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YEAR 1 Semester 2👩🏼‍🎓 > Neuro + Clinical🧠 > Flashcards

Neuro + Clinical🧠 Flashcards

1
Q

Development of nervous system

Up to day 20

A

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

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2
Q

Development of nervous system

From day 22

A

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

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3
Q

Development of neurons and glial cells

Gastrulation (Day 13-19)

A

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
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4
Q

Development of neurons and glial cells

Migration

A

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

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5
Q

Development of neurons and glial cells

Migration- when the cell reaches target tissue

A

Determined by chemoattractant/ repellant and growth cones

Produce small extensions (neurites) one is axon one is dendrite
Axon navigates to target once specified

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6
Q

Development of neurons and glial cells

Growth cones

A

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)

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7
Q

Development of neurons and glial cells

Neuron death

A

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

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8
Q

Postnatal neuroplasticity

A

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

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9
Q

Animal experimental studies- postnatal plasticity

A

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

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10
Q

Neuroplasticity in adults case studies

A

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

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11
Q

Brain injury

Different types

A

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

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12
Q

Causes of stroke

A

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

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13
Q

Punch drunk syndrome

A

Repeated blows to the head, increased likelihood of neurodegenerative diseases

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14
Q

Understanding normal function using damage knowledge

A

Localisation of function, individual variability
Dopamine related to reward system and inhibitory role
Limitations in distinguishing which areas affect function

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15
Q

Parkinson’s symptoms

A

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

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16
Q

Neuropathology of Parkinson’s

A

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

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17
Q

Parkinson’s cause evidence

A

Synthetic heroin-
users developed Parkinson symptoms MPTP unwanted by product converted to MPP+ which targets dopamine producing cells in substantia nigra

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18
Q

Treating Parkinson’s

A

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

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19
Q

Alzheimer’s symptoms

A

Changes in brain structure and volume, widespread neuronal loss
Most common cause of dementia
Memory loss, attention deficits, personality changes
Assessed with MMSE

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20
Q

Neuropathology in Alzheimer’s

A

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

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21
Q

Alzheimer’s link to Down’s syndrome

A

By age 40 Down’s syndrome patients develop amyloid plaques and neurofibrillary tangles ( at 21st chromosome location for both conditions)

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22
Q

Genetic risk factors Alzheimer’s

A

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)

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23
Q

Parkinson’s animal research

A

Transplant gene- recreate Parkinson’s characteristics
MPTP had no effect on rats, cats or dogs
Some effects in primates like humans

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24
Q

Alzheimer’s animal research

A 
Transgenic animals (genes implanted) recreates Alzheimer’s 
Too much APP, TAU and copies of aPOE

Treatments effective in animals but not in humans

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25
Q

Treatment of Alzheimer’s

A

inhibit cholinesterase to prevent breakdown

Cholinesterase breaks down acetylcholine

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26
Q

Epilepsy

A

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

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27
Q

Partial epilepsy

Simple and complex

A

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

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28
Q

Generalised epilepsy

Grand mal/petit mal

A

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

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29
Q

Epilepsy generalisation

A

Partial seizure in small specific area but spreads

May be able to remove problematic tissue

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30
Q

Epilepsy in EEG and animals

A

EEG- High amplitude spikes, synchronised firing

Animal models- inject excitatory agent to rat cortex causes epileptic activity and spreads

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31
Q

Epilepsy treatments

A

Pharmacological- GABA or Na+ channels dampen excessive neural firing, increase release of inhibitory GABA

Surgery- for drug resistant cases

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32
Q

Neurodegeneration

And types

A

Neural connections reduce by 50-90%

Anterograde-distal segment
Retrograde-proximal segment
Transneuronal-spreads by synapses

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33
Q

Neurodegeneration white and grey matter

A

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

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34
Q

Neural regeneration

A

Some species regrow limbs but human function is in PNS (damaged neurons) from growth cones
Wiring mixed, need myelin sheath to guide axons

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35
Q

Neural reorganisation

A

After damage, loses input but cells are still connected (phantom limb syndrome) intact areas expand to take over tissue that lost input

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36
Q

Neurocognitive disorders

A

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

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37
Q

DSM-5 neurocognitive disorder

A

Impairment in one cognitive domain

Sufficient for major NCD

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38
Q

Neurocognitive disorders

Amnesia deficits

A

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

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39
Q

Neurocognitive disorders

Language deficits: Aphasia

A

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

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40
Q

Neurocognitive disorders

Deficits in visuo-perceptual functioning: agnosia

A

Inability to process sensory information due to neural insult

Faces, music, movement (inability to recognise)

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41
Q

Neurocognitive disorders

Motor deficit: apraxia

A

Loss of ability to execute learned movements despite desire/ability to do so. May perform routine behaviour or be domain specific

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42
Q

Deficits in executive function

A

Associated with prefrontal cortex, often expressed as poor judgement, inappropriate behaviour or erratic mood swings

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43
Q

Major NCDs

A

Substantial cognitive impairment, requires assistance
Significant deterioration in at least one domain
Interferes with self reliance in activities

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44
Q

Minor NCDs

A

Moderate cognitive impairment
Requires some assistance
Deterioration in at least one domain, doesn’t interfere with self-reliance in activities

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45
Q

Neurocognitive disorders

Process of help

A

Determine nature of deficits, location of neural insult
Provide info about onset, type and severity
Discriminate neural and psychiatric symptoms
Focus for rehab

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46
Q

Neurocognitive disorders difficulties in diagnosis

A

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

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47
Q

Rehabilitation for neurocognitive disorders

A

Restore cognitive/developmental functions
Develop new skills
Therapy for comorbid disorders
Skills to structure living environment to accommodate cognition changes

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48
Q

Neurocognitive disorders

Biological treatments

A

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

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49
Q

Neurocognitive disorders

Cognitive rehabilitation

A

Extended practice of task with feedback or assistive technology
Holistic rehab addresses multiple aspects of dysfunction

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50
Q

Interventions for visuo-perceptual deficits: agnosia

A

Tracking and scanning movements, react to moving images

Compensatory strategies assist in recognition

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51
Q

Interventions for apraxia (struggle to learn movements)

A

Gestural training
Recognise gestures and postures to context
Demonstrate use of object, mimic
Train in virtual reality

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52
Q

Interventions for language deficits :aphasia

A

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

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53
Q

Interventions for memory deficits

A

Compensatory strategies e.g. labelling objects, diary
Pagers for prompts (may be unsuitable for aged)
Visual imagery mnemonics

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54
Q

Interventions for executive function impairments

A

Specific interventions for planning

Goal management training, problem solving to sustain attention and goals

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55
Q

Neurocognitive disorders tests and assessments

A

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

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56
Q

Biopsychology of emotion (Darwin)

A

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

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57
Q

Physiological theories of emotion

James-Lange theory

A

Stimuli-activates cortex-physiological arousal (automatic)-emotion is activated in physiology
Body not brain

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58
Q

Physiological theories of emotion

Cannon-Bard theory

A

Emotions from brain not body
Thalamus/hypothalamus generate emotion, cortex inhibits emotion

Emotional stimuli: physiological arousal and emotion work independently

59
Q 
Physiological theories of emotion 
Modern theory (two factor theory )
A

Use cognition to decide if stimulus is good/ bad when physiologically aroused

60
Q

Facial feedback hypothesis

A

Autonomic system

Similar nervous system patterns for emotions, expressions influence our emotions

61
Q

Fear

A

Easiest to infer, eyes open to take in info
Clenched muscles to run, motivated to avoid danger
Defensive behaviours

62
Q

Fear conditioning

A

Conditioned stimulus + unconditioned stimulus = conditioned response
Little Albert- Rat elicits fear without loud bang

63
Q

Fear and amygdala

A

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

64
Q

Kluver-Bucy monkeys and fear

A

Anterior temporal lobes removed

Decreased emotional reaction, hyper-sexuality, no fear

65
Q

Patient SM and fear

A

Bilateral amygdala destruction

No fear, can’t recognise fear expression

66
Q

Brain mechanisms in emotion

A

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

67
Q

Valence model

A

Right hemisphere specialised for processing negative emotion . Left hemisphere is specialised for positive

Left side more expressive when smiling

68
Q

Stress

A

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

69
Q

Stress short term

A

Anterior pituitary activated
ATCH secreted
Adrenal cortex releases glucocorticoids (cortisol)

Sympathetic nervous system
Adrenal medulla
Noradrenaline and adrenaline released

70
Q

4 types of stress

A

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

71
Q

Stress and the immune system

The two responses

A

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

72
Q

Specific phobias

A

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

73
Q

Types of phobias

A 
Animal 
Natural environment 
Blood-injection 
Situational
Other
74
Q

Phobias DSM 5

A

Disproportionate fear to specific object or situation
Actively avoid phobic stimulus
Significant distress in important areas of functioning

75
Q

Phobias psychoanalytic account-Freud

A

Defence anxiety =phobia
Id repressed from fear
Fear extended to external events, avoid conflict inside

76
Q

Phobias classical conditioning Little Albert

Negatives

A

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

77
Q

Phobias multiple pathways

A

Some direct trauma, others emotional

High disgust sensitivity= small animal phobia
Disease avoidance model (prevent illness)

78
Q

Phobias cognitive theory

and criticism

A

attentional bias to threat relevant info

Unclear if fear or bias came first

79
Q

Biological account phobias
(Preparedness theory)
Positives and negatives

A

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

80
Q

Phobia interventions

A

Exposure therapy- triggers cognitions and psychological response
Increase exposure to stimuli in fear hierarchy, address avoidance strategies

81
Q

PTSD

Types of trauma experienced

A

Experienced trauma prior to symptoms (not all develop)
Traumatic event (self or close family)
Exposure to traumatic details e,g, police

82
Q

PTSD DSM-5

A

Exposure- direct/witness
Intrusive- flashbacks/dreams
Avoid external or interval cues
Mood/cognition change-less interest activity
Increased reactivity- hyper-vigilance to cue

83
Q

PTSD biological predisposition

A

May have underdeveloped hippocampus (emotional memories)
Failure to control amygdala to appropriate response
Genetically heightened startle response, endocrine secretion

84
Q

PTSD vulnerability factors

A

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

85
Q

PTSD dissociation

A

Avoidance strategy

Distance self from trauma, risk of chronic PTSD

86
Q

PTSD conditioning theory

A

Avoid cues that trigger it
Store memories from event differently (emotional processing theory)
Cues override those of everyday life

87
Q

PTSD dual representation theory

A

Situationally accessible memory

Sensory channels not consciously processed, sounds and smells can trigger other memories

88
Q

PTSD interventions

Debriefing

A

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

89
Q

PTSD interventions

Cognitive restructuring

A

Target dysfunctional thoughts and beliefs which maintains PTSD
Believe they are incompetent and world is dangerous

90
Q

OCD

A

Obsessions- intrusive and recurring found disturbing and uncontrollable

Compulsions- relieve obsessive thoughts, repetitive or ritualised behaviour driven to perform. Reinforces obsession

91
Q

OCD DSM 5

A

Obsessions and compulsions
Believe behaviour will prevent bad event
Obsessions and compulsions hinder other functions

92
Q

OCD biological factors

A

Genetic, high monozygotic twin concordance
May be neuropsychological deficit
Traumatic brain injury can lead to OCD

93
Q

OCD and memory

A

Memory deficits, less confidence in memory

Deficit in ability to distinguish real/imagined actions

94
Q

OCD clinical constructs

A

Linking thoughts, beliefs and cognitive processes to symptoms

Inflated responsibility- causes anxiety
Thought action fusion-suppression/anxiety
Mental contamination- feel dirty from intrusive thoughts

95
Q

OCD thought suppression

A

Try to suppress distressing thoughts but causes more intrusive thoughts

96
Q

OCD interventions

A

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

97
Q

Generalised anxiety disorder

A

Worry about things, future and uncertainty. Chronic and uncontrollable, upsetting and stressful, disrupts life
Catastrophising- single fact to the extreme

98
Q

GAD DSM 5

A

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

99
Q

GAD biological theories

A

Inherited vulnerability to anxiety disorders

Higher amygdala response

100
Q

GAD environmental factors

A

Negative life events=lack of stability

Feel rejected by parents or over controlled, model anxious parents

101
Q

GAD cognitive biases

A

Hyper vigilant, seek things going wrong so can never relax. Less attention to positive stimulus, events interpreted as threatening and challenging

102
Q

GAD interventions

Pharmacological

A

Benzodiazepines-stimulate GABA to dampen excitatory effect, causing relaxation
Beta blocker- block effect of adrenaline, dampen stress response
SSRIs- antidepressants

103
Q

GAD interventions

Stimulus control treatment and CBT

A

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

104
Q

Panic disorder

A

Repeated panic or anxiety attacks
Heart palpitations, perspiring, dizziness
Activated sympathetic nervous system
Recurrent and unexpected, failure to regulate

105
Q

Panic disorder DSM 5

A

Spontaneous/unpredictable and recurrent
Worry about further panic attacks
Modify behaviours to avoid future attacks

106
Q

Hyperventilation

A

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

107
Q

Panic disorder cognitive model

Clarke’s panic cycle

A

Misinterpret body sensations as threatening leads to apprehension

108
Q

Panic disorder intervention

A

CBT- recognise cause of trigger, restrictive maladaptive beliefs and teach about flight or fight response

Drugs- b blockers, SSRIS, benzodiazepines

109
Q

Social anxiety disorders

A

Triggered in social situations, fear, embarrassment or negative evaluation. Cannot cope with anxiety

110
Q

Social anxiety disorder DSM 5

A

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

111
Q

Social anxiety disorder biological factors

A 
Increased vulnerability
Inhibited temperament (personality type)
112
Q

Social anxiety disorder cognitive model (before, at event, after)

A

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

113
Q

Social anxiety disorder interventions

A

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?

114
Q

Depression symptoms

A

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

115
Q

DSM 5 depression

A 
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
116
Q

Major depressive disorder and dysthymic disorder

A

Major depressive disorder- not an expected reaction to
bereavement or other disorders

Dysthymic disorder-depressed mood most of time for 2 years

117
Q

4 subtypes of depression

A

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

118
Q

Causes of depression (genetic, environment, diathesis)

A

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%

119
Q

Depression pharmacological treatments

Monoamineoxidase (MAO) inhibitors

A

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

120
Q

Depression pharmacological treatments

Tricyclic antidepressants, SSRIs and Lithium

A

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

121
Q

Monoamine theory of depression

Evidence

A

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

122
Q

Depression cognitive theory

Beck’s negative triad

A

Negative views of the world- future-self

Negative schemas and cognitive biases, self fulfilling prophecies of failure

123
Q

Depression learned helplessness (Seligman)

Research

A

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

124
Q

Seligman attribution model

A

Causes of negative events-

Internal vs external (blame self)
Global vs specific (everything bad)
Stable vs unstable (always bad)

125
Q

Rumination (depression)

A

Seek explanations for experiences. Predicts onset of depressive episodes. Driven by metacognitive belief that rumination resolves depression

126
Q

Depression interventions

Cognitive

A

CBT- Identify negative thoughts, dysfunctional/irrational and replace with more adaptive thoughts. Monitor

127
Q

Depression treatment evaluation

A

Expensive psychological treatments, has to engage
Drugs inexpensive but side effects
Both better than placebo for % responding to treatment
May be more effective together

128
Q

Significance of sleep

A

Amount of sleeping suggests it has significant biological function (each cycle about 90 mins)

129
Q

Sleep stages

A

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

130
Q

REM sleep and dreams

A

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.

131
Q

NREM dreams

A

Isolated experiences such as falling. More prevalent than assumed, sleep walking and talking (slow wave)

132
Q

Freud dreams

A

Manifest dreams-what we experience
Latent dreams-underlying meaning

No evidence

133
Q

Measuring sleep

A

Muscle movements EMG
Eye movements EOG
Brain activity EEG

134
Q

Activation synthesis (dreams)

A

Info supplied to cortex during REM is random, cortex tried to make sense of brain activity

135
Q

Sleep deprivation in animals

A

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

136
Q

Reticular formation

A

Found in centre of pons, faster rhythm than circadian

BRAC 90 mins

137
Q

Sleep deprivation in humans

A

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

138
Q

REM sleep deprivation

A

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

139
Q

Default theory of REM sleep

Support for this

A

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

140
Q

Efficient sleep from deprivation evidence

A

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

141
Q

Theories of why we sleep

Recuperation and adaptation

A

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

142
Q

Circadian rhythms and sleep

A

Sleep and wakefulness 24 hour

Endogenous but entrained by zeitgebers to adapt to environment

143
Q

Sleep brain regions

A

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

144
Q

OCD Perseverance and role of mood

A

Mood stop action when shows task is completed

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