Plateau Waves Research Articles

Open cranium model for the study of cerebrovascular dynamics in intracranial hypertension

BackgroundSignificant research has been devoted to developing noninvasive approaches to neuromonitoring. Clinical validation of such approaches is often limited, with minimal data available in the clinically relevant elevated ICP range. New MethodTo allow ultrasound-guided placement of an intraventricular catheter and to perform simultaneous long-duration ICP and ultrasound recordings of cerebral blood flow, we developed a large unilateral craniectomy in a swine model. We also used a microprocessor-controlled actuator for intraventricular saline infusion to reliably and reversibly manipulate ICP according to pre-determined profiles. ResultsThe model was reproducible, resulting in over 80 hours of high-fidelity, multi-parameter physiological waveform recordings in twelve animals, with ICP ranging from 2 to 78 mmHg. ICP elevations were reversible and reproducible according to two predetermined profiles: a stepwise elevation up to an ICP of 30–35 mmHg and return to normotension, and a clinically significant plateau wave. Finally, ICP was elevated to extreme levels of greater than 60 mmHg, simulating extreme clinical emergency. Comparison with existing methodsExisting methods for ICP monitoring in large animals typically relied on burr-hole approaches for catheter placement. Accurate catheter placement can be difficult in pigs, given the thickness of their skull. Additionally, ultrasound is significantly attenuated by the skull. The open cranium model overcomes these limitations. ConclusionsThe hemicraniectomy model allowed for verified placement of the intraventricular catheter, and reversible and reliable ICP manipulation over a wide range. The large dural window additionally allowed for long-duration recording of cerebral blood flow velocity from the middle cerebral artery.

A study on decompression wave propagation characteristics during CO2 pipeline leakage with consideration of gas‐liquid transition

AbstractPipelines stand as the most cost‐effective method for large‐scale transportation of CO2 from a source point to the storage site, especially over extensive distances. The potential for crack propagation following a pipeline rupture highlights the need for precise analysis of decompression wave propagation. To accurately model this, understanding the decompression wave's propagation laws becomes imperative. Although previous studies have predominantly focused on pipeline leaks within the dense phase or supercritical state, the transition from liquid to gas during leakage significantly affects the decompression wave propagation. When a gaseous CO2 pipeline ruptures, the high Joule‐–Thomson coefficient causes a swift temperature plunge, potentially leading to a gas–liquid transition. However, research on how this phase transition impacts the decompression wave characteristics is limited. To address this gap, this study proposes a transition computational fluid dynamics model to predict the decompression wave behavior. The model is validated with an industrial‐scale full‐bore rupture experiment. The results reveal that the gaseous CO2 leakage induces a pressure plateau at a certain distance from the leakage due to the gas‐liquid phase transition. The influences of initial conditions on this pressure plateau and decompression wave are also explored. This study provides valuable insights into understanding the decompression wave behaviors of gaseous CO2 pipelines, which are essential for ensuring the safety and reliability of CO2 transportation within the carbon capture and storage technology chain. © 2024 Society of Chemical Industry and John Wiley & Sons, Ltd.

Utility of intracranial pressure monitoring as a diagnostic tool in pediatric ventriculomegaly

ObjectiveIntracranial pressure (ICP) monitoring is commonly utilized for identifying pathologic ICP in cases of traumatic brain injury; however, its utility in hydrocephalic children has not been elucidated. Although patients with typical (pressure-active) hydrocephalus present with clear signs and/or symptoms and the need for cerebrospinal fluid (CSF) diversion is often clear, others may have arrested or pressure-compensated hydrocephalus with pathologic ICP elevation masked by ambiguous signs or are completely asymptomatic. Without treatment these pathologic ICP elevations may affect neurologic development or crescendo over time leading to neurological decline. The purpose of this study is to investigate the utility of ICP monitoring as a diagnostic tool in this relatively common patient population and identify ventriculomegaly patients with and without pathologic ICP, thus improving accuracy of identifying those with and without surgical needs. Methods36 patients (≤ 17 years old) underwent 41 inpatient ICP recording sessions between 2016 and 2022 and were retrospectively reviewed. This included patients with a history of severe, nonprogressive ventriculomegaly and normal fundoscopic examinations lacking traditional signs and symptoms concerning for elevated ICP. Nighttime pathological plateau waves were defined as sustained elevations of ICP ≥ 2x baseline for a duration of ≥ 5 minutes. ResultsThe mean age of patients was 5.5 years old (range 0–17 years old). 46.3% of patients had prior endoscopic third ventriculostomy (ETV), 14.6% had prior ventriculoperitoneal shunt (VPS), and 39% were without prior surgical intervention. Roughly half (51.2%) of patients had congenital ventriculomegaly while other patients had ventriculomegaly due to other pathologies such as germinal matrix hemorrhage/intraventricular hemorrhage (GMH/IVH) (29.3%), stroke (4.9%), cerebral infections/meningitis (2.4%), or unknown etiology (12.2%). The average procedure time was 19.1 ± 10.5 minutes, and mean length of stay was 2.8 ± 0.7 days. Pathologic ICP was demonstrated in 12 cases (29.3%), 4 (33.3%) of which were asymptomatic. Pathologic ICP was found in 7 of 19 (36.8%) in the prior ETV group, 1 of 6 (16.7%) in prior shunt group, and 4 of 16 (25%) in the non-surgical group (p = 0.649). Among those with pathologic ICP, 6 (50%) cases received an ETV, 5 (41.7%) cases underwent VPS placement, and 1 (8.3%) case underwent a VPS revision. There were no infectious complications or cases of hemorrhage. 4 patients required repositioning of the ICP monitor due to dislodgement. ConclusionInpatient ICP monitoring is a safe and effective diagnostic tool for evaluating the presence of pathologic ICP in severe, persistent non-progressive ventriculomegaly. The use of ICP monitoring may aid in identifying patients with pressure-compensated hydrocephalus who demonstrate pathologic ICP where surgical intervention may be warranted, while preventing unnecessary CSF diversion in those without pathology.

Quantitative analysis of similarity between cerebral arterial blood volume and intracranial pressure pulse waveforms during intracranial pressure plateau waves

IntroductionBoth intracranial pressure (ICP) and cerebral arterial blood volume (CaBV) have a pulsatile character related to the cardiac cycle. The evolution of the shape of ICP pulses under increasing ICP or decreasing intracranial compliance is well documented. Nevertheless, the exact origin of the alterations in the ICP morphology remains unclear. Research questionDoes ICP pulse waveform become similar to non-invasively estimated CaBV pulse during ICP plateau waves. Material and methodsA total of 15 plateau waves recorded in 15 traumatic brain injured patients were analyzed. CaBV pulse waveforms were calculated using global cerebral blood flow model from transcranial Doppler cerebral blood flow velocity (CBFV) signals. The difference index (DI) was used to quantify the similarity between ICP and CaBV waveforms. DI was calculated as the sum of absolute sample-by-sample differences between ICP and CaBV waveforms, representing the area between the pulses. ResultsICP increased (19.4 mm Hg [Q1–Q3: 18.2–23.4 mm Hg] vs. 42.7 mm Hg [Q1–Q3: 36.5–45.1 mm Hg], p < 0.001) while CBFV decreased (44.2 cm/s [Q1–Q3: 34.8–69.5 cm/s] vs. 32.9 cm/s [Q1–Q3: 24.7–68.2 cm/s], p = 0.002) during plateau waves. DI was smaller during the plateau waves (20.4 [Q1–Q3: 15.74–23.0]) compared to the baselines (26.3 [Q1–Q3: 24.2–34.7], p < 0.001). Discussion and conclusionThe area between corresponding ICP and CaBV pulse waveforms decreased during the plateau waves which suggests they became similar in shape. CaBV may play a significant role in determining the shape of ICP pulses during the plateau waves and might be a driving force in formulating ICP elevation.

Cerebral Perfusion Imaging and Plateau Waves

HomeStrokeAhead of PrintCerebral Perfusion Imaging and Plateau Waves No AccessCase ReportRequest AccessAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toNo AccessCase ReportRequest AccessCerebral Perfusion Imaging and Plateau Waves Diana Slawski, Kyle A. Lyman, Prateek Thatikunta, Carl A. Gold and Gregory W. Albers Diana SlawskiDiana Slawski Correspondence to: Diana Slawski, MD, Department of Neurology, Stanford University School of Medicine, 453 Quarry Rd, MC 5235, Stanford, CA 94305. Email E-mail Address: [email protected] https://orcid.org/0000-0001-5516-8968 Department of Neurology & Neurological Sciences, Stanford University School of Medicine, CA. Search for more papers by this author , Kyle A. LymanKyle A. Lyman https://orcid.org/0000-0002-3309-7211 Department of Neurology & Neurological Sciences, Stanford University School of Medicine, CA. Search for more papers by this author , Prateek ThatikuntaPrateek Thatikunta https://orcid.org/0000-0001-6542-2827 Department of Neurology & Neurological Sciences, Stanford University School of Medicine, CA. Search for more papers by this author , Carl A. GoldCarl A. Gold https://orcid.org/0000-0002-4868-4152 Department of Neurology & Neurological Sciences, Stanford University School of Medicine, CA. Search for more papers by this author and Gregory W. AlbersGregory W. Albers https://orcid.org/0000-0003-0263-4632 Department of Neurology & Neurological Sciences, Stanford University School of Medicine, CA. Search for more papers by this author Originally published6 Apr 2023https://doi.org/10.1161/STROKEAHA.122.042274Stroke. 2023;0FootnotesFor Sources of Funding and Disclosures, see page xxx.Correspondence to: Diana Slawski, MD, Department of Neurology, Stanford University School of Medicine, 453 Quarry Rd, MC 5235, Stanford, CA 94305. Email [email protected]edu Previous Back to top Next FiguresReferencesRelatedDetails Advertisement Article InformationMetrics © 2023 American Heart Association, Inc.https://doi.org/10.1161/STROKEAHA.122.042274PMID: 37021565 Originally publishedApril 6, 2023 Keywordsperfusion imagingedemamagnetic resonance imagingarousalangiographyPDF download Advertisement SubjectsCerebrovascular Disease/StrokeComputerized Tomography (CT)Magnetic Resonance Imaging (MRI)

Peak appearance time in pulse waveforms of intracranial pressure and cerebral blood flow velocity.

The shape of the pulse waveforms of intracranial pressure (ICP) and cerebral blood flow velocity (CBFV) typically contains three characteristic peaks. It was reported that alterations in cerebral hemodynamics may influence the shape of the pulse waveforms by changing peaks' configuration. However, the changes in peak appearance time (PAT) in ICP and CBFV pulses are only described superficially. We analyzed retrospectively ICP and CBFV signals recorded in traumatic brain injury patients during decrease in ICP induced by hypocapnia (n = 11) and rise in ICP during episodes of ICP plateau waves (n = 8). All three peaks were manually annotated in over 48 thousand individual pulses. The changes in PAT were compared between periods of vasoconstriction (expected during hypocapnia) and vasodilation (expected during ICP plateau waves) and their corresponding baselines. Correlation coefficient (rS) analysis between mean ICP and mean PATs was performed in each individual recording. Vasodilation prolonged PAT of the first peaks of ICP and CBFV pulses and the third peak of CBFV pulse. It also accelerated PAT of the third peak of ICP pulse. In contrast, vasoconstriction shortened appearance time of the first peaks of ICP and CBFV pulses and the second peak of ICP pulses. Analysis of individual recordings demonstrated positive association between changes in PAT of all three peaks in the CBFV pulse and mean ICP (rS range: 0.32-0.79 for significant correlations). Further study is needed to test whether PAT of the CBFV pulse may serve as an indicator of changes in ICP-this may open a perspective for non-invasive monitoring of alterations in mean ICP.

Multiscale Information Decomposition of Long Memory Processes: Application to Plateau Waves of Intracranial Pressure.

Traumatic Brain Injury (TBI) patients present high levels of physical stress, which in some situations can manifest as Plateau Wave (PW) episodes. This intense stress phenomenon can be evidenced by Heart Rate Variability (HRV). Thus, the multivariate and simultaneous analysis of cardio-cerebrovascular oscillations, involving the RR intervals, mean arterial pressure (MAP) and the amplitude of intracranial pressure (AMP), will be useful to understand the interconnections between body signals, allowing the interpretation of the combined activity of pathophysiological mechanisms. In this work, the multiscale representation of the Transfer Entropy (TE) and of its decomposition in the network of these three interacting processes is obtained, based on a Vector AutoRegressive Fractionally Integrated (VARFI) framework for Gaussian processes. This method allows to assess directed interactions and to quantify the information flow accounting for the simultaneous presence of short-term dynamics and long-range correlations. The results show that the baseline RR, but not MAP can provide information about the possibility of a PW arising. During PW, the long-term correlations highlight synergistic interactions between MAP and AMP processes on RR. The multiscale decomposition of the information along with the incorporation of the long term correlations allowed a better description of HRV during PW, highlighting the fact that the HRV mirrors this cerebrovascular phenomena.

Neurocritical Care

Neurologic critical care encompasses the management of many nervous system diseases when they present in the extremes of severity. Core conditions managed in the neuroscience intensive care unit (ICU) include stroke, cerebral hemorrhage, status epilepticus (SE), myasthenia gravis (MG), Guillain-Barré syndrome (GBS), traumatic brain and spinal cord injury, and high-risk postoperative neurosurgical patients. The skills and knowledge base required to care for patients with such conditions, and the life-threatening complications associated with them, are drawn from both traditional neurology and from critical care medicine. This chapter covers specialized monitoring in the neurologic intensive care unit and special conditions such as acute intracranial hypertension, acute ischemic stroke, intracerebral hemorrhage, venous sinus thrombosis, myasthenia gravis, GBS, seizure and status epilepticus, spinal cord injury, and traumatic brain injury. The chapter includes 8 tables and 5 figures. Tables provide common etiologies of acute intracranial hypertension; general prophylactic measures, medical interventions, surgical interventions, and stepwise treatment protocol for acute intracranial hypertension; drugs that can exacerbate weakness in myasthenia gravis, cholinergic drug dosage equivalents and duration of action, and antiseizure medications used in status epilepticus. Figures illustrate the Monro-Kellie Doctrine, intracranial pressure waveform and plateau waves, typical herniation patterns, large stroke with malignant edema, and examples of nontraumatic intracerebral hemorrhage. This chapter contains 114 references.

SIMULATION OF PANDEMIC DEVELOPMENT PROCESSES

The study is devoted to the development of mathematical models for predicting the incidence of COVID-19 using simulation tools. Methods of modeling the spread of infectious diseases have been studied since the beginning of the twentieth century. In the classical SIR model, the entire population was divided into three parts: «susceptible – infected – recovered». In the 1980s, the intermediate state – «infected, but not yet infectious» was added to the classical model. This model is called SEIR. The spread of the epidemic in both models is described by a system of differential equations, which is solved using numerical methods.&#x0D; Significantly new simulation modelling approaches are necessary to forecast evolution of the coronavirus pandemic. This study based on the classical SEIR model («susceptible – infected but not yet infectious – infected – recovered») suggests several methods for developing models: with a long plateau, with two or more waves. The modern tool used for the simulation is Anylogic 8.

Peopling History of the Tibetan Plateau and Multiple Waves of Admixture of Tibetans Inferred From Both Ancient and Modern Genome-Wide Data.

Archeologically attested human occupation on the Tibetan Plateau (TP) can be traced back to 160 thousand years ago (kya) via the archaic Xiahe people and 30∼40 kya via the Nwya Devu anatomically modern human. However, the history of the Tibetan populations and their migration inferred from the ancient and modern DNA remains unclear. Here, we performed the first ancient and modern genomic meta-analysis among 3,017 Paleolithic to present-day Eastern Eurasian genomes (2,444 modern individuals from 183 populations and 573 ancient individuals). We identified a close genetic connection between the ancient-modern highland Tibetans and lowland island/coastal Neolithic Northern East Asians (NEA). This observed genetic affinity reflected the primary ancestry of high-altitude Tibeto-Burman speakers originated from the Neolithic farming populations in the Yellow River Basin. The identified pattern was consistent with the proposed common north-China origin hypothesis of the Sino-Tibetan languages and dispersal patterns of the northern millet farmers. We also observed the genetic differentiation between the highlanders and lowland NEAs. The former harbored more deeply diverged Hoabinhian/Onge-related ancestry and the latter possessed more Neolithic southern East Asian (SEA) or Siberian-related ancestry. Our reconstructed qpAdm and qpGraph models suggested the co-existence of Paleolithic and Neolithic ancestries in the Neolithic to modern East Asian highlanders. Additionally, we found that Tibetans from Ü-Tsang/Ando/Kham regions showed a strong population stratification consistent with their cultural background and geographic terrain. Ü-Tsang Tibetans possessed a stronger Chokhopani-affinity, Ando Tibetans had more Western Eurasian related ancestry and Kham Tibetans harbored greater Neolithic southern EA ancestry. Generally, ancient and modern genomes documented multiple waves of human migrations in the TP’s past. The first layer of local hunter-gatherers mixed with incoming millet farmers and arose the Chokhopani-associated Proto-Tibetan-Burman highlanders, which further respectively mixed with additional genetic contributors from the western Eurasian Steppe, Yellow River and Yangtze River and finally gave rise to the modern Ando, Ü-Tsang and Kham Tibetans.

Intracranial pulse pressure waveform analysis using the higher harmonics centroid

BackgroundThe pulse waveform of intracranial pressure (ICP) is its distinctive feature almost always present in the clinical recordings. In most cases, it changes proportionally to rising ICP, and observation of these changes may be clinically useful. We introduce the higher harmonics centroid (HHC) which can be defined as the center of mass of harmonics of the ICP pulse waveform from the 2nd to 10th, where mass corresponds to amplitudes of these harmonics. We investigate the changes in HHC during ICP monitoring, including isolated episodes of ICP plateau waves.Material and methodsRecordings from 325 patients treated between 2002 and 2010 were reviewed. Twenty-six patients with ICP plateau waves were identified. In the first step, the correlation between HHC and ICP was examined for the entire monitoring period. In the second step, the above relation was calculated separately for periods of elevated ICP during plateau wave and the baseline.ResultsFor the values averaged over the whole monitoring period, ICP (22.3 ± 6.9 mm Hg) correlates significantly (R = 0.45, p = 0.022) with HHC (3.64 ± 0.46). During the ICP plateau waves (ICP increased from 20.9 ± 6.0 to 53.7 ± 9.7 mm Hg, p < 10−16), we found a significant decrease in HHC (from 3.65 ± 0.48 to 3.21 ± 0.33, p = 10−5).ConclusionsThe good correlation between HHC and ICP supports the clinical application of pressure waveform analysis in addition to the recording of ICP number only. Mean ICP may be distorted by a zero drift, but HHC remains immune to this error. Further research is required to test whether a decline in HHC with elevated ICP can be an early warning sign of intracranial hypertension, whether individual breakpoints of correlation between ICP and its centroid are of clinical importance.

Change in Blood Flow Velocity Pulse Waveform during Plateau Waves of Intracranial Pressure.

A reliable method for non-invasive detection of dangerous intracranial pressure (ICP) elevations is still unavailable. In this preliminary study, we investigate quantitatively our observation that superimposing waveforms of transcranial Doppler blood flow velocity (FV) and arterial blood pressure (ABP) may help in non-invasive identification of ICP plateau waves. Recordings of FV, ABP and ICP in 160 patients with severe head injury (treated in the Neurocritical Care Unit at Addenbrookes Hospital, Cambridge, UK) were reviewed retrospectively. From that cohort, we identified 18 plateau waves registered in eight patients. A “measure of dissimilarity” (Dissimilarity/Difference Index, DI) between ABP and FV waveforms was calculated in three following steps: 1. fragmentation of ABP and FV signal according to cardiac cycle; 2. obtaining the normalised representative ABP and FV cycles; and finally; 3. assessing their difference, represented by the area between both curves. DI appeared to discriminate ICP plateau waves from baseline episodes slightly better than conventional pulsatility index did: area under ROC curve 0.92 vs. 0.90, sensitivity 0.81 vs. 0.69, accuracy 0.88 vs. 0.84, respectively. The concept of DI, if further tested and improved, might be used for non-invasive detection of ICP plateau waves.

Errors and Consequences of Inaccurate Estimation of Mean Blood Flow Velocity in Cerebral Arteries.

Many transcranial Doppler ultrasonography devices estimate the mean flow velocity (FVm) by using the traditional formula (FVsystolic + 2×FVdiastolic)/3 instead of a more accurate formula calculating it as the time integral of the current flow velocities divided by the integration period. We retrospectively analyzed flow velocity and intracranial pressure signals containing plateau waves (transient intracranial hypertension), which were collected from 14 patients with a traumatic brain injury. The differences in FVm and its derivative pulsatility index (PI) calculated with the two different methods were determined. We found that during plateau waves, when the intracranial pressure (ICP) rose, the error in FVm and PI increased significantly from the baseline to the plateau (from 4.6±2.4 to 9.8±4.9cm/s, P<0.05). Similarly, the error in PI also increased during plateau waves (from 0.11±0.07 to 0.44±0.24, P<0.005). These effects were most likely due to changes in the pulse waveform during increased ICP, which alter the relationship between systolic, diastolic, and mean flow velocities. If a change in the mean ICP is expected, then calculation of FVm with the traditional formula is not recommended.

Plateau Waves of Intracranial Pressure: Methods for Automatic Detection and Prediction.

Plateau waves are recurrent phenomena observed in traumatic brain injury (TBI) patients, characterised by an increase in intracranial pressure (ICP) above 40mmHg combined with an almost zero arterial blood pressure (ABP) variation and, hence, a decrease in cerebral perfusion pressure (CPP). A raised ICP for a long period of time, namely plateau waves, can lead to a secondary brain injury. Due to the impaired cerebral autoregulation mechanism these TBI patients present, they are admitted to neurocritical care units (NCCUs) to be under continuous multimodal monitoring, which allows a correct diagnosis for each patient. Plateau waves can end naturally by activating a vasoconstriction mechanism which decreases the amount of blood available in the brain. Alternatively, the phenomenon can end with therapeutic treatment.In this sense, the present study consists in the development of an algorithm capable of automatically detecting plateau waves using offline data, i.e. data already collected from patients. This creates an extra tool which allows for faster detection of events to assist their identification and final diagnosis. Despite the additional steps that can be included to improve the algorithm, the results show good performance, and thus it may be applied in NCCUs.

Spectral Cerebral Blood Volume Accounting for Noninvasive Estimation of Changes in Cerebral Perfusion Pressure in Patients with Traumatic Brain Injury.

We present the application of a new method for non-invasive cerebral perfusion pressure estimation (spectral nCPP or nCPPs) accounting for changes in transcranial Doppler-derived pulsatile cerebral blood volume. Primarily, we analysed cases in which CPP was changing (delta [∆],magnitude of changes]): (1) rise during vasopressor-induced augmentation of ABP (N=16); and (2) spontaneous changes in intracranial pressure (ICP) during plateau waves (N=14). Secondarily, we assessed nCPPs in a larger cohort in which CPP presented a wider range of values. The average correlation in the time domain between CPP and nCPPs for patients undergoing an induced rise in arterial blood pressure (ABP) was 0.95±0.07. For the greater traumatic brain injury (TBI) cohort, this correlation was 0.63±0.37. ∆ correlations between mean values of CPP and nCPPs were 0.73 (p=0.002) and 0.78 (p<0.001) respectively for induced rise in ABP and ICP plateau wave cohorts. The area under the curve (AUC) for ∆CPP was of 0.71 with a 95% confidence interval of 0.54-0.88. To detect low CPP, AUC was 0.817 with a 95% confidence interval of 0.79-0.85. nCPPs can reliably identify changes in direct CPP across time and the magnitude of these changes in absolute values. The ability to detect changes in CPP is reasonable but stronger for detecting low CPP, ≤70mmHg.

Nonepileptic Electroencephalographic Correlates of Episodic Increases in Intracranial Pressure.

Continuous EEG can potentially be used as real-time brain telemetry for the early detection of neurologic decline. Scant literature on EEG changes related to elevated intracranial pressure (ICP) limits its use in this context. Retrospective, observational case series of patients in whom we noted EEG changes correlating with a clinical concern for elevated ICP, measured or unmeasured. We noted EEG changes of varying severity and duration correlating with either measured or unmeasured clinical concern for elevated ICP. In two patients with recurrent transient unresponsiveness (presumed from plateau waves), generalized rhythmic delta activity and attenuation of fast activity occurred 30 minutes before a clinical change. Elevated ICP in two patients, one related to progressive mass effect from infarctions, and the other to dialysis, correlated with generalized slowing and attenuation of fast activity up to 24 hours before clinical deterioration, leading to diffuse suppression. Two patients with intraventricular hemorrhage had cyclic patterns at ∼1 per minute and ∼6 per minute (similar frequency to described frequency of Lundberg B and C waves, respectively). Cyclic patterns and varying degrees of slowing and attenuation often preceded clinical deterioration associated with intracranial hypertension. Future systematic studies of EEG changes in this setting will facilitate early and noninvasive detection of elevated ICP.

CMET-24. PLATEAU WAVE EVENTS: A COMMON, CURABLE, AND ROUTINELY MISDIAGNOSED SYNDROME IN PATIENTS WITH NEOPLASTIC MENINGITIS (NM)

Abstract INTRODUCTION NM is defined clinically by multilevel neurologic dysfunction. Seizures occur in less than 15% of patients. We describe a curable phenomenon (“plateau wave events”) that mimics and may be more common than seizures, but is not responsive to anticonvulsant medication. METHODS We queried a multinational NM registry to identify patients with episodic neurologic dysfunction suspected of having seizures. Detailed demographic, disease, treatment, and outcome data were collected. RESULTS Forty-three patients (21.2% of 203) were identified. Twenty patients (46.5% of 43) demonstrated a stereotyped constellation of symptoms including episodic severe headache and loss (19 patients) or impaired level (1 patient) of consciousness, nausea, vomiting, and gait instability lasting 30–180 seconds, with abrupt resolution and without post-ictal symptoms. Events developed a median of 74 (0–350) days following NM diagnosis. Fourteen patients (74%) were female. Median age was 54.8 [IQR 46.8, 61.6] years. Fourteen patients had solid tumors (11 breast), 5 had hematologic malignancies, and 1 had a primary brain tumor. Thirteen (68%) had ventriculomegaly. All patients demonstrated increased ICP [median 30.0 cm H2O, IQR 22.5, 30.0]. CSF cytology was positive and CSF protein was increased in 100% of patients, but no demographic, laboratory, or disease characteristic was associated with plateau wave events on multivariate analysis. Inter-ictal EEG in 8 patients showed no epileptiform activity. One intra-ictal EEG showed marked brainwave slowing and bradycardia during the clinical event. One intra-ictal ICP tracing showed an abrupt and dramatic increase in intracranial pressure during the event. Nineteen patients underwent ventriculoperitoneal shunting and experienced immediate symptom resolution. Anticonvulsant medication, initiated in 11 of these patients prior to shunting, provided no benefit. CONCLUSIONS Plateau wave events are common in patients with NM. They are frequently mistaken for seizures but are easily recognized by a constellation of defining signs and symptoms. Ventriculoperitoneal shunting is curative.

Estimation of pulsatile cerebral arterial blood volume based on transcranial doppler signals

ObjectiveMathematical modeling of cerebral hemodynamics by descriptive equations can estimate the underlying pulsatile component of cerebral arterial blood volume (CaBV). This way, clinical monitoring of changes in cerebral compartmental compliances becomes possible. Our aim is to validate the most adequate method of CaBV estimation in neurocritical care. ApproachWe retrospectively reviewed patients with severe traumatic brain injury (TBI) [admitted from 1992–2012] and continuous transcranial Doppler (TCD) monitoring of cerebral blood flow velocity (FV) displaying either plateau waves of intracranial pressure (ICP), episodes of controlled, mild hypocapnia, or vasopressor-induced increases in arterial blood pressure (ABP). Each cohort was analyzed with continuous flow forward (CFF, pulsatile blood inflow and steady blood outflow) or pulsatile flow forward (PFF, both blood inflow and outflow are pulsatile) modeling approaches for estimating the pulse component of CaBV. Spectral pulsatility index (sPI, the first harmonic of the FV pulse/mean FV) can be estimated using the compliance of the vascular bed (Ca) and the cerebrovascular resistance (CVR – here, Ra). We compared three possible methods of assessing Ca (C1: the CFF model, C2 and C3: the PFF models based on ABP or cerebral perfusion pressure (CPP) pulsations, respectively) and combined them with three possible methods of assessing Ra (Ra1= ABP/FV, Ra2= the resistance area product, and Ra3= CPP/FV). Linear regression techniques were applied to describe the strength of each CaBV estimator (a combination of Ca and Ra) against sPI. Main ResultsThe combination of C1 and Ra3 (PI_C1Ra3) was the superior descriptor of CaBV as approximated by sPI for both the plateau waves and the hypocapnia cohorts (r = 0.915 and r = 0.955, respectively). The combination of C1 and Ra1 (PI_C1Ra1) was nearly as robust in the vasopressors cohort (r = 0.938 and r = 0.931, respectively). SignificanceTCD-based estimation of CaBV pulsations seems to be feasible when employing the CFF modeling approach.

Twenty-Five Years of Intracranial Pressure Monitoring After Severe Traumatic Brain Injury: A Retrospective, Single-Center Analysis.

Intracranial pressure (ICP) is a clinically important variable after severe traumatic brain injury (TBI) and has been monitored, along with clinical outcome, for over 25 yr in Addenbrooke's hospital, Cambridge, United Kingdom. This time period has also seen changes in management strategies with the implementation of protocolled specialist neurocritical care, expansion of neuromonitoring techniques, and adjustments of clinical treatment targets. To describe the changes in intracranial monitoring variables over the past 25 yr. Data from 1146 TBI patients requiring ICP monitoring were analyzed. Monitored variables included ICP, cerebral perfusion pressure (CPP), and the cerebral pressure reactivity index (PRx). Data were stratified into 5-yr epochs spanning the 25 yr from 1992 to 2017. CPP increased sharply with specialist neurocritical care management (P<0.0001) (introduction of a specific TBI management algorithm) before stabilizing from 2000 onwards. ICP decreased significantly over the 25 yr of monitoring from an average of 19 to 12 mmHg (P<0.0001) but PRx remained unchanged. The mean number of ICP plateau waves and the number of patients developing refractory intracranial hypertension both decreased significantly. Mortality did not significantly change in the cohort (22%). We demonstrate the evolving trends in neurophysiological monitoring over the past 25 yr from a single, academic neurocritical care unit. ICP and CPP were responsive to the introduction of an ICP/CPP protocol while PRx has remained unchanged.

Plateau waves of intracranial pressure mimicking seizure in a patient with fungal meningitis (P1.9-038)

Plateau waves of intracranial pressure mimicking seizure in a patient with fungal meningitis (P1.9-038)