POST-TRAUMATIC CEREBRAL INFARCTION. Neuroimaging findings, etiology and outcome

Server, Andrés; Dullerud, R.; Haakonsen, Monika; Nakstad, P; Johnsen, U. L.-H.; Magnæs, B.

doi:10.1034/j.1600-0455.2001.042003254.x

Cited by 31 publications

(52 citation statements)

References 42 publications

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Section: Ischemia and Infarctionmentioning

confidence: 99%

“…Post-traumatic cerebral infarction is an indication of a poor clinical outcome, especially among patients with associated subdural hematoma, brain swelling/edema and traumatic SAH [39]. The overall death rate has been reported to be more than 40% [39]. The most common cause of post-traumatic infarction is extrinsic compression of a blood vessel due to gross mechanical shift of the brain and herniation across the falx and/or tentorium, e.g., caused by an EDH or SDH.…”

Section: Ischemia and Infarctionmentioning

confidence: 99%

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New developments in the neuroradiological diagnosis of craniocerebral trauma

et al. 2005

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Accurate radiographic diagnosis is a cornerstone of the clinical management and outcome prediction of the head-injured patient. New technological advances, such as multi-detector computed tomography (MDCT) scanning and diffusion-weighted magnetic resonance imaging (MRI) have influenced imaging strategy. In this article we review the impact of these developments on the neuroradiological diagnosis of acute head injury. In the acute phase, multi-detector CT has supplanted plain X-ray films of the skull as the initial imaging study of choice. MRI, including fluid-attenuated inversion recovery, gradient echo T2* and diffusion-weighted sequences, is useful in determining the severity of acute brain tissue injury and may help to predict outcome. The role of MRI in showing diffuse axonal injuries is emphasized. We review the different patterns of primary and secondary extra-axial and intra-axial traumatic brain lesions and integrate new insights. Assessment of intracranial hypertension and cerebral herniation are of major clinical importance in patient management. We discuss the issue of pediatric brain trauma and stress the importance of MRI in non-accidental injury. In summary, new developments in imaging technology have advanced our understanding of the pathophysiology of brain trauma and contribute to improving the survival of patients with craniocerebral injuries.

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Section: Ischemia and Infarctionmentioning

confidence: 99%

Section: Ischemia and Infarctionmentioning

confidence: 99%

New developments in the neuroradiological diagnosis of craniocerebral trauma

et al. 2005

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“…Severe brain injury is known to cause cytotoxic and vasogenic edema formation. Swelling of brain tissue is also a critical factor after traumatic ASDH that is related to poor outcome (Gennarelli, 1993;Server et al, 2001). The assessment of brain water content reveals volume-dependent edema formation early after ASDH.…”

Section: Establishing a Porcine Model Of Asdh For Multiparametric Monmentioning

confidence: 99%

Acute Subdural Hematoma in Pigs: Role of Volume on Multiparametric Neuromonitoring and Histology

Timaru-Kast

Meissner²,

Heimann³

et al. 2008

Journal of Neurotrauma

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Traumatic brain injury (TBI) is often complicated by acute subdural hemorrhage (ASDH) with a high mortality rate. The pathophysiological mechanisms behind such an injury type and the contribution of blood to the extent of an injury remain poorly understood. Therefore, the goals of this study were to establish a porcine ASDH model in order to investigate pathomechanisms of ASDH and to compare effects induced by blood or sheer volume. Thus, we infused 2, 5, and 9 mL of blood (up to 15% of intracranial volume), and we compared a 5-mL blood and paraffin oil volume to separate out effects of extravasated blood on brain tissue. An extended neuromonitoring was applied that lasted up to 12 h after injury and included intracranial pressure (ICP), cerebral perfusion pressure (CPP), tissue oxygen concentration (ptiO(2)), biochemical markers (glutamate, lactate), somatosensory evoked potentials (SEP), brain water content, and histological assessment (Lesion Index [LI]). Volume-dependent changes were detected mainly during the first hours after injury. ICP increased to significant levels (p < 0.05) of 36.89 +/- 1.59, 15.52 +/- 0.48, and 11.25 +/- 0.35 mm Hg after 9, 5, and 2 mL of subdural blood, respectively (sham, 4.85 +/- 0.06 mm Hg). The ptiO(2) dropped drastically after 9 mL of subdural blood without recovery in both hemispheres to below 20% of baseline, but was affected little after 2 and 5 mL in the acute monitoring period (maximal drop to 71% of baseline). Later, 5 mL of blood led to a significant increase of ptiO(2) compared to 2 mL ipsilaterally (p < 0.05). Glutamate and lactate showed a comparable pattern with a long-lasting increase after 9 mL of blood and short-lasting changes after 2 and 5 mL. The two smaller volumes caused an increased brain swelling (2 mL, 80.60 +/- 0.34%; 5 mL, 81.20 +/- 0.66%; p < 0.05 vs. sham), a significant LI (sham, 6.4 +/- 1.4; 2 mL, 30.0 +/- 0.95; 5 mL, 32.1 +/- 1.2; p < 0.05 vs. sham), and a reduced SEP amplitude (5 mL, p < 0.05 vs. baseline) at the end of the experiment. A 9-mL led to herniation during the experiment causing dramatical brain swelling and acute histological damage. Comparison of blood volume with paraffin oil showed no significance, indicating that volume alone determines the acute pathophysiological processes leading to a rapidly developing histological damage. Additional effects due to blood contact with brain tissue (e.g., inflammation) may be detected only at later time points (>12 h).

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“…Ischemia and stroke are lesser-known complications of TBI, which occur in 1.9-10.4% of patients after trauma (Server et al, 2001). In a small retrospective study of 16 patients with trauma-related infarction, the cause of the infarction was focal mass effect and/ or herniation in 81% of patients, and direct vascular injury such as arterial dissection in 18% of patients.…”

Section: Strokementioning

confidence: 98%

“…Patients with carotid dissection classically present with Horner's syndrome and head and neck pain on the ipsilateral side, with or without symptoms of stroke. Another commonly recognized example of trauma-induced infarction is occipital stroke from posterior cerebral artery compression against the tentorium from herniation of the medial temporal lobe (Server et al, 2001).…”

Section: Strokementioning

confidence: 99%

Neurologic aspects of traumatic brain injury

Gottesman

Komotar

Hillis

2003

International Review of Psychiatry

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Traumatic brain injury is a common neurologic condition that can have a significant emotional and financial burden. Neurologic injury is classified on the basis of initial clinical status by the Glasgow Coma Scale, and also by the type and location of head injury. Complications in the management of these patients are reviewed, ranging from intracranial pressure management and stroke to post-traumatic epilepsy. In addition, predictive prognostic variables that can be used to predict outcome based on a patient's presentation at the time of a head trauma are discussed. Finally, interventions such as induced hypothermia that can be undertaken to try to optimize outcome, are discussed along with current data in support of or against such techniques.

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POST-TRAUMATIC CEREBRAL INFARCTION. Neuroimaging findings, etiology and outcome

Cited by 31 publications

References 42 publications

New developments in the neuroradiological diagnosis of craniocerebral trauma

New developments in the neuroradiological diagnosis of craniocerebral trauma

Acute Subdural Hematoma in Pigs: Role of Volume on Multiparametric Neuromonitoring and Histology

Neurologic aspects of traumatic brain injury

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