There have been several attempts to theorize about the origin of the brain and its modular functions by drawing upon the microevolutionary processes and their distal impact on macroevolution. Most of these attempts have focused on explaining the emergence and the expansion of the phylogenetically recent neopallium and its functions in behavioral and cognitive systems (Geary, 2005; McNally et al., 2012). In contrast, there has been little attempt to characterize the evolutionary basis of human emotions—a collection of systems with activity grounded in the phylogenetically ancient allocortex. Cognitive information processing is behaviorally and functionally distinct from affective processing—whereas the former involves the neocortical encoding of information gleaned from the environment through the senses, the latter originates from subcortical structures in the form of “diffuse global states” that may be cognitively processed into higher emotions.
Panksepp and Biven have now published a text that delves with great detail into the neural architecture of the human emotional life, with particular focus on its ancestral origins. This is a worthwhile endeavor, with implications for preclinical and clinical models of aberrant emotional behavior and regulation. In summary, Panksepp and Biven’s model is as follows. The emotional “brainmind” system is adaptive for providing humans and other living entities for which this structure has evolved intrinsic and evaluative information about their progress in the quest for survival. Whereas positive emotions are indicative of the experience of situations that are positively correlated with survival, negative emotions may be outcomes of the evaluation of situations that negatively correlate with survival. These “raw” emotions are “ancestral memories” that have been phylogenetically important for survival and, as such, have been genetically coded to be inborn capacities. The bulk of the text focuses on their essential nature as primary-process instinctual emotions—the most basic, primordial affective processes. Primary-process emotions are most important (or influential) in infants and other mammals. Here, these generate fixed (instinctual) behavioral responses and emotional arousal to a specific set or finite number of precipitating events. Although primary-process emotions initially control higher brain cognitive activities, with normal development, the higher cognitive abilities rooted in the neocortex come to control primary-process emotions. In Panksepp and Biven’s organization of the levels of emotional control, primary-process emotional networks regulate secondary-process emotions. Secondary-process emotions are unintentional learning and memory mechanisms grounded in the basal ganglia that include simple classical conditioning, instrumental and operant learning, and behavioral and emotional habits. During the course of development, these learning-memory mechanisms create object relations and contingencies that become linked to tertiary affects and neocortical awareness functions. Tertiary processes include emotional ruminations, evaluations, and thoughts that influence free will and intentions to act. Panksepp and Biven describe with illustrations the taxonomy of the primary-process affective network in mammals. This network comprises at least seven emotional systems, homologous across mammalian species, with neurobiology grounded in subneocortical structures. These include the seeking, rage, fear, lust, care, grief, and play network systems—the most important being the seeking system.
It is clear from the text that one of its goals was to underscore the continuity that exists between humans and other mammals in the neural archeology and experience of emotions. The authors do this by emphasizing commonalities across species in emotional action patterns, learning and memory, and neural circuits, but this is balanced with a discussion of species-specific differences. The book is a collaboration of a neuroscientist and a clinician; as such, although the basic neurobiology of “normal” and “aberrant” affective systems is often in view, Panksepp and Biven give extensive treatment to issues relevant to clinicians such as substance addiction (e.g., pp. 192, 326, 361, 384), aggression (pp. 157–158, 164–167), mood disorders (e.g., pp. 326–337, 335–339, 457–461, 479–483), anxiety disorders (e.g., pp. 176–191, 469–474), schizophrenia (e.g., pp. 108–110, 300, 441), psychological well-being (pp. 418–420), and psychotherapy (pp. 425–474). Clinicians involved in the treatment of posttraumatic stress disorder may find the authors’ favorable treatment of eye movement desensitization and reprocessing (EMDR) slightly one sided (pp. 468–474) for an intervention that remains questionable in the view of many psychologists with regard to its theoretical foundations (e.g., Herbert et al., 2000). Although EMDR’s therapeutic benefits are not in question, it has been argued that it simply capitalizes on prolonged exposure, much like several other treatments of anxiety disorders, and that its characteristic eye movements to facilitate accelerated processing are pseudoscientific claims. The authors venture an explanation of the benefits of eye movements—eye movements have neural circuits in the superior colliculi, which lie near the dorsal region of the periaqueductal gray (the negative affective regions of the periaqueductal gray). Eye movements may diffuse negative emotions by inhibiting neural networks that may contribute to negative emotions. The authors also venture the possibility that traumatic memories undergo modification (or recontextualization) during EMDR at a primary-process affective level, such that by the time the memories are reintegrated and reconsolidated into memory banks, these have been diffused of negative emotion. The authors acknowledge that there is no current neuroscientific evidence for this putative mechanism of action; however, some testable predictions that prove or disprove their hypothesis would have been welcome.
Our own interest in Panksepp and Biven’s view of the archaeology of emotions draws from clinical and research interest in the phenomenology and treatment of schizophrenia and other psychotic disorders. As noted by the authors, dopamine hyperactivity in the seeking system, particularly at D2 receptors, is implicated in psychosis. Although part of the same core abnormality, this cause-effect is more direct in frank hallucinations rather than strongly held delusional beliefs, which require disturbance in error-dependent updating of beliefs and inferences characterized by deviant Bayesian inferences, prediction error signaling, and jumping-to-conclusions as espoused by information processing models (Fletcher and Frith, 2009). Antipsychotic treatments operate by blocking dopamine activity at receptor sites but also have the unfortunate consequence of decreasing an individual’s natural seeking tendencies. This generally contributes to a constellation of behaviors that mimic negative symptoms in schizophrenia. One puzzling aspect of schizophrenia is the diminished expression of positive or negative emotions (i.e., restricted emotional range) and blunted affect in a subset of patients with schizophrenia with prominent, idiopathic negative symptoms (Kirkpatrick et al., 2001; Suslow et al., 2003) and increased negative emotionality in patients with nondeficit schizophrenia. Positive symptoms are less crucial to a deficit classification, although comparisons between patients with deficit and nondeficit schizophrenia suggest comparable degrees of severity in positive symptoms (Cohen et al., 2010; Galderisi et al., 2002). Panksepp and Biven’s model would seem less successful at explaining co-occurring or idiopathic negative symptoms in some people with schizophrenia given that symptoms of anhedonia, avolition, asociality, and affective flattening appear inconsistent with an overactive seeking system. There has also been some suggestion that anticipatory but not consummatory pleasure deficits may be more robust in people with schizophrenia (e.g., Gard et al., 2007), which appears to run counter to an overactive seeking system.
Similarly, whereas manic/hypomanic hyperactivation, cyclothymia, behavioral dysregulation, rapid cycling, and mixed episodes in people with bipolar spectrum disorders are explainable by an overactive seeking system, the “switch” process, mood episode sensitization, and extended depressive episodes may be inconsistent. Assuming that primary-process emotional systems cannot be both overactive and underactive, these issues may have required much more treatment in the text than the authors were willing to venture. With regard to the co-occurrence of positive and negative symptoms in schizophrenia, one possibility with origins in the pathology of the seeking system implicates the interconnectivity (via dopaminergic and glutamergic projections) of cortical and subcortical structures that may not only explain the co-occurrence of schizophrenia symptom domains but also shed light on emotional processing deficits (Laviolette, 2007). Dopamine hyperactivity in the emotional processing circuits of the subcortex (ventral tegmentum area, nucleus accumbence, and amygdala interconnections) may have an impact upstream on dopamine activity in the prefrontal areas, thereby contributing to hypofrontality. In addition, dopamine dysregulation along these circuits implicated in the processing of emotionally and/or motivationally salient information (these circuits include reciprocal projections into the prefrontal cortex) may contribute to disturbed learning and memory and negative symptoms.
The text provides a substantial discussion of the role of the neurohormone oxytocin in the lust, care, and play systems and notes recent findings that show that people with schizophrenia demonstrate disruptions in oxytocin signaling (see MacDonald and Feifel, 2012). The role of the neurohormone in social dysfunction and sociocognitive processing deficits is one that has garnered increased interest in the study of negative symptoms of schizophrenia. The text reviews studies in animal and humans that show that oxytocin acts in conjunction with other neurochemical and environmental variables to influence forms of social bonding grounded in the lust and care systems (little evidence for the play system) and does not unilaterally act as a “love hormone.” The authors suggest with evidence that oxytocin may influence social bonding by improving social confidence. The authors also underscore the role of other neuropeptides that may contribute to social behavior, for example, endogenous opioids, endogenous cannabinoid substance, and insulin-like growth factor–1. For clinicians, the authors discuss the putative therapeutic benefits of oxytocin as a putative treatment of postpartum depression, separation distress, marital distress, and social dysfunction and emotion processing deficits in people with schizophrenia.
In conclusion, the Archaeology of Mind provides a successful overview of the affective systems by underscoring the neural continuity that exists between humans and other mammals and, in some cases, birds. The authors accomplish this by reviewing an overwhelming plethora of evidence from animal studies that support their model. There is deference to traditional views of animal emotion, fear acquisition, learning, and memory processes, but, often, a review of their history is followed by a critical identification of their limitations. The text is, however, much more than a neuroscience or psychology text; it explores several issues of clinical relevance—the neural underpinnings of substance use problems, anxiety disorders, mood disorders, and psychotic disorders and psychopharmacological and psychosocial treatments of psychiatric illnesses. As such, the text would be of interest not only to basic scientists interested in preclinical modeling but also to clinicians and clinical researchers interested in the neurobiology of addiction, emotional disorders, and novel pharmacological and psychosocial interventions. The text provides an excellent discussion of depression in relation to underactivity in the seeking and hypersensitivity of the grief neural system; we would, however, like to see a more thorough treatment of the forms of emotional and social dysfunction that are characteristic to schizophrenia and bipolar disorder in future iterations of the model.
Anthony O. Ahmed, PhD
Peter F. Buckley, MD
Georgia Regents University
The author declares no conflict of interest.
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