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PubMed1997

Atrophy of the corpus callosum, cognitive impairment, and cortical hypometabolism in progressive supranuclear palsy.

Recent studies disclosed neurofibrillary degeneration in layer 3 of the association cortex in patients with progressive supranuclear palsy. This lesion may be associated with corpus callosum atrophy and may impair the function of cortical regions indispensable for complex cognitive activity. To investigate whether corpus callosum atrophy is associated with cognitive impairment and cerebral cortical hypometabolism, we studied 10 patients with progressive supranuclear palsy using magnetic resonance imaging and positron emission tomography with fluorodeoxyglucose as a tracer. Compared with 23 age-matched control subjects, the patients had significantly decreased callosal area-skull area ratios, with anterior predominance of the degree of atrophy. The corpus callosum atrophy was accompanied by a decreased mean cortical glucose metabolic rate, predominantly in the frontal region of the cortex, and poor performance on the picture arrangement subtest of the Wechsler Adult Intelligence Scale and the verbal fluency task. We conclude that corpus callosum atrophy with anterior predominance is present in progressive supranuclear palsy, and that this atrophy is associated with cognitive impairment and cerebral cortical hypometabolism, especially in the frontal cortical region. Corpus callosum atrophy may reflect the pathological changes in the cerebral cortex, accentuated in the frontal region, that contribute to the development of frontal lobe dysfunction in this disease.

Aged↗

PubMedDate not supplied

MR imaging of ventriculomegaly--a qualitative and quantitative comparison of communicating hydrocephalus, central atrophy, and normal studies.

Both communicating hydrocephalus and central atrophy cause ventricular dilatation. However, patients with hydrocephalus may require treatment. The aim of this study was to assess qualitatively and quantitatively the efficacy of MR imaging in the differentiation of communicating hydrocephalus from central atrophy. The midsagittal T1-weighted MR images of 33 patients with communicating hydrocephalus, 31 patients with central atrophy, and 23 normal subjects were evaluated qualitatively and quantitatively. This included configuration of the aqueduct; area of the septum pellucidum, third ventricle, and fourth ventricle; and morphology of the corpus callosum. Distal dilatation of the aqueduct was detected in 33.3% of patients with communicating hydrocephalus and in none of those with central atrophy. The corpus callosum was elevated in patients with communicating hydrocephalus when compared with that in patients with central atrophy. In conclusion, an analysis of midsagittal T1-weighted images has identified useful qualitative and quantitative criteria in the differentiation of communicating hydrocephalus from central atrophy. The configuration of the aqueduct with funneling at the fourth ventricular end strongly suggests the presence of communicating hydrocephalus rather than central atrophy alone.

Aged↗

PubMed2006

Relation of cerebral small-vessel disease and brain atrophy to mild Parkinsonism in the elderly.

The association between cerebral small-vessel disease, brain atrophy, and the risk and severity of mild parkinsonian signs (MPS) remains unclear. The objective of this study is to examine the effect of lacunar brain infarcts, cerebral white matter lesions (WMLs), and cortical atrophy on the risk and severity of MPS. This study is a cross-sectional community-based cohort study comprising 268 subjects, 65 to 83 years of age, residing in the Augsburg region of southern Germany, and without contraindications for magnetic resonance imaging (MRI) of the brain. Main outcome measures. Subcortical and periventricular WMLs, lacunar brain infarcts, and cortical atrophy determined using a standardized MRI protocol developed for the Rotterdam Scan Study and an established rating scale. MPS, assessed in a standardized neurological examination and based on the Unified Parkinson's Disease Rating Scale motor scale. Lacunar brain infarcts and large subcortical white matter lesions were associated with an elevated risk of resting tremor. More severe cortical atrophy was related to an increased risk of rigidity and bradykinesia. In a linear regression analysis relating each individual MRI measurement with the severity of MPS, the number of lacunar brain infarcts and the degree of brain atrophy were correlated with the severity of resting tremor, whereas the size of subcortical and periventricular WMLs was correlated with the severity of rigidity. A higher degree of brain atrophy was associated with increased severity of either cardinal sign. In our study, presence and volume of lacunar brain infarcts, cerebral WMLs, and cortical atrophy were associated with the risk as well as severity of MPS. Determining the presence of these brain changes using brain imaging might contribute to identify persons at risk for MPS.

Aged↗

PubMed1995

Axonal atrophy is a specific component of 2,5-hexanedione peripheral neuropathy.

To assess the relevance of previously identified axonal atrophy to hexanedione neuropathy, the present study quantitated fiber size in peripheral nerve of rats intoxicated with 2,5-hexanedione (HD) by either oral ingestion (0.4% in drinking water) or ip injection (0.4 g/kg/day). Prior to the appearance of neurobehavioral deficits, rats exposed to oral HD (77 days) exhibited axonal atrophy in proximal sciatic nerve and giant axonal swellings in distal tibial nerve. As oral-treated rats progressed to moderate (86 days) and severe (103 days) hindlimb weakness, both nerve regions contained a mixed population of atrophied and swollen axons. Rats injected with HD ip were sampled at behavioral endpoints that matched those of oral HD-treated rats. In sciatic and tibial nerves from rats treated ip, reductions in the axon area were similar to oral exposure. However, ip treatment did not produce giant axonal swellings in either nerve. Thus, although both routes of administration caused equivalent behavioral neurotoxicity, the expression of axonal swellings was route-dependent. This suggests that the production of swellings depends upon the HD exposure pattern. In contrast, axonal atrophy was prevalent in both nerve regions sampled and developed in parallel with behavioral deficits. In addition, atrophy was expressed regardless of the intoxication route which indicates that atrophy can occur independent of axonal swellings. Together, these attributes suggest that atrophy is a specific component of HD neurotoxicity.

Administration, Oral↗

PubMed1987

A quantitative study of physiological cerebral atrophy with aging. A statistical analysis of the normal range.

A new method of discriminating pathological cerebral atrophy from physiological atrophy during aging is reported. The authors advocate a pixel counting method using a minicomputer for the quantitative measurement of cerebral atrophy. Five hundred cases were studied with this quantitative method and the normal range of the physiological atrophy was determined statistically. In order to estimate the degree of cerebral atrophy easily, the conventional linear measurement methods were compared with the pixel counting method using multivariant analysis, and a simple formula for the calculation of the degree of cerebral atrophy is proposed. Using this formula and the normal range, pathological cerebral atrophy is easily detectable.

Adolescent↗

PubMed1986

Muscle fiber atrophy in the quadriceps in knee-joint disorders. Histochemical studies on 112 cases.

In order to determine whether there is a different susceptibility of muscle fiber types in the m. vastus lateralis (VL) in knee-joint disorders, histochemical studies were performed on 112 cases. Anterior cruciate ligament (ACL) injuries affected 51 patients; ACL injuries associated with meniscus (ACL + M) injuries affected 29. Twenty-five patients had sustained meniscus injuries and seven had injuries of the collateral ligaments (CL). Fifty-two were athletic and 60 were not. On each biopsy, fiber-type distribution was obtained and the degree of atrophy of each fiber type was estimated from two parameters, the mean diameter and the percentage of atrophied fibers. The distribution of type-1 fibers averaged 38.0% +/- 12.0%. There were no significant differences among disorders in the distribution of type-1 fibers. Both parameters of fiber atrophy revealed a difference in susceptibility between type-1 and type-2 fibers. Atrophy of type-1 fibers was found only in ACL and ACL + M injuries. Type-2 fibers were atrophied in all four disorders. Atrophy of type-2 fibers could be a nonspecific change due to the inactivity of the VL, but type-1 fiber atrophy may relate specifically to the condition of ACL insufficiency.

Adolescent↗

PubMed1993

Follow-up of neurophysiological tests and CT in late-onset cerebellar ataxia and multiple system atrophy.

The follow-up of neurophysiological tests (brain-stem auditory evoked potentials; blink reflex; sensory, motor and visual evoked potentials) and CT was investigated in 21 patients with late-onset cerebellar ataxia (CA) or multiple system atrophy. The study included an initial investigation and a follow-up examination on average 25.3 months later (minimum 8, maximum 36). Patients were divided into four groups: (1) those with pure CA after a minimum course of 5 years; (2) those with pure CA with pathological neurophysiological findings at the last examination; (3) those who at the first examination clinically presented with pure CA, but at the last examination were seen to have developed a multisystem disorder; (4) those with multiple system atrophy (mostly olivopontocerebellar atrophy) presenting additional non-cerebellar signs of involvement. Conforming to a strict interpretation of pure CA, group 1 patients invariably exhibited normal neurophysiological findings at all examinations. All patients in group 4, except for 2 only at the first examination, showed pathological changes in at least one of the neurophysiological tests. The main conclusion of this paper is that individuals who according to clinical criteria were initially classified as having CA but finally developed a multisystem disorder already had pathological neurophysiological findings at the initial examination (group 3). The increasing frequency of pathology in the several neurophysiological tests together with the progression of the disease is obviously of prognostic significance. CT revealed cerebellar atrophy without apparent involvement of brain-stem structures in all patients with CA; the majority of patients with multiple system atrophy also had atrophy of the brain-stem, pointing to olivopontocerebellar atrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1991

Computed tomography, magnetic resonance imaging and positron emission tomography with [18F]fluorodeoxyglucose in multiple system atrophy and pure autonomic failure.

We studied 45 patients who had autonomic failure with computed tomography, magnetic resonance imaging and positron emission tomography with [18F]fluorodeoxyglucose to characterize the neuroimaging features of multiple system atrophy and pure autonomic failure and determine the utility of these techniques in distinguishing multiple system atrophy from pure autonomic failure. There were 30 patients with multiple system atrophy and 15 with pure autonomic failure. In the multiple system atrophy group, eight patients had mainly cerebellar signs, seven extrapyramidal and 15 had combinations of cerebellar and extrapyramidal signs. Cerebellar atrophy on computerized tomography and magnetic resonance imaging, signal hypointensity in the posterolateral putamen on magnetic resonance imaging and a generalized reduction in glucose utilization rate with positron emission tomography with [18F]fluorodeoxyglucose, were the main findings and were seen only in the patients with multiple system atrophy. Decreased glucose utilization (hypometabolism) was most prominent in the cerebellum, brainstem, striatum and frontal and motor cortices. These results indicate clear differences, using neuroimaging studies, between multiple system atrophy and pure autonomic failure.

Atrophy↗

PubMed2002

Characteristic MRI findings in multiple system atrophy: comparison of the three subtypes.

We reviewed MRI findings in 29 patients with probable multiple system atrophy (MSA) to see whether there were common and or less common neuroradiological findings in the various clinical subtypes. We divided the patients into three clinical subtypes according to initial and predominant symptoms: 14 with olivopontocerebellar atrophy (OPCA), eight with the Shy-Drager syndrome (SDS) and seven with striatonigral degeneration (SND). The patients showed atrophy of the brain stem and cerebellum, high signal on T2-weighted images of the base of the pons and middle cerebellar peduncles, high and low signal on T2-weighted images of the putamen and atrophy of frontal and parietal lobes. The degree of atrophy of the middle cerebellar peduncle and cerebellum was greater in OPCA patients and a high-signal lateral rim to the putamen more frequent in SND. However, all findings were observed in all subtypes, and the degrees of atrophy of the putamen and pons and the frequency of high signal in the base of the pons were similar in the subtypes. We also found atrophy of the cerebral hemispheres, especially the frontal and parietal lobes, but its degree was not significantly different in the various subtypes. Our findings suggest that, although MSA can be divided clinically into three subtypes, most of the features on MRI are common and overlap in the subtypes, independently of the clinical presentation.

Brain↗

PubMed2006

Genetic mapping of loci controlling diethylstilbestrol-induced thymic atrophy in the Brown Norway rat.

Chronic estrogen administration can lead to thymic atrophy in rodents. In this article we report that the Brown Norway (BN) rat is sensitive to thymic atrophy induced by the estrogen diethylstilbestrol (DES). By contrast, DES does not induce significant thymic atrophy in the August x Copenhagen-Irish (ACI) strain. The sensitivity of the BN rat to DES-induced thymic atrophy appears to segregate as an incompletely dominant trait in crosses between the BN and ACI strains. In a (BN x ACI)F(2) population, we find strong evidence for three major genetic determinants of sensitivity to DES-induced thymic atrophy on rat Chromosome (RNO) 10 and RNO2. Genotypes at these loci, termed Esta1, 2, and 3, do not have a significant impact on the ability of DES to induce pituitary tumorigenesis or inhibit growth of these F(2) rats. These data indicate that the genetic factors that control DES-induced thymic atrophy are distinct from those that control the effects of DES on pituitary mass and body mass. The Esta intervals on RNO10 and RNO2 overlap with loci that control sensitivity to radiation-induced thymocyte apoptosis, as well as susceptibility to a variety of allergic and autoimmune pathologies, including allergic encephalitis, arthritis, and glomerulonephritis in rodents. These observations suggest that common genetic determinants may control sensitivity to estrogen-induced thymic atrophy, maintenance of thymocyte homeostasis, and immune function.

Aging↗

PubMed2006

Localization of grey matter atrophy in early RRMS : A longitudinal study.

Previous MR studies have established that grey matter (GM) atrophy occurs in multiple sclerosis (MS) from clinical onset. However, it is uncertain whether early GM atrophy is global or has certain local predilections: using Voxel-Based Morphometry this study aimed to address this question.Twenty-one patients with early RRMS (mean age 36 years, mean disease duration from symptom onset 25.8 months) and 10 healthy control subjects (mean age 37 years) were studied. T(1)-weighted three-dimensional MRI images were acquired at baseline and two year follow-up, and analysed with statistical parametric mapping software (SPM2). Two-sample t-tests (p < 0.05 corrected for multiple comparisons at cluster level) were used to compare GM maps from all patients and controls on a voxel-by-voxel basis. At baseline, no GM region appears significantly atrophic in MS subjects compared with controls. However, during the follow-up period significantly greater atrophy occurred in both thalami and the right lateral prefrontal cortex of MS patients when compared with controls. By year two, cross-sectional group comparison revealed GM atrophy in the thalami of MS patients relative to controls. The rate of thalamic atrophy in MS subjects was correlated with changes in EDSS during the follow-up period. This study suggests that early in the clinical course of RRMS, the thalamic atrophy is more consistently apparent than regional cortical atrophy.

Adult↗

PubMed2003

Factors associated with the development of chorioretinal atrophy around choroidal neovascularization in pathologic myopia.

PURPOSE: To examine the influencing factors on the development of chorioretinal atrophy, which is the main cause of long-term visual decrease in myopic choroidal neovascularization (CNV), in a large series of highly myopic patients. METHODS: Sixty-five patients (81 eyes) with myopic CNV were studied retrospectively. The influence of the patient's age, refractive error, axial length, visual acuity at onset of CNV, size of CNV, and grade of myopic retinopathy on the extent of chorioretinal atrophy more than 3 years after CNV onset was investigated by means of multiple linear regression analysis. RESULTS: Seventy-seven of 81 eyes (95.1%) developed chorioretinal atrophy around myopic CNV during the follow-up period. Multiple linear regression revealed that age was the most influencing factor for the development of chorioretinal atrophy in all the subjects. When we divided the subjects into two groups according to their age, however, CNV size was the only factor to influence the development of chorioretinal atrophy in the patients younger than 40 years, whereas age was still the only influencing factor in those older than 40 years. CONCLUSIONS: The factors influencing the development of chorioretinal atrophy differ according to patient age. Local factors, such as CNV size, determine the tendency to develop chorioretinal atrophy in young patients. Systemic factors, such as patient age, play a greater part in older subjects.

Atrophy↗

PubMed2004

Peripapillary atrophy in the unilateral exfoliation syndrome.

PURPOSE: To compare the areas of peripapillary atrophy between fellow eyes in patients with unilateral exfoliation syndrome. METHODS: Topographic measurements for peripapillary atrophy and the optic nerve head with confocal scanning laser ophthalmoscopy, using the Heidelberg Retina Tomograph were performed on 45 nonglaucomatous patients with unilateral exfoliation syndrome. The area of peripapillary atrophy was divided into an alpha and a beta zone. The areas of alpha and beta peripapillary atrophy and their angular extents around the disc were measured. The frequency distributions of the alpha and beta areas and their largest radial extents at different positions around the disc were calculated. RESULTS: An alpha area was detected in 84% of the exfoliative and 89% of the nonexfoliative fellow eyes, and a beta area in 31% and 42% of eyes, respectively. The exfoliative and the fellow nonexfoliative eyes did not differ in the sizes of the alpha (0.43+/-0.46 vs 0.33+/-0.18 mm(2), P=0.68) and beta (0.14+/-0.30 vs 0.17+/-0.34 mm(2), P=0.96) areas of peripapillary atrophy. The angular extents, the locations of the largest radial extent, and the frequency distributions of the alpha and beta peripapillary atrophy areas were similar in fellow eyes. CONCLUSION: Exfoliation syndrome itself is not a risk factor for peripapillary atrophy.

Aged↗

PubMed2005

Agreement between endoscopic and histological gastric atrophy scores.

BACKGROUND: This study was conducted to investigate the strength of agreement between the endoscopic atrophic border (EAB) and the histological score for atrophy. METHODS: A series of 298 dyspeptic Japanese patients underwent upper endoscopy. The grade of gastric atrophy was estimated according to the EAB. Antral and corpus biopsy specimens were taken and were evaluated semiquantitatively according to the updated Sydney classification system, including the score for atrophy. The StatExact software package was used to calculate the weighted kappa statistics. RESULTS: The strength of agreement between the endoscopic atrophy score (EAB) and the histological atrophy score was good, with a weighted kappa value of 0.51 (95% confidence interval, 0.44-0.59). CONCLUSIONS: The strength of agreement between the endoscopic and histological atrophy scores is not worse than the interobserver histological agreement between two pathologists. It is worthwhile to carry out further research on the use of the EAB to identify and score gastric atrophy.

Aged↗

PubMed2004

Histochemical study on the changes in muscle fibers in relation to the effects of aging on recovery from muscular atrophy caused by disuse in rats.

To investigate the effects of aging on the degree of muscular atrophy caused by disuse and its recovery, we evaluated the recovery from muscular atrophy induced in both young and old rats under the same conditions. The soleus was atrophied by immobilization of the foot joint in a hindlimb and unweighting of the bilateral hindlimbs for 2 weeks, and measurement of the wet weight of muscles and biochemical examination were performed 2, 4, and 6 weeks after the removal of unweighting and fixation during the recovery period of 6 weeks. There was no difference in the degree of atrophy in the fixed soleus between the young and old rats. The recovery from atrophy was delayed in the older rats compared to the young rats. In the unfixed hindlimb, the degree of atrophy was low in both the old and young rats, and the recovery was rapid. Because the recovery from disuse muscular atrophy is delayed with aging, it is necessary to avoid unweighting and immobilization, or to reduce the period spent under such conditions.

Age Factors↗

PubMed1986

The prevalence of alcoholic cerebellar atrophy. A morphometric and histological study of an autopsy material.

The Purkinje cell densities in the cerebellar vermis were determined in 31 male alcoholics and 34 non-alcoholic controls under 70 years of age. In addition, all cases were examined histologically for atrophy of the superior vermis. All analyses were performed independently of each other and on randomized slides. The alcoholics had significantly lower Purkinje cell densities than the controls in the superior and middle segments of the vermis. Histologically verified atrophy of the superior vermis was found in 13 of the alcoholics (42%) and in 3 of the controls (9%). There was a good accordance between the morphometric data and the histologic diagnoses. The cause of the cerebellar atrophy in the 3 control cases is uncertain. It could be due to hidden alcoholism or to premature ageing. In a series of non-alcoholic control cases above 70 years, one third of the cases showed atrophy of the superior vermis similar to that of alcoholics. The diagnosis alcoholic cerebellar atrophy should therefore be made with great caution in cases over 70 years. From previous morphometric data on symptomatic cases (Victor et al. 1959), it can be assumed that the majority of the present cases with histologically verified atrophy had overt clinical symptoms. It is concluded that almost one half of all severe alcoholics have atrophy of the superior vermis which can be recognized morphologically and probably also clinically.

Adult↗

PubMed2004

Utility of immunohistochemistry for alpha-methylacyl-CoA racemase in distinguishing atrophic prostate cancer from benign atrophy.

Small atrophic prostate cancers on needle biopsy are rare and difficult to distinguish from benign atrophy on needle biopsy. We report on a study of 23 needle biopsy specimens with small foci of atrophic prostate cancer from the consult service of one of the authors. In 19 cancer cases the atrophic component was pure; in 4 cases it was dominant with a minor (<5%) nonatrophic cancer component. These atrophic cancers and 16 cases of florid benign atrophy on needle biopsy were examined by immunohistochemistry for alpha-methylacyl-CoA-racemase (AMACR). All cases of cancer and atrophy were verified immunohistochemically with antibodies to basal cells (34betaE12 and p63). AMACR staining were scored as 1+ (5% to 25% of glands expressing AMACR), 2+ (26% to 50% of glands expressing AMACR), or 3+ (>50% of glands expressing AMACR). Positive staining was defined as staining above that of surrounding benign glands. AMACR was expressed in 69.6% of atrophic prostate cancers (3+, 11 cases; 2+, 3 cases; 1+, 2 cases); 30.4% (7 cases) of atrophic prostate cancer exhibited no AMACR expression. In the 4 cases with a few glands of ordinary (nonatrophic) prostate cancer, the nonatrophic cancer demonstrated more intense and a greater extent of AMACR staining. Fourteen cases (87.5%) of benign atrophy showed no AMACR expression. In 2 cases (12.5%) of benign atrophy, background immunostaining made it difficult to assess AMACR expression. We conclude that AMACR immunostaining alone is not sufficiently discriminatory in the differential diagnosis of atrophic prostate cancer versus benign atrophy. Atrophic prostate cancers are not as frequently or as strongly positive as ordinary prostate cancer. Using a panel of immunostains including AMACR, 34betaE12 and p63 (positive AMACR immunostaining along with negative basal cell markers) is recommended in the differentiation of atrophic prostate cancer and benign atrophy.

Adenocarcinoma↗

PubMed2004

Concomitant blockade of platelet-derived growth factor receptors alpha and beta induces intimal atrophy in baboon PTFE grafts.

OBJECTIVE: Although current treatments for restenosis attempt to prevent the development of intimal hyperplasia, an alternative strategy is to induce intimal atrophy after restenosis has developed. Because platelet-derived growth factor (PDGF) is a smooth muscle cell growth and survival factor, we tested the hypothesis that complete blockade of PDGF by using antibodies against PDGF receptors alpha and beta would cause intimal atrophy in a baboon vascular graft model. METHODS: We administered chimeric antibodies against PDGF receptor alpha or PDGF receptor beta, either separately or together, to baboons with bilateral prosthetic aortoiliac grafts, the intimas of which had reached maximal size before treatment was begun. High blood flow, which we have previously shown to cause intimal atrophy, was induced through one graft to serve as a positive control. After 2 weeks, the intima lining the grafts was assessed for cross-sectional area, cell proliferation, and apoptosis by standard morphologic and immunohistochemical techniques. RESULTS: Blocking both PDGF receptors simultaneously reduced the cross-sectional area of the normal-flow graft intima by 44% (P <.05 vs control), whereas treatment with the individual antibodies did not significantly alter intimal area. Blockade of both receptors also inhibited smooth muscle cell proliferation by 66% (P <.05 vs control), whereas neither antibody alone altered proliferation. In contrast, all treatments increased smooth muscle cell apoptosis threefold to fivefold. CONCLUSIONS: These data suggest that simultaneous inhibition of cell proliferation and stimulation of cell death by the administration of antibodies to both PDGF receptor alpha and receptor beta is required for intimal atrophy in this baboon graft model. In addition, these data provide an in vivo model for the pharmacologic induction of intimal atrophy and introduce a novel clinical approach to treat intimal hyperplasia. Clinical relevance This study introduces the concept of pharmacologic induction of intimal atrophy. Intimal hyperplasia plagues all forms of arterial reconstruction. Currently, the only effective treatment of these restenotic lesions is balloon angioplasty or operative revision. An alternative approach to patients with clinically significant intimal hyperplasia might be to stimulate intimal regression by modulating growth and survival factors required for intimal maintenance. Although PDGF is known to be critical in intimal formation, the results of this study suggest that PDGF is also critical for intimal maintenance. Inhibition of the PDGF system may prove to be a clinically applicable approach for inducing intimal atrophy.

Animals↗