The Impact of PBA on your Patients is Substantial1

Actor portrayal of patient with PseudoBulbar Affect (PBA) crying symptoms

Pseudobulbar affect (PBA) is not to be taken lightly. The uncontrolled laughing and/or crying episodes have a substantial impact—resulting in embarrassment for the patient and family. Because of the fear of having a PBA episode in public, patients may restrict their social interactions.

Patients with neurologic conditions including but not limited to stroke, dementia, traumatic brain injury (TBI), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), or multiple sclerosis (MS) may also be struggling with involuntary, sudden, frequent episodes of laughing and/or crying—treatable symptoms suggestive of PBA.

Robert, a real patient with Pseudobulbar Affect
Read all about Robert, a 64-year-old retired army paratrooper who suffered from PBA for 25 years.

Patients describe PBA in their own words

These short videos of real patients discussing PBA with an interviewer shed light on how PBA affects everyday life.

A real patient with TBI and PBA
Listen to a patient describe in her own words how PBA affected her life before she received treatment with NUEDEXTA.
A real resident who suffered a stroke and was diagnosed with PBA
Watch a resident in a long-term care facility discuss how her PBA symptoms impacted her life.
Real nurse discussing impact of Pseudobulbar affect on a resident of long-term care facility
A nurse talks about resident impact
Listen to Nurse Practitioner Cathy talk about a resident who suffered from the PBA symptoms of inappropriate laughing at inappropriate volume, and the impact this had on the resident's life.

PBA symptoms are prevalent in patients with various underlying neurologic conditions


The prevalence of PBA in the US is approximately 2 million among patients with underlying conditions. In a multicenter registry (N=5290), a CNS-LS score ≥13, suggesting the presence of PBA symptoms, was reported in 37% of patients with any 1 of 6 neurologic conditions.3,4

Presence of PBA symptoms in select neurologic conditions4,a

Neurologic Condition (n, mean age of patients)
CNS-LS ≥ 13
CNS-LS ≥ 21
Mean years from primary condition diagnosis to study enrollment
Traumatic brain injury (n=590, 46 yrs)
10.3 (n=347)
Multiple sclerosis (n=1215, 49 yrs)
9.9 (n=785)
Amyotrophic lateral sclerosis (n=125, 60 yrs)
2.3 (n=108)
Stroke (n=757, 68 yrs)
4.6 (n=395)
Alzheimer's disease (n=1799, 79 yrs)
3.7 (n=656)
Parkinson's disease (n=804, 73 yrs)
5.3 (n=386)

aCenter for Neurologic Study-Lability Scale (CNS-LS) is a 7-item self-report rating scale that measures perceived frequency and control over laughing and/or crying episodes. It was validated as a PBA screening tool in ALS and MS populations. The presence of PBA symptoms (uncontrollable episodes of laughing and/or crying) was defined as a CNS-LS score ≥13. Higher CNS-LS scores are indicative of more frequent uncontrollable laughing episodes or both laughing and crying episodes. This scale does not confer a PBA diagnosis.4,6-8

PRISM Study Design

PBA and the Brain

Neural damage can affect control over emotional expression9

PBA may involve a disruption of certain neurotransmitter functions1

Glutamate is thought to be one of the major neurotransmitters involved in PBA. N-methyl-D-aspartate (NMDA) is one of the main neurotransmitter receptors for glutamate.1 Glutamate receptors, including NMDA, exist throughout the brain and are also found in the neural network where PBA is thought to arise.1,11 Dextromethorphan (DM) is a sigma-1 receptor agonist and an uncompetitive NMDA receptor antagonist.2

Normal Glutamate Signaling
Normal Glutamate Signaling

Glutamate receptors, such as NMDA, are responsible for facilitating many neurologic functions, including emotional expression.9,12 Glutamate exerts its signaling function by binding to and activating receptor proteins.11

Abnormal Glutamate Signaling
Abnormal Glutamate Signaling

In a variety of neurologic conditions and brain injuries, including stroke and various neurodegenerative disorders, excess glutamate and excessive activation of glutamate receptors may lead to abnormal neurotransmission and cell dysfunction.11,12

References: 1. Ahmed A, Simmons Z. Pseudobulbar affect: prevalence and management. Ther Clin Risk Manag. 2013;9(1):483-489. 2. NUEDEXTA [package insert]. Aliso Viejo, CA: Avanir Pharmaceuticals, Inc. 3. Work SS, Colamonico JA, Bradley WG, Kaye RE. Pseudobulbar affect: an under-recognized and under-treated neurological disorder. Adv Ther. 2011;28(7):586-601. 4. Brooks BR, Crumpacker D, Fellus J, Kantor D, Kaye RE. PRISM: a novel research tool to assess the prevalence of pseudobulbar affect symptoms across neurological conditions. PLoS ONE. 2013;8(8):e72232. 5. Foley K, Konetzka T, Bunin A, Yonan C. Prevalence of pseudobulbar affect symptoms and clinical correlates in nursing home residents. Int J Geriatr Psychiatry. 2016;31(7):694-701. 6. Moore SR, Gresham LS, Bromberg MB, Kasarkis EJ, Smith RA. A self report measure of affective lability. J Neurol Neurosurg Psychiatry. 1997;63(1):89-93. 7. Smith RA, Berg JE, Pope LE, Callahan JD, Wynn D, Thisted RA. Validation of the CNS emotional lability scale for pseudobulbar affect (pathological laughing and crying) in multiple sclerosis patients. Mult Scler. 2004;10(6):679-685. 8. Smith RA, Berg JE, Pope LE, Thisted RA. Measuring pseudobulbar affect in ALS. Amyotroph Lateral Scler Other Motor Neuron Disord. 2004;5(suppl 1):99-102. 9. Miller A, Pratt H, Schiffer RB. Pseudobulbar affect: the spectrum of clinical presentations, etiologies and treatments. Expert Rev Neurother. 2011;11(7):1077-1088. 10. Purves D. Emotions. In: Purves D, Augustine G, Fitzpatrick D, Hall WC, LaMantia AS, White LE, eds. Neuroscience. 5th ed. Sunderland, MA: Sinauer Associates; 2011:647-667. 11. Pankevich DE, Davis M, Altevogt BM; for the Institute of Medicine Forum on Neuroscience and Nervous System Disorders. Glutamate-Related Biomarkers in Drug Development for Disorders of the Nervous System: Workshop Summary. Washington, DC: The National Academies Press; 2011. 12. Nguyen L, Lucke-Wold BP, Mookerjee SA, et al. Role of sigma-1 receptors in neurodegenerative diseases. J Pharmacol Sci. 2015;127(1):17-29.


NUEDEXTA® (dextromethorphan HBr and quinidine sulfate) is indicated for the treatment of pseudobulbar affect (PBA). PBA occurs secondary to a variety of otherwise unrelated neurologic conditions, and is characterized by involuntary, sudden, and frequent episodes of laughing and/or crying. PBA episodes typically occur out of proportion or incongruent to the underlying emotional state. PBA is a specific condition, distinct from other types of emotional lability that may occur in patients with neurologic disease or injury.



Quinidine and Related Drugs: NUEDEXTA contains quinidine, and should not be used concomitantly with other drugs containing quinidine, quinine, or mefloquine.

Hypersensitivity: NUEDEXTA is contraindicated in patients with a history of NUEDEXTA-, quinine-, mefloquine-, or quinidine-induced thrombocytopenia, hepatitis, bone-marrow depression, lupus-like syndrome, or known hypersensitivity to dextromethorphan (eg, rash, hives).

MAOIs: NUEDEXTA is contraindicated in patients taking monoamine oxidase inhibitors (MAOIs), or in patients who have taken MAOIs within the preceding 14 days, due to the risk of serious and possibly fatal drug interactions, including serotonin syndrome. Allow at least 14 days after stopping NUEDEXTA before starting an MAOI.

Cardiovascular: NUEDEXTA is contraindicated in patients with a prolonged QT interval, congenital long QT syndrome, history suggestive of torsades de pointes, heart failure, patients receiving drugs that both prolong QT interval and are metabolized by CYP2D6 (eg, thioridazine and pimozide), patients with complete atrioventricular (AV) block without implanted pacemaker, or at high risk of complete AV block.


Thrombocytopenia and Other Hypersensitivity Reactions: Quinidine can cause immune-mediated thrombocytopenia that can be severe or fatal. Non-specific symptoms, such as lightheadedness, chills, fever, nausea, and vomiting, can precede or occur with thrombocytopenia. NUEDEXTA should be discontinued immediately if thrombocytopenia occurs.

Hepatotoxicity: Hepatitis, including granulomatous hepatitis, has been reported in patients receiving quinidine, generally during the first few weeks of therapy. Discontinue immediately if this occurs.

Cardiac Effects: NUEDEXTA causes dose-dependent QTc prolongation. QT prolongation can cause torsades de pointes–type ventricular tachycardia, with the risk increasing as the degree of prolongation increases. When initiating NUEDEXTA in patients at risk for QT prolongation and torsades de pointes, electrocardiographic (ECG) evaluation of QT interval should be conducted at baseline and 3 to 4 hours after the first dose. Some risk factors include use with CYP3A4 inhibitors or drugs that prolong QT interval, electrolyte abnormalities, bradycardia, or left ventricular hypertrophy or dysfunction. If patients taking NUEDEXTA experience symptoms that could indicate the occurrence of cardiac arrhythmias (eg, syncope or palpitations), NUEDEXTA should be discontinued, and the patient further evaluated.

Concomitant Use of CYP2D6 Substrates: NUEDEXTA inhibits CYP2D6 and may interact with other drugs metabolized by CYP2D6. Adjust dose of CYP2D6 substrates as needed.

Dizziness: NUEDEXTA may cause dizziness. Take precautions to reduce the risk of falls.

Serotonin Syndrome: Use of NUEDEXTA with selective serotonin reuptake inhibitors (SSRIs) or tricyclic antidepressants increases the risk of “serotonin syndrome.”

Anticholinergic Effects of Quinidine: Monitor for worsening in myasthenia gravis.


The most common adverse reactions (incidence of ≥3% and two-fold greater than placebo) in patients taking NUEDEXTA are diarrhea, dizziness, cough, vomiting, asthenia, peripheral edema, urinary tract infection, influenza, increased gamma-glutamyltransferase, and flatulence.

These are not all the risks for use of NUEDEXTA. Please see Full Prescribing Information.

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