Alternate assumptions to naturalism in neuroscience

Thinking ManThis post is very different than anything I’ve previously written; it’s more philosophical than psychological and is an example of Theoretical and Philosophical Psychology, a small but important niche within psychology that provides critical analyses of the underlying assumptions [philosophies] of psychology and the related sciences. My post is not meant to attack the neurosciences (after all, that is my field of specialization); rather, it is meant to expose the philosophical underpinnings of neuroscience. The alternative assumptions I write about are not necessarily superior, just different. Feel free to contact me with any questions or if you are interested in the references I cite.

This post is an exposition of the naturalistic assumptions in the article An fMRI Study of Personality Influences on Brain Reactivity to Emotional Stimuli by Canli et al. (2001). It will also focus on alternative assumptions. I will first explore the assumption of materialism, one half of Descartes’ dualism, and contrast this assumption with a holistic monism. Then I will discuss biological determinism as well as an alternative assumption to it, namely agency.

Materialism accounts for one half of the Cartesian dualism (and thus has been termed a one-sided dualism), the theorized split between mind and matter. It is defined as the notion that “biological explanations will (eventually) be able to fully account for and explain…psychological phenomena” (Hedges, p. 3). Materialism assumes that biology is sufficient to explain behavior. This article is focused on “the neural correlates of emotion [and personality] in healthy people” (p. 33) by using brain imaging techniques. This is an example of materialism in that the authors are looking for “the biological basis [or an objective foundation] of emotion [a subjective phenomenon]” (p. 33). The authors’ assumption of materialism will become clearer with another example. Canli et al. state: “The similarity in the dimensional structure of personality and emotion is due to a common neural substrate where personality traits moderate the processing of emotional stimuli” (p. 33; italics added). What they are saying is that neurons (the brain) are the base and that emotional processing in the brain is affected by personality traits (which they state have a “common neural substrate” with emotions). This is a one-sided dualism—the researchers attempt to explain the subjective experiences of the mind (i.e., emotion) in terms of the material, or biological, body while not including the mind in their methods.

The authors of this study sought to understand emotional responses in terms of neuroimaging. This is an example of method-driven science in that the researchers “ignored…[the] notion of the mind [being immaterial and unpredictable] and focused…on the body” (Slife, p. 13). There is no way to image emotions directly, but by assuming that they are centered in biological reactions, these researchers were able to use traditional scientific methods to measure those reactions. This materialism, or one-sided dualism, has its shortcomings. An alternative way to approach the hypothesis of how personality serves as a “middleman” between the brain and emotions is to use the assumption of a holistic monism. Whereas the authors assume that the brain (body) is the foundation of emotional experience and thus sufficient for that experience, with a monistic assumption the researchers would recognize both body and mind as necessary but not separately sufficient. This would change their study because they would look at a more inclusive picture of people, not just biology and mind but context as well. All of these conditions interact and are only understood in relation to one another. The authors would also consider qualitative measures of life experience and meaning and research those, taking a pluralistic approach.

Another prevalent assumption, which is inseparable from materialism and is in fact a subset of it, is that of biological determinism. Whereas my materialism section focused on the authors’ attempts to explain subjective experiences by their “objective” methods, this one will focus on how they explain varying emotions as caused by variations in biological factors. The authors end their paper on a strong deterministic note: “The different brain activation patterns that these pictures produce…may result in two different subjective interpretations of the identical objective experience” (p. 39). Although they hedge their statement with a may, what they are saying is that their subjects all had the same “objective experience” but because of apparent differences in how their brains responded, this difference caused the variation in subjective emotional interpretation. They imply that people’s interpretations are determined by biology, which rules out agency.

Alternately, when viewing this article according to holistic monism, specifically agency, there are would be many changes in it. First off, it would not be a problem to recognize the role agency plays in the body. The authors would assume that the body affects agency and vice versa–they constitute each other. Instead of “different brain activation patterns” (p. 39) causing different interpretations of emotion it could be that the interpretations affect the neuronal firing instead (or an interplay of both). Also, with an alternative assumption, the following hypothesis would no longer be deterministic: “Extraversion is associated with greater brain reactivity to positive” (p. 34). The authors imply that personality traits are biologically based (see paragraph 2 of this paper)–even if behaviorally influenced; therefore, biology causes personality which causes changes in brain reaction (which are experienced subjectively by people as emotions). Alternatively, this can be explained by “agentic factors” (Slife, p. 25), such as people choosing (even unconsciously) how to respond to the pictures. Also, instead of personality being determined by the brain, manifestations of agency (choices) in a context (e.g., experiences) could shape personality.

Hippocampal Volume Loss and Major Depression

Mood disorders range from major depressive disorders to major manic episodes. These disorders are both unipolar and bipolar. One main area of mood disorder research is that of unipolar major depression. Major depression can last just one episode or it can be a disorder, which can last for years with multiple depressive episodes over this extended period. The psychological aspects of depression are well understood but the biological foundations are less understood. As some evidence of this, the DSM-IV manual does not include any neurological information concerning major depression. In this handbook, depression is treated purely as a mental condition without an explanation of the biological aspects of the disorder. On the other hand, there are many psychopharmaceuticals prescribed to people with depression, which suggests that there is more than a cursory acknowledgment of the biological basis of this mental illness. However, this biological focus is mainly a focus on neurotransmitters and not anatomy. Recently, there have been numerous studies conducted to investigate the relationship between brain structure and depression (see Videbech & Ravnkilde, 2004). One of the structures most often studied in connection with depression is the hippocampus, which is a key structure for memory. The purpose of this paper is to investigate whether the hippocampus specifically is negatively impacted in depressed patients.

Frodl et al. (2002) investigated hippocampal changes in patients with first episode major depression. The authors had 30 adult depressed subjects (mean age = 40.3) and 30 matched controls (mean age = 40.6). The mean time of the depressive episode for the depression group was 0.71 years. The researchers collected MR images for all subjects. They compared the hippocampal volumes of the depressed group with the control group with ANCOVAs. Depressed men had significantly smaller left hippocampal volume than did healthy male subjects but right hippocampal volume was not significantly different. Female depressed subjects had significantly larger right hippocampal volume than did their matched controls and left volume did not differ, which implicates differing effects of depression on men and women. There was a significant left-right hippocampal volume disparity in the depressed patients but there was not one in the healthy subjects. Overall, the difference in hippocampal volume was not significant between the depressed and control groups though. There was also no significant correlation between age and hippocampal volume for either group but this finding goes against that of other research (Frodl et al.). On the other hand, between groups there was a significant reduction of hippocampal white matter volume. In other words, both male and female depressed patients had on average a reduction in the hippocampal white matter compared to the control subjects.

The authors concluded that there are likely physiologic gender differences in how males and females react to stress, which would explain why depressed males had smaller hippocampal volume and females did not. They believe this may be an example of the protective effects of estrogen against stress seen in other studies. In any case, there was a tendency for both depressed males and females to have significant left-right hippocampal asymmetry and reduced white matter. They concluded that this represents the beginning of left hippocampus volume loss and disrupted axonal transmission, respectively. The researchers could not conclude, however, that depression caused the volume loss. It may be that the loss came in response to stress or some other factor, which in turn predisposed the depressed subjects to major depression. Alternatively, the depression could have been the catalyst for the reduction (Frodl et al., 2002). Further longitudinal research is needed to uncover the causal relationship between depression and hippocampal volume.

Continue reading “Hippocampal Volume Loss and Major Depression”

Dopamine, the Basal Ganglia, and Learning

A significant proportion of dopamine (DA) is produced in the substantia nigra pars compacta (SNpc) and is carried to the striatum via the nigrostriatal pathway. While this pathway has been traditionally linked with motor functioning, recent research has implicated striatal DA involvement in language (Crosson, 2003) and learning (Seger, 2006). One disease in which there is considerable DA disruption is Huntington’s Disease (HD). In HD the head of the caudate is typically the first brain structure affected by neuronal cell loss. This cell loss not only affects connections with the SNpc but also affects the connections between the striatum and the prefrontal cortex. In HD the disruption of these dopaminergic pathways leads to disruptions in motor and cognitive functioning.

How DA disruptions affect cognition has been explained by theories that are modifications of Mink’s model (1996) of center and surround (i.e., direct and indirect) basal ganglia regulation. Within the caudate there are two main families of DA receptors – D1 and D2. These receptors have been shown to have different functioning within the basal ganglia (Seger, 2006) – the D1 receptor is involved with the direct pathway and the D2 receptor is involved in the indirect pathway. The D1, or direct pathway, can be viewed as increasing the strength of the signal of the desired response while the D2, or indirect pathway, serves to reduce the noise of the competing undesired responses. Dopaminergic systemic disruption in HD should thus decrease the signal-to-noise ratio, which results in the person having a greater difficulty selecting the desired response (see model below).

Center-surround model of basal ganglia-based learning and memory

*Model based on Mink (1996) and Frank, Seeberger, and O’Reilly (2004)

There is evidence that in early stages of Huntington’s disease, D2 receptors are the first to be affected, with less binding occurring at D2 receptors presumably due to receptor loss. As the disease progresses, the D1 receptors also start to become depleted, with the end result of widespread DA dysfunction (Glass, Dragunow, & Faull, 2000). This DA dysfunction possibly affects verbal learning and recall by impacting the indirect pathway in the early stages of HD and indiscriminately the whole direct and indirect system in later stages of the disease process.

References

Crosson (2003). Left and right basal ganglia and frontal activity during language generation: Contributions to lexical, semantic, and phonological processes. Journal of the International Neuropsychological Society, 9, 1061-1077.

Frank, M. J., Seeberger, L. C., & O’Reilly, R. C. (2004). By carrot or by stick: Cognitive reinforcement learning in Parkinsonism. Science, 306, 1940-1943.

Glass, M., Dragunow, M., & Faull, R. L. M. (2000). The pattern of neurodegeneration in Huntington’s disease: A comparative study of cannabinoid, dopamine, adenosine and GABAA receptor alterations in the human basal ganglia in Huntington’s disease. Neuroscience, 97(3), 505-19.

Seger, C. A. (2006). The basal ganglia in human learning. Neuroscientist, 12(4), 285-290.

The basal ganglia and cognition

The basal ganglia are a collection of subcortical structures that were traditionally viewed as only being involved in movement. The basal ganglia include the caudate, globus pallidus, putamen, and nucleus accumbens (the subthalamic nucleus and the substantia nigra are also often included as part of the basal ganglia). Scientists have known about the basal ganglia’s role in movement for a number of years but have only recently really started studying their role in cognition, executive function, and memory.

Dissections of the brain have shown that there are a number of white matter “loops” exiting and entering the basal ganglia. We know that the striatum, which consists of the putamen and the caudate and is so named because there are connections between the two structures that look like stripes (striations), receives excitatory input from all over the cortex (Seger & Cincotta, 2002). The prefrontal cortex (roughly the very front of the brain) connects to the anterior putamen and the head of the caudate but the tail of the caudate and the posterior parts of the putamen receive inputs from parts of the temporal and parietal lobes. The frontal lobes are involved in tasks such as planning, remembering, organizing, and many other of the “higher-order” cognitive abilities. The parietal lobes are involved in visuo-spatial tasks and the temporal lobes are involved in memory and object recognition (these are gross simplifications of lobular function – all lobes have more functions than I wrote about). So if parts of the basal ganglia receive inputs from the frontal lobes, what are the basal ganglia doing if not just moderating movement?

Seger and Cincotta (2002) demonstrated that the striatum is involved in a type of learning. Lamar, Price, Libon, Penney, Kaplan, Grossman, and Heilman (2007) demonstrated that dementia patients with higher levels of white matter disruption (which likely interferes with basal ganglia connectivity) have poorer working memory performance. One example of what working memory is is performing a multiplication task in your head without using any paper – having to remember the digits and manipulate them is a process of working memory. Benke, Delazer, Bartha, and Auer (2003) reported on two clinical cases of patients with hematoma disrupting the left basal ganglia. Both patients had “executive function” disruption, short- and long-term memory impairment, and attentional difficulties. Many other researchers have demonstrated the role the basal ganglia has in cognition but we are still in the early stages of this area of research.

Overview of brain structure and function

I’ve posted links to slide providing a basic overview of brain anatomy and function. There are a number of copyrighted images in the slides so please do not use for non-personal information without permission. The information is in slide format so if anything is unclear please contact me for more information. Each PDF is about 1 MB so it could take a while to download with a slow connection.

Slides, part 1

Slides, part 2

Great neuroanatomy site

I came across this great site with “over 12 million megapixels of scanned images of serial sections of both primate and non-primate brains and that is integrated with a high-speed database for querying and retrieving data about brain structure and function over the internet.” They have some great high-quality images of brains – great for learning neuroanatomy.

Brainmaps.org