Dr. Grossi's Blog
One of the most common questions that arise in the office involves distinguishing between juvenile bipolar disorder and ADHD. Contributing to the difficulty is the finding that BPD and ADHD are co-morbid at least 50% of the time, i.e., those individuals meet criteria for both disorders. A further difficulty in drawing the distinction is that they are clinical diagnoses so by definition there is no test, scale, laboratory test or scan which precisely diagnoses the disorders.
There are historical and clinical characteristics that help to distinguish the two disorders. From a family history standpoint, children of parents who have BD are 13 times more likely to have BD than controls and twice as likely to have anxiety disorders as controls. From a clinical standpoint adolescents with BD tend to display shifts in energy level from high to low or vice versa. Moods accompanying these energy shifts range from silliness, meddlesomeness, intrusive behavior, elation, expansive, belligerent, angry,and irritable, to sadness, gloominess, depression, and suicidal preoccupation. Other features may include decreased need for sleep, increased talkativeness, and the sense that the child's thoughts are racing, increased destructibility, and increased in work out put and risk taking behaviors.
When comparing patients with ADHD to those with BD those with BD had more mood elevation, grandiosity, racing thoughts, decreased need for sleep and hypersexuality. Both groups shared hyperactivity, distractibillity, pressured speech. and irritability. These were thus not helpful in making the distinction.
ADHD is found in 6-7% of US children with a greater prevalence in boys than girls. BD is equally distributed in girls and boys. If one takes a cohort of 100 5 year olds who meet the criteria for ADHD and they are reassessed every year, when they reach 25 years of age only 66 % continue to meet criteria, the other 34 % fall out of the category. Those that continue to meet criteria at 25 will likely have the symptoms the rest of their lives. About 80% of children who meet criteria for ADHD meet criteria for at least one other disorder including learning disabilities, anxiety disorders, depression, and bipolar disorder. Children with ADHD have a low frustration tolerance which leads to aggressive behavior and anger episodes. In BD anger episodes and aggressive behavior arises out of irritable mood. While ADHD and BD can overlap, they each have some distinguishing features described above
There are some additional clinical findings found in BD children. Those include marked irritability, oppositional behavior, frequent mood swings, distractability, hyperactivity, impulsivity, restlessness, giddiness or goofiness, racing thoughts, aggressive behavior, grandiosity, carbohydrate cravings, depressed mood, exhaustion, low self-esteem, trouble getting up in the morning, and marked sensitivity to environmental stimuli and separation anxiety. Other symptoms somewhat less common include bed-wetting, night terrors, pressured speech, obsessional behavior, compulsive behavior, tics, learning disabilities, poor short term memory, poor organization, fascination with blood and guts, hypersexuality, manipulative behavior, bossy or bullying behavior, lying, suicidal thoughts, destructiveness, paranoia, and hallucinations and delusions.
The connection between humans and their dogs is fascinating and intriguing. I have many patients who are extraordinarily attached to their dogs, spend large sums of money on sick dogs, rejoice at their unconditional love and affection, and mourn when they die. How did dogs come to occupy this trusted friendship and powerful social attachment.
Dogs respond to pointing cues to find hidden food or other rewards. There are other social cues that dogs respond to such as gaze direction to which children also respond. Both children and dogs interpret eye contact as communication suggesting a similar or shared cognitive style.
What explains these human-like attributes in dogs? Genetic studies have established that dogs evolved from wolves; but, wolves do not seek human assistance in solving problems nor so they attend to social cues as dogs do. Since the dog's human-like tendencies do not appear to be genetic in origin, possibly they were shaped by domestication, i.e., selection based on temperament which allowed dogs to interact with humans like partners. If this is the case, then there should be underlying biological processes which support this social and cognitive evolutionary convergence.
In a prior blog I talked about the important role of oxytocin, a nonapeptide neuropeptide, in social interactions and formation of bonds between members of the same species. Can it also produce these effects in members of separate species? T. Romero et.al. and J. Oliva et.al. have studied the effect of administered oxytocin on dogs relative to other dogs and on the effect on dogs attending to human social cues. The results showed an increase in social contact between dogs, more social contact with humans, and more attendance to human social cues. Could this suggest that increased oxytocin in dogs leads to an increased oxytocin response in humans? Such a finding would suggest a dynamic similar to that found in a mother-infant bond.
Now comes Miho Nagasawa et. al. whose recent article in Science described an experiment in which the researchers watched 30 dog owners interacting with their dogs (varying breeds and ages) and measured the changes in urinary oxytocin before and after they interacted. The dogs that looked at their owners longest had the largest changes in urinary oxytocin. Their owners experienced a similar response. They could not replicate this with wolves. This supports the feedback loop described above and suggests that is transmitted partly by sustained eye contact between dog and human.
Is the relationship one of cause and effect? Nagasawa then administered oxytocin to another group of dogs before they interacted with their owners. They found an increase in mutual gaze between dog and owner. Strikingly they also observed an increase in oxytocin in the dog owners mediated by increase mutual gaze. This occurred in female dogs only.
These findings mirror findings in humans described by O. Weisman et.al. Nagasawa's results suggest that dogs have piggybacked on our parental behavior such as staring into our eyes to produce rewarding caretaking behavior. This phenomena is bidirectional and so dogs experience reward as well. These behaviors convey selective advantage with regard to human preferences. It appears that we are tuned into dogs in a similar way we are tuned into children. Our relationship to dogs thus appears to be based on human bonding pathways.
I have recently been thinking of the evolution of psychiatry from the later part of the nineteenth century and my own exposure, as a psychiatrist, to this evolution over the last half century. During the later part of the nineteenth century psychiatric illnesses were conceptualized as either organic or functional based on the findings at postmortem examination. At that time the tools for examination of the brain were too crude to reveal subtle organic changes to nerve cells and brain tissue. Thus alcoholism, Huntington's disease and Alzheimer's were classified as organic diseases but schizophrenia, bipolar disorder, mood disorders, and anxiety disorders were classified as functional mental illnesses because no brain pathology could be identified. These illnesses were often thought of as being in a person's head and were often considered a result of pathological rearing, e.g., the schizophrenogenic mother.
This distinction is no longer consistent with our modern concept of mental states. Psychiatrists no longer believe that only certain mental states are mediated by biological processes; but, now we believe that all mental processes are biological and are the result of cellular processes which are in turn dependent on biochemical processes and their genetic underpinnings. The process of coming to these conclusions has been convoluted and tortuous. Starting in the 1880s Freud began his investigation of hysteria. He developed a new method of investigating manifest and latent verbal content produced by patients. Freud's prolific and elegant writing (he was nominated for a Nobel prize in literature) propelled psychoanalysis into the dominant theoretical formulation of mental states for the first half of the twentieth century. During the 1950s the investigative power of psychoanalysis was exhausted and its reliance on the subjective interpretation of the psychoanalyst came under heightened scrutiny because it did not allow for empirical testing of its conclusions. It lost any claim to scientific inquiry and became more a therapeutic art which was exactly the opposite direction of the rest of medicine.
There were other developments which moved psychiatry away from psychoanalysis and toward biology and empirical testing. In 1952 chlorpromazine was discovered in France. It was the first of a class of tranquilizers which were used to suppress hallucinations and other psychotic phenomena. Derivatives of that class are still used today. Also in 1952 several new drugs were tested in the treatment of tuberculosis. The researchers found that patients treated with those agents became "energized, were inappropriately happy, and even discipline problems." Upon further investigation these drugs were discovered to function a monoamine oxidase inhibitors (MAOI). In the late fifties several drugs with this mode of action were introduced into the marketplace and promoted as antidepressants. Keep in mind that prior to 1952 there were no antidepressants and the word "antodepressant" was not even in the English language. People who were depressed prior to 1952 were given either opiates or stimulants.
In 1965 Joseph Schildkraut published an article in the American Journal of Psychiatry entitled "The Catecholamine Hypothesis of Affective Disorders". This article documented the neuropharmacological studies which suggested that the newly introduced antidepressants produced their clinical effects by altering catecholamine metabolism. This stimulated research which eventuated in the introduction of the SSRIs in the late 1980s and early 1990s. In the last fifteen years other attempts to elucidate higher order mental processes, emotions and thinking, using genetic tools have been gaining research prominence. Determining the genetics of mental illnesses has been much more challenging than neurological illnesses because there is no single gene causing the illness such as in Huntington's disease. The mental illnesses appear to be caused by many genes of small effect which interact with one another and with the environment to cause a genetic predisposition. Once certain environmental factors are added to this predisposition, the illness is expressed. A good example of this is the work done on identical twins where one twin meets criteria for the illness. Since the genes are identical in the twins, one would expect a concordance rate of 100%, that is, all of the twins would have the illness. Turns out that only 69 twin pairs have the illness.
I have tried to whistle a few bars of a very long and involved song and dance. I hope I have conveyed an overall sense of the trends in psychiatry over the last fifty years.