Psychopathology

EXPLAINING PHOBIAS:-

LITTLE ALBERT (WATSON & RAYNER, 1920):-

• Aim: to see if human emotional responses could be learned through classical conditioning.
• Procedure: A lab experiment with one participant, an 11-month-old boy who lived in the hospital where his mother was a nurse.  Albert was presented with various stimuli, e.g. a white rabbit, rat and cotton wool.  Reponses were filmed.  No fear reaction to any stimuli.  A fear reaction was induced by striking a steal bar with a hammer behind his head, making him cry.  He was then given a white rat to play with, so he was not scared.  As he touched the rat, the bar and hammer were struck.  This was repeated 3 times.  Variations of techniques continued for 3 months.  It was intended that his fear reactions would be de-conditioned but he was removed from the hospital before this could occur.
• Findings: when shown the rat, Albert would cry, roll over and crawl away.  Had developed a fear, which he displayed to similar animals with less intensity and to other white furry objects.
• Conclusions: Conditioned emotional responses, including love, fear and phobias, are acquired as a direct result of environmental experiences, which can transfer and persist, possibly indefinitely, unless removed by counter-conditioning.

EXPLAINING PHOBIAS:-

KING ET AL (1998):-

• Reported that case studies showed that children tended to acquire strong phobias through a traumatic experience, which further supports the idea of phobias being acquired through classical conditioning.

BAGBY (1922):-

• Reported on a case study of a woman who had a phobia of running water that origninated from her feet getting stuck in some rocks near a waterfall.
• As time went by she became increasingly panic-striken.
• Although she was eventually de-conditioned, the neutral stimulus of the sound of running water became associated with the fear she had felt and thus her phobia of running water was acquired.

TREATING PHOBIAS:-

BROSNAN & THORPE (2006):-

• Aim: To see whether a fear of computers could be successfully treated by systematic desensitisation.
• Procedure: In the first study, a sample of 16 ppts was used: 8 computer-anxious ppts and a control group of 8 non-anxious ppts.  A 10-week systematic desnsitisation programme was delivered to the computer-anxious ppts.  In the second study, 30 computer-anxious ppts were assigned to a treatment group or a non-treatment group.  There was also a non-anxious control group of 59 ppts.
• Findings: In the first study, computer anxiety and coping strategies were significantly improved in the computer-anxious group, becoming comparable to the non-anxious controls.  In the second study, testing established over the period of an academic year that the reduction in anxiety was 3 x greater in the treated group than the non-treated group.  By the end of the year, the treated group no longer differed from the control gorup, while the non-treated group reamined significantly more anxious.
• Conclusions: The behavioural therapy of systematic desensitisation is effective in reducing technophobia.

TREATING PHOBIAS:

WOLPE (1960):-

• Used flooding to remove a girls phobia of being in cars.
• The girl was forced into a car and driven around for 4 hours until her hysteria was eradicated, demonstrating the effectiveness of the treatment.

OST (1997):-

• Found that, flooding is a rapid treatment that often delivers rapid, immediate improvements, especially when a patient is encouraged to continue self-directed exposure to feared objects and situations outside of therapy sessions.

BARLOW (2002):-

• Reports that flooding has been shown to be equally as effective in treating phobias as systematic desensitisation, but systematic desensitisation is preferred, as it is better tolerated by most patients.

EXPLAINING DEPRESSION:

BEEVERS ET AL (2010):-

• Aim: Assess whether brain areas linked with cognitive control are affected by emotional stimuli in mild-moderate depressives.
• Procedure: 27 females (self-selected sample).  Depression measured with CESD scale: 13 ppts placed in low depression symptoms group and 14 in high depression group.  The mean CESD score for HDG group was indicative of mild-moderate symptoms of depression.  Cue stimuli = 3 facial types, happy, sad and neutral, with control condition of facial/geometric shape cues.  432 trials conducted: a single face/geometric shape cue presented on a screen along with 1 of 2 target stimuli.  Ppts press button indicating presented target stimuli and the time measure to do this was recorded.  Simultaneously fMRI brain scans conducted.
• Findings: Different brain activation recorded in LDG and HDG during presentation of happy/sad faces.  No difference in brain activation with neural facial/geometric shape cues.
• Conclusions: Mild-moderate individuals have difficulty activating brain areas associated with cognitive control of emotional information.  Poor cognitive control may indicate levels of vulnerability to more severe depression.

EXPLAINING DEPRESSION:

BOURY ET AL (2001):-

• Monitored students' negative thoughts with the Beck depression inventory, finding that depressives misinterpret facts and experiences in a negative fashion and feel hopless about the future, giving support to Beck's cognitive explanation.

SAISTO ET AL (2001):-

• Studied expectant mothers, finding that those who didn't adjust personal goals to match specific demands of the transition to motherhood, but indulged instead in negative thinking patterns, had increased depressive symptoms, supporting Beck's cognitive theory.

ALTERNATIVE GENETIC EXPLANATION OF DEPRESSION:-

WENDER ET AL (1986):-

• Found adopted children with depression were more likely to have a depressive biological parent, even though adopted children are raised in different environments, meaning biological factors are more important than cognitive ones.

ALTERNATIVE BEHAVIOURAL EXPLANATION OF DEPRESSION:-

LEWINSOHN (1974):-

• Proposed negative life events may incur a decline in positive reinforcements and lead to learned helplessness (learn through experience that they can't bring about positive life outcomes.

COLEMAN (1986):- (Supports Lewinsohn's Learning Theory)

• Found individuals receiving low rates of positive reinforcement for social behaviours became increasingly passive and non-responsive, leading to depressive moods.

TREATING DEPRESSION:-

EMBLING (2002);-

• Aim: To assess which types of depressive patients benefit most/least from CBT.  To explore the relationship between emotions and depression to assess which patients benefit most from CBT.
• Procedure: 38 patients diagnosed with depression and on antidepressants received 12 CBT sessions.  Compared to a control group on antidepressants but no CBT.  Patients recorded dysfunctional thoughts and rated negative emotions and their depression level was assessed pre-study and each week.
• Findings: The treatment group's average depression score decreased significantly while the contol group's stayed the same.  CBT was less effective for patients with greater need for social acceptance.
• Conclusion: CBT is more effective (combined with drug treatment) than drugs alone.  More effective for some people than others.

TREATING DEPRESSION:

LINCOLN ET AL (1997):-

• Used a questionnaire to identify stroke victims who had developed clinical depression.  19 patients were then given CBT sessions for 4 months, resulting in reduced symptoms, suggesting CBT to be a suitable treatment for specific groups of depressives.

DAVID ET AL (2008):-

• Found, using 170 patients suffering from major depressive disorder, that patients treated with 14 weeks of REBT had better treatment outcomes than those treated with the drug fluoxetine 6 months after treatment.  This suggests that REBT is a better long-term treatment than drug therapy.

GENETIC EXPLANATION TO OCD:

GROOTHEEST ET AL (2005):-

• Aim: To investigate the extent to which OCD is inherited and whether this differs between children and adults.
• Procedure: Meta-analysis of 28 twin studies of OCD.  9 of the studies (37 twin pairs) were conducted before 1965 (therefore diagnosed with OCD according to the old daignostic criteria). But the majority of studies (10000 twin pairs in total) were more recent (therefore diagnosed under current DSM criteria).
• Findings: IN CHILDREN - heritability of OCD symptoms ranged between 45 and 65%.  IN ADULTS - heritability of symptoms ranged between 27 and 47%.
• Conclusions: There is a genetic component to OCD.  The level of heritability of OCD is greater in children than among adults.

GENETIC EXPLANATION TO OCD:

LENANE ET AL (1990):-

• Performed a study into the prevalence of OCD among related family members, finding evidence for the existence of heritable contributors to the onset of the disorder, lending support to the genetic viewpoint.

SAMUELS ET AL (2007):-

• Used gene-mapping to compare OCD sufferers who exhibited compulsive hoarding behaivour with those who didn't, finding a link to chromosome 14, implying a genetic influence to compulsive hoarding behaviour, which may also indicate the existence of separate OCD sub-type.

NEURAL EXPLANATION TO OCD:

PICHICHERO (2009):-

• Reported case studies from US National Institute of Health showed children with steptococcal (throat) infections often displayed sudden indications of OCD symptoms shortly after being infected.  Some also often exhibited symptoms of Tourette's.  This supports the idea that infections may have an effect on neural mechanisms underpinning OCD.

FALLON AND NIELDS (1994):-

• Reported 40% of people with Lyme's disease incur neural damage resulting in psychiatric conditions, e.g. OCD, suggesting neural explanation can account for the onset of OCD.

ZOHAR ET AL (1987):-

• Gave mCPP (drug reducing serotonin levels), to 12 OCD patients and 20 non-OCD control ppts, finding OCD symptoms were significantly enhanced in OCD patients.  Suggests sufferers' condition was related to abnormal levels of serotonin.

NEURAL EXPLANATIONS TO OCD:

HU (2006):-

• Compared serotonin activity in 169 OCD sufferers and 253 non-sufferers, finding serotonin levels to be lower in the OCD patients, which supports the idea of low levels of serotonin being associated with the onset of the disorder.

SAXENA AND RAUCH (2000):-

• Reviewed studies of OCD that used PET, fMRI and MRI neuro-imaging techniques to find consistent evidence of an association between the orbital frontal cortex brain area and OCD symptoms.  This suggests that specific neural mechanisms are involved with the disorder.

TREATING OCD:

DRUG THERAPY:-

KORAN ET AL (2000):-

• Aim: To assess the ability of olanzapine augmented with an SRI to alleviate treatment resistant forms of OCD.
• Procedure: 10 adult OCD sufferers who had not responsed to treatment with the SSRI fluoxetine alone.  Continued taking the SSRI and added 2.5mg daily of the antipsychotic drug olanzapine. Then increased to 5mg/day for 2 weeks and later to 10mg/day for another 4 weeks.
• Findings: Overall the patients' symptoms dropped by 16%.
• Conclusions: SSRI treatment with the antipsychotic durg olanzapine improved OCD symptoms. Treatment with 2 drugs simultaneously is more effective than single treatment.
• Evaluation: Results would need to be confirmed by double-blind placebo controlled trials to be confirmed.  There is also a need to compare the effectiveness of risperidone and olanzapine when added to SRI treatments to see which is superior.

TREATING OCD:

DRUG THERAPY:

CICCERONE ET AL (2000):-

• Investigated the effect of low doses of the antipsychotic drugs risperidone in treating OCD, finding treatment effective due to the drug's dopamine lowering effect.

JULIEN (2007):-

• Reported that studies of SSRIs show that although symptoms do not fully disappear between 50 and 80% of OCD patients improve, allowing them to live a fairly normal lifestlye, which they wouldn't be able to do without the treatment.

TREATING OCD:

PSYCHOSURGERY:

RICHTER ET AL (2004):-

• Reported that 30% of OCD patients had a 35% or greater reduction in symptoms, but there were occasional complications, such as urinary incontinence and seizures.  As these were patients at risk of suicide who hadn't responded to drug therapies, the treatment can be considered relatively effective.

MALLETT ET AL (2008):-

• Evaluated deep-brain stimulation as a therapy for treatment resistant OCD, comparing it with pretend stimulation and found significant symptom reduction, which suggests the treatment to be effective.