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Presentan : dr . Yudi PrasetyonoModerator : dr . H. Ahmad Asmedi, M.Kes, SpS

Examiner : dr. H. Pernodjo Dahlan, SpS (K)dr. H. Abdul Gofir, SpS

Commentator : dr. Tetty KurniawatiMay, 11th 2006

Identity :

NameAgeSexOccupationEducationReligionAddressDate of admissonMedical Record

: Mr. BSP: 68 years: Male: Retired inspector of elementary school: College: Islam: Gunungsari, Bejiharjo, Karangmojo, Gunung Kidul: 14 April 2006: 1.23.65.34

Anamnesis :Obtained from the patient and his wife on April, 20 th, 2006

Chief complaint : Weakness of right arm and right leg The present history of illness :

About 15 hours before admission to hospital, when he waked up in the morning (06.00 a.m.), suddenly he complained weakness on the right arm and leg. He was unable to take up a glass with right hand but able to get up from seat, to walk assisted by his wife. He also complained speech lisp. Previously, he did not complain for headache. There were no unconsciousness, nausea or vomiting, vertigo, acute blindness or loss of partial visual field, numbness or without feeling a half of the body, wet the bed, seizure, fever. The patient never had head injury before.

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About 6 hours before admission to hospital, his complaint was worsening. He was unable to get up from seat, so he could only raise right arm and leg. His family brought his to paramedic, and than he reffered to Dr. Sardjito Hospital.

During 6 days stay in the hospital, the patient was still conscious and there was no fever. He did not complain headache, vomiting, and dyspnoe. The weakness of right extremities were not getting worse, the patient could to swallow the food and a drink without choke. The patient was also often quiet, but he could to communicate his complaint, and he was able to recognize his family. The problem of high blood pressure was controlled. The patient have been also consulted to internal and cardiac departments for management of hyperglycemia and cardiac problem.

The history of previous illness :- Patient suffered from hypertention about 5 years, he did not have his blood

pressure controlled regularly, and did not take many medicines.- Patient suffered from diabetes mellitus and already to take glibenclamide (1/2-0-

0) since 1 year- Patient had history smoking, but he stopped since 20 years ago- Patient did not know if he had a history of cardiac problem- Patient did not have a history of heart attack - Patient did not have a history of stroke and transtient ischemic attacks before- Patient did not know if he had a history of hypercholesterolemia

The history of family illness :No history of stroke, hypertension and diabetes mellitus

Systemic evaluation :Cerebrospinal system Cardiovaskuler system Respiratory system Gastrointestinal system Urogenital systemMuculosceletal systemIntegumental system

: weakness on the right extremities, speech lisp: no complaint: no complaint: no complaint: no complaint: no complaint: no complaint

Summary of anamnesis :

A man, 68 years old with chief complaint of weakness on the right arm and leg, with the sudden onset. The complaint occured when he waked up in the morning, and he was also complained speech lisp. The symptom was not accompany by headache and unconsciousness. No preceding of fever the body and head injury. The weakness right extremities became worse regularly. Patient had a history of uncontrolled hypertension, diabetes mellitus and smoking.

FIRST DISCUSSION

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Based on the anamnesis, we got symptom of weakness in the right extremities and speech lisp. The symptom onset was sudden and it occured when he waked up in the morning. There were no symptom of fever and progressive headache to suggest central nervous system infection, as well as no previously brain injury. The weakness right extremities became worse regularly. The patient had a history of uncontrolled hypertension, diabetes mellitus and smoking.

The classic vascular profile involves sudden onset with rapid progression to maximal deficit (instantaneously or in seconds) (Wiebers et al., 1997). These symptom of the patient lead to vascular lession, because the onset was sudden. These suggest to the diagnosis of stroke.

STROKE Stroke was defined as rapidly developing clinical symptoms and / or sign of focal and sometimes loss of cerebral function with the symptom lasting more than 24 hours or leading to death with no apparent cause other that of vascular (WHO cit Dahlan and Lamsudin, 1998) Stroke diagnosis was based on clinical examination, while type of pathology was based on result head CT scan or Magnetic Resonance Imaging (MRI) which is still limited in several hospitals in Indonesia. Some scorings such as Gadjah Mada Stroke Algorithm can be used to replace CT scan in pathological diagnosis of stroke whose parameters loss of consciousness, headache, and babinsky sign. (Dahlan and Lamsudin, 1998)

Patient acute stroke With or without

Unconsciousness, headache,and Babinsky reflex

There are three or two of Yes Intracerebral hemorrhagic these symptoms and signs () stroke No Unconsciousness () Yes Intracerebral hemorrhagic headache () and stroke Babinsky reflex () No Unconsciousness () Yes Intracerebral hemorrhagic headache () and stroke Babinsky reflex ()

No Unconsciousness () Yes Acute ischemic stroke headache () and or infarction stroke Babinsky reflex () No Unconsciousness () Yes Acute ischemic stroke headache () and or infarction stroke

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Babinsky reflex ()

Ischemic stroke or infarction strokeSymptoms of ischemia are consistent with neurologic dysfunction from a single

arterial territory or if improvement occurs rapidly or early in the clinical course. Ischemic cerebrovascular disorders are classified according to temporal profile, including transient ischemic attack (resolution of symptoms within the first 24 hours), reversible ischemic neurologic deficit (resolution of symptoms after 24 hours, within 3 weeks), progressive ischemic stroke (progressive deficit, often for as long as 24-72 hours), and completed ischemic stroke (resolution of symptoms after 3 weeks, if ever) (Wiebers et al., 1997).

Approximately 85 % of all stroke cases are caused by ischaemic or infarction that caused by decrease of blood suply to the brain. Normally the blood suply to the brain is 58cc/100gr brain tissue per minute. When the blood suply reduce to 18 cc/100 gr brain tissue per minute, the biochemistry cell and membrane causing the change of structure and function of universally infark teritory would change (Lindsay, 1997).Infarction stroke include subtype: thrombotic stroke, cardioembolic stroke and lacunar stroke. Thrombotic stroke:

An atherothrombotic stroke may be sudden, stuttering, or stepwise in onset (gradual). The classic history is a patient who awaken from sleep with the deficit. This stroke subtype result from thrombosis associated with atherosclerotic lession of the large and medium-sized arteries in the neck or brain. The mechanism of cerebral infarction in this setting is often artery-to–artery embolism of platelet-fibrin thrombi or atherosclerotic material rather than purely hemodynamic (Winikates, 2001). Cardioemboli stroke:

The typical cardioembolic stroke has an abrupt temporal profile, with deficit that are maximal at onset. Deficits may improved shortly afterward if the embolus breaks up and travel to more distal branches of the affected artery. The classic history is an onset of symptoms during activity or in association with palpitation or a valsava maneuver. The heart and aotric arch are sources of such emboli ( Winikates, 2001).Lacunar stroke :

The symptom may occur during sleep, and progression in a stepwise fashion during 1 to 4 days is not uncommon (Wiebers et al., 1997).

There are five classic lacunar symptoms (Wong, 2005):1. Pure motor stroke/hemiparesis

It consists of hemiparesis or hemiplegia tha typically affects the face, arm, and leg. Dysarthria, dysphagia, and transient sensory symptoms may be present. The lacune is usually in the posterior limb of the internal capsule or the basisi pontis.

2. Pure sensory strokeIt consists of persistent or transient numbness and/or tingling on one side of the body (eg, face, arm, leg, trunk). Occasionally, the complaint is of pain, burning, or other unpleasant sensation. The infarct is usually in the thalamus.

3. Dysarthria / Clumsy hand The main symptoms are dysarthria and clumsiness (ie, weakness) of the hand.

4. Ataxic hemiparesisIt consists of weakness and clumsiness on one side of the body. It usually affects the leg more than the arm. It is also know as homolateral ataxia and crural paresis.

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The most frequent sites of infarction are the posterior limb of the internal capsule, basis pontis and corona radiata.

5. Mixed sensorimotor strokeIt consists of hemiparesis or hemiplegia and ipsilateral sensory impairment. The infarct usually in the thalamus and adjacent posterior internal capsule.

Hemorrhagic stroke Hemorrhagic stroke have a clinical profile that may not be clearly distinguishable

from ischemic stoke, the onset has sudden. A prominenet decrease of level consciousness can be a clue. Headache, nausea, vomiting, severe hypertention, or other sign of raised intracranial pressure also suggest a hemorrhagic stroke (Winikates, 2001)

About 10 % of the stroke caused by intracerebral bleeding and about 5 % are subarachnoid bleeding, which is caused by the smash of aneurysma, malvormation arteriovenous, angioma cavernous, alcoholism, blood discrasia, antikoagulan therapy and angiopati amyloid ( Lindsay, 1997). Working diagnosis :

Clinical diagnosis

Topical diagnosis

Etiological diagnosis

: weakness of right extremities with sudden onset and worsen gradually, speech lisp: DD: left anterior watershed area left internal capsule: DD: lacunar stroke thrombotic stroke

Physical examination : The patient was examined in April 20th , 2006

General status

General ConditionConsciousnessBlood pressure PulseRespiratory rateTemperatureHeadNeckChestHeartLung AbdomenExtemity

: fair, within normal nutrition: compos mentis (GCS :E4,V5 M6): right: 160/90 mm Hg, left: 160/90 mm Hg: right: 84 x/minute, left: 84 x/minute: 20 x/minute: not febrile: conjunctiva not anemis: bruit carotis () : breath movement right and left is balance: irregular rythme (), murmur () : sonor, vesicular, ronchi (): lever and splen unpalpable, muscle rigidity () : unequal pulses ()

Psychiatric state :

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The psychiatric screening used UCLA Neuropsychiatric Inventory Result : suggest to disturbance in behavior domain depression and apathy

Neurological examination :Conciousness Head & eye

Neck

: compos mentis, GCS : E4,V5 M6 : mesocephal pupil isocor, diameter 3mm/3mm light reflex +/+, corneal reflex +/+: neck stiffness (-)

Cranialnerves

Description Right Left

n.I Smelling Wnl Wnln.II Visual Function >1/12 >1/12

Visual Field Wnl WnlColour Vision Wnl Wnl

n.III Ptosis (-) (-)Eye’s motion to medial Wnl WnlEye’s motion to below Wnl WnlEye’s motion to above Wnl WnlPupil 3 mm 3 mmKind of pupil Round RoundDirect of light reflex (+) (+)Indirect of light reflex (+) (+)Accomodation reflex (-) (-)

n.IV Strabismus divergen (-) (-)Eye’s motion to medial below (+) (+)Strabismus konvergen (-) (-)

n.V Biting Wnl WnlOpen mouth Wnl WnlSensibility of face Wnl WnlCorneal reflex Wnl WnlTrismus (-) (-)

n.VI Eye’s motion to lateral (+) (+)Strabismus konvergen (-) (-)Diplopia (-)

n.VII Blinking (+) (+)Nasolabial Fold Dissapeared WnlThe angle of the mouth Decreased WnlWrinkling of the forehead Wnl WnlWrinkling of the eyebrow Wnl WnlClose eye Wnl WnlGrimace Skewed mouth to leftBlowing Weak WnlTaste on the 2/3 anterior of the tongue

Wnl Wnl

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n.VIII Hearing of the whispered voice, ticking watch

Normal Normal

n.IX Arcupharyng SimetrisTaste on the 1/3 posterior of the tongue

Wnl Wnl

Vomiting Reflex (+) (+)Pronouncing the lingual (-)Retching (-)

n.X Pulse per minute 84 x 84 xArcupharyng SimetrisSpeech (+) Swallowing (+)

nXI Turning head Wnl WnlShoulder position SimetrisLift shoulder Wnl WnlTrofi of muscle shoulder Eutrophi Eutrophi

n.XII Tongue position Skewed to leftArticulation DysarthriaTremor of tounge (-) (-)Tounge protraction Skewed to rightTrofi of tounge’s muscle Eutrophi EutrophiFasiculation of tounge (-) (-)

BodyRight Left

Chest Breath movement is balanceSensibility: Protopatic Wnl Wnl Propioseptic :

Pression Wnl WnlVibration Wnl WnlPosition Wnl WnlDiscrimination Wnl Wnl

Abdominal Reflex Wnl WnlUpper Extremity

Movement Limited FreeStrength 3-3-3 5-5-5Tonus Normal NormalTrophy Eutrophi EutrophiPhysiological reflex (+) (+)Patological reflex (-) (-)Sensibility : Protopatic Wnl Wnl Propioseptic:

Pression Wnl WnlVibration Wnl WnlPosition Wnl WnlDiscrimination Wnl Wnl

Lower ExtremityMovement Limited FreeStrength 3-3-3 5-5-5

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Tonus Normal NormalTrophy Eutrophi EutrophiPhysiological reflex (+) (+)Patological reflex (+) (-)Sensibility : Protopatic Wnl Wnl Propioseptic:

Pression Wnl WnlVibration Wnl WnlPosition Wnl WnlDiscrimination Wnl Wnl

Vegetative function : within normal limitAbnormality movement : ()

Gadjah Mada Stroke Scale : 24Barthel index : 15Activities of Daily Living : 16

Cognitive function :

Mini Mental State Examination

Orientation : 8 (orientation of person and place were not impaired, but orientation of time was impaired)Regristration : 3Attention and calculation : 4Recall : 2 (new learning ability was impaired)Language : 4, the patient did not do the option of sentence command, because weakness in the right handConstruction : the imitating of picture was not examined, because of weakness in the right hand

D’esposito Attention : it was impaired, the patient did not do completely to mention the backward digit sequence and the backward month sequence Language : the patient could speak spontaneously, but it was not fluently; the mentioning, repetition, interpretation of verbal language and reading were not impaired, but the writing of sentence was not examined, because of weakness in the right hand, apraxia was not impaired Visuospatial : it was not impairedVisuoconstruction : it was not examined, because of weakness in the right handMemory : digit span was three (recent memory was impaired), recalling of 5 word was two (new learning ability was impaired), narrating of current public event was negativeExecutive function : it was impaired, mentioning of

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animal name within 1 minute was six, tcontinuing the alternating picture and the letter-digit sequence was not examined, because of weakness in the right hand

Conclusion : cognitive impairment especially in domain of attention, memory, and executive function

Hachinski score : 11

Supporting examination:

Laboratory finding (April, 14 th , 2006)Hb : 13,4 g/dL Difftel : AST : 36.3 IU/LAL : 8.100 / mm3 Neutrofil: 67.4 H% ALT : 37.2 IU/LAE : 5,84 x 106 / mm3 Limfosit : 27.1 L% BUN : 11.9 mg/dLHct : 43,1 L% Monosit : 4.6 L% Creatinin : 1.0 mg/dLAT : 214.000 / mm3 Eosinofil: 0.9 % Uric acid : 2,6 mg/dL Basofil : 0,0 % Random glucosa:235 mg/dL

Na : 138 mmol / L Chol : 311 mg/dL K : 3.4 mmol / L Tg : 115 mg/dL Cl : 100 mmol / L HDL : 51 mg/dL

LDL : 229 mg/dL

Laboratory finding Fast glucose : 209 mg/dLGlucosa 2 hour post prandial : 178 mg/dL

Radiology:Rontgen of thoracic ( April, 14 th 2006)Result: Pulmo : within normal limit, Cor: cardiomegali

Head CT Scan (April, 14 th 2006) Hipodens lession on left subcortical deep temporal lobe (diameter 2 mm) and leftperiventricular (diameter 5 mm)Result : infarction on left subcortical deep temporal lobe and left periventricular

Electrocardiography April, 14 th 2006:Synus Rhytm, Heart Rate 76 x/minute, ventricular extrasystole frequentApril, 16 th 2006:Synus Rhytm, Heart Rate 72 x/minute, ventricular extrasystole bigeminiApril, 20 th 2006:Synus Rhytm, Heart Rate 84 x/minute, ventricular extrasystole rare

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Consultations

Cardiology department (April, 14 th 2006): Result: ventricular extrasystole frequentTreatment : oxigenation via canule, amiodarone oral 3 x 100 mgEvaluation assessment (April, 16 th 2006): Result: ventricular extrasystole bigeminiTreatment : oxigenation via mask, amiodarone drip 450 mg/24 hoursEvaluation assessment (April, 20 th 2006): Result: ventricular extrasystole rareTreatment : oxigenation via canule, amiodarone drip 450 mg/24 hours

Internal department (April, 14 th 2006): Result: diabetes mellitus type 2 non obeseEvaluation assessment (April, 25 th 2006): Treatment: regular insulin 3 x 4 IU

Medical rehabilitation department (April, 16 th 2006): Result: Right hemiparesis on infarction stroke patientProgram: Exercise program Muscle strengthening Mobilization and ADL improvement

SECOND DISCUSSION

The results of physical examination, showed consciousness, right hemiparesis and right facial weakness (paresis of right facial nerve-upper motor neuron) and paresis of right hipoglossus nerve -upper motor neuron, vascular cognitive impairment. The patient had hypertension. Result of electrocardiography showed ventricular extrasystole and chest X ray show there was cardiomegaly. The result of Head CT scan examination showed infarction on left subcortical deep temporal lobe, left periventricular. The blood laboratory examination showed hyperglycemia, hypercholesterolemia. Consulting to the cardiology department there was frequent ventricular extrasystole which in the clinical course develop into bigemini ventricular extrasystole, while consulting to the internal department there was non obese diabetes mellitus type 2. Stroke is caused by multifactor disease such as hypertention, diabetes mellitus, cardiac disturbance, dyslipidemia and many other factors are listed as risk factors. This patient had uncontrolled hypertention, diabetes mellitus, ventricular extrasystole and dyslipidemia as the risk factors. The pathophysiology of hypertension, diabetes mellitus, dyslipidemia can cause stroke through atherosclerosis pathway.

Four major groups of diseases associated with ischemic cerebrovascular disorders are cardiac disorders (valve related emboli, intracardiac thrombus or tumor, systemic venous thrombi with right to left cardiac shunt), large vessel disease (atherosclerosis, carotid artery dissection, fibromuscular dysplasia), small vessel disease (hypertension,

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infectious and noninfectious arteritis), hematologic disease (polycythemia, thrombocythemia, thrombotic thrombocytopenic purpura) (Wiebers et al., 1997).

Lacunar infarct was defined as an acute stroke syndrome with a CT lesion compatible with the occlusion of a single perforating artery, consisting of a subcortical (basal ganglia, internal capsule, brainstem), small, sharply demarcated hypodense lesion with a diameter <15 mm. If no such lesion was visible or if no CT was performed, we used the established criteria of unilateral motor and/or sensory signs that involved the whole of at least 2 of the 3 body parts (face, arm, leg) without disturbance of consciousness, visual fields, language, or other cortical functions. We distinguished 4 lacunar syndromes: pure motor stroke, sensorimotor stroke, pure sensory stroke, and atactic hemiparesis/dysarthria clumsy hand syndrome (De Jong et al., 2002).

The small penetrating branches of the major intracranial arteries have poor collateral connections, obstruction of blood flow caused by fibrin deposition, lipohyalinosis, microatheroma, or thrombus leads to infarction in the limited distribution of one of these arteries (Wiebers et al., 1997). There isn a time profile for appearance of this lesion after the clinical event. Using CT imaging, the lowest prevalence of positive images occurs in the first week after the event. From reported data, early CT positivity for lesions congruent with a clinically defined lacunar infarct ranges from 12% to 50% of patients. In the first few days, MRI is reported to show a recent lacunar infarct in up to 94% of patients. Diffusion Weighted Magnetic Resonance Imaging (DW-MRI) performed after 3 days was 95% sensitive and 94% specific for revealing an acute lacunar infarct (Inzitari and Lamassa, 2003).

The study to determine the clinical presentation and aetiology of small subcortical infarctions as found on DW-MRI. Ninety three patients were identified showing subcortical or brainstem DWI lesions <1.5 cm in diameter within a maximum of 7 days from the onset of stroke symptoms (Seifert et al., 2005).

In study about effect of frequent ventricular extrasystole on brain circulation in patients with coronary heart disease, to demonstrated that reduction of cerebral blood flow can induced by frequent premature ventricular beats (Hagendorff et al., 1993).

On the cognitive function examination, the patient had MMSE examination to result in disturbance of orientation, attention and calculation, as well as registration. While in the D’esposito examination to result in disturbance of attention, memory, and executive function. Based on result of this examination, the patient had vascular cognitive impairment.

Subcortical ischemic vascular injury and lacunar infarctions relevant to vascular dementia tend to preventially involve the subcortical white matter of the frontal lobes and the anterior aspects of the basal ganglia including the caudate nucleus and globus pallidus. Patient with subcortical vascular dementia exhibit more severe impairment of executive function and less impairment of memory, particulary recognition memory (Cummings, 2003).

Final diagnosis :

Clinical diagnosis

Topical diagnosis

: lacunar stroke syndrome vascular cognitive impairment: posterior limb of left internal capsule

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Etiological diagnosis

left subcortical deep temporal lobe, left periventricular : hypertension small vessel disease, diabetes small vessel disease, hypercholesterolemia small vessel disease

Management

Oxygenation is a great importance during periods of acut cerebral ischemia in order to prevent hypoxia and potential worsening of the neurologycal injury (Adams, 2003).

Neuroprotectan drugs give variety result in stroke patient. The National Guideline of Stroke has not recommended neuroprotectan neither has AHA Guidelines . Neverthless Indonesian Neurological Association still recommended piracetam and citicholine as neuroprotectan drugs for stroke patients (Perdossi, 2004). Piracetam has two mechanisms affected to neuronal and vascular levels (Perdossi, 2004):

a. Neuronal level: related to phospolipid, cell membran fluidity repaired, neurotransmitter repair, adenylate cyclase stimulation.b. Vascular level: increase of erythrocyte deformability, decrease of platelet anti agregration, microcirculation repaired.

It is indicated to be given at seven hours of stroke onset. First 12 grams of piracetam per infussion over 20 minute, and then followed with 3 grams bolus every 6 hour or 12 grams every 12 hour until the fourth day. On day 5 until the end of 4 weeks, is piracetam given 4,8 gram divided 3 times a day orally, and on the week 5 until 12 it is given 2,4 gram twice a day ( Perdossi, 2004).

A randomized, double-blind parallel group design trial of 927 patients at 55 centers. Inclusion criteria are presenting within 12 hrs of onset of acute ischemic supratentorial stroke, disabling symptoms (Orgogozo scale score of >5 and <70) and arousable, the ages of 40 and 85. Patients received placebo or 12 g piracetam as an initial intravenous bolus followed by 12 g daily for 4 weeks and then 4.8 g daily for 8 weeks. The outcome assesment used Orgogozo scale and Barthel Index. Additional analyses of patients with moderate and severe stroke within the early treatment group also showed significant improvement on piracetam in both outcomes (p<0.02) (De Deyn, 1997).

Citicholine treatment will improve cerebral function passing through some ways as follow (Adibhlata et al., 2001):

a. Increase phosphatydil choline to make membrane repairb. Inhibit free fatty acid and free radicalc. Increase acetylcholine neurotransmitter production which has theurapetic effect as

long as ischemicd. As glutation resources which kind of primary endogenic antioxidant in the brain

For ischemic stroke, citicholoine should be given on first 24 hour since stroke attack at dose 250-1000 mg, intravenous 2-3 times a day over 2-14 day (Perdossi, 2004).

In systematic search of all prospective, randomized placebo-controoled, double blind trial, about oral citicoline treatment for acut ischemic stroke (various doses 500, 1000 and 2000 mg) to demostrated that citicoline within the first 24 hours after onset in patents with moderate to severe stroke increase the probability of complete recovery at 3 months (Davalos et al., 2002).

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Trial of CAPRIE was a randomised, blinded, international trial designed to assess the relative efficacy of clopidogrel (75 mg once daily) and aspirin (325 mg once daily) in reducing the risk of a composite outcome cluster of ischaemic stroke, myocardial infarction, or vascular death; their relative safety was also assessed. The interpretation this study is long-term administration of clopidogrel to patients with atherosclerotic vascular disease is more effective than aspirin in reducing the combined risk of ischaemic stroke, myocardial infarction, or vascular death. The overall safety profile of clopidogrel is at least as good as that of medium-dose aspirin (CAPRIE Steering Committee, 1999).

This multi-center study will recruit 2500 participants (20 percent of whom will be Hispanic Americans) to find out if using aspirin and clopidogrel together is more effective than using aspirin alone to prevent recurrent stroke in patients with lacunar stroke, and if lowering a patient’s blood pressure below the usual limits will also help prevent recurrent stroke and maintain thinking ability (Benavente, 2003). The flow chart of hypertension management in acute stroke (Perdossi, 2004):

Acute stroke

Sistolic 230 mmHg Sistolic 230 mmHg Sistolic 180 - 230 mmHg Sistolic 180 mmHg Diastolic 140 mmHg Diastolic 121 - 140 mmHg Diastolic 105 - 120 mmHg Diastolic 105 mmHg

Repeat to examination after 15 minute

Sistolic 230 mmHg Intracerebral hemorrhagic Diastolic 121 - 140 mmHg or disturbance of end organ

Positive Negative

Parenteral antihypertension Observation Drug Oral antihypertension drug give over the seventh until tenth day

The study about statin therapy to shows that statin therapy rapidly reduces the incidence not only of heart attacks but also of ischemic strokes, with no adverse effect on hemorrhagic strokes. Allocation to 40 mg simvastatin daily reduced the rate of ischemic strokes. Compared with the placebo group, the group assigned to 40 mg simvastatin daily had an average reduction in low-density lipoprotein cholesterol of 1 mmol/L. The investigators recommend that statins be routinely considered for all patients at high risk of stroke (Barclay, 2005).

Elevated blood glucose is common in the early phase of stroke. The prevalence of hyperglycemia, defined as blood glucose level >6.0 mmol/L (108 mg/dL), has been observed in two thirds of all ischemic stroke subtypes on admission and in at least 50% in each subtype including lacunar strokes. Extensive experimental evidence in stroke models

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supports that hyperglycemia has adverse effects on tissue outcome, and an association between blood glucose and functional outcome has been found in an increasing number of clinical studies. Although no interventional stroke studies have addressed the acute reversal of hyperglycemia, active lowering of elevated blood glucose by rapidly acting insulin is recommended in most published guidelines, even in nondiabetic patients (European Stroke Initiative [EUSI] guidelines >10 mmol/L, American Stroke Association [ASA] guidelines >300 mg/dL) (Lindsberg and Roine, 2003). Insulin infusion has an effect that is opposite to that of hyperglycemia. It not only lowers blood glucose levels but also exerts an antioxidant and anti-inflammatory effect. Insulin also improves NO production and results in improved blood circulation to the ischemic areas (Garg et al., 2006). Amiodarone is used to correct abnormal rhythms of the heart (an antiarrhythmic medication). Amiodarone is considered a "broad spectrum" antiarrhythmic medication, that is, it has multiple and complex effects on the electrical activity of the heart which is responsible for the heart's rhythm. Among its most important electrical effects are (Anonim, 2006):

1. A delay in the rate at which the heart's electrical system "recharges" after the heart contracts (repolarization);

2. A prolongation in the electrical phase during which the heart's muscle cells are electrically stimulated (action potential);

3. A slowing of the speed of electrical conduction (how fast each individual impulse is conducted through the heart's electrical system);

4. A reduction in the rapidity of firing of the normal generator of electrical impulses in the heart (the heart's pacemaker);

5. A slowing of conduction through various specialized electrical pathways (called accessory pathways) which can be responsible for arrhythmias.

A multicenter, international, randomized, placebo-controlled trial about efficacy and tolerability of donepezil in vascular dementia was randomized to 24 weeks of treatment with donepezil 5 mg/day and donepezil 10 mg/day, as well as placebo. At week 24, both donepezil groups showed significant improvement in cognition and global function versus placebo. Donepezil treated patient showed significant benefits in activities of daily living over placebo. Donepezil was well tolerated. Withdrawal rates do to adverse events were relatively low (Black et al., 2003). Medical rehabilitation program should be initiated since the patient admitted to the hospital. Commonly, in the first day after stroke attack, the active medical rehabilitation program, hasn’t been initialed. In general, first day program was aimed to against complication caused by prolonged bed rest, for example by doing proper bed positioning. There were a lot of opinion about bed rest period after stroke attack , but generally were recomended between 1-3 weeks (Santoso, 2004). Many opinions suggest active medical rehabilitation program to be done earlier. Criterion can be used as guide: active medical rehabilitation program can be started if patient condition were stabil there were no complication and there were no medical condition that endanger patient ( life-threatening) (Santoso, 2004). Early medical rehabilitation was aimed to maximize healing or repairing potention and prevent complication of prolong immobilization as soon as possible (Santoso, 2004).

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The target of medical rehabilitation program :a. To prevent, recognice and handle medical condition that accompany stroke, including

reccurent stroke, repairing hydration and nutrition.b. To maximize functional self-supporting through various exercise programc. To facilitate patient and family psychological and social living adaptationd. To support reintegration on society and work placee. To repair life quality of the patient

Rehabilitation is needed to gain functional recovery through relearning process. Before mobilizing and active exercising the patient is given positionong to recovery his body function and to protect spastisity (Aliyah, et a., 2001).

The patient had given therapies: General:Airway, Breathing and circulation maintenance:O2 3 L/minIVFD Ringer acetat 20 gtt per minPharmacotherapy Piracetam inj 4 x 3 gramCiticholin inj 2 x 500 mgClopidogrel 1 x 75 mgSimvastatine 1 x 10 mgAmiodarone drip 450 mg / 24 hoursPlanning therapy for vascular cognitive impairment: donepezil 1 x 5 mgDiet: diet DM 1900 kaloriPhysiotherapy

Prognosis

The study was to investigate the long-term prognosis of first-ever lacunar strokes and the possible role of clinical prognostic factors. A cohort of consecutive patients presenting with first-ever lacunar infarcts was prospectively evaluated after stroke onset at day 0 to 3 and/or day 7, every 3 months up to 1 year, and every 6 months thereafter. Five-year survival rate free of recurrent stroke was 63%, while 5-year survival rate was 86%. Age was the only significant predictor of survival free of recurrent stroke. Age and the degree of neurological dysfunction and functional disability at 7 days after the index stroke measured by the Toronto Stroke Scale and a Barthel Index score <40 were the only significant predictors of death. The 5-year probability rate of stroke-free recurrence was 72%. Sixty-three percent of the first recurrent strokes were lacunar infarcts (Salgado et al., 1996).

The results of study about functional outcome in patients with lacunar infarction was moderate or severe hemiparesis 1 month after stroke onset as the strongest predictor of physical dependence or death at 3 years (p<0,001), followed by white matter hyperintensities on MRI (p<0,001). Recurrent stroke increased disability and handicap but was not a statistically significant independent risk factor (Samuelsson et al., 1996).

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The cohort study in pure motoric stroke; age, male sex and nonuse of acetylsalicylic acid were stastitically significant for independent determinants of death. While, hypertension and diabetes mellitus were stastitically significant for independent risk factor of recurrent stroke (Staaf et al., 2001).

The study about two type of lacunar infarcts performed a follow-up in 333 patients

with first lacunar stroke, distinguishing those with 1 asymptomatic lacunar lesions (LACI+) from those without such lesions (LACI-). The conclusion to show prognosis for mortality, recurrent stroke, and overall functional outcome in lacunar stroke patients with 1 silent lacunar lesions is more unfavorable than in patients without such lesions. These

findings sustain the idea of 2 lacunar stroke entities (De Jong et al., 2002).

The patient had many problems including hypertension, diabetes mellitus, dyslipidemia, ventricular extrasystole, barthel index 15, and three lacunar lesion in the head CT scan finding with symptom pure motoric.

Based on these study, so the prognosis for this patient are:

Death Disease Discomfort Dissatisfaction Dissability Distitution

: dubia ad malam : dubia ad malam : dubia ad malam : dubia ad malam : dubia ad malam : dubia ad malam

Follow up

Follow up April, 22 th, 2006 April, 25 th 2006 April, 27 th 2006General conditionGCSVital sign

Fair, E 4V5M 6BP=170/100

P=88x, RR= 20xtemp=not febrile

Fair, E 4V5M 6BP=140/90

P=88x, RR= 20xtemp= not febrile

Fair, E 4V5M 6BP=140/90,

P=88x, RR= 20xtemp= not febrile

N.cranialis Paresis N.VII, XII dextra UMN

Paresis N.VII, XII dextra UMN

Paresis N.VII, XII dextra UMN

Ekstremity :Movement

Limited Free Limited Free Limited Free Limited Free Limited Free Limited Free

Strength 3/3/3 5/5/5 3/3/3 5/5/5 3/3/3 5/5/53/3/3 5/5/5 3/3/3 5/5/5 3/3/3 5/5/5

ECG

Laboratorium

Therapy

Ventricular extrasystole (), synus rythme

O2 3 L/minIVFD Ringer acetate 20 gtt per minPiracetam inj 4 x 3 gramCiticoline inj 2 x 500 mgClopidogrel 1 x 75 mg

Ventricular extrasystole (), synus rythme Fast BG : 2052 h PP BG : 278Albumin : 2.58O2 3 L/minIVFD Ringer acetate 20 gtt per minPiracetam inj 4 x 3 gr Citicoline inj 2x500 mgClopidogrel 1 x 75 mg

Ventricular extrasystole (), synus rythme

2 h PP BG : 176Albumin : 3.08To stop of O2, IVFD Piracetam oral 3x800 mg Citicoline oral 2x500 mgClopidogrel 1 x 75 mgLosartan 1 x 50 mgSimvastatine 1 x 10 mg

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Losartan 1 x 50 mgSimvastatine 1 x 10 mgAmiodarone drip stopDiet DM 1900 kaloriPhysiotherapy

Losartan 1 x 50 mgSimvastatine 1 x 10 mgRegular Insulin 3x4 IUAlbumin infuseDiet DM 1900 kalori Physiotherapy

Regular Insulin 3x4 IUPatient discharge from hospital, with educa tion: control to stroke unit, memory, endcrine and physiotherapy clinic

REFERENCES

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