Relationship between Intracranial Pressure and Cortical Spreading Depression following Fluid Percussion Brain Injury in Rats

Abstract

Traumatic brain injury (TBI) is known to be accompanied by an increase in intracranial pressure (ICP) and in some cases, by spontaneous generation of cortical spreading depression (CSD) cycles. However, the role of CSD in the pathophysiology of cerebral contusion is still unknown. A multiparametric monitoring assembly was placed on the right hemisphere of the rat brain to evaluate ICP, DC potential, extracellular K(+), cerebral blood flow (CBF), and electrocorticogram in 27 rats during 5 h. Fluid percussion brain injury (FPBI) with the magnitude of the impact 2.9, 3.3, 4.1, and 5.0 atmospheres was induced to the left parietal cortex in animal groups A, B, C, and D, respectively. A slow increase in ICP was evident, and was pronounced in group C and especially in group D, where four of nine animals died during the monitoring. At the end of the 5 h experiment, the mean ICP levels were 6.75 +/- 2.87, 8.40 +/- 2.70, 12.75 +/- 4.03, 29.56 +/- 9.25, and the mean total number of CSD cycles was 2.00 +/- 1.41, 4.29 +/- 4.23, 11.71 +/- 13.29, and 20.11 +/- 19.26 in groups A, B, C, and D, respectively. The maximal level of intensity of CSD cycle generation after FPBI was obtained in group D, where almost constant activity was maintained until the end of the experiment. A significant coefficient of correlation between ICP level and total number of CSD cycles was found for all ICP measurements (r = 0.47-0.63, p < 0.05, n = 27), however more significant (p < 0.001) was the coefficient during the period of monitoring between 2 and 4 h after FPBI. Our results suggest that numerous repeating CSD cycles are typical phenomena in moderate and especially severe forms of FPBI. The rising number of CSD cycles under condition of an ICP level >/=20 mm Hg may demonstrate, with high probability, the unfavorable development of TBI, caused by growing secondary hypoxic insult.

Clinical Relevance of Cortical Spreading Depression in Neurological Disorders: Migraine, Malignant Stroke, Subarachnoid and Intracranial Hemorrhage, and Traumatic Brain Injury

“…Rogatsky et al (2003) similarly simulated severe TBI with secondary deficits. Using fluid percussion injury in rats, different TBI severities resulted in substantial ICP elevations that significantly correlated with the number of CSDs.…”

The Acute Phase of Mild Traumatic Brain Injury Is Characterized by a Distance-Dependent Neuronal Hypoactivity

“…62 The processes that allow for persistence of this depression beyond a few hours are unknown; however, given the known link between CSD and cortical plasticity, 64 it seems likely that synaptic events such as long-term depression may be important. Cortical waves of depression have been monitored after injury induced with predominantly focal injury models, such as the LFPI, [65][66][67][68] Feeney's weight drop, 69 and the controlled cortical impact (CCI) model, 70 but have yet to be documented after a diffuse model of injury, such as the WDIA model. Nevertheless, our findings suggest that CSD is likely to be an important phenomenon after both diffuse and focal forms of injury, and may be important in establishing persistent cortical cellular changes.…”

The Utility of EEG, SSEP, and Other Neurophysiologic Tools to Guide Neurocritical Care

“…In human studies, cortical spreading depression has been associated with metabolic stress and injury, as measured by elevation in glutamate and lactate/pyruvate ratio, as well as low brain tissue oxygenation [78]. Its effects are not clearly mediated through or detected by rises in intracranial pressure [79], and thus CSD may result in secondary injury independent of intracranial pressure. Accordingly, CSD may represent either a therapeutic target in itself or a biomarker capable of guiding cerebral perfusion pressure and temperature management.…”