Psychopathology PDF

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this is actually from a-levels, im just trying to get some documents...

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PSYCHOPATHOLOGY

OCD  Co-morbid with Tourette’s and autism – argument that OCD isn’t a diagnosable disease but a …………………………………………………symptom  Persistently intrusive & irrational thoughts (obsessions) develop repetitive behaviours which reduces the anxiety and alleviates the obsessions. (false sense of control)  Compulsions act as a temporary cessation of anxiety  Sufferer is aware the obsession is irrational & that the compulsions are useless

Obsessions – behavioural characteristics

 Unable to perform everyday activities  Social impairment Obsessions – emotional characteristics  Extreme anxiety – the compulsions don’t solve the emotional disruption the ……………………...obsessions cause  Depression – severe distress can escalate to depression, a low mood  Irrational guilt over minor moral issues

Obsessions – cognitive characteristics    

Recurrent & persistent thoughts (90% - major cognitive issue is obsessive thoughts) Realisation of inappropriateness Hyper-vigilant – maintain constant alertness of potential hazards Attentional bias – sufferer chooses what to ignore and what to pay attention at

Compulsions – behavioural characteristics  Repetitive routines to temporarily alleviate stress from obsessions  Everyday behaviours impacted (FFA)  Reduced social interactions

Compulsions – emotional characteristics  Distress – compelled to carry out the behaviour

Compulsions – cognitive characteristics  Cannot stop the urge to carry out specific behaviour  Realisation of inappropriateness

BIOLOGICAL EXPLANATION TO OCD

1. GENETIC EXPLANATIONS  Taylor (2013) – 230 genes may be involved in the development of OCD (polygenic)  COMPT GENE  Inheriting susceptibility to certain behaviours  Certain allele common in OCD sufferers (regulates production of dopamine)  MZ twins have higher concordance rates than DZ twins in developing OCD  Turk et al (2013) – variation of COMPT allele found in OCD sufferers produces ……………………...abnormally large volumes of dopamine  SERT GENE  Regulated transportation of serotonin  Faulty gene causes too much serotonin being transported  Genes can be inherited or spontaneous abnormality

PSYCHOPATHOLOGY

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Ozaki et al (2003) – 2 unrelated families (gene variation NOT inheritance); 7 members ……………………….had OCD & faulty SERT gene, a cause of OCD may be a ……………………….faulty/abnormal variation of SERT gene  Groothest et al (2005) – Meta–analysis (smallest sample was 37 pairs, largest was …………………………….10,000 - inconsistency) quantifying the role genes play in …………………………….development of OCD. In children: 45-65% in adults: 27-47%. …………………………….Doesn’t account for subtypes  EPIGENETICS  Diathesis-Stress Model – genetic vulnerability/predisposition to developing OCD  Appropriate environmental triggers needed to activate the gene causing predisposition  Samuels et al (2007) – unrelated hoarders share abnormality in chromosome 14 …………….….……….. (D145588). Different subtypes have different genetic origins

AO3 BIOLOGICAL EXPLANATIONS Positives:  Many supporting studies (explanation is reliable)  Many findings suggest that OCD has genetic origins which increase a person’s susceptibility to the disorder  For example: - Samuels et al (2007) ………………..- Ozaki et al (2003) ………………..- Taylor (2013) ………………..- Nesdadt et al (2010) – 68% MZ twins shared OCD compared to ……………………………………………...31% DZ twins (concordance rates)  Large volume of supporting studies strengthens reliability of the theory

Negatives:  Reductionist  Twin studies strongly suggest that genetic variation is largely accountable for the development of OCD  Epigenetics suggests otherwise, since environmental factors control whether the gene is expressed or not (lack of evidence)  Less useful because biological explanation is too simple; development of OCD is dependent on much more than just genes.  Comer et al (2007) – Over ½ of OCD patients had a traumatic event and more ……………………...…severe cases of OCD had multiple traumas  Twin studies are not generalizable  Twins are very rare (3.3% in 2010) therefore are not representative of the overall population  Genetic influence may only be applicable to twins because of their almost identical genetic material and similar environments  Lack of twins also means the sample sizes in twin studies are severely limited therefore small sample sizes mean results are not reliable

2. NEURAL EXPLANATIONS  NEUROTRANSMITTERS (serotonin, dopamine)

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Low levels of serotonin mean normal transmission of mood-related hormones is disrupted. Common in OCD sufferers Excessive dopamine regulates caudate nucleus If caudate nucleus is dysfunctional due to abnormally high dopamine levels, it causes over-stimulation & impulsive thoughts. OCD symptom Dopamine influence concentration; OCD sufferers experience an inability to stop focusing on obsessive thoughts and repetitive behaviours

PSYCHOPATHOLOGY  BRAIN STRUCTURES (OFC, basal ganglia, PFC)  OCD co-morbid with Parkinson’s & Tourette’s – both caused by a dysfunctional basal ganglia  High levels of serotonin causes orbitofrontal cortex (OFC) and caudate nucleus (in basal ganglia) to malfunction – overstimulation & impulsive thoughts  Over-active pre-frontal cortex (PFC) causes exaggerated control of primal impulses  Once the appropriate behaviour to avoid danger is perform, the PFC reduces its activation (normally)  OCD sufferers’ PFC stays over-stimulated & they continue to carry out the behaviour (compulsion) – explains germophobic symptoms in OCD sufferers

AO3 NEURAL EXPLANATIONS Positives:  Supporting evidence  National Institute for Mental Health – DNA samples from sufferers, OCD ……………………………………………..associated with 2 mutations of the ……………………………………………..serotonin transport gene. Lowered mood  Hu (2006) – compared serotonin activity in OCD & non-OCD sufferers. ……………..Serotonin levels lower in OCD sufferers  Supports view that abnormally low serotonin contributes to the onset of OCD  However, supporting evidence is not consistent, whit very few studies supporting the dopamine and PFC explanation (lack of confident data)  Nevertheless, supporting evidence increases the validity

Negatives:  Role of neurotransmitters is unclear  Cannot establish whether the abnormal levels of neurotransmitters cause OCD  Causation cannot be inferred as only correlations have been identified  Serotonin-OCD link may be comorbid with depression as serotonin regulates mood  Lack of direct causational evidence questions the usefulness of the neural explanation to OCD; no treatment has been devised with it as a basis  Not all respond well to drugs raises serotonin & decreasing dopamine  Suggests that there are inconsistencies; not all OCD sufferers’ symptoms will improve on DT  Suggests serotonin & dopamine does not play a significant role in the onset of OCD

TREATMENTS FOR OCD 1.SSRI’s (Selective Serotonin Re-uptake Inhibitors)  Raises serotonin if too low  Control reuptake rate – SSRI’s leave more serotonin in the synapse for absorption by …………………………….the post-synaptic neuron  Knock-on effects include – improves mood, reduces anxiety & helps patient manage …………………………………the symptoms

2.TRYCYCLICS (Clomipramine)  Same as SSRI’s but targets serotonin & noradrenaline  Antidepressant

PSYCHOPATHOLOGY

3.ANTI-ANXIETY DRUGS (Valium)  Contains benzodiazepines (BZ’s) which enhances the effects of GABA (gamma amino butyric acid) which changes the electrical charge, opening the channel to increase flow of chloride ions, making it difficult for the post synaptic neuron to receive serotonin & noradrenaline

4.SNRI’S (Serotonin-Noradrenaline Re-uptake Inhibitors)  Alternative to SSRI’s

RESEARCH EVIDENCE  Pigott & Seay (1999) – SSRI’s most effective (least side effects & higher success rates …………………………..in the consistency of lowering symptoms of OCD) but …………………………..Clomipramine works for more patient but has serious side…………………………..effects  Julien et al (2007) – SSRI’s helped 50-80% of patients in the reduction/control of ……………………….symptoms. Improvement in quality of life, no social impairment

AO3 TREATMENTS OF OCD Positives:  Drug therapy does not require substantial effort from patient  Convenient form of treatment for the majority of the population  Widely available  More affordable than psychological treatments & cost effective  Accessibility to treatment is convenient for NHS as it is cheap & Is nondisruptive of the patient’s life  DT is effective  Julien et al (2007) – SSRI’s helped 50-80% of patients  Soomro et al (2009) – 17 studies showed significantly better results for the ………………………….SSRI’s than placebo condition ………………………..- SSRI’s most effective when paired with CBT  Typically, 70% patients see improvement from SSRI’s, alternative treatments are available for the other 30%  Effectiveness of DT advantageous because it suggests that OCD is genetically influenced

Negatives:  No cure  Drugs have to be taken indefinitely, body may get acclimatised to the drug & lose its effectiveness (neurological adaptation) – may need more potent drug or increased dosage  Psychosurgery may be a better alternative (destroying brain tissue to eradicate maladaptive processes)  Side-effects  Soomro et al (2008) – SSRI’s can cause insomnia, nausea. Tricyclics can ………………………….cause hallucinations & stomach problems. Unnecessary ………………………….side-effects outdo the benefits of the drug.  Intensity of side effects questions the usefulness of SSRI’s & tricyclics as a treatment for OCD

PHOBIAS

PSYCHOPATHOLOGY  Specific phobia – phobia of an object  Animal phobias - arachnophobia

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Situational phobias - fear of specific situations (claustrophobia, aerophobia)

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Natural environment phobias - Fear of storms (astraphobia) Blood-injection-injury (BII) phobias – fear of invasive medical procedures, such as …………...…………………………………blood tests or injections  Other phobias – fear of clowns (coulrophobia)  Social Anxiety (social phobia) – phobia of social situations  Fear of public speaking (glossophobia)  Agoraphobia – phobia of losing control in an unfamiliar environment with no escape route or ………………….emergency mechanisms

Behavioural characteristics  Panic – crying, screaming, running away. Children – freezing, clinging, tantrum  Avoidance – an agoraphobic may limit the time they spend outside which interferes ……………….with work, education & social life  Endurance – alternative to avoidance, phobic withstands high anxiety. Sometimes ……………….unavoidable (aerophobia)

Emotional characteristics  Anxiety – unpleasant state of high arousal, difficulty experiencing positive emotions  Anxiety is unreasonable, blown out of proportion/disproportionate to reality

Cognitive characteristics  Selective attention to phobic stimulus – best chance of reacting quickly to a threat the …………………………………………………phobic stimulus might impose. Not rational  Irrational beliefs – agoraphobics will be pressured to perform well in social situations due ……………………...to his irrational beliefs  Cognitive distortions – phobic’s perceptions of phobic stimulus are abnormal

BEHAVIOURAL EXPLANATION OF PHOBIAS

Mowrer (1960) – 2-Process Model  ACQUISITION BY CC  Watson & Rayner (1920) – Little Albert  Albert showed no unusual anxiety at beginning of study (9 months old)  Frightening noise + Rat = fear UCS + CS = CR  Phobia of white rat generalised to fluffy things eg. fur coats, non-white rabbit & cotton balls  MAINTENANCE BY OC  Mowrer (1960) buzzers thru CC – got electrocuted  Taught rats fear of when buzzer rang  Even when the buzzer was not paired with the electric shocks, the rats still jumped to avoid being electrocuted (negative reinforcement)  Behaviour (avoidance) reinforced negatively (removal of excessive fear caused by phobic stimulus)

PSYCHOPATHOLOGY

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DiGallo (1996) – 20% people involved in a car accident develop a phobia of travelling ……………………in cars - Car (NS) associated with accident (UCS) - Car (CS) becomes associated with panic (CR) - Attempts to avoid car journeys acts as a negative reinforcer (staying at home)

AO3 EXPLANATION OF PHOBIAS Positives:  2 process model has explanatory power  Goes beyond Watson & Rayner (CC) – suggests how phobias are maintained  Practical implication – patients need to be exposed to phobic stimulus in …………………………...therapies (SD & flooding) because this way they’re ……………………………restricted from practising avoidant behaviour. ……………………………Behaviour ceases (not –ively reinforced) so it declines  On the other hand, 2-PM ignores the possibility of vicarious acquisition  Nevertheless, practical implications improves explanation’s usefulness

Negatives:  Contradictory evidence  DiNardo et al (1988) – CC cannot explain acquisition of phobias for …………………………..everybody (questions generalisability). E.g. not …………………………..everyone who was bitten by a dog develops a phobia …………………………..of dogs (only 3% population has a phobia but much …………………………..more has had repeated fearful situations with the …………………………..same object )  Sue et al (1994) – recall of the 1st –ive event which was causation of the …………………….phobia motivates their ongoing fear  Contradictory evidence re-establishes the validity of Mowrer’s proposition of acquisition by CC & maintenance by OC

 Limited in the origins of phobia development (reductionist to an extant)  Overlooks the role of cognition which is problematic – irrational thinking is a ……………………………………………………………………key feature of phobias.

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PSYCHOPATHOLOGY Tomarken et al (1989) – presented a series of slides of snake and neutral ……………………………..images to phobic & non-phobic participants. The ……………………………..phobics tended to overestimate the number of ……………………………..snake images shown. Overlook evolutionary factors; phobias which have been a source of danger in the past (fear of snakes& spiders) are adaptive to prepare for danger Seligman (1971) – ‘biological preparedness’ – innate predisposition to ………………………………………………………...acquire certain phobias which ………………………………………………………...are adaptive of evolutionary past Evolutionary phenomena have an impact on the acquisition of phobias therefore the 2 process model’s incompleteness means it is partially unreliable

TREATMENTS FOR PHOBIAS 1.SD (Systematic Desensitisation)  Basis – a behavioural therapy which replaces maladaptive behaviour with ………...adaptive/appropriate behaviour acquired through a gradual process ………... (counter-conditioning)  Reciprocal inhibition – controlling physiological response to phobic stimulus by ……………………………consciously controlling stress to relax. (Relaxation inhibits ……………………………anxiety)  In vitro desensitisation – visualising (aerophobia) Not mutually  In vivo – suitable for simple phobias eg arachnophobia exclusive (can be combined)

 Processes: I. Anxiety hierarchy – list of situations involving the phobic stimulus which ……………………….provoke anxiety arranged in the least to most frightening  Therapist tackles the phobia one stage at a time II. Relaxation – teaches techniques for patient to be physiologically relaxed:  deep muscle relaxation  breathing exercises  imagining themselves in a relaxing situation  coping mechanisms eg fear of exams – time management  If unsuccessful, Valium restores the body to its parasympathetic (resting) state III. Exposure – to phobic stimulus while in relaxed state (starting from bottom of ……………..anxiety hierarchy) - progression measured by reduction of anxiety at each stage - success – when the patient is capable of remaining calm when ……………exposed to the most frightening situation in hierarchy

AO3 FOR SD Positives:  Widely available for a variety of phobias & patients compared to flooding & cognitive therapies

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PSYCHOPATHOLOGY Phobias – Such as arachnophobia & aerophobia (due to & dependent on ……………method – in vivo or vitro) Patients – those with learning disabilities cannot comprehend the process of ……………flooding & cognitive therapy - SD can be self-administered; convenient for those who cannot afford a therapist or stress-regulating medication Therefore, SD is useful due to wide availability to patients & variety of phobias

 Effective  McGrath et al (1990) – 75% treated when they undertake SD  Choy et al (2007) – in vivo>in vitro (provides alternative for extreme ………………………cases of phobic symptoms)  Gilroy et al (2003) – 42 arachnophobics treated with SD compared with control ………………………..groups treated with relaxation (w/out exposure). At 3 & 33 ………………………..months the SD group were less fearful than control group  Therefore due to successful treatment in both short & long terms, SD is an effective method of treating phobias

Negatives:  Low internal validity  due to the possibility that the patient becomes immune to the anxiety caused by the phobic stimulus because of repeated exposure (acclimatisation to phobic object) rather than relaxation  Ohman (1975) – less successful for survival related phobias. Basis of …………………..acquisition may be evolutionary, therefore the re…………………..learning/conditioning basis of SD may not cure certain , …………………phobias  questions internal validity because the treatment is not fixating on the right areas of treatment (including both methodology & basis)

2.FLOODING (implosion therapy)  Same basis of SD but instant rather than gradual (immediate exposure)  Patient required to apply relaxation technique under a highly stressful encounter with phobic stimulus with no escape route (no option of avoidance)  Body cannot be at a high level of stress indefinitely; eventually the body relaxes  In vivo or virtual reality (VR)  CS no longer elicits CR  Patients must give informed consent as the therapist is deliberately putting them in a strenuous situation that could possibly harm them psychologically

AO3 FOR FLOODING Positives:  Cost-effective  Marks (1981) – flooding successful for agoraphobics, some reported ..........................success after 9 years  Wolpe (1960) – drove around a girl with phobia of cars continuously for 4 ...........................hours; her fear reached hysterical heights but then receded ...........................& completely disappeared  Flooding may be better as a treatment than life-long reliance on drugs  

Negatives:

Ougrin (2011) – flooding is highly effective and is quicker than cognitive ,..........................therapies Treatment is abrupt and therefore cheaper than SD with the same outcome

PSYCHOPATHOLOGY  Flooding can be traumatic  Attrition rate is high because some patients will not be able to tolerate the high levels of panic induced by the therapy & are unwilling to face their phobia at such a degree of exposure  Problematic; Outcome of implosion is indefinite – taking part in flooding before completion is likely to aggravate rather than eradicate the phobia  Wolpe (1969) – reported the case of a client whose anxiety intensified to such ..........................a degree that flooding therapy resulted in her being ..........................hospitalized  Due to the chance of catastrophic outcomes & significant attrition rates, the effectiveness of flooding is therefore very limited  As it caters to only the most strong-willed & healthy patients e.g. those with heart problems are at life-threatening risk (Not suitable to majority of phobics – substandard availability)

DEPRESSION  Women mostly diagnosed during adolescence due to; - Body dissatisfaction - Hormonal changes - External pressures (e.g. social expectations) about body image - Low self esteem  Types: I. Unipolar (major depressive disorder) – consistent & severe low moods (delusions, ………………………………………………..difficulty engaging in social interactions) II. Dyst...