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Memory and treatment of cognitive impairments

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Presentation on theme: "Memory and treatment of cognitive impairments"— Presentation transcript:

1 Memory and treatment of cognitive impairments
MUDr. Tomáš Kašpárek Dep. of Psychiatry Masaryk University, Brno

2 Contents Introduction Physiology and classification Memory assessment
Disturbances in memory Treatment of cognitive impairment

3 Introduction Definition: ability to register, store, and recall information (three stages of memory) Memory: part of cognitive functions (involved in information processing; such as perception, thinking, attention) Dimensions of behavior cognition (reasoning) and emotionality

4 Stages of memory I: Registration
capacity to add new material (sensory, conceptual, perceptual) to memory new information need to be properly processed (percepted) – disturbing factors consciousness attention emotions repetition

5 „Life cycle“ of a memory trace
Immediate memory information stored for 15-20s Short-term memory consolidation of the memory trace – several minutes to 2 days medial temporal structures Long-term memory formed trace large cortical areas

6 Stages of memory II: Retention
ability to hold memories in a storage large # of neurons (changes in connectivity) involved in the storage of specific memory sensory specific fractions of complex perceptions in corresponding cortical areas

7 Stages of memory III: Recall
ability to return stored information active reconstructions adding together fractions of the exact recollection in a specific situation (=influence) – possibility of the failure to represent of past events properly awareness of the recollection, sureness, proper addressing of time and situation of recollection acquirement

8 Types of memory: Memory modules (Willingham 1997)
Explicit (declarative) memory – medial temporal cortex Procedural memory – sensory-motor functional systems Working memory – prefrontal cortex Classical conditioning – cerebellum; relation between motor function and perception Emotional conditioning – amygdala; relation between perception and emotion Priming - parietal, temporal and frontal cortex

9 Memory assessment Immediate recall Short-term memory Long-term memory
series of numbers (most adult recall 6 # forward and 3 in reverse) Short-term memory names of 3 inrelated objects after 5 min Long-term memory personal history (independent confirmation), general information (names of presidents...) Scales – MiniMental State Examination Specific tests – Wechsler Memory Scale III

10 Disturbances in memory

11 General notes memory = set of functions based on different neuronal processes = various dysfunctions according to the pathological process

12 Disturbances in registration
pathological process disturbed vigilance, attention head trauma, seizures, delirium, intoxication (BZD, sedatives), psychosis, depression, anxiety disturbed structures involved in memory consolidation hippocampus, mammillary bodies, fornix – i.e. mediotemporal structures short-term memory dysfunction, immediate recall may be spared

13 Disturbances in retention
pathological process impairment of large cortical areas posttraumatic amnesia cognitive disorders

14 Disturbances in recall
may reflect damaged storage may occur separately failure to recall with later proper recollection personality, situation attention, fatigue...

15 „Quantitative“ dysfunctions
Amnesia: short/long-term memory impairment in a state of normal consciousness anterograde: failure to form new information head trauma, state of CNS dysbalance, drug effect retrograde: failure to recall old information head trauma dissociative amnesia: patchy or selective Hypermnesia: unusually vivid memory mania, posttraumatic stress disorder (intrusive memories), obsessive or paranoid personality traits

16 „Qualitative“ dysfunctions
paramnesias – retrospective falsification of memories during its recollection (awareness of recalled memory, failure to proper class time and situation of memory acquirement) confabulation – filling memory gaps with inaccurate information; frontal lobe and self-monitoring? deja vu – sensation of previously experienced situation when experiencing the first time false awareness of memory common in normality, increased in fatigue, intoxication, complex partial seizures

17 Treatment of cognitive impairment

18 General notes no specific way to treat memory deficit
treatment modalities focused on the whole spectrum of impairments in cognitive disorders the most data available for Alzheimer's disease

19 Psychopharmacotherapy
Reinforcement of cholinergic mechanism Cholinesterase inhibitors (ChEIs) Prevention of excitotoxicity Memantine - NMDA antagonists

20 Cholinesterase inhibitors I
cholinesterases: acetylcholinesterase (AChE), butyrylcholinexterase (BChe)– hydrolysis of acetylcholin, thus decrease its amount in synapses molecular forms of AChe G4 (tetramer) – presynaptic membrane – both hydrolysis and feedback inhibition; decrease in AD and aging G1 (monomer) – postsynaptic membrane; no significant decrease

21 Cholinesterase inhibitors II
donepezil long-acting, selective, reversible AChEI metabolized by the liver microsome syst. rivastigmin pseudo-irreversible, both AChEI (G1) and BChEI no liver microsome metabolism galantamin reversibilie, competitive (increases AC only in areas with low AC concentration – lower central cholinergic side effects than noncompetitive inhibitors) AChEI + allosteric modulation of nACR

22 Cholinesterase inhibitors III – adverse effects
significant cholinergic side effects in 15% of patients receiving higher doses most common: GIT: nausea, vomiting, diarrhea, anorexia, weight loss CNS: headache, dizziness, insomnia, drowsiness, fatigue, agitation CVS: bradycardia, syncope generally mild in severity, short-lived, related to titration (slowly!) caution in patients with asthma, CHOPD, cardiac conduction defects/clinically significant bradycardia

23 Memantine I - Rationale
excessive glutamate release in Alzheimer's disease (as well as vascular dementia - ischemic damage) excitotoxic degradation of neurons progression of cognitive decline, severity of other symptoms neuronal degradation is linked with amyloid accumulation

24 Memantine II – Mechanism of action
non-competitive NMDA antagonist voltage dependent, fast receptor kinetics – enable physiologic function (LTP, memory) decreased activity of glutamate system hippocampus, neocortex decreased excitotoxicity - neuronal damage – amyloid accumulation i.e. slow down progression of the disease 5HT3 blockade facilitation of LTP antiemetic effect and regulation of GIT motility (combination with ACEI)

25 Memantine III – Clinical efficacy
slower progression of vascular and Alzheimer dementia fast onset of action – 2 weeks improvement of cognitive functions, vigility, daily activities reduction of the need for the help of caregivers efficacy even in the moderate to severe disease stages x ACEI

26 Memantine IV Adverse events Pharmacokinetics generally well tolerated
higher than placebo: insomnia, dizziness, headache, hallucinations (NMDA antagonist – PCP) Pharmacokinetics renal excretion no extensive metabolization no cytochrome P 450 inhibition dosage 20 mg pro die in 2 doses start: 5 mg, titration: 5 mg per week

27 References : Waldinger R.J.: Psychiatry for medical students, Washington, DC : American Psychiatric Press, 1997 Kaplan HI, Sadock BJ, Grebb JA.: Kaplan and Sadock´s synopsis of psychiatry, Baltimore: Williams and Wilkins, 1997

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