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1.11.1 Introduction
While many different theories exist as to the development of depression, there are two main schools of thought. The first emphasises the importance of biological substrates and clear neuroanatomical lesions. Depression therefore directly results from neuroanatomical and physiological damage. In contrast, others contend that the neuropathology is less important. After all, many individuals with extensive cerebral lesions show no change in mood and others with little abnormality visible on
CT scans, show extensive depression or behavioural change. This suggests that depression is caused by a maladaptive response to impairments caused by the injury. In this model the importance of premorbid psychosocial factors and susceptibility to depression is emphasised as well as post-injury behaviours and traits that prolong disability or a negative self-evaluation.
The older literature on depression often uses the terms “endogenous” and “reactive” as an early classification, although these terms have gone out of favour. Due to the lack of demographic and injury factors such as severity of TBI, to predict the likelihood of depression or the outcome, some authors suggest that the TBI is not related to the development of depression in these individuals and in this regard no different to any generalised trauma that an individual may undergo. This “reactive” model contends that depressive symptoms simply constitute a normal psychological response to a stressful event such as a trauma which negatively impacts upon that individual’s ability to adjust. In this regard some individuals are more predisposed to develop depression as a result of their premorbid personalities. There may also be a part played by lack of prompt medical attention or rehabilitation afterwards [Andelic 2012].
1.11.2 Biological substrates for depression
A number of studies have tried to correlate depression after TBI with neuro-anatomical findings and it is known that many of the areas associated with mood disturbance, are also damaged in TBI. A comprehensive study of this nature looked at 66 prospective admissions and examined the relationship between radiological findings and depression after injury [Federoff 1992]. They suggested that there was an increased early incidence of depression and left sided dorsolateral prefrontal cortex lesions and to a lesser extent, left sided basal ganglia lesions.
It has also been shown that after TBI there are volumetric changes in the left prefrontal cortex [Jorge 2005], in the orbitofrontal cortex bilaterally and the left anterior cingulate cortex [Hudak 2011]. Another recent study found marked asymmetry in frontal and parietal lobe volumes in depressed
individuals compared to non-depressed TBI [Koenigs 2008]. Areas of reduced neuron density are known to be rich in cholinergic innervation and interventions aimed at enhancing the cholinergic system have been shown to alter cognitive function [Salmond 2005]. Others have suggested that these lesions cause interruption and depletion of brain amines, particularly dopamine and serotonin and hence cause depression although a single neurotransmitter is unlikely to be the sole cause. It is also postulated that cerebral asymmetry in terms of the emotional processing may be caused by the left sided frontal lesions and altered activation or inhibition of a number of secondary brain centres then occurs [Schonberger 2011].
Studies show that over several weeks after TBI, cell damage and loss occurs in particularly vulnerable areas such as the prefrontal cortex, hippocampus, thalamus and amygdala [Raghupathi 2000, Grady 2003].
Many of these areas affected by TBI coincide with regions known to be important in regulating mood. The prefrontal cortex modulates a number of subcortical structures that evaluate aversive stimuli and their context [Finset 2000]. The orbitofrontal cortex is often affected by TBI and is important in regulating social behaviour [Fleminger 2008].
The regulation of mood is dependent on the coordination of neural networks within the cortex, limbic system and brain stem. Disruption of these neural circuits may constitute the substrate for cognitive and psychological impairments after TBI [Hariri 2003, Macgregor 2013] including depression [Jorge 2005].
Further development of such biological theories may be aided by newer and more sophisticated radiological techniques, particularly those that look at metabolic activity and brain function or which can more clearly define white matter tracts and lesions. Magnetic resonance spectroscopy has shown abnormalities of choline and N-acetyl aspartate in basal ganglia which are markers of neuronal integrity [Rao 2010]. Functional MRI scans (fMRI) and diffusion tensor imaging studies (DTI) show areas of heightened and decreased activity in areas of the cortex, particularly prefrontal [Matthews 2011]. DTI is particularly useful in identifying the integrity of white matter tracts and
SPECT (Single positron emission CT) is useful in studying areas of altered metabolic activity. New techniques may delineate and correlate brain function to specific cortical areas. This will allow better understanding of abnormalities such as mood and awaits wider availability of these techniques in clinical practice.
1.11.3 Psychosocial factors for depression
The neuroanatomical explanation for depression, described above, differs from the psychological theory. Many view the association between TBI and depression to be more likely to be mediated by psychological or psychosocial variables, particularly as time goes on.
Indeed
a later study by the same group that showed the early link with depression and left-sided lesions, found that the neuroanatomical lesions only correlated to presence of depression at an early phase, i.e. less than three months [Jorge 2005]. At a later date there was no link. They themselves suggest that psychosocial factors then become more significant in perpetuating depression than the anatomical substrates. Some individuals may have a pre-injury vulnerability to developing emotional difficulties and indeed pre-morbid psychiatric history prior to injury is often associated with a higher incidence of depression after TBI in the literature [Hart 2012]. Poor social circumstances after the injury such as lack of rehabilitation, poor family supports, ongoing substance or alcohol abuse may then perpetuate ongoing disabilities and the risk of depression [Helchem 2013]. Those individuals with fewer personal, social and financial resources, find themselves unable to resume their premorbid lifestyles and a consequence of this is poorer functional outcome and increased likelihood of depression. In this regard, depression can be considered a maladaptive psychological response to TBI and independent of the extent of injury or areas of brain affected [Hou 2012].It follows that symptoms are more likely to be maintained in individuals with adverse psychological factors [Sawchyn 2000, Cassidy 2014]. A belief that recovery is unlikely and that any disability will be prolonged, may also contribute to the development of depression in such individuals.
1.11.4 Working model
It is clear that the theoretical model for depression is complex and it is probably unlikely that a specific brain lesion or a single psychological factor is responsible alone for producing depression. While neuroanatomical biological substrates such as localised lesions and disturbances in various neurotransmitters are significant, these are also linked with poor premorbid psychosocial functioning and ongoing psychological distress with a failure to socially reintegrate or find appropriate support [Demakis 2007]. The role of personality traits is also significant with regards to those with a “helpless” or attributional style of coping, along with an external locus of control [Curran 2000]. Poor insight and ongoing cognitive impairments may also contribute. No single model can explain the complex interplay of biological, developmental and psychosocial factors that determine an individual’s susceptibility to depression after TBI. There is probably a heterogeneity of aetiologies [Busch 1998] with a variety of different factors but which ultimately end with a final common expression of psychological disturbance i.e. depression.
The combined theory postulates that the emotional disturbances in TBI can be attributed to complex networks of interaction between neurological impairment, pre-existing behaviours and maladaptive responses; in other words there are complex processes which implicate cerebral structures as well as the external psychosocial environment as involved in the manifestation of depression post-TBI.