Brain temperature monitoring and modulation in patients with severe MCA infarction

Schwab, Stefan; Spranger, Matthias; Aschoff, A.; Steiner, Th.; Hacke, Werner

doi:10.1212/wnl.48.3.762

Cited by 185 publications

(82 citation statements)

References 15 publications

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“…34 The brain temperatures of all 25 patients were consistently higher than body-core temperatures, confirming previous data that showed a significant gradient between body-core and brain temperatures in neurotrauma patients. 35,36 This may be explained by the high metabolic activity of cerebral tissue with considerable production of heat. 37 Another possibility is that in the early stages of infarct formation, a decrease in cerebral blood flow may result in a decreased capacity for the blood to carry off heat generated by local cerebral metabolism.…”

Section: Discussionmentioning

confidence: 99%

Moderate Hypothermia in the Treatment of Patients With Severe Middle Cerebral Artery Infarction

Schwab

Schwarz

Spranger

et al. 1998

Stroke

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599

351

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Background and Purpose-Animal research and clinical studies in head trauma patients suggest that moderate hypothermia may improve outcome by attenuating the deleterious metabolic processes in neuronal injury. Clinical studies on moderate hypothermia in the treatment of acute ischemic stroke patients are still lacking. Methods-Moderate hypothermia was induced in 25 patients with severe ischemic stroke in the middle cerebral artery (MCA) territory for therapy of postischemic brain edema. Hypothermia was induced within 14Ϯ7 hours after stroke onset and achieved by external cooling with cooling blankets, cold infusions, and cold washing. Patients were kept at 33°C body-core temperature for 48 to 72 hours, and intracranial pressure (ICP), cerebral perfusion pressure, and brain temperature were monitored continuously. Outcome at 4 weeks and 3 months after the stroke was analyzed with the Scandinavian Stroke Scale (SSS) and Barthel index. The side effects of induced moderate hypothermia were analyzed. Results-Fourteen patients survived the hemispheric stroke (56%). Neurological outcome according to the SSS score was 29 (range, 25 to 37) 4 weeks after stroke and 38 (range 28 to 48) 3 months after stroke. During hypothermia, elevated ICP values could be significantly reduced. Herniation caused by a secondary rise in ICP after rewarming was the cause of death in all remaining patients. The most frequent complication of moderate hypothermia was pneumonia in 10 of the 25 patients (40%). Other severe side effects of hypothermia could not be detected. Conclusions-Moderate hypothermia in the treatment of severe cerebral ischemia is not associated with severe side effects.Moderate hypothermia can help to control critically elevated ICP values in severe space-occupying edema after MCA stroke and may improve clinical outcome in these patients. (Stroke. 1998;29:2461-2466.)

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Section: Discussionmentioning

confidence: 99%

Moderate Hypothermia in the Treatment of Patients With Severe Middle Cerebral Artery Infarction

Schwab

Schwarz

Spranger

et al. 1998

Stroke

Self Cite

599

351

View full text Add to dashboard Cite

show abstract

“…This type of divergence has been demonstrated during neuropathological states, including ischemia and trauma, in both humans (Schwab et al, 1997;Henker et al, 1998) and animal models (Colbourne et al, 1993). If, during fever (or hyperthermia), core temperature rises disproportionately to that of brain, then threshold brain temperatures for the induction of seizures may not be reached.…”

Section: Introductionmentioning

confidence: 98%

Endogenous Neuropeptide Y Prevents Recurrence of Experimental Febrile Seizures by Increasing Seizure Threshold

Dubé

Brunson

Eghbal-Ahmadi

et al. 2005

JMN

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Febrile seizures (FSs) typically occur at the onset of fever and do not recur within the same febrile episode despite enduring or increased hyperthermia. Recurrent seizures during the same febrile episode are considered "complex," with potentially altered prognosis. A characterized immature rat model of FS was used to test the hypotheses that (1) a first FS influences the threshold temperature for subsequent ones, and (2) the underlying mechanisms involve the release and actions of the endogenous inhibitory hippocampal neuropeptide Y (NPY). Experimental FSs were induced two or three times, at 3-to 4-h intervals, and threshold temperatures measured. To determine the potential effects of seizure-induced endogenous NPY on thresholds for subsequent seizures, an antagonist of the major hippocampal NPY receptor (type 2) was infused prior to induction of the second seizure. As an indicator of NPY release, NPY expression was determined 4 and 24 h later. Threshold core and brain temperatures for hyperthermic seizures were consistent with those observed during human fever. Threshold temperatures for a second and third seizure were significantly and progressively higher than those required for the first. This "protective" effect involved induction of endogenous NPY because it was abolished by the NPY antagonist. In addition, NPY mRNA expression was increased in dentate gyrus, CA3 and CA1, after an experimental FS, consistent with peptide release. Collectively these data indicate that the absence of repetitive seizures during a febrile episode involves the inhibitory actions of endogenous NPY, suggesting that the signaling cascade triggered by this peptide might provide targets for therapeutic intervention.

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“…Mild hypothermia can reduce blood brain barrier disruption, preserve cell membrane integrity, and thereby decrease intracranial pressure (ICP)-related complications [49,50]. Damaged brain tissue can have higher temperature than noninjured areas [51][52][53]. The difference between brain and body temperature can increase in brain-injured patients by 0.1°C to 2°C [54,55].…”

Section: Detrimental Effects Of Fevermentioning

confidence: 99%

Therapeutic Hypothermia for Acute Neurological Injuries

2012

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Therapeutic hypothermia (TH) is the intentional reduction of core body temperature to 32°C to 35°C, and is increasingly applied by intensivists for a variety of acute neurological injuries to achieve neuroprotection and reduction of elevated intracranial pressure. TH improves outcomes in comatose patients after a cardiac arrest with a shockable rhythm, but other off-label applications exist and are likely to increase in the future. This comprehensive review summarizes the physiology and cellular mechanism of action of TH, as well as different means of TH induction and maintenance with potential side effects. Indications of TH are critically reviewed by disease entity, as reported in the most recent literature, and evidence-based recommendations are provided.

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Brain temperature monitoring and modulation in patients with severe MCA infarction

Cited by 185 publications

References 15 publications

Moderate Hypothermia in the Treatment of Patients With Severe Middle Cerebral Artery Infarction

Moderate Hypothermia in the Treatment of Patients With Severe Middle Cerebral Artery Infarction

Endogenous Neuropeptide Y Prevents Recurrence of Experimental Febrile Seizures by Increasing Seizure Threshold

Therapeutic Hypothermia for Acute Neurological Injuries

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