Cerebral Ventricular Enlargement Research Articles

Phase-contrast magnetic resonance imaging in evaluation of hydrocephalus in pediatric patients

BackgroundHydrocephalus is an increase in cerebrospinal fluid volume leading to cerebral ventricular enlargement (ventriculomegaly). Phase-contrast magnetic resonance imaging is a sensitive technique to cerebrospinal fluid flow allowing noninvasive quantitative and qualitative evaluation of cerebrospinal fluid flow.AimThe purpose of our study was to assess the role of cerebrospinal fluid flowmetry using phase-contrast magnetic resonance imaging in evaluation of hydrocephalus in pediatric patients.MethodsThis prospective study included a group of 50 patients with ventriculomegaly diagnosed by a previous magnetic resonance imaging study. A control group of 20 subjects of matched age group were also included. All the participants were subjected to cerebrospinal fluid flow study.ResultsAfter quantitative assessment of cerebrospinal fluid flow at aqueduct level, the mean values of flow and velocity parameters were compared in both patients and control groups. The mean values in patients with aqueduct stenosis and Dandy–Walker malformation were significantly lower than those of the control group (no flow with hypodynamic circulation) with p < 0.001, < 0.017 for mean velocity, respectively, the mean values in patients with brain atrophy and Arnold–Chiari malformation, bilateral obstructive hydrocephalus at foramen of Monro were significantly lower than those of the control group (diminished flow with hypodynamic circulation) with p < 0.001, < 0.001, 0.046 for mean velocity, respectively, and 0.002, 0.001, 0.160 for stroke volume, respectively, the mean values in patients with communicating hydrocephalus and unilateral obstructive hydrocephalus at foramen of Monro were significantly higher than those of the control group (hyperdynamic flow) with p < 0.001 for mean velocity and stroke volume, and the mean values in patients with arachnoid cysts were within normal as compared to control group (normal dynamic flow).ConclusionPhase-contrast magnetic resonance imaging is a noninvasive technicality used for evaluation of cerebrospinal fluid flow both qualitatively and quantitatively for determining the type of hydrocephalus seen.

Kidins220 deficiency causes ventriculomegaly via SNX27-retromer-dependent AQP4 degradation

Several psychiatric, neurologic and neurodegenerative disorders present increased brain ventricles volume, being hydrocephalus the disease with the major manifestation of ventriculomegaly caused by the accumulation of high amounts of cerebrospinal fluid (CSF). The molecules and pathomechanisms underlying cerebral ventricular enlargement are widely unknown. Kinase D interacting substrate of 220 kDa (KIDINS220) gene has been recently associated with schizophrenia and with a novel syndrome characterized by spastic paraplegia, intellectual disability, nystagmus and obesity (SINO syndrome), diseases frequently occurring with ventriculomegaly. Here we show that Kidins220, a transmembrane protein effector of various key neuronal signalling pathways, is a critical regulator of CSF homeostasis. We observe that both KIDINS220 and the water channel aquaporin-4 (AQP4) are markedly downregulated at the ventricular ependymal lining of idiopathic normal pressure hydrocephalus (iNPH) patients. We also find that Kidins220 deficient mice develop ventriculomegaly accompanied by water dyshomeostasis and loss of AQP4 in the brain ventricular ependymal layer and astrocytes. Kidins220 is a known cargo of the SNX27-retromer, a complex that redirects endocytosed plasma membrane proteins (cargos) back to the cell surface, thus avoiding their targeting to lysosomes for degradation. Mechanistically, we show that AQP4 is a novel cargo of the SNX27-retromer and that Kidins220 deficiency promotes a striking and unexpected downregulation of the SNX27-retromer that results in AQP4 lysosomal degradation. Accordingly, SNX27 silencing decreases AQP4 levels in wild-type astrocytes whereas SNX27 overexpression restores AQP4 content in Kidins220 deficient astrocytes. Together our data suggest that the KIDINS220-SNX27-retromer-AQP4 pathway is involved in human ventriculomegaly and open novel therapeutic perspectives.

Brain ventricular enlargement in human and murine acute intermittent porphyria.

The morphological changes that occur in the central nervous system of patients with severe acute intermittent porphyria (AIP) have not yet been clearly established. The aim of this work was to analyze brain involvement in patients with severe AIP without epileptic seizures or clinical posterior reversible encephalopathy syndrome, as well as in a mouse model receiving or not liver-directed gene therapy aimed at correcting the metabolic disorder. We conducted neuroradiologic studies in 8 severely affected patients (6 women) and 16 gender- and age-matched controls. Seven patients showed significant enlargement of the cerebral ventricles and decreased brain perfusion was observed during the acute attack in two patients in whom perfusion imaging data were acquired. AIP mice exhibited reduced cerebral blood flow and developed chronic dilatation of the cerebral ventricles even in the presence of slightly increased porphyrin precursors. While repeated phenobarbital-induced attacks exacerbated ventricular dilation in AIP mice, correction of the metabolic defect using liver-directed gene therapy restored brain perfusion and afforded protection against ventricular enlargement. Histological studies revealed no signs of neuronal loss but a denser neurofilament pattern in the periventricular areas, suggesting compression probably caused by imbalance in cerebrospinal fluid dynamics. In conclusion, severely affected AIP patients exhibit cerebral ventricular enlargement. Liver-directed gene therapy protected against the morphological consequences of the disease seen in the brain of AIP mice. The observational study was registered at Clinicaltrial.gov as NCT02076763.

A fetal case of microphthalmia and limb anomalies with abnormal neuronal migration associated with SMOC1 biallelic variants

Microphthalmia with limb anomalies (MLA, OMIM, 206920) is a rare autosomal-recessive disease caused by biallelic pathogenic variants in the SMOC1 gene. It is characterized by ocular disorders (microphtalmia or anophtalmia) and limb anomalies (oligodactyly, syndactyly, and synostosis of the 4th and 5th metacarpals), variably associated with long bone hypoplasia, horseshoe kidney, venous anomalies, vertebral anomalies, developmental delay, and intellectual disability.Here, we report the case of a woman who interrupted her pregnancy after ultrasound scans revealed a depression of the frontal bone, posterior fossa anomalies, cerebral ventricular enlargement, cleft spine involving the sacral and lower-lumbar vertebrae, and bilateral microphthalmia. Micrognathia, four fingers in both feet and a slight tibial bowing were added to the clinical picture after fetal autopsy. Exome sequencing identified two variants in the SMOC1 gene, each inherited from one of the parents: c.709G>T - p.(Glu237*) on exon 8 and c.1223G>A - p.(Cys408Tyr) on exon 11, both predicted to be pathogenic by different bioinformatics software. Brain histopathology showed an abnormal cortical neuronal migration, which could be related to the SMOC1 protein function, given its role in cellular signaling, proliferation and migration. Finally, we summarize phenotypic and genetic data of known MLA cases showing that our case has some unique features (Chiari II malformation; focal neuropathological alterations) that could be part of the variable phenotype of SMOC1-associated diseases.

Quantitation of specific binding ratio in 123I-FP-CIT SPECT: accurate processing strategy for cerebral ventricular enlargement with use of 3D-striatal digital brain phantom.

This study aimed to evaluate the effect of ventricular enlargement on the specific binding ratio (SBR) and to validate the cerebrospinal fluid (CSF)-Mask algorithm for quantitative SBR assessment of 123I-FP-CIT single-photon emission computed tomography (SPECT) images with the use of a 3D-striatum digital brain (SDB) phantom. Ventricular enlargement was simulated by three-dimensional extensions in a 3D-SDB phantom comprising segments representing the striatum, ventricle, brain parenchyma, and skull bone. The Evans Index (EI) was measured in 3D-SDB phantom images of an enlarged ventricle. Projection data sets were generated from the 3D-SDB phantoms with blurring, scatter, and attenuation. Images were reconstructed using the ordered subset expectation maximization (OSEM) algorithm and corrected for attenuation, scatter, and resolution recovery. We bundled DaTView (Southampton method) with the CSF-Mask processing software for SBR. We assessed SBR with the use of various coefficients (f factor) of the CSF-Mask. Specific binding ratios of 1, 2, 3, 4, and 5 corresponded to SDB phantom simulations with true values. Measured SBRs > 50% that were underestimated with EI increased compared with the true SBR and this trend was outstanding at low SBR. The CSF-Mask improved 20% underestimates and brought the measured SBR closer to the true values at an f factor of 1.0 despite an increase in EI. We connected the linear regression function (y = - 3.53x + 1.95; r = 0.95) with the EI and f factor using root-mean-square error. Processing with CSF-Mask generates accurate quantitative SBR from dopamine transporter SPECT images of patients with ventricular enlargement.

Uncommon runs of homozygosity disclose homozygous missense mutations in two ciliopathy-related genes (SPAG17 and WDR35) in a patient with multiple brain and skeletal anomalies

We describe a patient severely affected with multiple congenital anomalies, including brain malformations and skeletal dysplasia suggestive of cranioectodermal dysplasia (CED) ciliopathy, who unusually carries several homozygosity tracts involving homozygous missense mutations in SPAG17 (exon 8; c.1069G > C; p.Asp357His) and WDR35 (exon 13; c.1415G > A; p.Arg472Gln) as revealed by homozygosity mapping and next generation sequencing. SPAG17 is essential for the function and structure of motile cilia, while WDR35 belongs to the same intraflagellar transport (IFT) gene family whose protein products are part of functional IFT A and B complexes. Formerly, SPAG17 was related – through polymorphic variants – to an influence on individuals’ height; more recently, Spag17−/− mice models were reported to present skeletal and bone defects, reduced mucociliary clearance, respiratory distress, and cerebral ventricular enlargement. Homozygous or compound heterozygous mutations in WDR35 have mainly been related to CED2 or short-rib thoracic dysplasia 7, with only three cases showing some brain anomalies. Given that our patient presents these clinical features and the close functional relationship between SPAG17 and WDR35, it is feasible that the combined effects from both mutations contribute to his phenotype. To our knowledge, this patient is the first to harbor a likely pathogenic homozygous mutation in both genes at the same time. Thus, the resulting complex phenotype of this patient illustrates the heterogeneity associated with ciliopathies and further expands the clinical and mutational spectrum of these diseases. Finally, we highlight the combined use of high-throughput tools to diagnose and support the proper handling of this and other patients.

Case report Klinefelter syndrome and multiple sclerosis as the cause of psychosis

Introduction and goalsForty-three-year-old male diagnosed with Klinefelter syndrome and showing radiological findings suggesting a demyelinating pathology who presents several psychiatric manifestations including megalomaniacal ideation, delusion, lack of impulse control and behavioral alterations.Clinical caseForty-three-year-old male diagnosed with Klinefelter syndrome at the age of 31, presenting several psychiatric pathologies since adolescence: delusions, megalomania, mood fluctuation, and high impulsiveness. The patient had a poor therapeutic response to anti-psychotic drugs and ECT. He was hospitalized up to 9 times, but the full control of the symptomatology was not achieved. During his last hospitalization, a MRI revealed lesions compatible with a demyelinating pathology.DiscussionA higher prevalence of schizophrenia spectrum disorders has been described among patients suffering from Klinefelter syndrome, which might explain the role of the X chromosome in the susceptibility to psychiatric disorders, particularly to psychosis. Furthermore, the brain structure alterations presented by patients suffering from Klinefelter syndrome are similar to those described among schizophrenic patients: small brain volume, lateral cerebral ventricular enlargement and reduced temporal gyrus, amygdala, insula and cingulate cortex. Patients suffering from multiple sclerosis are more prone to psychiatric disorders, such as mood swing, aggressiveness or psychosis, which are not concurrent with the physical progression of the disease, sometimes being its first manifestation. Even when being patchy and multifocal, demyelination seems to be concentrated in the frontal lobes, related to the cognitive and affective functions and the personality.ConclusionsBoth multiple sclerosis and Klinefelder syndrome may alter the brain structure, mainly in the frontal lobe, and predispose to psychiatric disorders.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Normal Width of Third Ventricle In Nepalese Population: Assessment By CT Scan

Cerebral ventricular enlargement occurs as a natural aging process but also has been associated with many neurological disorders. Whether this enlargement is primary or secondary to these pathological conditions remains controversial. Objective of the study was to tabulate and create normal references values for maximum width of third ventricle in Nepalese population according to age group and gender. MTW was determined in two hundred (112 males and 88 females) and age ranging between 1- 93 years who had normal Computed tomography scan of the head .The data collected was analyzed with statistical program IBM SPSS version 20. Measurements of MTW in both males and females of the normal groups revealed no significant difference. No significant difference in MTW was noticed till the age of 49 years. Significant differences were noticed between 49 - 93 years of age. This study corroborated well with normal MTW values published in literatures from other parts of the world. However normal values specific to our local population becomes more relevant in interpreting CT scan of head in Nepal.

Cortical Overgrowth in Fetuses With Isolated Ventriculomegaly

Mild cerebral ventricular enlargement is associated with schizophrenia, autism, epilepsy, and attention-deficit/hyperactivity disorder. Fetal ventriculomegaly is the most common central nervous system (CNS) abnormality affecting 1% of fetuses and is associated with cognitive, language, and behavioral impairments in childhood. Neurodevelopmental outcome is partially predictable by the 2-dimensional size of the ventricles in the absence of other abnormalities. We hypothesized that isolated fetal ventriculomegaly is a marker of altered brain development characterized by relative overgrowth and aimed to quantify brain growth using volumetric magnetic resonance imaging (MRI) in fetuses with isolated ventriculomegaly. Fetal brain MRI (1.5 T) was performed in 60 normal fetuses and 65 with isolated ventriculomegaly, across a gestational age range of 22-38 weeks. Volumetric analysis of the ventricles and supratentorial brain structures was performed on 3-dimensional reconstructed datasets. Fetuses with isolated ventriculomegaly had increased brain parenchyma volumes when compared with the control cohort (9.6%, P < 0.0001) with enlargement restricted to the cortical gray matter (17.2%, P = 0.002). The extracerebral cerebrospinal fluid and third and fourth ventricles were also enlarged. White matter, basal ganglia, and thalamic volumes were not significantly different between cohorts. The presence of relative cortical overgrowth in fetuses with ventriculomegaly may represent the neurobiological substrate for cognitive, language, and behavioral deficits in these children.

Current status of transcranial color duplex ultrasound in the adult

Technical improvements accomplished over the last few years allow imaging of intracranial parenchymal structures as well as of basal cerebral arteries by ultrasound. Low frequency probes (2-2.5 MHz) and colour Doppler technology are required for these examinations. Recent experience in clinical practice proves that perfusion patterns in basal cerebral arteries can be depicted more accurately and with better reproducibility compared to conventional transcranial Doppler sonography. Simultaneous B-Mode imaging allows detection of cerebral haemorrhage, brain tumours and ventricular enlargement. Preliminary data on the sensitivity and specificity are promising and encourage further prospective studies.

Partial Trisomy of 7q: Case Report and Literature Review

This case describes a boy with pure partial trisomy of the long arm of chromosome 7. The only prenatal finding on the boy was cerebral ventricular enlargement. After birth, mild facial dysmorphic features and cardiac malformations (pulmonary valve dysplasia, interatrial and interventricular septal defects) were detected. The boy developed severe psychomotor retardation, failure to thrive, and poor interaction with the environment. Focal seizures occurred in the neonatal period. Left frontotemporal abnormalities were observed in the subsequent electroencephalograms. An area of subependymal nodular heterotopia in the right frontal region was detected. Eighteen cases of 7q pure trisomy have been described in the literature over the years. The present study confirms that, in 7q trisomy cases, there are several common, yet nonspecific, features: macrocephaly, frontal bossing, failure to thrive, psychomotor delay, low-set ears, short neck, and genital-urinary tract abnormalities. Shortened life span seems associated only with duplication of the entire arm, and correlation phenotype-genotype seems questionable.

Validation of linear cerebral atrophy markers in multiple sclerosis

Linear measures of cerebral ventricular enlargement may act as surrogate measures of cerebral atrophy in multiple sclerosis (MS). Linear atrophy markers were measured from routine MRI scans during a population survey of 171 Tasmanian MS patients and 91 healthy controls. Thirty-five Victorian MS clinic patients were recruited as a validation cohort with 14 of these re-assessed 4 years later. In the population survey, we measured three linear brain atrophy markers: inter-caudate distance (ICD), third ventricle width (TVW) and frontal horn width (FHW). TVW (OR 2.0, p = 0.001) and ICD (OR 16.1, p < 0.001) differentiated between MS cases and controls. In the validation study, we correlated the intercaudate ratio (ICR = ICD/brain width) and third ventricular ratio (TVR = TVW/brain width) with brain parenchymal volume. Cross-sectionally, ICR ( R = −0.453, p < 0.01) and TVR ( R = −0.653, p < 0.01) were correlated with brain parenchymal volume. Longitudinally, brain parenchymal volume loss was inversely correlated with increased ICD ( R = −0.77, p < 0.01) and TVW ( R = −0.71, p < 0.01). This study shows that ICD measurements obtained from clinical MRI scans are valid brain atrophy measures for use in monitoring MS progression.

Brain morphological abnormality in schizophrenia is independent of country of origin.

The disorder schizophrenia has a worldwide prevalence of 1% and is generally associated with lateral cerebral ventricular enlargement. Whether there is a relationship between these two findings is unclear but has aetiological relevance. Consecutively admitted Chinese patients (n = 19) with first episode of schizophrenia and healthy community volunteers (n = 29) underwent magnetic resonance imaging brain scan. The groups were balanced for age, sex, best social class and handedness. These patients were similar on clinical and socio-demographic indices to those who declined participation (n = 15). Semi-automated volumetric analysis of whole brain volume, cortical grey matter, cerebrospinal fluid, sulci and lateral ventricles was performed. Chinese patients in their first episode of schizophrenia have significant enlargement of lateral ventricles. Brain morphological abnormality in schizophrenia is present regardless of the country of origin. The importance of genes in driving normal brain development and stable prevalence suggests that aetiology may favour genes over environment.

Neurotoxicity, neuroplasticity, and magnetic resonance imaging morphometry: what is happening in the schizophrenic brain?

In an era of dramatic discoveries in neuroscience and genetics, it is likely that many popular theories and formulations about mental illness will need to be revised, if not discarded. The “neurodevelopmental hypothesis” is one of the popular theories about the origins of schizophrenia, which posits that abnormalities of early brain development increase risk for the subsequent emergence of the clinical syndrome. 1-3 An early piece of evidence in support of this hypothesis was the apparent lack of progression of cerebral ventricular enlargement observed with computed tomography during illness. 4-9 An important assumption of the neurodevelopmental hypothesis is that the putative primary pathologic condition of the brain is a reflection of abnormalities of early development. The neurodevelopmental hypothesis thus assumes that developmental neuropathologic conditions should arrest early in life and not continue to progress. The computed tomography results showing no apparent progression seemed consistent with this assumption. However, a recent series of magnetic resonance imaging (MRI) studies has called into question this assumption, by revealing changes in measurements of brain structures over short periods in patients who have been ill for varying durations and at various stages of life. These recent studies 10-14 have generated enthusiasm for a “neurodegenerative hypothesis,” harkening back to proposals of Kraepelin and other neuropathologists during the first quarter of the 20th century that there is destruction of neural tissue associated with psychosis. In fact, results of MRI measurements have been cited as support for a much broader conceptual revolution in psychiatry, a “neurotoxicity hypothesis” for many psychiatric illnesses, including affective disorders 15,16 and anxiety and stress disorders 17-19 and even jet lag. 20 This recent trend has been bolstered by basic discoveries about the adaptability of neuronal connections 21 and the viability and reproducibility of neurons in the adult brain (eg, apoptosis and neurogenesis). 22,23 These developments have led some to opine that the neurodegenerative hypothesis of schizophrenia may have been unjustly overshadowed by the ascendancy of the neurodevelopmental hypothesis. 24

Does schizophrenia result from developmental or degenerative processes?

The debate as to whether schizophrenia is a neurodevelopmental or a neurodegenerative disorder has its roots in the latter part of the 19th century when authorities such as Clouston (1891) posited that at least some insanities were "developmental" in origin. These views were soon eclipsed by Kraepelin's (1896) concept of dementia praecox as a degenerative disease, and the latter view carried not only the day but also much of the 20th century. Then, in the 1980s several research groups again began to speculate that schizophrenia might have a significant developmental component (Feinberg, 1982-1983; Schulsinger et al., 1984; Murray et al., 1985; Murray and Lewis, 1987; Weinberger et al., 1987). What became known as the "neurodevelopmental hypothesis" received support from neuropathological studies implicating anomalies in early brain development such as aberrant migration of neurons. Unfortunately, these studies proved difficult, if not impossible, to replicate (Harrison, 1999). The pendulum, therefore, began to swing again, and in the latter part of the 1990s came renewed claims that the clinical progression of the illness was accompanied by continued cerebral ventricular enlargement and reduction in the volumes of certain brain structures. Nevertheless, since few doubt that there is a developmental component to schizophrenia, the question which we will address in this paper is whether schizophrenia is a) simply the final consequence of a cascade of increasing developmental deviance (Bramon et al., 2001), or b) whether there is an additional brain degeneration following onset of psychosis which is superimposed on the developmental impairment (Lieberman, 1999).

Cerebral ventricular enlargement as a generalized feature of schizophrenia: a distribution analysis on 502 subjects

Enlargement of cerebral ventricles is one of the most replicated biological features, and the one quantitatively most deviant in schizophrenia. It occurs in the early phases of the disease and may have pathogenetic relevance. Whether this abnormality is limited to a specific subgroup of patients or is a common feature to most or all patients affected by schizophrenia, however, is still a matter of debate. The answer to this question would improve our comprehension of the nature of this abnormality and contribute to the debate between the competing hypotheses of biological homogeneity vs heterogeneity of schizophrenia. We performed a distribution analysis of lateral ventricular dimensions of 340 schizophrenic patients and 162 non-psychiatric controls. All subjects underwent cerebral computerized tomographic scan, and ventricular dimensions were expressed as ventricular brain ratio (VBR). After removing the effect of confounding variables (age, sex and type of scanner) on individual VBR, data were power-transformed and different distribution hypotheses were tested by means of the maximum log-likelihood ratio method. Our findings indicate that, in the mixed sample of patients and controls, a mixture of two gaussian curves represents the distribution better than a single gaussian curve, but no evidence emerged leading to rejection of the normality hypothesis in the schizophrenic patients sample. Lateral ventricular enlargement in schizophrenia is not a marker of a discrete subgroup of schizophrenia, but occurs in most, if not all, schizophrenic patients. This supports the hypothesis of biological homogeneity of the disease, at least relative to its major brain morphological abnormality.

Defining the course of brain structural change and plasticity in schizophrenia

Recent evidence from controlled CT and MRI longitudinal studies suggests that some cerebral ventricular enlargement and hemispheric volumetric reductions (e.g. cerebral atrophy) may have a progressive component in patients with schizophrenia. These studies vary in cohort composition, stage of illness examined, duration of follow-up interval, imaging techniques used, and specific brain regions with findings. They also conflict with earlier evidence suggesting that schizophrenia is a neurodevelopmental disorder with brain pathological deviance occurring prior to the illness onset. The newer brain imaging reports may be detecting subtle brain plasticity that results from a continuing cortical disruptive process, may be epi-phenomena caused by scanning and image analysis artifacts or may possibly reflect systemic physiological fluctuations. Future longitudinal studies of subjects at all stages of illness using a variety of new technologies are needed to clarify these findings.

Time course of cerebral ventricular enlargement in schizophrenia supports the hypothesis of its neurodevelopmental nature

In the absence of direct and conclusive data demonstrating the ‘neurodevelopmental hypothesis’ of schizophrenia, several neuromorphological findings provide relevant clues in support of it. In this paper, we review a number of results obtained by our group in this area of research. In particular, the demonstration of stability of cerebral ventricular dimensions both in chronic schizophrenia and around the onset of the disease, and that of an identical effect of ageing on this morphological feature in large samples of patients and controls, strongly support the neurodevelopmental nature of brain pathomorphology in schizophrenia.

De ontwikkelingsneurologische theorie van schizofrenie: bewijsmateriaal betreffende structuur en neuropsychologic.

Severe schizophrenics as a group show subtle abnormalities of cerebral structure. Cerebral ventricular enlargement is the best replicated finding, and this tends to be associated with impairment of neuropsychological performance. The idea that these abnormalities have a neurodevelopmental origin gains indirect support from the, admittedly less consistent, evidence of abnormalities of cerebral asymmetry and of neuronal migration in adult schizophrenics, as well as from the behavioural, psychomotor, and cognitive impairments reported in preschizophrenic children. However, the relationship between childhood and adult neuropsychological and brain structural findings has not been proven, and we do not know whether only some schizophrenics have a developmental origin, or whether patients differ only in the degree of developmental impairment that they show.

Reversibility of cerebral ventricular enlargement in anorexia nervosa, demonstrated by quantitative magnetic resonance imaging

OBJECTIVE: To determine the reversibility of the loss of brain parenchyma and ventricular enlargement in patients with anorexia nervosa after refeeding. STUDY DESIGN: Quantitative magnetic resonance imaging was performed on three groups of subjects: (1) 12 female adolescents hospitalized with anorexia nervosa, (2) the same 12 patients after nutritional rehabilitation, a mean of 11.1 months later, and (3) 12 healthy age-matched control subjects. Sixty-four contiguous coronal magnetic resonance images, 3.1 mm thick, were obtained. With a computerized morphometry system, lateral and third ventricular volumes were measured by a single observer unaware of the status of the patient. RESULTS: On admission, patients were malnourished and had lost an average of 11.7 kg (body mass index, 14.3 ± 2.0 kg/m 2). After refeeding, they gained an average of 9.7 kg (body mass index, 17.9 ± 1.5 kg/m 2). Total ventricular volume decreased from 17.1 ± 5.5 cm 3 on admission to 12.4 ± 3.0 cm 3 after refeeding ( p <0.01) and returned to the normal range. The degree of enlargement of the third ventricle was greater than that of the lateral ventricles. There was a significant inverse relationship between body mass index and total ventricular volume ( r = -0.63; p <0.05). CONCLUSION: In patients with anorexia nervosa, cerebral ventricular enlargement correlates with the degree of malnutrition and is reversible with weight gain during long-term follow-up. (J P EDIATR 1996;128:296-301)