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Basics of CT Scan Head and Trauma Radiographs
Published in Kajal Jain, Nidhi Bhatia, Acute Trauma Care in Developing Countries, 2023
Ujjwal Gorsi, Chirag Kamal Ahuja
Cerebral contusion is the most common parenchymal lesion in head trauma. Contusion results from impact of cerebral gyri to the inner table of the skull, hence seen often in basifrontal and anterior temporal regions due to presence of rough bony edges and ridges. It evolves from small petechiae to small haemorrhages and finally large haematomas over a period of time. Thus, it is important to image contusions at a periodic interval within the first few days to identify haematoma expansion and mass effect. Classical imaging appearance is that of low-density cortex (oedema) mixed with high-density blood (petechial haemorrhage) (Figure 29.5).
Application of the neuropsychological evaluation in vocational planning after brain injury
Published in Robert T. Fraser, David C. Clemmons, Traumatic Brain Injury Rehabilitation, 2017
Damage can present as brain contusions, which are bruises on the brain, much akin to bruises received on other parts of the body. (A contusion causes tissue damage and bleeding.) If a contusion is on the cerebral cortex, it is referred to as a cerebral contusion. If the bruising occurs in the brain stem area, it would be called a brain stem contusion. Damage to the brain can also occur as a result of a hematoma. A hematoma is a collection of blood in a certain confined space in the brain.
The brain, central nervous system and peripheral nerves
Published in Kevin G Burnand, John Black, Steven A Corbett, William EG Thomas, Norman L Browse, Browse’s Introduction to the Symptoms & Signs of Surgical Disease, 2014
Kevin G Burnand, John Black, Steven A Corbett, William EG Thomas, Norman L Browse
Cerebral contusion is focal brain injury caused by the impact of the brain surface against the internal ridges of the skull. Cerebral contusions are common in the frontal and temporal poles, as a result of impact against the corrugations in the floor of the skull.
The intersection of cerebral fat embolism syndrome and traumatic brain injury: a literature review and case series
Published in Brain Injury, 2020
Taron Davis, Alan Weintraub, Michael Makley, Eric Spier, Jeri Forster
To date, most of the literature describing CFES has been in case studies and case series (14–17). In more recent decades there has been an increase in the recognition of this condition and more published reports highlighting the importance of MRI in aiding in the diagnosis of CFES (7,8,11,15,18). While much of the literature on CFES highlights the transient nature of the neurologic symptoms which is associated with minimal long-term morbidity and mortality, there is a lack of meaningful data characterizing these “good outcomes” (7,18–20). These authors are presenting a qualitative series of cases reviewing the clinical and pathognomonic neuroimaging findings of 14 individuals with the diagnosis of an acquired brain injury (ABI) related to CFES, who were managed in an ABI rehabilitation program. This patient cohort represents the largest collection of individuals to be reviewed in the literature with the diagnosis of CFES. In addition, this is the only reported series discerning cerebral injury secondary to focal cerebral contusion (FCC), and DAI complicated by CFES. Two specific cases from this series are presented in order to highlight the differences in the presentation between individuals with a brain injury secondary to CFES alone, “isolated CFES,” and those presenting with a dual diagnosis of CFES along with a traumatic brain injury (TBI) related DAI/FCC. Lastly, we will offer considerations of risk factors and imaging recommendations for this high-risk patient population with a focus on prognosis and neurologic recovery outcomes.
“Five-layer gasket seal” watertight closure for reconstruction of the skull base in complex bilateral traumatic intraorbital meningoencephaloceles: a case report and literature review
Published in Brain Injury, 2018
Dan Zhao, Shanwei Tao, Dewei Zhang, Mengyang Qin, Yijun Bao, Anhua Wu
Traumatic meningoencephaloceles following traffic accidents that present with the symptoms of exophthalmos, traumatic CSF rhinorrhea, and dysosmia or dysopia are rare and can be easily neglected (1). This condition is typically accompanied by cerebral contusion or hematoma and can be life-threatening since cephalomeningitis occurs due to CSF leakage (2). The most common causes of meningoencephaloceles are trauma, tumors, and congenital skull malformations (3). Although congenital meningoencephaloceles have been clearly classified and well managed (4), it is obscure for the surgical standardization of traumatic meningoencephaloceles since this entity is more complicated than congenital meningoencephaloceles and usually combined with intricate craniofacial and basal fractures, brain injury, and CSF leak (5).
BIIB093 (IV glibenclamide): an investigational compound for the prevention and treatment of severe cerebral edema
Published in Expert Opinion on Investigational Drugs, 2019
Melissa Pergakis, Neeraj Badjatia, Seemant Chaturvedi, Carolyn A. Cronin, W. Taylor Kimberly, Kevin N. Sheth, J. Marc Simard
When head trauma results in a cerebral contusion, the hemorrhagic lesion often progresses during the first several hours after impact, either expanding or developing new, non-contiguous hemorrhagic lesions, a phenomenon termed hemorrhagic progression of a contusion (HPC). In animal models of contusion-TBI, a major effect of glibenclamide is to suppress contusion expansion. Blockade of SUR1 by glibenclamide or by antisense oligodeoxynucleotides significantly reduces the progression of brain contusions in treated animals, compared to vehicle [38,62]. Additional work by us [39] and by independent laboratories [40–43] has shown that in contusion-TBI, glibenclamide reduces hemorrhagic progression and edema, and improves neurological outcomes.