Neuropathic pain (NP) is a long-term recurrent disease caused by somatosensory nervous system injury, with spontaneous pain, hyperalgesia, ectopic pain, and paresthesia as the main clinical manifestations. It adversely affects patients' quality of life. NP treatments often include medication, physical therapy, and invasive therapy; the first two therapies are generally ineffective for some NP patients. These patients sometimes rely on invasive therapy to alleviate pain.Spinal cord stimulation (SCS) is a very effective therapeutic method. SCS is a neuroregulatory method that involves placing the electrodes on the corresponding painful spinal cords. Pain is greatly alleviated after SCS. SCS has been proven to be an effective therapeutic method for the treatment of neurological pain. Furthermore, SCS provides a feasible approach for patients with unsuccessful drug treatment. This paper reviews the relevant literature of spinal cord electrical stimulation, focusing on the mechanism of action, clinical application, clinical efficacy and technical progress of spinal cord electrical stimulation. SCS is widely used in the treatment of NP diseases such as postherpetic neuralgia, back surgery failure syndrome, and phantom limb pain. With advancements in science and technology, tremendous progress has also been made in the spinal cord electrical stimulation method and good momentum has been maintained.

Headache is a common refractory disorder among adults, especially in females, which can lower the quality of life in patients and increase medical costs. Nearly 90% of people have been affected by headache disorders during their lifetime. The severe situation of headaches has drawn the attention of researchers in recent years. Although the mechanism of headache has not been fully understood by us, there are many effective preventive drugs and treatments available. This review is aimed to sum up the progress in clinical trials of headaches in the past 5 years.

Cerebral ischemic disease is a group of diseases that cause insufficient blood supply to the cerebrum, cerebellum or brain stem for different reasons, resulting in corresponding nervous system symptoms. Cardiovascular disease is the leading cause of death in the world. Among them, the death caused by cerebral ischemia accounts for the vast majority, and it is one of the fatal diseases in the middle‐aged and elderly at present. Epidemiologic studies have projected increasing mortality due to cardiovascular disease worldwide (about 23.3 million people by 2030) because of the aging population. However, related studies have shown that insulin‐like growth factor I (IGF‐1) is a multifunctional cell proliferation regulator. It plays an important role in cerebral ischemia. It is effective in promoting cell differentiation, proliferation and individual development. Studies have shown that IGF‐1 signaling pathway is a key pathway controlling cell growth and survival. There may be five mechanisms in cerebral ischemia: prevention of intracellular calcium overload, inhibition of the upregulation of nNOS, IGF‐1upregulations activating HIF‐1α, regulation of Bcl‐2 to resist apoptosis, and enhancement of vascular endothelial function. Three critical nodes in the IGF‐1 signaling pathway have been described in cardiomyocytes: protein kinase Akt/mammalian target of rapamycin (mTOR), Ras/Raf/extracellular signal‐regulated kinase (ERK), and phospholipase C (PLC)/inositol 1,4,5‐triphosphate (InsP3)/Ca2+. IGF‐1 plays an important role in cerebral ischemia and myocardial ischemia, mainly by activating downstream of IGF‐1, controlling cell death and differentiation or transcription work, improving the function of heart muscle cells, reducing the myocardial cell apoptosis induced by myocardial infarction, regulating endogenous protection and restoration of cerebral ischemia injury, thus protecting cerebral and myocardial injury. Related studies have shown that bcl‐2 exerts great influence on both cerebral ischemia and myocardial ischemia. Therefore, the relevant pathways and targets of cerebral ischemia and myocardial ischemia and the role of IGF‐1 in protecting the heart are reviewed in this paper.

The loss of neuronal in the substantia nigra of the elderly contributes to striatal damage and plays a critical part in the common forms of neurodegenerative diseases such as Parkinson disease (PD). The deficit of dopamine is one of the most familiar neuropathological features of PD as well as α-Synuclein aggregation. The peripheral autonomic nervous system is al so affected negatively during the course of the disease, although the subsistent of dyskinesias and else major motor characteristic deficits take significant role in the diagnostic methods during clinical practice, which is related to a number of non-motor symptoms that might increase aggregate risks. Multiple pathways and mechanisms are involved in the molecular pathogenesis: α-Synuclein, neuronal homeostasis, mitochondrial function, oxidative stress, as well as neuroinflammation. Investigations in the last few years for diagnostic biomarkers used neuroimaging, including single photon emission computed tomography as well as cutting-edge magnetic resonance imaging techniques, which has been presented to facilitate discrepant diagnosis.Pharmacological treatment is also important and efficient in equal measure. In addition to reliance on striatal dopamine replacement therapy, many solutions that are used for motor or nonmotor symptoms in these patients are available.