Real-time detection of vascular occlusion and reperfusion of the brain during surgery by using infrared imaging

Watson, Joseph C.; Gorbach, Alexander M.; Pluta, Ryszard; Rak, Ramin; Heiss, John D.; Oldfield, Edward H.

doi:10.3171/jns.2002.96.5.0918

Cited by 37 publications

(28 citation statements)

References 25 publications

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“…10 The temperature measured on the tissue surface by means of IRT strongly correlates with the blood flow, and IRT is sensitive enough to quantify the effects of various levels of occlusion on the local organ perfusion. 1,28,38 Additional information on blood flow conditions in skeletal muscles can be provided by finite element (FE) simulations. For example, Vankan et al (1996) and van Donkelaar et al (2001) used FE to simulate perfusion in muscle tissue during tetanic, isometric contraction and maximal vasodilatation.…”

Section: Introductionmentioning

confidence: 99%

The Effects of Pressure and Shear on Capillary Closure in the Microstructure of Skeletal Muscles

Linder-Ganz

Gefen

2007

Ann Biomed Eng

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Deep tissue injury (DTI) is a severe pressure ulcer, which initiates in muscle tissue under a bony prominence, and progresses outwards. It is associated with mechanical pressure and shear that may cause capillaries to collapse and thus, induce ischemic conditions. Recently, some investigators stipulated that ischemia alone cannot explain the etiology of DTI, and other mechanisms, particularly excessive cellular deformations may be involved. The goal of this study was to evaluate the functioning of capillaries in loaded muscle tissue, using animal and finite element (FE) models. Pressures of 12, 37, and 78 kPa were applied directly to one gracilis muscle of 11 rats for 2 h. Temperatures of the loaded and contralateral muscles were recorded with time using infrared thermography (IRT) as a measure of the ischemic level. In addition, a non-linear large deformation muscle-fascicle-level FE model was developed and subjected to pressures of 12-120 kPa without and with simultaneous shear strain of up to 8%. For each simulation case, the accumulative percentage of open capillary cross-sectional area and the number of completely closed capillaries were determined. After 2 h, temperature of the loaded muscles was 2.4 +/- 0.3 degrees C (mean +/- standard deviation) lower than that of the unloaded contralateral limbs (mean of plateau temperature values across all pressure groups). Temperature of the loaded muscles dropped within 10 min but then remained stable and significantly higher than room temperature for at least 30 additional minutes in all pressure groups, indicating that limbs were not completely ischemic within the first 40 min of the trials. Our FE model showed that in response to pressures of 12-120 kPa and no shear, the accumulative percentage of open capillary cross-sectional area decreased by up to 71%. When shear strains were added, the open capillary cross-sectional area decreased more rapidly, but even for maximal loading, only 46% of the capillaries were completely closed. Taken together, the animal and FE model results suggest that acute ischemia does not develop in skeletal muscles under physiological load levels within a timeframe of 40 min. Since there is evidence that DTI develops within a shorter time, ischemia is unlikely to be the only factor causing DTI.

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Section: Introductionmentioning

confidence: 99%

The Effects of Pressure and Shear on Capillary Closure in the Microstructure of Skeletal Muscles

Linder-Ganz

Gefen

2007

Ann Biomed Eng

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“…Although brain insulation by cerebrospinal fluid, skull, scalp, and hair is also important (see detailed discussion in ref. 20), these effects are especially significant in small animals and͞or in case of exposed brain, where direct intraoperative temperature measurements (15,(22)(23)(24)(25) demonstrated that the superficial brain temperature is lower than the deep brain temperature by several degrees. A computer model of temperature changes in the human calcarine fissure during functional activation (26) predicted that the temperature changes in this structure could be both positive and negative, depending mostly on the distance from the brain surface.…”

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confidence: 99%

Theoretical model of temperature regulation in the brain during changes in functional activity

Sukstanskiı̆

Yablonskiy

2006

Proc. Natl. Acad. Sci. U.S.A.

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The balance between metabolic heat production, heat removal by blood flow, and heat conductance defines local temperature distribution in a living tissue. Disproportional local increases in blood flow as compared with oxygen consumption during functional brain activity disturb this balance, leading to temperature changes. In this article we have developed a theoretical framework that allows analysis of temperature changes during arbitrary functional brain activity. We established theoretical boundaries on temperature changes and explained how these boundaries depend on physiology (blood flow and metabolism) and external (heat exchange with the environment) experimental conditions. We show that, in regions located deep in the brain, task performance should be accompanied by temperature decreases in regions where blood flow increases (activated regions) and by temperature increases in regions where blood flow decreases (deactivated regions). The sign of temperature effect may be reversed for superficial cortex regions, where the baseline brain temperature is lower than the temperature of incoming arterial blood due to the heat exchange with the environment. Importantly, due to heat conductance, the temperature effect is not localized to the activated region but extends to a surrounding tissue at rest over the distances regulated by the temperature-shielding effect of blood flow. This temperature-shielding effect quantifies the means by which cerebral blood flow prevents ''temperature perturbations'' from propagating away from the perturbed regions. For small activated regions, this effect also substantially suppresses the magnitude of the temperature response, making it especially important for small animal brains.brain temperature ͉ cerebral blood flow ͉ cerebral metabolism ͉ functional brain activity B asic mechanisms underlying global temperature regulation in humans and animals have attracted substantial attention from scientists, and considerable progress has been achieved in this area both in health and disease (see, e.g., refs. 1-4). However, information on brain temperature regulation, especially its relationship to function, is conflicting. Indeed, although, numerous experimental studies have demonstrated changes in the brain temperature of humans and animals upon functionally induced changes in brain activity, the magnitude and even sign of reported temperature changes vary substantially. For example, localized temperature variations from 0.01°C to 0.2°C were observed in animal brains (5-13) under different stimuli (visual, auditory, somatic). As reported in ref. 6, the sign of temperature response to visual stimulation in cats depends on the frequency of flashing light; for low frequencies (2-12 Hz), the temperature increases, whereas at high-frequencies (42-62 Hz) the temperature decreased. Negative temperature changes, on average Ϫ0.2°C, were observed in the deep regions of the visual cortex in conscious intact human subjects by a magnetic resonance method (14), whereas positive temperature changes up...

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“…Subsequently, the initial values were gradually re-established but in some cases, continued to decline to 0 rise. The increase in brain temperature early after ischemia has been previously reported, but its significance to the pathogenesis of ischemic brain injury was not previously recognized 33,34 .…”

Section: The Ischemic Penumbramentioning

confidence: 96%

Basic physiology of hyperbaric oxygen in brain

Nemoto

Betterman

2007

Neurological Research

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Oxygen is the proverbial 'double-edged sword' in that it is a necessity for life in moderation and toxic and detrimental to life in excess. This too is the dilemma in hyperbaric oxygen (HBO) treatment in cerebral ischemic-anoxic insults such as stroke, head injury, near drowning, asphyxia, cardiac arrest, etc., i.e. the brain at risk, where regions of ischemia are beside regions of marked hyperemia. The natural heterogeneity of normal brain tissue oxygenation compounds the problem with different microvascular brain regions living at various levels of oxygenation from 0 to arterial PO(2) as an added complication. The application of HBO, whether normobaric or hyperbaric, will result in brain tissue oxygenation ranging from normoxic to highly hyperoxic with the latter possibly exacerbating the injury sustained. On this basis, the application of multiple therapeutic interventions may be considered, for example, HBO in combination with free radical scavengers or inhibitors of free radical generating enzymes. Despite these difficulties in moderating oxygen delivery to treat cerebral ischemic-anoxic insults, overwhelming preclinical evidence indicates that HBO administered during or within 2 hours post-insult effectively attenuates the severity of brain damage sustained. The primary disconnection between pre-clinical and clinical efficacy of HBO then appears to be the time of application. Clinically, HBO therapy is applied at the earliest 6 hours post-insult but usually between 12 hours or longer post-insult. Pre-hospital application of HBO may be required for clear-cut demonstration of clinical efficacy.

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Real-time detection of vascular occlusion and reperfusion of the brain during surgery by using infrared imaging

Cited by 37 publications

References 25 publications

The Effects of Pressure and Shear on Capillary Closure in the Microstructure of Skeletal Muscles

The Effects of Pressure and Shear on Capillary Closure in the Microstructure of Skeletal Muscles

Theoretical model of temperature regulation in the brain during changes in functional activity

Basic physiology of hyperbaric oxygen in brain

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