Intraventricular Intracranial Pressure Monitoring Research Articles

Waveform Morphology as a Surrogate for ICP Monitoring: A Comparison Between an Invasive and a Noninvasive Method.

BackgroundAlthough the placement of an intraventricular catheter remains the gold standard technique for measuring intracranial pressure (ICP), the method has several limitations. Therefore, noninvasive alternatives to ICP (ICPni) measurement are of great interest. The main objective of this study was to compare the correlation and agreement of wave morphology between ICP (standard intraventricular ICP monitoring) and a new ICPni monitor in patients admitted with stroke. The second objective was to estimate the discrimination of the noninvasive method to detect intracranial hypertension.MethodsWe prospectively collected data of adults admitted to an intensive care unit with subarachnoid hemorrhage, intracerebral hemorrhage, or ischemic stroke in whom an invasive ICP monitor was placed. Measurements were simultaneously collected from two parameters [time-to-peak (TTP) and the ratio regarding the second and first peak of the ICP wave (P2/P1 ratio)] of ICP and ICPni wave morphology monitors (Brain4care). Intracranial hypertension was defined as an invasively measured sustained ICP > 20 mm Hg for at least 5 min.ResultsWe studied 18 patients (subarachnoid hemorrhage = 14; intracerebral hemorrhage = 3; ischemic stroke = 1) on 60 occasions with a median age of 52 ± 14.3 years. A total of 197,400 waves (2495 min) from both ICP (standard ICP monitoring) and the ICPni monitor were sliced into 1-min-long segments, and we determined TTP and the P2/P1 ratio from the mean pulse. The median invasively measured ICP was 13 (9.8–16.2) mm Hg, and intracranial hypertension was present on 18 occasions (30%). The correlation and agreement between invasive and noninvasive methods for wave morphology were strong for the P2/P1 ratio and moderate for TTP using categoric (κ agreement 88.1% and 71.3%, respectively) and continuous (intraclass correlation coefficient 0.831 and 0.584, respectively) measures. There was a moderate but significant correlation with the mean ICP value (P2/P1 ratio r = 0.427; TTP r = 0.353; p < 0.001 for all) between noninvasive and invasive techniques. The areas under the curve to estimate intracranial hypertension were 0.786 [95% confidence interval (CI) 0.72–0.93] for the P2/P1 ratio and 0.694 (95% CI 0.60–0.74) for TTP.ConclusionsThe new ICPni wave morphology monitor showed a good agreement with the standard invasive method and an acceptable discriminatory power to detect intracranial hypertension.Clinical trial registration Trial registration: NCT05121155.

Cerebral perfusion pressure management through intraventricular intracranial pressure monitoring in spontaneous intracerebral hemorrhage: A case report

Cerebral perfusion pressure management through intraventricular intracranial pressure monitoring in spontaneous intracerebral hemorrhage: A case report

Inductive passive sensor for intraparenchymal and intraventricular monitoring of intracranial pressure.

Accurate measurement of intracranial hypertension is crucial for the management of elevated intracranial pressure (ICP). Catheter-based intraventricular ICP measurement is regarded as the gold standard for accurate ICP monitoring. However, this method is invasive, time-limited, and associated with complications. In this paper, we propose an implantable passive sensor that could be used for continuous intraparenchymal and intraventricular ICP monitoring. Moreover, the sensor can be placed simultaneously along with a cerebrospinal fluid shunt system in order to monitor its function. The sensor consists of a flexible coil which is connected to a miniature pressure sensor via an 8-cm long, ultra-thin coaxial cable. An external orthogonal-coil RF probe communicates with the sensor to detect pressure variation. The performance of the sensor was evaluated in an in vitro model for intraparenchymal and intraventricular ICP monitoring. The findings from this study demonstrate proof-of-concept of intraparenchymal and intraventricular ICP measurement using inductive passive pressure sensors.

Early Experience of Automated Intraventricular Type Intracranial Pressure Monitoring (LiquoGuard®) for Severe Traumatic Brain Injury Patients.

ObjectiveThe LiquoGuard® system is a new ventricular-type monitoring device that facilitates intracranial pressure (ICP)-controlled or volume-controlled drainage of cerebrospinal fluid (CSF). The purpose of this study is to report the authors' experience with the LiquoGuard® ICP monitoring system, as well as the clinical safety, usefulness, and limitations of this device in the management of patients with traumatic brain injury (TBI).MethodsIntraventricular ICP monitoring was performed on 10 patients with TBI using the LiquoGuard® monitoring system. ICP measurements, volume of drained CSF, and clinical outcomes were analyzed and discussed.ResultsICP monitoring was performed on 10 patients for a mean duration of 6.9 days. With a mean 82,718 records per patient, the mean initial ICP was 16.4 mm Hg and the average ICP across the total duration of monitoring was 15.5 mm Hg. The mean volume of drained CSF was 29.2 cc/day, with no CSF drained in 4 patients. Seven of 10 patients showed 1 or 2 episodes of abnormal ICP measurements. No patient exhibited complications associated with ICP monitoring.ConclusionThe LiquoGuard® system is a versatile tool in the management of TBI patients. Its use is both reliable and feasible for ICP monitoring and therapeutic drainage of CSF. However, episodes of abnormal ICP measurements were frequently observed in patients with slit ventricles, and further study may be needed to overcome this issue.

Zero drift of intraventricular and subdural intracranial pressure monitoring systems

ObjectiveTo assess zero drift of intraventricular and subdural intracranial pressure (ICP) monitoring systems. MethodsA prospective study was conducted in patients who received Codman ICP monitoring in the neurosurgical department from January 2010 to December 2011. According to the location of sensors, the patients were categorized into two groups: intraventricular group and subdural group. Zero drift between the two groups and its association with the duration of ICP monitor were analyzed. ResultsTotally, 22 patients undergoing intraventricular ICP monitoring and 27 receiving subdural ICP monitoring were enrolled. There was no significant difference in duration of ICP monitoring, zero drift value and its absolute value between intraventricular and subdural groups (5.38 d±2.58 d vs 4.58 d±2.24 d, 0.77mm Hg±2.18mm Hg vs 1.03mm Hg±2.06mm Hg, 1.68mm Hg±1.55mm Hg vs 1.70mm Hg±1.53mm Hg, respectively; all P>0.05). Absolute value of zero drift in both groups significantly rose with the increased duration of ICP monitoring (P<0.05) while zero drift value did not. Moreover, daily absolute value in the intraventricular group was significantly smaller than that in the subdural group (0.27mm Hg±0.32mm Hg vs 0.29mm Hg±0.18mm Hg, P<0.05). ConclusionThis study demonstrates that absolute value of zero drift significantly correlates with duration of both intraventricular and subdural ICP monitoring. Due to the smaller daily absolute value, ICP values recorded from intraventricular system may be more reliable than those from subdural system.

Moderately Elevated Intracranial Pressure after Diffuse Traumatic Brain Injury is Associated with Exacerbated Neuronal Pathology and Behavioral Morbidity in the Rat

Traumatic brain injury (TBI)-induced elevated intracranial pressure (ICP) is correlated with ensuing morbidity/mortality in humans. This relationship is assumed to rely mostly on the recognition that extremely elevated ICP either indicates hematoma/contusions capable of precipitating herniation or alters cerebral perfusion pressure (CPP), which precipitates global ischemia. However, whether subischemic levels of elevated ICP without hematoma/contusion contribute to increased morbidity/mortality remains unknown. To address this knowledge gap, we utilized a model of moderate diffuse TBI in rats followed by either intraventricular ICP monitoring or manual ICP elevation to 20 mm Hg, in which CPP was above ischemic levels. The effects of ICP elevation after TBI on acute and chronic histopathology, as well as on behavioral morbidity, were evaluated. ICP elevation after TBI resulted in increased acute neuronal membrane perturbation and was also associated with reduced neuronal density at 4 weeks after injury. Somatosensory hypersensitivity was exacerbated by ICP elevation and was correlated to the observed neuronal loss. In conclusion, this study indicates that morbidity and increased neuronal damage/death associated with elevated ICP can occur without concurrent global ischemia. Therefore, understanding the pathologies associated with subischemic levels of elevated ICP could lead to the development of better therapeutic strategies for the treatment and management of TBI patients.

Cortical Brain Biopsy in Long-Term Prognostication of 468 Patients with Possible Normal Pressure Hydrocephalus

Normal pressure hydrocephalus (NPH) can be alleviated by cerebrospinal fluid shunting but the differential diagnosis and patient selection are challenging. Intraventricular intracranial pressure monitoring as part of the diagnostic workup as well as shunting enable to obtain cortical brain biopsies to detect amyloid-β (Aβ) and hyperphosphorylated tau (HPτ), the hallmark lesions of Alzheimer’s disease (AD). In possible NPH, Aβ alone indicates an increased risk of AD and when present with HPτ probable AD, but the effect of those brain lesions on survival is not known. The aim of this study was to evaluate the predictive value of brain biopsy for the long-term outcome of possible NPH. Between 1991 and 2006, the Neurosurgery Department of the Kuopio University Hospital evaluated 468 patients for possible NPH by intraventricular intracranial pressure monitoring and frontal cortical brain biopsy immunostained against Aβ and HPτ. All patients were followed up until the end of 2008 (n = 201) or death (n = 267) with a median follow-up of 4.6 years (range 0–17). Logistic regression analysis with Cox models was applied. Out of the 468 cases, Aβ was detected in 197 (42%) cortical biopsies, and together with HPτ in 44 (9%). Aβ alone indicated increased risk of AD and with HPτ probable AD, but it did not affect survival. Vascular aetiology was the most frequent cause of death. Cortical biopsy findings indicate that NPH is at present a heterogeneous syndrome and has notable overlapping with AD. Brain biopsy did not predict survival but may open a novel research window to study the pathobiology of neurodegeneration.

In vivo accuracy of two intraparenchymal intracranial pressure monitors

To evaluate the in vivo accuracy of the new Pressio(®) device for intraparenchymal monitoring of intracranial pressure (ICP) versus the Codman(®) device and intraventricular measurement external ventricular drainage (EVD). Data were collected retrospectively for 30 consecutive patients admitted into a 25-bed neurosurgical intensive care unit of a university hospital between January and December 2009. Patients received both intraventricular and intraparenchymal ICP monitoring with Pressio(®) (n = 15) or Codman(®) (n = 15). We obtained 3,089 data points from the 30 patients. Mean difference between intraparenchymal and EVD pressure (bias) was -0.6 mmHg, and limits of agreement (1.96 SD of the bias) were -8.1 to 6.9 mmHg with Pressio(®) and 0.3 mmHg with limits of agreement of -6.7 to 7.1 mmHg with Codman(®) (NS). The temporal difference was -0.7 ± 1.6 mmHg/100 h of monitoring with Pressio(®) and 0.1 ± 1.6 mmHg/100 h of monitoring with Codman(®) over the study period (NS). Intraparenchymal pressure measured with both transducers approximates intraventricular cerebrospinal fluid pressure with an accuracy of ±7 mmHg.

Management of patients with severe traumatic brain injury guided by intraventricular intracranial pressure monitoring: a report of 136 cases

Objective To evaluate the effect of the treatment modality guided by intraventricular intracranial pressure (ICP) monitoring on patients with severe traumatic brain injury (TBI). Methods The clinical data of a group of 136 severely brain-injured patients admitted to Shanghai Neurosurgical Emergency Center from December 2004 to February 2006 were studied. Results The intraventricular ICP monitor was placed in all the 136 patients via Kocher's pathway, Paine's pathway or intraoperative opened ventricle. In this series, the probe was placed during the procedure of craniotomy in 98 patients; for other 38 patients, the probe was placed initially to measure or to monitor ICP. A stepwise protocol targeting at ICP control (≤20 mm Hg) and optimal cerebral perfusion pressure (CPP) maintenance (60–90 mm Hg) was deployed. Among them, 76 patients survived with good recovery, 14 with moderate disability, 24 with severe disability, 10 with vegetative state, and 12 died. Complications associated with intraventricular ICP monitoring included hemorrhage and infection. Hemorrhage occurred in 1 patient and infection in 5 patients. There were no unacceptable complications related to ICP monitoring. Conclusion Ventricular access for ICP monitoring can be safely and accurately achieved. ICP monitoring via ventriculostomy may facilitate an early and accurate intervention for severely brain-injured patients. The intraventricular ICP monitoring is a low-risk procedure and can yield great benefits for management of patients with severe TBI.

Ubiquitin C-terminal hydrolase is a novel biomarker in humans for severe traumatic brain injury*

Ubiquitin C-terminal hydrolase (UCH-L1), also called neuronal-specific protein gene product (PGP 9.3), is highly abundant in neurons. To assess the reliability of UCH-L1 as a potential biomarker for traumatic brain injury (TBI) this study compared cerebrospinal fluid (CSF) levels of UCH-L1 from adult patients with severe TBI to uninjured controls; and examined the relationship between levels with severity of injury, complications and functional outcome. This study was designed as prospective case control study. This study enrolled 66 patients, 41 with severe TBI, defined by a Glasgow coma scale (GCS) score of < or =8, who underwent intraventricular intracranial pressure monitoring and 25 controls without TBI requiring CSF drainage for other medical reasons. : Two hospital system level I trauma centers. Ventricular CSF was sampled from each patient at 6, 12, 24, 48, 72, 96, 120, 144, and 168 hrs following TBI and analyzed for UCH-L1. Injury severity was assessed by the GCS score, Marshall Classification on computed tomography and a complicated postinjury course. Mortality was assessed at 6 wks and long-term outcome was assessed using the Glasgow outcome score 6 months after injury. TBI patients had significantly elevated CSF levels of UCH-L1 at each time point after injury compared to uninjured controls. Overall mean levels of UCH-L1 in TBI patients was 44.2 ng/mL (+/-7.9) compared with 2.7 ng/mL (+/-0.7) in controls (p <.001). There were significantly higher levels of UCH-L1 in patients with a lower GCS score at 24 hrs, in those with postinjury complications, in those with 6-wk mortality, and in those with a poor 6-month dichotomized Glasgow outcome score. These data suggest that this novel biomarker has the potential to determine injury severity in TBI patients. Further studies are needed to validate these findings in a larger sample.

Clinical Significance ofαII-Spectrin Breakdown Products in Cerebrospinal Fluid after Severe Traumatic Brain Injury

Following traumatic brain injury (TBI), the cytoskeletal protein alpha-II-spectrin is proteolyzed by calpain and caspase-3 to signature breakdown products. To determine whether alpha -II-spectrin proteolysis is a potentially reliable biomarker for TBI in humans, the present study (1) examined levels of spectrin breakdown products (SBDPs) in cerebrospinal fluid (CSF) from adults with severe TBI and (2) examined the relationship between these levels, severity of injury, and clinical outcome. This prospective case control study enrolled 41 patients with severe TBI, defined by a Glasgow Coma Scale (GCS) score of < or =8, who underwent intraventricular intracranial pressure monitoring. Patients without TBI requiring CSF drainage for other medical reasons served as controls. Ventricular CSF was sampled from each patient at 6, 12, 24, 48, 72, 96, and 120 h following TBI and analyzed for SBDPs. Outcome was assessed using the Glasgow Outcome Score (GOS) 6 months after injury. Calpain and caspase-3 mediated SBDP levels in CSF were significantly increased in TBI patients at several time points after injury, compared to control subjects. The time course of calpain mediated SBDP150 and SBDP145 differed from that of caspase-3 mediated SBDP120 during the post-injury period examined. Mean SBDP densitometry values measured early after injury correlated with severity of injury, computed tomography (CT) scan findings, and outcome at 6 months post-injury. Taken together, these results support that alpha -II-spectrin breakdown products are potentially useful biomarker of severe TBI in humans. Our data further suggests that both necrotic/oncotic and apoptotic cell death mechanisms are activated in humans following severe TBI, but with a different time course after injury.

Fatal Severe Vasospasm Due to Rewarming Following Hypothermia. Case Report.

A 37-year-old female died of cerebral vasospasm as a complication of rewarming following hypothermia therapy for severe head injury. She presented with severe consciousness disturbance and anisocoria after falling down a flight of stairs. Computed tomography (CT) revealed a right acute subdural hematoma and temporal contusion. Following surgery, mild hypothermia was started and rewarming was completed by the 11th day. Neurological examination showed no abnormalities, but intracranial pressure (ICP) suddenly increased and she manifested anisocoria on the 13th day. Repeat CT revealed a low density area in the right middle cerebral artery region and cerebral angiography showed diffuse narrowing of the main arterial trunks. A cerebrospinal fluid (CSF) sample was collected using an intraventricular ICP monitoring catheter. The CSF level of 8-hydroxy-2'-deoxyguanosine was elevated during the rewarming period, indicating substantial deoxyribonucleic acid (DNA) oxidation. She died on the 15th day due to uncontrollable ICP. Histological examination at autopsy of the narrowed artery found the waving phenomenon in the internal elastic lamina and invasion of inflammatory cells into the adventitia. These findings constitute the possible evidence that free-radical-mediated oxidative DNA damage may be important in the genesis of severe vasospasm due to rewarming following hypothermia.

Late epilepsy after aneurysm operations.

The risk of late epilepsy was analyzed in a consecutive series of 177 patients operated on for supratentorial aneurysms. Late seizures occurred in 25 patients (14%); the seizures were recurrent in 21 patients (12%). Most seizures were partial, secondary generalized, or generalized tonic-clonic (72%). The mean latency between the operation and seizures was 8.4 months (range, 1 to 24 months), and in only 2 patients was the interval more than 12 months. The most important risk factors were preoperative and postoperative complications. Only 2.5% of the 81 Grade I patients developed epilepsy, compared to 33% of the 42 Grade III-IV patients. Other risk factors were location of the aneurysm in the middle cerebral artery, the presence of a large intracerebral hematoma, postoperative spasm with late ischemic infarction, and shunt-dependent hydrocephalus. The timing of operation or intraventricular intracranial pressure monitoring did not change the risk of late epilepsy. The fact that only 2 patients had early epilepsy may have been due to routine treatment with prophylactic anticonvulsants. The value of prophylaxis in late epilepsy is unproven, but prophylactic treatment could be useful in patients with a high risk of epileptic seizures.