Neuro + Clinical🧠 Flashcards
Development of nervous system
Up to day 20
Zygote divides
Day 4- morula solid ball 16 cells
Day 5- blastocyst separates to two groups, inner cell mass is embryo. Trophoblast (placenta)
Inner cell mass forms two layers: epiblast (embryo) hypoblast (gut)
Day 13-19 gastrulation, groove between epiblast and hypoblast
Ectoderm thickens to form neural plate
Day 20 uneven cell division forms groove, proliferation where neural plate meets ectoderm
Development of nervous system
From day 22
Day 22- neural tube (filled with liquid) becomes ventricles and central canal of spinal cord. Tube differentiates brain structures (neurulation)
Day 24-channel between spinal cord and brain partially closes, fluid pumped in and swells brain at different rates
3-4 weeks- tube bends (cephalon flexure) telencephalic tube grows over to form cerebral cortex. Folds back to form occipital and temporal lobes
6 month- Early gyri and sulci
9 month- same structure as adult
Development of neurons and glial cells
Gastrulation (Day 13-19)
Cells in ectoderm receive chemical signal (noggin) from notochord. Neural stem cells divide and proliferate, precursor neuron produces two other cells:
Primitive neuron (neuroblast) OR glial cell (glioblast) AND another Precursor neuron
Development of neurons and glial cells
Migration
Young neurons lack axons, dendrites and migrate with guidance mechanisms (glial cells)
Radial migration out towards outer wall of tube.
Tangential migration parallel to tube’s walls
When reach target tissue, decide what neuron/glial cell wants to be
Development of neurons and glial cells
Migration- when the cell reaches target tissue
Determined by chemoattractant/ repellant and growth cones
Produce small extensions (neurites) one is axon one is dendrite
Axon navigates to target once specified
Development of neurons and glial cells
Growth cones
Specialised terminals used by axons to find targets
Filopodia (fine processes) and lamellipodia (expansion)
Receptors in sense attractant or repellant chemical. Diffusible agents (chemoattractants/repellents)
Development of neurons and glial cells
Neuron death
Apoptosis- neurons destroy themselves (genetic) active and safe
Necrosis-Passive cell death
Some die if fail to obtain life preserving chemicals supplied by their targets
Postnatal neuroplasticity
Volume of brain quadruples between birth and adulthood (influenced by experience and postnatal wiring)
Synaptogenesis- cortical regions
Myelination- increase speed of atonal conduction. Sensory before motor then prefrontal cortex
Dendritic branching- from deeper to more superficial
Animal experimental studies- postnatal plasticity
Hubel and Wiesel- suture cat eyelid causes increased width of input columns from deprived eye
First 3 months critical period
Monkey 6 month critical period. Tissue not wasted, axons branch into deprived eye
Neuroplasticity in adults case studies
London taxi drivers bigger posterior hippocampus, related to time driving taxis
Late-blind people’s cortex responds to Braille
New neurons are generated in the olfactory bulb and hippocampus. Integrated into synaptic cleft. Newly generated granule cell is contracted by GABAergic synapse
Brain injury
Different types
Congenital- Genetic, affects neurodevelopment
Acquired-traumatic or non traumatic
Traumatic- sudden damage to blood supply, open or closed
Open-skull not intact, fragments cause wider damage
Closed- skull intact, coup and contra coup
Causes of stroke
Cerebral haemorrhage- blood leaks into brain, toxicity means neurons are not fed properly. Avoid strenuous activity, keep low blood pressure
Cerebral ischaemia- blocked blood vessel, affects blood supply to the brain. Caused by plugs (thrombus or emboli)or cardiovascular disease. Lack of oxygen/glucose leads to excitotoxicity and neuron death. Salvageable penumbra by reopening blocked blood vessel
Punch drunk syndrome
Repeated blows to the head, increased likelihood of neurodegenerative diseases
Understanding normal function using damage knowledge
Localisation of function, individual variability
Dopamine related to reward system and inhibitory role
Limitations in distinguishing which areas affect function
Parkinson’s symptoms
Loss of high level cognitive function, disorder of mood
Bradykinesia (slow movements) akinesia (no movement)
Rigidity, tremor (pill rolling) shuffling gait, cues can help movement
Neuropathology of Parkinson’s
Dopamine deficiency (in nigrostriatal dopamine pathway in basal ganglia) causes basal ganglia to be stuck on inhibition
Stops motor cortex communicates to motor system = no movement
Parkinson’s cause evidence
Synthetic heroin-
users developed Parkinson symptoms MPTP unwanted by product converted to MPP+ which targets dopamine producing cells in substantia nigra
Treating Parkinson’s
Lesion- symptoms relieved, not hugely
Levodopa- replace lost dopamine (brain makes from levodopa) side effects can be worse
Drugs- dopamine agonists, cannabis
Electrical stimulation- stops inhibitory output, can adjust since patient is conscious
Replace lost dopamine with stem cells- if early stage
Alzheimer’s symptoms
Changes in brain structure and volume, widespread neuronal loss
Most common cause of dementia
Memory loss, attention deficits, personality changes
Assessed with MMSE
Neuropathology in Alzheimer’s
Loss of acetylcholine
Brain shrinks, enlarged ventricles
Amyloid plaques: clumps of scar tissue (degenerating neurons and beta-amyloid protein)neurofibrillary tangles
Occurs from amyloid precursor protein (APP) cut in wrong place
Alzheimer’s link to Down’s syndrome
By age 40 Down’s syndrome patients develop amyloid plaques and neurofibrillary tangles ( at 21st chromosome location for both conditions)
Genetic risk factors Alzheimer’s
Early onset APP on chromosome 21
Genetic variation in alipoprotein alleles: too much E4 binds to beta-amyloid, developing amyloid plaque
Neurofibrillary tangles- too much Tau (microtubules in cytoskeleton) made from MAPS (microtubule associated proteins)
Parkinson’s animal research
Transplant gene- recreate Parkinson’s characteristics
MPTP had no effect on rats, cats or dogs
Some effects in primates like humans
Alzheimer’s animal research
Transgenic animals (genes implanted) recreates Alzheimer’s Too much APP, TAU and copies of aPOE
Treatments effective in animals but not in humans
Treatment of Alzheimer’s
inhibit cholinesterase to prevent breakdown
Cholinesterase breaks down acetylcholine
Epilepsy
Chronic, temporary changes in electrical function of the brain. Seizures affect awareness, movement and sensation
Idiopathic- no single cause
Auras- symptoms preceding partial seizures e.g. tastes, hallucinations from electrical activity
Partial epilepsy
Simple and complex
Simple- specific area, sensory/motor. Jacksonian seizures (start in arm, spread through body)
Complex-specific area, often restrained to temporal lobe. Diverse effects, compulsive and repetitive motor movements e,g. Chewing
Generalised epilepsy
Grand mal/petit mal
Grand mal- entire brain, lose consciousness, rigidity, extend limbs (tonic) and jerk (cloric)
Petit mal- can begin in many parts of brain, briefly absent, common in children
Epilepsy generalisation
Partial seizure in small specific area but spreads
May be able to remove problematic tissue
Epilepsy in EEG and animals
EEG- High amplitude spikes, synchronised firing
Animal models- inject excitatory agent to rat cortex causes epileptic activity and spreads
Epilepsy treatments
Pharmacological- GABA or Na+ channels dampen excessive neural firing, increase release of inhibitory GABA
Surgery- for drug resistant cases
Neurodegeneration
And types
Neural connections reduce by 50-90%
Anterograde-distal segment
Retrograde-proximal segment
Transneuronal-spreads by synapses
Neurodegeneration white and grey matter
Grey matter volume (cell bodies) decline with age from reduced connections and less support cells (glial)
White matter increases as connections improve, insulated with myelination
Frontal cortex last to be fully insulated
Neural regeneration
Some species regrow limbs but human function is in PNS (damaged neurons) from growth cones
Wiring mixed, need myelin sheath to guide axons
Neural reorganisation
After damage, loses input but cells are still connected (phantom limb syndrome) intact areas expand to take over tissue that lost input
Neurocognitive disorders
Damage/abnormalities in biology that underline thinking and behaviour
Can be caused by disease, trauma or genetic disposition
Deficits in cognitive function, perception and memory, language, executive function. Comorbid with depression and anxiety
Common causes: stroke, Parkinson’s, Alzheimer’s, injury
DSM-5 neurocognitive disorder
Impairment in one cognitive domain
Sufficient for major NCD
Neurocognitive disorders
Amnesia deficits
Inability to learn new info or recall, often damage to hippocampus or temporal lobe
Lack of attention, well learnt activities performed slower. Difficulty conversing
Frontal and parietal regions implicated, extends to subcortical regions
Neurocognitive disorders
Language deficits: Aphasia
Difficulty producing or comprehending speech, struggle to imitate or produce complex words
Broca’s: speech production affected, good comprehension but difficulty selecting words (anomia)
Wernicke’s: understanding words affected. Poor retrieval. Structurally intact speech but meaningless
Neurocognitive disorders
Deficits in visuo-perceptual functioning: agnosia
Inability to process sensory information due to neural insult
Faces, music, movement (inability to recognise)
Neurocognitive disorders
Motor deficit: apraxia
Loss of ability to execute learned movements despite desire/ability to do so. May perform routine behaviour or be domain specific
Deficits in executive function
Associated with prefrontal cortex, often expressed as poor judgement, inappropriate behaviour or erratic mood swings
Major NCDs
Substantial cognitive impairment, requires assistance
Significant deterioration in at least one domain
Interferes with self reliance in activities
Minor NCDs
Moderate cognitive impairment
Requires some assistance
Deterioration in at least one domain, doesn’t interfere with self-reliance in activities
Neurocognitive disorders
Process of help
Determine nature of deficits, location of neural insult
Provide info about onset, type and severity
Discriminate neural and psychiatric symptoms
Focus for rehab
Neurocognitive disorders difficulties in diagnosis
Symptoms often resemble other psychopathologies
Psychological problems also have cognitive decline
Symptom overlap, age as common risk factor
Closed head trauma may produce memory deficits resembling Alzheimer’s
Rehabilitation for neurocognitive disorders
Restore cognitive/developmental functions
Develop new skills
Therapy for comorbid disorders
Skills to structure living environment to accommodate cognition changes
Neurocognitive disorders
Biological treatments
Drugs-stabilise or slow degenerative disorders
Deep brain stimulation-blocks abnormal nerve signals to stabilise
Can improve quality of life but limited long term efficacy, masks symptoms. Side effects
Neurocognitive disorders
Cognitive rehabilitation
Extended practice of task with feedback or assistive technology
Holistic rehab addresses multiple aspects of dysfunction
Interventions for visuo-perceptual deficits: agnosia
Tracking and scanning movements, react to moving images
Compensatory strategies assist in recognition
Interventions for apraxia (struggle to learn movements)
Gestural training
Recognise gestures and postures to context
Demonstrate use of object, mimic
Train in virtual reality
Interventions for language deficits :aphasia
Speech therapy, production/comprehension
Practitioner and computerised therapy
Constraint induced movement therapy- practice verbal responses without gesturing
Group communication treatment- initiate communication through any means
Interventions for memory deficits
Compensatory strategies e.g. labelling objects, diary
Pagers for prompts (may be unsuitable for aged)
Visual imagery mnemonics
Interventions for executive function impairments
Specific interventions for planning
Goal management training, problem solving to sustain attention and goals
Neurocognitive disorders tests and assessments
Wechsler adult intelligence scale IV-aggregate scales for verbal comprehension, working memory, source of deficits, stage deficits emerged at
Trail-making task- quicker and more specific. Connect circles by alternating between letters and numbers. Evaluate processing speed, visual scanning
Biopsychology of emotion (Darwin)
Emotions displayed in living species, similar facial expressions in animals and humans
If beneficial evolves to enhance communication
Opposite signals: submissions different from aggression to be distinguished
Physiological theories of emotion
James-Lange theory
Stimuli-activates cortex-physiological arousal (automatic)-emotion is activated in physiology
Body not brain
Physiological theories of emotion
Cannon-Bard theory
Emotions from brain not body
Thalamus/hypothalamus generate emotion, cortex inhibits emotion
Emotional stimuli: physiological arousal and emotion work independently
Physiological theories of emotion Modern theory (two factor theory )
Use cognition to decide if stimulus is good/ bad when physiologically aroused
Facial feedback hypothesis
Autonomic system
Similar nervous system patterns for emotions, expressions influence our emotions
Fear
Easiest to infer, eyes open to take in info
Clenched muscles to run, motivated to avoid danger
Defensive behaviours
Fear conditioning
Conditioned stimulus + unconditioned stimulus = conditioned response
Little Albert- Rat elicits fear without loud bang
Fear and amygdala
Assess emotional significance of stimulus based on previous experience
Threatening sound alerts thalamus, auditory cortex and Amygdala
Amygdala alerts hypothalamus for sympathetic response
Amygdala alerts periacquiductal grey for behavioural response
Kluver-Bucy monkeys and fear
Anterior temporal lobes removed
Decreased emotional reaction, hyper-sexuality, no fear
Patient SM and fear
Bilateral amygdala destruction
No fear, can’t recognise fear expression
Brain mechanisms in emotion
Limbic system- Emotional processing
Hypothalamus-sends signals to the cortex, enabling us to respond
Hippocampus-learning and memory
Watching someone feel an emotion can make own corresponding brain areas light up
Valence model
Right hemisphere specialised for processing negative emotion . Left hemisphere is specialised for positive
Left side more expressive when smiling
Stress
Mental, physical, emotional and behavioural reactions to demands or threats.
Unusual demand depends how stressors is perceived
Can cause adaptation (healthy) or inability to cope
Historically needed to be adaptive and survive attacks
Stress short term
Anterior pituitary activated
ATCH secreted
Adrenal cortex releases glucocorticoids (cortisol)
Sympathetic nervous system
Adrenal medulla
Noradrenaline and adrenaline released
4 types of stress
Positive- brief increase in heart rate, mild stress hormone elevation. Energy to meet goal
Tolerable-temporary but has supportive relationships, boosts immune system
Toxic- prolonged activation of stress respond, no supportive relationships
Long term- affects body, mind, emotion, behaviour, can lead to depression and anxiety
Stress and the immune system
The two responses
Adaptive immune response- SLOWER Less lymphocytes when stressed, illness increases
Immune innate response- FASTER, non specific. Phagocytes eat pathogen. Triggers inflammation which causes long term health problems. Body attacks self
Specific phobias
Fear or anxiety about a specific object or situation
Avoidance to minimise contact, fight or flight psychological effects, aware of excessive fear
Phobia beliefs- maintain fear and avoidance
Types of phobias
Animal Natural environment Blood-injection Situational Other
Phobias DSM 5
Disproportionate fear to specific object or situation
Actively avoid phobic stimulus
Significant distress in important areas of functioning
Phobias psychoanalytic account-Freud
Defence anxiety =phobia
Id repressed from fear
Fear extended to external events, avoid conflict inside
Phobias classical conditioning Little Albert
Negatives
Learned behaviour, pair stimuli with outcomes
Not all phobias linked to trauma/develop into a phobia
More things likely to be scared
Incubation- fear not from successive encounters
Phobias multiple pathways
Some direct trauma, others emotional
High disgust sensitivity= small animal phobia
Disease avoidance model (prevent illness)
Phobias cognitive theory
and criticism
attentional bias to threat relevant info
Unclear if fear or bias came first
Biological account phobias
(Preparedness theory)
Positives and negatives
Pre-wired to develop phobias for life threatening objects
Avoid hazards that threatened our ancestors
More likely phobia of snake than flowers in conditioning. Amygdala relays signals to sympathetic system (fight/flight)
fMRI individual’s subjective response is correlated to amygdala
Post hoc though, no evidence what was a threat
Phobia interventions
Exposure therapy- triggers cognitions and psychological response
Increase exposure to stimuli in fear hierarchy, address avoidance strategies
PTSD
Types of trauma experienced
Experienced trauma prior to symptoms (not all develop)
Traumatic event (self or close family)
Exposure to traumatic details e,g, police
PTSD DSM-5
Exposure- direct/witness
Intrusive- flashbacks/dreams
Avoid external or interval cues
Mood/cognition change-less interest activity
Increased reactivity- hyper-vigilance to cue
PTSD biological predisposition
May have underdeveloped hippocampus (emotional memories)
Failure to control amygdala to appropriate response
Genetically heightened startle response, endocrine secretion
PTSD vulnerability factors
Personal responsibility felt
Developmental- unstable family life during early childhood
Family history of PTSD
Existing high anxiety and mental defeat (sees self as victim)
Low IQ, worse coping strategies
PTSD dissociation
Avoidance strategy
Distance self from trauma, risk of chronic PTSD
PTSD conditioning theory
Avoid cues that trigger it
Store memories from event differently (emotional processing theory)
Cues override those of everyday life
PTSD dual representation theory
Situationally accessible memory
Sensory channels not consciously processed, sounds and smells can trigger other memories
PTSD interventions
Debriefing
Discuss trauma, treat developing symptoms soon after event
Reassure people they are normal and event was abnormal
Discuss feelings of event
Graded exposure: detailed narrative, computer generated images, visualise trauma related scene
PTSD interventions
Cognitive restructuring
Target dysfunctional thoughts and beliefs which maintains PTSD
Believe they are incompetent and world is dangerous
OCD
Obsessions- intrusive and recurring found disturbing and uncontrollable
Compulsions- relieve obsessive thoughts, repetitive or ritualised behaviour driven to perform. Reinforces obsession
OCD DSM 5
Obsessions and compulsions
Believe behaviour will prevent bad event
Obsessions and compulsions hinder other functions
OCD biological factors
Genetic, high monozygotic twin concordance
May be neuropsychological deficit
Traumatic brain injury can lead to OCD
OCD and memory
Memory deficits, less confidence in memory
Deficit in ability to distinguish real/imagined actions
OCD clinical constructs
Linking thoughts, beliefs and cognitive processes to symptoms
Inflated responsibility- causes anxiety
Thought action fusion-suppression/anxiety
Mental contamination- feel dirty from intrusive thoughts
OCD thought suppression
Try to suppress distressing thoughts but causes more intrusive thoughts
OCD interventions
Graded exposure and ritual prevention-exposed to situation they avoid. Show no bad outcomes, reduces anxiety. Habituate links between obsessions and distress
CBT- challenge responsibility appraisals, show over importance of thoughts, exaggerated perception of threat
SSRIs- increase serotonin but may only work if comorbid depression
Neurosurgical treatments- destroy cells in cingulum if severe
Generalised anxiety disorder
Worry about things, future and uncertainty. Chronic and uncontrollable, upsetting and stressful, disrupts life
Catastrophising- single fact to the extreme
GAD DSM 5
Worry almost everyday at least 6 months
Restless and muscle tension
Avoid events with negative outcomes, reassurance seeking
Anxiety relates to at least two areas of activity
GAD biological theories
Inherited vulnerability to anxiety disorders
Higher amygdala response
GAD environmental factors
Negative life events=lack of stability
Feel rejected by parents or over controlled, model anxious parents
GAD cognitive biases
Hyper vigilant, seek things going wrong so can never relax. Less attention to positive stimulus, events interpreted as threatening and challenging
GAD interventions
Pharmacological
Benzodiazepines-stimulate GABA to dampen excitatory effect, causing relaxation
Beta blocker- block effect of adrenaline, dampen stress response
SSRIs- antidepressants
GAD interventions
Stimulus control treatment and CBT
SCT- Conditioning principle. Environments where anxiety occurs is linked. Limit worry to specific time/location
CBT- Target maladaptive cognitions, self monitoring
Relaxation training, cognitive restructuring challenges bias and behavioural rehearsal forms coping strategies
Panic disorder
Repeated panic or anxiety attacks
Heart palpitations, perspiring, dizziness
Activated sympathetic nervous system
Recurrent and unexpected, failure to regulate
Panic disorder DSM 5
Spontaneous/unpredictable and recurrent
Worry about further panic attacks
Modify behaviours to avoid future attacks
Hyperventilation
Dysfunctional breathing, oxygen delivered less efficiently to blood. Lowered pressure of carbon dioxide changes pH level
Heart pumps faster, symptoms show, apprehension about it and repeat
Panic disorder cognitive model
Clarke’s panic cycle
Misinterpret body sensations as threatening leads to apprehension
Panic disorder intervention
CBT- recognise cause of trigger, restrictive maladaptive beliefs and teach about flight or fight response
Drugs- b blockers, SSRIS, benzodiazepines
Social anxiety disorders
Triggered in social situations, fear, embarrassment or negative evaluation. Cannot cope with anxiety
Social anxiety disorder DSM 5
Distinct feat of social interactions and how they will be evaluated
Avoidance strategies, intense fear and anxiety
Last more than 6 months, significant distress and difficulty performing social or occupational activities
Social anxiety disorder biological factors
Increased vulnerability Inhibited temperament (personality type)
Social anxiety disorder cognitive model (before, at event, after)
BEFORE: existing negative belief about self, negative automatic thought of situation, physical anxiety symptoms (sympathetic) can lead to avoidance
AT EVENT: focus on self and how appear, increase physical symptoms, safety behaviours, try to retreat
AFTER: Negative thoughts, self evaluation, self doubt
Social anxiety disorder interventions
CBT-Build rapport, brief client, target factors maintaining disorder
Role play to identify safety behaviours to remove, focus on external situation rather than internal response
Social skill training and confidence building
Test fears and challenge (exposure) did outcome really occur?
Depression symptoms
Loss of capacity to experience pleasure (anhedonia)
Maladaptive thoughts, inability to function and uphold daily life
Affected sleep, suicidal thoughts, worthlessness
Lasts for 2 weeks or longer
Cognitive-difficulty concentrating or making decisions
Behavioural- social withdrawal and agitation
Physical-insomnia or hypersomnia
Mood-worthless or guilty
DSM 5 depression
At least 5: Depressed mood most of time Loss of interest, enjoyment Insomnia/excessive sleep, fatigue and lack of energy Worthless, guilt Lack of concentration, decision making Suicidal thoughts, attempts
Major depressive disorder and dysthymic disorder
Major depressive disorder- not an expected reaction to
bereavement or other disorders
Dysthymic disorder-depressed mood most of time for 2 years
4 subtypes of depression
Reactive depression- obvious trigger e.g. loss of job
Endogenous depression-no obvious trigger, bereavement previously excluded
Unipolar-extended periods of clinical depression, cause significant distress and impairment
Bipolar-periods of mania with depression. Type 1 loss of clarity and racing thoughts p. Type 2 (Hypomania) milder form of mania
Causes of depression (genetic, environment, diathesis)
Genetic- MZ 39% concordance DZ 27% concordance
Environmental- severe stress previous year 84% depressed
Diathesis- predisposed risk, stress in environment causes. Depression heritability about 50%
Depression pharmacological treatments
Monoamineoxidase (MAO) inhibitors
Ipromiazid- failed to treat tuberculosis but effective for depression. Increases monoamines by inhibiting MAO.
More noradrenaline and serotonin
Side effects- cheese effect blood pressure increases with cheese and wine. Tyramine (amine) normally broken down by MAO in liver
Depression pharmacological treatments
Tricyclic antidepressants, SSRIs and Lithium
Tricyclic- Imipramine blocks reputable of serotonin and noradrenaline, more in synapse
SSRIs- Prozac acts on serotonin alone, blocks reputable leaving more in synaptic cleft. Fewer side effects than tricyclic/ MAO inhibitors
Lithium- bipolar, relief from manic/depressive episodes
Monoamine theory of depression
Evidence
Antidepressants act on monoamines
Depression=deficit in monoamine neurotransmission
Some evidence elevated receptors in depressed patients (compensate for low levels of transmission) compensatory increase in receptors
Monoamine neurotransmitters could over activate the amygdala
Depression cognitive theory
Beck’s negative triad
Negative views of the world- future-self
Negative schemas and cognitive biases, self fulfilling prophecies of failure
Depression learned helplessness (Seligman)
Research
All experience unavoidable negative events
Creates cognitive set, learn to become helpless and depressed
Dogs who couldn’t avoid electric shock lay down and whined
Battered woman syndrome, behave powerless
Seligman attribution model
Causes of negative events-
Internal vs external (blame self)
Global vs specific (everything bad)
Stable vs unstable (always bad)
Rumination (depression)
Seek explanations for experiences. Predicts onset of depressive episodes. Driven by metacognitive belief that rumination resolves depression
Depression interventions
Cognitive
CBT- Identify negative thoughts, dysfunctional/irrational and replace with more adaptive thoughts. Monitor
Depression treatment evaluation
Expensive psychological treatments, has to engage
Drugs inexpensive but side effects
Both better than placebo for % responding to treatment
May be more effective together
Significance of sleep
Amount of sleeping suggests it has significant biological function (each cycle about 90 mins)
Sleep stages
Beta to alpha
Stage 1- wakefulness to sleep (theta) muscles still active, gentle eye rolling. High frequency
Stage 2-3- (theta and delta) deeper sleep, lower frequency and higher amplitude. K complexes (large negative waves followed by large positive)sleep spindles (quick wave burst)
Stage 4- deepest stage, reached in less than an hour, continues up to half an hour. High amplitude, mostly delta. Retreat back to stage one
REM sleep and dreams
EEG looks like an awake person. Increased wave frequency seen in autistic people
Story-like dreams, run in real time and can incorporate external stimuli, most dreams remembered.
NREM dreams
Isolated experiences such as falling. More prevalent than assumed, sleep walking and talking (slow wave)
Freud dreams
Manifest dreams-what we experience
Latent dreams-underlying meaning
No evidence
Measuring sleep
Muscle movements EMG
Eye movements EOG
Brain activity EEG
Activation synthesis (dreams)
Info supplied to cortex during REM is random, cortex tried to make sense of brain activity
Sleep deprivation in animals
All mammals and birds sleep, not higher order function. Not necessarily needed in large quantities. No relationship between sleep time and activity level
Experimental rat dunked in water when sleeping died after several days, extreme stress vs yoked rat. Difficult to separate effects of stressors from
effects of lost sleep
Reticular formation
Found in centre of pons, faster rhythm than circadian
BRAC 90 mins
Sleep deprivation in humans
3/4 less hour sleep=increased sleepiness. Fall asleep quicker, negative effect on mood, poor attention
Executive function: assimilation, lateral thought and reference memory affected
2-3 days continuous sleep deprivation=microsleeps (short second naps) less responsive to external stimuli
REM sleep deprivation
When woken each time REM occurs
REM rebound-more time spent in REM after deprivation. Proceed to REM more rapidly with more deprivation so have to be woken more on later days in experiment
Default theory of REM sleep
Support for this
Difficult to stay in NREM so brain switches to wakefulness (if needs to take care of body)or switch to REM to prepare for wakefulness
REM blocking drugs cause periods of wakefulness, no sleepiness or REM rebound when REM sleepers woken for 15 mins
Efficient sleep from deprivation evidence
More slow wave sleep (restorative) same amount as long sleepers
Naps without slow wave sleep do not decrease duration of sleep at night
Gradual reductions in sleep time lead to decreases in stages 1 and 2
Little sleepiness produced with repeated REM awakenings unlike slow wave sleep
Theories of why we sleep
Recuperation and adaptation
Recuperation theories- restores homeostasis, energy levels and clear toxins (beta amyloid)
Adaptation theories-sleep 24 hour timing mechanism, sleep at night to keep safe from dangers
Circadian rhythms and sleep
Sleep and wakefulness 24 hour
Endogenous but entrained by zeitgebers to adapt to environment
Sleep brain regions
Thalamus- homeostasis and circadian rhythms
Suprachiasmatic nucleus-Linked to retinohypothalamus tract (reacts to light)
Reticular formation- interconnected nuclei in brain stem produces wakefulness. Electrical stimulation here causes desynchronisation
OCD Perseverance and role of mood
Mood stop action when shows task is completed
