Brain infarction

XueD., Huang Z. G., Smith K. E., and Buchan A. M. (1992) Immediate or delayed mild hypothermia prevents focal cerebral infarction. Brain Res. 587, 66-72. 

Around acutely infarcted brain, there is an ischemic penumbra (Astrup et al. 1981). Here the blood flow is low, function depressed and the oxygen extraction fraction high. In other words, there is viable tissue with misery perfusion where the needs of the tissue are not being met The tissue may die or recover, depending on the speed and extent of restoration of blood flow. This concept opens up the possibility of a therapeutic time window during which restoration of flow or neuronal protection from ischemic damage might prevent both immediate cell death and the recruitment of neurons for apoptosis (see Ch. 21). 

Thrombolysis aims to reduce the volume of infarcted brain by recanalizing the occluded vessel and restoring blood flow. Restoration of blood flow may not necessarily always be beneficial. First, studies in animals suggest that reperfusion of acutely ischemic brain may actually be harmful, through the release of free radicals and toxic products into the circulation. Second, thrombolysis will probably not be of benefit if infarction is completed or if the ischemic penumbra is small. Finally, thrombolysis may cause hemorrhagic transformation of the infarct or extracranial bleeding. 

Videen TO, Zazulia AR, Mtmno EM, Derdeyn CP, Adams RE, Diringer MN, Powers WJ (2001) Mannitol bolus preferentially shrinks non-infarcted brain in patients with ischemic stroke. Neurology 57 2120-2122... 

Figure 31.5. Leukocyte migration into locally ischemic brain. Histologic and schematic representations of changes in leukocyte behavior in the brain microvessels after focal ischemia. Shortly (within 1-6 h) after experimental stroke, many of the leukocytes, primarily neutrophils, in the ischemic tissue vessels are adherent to the post-capillary venuole and capillary walls. This can modify and exacerbate the decreased blood flow occurring in the already ischemic brain. Then, these neutrophils can find their way outside the vascular walls into the focal ischemic cortex over the next 6-24h. Macrophages move into the brain later (i.e., over 1-5 days) and significantly accumulate in the infarcted brain. These changes in leukocyte behavior are mediated by increased brain inflammatory cytokine, adhesion molecule(s), and chemokine expression in the ischemic/injured brain. Reproduced from ref Barone FC, Feuerstein GZ. Inflammatory mediators and stroke new opportunities for novel therapeutics. J Cereb Blood Flow Metab 1999 19 819-834. With permission from Nature.

Hara, Y., Tooyama, I., Yasuhara, O., Akiyama, FI., McGeer, P. L., Handa, J., and Kimura, H., Acidic fibroblast growth factor-like immunreactivity in rat brain following cerebral infarction. Brain Res., 664, 101, 1994. 

Hiccup is a forceful, involuntary inspiration commonly experienced by fetuses, children, and adults. Its purpose is unknown, and its pathophysiology still poorly understood. Short hiccup bouts are mostly associated with gastric distention or alcohol intake. They resolve spontaneously or with simple folk remedies and do not require medical attention. In contrast, prolonged hiccup is a rare but disabling condition that can induce depression, weight loss, and sleep deprivation. A wide variety of pathological conditions can cause chronic hiccup myocardial infarction, brain tumor, renal failure, prostate cancer, and abdominal surgery are only a few of these conditions. 

Jones, R.D., Donaldson, I.M., and Parkin, P.J. 1989. Impairment and recovery of ipsilateral sensory-motor function following unilateral cerebral infarction. Brain 112 113-132. 

Nedergaard, M. (1987) Transient focal ischemia in hyperglycemic rats is associated with increased cerebral infarction. Brain Res., 408 79-85. 

CBF) at the left frontal and parietal lobe, d Analogue to the CBF the cerebral blood volume (CBV) parameter map shows extreme loss of blood volume corresponding to a dysfunction of vessel auto-regulation, a sign for infarction, e Nearly no contrast agent delivery to the infarcted brain territory during the whole scan period (40 s) is shown at the Time-to-peak (TTP) parameter map... 

An estimated oral dose of 260 mg endosulfan/kg caused severe seizures in a 43-year-old man, and brain death from cerebral herniation and massive cerebral edema occurred within 4 days of exposure (Boereboom et al. 1998) there were no signs of myocardial infarction and only slight congestion of the heart, but pulmonary congestion and atelectasis were evident at autopsy. 

CR is distributed in various organs with highest concentrations in skeletal muscle, myocardium, and brain and lesser amounts in the gastrointestinal tract, uterus, urinary bladder, and kidney ( ). The CR content of liver and red blood cells is negligible so that diseases of these tissues are unlikely to increase the serum CR activity. The serum CR level begins to increase in 2-4 hours after myocardial infarction and reaches a peak in 24-36 hours and returns to normal in about 3 days. 

The sensitivity and specificity of DWI depend to some extent on the technique being used and the amount of imaging time that can be dedicated to the DWI sequence. DWI pulse sequences typically require between approximately 30 seconds and 4 minutes of imaging time to image the entire brain and achieve sensitivity and specificity approaching 100% (Fig. 2.2). The rare infarcts that are not apparent on DWI are usually very small and are often located in the brainstem. 

Some have questioned the specificity of DWI in delineating particular areas of the brain that are destined for infarction, noting that some DWI lesions resolve at least partially in follow-up studies. However, it appears that reversibility of DWI lesions is quite unusual and typically involves only a small portion of initially abnormal tissue. One study found that reversal of a DWI abnormality occurred in 33% of patients following intra-arterial thrombolysis. However, in this study, the areas of reversal nevertheless went on to infarction in the majority of patients. ... 

The neurointerventionalist should limit the number of microcatheter injections performed during the exam, as there is growing evidence that this may increase the chances of hemorrhagic transformation of the infarcted tissue. Direct injection of contrast into stagnant vessels, which contains injured glial cells and thus breakdown of the blood-brain barrier, allows for contrast extravasation. Contrast is readily visualized on the immediate post-thrombolysis CT as an area of high attenuation in the parenchyma. In some instances, MRI with susceptibility-weighted sequences may be useful to differentiate contrast extravasation from Such a distinction... 

Hunter GJ, Silvennoinen HM, Hamberg LM, Koroshetz WJ, Buonanno FS, Schwamm LH, Rordorf GA, Gonzalez RG. Whole-brain CT perfusion measurement of perfused cerebral blood volume in acute ischemic stroke probability curve for regional infarction. 

In rodent stroke models, statin pretreatment has been shown to reduce infarct volumes and improve outcomes. Similarly, several clinical studies have shown that prior statin use reduced the severity of acute ischemic stroke and myocardial infarction. Recent studies indicate that beneftt can be achieved even when treatment is initiated after the onset of symptoms. In rodents, atorvastatin and simvastatin have been shown to reduce the growth of ischemic lesions, enhance functional outcome, and induce brain plasticity when administered after stroke onset. A retrospective analysis of the population-based Northern Manhattan Stroke Study (NOMASS) showed that patients using lipid-lowering agents at the time of ischemic stroke have a lower incidence of in-hospital stroke progression and reduced 90-day mortality rates. Retrospective analysis of data of the phase III citicoline trial showed... 

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