HUF 2-62 Association function and executive processing Flashcards
Association cortices
4 major lobes: frontal, parietal, temporal, occipital
Corpus callosum
1° areas: close links with specific motor structures or sensory receptors
2° areas: direct connections with 1° areas
Association areas: no direct connect with sensory and motor structures (“silent” areas)
* Receive info from higher-order sensory areas
Subdivision of association cortices
Higher functions: thought, perception, consciousness, emotion, memory, languages
- Prefrontal (ant.) association cortex
- Limbic “
- Parietal-temporal-occipital (pos.) “
Prefrontal cortex: behavioral control
- Frontal lobe ant. to premotor and motor cortices
- Excluding limbic cortical areas
- 1° motor cortex: simple movements
- Premotor cortex: complex movements
- DL/VL prefrontal cortex: cognition, rule-guided behaviour, decision-making
- Frontopolar cortex: long-term goals, multitasking
- Somatotopic map gradually lost in more ant. area
Prefrontal cortex: integrate diff. sensory input (esp. from pos. parietal cortex)
=> Select most appropriate motor responses
Frontopolar cortex: no direct sensory input at all
*Phineas Gage: normal intelligence; change in personality
Limbic association cortices
Cortical components of complex limbic system:
- Orbito-frontal cortex: medial and ventral surface of frontal cortex
- Cingulate gyrus: mid surfaces of cerebral cortex
- Insular cortex
- Parahippocampal gyrus of temporal lobe
Close relationship with other subcortical components of limbic system:
- Amygdala: fear response
- Hypothalamas: homeostatic drive
- Hippocampus: emotional memory
- Ventral striatum / septum: reward, pleasure
- More complex emotions (sadness, anger…) and related behaviours (e.g. aggression, defense)
Schizophrenia affects prefrontal and limbic system
Prefrontal cortex: prominent dopaminergic
Schizophrenics:
1. Smaller frontal lobe
2. No normal increase in BF in tasks involving the area
Prefrontal and limbic system malfunctions:
+ve symptoms: delusions, hallucinations
-ve symptoms: withdrawal
Antipsychotic drugs: DA receptor antag.
Parietal-temporal-occipital association cortex
- Parietal cortex pos. to somatosensory cortex
- Temporal cortex apart from auditory areas
∴ Junction between higher-order somatic, visual and auditory areas - Higher sensory area
1. Link and interpret info from diff. sensory modalities
2. Sensory perception, language and motor planning
Regional functional specialisation of parietal-temporal-occipital association cortex
Posterior parietal cortex:
- Locomotion of body parts and surroundings of body
- Project to motor cortex
Angular gyrus
- Visual processing of wards: reading and writing
Temporal association cortex:
- Input from visual areas => analyse visual info.
Wernicke’s area:
- Interpretation of languages (spoken and written)
Neural circuit of language
Wernicke-Geschwing model
- Auditory inputs (spoken words) from auditory cortex to Wernicke’s area
- Visual inputs (written words) from occipital cortex to angular gyrus to Wernicke’s area
- Language info to Broca’s area (in frontal lobe) via arcuate fasciculus
- Language response to motor cortices
- 1° motor cortex command ms. to produce language (speech, writing, sign language)
Higher order disorders of brain
- Lesions in ant. and pos. association cortices
=> Complex, subtle changes in sensory perception and motor functions (incl. language)
Broca’s (expressive) aphasia:
- Difficulty to construct language
Wernicke’s (receptive) aphasia:
- Cannot understand spoken words
Dyslexia:
- Cannot read and write (angular gyrus)
Apraxia:
- Disorders in high-level motor coordination (e.g. lesion in parietal and prefrontal cortex)
Agnosia:
- Lesions of pos. parietal lobe
=> Inability to recognise objects by touch or vision (neglect syndromes)
Cortex: collective properties and EEG
- Tendency to synchronise neuron activities in cortex because of interconnection
=> Collective (emergent) properties - Electroencephalogram (EEG): non-invasive, painless
=> Records activity of large population of cortical neurons simultaneously by macroelectrodes - EEG patterns occur differentially in diff. cortical areas; vary dramatically with particular states of behaviour and sensory influences
EEG and epilepsy
Normal vs. partial seizure vs. generalised seizure EEG
Epilepsy:
- Stereotyped and involuntary alterations in behaviour
- Simple jerking, convulsion, loss of consciousness
- ↓ synaptic inhibition through GABA
=> Cortical neurons firing simultaneously
- Drugs: ↓ excitability of cortical neurons
e. g. inactivation of Na-channels; ↑ GABA transmission
Depression
- Unpleasant mood, intense mental anguish, generalised loss of interest in world
- Disturbed sleep, diminished appetite…
- ↓ availability of biogenic amines (5-HT/NA/…) (?)
Drugs:
- Selective 5-HT reuptake blockers
- MAO inhibitors (↓ degradation of NT)
