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PubMed1994

Callosal atrophy in patients with lacunar infarction and extensive leukoaraiosis. An indicator of cognitive impairment.

BACKGROUND AND PURPOSE: It is unclear why only some patients with lacunar infarction and radiological evidence of diffuse white matter abnormalities have dementia. The purpose of this study is to investigate the value of callosal atrophy as an indicator of cognitive impairment. METHODS: We used magnetic resonance imaging to evaluate 11 right-handed male patients with lacunar infarction and extensive white matter hypodensities on computed tomography (8 with dementia and 3 without dementia). The midsagittal corpus callosum area on T1-weighted images was compared with the IQ determined by the Wechsler Adult Intelligence Scale. The relation between these parameters and cerebral oxygen metabolism measured with positron emission tomography was also evaluated in the 8 patients with dementia. RESULTS: All patients showed diffuse high-intensity areas in the bilateral hemispheric white matter on T2-weighted images. Compared with 19 age- and sex-matched right-handed normal control subjects, the patients had a significantly smaller callosal area. The severity of callosal atrophy, which varied from mild to severe, was significantly related to the total IQ. In the 8 demented patients, the total callosal area was significantly correlated with the mean level of oxygen metabolism in the cerebral white matter. CONCLUSIONS: In patients with lacunar infarction and diffuse white matter abnormalities, the presence of callosal atrophy may indicate cognitive impairment. Callosal atrophy may reflect the severity and extent of white matter damage associated with a decrease in oxygen metabolism, which may determine the severity of intellectual decline.

Adult↗

PubMed1998

Systolic ventricular dysfunction causes selective diaphragm atrophy in rats.

In order to examine the relative impairment of the diaphragm and other skeletal muscles in systolic ventricular dysfunction (VD), their structure and function were compared between rats with VD induced by left coronary artery ligation (n = 17) and sham-operated rats (Co, n = 10). In addition, in an attempt to unravel the mechanism of the observed impairment, we examined alterations in insulin-like growth factor-I (IGF-I) serum levels and IGF-I expression in the liver, diaphragm, and gastrocnemius. In a second series of rats (VD, n = 5 and Co, n = 5) hemodynamic measurements were performed. All measurements were performed 3 mo after the operation. Infarct size averaged 32 +/- 10 and 44 +/- 20% in the two series, respectively (NS). Hemodynamic measurements revealed a decrease in left ventricular peak systolic pressure of 19% (p < 0. 05). Significant diaphragm atrophy (weight: 622 +/- 52 mg in VD versus 750 +/- 54 mg in Co, p < 0.0005), without alterations in diaphragm contractile properties was present in VD animals. For all animals combined, the reduction in diaphragm weight was related to infarct size (r = -0.74, p < 0.001). No alterations were observed in the other inspiratory and peripheral muscles. ATPase staining of the diaphragm showed atrophy of type I and type IIx/b fibers, their cross-sectional area (CSA) being reduced by 13 and 16%, respectively (p < 0.05). There were no signs of myopathic alterations. IGF-I expression was increased by 55% in the diaphragm of rats with VD (p < 0.05). IGF-I expression in the liver and gastrocnemius and serum IGF-I levels were unaltered. These data suggest the presence of compensatory mechanisms aimed at minimizing diaphragmatic fiber atrophy. We conclude that systolic VD caused: (1) selective diaphragm atrophy, which was related to infarct size; (2) a decrease in diaphragm type I and IIx/b CSA not associated with myopathic changes; (3) an increase in the IGF-I mRNA content of the diaphragm. The selective diaphragm involvement in the present study may be related to the moderate degree of ventricular dysfunction induced.

Adenosine Triphosphatases↗

PubMed2002

Mechanical ventilation-induced diaphragmatic atrophy is associated with oxidative injury and increased proteolytic activity.

Prolonged mechanical ventilation (MV) results in reduced diaphragmatic maximal force production and diaphragmatic atrophy. To investigate the mechanisms responsible for MV-induced diaphragmatic atrophy, we tested the hypothesis that controlled MV results in oxidation of diaphragmatic proteins and increased diaphragmatic proteolysis due to elevated protease activity. Further, we postulated that MV would result in atrophy of all diaphragmatic muscle fiber types. Mechanically ventilated animals were anesthetized, tracheostomized, and ventilated with 21% O2 for 18 hours. MV resulted in a decrease (p < 0.05) in diaphragmatic myofibrillar protein and the cross-sectional area of all muscle fiber types (i.e., I, IIa, IId/x, and IIb). Further, MV promoted an increase (p < 0.05) in diaphragmatic protein degradation along with elevated (p < 0.05) calpain and 20S proteasome activity. Finally, MV was also associated with a rise (p < 0.05) in both protein oxidation and lipid peroxidation. These data support the hypothesis that MV is associated with atrophy of all diaphragmatic fiber types, increased diaphragmatic protease activity, and augmented diaphragmatic oxidative stress.

Animals↗

PubMed2006

Correlation between the area of increased autofluorescence surrounding geographic atrophy and disease progression in patients with AMD.

PURPOSE: To test the hypothesis that the extension of areas with increased fundus autofluorescence (FAF) outside atrophic patches correlates with the rate of spread of geographic atrophy (GA) over time in eyes with age-related macular degeneration (AMD). METHODS: The database of the multicenter longitudinal natural history Fundus Autofluorescence in AMD (FAM) Study was reviewed for patients with GA recruited through the end of August 2003, with follow-up examinations within at least 1 year. Only eyes with sufficient image quality and with diffuse patterns of increased FAF surrounding atrophy were chosen. In standardized digital FAF images (excitation, 488 nm; emission, >500 nm), total size and spread of GA was measured. The convex hull (CH) of increased FAF as the minimum polygon encompassing the entire area of increased FAF surrounding the central atrophic patches was quantified at baseline. Statistical analysis was performed with the Spearman's rank correlation coefficient (rho). RESULTS: Thirty-nine eyes of 32 patients were included (median age, 75.0 years; interquartile range [IQR], 67.8-78.9); median follow-up, 1.87 years; IQR, 1.43-3.37). At baseline, the median total size of atrophy was 7.04 mm2 (IQR, 4.20-9.88). The median size of the CH was 21.47 mm2 (IQR, 15.19-28.26). The median rate of GA progression was 1.72 mm2 per year (IQR, 1.10-2.83). The area of increased FAF around the atrophy (difference between the CH and the total GA size at baseline) showed a positive correlation with GA enlargement over time (rho=0.60; P=0.0002). CONCLUSIONS: FAF characteristics that are not identified by fundus photography or fluorescein angiography may serve as a prognostic determinant in advanced atrophic AMD. As the FAF signal originates from lipofuscin (LF) in postmitotic RPE cells and since increased FAF indicates excessive LF accumulation, these findings would underscore the pathophysiological role of RPE-LF in AMD pathogenesis.

Aged↗

PubMed1998

Apolipoprotein E epsilon 4 allele and whole brain atrophy in late-onset Alzheimer's disease.

OBJECTIVE: Diffuse brain atrophy is one of the gross pathological features of Alzheimer's disease and is a result of degenerative changes. The epsilon 4 allele of apolipoprotein E (APOE) is a risk factor or susceptibility gene in late-onset sporadic Alzheimer's disease and may influence the pathological changes associated with the disease. The aim of this study was to examine the relationship between the APOE epsilon 4 allele and whole brain atrophy. METHOD: Whole brain volume was quantified by using high-resolution magnetic resonance imaging and the computerized brain segmentation technique in 178 patients with late-onset sporadic Alzheimer's disease who carried no APOE epsilon 4 alleles (N = 62), one epsilon 4 allele (N = 93), or two (N = 23) and had comparable clinical severity of dementia. RESULTS: An apparent positive correlation was found between normalized whole brain volume (relative to total intracranial volume) and number of APOE epsilon 4 alleles; i.e., patients carrying two APOE epsilon 4 alleles had the least brain atrophy. This association between the APOE epsilon 4 allele and brain volume was similar in women and men and was independent of age, level of education, duration of illness since symptom onset, and severity of dementia. CONCLUSIONS: The results indicate that cognitive dysfunction progresses before severe brain atrophy develops in patients carrying the APOE epsilon 4 allele and suggest that an APOE epsilon 4-allele-related mechanism that affects neuronal function before a decrement in brain matter is involved in the development of dementia.

Aged↗

PubMed2005

Does donepezil treatment slow the progression of hippocampal atrophy in patients with Alzheimer's disease?

OBJECTIVE: The only approved pharmacological approach for the symptomatic treatment of Alzheimer's disease in Japan is the use of a cholinesterase inhibitor, donepezil hydrochloride. Recent in vivo and in vitro studies raise the possibility that cholinesterase inhibitors can slow the progression of Alzheimer's disease. The purpose of the present study was to determine whether donepezil has a neuroprotective effect in Alzheimer's disease by using the rate of hippocampal atrophy as a surrogate marker of disease progression. METHOD: In a prospective cohort study, 54 patients with Alzheimer's disease who received donepezil treatment and 93 control patients with Alzheimer's disease who never received anti-Alzheimer drugs underwent magnetic resonance imaging (MRI) twice at a 1-year interval. The annual rate of hippocampal atrophy of each subject was determined by using an MRI-based volumetric technique. Background characteristics, age, sex, disease duration, education, MRI interval, apolipoprotein E (APOE) genotype, and baseline Alzheimer's Disease Assessment Scale score were comparable between the treated and control groups. RESULTS: The mean annual rate of hippocampal volume loss among the treated patients (mean=3.82%, SD=2.84%) was significantly smaller than that among the control patients (mean=5.04%, SD=2.54%). Upon analysis of covariance, where those confounding variables (age, sex, disease duration, education, MRI interval, APOE genotype, and baseline Alzheimer's Disease Assessment Scale score) were entered into the model as covariates, the effect of donepezil treatment on hippocampal atrophy remained significant. CONCLUSIONS: Donepezil treatment slows the progression of hippocampal atrophy, suggesting a neuroprotective effect of donepezil in Alzheimer's disease.

Aged↗

PubMed2002

Frontal cortex atrophy predicts cognitive impairment in multiple sclerosis.

The association between regional measures of cortical atrophy and neuropsychological (NP) dysfunction was studied in 35 multiple sclerosis (MS) patients. Patients underwent neurological examination, MRI, and NP testing. Blind quantitative MRI analysis yielded total T(2) lesion area (TLA) and third ventricle width (3VW). Cortical atrophy, rated by blind visual inspection, was more extensive in superior frontal and parietal cortices than in other regions. No MRI measures were correlated with depression scores. TLA and 3VW were significantly correlated with each NP test. Cortical atrophy measures for bilateral superior frontal cortex were retained in regression models predicting impairments in verbal learning, spatial learning, attention, and conceptual reasoning. The authors conclude that cerebral atrophy predicts NP impairment while accounting for the influence of TLA or 3VW. Regions of cortex most susceptible to atrophic and cognitive changes in MS are the right and left superior frontal lobes.

Adult↗

PubMed1992

Fascia and perichondrium atrophy in tympanoplasty and recurrent middle ear atelectasis.

Fascia and perichondrium grafts to replace and reinforce thin, atrophic tympanic membranes (TMs) are recommended by several authors to correct middle ear atelectasis by forming a fibrous, collapse-resistant TM. This study reviewed the status of connective tissue grafts performed over the 10-year period from 1979 to 1988 to determine if these grafts would maintain sufficient strength and fibrous character to resist recurrent atelectasis. The author used fascia or perichondrium to repair 89 TM defects, and 63 ears were available for follow-up: 54 had cholesteatomas and 9 had perforations. Graft atrophy was judged by microscopic otoscopy and Kodachrome otophotography. Fascia TM grafts atrophied in 35 of 43 ears (80%), and perichondrium atrophied in 8 of 20 ears (40%). Grafts maintained their relatively thick and fibrous character in only 20 of 63 ears (32%). If fascia and perichondrium used to correct atelectasis were to atrophy at the same rate as the grafts in this series, atelectasis would recur after attempts to reinforce atrophic TMs. Atelectasis-prone middle ears require intubation despite surgery.

Adolescent↗

PubMedDate not supplied

Glutamine dipeptide-supplemented parenteral nutrition reverses gut atrophy, disaccharidase enzyme activity, and absorption in rats.

BACKGROUND: Total parenteral nutrition (TPN) is associated with intestinal atrophy and dysfunction possibly attributed to the absence of the nonessential amino acid glutamine from commercially available TPN solutions because of the instability of the monoamino acid during heat sterilization and storage. The use of stable dipeptides may overcome this problem. In this study we tested the hypothesis that glutamine dipeptide supplementation with alanyl-L-glutamine during TPN for 10 days would reverse small bowel atrophy and TPN-induced dysfunction in rats. METHODS: A conventional TPN solution (250 kcal/kg bw) was compared with an isocaloric and isonitrogenous TPN supplemented with alanyl-L-glutamine dipeptide. A food-fed control group was included (n = 6 each group). Jejunum mucosal architecture, absorption of water and glucose, and disaccharidase activity of maltase and alkaline phosphatase were evaluated. RESULTS: TPN-induced villous atrophy, significantly reduced absorption rate, and decreased activity of villous enzymes, compared with the TPN group, could be reversed by supplementation of glutamine dipeptide alanyl-L-glutamine to parenteral nutrition solutions with no difference to the control group. CONCLUSIONS: Glutamine dipeptide-enriched parenteral nutrition preserves mucosal structure and reversed atrophy-associated dysfunction.

Alkaline Phosphatase↗

PubMed1979

Reversal by testosterone of atrophy of accessory genital glands of castrated male sheep. A histologic and morphometric study.

The histologic features of male accessory genital glands of entire sheep (group I), castrated sheep (group II), castrated sheep treated with 40 daily intramuscular injections of 50 milligrams testosterone propionate (group III), and castrated sheep treated with 600 milligrams testosterone propionate 72 hours before death (group IV) were compared. Sheep were castrated at 3 months old and all sheep were killed when 15 months old. Volume fractions of glandular tissue, intralobular fibromuscular tissue and perilobular fibromuscular tissue of the seminal vesicles and Cowper's glands fluctuated significantly (P less than 0.05) during postcastration atrophy and after repeated testosterone treatment. Atrophy in sheep in group II was least in the prostate but greatest in Cowper's glands, seminal vesicles and ampullae of vasa deferentia. Seminal vesicle plexi, whose cytons had a statistically significant (P less than 0.05) degree of shrinkage, also were atrophied. After treatment with testosterone the postcastration atrophy of plexal neurons was almost reversed in sheep in group III. There also was hypertrophy of epithelial cells but the testosterone treatment failed to reduce to normal the fibromuscular volume fraction of the accessory genital glands. Testosterone propionate treatment of sheep in group IV failed to elicit appreciable morphologic changes. These results are compared with our previous findings on the content and uptake of zinc by the accessory genital glands. It is suggested that accumulation of zinc in the accessory genital glands of sheep is not necessarily closely linked to normal histologic appearance.

Animals↗

PubMed1980

[Potassium hydrogen phosphate induced nephropathy in the dog. I. Pathogenesis of tubular atrophy (author's transl)].

A nephropathy with severe tubular atrophy was observed in Beagle dogs after oral administration of K2HPO4 for 14 or 38 weeks. We describe the complete lysosomal degradation of atrophying tubular epithelial cells. During two experiments of 14 and 38 weeks duration, respectively, a total of 15 Beagle dogs received 0.8 g K2HPO4/kg body weight daily with their food. All dogs were examined clinically at regular intervals. Renal biopsies were taken in the fourth week from beagles of the 14-week study. Results were compared with those of control dogs. At the end of the experiments the animals were killed and necropsies done. Different stains and histochemical reactions were applied to paraffin sections of the kidneys. Acid phosphatase and beta-glucuronidase were found on cryostat sections. Kidneys fixed by perfusion of five Beagles from the 38-week study and three Beagles of the 14-week study, and from five control dogs, were examined electron microscopically. Ultrahistochemically, acid phosphatase was demonstrated. Clinically, the dogs in both experiments vomited, were cachectic, and had elevated creatinine and blood urea nitrogen. Morphologically, qualitatively identical changes were seen, but the renal damage was most marked at 38 weeks. There were disseminated tubular atrophy (usually of the proximal tubules), focal scar tissue and nephrocalcinosis. The following pathogenesis was established for the lesions of the proximal tubule: Tubular atrophy begins with loss of differentiation of epithelial cells. Enzyme histochemistry, ultrahistochemistry and electron microscopy show an increase in autophagic vacuoles and autophagolysosomes. The lysosomal bodies showing fusion enclose large parts of the cytoplasm as the process continues. Complete lysosomal degradation of epithelial cells and extrusion of large lysosomes into the tubular lumen follow. After complete enzymatic digestion of the intratubular detritus, the residue is empty, convoluted and collapsed tubular basement membrane. Atrophic tubular epithelial cells have many organelle-free zones at their base, which contain fine filamentous material resembling that of the basement membrane. The degradation process described here may explain why clinically the urinary sediment contains few cylinders and epithelial cells and why proteinuria decreases significantly toward the end of the experiment. So far, it is not clear whether the tubular basement membrane is synthesized by the tubular cells, by fibroblasts or by both cell types. The presence of basement membrane-like material in tubular epithelial cells and in parietal epithelial cells of the glomerulus favors the view that epithelial cells produce the basement membranes and that increased production of basement membrane-like material is a sign of loss of differentiation.

Animals↗

PubMed2001

Molecular genetic study of a childhood form of spinal muscular atrophy.

Molecular genetic studies were performed in 28 cases of childhood-onset spinal muscular atrophy (24 unrelated families). This consisted of type 1 (severe) (n = 5), type 2 (intermediate form) (n = 8), and type 3 (mild) (n = 15). Deletion of exons 7 and 8 of the SMNt gene was found in 100%, 100%, and 93%, respectively, in type 1, 2, and 3 spinal muscular atrophy. Deletion of exons 5 and 6 of the NAIP gene was found in 3 of 5 (60%) of type 1 and none of the type 2 and 3 cases. None of the 32 asymptomatic relatives had homozygous deletions in the SMNt and NAIP genes. Thus, the role of the NAIP gene needs to be specifically defined in spinal muscular atrophy. In a suspected case of spinal muscular atrophy, deletion of the SMNt gene is a useful laboratory marker for confirmation of the diagnosis.

Adolescent↗

PubMed2001

Long-term survival in a child with arthrogryposis multiplex congenita and spinal muscular atrophy.

Spinal muscular atrophy type 0 is a severe form of spinal muscular atrophy that is usually fatal in the first months of life. These children present with arthrogryposis multiplex congenita and respiratory compromise. We describe a child with spinal muscular atrophy and arthrogryposis multiplex congenita who has had a much better course and is alive without ventilator support at age 6 years. This case illustrates that the prognosis for spinal muscular atrophy and arthrogryposis multiplex congenita cannot always be predicted with certainty.

Arthrogryposis↗

PubMed1994

Efficacy of thyrotropin-releasing hormone in the treatment of spinal muscular atrophy.

Children with spinal muscular atrophy were treated by the administration of thyrotropin-releasing hormone. In three infants with spinal muscular atrophy type I, thyrotropin-releasing hormone showed little efficacy, but in children with types II and III, there was improvement in motor function and electromyographic findings after the thyrotropin-releasing hormone therapy. Thyrotropin-releasing hormone has a neurotrophic effect on the spinal anterior motor neurons of spinal muscular atrophy patients and thus may be warranted for the management of spinal muscular atrophy.

Age of Onset↗

PubMed1994

Pulmonary function in spinal muscular atrophy.

We present the first prospective study on pulmonary function in spinal muscular atrophy patients. Seventy-seven spinal muscular atrophy patients, ages 5 to 18 years, from three centers, were studied with regard to forced vital capacity, using height as a predictor. Patients were categorized into four motor function categories. The highest-functioning group had normal or near-normal values, and those who sat with support had the lowest values. Those with intermediate function had intermediate values. Forced vital capacity was studied longitudinally in 40 spinal muscular atrophy patients for 1.1 to 4.4 years. Eighty-eight percent of patients grew in height, but only 35% showed an increase in height-adjusted forced vital capacity percent. In those patients with the least function, 100% lost height-adjusted forced vital capacity over time. In those patients with the highest function, 57% lost height-adjusted forced vital capacity. In addition, the basic forced vital capacity, not correlated to height, decreased in 43% of cases. These pulmonary function alterations appear to be important determinants for function and survival in spinal muscular atrophy patients.

Adolescent↗

PubMed1996

Amylaceous (polyglucosan) bodies in familial cerebral atrophy of early onset.

An 8-year-old girl and her 4-year-old sister presented with psychomotor retardation during the 1st year of life. This was followed by spasticity, seizures, and in the older patient, progressive loss of faculties and death. Computed tomographic and magnetic resonance imaging scans demonstrated progressive cerebral atrophy in both patients. Postmortem examination in the older sibling showed diffuse atrophy of the supragranular layers of the cerebral cortex, atrophy and gliosis of the white matter, and accumulation of numerous amylaceous (polyglucosan) bodies within the cytoplasm of cell processes. The inclusions were closely associated with atrophy of the parenchyma. The findings suggest that this disorder is different from other childhood diseases in which amylaceous bodies accumulate within the brain.

Adipose Tissue↗

PubMed2005

Corpus callosum atrophy in Wernicke's encephalopathy.

BACKGROUND AND PURPOSE: Neuropathologic changes in Wernicke's encephalopathy (WE) involve variable brain structures. Corpus callosum involvement in WE, however, is largely unknown. The authors investigated the degree and the pattern of corpus callosum changes in WE according to the etiologies. METHODS: Nineteen patients with WE (between 34 and 81 years) and 19 age- and sex-matched control participants were included. The total cross-sectional callosal area and 5 callosal subregions (C1-C5) were measured by tracing outer margins in the midsagittal sections. Subregions were determined by placing radial dividers with 10 rays. The pixel numbers for corpus callosums were calculated, and the values obtained were adjusted for head size variations. RESULTS: The causes of WE were alcoholism (10), intestinal surgery (5), anorexia (3), and hyperemesis gravidarum (1). The mean size of the total corpus callosum was significantly reduced in alcoholic WE (P< .001; 527.8 +/- 70.8 mm2 for alcoholic WE; 664.6 +/- 58.1 mm2 for the corresponding controls), but not in nonalcoholic WE. In subregion analysis, prefrontal callosum (C2) atrophy was the most prominent in alcoholic WE. In contrast, only splenium (C5) was atrophied in nonalcoholic WE. The degree of atrophy did not change throughout the follow-up period (mean 5.3 weeks). CONCLUSION: This study suggests that the extent and location of corpus callosum atrophy differs between alcoholic WE and nonalcoholic WE, implying separate contribution of alcohol neurotoxicity and nutritional deficiency.

Adult↗

PubMed2000

Relationship of skeletal muscle atrophy to functional status: a systematic research review.

In the realm of muscle atrophy research, many studies address minute details of molecular function but few examine the effects of atrophy in terms of mobility, strength, endurance, and performance of activities of daily living. The relationship between impairment and functional limitation is the focus of this research review. A wide array of studies constitute this area of inquiry, including investigations as diverse and widely disparate as molecular chemistry and space travel and populations as different as rats, healthy young men, and elderly women. Thirty-four studies were selected based on their fit with the Enabling-Disabling Model. Three paradigms of atrophy and function emerged. Adaptation reflects the plastic nature of muscle when placed under certain conditions, ranging from disuse to high-resistance exercise. Injury/loss describes damage to muscle tissue from ischemia, medications, or reloading or reperfusion trauma. Also in this category is the loss of muscle that is seen with aging. Integrity relates to the muscle's tendency to protect itself and maintain structural adjacencies and cellular proportions. Based on the 3 muscle research paradigms, the relationship of muscle atrophy to function is portrayed as a bidirectional interaction wherein form and function have an influence on each other by way of physical changes, including those of adaptation, injury/loss, or integrity. A conceptual model is constructed to reflect this relationship.

Activities of Daily Living↗