Acta Neurochir (2010) 152:989–995. DOI 10.1007/s00701-010-0605-x
Purpose: In patients with idiopathic normal pressure hydrocephalus (iNPH) and ventriculomegaly, examine whether there is a gradient in pulsatile intracranial pressure (ICP) from within the cerebrospinal fluid (CSF) of cerebral ventricles (ICPIV) to the subdural (ICPSD) compartment. We hypothesized that pulsatile ICP is higher within the ventricular CSF.
Methods The material includes 10 consecutive iNPH patients undergoing diagnostic ICP monitoring as part of pre-operative work-up. Eight patients had simultaneous ICPIV and ICPSD signals, and two patients had simultaneous signals from the lateral ventricle (ICPIV) and the brain parenchyma (ICPPAR). Intracranial pulsatility was characterized by the wave amplitude, rise time, and rise time coefficient; static ICP was characterized by mean ICP.
Results None of the patients demonstrated gradients in pulsatile ICP, that is, we found no evidence of higher pulsatile ICP within the CSF of the cerebral ventricles (ICPIV), as compared to either the subdural (ICPSD) compartment or within the brain parenchyma (ICPPAR). During ventricular infusion testing in one patient, the ventricular ICP (ICPIV) was artificially increased, but this increase in ICPIV produced no gradient in pulsatile ICP from the ventricular CSF (ICPIV) to the parenchyma (ICPPAR).
Conclusions: In this cohort of iNPH patients, we found no evidence of transmantle gradient in pulsatile ICP. The data gave no support to the hypothesis that pulsatile ICP is higher within the CSF of the cerebral ventricles (ICPIV) than within the subdural (ICPSD) compartment or the brain parenchyma (ICPPAR) in iNPH patients.
J Neurosurg Anesthesiol 2009;21:339–345
Objective: To assess the intracranial hemodynamic modifica- tions induced by a decompressive craniectomy (DC) after severe traumatic brain injury (TBI), using transcranial Doppler (TCD) ultrasonography and intracranial pressure (ICP) sensor. Mor- tality rate and neurological outcomes were also evaluated after this procedure.
Design: A prospective study was carried out on 26 TBI patients, measuring transcranial Doppler and ICP before, immediately after, and 48 hours after the DC, allowing for statistical analysis of hemodynamic changes. The mortality rate and the neuro- logical outcomes were assessed.
Measurements and Results: After DC, ICP decreased from 37±17 to 20±13mm Hg (P=0.0003). The global cerebral blood flow was modified with diastolic velocities rising from 23±15 to 31±13cm/s (P=0.0038) and a pulsatility index decreasing from 1.70±0.66 to 1.18±0.37 (P=0.0012). This normalization of the global cerebral hemodynamics after the DC was immediate, symmetric, and constant during the first 48 hours. Outcome was evaluated at 6 months: good recovery or moderate disability was observed in 11 patients (42%), persistent vegetative state in 7 patients (27%), and 8 patients died (31%).
Conclusions: The DC results in a significant, immediate, and durable improvement of ICP associated with a normalization of cerebral blood flow velocities in most TBI patients with refractory intracranial hypertension.
J Neurosurg 111:910–915, 2009.DOI: 10.3171/2008.8.JNS0889
The aim of this study was to explore the relationship between hemodynamics (intracranial and systemic) and brain tissue energy metabolism, and between hemodynamics and glutamate (Glt)-glutamine (Gln) cycle activity.
Methods. Brain interstitial levels of lactate, pyruvate, Glt, and Gln were prospectively monitored in the neurointensive care unit for more than 3600 hours using intracerebral microdialysis in 33 patients with subarachnoid hemorrhage (SAH). Intracranial pressure (ICP), mean arterial blood pressure, and cerebral perfusion pressure (CPP) were recorded using a digitalized system.
Results. Interstitial Gln and pyruvate correlated with CPP (r = 0.25 and 0.24, respectively). Intracranial pressure negatively correlated with Gln (r = −0.29) and the Gln/Glt ratio (r = –0.40). Levels of Gln and pyruvate and the Gln/Glt ratio were higher and levels of Glt and lactate and the lactate/pyruvate ratio were lower during periods of decreased ICP (≤ 10 mm Hg) as compared with values in periods of elevated ICP (> 10 mm Hg). In 3 patients, a poor clinical condition was attributed to high ICP levels (range 15–25 mm Hg). When CSF drainage was increased and the ICP was lowered to 10 mm Hg, there was an instantaneous sharp increase in interstitial Glt and pyruvate in these 3 patients.
Conclusions. Increasing interstitial Gln and pyruvate levels appear to be favorable signs associated with improved CPP and low ICP. The authors suggest that this pattern indicates an energy metabolic situation allowing augmented astrocytic energy metabolism with accelerated Glt uptake and Gln synthesis. Moreover, their data raised the question of whether patients with SAH and moderately elevated ICP (15–20 mm Hg) would benefit from CSF drainage at lower pressure levels than what is usually indicated in current clinical protocols.
J Neurosurg Anesthesiol 2009;21:339–345
A prospective study was carried out on 26 TBI patients, measuring transcranial Doppler and ICP before, immediately after, and 48 hours after the DC, allowing for statistical analysis of hemodynamic changes. The mortality rate and the neuro- logical outcomes were assessed.
Measurements and Results: After DC, ICP decreased from 37±17 to 20±13mm Hg (P=0.0003). The global cerebral blood flow was modified with diastolic velocities rising from 23±15 to 31±13cm/s (P=0.0038) and a pulsatility index decreasing from 1.70±0.66 to 1.18±0.37 (P=0.0012). This normalization of the global cerebral hemodynamics after the DC was immediate, symmetric, and constant during the first 48 hours. Outcome was evaluated at 6 months: good recovery or moderate disability was observed in 11 patients (42%), persistent vegetative state in 7 patients (27%), and 8 patients died (31%).
Conclusions: The DC results in a significant, immediate, and durable improvement of ICP associated with a normalization of cerebral blood flow velocities in most TBI patients with refractory intracranial hypertension.
Neurosurgery 66 (6):1050–1057.
