• Principles inv in study of brain function
• Behavioural consequences of path affecting certain brain circuits
• Functional significance of following circuits: Prefrontal areas; Cortio-striato-pallido-thalamic loops; Limbic circuit

• Awareness of rich connectivity in areas responsible for higher level processing
• Systems rather than single structures
• Classical lesion-dysfunction approach may be inadequate (same lesion - different dysfunction; different lesion - same dysfunction)
• Paradigm-based neuroimaging studies help to clarify systems involved
• Integration important

Strong connections w/ temporal cortex (posterior brain) + limbic sys

• Gradation from limbic to isocortex
• Limbic cortex more interconnected/ primitive (like medial temporal lobe structure)
• Isocortex least interconnected - cross mainly to same level (like primary motor/ sensory cortices)
• Major ventral and dorsal systems
• (Barbas and Pandya, 1991)

• More available to study (primates, human injuries)
• Working memory: ST (hold info in mind for short time to enable work on it - eg. Phone number - analogous to computer RAM) - however, not only area determining working memory
• Cognitive and perceptual processes: most of these processes dep on working memory
• Lesion effects

1. Distractibility: attention easily diverted to unimportant stimuli (b/c working memory holds in mind what we want to do currently - therefore lose ST goals + respond to any stimulus that appears before us)
2. Sensory neglect: failure to appreciate a representation of the sensory space we are exposed to (similar to stroke in parietal cortex)
3. Response suppression: similar to distractibility; a particular stimulus in env will set off a particular response which is inappropriate in overall context
4. Sustained attention deficit
5. Reduced digit span (<7): MSE; number of numerical digits held in mind for ST, typical = 7

• Situated above orbit
• Stimulation effects

1. Stop feeding
2. Slow-wave sleep: not dreaming, deepest sleep
3. Reduced arousal

• Extensive Lesion Effects

1. Apathy: not interested in env
2. Reduction in arousal
3. Reduced social activity
4. Neglect childcare: normally instinctual
5. Solitary behaviour

• Less Extensive lesions (after acute phase)

1. Disinhibition
2. Euphoric
3. Labile: mood changeable
4. Overtalkative
5. Irresponsible: disregard for rules
6. Impulsive

• Perseveration: persistence of a response that was once appropriate beyond the time that is no longer relevant
• Reduced attention

• Includes anterior cingulate gyrus, supplementary motor area
• Lesion effects

1. Posturing
2. Waxy flexibility (a rigidity of the body in which the patient maintains whatever position he is placed in, the limbs having a heavy waxy malleability) and gegenhalten: an involuntary resistance to passive
3. movement, as may occur in cerebral
4. cortical disorders
5. Apathy
6. Utilisation behaviour: inability to suppress oneself from making use of an object that is placed in front of you
7. Alien hand syndrome: esp. supplementary motor area lesion, feeling that hand is acquired a life of its own

• Guiding complex movements
• Stimulation results in semi-purposeful movements, vocalisation etc.
• Active even when imagining complex action
• Active when acquiring new motor programs
• Lesion effects

1. Movements slow
2. Incoordination of repetitive movements
3. Mutism: inability or refusal to speak
4. Catatonia (gegenhalten and waxy flexibility): a wide group of motor abnormalities, most involving extreme under- or overactivity, associated primarily with catatonic schizophrenia.

• Fine motor movements
• Soft neurological signs
• Primitive reflexes (e.g. grasp reflex)

• To temporal and parietal areas
• Long association fibres
• Specific projection between posterior sensory areas and frontal areas
• Connections between isocortex and limbic cortex specific

1. C = Cortex
2. S = Striatum
3. P = Globus Pallidus; embedded in caudate and putamen complex
4. T = thalamus

DIAG: Motor CSPT

• Cortex: cortical neurones into striatum - from there to globus pallidus - from there to thalamus - from thalamus axons return to cortex

DIAG: Dorsal CSPT Circuits

• Divided into dorsal and ventral circuits for convenience only
• Glu = glutamate (+)
• GABA = (-)
• DA = dopamine; neuromodulator
• Basic circuit: cortex -> striatum -> pallidum -> thalamus -> cortex
• Basic loop: 2 inhibitory (GABA) interactions + excitatory (Glu) - net effect excitatory (+ve feedback). If there is a certain pattern in cortex, this pattern will tend to be maintained and may even intensify
• Therefore need pathway through SN to unlock the +ve feedback

DIAG: Ventral CSPT Circuits

• VTA = ventral tectal area
• Ventral area - more limbic part of cortex (emotion + high-level behaviour)

• Context-dependent behavioural learning (reward-related)
• Lesions:

1. Movement disorders
2. Disinhibition
3. Psychosis
4. Apathy
5. Catatonia and stupor (lowered level of consciousness; psychiatry: disorder marked by reduced responsiveness)
6. Hypermetabolism in OCD

• Co-ordination of Motor programme
• Switching of programme
• Mediate reward and motivational cues
• Lesions

1. Difficulty in fine tuning movement
2. Ballistic movement
3. Difficulty in switching to new prg

• Reciprocal connection with cortex
• Relay for sensory system
• Arousal
• Integration of sensory and motor inputs

• Hippocampus
• Amygdala
• Fornix
• Hypothalamic nuclei
• Anterior thalamus
• Cingulate cortex

DIAG: Penfield points for psychosis

• 1960-1970's
• Neurosurgery on Pt's under LA
• Electrical stimulation on different parts of brain - asked Pt's what they felt
• Superior temporal gyrus stimulation -> hallucination + psychosis

• Cortical structure
• Reciprocal connection with association cortex: hippocampus receives information about environment
• Connection with septal nucleus: deep in basal forebrain, next to hypothalamus
• Projection to hypothalamus: hypothalamus: humoral centre of brain (BP, autonomic responses, appetite, sex drive, energy levels)
• Tri-synaptic structure
• Fornix: tail of hippocampus, from posterior end, curves around and ends in hypothalamus, carries 5M fibres in parallel, one on each side
• Putative computation in hippocampus: associative memory formed + retrieved
• Lesion

1. Anterograde amnesia of declarative memory: classic amnesic syndrome
2. Bilateral lesion required
3. Amygdala lesion probably required

• Subcortical nucleus
• Connects via stria terminalis with medial hypothalamus
• Connected more with subcortical structures + hypothalamus
• Mediate emotional response + emotional learning
• Maintenance of mood state indep of env
• Med + lat amygdala
• More limbic parts of brain have richer connections
• Stimulation

1. "Fight or Flight"
2. Orienting response
3. Aroused and alert
4. EEG desynchronised
5. Skin conductance increase
6. Prolong stimulation: fight or flight response
7. Targeted attack behaviour

• Lesion

1. Tameness
2. Reduction of aggressive behaviour
3. If intensely provoked, short but fierce aggression can still result ("sham rage")
4. Mediated by hypothalamus
5. Failure of recognition of facial affect (others' emotions)
6. Indifferent response
7. Kluver-Bucy syndrome: exploratory activity with hands + mouth, new objects put into mouth (similar to early infancy)

SLIDE: emotion components

1. Autonomic
2. Humoral
3. Behavioural

SLIDE: explicit memory

• Hippocampus: involved only while memory trace is formed
• If hippocampus is destroyed after that period, memory already laid down is not affected, but cannot form new memory traces

SLIDE: implicit memory

• Reinforcement learning of CSPT loop
• Under a particular set of environmental conditions

SLIDE: emotional memory

• Not conscious
• Brain's characteristics in mediating emotional response in presence of particular set of env stimulus without having to explicitly remember
• Eg. PTSD - nightmares, fearful when encountering something similar (but not identical), over-intense connection between amygdala (between environment + connections)