Brain Metabolic Changes Associated with Post-Stroke Pathological Laughing and Crying: An 18 F-FDG-PET Study in Pontine Stroke

 Your competent? doctor should have created a protocol on curing pseudobulbar affect a long time ago. Or at least initiated research to solve the problem! But I bet your doctor DID NOTHING, LIKE USUAL!

Pseudobulbar affect (PBA) (6 posts to May 2013)

Brain Metabolic Changes Associated with Post-Stroke Pathological Laughing and Crying: An 18 F-FDG-PET Study in Pontine Stroke

Soojin Choi^1,2Dae Hyun Kim³Won Jun Kang^2,4YONGWOOK KIM^2,4*

• ¹Hanyang University Seoul Hospital, Seoul, Republic of Korea
• ²Yonsei University College of Medicine, Seodaemun-gu, Republic of Korea
• ³Samsung Medical Center, Gangnam-gu, Republic of Korea
• ⁴Severance Hospital, Seodaemun-gu, Republic of Korea

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Background: 

Pathological laughing and crying (PLC) is characterized by sudden, uncontrollable, and inappropriate episodes of laughter or crying. While previous studies have identified PLCassociated structural lesions, the underlying metabolic alterations in these patients remain unclear. 

Objective: 

We aimed to investigate cerebral metabolic alterations in patients with PLC following pontine stroke using 18 F-fluorodeoxyglucose-positron emission tomography imaging. 

Methods: 

In this retrospective study, we included 49 patients with pontine stroke admitted to a tertiary inpatient rehabilitation hospital between January 2011 and December 2021. Patients were classified into PLC (n = 20) and non-PLC (n = 29) groups. 18 F-fluorodeoxyglucose-positron emission tomography images obtained within 14 days of admission were analyzed using the SPM 12 software. Voxel-wise two-sample t-tests were performed to compare brain metabolism between the two groups (Pfamily-wise error-corrected < 0.05). Multiple regression analysis was conducted to identify brain regions significantly associated with PLC severity, adjusting for age and stroke lesion volume. 

Results: 

Compared with that of the non-PLC group, the PLC group exhibited significant hypometabolism in the right superior frontal gyrus (Pfamily-wise error-corrected < 0.05). Multiple regression analysis revealed that decreased metabolism in the right inferior and middle temporal gyri was significantly correlated with higher Pathological Laughter and Crying Scale scores, indicating greater PLC severity. No brain regions showed positive correlations with the Pathological Laughter and Crying Scale scores. 

Conclusions:

Our findings reveal that PLC following pontine stroke is associated with distinct patterns of hypometabolism, particularly in the right superior frontal gyrus and the right inferior and middle temporal gyri. These regions may contribute to the regulation of emotional expression and provide insights into the neural mechanisms underlying PLC.

Keywords: Pathological laughing and crying, Pontine stroke, brain metabolism, emotional regulation, PLACS

Received: 04 Jun 2025; Accepted: 10 Jul 2025.

Copyright: © 2025 Choi, Kim, Kang and KIM. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: YONGWOOK KIM, Severance Hospital, Seodaemun-gu, Republic of Korea

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

Last chance to register for a live webinar on PBA

What a fucking waste. I see nothing here that suggests they have solutions to cure your PBA, just manage it. We want cures you lazy fucking bastards. But then this is the NSA - National Stroke Association doing nothing to solve all the problems in stroke, you can expect nothing from them.
http://support.stroke.org/site/MessageViewer?em_id=32309.0&dlv_id=48545

Dear Friend, Are you or your loved one affected by PBA? PBA or pseudobulbar affect can impact as many as 28 percent of stroke survivors, causing sudden, unpredictable episodes of crying or laughing that seem overactive or out of place. Join us for a FREE, live, interactive online education program with PBA experts Erik Pioro, MD, PhD and Maileen Ulep-Reed, CNP. This program is presented in collaboration with NeuroCareLive, a PlatformQ Health learning channel. What: Living with the Burden of PBA: Education for patients and caregivers When: June 20, 2017 Time: 2:00 – 3:00 PM ET Topics covered will include: What is PBA? Managing Your PBA Self-Care, Resources, FAQ Register Now We hope you can join us for this educational webinar! Can’t make the live program? Go ahead and register and we will email you a link to the recording. In Health, Anna Taylor, MS Director of Programs

PRISM II: An open-label study to assess effectiveness of dextromethorphan/quinidine for pseudobulbar affect in patients with dementia, stroke or traumatic brain injury

If you have PBA then IF your doctor is any good at all s/he will be following this study closely and update your stroke protocols upon completion. But I can guarantee that unless YOU tell them about this nothing will happen. Your recovery is solely up to you, you can't depend on your doctors or therapists.
http://www.mdlinx.com/internal-medicine/medical-news-article/2016/06/10/dextromethorphan-quinidine-pseudobulbar-affect-dementia-brain/6712770/?news_id=881&newsdt=061116&subspec_id=488&utm_source=WeeklyNL&utm_medium=newsletter&utm_content=Weeks-Best-Article&utm_campaign=article-section&category=latest-weekly

In this open–label study, the physicians aim to assess the effectiveness of dextromethorphan/quinidine (DM/Q) for pseudobulbar affect (PBA) in patients with dementia, stroke or traumatic brain injury (TBI). This research found that DM/Q was an effective and well–tolerated treatment for PBA secondary to dementia, stroke, or TBI.

Methods

• A total of 367 patients participated with PBA secondary to dementia, stroke, or TBI.
• Participants received DM/Q 20/10 mg twice daily in this open-label, multicenter, 90-day trial.
• The primary outcome was the Center for Neurologic Study-Lability Scale (CNS-LS), assessing change in PBA episode frequency and severity.
• The authors compared the CNS-LS final visit score to baseline (primary analysis) and to the response in a previously conducted placebo-controlled trial with DM/Q in patients with ALS or MS.
• Secondary outcomes included change in PBA episode count and Clinical Global Impression of Change with respect to PBA as rated by a clinician (CGI-C) and by the patient or caregiver (PGI-C).

Results

• Mean (standard deviation [SD]) CNS-LS score improved significantly from 20.4 (4.4) at baseline to 12.8 (5.0) at Day 90/Final Visit (change, -7.7 [6.1]; P < .001, 95 % CI: -8.4, -7.0).
• This magnitude of improvement was consistent with DM/Q improvement in the earlier phase-3, placebo-controlled trial (mean [95 % CI] change from baseline, -8.2 [-9.4, -7.0]) and numerically exceeds the improvement seen with placebo in that study (-5.7 [-6.8, -4.7]).
• Reduction in PBA episode count was 72.3 % at Day 90/Final Visit compared with baseline (P < .001).
• Scores on CGI-C and PGI-C showed that 76.6 and 72.4 % of participants, respectively, were “much” or ”very much” improved with respect to PBA.
• IN this study the most frequently occurring adverse events (AEs) were diarrhea (5.4 %), headache (4.1 %), urinary tract infection (2.7 %), and dizziness (2.5 %); 9.8 % had AEs that led to discontinuation.
• Serious AEs were reported in 6.3 %; however, none were considered treatment related.

Go to PubMed Go to Abstract Print Article Summary Cat 2 CME

Dextromethorphan, Quinidine Effective for Pseudobulbar Affect Secondary to Dementia

This is PBA after dementia, what about after stroke? Whom is going to answer that question? ASA or NSA are you going to sponsor research to answer that f*ckingly simple question? Or are you going to continue to sit on your ass WAITING FOR SOMEONE ELSE TO SOLVE THE PROBLEM?
Dextromethorphan, Quinidine Effective for Pseudobulbar Affect Secondary to Dementia
 A fixed combination of dextromethorphan and quinidine has demonstrated efficacy in treating pseudobulbar affect (PBA) and depressive symptoms in patients with dementia, researchers reported here at the 168th Annual Meeting of the American Psychiatric Association (APA).
“The PRISM-2 is an open label study that enrolled patients with PBA secondary to dementia, stroke, or traumatic brain injury,” explained Andrew Cutler, MD, Florida Clinical Research Center, LLC, Sarasota, Florida.
The analysis focused on patients form PRISM-2 who had PBA secondary to dementia to determine if the medication had any impact on treating any depression that patients experienced.
“The way that this medication works suggests that it will affect mood,” said Dr. Cutler. “These were no patients who had significant clinical depression, but they had depressive symptoms.”
PBA symptoms were significantly enhanced from study entry to the 12-week mark, with a 67.7% decrease in PBA episodes and a mean change of -7.2 on the Center for Neurologic Study-Liability Scale (P< .001).
“By day 90, the PBA episodes were cut down to 3 a week,” said Dr. Cutler, noting patients had multiple PBA episodes daily at study entry. “There was tremendous improvement in episodes of PBA.”
The study also looked at depressive symptoms as measured by the Patient Health Questionnaire-9. They found an improvement on that scale that was statistically significant, with a change from 13.2 at study entry to 7.4 after 12 weeks (P< .001).
Of note, there was not a direct relationship between improvement in PBA symptoms and reduction in depressive symptoms.
The most common adverse events were headache, urinary tract infection, and diarrhoea.
The study was limited by the fact that it was not randomised; rather it was an open-label design.
Funding for this study was provided by Avanir Pharmaceuticals, Inc.
[Presentation title: Dextromethorphan Quinidine for Pseudobulbar Affect Secondary to Alzheimer’s Disease/Dementia: Effect on Mood Symptoms in PRISM-II Dementia Cohort. Abstract P8-085]

Dextromethorphan/Quinidine: A Review of Its Use in Adults with Pseudobulbar Affect

So maybe there is something for emotional lability Ask your doctor about this.

Dextromethorphan/Quinidine: A Review of Its Use in Adults with Pseudobulbar Affect

Yang LP¹, Deeks ED.

Author information

Abstract

Fixed-dose dextromethorphan/quinidine capsules (Nuedexta^®) utilize quinidine to inhibit the metabolism of dextromethorphan, enabling high plasma dextromethorphan concentrations to be reached without using a larger dose of the drug. The drug combination is the first treatment to be approved for pseudobulbar affect (PBA), a condition of contextually inappropriate/exaggerated emotional expression that often occurs in adults with neurological damage conditions, such as amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), stroke, traumatic brain injury, Alzheimer's disease or Parkinson's disease. Dextromethorphan/quinidine at the recommended dosages of 20/10 or 30/10 mg twice daily reduced the rate of PBA episodes and improved PBA severity in a 12-week, double-blind, placebo-controlled trial in adults with ALS or MS (STAR), with further improvements in the severity of the condition observed in a 12-week open-label extension phase. Dextromethorphan/quinidine 20/10 mg twice daily also improved PBA secondary to dementia in a cohort of a 12-week noncomparative trial (PRISM II). The drug combination was generally well tolerated in these studies, with no particular safety or tolerability concerns. Although longer-term efficacy and tolerability data for dextromethorphan/quinidine 20/10 or 30/10 mg twice daily would be beneficial, current evidence indicates that it is a useful option in the treatment of adults with PBA.

Lamotrigine Treatment for Post-Stroke Pathological Laughing and Crying

Well at least this one is only 11 years old, still incompent but not mind-boggling.
http://journals.lww.com/clinicalneuropharm/Abstract/2003/09000/Lamotrigine_Treatment_for_Post_Stroke_Pathological.6.aspx

Ramasubbu, Rajamannar

Abstract

Pathologic laughing and crying (PLC) is a common distressing and socially disabling condition in stroke patients. Antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs), have been increasingly recognized as the treatment of choice for pathologic crying (PC). However, little is known about etiologies and other treatment options for various clinical manifestations of PLC. This case report illustrates the beneficial effect of lamotrigine, a novel antiepileptic drug with antidepressant and mood-stabilizing properties in post-stroke PLC. A 60-year-old woman developed PLC after an ischemic stroke affecting the left frontal and temporal lobes. She was treated with lamotrigine initially at the dose of 50 mg a day, which was gradually increased to 100 mg a day over a 4-week period. There was a significant and rapid recovery in both laughing and crying components of PCL with lamotrigine treatment. The symptoms of pathologic laughing have shown a better response to lamotrigine than PC. Controlled investigations are needed to evaluate the beneficial as well as the differential effects of lamotrigine on PLC.

The syndrome of pathologic laughing and crying (PLC) involves uncontrollable motor expression of emotion in the absence of corresponding feelings of sadness or happiness. PLC is often precipitated by nonspecific stimuli. 1 Emotional lability is a second type of pathologic affect that represents a rapid fluctuation in emotional expression that is out of proportion to an appropriate stimulus or situation and is accompanied by an alteration in mood states. 1 The validity of the existence of these two types has not been substantiated because of a great deal of overlap in the phenomenology between PLC and emotional lability. 2 In this context, a commonly used instrument, namely the pathologic laughing and crying scale (PLCS), has included items to measure both the intensity of pathologic laughing (PL) and pathological crying (PC) and also the severity of emotional lability. 3 The other terms used in the literature to describe the pathologic affect of laughing and crying include emotionalism, 4 emotional incontinence, 5 and pseudobulbar affect. 6

PLC is a common emotional consequence of stroke. Approximately 15% to 20% of patients may experience this condition during the first year after stroke. 7 Pathologic crying is the most common manifestation in stroke patients. However, some patients may have episodes of laughing without episodes of crying and some display both laughing and crying. Brain stem lesions and right frontal damage are frequently associated with PLC. 7 Double-blind placebo-controlled studies documented the efficacy of both tricyclics (nortriptyline, amitriptyline) and selective serotonin reuptake inhibitors (SSRIs) (citalopram, fluoxetine, sertraline) in PLC. 3,8–11 However, since the controlled treatment studies to date focused largely on patients with PC and only a few patients with PL were in the cohort, our understanding of the efficacy of antidepressants in PL is limited. Furthermore, anecdotal reports described a rapid transition of PC to PL during treatment with SSRIs 12 and a slow transformation of PC to PL as a natural course of PLC in some patients. 13,14

L-dopa was reported to be effective in patients with PL in an open trial. 15 However, taking into account the depressogenic side effect of l-dopa 16 and the frequent co-occurrence of depression with PLC in stroke patients, 7 l-dopa may not be a suitable agent for post-stroke patients with PLC and depression. This report describes a case of post-stroke PLC that markedly improved with lamotrigine, a novel antiepileptic drug with antidepressant and mood stabilizing properties.

Brain System for Emotional Self-Control Discovered

Your doctor should be able to use this to determine why you have emotional lability or Pseudobulbar affect (PBA). So ask them.
http://www.sciencedaily.com/releases/2013/05/130509104354.htm
Different brain areas are activated when we choose to suppress an emotion, compared to when we are instructed to inhibit an emotion, according a new study from the UCL Institute of Cognitive Neuroscience and Ghent University.

---

In this study, published in Brain Structure and Function, the researchers scanned the brains of healthy participants and found that key brain systems were activated when choosing for oneself to suppress an emotion. They had previously linked this brain area to deciding to inhibit movement.
"This result shows that emotional self-control involves a quite different brain system from simply being told how to respond emotionally," said lead author Dr Simone Kuhn (Ghent University).
In most previous studies, participants were instructed to feel or inhibit an emotional response. However, in everyday life we are rarely told to suppress our emotions, and usually have to decide ourselves whether to feel or control our emotions.
In this new study the researchers showed fifteen healthy women unpleasant or frightening pictures. The participants were given a choice to feel the emotion elicited by the image, or alternatively to inhibit the emotion, by distancing themselves through an act of self-control.
The researchers used functional magnetic resonance imaging (fMRI) to scan the brains of the participants. They compared this brain activity to another experiment where the participants were instructed to feel or inhibit their emotions, rather than choose for themselves.
Different parts of the brain were activated in the two situations. When participants decided for themselves to inhibit negative emotions, the scientists found activation in the dorso-medial prefrontal area of the brain. They had previously linked this brain area to deciding to inhibit movement.
In contrast, when participants were instructed by the experimenter to inhibit the emotion, a second, more lateral area was activated.
"We think controlling one's emotions and controlling one's behaviour involve overlapping mechanisms," said Dr Kuhn.
"We should distinguish between voluntary and instructed control of emotions, in the same way as we can distinguish between making up our own mind about what do, versus following instructions."
Regulating emotions is part of our daily life, and is important for our mental health. For example, many people have to conquer fear of speaking in public, while some professionals such as health-care workers and firemen have to maintain an emotional distance from unpleasant or distressing scenes that occur in their jobs.
Professor Patrick Haggard (UCL Institute of Cognitive Neuroscience) co-author of the paper said the brain mechanism identified in this study could be a potential target for therapies.
"The ability to manage one's own emotions is affected in many mental health conditions, so identifying this mechanism opens interesting possibilities for future research.
"Most studies of emotion processing in the brain simply assume that people passively receive emotional stimuli, and automatically feel the corresponding emotion. In contrast, the area we have identified may contribute to some individuals' ability to rise above particular emotional situations.
"This kind of self-control mechanism may have positive aspects, for example making people less vulnerable to excessive emotion. But altered function of this brain area could also potentially lead to difficulties in responding appropriately to emotional situations."