STROKE / TBI RESEARCH

Comparison of the Effects of ExMI on Stress Incontinence and Stroke Related Urinary Incontinence.

(link:  https://openurl.ebsco.com/EPDB%3Agcd%3A1%3A10491745/detailv2?sid=ebsco%3Aplink%3Ascholar&id=ebsco%3Agcd%3A154848034&crl=c)

The aim of this study was to compare the effects of extracorporeal magnetic innervation (EXMI) treatment on stress incontinence (SI) and post-stroke urinary incontinence (PSUI).

Conclusion: EXMI is an effective treatment method in PSUI treatment.

Frequency-tuned electromagnetic field therapy improves post-stroke motor function: A pilot randomized controlled trial

(Link:  https://pubmed.ncbi.nlm.nih.gov/36452175/)

Impaired upper extremity (UE) motor function is a common disability after ischemic stroke. Exposure to extremely low frequency and low intensity electromagnetic fields (ELF-EMF) in a frequency-specific manner (Electromagnetic Network Targeting Field therapy; ENTF therapy) is a non-invasive method available to a wide range of patients that may enhance neuroplasticity, potentially facilitating motor recovery.

ENTF stimulation in subacute ischemic stroke patients was associated with improved UE motor function and reduced overall disability, and results support its safe use in the indicated population. These results should be confirmed in larger multicenter studies.

Pulsed Electromagnetic Fields: A Novel Attractive Therapeutic Opportunity for Neuroprotection After Acute Cerebral Ischemia

(Link:  https://pubmed.ncbi.nlm.nih.gov/34480781/)

Acute cerebral ischemia is characterized by several pathological processes evolving during time, which contribute to the final tissue damage. Secondary processes, such as prolonged inflammatory response, impaired mitochondrial function, and oxidative stress, are responsible for the progression of brain injury to the peri-infarct area, called “penumbra.” Adenosine has been shown to play a crucial role in regulating the inflammatory cascade following brain ischemia. Pulsed electromagnetic fields (PEMFs) act as modulators of adenosine receptors, increasing the functionality of the endogenous adenosine. In particular, PEMF exposure induces a significant upregulation of A2Aand A3adenosine receptors in different neuronal cell types. Several lines of evidence suggest that PEMF exposure might play a neuroprotective role after ischemic damage.

PEMFs counteract hypoxia-induced apoptosis and ROS production in neuronal-like cells and exert a strong anti-inflammatory effect on microglial cells. Data from stroke animal models showed that PEMFs exposure is able to reduce the size of the infarct area and decrease the levels of pro-inflammatory mediators. In clinical studies, PEMFs stimulation proved to be safe and well tolerated. Preliminary results on acute ischemic stroke patients showed a dose-dependent reduction in the lesion size.