high intracranial pressure

Microvascular shunts in the pathogenesis of high intracranial pressure

Authors: Nemoto EM, Bragin D, Stippler M, Pappu S, Kraynik J, Berlin T, Yonas H.

Hyperemia in the infarcted brain has been -suggested for years by "red veins" reported by neurosurgeons, shunt peaks in radioactive blood flow clearance curves, and quantitative cerebral blood flow using stable xenon CT. Histological characterization of infarcted brain revealed capillary rarefaction with prominent microvascular shunts (MVS). Despite abundant histological evidence, the presence of cerebrovascular shunts have been largely ignored, perhaps because of a lack of physiological evidence demonstrating the transition from capillary flow to MVS flow. Our studies have shown that high intracranial pressure induces a transition from capillary to microvascular shunt flow resulting in cerebral hypoperfusion, tissue hypoxia and brain edema, which could be delayed by increasing cerebral perfusion pressure. The transition from capillary to microvascular shunt flow provides for the first time a physiological basis for evaluating the optimal cerebral perfusion pressure with increased intracranial pressure. It also provides a physiological basis for evaluating the effectiveness of various drugs and therapies in reducing intracranial pressure and the development of brain edema and tissue hypoxia after brain injury and ischemia. In summary, the clear-cut demonstration of the transition from capillary to MVS flow provides an important method for evaluating various therapies for the treatment of brain edema and loss of autoregulation.

Effect of Cerebral Perfusion Pressure on Cerebral Cortical Microvascular Shunting at High Intracranial Pressure in Rats

Authors: Bragin DE, Bush RC, Nemoto EM.

BACKGROUND AND PURPOSE: Recently, we showed that decreasing cerebral perfusion pressure (CPP) from 70 mm Hg to 50 mm Hg and 30 mm Hg by increasing intracranial pressure (ICP) with a fluid reservoir induces a transition from capillary (CAP) to microvascular shunt (MVS) flow in the uninjured rat brain. This transition was associated with tissue hypoxia, increased blood-brain barrier (BBB) permeability, and brain edema. Our aim was to determine whether an increase in CPP would attenuate the transition to MVS flow at high ICP.
METHODS: Rats were subjected to progressive, step-wise increases in ICP of up to 60 mm Hg by an artificial cerebrospinal fluid reservoir connected to the cisterna magna. CPP was maintained at 50, 60, 70, or 80 mm Hg by intravenous dopamine infusion. Microvascular red blood cell flow velocity, BBB integrity (fluorescein dye extravasation), and tissue oxygenation (nicotinamide adenine dinucleotide) were measured by in vivo 2-photon laser scanning microscopy. Doppler cortical flux, rectal and cranial temperatures, ICP, arterial blood pressure, and gases were monitored.
RESULTS: The CAP/MVS ratio increased (P<0.05) at higher ICP as CPP was increased from 50 to 80 mm Hg. At an ICP of 30 mm Hg and CPP of 50 mm Hg, the CAP/MVS ratio was 0.6±0.1. At CPP of 60, 70, and 80 mm Hg, the ratio increased to 0.9±0.1, 1.4±0.1, and 1.9±0.1, respectively (mean±SEM; P<0.05). BBB opening and increase of reduced form of nicotinamide adenine dinucleotide occurred at higher ICP as CPP was increased.
CONCLUSIONS: Increasing CPP at high ICP attenuates the transition from CAP to MVS flow, development of tissue hypoxia, and increased BBB permeability.

"Moderate intensive insulin therapy" is associated with remission of high intracranial pressure in patients with vascular or infectious central nervous system diseases

Authors: Birnbaum T, Schmid SP, Feddersen B, Schankin CJ, Straube A.

Intensive insulin therapy (IIT), targeting blood glucose between 80mg/dL and 110mg/dL ("strict IIT"), has been associated with rapid remission of high intracranial pressure (ICP), but its use is limited due to a high risk of hypoglycemia. The aim of this retrospective study was to assess whether "moderate IIT" (target range for blood glucose: 80-140mg/dL) could have the same beneficial effect on ICP with a lower risk of hypoglycemia. We retrospectively analyzed the records of 64 patients with high ICP due to vascular or infectious central nervous system diseases. Patients treated with moderate IIT (n=32) after 2005 were compared with patients treated with a conventional approach (n=32, target <180mg/dL) before 2005. We assessed daily ICP during the first 14days. Secondary endpoints were the rate of hypoglycemic events and outcome. ICP was significantly lower during the second week in patients treated with moderate IIT (mean±standard deviation daily ICP on days 8-14: 16±5mmHg compared to 12±4mmHg, p<0.001). The risk of hypoglycemic events (<40mg/dL) did not differ significantly between the groups (0 vs. 1 patient, p=0.5). Moderate IIT is associated with remission of high ICP. In contrast to strict IIT, its use seems not to be limited by an increased risk of severe hypoglycemia.

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