A psicopatia e o criminoso nato: a modernização do positivismo criminológico / Psychopathy and the born criminal: the modernization of criminological positivism / Psicopatía y el criminal nato: la modernización del positivismo criminológico

O conceito de psicopatia é habitualmente associado a uma psicopatologia caracterizada pela falta de empatia, manipulação, agressividade, impulsividade, egocentrismo, crueldade e criminalidade. Já amplamente aceito pela comunidade científica, o conceito costuma ser utilizado em contextos jurídico-penais na validação de seu funcionamento punitivo. Dentre as concepções que alicerçaram o surgimento histórico desse conceito, destaca-se o papel do criminoso nato de Lombroso. Nesse sentido, este estudo buscou evidenciar como o conceito contemporâneo de psicopatia se firma enquanto modernização das concepções lombrosianas acerca do criminoso nato. Para isso, nos apoiamos na psicopatolologia para realizar um estudo comparativo entre as produções de Lombroso e as pesquisas contemporâneas acerca da psicopatia. Dentre as principais similaridades, destacamos a ênfase atribuída à suposta natureza criminal, etiologicamente decorrente de sua configuração orgânica. No mais, tais concepções também se assemelham no destaque de um déficit afetivo e moral, assim como na descrição da tendência a ser canhoto, egoísta, mentiroso, resistente à dor, narcisista, impulsivo, promíscuo, cruel, maléfico e inapto ao trabalho. Assim como fez Lombroso, as pesquisas acerca da psicopatia costumam ser realizadas com sujeitos já previamente criminalizados; condicionando uma seletividade étnico-racial e de classe. Descritos como sujeitos perigosos, incuráveis e intratáveis, ambas as concepções promovem a defesa do acirramento da punição jurídico-penal. Concluímos que a criminalidade nata de Lombroso continua a ser expressa no conceito de psicopatia, visto que as funções jurídico-penais e socioeconômicas de sua definição exercem o mesmo papel na legitimação científica da violência de Estado, encarceramento em massa e racismo estrutural.(AU)

Psychopathy is usually associated with a psychopathology characterized by a lack of empathy, manipulation, aggressiveness, impulsivity, egocentrism, cruelty, and criminality. Widely accepted by the scientific community, this concept is often used in legal and criminal contexts to validate its punitive functioning. Among the conceptions that underpinned the historical emergence of psychopathy, Lombroso's born criminal stands out. Hence, this study analyzes how the contemporary concept of psychopathy updates Lombrosian conceptions about the born criminal. To do so, we rely on psychopathology to conduct a comparative study between Lombroso's work and contemporary research on psychopathy. Among the main similarities, we highlight the emphasis given to the supposed criminal nature, etiologically arising from its organic configuration. Moreover, such conceptions emphasize an affective and moral deficit, and describe a tendency toward left-handedness, selfishness, lying, pain-resistance, narcissism, impulsivity, promiscuousness, cruelty, maliciousness and unfitness for work. As did Lombroso, research on psychopathy is usually conducted with individuals who have already been criminalized, conditioning an ethnic-racial and class selectivity. By describing these subjects as dangerous, incurable and intractable, both conceptions advocate for increased legal and penal punishment. In conclusion, Lombroso's natural criminality continues to underpin the concept of psychopathy, since its legal-criminal and socioeconomic functions play the same role in scientifically legitimizing state violence, mass incarceration, and structural racism.(AU)

La psicopatía es un concepto generalmente asociado a una psicopatología que se caracteriza por la falta de empatía, la manipulación, agresividad, impulsividad, egocentrismo, crueldad y criminalidad. Ya ampliamente aceptado por la comunidad científica, este concepto se utiliza a menudo en contextos legales para validar su funcionamiento punitivo. Entre los conceptos que fundamentaron el surgimiento histórico de este concepto, destaca el papel del criminal nato de Lombroso. En este contexto, este estudio buscó mostrar cómo el concepto contemporáneo de psicopatía se establece como la modernización de las concepciones lombrosianas sobre el criminal nato. Para eso, se utiliza la psicopatología para realizar un estudio comparativo entre las producciones de Lombroso y la investigación contemporánea sobre psicopatía. Entre las principales similitudes, destaca el énfasis atribuido a su supuesta naturaleza criminal, resultado etiológico de su configuración orgánica. Además, estas concepciones también son similares al resaltar un déficit afectivo y moral, así como al describir la tendencia a ser zurdo, egoísta, mentiroso, resistente al dolor, narcisista, impulsivo, promiscuo, cruel, malévolo e inadecuado para el trabajo. Como hizo Lombroso, los estudios sobre psicopatía se suelen realizar con sujetos que ya han sido criminalizados; condicionando una selectividad étnica, racial y de clase. Calificados como sujetos peligrosos, incurables e intratables, ambas concepciones promueven la defensa del aumento de la pena legal. Se concluye que la criminalidad nata de Lombroso continúa expresándose en el concepto de psicopatía, ya que las funciones penales y socioeconómicas de su definición juegan el mismo papel en la legitimación científica de la violencia estatal, encarcelamiento masivo y racismo estructural.(AU)

Increased functional connectivity of amygdala subregions in patients with drug-naïve panic disorder and without comorbidities / 中华医学杂志(英文版)

BACKGROUND@#Amygdala plays an important role in the neurobiological basis of panic disorder (PD), and the amygdala contains different subregions, which may play different roles in PD. The aim of the present study was to examine whether there are common or distinct patterns of functional connectivity of the amygdala subregions in PD using resting-state functional magnetic resonance imaging and to explore the relationship between the abnormal spontaneous functional connectivity patterns of the regions of interest (ROIs) and the clinical symptoms of PD patients.@*METHODS@#Fifty-three drug-naïve, non-comorbid PD patients and 70 healthy controls (HCs) were recruited. Seed-based resting-state functional connectivity (rsFC) analyses were conducted using the bilateral amygdalae and its subregions as the ROI seed. Two samples t test was performed for the seed-based Fisher's z -transformed correlation maps. The relationship between the abnormal spontaneous functional connectivity patterns of the ROIs and the clinical symptoms of PD patients was investigated by Pearson correlation analysis.@*RESULTS@#PD patients showed increased rsFC of the bilateral amygdalae and almost all the amygdala subregions with the precuneus/posterior cingulate gyrus compared with the HC group (left amygdala [lAMY]: t  = 4.84, P  <0.001; right amygdala [rAMY]: t  = 4.55, P  <0.001; left centromedial amygdala [lCMA]: t  = 3.87, P  <0.001; right centromedial amygdala [rCMA]: t  = 3.82, P  = 0.002; left laterobasal amygdala [lBLA]: t  = 4.33, P  <0.001; right laterobasal amygdala [rBLA]: t  = 4.97, P  <0.001; left superficial amygdala [lSFA]: t  = 3.26, P  = 0.006). The rsFC of the lBLA with the left angular gyrus/inferior parietal lobule remarkably increased in the PD group ( t  = 3.70, P  = 0.003). And most of the altered rsFCs were located in the default mode network (DMN). A significant positive correlation was observed between the severity of anxiety and the rsFC between the lSFA and the left precuneus in PD patients ( r  = 0.285, P  = 0.039).@*CONCLUSIONS@#Our research suggested that the increased rsFC of amygdala subregions with DMN plays an important role in the pathogenesis of PD. Future studies may further explore whether the rsFC of amygdala subregions, especially with the regions in DMN, can be used as a biological marker of PD.

Revealing the Precise Role of Calretinin Neurons in Epilepsy: We Are on the Way / 神经科学通报·英文版

Epilepsy is a common neurological disorder characterized by hyperexcitability in the brain. Its pathogenesis is classically associated with an imbalance of excitatory and inhibitory neurons. Calretinin (CR) is one of the three major types of calcium-binding proteins present in inhibitory GABAergic neurons. The functions of CR and its role in neural excitability are still unknown. Recent data suggest that CR neurons have diverse neurotransmitters, morphologies, distributions, and functions in different brain regions across various species. Notably, CR neurons in the hippocampus, amygdala, neocortex, and thalamus are extremely susceptible to excitotoxicity in the epileptic brain, but the causal relationship is unknown. In this review, we focus on the heterogeneous functions of CR neurons in different brain regions and their relationship with neural excitability and epilepsy. Importantly, we provide perspectives on future investigations of the role of CR neurons in epilepsy.

Effects of Chronic Restraint Stress on Apoptosis of Amygdala Cells in Rats / 法医学杂志

OBJECTIVES@#To explore the damage effects of chronic restraint stress (CRS) on amygdala cells through the rat CRS model.@*METHODS@#The rat CRS model was established, and the changes in body weight and adrenal mass in control group and CRS group were monitored at 1 d, 7 d, 14 d and 21 d. The behavior changes were evaluated by the percentage of retention time of open arms and open arm entries using the elevated plus maze (EPM). ELISA was used to detect the concentrations of rat's corticotropin releasing hormone (CRH), adrenocorticotropic hormone (ACTH) and cortisol. The changes of expression of glucocorticoid receptor (GR) and glial fibrillary acidic protein (GFAP) in amygdala were determined by immunohistochemistry and Western blotting. Ultrastructure changes of glial cell were observed by transmission electron microscopy. The apoptosis rate of amygdala was measured by flow cytometry.@*RESULTS@#Compared with the control group at the same time points, body weight of CRS 1 d, 7 d, 14 d and 21 d groups increased slowly, but adrenal mass increased significantly; the serum level of CRH, cortisol and ACTH increased significantly at 7 d, 14 d and 21 d respectively; the expression of GR in amygdala was increased while that of GFAP was decreased; EPM test suggested that the percentage of retention time of open arms and open arm entries decreased significantly after 14 d. The CRS group showed different degrees of glial cell damage in amygdala, and the apoptosis rate of glial cell was significantly increased in 21 d group.@*CONCLUSIONS@#This study successfully established a CRS model in rats, and anxiety-like behavioral changes in model rats may be caused by apoptosis of amygdala astrocytes.

Association of Increased Amygdala Activity with Stress-Induced Anxiety but not Social Avoidance Behavior in Mice / 神经科学通报·英文版

Chronic stress leads to many psychiatric disorders, including social and anxiety disorders that are associated with over-activation of neurons in the basolateral amygdala (BLA). However, not all individuals develop psychiatric diseases, many showing considerable resilience against stress exposure. Whether BLA neuronal activity is involved in regulating an individual's vulnerability to stress remains elusive. In this study, using a mouse model of chronic social defeat stress (CSDS), we divided the mice into susceptible and resilient subgroups based on their social interaction behavior. Using in vivo fiber photometry and in vitro patch-clamp recording, we showed that CSDS persistently (after 20 days of recovery from stress) increased BLA neuronal activity in all the mice regardless of their susceptible or resilient nature, although impaired social interaction behavior was only observed in susceptible mice. Increased anxiety-like behavior, on the other hand, was evident in both groups. Notably, the CSDS-induced increase of BLA neuronal activity correlated well with the heightened anxiety-like but not the social avoidance behavior in mice. These findings provide new insight to our understanding of the role of neuronal activity in the amygdala in mediating stress-related psychiatric disorders.

Inhibiting silence information regulator 2 and glutaminase in the amygdala can improve social behavior in autistic rats / 浙江大学学报·医学版

OBJECTIVE@#To investigate the underlying molecular mechanisms by which silence information regulator (SIRT) 2 and glutaminase (GLS) in the amygdala regulate social behaviors in autistic rats.@*METHODS@#Rat models of autism were established by maternal sodium valproic acid (VPA) exposure in wild-type rats and SIRT2-knockout ( SIRT2 -/-) rats. Glutamate (Glu) content, brain weight, and expression levels of SIRT2, GLS proteins and apoptosis-associated proteins in rat amygdala at different developmental stages were examined, and the social behaviors of VPA rats were assessed by a three-chamber test. Then, lentiviral overexpression or interference vectors of GLS were injected into the amygdala of VPA rats. Brain weight, Glu content and expression level of GLS protein were measured, and the social behaviors assessed.@*RESULTS@#Brain weight, amygdala Glu content and the levels of SIRT2, GLS protein and pro-apoptotic protein caspase-3 in the amygdala were increased in VPA rats, while the level of anti-apoptotic protein Bcl-2 was decreased (all P<0.01). Compared with the wild-type rats, SIRT2 -/- rats displayed decreased expression of SIRT2 and GLS proteins in the amygdala, reduced Glu content, and improved social dysfunction (all P<0.01). Overexpression of GLS increased brain weight and Glu content, and aggravated social dysfunction in VPA rats (all P<0.01). Knockdown of GLS decreased brain weight and Glu content, and improved social dysfunction in VPA rats (all P<0.01).@*CONCLUSIONS@#The glutamate circulatory system in the amygdala of VPA induced autistic rats is abnormal. This is associated with the upregulation of SIRT2 expression and its induced increase of GLS production; knocking out SIRT2 gene or inhibiting the expression of GLS is helpful in maintaining the balanced glutamate cycle and in improving the social behavior disorder of rats.

The antiepileptic activity of Safranal in kindling model of epilepsy in male rats

Abstract Recent studies suggested that safranal exerts anticonvulsant properties. The present study aimed to investigate the effect of safranal on epileptic activities in the amygdala electrical kindling model in male rats. Animals were implanted with a recording electrode on the skull and a tripolar in the amygdala. After 10 days of recovery, the afterdischarge (AD) threshold of each animal was determined and stimulated once daily the AD threshold for full kindling development. Then, parameters including afterdischarge duration (ADD), stage 4 latency (S4L), stage 5 duration (S5D), and stimulation threshold were determined before and after injection of safranal (0.05, 0.1, 0.2 ml/ kg; i.p). While the dose of 0.05 ml/kg had no significant effect, the dose of 0.1 ml/kg increased the AD threshold as well as S4L and decreased the S5D (P<0.05). Injection of 0.2 ml/kg of the safranal significantly decreased the ADD and S5D (P<0.05) and 83.3% of animals had no stage 4 and stage 5 of kindling (P<0.001). Based on the obtained data safranal has anticonvulsant effects dosedependently. It seems that a dose of 0.2 ml/kg is the minimum effective dose. Further investigation is warranted to conduct the clinical implications for the treatment of epileptic disorders

El término cuerpo amigdaloide en la terminología médica / The term amygdaloid body in medical terminology

RESUMEN: En terminología médica el término amígdala cerebral es utilizado para denominar a la estructura que según la Terminologia Neuroanatomica y Terminologia Anatomica se conoce como cuerpo amigadaloide, la cual está constituida por diversos núcleos y es responsable de las emociones, el comportamiento, regulación de la ansiedad, la agresión, el miedo, la memoria emocional, la cognición social y las respuestas al estrés. Siendo la amígdala cerebral una estructura tan importante el objetivo de este estudio fue: analizar el significado del término amígdala cerebral en la Terminologia Neuronatomica y en la Terminologia Anatomica y contrastar si el origen de sus raíces greco latinas concuerdan con la función de esta estructura acorde con los requerimientos de la FIPAT. Para ello se consultó los diccionarios de la Lengua Española, Diccionario DGE Griego Español, Diccionario VOX Griego Español, Diccionario Médico, Biológico, Histológico y Etimológico de la Universidad de Salamanca y Diccionario de Términos Médicos de la Real Academia Nacional de Medicina, así como algunos artículos y libros clásicos de anatomía. Los resultados indicaron que el término amígdala tiene el mismo significado en griego como en latín, en donde ἀμυγδαλέα, ἀμυγδαλέας (pr. amygdaléa, amygdaléas) es el árbol del almedro y ἀμυγδάλη, ἀμυγδάλης (pr. amygdále, amygdáles) significa almendra. Conociendo tanto la anatomía como la fisiología de esta estructura su forma no se asemeja a la de una almendra y su denominación actual no está acorde con los requerimientos de la FIPAT por lo cual consideramos que esta debe ser revisada.

SUMMARY: In medical terminology the term brain amygdala is used to refer to the structure that according to the Terminologia Neuroanatomica and Terminologia Anatomica is known as the amydaloid body, which is made up of various nuclei and is responsible for emotions, behavior, regulation of the anxiety, aggression, fear, emotional memory, social cognition, and responses to stress. Being the cerebral amygdala such an important structure, the objective of this study was: to analyze the meaning of the term cerebral amygdala in Terminologia Neuroanatomica and in Terminologia Anatomica and to contrast if the origin of its Greek Latin roots agrees with the function of this structure according to the requirements of the FIPAT. For this, the dictionaries of the Royal Spanish Academy, the DGE Greek Spanish Dictionary, the VOX Greek Spanish Dictionary, the Medical, Biological, Histological and Etymological Dictionary of the University of Salamanca, the Dictionary of the Royal National Academy of Medicine, as well as some articles and classic books of anatomy. The results indicated that the term amygdala has the same meaning in Greek as in Latin, where? ἀμυγδαλέα, ἀμυγδαλέας (pr. Amygdaléa, amygdaléas) is the almond tree andἀμυγδάλη, ἀμυγδάλης (pr. amygdále, amygdáles) means almond. Knowing both the anatomy and the physiology of this structure, its shape does not resemble that of an almond and its current name is not in accordance with the requirements of the FIPAT, for which we consider that it should be revised.

Association between poor tolerability of antidepressant treatment and brain functional activation in youth at risk for bipolar disorder

Objective: To investigate whether poor antidepressant tolerability is associated with functional brain changes in children and adolescents of parents with bipolar I disorder (at-risk youth). Methods: Seventy-three at-risk youth (ages 9-20 years old) who participated in a prospective study and had an available baseline functional magnetic resonance imaging (fMRI) scan were included. Research records were reviewed for the incidence of adverse reactions related to antidepressant exposure during follow-up. The sample was divided among at-risk youth without antidepressant exposure (n=21), at-risk youth with antidepressant exposure and no adverse reaction (n=12), at-risk youth with antidepressant-related adverse reaction (n=21), and healthy controls (n=20). The fMRI task was a continuous performance test with emotional distracters. Region-of-interest mean activation in brain areas of the fronto-limbic emotional circuit was compared among groups. Results: Right amygdala activation in response to emotional distracters significantly differed among groups (F3,66 = 3.1, p = 0.03). At-risk youth with an antidepressant-related adverse reaction had the lowest amygdala activation, while at-risk youth without antidepressant exposure had the highest activation (p = 0.004). Conclusions: Decreased right amygdala activation in response to emotional distracters is associated with experiencing an antidepressant-related adverse reaction in at-risk youth. Further studies to determine whether amygdala activation is a useful biomarker for antidepressant-related adverse events are needed.

The Periaqueductal Gray and Its Extended Participation in Drug Addiction Phenomena / 神经科学通报·英文版

The periaqueductal gray (PAG) is a complex mesencephalic structure involved in the integration and execution of active and passive self-protective behaviors against imminent threats, such as immobility or flight from a predator. PAG activity is also associated with the integration of responses against physical discomfort (e.g., anxiety, fear, pain, and disgust) which occurs prior an imminent attack, but also during withdrawal from drugs such as morphine and cocaine. The PAG sends and receives projections to and from other well-documented nuclei linked to the phenomenon of drug addiction including: (i) the ventral tegmental area; (ii) extended amygdala; (iii) medial prefrontal cortex; (iv) pontine nucleus; (v) bed nucleus of the stria terminalis; and (vi) hypothalamus. Preclinical models have suggested that the PAG contributes to the modulation of anxiety, fear, and nociception (all of which may produce physical discomfort) linked with chronic exposure to drugs of abuse. Withdrawal produced by the major pharmacological classes of drugs of abuse is mediated through actions that include participation of the PAG. In support of this, there is evidence of functional, pharmacological, molecular. And/or genetic alterations in the PAG during the impulsive/compulsive intake or withdrawal from a drug. Due to its small size, it is difficult to assess the anatomical participation of the PAG when using classical neuroimaging techniques, so its physiopathology in drug addiction has been underestimated and poorly documented. In this theoretical review, we discuss the involvement of the PAG in drug addiction mainly via its role as an integrator of responses to the physical discomfort associated with drug withdrawal.

Temporomandibular inflammation mobilizes parvalbumin and FosB/deltaFosB neurons of amygdala and dorsal raphe

Pathophysiological mechanisms involved in orofacial pain and their relationship with emotional disorders have emerged as an important research area for multidisciplinary studies. In particular, temporomandibular disorders (TMD) have been evaluated clinically from both physiological and psychological perspectives. We hypothesized that an altered neuronal activity occurs in the amygdala and the dorsal raphe nucleus (DR), encephalic regions involved in the modulation of painful and emotional information. Adult male Wistar rats were used in an experimental complete Freund's adjuvant (CFA)-induced temporomandibular joint (TMJ) inflammation model. CFA was applied for 1 or 10 days, and the animals were euthanized for brain samples dissection for FosB/ΔFosB and parvalbumin (PV) immunostaining. Our results were consistent in showing that the amygdala and DR were activated in the persistent inflammatory phase (10 days) and that the expression of PV+ interneurons in the amygdala was decreased. In contrast, in the DR, the expression of PV+ interneurons was increased in persistent states of CFA-induced TMJ inflammation. Moreover, at 10 days of inflammation, there was an increased co-localization of PV+ and FosB/ΔFosB+ neurons in the basolateral and central nucleus of the amygdala. Different nuclei of the amygdala, as well as portions of the DR, were activated in the persistent phase (10 days) of TMJ inflammation. In conclusion, altered activity of the amygdala and DR was detected during persistent inflammatory nociception in the temporomandibular joint. These regions may be essential for both sensory and affective dimensions of orofacial pain.

Áreas exofocales de lesión a mediano y largo término post-isquemia cerebral / Exofocal areas of medium- and long-term injury after cerebral ischemia

La isquemia cerebral es el tipo de accidente cerebrovascular más común, generando altas tasas de mortalidad y morbilidad a nivel mundial. El entendimiento de la fisiopatología de la lesión cerebral ha requerido de la implementación de modelos experimentales que permitan evaluar los fenómenos celulares, sobre todo aquellos a largo plazo. Por tal razón, el objetivo del presente trabajo fue evaluar las áreas exofocales a un mes y cuatro meses post-isquemia cerebral en un modelo experimental. Ratas Wistar fueron sometidas a una isquemia focal transitoria (t-MCAo) y un grupo fueron sacrificados al mes y otro grupo a los cuatro meses post-isquemia para su posterior análisis histológico. Los cortes fueron teñidos con Nissl y se realizó inmunohistoquímica de la proteína Tau. Nuestros resultados muestran tres áreas de lesión exofocal tanto al mes como a los cuatro meses post-isquemia: el giro dentado, la amígdala y el tálamo. Estas regiones se han asociado al control emocional, lo cual sugiere que a largo término post-isquemia se tengan en cuenta hallazgos clínicos que evalúen cambios emocionales en los pacientes que han sufrido un evento isquémico cerebral.

Cerebral ischemia is the most common type of stroke, which generates high mortality and morbidity rates worldwide. The understanding of the pathophysiology of brain injury has required the implementation of experimental models that allow the evaluation of cellular phenomena, especially those in the long-term. For this reason, the objective of the present work was to evaluate the exofocal areas at one month and four months after cerebral ischemia. Wistar rats were subjected to transient focal ischemia (t-MCAo) and one group was sacrificed one month and another group at four months' post-ischemia for subsequent histological analysis. The cuts were stained with Nissl and immunohistochemistry of the Tau protein was performed. Our results show three areas of exofocal lesion both one month and four months' post-ischemia: the thalamus, the dentate gyrus, and the amygdala. These regions have been associated with emotional control, which suggests that in the long-term post-ischemia clinical findings that evaluate emotional changes in patients who have suffered a cerebral ischemic event should be considered.

Clinico-pathological features of temporal lobe epilepsy with enlarged amygdala / 北京大学学报(医学版)

OBJECTIVE@#To summarize the clinical, video electroencephalogram (VEEG), radiological and pathological features of 3 patients of temporal lobe epilepsy (TLE) with amygdala enlargement (AE).@*METHODS@#Three TLE patients with AE who were hospitalized in Peking University International Hospital were collected. The above features were retrospectively analyzed, and the amygdala volume was measured as well.@*RESULTS@#Of all the 3 patients, 2 were females and 1 male, whose seizure onset ages varied from 21 to 40 years. Two cases presented with secondarily generalized tonicclonic seizures after falling asleep during the night. One of the 2 cases had complex partial seizures (CPSs) with episodic memory and automatism after one year, and the third one had CPSs with lip smacking and tongue wagging during the night. All the patients suffered from obvious anxious disorder. Unilateral AE by MRI was demonstrated in the 3 cases, one on the right side, and the other two on the left side. The average amygdala volume of the enlarged side and the other side were (2 123.7±131.8) mm3 and (1 276.3±156.9) mm3, respectively. Unilateral interictal epileptic discharges were ipsilateral to the AE in 2 cases, while the other patient showed bilateral interictal epileptic discharges. The ictal VEEG showed that the seizure onset zone was ipsilateral to the AE and was confined to the anterior and middle temporal regions in the 3 patients. The interictal single-photon emission computed tomography (SPECT) was negative in 2 cases. The interictal positron emission tomography (PET) showed hypometabolism in the AE in one case. The histological pathology revealed focal cortical dysplasia in the amygdala and temporal lobe in the 3 cases, and one of the 3 cases was combined with hippocampal sclerosis. All the patients became seizure free after surgery in the half year following-up. VEEG revealed slow wave activity and occasional spike wave in the operated side.@*CONCLUSION@#AE may be one subtype of TLE. It is necessary to recognize AE in TLE with MRI-negative. For those poorly responsive to antiepileptic drugs, surgical treatment could provide a better solution. Focal cortical dysplasia may be one of the most common pathological features of TLE with AE.

Biological and Clinical Markers in Panic Disorder

OBJECTIVE: Classifying mental disorders on the basis of objective makers might clarify their aetiology, help in making the diagnosis, identify “at risk” individuals, determine the severity of mental illness, and predict the course of the disorder. This study aims to review biological and clinical markers of panic disorder (PD). METHODS: A computerized search was carried out in PubMed and Science Direct using the key words: “marker/biomarker/clinical marker/neurobiology/staging” combined using Boolean AND operator with “panic.” In addition, the reference lists from existing reviews and from the articles retrieved were inspected. Only English language papers published in peer-reviewed journals were included. RESULTS: Structural changes in the amygdala, hippocampus, cerebral blood level in the left occipital cortex, serotonin 5-TH and noradrenergic systems activation, aberrant respiratory regulation, hearth rate variability, blood cells and peripheral blood stem cells, hypothalamic–pituitary–adrenal axis dysregulation were identified as potential candidate biomarkers of PD. Staging was identified as clinical marker of PD. According to the staging model, PD is described as follows: prodromal phase (stage 1); acute phase (stage 2); panic attacks (stage 3); chronic phase (stage 4). CONCLUSION: The clinical utility, sensitivity, specificity, and the predictive value of biomarkers for PD is still questionable. The staging model of PD might be a valid susceptibility, diagnostic, prognostic, and predictive marker of PD. A possible longitudinal model of biological and clinical markers of PD is proposed.

Role of nociceptin/orphanin FQ and nociceptin opioid peptide receptor in depression and antidepressant effects of nociceptin opioid peptide receptor antagonists

Nociceptin/orphanin FQ (N/OFQ) and its receptor, nociceptin opioid peptide (NOP) receptor, are localized in brain areas implicated in depression including the amygdala, bed nucleus of the stria terminalis, habenula, and monoaminergic nuclei in the brain stem. N/OFQ inhibits neuronal excitability of monoaminergic neurons and monoamine release from their terminals by activation of G protein-coupled inwardly rectifying K⁺ channels and inhibition of voltage sensitive calcium channels, respectively. Therefore, NOP receptor antagonists have been proposed as a potential antidepressant. Indeed, mounting evidence shows that NOP receptor antagonists have antidepressant-like effects in various preclinical animal models of depression, and recent clinical studies again confirmed the idea that blockade of NOP receptor signaling could provide a novel strategy for the treatment of depression. In this review, we describe the pharmacological effects of N/OFQ in relation to depression and explore the possible mechanism of NOP receptor antagonists as potential antidepressants.

Promising Neuroimaging Biomarkers in Depression

The neuroimaging has been applied in the study of pathophysiology in major depressive disorder (MDD). In this review article, several kinds of methodologies of neuroimaging would be discussed to summarize the promising biomarkers in MDD. For the magnetic resonance imaging (MRI) and magnetoencephalography field, the literature review showed the potentially promising roles of frontal lobes, such as anterior cingulate cortex (ACC), dorsolateral prefrontal cortex (DLPFC) and orbitofrontal cortex (OFC). In addition, the limbic regions, such as hippocampus and amygdala, might be the potentially promising biomarkers for MDD. The structures and functions of ACC, DLPFC, OFC, amygdala and hippocampus might be confirmed as the biomarkers for the prediction of antidepressant treatment responses and for the pathophysiology of MDD. The functions of cognitive control and emotion regulation of these regions might be crucial for the establishment of biomarkers. The near-infrared spectroscopy studies demonstrated that blood flow in the frontal lobe, such as the DLPFC and OFC, might be the biomarkers for the field of near-infrared spectroscopy. The electroencephalography also supported the promising role of frontal regions, such as the ACC, DLPFC and OFC in the biomarker exploration, especially for the sleep electroencephalogram to detect biomarkers in MDD. The positron emission tomography (PET) and single-photon emission computed tomography (SPECT) in MDD demonstrated the promising biomarkers for the frontal and limbic regions, such as ACC, DLPFC and amygdala. However, additional findings in brainstem and midbrain were also found in PET and SPECT. The promising neuroimaging biomarkers of MDD seemed focused in the fronto-limbic regions.

Morphologic Alterations in Amygdala Subregions of Adult Patients with Bipolar Disorder

OBJECTIVES: Previous studies have revealed inconsistent results on amygdala volume in adult bipolar disorder (BD) patients compared to healthy controls (HC). Since the amygdala encompasses multiple subregions, the subtle volume changes in each amygdala nucleus might have not been fully reflected in the measure of the total amygdala volume, causing discrepant results. Thus, we aimed to investigate volume changes in each amygdala subregion and their association with subtypes of BD, lithium use and clinical status of BD. METHODS: Fifty-five BD patients and 55 HC underwent T1-weighted structural magnetic resonance imaging. We analyzed volumes of the whole amygdala and each amygdala subregion, including the anterior amygdaloid area, cortico-amygdaloid transition area, basal, lateral, accessory basal, central, cortical, medial and paralaminar nuclei using the atlas in the FreeSurfer. The volume difference was analyzed using a one-way analysis of covariance with individual volumes as dependent variables, and age, sex, and total intracranial volume as covariates. RESULTS: The volumes of whole right amygdala and subregions including basal nucleus, accessory basal nucleus, anterior amygdaloid area, and cortico-amygdaloid transition area in the right amygdala of BD patients were significantly smaller for the HC group. No significant volume difference between bipolar I disorder and bipolar II disorder was found after the Bonferroni correction. The trend of larger volume in medial nucleus with lithium treatment was not significant after the Bonferroni correction. No significant correlation between illness duration and amygdala volume, and insignificant negative correlation were found between right central nucleus volume and depression severity. CONCLUSIONS: Significant volume decrements of the whole amygdala, basal nucleus, accessory basal nucleus, anterior amygdaloid area, and cortico-amygdaloid transition area were found in the right hemisphere in adult BD patients, compared to HC group. We postulate that such volume changes are associated with altered functional activity and connectivity of amygdala nuclei in BD.

Mechanism of Mindfulness-Based Intervention and Neurobiological Basis / 생물치료정신의학

Mindfulness is a process in which all thoughts, feelings, sensations, and all phenomena that happen to me are uncritically recognized as they are, so that they are eventually accepted and released without identifying or automatically responding to them. The clinical effects of mindfulness-based therapy have already been demonstrated in several studies. However, consistent results have not been reported for the mechanism of mindfulness-based treatment. Thus, this review aimed to describe a systematic review of the literature and research on the mechanisms of mindfulness-based interventions. Experienced meditators showed a physiological change in a ‘wakeful hypometabolic state’ during mindfulness meditation. In mindfulness meditation, it is known that certain areas other than brain activation during relaxation are additionally activated, particularly activation of fronto-limbic and fronto-parietal neural networks. The psychological mechanisms include meta-cognitive awareness, emotion regulation, reduction of automatic and self-referential thinking, concentration control, self-compassion, improvement of value clarification and self-regulation, exposure, extinction, and reconsolidation. Of the brain regions with changes in activity associated with mindfulness meditation, prefrontal cortex, the default mode network including cortical midline structures were associated with emotion regulation, concentration control, and reduction of automatic and self-referential thinking. In addition, brain regions associated with mindfulness meditation have been reported in the hippocampus, amygdala, and medical frontal cortices associated with memory reconsolidation and fear extinction. Thus, mindfulness-based interventions have a psychological and neurobiological effect with a special mechanism different from other psychological interventions, so that mindfulness based intervention can be an effective therapeutic intervention with a different mechanism from other psychological techniques.

Effects of CeA lesions on the initiation and expression of sodium appetite in sodium-deficient rats / 中国应用生理学杂志

OBJECTIVE@#To investigate the effects of central nucleus of amygdala (CeA) lesion on the initiation and expression of sodium appetite in sodium-deficient rats.@*METHODS@#Three groups of SD rats (n=6 in each group) were treated with bilateral CeA lesion, sham lesion or no lesion. After the recovery, the rats were fed with low-sodium diets for 14 days to establish a sodium-deficient rat model. The double-bottle selection in single cage test was used to observe the intake of 0.3 mol/L NaCl and DW in 5 timepoint with 24 hours in sodium-deficient rats. Immunofluorescence staining of aldosterone-sensitive neurons in the nucleus tractus solitarii (NTS)was used to investigate the effect of CeA lesion or not on the activity of aldosterone-sensitive neurons in rats with or without sodium deficiency.@*RESULTS@#After fed with low-sodium diet for14 days, the volume and preference rate of 0.3 mol/L NaCl intake of the rats within 24 h were significantly increased compared with those before low-sodium diet (P＜0.01). The intake volume and the preference rate of 0.3 mol/L NaCl in CeA lesion rats were significantly decreased than those in CeA sham lesion rats and normal rats in the sodium-deficient condition (P＜0.01). The CeA lesion had no effects on the activity of aldosterone-sensitive neurons in NTS in rats with low-sodium diet.@*CONCLUSION@#Low-sodium diet induces an increase in the expression of sodium appetite in rats. CeA lesions inhibit the behavioral expression of sodium appetite in sodium-deficient rats but have no effects on the initiation of sodium appetite in rats with sodium-deficient rats.

Efecto de la amigdalotomía e hipotalamotomía unilateral en pacientes con agresividad refractaria / Effect of tonsillotomy and unilateral hypothalamotomy in patients with refractory aggressiveness

Resumen Antecedentes: El tratamiento neuroquirúrgico, aunque polémico, se considera un recurso útil en el tratamiento de enfermedades psiquiátricas crónicas como la agresividad refractaria. Objetivo: Evaluar los resultados clínicos y los efectos colaterales de la hipotalamotomía posteromedial (HPM) asociada a amigdalotomía en pacientes con agresividad refractaria. Método: Se realizó un ensayo clínico en pacientes con agresividad crónica y refractaria a tratamiento farmacológico. Se les realizó amigdalotomía central asociada a HPM mediante termocoagulación por radiofrecuencia. El grado de agresividad se cuantificó mediante la escala global de agresividad de Yudofsky. Los cambios postoperatorios en la conducta agresiva continuaron siendo evaluados cada 6 meses durante al menos 36 meses. Resultados: Se observó un cambio estadísticamente significativo de la conducta agresiva, a lo largo de 36 meses de seguimiento. Se describen los efectos colaterales de la asociación de ambos procedimientos, siendo el de mayor frecuencia la somnolencia y algunos casos de reducción en la conducta sexual. Conclusión: Las lesiones unilaterales simétricas y simultáneas del núcleo central de la amígdala y del hipotálamo posteromedial contralaterales a la dominancia motora dan el mismo efecto clínico en la reducción de la agresividad patológica que las lesiones bilaterales.

Abstract Background: Neurosurgical treatment, although controversial, is considered a useful resource in the treatment of chronic psychiatric diseases such as refractory aggressiveness. Objective: To evaluate the clinical results and side effects of posteromedial hypothalamotomy associated with amygdalotomy in patients with refractory aggressiveness. Method: A clinical trial was conducted in patients with chronic aggressiveness and refractory to pharmacological treatment. A central amygdalotomy associated with posteromedial hypothalamotomy was performed using thermo-coagulation by radiofrequency. The degree of aggressiveness was quantified by the Yudofsky's global scale of aggression. Postoperative changes in aggressive behavior continued to be evaluated every 6 months for at least 36 months. Results: A statistically significant change in aggressive behavior was observed during 36 months of follow-up. The collateral effects of the association of both procedures are described, the most frequent being drowsiness and some cases of reduction in sexual behavior. Conclusion: Symmetric and simultaneous unilateral lesions of the central nucleus of the amygdala and the posteromedial hypothalamus contralateral to motor dominance give the same clinical effect in the reduction of the pathological aggression that the bilateral lesions.