Cortical States, Sleep and Attention - UCLan PDF

Cortical states, sleep and attention Where opportunity creates success Learning objectives Understand the chronobiology concept and its relationship with the SCN Describe the functional states of the brain Recognise the brain circuits underlying the functional states Associate the co...

Cortical states, sleep and attention Where opportunity creates success Learning objectives Understand the chronobiology concept and its relationship with the SCN Describe the functional states of the brain Recognise the brain circuits underlying the functional states Associate the cortical states with pathological conditions Contents ❖ Chronobiology Circadian rhythms Biological clocks Brain clock ❖ Sleep Sleep cycle Function of sleep Neural mechanism of sleep Narcolepsy ❖ Awake Resting state brain activity Attention Consciousness  Chronobiology Field of biology that examines periodic (cyclic) phenomena in living organisms and their adaptation to solar- and lunar-related rhythms Many important cycles: – Infradian rhythms→ cycles longer than a day – Ultradian rhythms→ which are cycles shorter than 24 hours – Tidal rhythms→ 12.4-hour transition from high to low tide and back – Lunar rhythms→ which follow the lunar month (29.5 days) – Circadian rhythms→ cycles during the 24-hour day  Circadian rhythm Circadian rhythm is a natural, internal process that regulates the sleep-wake cycle and repeats roughly every 24 hours – Diurnal: which describes organisms active during daytime – Nocturnal: which describes organisms active in the night Physiological and biochemical processes in the body rise and fall with daily rhythms – body temperature, blood flow, urine production, hormone levels, hair growth, and metabolic rate all fluctuate Is regulated by an endogenous clock – What happen when the cycles of daylight and darkness are removed from an animal’s environment? Biological clocks Zeitgebers – Environmental time cues – For mammals: primarily light–dark cycle – Free-running period completely deprived of zeitgebers humans it tends to be 24.5–25.5 hours Jet lag→ clock desynchronization  Brain clock Suprachiasmatic nucleus→ internal clock which maintain appropriate daily rhythms of homeostatic functions Input→ retinal ganglion cell detect the light (Melanopsin) SNC→ connect with pineal gland (Melatonin) – ↑ synthesis ↓ light – Use as insomnia treatment Output→ hypothalamus, midbrain and diencephalon GABA and vasopressin Molecular Mechanism of SCN SNC cells – Each one is a minuscule clock – Communicate their rhythmic message to the whole brain – Action potential ≠ Rhythm Clock genes – Per, cryptochrome, clock – Negative feedback loop→ clock gene is transcribed to produce mRNA that is then translated into proteins→ after a delay, proteins send feedback→ decrease in gene expression→ decreased transcription, less protein is produced→ gene expression again increases to start the cycle – takes about 24 hours How do the cells coordinate to express the same rhythm? Every cell of the body has a circadian clock Driven for the same gene transcription feedback Master control of SCN – Signalling pathways  Functional states of the brain 1. Awake Brain at rest (Brain’s default mode) Attention Consciousness 2. Sleep Non-REM sleep REM sleep Sleep  One-third of our lives sleeping Sleep deprivation is highly deleterious Why do we sleep? What purpose does it serve? Clinical importance of sleep Sleep→ is a readily reversible state of reduced responsiveness to the environment  The sleep cycle REM sleep – “Active brain in a paralysed body” – Dreaming sleep – Fast rhythm in EGG – ↑ oxygen consumption at the brain – Sympathetic activity – Atonia – Rapid eye movement (predictors of vivid dreaming) Non-REM sleep – “Idling brain in a movable body” – Slow rhythm in EGG – ↓ oxygen consumption and firing rate at the brain – Parasympathetic activity – ↓ body temperature and energy consumption – Involuntary movements 1. Waking state Beta activity (High-frequency and low-amplitude) 2. Non-REM sleep 75% total sleep time Divided into 4 stages: – Stage 1→ Theta activity – Stage 2→ sleep spindles and K complex – Stage 3→ Delta activity – Stage 4→ Delta activity 3. REM sleep Beta & gamma activity  Functions of sleep All mammals, birds, and reptiles appear to sleep— apparently needed by the brain Two main categories of theories of sleep function – Restoration Sleep to rest and recover, and prepare to be awake again – Adaptation Sleep to keep out of trouble, hide from predators Conserving energy Functions of dreaming and REM sleep REM sleep vs dreaming for research studies – Unclear why we dream—but body requires REM sleep Sigmund Freud – an unconscious way for us to express our sexual and aggressive fantasies, which are forbidden while we are awake – dream functions as wish fulfillment or conquer anxieties Hobson and McCarley→ activation–synthesis hypothesis – Dreams as associations and memories – Activation some part of cerebral cortex and synthesis of images and emotions Karni – certain memories require strengthening time period → REM sleep – Deprivation of REM sleep→ learning of the task did not improve overnight  Neural mechanism of sleep Sleep require a variety of brain regions – Diffuse modulatory neurotransmitter system 1. Noradrenergic and serotoninergic neurons→ waking state 2. Cholinergic neurons→ some enhance REM events, others active during waking 3. Control rhythmic behaviours of thalamus and therefore controls cortical EEG 4. Activity in descending branches of diffuse modulatory systems (e.g., inhibition motor neurons)  Wakefulness and the Ascending Reticular Activating System Brain stem lesions cause sleep, coma Moruzzi’s research (ARAS) – Lesions in midline structure of brain stem cause state similar to non-REM sleep. – Lesions in lateral tegmentum do not cause non-REM state sleep. – Electrical stimulation of midline tegmentum of midbrain changes cortex from slow, rhythmic EEGs of non-REM sleep to alert and aroused state Ascending Reticular Activating System Awakening and during various forms of arousal – neurons increase their firing rates – locus coeruleus→ norepinephrine – raphe nuclei→ serotonin – brain stem and basal forebrain→ acetylcholine – midbrain→ histamine – hypothalamus→ hypocretin Control of REM sleep – Before REM→ decrease firing rates locus coeruleus and the raphe nuclei – Increase in the firing rates Ach containing neurons in the pons→ induce REM stage? Falling Asleep and Non-REM State Sleep: progression of changes ending in non-REM state Non-REM sleep: decrease in firing rates of most brain stem modulatory neurons using NE, 5-HT, ACh Stages of non-REM sleep – EEG sleep spindles (pacemakers' thalamic neurons) – Spindles disappear – Replaced by slow, delta rhythms (less than 4 Hz)  Mechanism of REM sleep Many cortical areas are active as are during waking Limbic system more activated during REM Low activity in prefrontal lobe Brain stem systems→ inhibit our spinal motor neurons, preventing the descending motor activity→ REM atonia REM sleep behaviour disorder→ disruption of the brain stem systems Narcolepsia→ deficiency of hypocretin Sleep-promoting factors Adenosine – Antagonists: caffeine or theophylline – ↑ levels during waking – Inhibitory effect on the diffuse modulatory system Nitric oxide – Expressed by the cholinergic neurons of the brain stem – ↑ levels during waking – NO triggers the release of adenosine Interleukin-1 – interleukin-1 levels increase during waking – induces fatigue and sleepiness Melatonin – secreted by the pineal body – released at night, inhibited during daylight – helps initiate and maintain sleep – used to treat symptoms of jet lag and insomnia  Narcolepsy Long-term neurological disorder that involves a decreased ability to regulate sleep-wake cycles Symptoms often include periods of excessive daytime sleepiness and brief involuntary sleep episodes and sudden loss of muscle strength (cataplexy) ↓ levels of orexin Lifestyle changes include taking regular short naps and sleep hygiene Medications→ modafinil, sodium oxybate and methylphenidate Awake  Resting state brain activity Is the brain quiet in absence of any stimuli? Resting state activity – ↓ activity in areas during behavioural task ↑ activity at rest – Brain can be “busy” at rest Default mode network – Brain areas active in resting state – Default-mode network activity is anticorrelated with frontal-parietal attentional control regions – Medial prefrontal cortex, posterior cingulate cortex, posterior parietal cortex, hippocampus, lateral temporal Functions of the default network Sentinel hypothesis – Broadly monitoring the environment→ default network activated – Rare disorder: simultagnosia→ normal visual fields and are able to perceive individual objects, unable to integrate simultaneous information to understand a complex scene The Internal mentation hypothesis – Supports thinking and remembering, like daydreaming – Imaging: state like remembering  Brain structures controlling the default network Posterior cingulate cortex – Connections with medial temporal lobes autobiographical memory Alzheimer’s disease – Related with exploratory behaviour (future) ↑ activation of PCC during this tasks Schizophrenia and OCD Autism  Attention Describe as limited resource or bottleneck in brain processing→ Selective attention Attention driven in 2 ways – Exogenous attention—bottom–up attention Like animal detecting predator stimulus attracts our attention without any cognitive input – Endogenous attention—top–down attention Deliberately directed by the brain Limited capacity of attention – Attention-deficit hyperactivity disorder  Attention-deficit hyperactivity disorder Inattention, hyperactivity and impulsiveness More prevalent in children Potential causes – Anatomical→ prefrontal cortex and basal ganglia smaller in ADHD children – Genetic factors→ dopaminergic pathway – Nongenetic factors→ brain injuries and premature birth Treatment – Behavioural therapy – Psychostimulant drugs Behavioural effects of attention Overt attention vs covert attention Overt attention→ involves orienting the head and the eyes to a stimulus, thereby aligning visual and auditory processing with it and improving perception Covert attention→ involves somehow directing attention to the stimulus without moving the head or the eyes. Attention enhances visual sensitivity→ making things easier to detect Attention speed reaction times Physiological effects of attention Shifting Attention to something Functional MRI Imaging Spotlight of attention (spatial location) – stimulus consisted of patches of vertical and horizontal blue and orange lines arranged into 24 sectors – sequence of four sectors that a subject was cued to attend to – areas of enhanced brain activity move away from the occipital pole as the attended sector moves out from the fovea Brain activity shifts retinotopically Attention to features PET imaging Same–different discrimination task – An image was flashed on a computer screen→ after a delay period→ another image was flashed→ different elements Higher activity in different areas depending on the features’ stimuli – Colour and shape→ Ventromedial occipital cortex – Speed→ Parahippocampal gyrus – Motion→ Parietal cortex  Brain circuits for the control of attention Networks of cortical and subcortical structures involved are distributed across the brain Pulvinar nucleus of the thalamus Projects to many areas of cortex→ most visual cortical areas of the occipital, parietal, and temporal lobes, giving it the potential to modulate widespread cortical activity Regulates visual information flow→ synchronization between neural activity in the pulvinar, area V4, and area IT Frontal eye fields (FEF) Cortical area in frontal lobe Connections between FEF and V2, V3, V4, MT and parietal cortex Saccadic movements FEF neurons→ have motor fields→ small areas in the visual field FEF part of a system→ directing attention and enhancing visual performance Superior colliculus→ similar results Salience and priority maps in the parietal lobe Hypothesis of how certain visual features grab attention – Bottom–up attention – Salience map shows locations of salient features Top–down attentional modulation from cognitive input – Priority map shows locations where attention should be directed Based on stimulus salience and cognitive input Salience and priority maps cortical areas Lateral intraparietal cortex (area LIP) – priority map based on bottom–up and top–down inputs – Guides eye movements and attention Lesions in parietal cortex associated with neglect syndrome Frontoparietal attention network Bottom–up attention – Input from visual areas in the occipital lobe reaches area LIP. – Construction of salience map – Visual processing is enhanced; eyes may move. Top–down attention – Attention effects occur first in frontal and parietal areas. – Priority map in LIP and FEF – Visual processing is enhanced; eyes may move.  Neglect syndrome Deficit in attention to and awareness of one side of the field of vision is observed contralateral to the damaged hemisphere results most commonly from strokes and brain unilateral injury to the right cerebral hemisphere Spatial attention vs Spatial representation Neuropsychological diagnosis (tests) Neuropsychological treatment (prismatic adaptation→goggles that are made of prism wedges that displace the visual field laterally or vertically ) Pharmacological treatment (DA)  Balint’s syndrome Severe neuropsychological impairments – Inability to perceive the visual field as a whole (simultanagnosia) – Difficulty in fixating the eyes (oculomotor apraxia) – Inability to move the hand to a specific object by using vision (optic ataxia) Damage to the parieto-occipital lobes on both sides of the brain Lack of awareness of the syndrome may lead to misdiagnosis Neuropsychological treatment  Consciousness Materialist perspective – Consciousness arises from physical processes – Based on structure and function of nervous system Alternative: dualism – Mind and body are different things. – One cannot be fully explained by the other What is consciousness? Nature of human consciousness problematic – Even defining consciousness is controversial→ many definitions The easy problems of consciousness (David Chalmers, 1995) – Phenomena answerable by scientific methodology – Example: “It is sometimes said that we are conscious of things we pay attention to” The hard problem of consciousness – The experience itself – Why the experience is the way it is  Neural correlates of consciousness Christof Koch and Francis Crick NCC→ The minimal neuronal events sufficient for a specific conscious percept Experimental approach with bistable visual images—changes in neural activity? Binocular rivalry Different images seen by the two eyes – Perceptual awareness alternates Experimentally demonstrated – Neural recordings in monkey area IT show changes correlated with perceptions – Neural activity in IT may be neural correlate of this awareness Rivalry experiments in humans using fMRI to record brain activity – Using rival images of a face and a house – Recording in FFA (faces) and PPA (places) – Produced alternating patterns of brain activity in FFA and PPA Imagining imagery activates same visual processes – Similar results with neuronal probe recording in human subject  Challenges in the Study of Consciousness Small steps succeeding in studying neural correlates of consciousness (NCC) Challenges of interpreting NCC study data – What is “minimal” brain activity sufficient for conscious experience? – Is the neural activity a prerequisite for conscious experience or consequence of the experience but not NCC? – Can attention be confounded with awareness? The “hard problem” of consciousness remains Comatose states Pathological condition related with consciousness Unconscious state by apparent unresponsiveness to sensory stimuli After brain injury Prognosis is uncertain (days→ years) Controversial point of view→ persistent vegetative state EEG and neuro imaging as diagnosis tools