Perception & Action: Plasticity, Memory, Amnesia, and Phantom Phenomena

Perception & Action: Neural Plasticity, Memory, and Phantom Phenomena

• Theme across slides: how learning and experience shape brain structure and function; the role of synaptic changes, memory systems, brain localization, and remarkable phenomena like phantom limbs.

Strengthening synapses

• Synapses used often are strengthened; those not used are weakened and can become ineffective.
  • Visual shorthand from slides: Used lots → A, B positions indicating strengthened pathways; Not Used → weakened pathways.
• Core idea: use strengthens, disuse weakens; supports long-term changes in neural circuits that underlie learning and memory.

Hebb's Theory of Consolidation (1949)

• Short-Term Memory (STM)
  • Experience activates sensory pathways, which conduct neural impulses to the CNS.
  • STM is stored by neural activity reverberating in closed-loop CNS circuits.
• Long-Term Memory (LTM)
  • If reverberating activity is maintained long enough, structural changes occur in synapses, facilitating subsequent transmission over the same pathways.
  • Synaptic facilitation can influence motor output and thus behavior.
• Hebb rule (conceptual): a presynaptic neuron repeatedly participates in firing a postsynaptic neuron, the connection strengthens.
  • Formal expression (Hebbian form): $\frac{\Delta w<em>{ij}}{\Delta t} \propto x</em>i x<em>j$ where $xi$ and $x_j$ are the activity levels of pre- and post-synaptic neurons.
• Implication: memory emerges from activity patterns that reinforce specific neural pathways over time.

Memory consolidation and phases (Müller & Pilzecker influence)

• Consolidation is time-dependent: early changes support short-term memory; later changes support long-term memory.
• Key finding: short-term and long-term memory may involve distinct brain processes acting in parallel rather than being strictly sequential (challenging simple dual-trace ideas).
• Memory strength vs. time:
  • Short-term memory: $ext{duration} \approx \text{seconds to hours}$
  • Long-term memory: $\text{duration} \approx \text{hours to months}$
  • Long-lasting memory: $\text{duration} \approx \text{months to lifetime}$
• Later stages of consolidation likely involve interactions among multiple brain systems that reorganize and stabilize distributed connections.

Brain development and synaptic pruning

• Early life: brain grows rapidly; neurons mature and extend dendrites (input) and axons (output), increasing synaptic contacts.
• At birth: approx. 2,500 synapses per neuron in cerebral cortex.
• By age 2–3 years: approx. 15,000 synapses per neuron (Gopnik et al., 1999).
• Aging: synaptic pruning eliminates unused connections, refining neural networks.
• Concept: dynamic remodeling of synapses during development supports rapid learning and later optimization.

Memory systems and neuroanatomy

• Long-term memory can be categorized as Declarative (Explicit) vs Nondeclarative (Implicit).
  • Declarative memory: events (episodic) and world knowledge (semantic); supported by medial temporal lobe structures and prefrontal cortex.
  • Nondeclarative memory: procedural skills, perceptual priming, conditioning, and nonassociative learning; supported by basal ganglia, cerebellum, amygdala, and other circuits.
• Memory subsystems diagram (summary):
  • Declarative: Events, Facts — Episodic memory (personal experiences) and Semantic memory (world knowledge)
  • Nondeclarative: Procedural memory (skills), Perceptual priming, Habituation, Sensitization, Classical/Nonassociative learning
• Brain regions (typical mapping):
  • Medial temporal lobe (includes hippocampus, entorhinal cortex) and neocortex (prefrontal areas) for declarative memory
  • Basal ganglia and cerebellum for procedural and motor skills
  • Perceptual representation systems with distributed cortical involvement
• Note: The exact boundaries and interactions among these memory systems are complex and involve multiple interconnected regions.

Amnesia: Definitions and types

• Amnesia: partial or total loss of memory, often due to shock, brain injury, illness; can be organic or psychogenic.
  • Organic amnesia: due to physical brain damage (e.g., hypoxic episodes, infections, epilepsy, Alzheimer’s disease).
  • Psychogenic amnesia: due to psychological trauma; includes dissociative states and related disorders.

HM: A landmark case

• HM: bilateral medial temporal lobe lesions (including structures like hippocampus, amygdala, entorhinal cortex) due to prior surgeries for epilepsy.
• Lesion details (examples from slides):
  • Removal of entorhinal cortex, hippocampus, amygdala; rhinal cortex involvement; hemispheric specifics (bilateral with some sides relatively intact for comparison).
• Syndrome: severe deficit of global anterograde amnesia (inability to form new memories) with only mild retrograde amnesia.
• Everyday life indicators: forgets own physician, repeated reading of newspapers, inability to recall recent experiences or learn new information reliably; can show word lists, faces, objects memory deficits on formal tests.
• Conclusion: HM demonstrates the distinction between STM/working memory and LTM, and the crucial role of medial temporal structures in forming new long-term memories.

Retrograde vs. Anterograde Amnesia (HM as a case example)

• Retrograde amnesia: loss of memories formed before the trauma; can be time-limited (temporal gradient) with more recent memories impaired than remote memories.
• Anterograde amnesia: inability to learn new information after the trauma.
• HM had both retrograde (partial, lasting up to about 2 years post-trauma) and anterograde amnesia, illustrating dissociation of memory phases.
• Retrograde memory in HM showed preservation of older, remote memories (childhood memories largely intact).

Remote vs. Recent Memory (HM context)

• Recent memory deficit: loss of more recent information; remote memory: time-limited retrograde memory that spans years or decades earlier.
• Concept illustrated with HM’s memory profile: recent events poorly remembered; older memories more intact.
• Visual representation: memory performance vs. time since trauma shows a decline for recent memory while older memories remain relatively preserved.

Retrograde Amnesia: Retrograde tests (Rey–Osterrieth Figure)

• The Rey–Osterrieth figure test involves copying a complex figure and then reproducing it from memory after a delay.
• In HM-related studies and other cases (e.g., E.P., G.T.), some patients failed to recall previously copied figures (indicating retrograde deficits) while control subjects could reproduce with guidance.
• Example results (from figure): Some patients could not recall copying (E.P., G.T.); others drew strange images (e.g., horse head) indicating impaired memory for the copy after delay.

Other forms of amnesia and related disorders

• Unilateral hippocampal damage leads to material-specific deficits: left hemisphere -> words and names; right hemisphere -> faces and objects.
• Korsakoff’s psychosis: amnesia with confabulation (fabricated memories) due to severe thiamine (vitamin B1) deficiency.
• Frontal lobe damage: affects short-term/working memory, temporal ordering, and can produce confabulation.
• Electroconvulsive therapy (ECT/ECS) can also impact memory.

Anatomical localization: The hippocampus and surrounding regions

• Key structures around the hippocampus include: entorhinal cortex, amygdala, fornix, mammillary bodies, cingulate gyrus, corpus callosum, and thalamic connections.
• Importance: hippocampus and surrounding rhinal cortex regions are critical for declarative memory formation and episodic memory encoding.

Recap and connections

• Core themes: plasticity and memory; amnesia (HM) and memory localization; learning-induced brain changes; encoding and retrieval; brain changes due to learning; real-world examples (cab drivers, jugglers) demonstrating structural plasticity.
• The overarching idea: neural circuits adapt with experience, enabling new skills, memories, and perceptual representations.

Memory encoding strategies and testing insights

• Word memory and strategy use: memory for words can be good when encoding strategies are effective; retrieval is facilitated by strong encoding.
• Memory has sequence specificity: order and sequence can influence recall (illustrated by alphabet example and serial positions typical in memory tasks).

Structural brain changes with expertise and experience

• London cab drivers: show increased hippocampal gray matter, suggesting structural changes with long-term navigation experience.
• Question: do general skills (e.g., sports) induce similar brain changes? This remains an area of research.

Skill learning and brain plasticity: juggling study

• Experimental design:
  • Participants: 12 beginners assigned to a juggling group; 12 non-juggling controls.
  • Intervention: practice a three-ball cascade juggling routine until skilled (60 seconds of continuous juggling).
• Brain imaging findings:
  • Post-training scans showed changes in brain structure; percent change in gray/“green” matter across scans.
  • Data suggest learning new skills can alter brain structure, but exact causal mechanisms are unclear (changes could reflect new neurons, glial cells, or synapses).
• Important caveat: interpretation of structural changes requires caution; correlation does not imply sole causation, and multiple cellular processes may underlie observed MRI-detected changes.

Phantom limbs, cortical remapping, and neural plasticity

• Phantom limbs: vivid sensation that a lost limb is present; can be painful or distressing.
• Incidence and characteristics:
  • 90–98% of amputees experience phantom sensations; less common in early childhood.
  • Onset is immediate in about 75% of cases; duration ranges from days to decades (even up to ~57 years).
  • Affected body parts include arms, legs, breasts, face, and internal organs; habitual postures can sometimes change.
• Experimental findings (animals and humans):
  • Primate studies: middle finger amputation leads to hand cortex responding to adjacent finger stimulation; after long periods, hand cortex can respond to facial stimulation.
  • Human brain imaging: amputees show hand cortex activation when the face or upper arm is stimulated, indicating cortical reorganization.
• Referred sensations ( mappings from other body regions onto phantom limb):
  • Stimulation of the face can elicit sensations in phantom fingers (Ramachandran, 1993).
  • Mapping extends to adjacent cortical areas, including face-to-hand (e.g., lips, trunk, shoulder) and pharynx connections.
• Therapeutic interventions: mirror box therapy can alleviate painful phantom sensations or alter phantom limb posture.
• Implications of phantom limb research:
  • Brain topography is dynamic; neural organization adapts with changes in sensory input and motor use.
  • Phantom limb experiences have identifiable neural correlates, supporting a neurobiological basis for conscious experiences after limb loss.
  • Demonstrates neural plasticity in somatotopic maps and the potential for rehabilitation strategies leveraging cortical reorganization.
• Additional media: phantom limb case videos and demonstrations as educational exemplars.

Course overview and future directions

• Course themes covered: neural control of movement; neurophysiology, pathologies, and measurement techniques; plasticity and learning; perception and action.
• Future directions in research and application:
  • Advances in brain imaging: higher spatial and temporal resolution, real-time brain study.
  • Brain-machine interfaces and neural implants for rehabilitation.
  • Neuro-rehab engineering and potential development of artificial brains or augmentation technologies.

One more time… key takeaways

• Neural plasticity underlies learning, memory consolidation, and adaptation to injury.
• Memory involves multiple systems and regions; HM demonstrates the critical role of the medial temporal lobe in forming new long-term memories.
• Learning new skills can drive structural brain changes; the exact cellular underpinnings require careful interpretation.
• Phantom limbs illustrate that cortical organization is dynamic and can reorganize in response to sensory and motor changes, with practical therapeutic implications.

Final notes on connections and implications

• The dynamic nature of memory and perception emphasizes that the brain is not a fixed organ; experience shapes structure and function.
• Understanding these processes informs educational strategies, rehabilitation after injury, and therapies for sensory-motor disorders.
• Ethical and practical implications include real-time brain monitoring, brain implants, and neurorehabilitation technologies that may alter life quality for patients with neurological injuries or amputations.

Key equations and explicit notations

• Hebbian synaptic change (conceptual): $\Delta w<em>{ij} \propto x</em>i x_j$
• Memory duration concepts (terminology):
  • Short-term memory: $T_{STM} \in [\text{seconds}, \text{hours}]$
  • Long-term memory: $T_{LTM} \in [\text{hours}, \text{months}]$
  • Long-lasting memory: $T_{LLM} \in [\text{months}, \text{lifetime}]$
• Memory consolidation: consolidation can involve parallel, interacting processes across brain systems rather than strict sequential stages.

End of notes