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 865 records · Page 48Linked to original sources

PubMed2006

Relation of plasma thyroid-stimulating hormone levels to vascular lesions and atrophy of the brain in the elderly.

CONTEXT: Recent studies suggest that thyroid disease is associated with cardiovascular and peripheral vascular disease. However, little is known about the underlying pathophysiology and the relation with cerebrovascular disease or brain atrophy in the elderly. OBJECTIVE: To determine if plasma thyroid-stimulating hormone (TSH) levels are associated with vascular brain changes and cortical atrophy in the elderly. DESIGN: Community based, cross-sectional study. PARTICIPANTS AND SETTING: 268 participants of the Memory and Morbidity in Augsburg Elderly Study, 65-83 years of age and without contraindications for magnetic resonance imaging (MRI) of the brain. MAIN OUTCOME MEASURES: The presence of brain lesions and atrophy was determined using a standardized MRI protocol, an established rating scale and a single rater. Plasma TSH levels were assessed using standard laboratory methods. The association between plasma TSH levels and MRI findings was analyzed using logistic and linear regression models. RESULTS: Higher TSH levels within the normal clinical range were significantly associated with severer cortical atrophy (p = 0.04) and a higher proportion of infarct-like vascular lesions (p = 0.005) in men. These associations were independent of potential confounders, including thyroid hormone therapy, in multivariable regression analysis. No association between plasma TSH levels and both MRI outcomes were observed in women. In addition, neither in men nor in women was an association between TSH levels and white-matter lesions found. CONCLUSIONS: Increasing TSH levels even within the normal clinical range are associated with severer brain atrophy and infarct-like vascular lesions in elderly men.

Aged↗

PubMed1992

Relationship between levodopa-independent symptoms and central atrophy evaluated by magnetic resonance imaging in Parkinson's disease.

Thirty patients with Parkinson's disease were studied for the purpose of investigation relations between motor symptoms and cerebral atrophy evaluated by magnetic resonance imaging (MRI). Axial symptoms (gait disorder, postural instability and difficulty in arising from a chair), assessed at the time of maximum clinical improvement, were significantly correlated with frontal atrophy, while no correlation was found between the basal parkinsonian disability score and cerebral atrophy. It is suggested that frontal atrophy observed by MRI is linked with axial motor symptoms resulting from non-dopaminergic lesions. The origin of this atrophy is unknown.

Aged↗

PubMed1997

Qualitative assessment of cerebral atrophy on MRI: inter- and intra-observer reproducibility in dementia and normal aging.

To assess the reproducibility of a qualitative rating scale of cerebral atrophy on MRI in an aged population of demented and non-demented individuals, 4 raters independently judged cerebral atrophy (CA) in 13 regions on a 0-3 scale on 75 MRI scans, on two occasions. The level of agreement was expressed by kappa statistics as well as by analysis of variance for interexaminer reproducibility studies. The mean CA scores ranged from 13.3 to 21.2, indicating moderately high prevalence of cerebral atrophy in this sample. Complete agreement among observers was reached in 49.7% of the ratings during the first assessment and in 44.1% in the second assessment. The inter-observer agreement was poor in both sessions (mean overall kappas 0.34 and 0.24). The intra-observer agreement was moderate to good for all raters (mean overall kappa: 0.58). The average standard deviation of the differences between CA scores of the 4 raters was 5.12 in the first and 5.13 in the second session. The average standard deviation for the differences within raters was 2.4. We conclude that the assessment of cerebral atrophy using this rating scale on MRI in an aged population has a poor reproducibility among raters. However, it provides regional atrophy measurements and is quite reliable when performed by a single rater.

Aged↗

PubMed1982

Liver atrophy and encephalopathy after portacaval shunt in the rat.

The effect of various types of portal diversion (portacaval, mesocaval and pancreatico-splenocaval anastomoses, portacaval transposition and arterialization) on liver atrophy and post-shunt encephalopathy was studied in the rat. Among all diversions, only portacaval anastomosis produced dramatic liver atrophy and encephalopathy. Moreover, portacaval anastomosis was also the only portal diversion which induced low body weight gain. There was no correlation between blood ammonia levels and encephalopathy. Liver atrophy was always correlated to a decrease of hepatic blood flow. Diminution of liver blood flow was only slight following partial (either mesenteric or pancreatico-splenic) diversion of portal blood and nil after portacaval transposition or anastomosis. These results suggest that: (1) pancreatic (insulin-rich) blood is not essential for maintenance of liver trophicity. Hemodynamic factors seem to be predominant in the pathogenesis of post-shunt liver atrophy. (2) Post-shunt encephalopathy arises only when total diversion of the portal blood and liver atrophy are associated.

Ammonia↗

PubMed1988

Pericyte response during choriocapillaris atrophy in the rabbit.

The rabbit and rat choriocapillaris atrophies in response to experimental destruction of the retinal pigment epithelium by intravenous injection of sodium iodate. This provides a convenient model of capillary atrophy. We have observed that pericytes are spared during this process; the atrophy is due to loss of endothelium only. Extensive examination of thin sections obtained 1 day to 11 weeks after administration of iodate showed that pericytes retained their normal relationship to the remnant capillary basement membrane left behind as the endothelial tube atrophied. This was most conspicuously manifested in their retention of processes longitudinally disposed along the sleeves of remnant basement membrane. The processes retained bundles of actin filaments that had dense regions along them and inserted into subplasmalemmal densities at basement membrane attachment sites, i.e. they had the characteristics of stress fibers. The pericytes did not phagocytose the debris of endothelial necrosis, in spite of their known phagocytic abilities. Necrotic endothelial cells were eliminated by sloughing into the capillary lumen. The observations support the idea that the function of pericytes in the choriocapillaris, the major source of nutrition for the retinal photoreceptors, resides in their contractility, and that pericytes do not remove necrotic endothelium during capillary atrophy.

Actins↗

PubMed1990

Computerized tomography with longitudinal follow-up of brain atrophy in patients with Parkinson's disease.

Computerized tomographic (CT) studies with longitudinal follow-up of the relationship between supratentorial and infratentorial brain atrophy in Parkinson's disease (PD) using our new CT-derived brain atrophy index (BAI) are reported. In those patients with Parkinson's disease, CT analysis demonstrated a significant increase in brain atrophy compared with controls. Infratentorial BAI correlated significantly with supratentorial BAIs and the decrease in the infratentorial BAI correlated with a corresponding decrease in the supratentorial BAI in those with PD. It is postulated that the infratentorial brain atrophy found in patients with PD could well be secondary to supratentorial brain atrophy.

Adult↗

PubMed1983

Pathophysiology of hydronephrotic atrophy: the cause and role of active preglomerular vasoconstriction.

Unilateral complete ureteral occlusion is followed by a decreased blood flow in the ipsilateral kidney, which is established within 1 week, after which a steady state of whole renal blood flow is observed. Active preglomerular vasoconstriction is assumed to be the main factor causing renal flow reduction in the hydronephrotic kidney, resulting in rapid decrease of the initial elevated pelvic pressure within 24 h. The assumption of active preglomerular vasoconstriction also explains the observation that blood flow reduction clearly precedes renal atrophy after ureteral ligation. Neither alpha-receptor blocking agents nor angiotensin II blockage, nor denervation, reversed flow reduction in the first hours or weeks after ureteral ligation. A thromboxane synthesis inhibitor (imidazole) did reverse flow reduction completely without affecting the contralateral renal blood flow, indicating that active vasoconstrictive is present. In respect to renal hydronephrotic atrophy, compartment analysis of the blood flow of the obstructed kidney demonstrates that vasoconstriction contributes to ischemic atrophy at least in the cortex of the hydronephrotic kidney. Vasoconstriction cannot be reversed by prostaglandin synthesis inhibition after renal atrophy is established, although the renal blood flow is still sensitive to other vasodilating drugs like dopamine. From our data we conclude that prostaglandin-mediated active preglomerular vasoconstriction is a main factor causing renal atrophy by ischemia.

Animals↗

PubMed1993

Callosal atrophy with reduced cortical oxygen metabolism in carotid artery disease.

BACKGROUND AND PURPOSE: In cerebrovascular disease, brain atrophy may be a reflection of ischemic changes. Minor changes that are not detectable as infarction on computed tomography may result in atrophy with metabolic depression. We evaluated the relation between size of the corpus callosum and cerebral cortical oxygen metabolism in carotid artery disease. METHODS: We used magnetic resonance imaging and positron emission tomography to evaluate 13 right-handed male patients with transient ischemic attacks or minor strokes and unilateral internal carotid artery occlusive disease, two with stenosis and 11 with occlusion. Computed tomography showed only minor subcortical abnormalities in the affected hemisphere. Midsagittal corpus callosum areas on T1-weighted magnetic resonance images, white matter lesions on T2-weighted images, and the cerebral metabolic rate of oxygen measured by the oxygen-15 steady-state technique were analyzed. RESULTS: Compared with 13 age- and sex-matched control subjects showing the same degree of white matter areas of high intensity, the patients had significantly decreased callosal areas. The degree of corpus callosum atrophy was significantly correlated with the mean cortical oxygen metabolic rate. The same tendency was also found in five patients without infarcts on computed tomography. However, neither the callosal area nor the hemispheric metabolic rate was correlated with the extent of white matter lesions. CONCLUSIONS: These findings indicate that atrophy of the corpus callosum occurs in association with a decrease in cortical oxygen metabolism. Corpus callosum atrophy may be a useful morphological index that reflects the cerebral cortical metabolic state in carotid artery occlusive disease.

Aged↗

PubMed2006

Muscular atrophy of caveolin-3-deficient mice is rescued by myostatin inhibition.

Caveolin-3, the muscle-specific isoform of caveolins, plays important roles in signal transduction. Dominant-negative mutations of the caveolin-3 gene cause autosomal dominant limb-girdle muscular dystrophy 1C (LGMD1C) with loss of caveolin-3. However, identification of the precise molecular mechanism leading to muscular atrophy in caveolin-3-deficient muscle has remained elusive. Myostatin, a member of the muscle-specific TGF-beta superfamily, negatively regulates skeletal muscle volume. Here we report that caveolin-3 inhibited myostatin signaling by suppressing activation of its type I receptor; this was followed by hypophosphorylation of an intracellular effector, Mad homolog 2 (Smad2), and decreased downstream transcriptional activity. Loss of caveolin-3 in P104L mutant caveolin-3 transgenic mice caused muscular atrophy with increase in phosphorylated Smad2 (p-Smad2) as well as p21 (also known as Cdkn1a), a myostatin target gene. Introduction of the myostatin prodomain, an inhibitor of myostatin, by genetic crossing or intraperitoneal administration of the soluble type II myostatin receptor, another inhibitor, ameliorated muscular atrophy of the mutant caveolin-3 transgenic mice with suppression of p-Smad2 and p21 levels. These findings suggest that caveolin-3 normally suppresses the myostatin-mediated signal, thereby preventing muscular atrophy, and that hyperactivation of myostatin signaling participates in the pathogenesis of muscular atrophy in a mouse model of LGMD1C. Myostatin inhibition may be a promising therapy for LGMD1C patients.

Animals↗

PubMed1997

Vocal fold atrophy: quantitative glottic measurement and vocal function.

Videostroboscopic glottic measurements and vocal function were evaluated in 41 vocal fold atrophy patients with bowed vocal folds. The amount of bowing in the resting position and the glottal gap area and vibratory amplitude during phonation were measured from digitized videostroboscopic images. Vibratory amplitude was not decreased on atrophic vocal folds. With the same amount of total bowing, the glottal gap area for bilateral atrophy was smaller than for unilateral atrophy. These results suggest that vocal fold atrophy is not disadvantageous to thyroplasty type I, and that bilateral procedures may produce a better outcome than a unilateral procedure in the treatment of bilateral atrophy. Acoustic, aerodynamic, and perceptual parameters of vocal function were measured. The acoustic high-frequency power ratio and the H-index correlated with the glottal gap area. The mean flow rate correlated with the amount of bowing. The degree of dysphonia was related to the size of the glottal gap and bowing.

Adult↗

PubMed1975

Age-dependent resistance to transmissible gastroenteritis of swine. III. Effects of epithelial cell kinetics on coronavirus production and on atrophy of intestinal villi.

Coronavirus titers in small intestine, degree of villous atrophy and apparent rates of regeneration of intestinal villi were compared in newborn, 3-week-old and adult pigs for 1 week after they were exposed to the transmissible gastroenteritis virus of swine. The response within the newborn group was homogeneous, resulting in high virus titers, maximal villous atrophy and comparatively slow regeneration. In general, virus titers were lower, villous atrophy was less severe and regeneration more rapid in both older groups than in the newborn pigs. However, the response varied greatly in the older groups. The 3-week-old group was divided into two populations. The major population had low virus titers and developed partial villous atrophy, whereas the minor population had marked villous atrophy and virus titers comparable to those of the newborn pigs. These observations support the hyposthesis that the accelerated replacement of villous epithelium in the small intestine of pigs during the first 3 weeks contributes to the innate age-dependent resistance to transmissible gastroenteritis. The accelerated replacement of villous epithelial cells in older pigs contributes to resistance in two ways. The increased proliferative capacity of crypt epithelium results in a more rapid regeneration of atrophic villi; and the comparatively young villous absorptive cells resulting from accelerated replacement produce less virus per cell than the older ones of the newborn pig.

Age Factors↗

PubMed1985

The pathogenesis of persistent turbinate atrophy induced by toxigenic Pasteurella multocida in pigs.

Six one-week-old piglets were pretreated with a 1% acetic acid solution for two days in one or both nostrils. Three piglets were not treated with acetic acid. Three days after treatment all nine piglets were inoculated in both nostrils with a toxigenic type D strain of Pasteurella multocida. Three piglets were killed seven days after inoculation; one died spontaneously 13 days after inoculation and the remaining pigs were killed at approximately 90 kg body weight, i.e., five to six months of age. All acetic acid-treated animals developed severe atrophy of the turbinates in the treated nostrils. Untreated nostrils were normal. The present results showed that toxigenic P. multocida can induce turbinate atrophy that persisted until 90 kg body weight when the lesions were similar to spontaneous atrophic rhinitis in pigs. The turbinate atrophy was not accompanied by inflammatory reaction, atrophy of other bone structures, or lesions in other organs. The experiment showed furthermore that toxigenic P. multocida may be present in the tonsils of control animals without causing turbinate atrophy. A pathogenesis for atrophic rhinitis in pigs is proposed.

Acetates↗

PubMed1991

Selective type II muscle fiber hypertrophy in severe infantile spinal muscular atrophy.

The diagnostic muscle biopsy finding in severe infantile spinal muscular atrophy (Werdnig-Hoffmann disease, SMA type 1) is considered to be large-group atrophy with isolated clusters of hypertrophic type I myofibers. We present a unique case of severe infantile spinal muscular atrophy with selective hypertrophy of type II myofibers. A male infant presented at age 2 months with breathing difficulties and by age 4 months was hypotonic and weak. Electromyography revealed denervation in all extremity muscles, and nerve conduction velocities were normal but with small compound muscle action potentials. Quadriceps muscle biopsy revealed many hypertrophied type II myofibers (myofibers with a mean least diameter of 25.4 microns). In contrast, the largest type I myofibers were 20 microns in least diameter (mean diameter, 14.9 microns), and there was a normal-size population of type II fibers (mean diameter, 15.7 microns). In addition, sheets of atrophic type I and type II fibers averaged 2.0 microns in least diameter. Sural nerve biopsy was normal. Breathing difficulties progressed, with death ensuing at age 5 1/2 months. Autopsy revealed atrophy of ventral spinal roots with normal dorsal roots. There was loss of anterior horn cells, while remnant neurons were reduced in size. No other pathologic changes were identified. This case indicates that in severe infantile spinal muscular atrophy, relative sparing of the motor units with type II myofibers may occur.

Biopsy↗

PubMed1998

Axonal neuropathy and predominance of type II myofibers in infantile spinal muscular atrophy.

Two affected siblings with infantile spinal muscular atrophy (SMA I) presented with generalized muscular hypotonia, which progressed to early death. Quadriceps muscle biopsy did not show the typical neurogenic pattern of spinal muscular atrophy. The histochemical fiber type determination revealed a predominance of type II fibers without type I hypertrophy, an unprecedented finding in spinal muscular atrophy. Sural nerve biopsy exhibited findings typical for axonal neuropathy. In one patient, electrical stimulation of peripheral nerves showed an inexcitability of motor and sensory nerves. Genetic studies revealed homozygous deletions of the telomeric survival motor neuron (SMN) gene and the neuronal apoptosis inhibitory protein (NAIP) gene in the affected children. This is the second case report of molecular genetically proven spinal muscular atrophy associated with axonal neuropathy. We conclude atypical findings on muscle biopsy and evidence of axonal neuropathy are compatible with the diagnosis of infantile spinal muscular atrophy.

Adult↗

PubMed2004

Measurement of spinal cord atrophy in multiple sclerosis.

In multiple sclerosis (MS), the spinal cord is a common area of involvement, and its dysfunction is likely to be responsible for much of motor disability. It has been reported that atrophy in the cervical spinal cord occurs early and is detectable in patients presenting with a clinically isolated syndrome. This finding has important implications for the early treatment of patients with MS because atrophy is thought to reflect destructive, irreversible pathology and subclinical impairment. Recent clinical trials of disease-modifying agents have included spinal cord imaging and, in particular, the measurement of atrophy as a secondary or exploratory measure of treatment efficacy. This review summarizes the underlying pathology responsible for spinal cord atrophy and the methods available to measure it. The relationships between spinal cord atrophy, other magnetic resonance imaging parameters, and clinical disability are also discussed.

Atrophy↗

PubMed2006

The "cross" signs in patients with multiple system atrophy: a quantitative study.

Patients with multiple system atrophy (MSA) may show the "cross" sign in the pontine base that has been considered as an expression of the degeneration of pontine neurons and transverse pontocerebellar fibers. However, correlations between pontine base atrophy and existence of "cross" sign have not been fully investigated. The authors studied 68 patients with MSA (47 MSA-C [predominantly cerebellar ataxia], 21 MSA-P [predominantly parkinsonism], mean [+/-SD ] 58.7 +/- 10.9 years). T1-weighted (T1W) sagittal and axial images and T2-weighted (T2W) axial images were obtained for all patients and controls. To measure the areas of pontine basis and cerebellar vermis, the authors used midsagittal T1W images and analyzed a bit map transformed on a computer. They classified atrophy in the pontine base into 3 grades. There is significant correlation between atrophies of pontine base and existence of the cross sign. All patients with a smaller area of pontine base 2 standard deviations below those of normal controls had the cross sign. This supports that existence of the cross sign depends only on the extent of pontine base atrophies.

Adult↗

PubMed2000

Relationship between brain atrophy and disability: an 8-year follow-up study of multiple sclerosis patients.

Brain atrophy measurement can provide an estimate of the amount of tissue destruction due to the pathologic processes in multiple sclerosis. The potential usefulness of atrophy as a marker of disease progression depends upon the concurrent and predictive relationships between atrophy and disability. A follow-up study was performed to measure atrophy and disability scores in patients from the Multiple Sclerosis Collaborative Research Group's phase III trial of IFNbeta-1a (Avonex) in relapsing- remitting multiple sclerosis. New data were obtained on 160 out of 172 eligible patients from the original trial were enrolled in the follow-up study approximately 8 years after randomization. The follow-up visit consisted of several tests and questionnaires including a clinical exam to determine Expanded Disability Status Score (EDSS) and Multiple Sclerosis Functional Composite (MSFC), and a magnetic resonance imaging exam to calculate the brain parenchymal fraction. Brain parenchymal fraction was correlated with both EDSS and MSFC at each of the four time points for which data were available (baseline 1, 2 and 8 years). Furthermore, the change in BPF was correlated with the changes in disability scores from the end of the phase III trial to the follow-up exam. These data suggest that brain atrophy may be a useful and clinically relevant marker of disease progression in relapsing--remitting MS.

Adjuvants, Immunologic↗

PubMed2000

Single injections of a DNA plasmid that contains the human Bcl-2 gene prevent loss and atrophy of distinct neuronal populations after spinal cord injury in adult rats.

Spinal cord injury in adult mammals causes atrophy or loss of axotomized neurons. We have previously found that the product of the antiapoptotic gene Bcl-2, delivered by intraspinal injection of a DNA plasmid, reduces atrophy and loss of axotomized Clarke's nucleus neurons in adult rats. Here we studied whether the same treatment protects axotomized red nucleus (RN) neurons. Two months after the right dorsolateral funiculus was ablated in adult Sprague-Dawley rats by C3/C4 subtotal hemisection, there was approximately 48% loss of RN neurons in the magnocellular portion of the RN contralateral to the lesion and atrophy of many surviving neurons. When a DNA plasmid encoding the human Bcl-2 gene and the bacterial reporter gene LacZ, complexed with cationic lipids, was injected just rostral to the subtotal hemisection site, 87% of RN neurons survived, and there was partial, but robust, protection from atrophy. These and our previous results indicated that intraspinal administration of the Bcl-2 gene can prevent retrograde cell loss and reduce atrophy of axotomized RN and Clarke's nucleus neurons in adult rats and provide an effective means to rescue neurons whose survival depends on different growth factors.

Animals↗