Psychiatric Annals

Feature 

The Social Brain and the Psychiatrist in Training

Morton D. Sosland, MD

Abstract

As a child psychiatry fellow, I sensed psychiatry's division into biological and psychological sides. The division shows in explanations of why patients suffer as well as in treatment choices. It divides psychiatric faculty, affects psychiatry training received in residency and fellowship, and shapes how one considers available future professional opportunities. With 2 years of participation with the Group for the Advancement of Psychiatry (GAP) Research Committee sponsored by the GAP fellowship (I was a child fellow at Thomas Jefferson Memorial Hospital at the time), I found the “social brain” model helped me integrate the two spheres.

First, more about the problem. As T.M. Luhrmann discussed the following in her landmark work, Of Two Minds: The Growing Disorder in American Psychiatry:

“Young psychiatrists are supposed to learn to be equally good at both talk therapy and drug therapy, psychotherapy and biomedical psychiatry, and the American Psychiatric Association thinks that this integration is what training programs in psychiatry teach. Psychiatrists are supposed to understand these approaches as different tools in a common toolbox. Yet they are taught as different tools, based on different models, and used for different purposes. Some psychiatrists do integrate them to some extent. But those who do have to integrate two approaches that are different from the outset that carry with them different models of the person, different models of causation, and different expectations of how a person might change over time.”1

If psychiatrists experience division and confusion about the cause and treatment for an illness, patients doubtless feel equally or more confused. Is it a chemical imbalance or genetic in nature (biological)? Social or psychological? If it's chemical or genetic in causation, why use psychotherapy? If it's psychological or based on family interactions or upbringing, then what need for medication exists? Social brain explanations clarify psychiatric illness in my own mind, and in the minds of my patients, with more effective treatment strategies. But what exactly is the social brain?

I quote from the GAP Research Committee's definition of the social brain, further discussed elsewhere in this issue, which includes, “The social brain framework helps organize and explain all psychopathology. A single gene-based disorder like Huntington disease is expressed to a large extent as social dysfunction. Conversely, traumatic stress has structural impact on the brain as does the socially interactive process of psychotherapy.”

Overall, the social brain concept suggests a unifying explanation for how brains have developed, why mental illness exists, and how it affects us, and offers hope for how to treat mental illness more effectively using a unified approach. Psychiatric disorders fundamentally entail social communication problems for those afflicted. Successful human interaction depends on communication with other people. Attachment is based on collaborative communication. Secure attachment involves contingent communication, as the signals of one person gain direct response by the other. Children learn from parents' good, loving, and functional patterns of behavior or their dysfunctional behaviors, such as aggression, poor responses to stress, or substance abuse.

As detailed in other articles in this issue, the social brain rests on the shoulders of the biopsychosocial model. I know that today medical students and residents learn the biopsychosocial model but integrate it into practice only with difficulty. While at times mentioned in case formulations, the tripartite model in treatment most often helps merely to limit roles, the psychiatrist assuming responsibility for drugs and the psychologist and social worker for their respective parts of “biopsychosocial” — the term used quite literally.

Of course, when it is available and done in an integrated manner, the team approach works. However, all patients, even with no team involved, benefit when viewed…

As a child psychiatry fellow, I sensed psychiatry's division into biological and psychological sides. The division shows in explanations of why patients suffer as well as in treatment choices. It divides psychiatric faculty, affects psychiatry training received in residency and fellowship, and shapes how one considers available future professional opportunities. With 2 years of participation with the Group for the Advancement of Psychiatry (GAP) Research Committee sponsored by the GAP fellowship (I was a child fellow at Thomas Jefferson Memorial Hospital at the time), I found the “social brain” model helped me integrate the two spheres.

First, more about the problem. As T.M. Luhrmann discussed the following in her landmark work, Of Two Minds: The Growing Disorder in American Psychiatry:

“Young psychiatrists are supposed to learn to be equally good at both talk therapy and drug therapy, psychotherapy and biomedical psychiatry, and the American Psychiatric Association thinks that this integration is what training programs in psychiatry teach. Psychiatrists are supposed to understand these approaches as different tools in a common toolbox. Yet they are taught as different tools, based on different models, and used for different purposes. Some psychiatrists do integrate them to some extent. But those who do have to integrate two approaches that are different from the outset that carry with them different models of the person, different models of causation, and different expectations of how a person might change over time.”1

If psychiatrists experience division and confusion about the cause and treatment for an illness, patients doubtless feel equally or more confused. Is it a chemical imbalance or genetic in nature (biological)? Social or psychological? If it's chemical or genetic in causation, why use psychotherapy? If it's psychological or based on family interactions or upbringing, then what need for medication exists? Social brain explanations clarify psychiatric illness in my own mind, and in the minds of my patients, with more effective treatment strategies. But what exactly is the social brain?

The Social Brain Concept

I quote from the GAP Research Committee's definition of the social brain, further discussed elsewhere in this issue, which includes, “The social brain framework helps organize and explain all psychopathology. A single gene-based disorder like Huntington disease is expressed to a large extent as social dysfunction. Conversely, traumatic stress has structural impact on the brain as does the socially interactive process of psychotherapy.”

Overall, the social brain concept suggests a unifying explanation for how brains have developed, why mental illness exists, and how it affects us, and offers hope for how to treat mental illness more effectively using a unified approach. Psychiatric disorders fundamentally entail social communication problems for those afflicted. Successful human interaction depends on communication with other people. Attachment is based on collaborative communication. Secure attachment involves contingent communication, as the signals of one person gain direct response by the other. Children learn from parents' good, loving, and functional patterns of behavior or their dysfunctional behaviors, such as aggression, poor responses to stress, or substance abuse.

As detailed in other articles in this issue, the social brain rests on the shoulders of the biopsychosocial model. I know that today medical students and residents learn the biopsychosocial model but integrate it into practice only with difficulty. While at times mentioned in case formulations, the tripartite model in treatment most often helps merely to limit roles, the psychiatrist assuming responsibility for drugs and the psychologist and social worker for their respective parts of “biopsychosocial” — the term used quite literally.

Of course, when it is available and done in an integrated manner, the team approach works. However, all patients, even with no team involved, benefit when viewed with the three components combined. Instead of replacing the biopsychosocial model, the social brain perspective extends it. As the brain involved in and resulting from social interactions, the social brain defines a biological system at the biological, psychological, and social intersection. All thoughts and emotions stem from neural connections and neurotransmitters that have taken their places from learning in social interactions.

Such interactions have evolutionary origins across all human beings and across other species, as well as individual origins within our own early and lifelong development. The social brain also refers to language communication with others as well as how one communicates with oneself about oneself.

Psychiatry's Indelible Social Component

Psychiatry's social component figures critically in any diagnosis based on the Diagnostic and Statistical Manual of Mental Disorders (DSM). The patient's inability to function socially or occupationally (occupations represent social functions) makes a critical diagnostic distinction. Cardiologists do not define a myocardial infarction by how a patient functions socially, nor do endocrinologists define diabetes by the way a patient functions at work, but throughout the text revision of the fourth edition of DSM (DSM-IV-TR), we read the following criterion: “The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.”2 One must discern this to diagnose a major depressive episode, dementia, generalized anxiety disorder, personality disorders, and other conditions.

According to DSM-IV-TR, a manic episode must meet the following: “The mood disturbance is sufficiently severe to cause marked impairment in occupational functioning or in usual social activities or relationships with others, or to necessitate hospitalization to prevent harm to self or others, or there are psychotic features.” Schizophrenia includes a criterion referring to social or occupational dysfunction. Even the diagnosis of substance abuse includes the criterion of “failure to fulfill major role obligations at work, school, or home.” Many childhood psychiatric disorders possess definitions partially based on the child's poor social interactions. Of course, the pervasive developmental disorders quintessentially label the problems in social interaction.

In view of how almost all of our psychiatric disorders are defined, I feel we may do a disservice to our patients when these illnesses receive biological treatment only, as though therapy should focus on bad molecules alone. Using medication constitutes a critical starting point for many patients, but their social functioning must improve from the drug action (or its placebo effect). To help our patients heal fully, we must keep in central focus such social functioning.

The Social Environment and Brain

Scholarly and research literatures present difficulties for anyone making hard divisions between the components of “biopsychosocial.” Moreover, some examined ancient human ancestors to answer the question of how the social environment has affected human brains. A GAP-fostered article from its Child Committee stated about attention-deficit/hyperactivity disorder (ADHD), “Through an evolutionary biological lens, some mental disorders are better viewed as an adaptive response to early pathogenic environments and/or reflect the optimization of brain function to some environments at the cost of poorer response to the demands of other environments ... given the current estimated frequency of ADHD (3% to 5%), it is unlikely that such a ‘disorder’ could be as prevalent in the human species if not maintained within the species by selection forces that conveyed certain advantages to some ADHD characteristics or associated traits.”3

Early environmental experiences affect structural and functional aspects of cortical development, neuronal activity, and organization. Early pathogenic environments likely included the harsh prehistoric environments to which all humans have had to adapt. Both then and now, social environments may include trauma and neglect to which a child often has to adapt individually. The Child Committee article examined hunter–gatherer societies and stated that humans' survival may have depended on being hypervigilant (“integrating information through all senses at once”), impulsive (“quick to pounce”), and hyperactive (“foraging for food, moving toward warmer climes as seasons and ice ages come and go.” Also, the “response-ready” individual likely would have had an advantage under the brutal or harsh circumstances of the frozen steppe or humid jungle, whereas the excessively contemplative, more phlegmatic individual would have been “environmentally challenged.”

Anxiety disorders similarly may gain a fresh perspective using this lens. In the ancient past, the person whose breathing and heart rate increased rapidly and whose autonomic system had a low threshold for arousal might have escaped the tiger, but in today's environment, anxiety or panic attacks do not save us from workplace problems, however tiger-like a boss may seem. Exemplifying strong connections between social and biological processes, a neuroimaging study examined subjects rejected by peers in a computer game.4 The brain reacted to social rejection in the same way and in the same anterior cingulate cortex location as to pain.

Our brains wire us as social animals. In ancient times survival likely depended on group membership, and the pain of social rejection may have caused people to remain in social groups.

Research on relationships between genes and the environment (involving social interactions) examined the effects of the 5-HTT gene and life stressors on depression.5 Stressful life events included problems with employment, finances, housing, relationships, and the social stress of physical health problems. The 5-HTT gene has a promoter region with either a short allele (s) or a long allele (l). People with two copies of the short alleles (s/s) or at least one short allele (s/l) were more likely to be depressed than those people who had two copies of the long allele (l/l). For people with four or more stressful life events between ages 21 and 26, 33% of those with at least one short allele (s/s or s/l) became depressed compared with 17% of those with the l/l genotype.

The study also examined associations between childhood maltreatment (ages 3 to 11) and adult depression (ages 18 to 26). Childhood maltreatment significantly predicted adult depression only among people carrying an s allele, not among those with the l/l combination. This does not say that l/l abused children did not get depressed, but if they did, it failed to correlate with later depression, as was the case when subjects had the s allele. (The authors noted that more than half of the Caucasian population has an s allele but did not mention data on other racial populations.)

In addition to handling stress, adaptation over evolutionary time wired our brains to handle the social process of communication among people. The GAP Research Committee deliberated on the large proportion of the brain involved with communication, including a cerebral cortex devoted to verbal and non-verbal messaging and pattern recognitions and pattern generation for writing, as well as facial recognition, planning behaviors, and suppression of impulses that originate from lower centers. Perhaps most important, verbal communication reflects an extraordinary human capability critical for using detailed stories for informing, planning, bonding, gossip, entertainment, and helping one another in the many ways we do so.

Learning Through Social Interactions

As recent research on stress and genes indicates, the social interactions that affect our neural connections do not end in early development. While social interactions may have greater influence on the receptive brains of early years when our neurons have more plasticity, brains continue development throughout the lifespan. We change our neural connections through learning, which forms new connections in our brains. This happens through relationships in which we learn new ways of handling situations — which also happens through psychotherapy. The most important learning takes place with parents, siblings, spouses, friends, children, workplace, and community.

We frequently test beliefs and change them. In isolation, belief change occurs with greater difficulty; discussing personal ideas with another who either reinforces them or shows a new perspective more readily changes beliefs. While some remain stuck repeating dysfunctional patterns of behavior in relationships, those who truly thrive turn out to be those people remaining open to lifelong learning and who continue to work on improving relationships by continually testing old patterns of behavior, rejecting dysfunctional beliefs, and developing new ones as well as new approaches to life.

Social learning theory suggests that psychological functioning stems from continuous reciprocal interplay among behavioral, cognitive, and environmental influences.6 “Behavior, personal factors, and social forces all operate as interlocking determinants of one another — behavior stems from the environment and people play roles in creating the social milieu and other circumstances that arise in their daily transactions. Humans possess an advanced capacity for observational learning that enables them to expand their knowledge and skills on the basis of information conveyed by modeling influences.”7

Learning involves two memory systems used together, the declarative or explicit system and the procedural or implicit system, involving skills and habits in the striatum and emotional responses in the amygdala (as well as neocortex and cerebellum). Procedural memory involves unconscious physical and emotional memories. When a person learns something new, the memory initially stores in declarative memory and in procedural memory, to variable extents. Constant repetition transforms declarative memory into a procedural type, such as when one learns to drive a car.8

A person subjected to a frightening situation or a traumatic event finds that declarative memories in the hippocampus mix with emotional memories in the amygdala. A person may later feel depressed and anxious when emotional memories reactivate. Procedural and emotional memories in the amgydala may turn on the body's autonomic system, leading to fight-or-flight reactions so the person begins to breathe faster, the heart rate increases, and sweating begins — reactions comprising symptoms of posttraumatic stress disorder.

Lessons for Psychotherapy

Many recent studies show combining medication and psychotherapy works better than either modality alone. Even diagnoses viewed as primarily “biological” benefit from psychotherapy. ADHD exemplifies a psychiatric disorder with a large neurobiological and genetic component. In the National Institutes of Mental Health Collaborative Multisite Multimodal Study of Children with Attention-Deficit/Hyperactivity Disorder (MTA), combined medication and behavior management had a 68% success rate, medical management had a success rate of 56%, and behavior therapy alone had a success rate of 34%.9 The better results in the combined group proved a statistically significant result.

All now agree that a person with bipolar disorder should be on medication, yet psychotherapy makes a significant difference in the lives of patients with bipolar disorder. Using randomized controls, Lam and colleagues10 looked at cognitive therapy as an adjunct to mood stabilizers in 103 patients with bipolar disorder. The cognitive therapy group received 14 psychotherapy sessions during the first 6 months and two booster sessions during a second 6 months. Among controls, 75% relapsed during the year, compared with 44% of those receiving psychotherapy. The controls experienced more than threefold the amount of time in bipolar episodes (mean = 88 days) compared with the cognitive therapy group (mean = 27 days). Compared with 33% of the control group, only 15% of the patients in the cognitive therapy group needed admission to the hospital for bipolar episodes. Cognitive therapy helped the patients develop skills to monitor their moods and any prodromal symptoms, as well as modifying their moods and behavior before prodromal stages turned full-blown. Therapy also promoted the importance of sleep and routine, as well as medication compliance.

Schizophrenia also improves with appropriate psychotherapy added to medication. Psychotic beliefs blossom with continued isolation and lack of opportunity or desire to reality-test. When cognitive behavior therapists encourage patients to look at alternative explanations, the results can be profound, as the patients may come to realize that the auditory hallucinations are not an outside force but rather strong thoughts in their heads. The patient may also learn that behavioral techniques may help them stop their voices, a process that reduces the stress around the internal voice. This does not deny schizophrenia stems from changes in cells and molecules, but when the patient faces isolation with a lack of reality testing, the illness worsens.

When training, M.W. Deibler and I led a group for out-patients with schizophrenia. Several heard auditory hallucinations during the group sessions. Together, we focused on them testing out behavioral strategies, such as humming or reading, to control auditory experiences. We also examined alternative explanations for hallucinations. This very social form of group therapy proved helpful to several patients by changing the isolative hallucination experience into a potentially controllable experience with which others too were learning to cope.

Turkington's discussion of psychological meanings of psychosis helped me in psychotherapy used adjunctively to antipsychotic medication.11 He suggests that beneath systematized delusions and derogatory hallucinations lies a personalized meaning, or a schema, that drives symptoms. It may be, “I am a bad person,” and a voice will begin to express that derogatory belief. In response, the patient forms beliefs about the voice — that the devil speaks, or that alien sources produced the sounds. These frightening interpretations trigger both anxiety and withdrawal, which then worsens even more the hallucinations and other symptoms. Cognitive and behavioral interventions that help may include developing alternative explanations for the voices, relaxation training to reduce anxiety, activity scheduling, and a voice diary to encourage patients to dispute the content of the voices and to gain control over them.

Split Treatment

If we consider the social brain and all its implications, we more likely use psychotherapy and other social interventions in addition to medication. We're challenged by the fact that this combined approach may seem difficult in the era of managed care, where the split model of psychiatrist and therapist has taken root. We each have our separate functions determined by funding organizations. Many find ourselves working where our primary responsibility lies in medicating.

However, I assert again my feeling that we must maintain cognizance of the patients' social relationships to understand any recovery. We should enhance the placebo effect to the fullest, by engaging meaningfully with the patient. We must inquire about compliance and about the reasons for noncompliance. We must meet with families as well as patients as the circumstance warrants. (For children, this takes on critical dimensions.) We must incorporate abbreviated psychotherapy into the limited time we have with patients. Finally, if we work in the framework of the split treatment model, working closely with therapists and social workers means a more integrated approach.

Many psychiatrists, for a variety of reasons, choose to focus more on the biological side of psychiatry, limiting their model of diagnosis and treatment. However, I feel it would be a mistake for them to not recognize or appreciate the incredible importance of the social side of treatment, regardless of how the formal psychotherapeutic intervention happens. We need to assist our patients in social interactions in the community and with their own families, and think of vocational training or continuing education for our patients when appropriate. We may be using the newest antipsychotic or antidepressant, but if our patient is just sitting home alone and bored all day, they are more likely to relapse into depression or even psychosis. As one woman with schizoaffective disorder said to me, “An idle mind is the devil's workshop.” While vocational training doesn't work in all cases, when it does, it gives the person a purpose in life and enhances quality of life and self-esteem. It provides an identity beyond that of being a patient.

Summary

As a psychiatrist in training, I felt (as I still do today) excited about entering a field where I could use sociophysiological interventions in a variety of ways. Only by integrating both communication and medication effectively can one treat patients most effectively. Psychiatric Annals has offered issues on treatment-resistant depression with articles on electroconvulsive therapy, adjunctive medication, and cognitive-behavior therapy. Each possesses empirical support. To help our patients best, we must be willing to offer biological, psychological, and social interventions, depending on the patient's needs and the characteristics of the situation.

References

  1. Luhrmann TM. Of Two Minds: The Growing Disorder in American Psychiatry. New York, NY: Alfred A. Knopf; 2000:7.
  2. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Publishing; 1994.
  3. Jensen PS, Mrazek D, Knapp PK, et al. Evolution and revolution in child psychiatry: ADHD as a disorder of adaptation. J Am Acad Child Adolesc Psychiatry. 1997;36(12):1672–1679; discussion 1679–1681. doi:10.1097/00004583-199712000-00015 [CrossRef]9401328
  4. Eisenberger NI, Lieberman MD, Williams KD. Does rejection hurt? An fMRI study of social exclusion. Science. 2003;302(5643):290–292. doi:10.1126/science.1089134 [CrossRef]14551436
  5. Caspi A, Sugden K, Moffitt TE, et al. Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene. Science. 2003;301(5631):386–389. doi:10.1126/science.1083968 [CrossRef]12869766
  6. Hjelle LA, Ziegler DJ. Personality Theories: Basic Assumptions, Research, and Applications. 3rd ed. New York, NY: McGraw-Hill; 1992:336.
  7. Rockland LH. Supportive Therapy: A Psychodynamic Approach. New York, NY: Basic Books; 1989:250–251.
  8. Kandel ER. Biology and the future of psychoanalysis: a new intellectual framework for psychiatry revisited. Am J Psychiatry. 1999; 156(4):505–524.10200728
  9. Swanson JM, Kraemer HC, Hinshaw SP, et al. Clinical relevance of the primary findings of the MTA: success rates based on severity of ADHD and ODD symptoms at the end of treatment. J Am Acad Child Adolesc Psychiatry. 2001;40(2):168–179. doi:10.1097/00004583-200102000-00011 [CrossRef]11211365
  10. Lam DH, Watkins ER, Hayward P, et al. A randomized controlled study of cognitive therapy for relapse prevention for bipolar affective disorder: outcome of the first year. Arch Gen Psychiatry. 2003;60(2):145–152. doi:10.1001/archpsyc.60.2.145 [CrossRef]12578431
  11. Turkington D. Psychologic mechanisms of pychosis. Johns Hopkins University School of Medicine Advanced Studies in Medicine. 2003Sep;3:S773–S775.
Authors

Dr. Sosland is a private practice psychiatrist in Voorhees, NJ, and consultant psychiatrist, New-Point Behavioral Health Care, Woodbury, NJ.

Address reprint requests to: Morton D. Sosland, MD, 95 Route 73 South, Voorhees, NJ 08043.

10.3928/00485713-20051001-10

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