Dr. Philip Grossi
Tuesday, 22 October 2013

Bullying is defined as aggressive behavior directed at another in order to achieve or maintain a dominant position with the intention of causing mental or physical pain or harm. It influences the victim, bystanders, and the bully. It is not the same as teasing because teasing involves students of similar size or status. Bullying also tends to be repetitive and can be physical, social, or verbal.  Contrary to common belief that it is found mostly in grammar school, it is found through the high school school years.  Indeed bullying is more common in middle school and high school where the physical aggression of grammar school children is replaced by taunts, laughing at others, or name-calling. Often social media is used.  Boys and girls report being bullied almost equally but girls tend to report and seek help more often. Victims of physical violence or having property damaged are more likely to report bullyinig than those subjected to name-calling, exclusion, or having rumors spread about them.

Patients seen in the office who have suffered bullying often present with depression, anxiety, and a variety of somatic complaints such as stomachaches, headaches, and insomnia.  Interestingly, bullies often are depressed and suicidal.  Bullying situations often involve people taking different roles, i.e., sometimes as bully and sometimes as victim. Those individuals that take either role tend to manifest impaired, unsafe, and untrustworthy interpersonal relationships. Bystanders to bullying are also affected adversely. These individuals often feel hopeless and report negative emotions during bullying. Bullying often heralds other problems in the child's history.  They often come from families where violence is seen or physical or sexual abuse is present.  The depression , anxiety, and defiance often persist into adulthood and manifest with those same symptoms or fighting or domestic violence. 

For a much more comprehensive presentation on bullying, go to www.stopbullying.gov




Postpartum Depression

Dr. Philip Grossi
Monday, 30 June 2014

In the past year I have cared for a larger number of women who became pregnant than is usually the case.  In the last week a particularly challenging patient returned to the practice after a long absence.  She was five month pregnant and expressed substantial worry that she would suffer a postpartum depression as she had after one of her previous deliveries.  While she was not on any medications during the five months of this pregnancy, she wondered about starting medications several weeks or a month before her due date to forestall the development of depression. This is a strategy she had read about on the internet.

This started me thinking about the current diagnostic protocol for this disorder. DSM-5 does not recognize postpartum depression or psychosis as distinct disorders. Instead they call for the diagnosis of depression, mania, or other disorder with or without psychosis in the peripartum period. The reason for this change is simply that one half of all depressions start during pregnancy and the other half within four weeks of delivery.

The prevalence of postpartum blues in the population is about 65% and postpartum depression is 12%.  Postpartum psychosis is considerably rarer with a prevalence of 0.1 to 0.2%. In women who have previously been diagnosed with schizophrenia or bipolar I disorder, postpartum psychosis occurs in about 30%.  The risk of developing postpartum psychosis is affected by multiple factors.  Probably the two most important are a family history of postpartum psychosis, family history of bipolar disorder, and prior episodes of postpartum psychosis or psychosis unassociated with giving birth. Other significant factors include being off a mood stabilizer, sleep deprivation, and obstetrical complications.

An acute change in the mental status of a postpartum woman requires prompt and careful evaluation both of the patient's medical condition or medical complications and of psychiatric syndromes.  The clinical presentation can include disorientation, impaired concentration, agitation, restlessness, incoherent or rambling speech, delusions especially about the infant, hallucinations often commanding and often very unusual, and suicidal thinking. This is a definite psychiatric emergency and requires prompt and effective care. It should not be forgotten that the incidence of suicide in such women is 5% and of infanticide is 4%.  Therefore involving the family and educating them about the illness is necessary to get them shoulder what could well be a substantial burden.


Sleep Cycle

Dr. Philip Grossi
Sunday, 29 June 2014

Disturbances of the sleep cycle are among the most common disturbances associated with psychiatric disorders. The most common sleep disturbance is insomnia but oversleeping can also be an issue.  Insomnia can involve falling asleep (initial insomnia), staying asleep (middle insomnia), or early morning awakening (delayed insomnia). Usually people with this problem do not feel rested when awakened and usually experience irritability, anxiety, fatigue and reduced productivity the following day. I intend to set out the current understanding of the sleep/wake cycle in this blog.

Sleep is a regularly occurring state of unconsciousness resulting from two competing internal processes. Those processes are designated homeostatic which controls the amount of sleep and circadian which controls the timing of sleep. In the homeostatic process the longer one is awake the stronger the drive to sleep. So, as a normal day progresses the homeostatic drive increases and abates when one sleeps. If one is sleep deprived, then the homeostatic process increases to become overwhelming.  The circadian process is a synchronization of many bodily processes which starts with an area called the suprachiasmatic nucleus in the hypothalamus. Signals from that nucleus influence the sleep/wake cycle, hormone release, body temperature, and other physiological systems. It is the opposition of these two systems that consolidates sleep and wakefulness into discrete periods. The opposition can be thought of as similar to a teeter totter. When weight is added to one end that end falls, when weight is added to the other end or weight is taken from the original end, then the balance shifts. So the wake promoting and sleep promoting work to inhibit one another. If wake promoting activity is higher then sleep promoting is inhibited and one is awake. I sleep promoting activity is greater, then wake promoting is inhibited and one is asleep.

The neurobiology and neurophysiology underlying these competing systems is far from clear and established.  It would appear sleep promoting involves GABA, galanin, and melatonin whereas wake promoting involves orexin (hypocretin), norepinephrine, histamine, serotonin, and acetylcholine. GABA is the main inhibitory neurotransmitter in the human brain. Orexin is a peptide produced by neurons in the lateral hypothalamus and tilts the balance toward wakefulness. This discovery was made in narcoleptics who are orexin deficient. GABA is driven by the homeostatic process whereas orexin is driven by the circadian process.

Since the 1960s with the advent of the benzodiazepines the clinical treatment of sleep has focused on the sleep promoting side of the equation. The drugs thus used include all the household names. Doxepin was the first agent aimed to block wakefulness rather than promote sleep. Histamine levels increase during the night which is the likely explanation for H blockers promoting sleep maintenance. With the discovery of the orexin system and its wakefulness promoting actions, a whole new approach has opened for sleep therapeutics. Antagonists that block the orexin receptors inhibit excitatory input to arousal systems and create the conditions for sleep.  Such drugs are on the horizon and should be in the marketplace soon. One such drug, Suvorexant, has demonstrated efficacy at all doses and tolerability. It should be with us in months.