Mysteriously and in ways that are totally remote from normal exile, the grey drizzle of horror induced by depression takes on the quality of physical pain, William Styron wrote in Darkness Visible (Random House, 1990). Science of twentieth century can explain strange rare conditions, but common problems like depression – one of the most disabling sicknesses – remain without understanding. The classic literature of what was then called “physiological psychology” in the 1950s and 1960s concerned the neural substrates of emotion and related constructs such as depression.
However, it has been only recently that strong connections between this research tradition and the study of emotion in humans has been made (Berridge, 2002). While the emotional influences of human brain been a focus of scientists from the early days of neuropsychology and behavioural neurology, little systematic work on this topic was performed before the past two decades. It was not until 1996 that the very first article Critical evaluation of the article Brain Scans Provide Striking Insights Into Depression to use fMRI to study depression was published.
Since then a growing literature has accumulated that suggests different roles for the left and right prefrontal regions in different aspects of emotion, as well as specific roles for subcortical regions such as the amygdala. Some of the important findings from this collective body of the article will be summarized in this paper. Critical evaluation of the article Brain Scans Provide Striking Insights Into Depression Introduction How is it that our brain can affect our bodies and influence our health?
The mind/brain is quite literally housed within a body and causally exerts an influence over it. This relationship is decidedly not unidirectional but, rather, operates reciprocally. We are truly on the dawn of a new understanding of this relationship that is both breathtaking in range and focused on mechanism or process. The role of mental events such as emotions, moods, and attitudes in physical health and illness is becoming a tractable problem because we have new tools for interrogating brain function.
Since 1995, a growing number of studies using positron emission topography (PET) and a functional magnetic resonance imager (fMRI) to investigate the role of the amygdala in emotional processes have begun to appear. Many studies have reported more activation of the amygdala detected with either PET or fMRI when anxiety-disordered patients have been exposed to their specific anxiety-provoking stimuli than when they were exposed to control stimuli (Breiter et al. , 1996).
The findings from both the lesion and neuroimaging studies on the role of the amygdala in affective processes raise a number of important questions about the functional significance of amygdala activation and the precise role this structure may play in human emotion. The article Brain Scans Provide Striking Insights Into Depression describes findings of professor of psychology and psychiatry Richard Davidson. In his research Davidson studied the prefrontal cortex (PFC) and the amygdala, areas of the brain that have been identified as playing an especially important role in depression.
One key question is whether the amygdala influences emotion in general or primarily affects negative emotions. In this work I will provide some of the key concepts and findings that link different territories of the PFC and the amygdala to depression. In order to evaluate the reliability of the report I will also consider the acceptance of the research by the scientific community. The two key features of the brain underlying positive and negative affect highlighted in the article are the prefrontal cortex and the amygdala.
It has detailed studies on the basic function of the amygdala in depression. Specifically, he emphasizes the role of the amygdala in the depression, largely through the amygdala’s influence over brain areas. “Using PET to capture metabolic activity in both brain regions at the same time, we saw that, more than any other area, a portion of the left prefrontal cortex relates reciprocally to activity in the amygdala,” he said (Brain Scans Provide).
However, looking into scientific literature I discovered that the case for the differential importance of left and right PFC sectors for emotional processing was first made systematically in a series of studies on patients with unilateral cortical damage (Gainotti, 1972; Robinson, Starr, and Price, 1984; Sackeim et al. , 1982). Each of these works compared the mood of people with one-sided left or right brain injury and discovered a greater degree of depressive symptoms after left-sphere injury.
The general interpretation that has been placed on these studies is that depressive symptoms are increased after left-sided anterior PFC damage because this brain territory participates in a circuit that underlies certain forms of positive affect; damage to this region leads to deficits in the capacity to experience positive affect, which is a hallmark feature of depression (Watson et al. , 1995). In the research paper, Davidson also described a large group of individuals who had early damage to the two spheres of the brain.
The people, damaged early in life, both exhibited histories of oral and mental abusiveness and intermittent, fervent explosions of anger. A big collection of data at both the animals and people comprises different spheres of the PFC in emotion. Though the PFC is not a uniform zone of tissue, it has been distinguished in accordance with both cytoarchitectonic and functional reasoning. The three parts of the main PFC that have been consistently differentiated comprise the dorsolateral, ventromedial, and orbitofrontal areas.
There also appear to be significant functional diversities between the left and right parts among each of these sectors. Like Richard Davidson, Tomarken, Davidson, Wheeler, and Kinney (1992) used measurement of scalp-recorded brain electrical activity and discovered that indices of activation asymmetry connected with power spectral measures were steadfast over time and showed perfect internal permanency reliability thus implementing a number of significant psychometric criteria for an index of a characteristic construct.
In some studies, Davidson and Fox (1989) discovered that there are big individual differences in the size and direction of baseline dissymmetric process in brain electrical activity measurements found from prefrontal scalp sectors in both children and adults. Davidson and Fox (1989) discovered that 10-month-old infants who have larger relevant right-sided prefrontal activation in prefrontal scalp areas were more likely to shout in answer to a short period of maternal secretion than were their left-activated doubles.
Rickman (1999) found that infants and young children with larger relative right-sided prefrontal activation exhibited more behavioural inhibition and circumspection. Tomarken, Davidson, Wheeler, and Doss (1992) noticed that indults individual distinctions in such measures forecast dispositional mood, self-report measurements of behavioural activation and inhibition (Sutton and Davidson, 1997), repressive defensiveness, reactivity to positive and negative emotion elicitors (Tomarken, Davidson, and Henriques, 1990; Wheeler, Davidson, and Tomarken, 1993) baseline immune function (Kang et al.
, 1991), and reactivity of the immune system to depression (Davidson, Coe, Dolski, and Donzella, 1999). In his work, Larson (1998) noticed that individual distinctions in electrophysiological measurements of prefrontal asymmetry forecasted the significance of recovery after a negative affective stimulus. The data say that the prefrontal cortex may regulate the time course of emotional reacting or in the big inhibition of negative affect.
Richard Davidson also discovered that individual dissimilarities in these brain electrical measures of front asymmetry are connected with depressions. I found that Henriques and Davidson (1990) concluded that depressed people who are currently euthymic but have a history of past depression show less left prefrontal activation than do never-depressed controls. Davidson also found that when social phobics expect making a public speech, they exhibit large growth in right-sided prefrontal activation, though they do not vary from controls at baseline.
In a series of studies with Davidson, Kalin, and Shelton (1992), Kalin, Larson, Shelton, and Davidson (1998) have demonstrated that similar activation asymmetries can be measured in rhesus monkeys and that they predict similar types of behaviour and biology as we observe in humans. In the most recent effort of this kind, Kalin (1998) found that animals with greater relative right-sided prefrontal activation exhibit higher basal levels of the stress hormone cortical.
Similar data have recently been reported in humans by Buss, Dolski, Malmstadt, Davidson, and Goldsmith (1997). The data from the Larson et al. (1998) study referred to above indicated that people with greater relative left-sided prefrontal activation at baseline have bigger recovery of startle potentiation following the offset of a negative stimulus. Moreover, the measure of asymmetric prefrontal activation accounted for more variance in the magnitude of startle post-negative-stimulus offset (i.
e. , startle recovery) than it did during the stimulus. These findings confirm Davidson’s conclusion that individual differences in prefrontal activation asymmetry may play a role in regulating the time course of emotional responding and that those individuals with more leftsided prefrontal activation may recover more quickly than their right-activated counterparts from negative affect or stress.
A key to the mechanism that may underlie this consequence of left prefrontal activation is presented by a study from LeDoux’s laboratory, where Gewirtz, Fall, and Davis (1997) found that rats with lesions of the medial prefrontal cortex show dramatically slower extinction of a learned aversive response than do sham-operated controls. These findings imply that there is a descending pathway between the medial PFC and the amygdala (Amaral, Price, Pitkanen, and Carmichael, 1992) that is inhibitory and thus represents an active component of extinction.
In the absence of this normal inhibitory input, the amygdala remains unchecked and continues to stay activated. Abercrombie (1998) also used magnetic resonance imaging (MRI)-guided regions of interest to extract glucose metabolic rate measured with PET. He found that individual differences in metabolic activity in the right amygdala predict dispositional negative affect on the Positive and Negative Affect Schedule (PANAS; Watson, Clark, and Tellegen, 1988) in a group of depressed patients.
Using the same measure of negative affect Irwin, Davidson, Kalin, Sorenson, and Turski (1998) also found MR signal changes in the amygdala in response to negative versus neutral stimuli accounts for a substantial amount of variance in PANAS trait negative affect scores. There are reliable individual differences in baseline metabolic rate in the amygdala. This fact also requires comment, in light of the previous discussion about the amygdala’s significance in physic affective processes. There is apparently important neural activity in the amygdala, even when people sleep.
As a number of studies have now shown, baseline nontask (“resting”) levels of activation in the amygdala are associated with dispositional negative affect (Abercrombie et al. , 1998) and depression (Drevets et al. , 1992). I think that questions whether these baseline diversities in amygdala activation reflect activation in answer to the PET or whether such diversities forecast the magnitude of task-induced activation in the amygdala in answer to emotion elicitors must be studied in future research.
Conclusion After analysing of the scientific literature we can see that there is a well-established body of study to provide the theoretical support for findings presented in the article. Davidson highlights the role of the prefrontal cortex and the amygdala in depression. What is most significant about this research is that information about the neural systems underlying affect led to new insights about the mechanisms of emotion and emotion regulation.
The distinctions between pre-goal and post-goal attainment positive affect, between the initial learning of affective associations and their subsequent expression, and between emotional reactivity and emotion regulation were all informed by knowledge of the brain circuitry involved. The amygdala appears to play a considerable role in changing other brain systems. The prefrontal cortex is crucially involved in the representation of affective states in the absence of environmental stimuli.
In particular, the PFC is crucial for the anticipation of upcoming affective challenges and for the maintenance of affect following the offset of an emotional elicitor. In addition, the PFC appears to play an important role in emotion regulation, in part by modulating the reactivity of the amygdala. Of most importance for the research described here is the fact that there are reliable individual differences in the activation levels and those differences are systematically related to emotion. These individual differences play a key role in determining personality and vulnerability to psychopathology.
They also appear to be related to endocrine and immune function and, as such, likely will be important in our developing understanding of the mechanisms by which emotions influence physical health. Many neuroimaging studies that have produced actual emotion determine larder amygdala activation to negative than to positive elicitors. The data and conceptual frameworks that are emerging from this article offer the potential for developing new interventions that target emotion and behaviour change to facilitate health-promoting activity.
In addition, this body of research is presenting new insights into the way social and psychological factors appear to be related to the health outcomes. For the first time, we are able to go from the brain to the periphery and begin to characterize the detailed mechanisms by which central events influence bodily systems. And we have now begun to amass evidence and theory on the reverse pathway in this complex feedback system: the mechanisms by which bodily processes (including endocrine, immune, and autonomic processes) feed back on the brain and influence its functioning.
It has also helped to focus attention on the brain mechanisms that support emotion and the circuitry that underlies different aspects of emotional or affective style. References Amaral, D. G. , Price, J. L. , Pitkanen, A. , and Carmichael, S. T. (1992). Anatomical organization of the primate amygdaloid complex. In J. P. Aggleton (Ed. ), The Amygdala: Neurobiological Aspects of emotion, Memory and Mental Dysfunction (pp. 1–66). New York: Wiley-Liss. Brain Scans Provide Striking Insights Into Depression (October 25, 1996). Retrieved 27 September 2005, from http://www. healthemotions. org/news/pr002-1. html.
Breiter, H. C. , Rauch, S. L. , Kwong, K. K. , Baker, J. R. , Weisskoff, R. M. , Kennedy, D. N. , Kendrick, A. D. , Davis, T. L. , Jiang, A. , Cohen, M. S. , Stern, C. E. , Belliveau, J. W. , Baer, L. , O’Sullivan, R. L. , Savage, C. R. , Jenike, M. A. , and Rosen, B. R. (1996). Functional magnetic resonance imaging of symptom provocation in obsessivecompulsive disorder. Archives of General Psychiatry, 53, 595–606. Davidson, R. J. , and Fox, N. A. (1989). Frontal brain asymmetry predicts infants’ response to maternal separation. Journal of Abnormal Psychology, 98, 127–131. Davidson, R. J. , and Rickman, M. (1999).
Behavioural inhibition and the emotional circuitry of the brain: Stability and plasticity during the early childhood years. In L. A. Schmidt and J. Schulkin (Eds. ), Extreme Fear and Shyness: Origins and Outcomes (pp. 67–87). New York: Oxford University Press. Davidson, R. J. , Coe, C. C. , Dolski, I. , and Donzella, B. (1999). Individual differences in prefrontal activation asymmetry predicts natural killer cell activity at rest and in response to challenge. Brain, Behaviour, and Immunity, 13, 93–108. Irwin, W. , Davidson, R. J. , Kalin, N. H. , Sorenson, J. A. , and Turski, P. A. (2001).
Relations between human amygdala activation and self-reported dispositional affect. Journal of Cognitive Neuroscience, Suppl. S, 109. Kalin, N. H. , Larson, C. , Shelton, S. E. , and Davidson, R. J. (1998). Asymmetric frontal brain activity, cortisol, and behaviour associated with fearful temperament in Rhesus monkeys. Behavioural Neuroscience, 112, 286–292. Kang, D. , Davidson, R. J. , Coe, C. L. , Wheeler, R. E. , Tomarken, A. J. , and Ershler, W. B. (1991). Frontal brain asymmetry and immune function. Behavioural Neuroscience, 105, 860–869. Larson, C. L. , Davidson, R. J. , Abercrombie, H. C. , Ward, R. T. , Schaefer, S. M. , Jackson, D. C. , Holden, J. E. , and Perlman, S. B. (1998). Relations between PET-derived measures of thalamic glucose metabolism and EEG alpha power.
Psychophysiology, 35. 162–169. Morgan, M. A. , Romanski, L. , and LeDoux, J. E. (1993). Extinction of emotional learning: Contribution of medial prefrontal cortex. Neuroscience Letters, 163, 109–113. Sutton, S. K. , and Davidson, R. J. (1997). Prefrontal brain asymmetry: A biological substrate of the behavioural approach and inhibitor systems. Psychological Sciences, 8, 204–210. Tomarken, A. J. , Davidson, R. J. , Wheeler, R. E. , and Doss, R. C. (1992).
Individual differences in anterior brain asymmetry and fundamental dimensions of emotion. Journal of Personality and Social Psychology, 62, 676–687. Tomarken, A. J. , Davidson, R. J. , Wheeler, R. E. , and Doss, R. C. (1992). Individual differences in anterior brain asymmetry and fundamental dimensions of emotion. Journal of Personality and Social Psychology, 62, 676–687. Tomarken, A. J. , Davidson, R. J. , and Henriques, J. B. (1990). Resting frontal brain asymmetry predicts affective responses to films. Journal of Personality and Social Psychology, 59, 791–801. William Styron. (1990). Darkness Visible. Random House.