Degree Of Ventricular Enlargement Research Articles

Mediation of White Matter Alterations in the Association Between Ventricular Dilation and Cognitive Decline in Hydrocephalus Patients: An MRI Study.

Cognitive impairment is commonly observed in hydrocephalus patients. Ventricular enlargement compresses brain parenchyma, especially the white matter (WM). To investigate whether the relationship between ventricular dilation and cognitive decline in hydrocephalus patients is mediated by WM alterations. Retrospective. 51 communicating hydrocephalus patients (median age, 54 years), 50 obstructive hydrocephalus patients (median age, 49 years), and 53 control subjects (median age, 50 years). Diffusion tensors imaging, 3D T1 BRAVO, 3D FIESTA, CUBE T2, and FLAIR sequences at 3T. DTI parameters (skeletonized fractional anisotropy (FA), skeletonized mean diffusivity (MD), and peak width of skeletonized mean diffusivity p(PSMD)) were extracted using FSL software. Global, periventricular, and deep white matter hyperintensity (WMH) volumes, degree of ventricular enlargement (Evans index), and other conventional imaging markers (number of lacunes and perivascular spaces, intracranial and brain volume) were extracted using united imaging intelligence. Cognitive tests included Montreal cognitive assessment (MoCA), clock drawing test (CDT), and vocabulary fluency test (VFT). Multivariable linear regression analysis, mediation analyses, and dominance analysis. P-value <0.05 was considered significant. The degree of ventricular dilation, DTI parameters, and cognitive function scores were interrelated. The skeletonized FA values (β = -0.0917, 95% confidence interval (CI): -0.205, -0.024) and normalized global WMH volume (β = -0.0635, 95% CI: -0.13, -0.0005) together mediated 37.2% of the association between Evans index and MoCA. A comparable causal pathway was found for periventricular WMHs but not for deep WMHs. Dominance analysis indicated skeletonized FA values had a greater impact on cognition than WMH volume. The skeletonized FA values also mediated the association between Evans index and CDT (β = -0.0897, 95% CI: -0.165, -0.026) and VFT (β = -0.1589, 95% CI: -0.27, -0.083). WM alterations were causal mediators between ventricular dilation and cognitive decline in hydrocephalus patients. 3. Stage 3.

Macroscopic findings of brain with dementia.

In this paper, we have described the points to be noted when examining the macroscopic findings of the brain of patients with dementia. The characteristics of the macroscopic findings of the brain of patients with dementia are shown in the figure of the outer surface and the cut surface. Gross findings in the brain of patients with Alzheimer's disease should consider, in addition to the degree of limbic changes, whether the atrophy is diffuse, the degree of ventricular enlargement, and the complications of vascular changes. The macroscopic findings of the brain of patients with dementia with Lewy bodies are characterized by the absence of notable abnormal findings other than the depigmentation of the substantia nigra and locus coeruleus. In dementia with Lewy bodies, other types of dementia complications should be considered if abnormal findings are present. It should be noted that accurate diagnosis of argyrophilic grain dementia and senile dementia of neurofibrillary tangle type by macroscopic findings alone is often difficult to distinguish from a mild case of Alzheimer's disease and change by physiological aging in particular. In frontotemporal lobar degeneration, changes in the basal ganglia, brain stem, cerebellum and motor neurons should be observed to make a differential diagnosis of various types of frontotemporal lobar degeneration. It is important to understand the areas that are often damaged in different types of dementia and the extent of lesions, and to distinguish each type of dementia. Care should be taken as macroscopic findings are more complex when several types of dementia are mixed. It was shown that accurate understanding of macroscopic findings is essential for understanding clinical symptoms, imaging findings, differential diagnosis of dementia and disease pathogenesis.

Learning to combine complementary segmentation methods for fetal and 6-month infant brain MRI segmentation

Segmentation of brain structures during the pre-natal and early post-natal periods is the first step for subsequent analysis of brain development. Segmentation techniques can be roughly divided into two families. The first, which we denote as registration-based techniques, rely on initial estimates derived by registration to one (or several) templates. The second family, denoted as learning-based techniques, relate imaging (and spatial) features to their corresponding anatomical labels. Each approach has its own qualities and both are complementary to each other. In this paper, we explore two ensembling strategies, namely, stacking and cascading to combine the strengths of both families. We present experiments on segmentation of 6-month infant brains and a cohort of fetuses with isolated non-severe ventriculomegaly (INSVM). INSVM is diagnosed when ventricles are mildly enlarged and no other anomalies are apparent. Prognosis is difficult based solely on the degree of ventricular enlargement. In order to find markers for a more reliable prognosis, we use the resulting segmentations to find abnormalities in the cortical folding of INSVM fetuses. Segmentation results show that either combination strategy outperform all of the individual methods, thus demonstrating the capability of learning systematic combinations that lead to an overall improvement. In particular, the cascading strategy outperforms the ensembling one, the former one obtaining top 5, 7 and 13 results (out of 21 teams) in the segmentation of white matter, gray matter and cerebro-spinal fluid in the iSeg2017 MICCAI Segmentation Challenge. The resulting segmentations reveal that INSVM fetuses have a less convoluted cortex. This points to cortical folding abnormalities as potential markers of later neurodevelopmental outcomes.

Asymptomatic Severe Mitral Valve Regurgitation

Management of patients with mitral valve regurgitation (MR) has changed dramatically over the past 20 years; this change is largely attributable to 3 factors. First, there have been significant improvements in operative techniques that have led to predictable and durable results after valve repair. In current practice at our clinic, >95% of patients with pure MR caused by degenerative diseases have valve repair rather than prosthetic replacement, and with modern, simplified methods of leaflet repair and annuloplasty, the risk of reoperation after correction of MR is no greater than that after mitral valve replacement.1 Article p 797 The second major shift in mitral valve disease is the change in pathology and pathophysiology of MR. In current practice, almost 80% of patients having mitral valve operations have pure regurgitation rather than valve stenosis or mixed regurgitation and stenosis, and the cause is most often degenerative or myxomatous disease; there is a declining frequency of postinflammatory disease in North America and many other areas of the world. The third important change in the management of patients with mitral valve disease is the better understanding of the natural history of MR, which has been made possible by both detailed natural history studies and improved techniques of 2-dimensional and Doppler echocardiography.2–4 The article by Kang et al5 in this issue of Circulation provides important new and confirmatory information on the outcome of asymptomatic patients with severe MR. Before the 1990s, most clinicians viewed MR as a relatively benign condition, and surgery was reserved for patients who were severely symptomatic or failed medical management.6,7 Reluctance to proceed with operation was related to the likelihood of prosthetic valve replacement and to the notion that asymptomatic patients with severe MR were a …

O.064 Amyloid-beta clearance in experimental neonatal hydrocephalus

Structural and/or functional injury of the basal ganglia can lead to motor functional disabilities, abnormal gait and posture, and intellectual/emotional impairment, disorders also frequently seen in hydrocephalus. Previous reports have documented changes in dopamine levels in the neostriatum in experimental hydrocephalus. The present study was designed to investigate possible functional injury of cholinergic, GABAergic and dopaminergic systems in the basal ganglia immunohistochemically in a model of kaolin-induced hydrocephalus. Hydrocephalus was induced in 12 Wistar rats by intracisternal injection of 0.05 ml volume of 25% kaolin solution under microscopic guidance. Four controls received an equal volume of sterile saline. The animals were killed at 2, 4 and 8 weeks after injection. The numbers of choline acetyltransferase (ChAT)- and glutamic acid decarboxylase (GAD)-immunoreactive (IR) neostriatal neurons and tyrosine hydroxylase (TH) – IR nigral neurons, were counted in 60-μm thick representative sections and the IR cellular densities (counted cell number/neostriatal area) were calculated in the neostriatum. The number of total neostriatal neurons was also counted in 15-μm thick sections stained by cresyl violet (Nissl staining) to calculate the cellular density. The number and cellular density of neostriatal ChAT-IR neurons were significantly reduced at 2, 4, and 8 weeks after injection (P<0.05), while those of GAD-IR neurons decreased at 4 and 8 weeks (P<0.05). There was a linear correlation between degree of ventricular enlargement, and reduction in number of ChAT- and GAD-IR neurons (P<0.001) as well as in the cellular density (P<0.001). However, Nissl staining revealed no reduction in the cellular density of total neostriatal neurons (P<0.001). TH immunoreactivity was reduced in neostriatal axons and in nigral compacta neurons, particularly in the medial portion of the dopaminergic nigrostriatal pathway. These findings suggest that progressive hydrocephalus results in functional injuries of cholinergic and GABAergic neurons in the neostriatum and dopaminergic neurons in the substantia nigra compacta by mechanical distortion. The disturbance in balance of these neurotransmitter systems in the basal ganglia may explain some of motor functional disabilities in hydrocephalus.

Idiopathic hydrocephalus in children and idiopathic intracranial hypertension in adults: two manifestations of the same pathophysiological process?

Both idiopathic intracranial hypertension (IIH) in adults and idiopathic hydrocephalus in children have been shown to involve elevations in venous pressure that resolve once the cerebrospinal fluid pressure is reduced. It has been assumed that the venous pressure elevations in both conditions are not hemodynamically significant, but measurement of venous collateral flow in IIH has shown these pressure elevations to be of consequence. The authors used the same methodology to see if the venous pressure elevations noted in childhood hydrocephalus are important. Fourteen patients with idiopathic childhood hydrocephalus underwent magnetic resonance imaging with flow quantification. The degree of ventricular enlargement, total blood inflow, and superior sagittal/straight sinus outflow was measured. The degree of collateral venous flow was calculated for each venous territory. The findings were compared with findings in 14 age-matched controls. In children with hydrocephalus the cerebral blood inflow was normal, but the superior sagittal sinus (SSS) and straight sinus outflows were reduced by 27% and 38%, respectively, compared with measurements in controls (p = 0.03 and 0.002). These findings suggest that approximately 150 ml of blood per minute was returning via collateral channels from that portion of the brain drained by the SSS, and 60 ml/minute was returning from collaterals in the deep venous territory. Similarly to patients with IIH, children with hydrocephalus show a significant elevation in collateral venous flow, indicating that the same venous pathophysiological process may be operating in both conditions. Whether or not the ventricles dilate may depend on the differences in brain compliance between adults and children.

Neuroimaging Findings in Neurosyphilis

We report two cases of neurosyphilis with atypical clinical presentations that were compounded by atypical neuroimaging findings. In the first case, MRI brain scan findings were felt to be compatible with mesial temporal sclerosis or herpes simplex encephalitis. The second patient presented with a clinical picture compatible with normal pressure hydrocephalus as well as some degree of ventricular enlargement and prominent periventricular white matter changes by MRI brain scan. He actually underwent ventriculo-peritoneal shunting prior to determination that he had active syphilitic involvement of the central nervous system. Neurosyphilis, "the great imitator," is not only capable of mimicking various other neurological disease clinical presentations, it can also mimic neuroimaging features of various other disease processes as well.

NGF, NT-3 and Trk C mRNAs, but not TrkA mRNA, are upregulated in the paraventricular structures in experimental hydrocephalus.

This study was designed to detect possible alterations in the expression of neurotrophins and trks in kaolin-induced hydrocephalus by in situ hybridization. Sixteen rats were treated by injection of 25 mg kaolin suspended in 0.1 ml of physiological saline into the cisterna magna. Four rats were injected with saline and served as controls. The kaolin-treated rats were divided into two groups studied 1 and 4 weeks after treatment. Rats were anesthetized and killed, and their brains were rapidly dissected and frozen. DNA oligonucleotide probes for nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and trkA, trkB, and C were labeled with [(35)S]dATP using terminal deoxyribonucleotidyl transferase for in situ hybridization. Hydrocephalic brains were also classified according to the degree of ventricular enlargement. The results observed were as follows. (1) The medial septal and striatal NGF mRNA levels increased with severity in animals. (2) Hippocampal trkB and BDNF mRNA levels increased with time in animals with moderate ventricular enlargement. (3) Expression of hippocampal trkB, trkC, and NT-3 mRNA increased in animals with moderate ventricular enlargement, while it apparently decreased in the large ventricular enlargement group reaching normal ranges. (4) In the corpus callosum there was an apparent increase in NGF, NT-3 and trkC mRNA, but not in trkA, in hydrocephalic animals. NT-3 EIA confirmed the presence of NT-3 protein increases in corpus callosum. It is therefore possible that simultaneous NGF, NT-3, and trkC receptor upregulation occurred in glial elements of the white matter. These results demonstrate that neurotrophins and their receptors are overexpressed in many damaged structures of the severely hydrocephalic brain. There were discrepancies in the distribution of NGF and trkA mRNA, and we hypothesize that NGF mRNA in the damaged white matter structure might be due to the reduced availability of other receptors, such as the low-affinity NGF receptors.

Is the course of brain development in schizophrenia delayed? Evidence from onsets in adolescence

A degree of ventricular enlargement, together with a reduction of total cortical mass and loss of asymmetry is reported in schizophrenia, but the meaning is obscure. These changes may reflect an anomaly of brain development. Brain structure was assessed on a 1.5-Tesla MRI scan in a series of 29 adolescents at the time of a first episode of schizophrenia and compared with 15 adolescents with other serious psychiatric disturbance (mostly psychotic) and 20 normal adolescent controls. The age at scan ranged between 13 and 20 years. In the adolescents with a diagnosis of schizophrenia, total brain volume increased with age in a way that differed significantly ( p=0.007) from that seen in patients with other psychiatric disturbance and normal controls. Thus, brain growth, as assessed by this index, had reached a plateau in the control group by the age of 13 years, but this was not true of patients with schizophrenia. The measure that most clearly distinguished the groups ( p<0.001 after co-varying for height and sex) was the volume of the left lateral ventricle — the ventricle was significantly larger in patients with schizophrenic illness, and ventricular size increased with age to a greater extent in the patient group, although not significantly so, than in normal controls. Thus, aspects of brain growth are delayed in patients with early onset schizophrenia, and the greatest severity of illness is reflected in a component of growth that is lateralized to the dominant hemisphere. Individuals who develop serious psychiatric illness, including schizophrenia, represent a fraction of the population in whom a component of the relative development of the cerebral hemispheres occurs late.

Functional injury of cholinergic, GABAergic and dopaminergic systems in the basal ganglia of adult rat with kaolin-induced hydrocephalus

Structural and/or functional injury of the basal ganglia can lead to motor functional disabilities, abnormal gait and posture, and intellectual/emotional impairment, disorders also frequently seen in hydrocephalus. Previous reports have documented changes in dopamine levels in the neostriatum in experimental hydrocephalus. The present study was designed to investigate possible functional injury of cholinergic, GABAergic and dopaminergic systems in the basal ganglia immunohistochemically in a model of kaolin-induced hydrocephalus. Hydrocephalus was induced in 12 Wistar rats by intracisternal injection of 0.05 ml volume of 25% kaolin solution under microscopic guidance. Four controls received an equal volume of sterile saline. The animals were killed at 2, 4 and 8 weeks after injection. The numbers of choline acetyltransferase (ChAT)- and glutamic acid decarboxylase (GAD)-immunoreactive (IR) neostriatal neurons and tyrosine hydroxylase (TH) – IR nigral neurons, were counted in 60-μm thick representative sections and the IR cellular densities (counted cell number/neostriatal area) were calculated in the neostriatum. The number of total neostriatal neurons was also counted in 15-μm thick sections stained by cresyl violet (Nissl staining) to calculate the cellular density. The number and cellular density of neostriatal ChAT-IR neurons were significantly reduced at 2, 4, and 8 weeks after injection ( P<0.05), while those of GAD-IR neurons decreased at 4 and 8 weeks ( P<0.05). There was a linear correlation between degree of ventricular enlargement, and reduction in number of ChAT- and GAD-IR neurons ( P<0.001) as well as in the cellular density ( P<0.001). However, Nissl staining revealed no reduction in the cellular density of total neostriatal neurons ( P<0.001). TH immunoreactivity was reduced in neostriatal axons and in nigral compacta neurons, particularly in the medial portion of the dopaminergic nigrostriatal pathway. These findings suggest that progressive hydrocephalus results in functional injuries of cholinergic and GABAergic neurons in the neostriatum and dopaminergic neurons in the substantia nigra compacta by mechanical distortion. The disturbance in balance of these neurotransmitter systems in the basal ganglia may explain some of motor functional disabilities in hydrocephalus.

Correlates of leukoaraiosis and ventricular enlargement on magnetic resonance imaging: a study in normal elderly and cerebrovascular patients

Several studies have repeatedly demonstrated that leukoaraiosis as well as ventricular enlargement are common findings in normal elderly and in stroke patients, although there is no general consensus on prevalence rate as well as on their clinical correlations. It is also controversial whether white matter changes and ventricular enlargement are reciprocally related. In this study we investigated the prevalence and extent of white matter hyperintensities and the degree of ventricular enlargement on magnetic resonance imaging in 50 normal elderly individuals (mean age 62.1 ± 7.3 years) and in 50 consecutive chronic ischemic stroke patients (mean age 66.1 ± 7.7 years). All subjects underwent extensive clinical assessment. White matter hyperintensities were graded from 0 to 3 on a semi-quantitative scale, while bifrontal horn, bicaudate, and third ventricle ratio indices were used as measures of brain atrophy. Hypertension, diabetes, alcohol consumption, cardiac disease, carotid pathology occurred significantly more often in patients than in controls. Prevalence rates of white matter hyperintensities were 30% in controls and 82% in patients. Patients had significantly larger ventricular indices than controls. Significant univariate correlations for the extent of white matter hyperintensities were found with age, sex, hypertension, cardiac disease, carotid pathology, diabetes, history of stroke and ventricular enlargement. Age, sex, cardiac disease, alcohol habit, cerebrovascular disease and extent of white matter hyperintensities correlated with severity of ventricular enlargement. Multivariate regression analysis identified age, hypertension and history of stroke as independent predictors of white matter hyperintensities, while history of stroke, age and alcohol consumption were found as the only independent predictors of ventricular enlargement Separate analysis between periventricular, subcortical or deep white matter hyperintensities and each of the three ventricular indices failed to show a significant association after adjustment for clinical and demographic factors. We suggest that leukoaraiosis and ventricular enlargement are independent pathological processes associated with different risk factors in addition to age and stroke disease.

Functional importance of ventricular enlargement and cortical atrophy in healthy subjects and alcoholics as assessed with PET, MR imaging, and neuropsychologic testing.

The authors assessed the relationship between ventricular enlargement, cortical atrophy, regional brain glucose metabolism, and neuropsychologic performance in 10 alcoholics and 10 control subjects. Regional brain glucose metabolism was measured with fluorine-18 fluorodeoxyglucose (FDG) and positron emission tomography (PET). Cortical atrophy and ventricular size were evaluated quantitatively with magnetic resonance (MR) imaging. Alcoholics had decreased brain glucose metabolism and more cortical atrophy but did not have significantly greater ventricular size than did control subjects. The degree of ventricular enlargement and of cortical atrophy was associated with decreased metabolism predominantly in the frontal cortices and subcortical structures in both alcoholics and control subjects. There were no significant correlations between neuropsychologic performance and MR imaging structural changes, whereas various subtest scores were significantly correlated with frontal lobe metabolism. These data show that F-18 FDG PET is a sensitive technique for detecting early functional changes in the brain due to alcohol and/or aging before structural changes can be detected with MR imaging.

Effects of fructose loading in streptozotocin-diabetic and nondiabetic rats.

The present study compares the cardiovascular consequences of a 6-week fructose feeding in nondiabetic and streptozotocin-diabetic rats. Myocardial performance of these animals was determined using the isolated perfused working heart preparation. Systolic blood pressure, pulse rate, ventricular weight/body weight ratio, and plasma levels of glucose, insulin, triglycerides, and cholesterol were measured. In nondiabetic rats, fructose drinking caused significant increases in blood pressure, pulse rate, and plasma concentrations of insulin and triglycerides. Streptozotocin-diabetic animals exhibited significantly less body weight growth, slower pulse rate, higher plasma levels of cholesterol and triglycerides, ventricular enlargement, and functional impairment of the myocardium. The fructose-loaded diabetic rats had larger increases in plasma cholesterol and triglycerides than did control fructose-fed rats, but the fructose-induced increases in blood pressure and pulse rate were attenuated significantly. However, plasma levels of glucose and insulin and the degree of ventricular enlargement and myocardial dysfunction were not significantly different from those of control diabetic rats. These results show that fructose loading for 6 weeks can cause increases in blood pressure, pulse rate, and plasma lipids in both nondiabetic and diabetic rats. However, fructose ingestion does not significantly alter glycemic control or affect the development of myocardial dysfunction in streptozotocin-diabetic rats.

Myocardial performance of STZ-diabetic DOCA-hypertensive rats.

Myocardial performance of streptozotocin (STZ)-diabetic deoxycorticosterone acetate (DOCA)-hypertensive rats was examined using the isolated working heart apparatus at various time periods after induction of the experimental diseases. Blood pressure, pulse rate, and plasma levels of glucose, insulin, cholesterol, and triglycerides, as well as ventricular weight-to-body weight ratio, were also determined. In nondiabetic rats it was found that DOCA hypertension was associated with an increase in plasma cholesterol, a decrease in circulating insulin level, lower weight gain, and ventricular enlargement compared with control rats. Diabetic rats developed myocardial dysfunction in a time-dependent manner and exhibited hyperglycemia, hypoinsulinemia, bradycardia, and ventricular enlargement. Compared with the normotensive diabetic animals, STZ-diabetic DOCA-hypertensive rats showed a similar magnitude of myocardial dysfunction and a greater degree of ventricular enlargement, but significantly less severe hyperglycemia. It is concluded that DOCA-induced hypertension does not aggravate the severity of myocardial dysfunction developed in STZ-diabetic rats. It is also suggested that DOCA may have an action on glucose metabolism either directly or via an effect on insulin secretion.

Brain imaging in late‐onset schizophrenia and related psychoses

AbstractIn this article we review the published studies on brain imaging in late‐life psychoses, and present data from our study of magnetic resonance (MR) imaging of the brain in late‐onset schizophrenia (LOS). MR images were obtained in 11 patients with late‐onset schizophrenia (LOS), nine patients with probable Alzheimer's disease (AD), and nine normal controls comparable in age, gender, and education. Two of the LOS patients were excluded from further analysis due to the presence of diagnosable organic pathology (i.e. Alzheimer's disease and presence of a subaracnoid cyst). The MR images were subjectively rated for both degree of ventricular enlargement (VE) and degree of abnormal white matter hyperintensities (WHM) by an experienced, board certified neuroradiologist in a blind manner. No significant differences were found among the groups on degree of abnormal WHM. MR images of AD patients had a significantly greater degree of VE than normal controls, with LOS patients being intermediate. Our data, for LOS and have evidence of non‐specific abnormalities in brain morphology on MR imaging, yet do not have clinical or MR imaging evidence of a specific organic etiology for psychosis.

Intellectual sequelae of primary non-obstructive hydrocephalus in infancy: Analysis of 50 cases

In 50 cases of primary non-obstructive nonprogressive hydrocephalus in infancy, possibilities of predicting later intelligence were investigated. The mean IQ was 80 ± 24; in 50% of the cases IQ was normal, in 22% between 85 and 55 and in 28% below 55. The occipitofrontal circumference and the degree of ventricular enlargement had no correlation with the intellectual outcome in the children. Most prognostic value on the IQ had the age when reaching the developmental milestones, the degree of motor disability and the number of minor malformations. As there was no relation between the degree of hydrocephalus and the intellectual impairment, the conclusion can be made that associated anomalies of the CNS and defects in the cyto-architecture of the neocortex are more important factors in explaining mental retardation in cases of hydrocephalus.

Correlation between regional cerebral blood flow and brain atrophy in dementia. Combined study with 133Xenon inhalation and computerised tomography.

Measurement of the regional cerebral blood flow (rCBF) by the 133Xenon inhalation method and computerised tomography were performed in 25 patients with presenile and senile dementia. Reduction of rCBF and various degrees of ventricular enlargement and cortical sulcal widening were demonstrated in the majority of demented subjects. However, there was no correlation between rCBF values and the severity of ventricular dilatation or cortical atrophy. These findings suggest that loss of brain substance is not an important factor in the reduction of rCBF in dementia.