in certain chemicals in the brain - serotonin, endorphins, and some other
chemicals - which help in neural communication. This is similar to the biochemical
changes associated with migraine. Although it is not yet known how these chemicals
fluctuate, there is the assumption that this process activates pain pathways to the brain
and impairs the brain's ability to suppress pain. On the one hand, muscle tension in
the neck and scalp can cause headaches in people with chemical disorders.
Referensi: Sjaharir hasan. Fakultas kedokteran.mekanisme terjadinya nyeri
kepala dan prospek pengobatannya. Universitas Sumatra utara

4. Why patient look sleepy and difficult to communicate?

Jawab :

5. What is the pathomechanism of facial drop?

Jawab :
The upper muscles of the face get innervation from two sides. Therefore, there is a
difference between the symptoms of central and peripheral nerve palsy VII. In the central
disorder, around the eyes and forehead that gets innervation from two sides, is not paralyzed;
The lame is the bottom of the face. In the N interference VII kinds of peripheral (disturbance
is in the nucleus or nerve fibers) then all the facial muscles paralyzed and mugkin sesisi also
includes a nerve branch that takes care of tasting and the secretion of saliva which runs
alongside the facial nerve.
The core part motor takes care of the lower face gets innervation of the contralateral
motor cortex, while taking care of the upper face receive innervation from both sides of the
motor cortex (bilateral). Because damage to the upper side motor neurons from nerve VII
will result in paralysis of the lower facial muscles. While the top is not. In lower motor
neuron lesions, all ajah muscle movements, either volunteer, or involuntary, are paralyzed.
Supranuclear lesions of nerve VII are often part of hemiplagia. This can be seen in stroke
and lesion-need-space of the motor cortex, internal capsule, thalamus, pons above
mesensefalon and VII nerve nucleus. In such cases the tasting and salvias are not disturbed.
 Supranuclear VII nerve paralysis on both sides can be found in paralysis pseudobulber
So the lesion is divided into two: in the central facial paralysis (also called paralysis of lower
face) caused by supranuclear lesions (lesions kortikonuklear fibers, for example, as a result
of the internal capsule infarction). In contrast to lesions due infranuklear and bilateral
innervation of the mimic muscles in the eye and forehead, only the bottom and showing the
face contralateral motor defect. Infranuklear lesion (inferior facial nuclei), for example
caused by malignant parathyroid tumors, causing paralysis of all the facial motor branch N
[VII] side of the disorder (peripheral facial paralysis)

Reference :
Paulsen, F. 2013. Sobotta Atlas Anatomi Manusia. Edisi 23. Jilid 3. Jakarta : EGC.
Hal 310-311 Lumbantobing, S.M. Neurologi Klinik. Pemeriksaan Fisik dan
Mental. Jakarta : FK UI.

6. How to diagnose?
Jawab :
In order to establish a diagnosis of neurological diseases required anamnesis
examination, physical examination, mental examination and laboratory (support).
Neurological examination includes: examination of consciousness, excitement of the lining
of the brain, brain nerves, motor system, reflex sensory system and mental examination
(noble function).
Over the decades advanced science and medical technology have developed rapidly.
Many tools and facilities are available, and provide very important help in diagnosing the
disease as well as assessing the development or course of the disease. Currently we can easily
diagnose bleeding in the brain, or malignancy in the brain through imaging examination. We
can also easily determine the polyneuropathy and its development through electrical
inspection.
In addition to this rapid advancement, physical bedside and bedside checks still play an
important role. We can even improve the examination capabilities on the bedside with the
help of sophisticated technological tools. We can sharpen the ability of physical and mental
examination with the help of the advanced tools we have.
Until now we are still and have to cultivate our ability to see, hear, and feel, and observe
the state of the patient. With careful examination of history, physical and mental, we can
determine the diagnosis, and the necessary investigations.

Anamnesis
In examining neurological diseases, history of disease data is important. A doctor
may not have the opportunity to follow the disease from the beginning. Usually the
patient comes to the doctor at the time the illness is in progress, sometimes even
when the illness is healed and the complaints he suffered are residual symptoms. In
addition, there are also diseases whose symptoms occur at certain times; So, in the
form of an attack. Beyond the attack, the sufferer is in good health. If the patient
comes to a doctor outside of an attack, it is difficult for the doctor to make a
diagnosis of the illness, except with the help of the report presented by the patient
(anamnesis) and the person who witnessed it (allo-anamnesis).
Not infrequently also a disease has a certain journey. Because the course of the
disease often has a certain pattern, then in making the diagnosis we need to explore
the travel data of the disease. A physical disorder can be caused by various diseases.
By knowing the course of the disease, we can approach the diagnosis, and
unnecessary laboratory checks can be avoided. It is no exaggeration to say that: "A
good history brings us halfway to the right diagnosis."
To have a good history takes patience and attentive examiner, and adequate time.
Taking anamnesis should be done in a separate place, so as not heard by others.
Usually taking anamnesis follows two general patterns, namely:
1. The patient is allowed to express freely all his complaints and abnormalities.
2. The examiner (doctor) guides the patient to express his or her complaints by
questioning the question.
Taking a good history combines the two ways mentioned above. Typically
interviews with patients begin by asking for name, age, occupation, address. Then
asked the main complaint, the complaints that encourage patients come to see a
doctor.
In each complaint or abnormality it is worth exploring:
1. Since when started
2. Nature and severity
3. Location and spread
4. The relationship with time (morning, noon, night, sleep, time of menstruation,
after eating and so forth)
5. Other complaints related to the complain
6. Previous treatment and how the results
7. Factors that make complaints heavier or lighter
8. Travel complaints, whether sedentary, gaining weight, getting lighter, coming
in the form of an attack, and so forth

In each nerve disease patient should also be explored the possibility of

complaints or abnormalities below by asking the following questions:
1. Headache: Are you suffering from headaches? How is it, in the form of an
attack or continuously? Where is the location? Is progressive, getting heavier
or more frequent? Is it to interfere with daily activities?
2. Vomiting: Is it accompanied by nausea or not? Is this sudden vomiting,
suddenly, as if the contents of the stomach are thrown out (projectile)?
3. Vertigo: Have you ever felt as if you were moving, spinning or you felt
yourself moving or spinning? Does it have anything to do with changing
attitudes? Is it accompanied by nausea or vomiting? Is it accompanied by
tinnitus (ear ringing, hissing)?
4. Visibility Impairment (visus): Does your visual acuity decrease in one or both
eyes? Do you see a double (diplopia)?
5. Hearing: Is there a change in your hearing? Is there a tinnitus (ringing / hissing
in the ear)?
6. Other brain nerves: Are there interference with olfaction, tasting, salivation
(salivation), lacrimation (expression of tears), and feelings on the face? Are
 there any facial muscle weaknesses? Is it a lisp and a pelo? Does your voice
change, so hoarse, or bindeng (dysphonia), or so diminish / disappear
(afonia)? Is it a lisp and a pelo (dysarthria)? Is it difficult to swallow
(dysphagia)?
7. Sublime function: What about memory? Are you forgetful? Do you find it
difficult to express your thoughts (dysphasia, motor dysfasia) or understand
other people's conversations (dysphasia, sensory aphasia)? What about the
ability to read (aleksia)? Is it difficult to read, and understand what you read?
What about the ability to write, whether the ability to write changed, the form
of writing changed?
8. Awareness: Have you suddenly lost consciousness, not knowing what is going
on around you? Have you ever felt weak and like want to faint (syncope)?
9. Motoric: Are there any parts of your body that are weak, or lame (hands, arms,
legs, legs)? How is it, disappear, settled or diminished? Is your movement not
dexterous? Is there any movement on body part or abnormal body extremities.

Physical examination
a. General Inspection
Sensorium (awareness), Awareness level is divided into several:
o Normal: compost mentis
o Somnolen: Drowsiness. Awareness can be fully recovered when
stimulated. Somnolen is also called lethargy. This level of
consciousness is characterized by the ease with which the patient is
awakened, able to give verbal answers and fend off excitatory pain.
o Sopor (stupor): Deep sleepiness. The patient can still be awakened
with a strong stimulus, but his consciousness soon decreases again.
He was still able to follow a brief message and still looks
spontaneous movement. With excitatory pain the patient can not be
built perfectly. The reaction to the command is inconsistent and
 vague. Can not get verbal answers from patients. Motion motion to
fend off excitatory pain is still good.
o Coma - light (semi-coma): In this state there is no response to the
verbal stimuli. Reflexes (cornea, pupils etc.) are still good.
Movement mainly arises in response to excitatory pain. Patients can
not be awakened.
o Coma (in or complete): There is no spontaneous movement. There
is no answer at all to the excitement of the pain which however
powerful.
o Glasgow Coma Scale

b. Neurological Examination
1. Examination of awareness function.
Consciousness can be defined as a state that reflects the
integration of the afferent and afferent impulse, the whole of the
afferent impulse is called the central nervous system impulse and the
whole of the efferent impulse can be called the central nervous system
output. The current level of consciousness examination is the scale of
GLASGOW (Glasgow Coma Scale) that is more practical for general
practitioners and nurses because of clearer and more systematic
criteria. The scale of Glasgow is in addition to determining the level
of consciousness, it is also useful for determining the prognosis of the
treatment of a disease

2. Examination of noble cortical function.

Examination of mental status is an evaluation of cognitive and
emotional functions that must be done coherently and systematically.
Start with basic functions of awareness level, then basic cognitive
functions such as language and more complex examinations such as
arithmetic, consideration, etc.
 3. Examination of excitatory menses.
4. Check the coordination function.
5. Cranial nerve examination.
6. Examination of motor function: movement, muscle strength, and
muscle tone.
7. Examination of motor function: movement, muscle strength, muscle
tone.
8. Physiological reflex examination: bicep reflex, triceps,
brachioradialis, patellar, achilles, and abdominal.
9. Pathological reflex examination: Babinski, Hoffmann - Tromner,
Oppenheim and other variations.
10. Primitive reflex examination: Snout, Rooting, Palmomental, Glabella,
and Grasp reflexes.
11. Sensory function checks: pain, temperature, touchiness,
propioceptive, and discriminatory sensations.
12. Other physical neurological examinations: Chvostek, Laseque,
Patrick, and counter-Patrick.

c. Additional examination
According to Doenges, (2000) diagnostic tests that can be performed on
stroke are:
1. Cerebral angiography: helps determine the specific cause of stroke
such as bleeding, arterial obstruction or presence of occlusion /
rupture points.
2. CT-scan: attention to the presence of edema, hematoma, ischemia,
and the presence of infarction.
3. Lumbar puncture: indicates a normal pressure and usually there is
thrombosis, cerebral embolism, and TIA (Transient Ischaemia
Attack) or a cinematic ischemic attack. Increased pressure and
blood-borne fluid suggest subarachnoid hemorrhage or intra-cranial
 haemorrhage. The total protein content is increased in cases of
thrombosis due to the inflammatory process.
4. MRI (Magnetic Resonance Imaging): shows areas infarcted,
hemorrhagic, and arteriovenous malformations.
5. Doppler ultrasonography: identifies arteriovenous disease.
6. EEG (Electroencephalography): identifies the disease based on brain
waves and may show specific lesion areas.
7. X-ray: describes changes in pineal plate gland area opposite from the
expanding mass, internal carotid calcification is present in cerebral
thrombosis.

Referesi??

7. What is the differential diagnosis?

Jawab :
A. Hemorrhagic stroke
Definition
Stroke is a disease that occurs due to disruption of blood circulation of the brain
that can cause brain tissue death resulting in paralysis and even death in stroke
patients, stroke is divided into two types of hemorrhagic stroke and non
hemorrhagic stroke.
According to the World Health Organization (WHO) in Muttaqin (2011)
a stroke is defined as a disease caused by a sudden onset of blood disordered
diuretics with local and global clinical signs and symptoms that last for 24 hours
or more that can cause death. Hemorrhagic stroke is a bleeding that occurs
because the rupture of blood vessels in certain areas of the brain and non-
hemorrhagic stroke is the cessation of all or blood flow to the brain due to
blockage of blood vessels of the brain (Wiwit, 2010). Stroke is caused by
arteriosclerotic plaques that occur in one or more feeding arteries to the brain
that activate the blood clotting mechanism and inhibit blood flow in the arteries,
 causing acute brain function loss in the allocated area. Non hemorrhagic stroke
occurs in blocked blood vessels resulting in reduced blood flow in brain tissue,
cerebral thrombosis, atherosclerosis, and cerebral embolism, which is a blockage
of blood vessels arising from plaque formation resulting in narrowing of blood
vessels due to heart disease, diabetes, obesity, cholesterol, smoking, stress,
lifestyle, breakdown or destruction of upper motor neurons, , And hypertension.

Pathophysiology of Non Hemorrhagic Stroke

Non hemorrhagic stroke is closely related to arterosclerotic plaque that can
activate blood clotting mechanisms to form thrombus that can be caused by
hypertension. Thrombus can rupture from the blood vessel wall and will carry as
embolism in the bloodstream resulting in ischemia of the brain tissue and cause acute
or permanent brain function loss in the allocated area. Ischemia of the brain damages
the motor pathways of the cerebrum. Ischemia in the brain also results in brain stems
containing sensory and motor nuclei carrying motor and sensory function impaired
so that the whole body and balance settings are impaired. Areas in the brain that
require signals for movement and muscle coordination are not transmitted to the
spinal cord, nerves and muscles so that motor fibers in the nervous system are
impaired to control strength and movement and may result in disability in stroke
patients. Ischemia in the brain may also result in neurologic deficits.

Signs and Symptoms of Non Hemorrhagic Stroke

A stroke causes various neurological deficits, depending on which lesions or
blood vessels are blocked and the size of the area inadequately perfusinya. The
function of the damaged brain can not improve completely. Neurological deficits in
stroke include:
1. Motor deficit
The most common motor dysfunction is paralysis on one side or
hemiplegia due to lesions on the opposite side of the brain. At the start of the
stroke stage, the clinical picture that appears is paralysis and the loss or
decline of deep tendon reflexes or decreased muscle strength to do. If this
 internal tendon reflex reappears normally within 48 hours, an increase in tone
accompanied by spasticity or an increase in abnormal muscle tone in the
affected limb can be seen.

2. Communication deficit
Language and communication functionality can be manifested by the
following:
o Difficulties in forming the word (dysarthria), is indicated by the difficult
to understand speech caused by muscle paralysis responsible for
producing speech.
o Speech or defective speech loss (dysphasia or aphasia), which is
particularly expressive or receptive
o Inability to perform previously learned actions (apraxia) is seen when
the patient takes a comb and tries to comb his hair.

3. Sensory perception deficit

Sensory perception disorders are an inability to interpret sensations.
Sensory perception disorders in stroke include:
o Visual perception dysfunction, due to a primary sensory barrier
disorder between the eye and the visual cortex. The loss of half a field
of view is temporary or permanent (homonimus hemianopsia). The
affected visual side is related to the paralytic side of the body. The
head of the patient turns away from the sick side of the body and tends
to ignore that the place and space on that side are called
amorphosynthesis. In this situation the patient is only able to see food
on half a tray, and only half the room is visible.
o Impaired visual-spatial relationships that get the relationship of two or
more objects in the spatial area are often seen in patients with left
hemiplegia. Patients can not wear clothes without help because of the
inability to match clothes to body parts.
 Sensory loss, because a stroke can be mild or severe light damage with loss
of proprioception is the ability to sense the position and movement of the body
and difficulty in interpreting visual, tactile, and auditory stimuli.

4. Deficit of cognitive function and psychological effect

This dysfunction is shown in a limited field of vision, difficulty in
comprehension, forgetting, and lack of motivation that causes this sufferer to
face stress problems in the rehabilitation program.
5. Bladder deficit
Impaired motor and postural control causes post-stroke sufferers to
experience inability to use urinal, experiencing temporary urinary
incontinence due to confusion. Muscle tone increases and reflexes tendon
returns, increased bladder tone, and bladder spasticity may occur.

Management of Non Hemorrhagic Stroke

According to for the management of acute phase stroke patients if stroke patients
present with coma at admission may be considered to have a poor prognosis. Patients
are fully awake when hospitalized face the results that can be expected. The acute
phase lasts 48 to 72 hours by maintaining airway and ventilation
Adequate is a priority in this acute phase. Management in the acute phase includes:
1. The patient is placed in the lateral position with the head position of the bed
slightly elevated until cerebral venous pressure is reduced.
2. Endotracheal intubation and mechanical ventilation are necessary for patients
with massive strokes, as respiratory arrest may be a life-threatening factor in this
situation.
3. Monitor for pulmonary compliation such as aspiration, atelectasis, pneumonia
associated with ineffective airway, immobility or hypoventilation.
Hemorrhage Stroke
About 13 percent of strokes happen when a blood vessel ruptures in or near the brain. This is
called a hemorrhagic stroke as shown at right. When a hemorrhagic stroke happens, blood
collects in the brain tissue. This is toxic for the brain tissue causing the cells in that area to
weaken and die.

There are two kinds of hemorrhagic stroke. In both, a blood vessel ruptures, disrupting blood
flow to part of the brain.
Intracerebral hemorrhages (most common type of hemorrhagic stroke):
Occur when a blood vessel bleeds or ruptures into the tissue deep within the brain.
Are most often caused by chronically high blood pressure or aging blood vessels.
Are sometimes caused by an arteriovenous malformation (AVM). An AVM is a cluster
of abnormally formed blood vessels. Any one of these vessels can rupture, also
causing bleeding into the brain.

Subarachnoid hemorrhages:
Occur when an aneurysm (a blood-filled pouch that balloons out from an artery) on or
near the surface of the brain ruptures and bleeds into the space between the brain and
the skull.
Are often caused by high blood pressure.

In addition to high blood pressure, factors that increase the risk of hemorrhagic strokes
include:
cigarette smoking
use of oral contraceptives (particularly those with high estrogen content)
excessive alcohol intake
use of illegal drugs

How are hemorrhagic strokes diagnosed?

When someone has shown symptoms of a stroke or a TIA (transient ischemic attack), a doctor
will gather information and make a diagnosis. He or she will review the events that have
occurred and will:
get a medical history
do a physical and neurological examination
have certain laboratory (blood) tests done
get a CT or MRI scan of the brain
 study the results of other diagnostic tests that might be needed
Diagnostic tests examine how the brain looks, works and gets its blood supply. They can
outline the injured brain area. Diagnostic tests fall into three categories.
Imaging tests give a picture of the brain similar to X-rays.
Electrical tests record the electrical impulses of the brain (also called an EEG).
Blood flow tests show any problem that may cause changes in blood flow to the brain.

How are hemorrhagic strokes treated?

Because hemorrhages may be life-threatening, hospital care is required. Medication is
used to control high blood pressure. Other medicine may be given to reduce the brain swelling
that follows a stroke.
Surgery may be needed depending on the cause and type of the hemorrhage. Surgery is
often recommended to either place a metal clip at the base of an aneurysm or to remove the
abnormal vessels that make up an AVM.
Some procedures are less invasive and use of a catheter that goes in through a major
artery in the leg or arm. The catheter is guided to the aneurysm or AVM where it places a
device, such as a coil, to prevent rupture.

A. Non-hemorrhagic stroke
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B. Meningioma
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a. Definition
Three layers of membranes, called meninges, lying just under the skull, protect
the brain and spinal cord. From the outermost layer inward they are: the dura,
arachnoid, and pia. A meningioma grows from the arachnoid cells that form the
middle layer, and are firmly attached to the dura . Some meningiomas contain cysts
or calcified mineral deposits, and others contain hundreds of tiny blood vessels.
Because meningiomas tend to grow inward, they commonly cause pressure on the
brain or spinal cord. They can also grow outward causing the skull to thicken
(hyperostosis).

b. Epidemiology
 Meningiomas represent about 36% of all primary brain tumors and 12% of all
spinal cord tumors. They can occur in children, but most often occur in adults
between the ages of 40 and 60 years. Most meningiomas are benign (not cancer), as
less than 10% are malignant. While malignant meningiomas occur in both women
and men, benign meningiomas are three time more common in women.

c. Etiology
Scientists are not certain what causes meningioma tumors. Most agree that a
damaged chromosome is the most common abnormality in meningiomas, but the
cause of this abnormality is unknown. People with a genetic disorder
neurofibromatosis type 2 (NF2) are more likely to develop meningiomas. Of people
with malignant meningiomas, a higher percent have mutations in NF2. Studies show
that patients who received radiation treatment to the head for other conditions are at
higher risk for developing meningiomas later in life.

d. Symptoms
Meningiomas grow slowly; it may take years before they cause symptoms. Some
people with meningiomas have no symptoms. The tumor may be found incidentally
on a diagnostic scan performed for another reason. Symptoms of a meningioma vary
by the location and size of the tumor. They often first appear as headaches and
seizures, caused by increased pressure of the growing tumor. Weakness in the arms
or legs, or loss of sensation, may occur with spinal cord meningiomas.
Meningiomas are named according to their locationand cause various symptoms:
o Convexity meningiomas: grow on the surface of the brain. They may not
produce symptoms until they reach a large size. Symptoms include seizures,
neurological deficits, or headaches.
o Falx and parasagittal meningiomas: grow from the dura fold that runs
between the left and right sides of the brain. The falx contains two large
blood vessels (sinuses). Because of the danger of injuring the sinuses,
removing a tumor in this region can be difficult. Symptoms may include
personality changes, headache, vision problems, and arm or leg weakness.
 o Olfactory groove meningiomas: grow along the nerves that run between the
brain and the nose and often cause a loss of smell. They can compress the
frontal lobes causing personality changes that may be mistaken for
depression. They can also compress the optic nerves, causing visual
problems or even blindness.
o Tuberculum sella meningiomas: grow near the pituitary gland and optic
chiasm. They cause visual field problems and can extend into the optic canal.
o Sphenoid meningiomas: grow along the sphenoid ridge behind the eyes.
These tumors can cause visual problems, loss of sensation in the face, or
facial numbness. They often encase major blood vessels (e.g. cavernous
sinus, or carotid arteries) as well as the cranial nerves, making them difficult
to completely remove.
o Posterior fossa meningiomas: grow along the underside of the brain near the
brainstem and cerebellum. These tumors can compress the cranial nerves
causing facial symptoms or loss of hearing. Petroclival tumors can compress
the trigeminal nerve, resulting in facial pain (trigeminal neuralgia) or spasms
of the facial muscles.
o Foramen magnum meningiomas: grow near the area where the spinal cord
connects to the brain and can cause headaches, and signs of brainstem
compression, such as difficulty walking.
o Intraventricular meningiomas: grow inside the fluid-filled ventricles of the
brain. They block the flow of cerebrospinal fluid causing hydrocephalus,
headaches and dizziness.
o Intraorbital meningiomas: grow around the eye sockets of the skull and can
cause pressure in the eyes to build up, giving a bulging appearance. They
can also cause loss of vision.
o Spinal meningiomas: grow mainly in the thoracic spine. They can cause
back pain (typically at night) or loss of sensation and paralysis of the legs
from compression of the spinal nerves.

e. Diagnosis
 Anamnesis done through personal and family medical history and perform a
complete physical exam. In addition to checking your general health, the doctor
performs a neurological exam. This includes checks for mental status and memory,
cranial nerve function (sight, hearing, smell, tongue and facial movement), muscle
strength, coordination, reflexes, and response to pain. The doctor may order
diagnostic imaging such as computerized tomography (CT) or magnetic resonance
imaging (MRI) scans to help determine the size, location, and type of any tumor
(Fig. 2). For spinal cord tumors, a myelogram may be done, and in some cases,
angiograms, or x-rays of the blood vessels, are necessary.

f. Treatments
The treatment that is right for you will depend on age, general health status,
and the location, size, and grade of the meningioma. Each treatment has benefits,
risks and side effects that should be discussed and understood.
1. Observation (growth monitoring)
Because meningiomas grow slowly, patients with no or few symptoms
may be monitored instead of undergoing surgical removal of the tumor. The
doctor will monitor the growth of the tumor with periodic MRI scans. Patients
should immediately report any change in their symptoms.

2. Surgery
Surgical removal is the most common treatment for meningiomas that cause
symptoms. A surgeon performs a craniotomy to open the skull and remove the
tumor. A biopsy of tissue is examined by a pathologist to determine the tumor
grade. Although total removal can provide a cure for meningiomas, it is not
always possible. The tumor location determines how much can be safely
removed. If the tumor cannot be completely removed, radiation can treat the
remainder of the tumor. Technologies have improved the surgeons ability to
precisely locate the tumor, define the tumors borders, avoid injury to vital brain
areas, and confirm the amount of tumor removal while in the operating room.
These include:
o Image-guided surgery (IGS) is a technology that helps the surgeon
pinpoint the exact location of a tumor - similar to a GPS for the brain.
Before surgery, a special MRI scan is performed with fiducial
markers placed on the skin around the patients head. During surgery,
the fiducial markers correlate the real patient lying on the table to
a 3D computer model of the patient created from his or her MRI or
CT scans. Using a hand-held probe, the surgeon can track the probes
position in real time on the computer model of the patients anatomy.
IGS allows very precise planning of the approach by pinpointing the
tumor location and guiding the skin and bone openings.
o Brain mapping functional MRI (fMRI) creates a series of images
of the brain in action. The images capture blood oxygen levels in
parts of the brain that are responsible for movement, perception,
language and thinking (Fig. 4). By identifying and mapping these
eloquent areas, surgeons can remove tumors to the greatest extent
possible without harming areas that are critical to the patients quality
of life.
o Keyhole & endoscopic surgery are minimally invasive techniques
that enable surgeons to remove tumors at the skull base through small
keyhole openings, such as through the nose, eyelid or eyebrow.
Tumors that formerly required a large craniotomy and brain
retraction can be accessed with endoscopes through natural pathways
such as the nose and sinuses.
o Interventional MRI or CT is a specially designed operating room
in which the patient can undergo an MRI or CT scan before, during,
and after surgery while still under anesthesia. This enables the
surgeon to have real-time images of the patients brain and to know
exactly how much tumor has been removed prior to ending the
 procedure. This technology improves the ability for total tumor
removal and reduces the need for a second operation.

3. Radiation
Indications for radiation include: (1) incomplete tumor removal, (2)
inoperable tumors, (3) malignant meningioma, and (4) patient choice. In these
cases, radiation may be used to damage the DNA inside the cells, making them
unable to divide and reproduce. The goal of radiation treatment is to maximize
the dose to abnormal tumor cells and minimize exposure to normal healthy cells.
The benefits of radiation are not immediate but occur over time. Gradually, the
tumor will stop growing, shrink, and in some cases completely disappear. Benign
tumors, whose cells divide slowly, may take several months to a year to show an
effect. There are two techniques for delivering radiation: a single high dose
(stereotactic radiosurgery) or multiple low doses (fractionated radiotherapy).
o Stereotactic Radiosurgery (SRS) delivers a high dose of radiation
during a single session. Although it is called surgery, no incision is
made. Because a single radiosurgery dose is more damaging than
multiple fractionated doses, the target area must be precisely located
and completely immobilized with a stereotactic head frame or
facemask. Patients spend most of the day at the center while the
tumor is precisely located, a treatment plan is developed, and a
radiation dose is delivered.
o Fractionated Radiotherapy (FSR) delivers a low dose of radiation
daily over 5 to 6 weeks. A facemask is used to precisely localize the
tumor and accurately reposition the patient for each treatment
session. Delivering a fraction of the total radiation dose allows
normal cells time to repair themselves between treatments. It also
reduces side effects. Fractions are usually given five days a week
with a rest over the weekend.
 Referensi :
Ronald Warnick, MD. Meningiomas.University of Cincinnati Department of
Neurosurgery, Ohio. 4/2016. https://www.mayfieldclinic.com/PE-MENI.htm

4. What is the first management?

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5. How the Islamic perspective?

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