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To critically examine the relationship between evolutionary and developmental influences on human neocortex and the properties of the conscious mind it creates.
Using PubMed searches and the bibliographies of several monographs, we selected 50 key works, which offer empirical support for a novel understanding of the organization of the neocortex.
The cognitive gulf between humans and our closest primate relatives has usually been taken as evidence that our brains evolved crucial new mechanisms somehow conferring advanced capacities, particularly in association areas of the neocortex. In this overview of neocortical development and comparative brain morphometry, we propose an alternative view: that an increase in neocortical size, alone, could account for novel and powerful cognitive capabilities. Other than humans’ very large brain in relation to the body weight, the morphometric relations between neocortex and all other brain regions show remarkably consistent exponential ratios across the range of primate species, including humans. For an increase in neocortical size to produce new abilities, the developmental mechanisms of neocortex would need to be able to generate an interarchy of functionally diverse cortical domains in the absence of explicit specification, and in this respect, the mammalian neocortex is unique: its relationship to the rest of the nervous system is unusually plastic, allowing great changes in cortical organization to occur in relatively short periods of evolution. The fact that even advanced abilities like self-recognition have arisen in species from different mammalian orders suggests that expansion of the neocortex quite naturally generates new levels of cognitive sophistication. Our cognitive and behavioural sophistication may, therefore, be attributable to these intrinsic mechanisms’ ability to generate complex interarchies when the neocortex reaches a sufficient size.
Our analysis offers a parsimonious explanation for key properties of the human mind based on evolutionary influences and developmental processes. This view is perhaps surprising in its simplicity, but offers a fresh perspective on the evolutionary basis of mental complexity.
One of the most popular approaches in cognitive neuroscience has been to study the normal adult human brain. However, there are likely to be limits to the knowledge that can be obtained from such studies. If we assume that no single approach can ever provide us with knowledge of causative processes whereby the mind emerges from the brain, then we need to consider how to combine more disparate approaches. I aim to illustrate here how the parallel study of brain phylogeny, ontogeny and dysfunction may bring us towards an integrative understanding of fundamental aspects of cognitive neuroscience.
A review of published literature in these research areas was carried out and representative articles selected.
Comparative approaches, utilizing the extraordinary behavioural abilities as well as the structural and functional variants that evolution has thrown up across diverse groups of species, can inform the core neural systems that may be necessary and sufficient to support specific cognitive processes. Similarly, detailed studies of human brain development, focusing on structural and functional maturation correlated with temporal mapping of cognitive processes as they come ‘on-line’, may provide unique mechanistic insights. Finally, the study of brain dysfunction in neurological and psychiatric disorders such as Huntington’s disease, Alzheimer’s disease, schizophrenia and depression, may have the beneficial side-effect of greatly enhancing our understanding of healthy brain function.
Each approach has its own epistemological advantages and disadvantages, but combined they may lead to more sophisticated, and empirically testable, models. In this review, I outline evidence for their utility, illustrate the approaches using specific examples and suggest how new advances in fields such as genomics, neurophysiology and neuroimaging may provide unprecedented opportunities in cognitive neuroscience.
In the past decade, much has been written about ‘the hard problem’ of consciousness in the philosophy of mind. However, a separate hard problem faces the scientific study of consciousness. The problem arises when distinguishing the neural correlates of consciousness (NCC) and the neural constitution of consciousness. Here, I explain this correlation/constitution distinction and the problem it poses for a science of phenomenal consciousness. I also discuss potential objections to the problem, outline further hard problems in the scientific study of phenomenal consciousness and consider the ontological implications of these epistemological issues.
Scientific and philosophic analysis and discussion are presented.
The correlation/constitution distinction does indeed present a hard problem in the scientific study of phenomenal consciousness. Refinement of the ‘NCC’ acronym is proposed so that this distinction may at least be acknowledged in the literature. Furthermore, in addition to the problem posed by this distinction and to ‘the hard problem’, the scientific study of phenomenal consciousness also faces several other hard problems.
In light of the multiple hard problems, it is concluded that scientists and philosophers of consciousness ought to (i) address, analyze and discuss the problems in the hope of discovering their solution or dissolution and (ii) consider the implications of some or all of them being intractable. With respect to the latter, it is argued that ultimate epistemic limits in the study of phenomenal consciousness pose no threat to physicalist or materialist ontologies but do inform our understanding of consciousness and its place in nature.
To present the argument that the only secure foundation for a theory of behaviour, and ultimately of mind, rests at the level of single neurons, and to assess progress at this level of explanation.
Relevant data were obtained by a search of PubMed, last updated in January 2007, focused on implemented models from single-neuron studies.
Technical limitations on recording neural activity produce trade-offs between temporal and spatial resolution and the ability to track the massively parallel activity of the nervous system. The properties of the single neuron that would need to be measured and the techniques available to obtain the data are described. The concept of a fixed neuronal identity may be impeding progress and should be replaced with the concept of dynamically assigned neuron identity.
Modern data collection techniques make it possible to obtain data at the single-neuron level on the complete nervous systems of simple organisms. Present models based on this data do not provide an integrated explanation of behaviour. However, there do not appear to be insurmountable theoretical or practical obstacles to building such models in the future or of scaling the data collection up to more complex organisms.
Caloric vestibular stimulation (CVS) has traditionally been used as a tool for neurological diagnosis. More recently, however, it has been applied to a range of phenomena within the cognitive neurosciences. Here, we provide an overview of such studies and review our work using CVS to investigate the neural mechanisms of a visual phenomenon – binocular rivalry. We outline the interhemispheric switch model of rivalry supported by this work and its extension to a metarivalry model of interocular-grouping phenomena. In addition, studies showing a slow rate of binocular rivalry in bipolar disorder are discussed, and the relationship between this finding and the interhemispheric switch model is described. We also review the effects of CVS in various clinical contexts, explain how the technique is performed and discuss methodological issues in its application.
A review of CVS and related literature was conducted.
Despite CVS being employed with surprising effect in a wide variety of cognitive and clinical contexts, it has been a largely underutilized brain stimulation method for both exploratory and therapeutic purposes. This is particularly so given that it is well tolerated, safe, inexpensive and easy to administer.
CVS can be used to investigate various cognitive phenomena including perceptual rivalry, attention and mood, as well as somatosensory representation, belief, hemispheric laterality and pain. The technique can also be used to investigate clinical conditions related to these phenomena and may indeed have therapeutic utility, especially with respect to postlesional disorders, mania, depression and chronic pain states. Furthermore, we propose that based on existing reports of the phenomenological effects of CVS and the brain regions it is known to activate, the technique could be used to investigate and potentially treat a range of other clinical disorders. Finally, the effects of CVS (and its potential effects) on several phenomena of interest to philosophy suggest that it is also likely to become a useful tool in experimental neurophilosophy.
There has been a long interest in the relationship between folate and depression.
In this paper, we report baseline measures of red cell folate that were collected during a randomized trial of 107 patients with major depression. Red cell folate levels were examined for association with percentage improvement in depressive symptoms during treatment with fluoxetine or nortriptyline. The influences of possible confounding factors were assessed.
The low red cell folate group (defined in relation to the median) had a significantly poorer response to nortriptyline. This effect of red cell folate levels was not present in those treated with fluoxetine. No relationships were found between red cell folate levels and possible confounding factors of age, nutritional status, alcohol history, depression subtype, depression severity and chronicity of depression.
Response to nortriptyline was affected by red cell folate status. It may, therefore, be beneficial to consider folate augmentation in patients with major depression, particularly if treated with nortriptyline.
Deep brain stimulation (DBS) of the subthalamic nuclei (STN) can result in depression despite the obvious motor improvement.
Two patients with serious life-threatening depressive episodes are described. In the first case, the trigger for depression was a slight adjustment of the left stimulating electrode’s contact. In the second case, reducing both the dopaminergic therapy and the voltage of DBS resulted in the manifestation of depressive symptoms.
DBS-induced depression possibly has pathogenetic differences from ordinary Parkinson’s disease depression. The STN region seems to be a sensitive zone that influences emotions.