The method of iron-dependent cell death known as ferroptosis is distinct from apoptosis. The suppression of ferroptosis after intracerebral hemorrhage (ICH) will effectively treat ICH and improve prognosis. This paper primarily summarizes the mechanism of ferroptosis after ICH, with an emphasis on lipid peroxidation, the antioxidant system, iron metabolism, and other pathways. In addition, regulatory targets and drug molecules were described. Although there has been some progress in the field of study, there are still numerous gaps. The mechanism by which non-heme iron enters neurons through the blood–brain barrier (BBB), the mitochondrial role in ferroptosis, and the specific mechanism by which lipid peroxidation induces ferroptosis remain unclear and require further study. In addition, the inhibitory effect of many drugs on ferroptosis after ICH has only been demonstrated in basic experiments and must be translated into clinical trials. In summary, research on ferroptosis following ICH will play an important role in the treatment of ICH.

The blood–brain barrier (BBB) controls the flow of substances to maintain a homeostatic environment in the brain, which is highly regulated and crucial for the normal function of the central nervous system (CNS). Brain endothelial cells (bECs), which are directly exposed to blood, play the most important role in maintaining the integrity of the BBB. Unlike endothelial cells in other tissues, bECs have two unique features: specialized endothelial tight junctions and actively suppressed transcellular vesicle trafficking (transcytosis). These features help to maintain the relatively low permeability of the CNS barrier. In addition to the predominant role of tight junctions in the BBB, caveolae-mediated adsorptive transcytosis has attracted much interest in recent years. The active suppression of transcytosis is dynamically regulated during development and in response to diseases. Altered caveolae-mediated transcytosis of bECs has been reported in several neurological diseases, but the understanding of this process in bECs is limited. Here, we review the process of caveolae-mediated transcytosis based on previous studies and discuss its function in the breakdown of the BBB in neurological disorders.

Phantom limb pain (PLP) is a common sequela of amputation, experienced by 50-80% of amputees. Oral analgesics as the first-line therapy have limited effects. Since PLP usually affects activities of daily living and the psychological conditions of patients, effective treatments are imperatively needed. In this case study, a 49-year-old man was admitted to our hospital because of uncontrollable paroxysmal pain in his missing and residual leg. Due to severe injuries in a truck accident, the right lower limb of the patient was surgically amputated ~5 years ago. Around 1 month after amputation, he felt pain in his lost leg and PLP was diagnosed. Then, he started taking oral analgesics, but the pain still occurred. After admission on July 9, 2022, the patient received treatments of mirror therapy and magnetic stimulation to the sacral plexus. 1-month treatments reduced the frequency and intensity of pain in the phantom limb and the stump, without any adverse events. Analysis of high-resolution three-dimensional T1-weighted brain volume images at the end of 2-month treatments showed alterations in the thickness of cortex regions related to pain processing, compared to that before treatment. This case study gives us hints that one or both interventions of mirror therapy and sacral plexus magnetic stimulation effectively relieved PLP and stump limb pain. These non-invasive, low-cost and easily conducted treatments could be good options for PLP. But randomized controlled trials with a large number of cases are required to confirm their efficacy and safety.