Presented by : NATASHA ASTAR Group 3

Pembimbing: Prof. Dr. H. Basjiruddin A, Sp. S (K)

A 56 years old male presented with right upper and lower limb weakness since 4 days before admitted to hospital,

Chief Complaint Right upper and lower limb weakness

Current Illness History

Right upper and lower limb weakness since 4 days before admitted to Dr M Djamil Hospital. Earlier patient were brought to a general practitioner and then were admitted to Sijunjung Hospital for 2 days and then were refered here from Sijunjung Hospital

. Weakness are seen suddenly during activity (lifting farming items), and fall. Conscious after attack. The upper and lower limb weakness are equal. Now patient are unable to lift anything and have to be hold by family to walk. He also have difficulty in eating and drinking.

This complain are accompanied with wry mouth and patient cannot speak. Patient cannot understand conversation and cannot say any words. No complain of headache, vomiting, decreased consciousness, and seizures. No complain in sensing, miction and defecation

Past Illness History Known hypertensive since 3 years ago. No regular checkup to doctor. No previous history of stroke. No history of diabetes. Family History of Illness No family history of hypertension, diabetes, heart disease and stroke. Socioeconomic Background Patient is a farmer, smoke 12 stick of cigarette a day since 30 years ago.

General General Appearance: Moderately Ill Level of Consciousness: compos mentis cooperative Pulse Blood Pressure Temperature : 72 x/menit : 180/120 mmHg : 36,7oC Respiratory Rate : 20 x/menit

GCS 15 : E4 M6 Aphasia

Meningeal SIgn Neck stiffness: (-) Brudzinsky I : (-) Brudzinsky II : (-) Kernig Sign : (-)

Intracranial Pressure Examination

Vomiting (-) Progressive headache (-)

N. I N. II N. III, IV, VI

N. V N. VII

N VIII

: Difficult to evaluate : Difficult to evaluate : Light reflex +/+ Doll eye movement : difficult to evaluate : Right Nasolabial plica flatter than the left side, Eyelashes Reflex +/+ : difficult to evaluate

N IX NX N XI N XII

: Vomitting Reflex +, capable to swallow : Pharinx arch symmetric, Uvula on the midline : difficult to evaluate : difficult to evaluate

Motor Function Test

Upper Limb Movement Strength Tonus Trophy Fall Test Right Limited 0/0/0 eutonus eutrophy Left active 5/5/5 eutonus eutrophy

Right side lateralisation

Lower Limb Right Movement Limited Strength Tonus Trophy Fall test 0/0/0 eutonus eutrophy

Left active 5/5/5 eutonus eutrophy

Right side lateralisation

Sensibility Test Pain Sensibility +, Tactil Sensibility +.

Autonomous Nervous System

Mixturition : neurogenic bladder (-)

Defecation : normal Sweat secretion : normal

Reflex
Biceps Triceps

Right
+++ +++

Left
++ ++

APR
KPR

+++
+++

++
++

Reflex
Hoffman-Tromer Balbinsky

Right
+

Left
-

Chaddoks
Oppenheim Gordon

Schaeffer

Hemoglobin Leukocyte

: 14.7gr/dl : 10,500/mm3

Hematocryte
Thrombocyte Sodium Potassium Chloride Urea Creatinine

: 42%
: 140 000/mm3 : 148mmol/L : 3.5mmol/L : 104mmol/L : 60mg/dl : 1.4mg/dl

Random Blood Glucose: 125gr/dl

Other Examination

Blood : PT, APTT, total Cholesterol, uric acid, albumin, globulin, SGOT,SGPT, HDL, LDL, and Trygliceride. Chest X-Ray Non-contrast Brain CT scan Echocardiography

EKG : Atrial Fibrilation Normoventricular response

CT Scan : Gambaran infark luas frontotemporoparietal sinistra.

Clinical Diagnosis

Right Hemiparesis+Right NVII and NXII Paresis central type +Global aphasia
Topic Diagnosis Right brain hemisphere, Subcortical Etiology Cardioemboli Secondary Diagnosis Emergency Hypertension, Atrial Fibrillation Normoventricular Response

Supportive Head elevation 30degree

Oxygen 2L/minute
IVFD RL 12hour/kolf

Catheter (fluid balance)

Diet Soft Food, Low Sodium II

Medicinal Therapy Piracetam 4x3gr (IV) Bisoporolol 1x2.5mg (Oral) Aspilet 2x 80mg Herbesser Drip 50mg in 50cc Ringer lactate via syringe pump 50cc/hour

Medicinal Therapy

Dietary control Physical Therapy Family education and prevention on hypertension and stroke

1. History

Sudden weakness, conscious after attack, equal upper and lower limb weakness (hemiparesis), are the characteristic stroke. It is said subcortical because when a patient have equal upper and lower limb weakness, it shown that the disturbance are in brain area where all motor tract are bundled up together of subcortical cerebral function disturbance in that happen in non hemorrhagic

The patient also cannot speak or understand

speech. This is called aphasia. Aphasia can occur in subcortical ischemic stroke if the damage are extensive enough to cause disturbance in cortical area. as example this patient have wide frontotemporoparietal infarc from ct scan.

Wry mouth are caused by paresis of facial nerve and in this patient are found the central type paresis.

Patient also show major stroke risk factor of

smoking and hypertension and minor risk which is age. Smoking and hypertension contribute to artherosclerosis build up and could be a major risk of stroke. Stroke is characterized by the sudden loss of blood circulation to an area of the brain,

resulting in a corresponding loss of neurologic

function.

Strokes are classified as either hemorrhagic or

ischemic. Acute ischemic stroke refers to stroke caused by thrombosis or embolism and is more common than hemorrhagic stroke.

Ischemic strokes occur as a result of an

obstruction within a blood vessel supplying blood to the brain. The underlying condition for this type of obstruction is the development of fatty deposits lining the vessel walls.

This condition is called arteroscelrosis these fatty deposits can cause two types of obstruction:
a) Cerebral thrombosis refers to a thrombus (blood clot) that develops at the clogged part of the vessel. b) Cerebral embolism refers generally to a blood clot that forms at another location in the circulatory system, usually the heart and large arteries of the upper chest and neck. A portion of the blood clot breaks loose, enters the bloodstream and travels through the brain's blood vessels until it reaches vessels too small to let it pass.

A second important cause of embolism is an irregular heartbeat, known as atrial fibrillation. It creates conditions where clots can form in the heart, dislodge and travel to

the brain.

2. Physical examination

General physical examination reveals that the patient are in emergency hypertension state with

blood pressure of 180/120.

Emergency hypertension are blood pressure elevation with target organ damage. 12x/minute pulsus deficit are also found and this show cardiac insufficiency and shown as inability

to beat simultaneously with distal pulse. This

happens because of abnormality in cardiac output.

Neurological examination reveals this patient

GCS are E4 M6 Aphasia. Aphasia found are global aphasia. From reference, Aphasia is a disturbance of the comprehension and formulation of language, sensoric aphasia are caused by abnormality in Wernicke area as the receptive aphasia and

motoric area could be caused by abnormality in

Broca area as the expressive area.

Global aphasia results from damage to extensive

portions of perisylvian region of the brain. Patients with global aphasia have difficulty to understand both

spoken or written language and difficult to speak.

This patient have difficulty in naming, repeating, reading and writing which is the modality to assess aphasia. These problem usually occurs in left brain hemisphere. Stroke subcortical can disturb nerve impuls from and to this language areas.

Flatter right nasolabial plica are caused by right facial nerve paresis. In motor function test, limited movement and right upper and lower limb strength are 000 interpret as inability to move even the fingers of hand and feet. In Fall Test, Right side lateralisation are found and this shows the weakness in right side limbs.

Hyper reflex in all right side limbs are caused

by compensation mechanism by the spinal nerve because of the paresis. In other hand, positive Babinsky reflex shows that the lesion or the damage are in upper motor neuron but the actual pathophysiology about it remain unknown.

3. Laboratory and other findings.

No laboratory abnormality are found. But in patients with stroke, complete fat lab test such as total cholesterol, LDL, HDL, Triglyceride, and also uric acid are also done. This patients Electrocardiogram shows Atrial fibrillation Normoventrikular response. Atrial fibrillation are the high risk cause of stroke. Atrial fibrillation cerebral blood flow and slows blood flow risk of thrombus formation stuck as emboli at brain end artery. decrease increase

cause the thrombus to

Chest

X-Ray EKG

and

Echocardiography for further

are heart

recommended for this patient because of his abnormal finding investigation.

Echocardiogram could visualize every heart valve or space and could evaluate heart contraction abnormality

Non-contrast Brain CT scan are

recommended to visualize structural brain damage in patient and to confirm diagnosis. CT-scan are the gold standard to diagnose ischemic stroke or hemorrhagic stroke.

From the CT scan we could find the location,

volume and type of stroke for comfirming the

diagnosis

For ischemic stroke, the usual findings of

brain CT scan are hypodens lesion with perifocal oedema and for hemorrhagic stroke we will found hyperdens lesion with perifocal oedema, but sometimes we could also found

hypodens lesion in chronic hemorrhagic

stroke.

4. Therapy

In Supportive therapy, patients head are

elevated 30 degree to prevent high pressure

blood flow to further damage the brain. Oxygen 2L/minute, IVFD RL 12hour/kolf, Catheter (fluid balance), and Diet Soft Food, Low Sodium II are given to prevent further increase of blood pressure.

For Specific therapy, patients are given Piracetam 4x3gr (IV), Bisoporolol 1x2.5mg (Oral), Aspilet 2x 80mg and Herbesser Drip

50mg in 50cc Ringer lactate via syringe pump

50cc/hour.

The central goal of therapy in acute ischemic

stroke is to preserve the area of oligemia in the ischemic penumbra. The area of oligemia can be preserved by limiting the severity of ischemic injury (ie, neuronal protection) or by reducing the

duration of ischemia (ie, restoring blood flow

to the compromised area).

Recanalization

strategies,

including

IV

recombinant
activator approaches, revascularization injury occurs.

tissue-type
(rt-PA) so and to that attempt

plasminogen
intra-arterial establish in the cells

penumbra can be rescued before irreversible

Restoring blood flow can mitigate the effects

of ischemia only if performed quickly. Neuroprotective strategies are intended to preserve the penumbral tissues and to extend

the

time

window

for

revascularization

techniques; however, at the present time, no neuroprotective agents are available and approved for use in ischemic stroke.

The ischemic cascade offers many points at

which such interventions could be attempted. Multiple strategies and interventions for blocking this cascade are currently under investigation. The timing of the restoration of cerebral blood flow appears to be a critical factor.

Finally, education therapy are also given to

the patient such as physical therapy. Dietary

control few steps and family education are very recommended and it could be done through

4. Therapy
In Supportive therapy, patients head are elevated 30 degree to prevent high pressure blood flow to further damage the brain. Oxygen 2L/minute, IVFD RL 12hour/kolf,

Catheter (fluid balance), and Diet Soft Food,

Low Sodium II are given to prevent further

increase of blood pressure.

For Specific therapy, patients are given Piracetam 4x3gr (IV), Bisoporolol 1x2.5mg (Oral), Aspilet 2x 80mg and Herbesser Drip 50mg in 50cc Ringer lactate via syringe pump 50cc/hour.
The central goal of therapy in acute ischemic stroke is to preserve the area of oligemia in the ischemic penumbra. The area of oligemia can be preserved by limiting the severity of ischemic injury (ie, neuronal protection) or by reducing the duration of ischemia (ie, restoring blood flow to the compromised area).

Recanalization recombinant activator approaches, revascularization

strategies, tissue-type

including

IV

plasminogen intra-arterial to cells establish in the

(rt-PA)

and

attempt so that

penumbra can be rescued before irreversible injury occurs.

Restoring blood flow can mitigate the effects

of ischemia only if performed quickly.

Neuroprotective strategies are intended to preserve the penumbral tissues and to extend the time window for revascularization techniques; however, at the present time, no neuroprotective agents are available and approved for use in ischemic stroke.

The ischemic cascade offers many points at

which such interventions could be attempted. Multiple strategies and interventions for blocking

this cascade are currently under investigation.

The timing of the restoration of cerebral blood flow appears to be a critical factor. Finally, education therapy are also given to the

patient such as physical therapy. Dietary control

and family education are very recommended and it could be done through few steps