Selective anterograde amnesia associated with hippocampal and splenial damage after heat stroke

Cha, Seong-Yi; Kang, Tae Seok; Kim, Seong-Jang; Lee, Hyo-Young; Kim, Hak-Jin; Jung, Dae-Soo; Kim, Eun-Joo

doi:10.1016/j.clineuro.2013.03.003

Cited by 5 publications

(2 citation statements)

References 6 publications

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“…Several reports have described the characteristics of neurologic sequelae in patients with EHS. [ 13 – 15 , 29 ] However, as compared to CHS, since the prevalence of EHS and its neurological sequelae are relatively low, the sample sizes of these studies are rather small. To date, no study has yet reported the incidence of CNS sequelae in EHS survivors.…”

Section: Discussionmentioning

confidence: 99%

Outcome and risk factors associated with extent of central nervous system injury due to exertional heat stroke

Yang

Zhao

et al. 2017

Medicine

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To explore the relationship between the extent of central nervous system (CNS) injury and patient outcomes meanwhile research the potential risk factors associated with neurologic sequelae. In this retrospective cohort study, we analyzed data from 117 consecutive patients (86 survivors, 31 nonsurvivors) with exertional heat stroke (EHS) who had been admitted to intensive care unit (ICU) at 48 Chinese hospitals between April 2003 and July 2015. Extent of CNS injury was dichotomized according to Glasgow coma scale (GCS) score (severe 3–8, not severe 9–15). We then assessed differences in hospital mortality based on the extent of CNS injury by comparing 90-day survival time between the patient groups. Exploring the risk factors of neurologic sequelae. The primary outcomewas the 90-day survival ratewhich differed between the 2 groups (P = .023). The incidence of neurologic sequelae was 24.4%. For its risk factors, duration of recurrent hyperthermia (OR = 1.73, 95% CI: 1.20–2.49, P = .003), duration of CNS injury (OR = 1.39, 95% CI: 1.04–1.85, P = .025), and low GCS in the first 24 hours after admission (OR = 2.39, 95% CI: 1.11–5.15, P = .025) were selected by multivariable logistic regression. Cooling effect was eliminated as a factor (OR = 2641.27, 95% CI 0.40–1.73_107, P = .079). Significant differences in 90-day survival ratewere observed based on the extent of CNS injury in patients with EHS, and incidence was 24.4% for neurologic sequelae. Duration of recurrent hyperthermia, duration of CNS injury, and low GCS score in the first 24 hours following admission may be independent risk factors of neurologic sequelae. Cooling effect should be validated in the further studies.

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Section: Discussionmentioning

confidence: 99%

Outcome and risk factors associated with extent of central nervous system injury due to exertional heat stroke

Yang

Zhao

et al. 2017

Medicine

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“…[6] Human hippocampal and rat striatal glucose metabolism were inhibited in HS-related brain metabolism disorder and dysfunction. [5,[7][8][9] In hippocampal slices, HS also stimulated glutamate release and enhanced hypoxia, which were more dependent on temperature and adenosine triphosphate (ATP) than calcium. The depletion of ATP inhibited the uptake of glutamate World J Emerg Med, Vol 14, No 4, 2023 and aspartate acid.…”

Section: Introductionmentioning

confidence: 99%

Heat stroke alters hippocampal and cerebellar transmitter metabonomics

Guo-xin¹

2023

World Journal of Emergency Medicine

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BACKGROUND:The mechanisms underlying heat stroke (HS)-induced hippocampal injury remain unclear. This study aimed to evaluate the HS-induced metabonomics of hippocampal and cerebellar transmitters. METHODS:The HS model was established with male Sprague-Dawley rats subjected to heat exposure of up to 42 °C at a humidity of (55.0±5.0)%. The hippocampal and cerebellar transmitters and metabolites of rats were tested via ultra-high-performance liquid chromatography-mass spectrometry (UPLC-MS/MS). The primary transmitters and metabolites were identified by principal component analysis (PCA) and orthogonal partial least square-discriminant analysis (OPLS-DA). The major metabolic pathways for HS were selected after enrichment. The brain injury was evaluated by histological tests.RESULTS: HS induced hippocampal and cerebellar injuries in rats. HS upregulated the protein levels of hippocampal glutamate, glutamine, gamma-aminobutyric acid, L-tryptophan (Trp), 5-hydroxy-indoleacetic acid, and kynurenine; however, it downregulated asparagine, tryptamine, 5-hydroxytryptophan, melatonin, 3,4-dihydroxyphenylalanine (L-DOPA), and vanillylmandelic acid. HS also sharply elevated the protein levels of cerebellar methionine and Trp, and decreased the levels of serotonin, L-alanine, L-asparagine, L-aspartate, cysteine, norepinephrine, spermine, spermidine, and tyrosine. Hippocampal glutamate, monoamine transmitters, cerebellar aspartate acid, and catecholamine transmitters' metabolic pathways were identified as the main metablic pathways in HS. CONCLUSION:The hippocampus and cerebellum were injured in rats with HS, possibly induced the disorder of hippocampal glutamate and serotonin metabolism, cerebellar aspartate acid and catecholamine transmitter metabolism, and related metabolic pathways.

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Protective Effects of Hyperbaric Oxygen Therapy on Brain Injury by Regulating the Phosphorylation of Drp1 Through ROS/PKC Pathway in Heatstroke Rats

Nie

Xie

et al. 2020

Cell Mol Neurobiol

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Selective anterograde amnesia associated with hippocampal and splenial damage after heat stroke

Cited by 5 publications

References 6 publications

Outcome and risk factors associated with extent of central nervous system injury due to exertional heat stroke

Outcome and risk factors associated with extent of central nervous system injury due to exertional heat stroke

Heat stroke alters hippocampal and cerebellar transmitter metabonomics

Protective Effects of Hyperbaric Oxygen Therapy on Brain Injury by Regulating the Phosphorylation of Drp1 Through ROS/PKC Pathway in Heatstroke Rats

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