The future of the Affective Neuroscience Personality Scales: A reflection on seven pressing matters.

The Affective Neuroscience Personality Scales (ANPS) were designed to provide researchers in the mental sciences with an inventory to assess primary emotional systems according to Pankseppian Affective Neuroscience Theory (ANT). The original ANPS, providing researchers with such a tool, was published in 2003. In the present brief communication, about 20 years later, we reflect upon some pressing matters regarding the further development of the ANPS. We touch upon problems related to disentangling traits and states of the primary emotional systems with the currently available versions of the ANPS and upon its psychometric properties and its length. We reflect also on problems such as the large overlap between the SADNESS and FEAR dimensions, the disentangling of PANIC and GRIEF in the context of SADNESS, and the absence of a LUST scale. Lastly, we want to encourage scientists with the present brief communication to engage in further biological validation of the ANPS.

The Roles of Primary Emotional Systems and Need Satisfaction in Problematic Internet and Smartphone Use: A Network Perspective.

Problematic Internet and smartphone use (PIU and PSU, respectively) have received significant attention over the past years. In the current work, we studied the associations between PIU and PSU, primary emotional systems, and need satisfaction. The effective sample comprised 399 people who responded to scales measuring these variables. Bivariate correlation analysis showed that both PSU and PIU were positively associated with negative primary emotion traits (FEAR, ANGER, SADNESS) as well as lower scores on most of the need satisfaction factors. Network analysis showed that while PIU and PSU have a strong association with each other, in general, there were not many significant correlations between PSU, PIU, and other variables in the network. The associations being present were rather weak. Network analysis showed that PSU was positively associated with FEAR, ANGER, PLAY primary emotional systems. Both PSU and PIU had a negative association with safety and security and physiological needs satisfaction. Moreover, PSU had a positive link with belongingness need satisfaction, while higher PIU was associated with lower esteem and self-actualization need satisfaction. Addressing those unmet needs may be helpful in reducing problematic technology use, but further research testing this would be necessary.

A meta-analysis on individual differences in primary emotional systems and Big Five personality traits.

The Affective Neuroscience Personality Scales (ANPS) were constructed as a self-report assessment to measure individual differences in Jaak Panksepp's cross-species primary emotional systems: SEEKING, PLAY, CARE (positive emotions) and FEAR, SADNESS, ANGER (negative emotions). Beginning with the first published work on the ANPS in 2003, individual differences on the ANPS measures of these six primary emotional systems have been consistently linked to Big Five personality traits. From a theoretical perspective, these primary emotional systems arising from subcortical regions, shed light on the nature of the Big Five personality traits from an evolutionary perspective, because each of these primary emotional systems represent a tool for survival endowing mammalian species with inherited behavioral programs to react appropriately to complex environments. The present work revisited 21 available samples where both ANPS and Big Five measures have been administered. Our meta-analytical analysis provides solid evidence that high SEEKING relates to high Openness to Experience, high PLAY to high Extraversion, high CARE/low ANGER to high Agreeableness and high FEAR/SADNESS/ANGER to high Neuroticism. This seems to be true regardless of the ANPS inventory chosen, although much more work is needed in this area. Associations between primary emotional systems and Conscientiousness were in the lower effect size area across all six primary emotions, thereby supporting the idea that Conscientiousness rather seems to be less directly related with the subcortical primary emotions and likely is the most cognitive/cortical personality construct out of the Big Five. In sum, the present work underlines the idea that individual differences in primary emotional systems represent evolutionarily ancient foundations of human personality, given their a) meaningful links to the prominent Big Five model and b) their origins lying in subcortical areas of the human brain.

A comprehensive review of studies using the Affective Neuroscience Personality Scales in the psychological and psychiatric sciences.

Jaak Panksepp's Affective Neuroscience Theory (ANT) belongs to the most prominent emotion theories in the psychological and psychiatric sciences. ANT proposes the existence of seven primary emotional systems deeply anchored in the mammalian brain. These emotional/motivational systems have been shaped by evolutionary processes and function as tools for survival in mammalian species. The systems are called SEEKING, LUST, CARE, and PLAY, as well as ANGER, FEAR, and SADNESS. Panksepp carved out these emotional systems via means of deep brain stimulation, brain lesion and pharmacological manipulation studies. Davis et al. (2003) designed the Affective Neuroscience Personality Scales (ANPS) against the background of findings from ANT. This self-report inventory is meant to enable researchers to assess individual differences in primary emotional systems. Seventeen years have passed since the first version of the ANPS has been published. Therefore, we now provide a comprehensive overview on studies using the ANPS including work from personality science, psychiatry and the neurosciences.

The Affective Neuroscience Personality Scales: Linking the adjective and statement-based inventories with the Big Five Inventory in English and German-speaking samples.

Jaak Panksepp's Affective Neuroscience Theory is of high relevance not only for a better understanding of affective brain disorders but also in personality research. To make Panksepp's theory more accessible for psychologists and psychiatrists, Davis, Panksepp, and Normansell (2003) developed the Affective Neuroscience Personality Scales (ANPS). These scales assess the manifestation of the primary emotional traits in humans based on a personality trait approach. Given their putative foundation in old subcortical areas in the brain, these primary emotional traits (assessed via the ANPS) could represent the evolutionarily oldest manifestations of personality (but this notion is still a matter of a debate). However, the ANPS inventories were based on using contextual items (e.g., about specific attitudes, behaviors, and feelings in specific situations). Recently, an adjective-based ANPS (ANPS-Adjective Ratings or ANPS-AR) was developed for a less context-dependent and more efficient assessment of Panksepp's primary emotional systems in humans for use by both individuals and independent observer raters. The present work introduces the first German version of the ANPS-AR. Moreover, the current work investigates the original and ANPS-AR versions of the ANPS and their associations with the Big Five personality traits in two independent English- and German-speaking samples. The results show that the ANPS measures are very similarly correlated with the Big Five personality traits across different samples and scales. This work replicates the previous findings in an English version, and demonstrates the reliability and validity of the adjective-based German ANPS-AR.

Linking individual differences in satisfaction with each of Maslow's needs to the Big Five personality traits and Panksepp's primary emotional systems.

Maslow's hierarchy of needs is one of the most impactful theories in motivation psychology and personality science. Therefore, it is surprising that studies linking individual differences in a person's current satisfaction with each of Maslow's needs to the Big Five personality traits are rare. In the present study of 850 participants, associations between the Need Satisfaction Inventory and the Big Five personality traits were examined for the first time. In addition, the administration of the Affective Neuroscience Personality Scales provided an evolutionary framework for the present research. Individual differences in the Need Satisfaction Inventory were assessed, but participants were also asked about the current importance of each of Maslow's needs in their lives. This latter approach to viewing Maslow's needs (general rated importance of each need in the life of a person) showed strong deviations from Maslow's proposed order in the classic pyramid depicting the hierarchy of needs.

A Tribute to Jaak Panksepp (1943-2017).

This article gives a short overview on the life and achievements of Jaak Panksepp. Jaak Panksepp dedicated his life to the study of mammalian emotions. By means of electrical stimulation of the brain and psychopharmacological challenges he carved out seven primary emotional systems being highly conserved across different species of mammals including homo sapiens. The primary emotional systems are called SEEKING, CARE, LUST, PLAY (positive emotions), and FEAR, RAGE, SADNESS (negative emotions). While his early career was characterized by the direct study of these primary emotions in mammals, in his late career he invested more and more time in applying his knowledge to different fields of psychology including personality neuroscience and psychiatry.

Affective Neuroscience Theory and Personality: An Update.

The present work gives a short overview of central aspects of Jaak Panksepp's Affective Neuroscience Theory (AN theory) and its relevance for modern personality neuroscience. In contrast to the widely used Big Five approach to studying and understanding human personality, AN theory provides researchers with a distinct roadmap to the biological basis of personality, including molecular and neuroanatomical candidates, to understand individual differences in human behavior. Such molecular and neuroanatomical brain candidates have been derived by means of electrical brain stimulation and pharmacological challenges, while investigating primary emotional systems anchored in the subcortical mammalian brain. Research results derived from the study of emotions in mammals are also of relevance for humans because ancient layers of our minds-those layers where primary emotions originate-have been homologously conserved across species. From an evolutionary perspective, this makes sense because primal emotions represent "built-in tools for survival" for all mammals. In this context, Montag and Panksepp recently illustrated a potential ancient neurobiological effect by carving out robust associations between individual differences in primary emotions (assessed via self-report) and the Big Five in a cross-cultural study with data from the United States, Germany, and China. These associations together with some ideas derived from MacLean's Triune Brain concept highlighted (a) that primary emotions likely represent the phylogenetically oldest parts of human personality and (b) that primary emotions influence human personality in a bottom-up fashion given their localization in ancient subcortical brain regions. A comment on the work by Montag and Panksepp asked for insights on putative links between primary emotions and facets of the Big Five. Therefore, we provide some first insights into such associations from recent Germany data. In addition, the present work provides a new short version of the Affective Neuroscience Personality Scales to assess individual differences in primary emotions.

Selected Principles of Pankseppian Affective Neuroscience.

In the early nineties of the twentieth century Jaak Panksepp coined the term "Affective Neuroscience" (AN) today being accepted as a unique research area in cross-species brain science. By means of (i) electrical stimulation, (ii) pharmacological challenges, and (iii) brain lesions of vertebrate brains (mostly mammalian), Panksepp carved out seven primary emotional systems called SEEKING, CARE, PLAY, and LUST on the positive side, whereas FEAR, SADNESS, and ANGER belong to the negative affects. Abundant research into human clinical applications has supported the hypothesis that imbalances in these ancient primary emotional systems are strongly linked to psychiatric disorders such as depression. The present paper gives a concise overview of Panksepp's main ideas. It gives an historical overview of the development of Panksepp's AN thinking. It touches not only areas of neuroscience, but also shows how AN has been applied to other research fields such as personality psychology. Finally, the present work gives a brief overview of the main ideas of AN.

Localized cortical chronic traumatic encephalopathy pathology after single, severe axonal injury in human brain.

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild impact traumatic brain injury from contact sports. Recently, a consensus panel defined the pathognomonic lesion for CTE as accumulations of abnormally hyperphosphorylated tau (p-tau) in neurons (neurofibrillary tangles), astrocytes and cell processes distributed around small blood vessels at sulcal depths in irregular patterns within the cortex. The pathophysiological mechanism for this lesion is unknown. Moreover, a subset of CTE cases harbors cortical ß-amyloid plaques. In this study, we analyzed postmortem brain tissues from five institutionalized patients with schizophrenia and history of surgical leucotomy with subsequent survival of at least another 40 years. Because leucotomy involves severing axons bilaterally in prefrontal cortex, this surgical procedure represents a human model of single traumatic brain injury with severe axonal damage and no external impact. We examined cortical tissues at the leucotomy site and at both prefrontal cortex rostral and frontal cortex caudal to the leucotomy site. For comparison, we analyzed brain tissues at equivalent neuroanatomical sites from non-leucotomized patients with schizophrenia, matched in age and gender. All five leucotomy cases revealed severe white matter damage with dense astrogliosis at the axotomy site and also neurofibrillary tangles and p-tau immunoreactive neurites in the overlying gray matter. Four cases displayed p-tau immunoreactivity in neurons, astrocytes and cell processes encompassing blood vessels at cortical sulcal depths in irregular patterns, similar to CTE. The three cases with apolipoprotein E ε4 haplotype showed scattered ß-amyloid plaques in the overlying gray matter, but not the two cases with apolipoprotein E ε3/3 genotype. Brain tissue samples from prefrontal cortex rostral and frontal cortex caudal to the leucotomy site, and all cortical samples from the non-leucotomized patients, showed minimal p-tau and ß-amyloid pathology. These findings suggest that chronic axonal damage contributes to the unique pathology of CTE over time.

Convergent findings for abnormalities of the NF-κB signaling pathway in schizophrenia.

Neurons exhibit a constitutive level of nuclear factor-κB (NF-κB) signaling and this pathway plays a significant role in neurite outgrowth, activity-dependent plasticity, and cognitive function. Transcription factor analysis was performed in a microarray data set profiled in four different brain regions (n=54 comparison group; n=53 schizophrenia (SZ)). An independent postmortem cohort was used for gene expression (n=24 comparison group; n=22 SZ), protein abundance (n=8 comparison group; n=8 SZ), and NF-κB nuclear activity (n=10 comparison group; n=10 SZ) quantification. Expression quantitative trait locus analysis was performed using publicly available data. Prepulse inhibition (PPI) of the acoustic startle reflex was tested in healthy individuals (n=690). Comparison of microarray data showed that NF-κB was among the transcription factors associated with the differential expression of genes in cases vs controls. NF-κB gene and protein levels and nuclear activation were significantly decreased in the superior temporal gyrus of patients with SZ. Upstream NF-κB genes related to translocation were significantly dysregulated in SZ. The gene expression levels of an NF-κB-associated importin (KPNA4: one of the proteins responsible for the translocation of NF-κB to the nucleus) was decreased in SZ and an SNP within the KPNA4 locus was associated with susceptibility to SZ, reduced KPNA4 expression levels and attenuated PPI of the startle reflex in healthy control subjects. These findings implicate abnormalities of the NF-κB signaling pathway in SZ and provide evidence for an additional possible mechanism affecting the translocation of NF-κB signaling to the nucleus.

A system-level transcriptomic analysis of schizophrenia using postmortem brain tissue samples.

CONTEXT Schizophrenia is a common, highly heritable, neurodevelopmental mental illness, characterized by genetic heterogeneity. OBJECTIVE To identify abnormalities in the transcriptome organization among older persons with schizophrenia and controls. DESIGN Weighted gene coexpression network analysis based on microarray transcriptomic profiling. SETTING Research hospital. PATIENTS Postmortem brain tissue samples from 4 different cerebrocortical regions (the dorsolateral prefrontal cortex, the middle temporal area, the temporopolar area, and the anterior cingulate cortex) from 21 persons with schizophrenia and 19 controls. MAIN OUTCOME MEASURES Results from gene expression microarray analysis, from analysis of coexpression networks, and from module eigengene, module preservation, and enrichment analysis of schizophrenia-related genetic variants. RESULTS The oligodendrocyte, microglial, mitochondrial, and neuronal (GABAergic and glutamatergic) modules were associated with disease status. Enrichment analysis of genome-wide association studies in schizophrenia and other illnesses demonstrated that the neuronal (GABAergic and glutamatergic) and oligodendrocyte modules are enriched for genetically associated variants, whereas the microglial and mitochondrial modules are not, providing independent support for more direct involvement of these gene expression networks in schizophrenia. Interregional coexpression network analysis showed that the gene expression patterns that typically differentiate the frontal, temporal, and cingulate cortices in controls diminish significantly in persons with schizophrenia. CONCLUSIONS These results support the existence of convergent molecular abnormalities in schizophrenia, providing a molecular neuropathological basis for the disease.

Molecular and genetic evidence for abnormalities in the nodes of Ranvier in schizophrenia.

CONTEXT: Genetic, neuroimaging, and molecular neurobiological evidence support the hypothesis that the disconnectivity syndrome in schizophrenia (SZ) could arise from failures of saltatory conduction and abnormalities at the nodes of Ranvier (NOR) interface where myelin and axons interact. OBJECTIVE: To identify abnormalities in the expression of oligodendroglial genes and proteins that participate in the formation, maintenance, and integrity of the NOR in SZ. DESIGN: The messenger RNA (mRNA) expression levels of multiple NOR genes were quantified in 2 independent postmortem brain cohorts of individuals with SZ, and generalizability to protein expression was confirmed. The effect of the ANK3 genotype on the mRNA expression level was tested in postmortem human brain. Case-control analysis tested the association of the ANK3 genotype with SZ. The ANK3 genotype's influence on cognitive task performance and functional magnetic resonance imaging activation was tested in 2 independent cohorts of healthy individuals. SETTING: Research hospital. Patients  Postmortem samples from patients with SZ and healthy controls were used for the brain expression study (n = 46) and the case-control analysis (n = 272). Healthy white men and women participated in the cognitive (n = 513) and neuroimaging (n = 52) studies. MAIN OUTCOME MEASURES: The mRNA and protein levels in postmortem brain samples, genetic association with schizophrenia, cognitive performance, and blood oxygenation level-dependent functional magnetic resonance imaging. RESULTS: The mRNA expression of multiple NOR genes was decreased in schizophrenia. The ANK3 rs9804190 C allele was associated with lower ANK3 mRNA expression levels, higher risk for SZ in the case-control cohort, and poorer working memory and executive function performance and increased prefrontal activation during a working memory task in healthy individuals. CONCLUSIONS: These results point to abnormalities in the expression of genes and protein associated with the integrity of the NOR and suggest them as substrates for the disconnectivity syndrome in SZ. The association of ANK3 with lower brain mRNA expression levels implicates a molecular mechanism for its genetic, clinical, and cognitive associations with SZ.

The effects of hypertension and body mass index on diffusion tensor imaging in schizophrenia.

Recently, the negative effects of hypertension and elevated body mass index on cognitive functioning in schizophrenia have been reported (Friedman et al., 2010). Data suggests that cognitive changes in hypertensive patients from the general population may be mediated, in part, by white matter damage. Therefore, we performed diffusion tensor imaging (DTI) in the same subjects studied by Friedman et al. (2010) to investigate the effects of hypertension and elevated body mass index on the fractional anisotropy (FA) of several major white matter tracts. Significant interactions between a diagnosis of schizophrenia and hypertension on FA in several white matter regions were detected. Hypertension was associated with lower FA in the schizophrenic group and higher FA in the same tracts in the non-schizophrenic subjects. These results suggest hypertension-induced compensatory mechanisms in the brains of non-schizophrenic patients with hypertension which may be impaired in persons with schizophrenia.

Expression of mutant human DISC1 in mice supports abnormalities in differentiation of oligodendrocytes.

Abnormalities in oligodendrocyte (OLG) differentiation and OLG gene expression deficit have been described in schizophrenia (SZ). Recent studies revealed a critical requirement for Disrupted-in-Schizophrenia 1 (DISC1) in neural development. Transgenic mice with forebrain restricted expression of mutant human DISC1 (ΔhDISC1) are characterized by neuroanatomical and behavioral abnormalities reminiscent of some features of SZ. We sought to determine whether the expression of ΔhDISC1 may influence the development of OLGs in this mouse model. OLG- and cell cycle-associated gene and protein expression were characterized in the forebrain of ΔhDISC1 mice during different stages of neurodevelopment (E15 and P1 days) and in adulthood. The results suggest that the expression of ΔhDISC1 exerts a significant influence on oligodendrocyte differentiation and function, evidenced by premature OLG differentiation and increased proliferation of their progenitors. Additional findings showed that neuregulin 1 and its receptors may be contributing factors to the observed upregulation of OLG genes. Thus, OLG function may be perturbed by mutant hDISC1 in a model system that provides new avenues for studying aspects of the pathogenesis of SZ.

The brain's emotional foundations of human personality and the Affective Neuroscience Personality Scales.

Six of the primary-process subcortical brain emotion systems - SEEKING, RAGE, FEAR, CARE, GRIEF and PLAY - are presented as foundational for human personality development, and hence as a potentially novel template for personality assessment as in the Affective Neurosciences Personality Scales (ANPS), described here. The ANPS was conceptualized as a potential clinical research tool, which would help experimentalists and clinicians situate subjects and clients in primary-process affective space. These emotion systems are reviewed in the context of a multi-tiered framing of consciousness spanning from primary affect, which encodes biological valences, to higher level tertiary (thought mediated) processing. Supporting neuroscience research is presented along with comparisons to Cloninger's Temperament and Character Inventory and the Five Factor Model (FFM). Suggestions are made for grounding the internal structure of the FFM on the primal emotional systems recognized in affective neuroscience, which may promote substantive dialog between human and animal research traditions. Personality is viewed in the context of Darwinian "continuity" with the inherited subcortical brain emotion systems being foundational, providing major forces for personality development in both humans and animals, and providing an affective infrastructure for an expanded five factor descriptive model applying to normal and clinical human populations as well as mammals generally. Links with ontogenetic and epigenetic models of personality development are also presented. Potential novel clinical applications of the CARE maternal-nurturance system and the PLAY system are also discussed.

Microarray database mining and cell differentiation defects in schizophrenia.

The causes of schizophrenia remain unknown, but a key role of oligodendrocytes and of the myelination process carried out by them has gained increasing support. The adult human brain parenchyma contains a relatively large population of progenitor cells that can generate oligodendrocytes. Defects in these adult oligodendrocyte progenitor cells (OPCs) or in their proliferation/differentiation have received little attention as potential causes of schizophrenia yet. We compared the set of genes whose expression is modified in schizophrenia, as revealed by our microarray studies, with genes specifically expressed in stem cells, as revealed by studies on human embryonic stem cells. We also evaluated the genes that are upregulated when stem cells engage in differentiation programs. These genes can be viewed as fingerprints or signatures for differentiation processes. The comparisons revealed that a substantial fraction of the genes downregulated in the brains of persons with schizophrenia belong to the differentiation signature. A plausible interpretation of our observations is that a cell differentiation process, possibly of adult OPCs to oligodendrocytes, is perturbed in schizophrenia. These observations constitute an incentive for a new direction of study, aimed at investigating the potential role of OPCs in schizophrenia.

Pimozide augmentation of clozapine inpatients with schizophrenia and schizoaffective disorder unresponsive to clozapine monotherapy.

Despite its superior efficacy, clozapine is helpful in only a subset of patients with schizophrenia unresponsive to other antipsychotics. This lack of complete success has prompted the frequent use of various clozapine combination strategies despite a paucity of evidence from randomized controlled trials supporting their efficacy. Pimozide, a diphenylbutylpiperidine, possesses pharmacological and clinical properties distinct from other typical antipsychotics. An open-label trial of pimozide adjunctive treatment to clozapine provided promising pilot data in support of a larger controlled trial. Therefore, we conducted a double-blind, placebo-controlled, parallel-designed 12-week trial of pimozide adjunctive treatment added to ongoing optimal clozapine treatment in 53 patients with schizophrenia and schizoaffective disorder partially or completely unresponsive to clozapine monotherapy. An average dose of 6.48 mg/day of pimozide was found to be no better than placebo in combination with clozapine at reducing Positive and Negative Syndrome Scale total, positive, negative, and general psychopathology scores. There is no suggestion from this rigorously conducted trial to suggest that pimozide is an effective augmenting agent if an optimal clozapine trial is ineffective. However, given the lack of evidence to guide clinicians and patients when clozapine does not work well, more controlled trials of innovative strategies are warranted.

Linking oligodendrocyte and myelin dysfunction to neurocircuitry abnormalities in schizophrenia.

Multiple lines of evidence in schizophrenia, from brain imaging, studies in postmortem brains, and genetic association studies, have implicated oligodendrocyte and myelin dysfunction in this disease. Recent studies suggest that oligodendrocyte and myelin dysfunction leads to changes in synaptic formation and function, which could lead to cognitive dysfunction, a core symptom of schizophrenia. Furthermore, there is accumulating data linking oligodendrocyte and myelin dysfunction with dopamine and glutamate abnormalities, both of which are found in schizophrenia. These findings implicate oligodendrocyte and myelin dysfunction as a primary change in schizophrenia, not only as secondary consequences of the illness or treatment. Strategies targeting oligodendrocyte and myelin abnormalities could therefore provide therapeutic opportunities for patients suffering from schizophrenia.

The effects of hypertension and body mass index on cognition in schizophrenia.

OBJECTIVE: In recent years there has been a greater appreciation of the elevated prevalence of cardiovascular risk factors in the schizophrenia population and the liability some treatments have for their development. These vascular risk factors are in turn important risk factors in the development of dementia and more subtle cognitive impairments. However, their impact on the cognitive functions of patients with schizophrenia remains underexplored. The authors investigated whether vascular risk factors influence the cognitive impairments of schizophrenia and whether their effects on cognition in schizophrenia are different from those observed in nonpsychiatric comparison subjects. METHOD: The authors compared 100 patients with schizophrenia and 53 comparison subjects on cognitive test performance in 2×2 matrices composed of individual vascular risk factors and group (schizophrenia patients and comparison subjects). RESULTS: Hypertension exerted a significant negative effect on immediate delayed and recognition memory in both groups. Patients with schizophrenia and hypertension were adversely affected in recognition memory, whereas comparison subjects were not. A body mass index above 25 was associated with negative effects on delayed memory in both groups, although the association fell short of statistical significance. CONCLUSIONS: Given that patients with schizophrenia have a higher prevalence of vascular risk factors than the general population and are undertreated for them, treatment of these risk factors may significantly improve cognitive outcome in schizophrenia.