Introduction to Memory Introduction to Psychiatry�History Taking & MSE

Introduction to Memory

1. Memory Dr. Mostafa Mahmoud Alsabban Lecturer of Psychiatry Al Azhar University- Damietta

2. NEUROBIOLOGY OF MEMORY---AN UPDATE

3. INTRODUCTION Without memory, life would perpetually be spent in ‘here and now’. Memory provides the essential substrate for cognitive activities that define experience; development of personality and the possibility of growth and change

4. Disorders of memory and complaints about memory are common in association with neurological, psychiatric illness (anxieties, phobia, and maladaptive behaviors) and medical treatments. Definition of Memory: The process by which, what is experienced or learned is established as a record in the CNS, where it persists with a variable degree of permanence, and can be recalled or recollected from storage at will. (CTP)

5. PROCESSES INVOLVED IN MEMORY FUNCTION Encoding: The process of receiving sensory input and transforming it into a form of code, which can be stored in the brain ( registration) . Storage: The process of putting coded information to a stable record ( retention) . Information persists with a variable degree of permanence Retrieval: The process of gaining access to stored coded information when it is needed ( recall).

6. TYPES OF MEMORY Temporal : Short-term memory (STM) and Long-term memory (LTM). Form : Visual memory, verbal memory, nonverbal memory Process : Explicit vs implicit ( Tulving, Schacter and Stark, 1982) Declarative vs Non- declarative ( Cohen and Squire, 1980) Declarative Non-declarative Facts (semantic) Skills and habits Events(episodic) Priming Classical conditioning Non-associative conditioning

7. MODELS OF MEMORY Information Processing model (Atkinson and Shiffrin 1968) Levels of processing model (Craig and Lockhart 1972, Craig and Tulving 1975) Working memory model (Baddley and Hitch 1974)

8. Working memory model Central Executive Phonological loop Visuo-spatial scratch pad LTM

9. MEMORY STUDIES History Beginning of the 19 th century, Karl Lashley: entire cortex involved in all functions 1850-1909 : Herman Ebbinghaus, German psychologist, 1 st to study memory by experimental techniques, distinguished between STM and LTM 1882 : Theodore Ribot, observed memory impairment in brain-injured person Ribot’s law: amnesia affects the memories in reverse order of their development

10. 1875: S.S Korsakoff, Russian Neuropsychologist, studied long-term complication of chronic alcohol syndrome as prominent memory impairment (intact recent memory), loss of confusion, disorientation, irritability, polyneuropathy (“psychosis polyneurotica”) 1881: Carl Wernicke gave features of Wernicke’s syndrome as ataxia, vision disturbances and global confusion with an acute presentation. 1930: Wernicke’s syndrome and Korsakoff psychosis explained with a common mechanism (thiamine deficiency) due to a variety of causes (malabsorption syndrome, gastric carcinoma and toxemia of pregnancy)

11. 1950: Scoville and Milner described a patient HM with intractable seizures - surgical extirpation of MTL produced amnesia. Landmark study demonstrating role of MTL (particularly Hippocampus) in memory. Latter half of 20 th century: Study of disorders of memory in surgical patients prompted a vast range of pathological,, neuropsychological and neuroimaging studies in humans and animals.

12. Techniques Memory impairment disproportion to other cognitive functions noted in fully alert, conscious and responsive patients with different local brain illness or systemic illness affecting brain. This led to the study of different brain regions/anatomical lesions in animals and humans. In animal studies, the effects of carefully placed chemical or structural anatomical lesions on memory, amnesia was inferred from analogous nonlinguistic tasks; animals used were monkey, rat, and aplysia,

13. Various neuropsychological tests were applied to identify the severity and type of memory impairment. Finally, functional neuroimaging (NI) studies like PET / fMRI have become increasingly popular in last 10 years. In PET the neurotransmitters and their receptors can be studied. Although, the brain regions involved in performing a cognitive operation are identified,NI cannot tell what is unique about those regions. Also, when brain regions are simultaneously activated, NI can not detail their functional connectivity.

14. The baseline condition should be controlled to ensure that the finding is as specific as possible (e.g. particularly at MTL, activation during rest is higher than activation during controlled tasks). NI does not directly measure the neuronal activity; rather it relies on changes in rCBF resulting from metabolic demands of neuronal activity. Carrying out a memory task while bound in a machine can be constraining.

15. Human/Animal observations Infarctions: Posterior cerebral artery disease (hippocampus, limbic nucleus of thalamus, and mesial temporal lobe) result in amnesia. Thalamic strokes can present with dense retrograde amnesia Intracranial tumours: Hypothalamus and third ventricle tumours (e.g meningioma) cause dense anterograde amnesia. Infections: Herpes simplex infection involving hemorrhagic necrosis of temporal lobes produce profound amnesia.

16. Anoxia or Hypoxia: Exposure to neurotoxins (such as trimethyltin or carbon monoxide, inadequate oxygenation through respiratory, circulatory and hematological or metabolic compromise) leads to bilateral damage of hippocampus particularly CA1 regions results in chronic amnesia and and necrosis of hippocampus.

17. Alcohol and licit drugs: Classic alcoholic blackout—Inability to encode new memories during intoxication and inability to retrieve memories encoded proximate to the blackout. Cocaine and heroin are not associated with amnesia. Medications: Benzodiazepines and Barbiturates (IV), propofol and sildenafil, cause twilight or semiconscious states. Vitamin deficiencies: Particularly thiamine deficiency results in memory impairment.

18. ECT: Diminished ability to form new memories during/immediately following the period of treatment. Korsakoff’s syndrome (KS): Marked anterograde amnesia, some retrograde amnesia, confabulation, and poor insight. Neuropathology: neuronal loss, micro-hemorrhages, gliosis in paraventricular and periacqueductal grey matter. (Victor et al 1971) Sub-cortical dementias and basal ganglia lesions show impaired habit learning (Parkinson’s and Huntington’s disease) (Heindel et al 1998)

19. Semantic dementia is a variant of fronto-temporal dementia and Herpes encephalitis patients have profound loss of semantic knowledge, loss of meaning encompassing verbal and non-verbal material resulting in severe impairments in naming and word comprehension, perceptual and reasoning abilities. Episodic memory is relatively preserved. (Patterson and Hodges 1995) All these clinical observations lead to the idea of surgical manipulation of different brain regions