Neurology of Depression

Cognitive Psychology has in the recent years given explanations of depression and anxiety in both healthy and unhealthy populations. The explanation is given that there is a certain difference between those with anxious and depressive symptomatology, the symptoms of depression are supposedly caused by past loss or experience, anxiety by potential (or perceived) future threats. (Eysenck & Keane, 2010).

In cognitive psychology, ones vulnerability to experiencing the symptoms of anxiety and depression is due to the presence of certain cognitive biases. It is these biases which therapy’s, such as cognitive behavioural therapy (CBT) try to alter in order to help reduce the depressive/anxious symptomatology by eliminating/reducing these biases. These biases are as follows:

1. Attentional Bias: These occur when one focuses their attention onto a threat related stimuli which is often produced or experienced at the same time as a non threat related stimuli. (This can occur more so in the psychopathic population(s) than in the regular 'healthy' population as psychopaths have been suggested to focus their attentions on particular items or subjects.)
2. Interpretive Bias: This is where those things or situations with a dual meaning would be interoperated with the more threatening/sinister meaning instead of a positive or neutral meaning
3. Explicit Memory Bias: when the person holds a tendency to consciously recall only or more of the negative memories from their conscious memory than those positive memories.
4. Implicit Memory Bias: When the person tends to unconsciously recall negative or threatening memories.

In the cases of individuals who possess more of these, it would be rather obvious (and so needless to say) that it is those individuals who are more likely to display more depressive/anxious symptomatology. However, the big question in this area is which comes first, the symptoms of anxiety and depression, or the biases which clearly do not help the conditions?

Many theories have been composed in order to address the issue. Schema theories are among the popular ones. Beck (1976) as cited in Eysenck & Keane (2010). This places the vulnerability of depression and anxiety which some people hold on 'the formation of early life schemas and knowledge structure.'

In this they claim that all we do, with regard to cognition, is controlled by schemas, this meaning that those with 'anxious schemas' should see the more threatening information and be able to detect that easily and retrieve more easily, whereas those with depressive schemas will easily process and retrieve more depressive information. However, the claim is that the individual will likely not feel this all the time, and such schemas will not be active around the clock, instead only when they feel they are in an anxious or depressed mood. Thus making it more common in those with anxiety disorders (E.g. OCD, Paranoid Personality Disorder etc.) or Major Depressive Disorder – and thus may have implications on those with Bipolar and Schizaffective Disorder as these people are more likely to be in states of strong anxiety and/or depression and so are likely to suffer more from the unconscious thoughts which accompany these schemas – I am a failure.

Some criticisms have risen however with regard to this theory, the judgement of such schemas is often judged by the individuals behaviour (especially in clinical/diagnostic settings.) this then means that the schema is used as an explanation of the behaviour and not the other way around. It is for many psychologists to consider whether this is correct, in some cases it may be so that the schema influences the behaviour, however in many causes it could be that the behaviour influences (by creating, reinforcing or weakening) the schema, and this can also be so for the behaviour of those around the individual.

Beck's argument was that those with depression have entirely negative schema's this seems to be a mistake, for then it would be hard to effectively see recovery – change to a more positive schema – should the individual have a completely negative schema. Although therapies such as CBT do not always work in cases of depression, in those cases it does work, it would seem that the individual must have some form of positive schema.

A theory which seems slightly more reliable is one developed by Williams, Watts, MacLeod and Matthews (1997), as cited in Eysenck & Keane (2010). They made the suggestion that anxiety and depression serve different functions which are vital in the process of information processing and cognitive development. This theory is also one which is more generalisable, as it is easily applicable to both clinical and control populations. It would seem that anxiety is far more perceptual than is depression, and that depression is more specific in that they are likely to see more related stimuli to their situations.

It is the perceptual deductions which are the fast and automatic conclusions – which serve a more evolutionary function whereas conceptual processes are far more controlled but slower. It would seem that the conceptual processes are more human whereas perception seems to be far more evolutionary based and relevant to many species. It is the anxious perceptual nature which notices the threat and the depression and conceptual nature which interoperates the meaning of the threat. (Threat: Failing Exam (Anxiety) > Conclusion: I am a failure. (Depression).)

However we should consider that there are more biological reasons behind the states of such disorders'. For the sake of simplicity, I shall now focus my work purely onto depression and cut out the anxiety part, as it would seem that biologically, the causes of depression are less understood by most. For one to be diagnosed with depression (Major Depressive Disorder, the most common mood disorder) would mean that the person deviated from the norms of the emotion of sadness in that their level of negative emotion was detached from the reality of their circumstance and thus they felt more negative emotion than was 'normal' for their circumstance over a certain period of time – Approximately two years. (Holmes, 2010; Carlson, 2012).

The reason for my focusing attention upon the biological aspect of such is as follows. It would seem that disorders such as major depressive disorder (MDD) are heritable through family members, and studies have shown that people with relations suffering from affective psychosis have more chance of having children likely to develop MDD (1 in 10). (Rosenthal, 1971. As cited in Carlson, 2012). Thus this means that things such as MDD are likely down to a physiological cause and thus can be potentially be treated via medication – even though this may prove difficult - should one understand the processes and differences between those suffering from affective disorders such as MDD (or Bi Polar) and healthy controls.

Carlson (2012) states that there does appear to be a genetic link to certain affective disorders. Involved in MDD and its development, researchers seem to have found links to certain genes on chromosomes, these include defects to the genes involved in circadian rhythms in humans – and thus would explain the disordered sleeping patterns of those suffering from affective disorders – these genes include the RORA gene which holds the strongest link to the development of MDD and GRM8 which is involved in the production of some metabolic glutamate receptors (see, neurotransmission) has had a suggested involvement. However, as states by Carlson (2012) many of these studies are lacking in replication, thus no conclusive evidence has been found and we cannot confirm the exact genetic make up of those with MDD and Bipolar, this would be of advantage for a neurology/neuroscience basis, however we can assume from statistics that there is at least some genetic factor in the development of such disorders.

Further explanations have been given with regard to the time in which the baby was born. Sufferers of mental health problems such as Schizophrenia have correlated in that many birthdays fall under the late winter – early spring season. This has been suggested to have an increased likelihood of the child having schizophrenia in that the mother is more likely to develop flu in the second trimester (and critical period) of her pregnancy, thus this may cause physiological problems with the child which may lead to the development of schizophrenia. This has not been proven for affective disorders, however studies in Hungary in the thirties had indications that more people who committed suicide had a birthday in summer months, as >16% of MDD sufferers and >30% of those suffering from bi polar commit suicide, this could be a good indicate. However, there is as of yet, no conclusive evidence for this.

Biological techniques are often used in treating MDD, as therapies such as CBT often fail to work and many of these therapies – such as the use of receptor changing drugs – work well on patients. One proof comes from Lithium – a drug commonly used to treat Bipolar, has no effect on those suffering from MDD. This works are as a confirmation in that though the disorders have their similarities they would seem to have difference biological bases as they do not react to the same biologically stimulating drugs.

Many biological drugs work by selectively inhibiting (agonists) the reuptake of certain neurotransmitters. For example, many antidepressant drugs focus on the neurotransmitter serotonin (5-HTT) this is due to its emotional impact, some also focus on adrenaline. The most famous antidepressant would be selective serotonin reuptake inhibitors. (SSRIs) these drugs are designed to prevent the reuptake of serotonin into the neighbouring neural receptor (in the brain) and thus slowing the process of depression as it prolongs potentials in the first neuron.

Returning to aspects of biological development of MDD, it seems there has so far been little in the way of genetic evidence, however many techniques are improving and we should be able to develop more information about what causes (or potentially causes) MDD, yet there are suspicions – likely correctly – that MDD is caused by many genetic factors – plus some environmental and social factors also. Yet the biological effects of MDD have been suggested to have been at least considerable due to stroke patients, who, dependent upon which side of their prefrontal cortex they damaged displayed different alterations in their mood. (Fava & Kendler, 2000)

To conclude the findings of the above literature, it would seem most likely that depression is a genetic or at least biologically founded illness which is likely heritable, either directly through the genes given by parents – as there may be specific genome which actually and directly cause depression to occur in certain individuals or by providing a set of genes which make people more vulnerable to certain environmental factors which cause or influence the likelihood of one developing depression. (Caspi et al, 2003)

References

Carlson, N. R. (2012) Physiology of Behaviour. (11th Ed) New York: Pearson.

Caspi, A., Sugden, K., Moffitt, T. E., Taylor, A, Brain, I. W. Harrington, H., McClay, J., Mill, J., Martin, J., Braithwaite, A. & Poulton, R. (2003). Influence of Life Stress on Depression: Moderation by a Polymorphism in the 5-HTT Gene. Science. 301, 386-389

Eysenck, M. W. & Kaene, M. T. (201). Cognitive Psychology. (6th Ed) New York: Psychology Press

Fava, M. & Kendler, K. S. (2000) Major Depressive Disorder. Neuron. 28, 335 – 341

Holmes, D. A. (2010) Abornal, Clinical and Forensic Psychology. (1st Ed). London: Pearson