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PubMed1996

Correlation between peripapillary atrophy and optic nerve damage in normal-tension glaucoma.

PURPOSE: To investigate the correlation between peripapillary atrophy and visual field defects as well as optic nerve head configurations in patients with normal-tension glaucoma (NTG). METHODS: Topographic measurements for peripapillary atrophy and optic nerve head using confocal scanning laser tomography and automated static threshold perimetry were performed on 102 eyes of 51 patients with NTG. Peripapillary atrophy was divided into (1) a central zone (zone Beta) with visible, large choroidal vessels and sclera, and (2) a peripheral zone (zone Alpha) with irregular hyper- and hypopigmentation. The area, angular extent around the disc, and radial extent of each zone were measured. RESULTS: The area and extent of zone Beta increased significantly with increasing visual field defects expressed in terms of mean deviation, corrected pattern standard deviation, central visual field defects within 5 degrees of fixation, and superior hemifield defects (r = 0.3770-0.5291, P < 0.01). The angular extent of zone Beta represented localized field defects better (r = 0.5217, P < 0.001) than diffuse field defects (r = -0.3770, P < 0.01). Zone Beta significantly correlated with optic nerve head topography. Intraindividual right-left-side differences of corrected pattern standard deviation showed the highest correlation with the side differences of zone Beta area (r = 0.6305, P < 0.001). The location of visual field defects correlated significantly with the location of peripapillary atrophy (chi-square = 9.0484, P = 0.011). Zone Alpha was not significantly correlated with visual field defects or optic nerve head configurations (P > 0.05). CONCLUSION: Peripapillary atrophy is significantly associated with functional and structural optic nerve damage in NTG.

Adult↗

PubMed1996

Interobserver variation in the measurements of peripapillary atrophy in glaucoma.

PURPOSE: The purpose of this retrospective study is to compare the measurements of intrapapillary and peripapillary parameters between two observers and test the usefulness of measuring different types of crescents. METHODS: Optic disc photographs of 23 eyes of 23 patients with glaucoma and 23 age-matched normal eyes were measured in Oulu and in Erlangen using manual planimetric techniques. The authors measured the following magnification corrected intrapapillary and peripapillary areas: optic disc, neuroretinal rim, cup: disc area ratio, scleral ring, central (zone beta), and peripheral peripapillary atrophy (zone alpha). Twenty-one patients with glaucoma had a follow-up of 3.2 years (range, 1.1-4.7 years), and follow-up for 19 control eyes was 3.7 years (range, 2.5-5.9 years). The measurements were performed in a masked fashion for the diagnosis and temporal sequence of the photographs. RESULTS: Central peripapillary atrophy (zone beta) was statistically significantly largest in primary open-angle glaucoma in both centers (Oulu, P=0.003; Erlangen, P=0.004), whereas normal and exfoliative eyes did not differ significantly from each other. The results for peripheral peripapillary atrophy (zone alpha) and scleral ring were less consistent. Despite statistically significant interobserver correlations ranging from r=0.30 (scleral ring area; P=0.0472) to r=0.97 (optic disc area; P=0.0001), the means of all parameters, except for zone alpha and beta, differed statistically significantly between the two observers. CONCLUSIONS: The central peripapillary atrophy, or zone beta, is the most reproducible parameter when measuring peripapillary atrophy in glaucoma. Nonetheless, its measurement is of limited usefulness in the recognition of glaucoma or progression of glaucomatous nerve damage.

Adult↗

PubMed1987

Prevalence of brain atrophy in liver cirrhosis patients with chronic persistent encephalopathy. Evaluation by computed tomography.

Brain computerized axial tomography scans were performed in 18 consecutive liver cirrhosis patients with chronic persistent encephalopathy (8 alcoholic and 10 nonalcoholic) in order to evaluate the incidence of brain atrophy in this pathological condition. Fifteen patients of similar age with liver cirrhosis of Child's class B but with acute episodic hepatic encephalopathy were studied in parallel. Brain atrophy was detected in 87.5% of alcoholic and in 50% of nonalcoholic liver cirrhosis patients with chronic persistent encephalopathy, whereas the patients with acute episodic encephalopathy were normal. The high frequency of brain atrophy in alcoholic patients with chronic encephalopathy can be attributed at least in part to the toxic effect of alcohol. The presence of brain atrophy in nonalcoholic liver cirrhosis patients with chronic persistent encephalopathy seems to indicate that the chronic exposure to toxins which are involved in the pathogenesis of hepatic encephalopathy leads to neuronal alterations which develop mainly in the cortex and which can be demonstrated by in vivo imaging only in a long-lasting state of coma. Moreover, alcohol and toxins causing hepatic encephalopathy seem to potentiate each other in inducing brain atrophy.

Adult↗

PubMedDate not supplied

Age-dependent cerebral atrophy and cognitive dysfunction in SAMP10 mice.

Findings obtained from a series of studies to characterize age-dependent changes in brain morphology and behavior of inbred SAMP10 mice are reviewed. Following apparently normal development, SAMP10 mice developed brain atrophy with advancing age. The neocortex was diffusely atrophic in aged SAMP10 mice, with the frontal cortex being most affected. The entorhinal cortex, amygdala, and nucleus accumbens were also atrophic. Other subcortical structures were mildly atrophic, but the hippocampus was not atrophic. Mild to moderate hypertrophic astrocytosis was seen in the atrophied regions. Alzheimer's type pathology was not seen. The cortical atrophy was due to both loss and shrinkage of neurons. Brain atrophy was not remarkable in normal aging control SAMR10 mice. In accordance with above morphological changes, SAMP10 mice developed cognitive impairments with advancing age that were demonstrated by poor performance in passive avoidance and conditional avoidance tasks. All of these features of SAMP10 mice were inherited. SAMP10, therefore, is a unique model of age-dependent, inherited cerebral atrophy with cognitive dysfunction.

Aging↗

PubMed1999

Decreased formation of ethoxyacetic acid from ethylene glycol monoethyl ether and reduced atrophy of testes in male rats upon combined administration with toluene and xylene.

Male painters are commonly exposed to ethylene glycol monoethyl ether (EGE), a well known reproductive toxic agent causing testicular atrophy, in the form of solvent mixture containing toluene (TOL) and xylene (XYL). This study was carried out to determine the effect of exposing male rats to solvent mixture containing TOL and XYL on the EGE (200 mg/kg) on testicular atrophy and production of toxic metabolite, ethoxyacetic acid (EAA) from EGE. Compared to the extent of testes atrophy observed upon EGE administration alone, the combined administration of EGE (200 mg/kg) with TOL (250 mg/kg) and XYL (500 mg/kg) for 4 weeks has reduced the extent of testes atrophy by 25%. The combined administration delayed the time for appearance of the highest plasma concentration (t(max)) of EAA from 3 to 6 h and also decreased the highest concentration (Cmax) as well as the total amount of plasma EAA (AUC(0-18 h)) by 45 and 29%, respectively. This explained the diminished testicular atrophy in male rats observed when EGE was administered in a solvent mixture containing TOL and XYL. This study suggested that testicular toxicity observed in male painters caused by EGE may be decreased when they are exposed to EGE in the form of solvent mixture containing TOL and XYL.

Acetates↗

PubMed2002

Delayed tendon reattachment does not reverse atrophy and fat accumulation of the supraspinatus--an experimental study in rabbits.

Muscle atrophy and fat accumulation occur after rotator cuff tearing. Whether these changes are reversible after a successful repair is still unknown. Imaging allows only a semi-quantitative assessment of muscle atrophy and fat deposition. As only experimental studies permit a quantification of both, a unilateral detachment and wrapping in a polyvinylidine fluoride membrane of the supraspinatus was done in 22 rabbits. After 12 weeks, the polyvinylidine fluoride membrane was removed in 10 rabbits and the tendon inserted into a bony trough. The opposite shoulder served as control. All rabbits were killed at 24 weeks. Accumulation of fat on the muscle surface as well as between the muscle fascicles and occasionally in the sarcoplasm was increased in both experimental groups when compared to controls (non-reattached 12.8%, reattached 23.5% vs controls 5.4%; all p < 0.005). The muscle atrophy was significant (non-reattached 9.2 ml, reattached 9.1 ml vs controls 10.7 ml; both p < 0.005). Neither atrophy nor fat accumulation were reversed by surgical reattachment of the supraspinatus tendon. On the contrary, the fat accumulation was higher in the reattached group (p < 0.005). The trauma of reattachment, the delay between detachment and reattachment or an insufficient duration of recovery may have contributed to both, the lack of reversibility of supraspinatus atrophy and fat accumulation.

Adipose Tissue↗

PubMed2003

Early reattachment does not reverse atrophy and fat accumulation of the supraspinatus--an experimental study in rabbits.

INTRODUCTION: Reattachment of the supraspinatus (SSP) tendon after spontaneous rupture leads to improved shoulder function. Whether this improvement of function is due to a reversal of muscle atrophy and fat accumulation known to occur after SSP rupture is still debated. Our previous study of late reattachment of SSP (12 weeks) failed to confirm a reversal of muscle atrophy and of fat accumulation. PURPOSE: To find out whether earlier reattachment (6 weeks) reverses atrophy and fat accumulation of the SSP. MATERIAL AND METHODS: Reattachment group: in seven rabbits unilateral supraspinatus detachment, reattachment after 6 weeks and killing 6 weeks later. Detachment group: in seven rabbits unilateral supraspinatus detachment and killing 12 weeks later. The contralateral shoulders served as controls (n=14). Determination of the supraspinatus constituents: muscle, extra- and intramuscular fat in volume and cross-sectional area. RESULTS: Muscle tissue in the reattachment group (8.6 ml+/-1s.d.=0.6) and in the detachment group (8.9 ml+/-0.9) were less than in control supraspinati (10.2 ml+/-0.9, both p<0.05). Extra- and intramuscular fat in the reattachment group (8.7%+/-3.2) was greater than in both, the detachment group (4.6%+/-3.5), and control supraspinati (2.8%+/-1.7, both p<0.05). CONCLUSION: In the rabbit, reattachment of the SSP at 6 weeks did neither reverse muscle atrophy nor fat accumulation during the ensuing 6 weeks. However, earlier reattachment (6 weeks) when compared with later reattachment (12 weeks) prevented an increase in fat accumulation. On the other hand, the delay before reattaching the tendon did not lead to an increase in muscle atrophy.

Adipose Tissue↗

PubMed1993

Microvascular events in bone marrow related to development of and recovery from bone atrophy in thiotepa-treated rats.

To clarify the relationship of microvascular events in the bone marrow to the development of and the recovery from bone atrophy, we examined quantitatively and qualitatively trabecular bone, sinusoids and haematopoietic tissue in the metaphysis of the tibia of rats given thiotepa, an antitumour drug derived from nitrogen mustards. The administration of thiotepa rapidly reduced the number of haematopoietic cells causing significant dilatation of the sinusoids and atrophy of the trabecular bone 1 day after the injection. However, these changes were transient; regeneration of haematopoietic cells and normalization of the dilated sinusoids started 3 days after the injection, and the atrophied trabecular bone gradually returned to normal starting 6 days after the injection. These results imply that an extreme decrease in velocity and margination of sinusoidal blood flow following marked dilatation due to a decrease in haematopoietic cells cause atrophy of the trabecular bone, and that normalization of the sinusoidal blood flow following regeneration of haematopoietic cells leads to recovery from atrophy of trabecular bone.

Animals↗

PubMed2003

Alzheimer's disease and frontotemporal dementia exhibit distinct atrophy-behavior correlates: a computer-assisted imaging study.

RATIONALE AND OBJECTIVES: The purpose of this study was to test the hypothesis that distinct patterns of gray matter atrophy are responsible for unique interruptions of the naming process in Alzheimer's disease (AD) and frontotemporal dementia (FTD). MATERIALS AND METHODS: Voxel-based morphometry (VBM) was performed to characterize at the voxel level the neuroanatomic changes that occur in AD and FTD based on high-resolution T1-weighted three-dimensional (3D) spoiled-gradient echo images of patients (AD, n = 12; FTD, n = 29) and healthy control subjects (n = 12). The cortical atrophy measurements were correlated with performance on behavioral measures of naming and related processes to identify brain regions that may contribute to this language function. RESULTS: Both AD and FTD have significant naming difficulty, and this difficulty in naming correlates with a measure of lexical retrieval in both patient groups as well. However, only FTD patients showed a correlation with semantic memory. Areas of cortical atrophy common to AD and FTD were found in the anterior temporal, posterolateral temporal, and dorsolateral prefrontal regions of the left hemisphere. Correlation with naming in both AD and FTD was seen in the left anterior temporal cortex, suggesting that this area may play a role in the lexical retrieval component of naming. We also observed several unique areas of cortical atrophy in temporal and frontal cortices of these patients. Right anterior temporal and left posterolateral temporal regions of atrophy correlated with naming difficulty in FTD, suggesting that these areas may contribute to the semantic memory component of naming. Cortical areas correlating with naming that are not atrophic may represent regions that play an optional role in naming. CONCLUSION: VBM provides an important first step in analyzing brain-behavior relations in vivo in patients with neurodegenerative diseases. More refined analyses of brain morphology via high-dimensional normalization methods that are capable of modeling local as well as global variability in neuroanatomical structure promise to be even more informative.

Aged↗

PubMed2002

Diagnostic patterns of regional atrophy on MRI and regional cerebral blood flow change on SPECT in young onset patients with Alzheimer's disease, frontotemporal dementia and vascular dementia.

OBJECTIVES: Alzheimer's disease (AD), frontotemporal dementia (FTD) and vascular dementia (VaD) are the three most common causes of young onset dementias. Most neuroimaging studies of these disorders have involved comparisons with normal controls. The aims of this study were to examine the clinical diagnostic value of magnetic resonance imaging (MRI) and single photon emission computed tomography (SPECT) (in combination and in isolation) in the differentiation of one form of dementia from another from amongst a group of AD, FTD and VaD. METHODS: T1 weighted MRI images and 99mTc-HMPAO SPECT images were obtained from consecutive patients with FTD (n=21), AD (n=23) and VaD (n=20) and rated visually by experienced neuroradiologists and nuclear medicine physicians. RESULTS: Asymmetrical atrophy was seen only in FTD. Frontotemporal dementia patients were the most atrophic whereas severe atrophy was rarely observed in VaD. Severe frontal atrophy (unilaterally or bilaterally) and/or asymmetrical atrophy on MRI is highly diagnostic (sensitivity 0.71, specificity 0.93, LR 10.24) of FTD from within a group of FTD and non-FTD (AD, VaD) patients. Mild or severe parietal atrophy with severe reduction in parietal regional cerebral blood flow on SPECT is diagnostic (sensitivity 0.71, specificity 0.76, LR 3.02) of AD from within a group of AD and non-AD (VaD, FTD) patients. CONCLUSION: Anatomical (MRI) and functional (SPECT) imaging provide different information and a combination of these modalities improves diagnostic specificity.

Aged↗

PubMed2003

Proliferation and distribution of myoepithelial cells during atrophy of the rat sublingual gland.

BACKGROUND: The present study was aimed to determine the proliferation and distribution of myoepithelial cells during atrophy of rat sublingual glands. METHODS: The excretory duct of the right sublingual gland of rats was doubly ligated with metal clips to induce atrophy in the gland. The atrophic sublingual glands were taken from 1 to 28 days after duct ligation and examined with single immunohistochemistry for actin as a marker of myoepithelial cells and with immunohistochemical double staining for actin and proliferating cell nuclear antigen (PCNA) as a marker of proliferating cells. RESULTS: In unligated sublingual glands, myoepithelial cells embraced acini and intercalated ducts, but not striated and interlobular excretory ducts. In the early stages of atrophy, myoepithelial cells surrounded small ducts but not large ones. However, in the later stages of atrophy, myoepithelial cells were also observed at the periphery of the large ducts. The immunohistochemical double staining showed that there were PCNA-positive myoepithelial cells in the normal as well as in the atrophic sublingual glands. However, the PCNA labeling indices of myoepithelial cells were low in the unligated and atrophic sublingual glands, and there were no statistically significant differences in these labeling indices. CONCLUSION: The observations suggest that the distribution of myoepithelial cells change during atrophy of rat sublingual glands and that myoepithelial cells have low proliferative activity in both the normal and atrophic condition of rat sublingual glands.

Actins↗

PubMed1999

Interacting loci cause severe iris atrophy and glaucoma in DBA/2J mice.

Glaucomas are a major cause of blindness. Visual loss typically involves retinal ganglion cell death and optic nerve atrophy subsequent to a pathologic elevation of intraocular pressure (IOP). Some human glaucomas are associated with anterior segment abnormalities such as pigment dispersion syndrome (PDS) and iris atrophy with associated synechiae. The primary causes of these abnormalities are unknown, and their aetiology is poorly understood. We recently characterized a mouse strain (DBA/2J) that develops glaucoma subsequent to anterior segment changes including pigment dispersion and iris atrophy. Using crosses between mouse strains DBA/2J (D2) and C57BL/6J (B6), we now show there are two chromosomal regions that contribute to the anterior segment changes and glaucoma. Progeny homozygous for the D2 allele of one locus on chromosome 6 (called ipd) develop an iris pigment dispersion phenotype similar to human PDS. ipd resides on a region of mouse chromosome 6 with conserved synteny to a region of human chromosome 7q that is associated with human PDS. Progeny homozygous for the D2 allele of a different locus on chromosome 4 (called isa) develop an iris stromal atrophy phenotype (ISA). The Tyrpl gene is a candidate for isa and likely causes ISA via a mechanism involving pigment production. Progeny homozygous for the D2 alleles of both ipd and isa develop an earlier onset and more severe disease involving pigment dispersion and iris stromal atrophy.

Age Factors↗

PubMed1994

Gyrate atrophy of the choroid and retina with hyperornithinaemia, cystinuria and lysinuria.

The case of a 45-year-old woman with gyrate atrophy of the choroid and retina is documented. Additional features in this case, to the authors' knowledge not previously described in gyrate atrophy, are massive cystinuria, massive lysinuria, axial hypermetropia and diabetes. Gyrate atrophy is a rare autosomal recessive degenerative disease of the choroid and retina and is accompanied by defective ornithine metabolism. Simell and Takki demonstrated the association with hyperornithinaemia in 1973. The main metabolic features are those of hyperornithinaemia and ornithuria caused by a deficiency of the mitochondrial matrix enzyme, ornithine aminotransferase (OAT). The responsible human gene has been localised to chromosome 10. Despite the generalised deficiency of OAT, the literature indicates significant pathological involvement of the eye only. Ophthalmological features of the disease are myopia (up to 10-20 dioptres), night blindness, constricted visual fields and complicated cataracts. The clinical picture has been detailed previously by various authors. The case of a 45-year-old woman with gyrate atrophy and hyperornithinaemia is documented here. She has been followed up for 12 years and fully investigated. Additional features in this case, to our knowledge not previously described in gyrate atrophy, are massive cystinuria, massive lysinuria, axial hypermetropia and diabetes.

Adult↗

PubMed1987

Controlling for cerebral atrophy in positron emission tomography data.

This article outlines a simple method for estimating the degree of cerebral atrophy and subsequent experimental control for the effects of cerebral atrophy on regional metabolic values measured with positron emission tomography. It is suggested that rather than correcting derived values for atrophy, less potential error is introduced by experimentally controlling for regional atrophy when possible. By treating the derived metabolic rates and the measure of atrophy as two separate variables, it is also possible to establish whether there actually is a demonstrable relationship between the two measures.

Adolescent↗

PubMed2003

Signalling pathways that mediate skeletal muscle hypertrophy and atrophy.

Atrophy of skeletal muscle is a serious consequence of numerous diseases, including cancer and AIDS. Successful treatments for skeletal muscle atrophy could either block protein degradation pathways activated during atrophy or stimulate protein synthesis pathways induced during skeletal muscle hypertrophy. This perspective will focus on the signalling pathways that control skeletal muscle atrophy and hypertrophy, including the recently identified ubiquitin ligases muscle RING finger 1 (MuRF1) and muscle atrophy F-box (MAFbx), as a basis to develop targets for pharmacologic intervention in muscle disease.

Animals↗

PubMed2001

Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo.

Skeletal muscles adapt to changes in their workload by regulating fibre size by unknown mechanisms. The roles of two signalling pathways implicated in muscle hypertrophy on the basis of findings in vitro, Akt/mTOR (mammalian target of rapamycin) and calcineurin/NFAT (nuclear factor of activated T cells), were investigated in several models of skeletal muscle hypertrophy and atrophy in vivo. The Akt/mTOR pathway was upregulated during hypertrophy and downregulated during muscle atrophy. Furthermore, rapamycin, a selective blocker of mTOR, blocked hypertrophy in all models tested, without causing atrophy in control muscles. In contrast, the calcineurin pathway was not activated during hypertrophy in vivo, and inhibitors of calcineurin, cyclosporin A and FK506 did not blunt hypertrophy. Finally, genetic activation of the Akt/mTOR pathway was sufficient to cause hypertrophy and prevent atrophy in vivo, whereas genetic blockade of this pathway blocked hypertrophy in vivo. We conclude that the activation of the Akt/mTOR pathway and its downstream targets, p70S6K and PHAS-1/4E-BP1, is requisitely involved in regulating skeletal muscle fibre size, and that activation of the Akt/mTOR pathway can oppose muscle atrophy induced by disuse.

Animals↗

PubMed2006

A novel ubiquitin-binding protein ZNF216 functioning in muscle atrophy.

The ubiquitin-proteasome system (UPS) is critical for specific degradation of cellular proteins and plays a pivotal role on protein breakdown in muscle atrophy. Here, we show that ZNF216 directly binds polyubiquitin chains through its N-terminal A20-type zinc-finger domain and associates with the 26S proteasome. ZNF216 was colocalized with the aggresome, which contains ubiquitinylated proteins and other UPS components. Expression of Znf216 was increased in both denervation- and fasting-induced muscle atrophy and upregulated by expression of constitutively active FOXO, a master regulator of muscle atrophy. Mice deficient in Znf216 exhibited resistance to denervation-induced atrophy, and ubiquitinylated proteins markedly accumulated in neurectomized muscle compared to wild-type mice. These data suggest that ZNF216 functions in protein degradation via the UPS and plays a crucial role in muscle atrophy.

Animals↗

PubMed2003

Correlation between optic disc atrophy and aetiology: anterior ischaemic optic neuropathy vs optic neuritis.

BACKGROUND: The morphologic features of swollen disc in the acute stage of optic neuritis and anterior ischaemic optic neuropathy (AION) have been extensively investigated in contrast to the morphologic features of optic disc atrophy after these events. OBJECTIVE: : A prospective study to evaluate the morphologic features of optic disc atrophy 6 months or more after optic neuritis and nonarteritic AION. PATIENTS AND METHODS: A total of 35 optic discs after nonarteritic AION (n=27) and 24 after optic neuritis (n=19) in otherwise healthy subjects have been evaluated by direct fundoscopic examination with a +90 diopters lens and optic disc photography. The average age of patients at the onset of AION was 57.8 years (range: 38-80) and at the onset of optic neuritis was 32.6 (range: 19-46). The female:male ratio was 18 : 17 in the former and 15 : 9 in the latter. The evaluated parameters included: degree of rim pallor (0 to +3), location of rim pallor, height of rim above the retina, depth and width of cup, peripapillary retinal artery to vein (A : V) ratio, and peripapillary pigment epithelial atrophy. A comparison was made also with 17 age-matched normal discs of 17 patients. Statistical significance was calculated with chi(2) and Fisher's exact test. RESULTS: Most of the discs after AION were paler (+2: 70%, +3: 26%) than after optic neuritis (normal colour: 8%, +1: 58%, P< or =0.007). Rim segmental involvement after AION was usually either superior 'altitudinal' (53%) or inferior 'altitudinal' (29%), whereas after optic neuritis, it was usually either temporal-central (papillomacular) (42%) or diffuse temporal (42%, P<0.0001). Discs had lower A : V ratio (1 : 3, 40%) after AION compared with optic neuritis (1 : 3, 8%) (P=0.007). There were no significant differences between the two groups in height of the rim, cupping, and peripapillary atrophy. CONCLUSIONS: : A combination of the degree of rim pallor, location of rim pallor, and A : V ratio may be of value in assessing the aetiology of optic disc atrophy when no previous clinical data are available and a compressive lesion has been ruled out.

Acute Disease↗