Dr. Grossi's Blog
In recent days I began to redesign the initial evaluation form used in the office for new patients entering the practice. As I began this project a friend of mine became gravely ill and is about to die. This sparked my thinking about the similarities between the methods used by the psychiatrist and those used by the historian. We both use the case history method in which the psychiatrist relies on the patient's report of his/her past whereas the historian relies on documents of various sorts to draw conclusions about either the psychological makeup of an alive patient or a dead historical figure. There are strengths and weaknesses with each approach.
For the purpose of the current psychiatric evaluation I am thinking in categorical terms mostly but some dimensional ones as well. What then are the pieces of evidence I seek to support the conclusions I reach and the treatment recommendations I make. First there are symptoms, sometimes referred to as complaints., These are often non-specific and this suggestive of certain disorders but nowhere hear definitive. Then there is the course of illness whose diagnostic importance is unappreciated by most mental health professionals. It generates many questions. What was the age of onset? Are the symptoms constant or episodic? Is the central problem over time one of mood? Is the central problem over time one of distorted thinking? Do thinking and mood problems co-occur at times? etc. etc. etc. Then there is the genetic window to peer through. Psychiatric problems tend to run in families and I often observe more assortative mating than I would expect in the families I see. Schizophrenia and bipolar disorder are highly heritable disorders. Unipolar depression is less heritable and the environment is a greater participant in producing the clinical presentation. The fourth area of evidence is drawn from treatment response. This area is more difficult to appraise because some people never seek treatment and others receive treatment which is inadequate thus making it problematic to draw a reasonably accurate and firm conclusion. Yet, there are circumstances when a startlingly effective and rapid response to treatment can clearly point to a diagnosis. We are looking at the drug or other intervention as a probe. In the case of medications, where this is easiest to see, we know how a drug works. When I see certain responses from drugs, I can reason backward to a condition because I usually know what the drug effects. For example, when using an antidepressant I might produce a phenomena known as switching, i.e., converting a depressed patient into a hypomanic or manic one. This would directly support a diagnosis of bipolar disorder and would help to clarify the distinction between unipolar depression and bipolar disorder or bipolar depression. In the case where some social engineering is involved, for example, in urging a patient to leave an unhealthy relationship, I might observe a reduced reliance on medication over time as well as greater happiness and productivity. The use of this framework allows for the making of a psychiatric diagnosis in keeping with the categorical schema set out in DSM5.
This case method and categorical diagnosis will gradually be giving way to diagnosis based on a constellation of symptoms PLUS various laboratory findings which could include blood values, genetic study findings, brain scanning and other brain study results etc. Indeed in the current DSM5 the B 2 and 3 criteria for narcolepsy cites hypocretin deficiency and nocturnal sleep study showing REM sleep latency of less than or equal to 15 minutes as diagnostic criteria. These are the first citations of laboratory values in the DSM series.
The Research Domain Criteria (RDoC) which I discussed in one of my earliest blogs, has as its goal building the linkage between symptom complexes and underlying pathological mechanisms. The RDoC will be attempting to link symptoms to more biological and less biologically restricted categorizations than is found in the DSM5. The RDoC framework includes dimensional concepts, e.g., negative valences,, positive valences, social processes, cognition and arousal that mesh psychological and biological phenomena. Several biological concepts in the RDoC include physiological and genetic concepts. The RDoC also includes psychological constructs and implicates the neural circuits that underlie them. This acts to narrow the focus of the DSM5 and therefore will allow better tracking of many clinical findings which vary throughout the population and become pathological only at the extremes of population distribution. The probable outcome of RDoC is a faster evolution than the DSM has produced thus far and a more robust generation of hypotheses linking genetics and observed findings to interacting brain domains in mapped brain areas produced by modern neuroscience. This is likely to result in hybrid concepts linking biological mechanisms with psychological findings. Many psychiatrists and psychiatric researchers believe that psychiatric syndromes, DSM5 categories, are the result of dysfunctrional connectivity and not receptor malfunction. Therefore identifying specific circuit dysfunction and relating it to clinically observable phenomena is an important goal of RDoc and is likely the way forward from categorical diagnosis.
The title of this blog is the title of a book by John A. Nagle. I was reminded of the book, which I read many years ago, by the current news especially the unconventional conflict in Syria and with ISIS. The title clearly points to doing something that is unconventional. The book compares the British Army's response in Malaya to the American Army's response in Vietnam. The British adapted to the insurgency while the Americans continued a conventional war approach. The British won, the Americans lost.
I began to wonder whether the lessons of war could inform the skillful practice of psychiatry especially in a multicultural world. One of the first lessons of war is to understand the enemy, i.e., the enemy's values, beliefs, history, religious beliefs, economic organization, social structure, response to interventions, and their way of seeing the conflict. The understanding of these attributes of a human being is fundamental to good psychiatric practice. This understanding is usually referred to as empathy and involves listening to the patient and "climbing into their skin". This will inform the psychiatrist about their attitude toward treatment, medication, and interactions with other people and institutions as well as how these attitudes have developed and their consequent strength and constancy. This information is invaluable in developing an approach to a specific issue or problem that is effective and efficient. Simple reasoning to arrive at an approach is insufficient, empathic understanding is required to be successful . Contemporaneously, the military commander must be aware of current and past events that might be influencing his decision making in battle. Likewise, the psychiatrist must be aware of the impact of current and past events in his or her life that could be influencing the response to the patient. This is an active and dynamic process which often results in a response or feedback to a patient which should be framed in as many words as are necessary to convey the idea but not more.
In war there should be a proportionality between magnitude of the enemy's action and the response. So too, when assessing the severity of the patient's problem, including social, financial, vocational, and other environmental component contributions, the formulation of the response should be proportional to the severity of the gestalt which should maximize efficiency. With regard to individuals with psychotic problems, it is crucial to make the best selection of agents at an appropriately scaled dose which is an example of proportionality. In these cases it is important to hit the bullseye because the consequences of missing it can be substantial and might include unpredictable and disturbed acts in the community with possible self-harm or harm to others. it also supports or fosters the idea in the patient that psychiatric intervention is ineffective.
In war it is important to get the data and to constantly reexamine your thinking especially if failing to achieve goals. In psychiatric practice I have learned to value what I am seeing in front of me more than any belief based on education or experience. When facing poor clinical response, I am always prepared to reexamine the reasoning that got me to that point and I am always prepared to change my mind. In war one should be suspicious of the common or standard response to a problem. The most uncommon responses are often the most successful. So too in psychiatric practice the most uncommon interventions are often the most successful. Above all when choosing an intervention or strategy, never say never. Keep your mind as open as possible because we are dealing with the human mind which is the most complex object in the universe.
I wondered whether the lessons of war could inform the practice of psychiatry. The answer is yes. However, the reverse is also true, i.e., the lessons drawn from psychiatric practice can also inform the decision making in war.
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.
For many years I have believed that the benzodiazepines (diazepam, lorazepam, alprozolam, clonazepam etc.) are a much maligned and poorly understood family of drugs. This misunderstanding includes doctors, patients, and the government. My conclusion is based on many contacts with other doctors, many articles in the medical literature, and the thinking behind federal government's decision to exclude them as a benefit under Part D of Medicare. That last has been changed and they are now included as a benefit of Part D.
The misunderstanding has been perpetuated by a recent article in JAMA Psychiatry by Moore and colleagues. They questioned their clinical usefullness, emphasized their addictive potential, and suggested much tighter control of their usage. They demonstrated complete tunnel vision because they failed to take into account the issues set out in the following paragraphs.
All benzodiazepines have four actions. Those are: anti-anxiety, antispasmotic, anticonvulsant, and soporific (sleeper). They are also useful in a variety of medical procedures and as a tool in alcohol withdrawal. The indication found in the PDR or in online sites reflects a marketing decision by the manufacturing drug company. The manufacturing company decides to study a drug for a particular purpose and if the studies confirm its effectiveness and safety in the eyes of the FDA, then the FDA allows the company to promote the drug to the medical community for that purpose. The drug can be used for other purposes but it cannot be promoted for those other purposes. A good example of this is the study of clonazepam as an anti-convulsant for which it received an approval. The vast majority of its usage however is as an anti-anxiety agent. The company did this because it already had diazepam (Valium) which was a massive product in the anti-anxiety space and it did not want to introduce a competing product.
Benzodiazepines are an effective pharmacological treatment for anxiety disorders. Offidani et.al. published a meta-analysis of studies comparing benzodiazepines and antidepressants in Psychotherapy and Psychosomatics. The benzodiazepines showed superior efficacy and a more benign side effect profile. Furthermore, the discontinuation rate is much higher with the antidepressants.
Moore et. al. and the majority of the medical community are over-focused on dependency, addiction, toxicity, abuse, tolerance, and withdrawal syndromes. I have found that the rate of abuse is relatively low provided that the drugs are not given to alcoholics or individuals without anxiety disorders. People with anxiety disorders do not get addicted if the drugs are used properly. Antidepressants sometimes have very prominent withdrawal syndromes which can last weeks and are very uncomfortable. With regard to tolerance, this can definitely become an issue especially if these agents are need for a long period. There are a variety of strategies to prolong their clinical effect without raising the dose beyond acceptable limits. Contrary to popular opinion, these agents can be used for long periods with proper management and caution.
Some other oft expressed concerns include falls in the elderly, auto accidents, dementia, confusion, memory problems. While there is some merit in these concerns, if we compare these possible adverse events with those of the antidepressants and antipsychotics, the benzodiazepines look relatively better and less problematic in the long run. On the positive side of the ledger, these drugs enable individuals to relax, reduce anxiety, facilitate sleep and thus provide a better environment to work on longer term solutions to underlying problems.
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.