Meningitis Signs and Symptoms

Haidrani, Layla

doi:10.7748/ns.30.32.31.s33

Cited by 2 publications

(1 citation statement)

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“…In some cases, Cryptococcus can circulate through the bloodstream and reach the brain, causing meningitis ( Kwizera et al, 2021 ; Retchless et al, 2022 ). The disease presents with a range of symptoms, including headache, fever, nausea and vomiting, and stiff neck, among others ( Haidrani, 2016 ; Bårnes et al, 2018 ; Lin and Su, 2020 ). If left untreated, the disease can pose a significant risk to the patient life.…”

Section: Ferroptosis and Mitochondrial Dysfunction In Non-traumatic B...mentioning

confidence: 99%

Ferroptosis and mitochondrial dysfunction in acute central nervous system injury

Dong

Gong

Zhao

et al. 2023

Front. Cell. Neurosci.

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Acute central nervous system injuries (ACNSI), encompassing traumatic brain injury (TBI), non-traumatic brain injury like stroke and encephalomeningitis, as well as spinal cord injuries, are linked to significant rates of disability and mortality globally. Nevertheless, effective and feasible treatment plans are still to be formulated. There are primary and secondary injuries occurred after ACNSI. Most ACNSIs exhibit comparable secondary injuries, which offer numerous potential therapeutic targets for enhancing clinical outcomes. Ferroptosis, a newly discovered form of cell death, is characterized as a lipid peroxidation process that is dependent on iron and oxidative conditions, which is also indispensable to mitochondria. Ferroptosis play a vital role in many neuropathological pathways, and ACNSIs may induce mitochondrial dysfunction, thereby indicating the essentiality of the mitochondrial connection to ferroptosis in ACNSIs. Nevertheless, there remains a lack of clarity regarding the involvement of mitochondria in the occurrence of ferroptosis as a secondary injuries of ACNSIs. In recent studies, anti-ferroptosis agents such as the ferroptosis inhibitor Ferrostain-1 and iron chelation therapy have shown potential in ameliorating the deleterious effects of ferroptosis in cases of traumatic ACNSI. The importance of this evidence is extremely significant in relation to the research and control of ACNSIs. Therefore, our review aims to provide researchers focusing on enhancing the therapeutic outcomes of ACNSIs with valuable insights by summarizing the physiopathological mechanisms of ACNSIs and exploring the correlation between ferroptosis, mitochondrial dysfunction, and ACNSIs.

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