MRI Temporal Lobe Volume Measures and Neuropsychologic Function in Alzheimer's Disease
Charles D. SmithMonica MalceinKathy MeurerFrederick A. SchmittWilliam R. MarkesberyL. Creed Pettigrew
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The authors performed quantitation of the temporal lobes using magnetic resonance imaging in 20 patients with mild‐tomoderate Alzheimer's disease, 20 age‐matched aged control subjects, and 26 healthy young volunteers. Compared to young subjects, aged controls showed volume reductions in amygdala (17%, p =0.02), hippocampus (15%, p =0.0001) and temporal lobe (22%, p =0.0001). Compared to aged controls, Alzheimer's subjects showed further volume reductions in amygdala (33%, p =0.0001) and hippocampus (20%, p =0.006) but not temporal lobe (7%, p =0.15). In Alzheimer's subjects, left temporal lobe volume correlated strongly with the Mini Mental State (MMSE) score (adjusted r 2 =0.46, p =0.0006) whereas right amygdala volume correlated inversely with the noncognitive ADAS score (adjusted r 2 =0.46, p =0.0006). The authors conclude that significant volume changes occur in the temporal lobe in aging and in Alzheimer's disease, with the greatest percentage reductions in the amygdala in Alzheimer's disease. Temporal neocortical atrophy and temporal limbic atrophy might be associated with different patterns of performance and behavior in Alzheimer's patients.Multiple sclerosis (MS) has traditionally been considered to be primarily an inflammatory demyelinating disorder affecting the white matter. Nowadays it is recognized as both an inflammatory and a neurodegenerative condition involving the white and grey matter. Grey matter atrophy occurs in the earliest stages of MS, progresses faster than in healthy individuals, and shows significant correlations with cognitive function and physical disability; indeed, brain atrophy is the best predictor of subsequent disability and can be measured using magnetic resonance imaging (MRI). There are a number of MRI methods for measuring global or regional brain volume, including cross-sectional and longitudinal techniques. Preventing brain volume loss may therefore have important clinical implications affecting treatment decisions, with several clinical trials now demonstrating an effect of disease-modifying treatments (DMTs) on reducing brain volume loss. In clinical practice, it may therefore be important to consider the potential impact of a therapy on reducing the rate of brain volume loss. This article summarizes the knowledge on brain volume in MS.
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Background and Purpose: Brain atrophy can be regarded as an end-organ effect of cumulative cardiovascular risk factors. Accelerated brain atrophy is described following ischemic stroke, but it is not known whether atrophy rates vary over the poststroke period. Examining rates of brain atrophy allows the identification of potential therapeutic windows for interventions to prevent poststroke brain atrophy. Methods: We charted total and regional brain volume and cortical thickness trajectories, comparing atrophy rates over 2 time periods in the first year after ischemic stroke: within 3 months (early period) and between 3 and 12 months (later period). Patients with first-ever or recurrent ischemic stroke were recruited from 3 Melbourne hospitals at 1 of 2 poststroke time points: within 6 weeks (baseline) or 3 months. Whole-brain 3T magnetic resonance imaging was performed at 3 time points: baseline, 3 months, and 12 months. Eighty-six stroke participants completed testing at baseline; 125 at 3 months (76 baseline follow-up plus 49 delayed recruitment); and 113 participants at 12 months. Their data were compared with 40 healthy control participants with identical testing. We examined 5 brain measures: hippocampal volume, thalamic volume, total brain and hemispheric brain volume, and cortical thickness. We tested whether brain atrophy rates differed between time points and groups. A linear mixed-effect model was used to compare brain structural changes, including age, sex, years of education, a composite cerebrovascular risk factor score, and total intracranial volume as covariates. Results: Atrophy rates were greater in stroke than control participants. Ipsilesional hemispheric, hippocampal, and thalamic atrophy rates were 2 to 4 times greater in the early versus later period. Conclusions: Regional atrophy rates vary over the first year after stroke. Rapid brain volume loss in the first 3 months after stroke may represent a potential window for intervention. Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT02205424.
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Abstract We studied 74 consecutive patients with temporal lobe epilepsy who were treated surgically and in whom the volumes of mesial temporal structures were determined preoperatively by magnetic resonance imaging. We divided the patients into three groups according to the volumetric findings: unilateral (63.5% of the patients), bilateral (23%), or no atrophy (13.5%) of the amygdala–hippocampal formation. Two distinct surgical approaches were used: selective amygdalohippocampectomy (n = 37) or anterior temporal lobe resection (n = 37). Outcome was assessed at least 1 year after surgery, according to Engel's modified classification. Patients with unilateral mesial temporal atrophy had significantly better results compared with the other two groups ( p < 0.001): We found excellent results (class I or II outcome) in 93.6% of the patients with unilateral atrophy, in 61.7% of those with bilateral atrophy, and in 50% of the group with no significant atrophy of mesial temporal structures. The two different surgical techniques were equally effective, regardless of the pattern of atrophy. In conclusion, magnetic resonance volumetric studies in temporal lobe epilepsy proved to be an important preoperative prognostic tool for surgical treatment, but they did not provide guidance for selecting one surgical approach compared to the other.
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The loss of parenchymal brain volume per normative age comparison is a distinctive feature of brain atrophy. While the condition is the most prevalent to elderly, it has also been observed in pediatric ages. Various causes such as trauma, infection, and malnutrition have been reported to trigger the loss of brain tissues volume. Despite this literature based knowledge of risk factors, the magnitude of brain atrophy in pediatric age group is scantly addressed in most developing countries including Tanzania. The current study aims to understand the magnitude of brain atrophy in children residing in Northern Zone, Tanzania.A cross-sectional hospital survey was performed in which 455 children who were presented with various brain pathologies from the year 2013 to 2019 and whose brains examined by Computerized tomography (CT)-Scanners were recruited in the study. The brain statuses were examined using three linear radiological methods including the measure of sulcal-width, Evans index, and lateral ventricular body width.Results showed a significant number of atrophied brains among children in Northern Tanzania and that the condition was observed to have a 1:1 male to female ratio. The prevalence of pediatric brain atrophy was found to be 16.04%.The cortical subtype of brain atrophy presented as the most prevalent type of brain volume loss. The findings of this study suggest existence of considerable trends of brain atrophy in children which need special attention and mitigation plans.
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The relation of brain atrophy measured with computed tomography (CT) to mental deterioration on living people was studied. A newly improved technique for quantitative measurement of brain atrophy was developed. The pixels inside the head slices were divided into three parts; brain skull, and cerebrospinal fluid according to their CT number. The volume of brain, CSF, and cranial cavity were calculated by counting the number of pixels of each tissue. Results from 130 normal brains showed that the CSF volume was constant at about 16 ml through 20--39 years old. After 40 years the mean CSF volume increased drastically and reached 71 ml in the seventies. The volume of the brain was standardized for comparison between different-sized heads (brain volume index: BVI). The mean BVI decreased with statistical significance after 40 years of age. Mental function of these persons were evaluated using Hasegawa's dementia rating scale for the elderly. Progression of brain atrophy accompanied loss of mental activities (p less than 0.01).
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Preface.- Foreword.- History of the amygdala.- Formation of the amygdala.- Amygdala and Limbic system.- Functions of the amygdala.- Dissection of the amygdala.- Morphology of the amygdala.- Connections of the amygdala.- Projections from and toward amygdala.- The relationships of the amygdala.- The BST (bed nucleus of the stria terminalis).- The extended amygdala.- Vascularization of the amygdala.- Consequences of the ablation.- Conclusions and prospects.- Bibliography.- Index.
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Abstract Regional and global cerebral atrophy are inevitable features of Alzheimer's disease (AD). We assessed volumes and atrophy rates of brain structures in patients with familial AD during the period that they developed symptoms. Five patients with presymptomatic AD and 20 controls had two or more annual volumetric MRI brain scans. Volumes of brain, ventricles, temporal lobes, hippocampi, and entorhinal cortices (ECs) were measured. Rates of volume change were calculated from serial scans. There were no significant differences in baseline measures of whole brain, temporal lobe, or ventricular volume between patients and controls; averaged volumes of medial temporal lobe structures (both hippocampi and ECs) were 16.6% (95% confidence interval [CI], 3.3–28.0%) lower in patients. Atrophy rates for brain, temporal lobe, hippocampus, and EC were significantly increased in patients compared with controls ( p < 0.05). Averaged atrophy rates from both hippocampi and ECs were 5.1% (95% CI, 3.0–7.1%) greater in patients than controls. Linear extrapolation backward suggested medial temporal lobe atrophy commenced 3.5 years (95% CI, 0.7–7.5 years) before onset, when all patients were asymptomatic. We conclude that increased medial temporal lobe atrophy rates are an early and distinguishing feature of AD and that pathological atrophy probably is occurring several years before the onset of symptoms. Ann Neurol 2003;53:000–000
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