2 memory circuits ppt 18 th august (1).pptx

used this for a seminar in college

1. Anatomical substrates and circuits in memory function

2. Index Definition of memory Types of memory system Major neuroanatomical substrates Memory circuits Clinical syndromes Evaluation & management

3. Introduction - What is Memory?

4. Types of memory

5. Types of Memory Short-term memory (STM): Immediate, lasts seconds–minutes; relies on reverberating circuits in prefrontal cortex and hippocampus. Working memory: Active manipulation of information (e.g., mental arithmetic), dependent on dorsolateral prefrontal cortex. Long-term memory (LTM): More permanent storage, subdivided into: Declarative (explicit): Episodic (personal events) + Semantic (facts). Non-declarative (implicit): Procedural (skills), priming, conditioning. Consolidation: The process of converting STM → LTM, mediated by hippocampus–entorhinal circuits. Bradley’s Neurology)

6. Anatomical Substrates of Memory

7. Structural Anatomy Medial temporal lobe cornu ammonis (CA1–CA4), dentate gyrus, subiculum. Functional Anatomy Central role in declarative (explicit) memory, especially episodic and spatial memory. Essential for consolidation of short-term memory into long-term memory. Acts as a hub, binding sensory and contextual information from multiple cortical association areas. Clinical Relevance Bilateral hippocampal lesions (e.g., hypoxia, herpes encephalitis) → profound anterograde amnesia. CA1 region highly vulnerable to ischemia. Atrophy is an early biomarker of Alzheimer’s disease. In temporal lobe epilepsy, hippocampal sclerosis is a key pathological substrate. Hippocampus

8. Amygdala

9. Thalamus

10. Prefrontal Cortex

11. Basal Ganglia

12. Cerebellum

13. Association Cortices

14. Historical Perspective Papez (1937): Proposed first anatomical circuit for emotion and memory → the Papez circuit. Later expanded by MacLean into the concept of the limbic system. Modern neuroscience has redefined these as parallel but interconnected circuits, each contributing to aspects of memory like encoding, retrieval, emotional coloring , and consolidation.

15. Clinical relavance Bilateral hippocampal damage → profound anterograde amnesia (HM case). Early involvement in Alzheimer’s disease → episodic memory loss. Hippocampal sclerosis in temporal lobe epilepsy → seizure-related memory deficits. Functional MRI shows hippocampal activation during encoding and retrieval.

16. Examination Registration & recall of 3 objects after 5 minutes assesses episodic memory Story recall / logical memory detects hippocampal–cingulate dysfunction Orientation in time and place may be impaired with Papez circuit lesions Ref: de Jong; Bradley; Snell

17. Medial Limbic Circuit – Clinical Relevance Bilateral medial temporal lobe damage (e.g., herpes simplex encephalitis, hypoxic injury) produces severe anterograde amnesia with sparing of remote memory. Epileptic discharges in the medial limbic system cause déjà vu, jamais vu, and affect-laden auras. Atrophy of medial limbic structures is an early biomarker of Alzheimer’s disease.

18. Medial Limbic Circuit – Examination Immediate registration followed by delayed recall after interference is sensitive to consolidation deficits . Paired-associate learning tasks (recall of word pairs) highlight medial temporal involvement . Story recall testing further evaluates encoding and retrieval (Bradley) Ref: de Jong; Bradley; Snell

19. Diencephalic Circuit (Thalamic-Hypothalamic) Components: Mammillary bodies ↔ Anterior thalamic nuclei ↔ Cingulate cortex Function: Integrates memory encoding with executive function Clinical: Thalamic stroke → amnesia, Korsakoff syndrome Reference: Bradley’s Neurology, 8th ed.; Aggleton JP, Trends Cogn Sci. 2016

20. Clinical Relevance Lesions of dorsomedial thalamus → anterograde + retrograde amnesia. Korsakoff’s syndrome (thiamine deficiency) → memory loss + confabulation. Frontal-thalamic disconnection → impaired executive memory, planning, working memory. Ref: Bradley’s Neurology, 2016

21. Basal Forebrain–Hippocampal Circuit Components: Nucleus basalis of Meynert → Cholinergic projections → Hippocampus & Cortex Function: Attention and memory encoding Clinical: Early degeneration in Alzheimer’s → impaired episodic memory Ref: Snell RS. Clinical Neuroanatomy; Bradley’s Neurology; Hampel H, Lancet Neurol. 2018

22. Clinical Relevance Early degeneration of the nucleus basalis of Meynert is a hallmark of Alzheimer’s disease, producing impaired episodic memory. Basal forebrain lesions from aneurysm rupture or trauma cause amnesia with confabulation. Ref: Bradley’s Neurology

23. Clinical Relevance Dorsolateral prefrontal lesions impair working memory, planning, and source memory (facts recalled without context). Orbitofrontal damage leads to disinhibition, poor social memory, and confabulation. Frontal disconnection syndromes may mimic hippocampal amnesia. Ref:Bradley’s Neurology

24. Examination Prospective memory tasks (e.g., “Remind me about lunch in 10 minutes”) test executive memory. Source memory testing evaluates both content and context recall. Wisconsin Card Sorting Test and N-back tasks are gold standards for prefrontal working memory.

25. Cerebellar Contribution to Memory Components: Cerebellar cortex ↔ Dentate nucleus ↔ Thalamus ↔ Prefrontal cortex Function: Timing, sequencing, implicit motor memory Clinical: Cerebellar lesions → impaired motor learning, cognitive dysmetria

26. Clinical Relevance Cerebellar lesions → impaired motor learning and adaptation. Deficits in conditioned reflex learning (e.g., eyeblink conditioning). Contributes to cognitive memory via cerebello - thalamo -cortical pathways. Ref: Snell’s Neuroanatomy, 2020

27. Examination Motor sequence learning (finger tapping, pegboard tasks) assesses cerebellar contribution to memory Conditioned learning tasks such as eyeblink conditioning are impaired in cerebellar damage Timed coordination tasks with recall (dual motor + memory tasks) reflect cerebellar cognitive role . Ref: de Jong; Bradley; Snell