Impaired Intracranial Compliance Research Articles

The role of pulsatile and static intracranial pressure measurements in the management of children with craniosynostosis-an institutional experience from 49 patients.

Although measurement of intracranial pressure (ICP) has occasionally been utilized in children with craniosynostosis (CSS), data on parameters of pulsatile ICP in CSS are still lacking, and the role of pulsatile ICP measurements in the management of CSS is not well established. From our department's database, we retrieved the data from children in whom the measurement of static and pulsatile ICP was a part of the diagnostic work-up in different clinical situations related to CSS. Both clinical and ICP data were retrospectively reviewed and analyzed. We identified 49 children with CSS, median age 4.4years (range 0.2-18.9), in whom a total of 67 diagnostic ICP measurements were undertaken between 2002 and 2014. The CSS was syndromal in 23 cases. The rationale for ICP measurement was a question of indication for cranial vault expansion surgery (CVES) in 12 patients (Group 1), of its timing in 10 patients (Group 2), of suspected abnormally elevated ICP or hydrocephalus in 11 patients (Group 3), of indication for repeated CVES in 13 patients (Group 4), or shunt dysfunction in three patients (Group 5). The average mean ICP for the whole cohort was 15.1 ± 5.5mmHg and mean wave amplitude (MWA) 5.3 ± 2.2mmHg. There was no significant difference in ICP parameters when compared between Groups 1-5. Fundoscopy revealed papilledema in five out of 32 children (15.6%). There were significantly higher parameters of pulsatile ICP (MWA) in patients with papilledema, but no statistically significant difference in parameters of static ICP. In this cohort of pediatric patients with CSS presenting with various diagnostic challenges, we found the diagnostic measurement of static and pulsatile ICP useful in selecting the optimal treatment modality and timing of surgery. Papilledema was associated with elevated pulsatile ICP, a parameter that in previous studies has been shown to correlate with impaired intracranial compliance.

Magnetic resonance imaging biomarkers of cerebrospinal fluid tracer dynamics in idiopathic normal pressure hydrocephalus.

Disturbed clearance of toxic metabolites from the brain via cerebrospinal fluid is emerging as an important mechanism behind dementia and neurodegeneration. To this end, magnetic resonance imaging work-up of dementia diseases is largely focused on anatomical derangements of the brain. This study explores magnetic resonance imaging biomarkers of cerebrospinal fluid tracer dynamics in patients with the dementia subtype idiopathic normal pressure hydrocephalus and a cohort of reference subjects. All study participants underwent multi-phase magnetic resonance imaging up to 48 h after intrathecal administration of the contrast agent gadobutrol (0.5 ml, 1 mmol/ml), serving as cerebrospinal fluid tracer. Imaging biomarkers of cerebrospinal fluid tracer dynamics (i.e. ventricular reflux grades 0–4 and clearance) were compared with anatomical magnetic resonance imaging biomarkers of cerebrospinal fluid space anatomy (Evans’ index, callosal angle and disproportional enlargement of subarachnoid spaces hydrocephalus) and neurodegeneration (Schelten’s medial temporal atrophy scores, Fazeka’s scores and entorhinal cortex thickness). The imaging scores were also related to a pulsatile intracranial pressure score indicative of intracranial compliance. In shunt-responsive idiopathic normal pressure hydrocephalus, the imaging biomarkers demonstrated significantly altered cerebrospinal fluid tracer dynamics (ventricular reflux grades 3–4 and reduced clearance of tracer), deranged cerebrospinal fluid space anatomy and pronounced neurodegeneration. The altered MRI biomarkers were accompanied by pressure indices of impaired intracranial compliance. In conclusion, we present novel magnetic resonance imaging biomarkers characterizing idiopathic normal pressure hydrocephalus pathophysiology, namely measures of cerebrospinal fluid molecular redistribution and clearance, which add information to traditional imaging scores of cerebrospinal fluid space anatomy and neurodegeneration.

Failed Foramen Magnum Decompression in Chiari I Malformation Is Associated With Failure to Restore Normal Intracranial Compliance: An Observational Cohort Study.

The standard treatment for symptomatic Chiari malformation (CM) I is foramen magnum decompression (FMD) to facilitate cerebral spinal fluid flow through the foramen magnum, improve intracranial compliance, and alleviate symptoms (commonly headache). This procedure has a variable success rate, with a significant proportion of patients having persistent symptoms after surgery. To investigate intracranial pressure (ICP) hydrodynamics in symptomatic surgery-naïve patients with CM I and symptomatic patients who have had prior FMD. We undertook a retrospective, observational cohort study, extracting data from our departmental ICP database. Patients with untreated ("Virgin") Chiari malformations (VCM), patients with previous "failed" FMD (ie, with persistent classical Chiari symptoms) (fFMD) and a normal control group, all with existing continuous ICP monitoring date were included. Median ICP (mICP) and median pulse amplitude (mPA) were compared between the groups. A total of 33 CM patients (22 VCM and 11 fFMD) and 42 normal controls were included for analysis. mICP did not differ significantly between the normal control, VCM, and fFMD groups. mPA in the VCM and fFMD groups was significantly higher than the control group (P<.01 and P<.05, respectively). In this cohort, patients with persistent symptoms after FMD have persistently impaired intracranial compliance, similar to patients who have not undergone surgery at all when compared with a control group. The reasons for this are not clear, and further research is required to establish the causation and optimum management for failed FMD.

Cerebrospinal fluid volumetric net flow rate and direction in idiopathic normal pressure hydrocephalus

The aim of the present study was to examine cerebrospinal fluid (CSF) volumetric net flow rate and direction at the cranio-cervical junction (CCJ) and cerebral aqueduct in individuals with idiopathic normal pressure hydrocephalus (iNPH) using cardiac-gated phase-contrast magnetic resonance imaging (PC-MRI). An in-depth, pixel-by-pixel analysis of regions of interest from the CCJ and cerebral aqueduct, respectively, was done in 26 iNPH individuals, and in 4 healthy subjects for validation purposes. Results from patients were compared with over-night measurements of static and pulsatile intracranial pressure (ICP). In iNPH, CSF net flow at CCJ was cranially directed in 17/22 as well as in 4/4 healthy subjects. Estimated daily CSF volumetric net flow rate at CCJ was 6.9 ± 9.9 L/24 h in iNPH patients and 4.5 ± 5.0 L/24 h in healthy individuals. Within the cerebral aqueduct, the CSF net flow was antegrade in 7/21 iNPH patients and in 4/4 healthy subjects, while it was retrograde (i.e. towards ventricles) in 14/21 iNPH patients. Estimated daily CSF volumetric net flow rate in cerebral aqueduct was 1.1 ± 2.2 L/24 h in iNPH while 295 ± 53 mL/24 h in healthy individuals. Magnitude of cranially directed CSF net flow in cerebral aqueduct was highest in iNPH individuals with signs of impaired intracranial compliance. The study results indicate CSF flow volumes and direction that are profoundly different from previously assumed. We hypothesize that spinal CSF formation may serve to buffer increased demand for CSF flow through the glymphatic system during sleep and during deep inspiration to compensate for venous outflow.

Cerebrospinal Fluid Volumetric Net Flow Rate and Direction in Idiopathic Normal Pressure Hydrocephalus

The aim of the present study was to examine cerebrospinal fluid (CSF) volumetric net flow rate and direction at the cranio-cervical junction (CCJ) and cerebral aqueduct in individuals with idiopathic normal pressure hydrocephalus (iNPH) using cardiac-gated phase-contrast magnetic resonance imaging (PC-MRI). An in-depth, pixel-by-pixel analysis of regions of interest from the CCJ and cerebral aqueduct, respectively, was done in 26 iNPH individuals, and in 4 healthy subjects for validation purposes. Results from patients were compared with over-night measurements of static and pulsatile intracranial pressure (ICP). In iNPH, CSF net flow at CCJ was cranially directed in 17/22 as well as in 4/4 healthy subjects. Estimated daily CSF volumetric net flow rate at CCJ was 6.9 ± 9.9 L/24 hours in iNPH patients and 4.5 ± 5.0 L/24 hours in healthy individuals. Within the cerebral aqueduct, the CSF net flow was antegrade in 7/21 iNPH patients and in 4/4 healthy subjects, while it was retrograde (i.e. towards ventricles) in 14/21 iNPH patients. Estimated daily CSF volumetric net flow rate in cerebral aqueduct was 1.1 ± 2.2 L/24 hours in iNPH while 295 ± 53 ml/24 hours in healthy individuals. Magnitude of cranially directed CSF net flow in cerebral aqueduct was highest in iNPH individuals with signs of impaired intracranial compliance. The study results indicate CSF flow volumes and direction that are profoundly different from previously assumed. We hypothesize that spinal CSF formation may serve to buffer increased demand for CSF flow through the glymphatic system during sleep and during deep inspiration to compensate for venous outflow.

The pathophysiology of chronic noncommunicating hydrocephalus: lessons from continuous intracranial pressure monitoring and ventricular infusion testing.

OBJECTIVE The pathophysiology of chronic noncommunicating hydrocephalus (ncHC) is poorly understood. This present study explored whether lessons about the pathophysiology of this clinical entity might be retrieved from results of overnight monitoring of pulsatile and static intracranial pressure (ICP) and ventricular infusion testing. METHODS The study cohort included adult patients (> 20 years of age) with chronic ncHC due to aqueductal stenosis in whom symptoms had lasted a minimum of 6 months. A reference cohort consisted of age- and sex-matched patients managed for communicating HC (cHC). Information about symptoms and clinical improvement following surgery was retrieved from a quality register, and results of overnight ICP recordings and ventricular infusion testing were retrieved from the hospital ICP database. RESULTS The cohort with ncHC consisted of 61 patients of whom 6 (10%) were managed conservatively, 34 (56%) by endoscopic third ventriculostomy (ETV), and 21 (34%) using ETV and subsequent shunt surgery. In patients responding to surgery, pulsatile ICP (mean ICP wave amplitude) was significantly increased to a similar magnitude in patients with ncHC and the reference cohort (cHC). Furthermore, intracranial compliance (ICC) was reduced in clinical responders. The results of ventricular infusion testing provided evidence that patients responding to ETV have impaired ventricular CSF absorption, while those requiring shunt placement after ETV present with impaired CSF absorption both in the intraventricular and extraventricular compartments. CONCLUSIONS The study may provide some lessons about the pathophysiology of chronic ncHC. First, increased pulsatile ICP and impaired ICC characterize patients with chronic ncHC who respond clinically to CSF diversion surgery, even though static ICP is not increased. Second, in patients responding clinically to ETV, impaired ventricular CSF absorption may be a key factor. Patients requiring shunt placement for clinical response appear to have both intraventricular and extraventricular CSF absorption failure. A subgroup of patients with ncHC due to aqueductal stenosis has normal ventricular CSF absorption and normal ICC and may not be in need of surgical CSF diversion.

Astrogliosis and impaired aquaporin‐4 and dystrophin systems in idiopathic normal pressure hydrocephalus

Idiopathic normal pressure hydrocephalus (iNPH) is one subtype of dementia that may improve following drainage of cerebrospinal fluid (CSF). This prospective observational study explored whether expression of the water channel aquaporin-4 (AQP4) and the anchoring molecule dystrophin 71 (Dp71) are altered at astrocytic perivascular endfeet and in adjacent neuropil of iNPH patient. Observations were related to measurements of pulsatile and static intracranial pressure (ICP). The study included iNPH patients undergoing overnight monitoring of the pulsatile/static ICP in whom a biopsy was taken from the frontal cerebral cortex during placement of the ICP sensor. Reference (Ref) biopsies were sampled from 13 patients who underwent brain surgery for epilepsy, tumours or cerebral aneurysms. The brain tissue specimens were examined by light microscopy, immunohistochemistry, densitometry and morphometry. iNPH patients responding to surgery (n = 44) had elevated pulsatile ICP, indicative of impaired intracranial compliance. As compared to the Ref patients, the cortical biopsies of iNPH patients revealed prominent astrogliosis and reduced expression of AQP4 and Dp71 immunoreactivities in the astrocytic perivascular endfeet and in parts of the adjacent neuropil. There was a significant correlation between degree of astrogliosis and reduction of AQP4 and Dp71 at astrocytic perivascular endfeet. Idiopathic normal pressure hydrocephalus patients responding to CSF diversion present with abnormal pulsatile ICP, indicative of impaired intracranial compliance. A main histopathological finding was astrogliosis and reduction of AQP4 and of Dp71 in astrocytic perivascular endfeet. We propose that the altered AQP4 and Dp71 complex contributes to the subischaemia prevalent in the brain tissue of iNPH.

The association between the pulse pressure gradient at the cranio-cervical junction derived from phase-contrast magnetic resonance imaging and invasively measured pulsatile intracranial pressure in symptomatic patients with Chiari malformation type 1.

In symptomatic Chiari malformation type 1 (CMI), impaired intracranial compliance (ICC) is associated with an increased cranio-spinal pulsatile pressure gradient. Phase-contrast magnetic resonance imaging (MRI) represents a non-invasive modality for the assessment of the pulse pressure gradient at the cranio-cervical junction (CCJ). We wished to explore how the MRI-derived pulse pressure gradient (MRI-dP) compares with invasively measured pulsatile intracranial pressure (ICP) in CMI, and with healthy controls. From phase-contrast MRI of CMI patients and healthy controls, we computed cerebrospinal fluid (CSF) flow velocities and MRI-dP at the CCJ. We assessed bidirectional flow and compared the flow between the anterior and the posterior subarachnoid space at the CCJ. We computed total intracranial volume (ICV), ventricular CSF volume (VV), and posterior cranial fossa volume (PCFV). We analyzed the static and pulsatile ICP scores from overnight monitoring in CMI patients. Five CMI patients and four healthy subjects were included. The CMI group had a significantly larger extent of tonsillar ectopia, smaller PCFV, and a smaller area of CSF in the FM. The pulsatile ICP (mean ICP wave amplitude, MWA) was abnormally increased in 4/5 CMI patients and correlated positively with MRI-dP. However, the MRI-dP as well as the CSF flow velocities did not differ significantly between CMI and healthy subjects. Moreover, bidirectional flow was observed in both CMI as well as healthy subjects, with no significant difference. In symptomatic CMI patients, we found a significant association between the pulse pressure gradient at the CCJ derived from phase-contrast MRI and the pulsatile ICP (MWA) measured invasively. However, the MRI-dP was close to identical in CMI patients and healthy subjects. Moreover, the CSF flow velocities at the CCJ and the occurrence of bidirectional flow were not different in CMI patients and healthy individuals. Further studies are required to determine the diagnostic role of phase-contrast MRI in CMI patients.

Comparative observational study on the clinical presentation, intracranial volume measurements, and intracranial pressure scores in patients with either Chiari malformation Type I or idiopathic intracranial hypertension.

OBJECTIVE Several lines of evidence suggest common pathophysiological mechanisms in Chiari malformation Type I (CMI) and idiopathic intracranial hypertension (IIH). It has been hypothesized that tonsillar ectopy, a typical finding in CMI, is the result of elevated intracranial pressure (ICP) combined with a developmentally small posterior cranial fossa (PCF). To explore this hypothesis, the authors specifically investigated whether ICP is comparable in CMI and IIH and whether intracranial volumes (ICVs) are different in patients with CMI and IIH, which could explain the tonsillar ectopy in CMI. The authors also examined whether the symptom profile is comparable in these 2 patient groups. METHODS The authors identified all CMI and IIH patients who had undergone overnight diagnostic ICP monitoring during the period from 2002 to 2014 and reviewed their clinical records and radiological examinations. Ventricular CSF volume (VV), PCF volume (PCFV), and total ICV were calculated from initial MRI studies by using volumetric software. The static and pulsatile ICP scores during overnight monitoring were analyzed. Furthermore, the authors included a reference (REF) group consisting of patients who had undergone ICP monitoring due to suspected idiopathic normal-pressure hydrocephalus or chronic daily headache and showed normal pressure values. RESULTS Sixty-six patients with CMI and 41 with IIH were identified, with comparable demographics noted in both groups. The occurrence of some symptoms (headache, nausea, and/or vomiting) was comparable between the cohorts. Dizziness and gait ataxia were significantly more common in patients with CMI, whereas visual symptoms, diplopia, and tinnitus were significantly more frequent in patients with IIH. The cranial volume measurements (VV, PCFV, and ICV) of the CMI and IIH patients were similar. Notably, 7.3% of the IIH patients had tonsillar descent qualifying for diagnosis of CMI (that is, > 5 mm). The extent of tonsillar ectopy was significantly different between the CMI and IIH cohorts (p < 0.001) but also between these 2 cohorts and the REF group. Pulsatile ICP was elevated in both cohorts without any significant between-group differences; however, static ICP was significantly higher (p < 0.001) in the IIH group. CONCLUSIONS This study showed comparable and elevated pulsatile ICP, indicative of impaired intracranial compliance, in both CMI and IIH cohorts, while static ICP was higher in the IIH cohort. The data did not support the hypothesis that reduced PCFV combined with increased ICP causes tonsillar ectopy in CMI. Even though impaired intracranial compliance seems to be a common pathophysiological mechanism behind both conditions, the mechanisms explaining the different clinical and radiological presentations of CMI and IIH remain undefined.

The correlation between pulsatile intracranial pressure and indices of intracranial pressure-volume reserve capacity: results from ventricular infusion testing.

OBJECTIVE The objective of this study was to examine how pulsatile and static intracranial pressure (ICP) scores correlate with indices of intracranial pressure-volume reserve capacity, i.e., intracranial elastance (ICE) and intracranial compliance (ICC), as determined during ventricular infusion testing. METHODS All patients undergoing ventricular infusion testing and overnight ICP monitoring during the 6-year period from 2007 to 2012 were included in the study. Clinical data were retrieved from a quality registry, and the ventricular infusion pressure data and ICP scores were retrieved from a pressure database. The ICE and ICC (= 1/ICE) were computed during the infusion phase of the infusion test. RESULTS During the period from 2007 to 2012, 82 patients with possible treatment-dependent hydrocephalus underwent ventricular infusion testing within the department of neurosurgery. The infusion tests revealed a highly significant positive correlation between ICE and the pulsatile ICP scores mean wave amplitude (MWA) and rise-time coefficient (RTC), and the static ICP score mean ICP. The ICE was negatively associated with linear measures of ventricular size. The overnight ICP recordings revealed significantly increased MWA (> 4 mm Hg) and RTC (> 20 mm Hg/sec) values in patients with impaired ICC (< 0.5 ml/mm Hg). CONCLUSIONS In this study cohort, there was a significant positive correlation between pulsatile ICP and ICE measured during ventricular infusion testing. In patients with impaired ICC during infusion testing (ICC < 0.5 ml/mm Hg), overnight ICP recordings showed increased pulsatile ICP (MWA > 4 mm Hg, RTC > 20 mm Hg/sec), but not increased mean ICP (< 10-15 mm Hg). The present data support the assumption that pulsatile ICP (MWA and RTC) may serve as substitute markers of pressure-volume reserve capacity, i.e., ICE and ICC.

Comparison of pulsatile and static pressures within the intracranial and lumbar compartments in patients with Chiari malformation type 1: a prospective observational study.

In Chiari malformation type 1 (CMI), the obstruction of cerebrospinal fluid (CSF) flow through the foramen magnum is believed to cause alterations of intracranial pressure (ICP) pulsations. Foramen magnum decompression (FMD) is therefore considered a treatment of choice. However, the pathophysiology of CMI is poorly understood and it remains unknown how ICP alterations relate to symptoms and radiological findings. This study was undertaken to measure pulsatile pressure and its gradient between intracranial and lumbar compartments, and to determine its relationship to clinical and radiological findings. In patients with symptomatic CMI, we simultaneously measured ICP and lumbar CSF pressure, with particular focus on analysis of pulsatile pressure. Ventricular CSF volume (VV), intracranial volume (ICV) and posterior cranial fossa volume (PCFV) were calculated using volumetry software. In 26 patients (median 35 years), we found clearly abnormal or borderline values of pulsatile ICP in 18/26 patients (69 %; median 4.5 mmHg) and abnormal pulsatile pressure gradient in 17/24 patients (71 %; median 2.6 mmHg). The correlation between pulsatile ICP and the pulsatile pressure gradient was significantly positive (p < 0.001). We found no significant correlation between pulsatile or static pressure and extent of tonsillar ectopy, VV, ICV or PCFV. The pulsatile pressure gradient was significantly higher in patients with syringomyelia (p = 0.02). In this cohort, the pulsatile ICP was elevated in 69 %. The intracranial-lumbar pulsatile pressure gradient was abnormal in 71 % and significantly higher in patients with syringomyelia. The elevated pulsatile ICP significantly correlated with pulsatile pressure gradient; no similar correlation was found for static ICP. We interpret the results as providing evidence of impaired intracranial compliance as an important pathophysiological mechanism in CMI.

Antisecretory factor (AF) exerts no effects on intracranial pressure (ICP) waves and ICP in patients with idiopathic normal pressure hydrocephalus and idiopathic intracranial hypertension

BackgroundAntisecretory factor (AF) and derivates thereof counteract brain edema and inflammation, and normalize ICP dynamics. The aim of the present study was to assess whether AF normalized the abnormal ICP waves, indicative of impaired intracranial compliance, seen in patients with idiopathic normal pressure hydrocephalus (iNPH) and idiopathic intracranial hypertension (IIH). The hypothesis was that brain swelling contributes to the abnormal ICP waves. MethodsThe study enrolled patients undergoing diagnostic ICP wave monitoring for either iNPH or IIH. The ICP waves and ICP were recorded continuously before and after oral administration of Salovum® (0.5g/kg body weight/day divided by three doses), a freeze-dried egg yolk enriched in AF activity. Mean ICP wave amplitude (MWA), mean ICP wave rise time coefficient (MWRTC), and mean ICP were compared before and after Salovum® administration. ResultsA total of 10 iNPH patients and 8 IIH patients were included. No significant changes in the ICP wave indices or ICP were seen after Salovum® administration. Neither any significant time-dependent effect was observed. ConclusionThe lack of effect of Salovum® on ICP wave indices and ICP in iNPH and IIH may provide indirect evidence that brain swelling does not play a crucial role in the ICP wave indices or ICP of these conditions.

Thresholds for Hypoxic Cerebral Vasodilation in Volunteers

The effects of hypoxemia on the cerebral vasculature have been described in animal models, but data from human studies are limited and have often relied on invasive methodology.The ability to detect a threshold for hypoxic vasodilatation in humans may be clinically useful, particularly in patients with impaired intracranial compliance. Because physiology may differ among subjects, it would be advantageous to measure such thresholds using noninvasive bedside techniques that could be readily applied to individual patients. We have attempted to identify thresholds of hypoxic vasodilatation in volunteers using noninvasive methods of measurement. Thirteen healthy volunteers were studied using transcranial Doppler sonography. Time-averaged middle cerebral artery maximal flow velocity (MCA FVx), mean arterial blood pressure, peripheral oxygen saturation (SpO2), and partial pressure of endtidal CO2 were measured at baseline and during graded reduction in arterial SpO2 to 85%, at normocapnia. Flow velocity and estimated cerebrovascular resistance (CVRe) were indexed and plotted against SpO2. There was no significant change in mean arterial pressure during desaturation to 85%, although the mean heart rate increased from 65 to 82 bpm. An increase in MCA FVx and reciprocal decrease in CVRe were observed when SpO2 decreased to below 90%. These results suggest that hypoxemic cerebral vasodilatation may be measured noninvasively and that in normal human volunteers, the threshold is at an SpO2 of 90%, which is greater than that previously reported. Implications: The ability to detect the point at which cerebral blood vessels dilate using noninvasive techniques is clinically advantageous. We have attempted to do this using transcranial Doppler sonography in volunteers whose inspired oxygen concentrations were gradually decreased. Thresholds of cerebral vasodilatation were found to be higher than those previously reported. These thresholds are important with regard to adequate perfusion in various pathologic states. (Anesth Analg 1997;85:817-20)

Thresholds for hypoxic cerebral vasodilation in volunteers.

The effects of hypoxemia on the cerebral vasculature have been described in animal models, but data from human studies are limited and have often relied on invasive methodology. The ability to detect a threshold for hypoxic vasodilatation in humans may be clinically useful, particularly in patients with impaired intracranial compliance. Because physiology may differ among subjects, it would be advantageous to measure such thresholds using noninvasive bedside techniques that could be readily applied to individual patients. We have attempted to identify thresholds of hypoxic vasodilatation in volunteers using noninvasive methods of measurement. Thirteen healthy volunteers were studied using transcranial Doppler sonography. Time-averaged middle cerebral artery maximal flow velocity (MCA FVx), mean arterial blood pressure, peripheral oxygen saturation (Spo2), and partial pressure of endtidal CO2 were measured at baseline and during graded reduction in arterial Spo2 to 85%, at normocapnia. Flow velocity and estimated cerebrovascular resistance (CVRe) were indexed and plotted against Spo2. There was no significant change in mean arterial pressure during desaturation to 85%, although the mean heart rate increased from 65 to 82 bpm. An increase in MCA FVx and reciprocal decrease in CVRe were observed when Spo2 decreased to below 90%. These results suggest that hypoxemic cerebral vasodilatation may be measured noninvasively and that in normal human volunteers, the threshold is at an Spo2 of 90%, which is greater than that previously reported. The ability to detect the point at which cerebral blood vessels dilate using noninvasive techniques is clinically advantageous. We have attempted to do this using transcranial Doppler sonography in volunteers whose inspired oxygen concentrations were gradually decreased. Thresholds of cerebral vasodilatation were found to be higher than those previously reported. These thresholds are important with regard to adequate perfusion in various pathologic states.

Nonvolumetric methods of detecting impaired intracranial compliance or reactivity

The authors have attempted to find a clinically reliable method of measuring intracranial pressure (ICP) compliance or reactivity that does not require volumetric manipulation. An analysis was undertaken of ICP, pulse widths and of the presence or absence of B waves, both experimentally in dogs and clinically in postoperative human patients. In both dogs and humans, ICP pulse width generally increased with increasing ICP and with increasing intracranial mass, and definitely increased with systolic arterial blood pressure. Nonetheless, ICP pulse width commonly failed to increase with increasing cerebral reactivity, and low ICP pulse width measurements were at times recorded in distinctly pathological situations. From the clinical study it was found that B waves were encountered more commonly in patients with increased ICP or increased ICP pulse width. However, the correlation between B waves alone or in combination with increased ICP or ICP pulse width and quantitative measurements of ICP reactivity was not significant. Mean reactivity and the range of reactivity measurements were almost identical in patient groups with and without B waves. For the time being the "ICP reserve test" remains the most accurate, the safest, and the most clinically useful method of quantitating ICP reserve.