Ventricle-brain Ratio Research Articles

Biomarkers for Psychosis: Are We There Yet? Umbrella Review of 1478 Biomarkers.

This umbrella review aims to comprehensively synthesize the evidence of association between peripheral, electrophysiological, neuroimaging, neuropathological, and other biomarkers and diagnosis of psychotic disorders. We selected systematic reviews and meta-analyses of observational studies on diagnostic biomarkers for psychotic disorders, published until February 1, 2018. Data extraction was conducted according to the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guidelines. Evidence of association between biomarkers and psychotic disorders was classified as convincing, highly suggestive, suggestive, weak, or non-significant, using a standardized classification. Quality analyses used the Assessment of Multiple Systematic Reviews (AMSTAR) tool. The umbrella review included 110 meta-analyses or systematic reviews corresponding to 3892 individual studies, 1478 biomarkers, and 392210 participants. No factor showed a convincing level of evidence. Highly suggestive evidence was observed for transglutaminase autoantibodies levels (odds ratio [OR] = 7.32; 95% CI: 3.36, 15.94), mismatch negativity in auditory event-related potentials (standardized mean difference [SMD] = 0.73; 95% CI: 0.5, 0.96), P300 component latency (SMD = -0.6; 95% CI: -0.83, -0.38), ventricle-brain ratio (SMD = 0.61; 95% CI: 0.5, 0.71), and minor physical anomalies (SMD = 0.99; 95% CI: 0.64, 1.34). Suggestive evidence was observed for folate, malondialdehyde, brain-derived neurotrophic factor, homocysteine, P50 sensory gating (P50 S2/S1 ratio), frontal N-acetyl-aspartate, and high-frequency heart rate variability. Among the remaining biomarkers, weak evidence was found for 626 and a non-significant association for 833 factors. While several biomarkers present highly suggestive or suggestive evidence of association with psychotic disorders, methodological biases, and underpowered studies call for future higher-quality research.

Risk factors, treatment, and outcome in dogs and cats with subdural hematoma and hemispheric collapse after ventriculoperitoneal shunting of congenital internal hydrocephalus.

Overshunting and hemispheric collapse are well-known complications after ventriculoperitoneal shunt (VPS) implantation. Risk factors that predispose to overshunting, treatment options, and prognosis after therapeutic intervention have not been described. To identify preoperative risk factors for overshunting, the effect of surgical decompression, and their outcomes. Seventy-five dogs and 7 cats. Retrospective case cohort study. Age, breed, sex, body weight, number of dilated ventricles, ventricle brain ratio, intraventricular pressure, and implanted pressure valve systems were evaluated as possible risk factors. Overshunting had a prevalence of 18% (Cl 95% 9.9-26.66). An increase of 0.05 in VBR increased the risk of overshunting by OR 2.23 (Cl 95% 1.4-3.5; P = .001). Biventricular hydrocephalus had the highest risk for overshunting compared to a tri- (OR 2.48 with Cl 95% 0.5-11.1) or tetraventricular hydrocephalus (OR 11.6 with Cl 95% 1.7-81.1; P = .05). There was no influence regarding the use of gravitational vs differential pressure valves (P > .78). Overshunting resulted in hemispheric collapse, subdural hemorrhage, and peracute deterioration of neurological status in 15 animals. Subdural hematoma was removed in 8 dogs and 2 cats with prompt postoperative improvement of clinical signs. Biventricular hydrocephalus and increased VBR indicate a higher risk for overshunting. The use of differential valves with gravitational units has no influence on occurrence of overshunting related complications and outcomes. Decompressive surgery provides a favorable treatment option for hemispheric collapse and has a good outcome.

Longitudinal evaluation of ventricular volume changes associated with mild traumatic brain injury in military service members

ABSTRACTPrimary objective: To investigate differences in longitudinal trajectories of ventricle-brain ratio (VBR), a general measure of brain atrophy, between Veterans with and without history of mild traumatic brain injury (mTBI).Research design: Structural magnetic resonance imaging (MRI) was used to calculate VBR in 70 Veterans with a history of mTBI and 34 Veterans without such history at two time points approximately 3 and 8 years after a combat deployment.Main outcomes and results: Both groups demonstrated a quadratic relationship between VBR and age that is consistent with normal developmental trajectories. Veterans with history of mTBI had larger total brain volume, but no interaction between mTBI and age was observed for brain volume, ventricular volume, or VBR.Conclusions: In our longitudinal sample of deployed Veterans, mTBI was not associated with gross brain atrophy as reflected by abnormally high VBR or abnormal increases in VBR over time.

Abstract 23: BDNF val 66 met Genotype is Associated With Greater Brain Atrophy After Stroke

Background: Genetic factors may be useful to understand differences in outcomes post-stroke. We studied an imaging measure of brain atrophy in relation to two genotypes that may be associated with differences in stroke recovery, the val 66 met genotype for brain-derived neurotrophic factor (BDNF) and the ApoE e4 genotype. Each genotype has been associated with brain atrophy in non-stroke populations. The current study hypothesized that each genotype is associated with brain atrophy after stroke. Methods: The ICARE Study examined behavioral outcomes after stroke in relation to motor therapies. Of 361 ICARE enrollees, genetic and neuroimaging data were available in 127. The volume of the ventricles and the brain were measured, and brain atrophy expressed as the Ventricle-Brain Ratio (VBR). For MRI scans, VBR was first extracted from the scans using ALVIN then manually refined. For CT scans, VBR was extracted manually. All VBR measurements were verified by a neuroimaging expert. VBR was examined in relation to the two genotypes of interest, BDNF val 66 met and ApoE e4, controlling for the 3 covariates employed in ICARE: motor deficits, enrollment site, and time post-stroke at study entry. Results: There were 61 MRI and 66 CT scans. These were acquired 5±11 days post-stroke, which did not vary according to either genotype. Median ventricle volume=26.1 cc; brain volume=1,163 cc; and VBR=0.024. The BDNF val 66 met genotype was present in 23 subjects; ApoE e4, in 41; both were in HW equilibrium. Presence of the BDNF val 66 met genotype was associated with greater atrophy: median VBR increased 1.97-fold when this genotype was present vs. absent (p=0.01), controlling for above covariates; and remained significant (p=0.04) when also controlling for age. This BDNF gene-imaging correlate did not extend to gene-behavioral findings. The ApoE e4 genotype was not related to VBR (p=0.88). Conclusions: Median degree of brain atrophy is 97% greater in patients with stroke when the BDNF val 66 met genotype is present, at least for the mild-moderately impaired subjects enrolled in ICARE. Understanding the biology of inter-subject differences in brain anatomy after stroke can provide insights into patient heterogeneity and inform efforts to individualize stroke recovery therapies.

Effect of acetazolamide and subsequent ventriculo-peritoneal shunting on clinical signs and ventricular volumes in dogs with internal hydrocephalus

BackgroundAcetazolamide is recommended for the reduction of cerebrospinal fluid production in canine internal hydrocephalus. The efficacy of the drug in terms of alleviation of the clinical symptoms and the restoration of normal ventricular volume has not been documented. We hypothesize that acetazolamide inadequately improve clinical signs and has no effect on the ventricular volume. Six dogs with internal hydrocephalus underwent neurological examination and were examined by magnetic resonance imaging, on the day of the diagnosis, after treatment with acetazolamide directly before surgery, and 6 weeks after implantation of a vetriculo-peritoneal shunt due to lack of improvement after medical therapy with 10 mg/kg acetazolamide three times daily (TID). The ventricular volume in relation to the total brain volume was determined on each occasion. The changes in relative ventricular volume and of the neurological status were assessed and compared.ResultsMcNemar’s test revealed no significant differences in clinical symptoms before and after medical treatment (P > 0.05). However, clinical symptoms changed significantly after surgical treatment (P = 0.001). The ventricle-brain ratio was not significantly changed after therapy with acetazolamide (P > 0.05); however, after subsequent shunt implantation, it was significantly reduced (P = 0.001).ConclusionAcetazolamide (10 mg/kg TID) showed no effects on clinical signs or ventricular volume in dogs with internal hydrocephalus. After subsequent ventriculo-peritoneal shunting, the dogs had a significantly reduced cerebral ventricular volume and five out of six dogs had no abnormal findings in neurological examination.

Prevalence, incidence, and risk factors of lacunar infarcts in a community sample

Lacunar infarcts are small cavitated lesions no larger than 2 cm in diameter. Although often asymptomatic, they have been suggested as an important pathologic substrate of vascular dementia. The prevalence and risk factor profile of lacunar infarction has been variously reported, but the incidence data are scarce for large community-based data. Participants (n = 477) were recruited randomly from the electoral roll of community residents aged 60-64 years as part of the PATH Through Life Study. Demographic information and risk factor data were collected and MRI brain scans performed in two waves, 4 years apart. The number and locations of lacunar infarcts as well as other volumetric data were assessed on T1-weighted and T2-weighted fluid-attenuated inversion recovery images. In wave 1, 37 (7.8%) participants had at least one lacunar infarct. New lacunar infarcts were detected in 6 (6/375, 1.6%) participants at wave 2. Lacunes present at wave 1 increased significantly in mean volume from 53.90 to 69.86 mm(3) over 4 years. Hypertension (odds ratio [OR] = 1.6; 95% confidence interval [CI] = 1.01-2.60), anterior ventricle-brain ratio (%) (OR = 1.02; CI = 1.003-1.036), and volume of white matter hyperintensities (OR = 4.9; CI = 1.53-15.80) were independently associated with the prevalence of lacunar infarction. Lacunes were common incidental findings in the brains of individuals in their 60s, and their prevalence as well as size increased with age. Hypertension was the major treatable risk factor, and lacunar infarction was usually associated with severe white matter hyperintensities on T2-weighted imaging.

Ventricle brain ratio in the clinical course of HIV infection

As part of the computerized tomographic assessment of an unselected group of 47 patients in different stages of HIV infection we determined the ventricle brain ratio (VBR) and the width of several cortical sulci. We compared the findings for subgroups of patients defined by their stage in the Walter Reed Staging Classification. There was a significant increase in VBR only in the subgroup of patients with manifest acquired immune deficiency syndrome (AIDS) (WR 6). The findings are discussed in connection with the question of the likelihood that dementia will develop even in stages of HIV-infection preceding AIDS.

P1-337: Incidental lacunar infarcts, brain atrophy and white matter hyperintensities in a community population: The path through life study

Lacunar infarcts, brain atrophy and white matter hyperintensities (WMH) were commonly found in the ageing brain and have been associated with cognitive decline. However, the relationship between these structural changes has not been adequately addressed in a community sample. A total of 477 participants were recruited by electoral roll from the community residents aged 60–64 years old. Lacunar infarct was defined as small cavitated lesions with a diameter range of 3–20mm. The lesions were characterised by hypointense foci in T1-weighted and FLAIR images, while surrounded by a hyperintense rim on the latter. The WMH were detected and measured quantitatively by an automated procedure, applying a set of in-house computer algorithms and programs. The volume of WMH is a relative value which indicates the ratio of WMH to the total WM. The volumes of hippocampus and amygdala were determined by manual tracing performed by two trained researchers in accordance with an established protocol. Thirty-seven (7.8 %) participants had at least one lacunar infarct on MRI images. Participants with lacunar infarction showed greater total WMH volumes (p = 0.006), including periventricular WMH (p = 0.005), deep white matter WMH (p = 0.010) and amount of severe WMH (p = 0.032). The lacunar infarct group had a higher ratio of anterior ventricle-brain ratio (VBR) and larger hippocampus volumes compared with the group without lacunar infarct. However, this difference did not exist if intracranial volume (ICV) was taken into account. WMHs (OR = 4.9; CI = 1.53 -15.80) contributed to the risk of lacunar infarct independent of hypertension. It is suggested that lacunar infarcts are association with WMH and this association was not eliminated by including the effect of hypertension in this study. The link between lacunar infarction and WMH may reflect similar ongoing vasculopathy in small vessel which is not entirely due to hypertension. There was no evidence that lacunar infarcts were associated with global brain atrophy or hippocampus volumetric changes.

Cerebral lateral ventricular asymmetry on CT: how much asymmetry is representing pathology?

The purpose of this study was to evaluate the association of asymmetric lateral ventricle (ALV) with clinical and structural pathologies and assess its clinical importance. We analyzed 170 consecutive ALV cases on computed tomography (CT) and 170 control group patients with normal head CT. Patients who had apparent etiologic causes for ALV were excluded. The differential diagnosis of ALV and unilateral hydrocephalus (UH) was made by using three different ventricle-brain ratios (VBRs). The measurements of the ALV were made at the frontal horn level. Patients with asymmetry were divided into three subgroups including mild, moderate and severe groups to eloborate the grade of the ventricular asymmetry. Additional CT findings including septal deviation, diffuse enlargement, atrophy and the densities of constant sites were also recorded systematically for each patient. Clinical and handedness data were collected and analyzed. The prevalence of ALV in the study population was 6.1%. Headache was the most common reason for head CT examination and was significantly more common in the asymmetry group (61.7% in group A, 42.9% in group B, P = 0.001). Transient ischemic attack, focal neurologic findings, vertigo, ataxia, visual and hearing disturbances were similar in both groups (P > 0.5). There was no difference in smoking and alcohol habits in both patient groups. Ten (5.8%) patients in group A and 16 (9.4%) patients in group B had neuropsychiatric disorders, which did not achieve statistical significance. In group A patients, the larger ventricle was more common in the left side than in the right (left = 70.0%, right = 30.0%). Group A consisted of 57.0% mild (grade 1, n = 97), 26.5% moderate (grade II, n = 45) and 16.5% severe (grade III, n = 28) patients. There was no significant correlation between handedness and ALV. The density of different brain sites was found close similar on both sides in ALV and control group (P > 0.5). Choroidal cystic or solid neoplasm or periventricular dysplasia was detected in six ALV patients in group A (3.5%), on their additional MR examinations. The physician should not overlook an ALV finding on unenhanced CT, particularly in cases with severe degree of asymmetry or diffuse ventricular enlargement, and search for possible accompanying disorders.

MRI-based brain volumetry in chronic whiplash patients: no evidence for traumatic brain injury

Cognitive complaints, such as poor concentration and memory deficits, are frequent after whiplash injury and play an important role in disability. The origin of these complaints is discussed controversially. Some authors postulate brain lesions as a consequence of whiplash injuries. Potential diffuse axonal injury (DAI) with subsequent atrophy of the brain and ventricular expansion is of particular interest as focal brain lesions have not been documented so far in whiplash injury. To investigate whether traumatic brain injury can be identified using a magnetic resonance (MR)-based quantitative analysis of normalized ventricle-brain ratios (VBR) in chronic whiplash patients with subjective cognitive impairment that cannot be objectively confirmed by neuropsychological testing. MR examination was performed in 21 patients with whiplash injury and symptom persistence for 9 months on average and in 18 matched healthy controls. Conventional MR imaging (MRI) was used to assess the volumes of grey and white matter and of ventricles. The normalized VBR was calculated. The values of normalized VBR did not differ in whiplash patients when compared with that in healthy controls (F = 0.216, P = 0.645). This study does not support loss of brain tissue following whiplash injury as measured by VBR. On this basis, traumatic brain injury with subsequent DAI does not seem to be the underlying mechanism for persistent concentration and memory deficits that are subjectively reported but not objectively verifiable as neuropsychological deficits.

Schizophrenia is a disorder of aberrant neurodevelopment: A synthesis of evidence from clinical and structural, functional and neurochemical brain imaging studies

Byline: Ganesan. Venkatasubramanian Schizophrenia as a Disorder of Aberrant Neurodevelopment Several reasons have been advanced to support the view that schizophrenia is a neurodevelopmental disorder.[sup] [1] The primary reason is that the onset of schizophrenia has a cumulative age incidence distribution or developmental function, that is nonlinear with a peak change in slope or acceleration that usually takes to occur during young adulthood. Given the plausibility of the existence of brain abnormalities in schizophrenia at the onset of the illness, it further seems reasonable to conceive the onset of schizophrenia as a neurodevelopmental disorder. Further support has been provided by epidemiological studies showing premorbid intellectual deficits dating back to the early development[sup] [2] and neuropathological studies showing altered cerebral cytoarchitecture indicative of a developmental rather that acquired encephalopathy.[sup] [3] The main neurodevelopmental hypotheses for schizophrenia set forth in the last 10 years are relatively restricted and share three assumptions:[sup] [4] *The primary pathogenetic defect is an early derangement of the orderly development of the central nervous system that occurs in the pre- or perinatal period; *The period of active operation of the causative agent is of short duration, meaning that it is essentially static; *The behavioral consequences of this static process remain relatively latent until long after the primary pathogenetic process has run its course. Furthermore, aspects of illness suggesting neurodevelopmental deviation may not apply to all individuals and some authors have argued for neurodevelopmental and non-neurodevelopmental subtypes of the disorder[sup] [5] and even neurodegenerative subtypes of the disorder.[sup] [6] However, neurodegenerative hypotheses of schizophrenia have been criticized mainly because of the following reason: gliosis, which is regarded as a necessary neuropathological hallmark of neuronal degeneration, has not been found in a number of carefully controlled postmortem studies in patients with schizophrenia. These neuropathological studies provide strong evidence against a classic neurodegenerative pathogenesis of schizophrenia.[sup] [1],[4] In addition, the failure of the first prospective CT studies of schizophrenia to show the same age-disproportionate progressive increase in ventricle-brain ratio after onset of illness that is seen in disorders such as Huntington's disease also rejects neurodegeneration.[sup] [4] Some researchers have proposed another alternative that schizophrenia is a progressive neurodevelopmental disorder. This postulates that developmental mechanisms, such as apoptosis and pruning, can continue to go awry over many years without resulting in excessive gliosis. This accounts for both the neuropathological findings implicating prenatal pathology and the imaging findings (especially the recent Magnetic Resonance Imaging studies that report evidence for progressive brain changes in schizophrenia).[sup] [4] Thus, although schizophrenia is argued by a few as a neurodegenerative disorder,[sup] [6],[7] majority of the existing evidence points towards a neurodevelopmental etiopathogenesis.[sup] [1],[4] Neurodevelopmental Hypothesis of Schizophrenia - Evidence Base The tenets of the neurodevelopmental hypothesis of schizophrenia derive from observations of epidemiological, clinical and brain imaging evidence for neurodevelopmental deviance.[sup] [8] These include studies on schizophrenia patients examining obstetrical complications, age-at-onset (AAO), sex differences, minor physical anomalies (MPAs), neurological soft signs (NSS) and structural brain abnormalities. Other stigmata include abnormal dermatoglyphics and childhood neuromotor precursors of adult schizophrenic illness. This research paper attempts at providing an overview of evidence for neurodevelopmental basis for schizophrenia with specific focus on highlighting relevant Indian studies supporting this concept. …

Magnetic resonance imaging study of the ventricle–brain ratio in parents of schizophrenia subjects

Structural abnormalities found in probands with schizophrenia have been reported to occur to some degree in their unaffected relatives. However, there has yet to be a study that has focused on brain changes of parents of schizophrenics who are not the presumed obligate carriers. Using MRI, the authors studied the ventricle–brain ratio (VBR) of 9 pairs of parents of schizophrenics and 18 age- and sex-matched healthy controls. VBRs of the unaffected parents of schizophrenics were significantly larger than those of the controls. Our results suggest that large VBRs aggregate in the parents of schizophrenics and may serve as an indicator of vulnerability to the disorder.

Ventricular enlargement in schizophrenia related to volume reduction of the thalamus, striatum, and superior temporal cortex.

Enlargement of the lateral ventricles is among the most frequently reported macroscopic brain structural changes in schizophrenia, although variable in extent and localization. The authors investigated whether ventricular enlargement is related to regionally specific volume loss. High-resolution magnetic resonance imaging scans from 39 patients with schizophrenia were analyzed with deformation-based morphometry, a voxel-wise whole brain morphometric technique. Significant negative correlations with the ventricle-brain ratio were found for voxels in the left and right thalamus and posterior putamen and in the left superior temporal gyrus and insula. Thalamic shrinkage, especially of medial nuclei and the adjacent striatum and insular cortex, appear to be important contributors to ventricular enlargement in schizophrenia.

Relationship between plasma homocysteine levels and brain atrophy in healthy elderly individuals.

The authors examined the association of total plasma homocysteine (Hcy) levels with measures of atrophy and white matter disease on MRI scans in 36 healthy elderly individuals. Hcy had a significant positive relationship with lateral ventricle-brain ratios in the anterior (r = 0.49) and middle (r = 0.43) ventricular regions as measures of central atrophy, but not with cortical atrophy or white matter hyperintensities. In a logistic regression analysis, elevated Hcy was a significant determinant of increased anterior ventricle-brain ratio (> or =0.34) after controlling for age, folate, B12, creatinine, and white matter disease (OR = 2.3; CI, 1.03-5.09).

Correlations of brain MRI parameters to disability in multiple sclerosis

The objective was to correlate magnetic resonance imaging (MRI) T2-weighted lesion load and measures of white matter atrophy in the brain to disability in a population-based sample of patients with multiple sclerosis (MS). A well defined cohort of patients was drawn at random from the general MS population by using the Danish Multiple Sclerosis Registry. A semi-automated local thresholding technique was used to quantify T2-weighted lesions on MRI; whereas manual tracing was applied to measure the corpus callosum brain ratio (CCR) and the ventricle brain ratio (VBR). A sample of 86 patients with a mean age of 43.3 years (SD 4.3), mean disease duration of 13.6 years (SD 4.4) and a median Expanded Disability Status Score (EDSS) of 6.0 was identified. The correlation between total lesion area of the brain (TLA) and disability (EDSS) for the whole sample was moderate (Spearman rank correlation coefficient r=0.48, P<0.001). Also correlations of CCR and VBR to disability (r=0.32-0.46) were significant. Correlations of TLA and disability in this study were rather strong. Hence, T2-weighted MRI lesion load in the brain still plays an important role as a surrogate marker of disease and as a secondary outcome measure in phase III treatment trials.

Phasic and enduring negative symptoms in schizophrenia: biological markers and relationship to outcome

Negative symptoms have been associated with poor response to neuroleptics, enlarged ventricles, cognitive impairment, and poor outcome in schizophrenia. These associations appear, however, to be dependent on the phase of study, suggesting that acute-phase (phasic) negative symptoms may be pathophysiologically distinct from enduring negative symptoms that persist through the residual phase. To compare correlates of enduring and phasic negative symptoms, we studied 60 drug-free schizophrenic patients (DSM-III-R and SADS/RDC) at baseline, 4 weeks after neuroleptic treatment, and assessed the 1 year outcome. We rated positive and negative symptoms at baseline and 4 weeks after treatment. At baseline, premorbid function, neuropsychological function, ventricle–brain ratio (VBR) and symptom response to an anticholinergic agent were assessed, and a two-night sleep EEG and 1 mg dexamethasone suppression test (DST) were conducted. Phasic negative symptoms were defined as the change in negative symptoms (baseline to 4 weeks) and enduring negative symptoms as severity of negative symptoms at 4 weeks. Patients had varying proportions of phasic and enduring symptoms; the two did not define distinct subgroups. Phasic negative symptoms were significantly correlated with global treatment response, positive symptom treatment response, response to anticholinergic agent, baseline post-dexamethasone cortisol, and shortened REM latency. Enduring negative symptoms were significantly correlated with residual positive symptoms and global psychopathology, VBR, poor performance on neuropsychological testing, decreased slow-wave sleep, poor premorbid function, and poor 1 year outcome. These data suggest that phasic negative symptoms and enduring negative symptoms may be caused by different pathophysiological mechanisms.

Ventricular enlargement in schizophrenia spectrum patients with prodromal symptoms of obsessive–compulsive disorder

We hypothesized that male patients with schizophrenia spectrum disorders who have prodromal symptoms of obsessive–compulsive disorder (OCD) have ventricular enlargement compared with non-psychotic OCD patients, and that the difference in the ventricular size would offer a clue to the early detection of schizophrenia spectrum disorders. The ventricle–brain ratios (VBRs) in eight male patients with schizophrenia or schizotypal personality disorder (SPD) who had prodromal symptoms of OCD were compared with eight male patients with non-psychotic OCD and 14 normal male comparison subjects using three-dimensional magnetic resonance imaging (MRI). The VBR of the schizophrenia spectrum group was significantly larger than those of the OCD group or comparison subjects. Even the minimum VBR in the schizophrenia spectrum group was larger than the maximum VBR in the OCD group. These results may suggest the usefulness of three-dimensional MRI for early detection of patients with schizophrenia spectrum disorders who manifest OCD symptoms early in the course of the illness.

MRI changes during water loading in patients with polydipsia and intermittent hyponatremia.

Patients with polydipsia and intermittent hyponatremia have greater ventricle-brain ratios (VBRs) than matched patients without polydipsia and intermittent hyponatremia and normal subjects. Unlike previous studies, this study controlled for the impact of water loading when examining the volume of intracranial structures. Under controlled conditions, eight male schizophrenic patients with polydipsia and intermittent hyponatremia were first assigned to either normal fluid intake or oral water loading and then the alternative condition the following day. Magnetic resonance imaging (MRI) volumetric measurements were made with the use of a standardized protocol. During water loading, total VBR and lateral ventricle volume significantly decreased by 13.1% and 12.6%, respectively. A strong association between change in serum sodium concentration and change in VBR was noted across conditions. These findings indicate that 1) water loading does not account for the diminished brain volume observed in patients with polydipsia and intermittent hyponatremia in previous studies, and 2) hyponatremia can significantly alter brain morphology on MRI.

Brain computed tomography in geriatric manic disorder

Background: Excess brain changes in geriatric manic patients have been hypothesized. Few neuroimaging studies are available.Methods: Brain computed tomography scans in geriatric patients with manic disorder (n = 30) were compared to those in same-age control subjects (n = 18). Ratings of cortical sulcal widening (CSW), lateral ventricle–brain ratio (VBR), and related linear measures were determined.Results: Patients had greater CSW scores (Exact p =.002) and VBR (t = 2.51, df = 46, p < .02) compared to control subjects. CSW was positively associated with age at illness onset (rs = .46, p < .01) and age at first manic episode (rs = .53, p < .005). VBR was poorly correlated with CSW and was not associated with these indices of illness course.Conclusions: These findings support the need for further investigation of relationships between brain structure and clinical features in geriatric mania.

Brain Morphology and Response to Nortriptyline in Geriatric Depression

In geriatric patients with major depression (N=15), the authors compared response to treatment with nortriptyline as it relates to brain morphology assessed by computed tomography. There was a significant negative association between ventricle-brain ratio and response to nortriptyline (rs=-0.63; P=0.015).