Higher Cortical Functions and brain recovery

Association areas

integrate information from multiple cortical regions and sensory modalities to support complex cognition and behaviour. Primary site for higher cortical functions.

Higher cortical function

associative function that integrates and processes complex multisensory information, i.e. performs cognition, e.g. memory, executive function, language.

Mainly cortical, adaptative, awareness

List 3 features of higher cortical functions.

Memory consolidation

stabilises and reorganises newly acquired memories, helping integrate information into long-term memory.

Synaptic plasticity

supports changes in neural connections; including pruning synapses to forget unimportant associations, patterns, and behaviours.

Energy consolidation and metabolic maintenance

reduced metabolism and removal of waste products accumulated in wakefulness.

Neural maturation

supports plasticity, neural circuit maturation, and other metabolic processes during development.

Sleep

reversible behavioural state of perceptual disengagement from and unresponsiveness to the environment.

Rapid eye movement (REM) sleep

characterised by vivid dreaming and higher brain activity associated with memory consolidation and synaptic changes during this stage.

Non-rapid eye movement (NREM) sleep

characterised by unconscious or bland thoughts, energy consolidation and metabolic maintenance predominate. Can be further divided into 3 stages.

Less NREM, rapid phase alteration

List 2 features of the sleep cycle for elderly patients.

Insomnia

persistent difficulty initiating sleep, maintaining sleep or returning to sleep after early awakening, despite adequate opportunity to sleep, accompanied by daytime impairment.

Obstructive sleep apnea

intermittent cessation of breathing due to airflow blockage with collapse of tissue during sleep.

Transient hypoxemia

associated with sleep apnea, blood oxygen may drop to 70-80% for some time.

Obesity, old age, male

What are 3 key risk factors for obstructive sleep apnea.

Hypertension, stroke

What are 2 common outcomes of sleep apnea.

CPAP, lifestyle change, surgery

What are 3 possible treatments for sleep apnea.

Central sleep apnea

intermittent cessation of breathing due to CNS pathology interrupting neural signalling to respiratory muscles.

Stroke, heart failure, opioids, CPAP

What are 4 key risk factors for central sleep apnea.

Electroencephalography (EEG)

measures synchronised electrical activity of large populations of neurons; standard method to investigate sleep.

Amplitude

size of the recorded voltage fluctuations, usually measured in microvolts (µV).

Frequency

number of cycles per second, measured in hertz (Hz).

Phase

part of the oscillation the signal is in; more signals in phase between channels shows more synchrony.

Topography

distribution of EEG activity across different scalp locations.

Noise (artefact)

contributions to the electrical signal that are not wanted.

8-13 Hz frequency, low amplitude, less synchrony

Describe EEG reading during wakefulness.

<4-8 frequency, low to high amplitude, more synchrony

Describe EEG reading during NREM sleep.

Mixed frequency, low amplitude, less synchrony

Describe EEF reading during REM sleep.

Declarative (explicit) memory

conscious recollection of facts and events; may be episodic (from personal experiences) or semantic (recalling facts and knowledge).

Non-declarative (procedural, implicit) memory

associations, habits, and skills formed without conscious thought.

Ionic memory

extremely brief sensory memory of a stimulus that lasts only milliseconds, such as the visual image retained momentarily.

Short-term memory

declarative memory temporarily held for a limited amount of information for seconds to minutes and forgotten when attention is lost.

Intermediate-term memory

information stored for minutes to days, bridging short-term and long-term memory through changes in neuronal function.

Long-term memory

information stored for days to years or potentially a lifetime, supported by more persistent changes in synaptic connections and neuronal networks.

Encoding

process of converting incoming sensory information into a form that can be stored in short-term or working memory.

Consolidation

process of stabilising and strengthening a newly encoded memory into long-term storage, done by the hippocampus.

Retrieval

process of accessing and bringing stored information in long-term memory back into conscious awareness.

Reactivation

process of reactivating a stored memory, making it temporarily modifiable and allowing it to be updated or strengthened before being stored again (reconsolidation).

Hippocampus and medial temporal lobe

formation of long-term declarative memories; receiving converging information from cortical association areas to establish connections between the.

Neocortex

long-term storage of declarative memories; the cortical representations linked through hippocampal processing during memory formation.

Prefrontal cortex

short-term/working memory; maintain and manipulates information for current tasks.

Amygdala

emotional associations, including fear conditions.

Cerebellum

skeletal-muscular learning and adaptation; supports learned adjustments to motor performance.

Striatum

skills and habits; supports learning expressed through repeated actions and habitual behaviour.

Prism adaptation

sensorimotor rehabilitation technique; optical prism lenses displace visual field to adjust motor and spatial proprioception through repeated movements, allowing resetting of internal spatial map.

Place cells

hippocampal neurons that fire moving through a specific location; when coordinated in a population they can encode the entire environment supporting spatial learning and navigation.

Cortical association areas

unimodal and polymodal; process different information from an experience; e.g. sight, sounds, emotions.

Entorhinal cortex

major interface through which information converges between cortical areas and the hippocampus

Hippocampus

associated multimodal information from entorhinal cortex to form episodic memories and spatial-temporal representations.

HM clinical case

had bilateral removal of medial temporal lobes including much of the hippocampus and amygdala to treat severe epilepsy leading to anterograde and some retrograde amnesia.

Retrograde amnesia

loss of memories formed before the onset of amnesia.

Anterograde amnesia

inability to form memories after onset of amnesia.

Memory-system consolidation

long term memories may become more dependent on cortical areas compared to the hippocampus overtime.

Synaptic plasticity

ability of neuronal connections to change their strength in response to activity.

Neuronal ensemble

networks of neurons distributed throughout the brain that are activated together and thought to collectively represent a particular memory or experience

Hebb’s postulate

cells that fire together wire together; when activity in one neuron repeatedly contributes to firing of another neuron, the synapse is enhanced. e.g. Pavlovian fear conditioning.

Long-term potentiation

persistent increase in synaptic transmission typically following high frequency stimulation; maybe a cellular mechanism for learning and memory. Involves glutamate receptors →

AMPA receptor

mediates much of the baseline excitatory synaptic transmission; increased receptor function contributes to LTP expression.

NMDA receptor

detects coincident presynaptic input and postsynaptic depolarisation; calcium entry initiates LTP-related signalling.

Input specificity

only appropriately activated synapses are strengthened as the stimulated pathway receives the relevant synaptic activity.

Cooperativity

multiple inputs may be needed to produce sufficient depolarisation, i.e. combined inputs help relieve the NMDA receptor Mg²⁺ block.

Associativity

a weak input can be strengthen when active alongside a strong input, i.e. strong input depolarises postsynaptic cell helping relieve NMDA receptor Mg²⁺ block.

Dendritic spines

small postsynaptic structures where many excitatory synapses occur and may act as substrates for memory storage.

Long-term depression

persistent decrease in synaptic transmission typically following low-frequency stimulation (1 Hz per 15 minutes).

Phosphatase signalling

pathways leading to reduced AMPA receptor-mediated transmission in long term depression.

Intrinsic excitability

changes in ion channels alter how readily neurons fire action potentials.

Inhibitory plasticity

change to GABAergic synapses; alters the balance between excitation and inhibition.

Myelination

alter functional coupling between neuronal ensembles.

Neurogenesis

new neurons in the hippocampus contribute to hippocampus-dependent learning.

Epigenetic changes

DNA methylation, histone modifications and non-coding RNAs regulate gene expression.

Neuromodulators

chemical messages influencing how neurons respond to incoming information and whether synaptic changes persist.

Dopamine neurons

encode reward prediction and errors in those predictions to provide a teaching signal to determine which circuits are modified.

Neuroplasticity

ability of the nervous system to change its activity in response to intrinsic or extrinsic stimuli by reorganising its structure, functions, or connections.

Neurogenesis

development of new neurons in the brain, primary during development. Adult neurogenesis is vary limited.

Synaptic plasticity

development of experience-dependent, long-lasting changes in strength and number of neuronal connections. Main means of neuroplasticity in adults.

Long-term potentiation (LTP)

long-lasting increase in synaptic strength following repeated activation; can occur via mediation of many steps of synaptic signalling, e.g. receptor expression, neurotransmitter clearance.

Axonal sprouting

growth of new axonal branches (neurites) from existing neurons, potentially allowing them to establish new synapses (synaptogenesis) or a greater junctional area.

Equipotentiality

idea that different areas of the brain have the potential to perform other functions. Debunked by confirmation that lesions to particular areas lead to focal neurological deficits that cannot be recovered.

Vicariation

pathways within the same network or region can reorganise and compensate for the functions previously performed by a lesioned area.

Experience-dependent neuroplasticity

modifications of neural circuits through external or internal experiencing resulting in long-term structural and often functional changes.

Critical periods

limited developmental period where experience-dependent neuroplasticity is most facilitated. Occurs during brain development and shortly following brain lesion.

Maladaptive plasticity

neural changes that have negative consequences, such as reinforcing chronic pain pathways or contributing to abnormal movement patterns.

Specialised stroke unit and critical period rehabilitation

multidisciplinary therapy approach 60-90 days post-stroke which can maximising compensatory neuroplastic changes and protecting penumbra after stroke.

Functional electrical stimulation (FES) after stroke

repeated pairing of electrical stimulation of peripheral nerves with muscular movement causes cortical activation; may strengthen connection between neural activation and muscle movement.

Physical exercise in Parkinson’s disease

physical exercise may support synaptic function and reduce atrophy for long-term motor benefit in Parkinson’s disease.

Cognitive stimulation programs for dementia

activities repeatedly engaging cognitive networks may strengthen existing neural connections to counteract neurodegeneration for mild-moderate dementia.

Dorsal amygdalofugal pathway (stria terminalis)

travels from amygdala along the dorsolateral surface of the thalamus to reach hypothalamus and septal area.

Ventral amygdalofugal pathway

travels from amygdala reaching hypothalamus and brainstem.

Hypothalamus, septal area

Destinations of dorsal amygdalofugal pathway.

Hypothalamus, brainstem

Destinations of ventral amygdalofugal pathway

Ventral amygdalofugal pathway

amygdala output concerned with fast associative learning, reward/punishment coupling, and immediate motor/emotional drive.

Dorsal amygdalofugal pathway

amygdala output concerned with sustained stress, anxiety states (via BNST), and endocrine regulation.

Corticomedial nuclei

process olfactory information and contribute to innate behaviours, including feeding, reproduction, and responses to pheromones.

Basolateral nuclei

receive sensory information from cortex and thalamus and integrates it with emotional significance, supporting emotional learning and fear conditioning.

Central nucleus

main output region of the amygdala; coordinates autonomic, endocrine, and behavioural responses to emotional stimuli, particularly fear.

Olfactory processing, feeding/reproductive behaviours

describe functions of corticomedial amygdala nuclei.

Sensory processing, emotional significance and learning

describe functions of basolateral amygdala nuclei.

Outputs for emotional experience and expression

describe functions of central amygdala nucleus.

Cross-modal plasticity

reorganisation in which brain regions typically responsible for one sensory modality are recruited to process information from another modality.