Increase In Cerebrospinal Fluid Volume Research Articles

Cortical Reorganization following Injury Early in Life.

The brain has a remarkable capacity for reorganization following injury, especially during the first years of life. Knowledge of structural reorganization and its consequences following perinatal injury is sparse. Here we studied changes in brain tissue volume, morphology, perfusion, and integrity in children with hemiplegia compared to typically developing children, using MRI. Children with hemiplegia demonstrated reduced total cerebral volume, with increased cerebrospinal fluid (CSF) and reduced total white matter volumes, with no differences in total gray matter volume, compared to typically developing children. An increase in cortical thickness at the hemisphere contralateral to the lesion (CLH) was detected in motor and language areas, which may reflect compensation for the gray matter loss in the lesion area or retention of ipsilateral pathways. In addition, reduced cortical thickness, perfusion, and surface area were detected in limbic areas. Increased CSF volume and precentral cortical thickness and reduced white matter volume were correlated with worse motor performance. Brain reorganization of the gray matter within the CLH, while not necessarily indicating better outcome, is suggested as a response to neuronal deficits following injury early in life.

Mouse cerebral magnetic resonance imaging fails to visualize brain volume changes after experimental subarachnoid hemorrhage.

Brain atrophy after subarachnoid hemorrhage (SAH) has been detected in humans and might serve as a functional read-out parameter for neuropsychological deficits. To determine whether serial magnetic resonance imaging (MRI) can provide information on brain atrophy in animals as well, mice that had undergone experimental SAH were scanned repeatedly after the bleeding. Using a 7-T rodent MRI, six mice were evaluated for total hemispheric, cerebrospinal fluid (CSF) and hippocampal volumes on days 1, 2, 4, 21, 28, 42 and 60 after experimental SAH or sham operation, respectively. Repeated MRI scanning demonstrated a very high reproducibility with minimum standard deviation. Nevertheless, no significant differences were found between the two groups concerning hemispherical volumes or hippocampal volumes. A transient but significant increase in CSF volume was detected on days 2 and 60 after SAH. Compared with the existing method, no MRI data on brain atrophy in mice after experimental SAH have been published. Repeated brain MRI in mice after experimental SAH did not provide additional information on brain atrophy. Our data suggest that this is not due to a lack of sensitivity of the method. Despite all promising details about MRI, our results should initiate careful consideration (additional sequences/other questions) before its further use in this certain area, especially since it is expensive and associated with demanding logistics.

Brain Volume and Neurobehavior in Newborns with Complex Congenital Heart Defects

To investigate the relationship between tissue-specific alterations in brain volume and neurobehavioral status in newborns with complex congenital heart defects preoperatively. Three-dimensional volumetric magnetic resonance imaging was used to calculate tissue-specific brain volumes and a standardized neurobehavioral assessment was performed to assess neurobehavioral status in 35 full-term newborns admitted to the hospital before cardiopulmonary bypass surgery. Multiple linear regression models were performed to evaluate relationships between neurobehavioral status and brain volumes. Reduced subcortical gray matter (SCGM) volume and increased cerebrospinal fluid (CSF) volume were associated with poor behavioral state regulation (SCGM, P = .04; CSF, P = .007) and poor visual orienting (CSF, P = .003). In cyanotic newborns, reduced SCGM was associated with higher overall abnormal scores on the assessment (P = .001) and poor behavioral state regulation (P = .04), and increased CSF volume was associated with poor behavioral state regulation (P = .02), and poor visual orienting (P = .02). Conversely, acyanotic newborns showed associations between reduced cerebellar volume and poor behavioral state regulation (P = .03). Abnormal neurobehavior is associated with impaired volumetric brain growth before open heart surgery in infants with complex congenital heart defects. This study highlights a need for routine preoperative screening and early intervention to improve neurodevelopmental outcomes.

Reply—Spontaneous Cerebrospinal Fluid Otorrhea and Rhinorrhea in Idiopathic Intracranial Hypertension Patients

Background:Spontaneous cerebrospinal fluid (CSF) leakage may occur in patients with normal or increased intracranial pressure (ICP). We describe herein spontaneous CSF leakage as a result of chronic increased ICP in 4 patients with idiopathic intracranial hypertension (IIH). Although rhinorrhea prev

“Compensated hyperosmolarity” of cerebrospinal fluid and the development of hydrocephalus

Acute osmolar loading of cerebrospinal fluid within one lateral ventricle of dogs was examined as a cause of water extraction from the bloodstream and an increase in intracranial pressure. We have shown that a certain amount of 3H2O from the bloodstream enters osmotically loaded cerebrospinal fluid significantly faster, hence causing a significant increase in intracranial pressure. The noted phenomenon in which intracranial pressure still significantly increases, but in which the hyperosmolarity of the cerebrospinal fluid is no longer present, was named “compensated hyperosmolarity”. In the case of the sub-chronic application of hyperosmolar solutions into cat ventricles, we observed an increase in cerebrospinal fluid volume and a more pronounced development of hydrocephalus in the area of application, but without significant increase in intracranial pressure and without blockage of cerebrospinal fluid pathways. These results support the newly proposed hypothesis of cerebrospinal fluid hydrodynamics and the ability to develop new strategies for the treatment of cerebrospinal fluid-related diseases.

Cerebrospinal Fluid Space Alterations in Melancholic Depression

Melancholic depression is a biologically homogeneous clinical entity in which structural brain alterations have been described. Interestingly, reports of structural alterations in melancholia include volume increases in Cerebro-Spinal Fluid (CSF) spaces. However, there are no previous reports of CSF volume alterations using automated whole-brain voxel-wise approaches, as tissue classification algorithms have been traditionally regarded as less reliable for CSF segmentation. Here we aimed to assess CSF volumetric alterations in melancholic depression and their clinical correlates by means of a novel segmentation algorithm (‘new segment’, as implemented in the software Statistical Parametric Mapping-SPM8), incorporating specific features that may improve CSF segmentation. A three-dimensional Magnetic Resonance Image (MRI) was obtained from seventy patients with melancholic depression and forty healthy control subjects. Although imaging data were pre-processed with the ‘new segment’ algorithm, in order to obtain a comparison with previous segmentation approaches, tissue segmentation was also performed with the ‘unified segmentation’ approach. Melancholic patients showed a CSF volume increase in the region of the left Sylvian fissure, and a CSF volume decrease in the subarachnoid spaces surrounding medial and lateral parietal cortices. Furthermore, CSF increases in the left Sylvian fissure were negatively correlated with the reduction percentage of depressive symptoms at discharge. None of these results were replicated with the ‘unified segmentation’ approach. By contrast, between-group differences in the left Sylvian fissure were replicated with a non-automated quantification of the CSF content of this region. Left Sylvian fissure alterations reported here are in agreement with previous findings from non-automated CSF assessments, and also with other reports of gray and white matter insular alterations in depressive samples using automated approaches. The reliable characterization of CSF alterations may help in the comprehensive characterization of brain structural abnormalities in psychiatric samples and in the development of etiopathogenic hypotheses relating to the disorders.

Progressive Brain Changes in Children and Adolescents With First-Episode Psychosis

Progressive loss of brain gray matter (GM) has been reported in childhood-onset schizophrenia; however, it is uncertain whether these changes are shared by pediatric patients with different psychoses. To examine the progression of brain changes in first-episode early-onset psychosis and their relationship to diagnosis and prognosis at 2-year follow-up. Prospective, multicenter, naturalistic, 2-year follow-up study. Six child and adolescent psychiatric units in Spain. A total of 110 patients and 98 healthy controls were recruited between March 1, 2003, and November 31, 2005. Magnetic resonance imaging of the brain was performed for 61 patients with schizophrenia (n=25), bipolar disorder (n=16), or other psychoses (n=20) and 70 controls (both at baseline and after 2 years of follow-up). Mean age at baseline was 15.5 years (patients) and 15.3 years (controls). The GM and cerebrospinal fluid (CSF) volumes in the total brain and frontal, parietal, and temporal lobes. Compared with controls, patients with schizophrenia showed greater GM volume loss in the frontal lobe during the 2-year follow-up (left: -3.3 vs -0.6 cm(3), P=.004; right: -3.7 vs -0.8 cm(3), P=.005) and left frontal CSF volume increase (left: 6.7 vs 2.4 cm(3), P=.006). In addition to frontal volume, changes for total GM (-37.1 vs -14.5 cm(3), P=.001) and left parietal GM (-4.3 vs -2.2 cm(3), P=.04) were significantly different in schizophrenic patients compared with controls. No significant differences emerged for patients with bipolar disease. Greater left frontal GM volume loss was related to more weeks of hospitalization, whereas severity of negative symptoms correlated with CSF increase in patients with schizophrenia. Patients with schizophrenia or other psychoses showed greater loss of GM volume and increase of CSF in the frontal lobe relative to controls. Progressive changes were more evident in patients with schizophrenia than those with bipolar disorder. These changes in specific brain volumes after onset of psychotic symptoms may be related to markers of poorer prognosis.

Comment to the paper “Posterior fossa decompression and the cerebellum in Chiari type II malformation: A preliminary MRI study”

Set of Chiari malformations, per se, comprise an ensemble of interesting clinical forms, which are sometimes totally different from each other in regard to the clinical symptoms and accompanying pathological conditions of the central nervous system. Embryological background and development stages still require further explanations. There is still no single treatment mode that is widely accepted. Although most of the neurosurgeons accept early surgical correction for the symptomatic cases, treatment modality for nonsymptomatic cases is still under debate. Chiari type I and type I.5 cases are totally different story [1, 2]. The authors propose posterior fossa decompression in early infancy to prevent atrophy of cerebellum and other related posterior fossa structures in Chiari type II malformations. They calculated volumes of various structures in posterior fossa and came to a conclusion that cerebellar atrophy takes place in utero, and decompressive attempts do not help preventing cerebellar atrophy. However, they found that posterior fossa cerebrospinal fluid (CSF) volume improves and reaches to almost normal values after posterior fossa decompression as compared to normal individuals. In a recent investigation [3], total cerebellar volume was found to be significantly reduced in spina bifida myelomeningocele group as compared to the normal individuals. The results of this investigation coincide with the observations of the group, who proposes posterior fossa decompression in early infancy. The main question that suddenly rises in the mind is, while this posterior fossa decompression relieves the structures in the posterior fossa and causes an increase in CSF volume in Chiari type II cases, could this approach has any help to hydrocephalus in these patients, which is commonly attributed to the jam at foramen magnum level. The authors have found no improvement in cerebellar atrophy after decompressive surgery. On the other hand, this investigation showed that CSF volume (space as well) is augmented by posterior fossa decompression. The aim of all decompressive surgical attempts at posterior fossa is to relieve the level of foramen magnum and provide appropriate circulation of CSF for improvement of syringomyelia and brain stem compression. Although this kind of surgical approaches need more accumulated data related to the similar cases, in order to prevent forthcoming syringomyelia, to establish appropriate CSF circulation at level of foramen magnum, and to prevent brain stem compression, which can lead to lethal complications, this procedure may be helpful for the future prognosis of the patients. After the myelomeningocele operation, the timing of the posterior fossa decompression for Chiari II patients is another question to be answered as well.

Poster 6: Cerebrospinal Fluid (CSF) Volume Is the Main Marker of Huntington Disease Progression Severity and Age-at-Onset Prediction

Background Searching brain and peripheral biomarkers is a requisite to cure for Huntington's disease (HD). Mutated huntingtin exerts its main pathological effects on brain neurons. Neuronal dysfunction and degeneration cause progressively invalidating extrapyramidal symptoms, cognitive decline, and behavioral changes. Neuropathological studies showed progressive striatal dysfunction and degeneration since the beginning of the disease. Methods We analyzed the cross-sectional and longitudinal rate of brain atrophy, quantitatively measured by fully automated multiparametric magnetic resonance imaging, as fractional gray matter (GM, determining brain cortex volume), white matter (WM, measuring the volume of axonal fibers), and corresponding cerebrospinal fluid (CSF, a measure of global brain atrophy), in 94 gene-positive subjects with pre-symptomatic to advanced HD and age-matched healthy controls. Results and Discussion Each of the three brain compartments we studied (WM, GM, and CSF) had a diverse role, and their time courses differed in the development of HD. GM volume decreased early in life. Its decrease was associated with decreased serum brain derived neurotrophic factor and started even many years before onset symptoms, then decreased slowly in a nonlinear manner during the various symptomatic HD stages. WM volume loss also began in the pre-symptomatic stage of HD, a few years before manifest symptoms appear, rapidly decreasing near to the zone-of-onset. Finally, the CSF volume increase began many years before age at onset. Its volume measured in pre-symptomatic subjects contributed to improving the CAG-based model of age at onset prediction. The progressive CSF increase depended on CAG mutation size and continued linearly until the last stages of HD since the pre-symptomatic life stage, representing the best marker of progression rate and severity in HD ( R 2 = 0.25, p

Volumes of brain, grey and white matter and cerebrospinal fluid in schizophrenia in the Northern Finland 1966 Birth Cohort: An epidemiological approach to analysis

Magnetic resonance imaging (MRI) studies in schizophrenia have seldom involved a general population birth cohort or other epidemiological samples. We studied the Northern Finland 1966 Birth Cohort and identified all people with psychotic disorders. Along with an unaffected age-matched control sample ( n = 100) from the cohort, 54 subjects with schizophrenia underwent MRI brain scan at age 33–35 years from which we defined volumes of whole brain, grey and white matter and intracranial cerebrospinal fluid (CSF). Whole brain, grey and white matter volumes were 2–3% smaller in the schizophrenia subjects, who showed a 7% increase in CSF volume. These volume changes were independent of the effects of gender, family history of psychosis, perinatal risks or age at onset of illness. Moreover, there was no evidence that the effects were due to particular subgroups of cases having very low or high values. Rather, there were linear trends in the associations between whole brain and grey matter volume measures and schizophrenia. Our study replicates the previous findings of brain volume differences in schizophrenia on a general population level.

Brain structural damage in spinocerebellar ataxia type 2. A voxel‐based morphometry study

Voxel-based morphometry (VBM) enables an unbiased in-vivo whole-brain quantitative analysis of differences in gray matter (GM), white matter (WM) and cerebro-spinal fluid (CSF) volumes. We assessed with VBM 20 spinocerebellar ataxia Type 2 (SCA2) patients with mild or moderate cerebellar deficit and 20 age and sex-matched healthy controls. SCA2 patients showed a significant (P < 0.05 corrected for multiple comparison) symmetric loss of GM in the cerebellar vermis and hemispheres sparing lobules I,II, Crus II,VII, and X, and of the WM in the peridentate region, middle cerebellar peduncles, dorsal pons, and cerebral peduncles. The CSF volume was increased in the posterior cranial fossa. No GM, WM or CSF volume changes were observed in the supratentorial compartment. A mild (P < 0.05, >0.01) correlation was observed between the GM and WM loss and severity of the neurological deficit. In SCA2 patients with mild to moderate cerebellar deficit, GM and WM volume loss and CSF volume increase are confined to the posterior cranial fossa.

Progression of Brain Volume Changes in Adolescent-Onset Psychosis

Little is known about the changes that take place in the adolescent brain over the first few years following the onset of psychosis. The present longitudinal study builds on an earlier cross-sectional report demonstrating brain abnormalities in adolescent-onset psychosis patients with a recent-onset first episode of psychosis. Magnetic resonance imaging studies were obtained at baseline and 2 years later from 21 adolescents with psychosis and 34 healthy controls matched for age, gender, and years of education. Whole-brain volumes and gray matter (GM) and cerebrospinal fluid (CSF) volumes of the frontal, parietal, temporal, and occipital lobes were measured at baseline and at 2-year follow-up. In the frontal lobe, the rate of GM volume loss was significantly higher in male patients (2.9% and 2.0%, respectively, for left and right) than in controls (1.2% and 0.7%, respectively, for left and right). In the left frontal lobe, male patients showed a significantly higher rate of CSF volume increase than controls (8.6% vs 6.4%). These differences in rates of volume change were observed in male and female patients, although only males showed significant time x diagnosis interactions. This negative finding in females should be interpreted with caution as the study was underpowered to detect change in women due to limited sample size. An exploratory analysis revealed that schizophrenia and nonschizophrenia psychotic disorders showed similar volume change patterns relative to controls. Change in clinical status was not correlated with longitudinal brain changes. Our results support progression of frontal lobe changes in males with adolescent-onset psychosis.

Abnormal Cerebral Structure Is Present at Term in Premature Infants

Long-term studies of the outcome of very prematurely born infants have clearly documented that the majority of such infants have significant motor, cognitive, and behavioral deficits. However, there is a limited understanding of the nature of the cerebral abnormality underlying these adverse neurologic outcomes. The overall aim of this study was to define quantitatively the alterations in cerebral tissue volumes at term equivalent in a large longitudinal cohort study of very low birth weight premature infants in comparison to term-born infants by using advanced volumetric 3-dimensional magnetic resonance imaging (MRI) techniques. We also aimed to define any relationship of such perinatal lesions as white matter (WM) injury or other potentially adverse factors to the quantitative structural alterations. Additionally, we wished to identify the relationship of the structural alterations to short-term neurodevelopmental outcome. From November 1998 to December 2000, 119 consecutive premature infants admitted to the neonatal intensive care units at Christchurch Women's Hospital (Christchurch, New Zealand) and the Royal Women's Hospital (Melbourne, Australia) were recruited (88% of eligible) after informed parental consent to undergo an MRI scan at term equivalent. Twenty-one term-born infants across both sites were recruited also. Postacquisition advanced 3-dimensional tissue segmentation with 3-dimensional reconstruction was undertaken to estimate volumes of cerebral tissues: gray matter (GM; cortical and deep nuclear structures), WM (myelinated and unmyelinated), and cerebrospinal fluid (CSF). In comparison to the term-born infants, the premature infants at term demonstrated prominent reductions in cerebral cortical GM volume (premature infants [mean +/- SD]: 178 +/- 41 mL; term infants: 227 +/- 26 mL) and in deep nuclear GM volume (premature infants: 10.8 +/- 4.1 mL; term infants: 13.8 +/- 5.2 mL) and an increase in CSF volume (premature infants: 45.6 +/- 22.1 mL; term infants: 28.9 +/- 16 mL). The major predictors of altered cerebral volumes were gestational age at birth and the presence of cerebral WM injury. Infants with significantly reduced cortical GM and deep nuclear GM volumes and increased CSF volume volumes exhibited moderate to severe neurodevelopmental disability at 1 year of age. This MRI study of prematurely born infants further defines the nature of quantitative cerebral structural abnormalities present as early as term equivalent. The abnormalities particularly involve cerebral neuronal regions including both cortex and deep nuclear structures. The pattern of cerebral alterations is related most significantly to the degree of immaturity at birth and to concomitant WM injury. The alterations are followed by abnormal short-term neurodevelopmental outcome.

Improved Outcome in Thoracoabdominal Aortic Aneurysm Repair: The Role of Cerebrospinal Fluid Drainage

To evaluate the protective effect and the optimum duration of cerebrospinal fluid drainage (CSFD) during and after thoracoabdominal aortic aneurysm (TAAA) repair. From April 2001 to October 2003, we retrospectively compared 17 (n = 17) consecutive patients who have been electively operated on by Martin Grabenwoger for left heart bypass and selective perfusion of the visceral and renal organs. The first 7 patients had CSFD for 72 hours; the duration of CSFD was increased to 100 hours in the remaining 10 patients. Median drained cerebrospinal fluid (CSF) volume was 680 milliliters in the 72-hour group versus 1441 milliliters in the 100-hour group. A characteristic increase in CSF volume was noted between POD No. 2 and POD No. 4 indicating persistent spinal cord edema. Univariate and multivariate analysis demonstrated that CSFD for 100 hours is a significant predictor for decreased incidence of late onset paraplegia (p < 0.001). The overall incidence of postoperative neurological deficit was 17.6% (3 of 17). There was one patient (6%) who developed permanent paraplegia and two patients (12%) with transient paraplegia. These patients sustained late-onset paraplegia 72 hours after surgery for removal of a CSFD device. Complete motor function could be restored after re-insertion of a CSFD device. In one patient, permanent paraplegia was evident after awakening from anesthesia. Because of technical difficulties, only two intercostal arteries could be re-implanted, which was obviously not sufficient to restore spinal cord perfusion. In contrast, no neurological deficit occurred in patients in whom a CSFD instrument was left for 100 hours. The extended duration of CSFD may lower the risk of late-onset paraplegia and could improve outcome in patients undergoing thoracoabdominal aortic surgery.

Neuropsychological findings in congenital and acquired childhood hydrocephalus.

Hydrocephalus is an increase in cerebrospinal fluid volume that can be caused by a variety of etiologies. The most common connatal and acquired causes of hydrocephalus are spina bifida, aqueduct stenosis, and preterm low birthweight infants with ventricular hemorrhage. In general, the literature suggests mild neuropsychological deficits associated with hydrocephalus, which are predominant in visuospatial and motor functions, and other nonlanguage skills. Although the precise nature of the neuropsychological deficits in hydrocephalus are not completely known, several factors such as etiology, raised intracranial pressure, ventricular size, and changes in gray and white matter tissue composition as well as shunt treatment complications have been shown to influence cognition. In fact, the presence of complications and other brain abnormalities in addition to hydrocephalus such as infections, trauma, intraventricular hemorrhage, low birthweight, and asphyxia are important determinants of the ultimate cognitive status, placing the child at a high risk of cognitive impairment.

Unsupervised, automated segmentation of the normal brain using a multispectral relaxometric magnetic resonance approach.

The purpose of this study was the development and testing of a method for unsupervised, automated brain segmentation. Two spin-echo sequences were used to obtain relaxation rates and proton-density maps from 1.5 T MR studies, with two axial data sets including the entire brain. Fifty normal subjects (age range, 16 to 76 years) were studied. A Three-dimensional (3D) spectrum of the tissue voxels was used for automatic segmentation of gray matter (GM), white matter (WM), and cerebrospinal fluid (CSF) and for calculation of their volumes. Accuracy and reproducibility were tested with a three-compartment phantom simulating GM, WM, and CSF. In the normal subjects, a significant decrease of GM fractional volume and increased CSF volume with age were observed (P < 0.0001), with no significant changes in WM. This multispectral segmentation method permits reproducible, operator-independent volumetric measurements.

CSF, Sagittal Sinus, and Jugular Venous Pressures During Desflurane or Isoflurane Anesthesia in Dogs

Previous studies to determine whether desflurane increases cerebrospinal fluid (CSF) pressure are inconclusive because none have included all of the following: multiple doses of desflurane, administration for at least several hours, examination at normo- and hypocapnia, a concurrent comparison group, direct measurement of both intra- and extracranial CSF pressures, and measurement of venous pressures that influence CSF pressure. The present study was designed to determine whether CSF pressure increases during 4.0 h desflurane anesthesia using a study design that included the above elements. Catheters were placed in the lateral cerebral ventricle, cisterna magna, sagittal sinus, and jugular vein of 12 dogs anesthetized with thiopental 12 mg.kg-1.h-1 and halothane 0.5 to 0.8%. Catheter pressures were measured, and the CSF-sagittal sinus pressure gradient and slope of the gradient to CSF pressure relationship were determined during control conditions. Then, 6 dogs were anesthetized with desflurane and 6 dogs were anesthetized with isoflurane, and the same values were determined for 1.0 h at each of four experimental conditions: 0.5 and 1.0 minimum alveolar concentration (MAC) during normocapnia (PaCO2 35-39 mm Hg) and 0.5 and 1.0 MAC during hypocapnia (PaCO2 20-24 mm Hg). CSF and sagittal sinus pressures, but not jugular venous pressure, increased with both desflurane and isoflurane. The greater increase of CSF pressure with 4.0 h desflurane (to 40.2 +/- 12.7 cm H2O) than with 4.0 h isoflurane (to 26.2 +/- 11.5 cm H2O) was attributable to an increase of CSF pressure that was greater during 2.0 h desflurane and normocapnia than during 2.0 h isoflurane and normocapnia, and to an increase of CSF pressure during 2.0 h desflurane and hypocapnia that was similar to that during 2.0 h isoflurane and hypocapnia. The greater increase of CSF pressure during desflurane may have resulted, in part, from increased CSF volume as indicated by a positive CSF-sagittal sinus pressure gradient (in contrast, there was little or no CSF-sagittal sinus pressure gradient during isoflurane) and a steeper slope of the gradient to CSF pressure relationship.

Increase in brain cerebrospinal fluid volume is greater in older than in younger alcoholic patients: A replication study and CT/MRI comparison

This cross-sectional study used a semi-automated analysis technique to quantify regional brain cerebrospinal fluid (CSF) volumes derived from computed tomography (CT) in 84 healthy men ranging from 21 to 82 years of age and 28 patients meeting Research Diagnostic Criteria for alcohol dependence. The goals were to replicate an earlier CT study of an independent sample of alcoholic and control subjects (Pfefferbaum et al., 1988 a; Zipursky et al., 1988) and to compare CT assessments of brain changes with magnetic resonance imaging (MRI) assessments made in the same alcoholic patients (Pfefferbaum et al., 1992). Regional brain changes associated with normal aging were derived by regression analysis, using CT data collected from the healthy control subjects. As in the earlier CT study and in the concurrent MRI study, ventricular and sulcal CSF volumes in alcoholic patients were greater than would be expected for their age. Furthermore, the present CT study replicated the previous CT and MRI findings of a positive relationship between age and CSF volume enlargement in alcoholic patients over and above the normal age-related increase in CSF volume, suggesting greater vulnerability of the aging brain to alcohol. Comparison of CT-and MRI-derived estimates of ventricular and cortical sulcal volume revealed high correlations (>0.80). MRI and CT produced similar absolute ventricular volumes, while MRI produced larger sulcal volume estimates than did CT. The difference in sulcal volume estimate may be due to differences between CT and MRI in slice thickness and sensitivity to partial volume effects.

Isoflurane does not increase the rate of CSF production in the dog.

Using the open ventriculocisternal perfusion method, the rate of cerebrospinal fluid (CSF) production was examined in dogs anesthetized with isoflurane (1.4%) and nitrous oxide (66%) in oxygen. In one group (n = 6) the rate of CSF production did not change significantly when the expired concentration was decreased from 1.4% to less than 0.15%. In a second group (n = 6) maintained at isoflurane 1.4%, the rate of CSF production decreased by approximately 8%/h, similar to the time effect previously reported in controls with this model (a decrease of 4-9%/h). These data suggest that isoflurane causes no significant change in the rate of CSF production and that an increase in CSF volume does not occur during prolonged isoflurane anesthesia. In patients at risk due to increased intracranial pressure, isoflurane may be preferred to anesthetics that may increase intracranial volume, e.g., enflurane or ketamine.

Effects of Halothane and Fentanyl on the Rate of CSF Production in Dogs

Using the open ventriculocisternal perfusion method, the rate of cerebrospinal fluid (CSF) production was examined in dogs anesthetized with either halothane (0.8%) or fentanyl (3.0 micrograms/kg/min for 20 min, then 0.2 micrograms/kg/min, intravenously), and nitrous oxide (60-70%) in oxygen. Halothane decreased the mean rate of CSF production from 0.047 +/- 0.006 ml/min (mean +/- SEM) in controls to 0.033 +/- 0.005 ml/min. This effect persisted throughout 3.0-3.5 h of anesthesia. When the expired concentration of halothane was decreased from 0.8% to less than 0.1%, the mean rate of CSF production returned to control values within 45-50 min. Fentanyl produced no change in the mean rate of CSF production compared to controls. These data suggest that increased CSF volume does not contribute to increased intracranial pressure during prolonged halothane anesthesia. In patients at risk for increased intracranial pressure due to increased CSF volume, either halothane or fentanyl may be preferable to anesthetics that may increase CSF production, e.g., enflurane.