Vascular Dementia, With Lacunar Stroke

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    VASCULAR DEMENTIA, WITH LACUNAR STROKE

    Kelompok VII 2012 Palembang Class

    Tutor: dr. Alfian HasbiPresented by Timotius Wira Yudha

    Universitas Sriwijaya 2014

    Press CTRL + L to begin slideshow on Adobe Reader.

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    OVERVIEW

    Difficult terms Anatomy and Physiology

    Insight: Vascularisation, CBF Lacunar Stroke VASCULAR DEMENTIA

    Problem Map Conclusion

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    TERMINOLOGY

    Hemiparesis Topographical disorientation

    Grade II hypertension Presence of pathological reflexes BSS suggests untreated diabetes

    Forget consuming medication? VICIOUS CYCLE!

    Lacunar infarction MMSE

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    ANAT & PHYSIOL

    CNS Central Core Brain Limbic System Neocortex

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    http://missinglink.ucsf.edu/lm/ids_104_cerebrovasc_neuropath/Case3/Case3Images/CerArtDistBlum1.jpg
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    COMMON MECHANISMS FOR STROKAND VASCULAR DEMENTIA(Bezerra et al., 2012)

    LIPOHYALINOSIS RF: Hypertension, diabetes mellitus Tunica media thickening

    MICROATHEROMA RF: Hypertension, hypercholesterolaemy Classic atherosclerosis theory endothelial lesion

    BOTH ARE PRESENT

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    STROKE TYPE?

    Age = RISK FACTOR both ISCH / HAEM Physical Exam: HTN grade II

    Lab: Hyperglycaemie (DM II) NO Hyperlipidaemie / Hypercholesterolaemie

    HAEMORRHAGIC?

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    LACUNAR STROKE

    CT Scan: Lacunar infarction on lobustemporalis sinister.

    ISCHAEMY of arteries to brains internalstructures: A. lenticulostriata.

    Types Motor (pure) Ataxic Dysarthria Sensory (pure) Mixed sensorimotor

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    LACUNAR STROKE

    EMPHASIS: Motor Capsula interna, crus posterius

    Basis pontis Corona radiata

    Projection of axons from cortex that will be

    directed towards brainstem NO CNS axonal regeneration (which DOES

    occur in periphery)

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    http://missinglink.ucsf.edu/lm/ids_104_cerebrovasc_neuropath/Case3/Case3Images/CerArtDistBlum2.jpg
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    VASCULAR DEMENTIA

    Varying degrees of arterial occlusion createsdifferent clinical features: Consider simpleatherosclerosis vs large occlusion (STROKE).

    Memory is formed in FORMATIOHIPPOCAMPALIS

    Here occurs neurogenesis (Griggs, 2012:62) Supplied by A. cerebri posterior and A.

    choroidea anterior The same vessels supply Crus posterius of

    ca sula interna Gilro et al. 2009:609 .

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    http://missinglink.ucsf.edu/lm/ids_104_cerebrovasc_neuropath/Case3/Case3Images/CerArtDistBlum1.jpg
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    ATYPICAL?

    25% of infarcts to A. cerebri posterior causes amnesia (Brandt et al. quoted by Romn, 2005)

    LESION LOCALISATION LEFT: Verbal difficulties RIGHT: Visuospatial dysgnosie

    NY. LUNA: LEFT LESION, BUT WITH VISUO-SPATIAL DIFFICULTIES?

    ATYPICAL

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    DIAGNOSIS

    NINDS-AIREN (Romn, 2005) Simple, four characteristics

    Cognitive loss Cerebrovascular lesions demonstrated by brain

    imaging (CT, MRI) A temporal link between stroke and cognitive loss Exlusion of other causes of dementia (Alzheimer,

    Vitamin B12 deficincy)

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    THERAPY Focus on treating risk factors TO PREVENT

    ANOTHER STROKES. HYPERGLYCAEMY

    Biguanida (Metformin) Consider insulin if situation worsens

    HYPERTENSION Hydrochlorothiazide Consider selective beta-1 receptor antagonist

    Cholinesterase inh (Galantamine)? Aspirin (antiplatelet) prevent PLT aggregation.

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    PREVENTION

    Control risk factors! DITARY MODIFICATIONS

    Eat more UFA, Blueberry PHYSICAL ACTIVITIES

    3-5 days of 30 walking of 2.5 km

    REDUCE STRESS Spend more time for social interactions Play computer games

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    PROGNOSIS

    DUBIA AD MALAM BAD 5YSR: 39%

    Life expectancy is reduced on Men Low education Bad neuropsychological results

    (Alagiakrishnan, 2012)

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    MISCELLANEOUS

    SKDI Lacunar stroke: 2 (De facto 3B) Vascular dementia: 2To diagnose, refer, and treat fully after referral

    MMSE VS MOCA?

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    PROBLEM MAPDiabetes mellitus (uncontrolled) Hypertension Senilitas (penuaan)

    Stress oksidatif Vascular resistance \uparrow

    Penggunaan energi \uparrow Afterload \uparrow

    Deposit hyalin + tunica media Rawan lesi endothelial

    thickening (Lipohyalinosis)Macrophage attraction

    Microatheroma(Plaque buildup)

    Oklusi cabang2 lenticulair A. cerebri posterior and A. choroidea anterior

    Oklusi terjadi dengan derajat dan threshold yang berbeda

    Ischaemic stroke in Crus posterius capsulae internae Reduksi signifikan aliran darah ke Formatio hippocampalis

    Contralateral hemiparesis Presence of Problems in cognitive functioning, memorypathological reflexes

    Skor MMSE pathologik Suka lupa

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    CONCLUSION

    Ny. Luna, 69 tahun, mengalami gangguanfungsi luhur dengan emphasis memori etcausa dementia vasculare. Selain itu, ia jugamengalami hemiparesis et causa strokelacunair di Crus posterius capsulae internae.

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    REFERENCES Griggs, Richard A. 2012.Psychology: A Concise Introduction,

    Third Edition . New York: Worth Publishers. Romn, Gustavo C. 2005. Current Clinical Neurology .

    Clinical Forms of Vascular Dementia. Gilroy, Anne M., et al. 2009. THIEME Atlas of Anatomy . New

    York: Stuggart. Alagiakrishnan, Kannayiram et al. 2012. Vascular Dementia .

    http://emedicine . medscape.com/article/292105-overview,diakses 28 Oktober 2014, 13.01 WIB.

    Bezerra, D. C., et al. 2012. Neurology . Risk Factors forLacune Subtypes in the Atherosclerosis Risk in Communities(ARIC) Study.

    Guyton, Arthur C., John E. Hall. 2007.Buku Ajar FisiologiKedokteran . Editor: Luqman Yanuar Rachman. Jakarta: EGC.

    http://emedicine/http://emedicine/http://emedicine/
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