Billions of cells die in us every hour, and our tissues do not shrink because there is a natural regulation where Cell Death (CD) is balanced with cell division. The process in which cells eliminate themselves in a controlled manner is called Programmed Cell Death (PCD). The PCD plays an important role during embryonic development, in maintaining homeostasis of the body\'s tissues, and in the elimination of damaged cells, under a wide range of physiological and developmental stimuli. A multitude of protein mediators of PCD have been identified and signals have been found to utilize common pathways elucidating the proteins involved. This narrative review focuses on caspase-dependent and caspase-independent PCD pathways. Included are studies of caspase-dependent PCD such as Anoikis, Catastrophe Mitotic, Pyroptosis, Emperitosis, Parthanatos and Cornification, and Caspase-Independent PCD as Wallerian Degeneration, Ferroptosis, Paraptosis, Entosis, Methuosis, and Extracellular Trap Abnormal Condition (ETosis), as well as neutrophil extracellular trap abnormal condition (NETosis) and Eosinophil Extracellular Trap Abnormal Condition (EETosis). Understanding PCD from those reported in this review could shed substantial light on the processes of biological homeostasis. In addition, identifying specific proteins involved in these processes is mandatory to identify molecular biomarkers, as well as therapeutic targets. This knowledge could provide the ability to modulate the PCD response and could lead to new therapeutic interventions in a wide range of diseases.

UNASSIGNED: Metastatic brain tumors are a common complication of systemic cancer. They tend to have a chronic onset and are located at the gray-white junction of the cerebral hemispheres, those larger than 9.4 mm in diameter are often accompanied by substantial vasogenic edema. Herein, we report a rare case of calcified metastatic adenocarcinoma with Wallerian degeneration. In addition, we discuss the atypical manifestations of brain metastases.
UNASSIGNED: A 71-year-old man who went through stroke-like onset twice during 8 months with a history of resection of the left pulmonary adenocarcinoma 5 years prior was examined. Diffusion weighted magnetic resonance imaging of the brain showed an enlarged open-ring-shaped hyperintensity on the left periventricular white matter and basal ganglia, with Wallerian degeneration on the left cerebral peduncle. Brain computed tomography revealed nodular calcification of the lesion. The pathology of stereotactic biopsy indicated metastatic adenocarcinoma.
UNASSIGNED: When patients present with acute nervous system symptoms and a previous history of cancer, the possibility of metastases should be considered, even if neuroimaging is atypical.

Peripheral nerve injuries have been associated with increased healthcare costs and decreased patients\' quality of life. Aging represents one factor that slows the speed of peripheral nervous system (PNS) regeneration. Since cellular homeostasis imbalance associated with aging lead to an increased failure in nerve regeneration in mammals of advanced age, this systematic review aims to determine the main molecular and cellular mechanisms involved in peripheral nerve regeneration in aged murine models after a peripheral nerve injuries.
Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, a literature search of 4 databases was conducted in July 2022 for studies comparing the peripheral nerve regeneration capability between young and aged murine models.
After the initial search yielded 744 publications, ten articles fulfilled the inclusion criteria. These studies show that age-related changes such as chronic inflammatory state, delayed macrophages\' response to injury, dysfunctional Schwann Cells (SCs), and microenvironment alterations cause a reduction in the regenerative capability of the PNS in murine models. Furthermore, identifying altered gene expression patterns of SC after nerve damage can contribute to the understanding of physiological modifications produced by aging.
The interaction between macrophages and SC plays a crucial role in the nerve regeneration of aged models. Therefore, studies aimed at developing new and promising therapies for nerve regeneration should focus on these cellular groups to enhance the regenerative capabilities of the PNS in elderly populations.

A growing body of studies indicate that small noncoding RNAs, especially microRNAs (miRNA), play a crucial role in response to peripheral nerve injuries. During Wallerian degeneration and regeneration processes, they orchestrate several pathways, in particular the MAPK, AKT, and EGR2 (KROX20) pathways. Certain miRNAs show specific expression profiles upon a nerve lesion correlating with the subsequent nerve regeneration stages such as dedifferentiation and with migration of Schwann cells, uptake of debris, neurite outgrowth and finally remyelination of regenerated axons. This review highlights (a) the specific expression profiles of miRNAs upon a nerve lesion and (b) how miRNAs regulate nerve regeneration by acting on distinct pathways and linked proteins. Shedding light on the role of miRNAs associated with peripheral nerve regeneration will help researchers to better understand the molecular mechanisms and deliver targets for precision medicine.

Peripheral nerve injury (PNI) is a common disease in clinic, and the regeneration process of peripheral nerve tissue is slow, and patients with PNI often suffer from the loss of nerve function. At present, related research on the mechanism of peripheral nerve regeneration has become a hot spot, and scholars are also seeking a method that can accelerate the regeneration of peripheral nerve. Platelet-rich plasma (PRP) is a platelet concentrate extracted from autologous blood by centrifugation, which is a kind of bioactive substance. High concentration of platelets can release a variety of growth factors after activation, and can promote the proliferation and differentiation of tissue cells, which can accelerate the process of tissue regeneration. The application of PRP comes from the body, there is no immune rejection reaction, it can promote tissue regeneration with less cost, it is,therefore, widely used in various clinical fields. At present, there are relatively few studies on the application of PRP to peripheral nerve regeneration. This article summarizes the literature in recent years to illustrate the effect of PRP on peripheral nerve regeneration from mechanism to clinical application, and prospects for the application of PRP to peripheral nerve.

When temporal bone fractures are associated with facial palsy (FP) evolution the medical team have no much time to make a decision: to do or not to do a surgical approach? How to evaluate the necessity? When to do it and when is the correct time?

Peripheral nerves that are interrupted by trauma or surgical resection require reapproximation of their ends. When primary repair cannot be performed without undue tension, nerve grafting is required. Nerve repair with autograft is limited when there is insufficient amount of autologous nerves available for large nerve defects. This encouraged the search for alternative means of reconstruction in extensive nerve injuries. The cadaveric nerve allograft provides an unlimited graft source without the morbidities associated with autograft reconstruction; but these grafts are rapidly rejected unless appropriate recipient immunosuppression is achieved. An optimal treatment method for nerve allograft transplantation must minimize or prevent rejection while permitting nerve regeneration at the same time. In this report, the literature of nerve allograft transplantation experimental studies, strategies to prevent nerve allograft rejection, and reported clinical experiences are reviewed.

Fatigue is one of the most common and most disabling symptoms of multiple sclerosis (MS). Although numerous studies have tried to reveal it, no definite pathogenesis factor behind this fatigue has been identified. Fatigue may be directly related to the disease mechanisms (primary fatigue) or may be secondary to non-disease-specific factors. Primary fatigue may be the result of inflammation, demyelination, or axonal loss. A suggested functional cortical reorganization may result in a higher energy demand in certain brain areas, culminating in an increase of fatigue perception. Higher levels of some immune markers were found in patients with MS-related fatigue, whereas other studies rejected this hypothesis. There may be a disturbance in the neuroendocrine system related to fatigue, but it is not clear whether this is either the result of the interaction with immune activation or the trigger of this process. Fatigue may be secondary to sleep problems, which are frequently present in MS and in their turn result from urinary problems, spasms, pain, or anxiety. Pharmacologic treatment of MS (symptoms) may also provoke fatigue. The evidence for reduced activity as a cause of secondary fatigue in MS is inconsistent. Psychological functioning may at least play a role in the persistence of fatigue. Research did not reach consensus about the association of fatigue with clinical or demographic variables, such as age, gender, disability, type of MS, education level, and disease duration. In conclusion, it is more likely to explain fatigue from a multifactor perspective than to ascribe it to one mechanism. The current evidence on the pathogenesis of primary and secondary fatigue in MS is limited by inconsistency in defining specific aspects of the concept fatigue, by the lack of appropriate assessment tools, and by the use of heterogeneous samples. Future research should overcome these limitations and also include longitudinal designs.

A case of a 22-year-old woman with rare neurologic complications including encephalopathy and acute axonal sensorimotor polyneuropathy in the course of acute pancreatitis is reported. The encephalopathy emerged 3 weeks after the onset of the illness with complete remission being noted 1 week later. The polyneuropathy presented as quadriplegia and respiratory failure that required intubation and partially remitted gradually. There was no pancreatic lesion, no major pancreatic surgery, no sepsis, and no multiple organ failure, all of which had been proposed as the predisposing factors. Severe inflammatory response syndrome (SIRS) that developed during the clinical course of this patient might have induced these neurologic complications.

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