PART I

PRELIMINARY

1.1 Background
Anatomically Brain Stem covering the entire structure above the spinal cord
except the cerebrum, cerebellum, and white matter. So Rod brain consists of the
medulla oblongata, Pons, mesencephalon, thalamus, and basal ganglia. But the
more basal danGanglia thalamus leads to cerebral function and the relationship
between the cerebellum and the cerebrum. Motor function of the Brain Stem
mainly controls muscle tone and posture. The brain stem is also important in
reaction equilibrium.
The brain stem is the energy source of very powerful motor controlled by the
centers were higher during motor activity. When control of the centers of higher
against the motor activity of the brain stem is removed, the motor energy from the
brain stem and become unstoppable manifestations as rigidity (decerebrate
rigidity). When cutting height interkolikulus of mesensefalon so that the rostral
mesencephalon, thalamus and Corteks Cerebri eliminated its function there will
be a great hypertonia of all the extensor muscles. Limb will undergo rigid
extensions, back stiff and straight, with the head lifted upward and slightly
backward. Decerebrate rigidity result is due to the release of the centers of the
Brain Stem motor control centers of higher motor located at the slaughterhouse.
Reticular formation is part of the Brain Stem extends from the caudal medulla
oblongata, Pons and mesencephalon through into the thalamus.
Reticular formation is formed from a diffuse conglomeration of nerve cells
and nerve fibers of various sizes and types, so it is a complex matrix. Judging from its
effect on spinal refleksrefleks, the reticular formation can be divided into two
Fasilitatoris reticular formation (FRF) and reticular formation Inhibitoris (FRI) .FRF
receive eksitatoris strong intake of:

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1. ascendens sensory fibers, which through the Brain Stem heading to the thalamus
and cortex
cerebri
2. Vestibulo-cochlear nerve fibers (N.VIII)

These two sources provide a tonic against FRF eksitatoris intake so FRF tend
to generate strong activity. But with the influence of the Cortex Motoris, basal ganglia
and cerebellum FRF activity can be controlled. Without the control of the higher
structure, the FRF will be loose, and there was an increase in impulse downward and
affect the spinal reflexes. Impulses from FRF heading down through Retikulospinalis
tract, tract Vestibulospinalis and Tektospinalis tract. The influence of FRF primarily
aimed at the extension reflexes, although sometimes also ditingkatkan.Umumnya
flexion reflex FRF reciprocal influence, which he led to the facilitation of the
extensor and inhibisifleksor. One of the functions of the motor rod brain is to control
posture. So the effect of the extensor FRF is to be expected, therefore ekstensorlah
most important in maintaining posture.

Unlike the FRF controlled or suppressed by the function of Motor Cortex,

basal ganglia and cerebellum, the FRI actually need all three centers to stimulate a
motor is active. Without the effect of these motor centers of the FRI is not capable of
affecting spinal reflexes. FRI influence on spinal reflexes also are usually reciprocal
inhibition extensor and flexor facilitation.

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 CHAPTER II
LITERATURE REVIEW
2.1 Anatomy

Is the most caudal brainstem and Phylogenetic is the oldest part of the brain.
Overall the brain stem is divided into the medulla oblongata, pons, and
mesencepalon (midbrain). Medulla is a continuation towards the rostral spinal
cord, whereas mesensefalon located just below the diencephalon, the pons of the
brain stem bagiantengah. Ten of the 12 pairs of cranial nerves exit from the
brainstem and especially contribute to innervation of the head and neck.
In the volunteer movement, the brain stem excitatory impulses path traversed before reaching
the cerebrum. Excitatory impulses delivered by ascendentes tract (nerve fibers that conduct the
impulses to the brain) to be processed in the brain, then the impulse response delivered by
desendetes tract (Serrat nerve fibers that conduct impulses away from the brain). On the border
between the brain stem and spinal cord occur deccusatio (crossing)corticospinal
fibers ( d e s c e n d e n t e s n e r v e f i b e r s f r o m t h e c e r e b r u m t o spinal
cord). The fibers of the brain kortokospinal left crosses to the right side of the
brain fibers medullaspinalis and right crosses to the left side. This causes the
crossing parts of the body controlled by the right brain and the left of the left part
of the body is controlled by the right brain. The brain stem is the point of
attachment of the entirecranial nerveExcept nerve I andII attached to
thecerebrum (Big brain).

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The brain stem consists of three main parts:.
1. Mesencephalon or Central Brain (also called Mid Brain)
is the top of the brain stem that connects the Big Brain and Brain
Kecil.Mesencephalon composed of many nuclei and bundle of nerve fibers
ascending and descending, conical shape and is associated with the pons superior
and inferior side of the spinal cord. Is a part of the brain that connects the short
and terkontriksi pons and cerebellum. The function of the mesencephalon is as
conductor paths and reflexdan center also functions in response to control sight,
eye movement, enlarged pupils, regulate body movement and hearing.
Mesensepalon consists of 4 bagianyang protruding upward, over the next two are
called the corpus kuadrigeminus superior, 2 next UNDER called kuadrigeminus
inferior. Mesensefalon having fiber-seratsaraf trochlear nerve on duty to assist
the movement of the eyes and mengangkatkelopak eyes, and rolled her eyes and
the center of the eye. Sections mesencephalon, namely:
a. Corpora quadrigemina kolikulus superior (associated with visual reflex)
and inferior (related to auditory reflex).

b. Pedunkulus cerebralis two beams cylindrical fibers formed from

ascending and descending tracts that form the basis mesencephalon section.

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 c. C o n t a i n s a q u a d u c t u s S y l v i u s v e n t r i c u l a r c h a n n e l
c o n n e c t i n g w i t h Her other ventricle.

In mesencephalon contains cranial nerve nuclei III, IV

a n d V ( p a r t i a l l y ) . Ter d a p a t a l s o s u b s t a n c e N i g r a , a n a r e a o f
pigmented neurons that are important in fungsimotorik. There
w a s a l s o t h e r e d n u c l e u s , i e m a s a n e u r o n p i n k o v a l which plays a
role in muscle tone and posture.

Diensepalon, the top part of the brain, located between the cerebellum with
mesensepalon, a collection of nerve cells located in the front of the temporal lobe
ddanterdapat internal capsule facing sideways. The function of diensepalon namely
vasokontruktor that shrink blood vessels, respiratory namely to help the breathing
process, control the movement reflex, helps the heart work.

2. Punch
A transmitting station that sends data to the center of the
b r a i n a l o n g w i t h formasireticular. Pons that determines whether we are awake or
asleep. Pons is located in the anterior cerebellum, mesencephalon dar inferior and
superior of the medulla oblongata. Pons has a lot of fibers running transverse to the
anterior surface of the menghubungkankedua hemispheres cerebelli, many nuclei, and
the ascending and descending nerve fibers. Pons Consist substance alba, and connect
over the mountain medulla of the brain through pedunkulus cerebralis. Pons is
Pusatrespiratori, set the frequency and depth of breathing. And there are nukleisaraf
cranial V, VI, VII and VIII. Pons Varoli contains nerve fibers that connect the
cerebellum of the left and right, also connects major brain and spinal cord. Varol
bridge located in front of the cerebellum between the midbrain and medulla
oblongata. On the bridge there parol premotoksid that regulate breathing movements
and reflexes.

3. medulla oblongata

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 Is the part that connects between prosencephalon and rhombencephalon
contained in the narrow cavity called the mesencephalon Aquaeductus ventriculus
tertius cerebriyang connect with Quartus ventriculus. In many nuclei
oblongataterdapat medulla functioning nerve fibers ascending channel and
desenden.Memiliki length of about 3-4 cm, starting from the pons
f o r a m e n m a g n u m . T h e f r o n t medulla is the pyramid (bulge white substance,
which merupakanlanjutan of axons in pedunkulus cerebri). At the rear there are others
lanjutantraktus sensory medullooblongata. Nuclei is the center of information sent to
the transmitter pusatotak higher or to the cerebellum. Medulla is the center
berperandalam nuclei that control functions such as heart rate, BP, breathing,
coughing, swallowing and muntah.Dalam medulla are nuclei N IX, X, XI and XII.
The medulla oblongata or dial marrow function deliver impulses that come
darimedula otak.Medulla oblongata spinal heading to a part of the brain stem that
connects the bottom puncher Varoli with spinal cord marrow grafting also affect the
bridge, reflex physiology such as heart rate, blood pressure, volume dan speed of
respiration, digestion tool motion, and the secretion of digestive glands.
Other than that,marrow grafting also regulate other reflexes such as sneezing,
coughing and blinking.

2.2 Stem Brain Lesions

2.2.1 definition

All types of lesions involving the brainstem. Can be a vascular disorder

(Infarct or hemorrhage), tumors, inflammation and
degeneration.
The brain stem is an anatomical structure that is compact, functionally
barmacammacam, and clinically important. Even a single lesion relatively kecilpun
almost always damaging several nuclei, reflex center, tract, or pathways. Such lesions
are often vascular (eg, hemorrhage, ischemia occlusive), but the tumor, trauma, and
degenerative or demyelinating process can also damage the brain stem.

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 In Batang brain regions crossed by the pyramidal arrangement of the brain's
nerve roots of the 3rd, 6th, 7th and 12th, so the lesions that damage the brain stem
region pyramidal sesisi result hemiplegi involving typical brain nerve and called
hemiplegi alternans, Sesisi or hemilesi yangsering lesions occur in the brain are rarely
found in the spinal cord, so the UMN paralysis due to a lesion in the spinal cord is
generally a tetraplegia or paraplegia. Hemiplegia alternans due hemilesi in the
brainstem can be divided into:

1. Syndrome hemiplegia alternans in mesencephalon

2. Syndrome hemiplegia alternans in the pons
3. Syndrome hemiplegia alternans in the spinal cord

Unilateral damage to the pathways corticobulbar / corticospinal level

brainstem syndrome cause hemiplegia alternans. The syndrome consists of paralysis
that struck UMN muscles contralateral body parts that are below the level of the
lesion, while the level terdapatkelumpuhan LMN lesions, which hit the muscles by
the nervous disarafiCranial involved in the lesion. Depending on the location of the
lesion paralitiknya, it can be found in the mesencephalon syndrome, hemiplegia
alternans, Pons and medulla oblongata.

2.2.2 Weber Syndrome (Syndrome Cerebral Pedunkulus)

Weber syndrome is a collection of clinical symptoms and signs which
includes oculomotor nerve palsy (N.III) ipsilateral, contralateral spastic hemiparesis,
contralateral rigidity parkinsonism (substantia nigra), distaksia contralateral
(kortikopontis tract) as well as the cranial nerve deficits are likely due to a
disturbance in supranuclear innervation of the nerve VII, IX, X and XII.

Etiology:

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a.Penyumbatan the blood vessel side branches that berinduk on perforating ramus
medial basilar artery. Occlusion interpendikularis ramus posterior cerebral artery and
posterior artery khoroidalis.
b. Insufficiency bleeding resulting in lesions in the brain stem.
c.Lesi caused by neoplasmatik process as a result of the invasion of the thalamus or
cerebellum. Lesions neoplasmatik very difficult thing to show uniformity because the
process is in the form of pinealoma, glioblastoma and spongioblastoma of the
cerebellum. A rare cause is a tumor (glioma).
d. Lesions that damage the medial cerebral pedunkulus.
e. Stroke (hemorrhagic or infarct) in pedunkulus cerebral.
f. hematoma epiduralis
Clinical Manifestations:
These lesions are usually unilateral and affect the structure in the midbrain.

Table 1. Damage to the brain stem structures and their effects.

Structural damage Effect

substantia nigra Kontralteral parkinsonism

The fibers of the corticospinal
tract kortikobulbaris
Oculomotor nerve fibers (N.III)
contralateral hemiparesis
Kerusakah the muscles of the lower face and the
contralateral nerve function hipoglosus (N.XII
Ipsilateral oculomotor nerve palsy that causes drooping
eyelids and pupils were dilated.

Lesions caused by neoplasmatik process can damage buildings mesensefalon

as a result of the invasion of the thalamus or cerebellum, each corakan damage can
occur, so it is difficult sekalai neoplasmatik lesions showed a uniformity. Unilateral

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lesion in mesensefalon resulted in the emergence or hemiparesis contralateral
hemiparesis. Lesions that damage the medial cerebral pedunkulus will cause
hemiparesis accompanied ipsilateral oculomotor nerve paresis with pupils dilated and
fixed. The combination of these two types of paralysis known as hemiparesis
alternans oculomotor nerve or from Weber syndrome. Lesions of the medial
longitudinal fasciculus area will lead to the emergence hemiparesis alternans
oculomotor nerve (N.III) which is also accompanied by symptoms called ophthalmo-
internuklearis
Weber Syndrome Diagnosis can be confirmed by anmnesis about the history
of the disease, including a history of complaints of how long a complaint has been
perceived and whether the complaint occurred on one side or two sides. Neurological
exams usually do and was very helpful to determine the presence of Weber syndrome.
Examination of oculomotor nerve (nerve III) is usually carried out together with the
examination of trochlear nerve (nerve IV) and abdusen nerve (nerve VI).
The examination consists of:
a. Examination of the eyelids slit Patients were asked to look straight ahead, then
assessed the position of the eyelid towards the pupil and iris.
b. Examination of the pupil, which need to be examined are:
- Size: whether the normal diameter, miosis, mydriasis, pin-point pupils
- Form: whether normal, isokor, anisokor
- Position: whether central or eccentric
- pupillary
c. Eyeball movement Assessed by eyeball movement six directions, namely the
lateral, medial, lateral, medial upper and medial below to determine the
function of the muscles of extrinsic eyeball, by the way: the patient facing
forward and the eyeball is moved according to the command or following the
direction of the object in front of the patient.

2.2.3 syndrome Benedickt

Benedickt syndrome is a neurological syndrome oculomotor nerve
paralysis (N.III) due to trauma to the N.III and nucleus ruber. This happens

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due to blockage interpedunkularis branches of the basilar artery or
posterior serebralis or both in the midbrain. It was described as a paralysis
n. okulomorius ipsilateral accompanied by rhythmic or rhythmic tremor on
the right hand or leg contralateral enhanced by their sudden movement or
accidental, and disappears when it breaks. Which is the result of damage
to the nucleus ruber were heading out of the opposite side there is the
hemispheres of the cerebellum. There can also be hiperestesia
contralateral. Moreover, the disruption touch sensation, position, vibration
as well as the discrimination of two points contralateral (medial lemniscus
involvement); contralateral hyperkinesia (tremor, korea, Athetosis) from
involvement in the nucleus ruber; rigidity contralateral (substantia nigra)
Etiology Benedickt syndrome lesions in the nucleus ruber and oculomotor
nerve because of occlusion of the ramus interpedunkularis basilar artery or posterior
cerebral artery, or both in the midbrain, trauma or tumor
The clinical manifestations of the syndrome Benedickt nerve palsy III
ipsilateral to midrasis and fixed (interference fibers nerve roots III), Impaired touch
sensation, position and shakes the contralateral, Impairment of discrimination of two
points (engagement lemnikus medial and tract Spino talamikus), hyperkinesia
contralateral (tremor, khorea, Athetosis), akinesia contralateral contralateral Rigidity
(substantia nigra)

Table 2. Damage to the structure of the rod and effects that occur
Structures involved Clinical effects
Lemnikus medial Impaired touch sensation, position and shakes the
contralateral
nuclei ruber Contralateral hyperkinesia (korea Athetosis)
substantia nigra Akinesia (parkinsonism) contralateral
Root n. oculomotor Paralysis n. ipsilateral oculomotor with pupils dilated and
fixed.

2.2.4 Foville-Millard Gubler syndrome (Syndrome Pontis basis kaudalis)

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 Hemiplegia alternans due to a lesion in the pons is forever UMN paralysis
involving the contralateral side of the body parts, which is below the level of the
lesion combined with LMN paralysis of the muscles that disarafi by nerve VI or VII
nerve.

SThis occurs due to occlusion indrom ramus interpedunkularis basilar artery

and posterior cerebral artery. Millard Gubler syndrome and syndrome Foville
included also into part of the syndrome, hemiplegia alternans pons. This syndrome is
caused due to formation of a vascular lesion that is unilateral.Selaras with the
branching pattern of the arteries, the vascular lesion in the pons can be divided into:

- Paramedian lesions due to blockage of one of the branches of a medial

perforating branches. basilar
- Lateral lesions, which according to the bleeding area sirkumferens short
branch
- Lesions in the pons tegmentum caudal section, which seesuai the
bleeding area sirkumferens long.

Partial blockage to one of the branches of the medial perforating branches

basilar artery is often followed by the paramedian lesions. If the lesion was unilateral
paramedian and spacious it is, then the following corticospinal pathways
corticobulbar or with cores pes Pontis and pontoserebelar fibers will be damaged.
Tegmentum Pontis is not involved in these lesions.

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 Clinical manifestations:
Table 3. In fovile syndrome, lesion on the dorsal pons, causing:
Structures involved clinical effects
Lemnikus medial Impaired touch sensation, position, and shakes
contralateral
Lemnikus lateralis Deaf
Nucleus n. facial Paralysis n. ipsilateral peripheral facial
Spinatalamikus tract lateralis Analgesia and termanestesia half contralateral limb
pyramidal tract spastic hemiplegia
n. abducens Paralysis n. ipsilateral abducens peripheral.

Table 4. On the milliard-Gubler syndrome, lesion of the ventral pons and cause
Structures involved clinical effects
corticospinal tract contralateral hemiplegia
n. facial Ipsilateral facial paralysis
n. abdusens paralysis melirikipsilateral

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2.2.5 tegmentum syndrome Pontis kaudale

This syndrome is caused by occlusion of the basilar artery branch (ramus

sirkumferensialis longus and brevis).

Clinical features that can be found is abdusen nuclear palsy and ipsilateral
facial, nystagmus (medial longitudinal fasciculus), paresis gaze toward the side of the
lesion; hemiataksia and asinergia ipsilateral (pedunkulus serebralis medial);
termanestesia analgesia and contralateral (lateral spinothalamic tract); hypesthesia
and disturbance of position sense and shakes the contralateral side (medial
lemniscus); mioritmia palate and pharynx ipsilateral (tegmentalis central tract).

Clinical manifestations:

Table 5. Damage to the structure of the rod and effects that occur

damage to the structure Effect

Lemnikus medial Impaired touch sensation, and shakes contralateral
Lentikus lateralis Deaf
Nucleus n. facial Paralysis n. VII peripheral ipsilateral
Lateral spinothalamic tract Analgesia and termanestesia half contralateral limb
pyramidal tract Contralateral spastic hemiplegia
n. abducens Paralysis n. VI peripheral ipsilateral
2.2.6 tegmentum syndrome Pontis orale

Etiology This syndrome occurs due to occlusion of the ramus

sirkumferensialis longus basilar artery and the superior cerebellar artery.

Clinical features that can be found is the ipsilateral facial sensory loss
(interruption all the trigeminal nerve fibers) and paralysis of the muscles of
mastication (Motorius nucleus of the trigeminal nerve), hemiataksia, intention tremor,

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adiadokokinesia (superior cerebellar pedunkulus); interruption of all contralateral
sensory modality.
Clinical manifestations:
Table 6 rod structure damage and effects that occur
damage to the structure Effect
Cerebellar Pedunkulus superiuor - Hemiataksia
- intention tremor
- Adiadokokinesi
- cerebellar Disarteria
Nucleus prisipalis sensory n. trigeminal Gangguaan sensation epikritik face ipsiateral
Nucleus trakus spinal n. trigeminal Analgesia and ipsilateral facial termanestesia
Tegmentalis tract centralist Mioritmia palate and pharynx
tract tektospinalis The loss of blink reflex
Lateral spinothalamic tract Analgesia and termnestesia half contralateral limb
Lemnikus lateralis Deaf
Lemnikus medial Impaired touch sensation, shakes, and the position
of the contralateral body half
Kontinuklearis tract (lint out) Paralysis n. facial, n. glossopharyngeal, n.
hipoglosus.

2.2.7 Syndrome stale Pontis central part

The etiology of this syndrome appears to result from occlusion of the ramus
sirkumferensialis longus basilar artery and the superior cerebellar artery.

Clinical manifestations The clinical picture is hemianestesi all sensory

modalities ipsilateral, ipsilateral masticatory muscle flaccid paralysis, hemiataksia,
intention termor, adiadokokinesi, disatria sereblar and contralateral spastic
hemiparesis.

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Table 7. Damage to the structure of the rod and effects that occur
Structures involved clinical effects
Radikuds n. trigeminal - Hemianaesthesia all sensory modalities
ipsilateral
- Masticatory muscle paralysis ipsilateral fraksid
Pedunkulus medial cerebellar Hemiataksia and asinergia ipsilateral
corticospinal tract Spastic hemiparesis contralateral
nuclei pointis Diktaksia ipsilateral.

2.2. 8 Syndrome Wallenberg(Medullary syndrome Dorsolateralis)

Wallenberg syndrome or have other names syndrome or syndrome lateral

medullary posterior inferior cerebellar artery (PICA syndrome) is a disease in which
patients have neurological symptoms with sudden onset caused by occlusion or
embolism in the territory of the posterior inferior artery or vertebral artery. The
existence of this occlusion causes infarction of the lateral part of the medulla
oblongata. Occlusion is often derived from the vertebral artery which is the mother
branch of the posterior inferior cerebellar artery. This is often caused by trauma to the
neck, examples of activities ciropractic, yoga neck and head trauma. Vertebral artery
passes along her neck before stepping inside the head and branching into the posterior
inferior artery cerebeli
The main cause of vascular disorders that attack the vertebrobasilar system is
atherosclerosis, where plaque is formed in the walls of blood vessels that cause
lumennya narrowing and occlusion may occur. Atherosclerosis occurs in large blood
vessels.

The incident is different where the small blood vessels that invade the
diameter of 50-200 lm. In the small blood vessels called lipohyalinosis process that

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often occur associated with hypertension. Occlusion of small blood vessels will form
small infarcts and circular called lacunae which can appear solitary or multiple in the
subcortical and brain stem.
Lipohyalinosis weakens the walls of blood vessels in patients with
hypertension and arterial rupture can occur and cause hemorrhagic focal. Almost all
of intracerebral hemorrhage came from a small artery rupture which is the connector.
Due to the acquisition of the anatomical proximity between the vertebral artery and
cervical, these forms of manipulation of the neck can injure the vertebral artery in the
neck, and finally forming occlusion from the trauma inflicted. Embolic occlusion of
the vertebrobasilar system is not common.
Aterotrombotik plaques that occur in the blood vessels can extracranial
fibrinotik lysis due to the mechanism of the artery wall and blood, which causes the
formation of emboli, which will menyumblat smaller arteries, distal of the blood
vessels. Thrombi in blood vessels can also occur due to damage or ulceration of the
endothelium, resulting plaque becomes unstable and easily separated to form emboli.
Emboli can cause a blockage in one or more blood vessels. The emboli will contain
deposits of cholesterol, platelet aggregation and fibrin. Emboli will lysis, broken or
intact and clog blood vessels distal, depending on the size, composition, consistency
and age of the plaque, and also depending on the pattern and speed of blood flow.
A blockage in the blood vessels (especially the blood vessels in the brain) will
cause the death of brain tissue, where the abnormality is dependent on the existence
of adequate blood vessels. The brain is only 2% of total body weight, received a
bleeding 15% of the cardiac output and oxygen requires 20% of all essential, as the
energy needed to run the neuronal activity. The energy required is derived from the
metabolism of glucose, which is stored in the brain in the form of glucose or
glycogen to supply user for 1 minute, and require oxygen for metabolism, more than
30 seconds picture of EEG will be flat, within 2 minutes of activity brain tissue stop,
in 5 minutes then damage brain tissue begins, and more than 9 minutes, people will
die. When blood flow stops, the brain tissue of oxygen and glucose that is required

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for the formation of ATP will decrease, there will be a decrease in Na-K ATP ase, so
that the membrane potential will decrease. K + move to temporary space CES Na and
Ca ions gathered in the cell. This causes the surface of the cell becomes more
negative, causing membrane depolarization. When the initial depolarization of the
cell membrane is still reversible, but when permanent structural change room cause
death of brain tissue. This occurs immediately if perfusion decreases below the
threshold tissue death, which is when blood flow is reduced to below 10 ml / 100
gr.menit.
As a result of lack of oxygen acidosis which causes malfunctioning of
enzymes, because of the high ion H. Furthermore acidosis cause cerebral edema
marked swelling of cells, especially glia network, and result in the microcirculation.
Therefore, an increase in vascular resistance and then a decrease of perfusion
pressure, causing the expansion of the ischemic area
The role of Ca ions in the number of intra and extra cellular processes on the
state is now more clear, and it became the theoretical basis for reducing expansion of
the ischemic area to regulate the entry of ion Ca. Further complications of cerebral
ischemia is serbral edema. This incident occurred because of an increased amount of
fluid in the brain tissue as a result of the influence of local or systemic damage.
Immediately after ischemia arising serbral cytotoxic edema. As a result of osmosis
berpinda fluid cells from the extracellular space along with the content
makromolekulnya. This was followed by the pumping mechanism of Na / K in the
cell membrane where transport of Na and water back out into the extra cellular space.
In the state of ischemia, this mechanism is disrupted and the neurons become swollen.
Edema is an intracellular cytotoxic edema. If ischemia settled for a long time,
vasogenic edema may increase the cytotoxic edema. This occurs due to damage of the
blood-brain barrier, where the plasma fluid will flow into the brain tissue and into the
extracellular space along the nerve fibers in the white matter that occurs pengumpalan
cairann so that vasogenic edema serbral an extracellular edema

17
 There is an advanced stage of cerebral edema vasigenic fingerlike appears as a
picture in the white matter. In the early stages of cytotoxic edema serbral found
swelling in the area around the affected artery. Halini interesting that the blood-brain
barrier disruption berhungan with an increased risk of secondary bleeding after
recanalization (also called trauma reperfusy). Serbral extensive edema after ischemia
can be space-occupying lesion. Increased intracranial high pressure which causes
hilngnya ability to maintain fluid balance in the brain will cause suppression of the
ventricular system, so the cerebrospinal fluid will be reduced. If this continues, there
will be a herniation in all directions, and causing obstructive hydrocephalus. May
eventually lead to global ischemia and brain death
Clinical manifestations Clinical signs and symptoms that appear in this
syndrome depends on where the lesion is exposed. Clinical symptoms in Wallenberg
syndrome formed due to thrombosis atheromatous plaques that form in part a.
Vertebral. Only about 25% of this syndrome are derived completely cerebeli artery
occlusion of posterior inferior.

Table 8. Structure of the brain stem that looks and clinical effects on Wallenberg syndrome

Structures involved clinical effects

Inferior vestibular nucleus
Nucleus dorsalis n. vagus
Pedunkulus inferior cerebellar
nucleus ambiguous
Nucleus n. trochlear
Nucleus spinal tract n. trigeminal
The central sympathetic pathways
Nystagmus and the tendency of falling into the ipsilateral side
Tachycardia and dyspnea
Ataxia and ipsilateral asinergia
Paresis palate, larynx and pharynx ipsilateral, hoarseness
Deaf
Analgesia and ipsilateral facial termanestesia, corneal reflex
disappears
Horner's syndrome, hypohidrosis, ipsilateral facial vasodilator.

Treatment: There is no treatment that is typical in handling this case but

symptomatic therapy relieving symptoms and perform an active rehabilitation to
restore the daily activity of those who attacked stroke. No patients were difficult to

18
swallow, it is advisable to install a feeding tube inserted through the mouth or
gastrostomy given the risk of aspiration pneumonia can occur. In some cases,
medication may be used to reduce or eliminate pain. Some doctors report that the
anti-epilepsy drug gabapentin that seems to be an effective drug for individuals with
chronic pain. Baclofen may be effective in treating persistent hiccups.

2.2. 9 Sindrom Dejerin (Medial medullary syndrome)

SDejerin indrom is due to occlusion of the vertebral artery ramus

paramedianus or basilar artery, usually bilateral.

Clinical manifestations:

Table 9. Damage to the structure of the rod and effects that occur

Structures involved clinical effects

longitudinal fasciculus nystagmus
Lemnikus medial Impaired touch sensation, shakes, and the position
of the ipsilateral
Olivia Mioritmi palate and the position of the contralateral
Hipoglosus nerve (nerve XII) Flaccid paralysis nerve XII with tongue hemiatrofi
pyramidal tract Hemiplagia contralateral (not the Babinski reflex)

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 CHAPTER III

COVER

3.1Conclusion

Is the most caudal brain stem, is divided into the medulla oblongata,
pons and mesensefalon. The anatomy of the brain stem, including complex
structures with diverse functions and clinically significant, so that if there is a
lesion, single and no matter how small, it is almost always destructive lesions of
multiple nuclei, reflex center, tracts or pathways located in the brain stem. The
lesions are often vascular degenerative or demyelinating can also damage the
brain stem. A collection of symptoms that are typical and are alternans in the brain
stem to form a syndrome that later became known as the brainstem syndrome.
Brainstem syndrome is a group of symptoms characterized by disruption of one or
several functions of the cranial nerves and the sympathetic nerve lesion either by
mechanical processes such as invasion or trauma or as a result of a disturbance
vascularization. This syndrome is characterized symptoms distinct and alternans.

By knowing the various syndromes are expected for a clinician to help

determine the location of the lesions that occur based on clinical symptoms
appear. The prognosis of a variety of the syndrome depends on the underlying
cause of the disorder so in penatalaksanaanya also based on a disturbance or a
primary lesion which causes partial or some function of the cranial nerves

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3. Weber syndrome, downloaded from

http://dokmud.wordpress.com/2009/10/23/syndrome-weber/ 2009

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//emedicine.medscape.com/article/1220091-overview 2009

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http://emedicine.medscape.com/article/279394-overview, 2009.

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