Gangguan Psikiatri
pada orang berusia
lanjut
DR. Dr. Martina WS Nasrun, SpkJ (K) Divisi Psikiatri Geriatrik Dep Psikiatri FKUI / RSCMMasalah usila Indonesia
8,5 % jumlah penduduk 19 juta (2000 – 2005) Urutan ke 4 di dunia Sistim pelayanan usia lanjut? Jaminan kesehatan, akses kesehatan? Kesadaran masyarakat masih kurangMasalah Usia lanjut:
1. Kesehatan (fisik & mental) 2. Sosial 3. Ekonomi 4. Psikologis 5. Spiritualitas / religiusitas 6. Hak azasi (human right)Kesehatan
Multipatologi 80 % usila: 1 penyakit PHBS (life style) Asuransi kesehatan Successful aging Quality of lifeKesepian (loneliness)
Pensiun Anak sibuk Tak punya aktivitas Pasangan meninggal Terisolasi sosial Tak ada teman bicaraSosial
Peran sosial usia lanjut (masyarakat dan keluarga) Pergeseran peran (IRT, KK pasif) Kesepian, frustasi, depresi Post power syndrome Gangguan adaptasiEkonomi
Penghasilan menurun Masa persiapan pensiun, no pensiun Tingkatkan aktivitas, kreativitas Kembangkan hobi, ciptakan hobi Independensi keuangan?Psikologis
Kepribadian masa dewasa muda Coping mechanism, problem solving Kegagalan beradaptasi potensial gangguan jiwa dan fisik lainnya Integrity vs isolation Dignity in old age Arti hidup / cara pandang kehidupanSpiritualisme / religiusitas
Penghayatan keimanan Sikap hidup / persepsi diri Minat keagamaan meningkat Fungsi kognitif maningkat saat puasa Penelitian Larson: Non religius: kurang tabah, kurang kuat mengatasi stres, kurang tenang, takut mati dsb dibandingkan yang usia lanjut yang “religius”Hak azasi usia lanjut
Hindari abuse dan neglect (mental, emosional & fisik) Hak untuk mengatur diri sendiri Hak & kewajiban dalam masyarakat Hak berobat dan bertempat tinggal Mendapat perlakuan yang pantas Human right of people with dementia (Kyoto, 17 Oct 2004, ADI conference)Gangguan Psikiatri
pada
usia lanjut
Case finding: temuan kasus dini Intervensi segera Cegah disabilitas Optimalkan fungsi Identifikasi faktor risiko Kendalikan penyakitGangguan Psikiatri
pada usia lanjut:
Gangguan Depresi Gangguan Cemas Demensia (‘pikun’) Insomnia (gangguan tidur) Delirium (kebingungan akut)GANGGUAN DEPRESI
Tertekan, sedih, menetap dan tidak dapat berfungsi seharihari Penyebab: berbagai ‘kehilangan’ Sikap anggota keluarga Peka terhadap tandatanda dini Gejala depresi pada usia lanjut tidak khas, gejala somatik menonjol !4 Tanda pengenal
gangguan depresi:
Ada perasaan kosong / hampa
Pesimis, kuatir masa depan
Tak ada kepuasan hidup
Merasa hidupnya tidak bahagia
Gangguan Cemas
Gejala fisik muncul dahulu Cemas & kuatir berlebih Ketegangan fisik dan mental Gejala otonom (keringat, debardebar, sakit perut, pusing dll) Berlangsung kronis, hilang timbul PTSD: pada usila lebih beratDemensia
Kemunduran mental progresif Defisit berbagai fungsi kognitif Sindrom ABC (Activity, Behavior, Cognitive) Penyebab: AD, Stroke, Parkinson, dll Tanda – tanda dini demensia BPSD (behavior & psychological symptoms of dementia)
AD prognosis
Optimal case
en tal S tat e Exami nati on sc or e 25 | Symptoms 20 || Diagnosis 15 || Loss of functional independence 10 || Behavioral problems 5 ||Nursing home placement
Demensia: kumpulan gejalagejala
dis eksekutif
Aktivitas seharihari (ADL & IADL)
Amnesia Aphasia Agnosia Apraxia
Aspek neuropsikologis (kognitif) Gejala Psikiatrik / Psikologis Gangguan Perilaku Gejala neuropsikiatrik (nonkognitif: BPSD)
What is Dementia?
A: activity decline B: behavior disturbances C: cognitive impairment Sebab: gangguan fungsi otak! > kemunduran mental (De Ment)Activity decline
Instrumental ADL: Berkendaraan Bepergian sendiri Berbelanja Memasak Menggunakan telepon Mengelola keuangan Basic ADL: Makan Mandi Naik turun tangga Buang air besar / kecil BerpakaianBehavior disturbances
Apatis Pencuriga Mudah tersinggung Mudah marah Hiperaktif Insomnia Murung / sedihCognitive impairment:
Kelemahan memori (mudah lupa) Kesulitan berbahasa (afasia) Kesulitan mengeksekusi (rencana, kegiatan) Pengenalan benda, wajah, bentuk, ruang dll Kemerosotan daya nilai, abstraksi, judgment, dan fungsifungsi otak lainnyaHypothesized natural course of
sporadic Alzheimer’s disease (AD)
Asymptomatic Preclinical Clinical phase phase phase Onset of MCI* Clinical diagnosis of AD 0 25 50 75 100 % of end st age AD
MCI is a real entity and part of a continuum Normal – MCI Dementia An inbetween, transitional diagnosis A prodromal of dementia ! A good label for patients who are not normal, and clearly not yet demented
What is MCI?
MCI is also described as Age Associated Memory Impairment (AAMI) Age Related Cognitive Decline (ARCD) Questionable Dementia Mild Cognitive Disorder
MCI is a transitional phase
between aging and dementia
Mild (not demented; mild enough so that psychometric testing is needed to detect) Cognitive (more than memory other cognitive processes) Impairment (disease = real decline) MCI is not equivalent to Age Associated Cognitive Decline (which is considered “normal” when aging) but MCI is malignant in its evolution towards dementia
Definition of MCI
Mild cognitive impairment
Various definitions main features Subjective memory complaint by self or informant Objective findings: memory performance within 1 or 1–1.5 or 2 SD below age and education norms Normal global cognitive function And / or clinical dementia rating (CDR) 0.5 And / or global dementia scale (GDS) 3 Or MMSE below age and education cutoff norms Common denominator Normal activities of daily living (ADL), no dementiaEvolution of the Mayo Clinic criteria
for MCI
A Amnestic MCI AD B Multiple domains slightly impaired AD, normal aging? C Single nonmemory domain FTD PPA DLBDNormative Aging Dementia Stable ageappropriate memory impairment Reversible cognitive impairment (ie confusion) Incipient dementia • prodromal AD • prodromal VaD • prodromal mixed Dementia MCI Normative aging
Towards a broader concept of MCI
Considering heterogeneity of MCIH+ H+ Pyruvate Fatty acids Pyruvate Fatty acids Acetyl CoA e 2 H2O O2 O2 NADH H+ ADP + Pi ATP Citric acid cycle CO2 CO2 Matrix Inner membrane Inner membrane area Outer membrane ATPSynthase Complexes of the respiratory IV III I ++ ATP Membrane potential Ψ m Organisation and function of mitochondria
mtDNA mutations Genetic defects Respiratory chain Hypoxia Direct damage of respiratory chain + ++ +
Q
.O
2.ATP
↓ Xenobiotics Xray Aging Damaged respiratory chain Reduced mitochondrial membrane potential Causes of mitochondrial damageDOMINANTLY INHERITED
FORMS OF AD NONDOMINANT FORMS OF AD(Including "Sporadic" AD)
Missense mutations in the APP or
Presenilin 1 or 2 genes Failure of Aß clearance mechanisms(e.g., inheritance of APOE4, faulty Aßdegradation, etc.) Increased Aß42 production throughout life Gradually rising Aß levels with age Subtle effects of Aß42 oligomers on synaptic efficacy Gradual deposition of Aß42 oligomers as diffuse plaques Widespread neuronal/synaptic dysfunction and selective neuronal loss, with attendant neurotransmitter deficits Accumulation and oligomerization of Aß42 in limbic and association cortices
Aggressive resistance Physical aggression Verbal aggression ‘Aggression’ Hallucinations Delusions Misidentifications ‘Psychosis’ Withdrawn Lack of interest Amotivation ‘Apathy’