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PubMed2006

-765G > C COX-2 polymorphism may be a susceptibility marker for gastric adenocarcinoma in patients with atrophy or intestinal metaplasia.

AIM: To investigate the relationship between the -765G > C COX-2 polymorphism and the development of different gastric lesions: atrophy or intestinal metaplasia and gastric adenocarcinoma. METHODS: A cross-sectional study was performed involving 320 Portuguese individuals (210 without evidence of neoplastic disease, 73 patients with gastric adenocarcinomas and 37 with atrophy or intestinal metaplasia) using a PCR-RFLP method. RESULTS: -765C allele was overrepresented in the patients with gastric adenocarcinoma (51%) when compared either with the control group (38%) or patients with atrophy or intestinal metaplasia (27%). Callele was found to be very common in our population (0.22), and a multivariate logistic regression analysis revealed nearly 3-fold increased risk for the progression to gastric adenocarcinoma in patients with atrophy or intestinal metaplasia carrying the -765C allele (OR = 2.67, 95% CI = 1.03-6.93; P = 0.04). CONCLUSION: -765C carrier status should be considered as another susceptibility marker for gastric adenocarcinoma development in patients with atrophy or intestinal metaplasia.

Adenocarcinoma↗

PubMed1998

Quadriceps atrophy after partial resection of the patellar tendon: an experimental study in a rat model.

Quadriceps muscle atrophy of rats was examined after resection of the central third (group 1) or the lateral two thirds (group 2) of the patellar tendon, the tensor fascia lata (group 3), or the medial hamstring (group 4). The quadriceps atrophied in groups 1 and 2, and more so in group 2, but there was no atrophy in groups 3 or 4. Thus, after an anterior cruciate ligament reconstruction procedure using the patellar tendon, resection of the patellar tendon itself leads to quadriceps atrophy and the extent of atrophy is related to the resected width.

Animals↗

PubMedDate not supplied

Bilateral optic nerve hypoplasia associated with cerebral atrophy.

We present a series of 12 consecutive cases of optic nerve hypoplasia. Eight of these were unassociated with significant CNS malformations; of these, two had tomographic evidence of cerebral atrophy. This represents the first adequately documented cases of isolated cerebral atrophy associated with optic nerve hypoplasia. We discuss the increasing prevalence and marked variability of optic nerve hypoplasia, note the lack of clear distinction between primary failure of differentiation and secondary degeneration of optic pathways, and mention the inadequacy of the classic explanation of primary failure of ganglion cell development as the cause of hypoplastic nerves. The cause of cerebral atrophy are mentioned, and we hypothesize that the wide range of CNS insults resulting in atrophy may be responsible for a correspondingly wide range of abnormalities of the optic nerves. We speculate that cerebral atrophy may result in an inadequate cortical mass for induction of normal optic nerve growth, possibly by decreased retrograde axoplasmic flow and insufficient nerve growth factor. We encourage a complete neurologic evaluation, including CAT scan of the brain, in children with optic nerve hypoplasia.

Adolescent↗

PubMed2003

Cell proliferation arrest within intrathymic lymphocyte progenitor cells causes thymic atrophy mediated by the aryl hydrocarbon receptor.

Activation of the aryl hydrocarbon receptor (AHR), a basic helix-loop-helix transcription factor, in lymphocytes by the immunosuppressive environmental contaminant 2,3,7,8,-tetrachlorodibenzo-p-dioxin (TCDD) has been shown to cause thymic atrophy in every species studied. We set out to identify the specific hemopoietic cellular populations in which the AHR was activated to lead to thymic atrophy and to determine the effect of AHR activation in those cellular populations. Initially, we examined whether AHR activation in intrathymic dendritic cells could mediate TCDD-induced thymic atrophy. It was found that thymic atrophy occurred only when the AHR could be activated in the thymocytes but not hemopoietic-derived dendritic cells or other APCs. We next analyzed the effect of TCDD on the proliferation of thymocytes in vivo. There was a significant increase in the percentage of thymocytes in the G(1) phase of the cell cycle and a significant decrease in the percentage of S plus G(2)/M thymocytes, especially in the CD4(-)CD8(-)CD3(-) triple-negative intrathymic progenitor cell population 24 h after exposure to 30 micro g/kg TCDD. Furthermore, by 12 h after exposure to TCDD, we observed approximately 60% reduction of 5-bromo-2'-deoxyuridine incorporation in specific intrathymic progenitor cell populations. This reduction persisted for at least 6 days. These data indicate that intrathymic progenitor cells are direct targets of TCDD in the thymus and suggest that TCDD causes thymic atrophy by reducing entrance into cell cycle in these populations.

Animals↗

PubMed1976

[Hereditary optic atrophies].

Congenital or infantile autosomal recessive optic atrophy is rare. The autosomal recessive syndrome of optic atrophy associated with diabetes is less rare. Dominant juvenile optic atrophy occurs frequently. Behr's heredo-familial optic atrophy, with its neurological mainfestations and its recessive autosomal inheritance, is rare. Sex-linked optic atrophy is exceptional. Leber's optic neuritis occurs frequently. Its heredity is apparently sex-linked, but no classical mode of transmission can be applied. Cytoplasmic heredity is the most probable.

Diabetes Complications↗

PubMed1999

Atrophy of the posterior cricoarytenoid muscle as an indicator of recurrent laryngeal nerve palsy.

BACKGROUND AND PURPOSE: The posterior cricoarytenoid (PCA) muscle is one of the intrinsic muscles of the larynx innervated by the recurrent laryngeal nerve. As such, recurrent laryngeal nerve palsy should not only result in paralysis of the true vocal cord or thyroarytenoid muscle but also in a similar change in the PCA muscle. The ability of CT and MR imaging to depict denervation atrophy in the PCA muscle in patients with recurrent laryngeal nerve palsy was evaluated. METHODS: Two investigators reviewed the CT and/or MR studies of 20 patients with a clinical history of vocal cord paralysis. The appearance of the PCA muscle was given a rating of 0, 1, 2, 3, or 4, with 0 being definitely normal and 4 being definitely abnormal or atrophic. Each study was also reviewed for the presence or absence of other features of vocal cord paralysis: thyroarytenoid muscle atrophy, anteromedial deviation of the arytenoid cartilage, an enlarged piriform sinus and laryngeal ventricle, and a paramedian cord. RESULTS: Atrophy of the PCA muscle was shown unequivocally in 65% of the cases and was most likely present in an additional 20%. The frequency with which other features of vocal cord paralysis were seen was as follows: thyroarytenoid atrophy, 95%; anteromedial deviation of the arytenoid cartilage, 70%; enlarged piriform sinus, 100%; enlarged laryngeal ventricle, 90%; and a paramedian cord, 100%. CONCLUSION: Atrophy of the PCA muscle may be commonly documented on CT and MR studies in patients with recurrent laryngeal nerve palsy and vocal cord paralysis, and therefore should be part of the constellation of imaging features of vocal cord paralysis. This finding is particularly useful when other imaging findings of vocal cord paralysis are absent or equivocal.

Adolescent↗

PubMed1999

[Stereometry of temporal peripapillary atrophy in early-stage open-angle glaucoma].

PURPOSE: To study the significance of temporal peripapillary atrophy in the pathogenesis of open-angle glaucoma in its early stage. CASES AND METHOD: Sterometry of temporal peripapillary atrophy was performed in 46 eyes of 46 patients with early-stage open-angle glaucoma and in 38 eyes of 38 healthy persons using a Heidelberg Retina Tomograph. RESULTS: The area of peripapillary atrophy averaged 0.78 +/- 0.46 mm2 in glaucoma eyes and 0.55 +/- 0.33 mm2 in controls. The difference was significant (p < 0.002). Its volume averaged 0.04 +/- 0.04 mm3 in glaucoma eyes and 0.02 +/- 0.02 mm3 in controls. The difference was significant (p < 0.001). Both the area and volume of disc cupping were significantly greater in glaucoma eyes than in controls (p < 0.001). The volume of rim of the disc was significantly smaller in eyes with symmetrical cupping than asymmetrical one (p < 0.001). Both the area and volume of peripapillary atrophy were significantly greater in eyes with asymmetrical cupping than symmetrical one (p < 0.001 each). CONCLUSION: The presence, shape and size of temporal peripapillary atrophy are closely associated with the pathogenesis of open-angle glaucoma in its early stage.

Adult↗

PubMed1999

[Is hippocampal atrophy a specific change for Alzheimer's disease?].

Although detection of hippocampal atrophy has been proposed for the diagnosis of Alzheimer's disease (AD), atrophic changes in MRI can be found in other dementia diseases. This study was undertaken to determine whether hippocampal atrophy was a specific change for AD. Coronal T 1-weighted images were performed in 36 patients with AD, 40 patients with non-AD including vascular dementia, frontemporal dementia, Parkinson's disease with dementia, dementia with Lewy bodies, progressive supranuclear palsy, and normal pressure hydrocephalus, 9 patients with age-associated memory impairment (AAMI), and 24 control subjects. Hippocampal atrophy was graded subjectively on a 5-point scale. Scores of hippocampal atrophy for AD (2.11 +/- 0.95) and non-AD (1.80 +/- 0.91) were significantly higher than those for controls (0.79 +/- 0.72). Scores for AD were also significantly higher than those for AAMI (1.11 +/- 0.160), but no difference was found between AD and non-AD. These results suggest that hippocampal atrophy is not a specific marker for AD and appears to be a common phenomenon in dementia syndromes.

Aged↗

PubMed2000

Impact of Helicobacter pylori eradication on the development of MALT, gland atrophy and intestinal metaplasia of the antrum.

BACKGROUND: Chronic Helicobacter pylori infection leads to the development of mucosa-associated lymphoid tissue (MALT), gland atrophy, intestinal metaplasia, and in certain individuals, gastric lymphoma and adenocarcinoma. We conducted a prospective study to determine the effect of H pylori eradication on the development of MALT, gland atrophy and intestinal metaplasia. METHODS: From July 1995 to October 1996, 63 consecutive patients with H pylori-associated peptic ulcer disease were enrolled in a bacterial eradication trial. The grade of MALT and the degree of gastritis of the antrum were assessed using Wotherspoon's scale and the Sydney system before treatment, and at eight weeks and one year after H pylori eradication therapy. RESULTS: During the study period, 43 patients received complete follow-up. In the patient group with eradication failure (n = 22), MALT score was significantly decreased at the end of the eighth week (p < 0.05) but returned to the initial level by one year of follow-up. There were no changes in the scores for inflammation, neutrophil activity, gland atrophy or intestinal metaplasia at the end of the eighth week and at one year following H pylori eradication therapy. In contrast, there was a marked reduction in the MALT, inflammation, and activity scores at eight weeks (p < 0.01, < 0.05 and < 0.05, respectively) and one year after treatment (p < 0.05, < 0.001 and < 0.001, respectively) in the patient group with successful eradication (n = 21). However, no significant changes in gland atrophy and intestinal metaplasia were observed during the follow-up period. CONCLUSIONS: Eradication of H pylori leads to regression of MALT in the stomach, but the degrees of gland atrophy and intestinal metaplasia remain unchanged, even after one-year of follow-up.

Adult↗

PubMed2000

[A case of Gerstmann-Sträussler-Scheinker syndrome (P102L) accompanied by optic atrophy].

We report a patient with Gerstmann-Sträussler-Scheinker syndrome (GSS102) who developed optic atrophy. He had been complaining of slowly progressive postural unsteadiness and pain in both legs for 3 years. Visual acuity subacutely worsened in the last half year. His father and two aunts, who already died, had been diagnosed to have dementia. It is uncertain whether they had optic atrophy or not. He was alert but apathetic. Neurological examination revealed cerebellar ataxia, painful dysesthesia and loss of deep tendon reflexes in the lower limbs. Fundoscopic examination revealed bilateral optic atrophy without retinal degeneration, which has never been reported in GSS. A brain MRI showed mild atrophy of cerebellar hemispheres without signal abnormalities of optic nerves. DNA analysis of prion gene revealed point mutation at codon 102 (P102L), which was relatively common mutation in GSS. Other mutations were not found. Only two patients of Creutzfeldt-Jakob disease with optic atrophy have been reported. This case seems to be important to investigate why optic tracts are generally spared in prion disease.

Gerstmann-Straussler-Scheinker Disease↗

PubMed2001

Fundus autofluorescence and development of geographic atrophy in age-related macular degeneration.

PURPOSE: To describe the development of new and enlargement of preexisting atrophy confined to areas with abnormally high levels of in vivo autofluorescence in eyes with geographic atrophy (GA) associated with age-related macular degeneration (ARMD). METHODS: The spatial distribution and intensity of fundus autofluorescence as well as the spread of GA and occurrence of new GA was recorded over a period of 3 years in three patients with ARMD using a confocal scanning laser ophthalmoscope. RESULTS: A diffuse irregular increased autofluorescence at the posterior pole was recorded at baseline in the presence of unifocal or multifocal patches of geographic atrophy. Within these areas of elevated autofluorescence, new atrophic areas developed, and existing patches of atrophy enlarged during the review period, whereas this was not observed in areas with normal background autofluorescence. The total area of abnormal autofluorescence also showed enlargement over time. CONCLUSIONS: These preliminary findings suggest that areas of increased autofluorescence precede the development and enlargement of outer retinal atrophy in eyes with ARMD. Because the dominant fluorophores of fundus autofluorescence are part of lipofuscin granules of RPE cells, the observations indicate that excessive RPE lipofuscin accumulation may be of significance in the pathogenesis of GA associated with ARMD. With GA being a major cause for severe visual loss in ARMD, in vivo fundus autofluorescence recording over time may allow identification of prognostic determinants and may give important clues to the understanding of mechanisms of disease.

Aged↗

PubMedDate not supplied

Diffusion and perfusion MR imaging in cases of Alzheimer's disease: correlations with cortical atrophy and lesion load.

BACKGROUND AND PURPOSE: Perfusion and diffusion-weighted MR imaging are powerful new imaging techniques for evaluating tissue pathophysiology in association with many neurologic disorders, such as neurodegenerative diseases. The purpose of our study was to evaluate the sensitivity and specificity of dynamic susceptibility contrast-enhanced MR imaging and diffusion-weighted MR imaging in cases of Alzheimer's disease and to assess the role of atrophy in the quantification of cortical perfusion. METHODS: Thirty-nine participants were studied: 18 patients with moderate cognitive impairment with probable Alzheimer's disease, 16 patients with mild impairment with possible or probable Alzheimer's disease, and 15 group-matched elderly healthy comparison volunteers. Relative values of temporoparietal, sensorimotor, and hippocampal regional cerebral blood volume (rCBV) were measured as a percentage of cerebellar rCBV, and group classification was assessed with logistic regression. Brain atrophy was used as a covariate to assess its role in rCBV quantification. Regions of interest placed on orientation-independent apparent diffusion coefficient maps allowed the calculation of apparent diffusion coefficient values and relative anisotropic indices of the head of the caudate nuclei, thalamus, parietal, frontal, and hippocampal cortices bilaterally, genu and splenium of corpus callosum, and anterior and posterior white matter in patients with Alzheimer's disease and in control volunteers. RESULTS: Temporoparietal rCBV ratios were reduced bilaterally in the patients with Alzheimer's disease. Sensitivity was 91% in moderately affected patients with Alzheimer's disease and 90% in patients with mild cases. Specificity was 87% in healthy comparison volunteers. Lower values of sensitivity and specificity were obtained for sensorimotor (73%, 50%, and 67%, respectively) and hippocampal cortices (80%, 80%, and 65%, respectively). Using brain atrophy as a covariate, patients with Alzheimer's disease still showed a statistically significant reduction of rCBV compared with control volunteers. Diffusion-weighted MR imaging analysis only showed a trend, with no statistic significance, of reduction of anisotropy in posterior white matter. CONCLUSION: Dynamic susceptibility contrast-enhanced MR imaging of rCBV may be an alternative to nuclear medicine imaging for the evaluation of patients with Alzheimer's disease. When brain atrophy is used as a covariate, differences in rCBV still persist between patients with Alzheimer's disease and control volunteers, suggesting that perfusion impairment is unrelated to atrophy. No significant results for either white or gray matter were obtained using diffusion-weighted MR imaging.

Aged↗

PubMed2001

[Quantitative estimation of brain atrophy and function with PET and MRI two-dimensional projection images].

PURPOSE: The purpose of this paper is to estimate the extent of atrophy and the decline in brain function objectively and quantitatively. METHODS: Two-dimensional (2D) projection images of three-dimensional (3D) transaxial images of positron emission tomography (PET) and magnetic resonance imaging (MRI) were made by means of the Mollweide method which keeps the area of the brain surface. A correlation image was generated between 2D projection images of MRI and cerebral blood flow (CBF) or 18F-fluorodeoxyglucose (FDG) PET images and the sulcus was extracted from the correlation image clustered by K-means method. Furthermore, the extent of atrophy was evaluated from the extracted sulcus on 2D-projection MRI and the cerebral cortical function such as blood flow or glucose metabolic rate was assessed in the cortex excluding sulcus on 2D-projection PET image, and then the relationship between the cerebral atrophy and function was evaluated. This method was applied to the two groups, the young and the aged normal subjects, and the relationship between the age and the rate of atrophy or the cerebral blood flow was investigated. This method was also applied to FDG-PET and MRI studies in the normal controls and in patients with corticobasal degeneration. RESULTS: The mean rate of atrophy in the aged group was found to be higher than that in the young. The mean value and the variance of the cerebral blood flow for the young are greater than those of the aged. The sulci were similarly extracted using either CBF or FDG PET images. CONCLUSIONS: The purposed method using 2-D projection images of MRI and PET is clinically useful for quantitative assessment of atrophic change and functional disorder of cerebral cortex.

Adult↗

PubMed2001

Morphometric study of the midsagittal MR imaging plane in cases of hydrocephalus and atrophy and in normal brains.

BACKGROUND AND PURPOSE: Midsagittal morphologic changes often aid in the diagnosis of hydrocephalus. Stretching and upward displacement of the corpus callosum, widening of third ventricular recesses, and decreased mammillopontine distance have been described as indicating the possibility of hydrocephalus. Quantitative studies are scarce. We performed retrospective, quantitative analysis to verify and quantify changes in midline morphology that might differentiate hydrocephalus and ventriculomegaly due to atrophy. METHODS: Sagittal MR imaging studies of 22 patients with hydrocephalus and 32 patients with atrophy were analyzed, as were 42 studies with normal findings. The studied parameters included mammillopontine and mammillocommissural distances, callosal height at two points, and the distances between the lines passing through the chiasm (chiasmal line) and the edge of the callosal splenium. Various angles between the chiasmal line and surrounding structures were measured. Similar measurements were done with the line passing through the third ventricular floor segment anterior to the mammillary bodies (third ventricular line). RESULTS: In hydrocephalus, mammillopontine distance decreased, mammillocommissural distance increased, the third ventricular floor segment was concave in most cases, and the chiasmal line rotated clockwise. These changes were not seen in atrophy. Callosal height was increased in hydrocephalus significantly more than in atrophy. CONCLUSION: Specific changes of the midsagittal plane in hydrocephalus, some of which have not been described previously, can be observed and quantified, which might aid in differentiating this condition from atrophy.

Adolescent↗

PubMedDate not supplied

Patterns of cerebral atrophy in primary progressive aphasia.

The authors illustrate the spectrum of clinical and imaging patterns in primary progressive aphasia (PPA), a syndrome of slowly progressive speech and language impairment occurring with neurodegenerative disease. Although PPA presents with relatively isolated impairment in language, many patients progress to global cognitive or behavioral dysfunction. The syndrome may be associated with frontotemporal dementia (FTD)- or Alzheimer disease (AD)-type changes. Authors describe the clinical presentation in three cases of PPA and analyze the pattern of cerebral atrophy in each case with voxel-based morphometry. Two patients presented with nonfluent progressive aphasia. Subtle differences in the clinical features were suggestive of FTD in one case and AD in the other. Neuroimaging revealed a predominance of frontal atrophy in the first case and temporo-parietal atrophy in the second. The third case presented with the syndrome of semantic dementia and showed the typical behavioral problems associated with FTD and a pattern of left-greater-than-right temporal atrophy. Different clinical syndromes in PPA are associated with different patterns of atrophy. In the future, combined analysis of imaging and clinical characteristics may allow more accurate etiologic diagnosis.

Aged↗

PubMed2002

[Ultrasound differentiation between benign enlargement of the subarachnoid space and brain atrophy].

Fluid collections surrounding the brain (pericerebral fluid collections) in infants can be caused by a variety of conditions: benign enlargement of the subarachnoid space, passive dilatation of the subarachnoid space due to brain atrophy, subdural hygroma and subdural effusion as a result of meningitis or subdural haematoma. An enlarged frontal subarachnoid space and normal or minimally enlarged ventricular size, with normal or increase head circumference is relatively common finding in infancy. Without associated brain anomalies, this finding predicts normal development of the child. In our study, we have followed up psychomotor development of 22 children, with increased diameters of subarachnoid spaces, detected by ultrasound examination of the brain, without associated brain anomalies. The inclusion criterion for study was enlarged subarachnoid space, measured at the conventional coronal section at the level of the interventricular foramen. The upper limits of each measurements were: 3 mm for sinocortical width, 4 mm for craniocortical width and 6 mm for the interhespheric width. The patients have been followed up to the age of 24 months. Each of them had normal development. 16 of them had normal head circumference. 6 of them had head circumference above the 97th percentile and their head circumference measurements have been plotted for the next 6 months after the diagnosis, to be certain that growth is paralleling the normal curve. It is important to differ benign enlargement of subarachnoid space from brain atrophy, which is quite "serious" diagnosis, with poor neurodevelopmental prognosis. The brain atrophy has been presented with passive dilatation of subarachnoid space and ventriculomegaly, as well. In the case of benign enlargement of subarachnoid space normal or minimally enlarged ventricular size is present. For proper interpretation of this ultrasound finding, correlation with head circumference is necessary. We recommend the head circumference percentile chart to be enclosed to the each brain sonography finding. The algorithm of the further neurological evaluation differs significantly in the case of benign enlargement of subarachnoid space and brain atrophy. In the case of benign enlargement of subarachnoid space further neuroimaging procedures are not needed (in our study it has been done for 6 patients). If the brain atrophy is suspected, further complete neurological examination is necessary.

Atrophy↗

PubMed1992

Condylar atrophy in craniomandibular disorders.

In order to investigate the clinical characteristics of patients with condylar atrophy, we examined 146 patients with craniomandibular disorders using tomography. No statistical difference in occurrence of the condylar atrophy between males and females was observed. Patients with condylar atrophy was younger than those without condylar atrophy. And, condylar atrophy was closely related to craniomandibular disorders, especially to internal derangement or osteoarthrosis of the temporomandibular joint.

Adolescent↗

PubMed1992

Thymocyte injury after in vitro chemical exposure: potential mechanisms for thymic atrophy.

In addition to hepatic injury, thymic atrophy is a common observation in rodent subchronic toxicity studies. We have examined representative chemicals which produce thymic atrophy in rodents for their ability to cause direct thymocyte injury because the mechanism(s) responsible for these effects have not been determined. Although a number of the compounds examined failed to have any observable direct effect on thymocytes, others either inhibited lymphocyte proliferation or initiated cell death. In the latter group, thymocyte death was always preceded by increases in intracellular Ca++ and involved, to varying degrees, necrotic and apoptotic events. Apoptosis, as evidenced by cellular DNA cleavage into multiples of 180-200-base pair oligonucleotides and partial cell protection by cycloheximide treatment, was most evident after treatment with acetaldehyde or dibutyltin dichloride. A number of compounds that produce thymic atrophy also inhibited T lymphocyte proliferation without evidence of cell death. Considering that many of the compounds tested failed to produce any evidence of direct thymocyte injury (i.e., necrosis, apoptosis or inhibition of cell proliferation), indirect mechanisms may also be involved in thymic atrophy and may target prothymocytes in the bone marrow, after normal homing patterns or injure the thymic epithelium. Thus, it appears that a variety of mechanisms may be responsible for chemical-induced thymic atrophy and/or injury.

Animals↗