Advances in the diagnosis and management of post-stroke limb spasticity: a narrative review

 Where is the CURE SPASTICITY RESEARCH?

'Management' is NOT what survivors want! They want it CURED! Are you that stupid that you believe in the idiotic opinion of the infamous Dr. William M. Landau thinks spasticity is not worth treating!

Do you believe in the do nothingism of Dr. William M. Landau on spasticity?  

His statement from here:

Spasticity After Stroke: Why Bother? Aug. 2004

Wonder if he will be singing the same tune after he becomes the 1 in 4 per WHO that has a stroke, will he be satisfied with not getting recovered?

The latest here:

Advances in the diagnosis and management of post-stroke limb spasticity: a narrative review

• 

  Menghan Su 1,2

• M

  Mingqing Yu 1,2

• P

  Ping Xu 1,2

• 

  Yong Fei 2*

• 1. Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China

• 2. Department of Anesthesiology and Pain, The Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang, China

Abstract

Objective: 

This review aims to provide a comprehensive overview of the current understanding and clinical management of post-stroke limb spasticity.

Methods: 

Literature searches were conducted in PubMed and CNKI databases for articles published between January 2000 and June 2025, using keywords related to post-stroke spasticity, assessment, and interventions (botulinum toxin, rehabilitation, neuromodulation, surgery). The search was restricted to English-language articles addressing post-stroke limb spasticity. After screening, 68 studies were included and categorized by research theme.

Results: 

Several interventions were identified as effective in alleviating post-stroke limb spasticity. Specifically, botulinum toxin injection has emerged as the primary choice for managing focal spasticity. Neuromodulation methods, including transcranial magnetic stimulation, transcranial direct current stimulation, spinal cord stimulation, and vagus nerve stimulation, demonstrated significant therapeutic potential.(NOT GOOD ENOUGH! WHERE THE FUCK IS THE CURE?)

Conclusion: 

Neuromodulation techniques exert their effects by adjusting corticospinal tract excitability and promoting neural plasticity. However, additional randomized controlled trials are necessary to optimize stimulation settings and confirm their long-term effectiveness.

More at link.

A multicenter clinical nomogram for predicting post-stroke fatigue: development and validation

 

Will your competent? doctor and hospital ensure research is completed to determine WHAT WILL CURE POST STROKE FATIGUE? Not manage or anything less than a FULL CURE!

This prediction crapola is COMPLETELY FUCKING USELESS!

Let's see how long everyone in stroke has been incompetent at this problem!

• post stroke fatigue (60 posts to January 2018)

At least half of all stroke survivors experience fatigue Known since March 2017

Or is it 70%? Known since March 2015.

Or is it 40%? Known since September 2017.

A multicenter clinical nomogram for predicting post-stroke fatigue: development and validation

• X

  Xiaoqing Tao 1†

• S

  Shan Wang 2†

• L

  Li Pang 1

• Y

  Yiling Sun 1

• 

  Yifei Ji 1,2*

• 

  Yu Ren 1,3*

• 1. Department of Neurology, Beijing Anzhen Nanchong Hospital of Capital Medical University & Nanchong Central Hospital, Nanchong, Sichuan, China

• 2. Department of Neurology, The Second Clinical Medical College of North Sichuan Medical College, Nanchong, Sichuan, China

Abstract

Background and purpose: 

Post-stroke fatigue (PSF) is a common and disabling complication after stroke, yet its pathophysiological mechanisms remain unclear and reliable prediction tools are lacking. This study aimed to identify risk factors for PSF and develop a visualized nomogram for early prediction based on clinical and laboratory data.

Methods: 

We conducted a retrospective cohort study of stroke patients hospitalized in the Department of Neurology at the First Affiliated Hospital of Chongqing Medical University were randomly split into training (n = 592) and internal validation (n = 254) sets. An independent cohort of 440 patients from Nanchong Central Hospital was used as the external validation cohort. Fatigue was assessed at week 4 after admission using the Fatigue Severity Scale (FSS) and Fatigue Assessment Scale (FAS). Demographic, clinical, imaging, and laboratory data were collected. LASSO regression was used for variable selection, followed by multivariate logistic regression to construct a nomogram. Model performance was assessed using the area under the curve (AUC), calibration curves, and decision curve analysis (DCA), with internal and external validation via bootstrapping.

Results: 

A total of 846 stroke patients were enrolled and randomly split into training (n = 592), internal validation (n = 254) and external validation (n = 440) sets. Eight independent predictors of PSF were identified: brainstem, basal ganglia, and thalamic lesions, female sex, older age, modified Rankin Scale (mRS) score, white blood cell (WBC) count, and C-reactive protein (CRP) level (all p < 0.05). The nomogram showed good discrimination (AUC: 0.870, 0.862, and 0.672 for training, internal, and external validation sets, respectively), calibration, and clinical utility.

Conclusion: 

We developed a clinically applicable nomogram based on routinely available data for early prediction of PSF. The model demonstrated good accuracy and may aid in identifying high-risk patients to guide timely intervention.

Neuromodulation approaches and applications in the management of post-stroke pain: a comprehensive review

 

 So, this is what it is, does your incompetent? doctor have any recovery protocols on this?

Neuromodulation is a therapy that alters nerve activity by delivering electrical impulses or medications directly to the nervous system, essentially "reprogramming" abnormal nerve signals to treat conditions like chronic pain, Parkinson's, epilepsy, or bladder dysfunction, much like a pacemaker regulates heartbeats, using implanted devices or non-invasive methods. 

 Let's see how long your doctor has been incompetent! Over a decade and is still there? Massive incompetence of the board of directors in allowing it to fester for so long! Still no protocol on how to treat or prevent this pain!

• neuromodulation (27 posts to May 2015)
• post stroke pain (4 posts to August 2023)

Neuromodulation approaches and applications in the management of post-stroke pain: a comprehensive review

• 

  Stewart S. Cox 1

• M

  Marion Wood 1

• F

  Falon Sutton 1

• K

  Katherine Tucker 1

• N

  Nicole Cash 1

• R

  Ruxue Gong 1

• 

  Nathan C. Rowland 2,3

• 

  Steven A. Kautz 4,5,6

• 

• 

• 

  Xiaolong Peng 1*

• 1. Department of Psychiatry and Behavioral Sciences, College of Medicine, Medical University of South Carolina, Charleston, SC, United States

• 2. Department of Neurosurgery, College of Medicine, Medical University of South Carolina, Charleston, SC, United States

Abstract

Introduction: 

Post-stroke pain (PSP) remains a common and profoundly debilitating consequence of stroke, both in terms of a delay in recovery and in substantially reducing quality of life. Both invasive and non-invasive brain stimulation techniques are increasingly being explored as possible treatment modalities for various forms of PSP. This literature review examines the current body of evidence for all forms of neurostimulation for PSP.

Methods: 

In this paper, we provide a review of the most recent literature exploring neuromodulation for PSP, covering several key domains: an examination of various PSP subtypes and the underlying mechanisms; a consolidation to date of the literature examining both invasive and non-invasive neuromodulation techniques for forms of PSP, and a discussion of future directions for the field.

Results: 

The impact of neuromodulation techniques on PSP populations, focusing primarily on spasticity and central post-stroke pain (CPSP) is discussed.

Conclusion: 

To varying degrees, numerous invasive and non-invasive modalities are beginning to be explored for individuals suffering from PSP. While preliminary, there is promising evidence to suggest that neuromodulatory techniques may reduce or ameliorate PSP. Further evidence and large clinical trials are needed to compare these treatments to the standard of care, as well as each other, to optimize outcomes for patients. In a rapidly evolving field, this review helps to provide the current state of neuromodulation in research on PSP.

RNA gene expression and cognitive reserve as determinants of post-ischaemic stroke cognitive recovery

 How is your competent? doctor rebuilding your cognitive reserve enough to prevent dementia? This told me nothing.

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!

OH NO! your doctor KNOWS NOTHING AND DOES NOTHING! 

RNA gene expression and cognitive reserve as determinants of post-ischaemic stroke cognitive recovery

• Nurul Nadiah Muhamad, 
• MD Ali Katijjahbe, 
• Nor Azian Abdul Murad, 
• Wan Asyraf Wan Zaidi & 
• Suriati Mohamed Saini 

Scientific Reports , Article number:  (2026) Cite this article

We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.

Abstract

Cognitive impairment is a common yet under-recognised complication of ischaemic stroke (IS), with long-term effects on patient quality of life and rehabilitation outcomes. Identifying early biomarkers and protective factors such as cognitive reserve (CR) is essential for improving prognosis and guiding targeted interventions. This study aimed to determine the following: (i) RNA gene expression profiling during acute stroke and (ii) the associations between target genes as well as clinical factors and cognitive impairment during an acute event and at the 3-month follow-up. A three-month prospective cohort study involving 24 adults with mild to moderate IS and 24 age- and sex-matched controls admitted to Hospital Canselor Tuanku Muhriz, Malaysia, was conducted. Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA) within 48 h of stroke and at 3 months. Peripheral blood samples were collected for RNA extraction, and gene expression was analysed using RT² Profiler PCR arrays. Cognitive reserve was measured using the Cognitive Reserve Index Questionnaire (CRI-q). Statistical analyses included chi-square and independent t tests. At baseline, 83.3% of IS patients exhibited cognitive impairment (mean age 64.6 ± 10.5 years). Increased age (p = 0.006), low education level (p = 0.010), diabetes mellitus (p = 0.010), CRI-Education (p = 0.010) and CRI-Working Activity (p = 0.009) were significantly associated with baseline cognitive impairment. These clinical and CR factors survived False Discovery Rate (FDR) correction at the baseline stage (p < 0.05). However, at the 3-month follow-up, no clinical or CR factors remained statistically significant after FDR correction. Regarding gene expression, while MAPK1 (p = 0.029) and CAPZB (p = 0.042) were nominally upregulated in patients, and RCOR1 (p = 0.043) showed a nominal association with baseline impairment, no genetic markers survived FDR correction at either time point. Age, diabetes, and cognitive reserve are robust determinants of cognitive status during the acute phase of ischaemic stroke. The loss of significance at 3 months suggests these factors are primary drivers of initial functional buffering rather than long-term recovery trajectories in this cohort. CR should be utilised as a prognostic stratification tool during admission to identify high-risk patients rather than as a direct target for acute intervention. Future large-scale studies are required to validate whether the observed nominal gene expression trends can serve as reliable biomarkers for long-term recovery.

Data availability

The datasets presented in this article are not readily available because the data are part of an ongoing study. Requests to access the datasets should be directed to Dr. Nurul Nadiah, email: [p109270@siswa.ukm.edu.my] (mailto: p109270@siswa.ukm.edu.my) .

Targeting the microbiota-gut-brain axis in post-stroke insomnia: a phase-dependent therapeutic framework

 Wonderful descriptions; but complete failure at producing anything for stroke recovery!

Targeting the microbiota-gut-brain axis in post-stroke insomnia: a phase-dependent therapeutic framework

• 

  Yumin Zhou

• Y

  Yingying Huang

• 

  Xia Bi *

• Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital, Shanghai, China

Abstract

Post-stroke insomnia (PSI) is a critical biological barrier to neurorehabilitation afflicting over half of all stroke survivors. Traditional sedatives often force clinicians into a therapeutic dilemma between sleep efficacy and cognitive suppression. The microbiota-gut-brain (MGB) axis has recently emerged as a transformative target to resolve this impasse. Acute stroke triggers profound autonomic dysfunction, causing immediate intestinal barrier collapse. This “leaky gut” facilitates the systemic translocation of lipopolysaccharides (LPS) and activates the NLRP3 inflammasome. The resulting inflammatory storm hijacks central tryptophan metabolism via the indoleamine 2,3-dioxygenase (IDO) enzyme. This “tryptophan steal” diverts serotonin precursors toward neurotoxic kynurenine pathways, driving severe cortical hyperarousal. Sleep fragmentation then prevents the glymphatic system from clearing metabolic waste, further exacerbating neuroinflammation. To break this vicious cycle of neurotoxicity, we propose a phase-dependent therapeutic framework. During the highly vulnerable acute phase, interventions must prioritize gut barrier protection using postbiotics to mitigate infection risks under CNS injury-induced immunodepression (CIDS), often discussed as stroke-induced immunosuppression. As patients enter the chronic phase, therapy shifts toward metabolic restoration using live therapeutics, such as washed microbiota transplantation (WMT) and next-generation psychobiotics like Akkermansia muciniphila. Targeting the MGB axis offers a mechanism-based strategy to achieve precision sleep medicine, restoring the biological foundation necessary for optimal neuroplasticity and recovery.

1 Introduction

1.1 The silent epidemic: beyond symptomology

Stroke remains a formidable global health challenge, consistently ranking among the leading causes of mortality and long-term adult disability worldwide (GBD 2019 Stroke Collaborators, 2021; Feigin et al., 2025). While the advent of hyper-acute recanalization therapies—such as mechanical thrombectomy and intravenous thrombolysis—has improved acute outcomes, these advances have coincided with a growing population of survivors living with chronic sequelae (GBD 2019 Stroke Collaborators, 2021; Feigin et al., 2025). Among these, sleep–wake disturbances are pervasive yet frequently underestimated in routine clinical practice, often overshadowed by more visible motor deficits (Khot and Morgenstern, 2019). Epidemiological evidence suggests that sleep problems affect roughly half of stroke survivors, consistent with pooled estimates of poor sleep quality after stroke and broader post-stroke sleep-disorder burden (Khot and Morgenstern, 2019; Luo et al., 2023). Of these disorders, post-stroke insomnia (PSI) is commonly reported and can persist, presenting a barrier to effective neurorehabilitation (Wang et al., 2024; Sun et al., 2026). PSI is characterized not merely by difficulties in sleep initiation, but also by fragmentation of sleep continuity and non-restorative rest (Wang et al., 2024). The clinical ramifications of untreated PSI extend beyond subjective fatigue or daytime somnolence; disrupted sleep after stroke has been associated with poorer functional outcomes and increased risk of adverse vascular events in observational and review evidence (Khot and Morgenstern, 2019). Sleep is a fundamental physiological pillar for neuroplasticity and memory consolidation, and sleep disruption may therefore hinder recovery processes after stroke (Khot and Morgenstern, 2019). Indeed, disrupted sleep in the post-stroke period has been linked to worse functional recovery and mood and cognitive outcomes, supporting proactive recognition and targeted management rather than passive observation.

More at link.