Cerebrospinal Fluid Displacement Research Articles

Novel advanced imaging techniques for cerebral oedema.

Cerebral oedema following acute ischemic infarction has been correlated with poor functional outcomes and is the driving mechanism of malignant infarction. Measurements of midline shift and qualitative assessment for herniation are currently the main CT indicators for cerebral oedema but have limited sensitivity for small cortical infarcts and are typically a delayed sign. In contrast, diffusion-weighted (DWI) or T2-weighted magnetic resonance imaging (MRI) are highly sensitive but are significantly less accessible. Due to the need for early quantification of cerebral oedema, several novel imaging biomarkers have been proposed. Based on neuroanatomical shift secondary to space-occupying oedema, measures such as relative hemispheric volume and cerebrospinal fluid displacement are correlated with poor outcomes. In contrast, other imaging biometrics, such as net water uptake, T2 relaxometry and blood brain barrier permeability, reflect intrinsic tissue changes from the influx of fluid into the ischemic region. This review aims to discuss quantification of cerebral oedema using current and developing advanced imaging techniques, and their role in predicting clinical outcomes.

Head Elevation, Cerebral Venous System, and Intracranial Pressure: Review and Hypothesis

Background Facilitation of venous outflow from the brain is largely believed to be responsible for the beneficial effect of head elevation on intracranial pressure (ICP). However, the impact on cerebral perfusion pressure can be deleterious. Although the adverse effect of obstructing venous outflow in the setting of intracranial hypertension is well documented, the converse (improvement with augmented drainage) has not been demonstrated. Our hypothesis is that the effect of active augmentation of cerebral venous outflow on ICP, although unknown, could be potentially beneficial under conditions of intracranial hypertension. Methods Published literature was perused to ascertain known relationships between head elevation, ICP, cerebral perfusion pressure, and the cerebral venous system. Results Head elevation benefits ICP control in intracranial hypertension from improved venous outflow via various networks and craniospinal cerebrospinal fluid displacement; but patients on the severe spectrum have a high likelihood of experiencing cerebral perfusion pressure decline especially beyond 30°. In addition, the interaction between autoregulation, compliance, head elevation, ICP pulse amplitude, cerebral perfusion pressure, and ICP becomes increasingly dyssynchronous in the severely affected brain. Although the detrimental effects of obstructing venous drainage are well documented, the possibility of augmenting venous outflow by withdrawal of sagittal sinus blood has not been described previously. Conclusion There could exist a potential role for targeted sagittal sinus venous aspiration in favorably influencing control of increased ICP conditions, without significant risk to cerebral perfusion.

Characterization of Cardiac- and Respiratory-driven Cerebrospinal Fluid Motions Using a Correlation Mapping Technique Based on Asynchronous Two-dimensional Phase Contrast MR Imaging.

PurposeThe cardiac- and respiratory-driven components of cerebrospinal fluid (CSF) motion characteristics and bulk flow are not yet completely understood. Therefore, the present study aimed to characterize cardiac- and respiratory-driven CSF motions in the intracranial space using delay time, CSF velocity waveform correlation, and displacement.MethodsAsynchronous two-dimensional phase-contrast at 3T was applied to measure the CSF velocity in the inferior–superior direction in a sagittal slice at the midline (N = 12) and an axial slice at the foramen magnum (N = 8). Volunteers were instructed to engage in six-second respiratory cycles. The calculated delay time and correlation coefficients of the cardiac- and respiratory-driven velocity waveforms, separated in the frequency domain, were applied to evaluate the propagation of the CSF motion. The cardiac- and respiratory-driven components of the CSF displacement and motion volume were calculated during diastole and systole, and during inhalation and exhalation, respectively. The cardiac- and respiratory-driven components of the velocity, correlation, displacement, and motion volume were compared using an independent two-sample t-test.ResultsThe ratio of the cardiac-driven CSF velocity to the sum of the cardiac- and respiratory-driven CSF velocities was higher than the equivalent respiratory-driven ratio for all cases (P < 0.01). Delay time and correlation maps demonstrated that the cardiac-driven CSF motion propagated more extensively than the respiratory-driven CSF motion. The correlation coefficient of the cardiac-driven motion was significantly higher in the prepontine(P < 0.01), the aqueduct, and the fourth ventricle (P < 0.05). The respiratory-driven displacement and motion volume were significantly greater than the cardiac-driven equivalents for all observations (P < 0.01).ConclusionThe correlation mapping technique characterized the cardiac- and respiratory-driven CSF velocities and their propagation properties in the intracranial space. Based on these findings, cardiac-driven CSF velocity is greater than respiratory-induced velocity, but the respiratory-driven velocity might displace farther.

Respiratory cerebrospinal fluid flow is driven by the thoracic and lumbar spinal pressures.

Respiration plays a key role in the circulation of cerebrospinal fluid (CSF) around the central nervous system. During inspiration increased venous return from the cranium is believed to draw CSF rostrally. However, this mechanism does not explain why CSF has also been observed to move caudally during inspiration. We show that during inspiration decreased intrathoracic pressure draws venous blood from the cranium and lumbar spine towards the thorax. We also show that the abdominal pressure was associated with rostral CSF displacement. However, a caudal shift of cervical CSF was seen with low abdominal pressure and comparably negative intrathoracic pressures. These results suggest that the effects of epidural blood flow within the spinal canal need to be considered, as well as the cranial blood volume balance, to understand respiratory-related CSF flow. These results may prove useful for the treatment of CSF obstructive pathology and understanding the behaviour of intrathecal drug injections. It is accepted that during inspiration, cerebrospinal fluid (CSF) flows rostrally to compensate for decreased cranial blood volume, caused by venous drainage due to negative intrathoracic pressure. However, this mechanism does not explain observations of caudal CSF displacement during inspiration. Determining the drivers of respiratory CSF flow is crucial for understanding the pathophysiology of CSF flow disorders. To quantify the influence of respiration on CSF flow, real-time phase-contrast magnetic resonance imaging (MRI) was used to record CSF and blood flow, while healthy subjects (5:5 M:F, 25-50 years) performed either a brief expiratory or inspiratory effort between breaths. Transverse images were taken perpendicular to the spinal canal in the middle of the C3 and L2 vertebrae. The same manoeuvres were then performed after a nasogastric pressure catheter was used to measure the intrathoracic and abdominal pressures. During expiratory-type manoeuvres that elevated abdominal and intrathoracic pressures, epidural blood flow into the spinal canal increased and CSF was displaced rostrally. With inspiratory manoeuvres, the negative intrathoracic pressure drew venous blood from C3 and L2 towards the thoracic spinal canal, and cervical CSF was displaced both rostrally and caudally, despite the increased venous drainage. Regression analysis showed that rostral displacement of CSF at both C3 (adjusted R2 =0.53; P<0.001) and L2 (adjusted R2 =0.38; P<0.001) were associated with the abdominal pressure. However, with low abdominal pressure and comparably negative intrathoracic pressure, cervical CSF flowed caudally. These findings suggest that changes in both the cranial and spinal pressures need to be considered to understand respiratory CSF flow.

Reduction in Cerebrospinal Fluid Volume as an Early Quantitative Biomarker of Cerebral Edema After Ischemic Stroke.

Background and Purpose- Cerebral edema (CED) develops in the hours to days after stroke; the resulting increase in brain volume may lead to midline shift (MLS) and neurological deterioration. The time course and implications of edema formation are not well characterized across the spectrum of stroke. We analyzed displacement of cerebrospinal fluid (ΔCSF) as a dynamic quantitative imaging biomarker of edema formation. Methods- We selected subjects enrolled in a stroke cohort study who presented within 6 hours of onset and had baseline and ≥1 follow-up brain computed tomography scans available. We applied a neural network-based algorithm to quantify hemispheric CSF volume at each imaging time point and modeled CSF trajectory over time (using a piecewise linear mixed-effects model). We evaluated ΔCSF within the first 24 hours as an early biomarker of CED (defined as developing MLS on computed tomography beyond 24 hours) and poor outcome (modified Rankin Scale score, 3-6). Results- We had serial imaging in 738 subjects with stroke, of whom 91 (13%) developed CED with MLS. Age did not differ (69 versus 70 years), but baseline National Institutes of Health Stroke Scale was higher (16 versus 7) and baseline CSF volume lower (132 versus 161 mL, both P<0.001) in those with CED. ΔCSF was faster in those developing MLS, with the majority seen by 24 hours (36% versus 11% or 2.4 versus 0.8 mL/h; P<0.0001). Risk of CED almost doubled for every 10% ΔCSF within 24 hours (odds ratio, 1.76 [95% CI, 1.46-2.14]), adjusting for age, glucose, and National Institutes of Health Stroke Scale. Risk of neurological deterioration (1.6-point increase in National Institutes of Health Stroke Scale at 24 hours) and poor outcome (adjusted odds ratio, 1.34 [95% CI, 1.15-1.56]) was also greater for every 10% increase in ΔCSF. Conclusions- CSF volumetrics provides quantitative evaluation of early edema formation. ΔCSF from baseline to 24-hour computed tomography is a promising early biomarker for the development of MLS and worse neurological outcome.

Solving the Riddle of "Idiopathic" in Idiopathic Intracranial Hypertension and Normal Pressure Hydrocephalus: An Imaging Study of the Possible Mechanisms - Monro-Kellie 3.0.

Background:Idiopathic intracranial hypertension (IIH) and normal pressure hydrocephalus (NPH) represent a cluster of typical clinical and imaging findings, with no evident etiological cause noted. In this study, we have proposed a model for IIH and NPH called Monroe–Kellie 3.0 (MK 3.0). IIH and NPH may be entities which represent opposite sides of the same coin with venous system and cerebrospinal fluid (CSF) as core drivers for both these entities.Materials and Methods:IIH and NPH volume data were collected, voxel-based morphometry analysis was performed without normalization, and the distribution of the individual volumes of gray matter, white matter, and CSF was statistically analyzed. Visual morphometry analyses of segmented data were performed, and the findings in routine magnetic resonance imaging (MRI) were noted to build a model for IIH and NPH.Results:In IIH and NPH when the volumes were compared with controls, the distribution was similar. Furthermore, the morphometric changes noted in the MRI and segmented volume data were analyzed and the results were suggestive of changes in elastic property of brain causing a remodeling of brain shape and resulting in minor brain shift in the skull vault, and the resulting passive displacement of CSF which has been termed as MK 3.0.Conclusion:This model helps to put the clinical and imaging findings and complications of treatment in single perspective.

Ciliary Beating Compartmentalizes Cerebrospinal Fluid Flow in the Brain and Regulates Ventricular Development

SummaryMotile cilia are miniature, propeller-like extensions, emanating from many cell types across the body. Their coordinated beating generates a directional fluid flow, which is essential for various biological processes, from respiration to reproduction. In the nervous system, ependymal cells extend their motile cilia into the brain ventricles and contribute to cerebrospinal fluid (CSF) flow. Although motile cilia are not the only contributors to CSF flow, their functioning is crucial, as patients with motile cilia defects develop clinical features, like hydrocephalus and scoliosis. CSF flow was suggested to primarily deliver nutrients and remove waste, but recent studies emphasized its role in brain development and function. Nevertheless, it remains poorly understood how ciliary beating generates and organizes CSF flow to fulfill these roles. Here, we study motile cilia and CSF flow in the brain ventricles of larval zebrafish. We identified that different populations of motile ciliated cells are spatially organized and generate a directional CSF flow powered by ciliary beating. Our investigations revealed that CSF flow is confined within individual ventricular cavities, with little exchange of fluid between ventricles, despite a pulsatile CSF displacement caused by the heartbeat. Interestingly, our results showed that the ventricular boundaries supporting this compartmentalized CSF flow are abolished during bodily movement, highlighting that multiple physiological processes regulate the hydrodynamics of CSF flow. Finally, we showed that perturbing cilia reduces hydrodynamic coupling between the brain ventricles and disrupts ventricular development. We propose that motile-cilia-generated flow is crucial in regulating the distribution of CSF within and across brain ventricles.

Quantifying Infarct Growth and Secondary Injury Volumes: Comparing Multimodal Image Registration Measures.

Lesion expansion in the week after acute stroke involves both infarct growth (IG) and anatomic distortion (AD) because of edema and hemorrhage. Enabling separate quantification would allow clinical trials targeting these distinct pathological processes. We developed an objective and automated approach to quantify these processes at 24 hours and 1 week. Patients with acute ischemic stroke were scanned at presentation, 24 hours, and 1 week in a magnetic resonance imaging (MRI) cohort study. IG and AD were calculated from follow-up lesion masks after linear and nonlinear registration to a presenting MRI scan. Performance of IG and AD was compared with edema quantified using cerebrospinal fluid displacement. The use of alternative reference images to define AD, including template MRI, mirrored MRI, and presenting computed tomographic scan, was explored. Thirty-seven patients with nonlacunar stroke were included. AD was responsible for 20% and 36% of lesion expansion at 24 hours (n=30) and 1 week (n=28). Registration-defined IG and AD compared favorably with edema quantified using cerebrospinal fluid displacement, particularly at smaller infarct volumes. Presenting computed tomographic imaging was the preferred alternative reference image to presenting MRI for measuring AD. The contributions of IG and AD to lesion expansion can be measured separately over time through the use of image registration. This approach can be used to combine imaging outcome data from computed tomography and MRI.

Evidence for Decreased Brain Parenchymal Volume After Large Intracerebral Hemorrhages: a Potential Mechanism Limiting Intracranial Pressure Rises

Potentially fatal intracranial pressure (ICP) rises commonly occur after large intracerebral hemorrhages (ICH). We monitored ICP after infusing 100–160 μL of autologous blood (vs. 0 μL control) into the striatum of rats in order to test the validity of this common model with regard to ICP elevations. Other endpoints included body temperature, behavioral impairment, lesion volume, and edema. Also, we evaluated hippocampal CA1 sector and somatosensory cortical neuron morphology to assess whether global ischemic injury occurred. Despite massive blood infusions, ICP only modestly increased (160 μL 10.8 ± 2.1 mmHg for <36 h vs. control 3.4 ± 0.5 mmHg), with little peri-hematoma edema at 3 days. Body temperature was not affected. Behavioral deficits and tissue loss were infusion volume-dependent. There was no histological evidence of hippocampal or cortical injury, indicating that cell death was confined to the hematoma and closely surrounding tissue. Surprisingly, the most severe hemorrhages significantly increased cell density (~15–20%) and reduced cell body size (~30%) in regions outside the injury site. Additionally, decreased cell size and increased density were observed after collagenase-induced ICH. Parenchymal volume is seemingly reduced after large ICH. Thus, in addition to well-known compliance mechanisms (e.g., displacement of cerebrospinal fluid and cerebral blood), reduced brain parenchymal volume appears to limit ICP rises in rodents with very large mass lesions.

Mechanical Design and Analysis of a Unilateral Cervical Spinal Cord Contusion Injury Model in Non-Human Primates

Non-human primate (NHP) models of spinal cord injury better reflect human injury and provide a better foundation to evaluate potential treatments and functional outcomes. We combined finite element (FE) and surrogate models with impact data derived from in vivo experiments to define the impact mechanics needed to generate a moderate severity unilateral cervical contusion injury in NHPs (Macaca mulatta). Three independent variables (impactor displacement, alignment, and pre-load) were examined to determine their effects on tissue level stresses and strains. Mechanical measures of peak force, peak displacement, peak energy, and tissue stiffness were analyzed as potential determinants of injury severity. Data generated from FE simulations predicted a lateral shift of the spinal cord at high levels of compression (>64%) during impact. Submillimeter changes in mediolateral impactor position over the midline increased peak impact forces (>50%). Surrogate cords established a 0.5 N pre-load protocol for positioning the impactor tip onto the dural surface to define a consistent dorsoventral baseline position before impact, which corresponded with cerebrospinal fluid displacement and entrapment of the spinal cord against the vertebral canal. Based on our simulations, impactor alignment and pre-load were strong contributors to the variable mechanical and functional outcomes observed in in vivo experiments. Peak displacement of 4 mm after a 0.5N pre-load aligned 0.5-1.0 mm over the midline should result in a moderate severity injury; however, the observed peak force and calculated peak energy and tissue stiffness are required to properly characterize the severity and variability of in vivo NHP contusion injuries.

Blood flow velocities during experimental intracranial hypertension in pigs

Objectives: A purely hydraulic mechanism consisting in the pulsatile cuff-compression effect, by the cerebrospinal fluid displacement induced by the arterial pulsation, on the final portion of the bridging veins, has recently been hypothesized. This mechanism is able to maintain the constancy of cerebral blood flow (CBF) within the autoregulatory range, thus implying an exact balance between arterial inflow and venous outflow. In this study, we correlated arterial inflow and venous outflow during an experimentally induced condition of intracranial hypertension in pigs.Methods: Mock cerebrospinal fluid (CSF) was progressively infused until a condition of brain tamponade was reached. Blood flow velocities at middle cerebral artery and sagittal sinus sites were evaluated simultaneously.Results: Mean intracranial arterial blood flow velocity (IABFV), mean sagittal sinus blood flow velocity (SSBFV), and pulsatile-IABFV remained almost constant until cerebral perfusion pressure (CPP) dropped below 60–70 mmHg; then, a progressive decrease in mean IABFV and SSBFV, together with an increase in pulsatile-IABFV, was evident.Conclusion: The strict similarity between mean IABFV and SSBFV patterns suggests that CBF decrement is mainly due to a decrease in the venous outflow, which, in turn, produces an obstacle to the arterial inflow. The correspondent increase in pulsatile-IABFV confirms the presence of a distal outflow obstruction. All these findings point towards a purely hydraulic mechanism underlying the cerebral autoregulation which acts at the level of the so-called Starling resistor.

Dynamics of distribution of 3H-inulin between the cerebrospinal fluid compartments

Since the distribution of substances between various cerebrospinal fluid (CSF) compartments is poorly understood, we studied 3H-inulin distribution, over time, after its injection into cisterna magna (CM) or lateral ventricle (LV) or cisterna corporis callosi (CCC) in dogs. After the injection into CM 3H-inulin was well distributed to cisterna basalis (CB), lumbar (LSS) and cortical (CSS) subarachnoid spaces and less distributed to LV. When injected in LV 3H-inulin was well distributed to all CSF compartments. However, after injection into CCC 3H-inulin was mostly localized in CCC and adjacent CSS, while its concentrations were much lower in CM and CB and very low in LSS and LV. Concentrations of 3H-inulin in venous plasma of superior sagittal sinus and arterial plasma were very low and did not differ significantly, while its concentration in urine was very high. In 3H-inulin distribution it seems that two simultaneous processes are relevant: a) the pulsation of CSF with to-and-fro displacement of CSF and its mixing, carrying 3H-inulin in all directions, and b) the passage of 3H-inulin from CSF into nervous parenchyma and its rapid distribution to a huge surface area of capillaries by vessels pulsations. 3H-inulin then slowly diffuses across capillary walls into the bloodstream to be eliminated in the urine.

Posture-induced Changes in Intracranial Pressure: A Comparative Study in Patients with and without a Cerebrospinal Fluid Block at the Craniovertebral Junction

The aim of this study was to determine posture-induced changes in intracranial pressure (ICP) when patients with hydrocephalus or idiopathic intracranial hypertension remained supine for 1 hour and then sat up and remained sitting for 3 hours. Continuous ICP was monitored using a fiberoptic extradural sensor in: 1) 259 patients with hydrocephalus or idiopathic intracranial hypertension with free cerebrospinal fluid (CSF) flow through the craniovertebral junction and Sylvian aqueduct, 2) 20 patients with hydrocephalus secondary to aqueductal stenosis with free CSF flow through the craniovertebral junction, and 3) 97 patients with hydrocephalus associated with Chiari malformation. The maximum ICP difference (DeltaICP) was calculated as the difference between mean ICP in the supine position and minimum ICP value after changing body position. The mean ICP difference (DeltaICPmean) was calculated as the difference between the mean ICP in the supine position and the mean ICP while the patient was in a sitting position. In the complete sample, the median of DeltaICP was 13 mm Hg (interquartile range 10-17). The median of DeltaICPmean was 8 mm Hg (interquartile range 5-11). Both DeltaICP and DeltaICPmean were significantly greater in patients without obstruction in the craniospinal junction than in those with Chiari malformation (P = 0.005 and P = 0.014, respectively). No differences were found in DeltaICP or DeltaICPmean between patients with Sylvian aqueduct stenosis and those without (P = 0.777 and P = 0.346, respectively). ICP reduction after a change in body position is significantly greater in patients with free CSF flow through the craniospinal junction than in those with Chiari malformation, indicating the difficulty or impossibility of CSF displacement into the spinal canal in the latter.

The correction of vertebral joint dysfunctions changes cerebrovascular and cerebrospinal fluid functional parameters improving some Primary Respiratory Mechanism parameters

Introduction The driving force of the Primary Respiratory Mechanism (PRM) is the fluctuation of the Cerebrospinal Fluid (CSF) and the cerebrospinal vascular circulation. 1–4 Dynamic components are appreciated by osteopaths on palpation without reproducibility or research result concordance. 5 The aim of this study is to evidence, by using the equipment-based methods devised by Prof. Moskalenko, any PRM changes induced by osteopathic treatments. The study examines whether the momentary corrections of a given vertebral segment, previously diagnosed as the most important dysfunction at the spinal level (primary dysfunction), improve the rhythm, amplitude, and force of the cranial PRM. Design Pre–post randomised controlled double-blind clinical trial including placebos. Methods Participants: Eighteen male and female subjects aged between 18 and 100 divided into two even groups. Intervention: Step 1: objective osteopathic examination; Step 2: transcranial dopplerography (TCDG) and rheoencephalography (REG) at rest and with the application of functional tests (Transitional Respiratory Arrest and Stoockey Maneuver); Step 3: Group 1 received a vertebral manual input specific for the primary dysfunction while Group 2 received a specific vertebral manual input in a non-dysfunctional area; Step 4: step 2 repeated. Outcome Measures: Pre–post technique equipment-based evaluation using TCDG and REG with data analysed through spectral, pattern and phase analysis. Results PRM amplitude and rhythm showed an increase in Group 1: calculated from cerebrospinal flow and meningeal vasal tone parameters and cerebrospinal fluid displacement from the spine to the skull. Values showed greater changes in Group 1, while for Group 2 the changes were minor, absent or worsened. Conclusions The findings demonstrate cerebral flow and the change in brain vessel tone vary sufficiently after applying a vertebral manual input in the areas of maximum spinal restriction (Group 1). With regard to the vascular flow, an interesting fact is that there is no significant change in cerebral blood flow of the middle cerebral artery in both groups, however, a significant increase in blood flow was detected for both vertebral arteries only in Group 1 after the vertebral input. All changes, in particular the parameters concerning vascular and cerebrospinal fluid flows, could account for the marked increase in only one PRM parameter: amplitude.

The effect of position on intracranial pressure

The question as to whether the head and trunk of neurosurgery patients should be elevated remains controversial. This question is particularly important when intracranial hypertension is present. Head up position may have beneficial effects on intracranial pressure (ICP) via changes in mean arterial pressure (MAP), airway pressure, central venous pressure and cerebro spinal fluid displacement. However, in some circumstances, head up position may decrease MAP which in turn will result in a paradoxical rise in ICP through autoregulation mechanisms. Therefore, the degree of head elevation has to be titrated by evaluating the most adequate cerebral perfusion pressure (CPP) for each patient by means of transcranial Doppler or measurement of jugular venous blood oxygen saturation. Head elevation above 30 degrees should be avoided in all cases. In most patients with intracranial hypertension, head and trunk elevation up to 30 degrees is useful in helping to decrease ICP, providing that a safe CPP of at least 70 mmHg or even 80 mmHg is maintained. Patients in poor haemodynamic conditions are best nursed flat. CPP is thus the most important factor in assessment and monitoring when considering head elevation in patients with increased ICP.

The relationship of pulsatile cerebrospinal fluid flow to cerebral blood flow and intracranial pressure: a new theoretical model.

An electrical-equivalent circuit model of the cerebrovascular system is proposed, components of which directly relate to cerebrospinal fluid (CSF) compartment compliance and the determination of intracranial pressure (ICP). The model is based on three premises: 1) Under normal, physiologic conditions, the conversion of pulsatile arterial to nonpulsatile venous flow occurs primarily as a result of arterial compliance. Nonpulsatile venous flow is advantageous because less energy is required to maintain constant flow through the venous system, which comprises 75-80% of total blood volume. 2) Dynamic CSF movement across the foramen magnum is the primary facilitator by which intracranial arterial expansion occurs. Interference of the displacement of CSF during systole results in pulsatile venous flow and increased venous flow impedance. 3) Tissue hydrostatic pressure (here defined as ICP) is a dependent variable which is a function of capillary hydrostatic pressure and the osmotic/oncotic pressure gradient created by the blood-brain-barrier (BBB). An interference of transcranial CSF movement results in a decrease in cerebral blood flow (CBF) due to inertial effects impeding pulsatile venous flow. Feedback regulation in response to this decreased CBF leads to arteriolar vasodilatation (decreased resistance), thereby lowering the pressure difference between internal carotid and capillary pressures. Assuming no changes in the BBB potential, ICP increases linearly as capillary pressure increases.

Continuous spinal anaesthesia

Summary We have reviewed the history, advantages and disadvantages, technique, materials, and problems associated with continuous spinal anaesthesia. While the recent reports of cauda equina syndrome after continuous spinal anaesthesia prompted the FDA to remove microcatheters from the USA market, continuous spinal anaesthesia with small-bore catheters is still used without complications in many countries. The mechanism that caused cauda equina syndrome to develop after continuous spinal anaesthesia may be the displacement of cerebrospinal fluid and exposure of the cauda equina to poorly distributed local anaesthetics that, at certain concentrations, are neurotoxic per se . We suggest steps that can be taken to prevent this from happening and we believe it is therefore possible to do continuous spinal anaesthesia safely and advantageously in selected patients.

The mechanism of hydromyelia in Chiari type 1 malformations.

Abstract Experimental and clinical findings are presented to show that the magnitude of displacement of cerebro-spinal fluid from the basal cisterns during systole is an adequate force to cause hydromyelia in the presence of a Chiari malformation. The abnormal mechanism is discussed in detail and involves obstruction of the foramen magnum by the cone of depressed cerebellum adherent to the spinal cord, systolic deflection of the cerebro-spinal fluid from the basal cisterns into the 4th ventricle, and a milking action of the adherent cerebellum on the brainstem. These factors force cerebro-spinal fluid into the central canal of the spinal cord, tending to form a syrinx. Changes in epidural pressure associated with coughing and straining may cause extension of such a syrinx once it has formed.

Progressive ventricular dilatation following pneumonencephalography. A radiological sign of occult hydrocephalus.

✓ Eight patients with “normal pressure hydrocephalus” are presented who demonstrated radiographic and occasional clinical evidence of progressive dilatation of the ventricles following pneumoencephalography. The characteristic pneumographic signs of tentorial obstruction to the flow of cerebrospinal fluid (CSF) had been documented in the original air contrast study. The authors postulate that pneumoencephalography in patients with normal pressure hydrocephalus may result in a sudden displacement of CSF from the ventricles into the already compromised basal cisterns, leading to further obstruction of CSF outflow and progressive ventricular dilatation. Other mechanisms such as reduction in the potential resorptive capacity of the ventricular ependyma by air replacing ventricular fluid may play a part. The value of repeat radiological studies 24 and 48 hours after the original pneumogram is emphasized both as an aid in the radiological diagnosis of normal pressure hydrocephalus and as an additional parameter for studying problems in CSF flow and absorption.

INTRACRANIAL BLOOD FLOW IN DEMENTIA PARALYTICA, CEREBRAL ATROPHY AND SCHIZOPHRENIA

Recently an objective method for measuring a function of total intracranial blood flow has been developed,1which seems suitable for comparing the blood flow of groups of subjects. The following report is a comparative study of the total intracranial blood flow, as determined by this method, of patients suffering from dementia paralytica, from nonsyphilitic cortical atrophy and from schizophrenia. A group of 18 patients in the hospital who exhibited no clinical evidence of abnormal circulation in the brain or elsewhere served as controls. METHOD The method has been described in detail.1The relative intracranial blood flow was estimated by measuring the rate of cerebrospinal fluid displacement through a large lumbar puncture needle during sudden temporary compression of the veins of the neck. The studies were carried out with the cerebrospinal fluid pressure adjusted to 200 mm. of fluid. The veins were compressed by inflation of a freely distensible