Clinical biases in diagnosis

interview-2207741_640.jpg

In the abnormal psychology option, what is the difference between cognitive biases and clinical biases?

Clinical biases are cognitive biases that take place when a psychiatrist or psychologist is trying to make a diagnosis and label the behaviour. They can arise from experience (‘these symptoms nearly always mean this mental health problem’) and result in a misdiagnosis when other explanations for the behaviour are too readily discarded. This is a confirmation bias – symptoms are interpreted to confirm the mental health professional’s original swift diagnosis. It was demonstrated in Rosenhan (1973)  when the admitting medical staff interpreted the very vague symptoms described as schizophrenia, and even more clearly when the normal behaviour exhibited by the pseudo-patients was interpreted by medical staff to confirm the validity of the original diagnosis.

They can also arise from an existing societal and/or personal bias, such as an ethnic or gender bias. Jenkins-Hall and Sacco (1991) found that a sample of USA psychotherapists showed an ethnic bias against black clients in that they evaluated depressed black clients more negatively than depressed white clients. While both groups were diagnosed with depression, the black clients (ethnic minority in this case) were seen as being less socially capable and were evaluated as more seriously depressed, using a standardised scale. A larger study by Bertakis et al (2001) demonstrated that women were much more likely than men to be diagnosed as depressed by their primary care physicians, even with a similar number of visits. This showed a gender bias in diagnosis.

So, there is a clear link between this material and the study of cognitive biases, especially confirmation bias.

References

Bertakis, K.D., Helms, J., Callahan, E.J., Rahman, A., Leigh, P. & Robbins, J.A. (2001).  Patient Gender Differences in the Diagnosis of Depression in Primary Care.  Journal of Women’s Health & Gender-Based Medicine, 10(7), pp. 689-698.

Jenkins-Hall , K. & Sacco , W.P. (1991).   Effect of Client Race and Depression on Evaluations by White Therapists.  Journal of Social and Clinical Psychology, 10(3), pp. 322-333.

Rosenhan, D. L. (1973). On being sane in insane places. Science179(4070), pp. 250-258.

Taking a holistic approach to the course

connections jigsawI have been trying over the past few years to do this, and am sometimes asked what I mean by ‘a holistic approach.’  The easy way is to demonstrate using an example. If you are teaching/studying the abnormal psychology option, for instance, you will probably be doing this after you have spent some time looking at the core approaches to explaining human behaviour (biological cognitive and sociocultural) and also looking at research methods and ethics.

So, now comes the time to apply your learning to the content of this option. Explore the differences between psychiatry (more medically and biologically based) and psychology (more cognitively and socially based). Take major depressive disorder, for example: how might a psychiatrist explain it?  How might they look for evidence to see if their explanation is correct and what sort of evidence would they see as valuable? How valid is their method of looking for evidence? How reliable is it? Does it allow them to develop a theory of etiology of MDD that has good explanatory power? How might they want to treat MDD once they are sure a person is suffering from it? Discuss the benefits and limitations of this treatment. Are there any ethical considerations regarding this treatment? 

Now, how might a cognitive psychologist explain MDD? How would s/he look for evidence and what would they accept as evidence? How valid is this method? How reliable is it? Does it allow them to develop a theory of etiology of MDD that has good explanatory power? How would a cognitive psychologist treat MDD.  Discuss the strengths and limitations of this treatment. Are there ethical considerations regarding this treatment?

What about sociocultural arguments that childhood trauma, domestic violence, poverty and stress can all singly or in combination be responsible for MDD? That removing the conditions that lead to MDD is the best treatment? 

Finally, consider the eclectic approach that is more common nowadays. What is the evidence that a combined approach to both the diagnosis, explanation of* and treatment for MDD may be more successful than a single approach? What is the evidence that doing nothing also works? What about a choice of approaches, or sequential treatment?

If we start the abnormal psychology option with these questions and work together to answer them, then the specific content becomes easier to understand in context of perspectives on abnormal psychology, and within the framework of approaches to research. This can be put into practice in the other options as well. Put it all together!

*e.g. Interaction between genetic vulnerability, environmental trigger and possible faulty cognition.

Planning your course effectively – more overlaps

Cog blue corrected

Similarly to the biological approach, there are many overlaps between the cognitive approach and the options of abnormal psychology, development, health and human relationships.  For example, the psychology of cognitive processes and their reliability can explain clinical biases in diagnosis of disorders, debates regarding the etiology of  disorders and also inform their treatment.

Watch out for more of these!

Antagonists – what do they do?

dementia-3761172_640Antagonists are any chemicals that fit into receptor sites on the post-synaptic neuron, inhibiting the neuron from firing. Well-known antagonists for serotonin, which we looked at in the previous blog post, are anti-psychotic drugs like Clozapine, which acts on the HT2A serotonin receptors to decrease the effects of serotonin in the brain. Many ant-psychotic drugs also act as antagonists for dopamine, as an excess of both dopamine and serotonin has been associated with schizophrenia.

However, easy-to-understand studies referencing this effect of Clozapine are difficult to come by, so while this is useful knowledge for students on how anti-psychotic medication works, when teaching about antagonists there is more available research on the effects of scopolamine on acetylcholine, and hence on memory.  (And incidentally on motion sickness, as scopolamine is excellent at preventing nausea and vomiting!)

Scopolamine acts by blocking the acetylcholine receptors, specifically the muscarinic receptors (see the link below). Atri et al (2004)  reported how blocking the muscarinic acetylcholine receptors (mAChRs), by injecting scopolamine impairs learning of paired words.

As an age-related deterioration in cognitive function is thought to be predominantly related to a decline in cholinergic neurotransmission (relating to nerve cells in which acetylcholine acts as a neurotransmitter), scopolamine administration has often been used to model dementia. Scopolamine has therefore been extensively used for preclinical and clinical testing of treatments for cognitive impairment.  For example, Tröster et al (2013) found that scopolamine negatively affected anterograde short-term memory and verbal and nonverbal learning in middle-aged men.

Agonists – what are they?

fireworks-636983_640

Biological psychology has come to the fore over the past years.  The mapping of the human genome combined with improved brain-scanning techniques has meant that the biological correlation to psychological conditions is more easily identifiable, and it is clear that many mental disorders like major depressive disorder, anxiety disorders and schizophrenia are explainable through a gene x environment interaction.  This usually means that an inherited genetic pre-disposition to a disorder, or a certain behaviour or addiction is triggered environmentally.

Talking of genes takes us to neurotransmitters.  How? Genes make proteins which make neurotransmitters and genes also transport neurotransmitters across the synapse. (See Caspi et al._2003 and the 5HTTR serotonin transporter gene).  Neurotransmitters are agonists –they bind with receptor sites on the post-synaptic neuron and cause an action potential.  Drugs are also agonists that act in the same way, but they are not natural in our nervous system.  Neurotransmitters are known as endogenous agonists (internal agonists); drugs, or any chemicals taken into the body, to deliberately stimulate a certain neurotransmitter or group of neurotransmitters, are exogenous agonists (external agonists).

An exogenous agonist for serotonin is MDMA (Ecstasy).  It works by binding with the serotonin transporter genes and also with the receptor sites, temporarily increasing the serotonin in the synapse in the neocortex (part of the cerebral cortex), the amygdala, hippocampus and hypothalamus, affecting cognitions such as memory and perceptions, as well as mood. We party!

However, studies have suggested that there is a rebound effect, whereby damage to the serotonin transporters after several doses of MDMA over a period of a few days has resulted in an ultimate decrease of serotonin in the brain, and memory and mood impairment, leading to theories that this might be linked to a motivation to take more and eventually to possible addiction. (See McCann et al MDMA and memory).

Of course, the opposite to an agonist is…an antagonist, which will be the subject of the next blog post.

Research from Psychology Sorted: Poverty and childhood cognitive development – a biological approach.

This is the first in a series of posts using research directly from our new bookpoverty3349068_640 Psychology Sorted.  The study we’re looking at today is Luby et al. (2013) on how children’s brain development and therefore their cognitive development are affected by poverty. The researchers found that exposure to poverty in early childhood impacts cognitive development by school age. However, the effect is mediated positively by good caregiving and negatively by stressful life events.

This is highly relevant in light of reports from the UK, USA and  South-East Asia of the large, and in some cases growing, number of children living in poverty.  This research can be used as an example of both localization and neuroplasticity within the Biological Approach,  and to illustrate the influence of poverty/socio-economic status on cognitive development, for those studying the Developmental Psychology option.

This was a longitudinal study of 145 children from a sample of children already enrolled in a 10-year study of preschool depression who, prior to being scanned by MRI,  had undergone regular testing.  Once a year (for a duration of 3-6 years) the children had taken part in a series of tests aimed at measuring their cognitive, emotional and social aptitudes. The involvement of significant adults in their lives was also recorded (e.g. how close they were to their caregivers) as well as the occurrence of any negative and stressful events in their lives. Once this collection of information had been amassed, each child underwent two MRI scans – one of the whole brain and one of the hippocampus and amygdala only. This study can therefore also act as an example of the use of brain-imaging technology as a technique used to study the brain in relation to behaviour.

Both the hippocampus and the amygdala showed less white and grey matter in the MRI scans of the poorer children in this study, with a positive correlation between income/needs being met and brain volume. While both the hippocampus and amygdala showed less development in poverty-affected children the researchers found that in cases where the child experienced positive care there was less negative effect on the hippocampus. Difficult and stressful life events only affected the left hippocampus.

Of course, students and teachers need to evaluate the use of this research as well: how valid is the study as an illustration of both localization and neuroplasticity? This was a relatively small sample of pre-schoolchildren from the USA who exhibited symptoms of depression.  Moreover, attempting to measure complex variables (e.g. the nature of caregiving and behavioural responses) is beset with difficulties as these variables are not exact and may lack construct validity.  Nonetheless, there was triangulation of methods, with the background data from cognitive testing providing a rich backdrop for the results of the scans, and this research is supported by other studies, such as that by Duval et al. (2017). 

Encourage your student to find and read media and academic examples of evidence and counter-evidence, and to engage in critical thinking and evaluation. For example, some poor families often cannot afford pre-school kindergartens for their children, who may be raised to some extent in isolation as well as in poverty.  This could be a confounding variable. Are there others? The student who is thinking like this is well on the way to writing a good argumentative essay on the effects of poverty on childhood cognitive development.

Coming soon – ‘Psychology Sorted’, the book!

Hi Psychology teachers from all over the world! Yes, I know that summer is beckoning but wouldn’t you like a sneaky peak at a BRAND NEW RESOURCE that is due to be out around October 1st? Written by Laura Swash and Claire Neeson, this resource will solve all those pesky teaching dilemmas such as: ‘Which studies should I use for each topic and how can I re-use them to create less bulk for the students to learn?  How can I find a streamlined, easy, cross-referenced resource that’s user-friendly (for me and my students)?  What can I use for both teaching AND revision?’ Here is a sample for you to taste, to get the ‘flavour’ of what we’re doing. Add us to your school shopping list: #1 Order ‘Psychology Sorted’ next term.  Sorted!

Sample_Section 1_Bio. updated

Bio KS1 Fisher et al_2005