Please enable JavaScript.
Coggle requires JavaScript to display documents.
DEPRESSION, STUDIES & DIAGNOSIS, :check:Lewinson et al found from…
DEPRESSION, STUDIES & DIAGNOSIS
Carlsson
Results
- Support role of low levels of glutamate in dev of psychotic symptoms
- Found PCP acts as antagonist of glutamate receptor [NMDA]
--> PCP inhibits action of glutamate & reducing action in areas of brain
- PCP found to be more likely to result in psychosis in users even more than users of amphetamine
- Reduced levels of glutamate are associated with increased dopamine release
Results
- Clozapine is a highly effective treatment for Sz - fewer negative symp
- Shown to be antidopaminergic and antiserotonergic functions --> meaning it reduces levels of dop & serotonin in the brain
- Highly effective in patients who have previously not responded to treatment
--> relationship between serotonin and glutamate
- therefore some non treatment patients may belong to subgroup whose disorder is explained by hypoglutamatergia
Key points
- Further research must be carried out to dev drugs to treat negative side effects
- Consider role of other NT [serotonin, glutamate]
:red_cross: Research taken from other researchers so low reliability and validity
:check: Secondary research useful to gather larger amount of info quickly & gain wider picture
:check: Many of the pieces of research used came from reliable methods eg PET scans which take obj measures of activity in diff areas of the brain
:check: Research helpful to dev more effective treatments for p who are treatment resistant
Aim
- Review studies of the relationship between levels of NT [especially serotonin and glutamate] on symptoms of Sz
Diagnosis
4 Ds
- Deviance -behav considered rare
- Dysfunction -behav interfering with person's life
- Distress -Behav upsets indiv
- Danger -behav dangerous to themselves and/ or to others
ICD-10
- includes conditions and diseases which are related to the entire human physiology
- Section F specially for MHD
- Each disorder is grouped into "families" which are represented by a number eg depression part of the mood disorders [3]
- Following number represents specific disorder eg F32 is depression
- decimal digits represent specific sub-type eg F32.0 = mild depression
DSM V
- strictly intended for MHD
- contains the ICD-10 code next to MHD so clinician can refer to both manuals
Rosenhan
Aim
- To challenge diagnostic system for MHD as it puts emphasis on the individual as the source of symp used to classify disorders as opposed to environmental context in which symp arose
Procedure
- Claiming to hear voices : "empty" "hollow" "thud" in their own gender
--> stimulated "existential crisis"
- 7 out of 8 patients diagnosed with Sz
- 1 patient diagnosed with
Ppts + hospitals
- 8 patients [3W & 5M]
- none had MHD history
- not showered for 2 weeks = unkempt
- 12 hospitals [range of good & bad, old & new, refurb & non-refurb]
- hospitals across 5 states
Results
- Av stay = 19 days
- longest stay = 52 days
- Shortest stay = 7 days
- 1/3 of patients challenged pseudopatients
- normal behav was pathologized eg : note taking = "writing behav" , Pacing corridors = "nervousness", waiting for lunch = "oral aquisitive syndrome"
- staff Depersonallisation of patients eg : 71% ignored by nurses when p approached, eye contact made 23% of time, verbal responses only 2% of time
and ZERO senior staff answered verbally
- Nurses stayed in office for 90% of the time
- Patients spent less than 7 mins per day with the staff
-
-
-
:check:Lewinson et al found from research into adolescent depression - when stressed, dysfunctional attitudes rather than environmental factors was the strongest predictor of adolescent major depressive disorder
--> Shows link between negative thinking and depression
BUT little evidence showing negative thinking was present before the onset of depression as suggested by Beck
:red_cross: Fails to explain gender bias with women suffering more frequently than men with depression - no evidence that suggests females have more negative schemas than males do
:check: Antidepressant drugs inhibit the activity of MAO-A --> leading to more monoamine activity and a reduction in symp of depression [MAOI]
:red_cross: But drugs only "mask" the symptoms & have unpleasant side effects. Research into 5- HTT gene offers hope that future therapies will help increase the S levels of those who show early symptoms of depression --> preventing development of dep in the first place
:check: Andreoli et al found that antidepressants known to increase N levels are just as effective as those that increase S levels
However NRIs not always successful for all depressed p and seem to be more effective with endogenous than reactive depression types
:check: Supported by D'Alessandro who found students'
- with negative views about their futures were strongly associated with an increase in depressed mood
- with dysfunctional beliefs about themselves who didn't get into their first choice of college then doubted their futures and developed depressive symp
-
:check:Rosenthal - diathesis stress model explains that a gene that produces a MHD can be "triggered" a stressful environment
:red_cross: Kirsch believes antidepressants cause a placebo effect because they block the reuptake of serotonin so it is available in synaptic gap to be taken up by postsynaptic receptors which elevates mood
:check: Versiani et al used a double-blind trial of NRIs & a placebo drug to find a marked improvement in mood in depressed patients with NRI compared to the placebo drug - antidepressants more eff
:red_cross: Correlation doesn't show cause - whether abnormal brain activity causes depression or whether depression causes abnormal brain activity
- or if there is another factor causing abnormal activity and depression
:red_cross: Angoa- Perez found mice lacking gene for trytophan [enzyme for serotonin production] didn't show any signs of depression in tests nor were they responsive to antidepressant med
--> cause must be more than low levels of serotonin & other factors involved
:red_cross: Treatment aetiology fallacy - we assume that because the antidepressants are effective in reducing the symp, that the target of the treatment [monamine] must be the cause. But this is not correct, it is not proven that serotonin and noradrenalin levels cause depression.
:red_cross: Sullivan et al found that there was a 40% increased risk of developing the disorder when a first degree relative has depression.
Found within meta-analysis of family, twin & adoption studies.
--> evidence that there is a familial transmission of depression so could indicate a genetic vulnerability to NT dysfunction
:red_cross: Challenged because humans have much higher levels of cognitive functining and may behave differently to how the dogs did. :check:But the research has been replicated with humans and findings were the same
-
:red_cross: Individuals may be more vulnerable to depression if certain life events trigger the genetic predisposition
- Brown and Harris found that major life events tended to occur in a depressed ladies life from London, before an episode of depression.
- However it is difficult to establish a causal relationship because depression may cause the life difficulties rather than the other way round
-
-
-