Simultaneous Intracerebral Microdialysis and Positron Emission Tomography in the Detection of Ischemia in Patients with Subarachnoid Hemorrhage

Enblad, Per; Valtysson, Johann; Andersson, Jesper; Lilja, Anders; Valind, Sven; Antoni, Gunnar; Långström, Bengt; Hillered, Lars; Persson, Lennart

doi:10.1097/00004647-199607000-00014

Cited by 160 publications

(113 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Thus, it is possible that seizures resulted in worsening brain edema and hence elevation in ICP. (2,14,17). We have demonstrated that LPR is elevated for 1 wk in previous studies (18).…”

Section: Potential Role Of Electrographic Seizures On Brain Swelling mentioning

confidence: 53%

“…LPR is thought to represent alterations of mitochondrial function and redox state of the cell (16). LPR can increase with brain ischemia, under conditions of severely limited cerebral blood flow (2,14,17). We have demonstrated that LPR is elevated for 1 wk in previous studies (18).…”

Section: Seizures Are Associated With Prolonged Metabolic Distressmentioning

confidence: 70%

“…Alternatively, the seizures may have resulted in an increase in extracellular edema and hence increased ICP. In the past, we reported increases in glutamate (14) and increased brain edema (15) with seizure activity after TBI and intracerebral hemorrhage, respectively. In the present series, we again demonstrated an increase in glutamate during the seizures.…”

Section: Potential Role Of Electrographic Seizures On Brain Swelling mentioning

confidence: 97%

See 2 more Smart Citations

Nonconvulsive electrographic seizures after traumatic brain injury result in a delayed, prolonged increase in intracranial pressure and metabolic crisis

Vespa

Miller²,

McArthur³

et al. 2007

Critical Care Medicine

367

148

View full text Add to dashboard Cite

Objective-To determine whether nonconvulsive electrographic post-traumatic seizures result in increases in intracranial pressure and microdialysis lactate/pyruvate ratio. Design-Prospective monitoring with retrospective data analysis.Setting-Single center academic neurologic intensive care unit.Patients-Twenty moderate to severe traumatic brain injury patients (Glasgow Coma Score 3-13). HHS Public Access Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptMeasurements and Main Results-Continuous electroencephalography and cerebral microdialysis were performed for 7 days after injury. Ten patients had seizures and were compared with a matched cohort of traumatic brain injury patients without seizures. The seizures were repetitive and constituted status epilepticus in seven of ten patients. Using a within-subject design, post-traumatic seizures resulted in episodic increases in intracranial pressure (22.4 ± 7 vs. 12.8 ± 4.3 mm Hg; p < .001) and an episodic increase in lactate/pyruvate ratio (49.4 ± 16 vs. 23.8 ± 7.6; p < .001) in the seizure group. Using a between-subjects comparison, the seizure group demonstrated a higher mean intracranial pressure (17.6 ± 6.5 vs. 12.2 ± 4.2 mm Hg; p < .001), a higher mean lactate/pyruvate ratio (38.6 ± 18 vs. 27 ± 9; p < .001) compared with nonseizure patients. The intracranial pressure and lactate/pyruvate ratio remained elevated beyond postinjury hr 100 in the seizure group but not the nonseizure group (p < .02).Conclusion-Post-traumatic seizures result in episodic as well as long-lasting increases in intracranial pressure and microdialysis lactate/pyruvate ratio. Intracranial pressure (ICP) remains one of the principal treatment targets for traumatic brain injury (TBI) (1). Elevation of ICP is due to brain edema, mass effect from hemorrhagic lesions, and possibly from disrupted pressure autoregulation. The treatments for ICP have been focused on these pathophysiologic mechanisms. While the treatment principals for elevated ICP have been codified into guidelines and practiced by many intensivists, ICP often remains refractory to treatment. Indeed, treatment failure resulting in herniation and death occurs frequently. The mechanisms for persistently elevated ICP have not been well elucidated, but candidate mechanisms include sustained hyperemia, excitotoxicity, and osmotic rebound. In contrast, little attention has been paid to the adverse effects of epileptic activity upon the extent or duration of elevated ICP after TBI.In recent years, post-traumatic seizures have been documented to occur frequently after human TBI (2). Indeed, seizures are frequent after a variety of hemorrhagic injuries to the brain (3, 4). The incidence of seizures increases as a function of the severity of injury, and other selected features of the injury such as the presence of hemorrhagic contusions. Posttraumatic seizures previously have been associated with increased glycolysis in both animal and human metabolic imaging studies (5, 6) and have been associated with alterat...

show abstract

“…Thus, it is possible that seizures resulted in worsening brain edema and hence elevation in ICP. (2,14,17). We have demonstrated that LPR is elevated for 1 wk in previous studies (18).…”

Section: Potential Role Of Electrographic Seizures On Brain Swelling mentioning

confidence: 53%

Section: Seizures Are Associated With Prolonged Metabolic Distressmentioning

confidence: 70%

Section: Potential Role Of Electrographic Seizures On Brain Swelling mentioning

confidence: 97%

See 1 more Smart Citation

Nonconvulsive electrographic seizures after traumatic brain injury result in a delayed, prolonged increase in intracranial pressure and metabolic crisis

Vespa

Miller²,

McArthur³

et al. 2007

Critical Care Medicine

367

148

View full text Add to dashboard Cite

show abstract

“…However, there is no evidence that 1 method is more efficient and reliable than other methods. [37][38][39] Cumulative meta-analysis, including 1981 patients altogether, demonstrated that the frequency of shunt-dependent hydrocephalus was not significantly different between coiling and clipping. This result differs with the prior meta-analysis conducted in 2007, 40 which showed that the risk of shuntdependent hydrocephalus was significantly higher after coiling than clipping for ruptured intracranial aneurysms.…”

Section: Secondary Outcomesmentioning

confidence: 98%

Clipping Versus Coiling for Ruptured Intracranial Aneurysms

Li¹,

Pan²,

Wang³

et al. 2013

Stroke

258

152

View full text Add to dashboard Cite

Background and Purpose-Endovascular treatment has increasingly been used for aneurismal subarachnoid aneurismal hemorrhage. The aim of this analysis is to assess the current evidence regarding safety and efficiency of clipping compared with coiling. Methods-We conducted a meta-analysis of studies that compared clipping with coiling between January 1999 and July 2012. Comparison of binary outcomes between treatment groups was described using odds ratios (OR; clip versus coil). Results-Four

show abstract

“…13,14 An increase in lactate to pyruvate (L/P) ratio is a sensitive indicator of brain ischemia, and increases in L/P ratio have been observed after subarachnoid hemorrhage. 15,16 Brain edema of cellular nature is frequently observed, which results in an increase of intracranial pressure (ICP) for more than 5 days. 17 Increased ICP causes structural damage and herniation and reduces cerebral perfusion pressure and cerebral blood flow, leading to further exacerbation of ischemia.…”

Section: Pathophysiology Of Traumatic Brain Injurymentioning

confidence: 99%

Use of Magnesium in Traumatic Brain Injury

Sen¹,

Gulati

2010

Neurotherapeutics

View full text Add to dashboard Cite

Summary: Depletion of magnesium is observed in animal brain and in human blood after brain injury. Treatment with magnesium attenuates the pathological and behavioral changes in rats with brain injury; however, the therapeutic effect of magnesium has not been consistently observed in humans with traumatic brain injury (TBI). Secondary brain insults are observed in patients with brain injury, which adversely affect clinical outcome. Systemic administration studies in rats have shown that magnesium enters the brain; however, inducing hypermagnesemia in humans did not concomitantly increase magnesium levels in the CSF. We hypothesize that the neuroprotective effects of magnesium in TBI patients could be observed by increasing its brain bioavailability with mannitol. Here, we review the role of magnesium in brain injury, preclinical studies in brain injury, clinical safety and efficacy studies in TBI patients, brain bioavailability studies in rat, and pharmacokinetic studies in humans with brain injury. Neurodegeneration after brain injury involves multiple biochemical pathways. Treatment with a single agent has often resulted in poor efficacy at a safe dose or toxicity at a therapeutic dose. A successful neuroprotective therapy needs to be aimed at homeostatic control of these pathways with multiple agents. Other pharmacological agents, such as dexanabinol and progesterone, and physiological interventions, with hypothermia and hyperoxia, have been studied for the treatment of brain injury. Treatment with magnesium and hypothermia has shown favorable outcome in rats with cerebral ischemia. We conclude that coadministration of magnesium and mannitol with pharmacological and physiological agents could be an effective neuroprotective regimen for the treatment of TBI.

show abstract

Simultaneous Intracerebral Microdialysis and Positron Emission Tomography in the Detection of Ischemia in Patients with Subarachnoid Hemorrhage

Cited by 160 publications

References 19 publications

Nonconvulsive electrographic seizures after traumatic brain injury result in a delayed, prolonged increase in intracranial pressure and metabolic crisis

Nonconvulsive electrographic seizures after traumatic brain injury result in a delayed, prolonged increase in intracranial pressure and metabolic crisis

Clipping Versus Coiling for Ruptured Intracranial Aneurysms

Use of Magnesium in Traumatic Brain Injury

Contact Info

Product

Resources

About