Presentation Kul Nbh
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KULIAH
NEUROBEHAVIOUR
Dr. Listyo Asist Pujarini, MSc., sPs
Senin, 14 September 2009
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Pelayanan kesehatan membaik
Jumlah Lansia meningkat
Proses degenerasi tak dapat dihindari
Kemunduran fungsi mental demensia
Penurunan kualitas hidup, beban kel & masyarakat
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OTAK MENUA (1)1. Proses menua (aging) menyebabkan proses penuaan
sekujur tubuh, tak terkecuali otak.2. Pada proses penuaan otak, terjadi penurunan jumlah sel
neuron secara bertahap. a. Girus temporal superior, pelipis:
(memori), pl cepat kehilangan neuron. b. Girus pre sentralis, otak depan :
kemampuan eksekusif. c. Area striata, dan yang tak berubah girus
post sentralis.
Kusumoputro. S, 2003
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OTAK MENUA (2)Secara Patofisiologis
1. Penurunan jumlah neuron kolinergik, menyebabkan berkurangnya neurotransmiter Asetilkolin (ACh).
2. Sehingga dapat menimbulkan “sindrom gangguan ABC” yaitu :
A : ADL terganggu. B : Behavior berubah. C : Cognition menurun.
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OTAK MENUA (3)Peran AChE dan BuChE
1. AChE : Asetilkolin Esterase.
2. Terdapat di otak dan eritrosit.
3. Ikut mengatur Ach dgn menghidrolisis Ach di celah sinaps.
1. BuChE :Butirilkolin Esterase.
2. Terdapat lebih banyak di : otot jantung, o.polos, kulit dan plasma.
3. idem.
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KEMATIAN NEURON Secara Neurohistopatologi
1. Bercak saraf t.d. protein beta amiloid, disebut: neurotic plaque.
2. Kekusutan serat saraf, neuro fibrillary tangels, yg tbtk dari protein tau yg alami ggn shg bergulung & kusut.
1. Usila N -- AD (+) ----- (++:+++)
2. (+) ---- (++:+++)
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plaque
tangles
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8
Neuritic plaques & neurofibrillary tangles
plaques
tangles
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KEMATIAN NEURON Secara Kontinum
1. Jumlah Berkurang Sakit neuron bertahap 100% 40-60-80% 20%2. Disfungsi - +/- + +++ neurologis3. Waktu 20 – 30 tahun4. AD 65th 80th 90th 8% 25% 40%
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FUNGSI KOGNITIF
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Neurokognitif
• Atensi• Memori• Bahasa• Ketrampilan visuospasial• Fungsi eksekutifDitambah pengolahan informasi
emosional
(Jeffrey, 2003)
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Atensi
• Adalah kemampuan untuk memusatkan dan mengolah kognitif langsung dan menolak kebingungan.
• Diperiksa dengan digit span test,
(Jeffrey, 2003)
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Memori
Terdiri dari 2 tipe yaitu amnestic disorder dan retrieval deficit syndrome.
Amnestic disorder: disfungsi limbik medial dan hipokampus, pasien tidak dapat memperhatikan dan menyimpan informasi baru dan menunjukkan defisit recall dan recognition.
Retrieval deficit syndrome: disfungsi sirkuit frontal subkortikal, pasien kesulitan dalam recalling tetapi baik dalam recognition.
Dinilai dengan ingatan 3 sampai 10 kata (Jeffrey, 2003)
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Bahasa
Verbal output disoreder meliputi artikulasi (disartri), volume (hipofonia), prosodi (abnormal vocal inflection), proportional language (afasia).
Klasifikasi afasia tergantung pada penilaian fluency, comprehension, repetition.
Tes untuk penilaian afasia meliputi naming, reading, writing, singing, automatic speech
(Jeffrey, 2003)
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Repetitionintact
Repetitionimpaired
Repetitionintact
Repetitionimpaired
Repetitionintact
Repetitionimpaired
Repetitionintact
Repetitionimpaired
Conduction
Transcortical sensory
Wernicke’s
Transcorticalmotoric
Broca’s
Isolation
Global
AnomicComprehension
intact
Comprehensionimpaired
Comprehensionintact
Comprehensionimpaired
Fluent
Nonfluent
Aphasia
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Ketrampilan visuospasial
• Visuospasial kompleks tegantung pada atensi, memori dan fungsi eksekutif yang terintegrasi.
• Gangguan visuospasial menunjukkan disfungsi aspek posterior hemisfer kanan.
• Dinilai dengan kemapuan meniru atau menggambar stimuli visual.
(Jeffrey, 2003)
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Fungsi eksekutif
Memori
Pilihan kemauanEmosi
Input sensoris Mengatur
ProgramRencana
Aksi
Monitor
(Jeffrey, 2003)
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- Contralateral limb weakness- Contralateral sensory loss- Disfasia- Disleksia, disgrafia, diskalkulia- Disorientasi spasial
HemianopsiaHomonim Kontralateral
NistagmusDisartriaAtaksia- Ggn saraf kranial
- Ggn fx vital
- Ggn bahasa- Ggn memori- Ggn mood- Ggn perilaku- Hearing & vision pathways
- Demensia- Ggn mood- Ggn perilaku- Inkontinensia- disfungsi olfaktorius- Disfungsi opticus
(Wilkinson, 1997)
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Domain Cognition
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KONSEP KONTINUM GANGGUAN KOGNITIF
1. Menua sukses,atau normal.2. Menua normal tetapi MUDAH LUPA :
Forgetfulness, Benign Senescent Forgetfulness :BSF, Mudah lupa terkait usia :Age-Associated Memory Impairment : AAMI.
3. Kelemahan Kognitif Ringan, Mild Cognitive Impairment : MCI
4. Penyakit Alzheimer. Stadiun Awal, Menengah, Lanjut.
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MUDAH LUPA RINGAN (1)1. Keluhan mudah lupa (BSF & AAMI) , banyak
dijumpai pd warga usia lanjut (Wulan).
2. Gangguan mengingat kembali, recall, ini masih fisiologis, disebut : a senium naturale.
3. Pasien sadar kekurangannya & melakukan kompensasi :sirkumlokusi, yaitu penjelasan berbelit-belit seakan minta bantuan.
4. BSF digunakan bergantian dg AAMI.
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MUDAH LUPA RINGAN (2)
BSF1. Mudah lupa
dibanding dg kelompok sebaya (peer group)
2. Kognitif normal.
3. Belum menunjukkan gejala demensia.
AAMI1. Sama.
2. Dengan kemunduran kognitif nyata.
3. Belum menunjukkan gejala demensia.
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MUDAH LUPA
Dalam kriteria :
1. Mudah lupa nama: benda, orang, peristiwa.2. Terdapat gangg. mengingat kembali : recall.3. Terdapat gangg. utk mengambil kembali apa yg pernah
diingat : retrieval.4. Mudah mengingat kembali bl diberi bantuan/ isyarat.5. Sering menjabarkan fungsi pada istilah yg lupa.
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PENYEBAB MUDAH LUPA PADA WULAN
1. Proses berpikir yg jadi lamban.2. Sulit memusatkan perhatian .3. Mudah beralih ke hal yg tidak penting.4. Perlu lebih banyak waktu utk belajar hal yg baru.5. Kurang dpt menggunakan strategi memori yg
tepat.6. Perlu lebih banyak bantuan pengenalan/ isyarat
utk mengingat kembali.
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M C I = KELEMAHAN KOGNITIF RINGAN adalah salah satu gangguan kognitif,
termasuk kelompok perantara, fase transisi antara “Mudah lupa terkait usia” (AAMI) dengan demensia Alzheimer.
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M C I Batasan operasional :Terdapat keluhan gangguan memori secara subyektif.Gangguan memori tersebut terbukti secara tes memori, yang disesuaikan tingkat pendidikan dan usia.Penampilan kognitif secara global normal.Aktifitas hidup shr-hr (ADL) masih normal.Belum masuk kriteria demensia.
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Terapi Preventif MCI
• Penggunaan statin untuk penurunan kolesterol
(Dekosky S, Am. J. Med, 2005)• Penggunaan anti hipertensi
(Quicx, et al, Neurology 2003)• Kombinasi Vit.C & Vit.E
(Kerwind, 2005)
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Terapi Preventif MCIResiko tinggi pada keadaan :• Tekanan darah diastolik usia pertengahan
dengan APO.E4 (Decarti. C, et al, Arch Neuro 2001)
• Tekanan darah sistolik usia pertengahan & kolesterol tinggi
(Kivipello. NA, et al, Lancet Neurology 2005)• Defisiensi asam folat & B 12
(Wang. HX, et al, Neurology 2001)• Kadar Homocysteine tinggi pada usia
pertengahan (Sachdey P, et al, Arch Neurol, 2004)
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dementia
normal
forgetfulnes
mild cognitive impairment
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PROGNOSISMCI
• Membaik• Stabil (status quo)• Progres > VaD > AD > Demensia lain
(Golomb J., et al.,2001; Jelic V&Winbald B., 2003)
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DemensiaKondisi mental berupa kemerosotan
fungsi kognif-intelektual yang berlansung perlahan tapi semakin
memberat yang mengganggu aktifitas kehidupan sehari-hari
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Prevalence of Dementia-- of those 85+ years and who suffer from dementia, almost 50% live in the community -- those 85+ who have dementia and live in the community
- 45.5% have mild dementia- 44.5% have moderate dementia- 10.0% have severe dementia
-- the prevalence of dementia rises with age
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Definition – Diagnostic criteria for Dementia
A. Development of multiple cognitive deficits manifested by both:
1. memory impairment (impaired ability to learn new information or to recall previously learned information);
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Criteria for dementia (cont’d)
2. One (or more) of the following cognitive disturbances:
--Aphasia (language disturbance)-- Apraxia (impaired ability to carry out motor
function despite intact motor function--Agnosia (failure to recognize or identify
objects despite intact sensory function)
--Disturbance in executive functioning
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Etiologies of DementiaDementia Frequency
(%)Alzheimer’s disease 50-60Vascular dementia 10-30Depression 5-15Alcohol-related dementia 1-10Metabolic disturbances 1-10Toxic disturbances 1-10Hydrocephalus 1-5Anoxia brain injury 1-2Central nervous system infections 1-2Brain tumors 1-2Brain trauma 1-2Subdural hematoma 1-2Other 10-20
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CAUSES OF DEMENTIA
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Alzheimer disease
Jenis demensia yang sering mengenai orang tua, disebabkan oleh degenerasi neuronal
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Pathophysiology of A.D.The presence of neurofibrillary tangles and neuritic plaques
1) neuritic plaques increase in number and are abnormally distributed
2) neurofibillary tangles – abnormal bundles of protein ( B amyloid) that interfere with nerve functioning
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Pathophysiology of A.D. (cont’d)
3) decrease in neurotransmitter acetylcholine 4) several point mutations in the gene coding of ApoE (it is involved in synaptic repair) 5) accumulation of homocysteine
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Kriteria dx AD sesuai DSM IV:A. Defisit kognitif komplek: 1. Gangguan memori 2. Satu/> afasia, apraksia,
agnosia, ggn fx eksekutifB. Defisit kognitif AI &A2 ggn ADL
&menggambarkan penurunan tk kemampuan scr jelas
C. Awitan berthp &semakin menurun
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D. Defisit kognitif tdk disebabkan ggn ssp, sistemik atau intoksikasi
E. Tdk terjd slm deliriumF. Tdk ada ggn jiwa
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43
GEJALA ALZHEIMER
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44
GEJALA ALZHEIMER
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Vascular Dementia
Semua kasus demensia yg disebabkan oleh gangguan serebrovaskuler, anoksik, hipoksik otak
dengan penurunan kognisi dari yang ringan sampai paling berat dan meliputi semua domain
(tidak harus gangguan memori yg menonjol)
Kriteria dx VaD
• Ada 4 konsensus (DSM IV, ICD X, ADDTC, NINDS AIREN)• Yang paling sering:NINDS AIREN
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Probable VaDNINDS-AIREN
• Demensia• CVD yg ditandai dg defisit neuro fokal pd px fisik:
hemiparesa, paresa n VII, gangguan sensorik, hemianopsia, disatria, dll yg konsisten dg stroke (rwyt stroke+/-), bukti yg relevan adanya CVD (HCTS/MRI), meliputi stroke multiple pembuluh darah besar/infark tunggal yg strategis/infark lakuner multiple/kombinasi
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• Terdapat hub ant ke2 gangguan diatas dg 1/>gx dibawah ini:
– awitan demensia berada dalm kurun 3 bln post stroke
– deteriorasi fg kognisi yg mendadak/ berfluktuasi /progresif
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Perbedaan AAMI, MCI dan DemensiaGejala AAMI MCI Demensia
Keluhan memori oleh :-Penderita-Keluarga
+-
-/++
-+
ADL abnormal-dasar-kompleks
--
-+
++
Perilaku abnormalMemori abnormal-tes skriningTes neuropsikologi
-
--
+/-
+/-+
+
++
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Risk factor dementia vasculer
1. Brain vasculer dissorder 2. Stroke 3. Hipertension 4. Diabetes melitus with dislipidemi 5. Increase LDL 6. Smoking 7. Non vasculer
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Faktor Risiko• Stroke iskemik pada usia >65 thn : 25-33%
demensia :
usia tua, tingkat pendidikan dan pendapatan yang rendah, merokok, tekanan darah yang rendah atau hipotensi ortostatik, stroke berulang dan stroke yang lebih luas, lesi di substansia alba yang lebih besar, stroke di hemisfer kiri, dan komplikasi stroke akut yang berupa hipoksia dan iskemia (kejang, aritmia jantung, pneumonia aspirasi, hipotensi) disfagia, masalah-masalah gait, dan gangguan buang air kecil; perokok; tekanan darah rendah, hipotensi ortostatik, WML dan atrofi kortikal.
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Pathofisiologi dementia vasculer
Vasculer degeneration : DM, Hipertension,stroke Neurotransmiter decreaseNeuronal degeneration : Ach, NA, 5 HT Pure degeneration ( Alzeimer ) Aquisital (alkohol,drug ) VaD
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Patofisiologi VaDIschemia
HipoperfusionHemorrhage
Heterogeneous brain lessions
Inflamatorymechanism
Alteration of O2metabolism
Reduction ofCerebral flow
VaD
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Iadecola,2003
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Delirium DemensiaAkut, awitan diketahuiBerhari-hari sd mingguanBiasanya reversibleDisorientasi pd awal Fluktuasi dari jam ke jamPerubahan fisiologis nyataTingkat kesadaran fluktuasiGangg siklus tidur jam ke jam
Gangg psikomotor pd awal
Awitan tak jelasPerlahan, bertahapBiasanya irreversibleDisorientasi pd fase lanjut Fluktuasi dr hari ke hariPerubahan fisiologis tak nyataKesadaran berkabut (fase akhir)Gangg siklus tidur siang ke malamGangg psikomotor pd fase lanjut
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Differentiation of VaD and ADNINDS-AIREN Criteria for VaD
NINCDS-ARDRA Criteria for AD
Onset Abrupt (Insidious)
Course Fluctuating, stepwise (progressive, stable)
Progressive, plateaux
Cerebrovascular Disease (CVD)
Clinical signs Absence
Computed Tomography (CT) and/or Magnetic Resonance Imaging (MRI)
Relevant CVD Absence of CVD
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Distinguishing Characteristics of Cortical and Subcortical Dementias
Function Cortical Dementia
Subcortical Dementia
Psychomotor speed Normal Slowed
Language Involved Spared
Memory:-Recall-Recognition-Remote
-impaired-impaired-temporal gradient present
-impaired-spared-temporal gradient absent
Executive function Less involved More involved
Depression Less common More common
Apathy Less common More common
Motor system Spared until late Involved early
Anatomy Cerebral cortex Subcortical structures and dorsolateral prefrontal cortex projecting to head of caudate nucleus
Examples Alzheimer’s disease Huntington’s disease, HIV encephalopathy, lacunar state
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Types of dementia
• Multi-infarct dementia• Pick’s disease• Frontal-lobe dementia• Lewy-body dementia
– Plaques and tangle plus Lewy bodies– Parkinson-like symptoms, hallucinations
• Parkinson’s disease• Subcortical dementia• Alcoholic, HIV, infection
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“Reversible Dementias”– More properly called “potentially reversible
cognitive impairments”– Candidates: Drug induced, depression, thyroid,
B12, NPH, subdural hematoma– Truly reversible <1-3%– Most patients go on to develop dementia– Depression: 4-7X increase risk of dementia– B12: 5-15% treatment responsive
Clarfield1994, Larson 1985, Patterson 1999, Freter 1998
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Multi-infarct (vascular) dementia
• The second most common cause of dementia
• Arises from many small infarcts (strokes)• Patients seem particularly impaired at
motor tasks
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Pick’s disease
• Shrinking of the tissues of the brain and presence of abnormal bodies (Pick's bodies) in nerve cells
• Affects 1 out of 100,000 people• More common in women than men• May occur as early as 20 years old, but usually begins
between ages 40 to 60 (average 54)• Onset more slow, insidious, earlier than AD
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DEMENSIAdiagnosis etiologi
Tak diketahui :• Alzheimer’s diseaseNeurodegeneratif :• Pick’s disease• Parkinson’s disease• Khorea Huntington• Demensia Lewy Bodies
Infeksi :• Kompleks demensia AIDSTrauma : trauma kepalaMetabolik :• Hipoglikemia lama• Hipotiroidisme • Paratiroidisme
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Kriteria Dx Demensia Lewy Bodies(DLB) (Lovestone&Gauthier, 2001
Pasien mengalami penurunan kognisi yg jelas yg mengganggu f.sosial&okupasi
• Fluktuasi kognisi jelas• Halusinasi visual berulang• Gambaran motorik seperti parkinsonSatu gejala: Possible DLB Dua Gejala:Probable DLB
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Gamb.Klinis Demensia L.Fronto Temporal (Lovestone&Gauthier,2001)
• Awitan perlahan, tidak jelas, progresivitas lambat• Ggn kepribadian yg berat pd fase dini,euforia, emosi
tumpul,disinhibisi,apatis atau gelisah• Penurunan fungsi mental• Gangguan berbicara• Pem. terdapat refleks primitif, inkontinensia,
akinesia, rigiditas• Atrofi lobus frontotemporal yg jelas
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CLOCK DRAWING TEST
•
Patients are asked to draw a clock with all the numbers, and make the hands point to certain time, eg, 20 minutes before 2 o'clock. The clocks shown above are considered poor (0), fair (1), good (2), and excellent (3). Source: Reprinted with permission from Strub RL, Black FW. The Mental Status Examination in Neurology. 3rd ed. Philadelphia, PA: FA Davis; 1993.
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LABORATORY TESTS (routine)(less history usually found in NH setting)
• BLOOD TESTS– electrolytes, liver, kidney function tests, glucose– thyroid function tests (T3, T4, FTI, TSH)– vitamin B12, folate– complete blood count,
• EKG• CHEST X-RAY• URINALYSIS• ANATOMICAL BRAIN SCAN – CT / MRI
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Neuro Imaging
• Head CT Scan Lesi periventrikuler & sub alba luas:patchi/difus simetris
dg densitas mengah ant subs alba & likuor dlm ventrikel dg pinggir yg tdk tegas yg meluas ke centrum semiovale dan paling sdkt satu infark lakuner, disertai
hal: tdk ditemukan infark diteritori non lakuner di kortikal, kortiko-subkortikal dan infark watershed,
perdarahan yg menunjukkan pykt vasa besar, tanda hidrosephalunormal pressure & psb spesifik subs alba
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Computed tomography of the brain of patient with multi-infarct dementia showing multiple cortical infarct
Multiple cortical infarcts are commonly the result of thromboembolic disease--for example, from a cardiac or carotid source--but can also be caused by cerebral vasculitis.
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Terapi dg pemahaman patofisiologi demensia
I. Penghilangan simtom primer
A.Modulasi neurotransmiter neuropetid (takrin terbukti)
II. Progresifitas diperlambat / menunda awitan penyakit
B. Peningkatan metabolisme neuronal dg agen nootropik (ko-dergocrin mesilat)
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TerapiI. Penghilangan
simtom primer (memori melemah)Simtom sekunder (depresi, agitasi)
Tanpa mempengaruhi proses dsr neurodegnratif
A. Modulasi neurotransmiter & neuropetid: B. Peningkatan metabolisme
neuronal dg agen nootropik Asetilkolin
Monoamin
Indolamin
As. Amino eksitatori
Somatostatin
Neuropeptid lain
ko-dergocrin mesilat serebrolisin
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TerapiII. memperlambat progresivitas
menunda awitan penyakitObat anti
inflamasiPenyekatsaluran Ca
Penyekat radikal bebas
Faktor neurotropikestrogen
Apolipoprotein E
Protein tau
Protein prekursor amiloid & beta amiloid cara:
modulasi/
target
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Golongan NootropikGolongan Nootropik
• Sebagai penguat metabolik sel otak• Meningkatkan fungsi learning & memori• Bila digabung dgn stimulasi kognitif hasilnya
lebih baik.• Banyak dipasaran (nootropil, neurotam dsb)
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Terapi Simptomatik : Nootropic
Piracetam : Perbaikan memori pada non Demensia efek positif pada test atensi & memori. Piracetam dan training memori efektif perbaikan kognitif
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Neuroprotektif lainNeuroprotektif lain
• Ginggobiloba ;– Banyak dipublikasikan tetapi masih kontroversial
hasilnya.• Estrogen ;
– Dapat memperbaiki performance penderita Alzheimer
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Anti - oksidanAnti - oksidan
• Anti radikal bebas di otak• Dapat menghambat deteriorisasi penyakit• Tidak memberi efek pada kognitif• Vitamin E, C, selegiline
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NSAIDNSAID
• Pada otak DA dapat dijumpai proses peradangan
• Deposit B amiloid peptide ada hubungannya dgn proses peradangan kronis
• Dasar dari penggunaan NSAID
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Terapi Non Farmakologis
• Psikososial (Komunikasi, Informasi, dan Edukasi)• Program terapi
- Pelatihan memori- Rekreasi terapi
* Terapi Reminens * Orientasi nyata* Stimulasi kognitif
- Latihan fisik (GLO)
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