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.

Tuesday, March 11, 2025

Effect of phototherapy on event-related potentials in patients with post-stroke depression through serum tetrahydrobiopterin level intervention: a clinical study

 Since this seems to work, you'll have to DEMAND YOUR COMPETENT? DOCTOR gets it installed in their hospital.

Do you prefer your doctor incompetence NOT KNOWING? OR NOT DOING?

Effect of phototherapy on event-related potentials in patients with post-stroke depression through serum tetrahydrobiopterin level intervention: a clinical study

Abstract

Background

This study investigated the effects of phototherapy on serum BH4 levels, evoked potentials, and cognitive impairment in post-stroke depression patients.

Methods

We conducted a prospective study with 160 post-stroke depression patients, randomly assigned to an experimental group receiving daily 40 min of phototherapy alongside routine treatment, and a control group receiving only routine treatment. Serum tetrahydrobiopterin (BH4) levels were measured via ELISA. Evoked potentials were assessed using an ERP recorder, depressive symptoms were evaluated with the Hamilton Depression Scale (HAM-D), and cognitive function was analyzed using the Montreal Cognitive Assessment (MoCA). Inflammatory factor expression was detected via RT-PCR.

Results

Both groups exhibited increased BH4 levels, but the phototherapy group had significantly higher levels (P < 0.05). The phototherapy group also demonstrated improved ERP parameters, with higher MMN latency, P300 latency, and amplitudes compared to controls (P < 0.05). HAM-D scores decreased more in the phototherapy group (P < 0.05), while MoCA scores increased significantly (P < 0.05). Additionally, inflammatory markers IL-6, TNF-α, and IL-1β were lower in the phototherapy group (P < 0.05).

Conclusions

Phototherapy positively influenced BH4 levels, improved evoked potentials, alleviated depressive symptoms, enhanced cognitive function, and reduced inflammation in post-stroke depression patients.

Peer Review reports

Introduction

Post-stroke depression is widely recognized as a common complication among stroke patients, significantly hindering their rehabilitation process [1, 2]. Phototherapy, a therapeutic approach designed to alleviate depressive symptoms, operates by adjusting the biological clock. This method simulates the characteristics of natural light to regulate the secretion of neurotransmitters and hormones in the brain, thereby influencing the mood and physiological state of patients. In the realm of post-stroke depression research, event-related potentials (ERPs) are frequently employed as a neurophysiological index to study the impact of stimulating events on EEG activity [3, 4]. By recording patients’ EEG activities during specific stimulation tasks, ERPs facilitate the exploration of changes in brain function. Previous studies have identified significant abnormalities in ERP parameters among patients with post-stroke depression, including alterations in P300 and N400 components, which are linked to cognitive function and emotional regulation [5, 6]. However, current research on the influence of phototherapy on ERPs in patients with post-stroke depression is still relatively limited.

Moreover, serum tetrahydrobiopterin (BH4), a critical cofactor involved in neurotransmitter synthesis, plays a crucial role and may be associated with the neurological dysfunction observed in patients with post-stroke depression [7]. Among numerous inflammatory factors, 16 may be linked to post-stroke depression, including pro-inflammatory factors (interleukin-1 β, interleukin-6, interleukin-8, interleukin-18, tumor necrosis factor alpha, and interferon gamma), anti-inflammatory factors (interleukin-4, interleukin-10, and transforming growth factor beta 1), and other non-specific factors (C-reactive protein, neopterin, adiponectin, NLRP3 inflammasome, matrix metalloproteinase 9, growth differentiation factor 15, and serum amyloid A) [8]. Counteracting the expression of pro-inflammatory factors or supplementing exogenous anti-inflammatory factors can help alleviate post-stroke depression symptoms, and treatments for post-stroke depression can alter serum inflammatory factors. These inflammatory factors contribute to post-stroke depression by interacting with their receptors, intracellular signaling pathways, neurotransmitters, or the hypothalamic-pituitary-adrenal axis. Detecting serum inflammatory markers or gene polymorphisms holds significant predictive value for diagnosing post-stroke depression.

ERP measures the electrical potential changes produced by the brain in response to specific events [9]. The principle involves recording brain electrical activity under specific stimuli through electrodes. The measurement process includes preparing the testing environment, administering stimuli, and recording and analyzing potential changes. BH4, as a significant regulator of nerve conduction, impacts ERP waveform. Changes in BH4 levels can affect T cell activity, influencing ERP components such as N1 and P2, though its specific mechanism remains to be further explored [7]. As a coenzyme factor, BH4 plays a vital role in neurotransmitter synthesis and regulation, indirectly affecting ERP production [10]. By regulating neurotransmitters like dopamine and serotonin, BH4 may influence the waveform and latency of ERPs. The relationship between BH4 levels and ERP performance is close, as BH4 directly impacts the amplitude of ERP components. A decrease in BH4 levels corresponds with an increase in ERP wave amplitude, reflecting the brain’s need to mobilize more cognitive resources in response to cognitive challenges.

Phototherapy, a non-pharmacological treatment, is significant in treating post-stroke depression [11]. It not only improves depressive symptoms but also regulates the biological clock and neurotransmitters, aiding recovery. Phototherapy enhances the emotional and cognitive function of post-stroke depression patients by regulating neurotransmitters such as serotonin and norepinephrine and promoting the synthesis and release of melatonin, which influences the brain’s biological clock and endocrine system [11]. By affecting the release and reuptake of neurotransmitters, phototherapy regulates the concentration of neurotransmitters like dopamine and serotonin in the brain, playing a crucial role in emotional regulation. Simulating natural light, particularly blue and white light, phototherapy stimulates photosensitive cells in the retina, transmitting signals to the brain and regulating the biological clock’s rhythm. This regulation helps restore normal circadian function, improving sleep quality and emotional state in post-stroke depression patients. By simulating natural light and regulating the patient’s biological clock and hormone secretion—especially melatonin and serotonin—phototherapy alleviates emotional depression and anxiety, enhancing psychological adaptability and quality of life [12].

Furthermore, inflammatory factors such as TNF-α and IL-6 induce neuronal apoptosis, affect neuronal communication and metabolism, and activate glial cells, leading to functional abnormalities and cerebrovascular dysfunction [13]. These pathways collectively impact cognitive function, contributing to cognitive disorders. Inflammatory factors like CRP, IL-6, and TNF-α are significantly correlated with cognitive dysfunction, influencing cognitive function by inducing neuronal apoptosis, affecting neuronal communication and metabolism, activating glial cells, and damaging cerebral blood vessels.

Despite these insights, studies exploring the effects of phototherapy on BH4 levels and its relationship with ERPs are scarce. Therefore, this study aimed at investigating the effects of phototherapy on serum BH4 levels, evoked potentials, and cognitive impairment in post-stroke depression patients, offering a novel treatment strategy.

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