Characterisation of Brain Edema Following “Controlled Cortical Impact Injury” in Rats

Unterberg, A.; Stroop, Ralf; Thomale, Ulrich-Wilhelm; Kiening, Karl; Päuser, S.; Vollmann, W.

doi:10.1007/978-3-7091-6837-0_33

Cited by 53 publications

(63 citation statements)

References 6 publications

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“…The exact etiology of vasogenic edema in DAI is currently not yet fully understood. Animal and human studies have confirmed that vasogenic edema occurs in DAI [17,18] and has been reported to be potentially partially reversible. Type-2 lesions represent lesions with restricted or decreased diffusion.…”

Section: Discussionmentioning

confidence: 71%

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Diffusion-weighted MRI in diffuse axonal injury of the brain

et al. 2002

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The goal of this study was to identify and describe the different types and patterns of tissue injury which are encountered by diffusion-weighted imaging (DWI) in diffuse axonal injury (DAI) of the brain. The DWI data sets of 98 patients who suffered from a closed-head injury were retrospectively evaluated. Medical records were reviewed to rule out pre-existing neurological diseases. Lesions were studied for their DWI signal characteristics and lesion size or extension. Traumatic lesions were classified into three categories depending on their signal characteristica on DWI and apparent diffusion coefficient (ADC) maps: type 1, DWI- and ADC-hyperintense most likely representing lesions with vasogenic edema; type 2, DWI-hyperintense, ADC-hypointense indicating cytotoxic edema; type 3, central hemorrhagic lesion surrounded by an area of increased diffusion. According to the size and extent of lesions, injury was classified into three groups: group A, focal injury; group B, regional/confluent injury; and group C, extensive/diffuse injury. Our study showed that diffusion-weighted imaging differentiates between lesions with decreased and increased diffusion in patients with DAI. Different degrees of tissue injury extent were noticed. Future prospective studies should study if this additional information can be used as a predictor of injury reversibility, final outcome and prognosis.

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Section: Discussionmentioning

confidence: 71%

“…One likely, important contributor is cytotoxic edema. Cytotoxic edema has been observed in multiple studies involving traumatic brain injury [17,18,19]. An animal study using a controlled cortical impact injury in rats showed that vasogenic and cytotoxic edema can occur simultaneously.…”

Section: Discussionmentioning

confidence: 99%

Diffusion-weighted MRI in diffuse axonal injury of the brain

et al. 2002

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“…Thus, the overall increase in T 1 is probably due to an increase in tissue water content within the contusion. The cellular disintegration and breakdown of macromolecules in the contusion has recently been theorized to cause a rapid increase in osmolality (29) and thus may be an important contribution to edema, although ischemic and vasogenic contributions may also be important (10).…”

Section: T 1obs Heterogeneitymentioning

confidence: 99%

“…Cerebral edema often accompanies the development of early posttraumatic hypoperfusion, particularly in the most severely injured regions (1,10). This co-existence of regions of edema and perfusion deficit should create spatial heterogeneity of the in vivo spin-lattice relaxation time (T 1obs ) of tissue water in models of focal contusion, such as the CCI model of TBI in the rat.…”

mentioning

confidence: 99%

Early perfusion after controlled cortical impact in rats: Quantification by arterial spin-labeled MRI and the influence of spin-lattice relaxation time heterogeneity

et al. 1999

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“…Both measurements allow for a more individualized (targeted) ICP/CPP therapy. 74,90 In the last decade the so-called bedside-or onlinemicrodialysis has been introduced in neurocritical care. This method is based on a double-lumen microcatheter with a semipermeable membrane in the cerebral parenchyma.…”

Section: Traumatic Head Injurymentioning

confidence: 99%

Current Concepts in Diagnosis and Treatment of Traumatic Brain Injury: Implications for Healthcare in Nepal

Sakowitz

Sharma

Kiening³

2005

Nep J Neurosci

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Taumatic brain injury (TBI) is a leading cause of disability and death in the industrialized and in the developing world. With an incidence of 200-400 cases per 100.000, head injuries are a major contributor to socio-economic costs. The 20% suffering from severe head injury (SHI) requiring prolonged intensive care and/or neurosurgical intervention are of particular interest to specialist practitioners from multiple disciplines.This review covers the current concepts of diagnosis and treatment in these patients in the Western world, i.e. mainly the US and Western Europe. Special emphasis is laid upon evidence-based guidelines established during the last decade. Comparison is drawn to the current status of trauma care in Nepal.Management strategies for TBI can not be applied to Nepalese healthcare entirely. Effective management of head injured persons in Nepal is affected by its difficult geographical location, unavailability of trained personnel in the field, and difficulty in transporting the patients due to the lack of motorable roads. While some of the equipment for the treatment of TBI victims is readily available (e.g. ventricular drainage), others are scarce (e.g. operating room capacity, intensive care facilities) or completely unavailable (e.g. emergency medical service providers, specialized monitoring equipment). Realistic proposals for improvement of the current situation are made. Nepal Journal of Neuroscience, Volume 2, Number 1, 2005, page: 29-51

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Characterisation of Brain Edema Following “Controlled Cortical Impact Injury” in Rats

Cited by 53 publications

References 6 publications

Diffusion-weighted MRI in diffuse axonal injury of the brain

Diffusion-weighted MRI in diffuse axonal injury of the brain

Early perfusion after controlled cortical impact in rats: Quantification by arterial spin-labeled MRI and the influence of spin-lattice relaxation time heterogeneity

Current Concepts in Diagnosis and Treatment of Traumatic Brain Injury: Implications for Healthcare in Nepal

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