Week 22

Question 1

Major depressive disorder

Answer 1

• intense, prolonged feelings of sadness, lack of motivation and heaviness, having lack of energy, concentration and sleep problems
• the absence of happiness appears to be a more reliable symptom than an increase in sadness
• depressed patients react normally to sad or distressing images but rarely smile at the comical ones
• behavioural symptoms: depressed people are usually less active
• cognitive symptoms: negative self-view; extremely pessimistic; feeling of helplessness
• physical symptoms: frequent headaches, indigestion, constipation, dizziness and general pain; disturbed sleep and appetite
• more common to have periods of normal mood than to have long-term episodes of depression
• general argument that the brain learns how to be depressed and gets better at this over time and the more often you experience an episode, the easier it is to have another one –> basically early treatment is the best option

Question 2

Genetics of depression

Answer 2

• moderate degree of heritability but no one gene shows a strong link to depression
• genetic link could be masked by different onset types: early onset (before age of 30) - 40-50% of other relatives with depression/mental health disorders vs late onset (after age of 45) - high probability of relatives with circulatory problems

Question 3

Serotonin uptake transporter gene

Answer 3

• regulates the ability of axons to reabsorb serotonin after its release
• influence of a stressful environmental effect occurring on developing depression: for people with two long forms of this transporter gene, the environment had a minor impact
• short forms of the gene showed a marked environmental effect on the probability of developing depression
• however, this is very subjective and study did not account for the severity of the stress experienced from each event
• also the same gene increases emotional activity across a range of positive and negative emotions, not specific to depression

Question 4

Other biological factors

Answer 4

• Borna disease (produces periods of frantic activity followed by lethargic activity like in bipolar disorder, in farm animals): found in 1/3rd of cases of depression in humans even though it is only found in 5% of the general population (potential viral link)
• hormones (cortisol is linked to stress and therefore depression; post-natal depression occurs in 20% of women with a drug-induced drop in estradiol and progesterone - which is what happens after giving birth; decline in testosterone in older men leads to increased risk of depression)

Question 5

Brain hemispheres

Answer 5

• positive mood associated with activation of the left PFC in normal population
• depressed people have decreased activity in the left and increased activity in the right PFC
• may reflect a biological predisposition rather than a predictive factor (imbalance remains stable over many years despite changes in symptoms)

Question 6

Antidepressant drugs

Answer 6

• tricyclics (e.g. amitriptyline): block serotonin/dopamine reuptake transporters to prolong the presence of the neurotransmitters in the synaptic cleft; however they also block histamine/acetylcholine receptors and some sodium channels leading to side effects (drowsiness, heart irregularities and nausea) so not suitable for long term use
• SSRIs (e.g. citalopram, fluoxetine): specific to serotonin reuptake transporters leading to milder side effects but similar treatment outcomes
• MAOIs: block monoamine oxidase that metabolises catecholamines and serotonin to render them inactive so there is more neurotransmitter available for release
• atypical antidepressants: dopamine and noradrenaline reuptake inhibitors; st Johns Wort (risky as it renders other medication ineffective)

Question 7

Effectiveness of antidepressants

Answer 7

• in mild stages of severity, there is no real difference shown between drug and placebo
• but in more severe episodes, antidepressants have been found to show a relatively significant effect

Question 8

Electroconvulsive therapy (ECT)

Answer 8

• electrically induced seizures to treat depression
• issues with this being used inethically and without consent but is now used in severe cases of depression where drugs are ineffective
• appears to alter the expression of more than 100 genes in the hippocampus and frontal lobes
• side effects cause transient memory loss (reduced if you confine treatment to the right hemisphere)

Question 9

Transcranial magnetic stimulation (TMS)

Answer 9

• similar but more modern technique
• stimulates axons near the surface of the brain
• still unclear why this is effective

Question 10

Lifestyle changes

Answer 10

• CBT
• exercise (shown to have antidepressant effects particularly in older adults)
• dietary changes (Omega-3 fatty acids)

Question 11

Seasonal affective disorder (SAD)

Answer 11

• form of depression more prevalent in polar regions of the world where winter nights are the longest
• seldom as severe as major depression
• treatment with bright light is very effective
• possible links with vitamin D deficiency

Question 12

Anxiety Disorders

Answer 12

• anxiety disorders involve irrational worries and fears that undermine wellbeing and cause dysfunction
• GAD: generalised and chronic anxiety
• phobia disorders: when anxiety may be tied to a specific object or situation
• panic disorder: when people experience sudden and intense anxiety attacks
• OCD: experiencing repetitive, anxiety-provoking thoughts that compel people to engage in ritualistic, irrational behaviour
• PTSD: characterised by recurrent thoughts about a traumatic event that can appear weeks or months later

Question 13

Dissociative Disorders

Answer 13

• involve severely disjointed and fragmented cognitive processes, reflected in significant disruptions in memory, awareness or personality
• DID: when people shift between multiple identities that are distinct from each other in personal memories, behaviour and attitudes
• dissociative amnesia and fugue: involve significant memory loss that is not the result of normal forgetting; can be attributed to brain injury, drugs, another mental disorder or a significantly stressful life circumstance; fugue involves assumption of a new identity completely

Question 14

Personality Disorders

Answer 14

• deeply ingrained, inflexible patterns of thinking and feeling or controlling impulses that cause distress or impaired functioning
• three clusters of personality disorders: odd/eccentric, dramatic/erratic and anxious/inhibited
• these are generally just extreme versions of personalities and are frequently comorbid with other disorders
• antisocial personality disorder: associated with lack of moral emotions and behaviour; people can be manipulative, dangerous and reckless; includes sociopaths and psychopaths; often found in prison populations

Question 15

Diasthesis-stress Model

Answer 15

suggests that a person may be predisoposed to a mental disorder that remains unexpressed until triggered by a stressful event

Question 16

Bipolar disorder

Answer 16

• depression can be unipolar or bipolar (varying between mania and depression)
• mania reflects periods of restless activity, excitement, self-confidence, loss of inhibition etc.
• bipolar symptoms also include attention problems, poor self control and issues with verbal memory
• bipolar I disorder: people with full blown episodes of mania; bipolar II disorder: people with milder episodes of mania (hypomania)

Question 17

Genetics (bipolar)

Answer 17

• genetic predisposition supported by twin and adoption studies
• two genes identified to increase probability of bipolar II
• genetic link between major depression and bipolar disorder (generally shows increased risk)

Question 18

Drug treatments (bipolar)

Answer 18

• lithium salts (stabilise mood to prevent a relapse into mania or depression but risk of toxicity in high doses
• valproate and carbamzepine (appear to reduce the number of AMPA type glutamate receptors in the hippocampus that are linked with mania + block synthesis of arachidonic acid produced when brain is inflamed –> linked to bipolar which appears to show increased brain inflammation)

Question 19

Other treatments

Answer 19

• intensity of mood swings can be reduced by encouraging a healthy sleep cycle in a quiet dark room –> bipolar leads to circadian rhythm being affected (depressed phase = long periods in bed and manic phase = getting very little sleep)
• eating more foods containing omega-3 fatty acids (shown to counter arachidonic acid build up)

Question 20

Schizophrenia

Answer 20

• refers to the dissociation between emotional and intellectual aspects of experience
• deterioration in everyday functioning (work, relationships, personal care etc.) for at least 6 months and must exhibit at least 2 of the following symptoms:
• positive symptoms (behaviours that are present but shouldn’t normally be there - dellusions, hallucinations, disorganised speech, catatonic behaviour)
• negative symptoms (behaviour that are absent but should be present - weak or absent signs of emotion/speech/socialisation; these are usually stable over time but are difficult to treat)
• cognitive symptoms: generally lower IQ; deficits in attention and working memory; issues with understanding abstract concepts
• significantly more common in cities than rural areas and more common in the HICs than LICs (diets higher in sugar and saturated fat are more common aggravating schizophrenia; whereas omega-3 fatty acids alleviate it)

Question 21

Genetics (schizophrenia)

Answer 21

• as the genetic link increases, so does the probability of developing schizophrenia (e.g. 13% for one schizophrenic parent; 48% for monozygotic twins)
• also influence of environmental conditions on developing schizophrenia
• appears to be no common gene directly linked to schizophrenia; rare mutations that alter the structure of proteins at synapses or interfere with the immune system; microdeletions in chromosomes (perhaps disrupting the development of the brain and therefore increases likelihood of schizophrenia)

Question 22

Neurodevelopmental hypothesis

Answer 22

• also prenatal environmental influences (schizophrenic mothers more likely to drink, smoke, take drugs during pregnancy so increased risk of complications; highest incidence of schizophrenia occurs in adopted children with biological schizophrenic parents and a disordered adoptive family –> double link)
• genetics + prenatal influences + environment may lead to abnormalities in the developing brain which may leave it more vulnerable to other factors at critical periods of development (e.g. traumatic experiences, dietary deficiencies, exposure to toxins etc.)
• possible that early developmental abnormalities can impair behaviour in adulthood

Question 23

Risk of schizophrenia is elevated by:

Answer 23

• poor nutritional intake of the mother during pregnancy
• premature birth/low birth weight
• pregnancy complications
• exposure of mother to extreme stress
• head injuries during childhood
• being born in winter (increased risk of viral infections)
• acute infections during adolescence
• Toxoplasma Gondii (infected infants have impaired brain development) –> adults with schizophrenia more likely to have had a pet cat in childhood and blood tests show higher concentration of toxoplasma antibodies in schizophrenics

Question 24

Brain abnormalities

Answer 24

• schizophrenics associated with larger brain vesicles than average (e.g. comparing one schizophrenic twin with the other non-schizophrenic)
• also have less than average gray matter and white matter (largest difference in temporal and prefrontal brain areas - hence deficits in memory and attention which are PFC functions)

Question 25

Dopamine hypothesis

Answer 25

• antipsychotic drugs (e.g. clopromazine, haloperidol): used to treat schizophrenia that block dopamine synapses
• elevated dopamine is a key symptom in schizophrenic episodes plus lower release of glutamate and fewer number of receptors in PFC and hippocampus
• narcotics (e.g. amphetamine, cocaine) increase dopamine at the synapses which cause hallucinations and delusions like in schizophrenia
• experimentally, studies have shown that schizophrenics have twice the number of D2 receptors occupied at any given time than members of the normal population

Question 26

Glutamate hypothesis

Answer 26

• in many brain areas, dopamine inhibits glutamate so an increase in dopamine = decrease in glutamate
• narcotic PCP inhibits glutamate receptors and can produce both the positive and negative symptoms of schizophrenia
• suggests that glutamate is involved but this is one of the most widespread neurotransmitters so simply increasing this could be detrimental to overall health

Question 27

Declarative memory

Answer 27

• open to conscious exploration
• influence of episodic and semantic memory

Question 28

Amnesia

Answer 28

• anterograde: unable to form memories of events following surgery
• retrograde: unable to retrieve memories prior to the surgery

Question 29

Case of HM

Answer 29

• bilateral removal of hippocampus and medial temporal lobe - anterograde and retrograde amnesia for 1-3 years prior (led to the thought process that the hippocampus stores episodic memories in short term before they are moved to the cortex); his long-term memory deficit was limited to declarative memory but his non-declarative memory was still intact, as was his short-term working memory and IQ level
• the above was demonstrated experimentally: showing recency effect based on short-term memory is still intact but primacy effect based on long-term memory is altered
• the case of HM tells us the medial temporal lobe area is important for long-term declarative memory and transferring things into long-term memory; but less so for working memory/procedural memory/

Question 30

Double dissociation in STM and LTM

Answer 30

• patient KF has damage to left temporo-parietal area (does not show recency effect in memory; has impaired STM and preserved LTM)
• patient MH has damage to bilateral temporal lobes (preserved STM and impaired LTM)
• this gives clear evidence that the MTL supports LTM and TPC supports STM

Question 31

Spatial memory

Answer 31

• Morris water maze shows how the hippocampus of rats allow it to move round a maze and built up a spatial map of an area through practice and reinforcement
• if you damage the hippocampus of a rat that has learnt the location of a platform, it reverts back to random patterns of searching (particularly effect of right hippocampus)
• also proven that neurons in the hippocampus fire at different locations in space depending on the direction you are facing
• also evidence in birds: largest hippocampus = best spatial memory (Clark’s nutcracker)

Question 32

Cognitive map theory

Answer 32

• London taxi drivers have been trained to memorise a spatial map of the city’s streets
• greatest hippocampal activity when answering questions about routes through the city compared to when answering non-spatial questions
• also taxi drivers have a larger than average posterior portion of the hippocampus (size correlating to experience as a driver)

Question 33

Relational memory theory

Answer 33

• hippocampus does not necessarily represent space but more the relationships among overlapping cues in the environment
• including spatial maps but also other overlapping associations (e.g. reward and temporal cues) –> evidence that rats learn the relative rewards associated with pairs of odours placed into cups of sound; whereas rats with a lesion to the formix that disrupts hippocampal output to the cortex are impaired at learning these overlapping relations
• specific links to the left hippocampus for specific memory problems associated with overlapping regions

Question 34

Episodic memory theory

Answer 34

• postulates that the hippocampus is critical for episodic but not semantic memory
• evidence from retrograde amnesia patient KC (damage to hippocampus): lifelong retrograde amnesia in episodic memory but preserved intellectual and skilled abilities; was still able to retrieve semantic memories acquired before the accident (but no personal/emotional memories)
• evidence from anterograde amnesia patient HM: patients are able to learn a few new semantic facts (but not store new episodic memories)
• evidence from congenital amnesia: hippocampal lesions lead individuals to perform poorly on tests of episodic but not working memory and are able to learn normally in school (semantic memory intact)
• evidence from double dissociations: in semantic dementia, left lateralised damage to anterior temporal lobe (not hippocampus) leads to alterations in semantic memory; patient AM has preserved episodic memory for events but severely impaired semantic memory in tests given

Question 35

Integrating theories of hippocampal memory function

Answer 35

• hippocampus is essential for: explicit/declarative/episodic memory; spatial memory and encoding overlapping relationships
• it is less essential for semantic memory (anterior temporal cortex) and working memory (intact in amnesic patients with MTL damage)
• spatial map appears to be linked to right posterior hippocampal processing
• relational functions are associated with left anterior hippocampal processes
• suggestions that relational and episodic memory are closely related through episodic recollection

Question 36

Working memory model

Answer 36

• working memory is more about maintaining information whilst we are working with it, rather than just simply stage
• central executive, visuo-spatial sketchpad and phonological loop
• e.g. delayed response task: animal presented with food reward and response delay with screen coming down meaning the animal has to remember the location by maintaining the info in working memory –> PFC cells continue to remain active during delay suggesting their role in the maintenance of information in our working memory

Question 37

Phonological Loop

Answer 37

• increased activation with increased verbal memory load (more syllables) as this requires increased maintenance rehearsal –> posterior lateral inferior prefrontal cortex
• also increased activation with increased verbal similarity (increased demand on the stores by adding additional complications) –> supramarginal gyrus
• damage to the temperoparietal area leads to very poor short term memory particularyl the phonological loop

Question 38

Visuo-spatial working memory

Answer 38

• experiment where faces, houses and locations are presented, followed by a delay and then question about if the image matches
• found that faces activate the FFA and houses activate the PPA; faces and houses both activate the left inferior fusiform gyrus; general location activates more of the dorsal/caudal area and inferior/superior parietal lobe bilaterally

Question 39

Building blocks for working memory

Answer 39

• emerging from interactions among process components, of which selective attention to perceptual and long-term memory representations is central
• process components: selective attention, rehearsal, pattern recognition, update, sustained attention etc.
• perceptual and LTM representations: verbal and object representations; and numerical and alphabetical procedures
• there is also an inherent link between goal/task sets (maintenance, encoding or response goals) which involve different processing aspects of working memory to be carried out (e.g. may require a specific rehearsal process or type of pattern recognition)

Question 40

Maintenance

Answer 40

• e.g. for a single delayed match to sample task
• selective attention required to encode object
• rehearsal and sustained attention to maintain object in working memory during the delay
• selective attention and pattern recognition for the response in identifying the object

Question 41

Manipulation

Answer 41

• e.g. for mental arithmetic
• selective attention for encoding verbal cues (e.g. a sum)
• sustained attention, update and inhibition required during the delay stage (use of procedural long-term memory to separate the sum into different parts and recall the skills required to process mental arithmetic and inhibit only certain numbers at different stages so you do not get confused)
• selective attention in response phase to give verbal answer

Question 42

Neural processes

Answer 42

• percept perceived in visual cortex
• passes along ventral stream to long-term memory representations of objects (activation of modality-specific areas depending on what it is)
• during delay period, rehearsal occurs by activating the frontal lobe and maintaining attention via parietal cortex
• process keep repeating in a cycle to maintain information in working memory
• overall, regions of the PFC and parietal cortex are involved in executive/attentional functions in working memory
• areas of association cortex appear important in the storage of specific material during working memory delay
• lesions to temporal cortex affect visual working memory but leave spatial working memory intact –> parietal lesions affect spatial working memory

Question 43

Verbal working memory regions

Answer 43

• much more left lateralised processing
• Broca’s area, LMTG, LIPL, DLPFC

Question 44

Central executive regions

Answer 44

• e.g. in sustained attention (modality-general functions)
• dorsolateral PFC

Question 45

Visual working memory regions

Answer 45

• ventral stream
• activating representations in temporal cortex, IPS for spatial locations and FEF

Question 46

Decline in memory with age

Answer 46

• older humans have impaired working memory abilities –> seemed to be linked to reduced PFC activity and potentially reduced input connections to the PFC
• also people with more intact working memory ability show greater PFC activation
• potential for use of stimulant drugs activating dopamine receptors in treating decline in memory function

Question 47

Declarative memory summary

Answer 47

• short-term declarative memory (working memory) is subserved by a network of brain areas including frontal and posterior attentional processing areas and stimulus dependent visuo-spatial processing regions (FFA/PPA/parietal lobe)
• medial temporal lobe most closely associated with declarative memory and amnesia –> also associated with spatial memory/episodic memory
• semantic memory spared in amnesic patients (more reliant on temporal pole)
• working memory relatively spared but some issues due to proximity with inferior temporal areas (words, images, faces etc.)

Question 48

Non-declarative memory

Answer 48

• a collection of various forms of memory that operate automatically and accumulate information that is not accessible to recollection (e.g. skills and priming)
• crucially this is utilised when people become very good at a task without being able to declare their strategy (basal ganglia has learnt the skills/technique required to carry out a task automatically)

Question 49

Skill learning

Answer 49

• requires extensive training (e.g. playing a musical instrument) that takes place over a long period of time
• could include a perceptual, motor or cognitive skill
• some situations require the use of knowledge built up over many prior experiences; in this case, episodic memory is not enough as it takes many episodes to generate a reliable predictive model so implicit/non-declarative learning is more useful
• e.g. probabilistic learning (weather task)

Question 50

Basal ganglia

Answer 50

• situated at the base of the forebrain
• strongly interconnected with the cerebral cortex, thalamus and brainstem
• crucial for non-declarative learning and memory
• Parkinson’s Disease has significant impacts on this region due to a deficit in the dopaminergic neurons present here

Question 51

Probabilistic Learning

Answer 51

• noted that amnesic patients are not good at episodic memory recall (hippocampus required for this) whereas control and PD patients are; yet when the probabilistic model is built up the control and amnesic patients are good at the task, whereas PD patients are severely impaired (basal ganglia damage)
• in this case, after many repetitions control patients begin using declarative memory as the basal ganglia has stored the probabilistic relations implicitly (rather than using declarative episodic memory which can only store small amounts of information and not apply a strategy)
• PD patients are less successful as their basal ganglia is impaired and so cannot adopt the non-declarative memory strategy
• whereas amnesics have an intact basal ganglia so show gradual improvements as they begin to adopt the non-declarative learning approach
• clear demonstration that hippocampus is required for explicit/declarative memory whereas basal ganglia is important for implicit/non-declarative memory but most learning is maximised by both being active

Question 52

Perceptual priming (direct/repetition priming)

Answer 52

• given the prime initially then you are asked to do something (e.g. given stem of the word and asked to recall)
• greater number of words from the initial read list are completed correctly compared to ones that were not initially given beforehand –> demonstrates priming effect
• brain scans show left ventrolateral PFC and left occipital cortex appear to be associated with stem completion
• left ventrolateral PFC, left occipital cortex and fusiform cortex appear to show a reduction during repetition suppression –> suggesting involvement in processing and completing word stems (show a deactivation when the same words are repeated)
• For above: left hemisphere shows a repetition suppression effect for the same and different exemplars (e.g. different types of umbrella, different fonts of words)
• whereas right hemisphere only shows a repetition suppression effect for the same exemplars
• for the above: for images, it is the left/right fusiform gyrus that is involved and for words it is the left fusiform cortex and right occipital cortex
• illustrates that the left hemisphere is more focused on language elements and the right hemisphere is governed by more perceptual/visual aspects of the stimulus –> explains why it only responds to exact replicas

Question 53

Repetition suppression

Answer 53

• neural responses diminish to subsequent presentations of the same items
• this is a form of neural sharpening, where non-essential neurons respond less and less to each repeat as the same stimulus is given
• leads to reduced haemodynamic response functions detected by MRI so you are left with only the most selective neurons critical for the response to that particular stimuls

Question 54

Conceptual priming (direct/repetition priming)

Answer 54

• given prime initially, then given a related cue (such as category the word falls into) and then asked to give the same word as the answer
• within this, there is a within-task repetition on each row but there is also a between-task repetition but these are different between trials
• in the left anterior IPFC, this only seems to respond to within-task repetitions (repetition suppression effect) –> appears to be related to conceptual processing
• whereas left posterior IPFC shows suppression effects within and between task repetition (non-semantic processing)
• posterior regions are more language-specific/perceptual (phonological and non-semantic - suppression within and across tasks) whereas anterior regions are more semantic/conceptually specific (suppression within tasks only)

Question 55

Semantic priming (indirect priming)

Answer 55

• given initial prime word and the answer is a related word as it is in the same semantic category (determining whether there is a semantic relation)
• brain regions show repetition suppression effect for semantically related words and an increased activation for unrelated words (no sharpening)
• shown to be a reduction in activity in the anterior temporal lobe (left temporal pole) only for semantic repetition, linking this region to semantic processing (consistent with links between this area and semantic dementia)

Question 56

Priming summary

Answer 56

• perceptual priming: posterior sensory regions are important; for words - left VLPFC (frontal lobe), left FG and visual cortex show repetition effects –> left hemisphere involved in language processing; for pictures - left FG for same and different exemplars –> more related to language and right FG only for exact same exemplars –> responding to visual aspects
• conceptual priming: frontal lobe distinction; anterior left inferior frontal gyrus (semantic processing) and posterior left inferior frontal gyrus (phonological aspects)
• semantic priming: left anterior temporal lobe involved