Sagittal Sinus Pressure Research Articles

The correlation between intracranial pressure and venous sinus pressures changes after venous sinus stenting

BackgroundThe pathophysiology of idiopathic intracranial hypertension (IIH) and other cerebral venous outflow disorders (CVD) has largely been unexplored. While a correlation between venous sinus pressure and opening pressure (OP) has...

Elevated systemic venous pressures as a possible pathology in prepubertal pediatric idiopathic intracranial hypertension.

Pediatric idiopathic intracranial hypertension (IIH) is a rare and challenging condition. As implied by the nomenclature, the etiologies remain unknown, and multiple etiologies are being investigated. In this study, we explored the potential role of increased systemic or cerebral venous pressure in the pathogenesis. An observational cohort study following the STROBE guidelines, including prepubertal children with clinical symptoms and imaging findings consistent with IIH referred to the neurosurgical department, was conducted. The patients underwent a comprehensive diagnostic protocol, including MRI, continuous intracranial pressure (ICP) monitoring, and endovascular venography with venous pressure measurements. The study included 11 consecutive patients (six boys and five girls) with an average age of 2.3years, and an average BMI of 18.4. Among these, one patient was found to have venous stenosis with a gradient; the other 10 patients presented with normal intracranial anatomy. All patients exhibited elevated venous pressures, with an average superior sagittal sinus pressure of 18.9mmHg, average internal jugular vein pressure of 17.0mmHg, and average central venous pressure of 15.9mmHg. Daytime ICP averaged 12.9mmHg, whereas nighttime ICP averaged 17.2mmHg with either A- or B-waves in 10 of the 11 patients. Despite pathological ICP, only three patients had papilledema. All patients had an increased systemic venous pressure, indicating a possible pathological factor for prepubertal IIH. Additionally, our findings show that young children often only partly meet the Friedman criteria due to a lack of papilledema, emphasizing the need for pediatric-specific diagnostic criteria. Further large-scale studies are needed to confirm these findings and to explore the underlying reasons for this increase in venous pressure and potential new treatment avenues.

A descriptive study of venous pressures and gradients while awake and both pre- and post-stent under anesthesia in patients with idiopathic intracranial hypertension

BackgroundThis study aims to explore factors that affect venous sinus pressures and associated gradients while awake and under general anesthesia (GA) both before and after venous sinus stenting (VSS) in...

Pentadecapeptide BPC 157 Counteracts Hemodynamic and ECG Disturbances Induced by Sotalol in Rats

Cytoprotective and organoprotective pentadecapeptide BPC 157 demonstrated particular beneficial cardiovascular effects (Curr Pharm Des. 2014;20(7):1121‐1125). Antiarrhythmic effects counteracted digoxin toxicity (Regul Pept. 2009;156(1‐3):83‐89), major blood vessel occlusions (Biomedicines 2021, 9,1029; 2021, 9,609; 2021, 9, 792) and lidocaine toxicity (Emerg Med Int. 2020;2020:6805354). Now, we reveal, by BPC 157, mitigation of hemodynamic and ECG disturbances of sotalol, a class III antiarrhythmic with non‐selective beta‐blocking activity.Albino Wistar rats received sotalol (80mg/kg, intragastrically), and at 5 min thereafter were treated with saline or BPC 157 (10ng/kg, intragastrically. Seven standard and one precordial ECG leads were recorded (baseline; after application of sotalol; and 10, 30, 90, 120 and 150 minutes after application of sotalol). Heart rate, QRS complex, PR and QT intervals were analyzed. Corrected QT intervals (QTc) were calculated according to Fridericia formula.Baseline ECG readings included average heart rate of 275.5 ± 25 bpm, average PR 54.8 ± 3.4 ms, average QRS complex 25.0 ± 4.23 ms and average QTc 166 ± 9.7 ms. Sotalol caused bradycardia (245 ± 23.5 bpm), PR prolongation (57.3 ± 2.7 ms), QRS widening (26.3 ± 3.2 ms), and QTc prolongation (173 ± 9.1 ms), measured 10 minutes after application. In BPC 157 treated animals (5 minutes after BPC‐157 application, 10 minutes after sotalol application), these effects were attenuated (heart rate 306 ± 31.7 bpm, average PR 52.3 ± 1.6 ms, average QRS 23.7 ± 5.4 ms and average QTc 159 ± 21.2 ms). This attenuation was lost in later measurements, for QRS ‐ 25 minutes after BPC 157 application, for frequency after 55 minutes, for PR after 115 minutes and for QTc after 145 minutes. In animals treated with sotalol, an increase in superior sagittal sinus pressure (10 ± 5 mmHg), as well as an increase in portal vein (17 ± 4 mmHg) and inferior caval vein pressures (12 ± 6 mmHg) were noted, along with the decrease in abdominal aortic pressure (53 ± 10 mmHg). These effects were attenuated in BPC treated animals (‐1 ± 1 mmHg for superior sagittal sinus, 7 ± 1 mmHg in portal vein, 5 ± 1 mmHg in inferior caval vein, and 81 ± 7 mmHg in abdominal aorta).In conclusion, BPC 157 attenuated deleterious hemodynamic effects of sotalol while the effects on the ECG parameters were also noted, although not long lasting, supporting the view of BPC‐157 as a rapid‐acting protective agent.

Pentadecapeptide BPC 157 Anti‐Ulcer Effect After Stomach Perforation also Opposed the Intracranial Hypertension (Superior Sagittal Sinus), Portal and Caval Hypertension and Aortal Hypotension

We report that rat stomach perforation (surgery with 5‐mm diameter metal needle on the ventral side in the prepyloric area) induced a defect that would not heal. Also, stomach perforation rapidly induced the intracranial hypertension (superior sagittal sinus), portal and caval hypertension and aortal hypotension. Stable gastric pentadecapeptide BPC 157 largely attenuated or eliminated these pressure disturbances. Finally, BPC 157 completely healed stomach defect. Previously, BPC 157 largely attenuated or even eliminated the consequences of Budd‐Chiari syndrome in rats, in particular, portal and caval hypertension and aortal hypotension, and then, huge thrombosis in both veins and arteries, and multiple organ dysfunction syndrome, heart, lung, liver, kidney and gastrointestinal lesions. These beneficial effects may relieve a Virchow's triad situation that may be commonly presented as well as counteracted (i.e.,duodenal venous congestion lesions (World J Gastroenterol 2018), perforated cecum (World J Gastroenterol 2018), bile duct ligation induced liver cirrhosis and portal hypertension (Eur J Pharmacol 2109), Pringle maneuver, ischemia, reperfusion (World J Hepatol 2020), and suprahepatic occlusion of the inferior caval vein (Budd‐Chiari‐syndrome) (World J Gastrointest Pathophysiol 2020)). Likewise, given in reperfusion, after clamping of the common carotid arteries, BPC 157 counteracted stroke (i.e., both early and delayed neural hippocampal damage, achieving also full functional recovery) (Brain Behav 2020).MethodsTherapy (BPC 157 (10 µg or 10 ng/kg) or saline (5 ml/kg)) was given intragatrically, at 1 min after stomach perforation. At 5 min after stomach perforation, as described before (World J Hepatol 2020), recordings were made in deeply anesthetized rats. Briefly, a cannula (BD Neoflon™ Cannula) was connected to a pressure transducer (78534C MONITOR/ TERMINAL; Hewlett Packard, USA) inserted into the superior sagittal sinus, and portal vein, and inferior vena cava, and abdominal aorta at the level of the bifurcation. We used five minutes recording. For superior sagittal sinus pressure recording, we made a single burr hole in the rostral part of the sagittal suture, above the superior sagittal sinus, and cannulated superior sagittal sinus anterior part by Braun intravenous cannulas, and then, in laparatomized rats, we recorded portal vein, inferior vena cava and abdominal aorta pressure.ResultsWithout therapy, the severely increased intracranial hypertension (10±2 mmHg in superior sagittal sinus), portal (33±4 mmHg) and caval (28±3 mmHg) hypertension and aortal hypotension (59±3 mmHg) occurred rapidly. Both BPC 157 regimens markedly counteracted intracranial hypertension (‐6±2 mmHg in superior sagittal sinus), portal (6±2 mmHg) and caval (5±2 mmHg) hypertension and aortal hypotension (81±3 mmHg) (i.e., 10 ng).ConclusionBPC 157 anti‐ulcer effect also opposed the intracranial hypertension (superior sagittal sinus), portal and caval hypertension and aortal hypotension.

Cerebrospinal fluid dynamics in idiopathic intracranial hypertension: a literature review and validation of contemporary findings

BackgroundIdiopathic intracranial hypertension (IIH) is a rare disease of unknown aetiology related possibly to disturbed cerebrospinal fluid (CSF) dynamics and characterised by elevated intracranial pressure (ICP) causing optic nerve atrophy if not timely treated. We studied CSF dynamics of the IIH patients based on the available literature and our well-defined cohort.MethodA literature review was performed from PubMed between 1980 and 2020 in compliance with the PRISMA guideline. Our study includes 59 patients with clinical, demographical, neuro-ophthalmological, radiological, outcome data, and lumbar CSF pressure measurements for suspicion of IIH; 39 patients had verified IIH while 20 patients did not according to Friedman’s criteria, hence referred to as symptomatic controls.ResultsThe literature review yielded 19 suitable studies; 452 IIH patients and 264 controls had undergone intraventricular or lumbar CSF pressure measurements. In our study, the mean CSF pressure, pulse amplitudes, power of respiratory waves (RESP), and the pressure constant (P0) were higher in IIH than symptomatic controls (p < 0.01). The mean CSF pressure was higher in IIH patients with psychiatric comorbidity than without (p < 0.05). In IIH patients without acetazolamide treatment, the RAP index and power of slow waves were also higher (p < 0.05). IIH patients with excess CSF around the optic nerves had lower relative pulse pressure coefficient (RPPC) and RESP than those without (p < 0.05).ConclusionsOur literature review revealed increased CSF pressure, resistance to CSF outflow and sagittal sinus pressure (SSP) as key findings in IIH. Our study confirmed significantly higher lumbar CSF pressure and increased CSF pressure waves and RAP index in IIH when excluding patients with acetazolamide treatment. In overall, the findings reflect decreased craniospinal compliance and potentially depleted cerebral autoregulation resulting from the increased CSF pressure in IIH. The increased slow waves in patients without acetazolamide may indicate issues in autoregulation, while increased P0 could reflect the increased SSP.

Superior sagittal sinus dural arteriovenous fistula caused by treatment of meningioma masquerades as sinus thrombosis

Dural arteriovenous fistulas (DAVF) are rare acquired lesions resulting from abnormal shunting between intracranial dural arteries and venous system. Typically arising from structural weakness of the dura and a coinciding trigger factor, DAVFs can present with similar clinical and imaging characteristics to sinus thrombosis. A 61-year-old male with a history of meningioma previously managed with subtotal resection and stereotactic radiosurgery presented with progressive right-sided vision loss and bilateral papilledema. Initial imaging suggested possible sinus occlusion. Catheter angiogram revealed a Borden-Shucart grade III DAVF of the superior sagittal sinus and elevated venous pressures and the patient subsequently underwent endovascular transarterial intervention twice. We report on the first case of a superior sagittal sinus DAVF occurring after surgical resection of a parasagittal meningioma.

Correlation between intracranial pressure and venous sinus pressures in patients undergoing cerebral venography and manometry

BackgroundThe pathophysiology of idiopathic intracranial hypertension (IIH) is complex but is directly related to cerebral venous hypertension. Few studies have simultaneously recorded venous sinus pressures and lumbar puncture (LP) opening...

Changes in mean arterial pressure and end-tidal carbon dioxide content affect venous sinus pressures in patients with idiopathic intracranial hypertension: a randomized study

IntroductionLittle is known about how changes in physiologic parameters affect venous sinus pressure measurements, waveforms, or gradients associated with sinus stenosis.ObjectiveTo evaluate the effect of changes in cardiovascular and respiratory...

Coupling of CSF and sagittal sinus pressure in adult patients with pseudotumour cerebri

ObjectivePseudotumour cerebri syndrome (PTCS including idiopathic intracranial hypertension) is characterised by the symptoms and signs of raised cerebrospinal fluid pressure (CSFp) in the absence of ventricular dilatation or an intracranial mass lesion. Its aetiology is unknown in the majority of cases but there is much evidence for impaired CSF absorption. Traditionally, sagittal sinus pressure has been considered to be independent of CSF pressure in adults. However, the discovery of stenoses of intracranial venous sinuses and introduction of venous sinus stenting has highlighted the importance of the venous drainage in PTCS. In this study, we have explored the relationship between CSFp and SSp before and during a CSF infusion test and during CSF drainage.Materials and methodsTen patients (9 females:1 male) with PTCS underwent infusion studies in parallel with direct retrograde cerebral venography. Both SSp and CSFp were recorded at a baseline and during CSFp elevation in a course of a CSF infusion test. The drainage of CSF after the CSF infusion was performed in 7 patients. In 5 cases, jugular venous pressure was also measured.ResultsCSFp and SSp including their amplitudes correlated significantly and strongly both at baseline (R = 0.96; p = 0.001) and during infusion (R = 0.92; p = 0.0026). During drainage, this correlation was maintained until SSp reached a stable value, whereas CSFp continued to decrease.ConclusionsIn this series of ten patients with PTCS, CSFp and SSp were coupled, both at baseline and during infusion. The implications of such coupling for the calculation of CSF outflow resistance are discussed.

A descriptive study of venous sinus pressures and gradients in patients with idiopathic intracranial hypertension

ObjectiveTo determine the relationship between normal physiologic and pathologic venous sinus pressures in patients with idiopathic intracranial hypertension (IIH), which is poorly understood.MethodsRetrospective analysis was performed to identify patients with...

Cerebrospinal fluid dynamics in pediatric pseudotumor cerebri syndrome

PurposeThere is a growing body of evidence highlighting the importance of comprehensive intracranial pressure (ICP) values in pseudotumor cerebri syndrome (PTCS). Due to the highly dynamic nature of ICP, several methods of ICP monitoring have been established, including the CSF infusion study. We have performed a retrospective review of the CSF dynamics measurements for all pediatric patients investigated for PTCS in our center and examined their diagnostic value compared with clinical classification.MethodsWe retrospectively recruited 31 patients under 16 years of age investigated for PTCS by CSF infusion test. We used the clinically provided Friedman classification 13/31 patients with definite PTCS (group A), 13/31 with probable PTCS (group B), and 5/31 not PTCS (group C), to compare CSF dynamics in the 3 groups.ResultsCSF pressure (CSFp) was significantly increased in group A (29.18 ± 7.72 mmHg) compared with B (15.31 ± 3.47 mmHg; p = 1.644e-05) and C (17.51 ± 5.87; p = 0.01368). The amplitude (AMP) was higher in the definite (2.18 ± 2.06 mmHg) than in group B (0.68 ± 0.37; p = 0.01382). There was no in either CSFp or AMP between groups B and C. No lower breakpoint of the AMP-P line was observed in group A but was present in 2/13 and 2/5 patients in groups B and C. In group A, sagittal sinus pressure (SSp) and elasticity were the only parameters above threshold (p = 4.2e-06 and p = 0.001953, respectively), In group B, only the elasticity was significantly higher than the threshold (p = 004257). Group C did not have any of the parameters raised. The AUC of CSFp, elasticity, and SSp for the 3 groups was 93.8% (84.8–100% CI).ConclusionsMonitoring of CSFp and its dynamics, besides providing a more precise methodology for measuring CSFp, could yield information on the dynamic parameters of CSFp that cannot be derived from CSFp as a number, accurately differentiating between the clinically and radiologically derived entities of PTCS.

Validation of Davson's equation in patients suffering from idiopathic normal pressure hydrocephalus.

The so-called Davson's equation relates baseline intracranial pressure (ICP) to resistance to cerebrospinal fluid outflow (Rout), formation of cerebrospinal fluid (If) and sagittal sinus pressure (PSS) There is a controversy over whether this fundamental equation is applicable in patients with normal pressure hydrocephalus (NPH). We investigated the relationship between Rout and ICP and also other compensatory, clinical and demographic parameters in NPH patients. We carried out a retrospective study of 229 patients with primary NPH who had undergone constant-rate infusion studies in our hospital. Data was recorded and processed using ICM+ software. Relationships between variables were sought by calculating Pearson product correlation coefficients and p values. We found a significant, albeit weak, relationship between ICP and Rout (R = 0.17, p = 0.0049), Rout and peak-to-peak amplitude of ICP (AMP) (R = 0.27, p = 3.577e-05) and Rout and age (R = 0.16, p = 0.01306). The relationship found between ICP and Rout provides indirect evidence to support disturbed Cerebrospinal fluid circulation as a key factor in disturbed CSF dynamics in NPH. Weak correlation may indicate that other factors-variable PSS and formation of CSF outflow-contribute heavily to linear model expressed by Davson's equation.

Cerebral spinal fluid dynamics: effect of hypoxia and implications for high-altitude illness.

The pathophysiology of acute mountain sickness and high-altitude cerebral edema, the cerebral forms of high-altitude illness, remain uncertain and controversial. Persistently elevated or pathological fluctuations in intracranial pressure are thought to cause symptoms similar to those reported by individuals suffering cerebral forms of high-altitude illness. This review first focuses on the basic physiology of the craniospinal system, including a detailed discussion of the long-term and dynamic regulation of intracranial pressure. Thereafter, we critically examine the available literature, based primarily on invasive pressure monitoring, that suggests intracranial pressure is acutely elevated at altitude due to brain swelling and/or elevated sagittal sinus pressure, but normalizes over time. We hypothesize that fluctuations in intracranial pressure occur around a slightly elevated or normal mean intracranial pressure, in conjunction with oscillations in arterial Po2 and arterial blood pressure. Then these modest fluctuations in intracranial pressure, in concert with direct vascular stretch due to dilatation and/or increased blood pressure transmission, activate the trigeminal vascular system and cause symptoms of acute mountain sickness. Elevated brain water (vasogenic edema) may be due to breakdown of the blood-brain barrier. However, new information suggests cerebral spinal fluid flux into the brain may be an important factor. Regardless of the source (or mechanisms responsible) for the excess brain water, brain swelling occurs, and a "tight fit" brain would be a major risk factor to produce symptoms; activities that produce large changes in brain volume and cause fluctuations in blood pressure are likely contributing factors.

Case report: atypical presentation of jugular foramen mass

IntroductionJugular foramen lesions are often associated with pathology of adjacent structures due to either compression or direct invasion. Common presenting symptoms include pulsatile tinnitus, a neck mass, hearing loss, and cranial nerve palsies, leading to changes in taste, vocal cord paralysis, dysphagia, and sternocleidomastoid/trapezius weakness (A. Hakuba, K. Hashi, K. Fujitani, et al., Jugular foramen neurinomas. Surg Neurol 1979; 11:83-94). This patient was found to have a jugular foramen mass after presenting with the unusual constellation of visual changes and headache. Case presentationA jugular foramen mass in a young woman was discovered after presenting with visual changes and headache; the patient was found to have papilledema on initial examination. Otologic and head and neck examination were normal. Subsequent imaging demonstrated a mass at the right jugular foramen with compression of this structure; a contralateral transverse sinus stenosis was also seen. This latter abnormality (along with obstruction of the jugular foramen) impeded venous drainage leading to papilledema and visual changes. DiscussionIn a patient presenting with papilledema and severe headache with an associated jugular foramen mass, a multidisciplinary approach benefits the patient with input from interventional neuroradiology, neurosurgery, and neuro-ophthalmology. Venous outflow was compromised through the left stenotic transverse sinus, and the normal outflow on the right side through the jugular bulb was impeded by the tumor; obstructions of both led to symptomatic impeded venous outflow. This compromise in venous outflow led to an increase in superior sagittal sinus pressure, with subsequent increase in intracranial pressure and resultant papilledema. In an attempt to increase blood flow, an angioplasty was performed on the patient's affected transverse sinus. In addition, symptomatology consistent with pseudotumor cerebri prompted the use of acetazolamide for medical management. After both therapies, the patient's symptoms dramatically improved and were stable. The tumor has also remained stable, with no immediate need for surgical resection, stereotactic radiation, or consideration of an intraluminal transverse sinus stent placement or shunting. ConclusionThe unique presentation of a jugular foramen mass in a young woman leading to papilledema highlights the need for high clinical suspicion of potential etiologies necessary for diagnosis. Despite the benign nature of her disease process, an unusual constellation of anatomical factors lead to the need for acute intervention.

An experimental study on artificially induced CSF pulse waveform morphological modifications

Objective: The analysis of cerebrospinal fluid (CSF) pulse pressure waveform has been considered as a reliable method to investigate the intracranial system (ICS) dynamics. We have examined the morphological changes of the CSF pulse wave and of the sagittal sinus pressure (SSP) wave during a progressive increase in intracranial pressure (ICP) in order to investigate the ICS dynamics.Methods: Four dogs were anesthetized. Blood pressure, ICP, and SSP were simultaneously recorded. Two vertical tubes were inserted inside one lateral ventricle, thus allowing the half-opening (one tube open) and opening (both tubes open) of the ICS. ICP was modified by varying the height of the liquid column into the tubes. Pressures were analyzed by applying the fast Fourier transformation on each pulse pressure wave. We distinguished two peaks (first and second peaks) and a notch in each pulse pressure wave. The pressure was raised from resting pressure up to 50 mmHg.Results: A progressive and distinct change in the CSF pulse pressure shape was evident when opening the ICS to the atmosphere: a reduction in the height of the dicrotic notch and in the amplitude of the second peak and a corresponding positive shift of the first harmonic with respect to the onset of the CSF pulse pressure wave.Discussion: A decrease in the amplitude of the CSF pulse waveform second peak and a positive phase shift of its first harmonic indicate an opening of the ICS to the atmosphere, i.e. an increase in the intracranial compliance.

Transverse Sinus Stenting for Idiopathic Intracranial Hypertension: A Review of 52 Patients and of Model Predictions

Transverse sinus stenosis is common in patients with IIH. While the role of transverse sinus stenosis in IIH pathogenesis remains controversial, modeling studies suggest that stent placement within a transverse sinus stenosis with a significant pressure gradient should decrease cerebral venous pressure, improve CSF resorption in the venous system, and thereby reduce intracranial (CSF) pressure, improving the symptoms of IIH and reducing papilledema. We aimed to determine if IIH could be reliably treated by stent placement in transverse sinus stenosis. We reviewed the clinical, venographic, and intracranial pressure data before and after stent placement in transverse sinus stenosis in 52 of our own patients with IIH unresponsive to maximum acceptable medical treatment, treated since 2001 and followed between 2 months and 9 years. Before stent placement, the mean superior sagittal sinus pressure was 34 mm Hg (462 mm H(2)0) with a mean transverse sinus stenosis gradient of 20 mm Hg. The mean lumbar CSF pressure before stent placement was 322 mm H(2)O. In all 52 patients, stent placement immediately eliminated the TSS pressure gradient, rapidly improved IIH symptoms, and abolished papilledema. In 6 patients, symptom relapse (headache) was associated with increased venous pressure and recurrent stenosis adjacent to the previous stent. In these cases, placement of another stent again removed the transverse sinus stenosis pressure gradient and improved symptoms. Of the 52 patients, 49 have been cured of all IIH symptoms. These findings indicate a role for transverse sinus stent placement in the management of selected patients with IIH.

Nonischemic cerebral venous hypertension promotes a pro-angiogenic stage through HIF-1 downstream genes and leukocyte-derived MMP-9

Cerebral venous hypertension (VH) and angiogenesis are implicated in the pathogenesis of brain arteriovenous malformation and dural arteriovenous fistulae. We studied the association of VH and angiogenesis using a mouse brain VH model. Sixty mice underwent external jugular vein and common carotid artery (CCA) anastomosis (VH model), CCA ligation, or sham dissection (n=20). Hypoxia-inducible factor-1alpha (HIF-1alpha), vascular endothelial growth factor (VEGF) and stromal-cell-derived factor-1alpha (SDF-1alpha) expression, and matrix metalloproteinase (MMP) activity were analyzed. We found VH animals had higher (P<0.05) sagittal sinus pressure (8+/-1 mm Hg) than control groups (1+/-1 mm Hg). Surface cerebral blood flow and mean arterial pressure did not change. Hypoxia-inducible factor-1alpha, VEGF, and SDF-1alpha expression increased (P<0.05). Neutrophils and MMP-9 activity increased 10-fold 1 day after surgery, gradually decreased afterward, and returned to baseline 2 weeks after surgery. Macrophages began to increase 3 days after surgery (P<0.05), which coincided with the changes in SDF-1alpha expression. Capillary density in the parasagittal cortex increased 17% compared with the controls. Our findings suggest that mild nonischemic VH results in a pro-angiogenic stage in the brain by upregulating HIF-1 and its downstream targets, VEGF and SDF-1alpha, increasing leukocyte infiltration and MMP-9 activity.

Cerebrospinal fluid dynamics

The pathophysiology of hydrocephalus can be modelled and described in terms of altered biomechanical parameters. Shunting is aimed to correct the patient's cerebrospinal fluid dynamics, compensating for inadequate cerebrospinal fluid re-absorption or insufficient volume buffering reserve. Computerized infusion studies implement intracranial pressure and arterial pressure signal processing and model analysis to allow the estimation of cerebrospinal dynamics variables such as cerebrospinal fluid outflow resistance, brain compliance and pressure-volume index, estimated sagittal sinus pressure, cerebrospinal fluid formation rate, compensatory reserve and cerebral vasoreactivity. Infusion studies can assist in the prognostication of normal pressure hydrocephalus and in the diagnosis of idiopathic intracranial hypertension. The technique is also helpful in the assessment of shunt malfunction, including posture-related over-drainage and shunt obstruction.

Effects of dexmedetomidine on cerebral circulation and systemic hemodynamics after cardiopulmonary resuscitation in dogs

Our purpose was to examine the effect of dexmedetomidine, when used with phenylephrine during cardiopulmonary resuscitation (CPR), on the cerebral and systemic circulations. In pentobarbital-anesthetized, mechanically ventilated dogs, we evaluated pial vessel diameters, cerebral oxygen extraction, and systemic hemodynamics before and after cardiac arrest (5 min) and resuscitation, in the presence or absence of dexmedetomidine (n = 7 each; dexmedetomidine or control group). In both groups: (a) pial arterioles were dilated at 5 and 15 min after CPR, and had returned to baseline diameters at 30 min; (b) sagittal sinus pressure was significantly raised at 5 and 15 min after CPR; and (c) cerebral oxygen extraction was decreased at 5, 15, and 30 min after CPR, and had returned to baseline level at 60 min after CPR. We could find no differences between the two groups in the cerebral circulation after CPR. However, the number of defibrillation electric shocks required to restore spontaneous circulation (5.5 vs 3.6; P < 0.05), the dose of phenylephrine used for CPR (1193 microg vs 409 microg; P < 0.01), and the number of postresuscitation ventricular ectopic beats observed during the first 120 min after successful resuscitation (1606 vs 348; P < 0.05) were all significantly lower in the dexmedetomidine group. Although intravenous dexmedetomidine, as used for CPR, does not have a beneficial effect on either cerebral vessels or cerebral oxygen extraction, it may reduce the number of defibrillation shocks needed and the number of postresuscitation ventricular ectopic beats, and help to bring about stable systemic circulation after CPR.