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Parenchyma, brain

FIGURE 2.6 Dynamic susceptibility contrast imaging. Axial images of the brain are acquired repeatedly, in this case every 1.5 seconds. As a bolus of intravenously injected contrast material enters the brain, first arteries, then brain parenchyma, and finally veins demonstrate a transient loss of signal intensity. In this acute stroke patient, hypoperfusion of the left middle cerebral artery territory results in delayed arrival of the contrast bolus and prolonged stasis of contrast within the tissue. [Pg.16]

Tris-hydroxymethyl-aminomethane (THAM) has been evaluated in ischemic stroke to reduce mass effect and ICP. It acts as a bulfer, neutralizing acidosis on a local level, including in the brain parenchyma. It has been studied in animal models of stroke, showing an effect in reducing the size of and swelling from cerebral infarction. To date, however, THAM has not been studied in a controlled fashion in humans with ischemic stroke. [Pg.175]

Other methods for ICP monitoring include Camino ICP monitors, which are positioned into the brain parenchyma, but do not transverse the hemisphere nearly to the degree that EVDs do, and are associated with a lower risk of intracerebral hemorrhage. The ICP is measured by a fiberoptic transducer at the tip of the cathe-ter. ° ICP monitors, however, are subject to inaccuracy over time, so-called drift, and thus may become less reliable after the first few days post-insertion. Epidural and subarachnoid bolts/catheters are the least invasive, placed external to or just within the dura, thereby carrying a much lower risk of hemorrhage and infection, but with unfortunately compromised accuracy. [Pg.186]

Nimmeijahn A, Kirchhoff F, Helmchen F. Resting microglial cells are highly dynamic surveillants of brain parenchyma in vivo. Science 2005 308 1314-1318. [Pg.368]

The biosynthesis of adenosine is theoretically controlled by several processes namely (1) the biosynthesis of adenosine from AMP by 5 -nucleotidase [EC 3.1.3.5], (2) from S-adenosyl homocysteine by S-adenosyl homocystine hydrolase [EC 3.3.1.1], (3) the metabolism of adenosine to AMP by adenosine kinase [EC 2.7.1.20], and (4) to inosine by adenosine deaminase (ADA) [EC 3.5.4.2], Interestingly, both 5 -nucleotidase and ADA activities were found to be highest in the leptomeninges of rat brain in contrast, the adenosine kinase activity was widely distributed throughout the brain parenchyma, which has negligible ADA activity... [Pg.372]

Hemorrhagic strokes account for 12% of strokes and include subarachnoid hemorrhage, intracerebral hemorrhage, and subdural hematomas. Subarachnoid hemorrhage may result from trauma or rupture of an intracranial aneurysm or arteriovenous malformation. Intracerebral hemorrhage occurs when a ruptured blood vessel within the brain parenchyma causes formation of a hematoma. Subdural hematomas are most often caused by trauma. [Pg.169]

The presence of blood in the brain parenchyma causes damage to surrounding tissue through a mass effect and the neurotoxicity of blood components and their degradation products. Compression of tissue surrounding hematomas may lead to secondary ischemia. Much of the early mortality of hemorrhagic stroke is due to an abrupt increase in intracranial pressure that can lead to herniation and death. [Pg.170]

The blood-brain barrier forms the interface between the bloodstream and the brain parenchyma and thus controls the passage of endogenous substances and xenobiotics into and out of the central nervous system. Brain microvessels exhibit a variety of unique structural features, such as an extremely tight endothelium without fenestration, a very low rate of pinocytosis, tight junctions between endothelial cells excluding paracellular permeability, and a series of polarized transport proteins. The following chapter describes the structural and functional characteristics of the blood-brain barrier with emphasis on transport proteins, as well as in vitro techniques, which allow studying this complex barrier in the brain. [Pg.398]

The blood-CSF barrier is relatively permeable to hydrophilic macromolecules, (i.e., ai-macroglobulin and IgM). In addition, the passage of smaller molecules, which are larger than 500 Da, is facilitated by lipophilicity (i.e., by antibiotics and cytostatic drugs). The composition of the extracellular fluid of the brain parenchyma is unknown. It resembles CSF only in a narrow margin of a few millimeters adjacent to the free CSF space, a zone where a limited diffusion of water-soluble molecules is possible (F2). The composition of CSF is well known because the subarachnoid space can be tapped at its lowest point. Despite the great distance from the site of production, the choroid plexus, it shows all of the characteristics of a filtrate, even in the lumbar sac. [Pg.8]

A 15-year-old Hispanic boy is brought in with seizures. No prior history of fever, chills, trauma, or headaches was reported on admission. Computed tomography reveals three ring-enhancing cystic lesions in the brain parenchyma, and a diagnosis of neurocysticercosis is made. Initial therapy in the management of this condition should include... [Pg.627]

The distribution of LCM in the brain parenchyma was further analyzed using fluorescently labeled LCM and confocal laser scanning microscopy. As in the case of unlabeled LCM, rats bearing 9L gliosarcoma tumors were injected intravenously (i.e., via tail vein) with diO-LCM and sacrificed 2 min later. The brains were processed as described elsewhere (ref. 531). In this case,... [Pg.223]

Fig. 13.3. This figure demonstrates the distribution of fluorescently tagged LCM in brain parenchyma analyzed by confocal laser scanning microscopy. Rats bearing 9L tumors were administered diO-LCM and sacrificed 2 minutes later. Vibratome sections were counterstained with TR-WGA which binds to tumor cells and distinguishes the tumor area from the surrounding normal tissue. Comparison of the area stained with TR-WGA (tumor cells) (B) and that stained with diO (A) indicates that LCM were associated with a large portion of the tumor. (Taken from ref. 531.)... Fig. 13.3. This figure demonstrates the distribution of fluorescently tagged LCM in brain parenchyma analyzed by confocal laser scanning microscopy. Rats bearing 9L tumors were administered diO-LCM and sacrificed 2 minutes later. Vibratome sections were counterstained with TR-WGA which binds to tumor cells and distinguishes the tumor area from the surrounding normal tissue. Comparison of the area stained with TR-WGA (tumor cells) (B) and that stained with diO (A) indicates that LCM were associated with a large portion of the tumor. (Taken from ref. 531.)...
Confocal laser scanning microscopy was used to determine the spatial relationship of LCM with tumor cells. Serial optical sections of 9L tumor cells situated in the brain parenchyma of rats having received diO-LCM were taken at 0.8 pm intervals. A series of nine consecutive sections was obtained all nine of these are... [Pg.225]


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See also in sourсe #XX -- [ Pg.9 , Pg.18 , Pg.43 , Pg.49 , Pg.134 , Pg.151 , Pg.160 , Pg.272 ]




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