Neuromodulation is a distinctive technology that modifies neural activity by delivering electrical impulses or pharmaceutical agents directly to specific regions of the brain or spinal cord. Spinal neuromodulation refers to therapeutic interventions designed to alter the activity of the spinal cord and nerve roots in order to relieve pain and other neurological symptoms. This approach primarily utilizes devices such as spinal cord stimulation systems, intrathecal drug delivery systems, and other advanced neuromodulatory technologies. Spinal neuromodulation devices function either by electrically stimulating nerves to produce natural biological responses or by administering precise, targeted doses of pharmaceutical agents directly to the site of action. These treatments have proven transformative for many patients, offering the potential for fewer side effects, greater patient comfort, and overall improvements in quality of life. The primary modalities discussed in this article include spinal cord stimulation, sacral neuromodulation, and intrathecal baclofen therapy. Spinal cord stimulation has long been a preferred treatment for chronic low back pain, chronic pain after spinal surgery, complex regional pain syndrome, and painful diabetic peripheral neuropathy. Recent technological advances have expanded its use to additional spinal disorders, and ongoing research is exploring its potential for promoting neurological recovery in individuals with paraplegia. Sacral neuromodulation is an interventional technique used to modulate sacral reflex arcs for the management of neurogenic bladder and neurogenic bowel dysfunction. Intrathecal baclofen therapy is a minimally invasive treatment indicated for severe poststroke spasticity and other forms of spasticity. This article reviews the clinical benefits of these therapies, as well as considerations related to safety, cost-effectiveness, and the quality of supporting evidence.

OBJECTIVE: To examine the role of carvacrol in modulating PI3K/AKT signaling involved in human breast cancer pathogenesis using in vitro experimental model MCF-7 cells. METHODS: MTT and lactate dehydrogenase assays were performed with cells treated with different doses of carvacrol (0-250 p mol/L) at different time points (24 and 48 h). The nuclear morphology was assessed in MCF-7 cells with propidium iodide (PI) and acridine orange/ethidium bromide (AO/EB) staining and analyzed by fluorescence microscopy. Events like cell cycle arrest, apoptosis was observed by flow cytometric analysis and expressions of p-Rb, cyclin D1, cyclin-dependent kinase 4 (CDK4), CDK6, Bax, Bcl-2, PI3K/p-AKT was analyzed by immunoblot. RESULTS: Carvacrol significantly reduced cell viability with the half maximal inhibitory concentration value of 200 µmol/L at 24 and 48 h (P<0.05). importantly, there was a significant increase in the accumulation of the G CONCLUSION Carvacrol significantly inhibited the breast cancer MCF-7 cell proliferation and induced apoptosis via suppressing PI3/AKT signaling pathway.