Insights & Implications in Gerontology: Understanding Pseudobulbar Affect by GSAStrategicAlliances

insights

JULY 2022

& Implications

I N GERONTOLOGY

faculty

Jill Farmer, DO, MPH

Director, Parkinson’s Disease and Movement Disorders Program Global Neurosciences Institute Assistant Professor of Neurology Drexel University College of Medicine

Lynn Shaughnessy, PsyD, ABPP/CN

Director, Neuropsychology Cognitive Neurology Unit Beth Israel Deaconess Medical Center Instructor, Harvard Medical School

Michael Sarai, DO

Geriatric Medicine Fellow Department of Internal Medicine Saint Louis University School of Medicine

Understanding Pseudobulbar Affect What is PBA? Pseudobulbar affect (PBA) is a condition characterized by bouts of uncontrolled crying or laughing that are disproportionate or inappropriate to the social context and are not associated with depression or anxiety.1,2 Episodes of laughing or crying are often disconnected to the mood or feelings of the individual, with intense crying or laughing that persists for

some time and cannot be suppressed (Figure 1). For example, an experience that might typically result in a sad sigh could trigger uncontrolled weeping. Patients may describe the laughter or crying as “coming out of nowhere,” or report that “I get set off by little things and I can’t stop it.” The symptoms of PBA can be severe, with persistent, unremitting episodes having a sudden or unpredictable onset.1 Outbursts might last a few seconds to several minutes and can occur several times daily. Other terms that have been used to describe PBA include involuntary emotional expression disorder, emotional lability, emotional dysregulation, pathological laughter and crying, emotional incontinence, and emotionalism.2

George T. Grossberg, MD

Professor and Director of Geriatric Psychiatry Department of Psychiatry and Behavioral Neuroscience Saint Louis University School of Medicine

Figure 1. Symptoms of Pseudobulbar Affect

Excessive crying in response to mildly sad or touching situations

Uncontrollable laughter in response to mildly amusing situations

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Episodes of crying or laughter may persist for several minutes

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contents

This publication is available on www.geron.org/insights

What is PBA?

Diagnosing PBA

Interdisciplinary Insight: Being Alert for PBA

Options for Treating PBA

Interdisciplinary Insight: Managing Medications in Patients With PBA

Brain Health and PBA

Summary

Resources

PBA typically occurs in patients who have a brain injury or neurologic disorder, such as amyotrophic lateral sclerosis (ALS), extrapyramidal and cerebellar disorders (e.g., Parkinson’s disease, multiple system atrophy, progressive supranuclear palsy), multiple sclerosis (MS), traumatic brain injury, Alzheimer’s disease and other dementias, stroke, and brain tumors.2 The exact cause is unknown, but it appears that the disease or injury disrupts the neural networks and neurotransmitters that are responsible for expression of emotion, especially in the cerebellum.2

In patients with PBA, serotonin, norepinephrine, and dopamine levels are decreased and glutamate levels are increased, which results in socially inappropriate or situationally disproportionate emotional expression. The cerebellum, which plays a role in modulating emotional responses, is involved with pathways that are affected by these neurotransmitters.2,3 This disruption lowers inhibitory mechanisms, which lowers the threshold for activating laughing or crying pathways in the brainstem that do not align with the patient’s actual feelings (Figure 2).4,5

Figure 2. Disrupted Neural Pathways in PBA

PBA = pseudobulbar affect. Source: Pseudobulbar affect: the spectrum of clinical presentations, etiologies and treatments. Miller, A., Pratt, H., & Schiffer, R.B., Expert Review of Neurotherapeutics. January 9, 2014, Taylor & Francis Ltd, http://www.tandfonline.com, reprinted with permission of the publisher.

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An estimated 2 million to 7 million individuals in the United States have PBA.3 Prevalence varies among populations with various neurologic disorders. For example, PBA has been estimated to occur in approximately 10% of patients with MS and up to 50% of patients with ALS.1,6 An online survey of 2,318 patients with Alzheimer’s disease, ALS, MS, Parkinson’s disease, stroke, or traumatic brain injury found that the prevalence ranged from 9.4% to 37.5%, depending on which screening instrument and threshold was used.6 PBA symptoms can cause embarrassment for the patient, family, and caregivers, resulting in restricted social interactions, withdrawal, and social isolation. Thus, patients with neurologic disorders and PBA experience additional burden of disease and reduced quality of life.2 Patients with PBA have higher levels of anxiety, higher prevalence of psychiatric disorders (e.g., clinical depression), and poorer social functioning than those without PBA.2 Clinicians who recognize PBA and offer treatment to affected patients have the potential to improve patient well-being. Early detection and management of PBA is important for minimizing the impact on quality of life and the patient’s social networks.

Diagnosing PBA PBA is typically diagnosed based on patient history as part of a neurologic evaluation by a clinician such as an internist or a specialist such as a neuropsychologist, neurologist, or psychiatrist. However, it is often underdiagnosed or misdiagnosed and can be mistaken for mood disorders (e.g., depression, bipolar disorder) or post-traumatic stress disorder. Further, PBA is often undertreated even when it has been diagnosed.6 Importantly, PBA can often co-occur with depression and other mood disorders, but it can be distinguished from depression based on several criteria (Table 1).7,8

Criteria used for diagnosing PBA include:3

• Is the emotional response (crying or laughing) occurring involuntarily, suddenly, and without the patient’s ability to control the emotion?

• Is the emotional response inconsistent with or

disproportionate to the patient’s mood or inner feelings?

• Does expression of the emotion provide a feeling of relief?

• Does the emotional response cause significant distress or limit the ability to work or interact socially?

• Is the emotional response caused by another psychiatric or neurologic disorder?

• Is the emotional response due to a drug? Validated rating scales for assessing PBA have also been developed, including the Center for Neurologic Study–Lability Scale (CNS-LS) and the Pathological Laughter and Crying Scale (PLACS).9,10 These scales can help to assess the extent to which patients’ symptoms align with these criteria. The CNS-LS is a self-administered survey that assesses control of laughter and crying with total scores ranging from 7 (no excess emotional lability) to 35 (severe excess emotional lability).9 Patients use a 5-point Likert scale (1 = never, 2 = rarely, 3 = occasionally, 4 = frequently, 5 = most of the time) to indicate whether the following items apply:

• There are times when I feel fine 1 minute, and then I’ll become tearful the next over something small or for no reason at all.

• Others have told me that I seem to become

amused very easily or that I seem to become amused about things that really aren’t funny.

• I find myself crying very easily.

An estimated 2 million to 7 million individuals in the United States have PBA.3 Prevalence varies among populations with various neurologic disorders.

• I find that even when I try to control my laughter, I am often unable to do so.

• There are times when I won’t be thinking of any-

thing happy or funny at all, but then I’ll suddenly be overcome by funny or happy thoughts.

• I find that even when I try to control my crying, I am often unable to do so.

• I find that I am easily overcome by laughter. insights & Implications IN GERONTOLOGY

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Understanding Pseudobulbar Affect

Table 1. Distinguishing Between PBA and Depression

Clinical Component

PBA

Depression

Spectrum of emotional lability

Crying, laughing, or both

Crying, loss of interest, thoughts of worthlessness or suicide

Episode duration

Seconds to minutes, sporadic

Weeks to months

Stimulus

No evident stimuli

Specific mood-related scenarios

Episode control

None

Coping mechanisms may shorten episodes

Underlying neurologic condition

Neurologic disease of brain injury always present

May or may not possess underlying neurologic condition

Affect

Exaggerated or incongruent with situational context

Flattened, saddened, or apprehensive; rarely demonstrate elation

Thoughts of death, dying, or suicide

Absent

May be present

Appetite

Usually unaffected

May be increased or decreased

PBA = pseudobulbar affect. Source: References 7 and 8.

A score of 13 or greater was found to predict neurologists’ clinical diagnoses of PBA in 82% of patients with ALS, but produced more false positives in patients with MS. A score of 17 in patients with MS reduced false positives without reducing sensitivity.

• Have these episodes occurred without any cause

The 18-item PLACS is an interviewer-administered tool that assesses sudden episodes of laughter and crying. A cutoff score of 13 was associated with high sensitivity and specificity in patients with stroke.10 Clinicians ask patients two questions to determine the frequency of sudden episodes of laughter or crying. Patients who report that they experience such episodes are also asked to respond to the following questions about the episodes using a 4-point Likert scale (0 = rarely or not at all, 1 = occasionally, 2 = quite often, 3 = frequently):10

• Have these episodes been uncontrollable

in your surroundings?

• Have these episodes lasted for a long period of time?

by you?

• Have these episodes occurred as a result of feelings of happiness/sadness?

• Have these episodes occurred in excess of feelings of happiness/sadness?

• Have these episodes of crying/laughter

occurred with feelings of sadness/happiness?

• Have these episodes occurred with any

emotions other than happiness or sadness, such as nervousness, anger, fear, etc.?

• Have these episodes caused you any distress or social embarrassment?

Depending on the underlying neurologic condition, patients may be unaware of their symptoms or lack insight into their experience. In such situations, gathering information from reliable informants, such as family or caregivers, can help inform the diagnosis.

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Interdisciplinary Insight: Being Alert for PBA As a neurologist who specializes in Parkinson’s disease (PD), Jill Farmer, DO, MPH, frequently sees patients with pseudobulbar affect (PBA). “PBA is a common condition associated with multiple other neurologic conditions and it should be one of the foundational considerations when evaluating patients,” she observes. “It is a pathway problem in the brain commonly seen in patients with neurodegenerative disease or structural abnormalities due to conditions such as traumatic brain injury, tumor, or stroke,” she explains. Dr. Farmer notes that although PBA is not as common as anxiety or depression in patients with PD, it does impact roughly 10% to 15% of the patients who she sees at the Global Neurosciences Institute. Distinguishing PBA from depression or anxiety can sometimes be a challenge. “In an ideal world, I would work with a psychologist or psychiatrist to diagnose patients, but access is a huge challenge.” The assessment of patients with neurologic conditions should incorporate questions about mood and emotion, including assessment of whether responses to certain environments are out of proportion to what would be expected for other conditions such as anxiety and depression. In some cases, distinguishing PBA from depression is difficult, and a diagnosis of PBA is arrived at empirically based on response to treatment. “Because the treatment of PBA is very simple, I will sometimes initiate treatment if I suspect PBA. If the medication reduces the occurrence of episodes, it confirms the diagnosis of PBA,” explains Dr. Farmer. “On the other hand, if the medication does not have an impact, we can discontinue it.” Regardless, it is essential to concomitantly manage all comorbid conditions.

For example, patients with diagnosed depression may continue to have crying episodes despite effective treatment of depression. Consideration of a PBA diagnosis is relevant in these situations of continued emotional lability. In other cases, a diagnosis of PBA may be suspected based on actual observation of episodes during clinical encounters. Dr. Farmer describes a patient case:

“I had a patient, M.P., with young-onset PD in her late 50s. M.P. was originally diagnosed with Alzheimer’s and severe depression. After a thorough evaluation, we determined that she had PD and not Alzheimer’s. Her cognition was not substantially impaired, although we considered that she may have had a pseudodementia due to untreated depression. M.P. had a lot of anger about her diagnosis and would cry frequently. We initially considered that these symptoms were a component of the mood disorder. “We initiated treatment for PD with a dopamine agonist to address tremor. M.P. also received speech therapy, physical therapy, and cognitive therapy. Although she responded well to these interventions and said her mood felt better, she still experienced frequent crying episodes. Based on the ongoing crying episodes, we realized that she had comorbid PBA and initiated medication therapy. “M.P. has continued medication therapy for PBA for years now. She still fluctuates with her mood, but outbursts and crying are still reduced significantly. We continue to monitor her response to treatment and include discussion of the purpose of all her medications during regular medication reviews every 3 to 4 months.”

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Understanding Pseudobulbar Affect

Options for Treating PBA Goals of treatment for PBA include reducing severity and frequency of episodes. Behavioral strategies should always be considered for patients and caregivers—particularly when symptoms are mild or do not impact the patient’s quality of life—and may be adequate for treatment of PBA. Pharmacologic options may also provide benefit for appropriate patients. Implementing nonpharmacologic behavioral strategies along with pharmacologic treatment may produce a synergistic effect.

Behavioral Strategies

Behavioral strategies for patients with PBA include educating family and friends so that they better understand the condition, its symptoms, and expectations for behavior, including how to respond during an episode. The preferred responses to episodes should be discussed in advance with the person with PBA. Strategies to help the patient cope with an episode include relaxation practices (e.g., slow deep breathing) and distraction techniques (e.g., thinking or focusing on something else, changing body position). Mindfulness techniques, such as grounding, may also be helpful. Patients may want to remove themselves from social situations until episodes pass. Behavioral interventions for PBA can include occupational therapy designed to help patients perform everyday tasks. For some patients, maintaining a diary to track when symptoms occur, along with preceding factors, can help to identify episode triggers (that may possibly be avoided in the future). Caregivers can support a loved one with reassurances that they understand the emotional episodes cannot be avoided through self-control and are not the person’s fault. Caregivers should assure the patient that they are not embarrassed by the episodes. They can support the patient in social situations by making plans for how to manage episodes, if they arise. For example, determining when to leave a situation and knowing alternate locations for privacy can be helpful. Caregivers should communicate with the patient to learn how that individual wants personal information about the condition shared with others. In some cases, patients or caregivers carry a card explaining the condition, which can be handed to observers when episodes occur.

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Pharmacologic Options

There are several pharmacologic options for the management of PBA (Figure 3).1,2,11-13 The appropriate selection of medications to treat PBA includes consideration of drug–drug interactions, adverse effects, impact on patient comorbidities (including neurologic conditions), contraindications, and impact on symptoms of PBA. Because dextromethorphan/ quinidine is currently the only medication approved by the U.S. Food and Drug Administration (FDA) for the treatment of PBA, it is often used as first-line therapy (Figure 3). Dextromethorphan hydrobromide 20 mg combined with quinidine sulfate 10 mg (DMQ; Nuedexta) is available as a capsule for oral administration. Dextromethorphan is a sigma-1 receptor agonist and an uncompetitive N-methyl-d-aspartate (NMDA) receptor antagonist with an unknown mechanism of action in the treatment of PBA. Dextromethorphan increases levels of serotonin and norepinephrine while inhibiting excessive glutamate activity. Quinidine is an inhibitor of cytochrome P450 2D6 (CYP2D6), which increases and prolongs plasma concentrations and half-life of dextromethorphan.1,11 The recommended starting dose of DMQ is one capsule daily by mouth for the initial seven days of therapy. On the eighth day of therapy and thereafter, the daily dose should be a total of two capsules a day, given as one capsule every 12 hours. The need for continued treatment should be reassessed periodically, as spontaneous improvement of PBA occurs in some patients.1 Three clinical trials of DMQ found patients experienced significant reductions in the rate of PBA episodes, compared with patients who received placebo, as well as more episode-free days and rates of remission at 12 weeks.1 In the first (dose-ranging) trial of 326 patients, mean changes from baseline in the number of laughing and crying episodes per day after 12 weeks of treatment were −4.1 (P = 0.0099) in the dextromethorphan 30mg/quinidine 10-mg arm, −3.9 (P = 0.0048) for the dextromethorphan 20-mg/quinidine 10-mg arm, and −3 (P = 0.0099) in the placebo arm. The mean change from baseline in CNS-LS scores was −8.2 for dextromethorphan 30 mg/quinidine 10 mg (P = 0.0002), −8.2 for dextromethorphan 20 mg/quinidine 10 mg (P = 0.0113), and −5.7 for placebo.1

Figure 3. PBA Treatment Algorithm

First-line treatment

Second-line treatment

Third-line treatment

• Dextromethorphan/ quinidine

• Selective serotonin reuptake inhibitors or • Tricyclic antidepressants

• Levodopa, reboxetine, venlafaxine, mirtazapine, lamotrigine, methylphenidate, dexamphetamine, or amantadine

For all patients, incorporate behavioral management strategies and caregiver support When selecting medications, consider: drug-drug interactions, advere effects, impact on patient comorbidities (including neurological conditions), contraindications, and impact on symptoms of PBA

PBA = pseudobulbar affect. Sources: References 1, 2, 11-13.

In the second study of 150 patients with MS, adjusted mean changes from baseline in CNS-LS scores were 7.7 in the dextromethorphan/quinidine group and 3.3 in the placebo group, (P <0.0001). The mean numbers of episodes per week of inappropriate crying and laughing were 4.7 ± 10.9 with the study drug and 11.5 ± 19.4 with placebo (P = 0.0002).1 In the third study of 140 patients with ALS, adjusted mean changes from baseline in CNS-LS scores were 7.4, 4.1 (P = 0.001), and 3.7 (P <0.001) for dextromethorphan/quinidine 10 mg, dextromethorphan, and quinidine, respectively.1 DMQ was generally well tolerated in clinical trials.11 Among adverse events reported by 5% or more of patients in the dose-ranging study, dizziness and diarrhea were more frequent in both DMQ groups than in the placebo group. Nausea and urinary tract infections were highest in the DMQ 30-mg/10-mg group but were comparable to placebo in the 20-mg/10-mg group.11 DMQ is contraindicated in patients with:

• Concomitant use of other medications that

contain quinidine, quinine, or mefloquine; prolong the QTc interval; or are metabolized by the CYP2D6 isoenzyme, such as thioridazine and pimozide because of the potential additive effects on the QTc interval. (Patients’ entire medication regimens should be assessed for potential drug interactions. For example, post-stroke patients may be on digoxin; quinidine increases digoxin levels.)

• History of thrombocytopenia, hepatitis, bone

marrow depression, or lupus-like syndrome induced by the quinidine-related drugs mentioned.

• Concomitant use of monoamine oxidase (MAO)

inhibitors or the recent use of MAO inhibitors within 14 days. (The interaction applies to general MAO inhibitors and not selective MAO type B inhibitors, which are commonly used by patients with Parkinson’s disease.)

• Hypersensitivity to dextromethorphan, as

commonly seen in over-the-counter cough preparations.

• History of atrioventricular (AV) block (complete,

without implanted pacemaker) or at high risk of AV block.

• Heart failure. • Prolonged QTc interval, congenital long-QTc syn-

drome, or history suggesting torsades de pointes.

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Understanding Pseudobulbar Affect

Importantly, quinidine inhibits CYP2D6. Therefore, the patient’s care team should assess the metabolism of other medications that the patient takes before starting DMQ; dosage adjustments may be necessary to maintain the efficacy and safety of these medications. (Approximately 25% of medications are metabolized by CYP2D6, including antipsychotic/dopamine antagonists, antiarrhythmics, beta-blockers, neuroleptics, tricyclic antidepressants [TCAs], and selective serotonin reuptake inhibitors [SSRIs].12) Additionally, quinidine is a substrate for CYP3A4. Other medications that inhibit or induce CYP3A4 (e.g., amiodarone, clarithromycin) may impact quinidine’s metabolism.12 According to the DMQ package labeling, “approximately 7% to 10% of Caucasians and 3% to 8% of African Americans lack the capacity to metabolize CYP2D6 substrates and are classified as poor metabolizers (PMs). The quinidine component of [DMQ] is not expected to contribute to the effectiveness of [DMQ] in PMs, but adverse events of the quinidine are still possible. In those patients who may be at risk of significant toxicity due to quinidine, genotyping to determine if they are PMs should be considered prior to making the decision to treat with [DMQ].” Medications that are used off-label for the treatment of PBA include various antidepressants such as SSRIs (e.g., citalopram, fluoxetine, sertraline, fluvoxamine), TCAs (e.g., nortriptyline), and norepinephrine/serotonin reuptake inhibitors (e.g., venlafaxine, duloxetine). In patients with comorbid depression, improvement in emotional lability seen with antidepressants is independent of depression status.10 Antidepressants increase levels of neurotransmitters, including serotonin and norepinephrine in the corticolimbic and cerebellar pathways of the brain.

Dosages of antidepressants for treating PBA (Table 2) are lower than those used for treating depression. Data to support the use of these agents are limited to small trials and case studies.12 Adverse events that are common with SSRIs include insomnia, drowsiness, anxiety, headache, and diarrhea. Those associated with TCAs include weight gain, hypotension, dry mouth, constipation, confusion, sedation, sleep disturbances, and potential cardiotoxicity. Frequency and severity of adverse events vary among agents.12 Other pharmacologic treatments may be attempted if initial treatments are ineffective or cannot be tolerated.2 These treatments include levodopa, reboxetine, venlafaxine, mirtazapine, lamotrigine, methylphenidate, dexamphetamine, and amantadine.13

Guidelines for Treating PBA

There are few guidelines that address the treatment of PBA. Those that exist are specific to the presence of PBA in certain conditions, including the American Academy of Neurology (AAN) guideline for the care of patients with ALS and the AAN guideline for management of psychiatric disorders in patients with MS.14,15 The AAN guideline for ALS was published in 2009 before DMQ was approved and states that, “For treatment of pseudobulbar affect, dextromethorphan and quinidine should be considered if approved by the U.S. Food and Drug Administration.” The authors note that DMQ “is probably effective for pseudobulbar affect in ALS” and include a recommendation stating, “if side effects are acceptable, DMQ should be considered for symptoms of pseudobulbar affect in patients with ALS (Level B).”14 The AAN guideline for psychiatric disorders in MS provides a Level C recommendation, describing DMQ “is possibly effective and safe and may be considered for treating individuals with MS with PBA.”15 This more recent guideline also recognizes that SSRIs and TCAs are used in clinical practice, but notes that there are not any published randomized placebo-controlled trials to support their use.15

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Table 2. Common Antidepressant Dosages Used in the Treatment of Pseudobulbar Affect

Medication

Dosage Range

Selective Serotonin Reuptake Inhibitors Citalopram

10–20 mg/day

Fluoxetine

20–40 mg/day

Fluvoxamine

100 mg/day

Sertraline

50–100 mg/day

Tricyclic Antidepressant Nortriptyline

20–100 mg/day

Source: References 8 and 12.

Interdisciplinary Insight: Managing Medications in Patients With PBA Because PBA typically occurs in patients who are taking medications for multiple conditions, the risks of polypharmacy are increased.

Patient Case: Polypharmacy Presentation

G.L. is a 72-year-old woman with a 2-day history of altered mental status presenting to the emergency department (ED) from a nursing home.

Past Medical History

G.L.’s past medical history includes heart failure and atrial fibrillation. She was hospitalized 4 weeks ago due to a stroke and subsequently discharged to the nursing home for physical therapy. Her nursing home course was complicated by PBA and failure to thrive, manifesting as lethargy and weight loss. Her medications in the nursing home included dabigatran, diltiazem, digoxin, bumetanide, simvastatin, losartan, and dextromethorphan/quinidine.

Patient Assessment

In the ED, G.L.’s physical exam was notable for bradycardia (heart rate in the 30s) and bilateral lower extremity edema. Initial lab work was notable for hypokalemia and elevated creatinine levels. Geriatric medicine was consulted for further work-up of her bradycardia, delirium, failure to thrive, and acute kidney injury. In the telemetry unit, G.L. had multiple arrhythmias, including sinus bradycardia, AV block, and frequent bigeminy. The digoxin level was 2 ng/mL. Her arrhythmias, failure to thrive, and weight loss were attributed to digoxin toxicity. Digoxin was discontinued before discharge.

Comments

G.L. had multiple risk factors for digoxin toxicity, including concomitant prescription of dextromethorphan/quinidine. Quinidine is a P-glycoprotein inhibitor and, therefore, may increase the serum concentration of digoxin. Prescribers must be attentive to drug interactions when prescribing dextromethorphan/quinidine for medically complex patients.

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Understanding Pseudobulbar Affect

Brain Health and PBA

Brain health may be defined as “a state of complete physical, mental, and social wellbeing through the continuous development and exercise of the brain.”16

Health care providers are increasingly recognizing PBA as a behavioral symptom that is connected to brain health, and they are assessing for PBA as part of brain health management efforts. Brain health may be defined as “a state of complete physical, mental, and social wellbeing through the continuous development and exercise of the brain.”16 This definition combines neurologic, psychiatric, and social concepts to take a broader view of well-being.16 Addressing all of these elements in a unified approach is intended to support overall brain health. Strategies that manage health and wellness overall (e.g., exercise, social stimulation, management of vascular risk factors) are also important for primary prevention of multiple neurologic conditions. To achieve greater awareness of cognition and brain health in older adults, The Gerontological Society of America Workgroup on Cognitive Impairment Detection and Earlier Diagnosis created the KAER framework. This framework encourages individuals to be more aware of brain health–related changes and creates an environment where patients may feel more comfortable sharing their concerns. The KAER framework has four steps—Kickstart, Assess, Evaluate, and Refer—that are intended to improve health‐related outcomes and well‐being. These steps may increase detection of cognitive impairment, initiate earlier diagnostic evaluation, and generate referrals for educational and supportive community services related to brain health.17

This framework can be used to incorporate assessment for PBA as a part of overall brain health assessments. Clinicians can ask patients and caregivers questions about emotional expression such as:

• Have you noticed any changes in your emotional expression that concern you?

• In the past few months, have you had problems

with episodes of uncontrolled laughing or crying?

Note that the first question asks about concerns and the second question asks whether the patient is experiencing problems. Additionally, regular screenings conducted for patients with neurologic conditions could include a question about PBA symptoms such as:

• Can you tell me about any changes in your laughter or crying since the onset of your [underlying neurologic diagnosis or brain injury]?

If patients report concerns about uncontrolled bouts of laughter or crying, a validated screening tool may be used for assessment. Care providers (including family members and staff at long-term care facilities who observe patients laughing or crying inappropriately) may consider having the patient evaluated for PBA, especially if the patient has a neurologic condition or brain injury. Further, it is important to recognize that PBA often occurs in conjunction with cognitive symptoms and frontally mediated cognitive challenges that can further impact patient care and quality of life. Finally, managing PBA can be difficult due to the heterogeneity of comorbid conditions with which it may be associated. Patients are often seen by multiple health care providers to manage various conditions. Therefore, interprofessional care is essential to support collaborative team care for the patient (Figure 4).

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Resources

Figure 4. Interprofessional Wheel of Care Primary Care Provider

Disease-Specific Resources Neurologists/ Other Specialists

Caregivers

Alzheimer’s Association www.alz.org

American Stroke Association

P AT I E N T

Nurses

Occupational Therapists

www.stroke.org/en/about-stroke/effects-of-stroke/emotional-effects-ofstroke/pseudobulbar-affect

National Multiple Sclerosis Society Social Workers Pharmacists

https://www.nationalmssociety.org/NationalMSSociety/media/MSNationalFiles/ Brochures/Clinical_Bulletin_Pseudobulbar-Affect-Uncontrollable-Laughingand-or-Crying.pdf

PBA Info www.pbainfo.org

Summary PBA is a relatively common disorder in patients with neurologic conditions that can have a substantial negative impact on quality of life.

Pseudobulbar Affect in Alzheimer’s Disease alzheimersnewstoday.com/pseudobulbar-affect-alzheimers-disease/

Pseudobulbar Affect in Parkinson’s Disease www.parkinsonsnewstoday.com/pseudobulbar-affect-parkisons-disease/

Treatment options available for PBA can reduce symptoms and improve quality of life. Coordinated care from the interprofessional health care team, along with the patient’s caregivers, can optimize management and outcomes for patients. However, PBA is often underrecognized and undertreated. Incorporation of screening questions into regular health assessments can help to identify patients who can benefit from interventions to manage PBA.

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Resources for Caregivers

Caregiver Action network www.caregiveraction.org

National Alliance for Caregiving www.caregiving.org

Our PBA Support Group (Facebook Private Group) www.facebook.com/groups/ourpbasupportgroup/

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Understanding Pseudobulbar Affect

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