Heat stroke: typical MRI and 1H-MRS features

Li, Jun; Zhang, Xueyan; Zou, Zhimeng; Wang, Bin; Xia, Ji-kai

doi:10.1016/j.clinimag.2014.12.011

Cited by 17 publications

(19 citation statements)

References 5 publications

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“…Patchy cortical lesions may also be seen (Muccio et al, 2013). Punctate hemorrhagic lesions have been described in the cerebellar hemispheres, brain stem, corona radiata, and frontal lobes on susceptibility-weighted images (Li et al, 2015a;Zhang and Li, 2014;Murcia-Gubianas et al, 2012). Diffusion tensor imaging has shown fractional anisotropy of cerebellar white and gray matter (Li et al, 2015b).…”

Section: Hyperthermiamentioning

confidence: 99%

Thermoregulatory disorders and illness related to heat and cold stress

Cheshire

2016

Autonomic Neuroscience

260

184

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Thermoregulation is a vital function of the autonomic nervous system in response to cold and heat stress. Thermoregulatory physiology sustains health by keeping body core temperature within a degree or two of 37°C, which enables normal cellular function. Heat production and dissipation are dependent on a coordinated set of autonomic responses. The clinical detection of thermoregulatory impairment provides important diagnostic and localizing information in the evaluation of disorders that impair thermoregulatory pathways, including autonomic neuropathies and ganglionopathies. Failure of neural thermoregulatory mechanisms or exposure to extreme or sustained temperatures that overwhelm the body's thermoregulatory capacity can also result in potentially life-threatening departures from normothermia. Hypothermia, defined as a core temperature of <35.0°C, may present with shivering, respiratory depression, cardiac dysrhythmias, impaired mental function, mydriasis, hypotension, and muscle dysfunction, which can progress to cardiac arrest or coma. Management includes warming measures, hydration, and cardiovascular support. Deaths from hypothermia are twice as frequent as deaths from hyperthermia. Hyperthermia, defined as a core temperature of >40.5°C, may present with sweating, flushing, tachycardia, fatigue, lightheadedness, headache, and paresthesia, progressing to weakness, muscle cramps, oliguria, nausea, agitation, hypotension, syncope, confusion, delirium, seizures, and coma. Mental status changes and core temperature distinguish potentially fatal heat stroke from heat exhaustion. Management requires the immediate reduction of core temperature. Ice water immersion has been shown to be superior to alternative cooling measures. Avoidance of thermal risk and early recognition of cold or heat stress are the cornerstones of preventive therapy.

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Section: Hyperthermiamentioning

confidence: 99%

Thermoregulatory disorders and illness related to heat and cold stress

Cheshire

2016

Autonomic Neuroscience

260

184

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“…The lesions of the cerebellum are mainly concentrated in the cerebellar cortex, superior cerebellar peduncle, vermis of the cerebellum, and corpora dentatum. In addition, the common lesion site is the caudate nucleus of the basal ganglia [6,7,9,[11][12][13][14][15][16][17][18]. However, our case involved symmetrical lesions in both sides of the posterior limb of the internal capsule, putamen, external capsule, insular lobe, and subcortical white matter, which has not been reported before.…”

Section: Discussionmentioning

confidence: 63%

Magnetic resonance imaging and magnetic resonance venography features in heat stroke: a case report

Cao

Wang

Gao

et al. 2019

Preprint

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Background: Heat stroke (HS) is a critical illness that can cause multiple organ dysfunction, including damage to the central nervous system (CNS), which can be life-threatening in severe cases. Brain lesions in patients with HS who present with CNS damage have been rarely reported before, and they usually vary in different cases, hence, patients with such lesions may present a clinical challenge in terms of diagnosis and management. Cerebral venous thrombosis (CVT) is a rare cause of stroke that mostly affects young individuals and children. The pathogenesis of brain damage caused by HS is complex, and CVT may be involved in the pathogenesis of HS with CNS damage. In this manuscript, we have reported a case of a patient with HS having CVT with symmetrical lesions in the bilateral putamen, posterior limb of the internal capsule, external capsule, insular lobe, and subcortical white matter in the brain. Case presentation: We encountered a 48-year-old man who presented with HS in the summer season. During admission, he had a high body temperature and was in coma and shock. Then, he developed rhabdomyolysis syndrome, acute kidney and liver damage, electrolyte imbalance, and acid–base balance disorders, and his D-dimer level was elevated. After several days of anti-shock treatment, the patient’s level of consciousness improved. However, he experienced a decline in vision. Cerebral magnetic resonance imaging (MRI) showed symmetrical lesions in the bilateral posterior limb of the internal capsule, putamen, external capsule, insula, and subcortical white matter, and cerebral magnetic resonance venography (MRV) showed the development of CVT. Therefore, anti-coagulation treatment was provided. After timely clinical intervention, the symptoms of the patient gradually improved. Conclusions: This case showed that HS can cause CVT. Therefore, cerebral MRI findings in HS must be assessed; in addition, early MRV can help in the diagnosis of the disease, which can effectively improve prognosis.

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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%

“…[ 11 , 12 ] Notably, approximately 20% to 30% of CHS survivors experience neurologic sequelae (eg, cerebellarataxia, dysarthria, cognitive disorders, and anterograde amnesia) within a few days, weeks, or months of CHS onset despite rapid initiation of aggressive clinical treatments, including lowering of core body temperature and support of organ function. [ 3 , 7 , 13 – 16 ] Bazille et al [ 16 ] performed neuropathologic studies in 3 patients who died from HS which identified Purkinje cells in cerebellum showed diffuse loss. We also noticed that the body core temperature of the 3 patients are over 42 °C.…”

Section: Introductionmentioning

confidence: 99%

“…We also noticed that the body core temperature of the 3 patients are over 42 °C. In the study of Li et al, [ 13 ] hyperthermia for HS patients close to 40 °C, abnormal signals in cerebellum were observed by magnetic resonance imaging. About 10 years ago, the American College of Sports Medicine (ACSM) had recognized that cooling rapidly could reduce neurological complications of EHS patients greatly, and body core temperature below 40.5 C in 60 minutes seldom result in lasting sequelae.…”

Section: Introductionmentioning

confidence: 99%

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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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Heat stroke: typical MRI and 1H-MRS features

Cited by 17 publications

References 5 publications

Thermoregulatory disorders and illness related to heat and cold stress

Thermoregulatory disorders and illness related to heat and cold stress

Magnetic resonance imaging and magnetic resonance venography features in heat stroke: a case report

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

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