PSY 595 Cognitive Neuroscience. J.P. Toth. Fall A Selective History of Cognitive Neuroscience

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Reynold Ramsey
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A Selective History of Cognitive Neuroscience Key Question: Can cognitive functions or processes be localized to specific neural areas or processes?

1 A Selective History of Cognitive Neuroscience Key Question: Can cognitive functions or processes be localized to specific neural areas or processes? - what do we mean by "cognitive function" or "cognitive process"? - how do we go about identifying relevant neural "areas" or "processes"? A. Major figures in the localization/equipotential debate. 1. Gall & Spurzheim (early 1880s): Phrenology; First "strict localization" theory. 2. Pierre Flourens (early 1800s): First true ablation experiments; Anti-localization/Equipot. 3. Paul Broca (mid 1800s): Broca's area (BA 44/45); Expressive aphasia: Localization. 4. Carl Wernike (late 1800s): Wernicke's area (BA 22); Fluent aphasia: Connectionism. 5. Fritsch & Hitzig (1870s): "On the Electrical Excitability of the Cerebrum". Localization. 6. F.L. Goltz (1892): Ablated area studied by Fritsch & Hitzig. Anti-localization. 7. John Hughlings-Jackson (mid to later 1800s): Partial/Graded Localization. are we localizing functions or symptoms? [cf. questions with lesion method]. cf. diaschisis; disconnection syndromes; primitive forms of behavior & cognition. notion that brain is hierarchically organized with complex functions built on simpler ones; thus, damage can produce regression to earlier forms (cf. "microgenesis"). "ask not what an area does, but what contribution it makes". Advocates: A. Luria; K. Pribram; N. Geschwind; R. Sperry; M. Mesulam; A. Damasio. B. Discovery of Neurons (early 1900s). 1. Separate but interacting neurons (Cajal) vs. the nerve-net ('syncytium') hypothesis (Golgi). 2. Two major principles of neurons (Cajal). a. Connectional specificity (no shared cytoplasm; connections not random). b. Dynamic polarization (neurons have an input/output structure). 3. The Hebbian synapse. C. Disciplines Contributing to Modern Cognitive Neuroscience. 1. Cognitive Psychology (methods, tasks, theories, and models). 2. Advances in neural imaging and electrophysiology. 3. Clinical Neuropsychology. Emphasis on psychological deficits and lesion location. a. Behavioral neurology [cf. Neurology; Neurosurgery]. b. Psychometric approach to neuropsychological testing. 4. Experimental Neuropsychology. Emphasis on case-studies and models of normal function (UK).

2 Anatomy I: Cellular Organization of the Brain A. Cell types. 1. Neurons: Sensory Neurons > Inter-Neurons > Motor Neurons. 2. Glial (glue) cells (Astrocytes; Microglia; Oligodendroglia; Schwann cells). 3. Grey matter & white matter. B. Neurons. 1. Major structural features. a. Cell body (soma); axon hillock. b. Dendrites (tree); dendritic spines. c. Axons (axle); collaterals > teleodendria > terminal buttons. i. Myelin sheath & nodes of Ranvier. 2. Generalizations about neurons (integration units; vary greatly in size & shape; aggregate into nuclei; "shaped" by experience; can malfunction; can be regenerated). C. Neural signaling. 1. Resting potential (~ -70 mv); maintained by NA+/K+ pump. 2. Graded potential (aka electrotonic conduction). a. Passive/additive voltage change; dissipates over time & distance. b. Spatial & temporal summation (synaptic integration). 3. Action potential (~ -50 mv). a. Active voltage change. b. Saltatory (skip) conduction. c. Neural refractory period. 4. Neural coding (place, frequency, temporal, sparse, coarse/population). D. Synaptic transmission. 1. Structure of the synapse (buttons > cleft > vesicles > post-synaptic membrane). 2. Steps in synaptic transmission (fuse > release > bind > re-uptake). 3. Neurotransmitters. a. Small-molecule ("classic") neurotransmitters. About 10 currently known. i. Acetylcholine (widespread; excitatory & inhibitory; movement; memory). ii. Norepinephrine/NE (widespread; excitatory; sleep & arousal). iii. Dopamine/DA (voluntary movement; EFs/WM; motivation & reward). iv. Serotonin/5-HT (mood/emotion; sleep & arousal; memory) v. Glutamate (widespread; excitatory; memory & thought). vi. GABA (widespread; inhibitory; movement; memory). b. Peptides (e.g., opiates). c. Gases (e.g., Nitrous Oxide/NO, Carbon Monoxide/CO).

3 Anatomy II: Major Structures of the Central Nervous System A. Forebrain Cortex (bark) [aka neo-cortex; "cold cognition"/information processing]. - Gyri (ridges), Sulci (crevices), & Fissures (deep sulci). - Hemispheres (half globes) & Corpus Callosum (hard body). - Primary, secondary, and tertiary (association) cortex. - Occipital Lobe [vision]. - Parietal Lobe [somatosensation (body); spatial processing; attention]. - Temporal Lobe [audition; language comp.; object recog & knowledge; memory]. - Frontal Lobe [motor behavior; executive functions/wm/metacog; social/personality]. - Prefrontal Cortex: DLPFC, VMPFC, & Orbital PFC. Limbic lobe ["hot cognition"/emotion; declarative/explicit memory]. - Hippocampus (sea horse). - Amygdala (almond). - Cingulate (girdle). - Septum (partition), Fornix, & Mamillary bodies [hippocampal output]. - Olfactory bulb. Basal ganglia [motor control; procedural/implicit memory; motivation & reward*]. - Putamen (shell). - Caudate (tailed nucleus). - Globus Pallidus (pale globe). Diencephalon (between brain). - Thalamus (inner chamber) [sensory relay station]. - Pulvinar (excitatory); Reticular Nucleus (inhibitory). [attention gating]. - Hypothalamus [autonomic and endocrine functions; homeostasis; emotion]. B. Brainstem Midbrain - Tectum. - Superior Colliculus [eye movements] and Inferior Colliculus [audition]. - Tegmentum (cranial sensory nerves & motor nuclei). - Substantia Nigra/DA; Ventral Tegmental Area (VTA); Nucleus Accumbens. Hindbrain - Cerebellum (little brain) [fine motor control; timing]. - Pons & Medulla. - Ascending neurotransmitter pathways (LC/NE, RN/5-HT). - Reticular Activating System [sleep/wake; states of consciousness; attention]. C. Spinal Cord

4 Methods A. Cognitive/behavioral measures & approaches. 1. Reaction time (RT) & Accuracy. 2. Questionnaires (e.g., CFQ) & Self-report (e.g., Remember/Know). 3. Eye-movements & pupilometry. 4. Modeling & Process Estimation (SDT, PDP, MPT, Additive Factors, etc.). B. Neuropsychological Tests (e.g., JOL, Digit Span, WCST, etc.). 1. Lesion localization. 2. Establish baseline functioning and equate groups. C. The Lesion Method. 1. Assumptions: Modularity, Transparency, & Homogeneity. 2. Problems: Disconnection, modulation, diaschisis, reorganization, compensation, multiple strategies, practice effects. 2. Single and double dissociations. 3. Group versus case studies. (cf. lesion-overlap method). 4. Animal models (cf. functional lesions via cooling, pharma, TMS). D. Connectionist models & Lesion simulation. E. Electrophysiological stimulation. 1. Direct stimulation of the brain (surface or depth electrodes). 2. Transcranial magnetic stimulation (TMS). F. Electrophysiological recording. 1. Skin conductance (SCR/GSR). 2. Electroencephalography (EEG) [cf. synchronized oscillations]. 3. Event-related potentials (ERP) [cf. the inverse-mapping problem]. G. Neuroimaging. 1. Structural ( hardware ). a. Computerized Tomography (CT). b. Magnetic Resonance Imaging (MRI). c. Diffusion Tensor Imaging (DTI) [white-matter integrity]. 2. Functional ( software/wetware ). a. Positron Emission Tomography (PET). i. SNRFing (smooth, normalize, rotate, and filter). ii. Subtraction method (linear/additive assumtion). b. Function Magnetic Resonance Imaging (fmri). c. Magnetoencephalography (MEG). d. Optical Imaging (NIRS). e. Analyses: ROIs vs. correlated activity & path analysis.

5 Methods - Appendix A Potential problems in using lesions to localize cognitive processes: Disconnection between two or more (potentially distant) areas. Conduction aphasia; alexia; apraxia. Modulation effects (altered levels of facilitation and inhibition). Sustained attention; attentional. Diaschisis (functional de-activation of a distant, but connected, area). Patient RV (Kosslyn et al., 1991): Left frontal damage > left occipital-temporal deactivation > object recognition deficits. Compensation (redistribution of function, usually by surrounding tissue). Pasticity (e.g., rapid re-mapping of somatosensory cortex). Re-organization (development of alternate routes for processing). Patient LD: Semantic memory taking over episodic functions. Strategy change (a change in how a task is performed). Verbal control of behavior after right frontal damage (Stuss). Surface dyslexia: letter-by-letter reading. Practice effects (automating tasks or subprocesses supporting a task). Reduction of frontal activation after 2-3 repetitions of a word-generation task (Petersen); suggests rapid change in the organization of both cognitive and neural processing. Shared function in clustered neural tissue (one lesion, multiple impairments). Gertsmann's syndrome (supramarginal/angular gyrus): L/R confusion; finger agnosia; agraphia; acalculia. Amygdala: Emotional experience vs. memory vs.. cf. Kosslyn & Von Kleeck's (1990) 3 dimensions. Distributed functions (distinct lesions, similar functional impairments). Apraxia: motor cortex, sensory cortex (kinesthetic feedback), motor programming (SMA or parietal); frontal/intentional processes.

6 Methods - Appendix B Using lesions to localize cognitive function The basic idea: If damage to area X causes loss of cognitive function Y, then X must have been responsible for Y. "Focusing on the hole instead of the doughnut" (Smith). "Symptoms must be viewed as expressions of disturbance in a system, not as direct expressions of focal loss of neuronal tissue" (Benton). Lesions can be localized, not functions (Hughlings-Jackson). How can lesions be fruitfully used to constrain cognitive theories? Single Dissociation: Jack sustains brain damage to area X and then shows an impairment on task A (face recog) but not task B (object recog). What can we conclude? (1) Area X underlies task A.... but Joe may be impaired on tasks other than A (e.g., dog recognition). (2) Task A and B represent separate ( dissociable ) functions. but task A may simply be easier than task B. Double Dissociation: Jill sustains brain damage to area Y and shows the reverse pattern (an impairment on task A but not task B). What can we conclude? (1) Different cognitive processes are involved in tasks A & B. but what if performance on the preserved task is impaired relative to normals? - separation of processes, but maybe not complete separation. Associations: Joe is not only impaired on task A, but also C and D. [e.g., left occipital-parietal damage often impairs the spatial organization of perception and motor movements, but also arithmetic (e.g., "what is 41-6?") and grammar problems (e.g., "If Sue is Brenda's mother, and Faye is Sue's sister, how are Faye and Brenda related?"). What can we conclude? - Is damage specific to a particular (multi-use) cognitive process? - Or are 'different' cognitive processes being carried out by the same neural tissue?

7 Principles of Neural Organization A. Structural Organization of the Cortex. 1. Cortical Layers. a. Reentrant (reciprocal/feedback) processing. 2. Cortical Columns (as Information Processing Modules?). 3. How might neurons participate in cognitive functions? (Kosslyn & von Kleeck, 1990) a. Dedicated vs. Shared function. b. Clustered vs. distributed. c. Number of neurons involved (sparse vs. coarse coding). B. Brain Maps. 1. Anatomical Maps. a. Major anatomic divisions (gyri & sulci). b. Cytoarchitectonics: Brodmann Areas (1909). b. Rate of Myelination: Fleshig (1920). 2. Projection Maps. a. Axonal tracing. b. Connectivity mapping. 3. Functional Maps. a. Based on (i) performance following brain injury or electrical stimulation; and (ii) electrical activity (EEG/ERP), magnetic activity (MEG), or metabolic processes (PET/fMRI) during sensory stimulation, motor behavior, or cognitive performance. b. Topographic maps (retinotopic, tonotopic, somatotopic). B. Theories of Functional Organization. 1. Strict Localization (Gall; Broca; Fritsch & Hitzig). - e.g., Broca's aphasia; Anterograde amnesia. 2. Holism (Equipotentiality / Mass Action) (Flourens; Goltz; Lashley). - e.g., decerebrate & decortication studies. 3. Connectionism (Wernicke; Geshwind). - e.g., conduction aphasia; diaschisis. 4. Hierarchical Organization (Hughlings-Jackson). - devolution; microgenesis. - cf. MacLean's (1949) Triune Brain Hypothesis. 5. Functional Hierarchies (Luria). a. The sensory & motor units. b. Primary, secondary, and tertiary (association) cortex. c. Processing as hierarchical, serial, & convergent. 6. Distributed/Reciprocal Hierarchies (Felleman & Van Essen). a. Processing as reciprocal, parallel, & distributed. i. Shared/multiple functions. ii. The binding problem.

Neural Communication. Central Nervous System Peripheral Nervous System. Communication in the Nervous System. 4 Common Components of a Neuron

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