Anticonvulsant properties of hypothermia in experimental status epilepticus

Schmitt, Friedhelm C.; Buchheim, Katharina; Meierkord, Hartmut; Holtkamp, Martin

doi:10.1016/j.nbd.2006.05.008

Cited by 112 publications

(74 citation statements)

References 50 publications

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“…34 This discrepancy may be related to the earlier and deeper cooling used in animal models. 32,33 Most studies rely on clinical evaluation for seizure diagnosis and classification of seizure severity in newborns. 35,36 However, it is known that the majority of seizures, especially in critically ill infants, do not have a clinical correlate and will not be recognized without continuous EEG.…”

Section: Resultsmentioning

confidence: 99%

Video-EEG monitoring in newborns with hypoxic-ischemic encephalopathy treated with hypothermia

Nash¹,

Bonifacio²,

Glass³

et al. 2011

Neurology

169

128

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Section: Resultsmentioning

confidence: 99%

Video-EEG monitoring in newborns with hypoxic-ischemic encephalopathy treated with hypothermia

Nash¹,

Bonifacio²,

Glass³

et al. 2011

Neurology

169

128

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“…There are various ways that inflammation of the colon could cause an alteration in PTZ seizure threshold. As seizure generation is highly sensitive to brain temperature (29), it is possible that the peripheral inflammation caused a high fever that made the brain more susceptible to the PTZ. This is unlikely, however, as animals with TNBS colitis do not display fever (15,30).…”

Section: Discussionmentioning

confidence: 99%

Microglial activation and TNFα production mediate altered CNS excitability following peripheral inflammation

Riazi

Galic²,

Kuzmiski³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

366

307

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Peripheral inflammation leads to a number of centrally mediated physiological and behavioral changes. The underlying mechanisms and the signaling pathways involved in these phenomena are not yet well understood. We hypothesized that peripheral inflammation leads to increased neuronal excitability arising from a CNS immune response. We induced inflammation in the gut by intracolonic administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) to adult male rats. To examine the excitability of the brain in vivo, we administered pentylenetetrazole (PTZ; a GABAergic antagonist) intravenously to evoke clonic seizures. Rats treated with TNBS showed increased susceptibility to PTZ seizures that was strongly correlated with the severity and progression of intestinal inflammation. In vitro hippocampal slices from inflamed, TNBS-treated rats showed increased spontaneous interictal burst firing following application of 4-aminopyridine, indicating increased intrinsic excitability. The TNBS-treated rats exhibited a marked, reversible inflammatory response within the hippocampus, characterized by microglial activation and increases in tumor necrosis factor ␣ (TNF␣) levels. Central antagonism of TNF␣ using a monoclonal antibody or inhibition of microglial activation by i.c.v. injection of minocycline prevented the increase in seizure susceptibility. Moreover, i.c.v. infusion of TNF␣ in untreated rats for 4 days also increased seizure susceptibility and thus mimicked the changes in seizure threshold observed with intestinal inflammation. Our finding of a microglia-dependent TNF␣-mediated increase in CNS excitability provides insight into potential mechanisms underlying the disparate neurological and behavioral changes associated with chronic inflammation.4-aminopyridine ͉ cytokine ͉ pentylenetetrazole ͉ seizure ͉ colitis

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“…The anticonvulsant property of hypothermia has been recognized for decades in clinical and preclinical studies of refractory status epilepticus (Schmitt et al, 2006;Corry et al, 2008) and brain injury-induced seizures (Clifton et al, 1993;Hayes, 2009). In most clinical cases, whole-body hypothermia therapy requires a prolonged period of maintenance, for example, 24-48 hours, to cover the high-risk period of seizure occurrence (McIntyre et al, 2003;Bernard and Rosalion, 2008;Diller and Zhu, 2009).…”

Section: Fig 5 (A)mentioning

confidence: 99%

Comprehensive Evaluation of Neuroprotection Achieved by Extended Selective Brain Cooling Therapy in a Rat Model of Penetrating Ballistic-Like Brain Injury

Shear

Deng-Bryant

et al. 2016

Therapeutic Hypothermia and Temperature Management

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Brain hypothermia has been considered as a promising alternative to whole-body hypothermia in treating acute neurological disease, for example, traumatic brain injury. Previously, we demonstrated that 2-hours selective brain cooling (SBC) effectively mitigated acute (p24 hours postinjury) neurophysiological dysfunction induced by a penetrating ballistic-like brain injury (PBBI) in rats. This study evaluated neuroprotective effects of extended SBC (4 or 8 hours in duration) on sub-acute secondary injuries between 3 and 21 days postinjury (DPI). SBC (34°C) was achieved via extraluminal cooling of rats' bilateral common carotid arteries (CCA). Depending on the experimental design, SBC was introduced either immediately or with a 2-or 4-hour delay after PBBI and maintained for 4 or 8 hours. Neuroprotective effects of SBC were evaluated by measuring brain lesion volume, axonal injury, neuroinflammation, motor and cognitive functions, and post-traumatic seizures. Compared to untreated PBBI animals, 4 or 8 hours SBC treatment initiated immediately following PBBI produced comparable neuroprotective benefits against PBBI-induced early histopathology at 3 DPI as evidenced by significant reductions in brain lesion volume, axonal pathology (beta-amyloid precursor protein staining), neuroinflammation (glial fibrillary acetic protein stained-activated astrocytes and rat major histocompatibility complex class I stained activated microglial cell), and post-traumatic nonconvulsive seizures. In the later phase of the injury (7-21 DPI), significant improvement on motor function (rotarod test) was observed under most SBC protocols, including the 2-hour delay in SBC initiation. However, SBC treatment failed to improve cognitive performance (Morris water maze test) measured 13-17 DPI. The protective effects of SBC on delayed axonal injury (silver staining) were evident out to 14 DPI. In conclusion, the CCA cooling method of SBC produced neuroprotection measured across multiple domains that were evident days/weeks beyond the cooling duration and in the absence of overt adverse effects. These ''proof-of-concept'' results suggest that SBC may provide an attractive neuroprotective approach for clinical considerations.

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Anticonvulsant properties of hypothermia in experimental status epilepticus

Cited by 112 publications

References 50 publications

Video-EEG monitoring in newborns with hypoxic-ischemic encephalopathy treated with hypothermia

Video-EEG monitoring in newborns with hypoxic-ischemic encephalopathy treated with hypothermia

Microglial activation and TNFα production mediate altered CNS excitability following peripheral inflammation

Comprehensive Evaluation of Neuroprotection Achieved by Extended Selective Brain Cooling Therapy in a Rat Model of Penetrating Ballistic-Like Brain Injury

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