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PubMed2006

Cerebral atrophy measurements using Jacobian integration: comparison with the boundary shift integral.

We compared two methods of measuring cerebral atrophy in a cohort of 38 clinically probable Alzheimer's disease (AD) subjects and 22 age-matched normal controls, using metrics of zero atrophy, consistency, scaled atrophy and AD/control group separation. The two methods compared were the boundary shift integral (BSI) and a technique based on the integration of Jacobian determinants from non-rigid registration. For each subject, we used two volumetric magnetic resonance (MR) scans at baseline and a third obtained 1 year later. The case of zero atrophy was established by registering the same-day baseline scan pair, which should approximate zero change. Consistency was established by registering the 1-year follow-up scan to each of the baseline scans, giving two measurements of atrophy that should be very similar, while scaled atrophy was established by reducing one of the same-day scans by a fixed amount, and rigidly registering this to the other same-day scan. Group separation was ascertained by calculating atrophy rates over the two 1-year measures for the control and AD subjects. The results showed the Jacobian integration technique was significantly more accurate in calculating scaled atrophy (P < 0.001) and was able to distinguish between control and AD subjects more clearly (P < 0.01).

Aged↗

PubMed2004

Sleep disordered breathing in spinal muscular atrophy.

Sleep disordered breathing is a common but under-diagnosed complication causing sleep disturbance and daytime symptoms in children with spinal muscular atrophy. Non-invasive (positive pressure) ventilation is an established treatment of respiratory failure; its role in treatment of sleep disordered breathing though remains controversial. Aim of this study was to verify the hypothesis that nocturnal non-invasive ventilation has beneficial impact on breathing during sleep, sleep quality and daytime complaints in children with spinal muscular atrophy. Twelve children with spinal muscular atrophy type I or II (7.8+/-1.9 years) underwent polysomnography and were asked to fill out a symptom questionnaire. Seven patients (six with spinal muscular atrophy I and one with spinal muscular atrophy II) had sleep disordered breathing and received non-invasive ventilation during sleep. Five less severely affected patients (one with spinal muscular atrophy I and four with spinal muscular atrophy II) had no sleep disordered breathing and served as reference group. Patients were restudied after 6-12 months. In patients with sleep disordered breathing both sleep architecture and disease related symptoms were significantly worse than in the reference-group. Non-invasive ventilation during sleep completely eliminated disordered breathing, normalized sleep architecture and improved symptoms (P<0.05 for all). In children with spinal muscular atrophy sleep disordered breathing may cause relevant impairment of sleep and well-being. Both can be highly improved by nocturnal non-invasive ventilation.

Child↗

PubMed1997

Delayed stimulation of the latissimus dorsi may result in disuse atrophy.

BACKGROUND: The latissimus dorsi is usually left unstimulated for 2 weeks after cardiomyoplasty to allow the muscle to recover from the loss of the collateral circulation. To determine whether the 2-week delay may cause muscle atrophy, we randomized 15 mongrel dogs to a control group or a disuse atrophy group. METHODS: The collateral circulation to the latissimus dorsi was ligated in all animals before cardiomyoplasty to reduce the risk of ischemic injury to the muscle during mobilization. Two weeks after collateral ligation, the atrophy group had the tendinous attachment of the latissimus dorsi severed and then 2 weeks later underwent cardiomyoplasty. The control group had a 2-week delay after collateral ligation followed by cardiomyoplasty. Biopsies were performed before collateral ligation and before cardiomyoplasty. After heart failure was induced, hemodynamic function was assessed during synchronized contraction of the latissimus dorsi by measuring the maximum systolic elastance, stroke volume, preload recruitable stroke work index, and diastolic compliance. RESULTS: Comparison of muscle morphology between the two groups demonstrated the presence of muscle atrophy in those animals that had been randomized to the atrophy protocol. During synchronized contraction of the latissimus dorsi, there was no significant increase in maximum systolic elastance in either group. However, both stroke volume and pulmonary recruitable stroke work index were significantly higher in the control animals during assisted beats. The left ventricle was less compliant in the atrophy group, suggesting that muscle atrophy had adversely affected diastolic function. CONCLUSIONS: Delayed electrical stimulation of the latissimus dorsi may result in atrophy and loss of function.

Animals↗

PubMed2000

Concordance of parapapillary chorioretinal atrophy in ocular hypertension with visual field defects that accompany glaucoma development.

OBJECTIVE: To determine whether the extent and location of progressive parapapillary chorioretinal atrophy noted in some patients with ocular hypertension are correlated with the extent and location of visual field defects that occur with progression to glaucoma. STUDY DESIGN: Retrospective cohort study. PARTICIPANTS: Thirty patients with ocular hypertension who had progressive changes of parapapillary atrophy develop before clinically detectable optic disc or visual field damage. MAIN OUTCOME MEASURES: Assessment of changes in the parapapillary atrophy and visual field parameters. METHODS: Baseline and follow-up optic disc photographs and visual field test results were retrospectively analyzed. The relationship between the extent of parapapillary atrophy observed during the ocular hypertension period and initial visual field abnormalities detected after glaucoma development, as well as their spatial relationship, was statistically analyzed. RESULTS: The extent of progressive changes of the parapapillary atrophy detected during the ocular hypertension period was correlated with the extent of changes in the visual field parameters, including corrected pattern standard deviation and mean deviation measured after glaucoma development (Mantel-Haenszel chi-square test, P = 0.026, P = 0.037, respectively). In addition, the visual field abnormalities occurred in the corresponding quadrants of the progressive parapapillary atrophy. Analysis of the spatial relationship revealed that the location of progressive changes of the parapapillary atrophy was concordant with the location of visual field abnormalities in 78% of the quadrants (94 of 120 quadrants) (chi-square test, P = 0.001). CONCLUSIONS: The extent and location of visual field abnormalities that develop in ocular hypertensive eyes with progression to glaucoma exhibit a concordance with the extent and location of progressive parapapillary atrophy noted in the ocular hypertension period. This suggests the importance of detailed examination of the parapapillary area in ocular hypertensive eyes.

Choroid↗

PubMed1988

Cerebellar atrophy in epileptic patients.

High-resolution CT scans of the brain and posterior fossa were performed on 106 phenytoin (PHT)-treated epileptics, 28 de novo epileptics and 43 control subjects. A higher incidence of cerebellar and brainstem (CBS) atrophy was observed in chronic PHT- or PHT+ phenobarbital-treated epileptics compared to the two other groups. Some control subjects and de novo epileptics presented mild CBS atrophy, whereas moderate to severe atrophy was noted exclusively in chronically-treated patients. In attempting to delineate the etiology of CBS atrophy, epileptic patients were divided in three groups: 55 subjects with normal CT scans, 30 with both cerebral and CBS atrophy, and 49 with pure CBS atrophy. Their ages, length of illness, number of generalized seizures, number of other seizures, and amount of PHT received during their lifetime were assessed. Statistical analysis revealed that posterior fossa atrophy in epileptics was significantly correlated with both the length of the illness and the amount of PHT ingested during the patient's lifetime. The number of seizures appears to not be related to CBS atrophy.

Adolescent↗

PubMed2002

Sensitivity of biopsy site in evaluating regression of gastric atrophy after Helicobacter pylori eradication treatment.

BACKGROUND: Helicobacter pylori infection is a major cause of the progress of gastric glandular atrophy, a high-risk background factor in the development of gastric cancer. Regression of gastric atrophy is critical to prevention of cancer by H. pylori eradication treatment. However, it is controversial whether gastric atrophy regresses after H. pylori eradication. AIM: To determine the most sensitive and appropriate biopsy site for evaluation of regression of atrophy after treatment. SUBJECTS AND METHODS: Thirty-eight patients who showed regression of gastric atrophy in histology after treatment were investigated. Four biopsy specimens from the lesser and greater curvatures in the antrum and corpus were evaluated before and after treatment according to the Updated Sydney System. RESULTS: Regression of atrophy after treatment was seen in 30 of 38 biopsy specimens from the lesser curvature of the corpus (79%), and this site was most sensitive. Odds ratio of this site to the others was 8.28. Regression of atrophy in this site was observed at 12.2 months in the younger patients and 15.9 months in the elder patients. CONCLUSION: Biopsy sampling from the lesser curvature of the corpus is the most sensitive and appropriate for evaluation of regression of gastric atrophy after H. pylori eradication treatment.

Adult↗

PubMed1999

External anal sphincter atrophy on endoanal magnetic resonance imaging adversely affects continence after sphincteroplasty.

BACKGROUND: There is still considerable debate about the value of preoperative anorectal physiological parameters in predicting the clinical outcome after sphincteroplasty. Recently it has been reported that atrophy of the external anal sphincter can be clearly shown with endoanal magnetic resonance imaging (MRI). The aims of this study were to investigate the prevalence of external anal sphincter atrophy in women with anterior sphincter defects due to obstetric injury and to determine the impact of external anal sphincter atrophy on the outcome of sphincteroplasty. METHODS: In this prospective study, 20 consecutive women (median age 50 (range 28-75) years) with faecal incontinence due to obstetric trauma were assessed before operation with endoanal ultrasonography and endoanal MRI. The external anal sphincter was examined and evaluated for the presence of atrophy. The clinical outcome of sphincteroplasty was interpreted without knowledge of the magnetic resonance and ultrasonographic images. RESULTS: In all patients anterior sphincter defects could be demonstrated with ultrasonography and MRI. External anal sphincter atrophy could only be demonstrated on MRI. Eight of 20 patients had external anal sphincter atrophy. Continence was restored in 13 patients. Outcome was significantly better in those without external anal sphincter atrophy (11 of 12 patients versus two of eight; P = 0.004). CONCLUSION: External anal sphincter atrophy can only be visualized on endoanal MRI and affects continence after sphincteroplasty. Endoanal MRI is valuable in the preoperative assessment of patients with faecal incontinence. Presented to the American Society of Colon and Rectal Surgeons in Philadelphia, Pennsylvania, USA, June 1997

Adult↗

PubMed2001

Morphometric assessment of gastric antral atrophy: comparison with visual evaluation.

AIMS: As part of a multinational effort to reach a consensus in the definition and evaluation of atrophic gastritis, we applied morphometric techniques to 22 antral biopsy specimens examined visually by 12 experienced gastrointestinal pathologists. METHODS AND RESULTS: Atrophy was defined as loss of glands. Each pathologist graded atrophy with both non-standardized and standardized approaches. Discriminant function analyses of morphometric measurements were conducted to validate and grade atrophy. Kappa statistics were used to compare the performance of each pathologist against the group mode and against the discriminant functions' grading of atrophy. Three morphometric indexes showed significant differences among categories of atrophy utilizing non-standardized as well as standardized visual atrophy grades: (i) the ratio of glandular length to total mucosal thickness; (ii) the proportion of the secretory compartment area occupied by glands; and (iii) the number of glandular cross sections per 40x microscopic field. The discriminant function analyses verified all cases classified visually as either non-atrophic, or moderately/severely atrophic; it verified as mildly atrophic 40% of the cases classified visually as mildly atrophic; and classified the remaining 60% as moderately or severely atrophic. The kappa statistics were good or excellent for the majority of pathologists. CONCLUSIONS: The evaluation of antral atrophy, simply defined as loss of glands, can be reliable and reproducible. The visual grading of atrophy as absent, moderate and severe is entirely consistent with objective morphometric observations.

Atrophy↗

PubMed2001

[Optical coherence tomography in geographic atrophy--a clinicopathologic correlation].

BACKGROUND: Optical coherence tomography was used for the examination of patients with geographic atrophy in different stages of age-related macular degeneration. Always compared with biomicroscopy and fluorescein angiography [4,7,8,10]. PATIENTS AND METHODS: 37 patients with geographic atrophy (n = 55 eyes) out of 150 with AMD (n = 169 eyes) were examined. The results of biomicroscopy, fluorescein angiography, optical coherence tomography and histological knowledge in age-related macular degeneration were studied. RESULTS: Fluorescein angiography always identified geographic atrophy and in 13.5% the findings additionally were similar to an occult choroidal neovascularisation with circular hyperpigmentation. Geographic atrophy shows a significant thinning of the neurosensory retina of 135 microns as an average in optical coherence tomography (p < 0.0005) which did not correlate to visual acuity. Typically an enhanced vertically sharp demarcated reflectivity of the choroid is found because of the lacking pigment epithelium. 43% of the geographic atrophies were identified by optical coherence tomography. 3 out of 55 eyes (5%) in optical coherence tomography only show macular holes additionally to geographic atrophy. CONCLUSION: A typical pattern of reflectivity is found by optical coherence tomography with enhanced reflectivity of the choroid because of lacking pigment epithelium and significant thinning of the fovea. Atypical macular holes moreover are found in 5% neither appearing in biomicroscopy nor in fluorescein angiography. An occult choroidal neovascularisation can be differentiated by optical coherence tomography from geographic atrophy because there is no spindle-like thickening of the pigment epithelium and no enhanced choroidal reflectivity. In borderline cases optical coherence tomography may be helpful and therapeutically decisive in differentiating geographic atrophy and occult choroidal neovascularisation and in detecting atypical macular holes.

Aged↗

PubMed2005

How good is zoom endoscopy for assessment of villous atrophy in coeliac disease?

BACKGROUND AND STUDY AIMS: The advent of magnification endoscopy may allow the macroscopic detection of unrecognised villous atrophy in patients with unsuspected coeliac disease. In addition, it may also be possible to use this method to assess the degree of villous atrophy. The aim of this study was to determine the accuracy of zoom endoscopy for the macroscopic evaluation of villous atrophy, in comparison with histological evaluation. PATIENTS AND METHODS: The zoom endoscope provided a magnification capability of x 115. A scoring system (Z score) was devised for grading the appearances of villous atrophy: "Z1" for normal mucosa, "Z2" for stunted villi, "Z3" for markedly stunted villi (with ridges and pits) and "Z4" for a flat mucosa. A total of 53 consecutive patients with treated coeliac disease were followed up over almost 2 years using the Olympus GIF-Q240Z zoom endoscope; a total of 80 procedures were carried out. Four biopsies from the second part of the duodenum were taken from each patient for histological assessment. Histological assessment of villous atrophy was made by a pathologist blinded to the Z score. The correlation between the Z score and the histological score was assessed using the weighted kappa method. RESULTS: The kappa score for the correlation between the macroscopic assessment of villous atrophy and the histology was 0.631, indicating fair to good reproducibility. Agresti's method revealed a very strong baseline association between the two methods ( P < 0.001). Zoom endoscopy had a positive predictive value of 83 % and a negative predictive value of 77 % in detecting villous atrophy. CONCLUSIONS: Our findings suggest that zoom endoscopy may be valuable in assessing the degree of villous atrophy. However, further studies are needed to assess its efficacy in routine practice as a screening or case-finding tool.

Adult↗

PubMed2002

Mapping the evolution of regional atrophy in Alzheimer's disease: unbiased analysis of fluid-registered serial MRI.

Alzheimer's disease (AD) is characterized by progressive cerebral atrophy, which may be assessed by using volumetric MRI. We describe a voxel-based analysis of nonlinear-registered serial MRI to demonstrate the most statistically significant (P < 0.001) regions of change at different stages of the disease. We compared presymptomatic (n = 4), mild (n = 10), and moderately affected (n = 12) patients with early- and late-onset AD, with age- and sex-matched controls, and demonstrated increasing global atrophy with advancing disease. Significantly increased rates of hippocampal atrophy were seen in presymptomatic and mildly affected patients. There was a shift in the distribution of temporal lobe atrophy with advancing disease; the inferolateral regions of the temporal lobes showed the most significantly increased rates of atrophy by the time the patients were mildly or moderately affected. Significantly increased rates of medial parietal lobe atrophy were seen at all stages, with frontal lobe involvement occurring later in the disease. Our results suggest that the sites showing the most significant rates of atrophy alter as the disease advances, and that regional atrophy is already occurring before the onset of symptoms. This technique provides insights into the natural history of AD, and may be a valuable tool in assessing the efficacy of disease-modifying treatments, especially if these treatments were to have region-specific effects.

Alzheimer Disease↗

PubMed2000

Distribution of atrophy in Helicobacter pylori-infected subjects taking proton pump inhibitors.

BACKGROUND: Gastric atrophy is associated with Helicobacter pylori infection. Conflicting results have been obtained as to whether acid suppressant therapy hastens the development or changes the distribution of atrophy in the stomach. The aim of this study was to investigate whether concomitant proton pump inhibitor (PPI) therapy in H. pylori-infected individuals resulted in an increase or an alteration in atrophy distribution and whether this was reflected by the plasma gastrin. METHODS: Multiple gastric biopsy specimens were taken from the antrum and corpus from 46 H. pylori-infected subjects, 18 of whom were taking PPIs, and assessed histologically by the updated Sydney System. The control group was age- and sex-matched to the index group. Fasting gastrin levels were measured. RESULTS: In the control group there was no significant tendency for either antral or corpus atrophy to predominate (P = 0.44). In the treatment group there was a significant tendency for corpus as opposed to antral atrophy to develop (P < 0.001). There was no significant difference in the overall atrophy score between the treated and untreated groups (P = 0.76). Fasting gastrin levels were significantly higher in the treated group (P < 0.001). CONCLUSIONS: Treatment with PPIs in H. pylori-infected subjects does not lead to an overall increase in gastric atrophy. It does, however, result in an increased prevalence of corpus as opposed to antral atrophy. This is associated with a significantly higher gastrin level.

Adult↗

PubMed2001

Duodenal disaccharidase activities in the follow-up of villous atrophy in coeliac disease.

BACKGROUND: In active coeliac disease, mucosal atrophy is associated with a marked decrease in intestinal disaccharidase enzyme activities. We investigated the value of duodenal mucosal disaccharidases to predict the severity of mucosal villous atrophy and its recovery in 50 patients with coeliac disease. METHODS: Duodenal mucosal histology and disaccharidase activities were studied at least twice with a mean interval of 9 months. Histology of specimens from all patients was examined by the same pathologist blinded to the data on disaccharidase activities. Mucosal damage was scored into four groups as follows: Grade 0 = normal mucosa; grade I = slight villous atrophy, that is, cryptic component 30%-50%; grade 2 = moderate villous atrophy, that is, cryptic component 50%-90%; grade 3 = severe villous atrophy, that is, cryptic component >90%. The enzyme activities of the disaccharidases were determined as U/g protein. RESULTS: Duodenal mucosal disaccharidase activities were good predictors of the grade of mucosal villous atrophy. Positive predictive values for moderate or severe villous atrophy were 90% for maltase (maltase activity <150 U/g protein), 86% for sucrase (<40 U/g protein) and 71% for lactase (<20 U/g protein). Accordingly, negative predictive values, that is, none or only minimal villous atrophy (grades 0 or 1) with normal disaccharidase activities, were 71% for maltase, 70% for sucrase and 63% for lactase. CONCLUSIONS: The increase in duodenal disaccharidase activities correlated with recovery of the mucosa based on histology. Besides the histological examination, measurement of disaccharidase activities offers an additional tool to evaluate response to a gluten-free diet in patients with coeliac disease.

Adult↗

PubMed2002

Measurement of atrophy in multiple sclerosis: pathological basis, methodological aspects and clinical relevance.

MRI methods are widely used to follow the pathological evolution of multiple sclerosis in life and its modification by treatment. To date, measures of the number and volume of macroscopically visible lesions have been studied most often. These MRI outcomes have demonstrated clear treatment effects but without a commensurate clinical benefit, suggesting that there are other aspects of multiple sclerosis pathology that warrant investigation. In this context, there has been considerable interest in measuring tissue loss (atrophy) as a more global marker of the adverse outcome of multiple sclerosis pathology, whether it arises in macroscopic lesions or in the normal appearing tissues. An International Workshop recently considered the measurement of atrophy in multiple sclerosis and provided the basis for this review. Brain white matter bulk consists predominantly of axons (46%) followed by myelin (24%), and progressive atrophy implies loss of these structures, especially axons, although variable effects on tissue volumes may also arise from glial cell proliferation or loss, gliosis, inflammation and oedema. Significant correlations found between brain volume and other putative MR neuronal markers also indicate that atrophy reflects axonal loss. Numerous methods are available for the measurement of global and regional brain volumes and upper cervical cord cross-sectional area that are highly reproducible and sensitive to changes within 6-12 months. In general, 3D-T(1)-weighted acquisitions and largely automated segmentation approaches are optimal. Whereas normalized volumes are desirable for cross-sectional studies, absolute volume measures are adequate for serial investigation. Atrophy is seen at all clinical stages of multiple sclerosis, developing gradually following the appearance of inflammatory lesions. This probably reflects both inflammation-induced axonal loss followed by Wallerian degeneration and post-inflammatory neurodegeneration that may be partly due to failure of remyelination. One component of atrophy appears to be independent of focal lesions. Existing immunomodulatory therapies have had limited effects on progressive atrophy, concordant with their modest effects on progressive disability. Atrophy provides a sensitive measure of the neurodegenerative component of multiple sclerosis and should be measured in trials evaluating potential anti-inflammatory, remyelinating or neuroprotective therapies.

Atrophy↗

PubMed2001

Association of polymorphism in the alcohol dehydrogenase 2 gene with alcohol-induced testicular atrophy.

BACKGROUND: Alcohol abuse can induce testicular atrophy, but it only occurs in some alcoholics. Alcohol dehydrogenase (ADH) is located principally on the Leydig cells. METHODS: To investigate whether genetic polymorphism of alcohol dehydrogenase (ADH) 2 and aldehyde dehydrogenase (ALDH) 2 was related to alcoholic testicular atrophy, we determined restriction fragment-length polymorphisms of the ADH2 and ALDH2 genes in 43 Japanese male alcoholics and 50 healthy subjects. An orchidometer was used to determine the testicular size. RESULTS: Less than 16 ml in testicular size was defined as testicular atrophy. Testicular atrophy was found in 24 (55.8%) cases out of 43 alcoholics. Digestion with MaeIII and MboII after polymerase chain reaction amplification showed that the ADH21 allele frequency was significantly higher in patients with testicular atrophy than in those without testicular atrophy (chi2 = 4.665, p = 0.031), whereas no significant association was observed between testicular atrophy and the ALDH2 gene. CONCLUSIONS: The ADH21 allele may be associated with alcoholic testicular atrophy.

Adult↗

PubMed2005

Muscle atrophy after treatment with Halovest.

STUDY DESIGN: A prospective study was conducted on the sequential changes in the muscles around the cervical spine following external fixation for an extended period. OBJECTIVE: Muscular atrophy around the cervical spine following prolonged external fixation with a Halovest and subsequent recovery from the atrophy were examined. SUMMARY OF BACKGROUND DATA: There are a number of reports on the usefulness of the Halovest. However, there have been no descriptions about muscular atrophy following fixation by the Halovest. METHODS: The study participants were 10 patients who were conservatively treated by the Halovest. Imaging by CT was performed periodically following fixation by the Halovest. The cross sections of the sternocleidomastoid muscle and the nuchal muscle group at C5-C6 were computed by using NIH Image Software. The results were used to evaluate muscular atrophy following fixation by the Halovest and the subsequent recovery after removal of the fixation. RESULTS: Following fixation by the Halovest, atrophy of the muscles around cervical spine sequentially progressed. Three months after fixation, muscular atrophy was about 15% at the sternocleidomastoid muscle and 22% for the nuchal muscle group, but the patients recovered from the atrophic state following the removal of the device. CONCLUSION: Following fixation by the Halovest, muscular atrophy around the cervical spine sequentially progressed. After the device was removed, however, the muscles recovered from the atrophic state. Muscular atrophy caused by prolonged fixation by the Halovest was a reversible change.

Adolescent↗

PubMed2006

Insights into muscle atrophy and recovery pathway based on genetic models.

PURPOSE OF REVIEW: Muscle atrophy is a pervasive problem that occurs with disuse, aging, and a myriad of disease conditions. The purposes of this review are to describe recent advances in studying muscle atrophy that have elucidated pathways involved at the molecular level; to compare different types of atrophy--primary (e.g. bed rest, immobilization) and secondary (when the atrophy is related to pathology as well as disuse, e.g. injury, sepsis etc.) and their multiple common features; to review progress in studying the recovery process and clinical status. RECENT FINDINGS: Major advances have been made at the molecular level. There are two phenotypes for muscle atrophy--primary, which is mainly related to disuse (e.g. bed), and secondary, when the atrophy is related to pathology as well as disuse. It appears that the two forms have multiple elements in common. Studies on the recovery process reveal a very complex sequence of events that are not the simple reverse of the muscle loss process. In contrast to the progress at the molecular level, progress in treating muscle atrophy or accelerating recovery has been disappointing. SUMMARY: Although nutritional supplementation and pharmacological agents continue to have the potential to minimize muscle atrophy, given its minimal risks, exercise sets a very high standard for treatment options when medically appropriate. Identification of pathways and control points offers the potential for new approaches.

Bed Rest↗

PubMed2006

Phenomenological model of diffuse global and regional atrophy using finite-element methods.

The main goal of this work is the generation of ground-truth data for the validation of atrophy measurement techniques, commonly used in the study of neurodegenerative diseases such as dementia. Several techniques have been used to measure atrophy in cross-sectional and longitudinal studies, but it is extremely difficult to compare their performance since they have been applied to different patient populations. Furthermore, assessment of performance based on phantom measurements or simple scaled images overestimates these techniques' ability to capture the complexity of neurodegeneration of the human brain. We propose a method for atrophy simulation in structural magnetic resonance (MR) images based on finite-element methods. The method produces cohorts of brain images with known change that is physically and clinically plausible, providing data for objective evaluation of atrophy measurement techniques. Atrophy is simulated in different tissue compartments or in different neuroanatomical structures with a phenomenological model. This model of diffuse global and regional atrophy is based on volumetric measurements such as the brain or the hippocampus, from patients with known disease and guided by clinical knowledge of the relative pathological involvement of regions and tissues. The consequent biomechanical readjustment of structures is modelled using conventional physics-based techniques based on biomechanical tissue properties and simulating plausible tissue deformations with finite-element methods. A thermoelastic model of tissue deformation is employed, controlling the rate of progression of atrophy by means of a set of thermal coefficients, each one corresponding to a different type of tissue. Tissue characterization is performed by means of the meshing of a labelled brain atlas, creating a reference volumetric mesh that will be introduced to a finite-element solver to create the simulated deformations. Preliminary work on the simulation of acquisition artefacts is also presented. Cross-sectional and longitudinal sets of simulated data are shown and a visual classification protocol has been used by experts to rate real and simulated scans according to their degree of atrophy. Results confirm the potential of the proposed methodology.

Alzheimer Disease↗