PTSD in late life can result from trauma that occurred much earlier or can follow traumatic events that occurred for the first time in old age. When trauma took place when the person was younger, PTSD in later life might represent the re-emergence after a period of extended quiescence or be the continuation of a chronic disorder experienced throughout adult life. DSM-5 criteria for the diagnosis of PTSD in older adults are no different from those for other age groups, with the exception of modified criteria for preschool children aged 6 years or younger.

DSM recommends using a “Delayed Expression” specifier when symptoms emerge more than 6 months after the index trauma, and the literature is replete with descriptions of older adults who experience the complete PTSD syndrome for the first time decades after the index trauma. Identifying chronic PTSD that has been present throughout most of adult life might be straightforward, although PTSD did not exist as a diagnostic entity when the older adult first developed the clinical syndrome. One Pearl Harbor survivor described his symptoms as “a non-stop movie playing in my head” that began soon after the attack. Decades later he received a diagnosis of PTSD and was subsequently treated with medications and psychotherapy.

Identification and treatment of PTSD in later life can present multiple challenges, starting with the unique aspects of the symptomatology of the disorder in older adults and from the issues with their treatment-seeking. For example, older adults might report somatic presentations over emotional-psychological symptoms. A higher intensity of hyperarousal symptoms, especially if the trauma occurred later in life, are reported while intrusive re-experiencing symptoms are not mentioned. Cognitive impairment and dementia-the risk of which is increased from a lifetime diagnosis of PTSD-might also interfere with the older adult’s ability to interpret and communicate symptoms.

Mini Quiz: PTSD Assessment and Treatment in an Elderly Patient

Another aspect of PTSD in later life that can be a factor in appropriate diagnosis and the decision about whether to institute treatment is that older adults frequently experience symptoms in numbers insufficient to cross the threshold of DSM criteria for a diagnosis of PTSD. Such trauma-related symptoms were observed to be at least as, if not more, common than threshold-level PTSD in clinical populations.

 Since the diagnostic significance of sub-threshold symptoms (ie, partial PTSD) had been unclear, clinicians had no clear understanding about the appropriate course of action for such symptoms.

Our research demonstrated that older adults with DSM-IV-defined PTSD at the time of initial assessment might have partial PTSD after a follow-up period of 3 to 6 months.

 Along similar lines, older adults with partial PTSD at initial assessment could receive a diagnosis of syndrome-level PTSD during follow-up. (These variable trajectories are summarized in the Figure.)

Furthermore, fluctuations in the symptom profile during the longitudinal course of PTSD were observed to be independent of other psychiatric comorbidities. This suggests that PTSD might be the rare DSM disorder that requires the presence of an external event(s) for diagnosis, but once manifest, it is no different from other psychiatric conditions (eg, mood or substance-use disorders) in having a relapsing and recurring course.

Findings also indicate that older adults with PTSD have fewer friends and have greater difficulty in making ends meet.

 They are also more likely to feel stigmatized and think that their peers would view them negatively if they sought treatment for their symptoms. These observations have implications for the identification and treatment of PTSD in later life. However, there is little information regarding routine screening for or treatment of PTSD in older adults in the few available practice guidelines.

It is important to point out that older adults who have experienced a traumatic event but who do not exhibit trauma-related symptoms have a better quality of life than those who have not experienced the adversity of trauma.

 Studying resiliency in this group could offer insights into how to optimize treatment to aid recovery.

Treatment planning for patients with PTSD in later life presents its own challenges, which stem from a scant evidence base of interventions tested specifically in older adults. Few in the geriatric age group are accepted into randomized trials, and there are no published subgroup analyses from this population. The published literature on psychotherapies with proven effectiveness is only marginally better.

 However, older adults have been treated with the same interventions that have demonstrated efficacy in younger populations, and there is no evidence that these interventions have not been effective in the geriatric population.

Practice guidelines make no specific recommendations for the treatment of late-life PTSD, although the American Academy of Child and Adolescent Psychiatrists has guidelines for the pediatric population. Most guidelines could benefit from updates and inclusion of recent literature-with the notable exception of the Veterans Affairs/Department of Defense (VA/DoD) guidelines, which were updated in October 2017.

A number of therapeutic interventions show promise, although the practicality of their use in older adults is yet to be explored. Both medications and various types of trauma-focused psychotherapies, especially those that have been manualized, are available for use. The ease with which these interventions can be employed, based on the strength of the evidence for their usefulness, is summarized in the Table.

If resources are available, it might be optimal to combine psychotherapy and psychopharmacological interventions. At least one trial in survivors with PTSD from the World Trade Center attack demonstrated that treatment involving psychotherapy combined with medication was superior when compared with the same therapy along with placebo.8 Assessment for other psychiatric and medical disorders that are commonly comorbid with PTSD in later life is strongly encouraged, as is the potential use of a severity or symptom rating scale to document any improvements.

Sertraline and paroxetine have FDA approval for the treatment of PTSD; the VA/DoD guidelines also recommend either fluoxetine or venlafaxine as first-line monotherapy options. Of these 4 agents, paroxetine and venlafaxine have noticeable anticholinergic adverse effects and fluoxetine has a long half-life and significant drug-drug interactions, which suggests the need for monitoring if any of the medications besides sertraline are used in older adults.

Prazosin, an alpha-adrenergic blocker, has shown benefits for PTSD symptoms of re-experiencing (eg, nightmares) and an independent beneficial effect on sleep quality in multiple trials. However, in spite of the positive results, the VA/DoD guidelines state that the data are inconclusive and make no recommendation for the use of prazosin (either as monotherapy or for augmentation) because a large multicenter trial, the results of which are suspected to be negative, remains unpublished. Prazosin has the additional effect of lowering blood pressure and can result in significant orthostatic hypotension. The lore among clinicians is that prazosin is helpful; close collaboration with a primary care physician/geriatrician to first lower the dose(s) of existing antihypertensive medications is recommended before initiating prazosin.

Clinical trials with multiple other classes of medications (eg, mood stabilizers, D-cycloserine) have been attempted with inconsistent results. Based on a risk-to-benefit analysis, it is best to avoid trials of second-generation antipsychotics (especially risperidone) even though there might be instances when psychotic symptoms, rarely present with PTSD, might improve. Similarly, monotherapy with benzodiazepines should be avoided even though they typically offer immediate relief from anxiety in the short term. Not only do benzodiazepines present a host of risks of their own and impair cognition, but they are also likely to interfere with habituation and learning that might occur through psychotherapy.

Prolonged exposure therapy, which involves emotional processing of the traumatic events, is the most extensively researched psychotherapeutic intervention for PTSD. The evidence for other similar therapies such as cognitive processing therapy, eye movement desensitization and reprocessing, and cognitive behavioral therapies specific for PTSD is robust. The VA/DoD practice guidelines also include brief eclectic psychotherapy, narrative exposure therapy, and written narrative exposure, but almost all the evidence comes from trials in younger adults.

The evidence for the “trauma-focused” psychotherapies for older adults is much less extensive. Nonetheless, case studies of prolonged exposure for older adults without cognitive impairment were among the earliest psychotherapeutic interventions reported, and such therapy seemed to be well tolerated without any adverse effects on cardiac comorbidities or treatment dropout. All of the exposure-based psychotherapies have shown at least some improvement for all domains of PTSD symptoms, and the benefits have persisted after the therapy was stopped.

Although there are more treatment options now than in 1980, when PTSD was formally recognized as a psychiatric condition by DSM-III, many persons with PTSD experience only partial relief of their symptoms. A number of alternative treatments have been explored, and adjunctive use of mindfulness and meditation-based treatment approaches have shown some incremental improvement for PTSD and any accompanying depression.

 Small samples and open-label trials limit conclusions as to when and for whom these interventions might be recommended.

The Multidisciplinary Association for Psychedelic Studies (MAPS), a non-profit research and educational institution announced that the FDA had recently granted methylenedioxymethamphetamine (MDMA)-assisted psychotherapy a Breakthrough Therapy designation-thereby paving the way for a phase 3 trial.

 Conversely, there is no evidence that marijuana is beneficial for PTSD, and the American Psychiatric Association does not support its use. It is important for clinicians to be aware of the risks and harm, including exacerbation of psychiatric illness, even as 28 states and the District of Columbia now have legislation allowing for the use of cannabis products for PTSD.

It is important to note that while there are no published studies of late-life PTSD using DSM-5 criteria and no medication trials specifically in older adults, interventions that are useful for PTSD in other age groups can be used in later life and based on clinical experience are well tolerated. Manualized, trauma-focused psychotherapies such as prolonged exposure have the greatest evidence. Antidepressants, especially SSRIs, have potential benefit as well. Nonetheless, there is much that remains to be learned about late-life PTSD.

-I am grateful to Avron Spiro, III, PhD, who reviewed this manuscript.

Dr. Chopra reports no conflicts of interest concerning the subject matter of this article.

 Durai NL, Chopra MP, Coakley E, et al. Exposure to trauma and posttraumatic stress disorder symptoms in older veterans attending primary care: comorbid conditions and self-rated health status. 

Chopra MP, Zhang HM, Pless Kaiser A, et al. PTSD is a chronic, fluctuating disorder affecting mental quality of life in older adults. 

 Pless Kaiser A. Seligowski A, Spiro 3rd A, Chopra M. Health status and treatment-seeking stigma in older adults with trauma and posttraumatic stress disorder. 

Forbes D, Creamer M, Bisson JI, Cohen JA, et al. A guide to guidelines for the treatment of PTSD and related conditions. 

 Cook JM, McCarthy E, Thorp SR. Older adults with PTSD: brief state of research and evidence-based psychotherapy case illustration. 

VA/DoD Clinical Practice Guidelines for PTSD. 

https://www.healthquality.va.gov/guidelines/MH/ptsd/

American Psychiatric Association. Practice Guidelines for the Treatment of Patients With Acute Stress Disorder and Posttraumatic Stress Disorder. Arlington, VA: American Psychiatric Publishing, Inc; 2004. Also available at: 

https://psychiatryonline.org/pb/assets/raw/sitewide/practice_guidelines/guidelines/acutestressdisorderptsd.pdf

 Schneier FR, Neria Y, Pavlicova M, et al. Combined prolonged exposure therapy and paroxetine for PTSD related to the World Trade Center attack: a randomized controlled trial.

Hilton L, Maher AR, Colaiaco B, et al. Meditation for posttraumatic stress: systematic review and meta-analysis. 

Multidisciplinary Association for Psychedelic Studies (MAPS). A Phase-3 Program of MDMA-Assisted Psychotherapy for the Treatment of Severe Posttraumatic Stress Disorder (PTSD). 

http://www.maps.org/research/mdma/ptsd/phase3

 O’Neil ME, Nugent SM, Morasco BJ, et al. Benefits and harms of plant-based cannabis for posttraumatic stress disorder: a systematic review. 

Articles

PTSD in late life can result from trauma that occurred much earlier or can follow traumatic events that occurred for the first time in old age.

PTSD in Late Life: Special Issues

Dr. Swartz is Affiliate Faculty, Oregon Health & Science University, Portland; Emeritus Faculty, Southern Illinois University School of Medicine, Springfield, Illinois; and Medical Director, Lutheran Community Services Northwest, Vancouver, Washington.

Visual Hallucinations Linked to Timolol Eye Drops

The visual hallucinations from timolol eye drops reported in your January cover story apparently resulted from local effects on retinal circulation rather than systemic effects.

 The hallucinations described were of geometric shapes. This resembles phosphenes, an ordinary response to disruption of retinal circulation, as from closing eyelids tightly for 5-10 seconds or from orthostasis. Phosphenes can also result from diseases affecting the retina (eg, MS).

For mechanism, the Psychiatric Times piece hypothesized only similar systemic effects of eye drops and a 10-mg oral dose. A drop of timolol 0.5% in each eye contains just one twentieth of 10 mg, so its systemic effects cannot be compared. Moreover, timolol is hydrophilic, so after systemic absorption, it does not normally enter the brain.

In treating anxiety disorders over 25 years I have given CNS-active beta-blockers to over 2000 patients with clinical benefit. For elderly patients I prefer pindolol, in younger adults betaxolol.

 None of the patients reported visual hallucinations or showed (or mentioned) cognitive impairment. Beta-blockers are well tolerated and safer than antipsychotics in anxiety disorders. The report about timolol should not be understood as stating that timolol causes psychosis. Moreover, changes in color vision are distortions, and your article should not have called them hallucinations.

This article was originally published on February 1, 2018 and has since been updated.

Visual hallucinations linked to timolol eye drops

3. Swartz CM. Sympathy for the sympathetic (nervous system). In series "Clinical Controversies." 

Timolol Does Not Cause Psychosis

s Clinical Pharmacy Specialist, Mental Health, VA Ann Arbor Healthcare System

is a PharmD Candidate, University of Michigan College of Pharmacy;

is Associate Chair and Clinical Associate Professor, Department of Clinical Pharmacy, University of Michigan College of Pharmacy and Clinical Pharmacist in Psychiatry, Michigan Medicine, Ann Arbor, MI.

In the past decade, the effects of antidepressants on the QT interval and the subsequent risk of cardiac arrhythmias have become a notable concern. When the FDA released a 

 about the risk of abnormal changes in the electrical activity of the heart with citalopram, providers learned to consider this risk as not only an adverse effect of a specific medication, but also the consequence of drug-drug interactions.

While the caution exhibited by prescribers following the FDA warning about citalopram is understandable, the recommended changes in the prescribing of citalopram based solely on QT interval prolongation have had unintended consequences. Recent studies that evaluated the impact of these prescribing changes have shown increased rates of hospitalizations, along with increases in the number of prescriptions for benzodiazepines and sedative-hypnotics, since the lower maximum dose was instituted. Moreover, the association between citalopram and ventricular arrhythmias and mortality has not been verified in studies of citalopram doses greater than 40 mg. Therefore, clinical judgment and risks versus benefits need to be considered when prescribing antidepressants that may affect the QT interval.

When a patient is assessed for antidepressant therapy, providers should keep the risk factors for QT prolongation in mind (

). A thorough medical history, laboratory monitoring, and a baseline electrocardiogram (ECG) may be necessary to identify patients at risk for QT prolongation before starting an antidepressant that may prolong QT interval. Significant QT prolongation may occur through drug-drug interactions when another medication known to affect the QT interval is used concomitantly or when a medication alters the metabolism of another drug with known effects on the QT interval. This potential should always be considered when a new medication is added, even when therapy is brief, such as with antibiotics or antiemetics.

QT prolongation risk varies with each antidepressant, and specific medications should be chosen with consideration of these differences. Case reports of QT prolongation have been published with all of the SSRIs, with the exception of paroxetine, but many of these events were in the context of an overdose, inherent risk factors, and concomitant use of other medications known to increase the QT interval, which makes it difficult to draw conclusions.

 emphasize that SSRIs, including fluoxetine and paroxetine, are not statistically significantly associated with QT prolongation, as indicated by comprehensive, prospective studies regarding the corrected QT (QTc) interval. More caution should be used with escitalopram than with other SSRIs (excluding citalopram) because it causes a slight increase in the QTc interval. However, the 

 is less than the increase associated with therapeutic doses of 

, and it is within the FDA-approved dosing range (

 (Although the FDA has not issued any warning about QT prolongation with escitalopram, other countries’ regulatory bodies have issued warnings similar to those for citalopram.)

TCAs and SNRIs have also been shown to prolong the QT interval to varying degrees. Certain TCAs (eg, amitriptyline, maprotiline) may lead to QT prolongation, although others do not (eg, clomipramine).

 The risk of QT prolongation is similarly low for the SNRIs, including duloxetine and desvenlafaxine.

 Venlafaxine may require more caution, particularly in cases of overdose, and in elderly patients or those with hepatic impairment. Therapeutic use of bupropion and mirtazapine is likely safe; however, bupropion overdoses have been associated with 

 provides a comparison of QT prolongation risk among antidepressants. Selecting an alternative antidepressant to citalopram or agents that may be considered “higher risk” can be useful for patients with many risk factors for QT prolongation. This is not always necessary in healthy patients or in patients who are responding well to the medication with normal laboratory parameters and ECG. Treatment decisions must be individualized, based on patients’ risk factors, target symptoms, cost, etc.

Increases in the QT interval are significant because they increase the risk of torsades de pointes and other serious cardiac events. However, increases, such as the reported average 18.5-ms increase associated with 60 mg of citalopram, may not be clinically significant, because QT prolongation indicates only the potential for an event to occur.

 Use of citalopram and other antidepressants associated with an increased risk of QT interval prolongation is possible through proper monitoring and judicious use.

Monitoring throughout the course of treatment is necessary because 

 can occur anywhere from the first 5 days of treatment to after 30 days of treatment.

 To monitor a patient’s QT interval, an initial baseline ECG and electrolyte panels are recommended with periodic monitoring to follow.

 recommend that patients with one or more risk factors, such as female sex or age older than 65 years, should be monitored more closely with ECGs and electrolyte panels every month for the first 6 months and monitored once every 6 to 12 months thereafter. QTc is most commonly obtained through Bazett’s formula, although it is unable to correct for fast and slow heart rates. In general, any QTc above 500 ms requires discontinuation of the medication, while a modification of therapy may be necessary with intervals of 470 to 500 ms in males and 480 to 500 ms in females.

 that highlights the risk of QT prolongation associated with citalopram illustrates concerns about drug-induced QT prolongation; however, the risk with citalopram is not much higher than that associated with other medications and is typically clinically insignificant. Unnecessary changes in therapy in patients whose condition is stable on citalopram can prove harmful. Antidepressants, like all other medications, come with risks, but with knowledge and proper monitoring, the risk associated with QT interval prolongation can be safely managed.

The authors report no conflicts of interest concerning the subject matter of this article.

Unintended consequences of adjusting citalopram prescriptions following the 2011 FDA warning

 Beach SR, Celano CM, Noseworthy PA, et al. 

QTc prolongation, torsades de pointes, and psychotropic medications

A comparison of the risk of QT prolongation among SSRIs

Risk of QT/QTc prolongation among newer non-SSRI antidepressants

 Trinkley KE, Page RL II, Lien H, et al. 

QT interval prolongation and the risk of torsades de pointes: essentials for clinicians

 US Food and Drug Administration. FDA Drug Safety Communication: Revised Recommendations for Celexa (citalopram hydrobromide) Related to a Potential Risk of Abnormal Heart Rhythms With High Doses. 

In the past decade, the effects of antidepressants on the QT interval and the subsequent risk of cardiac arrhythmias have become a notable concern. When the FDA released a drug safety communication about the risk of abnormal changes in the electrical activity of the heart with citalopram, providers learned to consider this risk as not only an adverse effect of a specific medication, but also the consequence of drug-drug interactions.

QT Prolongation and Antidepressants

practices psychiatry in Manhattan, New York. He continues to publish frequently on film, media, and popular culture. For many years, his cinema column appeared in Psychiatric Times. He has appeared frequently on national and international network and cable television programs including Good Morning America, Today, CBS Evening and Sunday News, PBS, CNN, Showtime, and BBC-TV. Please address communications to Dr. Greenberg at 

I’ve written about poker nearly as long as I’ve been playing it. I observed in these pages years ago that the game can be a great revealer of-but sometimes a great destroyer of-character, especially when one harbors the psycho-social and hereditary/genetic potential for compulsive gambling.

Gambling humor embraces the dark side. Poker argot is especially mordant. “Where’s Lennie?” asked one of my high-rolling patients about a legendary loser, absent from the tables for several months.

Came the laconic reply: “Lennie is in Poker Hospital…” meaning he was broke beyond redemption…possibly disappeared himself to elude loan shark thugs who would assuredly be playing castanets on his kneecaps with hammers if he didn’t pay up.

Molly Bloom, feisty heroine of the eponymous 

, wound up in poker hospital not from playing, but from running lavish underground poker games in LA and NY. Her “clients” were major Wall Street sharks, glitterati from the worlds of entertainment, sports, politics, and-to her final undoing-kingpins of the Russian mob.

No-Limit Texas Hold-em is the most popular form of poker today. You can easily google the rules, but it’s more enjoyable to learn them by watching 

(1998), the best poker picture ever lensed.

Each player-10 maximum-is dealt 2 down cards, which are then combined with a “window” of 5 common pasteboards. Betting proceeds before and after the window is flopped. The best 5-card hand wins.

The game looks disarmingly simple. In fact, it’s alarmingly complex. Any player can go “all in”-bet his or her entire stack-at any time during a round. The ability to bluff and suss out bluffing is crucial. Played for high stakes, the game requires extraordinary patience and battlefield courage. You strive to keep your head on straight during hours of boredom, punctuated by moments of sheer terror.

Fine players carefully bide their time until the right terrifying moment comes along. But Molly’s punters were action junkies, many pathological gamblers who were always all in, creating stratospheric pots. Molly was especially adept at winkling out “fish,” poor players with deep pockets, able to sustain formidable losses and come back week after week for more .

She took great pride running a legitimate game in a milieu prone to knavery. She paid her employees-dealers, servers, security-on the books, kept scrupulously to the letter of ambiguous gaming laws. She lived large, but only on big weekly tips.

Aaron Sorkin’s previous TV and theatrical work-eg, in 

-featured high octane plotting and rat-a-tat dialogue reminiscent of the screwball comedies and sizzling crime pictures of Hollywood’s studio era. 

 marks his debut as a film director; he also adapted the film from Bloom’s autobiography.

Sorkin’s skillset satisfyingly drives the picture until an unfortunate conclusion, of which more presently. (Molly is stunningly played by Jessica Chastain). In the scorching establishing sequence, Federal agents summarily yank Molly out of bed and into the slammer for illegal gambling. Her arrest came several years after she had closed her operations.

The feds actually cared little about Molly’s games. They jailed her with the goal of compelling her to rat out 30 badfellas under indictment who had played at her tables. But Molly refused to co-operate. She had substantial knowledge about her players’ private lives, and refused to break confidentiality so as not to shame them and their families. Their outside business wasn’t her business.

Sorkin adroitly interpolates Molly herself relating her picaresque, often harrowing backstory, and third person narration of her quest to escape incarceration. Her voiceover delivery is fast paced, ironic, curiously distanced-as if she’s describing someone else’s life in a galaxy far away. Staccato cutting accentuates Molly’s fragmentated modus vivendi-initially exciting, and terminally desolating.

Molly’s father (a one-note gruff Kevin Costner) is a charismatic psychology professor, who relentlessly helicoptered Molly and her 2 brothers to become academic and athletic super achievers.

We infer that the brothers accepted, indeed flourished, under their father’s iron tutelage. Molly brashly challenged and disrespected him at every step; yet identified with his Ayn Randish vision of a world in which the meek are crushed and the elite rewarded.

Molly rose to early prominence in breakneck downhill ski racing, until a freak accident demolished her career. She migrated to LA against her father’s wishes and without his support. She became the factotum of a repellant Hollywood wanabee mogul. She serviced, then stole his game; eventually moved to Manhattan, where she ran more games at higher stakes.

Her judgement eventually deteriorated under escalating self-generated stress. She became drug-addicted, brought key Russian mobsters and an FBI informant to her tables. After refusing to partner up with the Mafia, she was shockingly beaten, then recovered her senses; fled back to California, got herself straight, and lived under the radar until her arrest. Making bail reduced her to penury. The Feds had already confiscated her savings, and taxed them to boot.

Molly’s players were all men; and crooked timber to a man. Their crude narcissism could gag a goat. The majority constituted an omnium gatherum of gambling addicts-perennial chasers after Lady Luck-massive losers who offered every rationale in the sordid book for behavior ruinous to others as themselves. Her biggest winner, no addict, was an odious predator who delighted in demolishing his opponents’ self-esteem as much as savaging their bankroll. Molly’s prosecutors are portrayed as no less repugnant. Utterly devoid of pity, they’d happily let her rot in jail if she didn’t co-operate. (Intriguingly, her punters from the Russian mob left their vicious psychopathy outside Molly’s doorstep: in the film they come across as hapless, even likeable schlubs.)

Charlie Jaffey (the estimable Idris Elba), a prominent criminal lawyer, proves a shining exception to the prevailing male grottiness. Jaffey’s fee is high as his probity. He takes her case-probably pro bono-because he’s captivated by her sass, wit, and staunch, if naÃ¯ve to compromise her people. By her lights, what went on outside the game room-sports betting, prostitution-weren’t her concern. All that mattered was running a pleasurable, profitable man-cave.

At the end, her case is unexpectedly thrown out by a benevolent judge. Her father also shows up with glib park bench psychoanalyzing, and a sappy declaration of love, dripping with crocodile tears. The reconciliation sequence strikes precisely the wrong bathetic note, in a solidly winning picture with a hollow Tinseltown heart. Watching it is akin to quaffing a good wine with a two-buck-chuck finish.

 has generally drawn excellent reviews. A few dissenters complained that Molly comes across as a stick figure, sans depth and complexity. Hollywood usually doesn’t “get” pathological gambling, glamorizing or demonizing it. Whatever his penchant for wearisome liberal pieties, Sorkin deserves credit for being spot on about the disorder’s psychopathology.

Pace the Goldwater ruling, the onscreen Molly Bloom’s shallowness isn’t due to vapid scripting, but the peculiar alexithymia native to the pathological gambler’s persona, which breeds massive unknowningness about inner life and motivations.

By this token, Molly is absolutely unable to register the dubious legality-and morality-of her games. Her insensate craving for “action” is another classic manifestation of the disorder: it precipitated the sinister slalom that ground down her ego strength and eroded her mortality (one notably sees this in end-stage gambling).

Molly also is fatally susceptible to the “gambler’s fallacy”-the unshakeable conviction that no matter how dire her straits, the odds will inevitably turn in her favor. Her gallows humor comprises yet another signature of the disorder.

I’ve elsewhere described pathological gambling as the dark underbelly of the American dream. It’s implied that by nurture or nurture, Molly has inherited her father’s cynical world view: if you’re not a stone-hearted winner, you’re a feckless loser.

Sorkin leaves Molly existentially unmoored, broke but not broken, already scanning the horizon to reinvent herself in some fashion. Given the dog-eat-dog tenor of the (Washington) times, her character pathology, ferocious intelligence, and ruthless ambition would seem to make going into politics a viable career option.

NB: For more information on pathological gambling, the reader is directed to Dr. Greenberg’s chapter on the subject in the latest edition of the Comprehensive Textbook of Psychiatry. His review of Rounders, which originally appeared in the now defunct Poker Pro magazine, can be found on the internationalpsychoanalysis.net website. 

This article was originally published on February 13, 2018 and has since been updated. 

The game looks disarmingly simple. In fact, it’s alarmingly complex.

Molly’s Game: Poker Hospital and Pathologic Gambling 

After he juggles three chainsaws and spins

twenty plates balanced on sticks, he moves

to the grand finale: ten Bowler hats tossed

across the arena and stacked on the ringmaster’s

head. He gets to nine and misses, and misses

the tenth three more times, cheers rising

to a roar with each failure, until the drum

rolls and the spotlight finds him for the final

of the stack and the audience stomps their praise.

it hits me: the misses were part of the act,

the juggler knowing the crowd would admire

his skill, but would love him even more for

at my office, where there are no stage lights,

I work will only suffer more if I screw up,

Dr. Berlin is Senior Affiliate in Psychiatry at the University of Massachusetts Medical School. E-mail: 

After he juggles three chainsaws and spins twenty plates balanced on sticks, he moves to the grand finale: ten Bowler hats tossed across the arena and stacked on the ringmaster’s head.

The Juggler

is President, Academy of Psychosomatic Medicine.

In October 2017, the American Board of Medical Specialties (ABMS), acting on recommendations by the American Board of Psychiatry and Neurology (ABPN), American Psychiatric Association (APA), and Academy of Psychosomatic Medicine (APM), voted to change the name of the subspecialty Psychosomatic Medicine to Consultation-Liaison Psychiatry. The following month, APM voted to change its name to the Academy of Consultation-Liaison Psychiatry. The Academy’s name change will be effective on April 16, 2018.

The Academy of Psychosomatic Medicine initiated the name change process after hearing from its members for many years that the name Psychosomatic Medicine was problematic.

 Many expressed the concerns that the name had a pejorative connotation, had a negative impact on recruiting into the field, and was not widely used by actual clinicians and academic departments. The name Psychosomatic Medicine had been selected by the ABMS for the official approval of subspecialty certification during deliberations conducted between 2000 and 2003.

 From the beginning, there was controversy and general dissatisfaction with the chosen name, although there were ongoing efforts to improve the brand of the name.

The APM conducted several surveys to determine whether there was a consensus for a name change. In early 2016, APM members were asked for their opinion whether an alternative name should be chosen for the field. Of the 780 respondents, a majority of Academy members, 68% supported a name change, 16% were neutral, and 16% disagreed with changing the name. A second survey was conducted later that year, focused on how APM members were currently describing their field. Of the 350 responses received, the majority (55%) said they were using the name “Consultation-Liaison Psychiatry;” only 17% said they used the term “Psychosomatic Medicine.”

In December of 2016, a final survey was conducted in which members were asked: “If other key national organizations were in favor, would you support changing the name of the field to Consultation-Liaison Psychiatry, which would include also changing the name of the Academy to mirror that term?” Of the 668 respondents, representing more than half of the Academy's membership, 81% endorsed the name change.

The APM then requested and received the support of the APA Board of Directors in December 2016. The next step was to petition the ABPN; the organization within ABMS that oversees accreditation in psychiatry. In February 2017, the ABPN Board of Directors voted to the support the name change request. The ABPN then took this request to the ABMS. The ABMS held an open comment period and then approved the name change at their annual meeting in October 2017. Finally, following this official name change of the subspecialty, APM’s Council recommended to Academy members that they support changing APM’s name to the Academy of Consultation-Liaison Psychiatry, and the vote to change the name was approved at the November 2017 annual meeting.

The Academy’s “go-live” date for its name change is April 16, 2018. This date provides sufficient time for all preparations and initiates the formal name change before the annual meeting of the American Psychiatric Association. The Academy will use the large stage of the APA 2018 annual meeting to market and brand the name change.

Over two dozen specific tasks need to be completed to be ready for the go-live date, for example:

• Change the name in Academy documents and publications

• Coordinate with the Academy’s journal, Psychosomatics

• Identify branding opportunities, including at the 2018 APA annual meeting

• Integrate the name change into plans for the 2018 Academy annual meeting

• Coordinate with the Academy’s foundation

• Notify sister medical organizations in the US and abroad

• Consult with fellowship program directors

The Academy’s Council hopes to take advantage of this opportunity of a name change to prioritize the branding of the field of Consultation-Liaison Psychiatry and the organization. The “new name” is actually the subspecialty’s old name. It comes from a time when most of the clinical work was in inpatient medical-surgical units. Much has changed since then and the Council is focused on finding ways to market an expanded brand that captures a broad and deep set of practice settings when seeing or hearing the word “liaison.” The word liaison will be branded by the Academy to mean integrated care in primary and specialty outpatient care settings, in addition to the important work done integrating psychiatric care into inpatient medical-surgical, critical care, and rehabilitation units.

The theme of the 2018 Annual meeting in Orlando (November 13-17, 2018) is “Branding Consultation-Liaison Psychiatry, Defining the Breadth and Depth of our Subpecialty.” The meeting will highlight the clinical, academic, and research work done in outpatient and inpatient clinical settings. The meeting sessions will be presented by the Academy’s Special Interest Groups that represent areas of expertise within the field. These groups are incredibly active and represent the breadth and depth of knowledge in several areas of outpatient or inpatient practice at the interface of psychiatry and medicine.

Information about the Academy, its Special Interest Groups, and the upcoming annual meeting, can be found on the Academy’s webpage-

-The author acknowledges the Academy of Psychosomatic Medicine for helping to bring this article to fruition. The Academy is the professional home for psychiatrists providing collaborative care bridging physical and mental health. Over 1200 members offer psychiatric treatment in general medical hospitals, primary care, and outpatient medical settings for patients with comorbid medical conditions.

 Montalvo C, Robinson DM. What is psychosomatics? Lessons learned regarding the importance of a name. Psychosomat. 2017;58:215-216.

Gitlin DF, Levenson JL, Lyketsos CG. Psychosomatic medicine: a new psychiatric subspecialty. Acad Psychiatry. 2004;28:4-11.

 Lipsitt DR. Consultation-liaison psychiatry and psychosomatic medicine: the company they keep. Psychosom Med. 2001;63:896-909.

 Ali S, Ernst C, Pacheco M, Fricchione G. Consultation-liaison psychiatry: how far have we come? Curr Psychiatry Rep. 2006;8:215-222.

[Editor’s note: Members of The Academy of Psychosomatic Medicine are frequent contributors to Psychiatric Times. Articles and authors can be seen at 

www.PsychiatricTimes.com/authors/academy-psychosomatic-medicine

The name of the subspecialty Psychosomatic Medicine has become Consultation-Liaison Psychiatry. And the Academy of Psychosomatic Medicine has changed its name to the Academy of Consultation-Liaison Psychiatry. Here's why.

What’s in a Name? Name Changes for Subspecialty and the Academy of Psychosomatic Medicine

All other clinicians either will receive a CME Attendance Certificate or may choose any of the types of CE credit being offered.

To understand the role of stress in the manifestation of depressive symptoms.

At the end of this CE activity, participants should be able to:

• Describe the brain circuits associated with depressive symptom clusters

• Identify the multiple functions associated with reward systems (eg, anticipatory, consummatory)

• Explain how the frontal cortex affects cognition in depression

This continuing medical education activity is intended for psychiatrists, psychologists, primary care physicians, physician assistants, nurse practitioners, and other health care professionals who seek to improve their care for patients with mental health disorders.

:This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of CME Outfitters, LLC, and Psychiatric Times. CME Outfitters, LLC, is accredited by the ACCME to provide continuing medical education for physicians.

CME Outfitters designates this enduring material for a maximum of 1.5 

™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Note to Nurse Practitioners and Physician Assistants: AANPCP and AAPA accept certificates of participation for educational activities certified for 

It is the policy of CME Outfitters, LLC, to ensure independence, balance, objectivity, and scientific rigor and integrity in all of their CME/CE activities. Faculty must disclose to the participants any relationships with commercial companies whose products or devices may be mentioned in faculty presentations, or with the commercial supporter of this CME/CE activity. CME Outfitters, LLC, has evaluated, identified, and attempted to resolve any potential conflicts of interest through a rigorous content validation procedure, use of evidence-based data/research, and a multidisciplinary peer-review process.

The following information is for participant information only. It is not assumed that these relationships will have a negative impact on the presentations.

Serge Campeau, PhD, has no disclosures to report.

Bruce S. McEwen, PhD, (peer/content reviewer) has no disclosures to report.

 staff and CME Outfitters staff have no disclosures to report.

Faculty of this CME/CE activity may include discussion of products or devices that are not currently labeled for use by the FDA. The faculty have been informed of their responsibility to disclose to the audience if they will be discussing off-label or investigational uses (any uses not approved by the FDA) of products or devices. CME Outfitters, LLC, and the faculty do not endorse the use of any product outside of the FDA-labeled indications. Medical professionals should not utilize the procedures, products, or diagnosis techniques discussed during this activity without evaluation of their patient for contraindications or dangers of use.

is Associate Professor, Departments of Psychiatry and Medical Genetics, University of British Columbia, Vancouver, BC

Clinicians across all disciplines-including psychiatry-are increasingly feeling pressure to incorporate genetics into their clinical practice. Psychiatrists can find themselves confronted with their patients’ questions about whether genetic testing is an option that might provide useful answers for them. However, many psychiatrists lack confidence in their abilities to integrate genetics into their patient care.

Genetic counseling is a field at the forefront of the integration of genetics into clinical practice across a wide variety of medical specialties. In this article, I draw on experience from our specialist psychiatric genetic counseling service to provide practical guidance for psychiatrists who wish to confidently address the questions regarding genetics that may be posed by patients and their families.

Given that there are misconceptions about genetic counseling, before considering what it IS, it is first important to explicitly consider what it is NOT:

1. Genetic counseling is not genetic testing: Genetic counseling does not require genetic testing, nor in fact, even the availability of genetic testing for meaningful patient benefits to be derived from genetic counseling.

2. Genetic counseling is not simply a discussion with a family of a child’s risk for a condition of concern. Within the field of medicine, there is a perception that a conversation between a health care professional and a patient that concerns a child’s risk for an indicated heritable condition is “genetic counseling.” In fact, genetic counseling is a 50-year-old professional discipline, with accredited MSc level training programs throughout North America, certification boards, and in some states, licensure.

The work can involve addressing issues about a child’s risk for a condition of concern when it is relevant; but this constitutes only one facet of a wide range of issues that can be addressed. Genetic counselors work across an enormous range of medical specialties (eg, psychiatry, oncology, neurology, cardiology).

3. Genetic counseling is not a purely educational/informational intervention. Although information is a critical component, ideally the information is not simply delivered, but rather it is a discussion in the context of a psychotherapeutically-oriented encounter.

4. Genetic counseling is not limited to a discussion of the genetic contributions to a specific illness. In the context of a serious illness (eg, a psychiatric disorder), genetic counseling involves discussion of how genes, environmental exposures, and experiences interact to precipitate illness.

 by the National Society of Genetic Counselors (NSGC) as the: “process of helping people understand and adapt to the medical, psychological, and familial implications of genetic contributions to disease.”

Practical guidance for psychiatrists who wish to confidently address questions regarding genetics that may be posed by patients and their families.

Vol 35 No 3

PTSD in Late Life: Special Issues

Timolol Does Not Cause Psychosis

QT Prolongation and Antidepressants

Molly’s Game: Poker Hospital and Pathologic Gambling

The Juggler

What’s in a Name? Name Changes for Subspecialty and the Academy of Psychosomatic Medicine

Genetics in the Clinical Setting: The Role of Psychiatric Genetic Counseling

Advantageous Adages in Psychodynamic Psychotherapy

Lies, Damn Lies, and Statistics

HOCUS POCUS: How the NIMH Made 2 Million People With Schizophrenia Disappear

On the Prevalence of Schizophrenia and Transforming Care Through Research