Dr Jay Seitz

I asked in an earlier blog, The social construction of mental illness, why attention deficit disorders in children, adolescents, and adults are uncommon, if non-existent, in other cultures such as East Asian societies?  Why is there such a rash of these disorders in often high-functioning individuals across the US?  The concept of attention is much maligned and there seems to be some confusion about what it actually is as well as the role it actually plays in humans.

There are two fields that study attention: Cognitive psychology, which since the 1950s, seeks to understand the nature of human thought processes; and cognitive neuroscience, which is even a newer field, which investigates the brain bases of human mental processes like thought, attention, memory, language, consciousness, perception, and so on.

Let’s start with the doyen of human mental processes, William James (the brother of Henry James, the novelist), early prognostications on the subject:

“Everyone knows what attention is. It is the taking possession by the mind in clear and vivid form, of one out of what seem several simultaneously possible objects or trains of thought…It implies withdrawal from some things in order to deal effectively with others.” (The Principles of Psychology, 1890).

Or, to put it in the language of science, something like selecting targets from competing inputs. That is, it involves increasing neural thought activity in one’s area of concern and decreasing or inhibiting other thought processes that are not in one's immediate area of concern.  For example, deciding what you would like to have for dinner and selecting a way to get there: Recipes, leftovers, quick stop at the store, pushing some buttons on the microwave, and the like.  That is, we frequently choose to focus our attention on a specific activity (improving our golf swing) and pay less attention to the immediate environment such as a noisy neighbor or an annoying itch on our leg.

There are many varieties of attention, however, such as concentrating on one thing while ignoring others (typing on one’s Blackberry and ignoring the conversation next to you), doing two things at once (talking on a cell phone while driving) or sustaining an activity over time (e.g., reading a book).  Of the latter, we may even find that we need to be vigilant about an anticipated knock on the door or an infant’s cry–-a special kind of sustained attention.  Yet, some processes of attention are preconscious, meaning the mind carries them out without conscious awareness (avoiding obstacles as we walk down a busy sidewalk) and automatic (one’s morning ritual after arising from bed).  These preconscious and automatic processes often and characteristically go awry.  For instance, when we are having a stressful day and are overwhelmed, but more commonly we refer to these not so infrequent moments as cognitive slips when the order of, or choosing of alternatives, breaks down: You inadvertently place a box of cereal in the refrigerator and carry the milk to the pantry cabinet.

Let's look at some ways that "attention" gets misunderstood:

From a neural perspective, attentional processes are widely distributed in the brain and it would be rather remarkable for these to break down en masse or even en part (if they did, we wouldn’t be talking about the waxing and waning of attentional processes anymore but more severe causes such as a stroke or a severe epileptic seizure or the like).  On the other hand, there is some evidence that the maturation of the frontal lobes is not completed until late adolescence so adolescents with attentional issues may be demonstrating the normal development of the brain, rather than underlying pathology.  Parenting skills and providing a healthy home and social environment may be more relevant during this period than reflexive use of medication or psychotherapy.  Moreover, there are many kinds of “attention” and each of these attentional processes involves different cognitive processes and underlying brain systems as well as their activation or inhibition.  Attention is not unitary.

The parietal lobe, for instance, is involved in switching among visual tasks (reading the newspaper or surfing the web); the pulvinar nucleus of the thalamus in focusing on a target from an array of choices (choosing the chocolate cake from the dessert menu); areas of the thalamus and the visual cortex for awareness of one’s immediate environment; frontal and parietal areas for focusing on color, form, and location information; the interplay of frontal areas, the basal ganglia, and the anterior cingulate cortex (which translates decisions into actual physical activity) for searching for appropriate targets (Which book should I choose from my bookshelf?) and it’s even more complicated because the left frontal areas are more concerned with semantic content (Which book will help me better understand Middle East politics?) and the right posterior areas are more concerned with the features of objects (Apple or a pear?); the dorsolateral prefrontal cortex for holding this information in immediate memory; and various areas of the frontal cortex for sustained vigilance.

If someone complains of an “attentional deficit” or a “problem concentrating” just exactly what is being stated?  These attributions are almost meaningless without a knowledge of the cultural and environmental context in which they occur.  Not to mention an individual’s personality and disposition as well as the impact of psychosocial stress and lifestyle choices on an individual.

There is also an issue about which sensory modalities are involved.  Since attention can be focused on what people say or what they look like or the feelings they arouse in us or the touch of someone’s hand on our shoulder or the aroma of freshly brewed coffee.  Or, the taste of a favorite meal or the physical feedback we receive from internal receptors in our bodies.  Inattention deficit in what sense?  Problem concentrating on what?  Often, these questions are never asked by mental health professionals but taken at face value.

Indeed, theories of attention are derived from studies of individuals with obvious and pronounced damage to the brain as well as studies of normal individuals and how their brain systems interact in sundry types of everyday attentional processes (i.e., focal, divided, and sustained attention as well as preconscious and automatic processes of attention).  There is no hard scientific evidence, that I am aware of, for the collapse of cognition or its brain basis in common, everyday complaints of inattention or problems in concentration.

Insomnia, drugs (both the licit and illicit kind, such as excessive use of caffeine or sleeping pills), psychosocial stressors (work, school, family, and financial stress), and diet and physical exercise (or lack of it) can have a significant impact on cognition.  There are even suggestions that infection or immune activation may break down cognitive processes and hormonal changes in the body have also been documented (e.g., estrogen suppression in women).  Indeed, the augmentation or suppression of neurotransmitter systems (e.g., acetycholine, involved in memory; dopamine, involved in needs and desires) can affect cognitive function and have many causes and consequences.  Yet, it is uncommon for these possibilities for “attention deficit” or “problems in concentrating” even to be considered in the diagnosis and treatment of attentional issues.  The focus is on symptoms, not underlying causes.

In Part II, I’ll examine the psychopharmacology of attention and the role of psychiatric treatment including psychotherapy.  I will also look at normal overactivity (particularly in males) and consider the special case of situational hyperactivity, especially in children.

Some suggested readings:

Fuster, J. M. (2003).  Cortex and mind: Unifying cognition.  Oxford: Oxford University Press.

Gazzaniga, M. S., Ivry, R. B., & Mangum, G. R. (2002).  Cognitive neuroscience: The biology of mind (2nd ed.).  NY: W. W. Norton (Chapter 6: Attention and selective perception).

Kolb, B., & Whishaw, I. Q. (2003).  Fundamentals of human neuropsychology (5th ed.).  NY: Worth (Chapter 22: Attention, mental images, and consciousness).

Sternberg, R. S. (2006).  Cognitive psychology (4th ed.).  Belmont, CA: Thomson Wadsworth (Chapter 3: Attention and consciousness).

About 20% of visits to health care providers involve difficulties with anxiety and depression and their various manifestations: Bipolar disorder as well as anxiety- and depression-spectrum disorders.  These include generalized anxiety disorder (GAD) and major depressive disorder (MDD).  Since anxiety and depression are related, you get mixed anxiety depression (MAD) and its lesser form, “anxious dysthymia,” since more milder forms of depression are called dysthymia.  In addition, you have panic disorder, which is related to anxiety–they often co-occur–and the resulting spectrum of disorders are called anxiety or depression spectrum disorders.

What are the putative biological origins of anxiety and depression?

Let’s count the number of ways that anxiety and depression have been theorized to arise.  Here are some of the major ones: The monoamine hypothesis, the neurotransmitter receptor hypothesis that posits the occurrence of abnormal receptors in the brain or aberrant signal transduction, insufficient genetic expression of relevant brain neurons, and the neurokinin hypothesis of emotional dysfunction.

The basis of the monamine hypothesis is that there is insufficient serotonin in the brain in individuals with anxiety and depression and females, on average, have about 1/3 less than males, leading to about a 2:1 ratio of female:male depressives or anxious individuals.  In the case of the neurotransmitter receptor hypothesis, the lack of serotonin affects the receptors on neighboring neurons or the ability to transduce signals to neighboring neurons leading to anxiety and depression.  The monoamine hypothesis of gene expression argues that the gene for brain-derived neurotrophic factor is repressed under stress undermining the viability of brain neurons, atrophy, apoptosis),

The neurokinin hypothesis of emotional dysfunction claims that the neurokinins in the brain, such as substance P, are causing anxiety and depression and by decreasing the availability of neurokinins, the regulation of emotions by individuals may be improved.

When the predominant symptoms are anxiety, it has been suggested that there is an overproduction of norepinephrine in the locus coeruleus deep within the subcortex of the brain and by blocking receptors on the surface of neurons that are sensitive to noreprinephrine, anxiety is reduced.

When the predominant symptoms are panic disorder, it has been posited that overproduction of norepinephrine in the locus coerleus is, rather, a result of abnormal discharge of norepinephrine neurons suggesting that panic attacks are similar to seizure-like activity in the areas of the brain that subserve emotions.

Post-traumatic stress disorder may also be due to overproduction of noreprinephrine in the locus coerleus but with accompanying arousal of the autonomic nervous system, an abnormal stress response, and an inflated startle response.

Cognitive-behavioral therapy (CBT) is effective for anxiety, depression, and panic disorder but in more moderate to severe cases, the addition of anxiolytic or anti-depressive medication may be more effective than CBT or medication alone.  In very severe cases of depression and bipolar disorder–the occurrence of both depression and mania–electroconvulsive shock therapy (ECT) is still widely practiced in the psychiatric profession.

What about medication for anxiety and depression?  The response rate for anti-depressant medication is only about 67% whereas the response rate for a placebo is around 33% suggesting that antidepressant medication is often not effective alone.  For instance, when individuals who responded positively to a placebo are given an antidepressant, there is a 50% relapse rate while the rate of relapse is only 10% without a placebo.  However, often many medications must be tried before the right one or more is found and then a “cocktail” of various psychoactive medications may be employed to get a favorable therapeutic dosage.

For instance, lithium is often prescribed for severe depression.  Anticonvulsants (e.g., carbamazepine, galapentin, lamotrigine, and topiramate, and valproic  acid), benzodiazipines such as diazepam and fluzazepam, which facilitate the production of gamma amino butyric acid or “GABA” that inhibits activity of the amygdala (one of the emotional centers of the brain), and atypical antipsychotics (i.e., clozapine, risperidone, olanzapine, quetiapine, and ziprasidone) are often used to stabilize mood and reduce manic symptoms.  The benzodiazipine, Alprazolam, is often used to treat panic disorder.  Estrogen supplements and stimulants such as dextroamphetamine are also sometimes used.  Beta adrenergic blockers or psychoactive drugs that block epinephrine, another important neurotransmitter, and Paxil, a selective serotonin reuptake inhibitor, are often used to treat social phobias such as fear of public speaking.

What are some of the other medications used to treat anxiety and depression spectrum disorders?

Remeron (mirtazapine) and Serzone (nefazodone) are often prescribed for GAD and Effexor (Venlafaxine XR) to stabilize mood.  Monoamine oxidase (MAO) inhibitors such as Aurorix, Marplan, Nardil, Parnate, and Selegiline are often effective in preventing the decay of another important neurotransmitter in the brain linked to depression, noreprinephrine.  By inhibiting MAO, more noreprinephrine is made available to brain systems.

Tricyclic antidepressants such as Anafranil, Asendin, Elavil, Ludiomil, Norpramin, Parmelor, Sinequan, Surmontil, Tofranil, and Vivactil impede the reuptake of noreprinephrine and serotonin in the nerve synapse increasing the availability of these two neurotransmitters to brain systems.

The most common antidepressants and anxiolytics are selective serotonin reuptake inhibitors such as Celexa, Luvox, Paxil, Prozac, and Zoloft.  They make more serotonin available to brain systems by preventing its “reuptake” in the nerve synapse.  They are the treatment of choice in treating post-traumatic stress disorder.

There are also selective noradrenergic reuptake inhibitors such as reboxetine, noreprinephrine and dopamine reuptake inhibitors such as bupropion, serotonin-norepinephrine reuptake inhibitors such as venlafaxine and Effexor, alpha 2 antagonists or noradrenergic and specific serotonergic antidepressants such as mirtazapine, which increases the availability of serotonin and norepinephrine to brain systems, and serotonin 2A antagonist/reuptake inhibitors such as nefazodone and trazodone.

“Buspar” (buspirone) is a partial (serotonin) agonist and is often used to treat anxiety.

Anxiety spectrum disorders (GAD) are also treated with sedating antihistamines; beta adrenergic blockers; alpha 2 agonists such as clonidine; non-benzodiazepine short-acting hypnotics such as zalepon, zolpidem, and zopiclone; sedating antidepressants such as mirtazapine, nefazodone, and trazodone; sedating antihistamines such as diphenhydramine, doxylamine, and hydroxyzine; sedating anticholinergics such as scopolamine; and sedative-hypnotics such as choral hydrate, melatonin, and valerian.  The latter two are available through your local health food store.

In all, quite a wide range of possible biological solutions.

Some suggested reading:

Beck, J. S. (1995).  Cognitive therapy: Basics and beyond. NY: Guilford.

Stahl, S. M. (2000).  Essential psychopharmacology: Neuroscientific basis and practical applications (2nd. ed.).  Cambridge: University of Cambridge Press.

According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), borderline personality disorder (BPD) has the following characteristics:

“A pervasive pattern of instability of interpersonal relationships, self-image, and affects, and marked impulsivity beginning by early adulthood and present in a variety of contexts…”

Dr. Margaret Linehan, a pioneer in treating borderline personality disorder with a variant of cognitive-behavioral therapy called “dialectical behavior therapy,” has noted five (5) essential criteria for BPD:

Emotional dysregulation: Individuals with BPD have a emotional system that is very labile and overreactive and may include issues with anger management, irritability, and accompanying anxiety or depression.

Interpersonal dysregulation: Marked problems in interpersonal relationships.

Behavioral dysregulation: Impulsive and suicidal behaviors are common.

Cognitive dysregulation: Cognitive rigidity and deficient social cognition or the ability to understand others and use their social intelligence successfully in emotionally stressful situations.  Such individuals are not “manipulative,” however, because they have not necessarily sought that effect in others.  However, depersonalization, dissociation, and delusions are common.

Self dysregulation: Weak sense of a core self and often accompanied by shameful feelings due to the expression of negative and irrepressible emotions.

Typically, individuals who meet DMS-IV-TR criteria for BPD are female and also engage in self-injurious and parasuicidal behaviors.  Of the latter, the participation in self-injurious behavior may result in bodily harm, physical illness or risk of death.  BPD is often accompanied by a major affective disorder (e.g., bipolar disorder or depression) or dysthymia.

Dialectical behavior therapy (DBT)

DBT emphasizes the remediation of five essential emotional and social “skill” areas:

Emotional regulation: Learning to modulate one’s mood and lessening the tendency to be overreactive in interpersonal relationships.

Interpersonal effectiveness: Being more interpersonally effective in one’s close social relationships.

Distress tolerance: Learning to be more tolerant of distress in oneself through employing distracting activities, self-soothing by finding pleasure through one’s five sensory modalities, and living fully in the present moment by employing the use of imagery, relaxation techniques, and using self-encouragement, among other things.

Core mindfulness skills: These mental skills include being less judgmental towards others and one’s interpretation of events and instead observing, describing, and participating without judgment.

Self-management skills: Being realistic in one’s assessment of others and events  and attenuating crisis generating behaviors.

Some suggested reading:

American Psychiatric Association (2000).  Diagnostic and statistical manual of mental disorders (4th ed., text revision).  Washington, D.C.:  American Psychiatric Association.

Linehan, M. M. (1993).  Cognitive-behavioral treatment of borderline personality disorder. NY: Guilford Press.

Obviously, as a practicing neuropsychologist, I believe that genetics and brain structure and function have a tremendous influence on behavior.  But, is errant behavior always a result of biology gone awry?

According to Allan Horwitz, a sociologist of mental health at Rutgers, cultures and subcultures “provide publically available and shared meanings that facilitate certain kinds of symptoms interpretations while discouraging others.”

Are many normal behaviors pathologized because they are the brain’s normal accommodations to the stresses of daily living?  Psychosocial stress can have profound effects on the central nervous system and on the body as I detail on my web pages.

For example, attention deficit disorders in children and adolescents are uncommon, if non-existent, in other cultures such as East Asian societies.  Why is there such a rash of these disorders in often high-functioning individuals across the US?  Why is there such seemingly high rates of diagnosed anxiety and depression in Western cultures?

One problem, noted by many, is the diagnostic system.  Symptom-based measures tend to pathologize normal behavior leading to a gross overestimation of the occurrence of actual mental disorders.  Inflated statistics of prevalence rates of mental disorders are repeatedly cited in the mass media and are misleading.  Probably, a better estimate of actual prevalence rates is that something like 50% of individuals who receive mental health treatment have no diagnosable mental health conditions.  What’s going on?  Why are narcissistic personality disorders and bipolar disorders (cycles of mania and depression) largely found only in cities?  Why is the diagnosis of multiple personality disorder more likely to be diagnosed in a clinician that is invested in the diagnosis?

One’s social network (family, friends, co-workers, and acquaintances), forms of social support (community and religious groups), quality of work and family life, as well as one’s financial condition can greatly alleviate distress and human mental suffering.  Often individuals lack these significant factors in their life and unknowingly attribute mental distress to internal causes alone.

Women tend to refract stress as anxiety and depression, anorexia, and various forms of panic disorder (given their underlying biology) whereas as men refract stress as impulse control disorders, obsessive-compulsive behaviors (substance abuse, sex, and gambling), and attentional issues (given their underlying biology).  These behaviors are structured by sociocultural factors.

As regards treatment, psychoactive drugs can be helpful, but often have mixed or illusory effects.  Typically, about a third of individuals, even on combinations of psychoactive medications, show no response at all.  Moreover, about a third of individuals respond positively to placebos, substances without therapeutic effect, to make matters even more confusing.  Of course, given the intimate and inextricable relationship between mind and body, this is not surprising.  The underlying biological mechanisms, unfortunately, are not well understood as are the effects of psychosocial stress and the environment on individuals.  In addition, psychotherapy can be effective but it also has mixed results.  As Horwitz argues: “Psychotherapy is an undefined technique applied to unspecified problems with unpredictable outcome.  For this technique we recommend rigorous training.”  Like psychoactive medications and placebo effects, psychotherapy (both the cognitive-behavioral and interpersonal varieties) can be effective with some individuals but less so with others, but efficacy is often considerably enhanced when combined with medication and stress-reduction techniques.  The reasons for these heterogenous outcomes, however, are unclear.

The take-home point:  Mental distress is rooted in social experiences and social connections.  These are structured by the culture and the environment.  Psychosocial stress has profound effects on the central nervous system.  As does genetics and biology.  Unfortunately, normal behavior as a reaction to stressful environments, is pathologized in otherwise mentally healthy individuals.  What many distressed individuals need is care and concern and social support from others rather than the reflexive attribution of their behavior to solely internal causes.

Some suggesting reading:

American Psychiatric Association.  (2000).  Diagnostic and statistical manual of mental disorders (4th ed., text revision).  Washington, D.C.:  American Psychiatric Association.  

Horwitz, A. (2002).  Creating mental illness.  Chicago: University of  Chicago Press.

PDM Task Force.  (2006).  Psychodynamic diagnostic manual.  Silver Spring, MD: Alliance of Psychoanalytic Organizations.

Stahl, S. M. (2000).  Essential psychopharmacology: Neuroscientific basis and practical applications (2nd. ed.).  Cambridge: University of Cambridge Press.

World Health Organization (2004).  International classification of diseases (10th rev.).  Geneva: World Health Organization.

There are three major theories of stuttering that emphasize their biological roots or relevant psychological factors: Neurogenic, developmental, and psychogenic stuttering.

The basis of the “neurogenic theory of stuttering” is that the problem originates in the inability of the basal ganglia to generate neural feedback for appropriate timing of the next segment in the speech stream.  If this problem arises in early childhood it is called “developmental stuttering” with mean age of onset around 2.5 to 3 years.  If psychological factors are significantly involved, such as social anxiety or depression, dysfluent speech may be affected for the worse.

The basal ganglia, in the subcortex, just below the cerebral cortex or “thinking” part of the brain, is interconnected with the cortex as well as the amygdala, brainstem, and thalamus.  These collective circuits are known as “basal ganglia-thalamocortical loops” with direct links to “limbic” structures such as the amygdala.  The latter is central to the emotions of fear and anxiety and plays a prominent role in social anxiety and depression.  Indeed, negative emotions can exacerbate stuttering in the presence of others.

But, there is also involvement of the neurotransmitter, dopamine, in the etiology of stuttering.  Dopamine projections from the substantia nigra pars compacta (SNc) project to the striatum part of the basal ganglia.  When the levels of dopamine in the striatum decrease, there is a lowering or cessation of stuttering, whereas when levels of dopamine increase, there is an augmentation of stuttering as well as associated motor and behavioral impulses.  That is one reason stuttering might be thought of as a “tic”disorder akin to obsessive-compulsive disorders such as Gilles de Tourette syndrome that I discussed in an earlier blog.

There are other possibilities on the biological origins of stuttering such as dystonic activity in the facial musculature, that is, opponent muscle groups at odds with each other producing involuntary motor activity.  Or, a disorder in the sensorimotor area of the cortex in the region known as the oropharynx that controls the motor articulatory apparatus used in speaking.

While the mean age of onset of developmental stuttering is in the range of 2.5 to 3 years, it is typically more prominent in boys (2:1; male:female).  The recovery rate is in the range of 60-70% within two years after the onset of stuttering but, what is most surprising, is that these early stutterers often demonstrate advanced development of language abilities.

What might be some ways to relieve stuttering?

a) Haloperidol (“Haldol”), a dopamine antagonist, attenuates motor activation and may reduce stuttering.

b) Speaking at the pace of a metronome (known as the “rhythm effect”) can reduce stuttering by compensating for inappropriate timing cues originating in the basal ganglia.

c) Reading in unison with others (“chorus speech”) as well as singing can also relieve stuttering, because music provides a separate mechanism for generating internal timing cues when there is aberrant output from the basal ganglia; most likely by way of the premotor cortex.

d) There is also some evidence that modified auditory feedback can improve dysfluent speech in those that stutter.

Some suggested reading:

Alm, P. A. (2004).  Stuttering and the basal ganglia circuits: A critical review of possible relations.  J. of Communication Disorders, 37, 325-369.

LeDoux, J. (1998).  The emotional brain: The mysterious underpinnings of emotional life. NY: Simon & Schuster.