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Traumatic Cerebral Contusion: Pathobiology and Critical Aspects

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Traumatic Cerebral Contusion: Pathobiology and Critical Aspects Romanian Neurosurgery (2013) XX 2: 125 – 137 125 DOI: 10.2478/romneu-2013-0001 Traumatic cerebral contusion: pathobiology and critical aspects Hernando Alvis-Miranda, Gabriel Alcala-Cerra, Luis Rafael Moscote-Salazar Universidad de Cartagena Abstract term repercussions of TBI are substantial Traumatic brain injury is a major cause especially among adolescents and young of mortality in developed countries. adults, whose brains continue to mature Cerebral parenchymal injury is evidenced and develop (5). by a significant percentage of patients. The Focal brain injury, is defined as a most important structural lesion of the localised damage to the brain in form of brain is the cerebral contusion, which is a laceration, contusion and haematoma complex and dynamic area, a result of the occurring in the presence or absence of a primary lesion and which is associated with skull opening from either a pre-trauma ischemic and inflammatory phenomena trephination or a mechanic fracture caused that need to be known by the by the impact itself (6). From the focal neurosurgeon. We present a review of the brain injuries, cerebral contusions (CC) are most important aspects of brain contusion. one of the most common traumatic Key words: brain contusion, focal findings, being present in up to 31% of traumatic brain injuries, traumatic brain initial imaging studies (CT-scans) of injury. patients with TBI (7). It has been reported that contusions occurred in 89% of brains Introduction examined postmortem (8). CC is a type of focal TBI, resulting from Traumatic brain injury (TBI) is an direct loading and often occurs in the important public health problem and is the absence of widespread injury (9), leading cause of mortality, morbidity, and representing focal regions of trauma- disabilities in children and young adults, induced subpial hemorrhage and swelling, especially in young males (15-35 years old) zones of cellular injury where the (1). Internationally, TBI accounts for microvasculature is also disrupted (10). significant socio-economic implications; in Pure CC are fairly common, found in 8% the US alone, over 1.7 M individuals suffer of all TBI (11, 12) and 13% to 35% of a TBI each year (2). One of the main severe injuries (11). characteristic of TBI is that patients without The vast majority of contusions occur in a severe TBI, can experience subsequent the frontal and temporal lobes, although mental and/or medical problems (3, 4). The they can occur at almost any site, including acute consequences of TBI are just only a the cerebellum and brainstem (13). half of the complete problem, the long- Ratnaike et al (14) founded retrospectively 126 Alvis-Miranda et al Traumatic cerebral contusion that most blows causing CC are to back of caused by the initial mechanical impact, the head, being most contusions resulting in skull fracture, CC, and vascular contrecoup lesions affecting the frontal and and parenchymal injury causing intracranial temporal lobes. Any intracranial contusion, bleed and ICH. An inflammatory process, as other focal injuries such as hematoma, or edema formation, and excitotoxicity follow, brain laceration falls within the category of resulting in further increase in ICP and severe TBI (15). reduced cerebral perfusion pressure (CPP) This work aims to review critical aspects (17, 18). of CC in clinical practice, such as Despite the prevalence of such injury, pathophysiology, diagnosis and the injury mechanism leading to CC has management. long been studied but still remains unclear. As part of TBI, CC is a complex Characterization neurological event that results in the CC are more common in regions that disruption of numerous cellular and contact bony surfaces in the cranial vault physiological processes (19). during trauma: frontal and temporal poles, Biomechanical forces orbitofrontal gyri, perisylvian cortices, and TBI results from the transfer of energy inferolateral temporal lobe surfaces (16). from the environment to brain tissue that is Contusions can be characterized by greater than the amount that can be mechanism, anatomic location, or adjacent absorbed without dysfunction. Traumatic injuries. Table 1 summarizes main insults generally occur over short periods of characteristics of each one. time and are referred to as dynamic loading, and includes both direct or impact loading, Pathophysiology as well as impulsive loading whereby no In TBI, the primary injury to the brain is physical contact occurs (9). TABLE 1 Characterization of cerebral contusions Fracture Result from direct contact injuries and occur immediately adjacent to a contusions skull fracture. Coup contusions Refer to those that occur at the site of impact in the absence of a fracture. Contrecoup Are those that are diametrically opposite to the point of impact. contusions Are focal hemorrhages involving the cortex and adjacent white matter of Gliding the superior margins of the cerebral hemispheres; they are due to contusions rotational mechanisms rather than contact forces. Intermediary Are lesions that affect deep brain structures, such as the corpus callosum, contusions basal ganglia, hypothalamus, and brainstem. Can occur in areas where the medial parts of the temporal lobe contact Herniation the tentorial edge (i.e., uncal herniation) or where the cerebellar tonsils contusions contact the foramen magnum (i.e., tonsillar herniation). Adapted from (16) Romanian Neurosurgery (2013) XX 2: 125 – 137 127 DOI: 10.2478/romneu-2013-0001 The loads absorbed by the brain after the potential to cause prolonged and trauma generally include linear and deteriorated neurological and rotational components called angular loads. neuropsychological change (20). The rate and duration of the insult are There have been arguments regarding important because loads applied at high whether intracranial pressure (ICP) or rates tend to result in more damage (9). tissue strain causes CC (21). Traditionally, CC and other focal injuries result from positive (compressive) ICP has been direct loading and often occurs in the believed to induce CC under the impact absence of widespread injury (9). site (22). Pericontusional zone (PCZ) is Cerebral and systemic changes induced recognized as the rim of edematic non- by cerebral contusion necrotic tissue surrounding the central Following TBI, an abundance of necrotic core in the acute phase of biochemical events is directed to the traumatic cerebral contusion (20). PCZ has ensuing brain parenchyma destruction. Figure 1 Schematic cascade of events triggered by TBI Adapted from (24) 128 Alvis-Miranda et al Traumatic cerebral contusion Focal vascular alterations restrict the on alterations in the neural tissue, giving delivery of substrates to the brain such as less emphasis to the mechanisms that give oxygen and glucose, driving to energy rise to ischemic brain damage. However the depletion, ionic gradients that are necessary evidence indicates that three major factors to maintaining membrane potential are lost, are involved, these are (32): resulting in neuronal and glial 1. Increases in the intercellular cytosolic depolarizations (23). calcium concentration The pathogenesis of CC results from 2. Acidosis interrelated multifactorial phenomena 3. Free radical production involving anatomical and functional In severe TBI, CPP, which is defined as microcirculatory alterations; all are a the difference between mean arterial continuum of deleterious effects that drives pressure and ICP, at a level lower than 70 brain parenchyma to suffering and death, mmHg serves as a clinical threshold for Figure 1, schematizes these effects. adverse outcome (33). TBI is associated with a cerebral In 1957, Freytag and Lindenberg inflammatory response characterized by demonstrated two components of CC: the microglial and astrocytic activation, as well central core area in which cells undergo as release of inflammatory mediators (25). necrosis and the peripheral (rim) area in Pro-inflammatory cytokines such as IL- which cellular swelling occurs (34) Hacer 1β, IL-6 and TNF-α have been linked to Imágen. the early events mediating BBB breakdown In the central core area, the CBF is 4.7 and subsequent development of cerebral ml/100g/min, and of 16-18 ml/100g/min in edema (26). the peripheral zone (24). TNF-α directly disturbs BBB integrity, Normally, CBF is >50 ml/100g/min, leading to cerebral edema and leukocyte and the ischemic threshold is commonly infiltration (27). considered to be 18-20 ml/100g/min (35– Vascular Alteration – Cerebral Blood Flow 37). and Perfusion The decrease of ABP, the development Head trauma causes rupture of cerebral of ICH, and decrease in CPP are related to small blood vessels at an early period, disturbances in blood vessel sensitivity in especially in white matter. Spasm of the the hypoperfusional zone (36, 38–40). larger cerebral arteries after head trauma has In the clinical setting, low GCS been postulated in several works to be the associated with vasospasm has reported main cause of cerebral ischemia; however, deficiencies in cerebral perfusion (41). measurements of cerebral blood volume are The low cerebral perfusion following more compatible with compromised TBI is accompanied by a parallel decrease in microcirculation in the cerebral tissue (28). BTpO2 (42). Ischemia and contusion are directly Katayama et al have reported that blood correlated with the severity of the injury flow decreases 3 hours after the harmful (29–31). Unfortunately the contusion- event, implying the impact of adequate associated microvascular alterations
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