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Management of Common Neuropsychiatri c Problems

Management of Common Neuropsychiatri c Problems. ศ.นพ.สุชาติ พหลภาคย์ ภาควิชาจิตเวชศาสตร์ รศ . นพ . สมศักดิ์ เทียมเก่า ภาควิชาอายุรศาสตร์ อ . นพ . สุรินทร์ แซ่ตัง รพ . ขอนแก่น. Management of Common Neuropsychiatri c Problems. Mild cognitive impairment

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Management of Common Neuropsychiatri c Problems

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  1. Management of Common Neuropsychiatric Problems ศ.นพ.สุชาติ พหลภาคย์ภาควิชาจิตเวชศาสตร์ รศ.นพ.สมศักดิ์ เทียมเก่า ภาควิชาอายุรศาสตร์ อ.นพ. สุรินทร์ แซ่ตัง รพ. ขอนแก่น

  2. Management of Common Neuropsychiatric Problems Mild cognitive impairment Medication-induced movement disorder ศ.นพ.สุชาติ พหลภาคย์ ภาควิชาจิตเวชศาสตร์ คณะแพทยศาสตร์ มหาวิทยาลัยขอนแก่น

  3. Management of Common Neuropsychiatric Problems รศ.นพ.สมศักดิ์ เทียมเก่า ภาควิชาอายุรศาสตร์ Headache

  4. Management of Common Neuropsychiatric Problems ศ.นพ.สุชาติ พหลภาคย์ภาควิชาจิตเวชศาสตร์ รศ.นพ.สมศักดิ์ เทียมเก่า ภาควิชาอายุรศาสตร์ อ.นพ. สุรินทร์ แซ่ตัง รพ. ขอนแก่น Case discussion

  5. Management of Common Neuropsychiatric Problems Mild cognitive impairment Medication-induced movement disorder ศ.นพ.สุชาติ พหลภาคย์ ภาควิชาจิตเวชศาสตร์ คณะแพทยศาสตร์ มหาวิทยาลัยขอนแก่น

  6. Neuropsychiatry สาขาหนึ่งของการแพทย์ เป็นการเรียนรู้เกี่ยวกับโรคที่มีอาการทั้งทางจิต cognition และประสาทวิทยา

  7. Mx of common neuropsychiatric problems 1. Mild cognitive impairment 2. Medication - induced movement disorders

  8. Mild Cognitive Impairment (MCI) defn • Remains a research construct • Memory loss in the transitional zone between normal aging memory loss and very early Alzheimer’s disease = Dementia prodrome, incipient dementia, isolated memory impairment, cognitive impairment no dementia. = Pathological, not a manifestation of aging

  9. MCI its construct MCI has been proposed to identify the individual at an earlier point in the cognitive decline such that if therapeutic interventions become available, clinician can intervene at this juncture

  10. MCI types 1. a-MCI => memory impairment (amnesia) 2. md MCI=>multiple domain MCI=> language, executive function and visuospatial skills 2.1 md -MCI+a 2.2 md -MCI-a 3. Single nonmemory domain MCI

  11. a-MCI : Diagnosis criteria 1. Memory complaint usually corroborated by an informant 2. Objective memory impairment for age (test = -1.5 SD) 3. Essentially preserved general cognitive function 4. Largely intact functional activities 5. Not demented

  12. MCI :- objective memory test :- • Word list learning • Paragraph recall • No generally accepted instrument for this determination • Neuropsychological testing may be useful

  13. Table 1. The Short Test of Mental Status Maximum Subtests Testing score Orientation Name; address; current location 8 (building); city; state; date (day); month; year Attention Digit span (present at 1 per second;) 7 record longest correct span) 2-9-6-8-3 5-7-1-9-4-6 2-1-5-9-3-6-2 Learning and Learn our unrelated words:apple, 4 immediate recall Mr Johnson, charity, tunnel. Record the number of trials for acquisition (maximum of 4 trials) Calculation 5 * 13 = 4 65-7 = 58/2 = 29 + 11 = Abstraction/ Similarities: orange/banana, 3 similarities dog/horse, table/bookcase. Information President; first president; number of 4 weeks per year; define an island Construction Copy the Necker cube. Draw a clock 4 face showing 11:10. Recall The 4 words apple, Mr Johnson, 4 charity, tunnel. Total Score* 38 * Total score = sum of the subtest scores - (number of trials for acquisition -1). For example, if a patient learned all 4 words no the first trial nothing is subtracted from the sum of the subtest scores. If a patient required 4 trials to learn the 4 words, then 3 was subtracted from the sum of the subtest score.

  14. MCI : Biological abnormalities 1. Over - representation of the apolipoprotein E4 allele 2. Volumetric loss in entorhinal cortex and hippocampus measured by MRI neuronal counts in postmortem 3. Increased brain markers of oxidative stress 4. Abnormalities of the cholinergic system 5. Depression or medical co-morbidity So-MCI is heterogeneous and not all MCI will progress to AD

  15. MCI : treatment - No FDA approved medicine But if Dr is convinced that the attending MCI is an incipient AD, then he may wish to Rx with cholinesterase inhibitor or memantine

  16. MCI : treatment Donepesil risk of developing A.D. during the first year but by the end of 3 year the risk was the same as these taking Vit E or placebo Galantamine (Reminyl) = no improvement

  17. Currently available treatment 1. Acetylcholinesterase inhibitors = 1st choice donepezil , rivastigmine ,galantamine some research said donepezil lowered the risk of developing AD only during the first year 2. Putative treatments 2.1 antiglutamatergic drugs = memantine 2.2 nootropics = piracetam 2.3 antioxidants :- ginko biloba, VitA, C, E, selegiline, MAOI, 3. Anti-inflammatory drugs 3.1 aspirin 3.2 NSAID

  18. Currently available treatment 4. ERT 5. Visionary interventions 5.1 targeting neuropatholgical substrates 5.2 regulation of neuronal plasticity 6. Treating co-morbidity, controlling risk factors 7. Psychosocial intervention

  19. MCI Rx of the co-morbidity Vascular risk factors :- high BP High serum cholesterol High midlife diastolic BP White matter hyperintensity Presence of apolipoprotein E4 genotype Low serum B12 and folate

  20. Psychosocial intervention emotional and mental stimulation 1. Extensive social network 2. Participating cognitively stimulating activities

  21. MCI : Rx with AChE • Autopsy-based study reported similar reductions in basal forebrain immunoreactive neurons = selective loss of cholinergic neurons in MCI and AD => cholinergiic differentiation of the cerebral cortex • Long term effects will be via modification of APP metabolism • However a study observered specific upregulation of choline acetyltransferase in MCI subjects = compensatory process in preclinical phase and suggest limitation of AChE inhibitor efficacy at this stage

  22. MCI : Rx with antiglutamatergic drugs • Overactivity of excitatory amino acid glutamate neurotoxcity • NMDA- mediated excitotoxicity tau phosphorylation NT = one of the major pathological substrates of AD • Memantine = NMDA - receptor antagonist

  23. MCI : Rx with nootropics • Piracetam • Enhance memory function • Nonspecific action :- energy metabolism, cholinergic mechanism, excitatory amino acid receptor - mediated function and steroid sensitivity

  24. MCI : Rx antioxidants • Large amounts of unsaturated lipids and catecholamines in the brain , β - protein precursor, Aβ, presenilins and APOE are link to reactive oxygen species (ROS) production apotosis • Oxidative stress atherogenesis • Higher ascorbic acid and β- carotene plasma level better memory • Ginko biloba, VitA, C, E = free radical scarvenger, MAOI = reduce free radical formation

  25. MCI : Rx with anti inflammatory drugs • Inflammatory process are involved in the pathogenesis of AD • AD pt has upregulation of cytokines, acute phase proteins, activation of the complement regulatory proteins, accumulation of activated microglia • Reduced prevalence of AD in pt with arthritis • Rx with aspirin, NSAID, COX-2 inhibitors

  26. MCI : Rx with ERT • Estrogen acts via ERα และ ERβ activate nerve growth factors, synaptogenesis, modulate function of ACh, 5-HT, DA, NA, and cerebral blood flow • Estrogen has intrinsic antioxidant activity, neuroprotective effect by promoting nonamyloidgenic β- secretase processing of APP

  27. Targeting neuropathological substrates 1. Reduction of Aβproduction 2. Inhibitors of Aβaggregation However APP transgenic animals develop behavioral abnormality before extensive amyloid deposition occurs 3. Neurofibrillary changes better correlate with disease severity than amyloidosis 4. Intervention in tau hyperphosphorylation

  28. Regulation of neuronal plasticity 1. Nerve growth factor (NGF) =neurotropic factor for the basal forebrain cholinergic neuron

  29. Medication - induced movement disorders 1. All first generation antipsychotics : Chlorpromazine Thioridazine Perphenazine Haloperidol 2. Some second generation anti-psychotics ; usually dose related

  30. Medication - induced movement disorders 3. Nonantipsychotic psychotripics Lithium Anticonvulsants Antidepressants 4. Nonpsychotropics Prochlorperazine Metoclopramide

  31. Neuroleptic - induced movement disorders 1. Acute dystonia 2. Akathisia 3. Parkinsonian - like 4. Tardive dyskinesia

  32. Neuroleptic - induced acute dystonia : Pathophysiology = not known, may be acute saturation of D2 receptors

  33. Neuroleptic induced acute dystonia • Early - onset during the course of treatment with neuroleptic • M > F, age < 30 years > • Receive high potency anti-psychotic medication

  34. Neuroleptic induced acute dystonia :Dx A. 1 (or more) of the following signs or symptoms has developed in association with the use of neuroleptic medication 1. Abn positioning of the head and neck in relation to body (retrocollis, tortiollis) 2. Spasms of the jaw muscles (trismus, gaping, grimacing )

  35. Neuroleptic induced acute dystonia :Dx 3. Impaired & wallowing (dyspepsia) speaking or breathing 4. Thickened or slurred speech due to hypertonic or enlarged tongue 5. Eye deviated up, down, or sideward (oculogyric crisis )

  36. Neuroleptic induced acute dystonia :Dx 6. Tongue protrusion or tongue dysfunction 7. Abn positioning of the distal limb or trunk

  37. Neuroleptic induced acute dystonia :Dx B. A developed within 7 days of starting or rapidly raising the dose of neurolepticmedication or of reducing a medication to or prevent acute EPS

  38. Treatment : 1. Anticholinergic or antihistaminergic drugs 2. If fails to respond to 3 doses of these drug with in 2 hrs, then consider other causes for the dystonia 3. After resolution of the acute episode, give oral anticholinergic agents

  39. Neuroleptic - induced acute akathisia : Pathophysiology = DA neurons in the ventral tegmental area

  40. Neuroleptic - induced tardive dyskinesia : Pathophysiology 1. Sustained D2 receptor blockade receptor hypersensitivity 2. Blockade of presynaptic DA receptors glutamatergic transmission oxidative stress cell death

  41. Neuroleptic - induced acute akathisia • Risk = middle aged women • Occurs at some point in the course of medication (antipsychotics, antidepressants and sympathomimetics)

  42. Neuroleptic - induced acute akathisia : Dx A. subjective complaints of restlessness after exposure to a neuroleptic medication B. At least one-of the following 1. fidgety movement or swinging of the legs 2. rocking from foot to foot while standing 3. pacing to relieve restlessness 4. inability to sit or stand still for at least several minutes

  43. Neuroleptic - induced acute akathisia : Dx C. onset of A and B occurs within 4 weeks of initiating or increasing the dose of neuroleptic , or of reducing medication used to Rx or prevent acute EPS

  44. Neuroleptic - induced acute akathisia : Rx 1. Reduce neuroleptic medication dosage 2. Attempt to treat with B - adrenergic receptor antagonists, anticholinergic drugs, cyproheptadine 3. Considering changing the neueroleptics

  45. Neuroleptic induced parkinsonism :Pathophysiology = DA activity, this can be induced by 1. Depletion of DA in presynaptic stores (reserpine) 2. DA receptor blocking = antipsychotic and atypical calcium blocking agent (cinnarizine)

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