Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Saturday, July 12, 2025

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 ChoiSoojin Choi1,2Dae Hyun KimDae Hyun Kim3Won Jun KangWon Jun Kang2,4YONGWOOK KIMYONGWOOK KIM2,4*
    • 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

    The final, formatted version of the article will be published soon.

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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.

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