SEARCH · PubMed Health

Results for “Atrophy”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources

PubMed1995

Scanning laser ophthalmoscopic analysis of the pattern of visual loss in age-related geographic atrophy of the macula.

PURPOSE: We explored the clinical impression that geographic atrophy of the retinal pigment epithelium, a form of advanced age-related macular degeneration, is perceived by the patient as progressing gradually, even when fixation switches from foveal to extrafoveal. METHODS: We analyzed the responses of 60 patients with geographic atrophy to a questionnaire administered as part of a five-year study of the natural course of geographic atrophy, funded by the National Eye Institute. We performed scanning laser opthalmoscope perimetry on all patients. We examined two additional patients with geographic atrophy who reported abrupt visual loss. RESULTS: No eye with geographic atrophy was reported by any patient to have had sudden visual loss. Although most patients with geographic atrophy show foveal fixation until the fovea is atrophic and then show extrafoveal fixation, scanning laser ophthalmoscope perimetry in three patients with geographic atrophy showed alternation between a foveal and an extrafoveal retinal locus for fixation. Two patients with geographic atrophy who complained of abrupt visual loss were found to have occult choroidal neovascularization, which evolved in one patient to classic choroidal neovascularization. The neovascularization was difficult to detect because of the presence of geographic atrophy and its associated ophthalmoscopic and fluorescein angiographic features. CONCLUSIONS: Visual loss in geographic atrophy is nearly always perceived by the patient as being gradual, even when considerable decreases in visual acuity occur and when foveal vision and fixation are lost. A possible explanation for this perception is that there is a transitional period during which a patient uses both a foveal and extrafoveal site for fixation. The complaint of abrupt visual loss in a patient with geographic atrophy should raise the suspicion of choroidal neovascularization, which may be occult and difficult to detect.

Aged↗

PubMed1999

Parapapillary atrophy in patients with focal visual field loss.

PURPOSE: To examine parapapillary atrophy in normal subjects and patients with primary open-angle glaucoma with focal visual field loss. METHODS: Twenty-nine patients with repeatable early focal visual field loss according to standard automated perimetry (Humphrey program 24-2) and 29 matched (age and disk area) normal subjects were included. Parapapillary atrophy area and optic disk topography were evaluated with a confocal scanning laser ophthalmoscope. The difference in parapapillary atrophy area between normal subjects and patients with glaucoma was examined. Optic disk topography was evaluated by means of the rim-disk area ratio in 36 10-degree sectors and classified into diffuse and focal patterns of neuroretinal rim thinning. In patients with a focal pattern, the locations of rim thinning and parapapillary beta zone atrophy were compared. RESULTS: Beta zone atrophy was detected more frequently in patients with glaucoma (45% [13/29]) than in normal subjects (7% [2/29]), and it was located both superiorly and inferiorly in 92% (12/13) of the glaucoma patients. Alpha zone atrophy was significantly larger in patients with glaucoma than normal subjects (P = .009) but not more frequent (97% [28/29] in both groups). Sixty-one percent (8/13) of glaucoma patients with beta atrophy had diffuse thinning and 31% (4/13) had focal thinning. Eight percent (1/13) did not have neuroretinal rim thinning. In the four patients with both focal rim thinning and beta zone atrophy, the location of rim thinning corresponded to the location of the beta zone atrophy (100% [4/4]). CONCLUSIONS: In patients with early focal glaucomatous visual field loss, the presence and location of parapapillary beta zone atrophy and neuroretinal rim thinning are in good correspondence. Observation of localized parapapillary beta zone atrophy in clinical practice should direct one to more closely examine the optic disk in this region, as it may reveal localized rim thinning in a disk previously considered to be normal. Moreover, diffuse structural change in an eye with only focal functional change, as determined by standard automated perimetry, is consistent with the possibility that structural damage may be more widespread than functional damage in these patients.

Adult↗

PubMed1998

Increasing peripapillary atrophy is associated with progressive glaucoma.

OBJECTIVE: This study aimed to determine the incidence and degree of progression of peripapillary atrophy in progressive and nonprogressive glaucoma. STUDY DESIGN: A retrospective cohort study. PARTICIPANTS: A total of 75 eyes of 75 patients were examined. MAIN OUTCOME MEASURES: Qualitative assessment of optic disc, peripapillary atrophy,and visual field change was performed by three experienced, masked, independent observers. METHODS: Rim-disc area ratio and peripapillary atrophy-disc area ratio were measured at baseline and follow-up with computer-aided planimetry. RESULTS: Among 75 eyes studied with an average duration of follow-up of 8 years (range, 4-19 years), 33 (44%) showed progressive optic disc damage. Twenty-one (64%) of 33 eyes with progressive disc damage showed peripapillary atrophy progression, and 7 (17%) of 42 eyes without progressive disc damage showed peripapillary atrophy progression; this difference was significant (P < 0.01). In groups with and without peripapillary atrophy, no statistically significant differences were found for mean intraocular pressure, baseline rim-disc area ratio, or baseline peripapillary atrophy-disc area ratio. However, optic disc progression and visual field progression were statistically more frequent in the group with peripapillary atrophy progression (75% and 54%, respectively) than in the group without peripapillary atrophy progression (26% and 11%, respectively) (P < 0.01). There was a statistically significant correlation between measurements of peripapillary atrophy area increase and disc rim loss over time (r = -0.35, P = 0.002). CONCLUSION: Progression of peripapillary atrophy is associated with progressive optic disc damage and progressive visual field loss in glaucoma and may be used as a marker for progressive glaucomatous damage.

Adult↗

PubMed2003

Neuropsychological-neurophysiological alterations and brain atrophy in cirrhotic patients.

Psychometric performance has been reported to be related to brain atrophy in cirrhotics, but the relationship between brain atrophy and EEG findings is still unknown. The aim of this study was to ascertain the relationship among brain atrophy, EEG, and cognitive performance in cirrhotics. Sixty-eight cirrhotics (age = 55 +/- 10 years; males-66%) underwent psychometric evaluation (Symbol Digit Test, Trail Making Test-Part A, Scan test), EEG recording and spectral analysis (S-EEG), and brain CT scan. Central brain atrophy was ascertained by the following indexes of brain atrophy: the Evans' index, the bicaudate index, the cella media index, the bifrontal index, and the ventricular index; cortical brain atrophy by the sulci index. The severity of liver failure was assessed by the Child-Pugh score: 18% of patients were Child-Pugh Class A, 50% Class B, and 32% Class C. Central and cortical atrophies were found to be correlated with age, but not with the Child-Pugh score. Psychometric performance and the EEG mean dominant frequency (MDF) were found to be correlated with brain atrophy. Multivariate analysis showed that a poor psychometric performance was independently predicted by EEG slowing (MDF: p < 0.01) and by central brain atrophy (cella media index: p < 0.01). In conclusion, brain atrophy was associated with a poor psychometric performance and EEG alterations in cirrhosis. Both brain atrophy and EEG alterations independently predicted cognitive dysfunction in cirrhotic patients.

Adult↗

PubMed2004

Clinical rating of cortical atrophy and cognitive correlates following traumatic brain injury.

We report on the utility of using a rapid, easy-to-use, visually based semi-quantitative neuroimaging atrophy rating scale in individuals with traumatic brain injury (TBI) and normal control subjects. Magnetic resonance (MR) scans were rated using a standardized semi-quantitative MR rating method. A four-point scale was used to rate each scan for atrophy in frontal, temporal, and parietal areas. Seventy-five TBI subjects (50 males, 25 females) and 75 age- and gender-matched control subjects were compared for atrophy ratings. Clinical atrophy ratings were also compared to a quantitative measure of atrophy, the ventricle-to-brain ratio, and with the TBI subjects' scores on standard neuropsychological tests. TBI patients had significantly higher clinical atrophy ratings in frontal and temporal lobe areas compared to controls. The clinical atrophy ratings significantly correlated with the ventricle-to-brain ratio, a quantitative measure of atrophy in the same TBI subjects. Higher clinical ratings of frontal and temporal atrophy correlated with deficits in memory and executive function. These findings indicate that clinical ratings of trauma-induced atrophy can be reliably performed and are associated with neuropsychological outcome and quantitative measures of cerebral atrophy.

Adolescent↗

PubMed2005

Ultrasound diagnosis of brain atrophy is related to neurodevelopmental outcome in preterm infants.

BACKGROUND: Intraventricular haemorrhage and periventricular leukomalacia are associated with poor outcome of very preterm infants, while the role of more subtle cerebral alterations, as detected by cranial ultrasound, is less clear. AIM: In this study, we related periventricular echodensities and signs of brain atrophy to neurodevelopmental outcome at 3 y of age. PATIENTS AND METHODS: All preterm infants born in 1997 in our institution with a gestational age <32 wk or birthweight <1500 g were subjected to repeated standardized cranial ultrasound examinations until discharge. Survivors were examined at 3 y of age employing the Bayley Scales of Infant Development II. RESULTS: Eighty-seven infants were enrolled (birthweight 430-2500 g (median 1200 g), gestational age 24-34 wk (median 29 wk)). Periventricular echodensities were detected in 42 infants (48%); in 12 cases persisting <7 d, in 30 cases >7 d. At discharge, 18 infants (22%) had signs of brain atrophy. Neurodevelopmental outcome was assessed in 64 infants. Infants with signs of brain atrophy scored significantly lower on MDI (atrophy 91.8, no atrophy 101.9; p=0.02), PDI (atrophy 91.4, no atrophy 106.5; p=0.001) and Behaviour Rating Scale (atrophy 41.1, no atrophy 66.4; p=0.01) than infants without atrophy. Periventricular echodensities were not related to outcome. CONCLUSION: Our data show that infants with sonographic signs of brain atrophy at discharge achieve lower scores in neurodevelopmental testing at 3 y.

Atrophy↗

PubMed2005

Hippocampal atrophy on MRI in frontotemporal lobar degeneration and Alzheimer's disease.

BACKGROUND: Hippocampal atrophy on magnetic resonance imaging (MRI) is an early characteristic of Alzheimer's disease. However, hippocampal atrophy may also occur in other dementias, such as frontotemporal lobar degeneration (FTLD). OBJECTIVE: To investigate hippocampal atrophy on MRI in FTLD and its three clinical subtypes, in comparison with Alzheimer's disease, using volumetry and a visual rating scale. METHODS: 42 patients with FTLD (17 frontotemporal dementia, 13 semantic dementia, and 12 progressive non-fluent aphasia), 103 patients with Alzheimer's disease, and 73 controls were included. Hippocampal volumetry and the easily applicable medial temporal lobe atrophy (MTA) rating scale were applied to assess hippocampal atrophy. RESULTS: Multivariate analysis of variance for repeated measures showed an effect of diagnostic group on hippocampal volume. There was a significant diagnosis by side (left v right) interaction. Both FTLD and Alzheimer's disease showed hippocampal atrophy compared with controls. Results of the visual MTA rating scale confirmed these findings. Within the FTLD subtypes there were marked differences in hippocampal atrophy. Frontotemporal dementia and semantic dementia showed bilateral hippocampal atrophy, and in semantic dementia the left hippocampus was smaller than in Alzheimer's disease. No significant hippocampal atrophy was detected in non-fluent progressive aphasia. CONCLUSIONS: Hippocampal atrophy is not only a characteristic of Alzheimer's disease but also occurs in FTLD. The three clinical subtypes of FTLD show different patterns of hippocampal atrophy.

Aged↗

PubMed2006

Role for IkappaBalpha, but not c-Rel, in skeletal muscle atrophy.

Skeletal muscle atrophy is associated with a marked and sustained activation of nuclear factor-kappaB (NF-kappaB) activity. Previous work showed that p50 is one of the NF-kappaB family members required for this activation and for muscle atrophy. In this work, we tested whether another NF-kappaB family member, c-Rel, is required for atrophy. Because endogenous inhibitory factor kappaBalpha (IkappaBalpha) was activated (i.e., decreased) at 3 and 7 days of muscle disuse (i.e., hindlimb unloading), we also tested if IkappaBalpha, which binds and retains Rel proteins in the cytosol, is required for atrophy and intermediates of the atrophy process. To do this, we electrotransferred a dominant negative IkappaBalpha (IkappaBalphaDeltaN) in soleus muscles, which were either unloaded or weight bearing. IkappaBalphaDeltaN expression abolished the unloading-induced increase in both NF-kappaB activation and total ubiquitinated protein. IkappaBalphaDeltaN inhibited unloading-induced fiber atrophy by 40%. The expression of certain genes known to be upregulated with atrophy were significantly inhibited by IkappaBalphaDeltaN expression during unloading, including MAFbx/atrogin-1, Nedd4, IEX, 4E-BP1, FOXO3a, and cathepsin L, suggesting these genes may be targets of NF-kappaB transcription factors. In contrast, c-Rel was not required for atrophy because the unloading-induced markers of atrophy were the same in c-rel(-/-) and wild-type mice. Thus IkappaBalpha degradation is required for the unloading-induced decrease in fiber size, the increase in protein ubiquitination, activation of NF-kappaB signaling, and the expression of specific atrophy genes, but c-Rel is not. These data represent a significant advance in our understanding of the role of NF-kappaB/IkappaB family members in skeletal muscle atrophy, and they provide new candidate NF-kappaB target genes for further study.

Animals↗

PubMed2004

Role of MRI in multiple sclerosis II: brain and spinal cord atrophy.

A growing body of evidence indicates that irreversible tissue destruction including axonal and neuronal degeneration is a key component of the multiple sclerosis (MS) disease process. Magnetic resonance imaging (MRI) is a powerful technique that can be combined with semiautomated or automated computer assisted analysis approaches to detect progressive atrophy of the brain and spinal cord with high sensitivity and reproducibility. The pathophysiology of central nervous system (CNS) atrophy in MS is unknown but likely represents an epiphenomenon related to the effects of inflammation including chronic demyelination, axonal injury, neuronal loss and Wallerian degeneration. Other factors that may contribute to tissue atrophy include injury to the normal appearing gray and white matter by mechanisms such as loss of growth factors, altered electrical conduction and pathologic iron deposition. Prospective studies have suggested that atrophy in MS is predicted by previous inflammatory activity as measured by overt MRI lesions. Gadolinium (Gd)-enhancing lesions have shown a particularly strong predictive value in some but not all longitudinal studies of brain atrophy. Brain atrophy has also been related in cross-sectional and longitudinal studies to T2-hypointense lesions in deep grey matter, suggesting a link between tissue iron deposition and atrophy. The measurement of brain atrophy seems to be of growing clinical relevance as a biomarker of the MS disease process. Atrophy should now be included as a secondary endpoint in trials of therapies aimed at limiting disease progression. Currently available anti-inflammatory immunomodulatory agents and immunosuppressive treatments, while effective at preventing clinical deterioration, have shown at best partial effects in preventing CNS atrophy. Thus, there is a need to further validate atrophy as an outcome measure and ultimately develop treatment strategies that will protect against the destructive aspects of the disease process. This should in turn lead to better long term neurologic functioning and a better quality of life for patients with MS.

Atrophy↗

PubMed2005

Regional brain atrophy evolves differently in patients with multiple sclerosis according to clinical phenotype.

BACKGROUND AND PURPOSE: Progressive brain atrophy is a well-known feature of multiple sclerosis (MS). We characterized the spatial evolution of atrophy in different MS phenotypes. METHODS: Dual-echo and T1-weighted MR images were obtained in 70 patients with MS and 10 healthy control subjects at entry and after 15 months. Within-group changes in regional atrophy were assessed by applying Structural Image Evaluation Using Normalization of Atrophy software and statistical parametric mapping analysis. Reported differences are for P <.001. RESULTS: During follow-up, patients with relapsing-remitting MS (RRMS) differences significant atrophy around the ventricular system; pericerebellar spaces; cerebellar tentorium; putamen; corpus callosum; cingulate sulcus; hippocampus; parieto-occipital fissure; lateral fissure; and frontal, parietal, temporal, and occipital cortex. Patients with secondary progressive MS developed significant atrophy of the cingulate sulcus; pulvinar; caudate nucleus; anterior orbital gyrus; mammillary body; fourth ventricle; and regions of frontal, parietal, temporal, and occipital cortex. Patients with primary progressive MS developed significant atrophy of the bilateral central sulcus; caudate nucleus; prepontine and quadrigeminal cisterns; lateral ventricle; and regions of frontal, parietal, temporal, and occipital cortex. In all phenotypes, the development of atrophy in some regions was significantly correlated with the accumulation of T2- and T1-visible lesions and clinical disability (r = -0.57 to -0.86). CONCLUSION: In MS, brain atrophy develops involving different structures in the different phenotypes. While ventricular enlargement is predominant in RRMS, cortical atrophy seems to be more important in the progressive forms. Measures of regional brain atrophy were significantly correlated with disability, suggesting that this approach is promising for bridging the gap between clinical and MR imaging findings in MS.

Adult↗

PubMed2005

Visual assessment of atrophy on magnetic resonance imaging in the diagnosis of pathologically confirmed young-onset dementias.

OBJECTIVES: To investigate the diagnostic accuracy of visual inspection of magnetic resonance imaging (MRI) in a range of pathologically confirmed diseases causing young-onset dementia and to assess the sensitivity and specificity of atrophy patterns for Alzheimer disease (AD) and frontotemporal lobar degeneration (FTLD). DESIGN: Sixty-two patients with pathologically confirmed diseases that may present as young-onset dementia were selected from a biopsy and postmortem series. The first diagnostic T1-weighted volumetric MRI was obtained for each patient, together with images from 22 healthy control subjects. All MRIs were assessed for regional atrophy independently by 3 neuroradiologists, blinded to all clinical details except age. Observers were also asked to use their clinical judgment to form a diagnosis. RESULTS: Eighty-seven percent of dementia cases were distinguished from controls after visual inspection of MRI, and a correct pathologically confirmed diagnosis was given in 58% of cases. Hippocampal atrophy was noted in 92% of AD cases but was commonly seen in other dementias and controls. A bilateral symmetrical pattern of hippocampal atrophy discriminated AD from FTLD with 47% specificity, while posterior greater than anterior gradient of atrophy was 92% specific for AD. Atrophy of the anterior, inferior, and lateral temporal lobes was suggestive of FTLD pathology (> or =90% sensitivity), while anterior greater than posterior gradient of atrophy and hemispheric asymmetry of atrophy were each at least 85% specific for FTLD. CONCLUSION: Despite variation and overlap of atrophy patterns, visual inspection of regional atrophy on MRI may aid in discriminating AD and FTLD.

Aged↗

PubMed1986

Diagnosis of cerebral atrophy in infants by near-field cranial sonography.

Cranial sonography is the ideal imaging tool for use in infants. However, it has not been used for the diagnosis of cerebral atrophy in infants as the subarachnoid space has been a "blind spot" with ultrasound. We evaluated cerebral atrophy by a unique application of cranial sonography that we have termed the near-field method, and compared these results with those of cranial computed tomography (CT). We examined 106 infants with the near-field method of cranial sonography. Eleven patients fitted our sonographic criteria for cerebral atrophy. Cranial CT was done in eight of the 11 patients with sonographic findings of cerebral atrophy and was consistent with the diagnoses of cerebral atrophy in all cases. Of these eight patients, one had cerebral atrophy and subdural effusion seen by both near-field sonography and cranial CT. Cranial CT was performed in eight of the 95 patients with normal sonographic findings, and all results were normal. All patients with cerebral atrophy determined by cranial CT were found to have cerebral atrophy by near-field sonography. Likewise, all patients without cerebral atrophy by cranial CT were not found to have cerebral atrophy CA by near-field sonography. The near-field method of cranial sonography therefore appears to have a sensitivity and specificity of 100% with cranial CT as a referral method.

Atrophy↗

PubMed2002

Mapping of autosomal recessive chronic distal spinal muscular atrophy to chromosome 11q13.

Distal spinal muscular atrophy is a heterogeneous group of neuromuscular disorders caused by progressive anterior horn cell degeneration and characterized by progressive motor weakness and muscular atrophy, predominantly in the distal parts of the limbs. Here we report on chronic autosomal recessive distal spinal muscular atrophy in a large, inbred family with onset at various ages. Because this condition had some of the same clinical features as spinal muscular atrophy with respiratory distress, we tested the disease gene for linkage to chromosome 11q and mapped the disease locus to chromosome 11q13 in the genetic interval that included the spinal muscular atrophy with respiratory distress gene (D11S1889-D11S1321, Z(max) = 4.59 at theta = 0 at locus D11S4136). The sequencing of IGHMBP2, the human homologue of the mouse neuromuscular degeneration gene (nmd) that accounts for spinal muscular atrophy with respiratory distress, failed to detect any mutation in our chronic distal spinal muscular atrophy patients, suggesting that spinal muscular atrophy with respiratory distress and chronic distal spinal muscular atrophy are caused by distinct genes located in the same chromosomal region. In addition, the high intrafamilial variability in age at onset raises the question of whether nonallelic modifying genes could be involved in chronic distal spinal muscular atrophy.

Adult↗

PubMed2006

Noninvasive versus histologic detection of gastric atrophy in a Hispanic population in North America.

BACKGROUND & AIMS: Cancer risk is directly correlated with the severity and extent of mucosal atrophy, making identification of atrophy a goal in cancer prevention programs. The aim of this study was to compare targeted histology with noninvasive testing for the identification of antral and/or corpus atrophy in North America. METHODS: In a cross-sectional study of a random sample of households, 8 gastric biopsy specimens were obtained from defined locations in the antrum and corpus. Biopsies were scored for the presence of Helicobacter pylori and gastric atrophy (defined as loss of normal glandular components). Atrophy was scored by using the Sydney system and a system based on the number and location of corpus biopsies with atrophy. Patients' sera were examined for pepsinogen I, pepsinogen II, and gastrin-17 (fasting and stimulated). RESULTS: One hundred eighty volunteers, approximately 30 per age group and ranging in age from 18-82 years, participated. There were 76 men. The overall weighted prevalence of a corpus atrophy was 4.7% (95% confidence interval, 2.3-7.0). There was a significant inverse relationship between the grade of corpus atrophy and the pepsinogen I/pepsinogen II ratio (R = -0.31, P < .01). We failed to confirm the usefulness of the proposed algorithm by using gastrin-17, H. pylori serology, and serum pepsinogens to categorize the gastric histology. The Sydney system underestimated the prevalence of corpus atrophy by approximately 25%. CONCLUSION: Noninvasive testing is both possible and practical by using pepsinogen assays for the identification of the precancerous condition of moderate to severe corpus atrophy in North American Hispanic patients.

Adolescent↗

PubMed2005

Atrophy in prostate needle biopsy cores and its relationship to prostate cancer incidence in screened men.

OBJECTIVES: To evaluate whether the incidence of atrophy reported on sextant biopsies is associated with subsequent prostate cancer detection and to obtain a more thorough analysis of the different categories and extent of atrophy, we performed a review of benign biopsy cores. METHODS: In the Rotterdam section of the European Randomized Study of Screening for Prostate Cancer, 4117 and 1840 men underwent sextant biopsy in the first and second screening round (4-year interval), respectively. Sextant biopsy was prompted by elevated prostate-specific antigen levels. For review, randomly taken benign sextant biopsies (n = 202) with a follow-up of at least 8 years were chosen. RESULTS: Before review, atrophy was reported in the biopsies of 11.4% and 8.7% of the first and second round, respectively. The prostate cancer incidence during 8 years of follow-up after an initial diagnosis of atrophy was 10.4%, which was not significantly different than the 12.3% of cancers detected after a benign diagnosis without reference to atrophy. After review, the incidence of simple atrophy, post-atrophic hyperplasia, and sclerotic atrophy in sextant biopsies was 91%, 47%, and 9%, respectively. Extensive atrophy was observed in 5% of biopsies. Only 2 men (4.7%) in the reviewed group had a subsequent diagnosis of prostate cancer in the 8 years of follow-up. Additionally, prostatic intraepithelial neoplasia was diagnosed in 3 men (7.0%) in the second screening round. CONCLUSIONS: Atrophy, especially its simple form, is a very common lesion in prostate biopsy cores (94%). Atrophy in an asymptomatic population undergoing screening was not associated with a greater prostate cancer or prostatic intraepithelial neoplasia incidence during subsequent screening rounds.

Aged↗

PubMedDate not supplied

The MRI pattern of frontal and temporal brain atrophy in fronto-temporal dementia.

OBJECTIVE: To compare patterns of brain atrophy in fronto-temporal dementia (FTD) and Alzheimer's disease (AD) since atrophy in individual areas may not be sufficiently specific as diagnostic marker. METHODS: Frontal, temporal and hippocampal atrophy was measured from MRI of 10 FTD patients, 27 AD, and 27 controls. Corrected atrophy and asymmetry were computed (W-scores). RESULTS: FTD had mild atrophy in the hippocampus (average W-score=-1.3), severe in the frontal (W-score=-2.4) and very severe in the temporal lobes (W-score=-2.9). AD had moderate atrophy in the hippocampus and temporal lobes (W-score=-1.8 and -1.9, respectively), and very mild frontal atrophy (W-score=-0.9). Atrophy was more asymmetrical in FTD (left more atrophic) than in AD patients, particularly in the temporal lobes. A discriminant function including the asymmetry values of frontal and temporal regions could separate FTD from AD with 90% sensitivity and 93% specificity. CONCLUSIONS: FTD is characterized by a specific pattern of atrophy, more useful than atrophy of single regions in the differential diagnosis.

Aged↗

PubMed1987

Histopathology of different types of atrophy of the human tongue.

Numerous studies have been devoted to the various histopathologic changes of the surface of the tongue. The muscles of the tongue and their changes in the process of ageing as well as in neurogenic atrophies, however, have not been systematically examined so far. Enlarging upon previous studies, an autopsy material of 170 tongues from all age groups was histologically examined in order to identify the steps in the development of age-related atrophy. These are characterized by a histometrically documented atrophy of the musculature with progressive lipomatosis. Fatty infiltration starts in the 2nd/3rd decade at three sites of predilection: body, root and tip of the tongue in the region of the anterior lingual gland (NUHN). The age-dependent atrophy and the known clinical behaviour of neurogenic atrophies of the tongue are correlated with the histopathology of three typical forms: a neurogenic myasthenic atrophy of the tongue with high-grade symmetrical fatty replacement as an expression of a progressive myasthenic denervation; a lipomatous atrophy of the tongue as a late stage of poliomyelitis and long-term treatment in the "Iron Lung", and a lipomatous hemiatrophy due to posttraumatic extracranial hypoglossus paresis. The paretic part of this tongue consists of 85-90% fatty tissue. The different degrees of muscular atrophy of the tongue are largely compensated by metaplasia of fatty tissue in the perimysium following muscular degeneration (in the sense of a fatty replacement). With the exception of general and severe myasthenic atrophy, size, form and function of the tongue fail to show any significant changes in age-related atrophy and hemiatrophy.

Adolescent↗

PubMed2003

Macular atrophy after photocoagulation of soft drusen.

PURPOSE: To analyze the appearance and characteristics of macular atrophy after photocoagulation of soft drusen. PATIENTS AND METHODS: The authors studied the development of macular atrophy in 52 consecutive eyes (52 patients) that underwent green argon laser photocoagulation for the treatment of soft drusen. The mean age was 71.4 +/- 5.1 years (range, 61-85 years). Twelve eyes (23%) were in men and 40 (77%) were in women. Follow-up averaged 50.1 +/- 21.3 months (range, 6-96 months). RESULTS: Macular atrophy occurred in nine eyes (17.7%), including five (56%) women and four (44%) men. The time interval between photocoagulation and macular atrophy averaged 37.2 +/- 21.2 months (range, 7-75 months). The mean age of patients with macular atrophy was 68.1 +/- 4.6 years (range, 61-75 years). Mean best-corrected visual acuity (BCVA) after soft drusen photocoagulation and before macular atrophy development was 20/55 (range, 20/28-20/200). After the appearance of macular atrophy, mean BCVA was 20/126 (range, 20/50-20/900). Differences between BCVA before and after macular atrophy were statistically significant (P = 0.02, student's paired t-test). CONCLUSIONS: Macular atrophy can occur after photocoagulation of soft drusen, as applied according to our treatment protocol. The development of macular atrophy was associated with a significant decrease in BCVA.

Aged↗