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Climate medicine: What was once on the radar of just a handful of physicians has exploded into awareness, alarm, and sometimes debate and skepticism. No matter how you look at it, psychiatrists are on the front lines.

Climate Psychiatry Year in Review

You are referred a patient with a 3-year history of multiple vague health and cognitive complaints including pain, nausea, memory and concentration difficulties, and fatigue. Despite an exhaustive battery of tests, 

 has been found for the patient's symptoms.

Additionally, the reported severity of her complaints appears grossly out of proportion given gathered information and your own clinical observations. She does appear genuinely and significantly distressed by her reported issues but otherwise denies depressive symptoms.

After meeting with the patient, reviewing medical records (which include valid performance on neuropsychological validity testing), and interviewing multiple collateral sources, you come to the opinion that the patient is not intentionally falsifying or exaggerating her symptoms.

The patient does claim that she is no longer able to work due to the severity of her difficulties and states that she intends to file for disability.

Given this information, which of the following would be the most appropriate diagnosis for this patient?

The reported severity of the complaints in this patient appears grossly out of proportion given gathered information and clinical observations. What's your diagnosis?

Mini Quiz: Assessment of Malingering

Psychosomatic medicine, or medical psychiatry-also known as consultation-liaison (CL) psychiatry-specializes in the diagnosis and treatment of psychiatric disorders and psychiatric manifestations of complex medical illness.

 CL psychiatrists treat a challenging and diverse patient population both in the general hospital setting and in the outpatient setting. They specialize in the care of patients with comorbid psychiatric and medical illnesses, as well as patients whose psychiatric illness is a direct consequence of a primary medical condition.

Psychosomatic medicine psychiatrists also have expertise in managing psychiatric effects of medical treatments and medications. Their roles include consulting to the patient’s primary medical team, serving as a liaison between the psychiatry service and the primary medical service, and treating patients’ psychiatric disorders while active medical care is being provided.

 Consultation psychiatrists have the unique ability to do this work while navigating the logistics of managing psychiatric treatment of sometimes very complex patients in the general hospital setting.

 issues-the last article in that series appears on page 32 of this issue-includes articles on the management of some of the more challenging consultations seen in the general medical hospital. Topics in neuropsychiatry, oncology, and pediatrics were selected not only to illustrate interesting and challenging issues but also to represent the diversity of the field of psychosomatic medicine.

 (PNES). They review the history, epidemiology, diagnosis, and treatment of PNES. The authors provide an interesting look into the diagnosis with a discussion of the significance non-epileptic seizures hold in the context of a patient’s medical illness, and they suggest ways of communicating with patients who have this disorder.

, its diagnosis, incidence, and possible etiologies as well as its relationship to delirium. They present the broad and often confusing differential diagnosis for catatonia as well as treatment strategies.

Also included is an article on the role of psychiatric care for patients living with cancer. 

 address some of the varied psychiatric issues that the consultant must take into account when caring for these patients. They discuss the importance of coordination of care, management of medications (including attention to pain control), and the involvement of a supportive care team.

 present a case, supplemented with a comprehensive discussion, of pediatric auto-immune neuropsychiatric disorder associated with streptococcal infection (PANDAS). The authors characterize the roles of infection, immune dysregulation, and inflammation in the development of this disorder. They also address psychiatric effects of the illness and of psychiatric treatments.

Finally, in this issue, Dr. Certa discusses the topic of determining where patients with both significant psychiatric symptoms and medical illness should be treated. There is little literature on this issue, but it remains a common challenge for both the hospitalist and the consulting psychiatrist. He discusses the evolution of the psychiatric hospital housed within the general hospital and some of the more common factors that might pose as barriers to the transfer of patients from the general to the psychiatric ward.

The authors and I hope that you find these articles useful and informative!

I am Director of the Psychiatric Hospital and Consultation Liaison Services at Thomas Jefferson University Hospital, a 965-bed academic general hospital in Center City, Philadelphia, Pa. In addition, I am the Program Director for the Psychosomatic Medicine Fellowship. As the medical student clerkship site director for the Consultation Liaison rotation, I’ve mentored and taught over 700 medical students in hospital psychiatry over the past 10 years.

My areas of clinical expertise are general hospital psychiatry and psychiatric treatment of women during the peripartum period. I’ve published on and lecture locally and nationally on women’s mental health. I am proud to serve as a council member for the Academy of Psychosomatic Medicine. I also chair their Fellowship Education Subcommittee, where I have the pleasure of working with some of the brightest and most talented psychosomatic medicine Program Directors from around the country.

Working in the field of consult psychiatry constantly reminds us that we must treat the whole patient, both in mind and body, and that these are not disparate. Entering the room as a psychiatric consultant, at a time when a patient is ill and most vulnerable, is the most rewarding work I do as a psychiatrist. The hospital is an ideal setting to teach future physicians. In this setting, it becomes most apparent that psychiatry is truly an essential specialty of medicine. Teaching psychiatry allows us to show trainees that psychiatric illness can be understandable and is treatable.

As an undergraduate at Drew University, I double majored in art and psychology. I worked as an art therapist for several years while in graduate school. I have two Masters Degrees-one in psychology from New York University and one in clinical health psychology from Albert Einstein College of Medicine; my medical degree is from Jefferson Medical College. I completed my residency in psychiatry at the University of Pennsylvania.

Even before medical school, I had been interested in integrative medicine and the integrative approach to patient care. I pursued multiple opportunities to increase my knowledge of the treatment of patients, including a fellowship at the Psychoanalytic Center of Philadelphia and also graduate training in Mindfulness Based Stress Reduction. Having skills in different modalities for treating patients is helpful for delivering care to a diverse patient population. It also helps me to keep an open mind when approaching each patient.

The study of traditional yoga has been one of my great interests as well. I have practiced regularly for the past 9 years and recently obtained yoga instructor certification after intensive training and study on weekends over the past 7 months. The foundations of yoga and meditation can help people control their breath, body, thoughts, and behavior. It provides people with insight into themselves and can help them be more attentive to their actions. I continue to paint and sketch when time allows. Last fall, I travelled to Sicily and found it to be the most peaceful and beautiful place that I have ever visited.

 This introduction to our Special Report on psychosomatic medicine should have run in the March issue with the bulk of the articles on that broad topic. We are grateful for the time and expertise Dr. Becker put into the articles of that Special Report, which you can find on our 

Dr. Becker is Director, Consultation-Liaison/Hospital Psychiatry and Program Director, Psychosomatic Medicine Fellowship, Thomas Jefferson University Hospital, Department of Psychiatry and Human Behavior, Philadelphia, PA.

American Psychiatric Publishing Textbook of Psychosomatic Medicine: Psychiatric Care of the Medically Ill

. 2nd ed. Arlington, VA: American Psychiatric Association Publishing; 2011.

. 3rd ed. New York: Oxford University Press; 2015.

Psychogenic non-epileptic seizures: clinical issues for psychiatrists

Update on medical catatonia: highlights on delirium

Depression and anxiety disorders in patients with cancer.

Sudden onset of tics, tantrums, hyperactivity, and emotional lability: update on PANS and PANDAS

Psychosomatic medicine psychiatrists specialize in managing psychiatric effects of medical treatments and medications.

Challenging Consultations

To view a PDF, of this slideshow, click here.

Beyond psychosocial implications of anxiety disorders, an array of physiological effects may ensue. 

7 Medical Illnesses That May Present as Anxiety

 is admitted to the hospital with rash, arthralgias, and altered mental status. On examination, the patient displays stupor, mutism, posturing, and echopraxia while vital signs, creatine kinase, and brain MRI are all normal. Lorazepam 2mg IV q6 partially improves her symptoms, but higher doses cause more sedation. How would you proceed?

B. Switching from lorazepam to oral diazepam

A patient with lupus presents with rash, arthralgias, and altered mental status. Various symptoms, including stupor and mutism, improve with treatment but higher doses of the drug cause more sedation. How would you proceed?

Mini Quiz: Medical Catatonia

An update on emerging trends in psychosomatic medicine to help clinicians address mental health stressors in psychiatric and medical settings. 

Comorbidity Conundrums and Other Brain Teasers

Although psychogenic non-epileptic seizures (PNES) are events that appear to be similar to seizures, they are not caused by abnormal electrical brain activity. Instead, they are thought to have an underlying psychological cause.

PNES is classified as a subtype of conversion disorder under the category, somatic symptom and related disorders in DSM-5. When coding for PNES as a conversion disorder using ICD-10, the diagnosis must include the specifier “with attacks or seizures” (ICD-10 code F44.5) to differentiate it from other conversion symptoms (eg, dysarthria, sensory loss), which are coded separately. Alternate names frequently used for PNES are non-epileptic attack disorder, functional seizures, stress seizures, psychogenic seizures, and pseudoseizures. The last has largely fallen out of favor because of the pejorative nature of the term “pseudo,” which may imply that the symptoms are not real and therefore undermine the impact of the disorder on a patient’s life. It is not uncommon to see both PNES and epileptic seizures in the same patient.

PNES has a long history in the medical literature, where it has been described by several aliases, the most common being hysteria. Equally as varied were the many hypotheses for the causes of hysteria. Because of its observed frequency in females, hysteria was conceptualized as the result of a “wandering uterus” that had been displaced in the body and subsequently inhabited other organs and appendages, applying pressure and leading to the manifestation of physical symptoms. This theory eventually lost prominence as symptoms of hysteria were increasingly reported in males.

Update on Psychogenic Nonepileptic Seizures

In the 19th century, the phenomenon became a passion of French neurologist Jean Charcot, who identified it primarily as a neurological disorder with psychological underpinnings that could, in some cases, be treated by hypnosis. Sigmund Freud, after studying under Charcot, theorized the symptoms as a conversion of repressed libidinal impulses into physical form, which brought about its current title of conversion disorder. Alternatively, Pierre Janet suggested hysteria was more of a dissociative phenomenon that occurred at times of stress with the purpose of allowing an individual to re-experience a traumatic event while separating the memory from conscious awareness.

Clues to a possible diagnosis of PNES can be discovered by eliciting a seizure history including onset, typical semiology of the seizure, and treatment. Patients with PNES are likely to have seizures more frequently with more hospital visits than patients with epilepsy. They may often carry a diagnosis of refractory epilepsy, and it is not uncommon for patients to have current or past prescriptions of antiepileptic drugs. Antiepileptic drugs, however, are not effective in treating PNES and may either worsen the symptoms or cause only a transient partial response.

Psychiatric comorbidity is quite common in patients with PNES. The most frequently co-occurring disorders are PTSD, anxiety disorder, personality disorder, and depression (

). Patients with comorbid psychiatric disorders may also have more severe dysfunction and higher levels of stress. Identifying a comorbid psychiatric condition can result in more specific treatments that target those symptoms as well as better outcomes for patients.

In addition to performing a psychiatric review of systems, inquire about any history of medically unexplained symptoms (hand tingling, paralysis, etc) and screen for possible somatoform disorders. Patients with PNES may frequently report pain as other somatic symptoms. Prescriptions for pain medication were found to have a positive predictive value of 76.9% in patients with PNES compared with patients with epilepsy.

Attempts to identify typical psychological features of PNES have been largely unsuccessful. 

, coined by Freud in his observation of patients with conversion disorder, has been thought to be a classic characteristic; however, a systematic review of the literature found this feature was observed in only a minority of those with conversion disorder and not at a significantly higher rate than in controls.

 Alexithymia was thought to be more common in this patient population but has been found to occur at similar rates in patients with PNES and in patients with epilepsy or other medical disorders.

 Patients with PNES can be divided based on problems with emotional regulation: one group has a tendency toward emotional dysregulation, and the other is emotionally over-regulated.

The precipitating psychological stressor criterion to confirm a diagnosis of PNES was removed from the criteria for conversion disorder in DSM-5. Rates of precipitation trauma are between 44% and 100% in patients with PNES; however, most patients do not report a trigger or stressor during the initial psychiatric assessment. That is not to say traumatic factors will not be discovered once the patient engages in treatment. Lifetime physical and sexual abuse in particular are reported at rates of 23% to 77% and childhood sexual or physical abuse at 32.4% to 88%.

 Outside of abuse, bereavement and being in or witnessing an accident are other possible antecedent factors. Early-onset (adolescence) PNES has been associated with bullying; late-onset PNES has been associated with health-related trauma.

When assessing triggers, keep in mind that one-third of epilepsy patients also report childhood physical or sexual abuse. Moreover, stress can trigger epileptic seizures.

The gold standard for diagnosing PNES is continuous video electroencephalography, or vEEG. This should be done only after carefully eliciting a description of the typical seizure presentation, also known as semiology, from the patient or a family member. Only a video recording that captures an episode resembling the reported semiology with no concomitant epileptiform activity seen on EEG (vEEG) can be used to make a definitive diagnosis. If multiple seizure types are reported, then each type of seizure should be visualized on vEEG because of the possible co-occurrence of PNES with epileptic seizures.

vEEG usually requires inpatient admission to an epilepsy monitoring unit, which is not found at all hospitals. Such admissions are also costly and may have long wait times. However, a routine EEG that lasts 20 to 30 minutes has a 1% chance of capturing even an epileptic seizure and is an insufficient substitute. Ambulatory EEG has also not been shown to be a reliable diagnostic test for PNES. The Nonepileptic Seizures Task Force for the International League Against Epilepsy published a staged diagnostic approach to PNES.

 Some of their recommendations are reviewed here; however, we encourage readers to refer to the article for a more comprehensive review.

When vEEG is not available, a seasoned clinician could possibly diagnose PNES by observing specific semiology alone. Bedside tools based on data from several studies have been created to aid in visual diagnosis of PNES episodes (

). However, the studied semiologic differences are specifically between convulsive-type PNES and generalized tonic-clonic (GTC) seizures. PNES as well as epileptic seizures have various presentations (eg, absence seizures, frontal seizures) that significantly reduce the ability to diagnose PNES by observation alone and can lead to misdiagnosis. In such cases, a push for vEEG referral by the consulting psychiatrist is warranted.

In regards to observed semiologic differences, convulsion-type attacks in PNES tend to be asymmetrical and asynchronous, have a more fluctuating inconsistent course, and may respond to bystander intervention. Preserved awareness during events, especially with bilateral limb movements, should raise suspicion for PNES. Pelvic thrusting has been observed more frequently in PNES; however, it can occur in GTC seizures as well. Side-to-side head and body movement along with eye and mouth closure have been more readily associated with PNES than with GTC seizures. Urinary incontinence and tongue biting have not been shown to be useful in differentiating PNES from GTC seizures. The latter rarely last more than 2 minutes.

Post-ictally, patients with PNES are more likely to regain awareness quickly, recall the seizure event, and not have symptoms of fatigue or headache. PNES episodes are also more typically followed by rapid shallow breathing that quickly subsides, whereas GTC seizures are frequently followed by prolonged harsh, loud, deep breathing.

Non-epileptic status, a prolonged episode of seizure-like symptoms that lasts more than 30 minutes, was reported by one-third of patients in one study.

 However, unlike status epilepticus, non-epileptic status does not pose an imminent risk of brain injury.

Along with semiology, there are a handful of soft signs that may heighten suspicion of PNES. One is the teddy bear sign, in which an adult patient keeps a stuffed animal in the hospital bed. The specificity of this soft sign was rated highly by a retrospective chart review.

 However, a prospective study that looked at the presence of a stuffed animal at the time of admission in 264 patients found that of the 34 patients who presented with a stuffed animal, 56% had a diagnosis of epilepsy and 39% had a diagnosis of PNES, which gives the sign poor predictive value.

Another soft sign for PNES is the number of allergies a patient reports. Independent of other risk factors, patients who reported more than 12 allergies had a 6-fold higher likelihood of a PNES diagnosis.

As mentioned above, one of the conditions in the differential diagnosis of PNES is epilepsy. 

 summarizes various sites of seizure origin and likely semiology. (For a more complete description of epileptic semiology, see the article by Noachtar and Peters.

Another condition in the differential may be periodic limb movements of sleep, which are highly correlated with restless legs syndrome. They occur only during sleep with very repetitive, stereotyped limb movements; are more likely to involve the lower extremities; and can be bilateral.

Up to 13% of patients who are referred to an epilepsy clinic may have neurocardiogenic syncope, a syndrome that can mimic epileptic seizures. There are multiple precipitating factors, one of which is emotional stress. On rare occasions, patients can have seizure-like activities during syncopal episodes. Patients would likely lose consciousness first and fall before uncontrolled muscle movements.

It is important to recognize when seizure-like symptoms are being volitionally produced for the purpose of maintaining a sick role or for secondary gain. Unfortunately, vEEG may not be able to separate conversion disorder from factitious disorder. However, a study that looked at the possibility of physical symptoms in PNES serving as an unconscious motivation to acquire “the sick role” found that there were no differences between patients with PNES and controls in attitudes toward illness or the desire to be sick.

While the desire to maintain a sick role in factitious disorder may be unconscious, the act of deception itself is conscious and purposely perpetrated. Clinical scenarios that may heighten suspicion of factitious disorder are those where the symptoms seem to occur or increase in severity when requests for unnecessary interventions are declined by the treatment team. Another example is a sudden increase in seizure frequency when a patient is informed that discharge from the hospital is imminent.

The prognosis of the disorder, like its etiology, is varied. With no intervention, slightly more than one-third of 260 patients with PNES were seizure-free at 1-year follow-up.

 Psychological factors that predict poor prognosis include dissociative tendencies, somatization, negativism, and depression. Keep in mind, however, that seizure frequency may not always correlate with quality of life, and patients who are seizure-free with untreated comorbid psychiatric disorders may be as impaired as those who continue to experience seizures.

Patients with PNES who receive the diagnosis without any intervention continue to be high health care utilizers; however, the chief complaint becomes pain rather than seizures.

 The frequency of total outpatient visits, while also unchanged, shifts in specialty with patients having frequent visits to outpatient psychiatry clinics rather than neurology. Having an internal locus of control and being currently employed were the 2 factors found to predict a reduction in health care utilization.

There has been a recent focus on psychoeducation and cognitive behavioral therapy (CBT) as primary methods for first-line interventions in patients with PNES. Most of the available small randomized clinical trials have shown positive results. There is also some evidence for the effectiveness of psychodynamic and mindfulness-based therapies. These specific forms of intervention may be useful if either first-line intervention is not effective or the evaluating psychiatrist deems it appropriate given the underlying psychological stressor.

Research into pharmacological treatment for PNES has focused on SSRIs as first-line treatment. LaFrance and colleagues

 randomized 34 patients to CBT only, CBT with flexible-dose sertraline, antidepressant only, and treatment as usual. Patients in the CBT-only group and the CBT-plus-flexible-dose-sertraline group showed a significant reduction in seizure frequency. In another study comprising 38 patients, LaFrance and colleagues

 found no statistical difference in the SSRI group and placebo group in seizure reduction. However, a within-group analysis showed a 45% reduction in seizure events in the SSRI group at 12 weeks.

The results from a small (N = 19) open-label, 5-month prospective study of patients with PNES showed that venlafaxine reduced the number of seizures by more than 50% in 15 patients with an average dose of 189.71 mg daily.

 It should be noted that participants with psychiatric comorbidities were not excluded from SSRI studies.

There is a possibility that the use of antidepressants in PNES could improve outcomes by treating comorbid psychiatric issues rather than by having a direct effect on PNES. The quest for a pharmacological solution for PNES will have to continue. Much more research is needed before we have a first-line pharmacological treatment specifically for PNES.

While there have been strides over the years in our ability to diagnose PNES, its etiology and treatment remain elusive. It is imperative, however, that psychiatrists assist in early diagnosis and treatment interventions to decrease the severity of burden from this disorder. The current empirical studies may help us discover what Charcot alluded to in his anecdotal experiences-that PNES may be a symptom of a variety of mental and biological processes rather than a specific disorder unto itself, requiring personalized treatments instead of a one-size-fits-all intervention. The goal for PNES treatment may also not be the complete elimination of seizures, but rather a focus on seizure reduction and patient functioning.

Dr. Abbasi is Consulting Psychiatrist for the Jefferson Comprehensive Epilepsy Center, and Assistant Professor, Psychiatry and Human Behavior, Sidney Kimmel College of Medicine at Thomas Jefferson University Hospitals, Philadelphia, PA. Dr. TsungWai is a Second-Year Resident, Department of Psychiatry and Human Behavior, Thomas Jefferson University Hospitals. 

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

 Gazzola DM, Carlson C, Rugino A, et al. Psychogenic nonepileptic seizures and chronic pain: a retrospective case-controlled study. 

 Stone J, Smyth R, Carson A, et al. La belle indiffÃ©rence in conversion symptoms and hysteria: systematic review. 

 Brown RJ, Reuber M. Towards an integrative theory of psychogenic non-epileptic seizures (PNES). 

 Brown RJ, Reuber M. Psychological and psychiatric aspects of psychogenic non-epileptic seizures (PNES): a systematic review. 

 Fiszman A, Vieira S, Leon A, et al. Traumatic events and posttraumatic stress disorder in patients with psychogenic nonepileptic seizures: a critical review. 

 Reuber M. Psychogenic nonepileptic seizures: answers and questions. 

 Duncan R, Oto M. Predictors of antecedent factors in psychogenic nonepileptic attacks: multivariate analysis. 

 LaFrance WC Jr, Baker GA, Duncan R, et al. Minimum requirements for the diagnosis of psychogenic nonepileptic seizures: a staged approach: a report from the International League Against Epilepsy Nonepileptic Seizures Task Force. 

 Reuber M, Pukrop R, Mitchell AJ, et al. Clinical significance of recurrent psychogenic nonepileptic seizure status. 

 Burneo JG, Martin R, Powell T, et al. Teddy bears: an observational finding in patients with non-epileptic events. 

 Robbins NM, Larimer P, Bourgeois JA, Lowenstein DH. Number of patient-reported allergies helps distinguish epilepsy from psychogenic nonepileptic seizures. 

 Park JH, Bokma J, Chapple K, Caplan JP. A retrospective study of polyallergy as a marker of nonepileptic seizures in the epilepsy monitoring unit. 

 Reeves AL, McAuley JW, Moore JL, Capestany J. Medication use, self-reported drug allergies, and estimated medication cost in patients with epileptic versus nonepileptic seizures. 

 Noachtar S, Peters AS. Semiology of epileptic seizures: a critical review. 

 Testa SM, Brandt J. Do patients with psychogenic nonepileptic seizures have positive covert attitudes toward sickness? 

 McKenzie P, Oto M, Russell A, et al. Early outcomes and predictors in 260 patients with psychogenic nonepileptic attacks. 

 Salinsky M, Storzbach D, Goy E, et al. Health care utilization following diagnosis of psychogenic nonepileptic seizures. 

 Duncan R, Anderson J, Cullen B, Meldrum S. Predictors of 6-month and 3-year outcomes after psychological intervention for psychogenic non epileptic seizures. 

 LaFrance WC Jr, Baird GL, Barry JJ, et al. Multicenter pilot treatment trial for psychogenic nonepileptic seizures: a randomized clinical trial. 

 LaFrance WC Jr, Keitner GI, Papandonatos GD, et al. Pilot pharmacologic randomized controlled trial for psychogenic nonepileptic seizures. 

 Pintor L, Bailles E, Matrai S, et al. Efficiency of venlafaxine in patients with psychogenic nonepileptic seizures and anxiety and/or depressive disorders. 

 Diprose W, Sundram F, Menkes DB. Psychiatric comorbidity in psychogenic monepileptic seizures compared with epilepsy. 

 DePaola L, Terra VC, Silvado CE, et al. Improving first responders’ psychogenic nonepileptic seizures diagnosis accuracy: development and validation of a 6-item bedside diagnostic tool. 

The authors shed light on a disorder that is difficult to diagnose and manage, and offer insights on how to develop an appropriate treatment plan.

Psychogenic Non-Epileptic Seizures: Clinical Issues for Psychiatrists

Catatonia, described in 1874 by K. L. Kahlbaum, is a distinct and heterogeneous neuropsychiatric syndrome, with both motoric and behavioral signs. It may be hypokinetic, hyperkinetic, or mixed and includes volitional signs, such as mutism, negativism, and automatic obedience. It was formerly relegated to a schizophrenia subtype, or considered extinct after the advent of modern psychopharmacology. Renewed interest and emerging systematic data have highlighted the frequency and pattern of catatonic presentations in psychiatric and medical settings, including in critical illness.

Historically, up to 40 signs were recognized, and most are now included in the published scales for detecting and rating the severity of catatonia. The Bush-Francis Catatonia Rating Scale (BFCRS) is widely used in both clinical and research settings, shows high inter-rater reliability and favorable sensitivity and specificity, and was validated in a mixed medical and psychiatric sample.

 The 23-item BFCRS was derived from classic descriptions of catatonia and modern diagnostic criteria. Cases are defined by the presence of 2 or more of the first 14 signs.

DSM-5 criteria require 3 or more from a similar list of 12 common catatonic signs. The BFCRS or DSM-5 items identify diverse clinical features, including motoric, behavioral, volitional, and autonomic signs. Statistical analyses identified subtypes of catatonia, including a retarded and an excited form. Malignant catatonia-a severe form with fever and autonomic instability-is uncommon but is important to identify as it may be fatal if not recognized and aggressively treated.

Despite effective treatments, patients with any form of catatonia remain at risk from serious complications such as dehydration, muscle breakdown, aspiration, or embolic phenomena. Once catatonia is recognized, these risks can be mitigated by effective treatments. Among the most studied treatment modalities, regardless of the underling etiology, prompt administration of gamma-aminobutyric acid (GABA) receptor agonists or ECT for severe or resistant cases usually relieves the symptoms and may be lifesaving.

Pathology of catatonia in the context of medical illness

The exact pathogenesis of catatonia remains unknown. Systematic examination of catatonia with genetic and brain imaging studies has been slow to develop. Familial aggregation has been reported for periodic catatonia, and preliminary evidence associated this with 15q15 chromosome.

 Single photon emission CT studies using a GABA-A ligand revealed reduced binding in areas of the frontal lobe.

 More recent studies showed increased cerebral blood flow in the supplementary motor cortex, which correlated with BFCRS severity scores, and apparent loss of frontal and insular gray matter in catatonic schizophrenia.

For catatonia in medical populations, the pattern or frequency of catatonic signs does not distinguish psychiatric from medical catatonia. A review of case reports on catatonia associated with brain lesions found an association with frontal and basal ganglia damage. The most recent systematic reports of medical catatonia confirm that non-localizing encephalopathies were the most common primary diagnoses associated with catatonia; a variety of non-specific EEG findings were also seen.

 Catatonia is generally thought to be under-recognized in the medically ill.

Of particular interest and potentially of great clinical significance is the relationship between catatonia and delirium. Delirium is the classic syndrome of acute brain dysfunction-with disturbed attention, awareness, and cognition-and is predictive of excess mortality, longer hospitalization, costlier care, and long-term cognitive impairment. While delirium is often assessed in critical settings such as the ICU, catatonia is not. Recognition and study of ICU catatonia have until recently been hindered by recent editions of DSM, which consistently hold that catatonia cannot be diagnosed in the presence of delirium. However, there is no clear evidence to support the exclusion.

Despite the DSM exclusion, delirium might coexist with catatonia, perhaps most prominently in the hypoactive motoric subtype of delirium. Hypoactive delirium includes decreased motor activity, decreased speech, and behavioral withdrawal-all of which map to catatonic features.

The first prospective report of catatonia with delirium was published in 2014.

 The data showed that 13% of 205 consecutive delirium cases met DSM-5 criteria for catatonia, and 32% met BFCRS criteria for catatonia. However, no treatment or outcome data were presented.

The many implications of more clinical attention and systematic study of comorbid delirium and catatonia include prognosis and management. For catatonia, active treatment consists of benzodiazepines (typically lorazepam) and/or ECT; antipsychotics are generally avoided because they may worsen catatonia or precipitate a lethal or malignant form similar to neuroleptic malignant syndrome (NMS). Conversely, treatment of delirium addresses the underlying medical condition and environmental factors, and antipsychotics are often used; however, benzodiazepines are generally avoided (except for known substance-withdrawal delirium).

There are no prospective data on the management or outcome of catatonia with delirium that address this apparent dilemma. However, a recent study of medical inpatients identified 54 cases of catatonia of whom 43% had a prior psychiatric history, while 54% had suspected delirium.

 When medical catatonia was compared to that attributed to psychiatric disorders, there was no statistical difference in the rates of treatment attempts using lorazepam nor in response, which was greater than 80%. However, cases of catatonia comorbid with suspected delirium were less likely to respond to lorazepam (71%) than cases without delirium (100%), regardless of etiology. While this was a retrospective study, it supports the assertion that catatonia and delirium can be comorbid and suggests that in many cases the treatment of catatonia with benzodiazepines may be successful in the presence of a delirium.

A variety of medical conditions can produce stupor, which is a decreased awareness and interaction with the external environment. Stupor can occur with preserved alertness, more often seen in catatonia, or with lethargy, more often seen in delirium. Stupor that is associated with a metabolic disorder or that is associated with delirium may present with catatonic features. The 

 presents examples of medical conditions associated with catatonia.

NMS, serotonin syndrome, and non-convulsive status epilepticus are other examples of stuporous states associated with catatonia. It may be that NMS and serotonin syndrome are actually medication-induced malignant catatonia.

Delirious mania is a rare syndrome linked to bipolar disorder characterized by the rapid onset of delirium, mania, and psychosis, with prominent hyperactive catatonia. Delirious mania can be construed as a malignant hyperactive form of catatonia, as well as a hyperactive delirium. Delirious mania has been associated with medical disorders. The newly characterized excited delirium syndrome, induced by cocaine or other stimulants, has been likened to delirious mania. Delirious mania was reported after cerebellar/pontine stroke, which produced delirium that was treated with antipsychotics that led to a catatonic state; this ultimately resolved with continuation of valproate, removal of antipsychotics, and administration of lorazepam.

Differences between etiologies (psychiatric vs medical) do not appear to alter the general treatment approach for catatonia. Removal of suspected offending agents, treatment of the underlying medical condition, or management of drug withdrawal are essential for both forms of catatonia.

For persistent catatonia, rapid initiation of lorazepam or a related benzodiazepine, which may require cautious titration to higher dosages (eg, 8 mg/d or more of lorazepam), usually leads to improvement of symptoms. Benzodiazepines (and related agents such as amobarbital and zolpidem) may counteract hypothesized GABA-receptor hypofunction in catatonia. Intravenous lorazepam has more assured absorption and may exert more prolonged clinical effects than the oral form based on differing drug distribution.

Potential adverse effects of high-dose intravenous lorazepam include anion gap acidosis from its solvent, propylene glycol. This risk increases with higher doses and in renal impairment, but toxicity has been reported with as little as 2 mg per hour. The osmolar gap (a marker for glycol toxicity) should be monitored every other day if the lorazepam infusion reaches 1 mg/kg daily.

Augmentation with memantine or amantadine may also be helpful. Their hypothesized mechanism is N-methyl-d-aspartic acid (NMDA) receptor antagonism, which may be linked to GABA hypofunction. Memantine can be started at 5 to 10 mg daily and titrated based on medical status with monitoring of the QT interval. Improvement from memantine seems slower than with lorazepam, but both can be co-administered. Amantadine is started at 100 to 200 mg daily and titrated, but it should be used with caution if renal impairment or seizure risk is present. Mania, suicidal ideation, and withdrawal-emergent NMS have also been reported with administration of amantadine.

ECT can be considered for inadequate medication response for persistent and severe catatonia and may be used more emergently for malignant features (autonomic instability and hyperthermia). Use of ECT for catatonia in medical settings or with uncertain CNS pathology should be approached cautiously, and the potential benefit weighed against the known adverse risk of severe and prolonged catatonia. Some reports show a benefit of ECT for catatonia for various acute neurological illnesses.

 However, no benefit was seen with the use of ECT in catatonia after cerebral hypoxia; in this setting, it may worsen neurological status.

Atypical antipsychotics were reported to benefit some cases of non-medical catatonia after other treatments had failed, or for coexistent catatonia and psychosis when ECT was not feasible.

 Serum iron should be measured, since low levels may be predictive of conversion to malignant catatonia. Benzodiazepines should be continued concurrently with the antipsychotic, with monitoring for extrapyramidal or autonomic symptoms that portend malignant catatonia or NMS. Antipsychotics in medical catatonia or delirium with catatonia have not been studied, and caution is advised with their use.

When medical catatonia is identified, the primary hospital service may initially resist lorazepam treatment, particularly when the patient is medically compromised. Under-dosing of lorazepam and treatment failure may result if the rationale for its use is not clearly expanded. Inviting the primary care team to witness a lorazepam or zolpidem challenge may help medical specialists appreciate that a sedating agent can improve catatonic stupor.

Frequent vital sign assessments, monitoring of the osmolar gap, and pulse oximetry can improve safety, along with ready access to flumazenil for reversal of potential adverse effects of benzodiazepines. If sedation is a concern, adding non-sedating memantine or amantadine may allow for lower benzodiazepine dosing.

When multiple hospital consultants are involved in complex cases, interdisciplinary meetings are strongly recommended. In such situations, we encourage a clear consensus that identifies specific targets for defining both treatment response and adverse effects.

Dr. Wilson is Instructor in the Department of Psychiatry and Behavioral Sciences at Vanderbilt University Medical Center, Nashville, TN. Dr. Denysenko is Assistant Professor in the Department of Psychiatry at Rowan University School of Osteopathic Medicine, Cherry Hill, NJ. Dr. Francis is Professor of Psychiatry at Penn State Medical School, Hershey, PA.

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 StÃ¶ber G, Saar K, RÃ¼schendorf F, et al. Splitting schizophrenia: periodic catatonia: susceptibility locus on chromosome 15q15. 

 Northoff G, Steinke R, Czervenka C, et al. Decreased density of GABA-A receptors in the left sensorimotor cortex in akinetic catatonia: investigation of in vivo benzodiazepine receptor binding. 

 Walther S, SchÃ¤ppi L, Federspiel A, et al. Resting-state hyperperfusion of the supplementary motor area in catatonia. 

 Smith JH, Smith VD, Philbrick KL, Kumar N. Catatonic disorder due to a general medical or psychiatric condition. 

 Llesuy JR, Coffey MJ, Jacobson KC, Cooper JJ. Suspected delirium predicts the thoroughness of catatonia evaluation. 

. November 30, 2016; Epub ahead of print.

 Grover S, Ghosh A, Ghormode D. Do patients with delirium have catatonic features? An exploratory study. 

 Bobo WV, Murphy MJ, Heckers SH. Recurring episodes of Bell’s mania after cerebrovascular accident. 

 Rasmussen KG, Hart DA, Lineberry TW. ECT in patients with psychopathology related to acute neurologic illness. 

 Quinn DK, Abbott CC. Catatonia after cerebral hypoxia: do the usual treatments apply? 

 Sienaert P, Dhossche DM, Vancampfort D, et al. A clinical review of the treatment of catatonia. 

 Denysenko L, Freudenreich O, Philbrick K, et al. Catatonia in Medically Ill Patients: An APM-EAPM Clinical Monograph. April 2015. 

http://www.apm.org/library/monographs/catatonia/Catatonia_APM-EAPM_2015-04-17.pdf

Renewed interest and emerging systematic data have highlighted the frequency and pattern of catatonic presentations in psychiatric and medical settings, including in critical illness.

Update on Medical Catatonia: Highlight on Delirium

Over 15.5 million cancer survivors are alive today in the US, which is similar to the populations of New York City, Los Angeles, and Chicago combined. The number of survivors continues to grow, not just because of earlier detection and treatment, but because of revolutionary new therapies that have been emerging over the past decade. Now, patients with poor-prognosis metastatic cancers such as lung cancer and melanoma can live many years with good quality of life while on active treatment. For many individuals, this changes the landscape from a terminal illness to more of a chronic illness.

Concurrent with advances in cancer treatment, the importance of psychosocial care of individuals with cancer is being increasingly recognized. In 2008, the Institute of Medicine published 

Cancer Care for the Whole Patient: Meeting Psychosocial Health Needs

, which documented under-detection and failure to optimally manage psychiatric disorders and psychosocial needs in patients with cancer and their families.

 Unmet needs can have negative consequences for quality of life, treatment adherence, and survival. Subsequently, the American College of Surgeons Commission on Cancer started requiring cancer centers to screen patients for psychosocial distress as part of accreditation, and the American Society of Clinical Oncology developed practice guidelines for managing depression and anxiety.

Although most cancer centers provide some psychosocial services, increased attention to the psychosocial needs of patients with cancer may result in increased referrals to mental health professionals in other settings. Some basic knowledge about a patient’s cancer and treatment are essential for psychiatric management.

Studies have documented that a cancer diagnosis results in high levels of emotional distress.

 Patients go through an adjustment period for about 4 to 6 weeks after diagnosis. Cancer for many patients is synonymous with death and debilitating treatments, with images of a prolonged painful dying process. Patients often say they feel overwhelmed trying to assimilate medical information and make treatment decisions-all while continuing to manage family, work, and other responsibilities. However, for the majority of patients, once they receive a plan of action and begin treatment, their emotions tend to level out. Yet, cancer should not be considered as one discrete crisis, but rather as a series of crises that may occur at any time in the disease trajectory from diagnosis, treatment, cycles of recurrences and remissions, post-treatment, and sometimes palliative care.

In terms of psychiatric disorders among cancer patients, there is significant variability in the prevalence rates reported due to different assessment methods (clinical interview versus standardized measures), diagnostic criteria, type of cancer, and stage of disease among other variables. Recently, Mehnert and colleagues

 reported a 31% prevalence rate for any psychiatric disorder in cancer patients. Adjustment disorders tend to be the most commonly diagnosed, with the rates ranging from 11% to 35%.5 Rates for depression vary from 11% to 37%, and anxiety disorders show rates from 2.6% to 19.4%.

 The rate for depression in the general population is 7%-and thus lower than among cancer patients-but the rates for overall anxiety disorders seem to be comparable.

The Case Vignette presents specific issues important for psychiatrists to consider when treating patients with cancer.

Mrs. T is a 53-year-old postmenopausal married woman with 2 teenage daughters who recently received a diagnosis of stage IV breast cancer metastatic to pelvic bone. Up until 2 months ago, she had been working full-time as an attorney but had to stop because of severe pain that progressively worsened. A medical workup showed an estrogen and progesterone receptor–positive, human epidermal growth factor receptor 2 (HER2)-negative tumor. She was treated with local pelvic bone radiation to help manage the pain, tamoxifen, and zoledronic acid. She was reluctant to take pain medications because of fear of addiction.

She does not have a psychiatric history or comorbid illnesses. Soon after starting tamoxifen, she began to feel very sad, anxious, irritable, and fatigued; cried easily; and had trouble sleeping because of hot flashes. She ruminates on dying and leaving her daughters. She denies hopelessness and suicidal ideation, and quite the contrary she very much wants to live.

. With the patient’s permission, consulting and informing the oncology team of your involvement is critical. As mentioned earlier, psychiatrists need to understand the patient’s cancer diagnosis, staging, treatments, adverse effects of treatment, and prognosis to appreciate the challenges the patient is coping with throughout treatment as well as survivorship or end-of-life. Medical concerns can cause or exacerbate depression and anxiety. For example, in this case, knowing that survival with metastatic breast cancer can be years is critical in providing psychiatric care for the patient. Remaining silent as the patient expresses fear of death within the next few months can be taken by the patient as agreement and can exacerbate anxiety. Psychiatrists contribute to oncology care by providing information to the oncology team regarding the patient’s emotional status and potential barriers to care and treatment adherence.

. While there may be overlap between symptoms of depression and anxiety and cancer- and treatment-related adverse effects (fatigue, changes in sleep and appetite), treatment of the psychiatric disorder is primary rather than a focus on differentiating the causes of the symptoms. The most prescribed antide­pressants in cancer patients are SSRIs, particularly escitalopram and sertraline, because of their tolerability, few drug-drug interactions (no significant inhibition of cytochrome P450 [CYP450] enzymes), and minimal discontinuation syndrome.6,8 At times the choice of an antidepressant is made based on the antidepressant adverse-effect profile. For example, mirtazapine can be sedating and cause increased appetite, which may be helpful for the cancer patient with insomnia, loss of appetite, and weight loss.

Some psychiatric medications may adversely affect the efficacy of commonly used systemic cancer therapies. Although the full clinical sig­nificance is still unclear, some SSRIs may interfere with tamoxifen being metabolized into its active metabolite, endoxifen, through inhibition of CYP2D6. Venlafaxine may be a good option in this situation, especially with evidence that it reduces hot flashes, another adverse effect of treatment.

Be aware that some systemic cancer treatments are associated with psychiatric adverse effects. Vincristine and vinblastine, used to treat leukemia and some lymphomas, may cause depression. Interferon at high doses can cause depression and even suicidal ideation. The chemotherapy agent procarbazine at high doses can cause lethargy, depression, mania, confusion, and hallucinations. It crosses the blood-brain barrier and acts as a monoamine oxidase inhibitor, so it can potentiate the effects of alcohol, opioids, and tricyclic antidepressants. Glucocorticosteroids such as prednisone and dexamethasone are widely used in cancer care. They can cause a range of psychiatric symptoms, from emotional lability, depression, anxiety, restlessness, irritability, and insomnia to paranoia, delusions, and hallucinations. Symptoms may develop within a couple of days of the start of treatment and are also common if the dose is rapidly tapered off. But psychiatric symptoms can develop even on a stable dose.

. Suffering from uncontrollable pain is one of the most common fears of cancer patients. Unfortunately, pain is under-recognized and undertreated in patients with cancer. Bone pain experienced by cancer patients can be excruciating, and explaining to the patient that at times she may need to use opioids under the care of her oncologist without fearing addiction can prevent the patient from suffering unnecessarily. Poorly managed pain can lead to depression and anxiety. Once pain is appropriately managed, depressive and anxiety symptoms often diminish or resolve.

While some psychiatrists and oncologists have expertise in pain management, others may not and are reluctant to prescribe the necessary medications at the appropriate doses. Speaking with the oncology team and helping to get appropriate referral to a cancer pain specialist or palliative care team is crucial to the quality of life of cancer patients, especially those with advanced disease.

Before the patient’s visit with the pain specialist, it is helpful for the psychiatrist to provide education and correct some common misconceptions. The following 3 key issues should be considered regarding referral for pain management:

 A majority of cancer patients do not have a history of addiction and actually fear becoming addicted to pain medications

 Patients view the taking of pain medications as associated with death and dying: “Only a patient who is dying takes morphine”

 Patients may need education on the difference between addiction and tolerance, in order to comply with prescribed pain medications

Psychiatrists need to understand the patient’s cancer diagnosis, staging, treatments and their adverse effects, and prognosis to appreciate the challenges the patient is coping with throughout treatment as well as survivorship or end-of-life.

Somatoform Disorder