Bradley S. Peterson | |
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Occupation(s) | Adult and child psychiatrist, developmental neuroscientist, academic and author |
Academic background | |
Education | B.S., Philosophy M.D. |
Alma mater | Tulane University St. Catherine’s College, Oxford University University of Wisconsin–Madison Medical School Harvard University Yale University |
Academic work | |
Institutions | Yale University Columbia University University of Southern California |
Bradley S. Peterson is an American psychiatrist,developmental neuroscientist,academic and author. He is the Inaugural Director of the Institute for the Developing Mind at Children's Hospital Los Angeles (CHLA),and holds the positions of Vice Chair for Research and Chief of the Division of Child &Adolescent Psychiatry in the Department of Psychiatry at the Keck School of Medicine at the University of Southern California. [1]
Peterson is most known for his neuroscience research on neuropsychiatric disorders including autism,depression,bipolar disorder,ADHD,Tourette syndrome,obsessive-compulsive disorder,schizophrenia,and eating disorders,as well as premature birth,the effects of environmental toxins on brain development,and brain mechanisms that mediate the effects of treatments on clinical outcomes. He has also studied normal brain development,and brain processes that support normal cognitive and emotional processes. [2]
Peterson was named Outstanding Mentor by the American Academy of Child &Adolescent Psychiatry in 2006 and 2014, [3] and he is the recipient of the 2007 Columbia University John J. Weber Prize for Outstanding Research, [4] the 2012 American Psychiatric Association Blanche Ittleson Award, [5] the 2024 Leadership in Child,Adolescent and Young Adult Psychiatry from the American College of Psychiatrists,the 2012 Excellence in Teaching Award from the New York Presbyterian Hospital of Columbia and Cornell Universities,and the 2017 and 2020 USC Keck School of Medicine Dean's Teaching Award. [1]
Peterson is a Fellow of the American College of Neuropsychopharmacology and the American College of Psychiatrists. [6] He is the Editor for the Neuroscience Section of the Journal of Child Psychology &Psychiatry . [7]
Peterson graduated with a bachelor's degree in Philosophy from Tulane University in 1983 and an M.D. from the University of Wisconsin–Madison Medical School in 1987 and also studied philosophy at St. Catherine's College of Oxford University. [1]
Peterson began his academic career at the Yale School of Medicine as an Assistant Professor in Child Psychiatry in 1994,the Elizabeth Meers and House Jameson Assistant/Associate Professor in 1996 and associate professor in 2000. In 2001,he became an Associate Professor in Child Psychiatry at the Columbia College of Physicians &Surgeons from 2001 to 2014 and a professor in psychiatry from 2005 to 2014. [8] Subsequently,he joined the University of Southern California as a professor in the Department of Psychiatry in 2014. [1]
Since 2017,he has been the Director of Child &Adolescent Psychiatry since 2014 and the Vice Chair for Research in the Department of Psychiatry of the Keck School of Medicine at the University of Southern California. [1] He has been the Director of the Institute for the Developing Mind at Children's Hospital Los Angeles since 2014,where he has also served as Interim Chief Scientific Officer from 2016 to 2018,Chief of Psychiatry since 2019,and co-director of the Behavioral Health Institute since 2022. [9]
Peterson has studied normal brain development across the life span,normal and pathological impulse control,prenatal exposures,emotional processing and mood disorders,Autism Spectrum Disorders,and the development of new MRI methods. [2]
Peterson has investigated normal brain development,normal aging,normal cognitive and emotional processes,and self-regulatory control. He and his colleagues demonstrated that gray matter density declines nonlinearly with age in frontal and parietal cortices from early childhood to approximately age 40,and declining in the left posterior temporal region beginning approximately at age 60,indicating that cortical maturation and aging trajectories vary across the brain. [10] In addition,he showed that brain tissue microstructure and metabolites mature in frontal and cingulate cortices and contribute to improved self-regulation during the transition from childhood to adolescence. [11] He further demonstrated age-related increases in prefrontal cortex and basal ganglia activation during a Stroop task was associated with improved self-regulatory control,indicating maturation of frontostriatal systems from childhood through adulthood in healthy individuals. [12]
Peterson has studied normal cognitive and emotional processing in the brain as well. He and his colleagues,including James Russell,developed an emotion processing task based on the Circumplex Model of Affect [13] that explored with functional MRI the neural systems that independently subserve the valence and arousal components of a full range of normal emotions evoked by emotional words, [14] faces, [15] [16] and induced moods. [17] In collaboration with Mark Packard,he developed a virtual reality platform for use during functional MRI scanning to study procedural and declarative learning processes in both health [18] [19] and illness. [20]
Peterson has researched disorders of impulse control,including Tourette's Syndrome (TS),Obsessive-Compulsive Disorder (OCD),and Attention-Deficit/Hyperactivity Disorder (ADHD). His imaging studies of TS subjects and controls across the lifespan have demonstrated larger prefrontal cortices in TS children,with an inverse association of these regional volumes with tic symptom severity. [21] Prefrontal volumes in TS adults,however,were smaller than control values,likely due to the ascertainment bias of studying still-symptomatic adults,given that tic symptoms usually substantially improve by adulthood. [22] These findings,along with earlier observations of significant prefrontal activation during tic suppression,suggested that compensatory responses involving activity-dependent plasticity and prefrontal hypertrophy play a role in controlling tic symptoms. [23] [24] He also established that caudate volumes in TS children predict the severity of both tics and OCD symptoms in early adulthood,even after adjusting for potential confounds. [25] These collective results suggested that prefrontal hypertrophy acts as a compensatory response to the presence of tics,attenuating symptoms in temporal proximity to the time of volume measurement. Conversely,the magnitude of the abnormality in the caudate nucleus is more critical in predicting the long-term outcome of symptom severity in TS. [26]
In addition,Peterson showed the presence of prominent cortical thinning in ventral portions of the sensory and motor homunculi that control the facial and vocal muscles that are commonly involved in tic symptoms. [27] More severe thinning was associated with more severe tic symptoms,suggesting that these sensorimotor regions are important in producing tics. He also explored neural mechanisms that generate the tics,comparing brain activation during spontaneous tics in persons with TS and mimicked tics in healthy controls. Finding showed that the sensory urges that generate tics derive from greater neural activity in somatosensory cortices,putamen,and amygdala/hippocampus complex,whereas progressively weaker activity in cortical-subcortical regulatory circuits (especially the caudate and anterior cingulate cortex) accompany proportionately more severe symptoms,highlighting that faulty activity in these circuits fail to control tic behaviors and the sensory urges that generate them. [28] Faulty activity within the subcortical portions of these circuits was further implicated in his showing that habit learning processes based within the striatum (caudate and putamen) are impaired in persons with TS in direct proportion to the severity of tic symptoms. [29]
Peterson's functional and anatomical studies have helped to define the neural basis of ADHD. A morphological study of the cortical surface,published in The Lancet,revealed smaller volumes of inferior prefrontal and anterior temporal regions in children with ADHD,supporting the hypothesis of involvement of these regions in the pathophysiology of the disorder. [30] Several of his functional imaging studies documented the significance of these regions in attention and behavior regulation. He demonstrated abnormal default-mode activity in ventral anterior cingulate and posterior cingulate cortices in ADHD youth,with these abnormalities normalizing in response to stimulant medications. [31] Additionally,he showcased that stimulant medications may reverse morphological abnormalities in the basal ganglia and thalamus of youth with ADHD. [32] [33] He also presented evidence for neuroplastic hypertrophy in the hippocampus and amygdala of ADHD youth,potentially serving as a compensatory response to dysfunctional frontostriatal circuits elsewhere in the brain and contributing to the attenuation of ADHD symptoms. [34]
Peterson's work on neonatal risks focused on conditions that confer risk for disturbances in development of the neonatal CNS,including premature birth,prenatal exposure to drugs of abuse,and prenatal exposure to various common environmental toxins. [2]
Peterson published the first quantitative study of the long-term effects of preterm birth on brain development,revealing large reductions in the volumes of specific cortical regions in the preterm children,most prominently in sensorimotor regions but also in premotor,midtemporal,parieto-occipital,and subgenual cortices,correlating with IQ at age 8 and gestational age at birth,indicating that younger birth age is associated with greater abnormalities in brain structure,and larger abnormalities in brain structure are associated with lower IQ. [35] Using fMRI in the same group,he demonstrated that while term-born children activated typical language areas during meaningful speech perception,prematurely born children activated these regions during meaningful speech similarly to how term-born children responded to nonsensical,phonemic sounds. [36] He concluded that the unusual activation during meaningful speech in preterm children was linked to lower verbal IQ and reduced comprehension of meaningful stories. [37] Subsequently,he examined brain volumes in preterm and term infants near their term due dates,observing a consistent pattern of anatomical abnormalities similar to those identified in 8-year-old prematurely born infants,suggesting that specific brain region morphological abnormalities are present soon after preterm birth. [38]
In addition,Peterson conducted imaging on a cohort of over 180 newborns,with 45 exposed in utero to crack cocaine,45 to narcotics,45 to cannabis,and 45 unexposed to any drugs of abuse,finding notable abnormalities in brain structure,connectivity,and function in drug-exposed infants at birth. [39] He collaborated with researchers at Columbia's School of Public Health,scanning 450 children in a longitudinal study on the impact of prenatal exposure to environmental toxins,including household insecticides,and found that prenatal exposure to the organophosphate insecticide chlorpyrifos increased white matter volumes in specific brain regions in proportion to cumulative exposure and associated IQ impairment,influencing an FDA review of chlorpyrifos use in the U.S. as an agricultural pesticide. [40] Furthermore,he showcased that prenatal exposure to PM2.5 and PAH disrupts brain development in youth,affecting anatomy,microstructure,and function,with implications for cognitive,emotional,and behavioral outcomes. [41]
Peterson has studied the brain bases of affective disorders,including Bipolar Disorder and Major Depression. Using a self-regulatory task,he found that adults with BD exhibited deficient left inferior prefrontal cortex activation,indicating a potential trait abnormality. The BD group also showed reduced amygdala (16%) and hippocampus (5%) volumes,likely emerging early in the illness course. [42] These and other related findings suggested the presence of faulty circuits that regulate emotions,with mesial temporal lobe structures losing normal top-down control from frontal cortices,potentially generating the mood changes of BD. [43]
Peterson,along with Myrna Weissman and colleagues,identified a brain-based endophenotype for Major Depressive Disorder (MDD),characterized by cortical thinning across the lateral surface of the right hemisphere and associated white matter abnormalities. [44] [45] This endophenotype,linked to familial risk for MDD,correlated with inattention and poor visual memory. He established neural patterns associated with depression risk (cortical attention circuits),resilience (dorsal anterior cingulate cortex),and enduring effects following illness (default mode circuits) as well,highlighting potential endophenotypes for novel interventions. [46]
Additionally,Peterson demonstrated that treatment with duloxetine attenuates and normalizes excessive activity and network connectivity in dysthymic individuals. [47] His research also illuminated that in patients with depressive disorders,duloxetine treatment induces changes in cortical gray matter morphology that likely represent neuroanatomical plasticity,and it normalizes N-acetyl-aspartate (NAA) concentrations by modulating depressive symptom severity,revealing the relationship between neurochemistry and depressive symptoms. [48] [49]
Peterson used multiple MRI modalities to explore the brain basis for the heterogeneity of symptoms in Autism Spectrum Disorder (ASD). He observed that brain lactate,indicating the presence of mitochondrial dysfunction,was significantly greater in individuals with ASD,suggesting a possible neurobiological subtype of ASD. [50] He also found that metabolite concentrations were altered in regions of the brain subserving socialization in persons with ASD,and in proportion to the severity of ASD symptom scores. [51] In another study,participants with ASD showed widespread alterations in regional brain blood flow,correlating with socialization deficits and suggesting potential metabolic disturbances that impact neural efficiency and trigger compensatory glial responses. [52] Alongside colleagues,he showed that ASD participants exhibited altered white matter microstructure that adversely impact blood flow,symptoms,and cognitive abilities. [53] He further used functional MRI to demonstrate that persons with ASD processed and likely experienced emotional stimuli very differently from the way typically developing persons did,and moreover that these differences were specific to the arousal components of facial emotions but not valence components. [54]
Peterson led a research program with collaborators that developed new methods for acquisition and processing of MRI data,including deformation-based analyses for anatomical data processing,noise reduction in diffusion tensor images, [55] statistical techniques for intergroup comparison of diffusion tensor images,enhanced signal-to-noise ratios in spectroscopic images, [56] and improved head coils for human and animal imaging. [57] His team developed software supporting virtual reality platforms for use in fMRI scanning. [58] Furthermore,he and Ravi Bansal developed software capable of diagnosing psychiatric disorders based solely on an individual's anatomical brain image. [59] [60]
Tourette syndrome or Tourette's syndrome is a common neurodevelopmental disorder that begins in childhood or adolescence. It is characterized by multiple movement (motor) tics and at least one vocal (phonic) tic. Common tics are blinking,coughing,throat clearing,sniffing,and facial movements. These are typically preceded by an unwanted urge or sensation in the affected muscles known as a premonitory urge,can sometimes be suppressed temporarily,and characteristically change in location,strength,and frequency. Tourette's is at the more severe end of a spectrum of tic disorders. The tics often go unnoticed by casual observers.
Lissencephaly is a set of rare brain disorders whereby the whole or parts of the surface of the brain appear smooth. It is caused by defective neuronal migration during the 12th to 24th weeks of gestation resulting in a lack of development of brain folds (gyri) and grooves (sulci). It is a form of cephalic disorder. Terms such as agyria and pachygyria are used to describe the appearance of the surface of the brain.
Deep brain stimulation (DBS) is a surgical procedure that implants a neurostimulator and electrodes which sends electrical impulses to specified targets in the brain responsible for movement control. The treatment is designed for a range of movement disorders such as Parkinson's disease,essential tremor,and dystonia,as well as for certain neuropsychiatric conditions like obsessive-compulsive disorder (OCD) and epilepsy. The exact mechanisms of DBS are complex and not entirely clear,but it is known to modify brain activity in a structured way.
Coprolalia is involuntary swearing or the involuntary utterance of obscene words or socially inappropriate and derogatory remarks. The word comes from the Greek κόπρος,meaning "dung,feces",and λαλιά"speech",from λαλεῖν"to talk".
A tic is a sudden and repetitive motor movement or vocalization that is not rhythmic and involves discrete muscle groups. It is typically brief and may resemble a normal behavioral characteristic or gesture.
Sensory overload occurs when one or more of the body's senses experiences over-stimulation from the environment.
Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) is a controversial hypothetical diagnosis for a subset of children with rapid onset of obsessive-compulsive disorder (OCD) or tic disorders. Symptoms are proposed to be caused by group A streptococcal (GAS),and more specifically,group A beta-hemolytic streptococcal (GABHS) infections. OCD and tic disorders are hypothesized to arise in a subset of children as a result of a post-streptococcal autoimmune process. The proposed link between infection and these disorders is that an autoimmune reaction to infection produces antibodies that interfere with basal ganglia function,causing symptom exacerbations,and this autoimmune response results in a broad range of neuropsychiatric symptoms.
The posterior cingulate cortex (PCC) is the caudal part of the cingulate cortex,located posterior to the anterior cingulate cortex. This is the upper part of the "limbic lobe". The cingulate cortex is made up of an area around the midline of the brain. Surrounding areas include the retrosplenial cortex and the precuneus.
Tourette syndrome is an inherited neurodevelopmental disorder that begins in childhood or adolescence,characterized by the presence of motor and phonic tics. The management of Tourette syndrome has the goal of managing symptoms to achieve optimum functioning,rather than eliminating symptoms;not all persons with Tourette's require treatment,and there is no cure or universally effective medication. Explanation and reassurance alone are often sufficient treatment;education is an important part of any treatment plan.
Causes and origins of Tourette syndrome have not been fully elucidated. Tourette syndrome is an inherited neurodevelopmental disorder that begins in childhood or adolescence,characterized by the presence of multiple motor tics and at least one phonic tic,which characteristically wax and wane. Tourette's syndrome occurs along a spectrum of tic disorders,which includes transient tics and chronic tics.
The obsessive–compulsive spectrum is a model of medical classification where various psychiatric,neurological and/or medical conditions are described as existing on a spectrum of conditions related to obsessive–compulsive disorder (OCD). "The disorders are thought to lie on a spectrum from impulsive to compulsive where impulsivity is said to persist due to deficits in the ability to inhibit repetitive behavior with known negative consequences,while compulsivity persists as a consequence of deficits in recognizing completion of tasks." OCD is a mental disorder characterized by obsessions and/or compulsions. An obsession is defined as "a recurring thought,image,or urge that the individual cannot control". Compulsion can be described as a "ritualistic behavior that the person feels compelled to perform". The model suggests that many conditions overlap with OCD in symptomatic profile,demographics,family history,neurobiology,comorbidity,clinical course and response to various pharmacotherapies. Conditions described as being on the spectrum are sometimes referred to as obsessive–compulsive spectrum disorders.
Tourette syndrome (TS) is an inherited neurological disorder that begins in childhood or adolescence,characterized by the presence of multiple physical (motor) tics and at least one vocal (phonic) tic.
Attention deficit hyperactivity disorder management options are evidence-based practices with established treatment efficacy for ADHD. Approaches that have been evaluated in the management of ADHD symptoms include FDA-approved pharmacologic treatment and other pharmaceutical agents,psychological or behavioral approaches,combined pharmacological and behavioral approaches,cognitive training,neurofeedback,neurostimulation,physical exercise,nutrition and supplements,integrative medicine,parent support,and school interventions. Based on two 2024 systematic reviews of the literature,FDA-approved medications and to a lesser extent psychosocial interventions have been shown to improve core ADHD symptoms compared to control groups.
The causes of schizophrenia that underlie the development of schizophrenia,a psychiatric disorder,are complex and not clearly understood. A number of hypotheses including the dopamine hypothesis,and the glutamate hypothesis have been put forward in an attempt to explain the link between altered brain function and the symptoms and development of schizophrenia.
The cause of obsessive–compulsive disorder is understood mainly through identifying biological risk factors that lead to obsessive–compulsive disorder (OCD) symptomology. The leading hypotheses propose the involvement of the orbitofrontal cortex,basal ganglia,and/or the limbic system,with discoveries being made in the fields of neuroanatomy,neurochemistry,neuroimmunology,neurogenetics,and neuroethology.
Schizophrenia is a primary psychotic disorder,whereas,bipolar disorder is a primary mood disorder which can also involve psychosis. Both schizophrenia and bipolar disorder are characterized as critical psychiatric disorders in the Diagnostic and Statistical Manual of Mental Disorders fifth edition (DSM-5). However,because of some similar symptoms,differentiating between the two can sometimes be difficult;indeed,there is an intermediate diagnosis termed schizoaffective disorder.
The delayed-maturation theory of obsessive–compulsive disorder suggests that obsessive–compulsive disorder (OCD) can be caused by delayed maturation of the frontal striatal circuitry or parts of the brain that make up the frontal cortex,striatum,or integrating circuits. Some researchers suspect that variations in the volume of specific brain structures can be observed in children that have OCD. It has not been determined if delayed-maturation of this frontal circuitry contributes to the development of OCD or if OCD is the ailment that inhibits normal growth of structures in the frontal striatal,frontal cortex,or striatum. However,the use of neuroimaging has equipped researchers with evidence of some brain structures that are consistently less adequate and less matured in patients diagnosed with OCD in comparison to brains without OCD. More specifically,structures such as the caudate nucleus,volumes of gray matter,white matter,and the cingulate have been identified as being less developed in people with OCD in comparison to individuals that do not have OCD. However,the cortex volume of the operculum (brain) is larger and OCD patients are also reported to have larger temporal lobe volumes;which has been identified in some women patients with OCD. Further research is needed to determine the effect of these structural size differences on the onset and degree of OCD and the maturation of specific brain structures.
The Yale Global Tic Severity Scale (YGTSS) is a psychological measure designed to assess the severity and frequency of symptoms of disorders such as tic disorder,Tourette syndrome,and obsessive-compulsive disorder,in children and adolescents between ages 6 and 17.
Hilary Patricia Blumberg is a medical doctor and the inaugural John and Hope Furth Professor of Psychiatry at the Yale School of Medicine. She is also a professor of Radiology and Biomedical Imaging,and works in the Child Study Center at Yale where she has been a faculty member since 1998. She attended Harvard University as an undergraduate,and completed medical school at Cornell University Medical College (1990). She completed her medical internship and psychiatry residency at Cornell University Medical College/New York Hospital,and her neuroimaging fellowship training at Cornell University,Weill Medical College. She has received the 2006 National Alliance for Research in Schizophrenia and Depression (NARSAD) and the Gerald L. Klerman Award for Clinical Research. Blumberg has authored a number of scientific articles that focus on bipolar disorder,neuroimaging,and effects of specific genetic variations,developmental trajectories and structure-function relationships.
The Tourette's Disorder Scale (TODS) is a psychological measure used to assess tics and co-occurring conditions in Tourette syndrome,a disease characterised by simple and complex motor and vocal tics and a wide range of behavioural and emotional symptoms. There are two versions of TODS (TODS-CR and TODS-PR),each being a 15-item scale that helps clinicians evaluate the severity of various symptoms associated with tics,inattention,hyperactivity,obsessions,compulsions,aggression and emotions.