An investigation of cerebral edema and injury volume assessments for controlled cortical impact injury.

An investigation of cerebral edema and injury volume assessments for controlled cortical impact injury.

J Neurosci Methods. 2007 Nov

Elliott MB, Jallo JJ, Tuma RF.
Department of Physical Therapy, Temple University, 3307 North Broad Street, Philadelphia, PA 19140, United States.

Using the controlled cortical impact (CCI) model, our laboratory compared edema in contralateral and ipsilateral regions to help clarify conflicting reports of contralateral edema and for enhanced assessment and interpretation of CCI injury pathophysiology. This investigation examined regional edema in response to graded injury severities over time with regards to tissue damage. Prior to injury rats were anesthetized with ketamine and xylazine (1:1). CCI injury parameters were set at 4.0m/s and 120 to 130ms. Rats were randomized to receive moderate or severe injuries set at 2.0 and 3.0mm depths, respectively. Cerebral edema and injury volume were examined separately following euthanasia with pentobarbital. Cerebral edema was measured using the wet-dry weight technique at 24 or 48h after injury. Sham animals underwent all surgical procedures except the impact injury. Injury volume was quantified using 2,3,5-triphenyltetrazolium chloride staining at 24h or 7 days after injury. The results of this investigation confirm that cerebral edema is absent in the uninjured, contralateral hemisphere after moderate and severe CCI injury. There were regional differences in cerebral edema formation in the hemisphere ipsilateral to injury that were dependent on injury severity and the length of time after injury. Tissue damage was reduced over 7 days following moderate CCI injury. Conclusions: (1) the absence of edema in the contralateral hemisphere allows it to serve as a valid control for edema formation, (2) misrepresenting injury volume because of edema continues to be a problem for evaluating CCI injury and treatment efficacy, and (3) reduced injury volume over 7 days following CCI injury suggests tissue recovery after initial dysfunction.

PMID: 18076998 [PubMed - as supplied by publisher]

Sudden Death in Toddlers with Viral Meningitis, Cerebral Edema, Lund Edema

Sudden Death in Toddlers with Viral Meningitis, Massive Cerebral Edema, and Neurogenic Pulmonary Edema and Hemorrhage: Report of Two Cases.
Pediatr Dev Pathol. 2007 Mar

Krous H,
Chadwick A,
Miller D,
Crandall L,
Kinney H.

Viral (lymphocytic) meningitis typically does not cause sudden death, especially in the absence of severe inflammation in the brain or other organs. We report two toddlers with clinical evidence of a viral infection who died unexpectedly and were found at autopsy to have lymphocytic meningitis associated with severe brain edema, transtentorial herniation, neurogenic pulmonary edema and hemorrhage, and cardiomegaly. Influenza A, demonstrated in tracheal epithelium by immunocytochemistry, is the presumed cause of the mild meningitis in one case; adenovirus was cultured from swabs of the brain and anus in the second case.

Current concepts of neurogenic pulmonary edema and acute cardiac dysfunction associated with intracranial disease are discussed in considering the mechanism of sudden death in these toddlers. These cases emphasize the possibility that mild intracranial viral infections may be a rare cause of sudden death via lethal cardiopulmonary complications. They also underscore the importance of a comprehensive autopsy, including detailed neuropathologic examination and viral testing, in determining of the cause of unexpected death in toddlers.

PMID: 17378656 [PubMed - as supplied by publisher]