Studies of the Choroid Plexus and Its Associated Epiplexus Cells in the Lateral Ventricles of Rats Following an Exposure to a Single Non-Penetrative Blast.

Kaur, Charanjit; Singh, Jeffrey M.; Lim, Michael; Ng, B. L.; Yap, Eric P.H.; Ling, Eng‐Ang

doi:10.1679/aohc.59.239

Cited by 33 publications

(25 citation statements)

References 12 publications

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“…This pathology seems best explained by direct effects of blast on the choroid plexus leading to vascular rupture and blood leakage into the ventricles. These results are in agreement with a previous study indicating that the choroid plexus is extremely sensitive to the blast wave [24]. …”

Section: Discussionsupporting

confidence: 94%

Blast overpressure induces shear-related injuries in the brain of rats exposed to a mild traumatic brain injury

Sosa

Gasperi

Paulino

et al. 2013

acta neuropathol commun

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BackgroundBlast-related traumatic brain injury (TBI) has been a significant cause of injury in the military operations of Iraq and Afghanistan, affecting as many as 10-20% of returning veterans. However, how blast waves affect the brain is poorly understood. To understand their effects, we analyzed the brains of rats exposed to single or multiple (three) 74.5 kPa blast exposures, conditions that mimic a mild TBI.ResultsRats were sacrificed 24 hours or between 4 and 10 months after exposure. Intraventricular hemorrhages were commonly observed after 24 hrs. A screen for neuropathology did not reveal any generalized histopathology. However, focal lesions resembling rips or tears in the tissue were found in many brains. These lesions disrupted cortical organization resulting in some cases in unusual tissue realignments. The lesions frequently appeared to follow the lines of penetrating cortical vessels and microhemorrhages were found within some but not most acute lesions.ConclusionsThese lesions likely represent a type of shear injury that is unique to blast trauma. The observation that lesions often appeared to follow penetrating cortical vessels suggests a vascular mechanism of injury and that blood vessels may represent the fault lines along which the most damaging effect of the blast pressure is transmitted.

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Section: Discussionsupporting

confidence: 94%

Blast overpressure induces shear-related injuries in the brain of rats exposed to a mild traumatic brain injury

Sosa

Gasperi

Paulino

et al. 2013

acta neuropathol commun

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“…Based on animal model studies, early changes after exposure to BSWs mainly include increased intracranial pressure (Leonardi et al, 2011), deformation of brain areas in some cases (Bayly et al, 2006), considerable oxidative stress in brain capillaries and BBB disruption. This is typically followed by neuroinflammation typified by the appearance of activated microglia and increased concentration of pro-inflammatory cytokines and neurodegeneration in perivascular regions (Kaur et al, 1995, 1996, 1997; Abdul-Muneer et al, 2013), and atypical distribution of phosphorylated neurofilaments in neurons (Säljö et al, 2000). Furthermore, a mouse study has reported that multifocal axonal injury in white matter tracts typically occurs only when the torso of animal is not shielded during the exposure to shock waves (Koliatsos et al, 2011).…”

Section: Links Between Shock-wave Induced Early Changes Such As Bbb Dmentioning

confidence: 99%

Blood brain barrier dysfunction and delayed neurological deficits in mild traumatic brain injury induced by blast shock waves

Shetty

Mishra

Kodali

et al. 2014

Front. Cell. Neurosci.

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Mild traumatic brain injury (mTBI) resulting from exposure to blast shock waves (BSWs) is one of the most predominant causes of illnesses among veterans who served in the recent Iraq and Afghanistan wars. Such mTBI can also happen to civilians if exposed to shock waves of bomb attacks by terrorists. While cognitive problems, memory dysfunction, depression, anxiety and diffuse white matter injury have been observed at both early and/or delayed time-points, an initial brain pathology resulting from exposure to BSWs appears to be the dysfunction or disruption of the blood-brain barrier (BBB). Studies in animal models suggest that exposure to relatively milder BSWs (123 kPa) initially induces free radical generating enzymes in and around brain capillaries, which enhances oxidative stress resulting in loss of tight junction (TJ) proteins, edema formation, and leakiness of BBB with disruption or loss of its components pericytes and astrocyte end-feet. On the other hand, exposure to more intense BSWs (145–323 kPa) causes acute disruption of the BBB with vascular lesions in the brain. Both of these scenarios lead to apoptosis of endothelial and neural cells and neuroinflammation in and around capillaries, which may progress into chronic traumatic encephalopathy (CTE) and/or a variety of neurological impairments, depending on brain regions that are afflicted with such lesions. This review discusses studies that examined alterations in the brain milieu causing dysfunction or disruption of the BBB and neuroinflammation following exposure to different intensities of BSWs. Furthermore, potential of early intervention strategies capable of easing oxidative stress, repairing the BBB or blocking inflammation for minimizing delayed neurological deficits resulting from exposure to BSWs is conferred.

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“…Blast injury is known to cause injury confined to the choroid plexus of lateral ventricles and surrounding tissue (31).…”

Section: Discussionmentioning

confidence: 99%

“…Kaur et al (31) reported that the choroid plexus in rats exhibited ultrastructural changes following an open-field blast and that the intercellular spaces between the choroid plexus epithelial cells were greatly widened, coupled with the massive eruption and possible extrusion of the apical cytoplasm into the ventricular lumen. Garman et al (32) observed blood-brain barrier permeability around the circumventricular organs following the blast using the tube-blast injury model.…”

Section: Discussionmentioning

confidence: 99%

Pathophysiology of microwave-induced traumatic brain injury

et al. 2015

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Microwave technology has been widely used in numerous applications; however, excessive microwave exposure causes adverse effects, particularly in the brain. The present study aimed to evaluate the change in the number of neural cells and presence of apoptotic cells in rats for one month after exposure to excessive microwave radiation. The rats were exposed to 3.0 kW of microwaves for 0.1 sec and were sacrificed after 24 h (n=3), or 3 (n=3), 7 (n=3), 14 (n=3) or 28 days (n=4) of exposure. The neural cells were counted in the motor cortex and hippocampus [cornu ammonis 1 (CA1) and CA2] and the percentage of positive cells stained with terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) were also measured, which detected apoptotic cell death in the choroid plexus in the lateral ventricle, motor cortex and hippocampus. In the CA1, the number of neural cells decreased significantly by day 28 compared with that in the control (60.7 vs. 50.6, P=0.0358), but did not decrease before day 28. There were no significant differences on any day in the CA2 and the motor cortex. The number of cells showed a significant increase on day 7 compared to the control in the choroid plexus (2.1±1.1 vs. 21.8±19.1%, P=0.0318). There were no significant differences from the controls in the percentage of TUNEL-positive cells in the motor cortex and hippocampus. The effects of microwave exposure on the brain remain unclear; however, microwave-induced neurotrauma shows the same pathological changes as blast traumatic brain injury.

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Studies of the Choroid Plexus and Its Associated Epiplexus Cells in the Lateral Ventricles of Rats Following an Exposure to a Single Non-Penetrative Blast.

Cited by 33 publications

References 12 publications

Blast overpressure induces shear-related injuries in the brain of rats exposed to a mild traumatic brain injury

Blast overpressure induces shear-related injuries in the brain of rats exposed to a mild traumatic brain injury

Blood brain barrier dysfunction and delayed neurological deficits in mild traumatic brain injury induced by blast shock waves

Pathophysiology of microwave-induced traumatic brain injury

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