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209 Cards in this Set
- Front
- Back
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What was the biological approach to mental illness in late 1800s? |
Proposed chemical imbalance (e.g. in metabolism) ascausal of MHP Advances in identification and treatment made Established systems of classification according tomedical knowledge not social prejudice |
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What was the psychological approach to mental illness in late 1800s? |
“biological” symptoms of psychologicaldistress (psychogenic) described byNeurologists and Physicians |
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What was the socio-behavioural approach to mental illness like in the past? |
Watson (1920’s) described inducing a phobia in achild by pairing an innocuous stimulus with a frightening one |
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What are the two senses of consciousness? |
state (wakefulness, alertness) content (awareness, experience) |
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Can state be described accurately using objectivecriteria? |
yes, e.g. the coma scale |
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What are the five parts to self-consciousness? |
self perception self monitoring self recognition awareness of awareness self knowledge |
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What is self-perception? |
proximal stimuli/ internal states- being aware of astimulus that is hinging on you |
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What is self-monitoring? |
metacognition- making a prediction of whetheryou’re going to remember something |
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What is self recognition? |
knowing that we are the person in the mirror |
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What is awareness of awareness? |
theory of mind- we are able to understand that othersare aware |
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What is self knowledge? |
auto noetic consciousness- subjects of a personalhistory |
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What three states are people usually in? |
awake, rapid eye movement sleep (REM) or non-rapideye movement sleep (NREM) |
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How many cycles of sleep are there roughly in a night? |
5 |
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What does slow wave sleep do? |
(mind is pretty empty, big effort to wake up) particularly restorative as it is particularly crucial for restoring mental andphysical function |
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What might fast rhythms do? |
play a part in binding mental content in thebrain |
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What are some neurotransmitter systems that are involved in sleep cycle and wakening? |
dopamine, serotonin etc |
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What happens if you block out Area V5 in your brain? |
you may lose the ability to judging motion |
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If stimulus is weak and you are not focusing on it, what will there be a rise in? |
there will be a rise in activity in brain but will not give you a conscious experience (subliminal) |
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What was Giulio Tononi's integratedinformation theory of consciousness? |
Consciousness occurs when youhave integration of modular activity that is widespread in the system Developed mathematical way ofquantitating the likelihood that there is consciousness in the system |
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What is a coma? |
state in which people don’t appear to be awake, andare not enjoying any experience. |
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What are some signs of a coma? |
Absence of arousal or awarenessof self or surroundings Eyes closed, absent sleep wakecycle Not obeying commands Reflex activity only Glasgow coma score of below 7 Variable respiratory function Usually the EEG will give slow waves |
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What does vegetative mean? |
a state of wakefulness without awareness No evidence of a functioning mind (nocommunication, no purposeful action, no evidence of discriminative perception) |
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What is compatible behaviour? |
Non-specific arousal response ‘Irrelevant’ spontaneous behaviour Momentary orienting behaviour |
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What is incompatible behaviour? |
Attempt to communicate Response to command Purposeful action Discriminative perception |
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When might a vegetative state occur? |
after extensive damage to cerebralcortex, cerebral white matter, or thalamus |
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What does minimally conscious mean? |
people who are beginning to emerge from avegetative state |
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What does 'locked in' mean? |
not a disorder of awareness but a disorder when itcomes difficult to communicate you are aware Quadriplegia and anarthria brought about by thedisruption of corticospinal and corticobulbar pathways Defining feature is the relative preservation ofcognition |
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What does 'brain death' mean? |
state in which the brain has died, you are nolonger aware or awake |
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What is the risk with misdiagnosis of altered states? |
A third of those diagnosed in vegetative state arenot actually in the vegetative state |
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What are some remedies for misdiagnosis of altered states? |
education/ structured observation using behaviouralscales (e.g. CRS-R)/ repeated observation |
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What is REM sleeping behaviour disorder? |
acting out your dreams |
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How can you diagnose awareness? |
you can give a pulse of activity to the brain andsee how that pulse spreads around the brain |
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What does medically unexplained symptoms refer to? |
patients who experience physical symptoms for whichthere is no known organic pathologyidentified |
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Do MUS patients express higher levels ofdistress and disability in comparison to those with organic presentations? |
yes |
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How are MUS symptoms understood? |
unconscious process: somatoform disorder (e.g. Somatization disorder, Conversion disorder,Hypochondriasis) conscious process: goal is psychological (primary pain)- Malingering/ Goal is external (secondarygain)- Factitious disorder |
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Name three common diagnoses for MUS disorders? |
Cardiology (atypical chestpain) Maxofacial (TMJ) ENT (tinnitus, dizziness) |
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What is the assessment and diagnosis process of MUS? |
History- adverse events mayoccur more than a year before symptoms Identification of precipitatingfactors- making links between psychological functioning and symptoms Time to diagnosis- linked tooutcome (sooner you make the diagnosis of MUS, the better) Communication of diagnosislinked to outcome Systematic protocol forcommunicating diagnosis- minimize rejection |
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Why might a disorder be selected for a MUS patient? |
because patient has previouslyexperienced the symptom on an organic basis. It reappears at time ofpsychosocial stress |
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What are some contributory factors of MUS? |
Somatised presentations may belegitimized by repeated medical investigations May validate patient’serroneous attribution and make disorder more resistant to re-framing inpsychological terms Physician’s ability to toleraterisk of missing a rare condition may also influence patient behaviour Invasive procedures risk ofiatrogenic disorder which, therefore, confirms belief of physical illness Risk of litigation may affectmedical practice |
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What factors influence diagnosis of MUS? |
Patient attitude to role ofdoctor- only legitimate to discuss physical symptoms Time available in consultation Behaviour of healthprofessionals- clarification of complaint, attention to verbal and non verbalcues GPs who encouraged psychosocialdiscussion less likely to refer on |
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Name three ways MUS may present itself |
Pain in a variety of locations Fatigue May be difficult to describe symptoms |
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Why is MUS diagnosis unpopular with patients? |
Don’t see themselves asmentally ill Diagnosis not made, but as aresult of exclusion Patients don’t maintaindiagnosis Few referred, fewer attend,fewer accept help |
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Why is MUS diagnosis unpopular with professionals? |
Can we exclude neurologicaldisorder? Can we be sure it’s notfactitious? Are psychological factorsimportant? Patients seen as tiresome andcauses despondency in professionals- picked up by patient- exacerbatessituation Excessive use of NHS resources |
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What are some other terms used to describe MUS? |
psychosomatic, conversion, psychogenic,abnormal illness behaviour |
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What is the benefit of 'functional' language? |
Can give clear ‘diagnosis’- youhave ‘functional’ weakness Can talk about disruption in‘functioning’- mechanism aetiology (computer metaphor) Allows ‘physical’ vs.‘psychological’ Allows possibility forimprovement- way into treatment function Allows for both physical andpsychological treatment strategies |
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What do MUS patients want? |
Clear communication ofdiagnosis Joined up services Information about symptoms andcauses Coping strategies To be believed Not to be abandoned |
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Define anxiety |
An unpleasant emotional state characterized byfearfulness & unwanted and distressing physical symptoms and thoughts |
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Name five anxiety disorders |
Phobias Panic Disorder Generalized anxiety Obsessive Compulsive Disorder(OCD) Post traumatic Stress Disorder(PTSD) |
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When is a phobia diagnosed? |
when a fear that is out of proportion to the actualthreat of the object/situation (e.g. of spiders in UK, but not Oz), it is recognizedby person as largely groundless or is disrupting to their life |
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What is the biological explanation of the cause of phobias? |
evolutionary preparedness fight or flight response genetic risk |
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What is evolutionary preparedness? |
Good evolutionary reasons to be altered to thingsthat we need to, quickly, avoid |
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What is the fight or flight response? |
evolutionary mechanism involving primitive brainareas and decision making (limbic & frontal, R) (transmits “adrenaline”surge/ heart races (blood to arms legs, away, e.g. from stomach)/ muscle tenseup/ pupils dilate etc.) |
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What is the genetic risk of phobias? |
there may bedistribution of those who have more or less “autonomic lability” (readiness toarousal) Those with close (1stdegree) relative with agoraphobia have greater risk of agoraphobia & otherphobias, but role-modeling of fear important factor |
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What is the behavioural explanation of the cause of phobias? |
avoidance conditioning vicarious conditioning |
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What is avoidance conditioning? |
learn to fear a neutral stimulus if it is pairedwith an intrinsically fearful stimuli reinforced for avoiding situations by drop off inarousal state |
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What is vicarious conditioning? |
role modeled fear/anxiety by parent/friend reinforced by others Media influence (e.g. Jaws and shark phobias) |
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What are some treatments of phobias? |
systematic desensitisation reinforcing coping responses by others flooding |
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What is generalised anxiety disorder? |
often triggered by stressful events (see depression lecture) co-morbidity with depression fears over not being able to cope |
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What is obsessive compulsive disorder? |
pre-occupation &/or compulsive repetitive behaviours self-doubt, indecision |
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What is panic disorder? |
very common co-morbidity with other specific anxietydisorders/depression Understanding Fight/flight, graded exposure etc.. |
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What are some treatments for PTSD? |
CBT debriefing may reduce symptoms eye movement desensitisation group therapy medication may help ease associated symptoms of depression and anxiety &promote sleep |
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What are psychological mechanisms for PTSD? |
cognitive behavioural: Fear Conditioning & avoidance learning cognitive: how the survivor experiences a shift inself-efficacy (sense of control in the world) |
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What are biological mechanisms for PTSD? |
Biological readiness for “fearconditioning response” Good evolutionary reasons to bealerted to things that we need to, quickly, avoid flight or fight response system genetic predisposition? may be adistribution of those who have more or less “autonomic lability” (readiness toarousal) Stress hormone levels beingelevated within a few hours of “common civilian trauma” related to developmentof PTSD |
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What are some factors contributing to the development of PTSD? |
Pre-morbidhistory (early separation/ family history/ general anxiety/ PtSD) Femalegender (more reporting?/ Issues re: social power/abuse?/ Under-reporting bymen, masked by increased alcohol use/etc.?) Nature ofevent (severity/ exposure level/ control over event(s)) |
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What is the diagnosis of PTSD? |
Mostpeople exposed to trauma develop stress symptoms (anxiety), symptoms typicallybegin within 3 months of a traumatic event PTSD isdiagnosed when symptoms last more than 1 month (If they suffer for days to thenclassed as Acute Stress Disorder (ASD)) Theseverity and duration of the illness varies. Some people recover within 6months, while others suffer for decades |
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What are the symptoms of Coexisting: “Bimodalreactions”? |
Fight/flight (Flashbacks,nightmares, hyper arousal to reminders of trauma, hyper vigilance for danger toself/others) Freeze (avoidance behaviour,numb & blunted affect, amnesia states, Derealisation, disassociation) |
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What is the pleasure principle? |
James Olds (1959)- rewardpathway Dopamine plays an importantrole in the reward centre and is triggeredwhen we do pleasurable things from eating good food to having sex as well as take drugs |
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What does cannabis do? |
disrupts the way nerves fire in the brain's memory centre |
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What areas are affected by cannabis? |
Dorsolateral prefrontal cortex (involved in balancing act of decidingwhether or not to do something) Circuitry sub-serving control of impulses, judgment, and decision-making Implications of late maturationof this area have entered educational, social, political, and judicialdiscourse |
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What is cannabis associated with? |
paranoia |
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What is substance misuse (in terms of alcohol)/ what are its problems? |
Periodic (binge) or Chronic Put self at risk Detrimental effect on socio-occupational functioning Legal problems (e.g. drunk and disorderly) Persistent relationship problems |
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What is a dependence on alcohol? |
Larger doses needed for same effect Appears to function normally on amount that would impair others Withdrawal symptoms (Delirium tremens/ Nausea) Activities curtailed for getting alcohol |
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What are social problems with alcohol? |
Relationship problems Work/financial problems Legal problems/ violentbehaviour |
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What are medical problems with alcohol? |
80% of long term alcohol mis-users have a medical condition Multi-system: Cardiovascular/ Gastrointestinal /Cancers & Cirrhosis Neurological – Alcohol use implicated in in 50% (?) of head injuries Heavy alcohol use related to korsakoffs psychosis (thiamine deficiency) |
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What are psychiatric problems with alcohol? |
Affective states (depression /anxiety) Personality change Sexual problems Hallucinations |
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What are biological risk factors of alcoholism? |
Twin studies (MZ 54% concordance of alcohol problems, DZ 28%) Dopamine-2 Receptor gene (Abnormality in “majority”of “dependent” & 20% of non-dependent) May be linked to 'reward centre' |
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What are psycho-social risk factors of alcoholism? |
Men x 2 more likely thanwomen Particular occupationsmore at risk 1/3 of homeless havealcohol dependency problem |
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What are the Psychological Models of Alcohol Misuse & Dependency? |
socio-cultural psychodynamic cognitive behavioural |
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What is socio-cultural reason for alcohol misuse? |
Stressful socio-economic conditions = higher rates of problem, e.g.unemployment Sub-culture/peers/parent value alcohol and/or drink alcohol = higherrates |
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What is psychodynamic reason for alcohol misuse? |
Dependent personality developed due to needs unmet in childhood stages Set up to develop a “dependent relationship” with alcohol |
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What is cognitive behavioural reason for alcohol misuse? |
Behaviour reinforced by: Positive reward of euphoria/ social acceptance and Negative reinforcement of avoiding tension Self-medicating a mood disorder |
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How can you recognise a problem with alcohol misuse? |
Consumption over safelimits Time of first alcoholdrink of the day Presence ofwithdrawal symptoms Morning shakes/nausea CAGE questions (e.g.Have you ever felt the need to cut down?) |
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What range of support is needed for alcoholics? |
Individual and Groupapproaches Outpatient/ Inpatient General Supportgroups Residentialself-help/therapeutic community Carer support Community preventionprogrammes |
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What are biological treatments for alcohol misuse? |
Detoxification (Either in stages orby use of drugs to nullify symptoms. Relapse rates high ifno psychotherapy) Antagonistic drugs (Block effects ofaddictive drug, e.g. Antabuse for alcohol. Produces nausea/dizzinessetc. if taken with alcohol, therefore also form of behavioural (aversion)therapy) |
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What are behavioural treatments for alcohol misuse? |
Developing alternatebehaviour, e.g. meditation/assertiveness to manage peers etc. Relapse rate high ifnot combined with biological/cognitive Learning the effectit has on their lives |
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What are cognitive behavioural treatments for alcohol misuse? |
Tends to be mosteffective for misuse problems Need to be incombination with detox for dependence Consider level of motivationfor change (Motivational enhancement therapy) |
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What are the key components to cognitive behavioural treatments of alcohol misuse?
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Educationon alcohol Havecontract Identify triggersand coping strategies Develop Goals |
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Until recently, what wasn't dementia considered the cause of? |
death |
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What is the diagnosis for dementia? |
non specific syndrome, set of symptoms core characteristic: abnormal cognitive functions DSM-IV: memory impairment, progressive nature, problems with daily activities |
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What is Alzheimer's? (AD) |
protein abnormalities in neurone gross atrophy of affected regions (temporal lobe, parietal lobe) lower brain activity during cognitive task |
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What are common early symptoms of Alzheimer's? |
agnosia (problems producing names or right object name) forgetting what was just read mood changes |
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What are later symptoms of Alzheimer's? |
wondering restlessness, agitation older memories are resistant, trouble with making new ones |
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What is an ischemic stroke? |
blocked blood flow to parts of the brain |
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What is a hemorrhagic stroke? |
bleeding inside/ around brain tissue
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What is vascular dementia? |
any cognitive domain can be impaired often it happens suddenly |
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What is lewy bodies dementia? |
results from clumps of neuroproteins fluctuating cognitive processes, variations in alteration spontaneous Parkinson's visual hallucination |
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What is frontotemporal dementia? |
particularly difficult to diagnose dramatic change of personality disinhibited, odd social behaviour euphoria, apathy repetitive compulsive behaviour (e.g. extreme hoarding) |
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What are five ways you can measure change in dementia patients? |
MMSE (mini-mental state examination) AMT (Hodginson Abbreviated mental test) MIS (memory impairment screen) Min-cog GPCOG |
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What are some less brief ways of measuring dementia? |
Addenbrooke's cognitive examination Geriatric depression inventory |
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What are some biological treatments for dementia? |
there are no medical treatments to reverse the effects of dementia there are drugs that help manage the symptoms |
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What are some psychological interventions for the treatment of dementia? |
behaviour management cognitive stimulation |
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What are some factors that increase risk of dementia? |
age poor living conditions genetics high fat intake diet low levels of vitamin D extensive drinking smoking coronary bypass no physical activity |
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What are the emotional readingskills developed across the span of childhood into late adolescence? |
From birth: intrinsic bipolar emotional related to arousal- distress andpleasure Six months: primary emotions- surprise, interest, anger, sadness and fear 1 year (girls): ‘empathising’ 3 years: Theory of Mind 7-9 years: Complex theory of mind (e.g. detecting faux pas) Continues to develop in late adolescence (14-17 years: ToM) |
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Define Theory of Mind |
to attribute mentalstates to others, to know they have beliefs, desires and intentions thatdifferent from one’s own |
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Define empathy |
to understand another’sstate of mind and “co-experience” their outlook or emotions within oneself |
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What is cognitive empathy? |
know differentperspectives |
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What is affective empathy? |
what their mood is (andfeel “their” emotion) |
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What is the normal development and communication of children? |
Most children have innate preferences for social attentiveness whichallows them to develop pre-verbal social skills The use of gestures (e.g.pointing at objects) leads to shared communication and shared perspective Normal communicationallows the child to share in the perceptions and thoughts of those around them-to make sense of the world They develop ToM |
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What are survival reasons for children attending to “faces”,following gaze, communicative noises, facial expressions etc? |
Detecting threatsfrom cues such as angry faces has an obvious benefit for survival |
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What are social reasons for children attending to “faces”, following gaze, communicative noises, facial expressions etc? |
Detecting theemotions of others helps to understand their thoughts and behaviour For forming socialbonds with others |
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What are some characteristics of Autism? |
Delayed developmentally Limited communicative intent- echo laic Obsessive rituals Oppositions when disturbed Sensitivity |
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Why, historically, were parents blamed as cause of Autism? |
A child and mother notbonding (attachment theory The theory became quitewidely known as “refrigerator mother” Very damaging theory inmany ways and no evidence for it whatsoever |
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What is the evidence for the MMR vaccine causing Autism? |
Incidence hasincreased from 0.3 per 10,000 since 1988 to 2.1 per 10,000 in 1999 MR vaccination was atsame level Not thought to be dueto more awareness Increased risk“remains uncertain” |
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What characteristic can be seen in Autistic patients? |
Triad of Impairment (in areas of socialisation/ language development/ behaviour) |
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What are the biological causes of Autism? |
Genetics: 91%concordance in MZ twins, nearly 0% DZ twins and about 3% of siblings of peopleare also affected Illness: rubella,meningitis, tuber sclerosis, encephalitis as a direct cause- in a significant numberof people there are often signs of increased neurological abnormality (EEG,MRI) |
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What are some signs of social impairment in someone with Autism? |
Absent/ impairedimitation (does not wave bye; mechanical imitation of others’ actions out ofcontext) Absent/ abnormalsocial play (e.g. preference for solitary play) Impaired ability tomake friendship (e.g. can range from someone lacking understanding ofconventions of social interactions or complete withdrawal) No or lack of wantingto seek comfort from others at times of distress |
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What is the social impairment in someone with Autism due to? |
People with autismlack “Theory of Mind” (An in-ability to think about their own and others' mental states) Evidence from “Sally Anne” experiments suggests that peoplewith autism are severely delayed in developing this ability, if ever able to atall |
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What are some signs of language impairment in someone with Autism? |
No developmentallyappropriate mode of communication (e.g. babbling, mime or speech) Absent or abnormalnonverbal communication (eye-gaze, facial expression or gestures) Abnormalities in formof speech (e.g. stereotyped and repetitive use of speech (echolalia)) Pronominal reversals(use of "he" instead of "I", "He wants tea“) Abnormalities inproduction of speech (volume, stress, rhythm etc. e.g. asking question) Lack of understandingabout symbolic (abstract) nature of language, stuck on concrete (eg. "Justgive me a hand.....“) |
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What is the language impairment in someone with Autism due to? |
Possibly due to people with autism not having the insight intocommunication (motivated) to learn language skills |
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What are some signs of a restricted behavioural repertoire in someone with Autism? |
Stereotyped bodymovements (e.g. hand flicking, rocking, head banging etc) Preoccupation withparts of objects or attachemtn to unusual objects (e.g. spinning wheels on toycar, carrying particular tin around) Marked distress overchanges made in trivial aspects of environment (e.g. vase moved out ofposition) also known as 'neophobia': fear of new things Insistence onfollowing routines in detail Absence ofimaginative activity Stereotyped andrestricted patterns of interest (e.g. preoccupation with lining things up,preoccupation with bus timetables) |
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What are the goals of intervention with someone with Autism? |
Provide with adaptive skills for engaging and making sense of greaterpart of the world and promote independence Relieve symptoms of anxiety, frustration, and possibly difficultbehaviour(Especial emphasis oncommunication skills) |
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Why is it difficult for interventions with someone with Autism? |
Rigidity withroutines: educational approaches rely on changing routines Usual rewards not rewarding, e.g. social praise etc., for encouragingparticipation: the search for rewards is difficult |
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What is a personality disorder? |
Persistent pervasive abnormality of social relationships and socialfunctioning. |
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Why is studying personality disorders· Little evidence of a link to schizophrenia or Mood Disorder· Heritability (Torgersen, 2000)o Aggressive antisocialbehaviour more heritable than non aggressive (Eley et al, 1999) important? |
Common Presents with significant levels of morbidity and mortality When present co-morbid conditions are more difficult to treat It represents a substantial health economic burden It is treatable |
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What are some co-morbid health problems with personality disorders? |
Substance misuse ADHD Eating Disorders Somatisation |
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What are genetic studies of personality disorders? |
Little evidence of a link to schizophrenia or Mood Disorder Heritability (Torgersen, 2000) - Aggressive antisocialbehaviour more heritable than non aggressive (Eley et al, 1999) |
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What is the attachment theory? |
Increasedanxious-ambivalent or avoidant attachment in BPD Unresolved trauma onAAI (Patrick, 1994) |
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What is Mentalisation BasedTherapy? |
Reflective Functionand Attachment(Strong relationshipbetween RF and scores in Strange Situation Test (Ainsworth 1978)/ Intergenerationaltransmission) Metalizing and secureattachment go together in the care giver associated with a coherent workingmodel of the child richly imbued with representations of internal states |
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What is The NeurologicalBasis of Mentalisation? |
Right Hemispherespecialised for emotion and Social Cognition (Schore, 2001) Optimal developmentis associated with the development of affect regulation associated with theVMPF cortex (Theory of Mind) |
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What is Transference Focussed Therapy? |
Kernberg (2002) Object relationsdyads Positive and negativeobject representations kept apart |
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What was the historical perspective as a reason behind eating disorders? |
Lots of accounts ofpeople dying of a broken heart (renaissance period) Religious orders(excessive dietary rules- fasting) |
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What was the cross-cultural perspective as a reason behind eating disorders? |
Western thin/ attractiveideal(Fiji before and aftertelevision study (natural experiment found western television had profoundeffects on body dissatisfaction)) Survival advantage infamine? |
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Name 5 eating disorders |
Anorexia Nervosa (AN) Bulimia Nervosa (BN) Binge Eating Disorder (BED) Eating Disorder Not Otherwise Specified (EDNOS)/ Other Specified Feedingand Eating Disorder (OSFED) Orthorexia |
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What is the DSM5 diagnosis for Anorexia Nervosa? |
1. Restriction of energy intake relative to requirements leading to asignificantly low body weight in the context of age, sex, developmentaltrajectory, and physical health. 2. Intense fear of gaining weight or becoming fat, even thoughunderweight. 3. Disturbance in the way in which one's body weight or shape isexperienced, undue influence of body weight or shape on self-evaluation, ordenial of the seriousness of the current low body weight. |
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What is the DSM5 diagnosis for Bulimia Nervosa? |
1. Recurrent episodes of binge eating characterized by BOTH of thefollowing: Eating in discreteamount of time (within a 2 hour period) large amounts of foodand sense of lack ofcontrol over eating during an episode 2. Recurrent inappropriate compensatory behaviour in order to prevent weightgain (purging). 3. The binge eating and compensatory behaviours both occur, on average, atleast once a week for three months. 4. Self-evaluation is unduly influenced by body shape and weight. 5. The disturbance does not occur exclusively during episodes of anorexianervosa. |
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What are some Other SpecifiedFeeding and Eating Disorders (OSFED)? |
Atypical Anorexia Nervosa Bulimia Nervosa (of low frequency and/or limited duration) Binge Eating Disorder (of low frequency and/ or limited duration) Purging Disorder Night Eating Syndrome |
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What are effective treatments for AN? |
Food! (in the short term) Family-based interventions No NICE-approved ‘first line’treatment |
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What are effective treatments for BN? |
CBT-E – Chris Fairburn |
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What causes eating disorders? |
Personality (perfectionists?) Parts of the brain Social pressure Bad experiences around food Family factors |
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What are some factors during birth/ infancy that can increase the risk of an eating disorder? |
Gender Genetic factors Obstetriccomplications (somatic bodily complications that occur during pregnancy andchildbirth) Early feedingdifficulties High concernparenting |
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What are some factors during childhood that can increase the risk of an eating disorder? |
Childhood obesity Childhood anxietydisorders Sexual abuse Obsessive compulsivepersonality disorder Adverse life events |
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What are some factors during adolescence that can increase the risk of an eating disorder? |
Puberty Body dysmorphicdisorder High level exercise(TOYA study) DIETING OCD/ Perfectionisms Negativeself-evaluations |
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What is the formulation of an eating disorder? (five P's) |
Predisposing (Epigeneticfactors/ genetic profile/ neurobiological state) Precipitating(Vulnerability/ puberty/ dieting/ stress or trauma) Presenting Perpetuating (Managementby family or clinicians/ perceived advantages of AN/ Stress or trauma/Socio-cultural context) Protective |
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What are five Neuropsychological processing styles? |
Visual spatialprocessing Cognitive flexibility Central coherence Risk/Reward processing Emotion processing |
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What is Visual spatial processing? |
The way the brainprocesses visual information Appears to be subtlyimpaired in AN, even following weight recovery Could this be linked to body imagedisturbance? |
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What is Cognitive flexibility? |
The ability to shift betweendifferent ways of thinking Appears to be impaired in AN andBN, even following weight recovery Could be a genetic factor? Could this be linked to gettingstuck with thoughts and rituals about eating? |
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What is Central coherence? |
The ability to integrate detailand global perspectives (to see the wood and the trees): Ability to see finedetail and the big picture Global processing difficulties inAN and BN (Lopez et al, 2008) Could this be linked to a detailedfocus on weight and calories, rather than the bigger picture of life? |
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What is Risk/Reward processing? |
The ability to identify riskychoices and avoid impulsive responses Appears to be impaired in BN (andto some extent in AN) Could this be linked to bingeeating in BN and to altered reward value of food in AN and BN? |
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What is Emotion processing? |
The ability to interpret what thebody is telling us (turning emotions into feelings) Appears to be impaired in AN(though we’re not as good at measuring it) Could this be linked to distortedbody image, intuition difficulties (gut feelings) and alexithymia (lackingwords for feelings) |
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What are some potential treatments for eating disorders? |
Cognitive Remediation Therapy (CRT) Cognitive flexibility Switching Central coherence Spatial relationships Planning Neurobiofeedback |
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What is Cognitive Remediation Therapy (CRT)? |
Originally developed for thetreatment of cognitive impairments in psychosis, based on cognitive remediationof acquired brain injury Based in neurocognitive deficitsidentified in AN Targets processes of thinkingrather than content Patients practice more flexibleways of thinking 10 individual sessions (45-min duration,twice a week). Relating the skills practiced toeveryday activities |
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What is Neurobiofeedback? |
Meditation and Buddhist monks mentalisation-based therapy Real time fMRI changing blood flow to the insula |
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What medication is given to those with an eating disorder? |
Noradrenaline Serotonin Dopamine |
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What is a mood disorder? |
Disorder in which primary disturbance appears to be one of mood Can be unipolar (low mood only) or bipolar (high mood, usually also withlow mood) |
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What does Unipolar depressivedisorders include? |
major depression, minor depression, dysthymia |
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What does Bipolar depressive disorders include? |
Bipolar I Disorder,Bipolar II Disorder, cyclothymia, hyperthymia |
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What are some symptoms of depression? |
Sadness, loss of pleasure Worthlessness Guilt Foreboding Poor sleep Appetite changes |
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What are some signs of depression? |
Withdrawn socially Fatigue Poor concentration Inactivity Restlessness |
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What is the diagnosis of a Major Depressive Episode? |
1. Low mood/ Anhedonia 2. Plus at least five of the following: Changes in weight and/or appetite Psychomotor agitation orretardation Fatigue, loss of energy Insomnia or hypersomnia Feelings of worthlessness orinappropriate guilt Difficulty thinking,concentrating, making decisions Recurrent thoughts of death orsuicidal ideation 3. Symptoms must be present nearly every day for at least two weeks 4. Symptoms must cause clinically significant distress and/or impairment insocial, occupational, or other important areas of functioning 5. Symptoms not due to drugs, alcohol, or other medical problem |
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What is the diagnosis for Dysthymia (DSM-IV) or PersistentDepressive Disorder (DSM-V)? |
Depressed mood, at least 50% of the time (i.e., for more days thannot), for at least two years When low mood is present, accompanied by at least two othersymptoms of depression (previous slide) Chronic depression, often starts early in life and precedes firstinstances of major depressive episodes May report: feeling drained, pessimistic, avoiding others, socialdifficulties, always been this way |
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What is double depression? |
Dysthymia + MajorDepressive Episode |
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What are some of the consequences of depression? |
Negative impact on parent-child and romantic relationships Theno. 1 cause of disability in the world 2 - 9% of people withdepression commit suicide, compared to 1% in general population Greater risk of heart disease,diabetes, stroke |
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What percentage of depressive episodes recover on their own within 6-9 months? |
70% |
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What are biological factors of depression? |
Physical illness can lead to depression, and viceversa(Nervous system diseases (e.g.,Parkinson’s disease)/ Vascular diseases (e.g., heartdisease)/ Endocrine diseases (e.g.,hypothyroidism)) There is a genetic risk (cf. kindling hypothesis) |
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Name two biological treatments of depression |
SSRIs = Selective Serotonin ReuptakeInhibitors ECT = Electroconvulsive Therapy |
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What are SSRIs? |
Less side-effects than olderanti-depressants Not “happy pills” Generally effective in managingbiological signs and symptoms Less effective at preventing riskof relapse |
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What is ECT? |
Highly controversial, waswidespread, now limited and last treatment option for very depressed andsuicidal people but has major ethical implications |
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What are cognitive factors of depression? |
Aaron Beck’s cognitivetheory: Depressed people are not to blame for their depression Forces have shaped their thinking patterns and behaviours: Family life/ Adolescence/ Peers/ Losses and stresses |
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What are cognitive treatments for depression? |
Thoughts and behaviour patterns can be re-shaped Do not need to look to the past, childhood (i.e., deal with the here andnow, for tomorrow) |
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What is the Cognitive behavioural model of depression? |
Negative triad of beliefs in depression Inner speech seen as full of negative propaganda (voice of criticism) –labeled as Negative Automatic Thoughts (NATs) NATs based on negative core beliefs about the self Viciousspiral of depression |
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What is the negative triad of beliefs in depression? |
Negative views of the self,the world, and the future (“I can’t do anythingright… I’ll never be better at things… Ican’t trust anyone...”) |
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What are the treatments involved in CBT for depression? |
Behaviour experiments Tracking NATs Challenging NATs, and by checkingthem… Challenging core beliefs By reviewing evidence In the therapeutic alliance |
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What increases risk for depression? |
Being female: Females attwice the risko Family history of depression (50-80%) Past history of depression (> 3 episodes, risk x 2) Loss or stressful events (e.g.,a break-ups, exams, moving away from home, illness, bereavement) Poor housing, low income,debts Negative styles of thinking:Dwelling on problems, rumination, poor memory of past events |
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Define Mania |
A distinct period of abnormally and persistently elevated, expansive, orirritable mood and abnormally and persistently increased goal-directed activityor energy, lasting at least 1 week and present most of the day, nearly everyday (or any duration if hospitalization is necessary). |
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What is hypomania? |
Fourdaysor more of persistently elevated, expansive or irritable mood and persistentlyincreased activity or energy As with mania, three / four or more of other symptoms Notsevere enough to cause marked impairment, hospitalisation not necessary, no psychoticfeatures Unequivocal change in functioning & observable by others |
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What is Cyclothymia? |
Brief spells of mild hypomania and mild depression (not sufficient tomeet clinical criteria) with rare occasions when no symptoms Lasts > 2 years, often much longer 15-20% develop bipolar I or II |
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Why is there a link between people with BD and more creative hobbies? |
No firm evidence forBD and divergent thinking Personalitycorrelates: impulsivity, openness to experience, drive and ambition Association betweenenergised positive mood / mania symptoms and fluency / creativity |
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What are biological factors of Bipolar disorder? |
Fairly high heritability rate of around 80% (McGuffin et al. 2003) 10% chance of BP in 1st degree relatives of BP Mania and depression may be separately heritable (McGuffin et al. 2003) Treatment often with medication |
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What are the targets of CBT for BD? |
Prodromes Identifying andresponding to prodromes associated with reduced chance of illness Psychoeducation Social rhythm stabilisation Medication adherence Stressful life events Dysfunctional cognitions |
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What are prodromes? |
“warning signs” of an episode of illness |
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What is involved with Relapse prevention CBT? |
Assessment and formulation: could include life chart Psychoeducation Activity monitoring andscheduling Identify and explore problematic thinking patterns Socratic questioning, behavioural experiments Detection and management of prodomes Future self-management |
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What is activity monitoring and scheduling? |
Monitoring: seerelationship of activities with mood; monitor outcome of changes made in CBT Scheduling: Stabiliseroutine; balance task-oriented behaviours |
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What are the biological causes of psychosis? |
Genetic risk Brain anomalies |
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What are the psychological causes of psychosis? |
“View one takes”(cognitive distortion) Developmentalfactors…attachment, early history, general stresses, major stress (PTSD) |
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What are the social factors that cause psychosis? |
Deprivation as a riskfactor? Isolation? Alienation |
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What is the difference between psychotic and schizophrenia? |
Psychosis = loss of “shared” senseof reality Schizophrenia = split mind,real & imagined< associated with additional symptoms… |
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What are the main features of Psychosis? |
Loss of awareness of sociallyperceived (shared) reality |
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What are the main features of schizophrenia? |
Delusional beliefs Hallucinations |
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What is the difference between 'Positive' and 'Negative' symptoms of schizophrenia? |
Positive - “excess cognition” (e.g. Hearing voices/ Delusions/ Disorganized speech) Negative- “deficits in behaviour” (e.g. Avolition/ Alogia - poverty of speech/ Anhedonia/ Flat affect (outward expressionbut probably not actual experience)) |
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What are the three main forms of schizophrenia? |
disorganised catatonic paranoid |
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What is disorganised schizophrenia? |
Content of speech disordered &bizarre associations Behaviour disorganized, notcongruent with social cues |
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What is catatonic schizophrenia? |
Apathy, withdrawal states, leadinginto immobility but with islands of excitement & agitation. May laterrecall experience. Kicks in after other symptoms |
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What is paranoid schizophrenia? |
Delusions prominent, esp.persecutory, e.g. ideas of reference, that snippets of overheard conversationapplies to them Hallucinations |
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What are some of the most common positive symptoms of schizophrenia? |
Lack of insight Auditory hallucinations Ideas of reference Delusions of reference Suspiciousness |
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What are the biological factors of schizophrenia? |
genetics dopamine |
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What is the effect of genetics on schizophrenia? |
Twin studies, Gottesmann& Shields (1972): MZ 42%, DZ 9% concordance rate It may be that geneticrisk is for a range of related disorders that share common neuro-chemicalunderpinnings |
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What is the effect of dopamine on schizophrenia? |
Biochemical: Symptoms may be triggered bychemical “imbalances” |
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What is the difference in the brain systems of those with schizophrenia compared to those without? |
Patients with schizophrenia experienced excess activity in the substantianigra (RED), decreased activity in the prefrontal corte (BLUE), and diminishedfunctional connectivity between these regions, suggesting that communicationamong these regions was out of sync. Additionally, the higher the level of connectivity between the substantianigra and the striatum, the higher the level of psychosis seen in the patientswith schizophrenia |
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What psychological stress may trigger episodes of psychosis? |
social factors stressful life events family environment |
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What do Medicaland psychological models suggest about psychosis? |
Not a disease entity but a bio-psycho-social condition, with oneor more of each factor being influential |
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What are some psychological interventions for psychosis? |
Family Therapy (FT) Behaviour Therapy Management of triggers for voices/delusions Cognitive therapy ABC in CBT |
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What is family therapy? |
Aimed at preventing relapse/ Educative & to change patterns from confrontative (EE) to collaborative & constructive |
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What is behaviour therapy? |
Often used to develop socialskills/daily living skills (esp. for those with negative symptoms) Use of token economy |
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What is Management of triggers for voices/delusions? |
Staff/carers noting anyantecedents (circumstances) that triggered Changing environment Building up otherresponses |
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What is cognitive therapy? |
Self-monitoring for useof medication Investigated content ofbeliefs and sources of voices |
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What is ABC in CBT forPsychosis? |
Based on a scale of 0 to 10, the patient rates the intensity of distress. The consequence (C) is assessed and divided into emotional and behavioralCs. The patient gives his own explanation as to what activating events (As)seemed to cause C; and the therapist ensures that the factual events are not“contaminated” by judgments and interpretations. |
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What "thinking" problems may offenders have? |
Lack of impulsecontrol Poor at controllingemotions Poor problem solving Rigid and inflexiblethinking Unable to seeother people’s views Recognising consequences of behaviour |
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What effect can a TBI have on crime? |
TBI earlier than age 12 were found to havecommitted crimes significantly earlier than those who had a head injury later Those with TBI = moreconvictions Young offenders with substantial TBI were significantlyimpaired on the expression recognition task |
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Is TBI causal or coincidental in crime? |
Violent crime, is likely to result from complexinteraction of factors such as genetic pre-disposition, emotional stress,poverty, substance abuse and child abuse |
