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PubMed1997

Partial loss of NADPH-diaphorase/nitric oxide synthase-complex in amyotrophic lateral sclerosis and human type-II myofiber atrophy.

To substantiate the role of nitric oxide synthase type-I (NOS-I) in neurogenic muscular disorders we investigated human biopsy samples of type-II fiber atrophy and amyotrophic lateral sclerosis (ALS) by NOS-I immunoreactivity (-IR), NOS-associated NADPH-dependent diaphorase activity (NOSaD) and Western blot analysis. In type-II atrophy, loss of NOSaD and reduced NOS-I-IR was apparent in atrophic myofibers. In atrophic fiber groups lacking NOSaD, both NOS-I and dystrophin-IR was decreased while sarcolemmal beta-dystroglycan- and adhalin-IR (markers of the sarcolemmal dystrophin-glycoprotein complex) was normal. In ALS, groups of scattered angulated atrophic fibers revealed partial loss of NOS-I-IR/NOSaD. Atrophied fibers of either type-I or type-II thus revealed differential sarcolemmal NOS/NOSaD pattern thereby reflecting myopathological alterations of the NO-system in human type-II atrophy and ALS.

Adult↗

PubMed1994

Atrophy of the tongue with persistent articulation disorder in myasthenia gravis: report of 10 patients.

Ten patients with atrophy of the tongue, from a group of 752 with generalized acquired myasthenia gravis (MG), were studied. Tongue atrophy developed late in the majority of patients and was accompanied by tongue paresis (70% of the cases) and eventually associated to atrophy of other muscles of the palate, especially the uvula. All the patients exhibited severe forms of MG with bulbar involvement, mainly persistent dysphonia and dysphagia, almost always refractory to treatment. There is no correlation among atrophy of the tongue, sex, and thymus pathology. There is correlation between severeness of symptoms and early, persistent and treatment refractory dysphonia and dysphagia.

Adult↗

PubMed2001

The significance of type 1 fiber atrophy (hypotrophy) in childhood neuromuscular disorders.

To determine the incidence of selective type 1 fiber atrophy (hypotrophy) and its possible significance in various muscle diseases of childhood, we reviewed 2212 muscle biopsies from children which we had examined in the past 20 years histochemically with ATPase staining. Type 1 fiber atrophy was seen in a variety of neuromuscular disorders, but predominantly in congenital myopathies, including all patients with congenital fiber type disproportion myopathy (20 patients), central core disease (12 patients) and multicore disease (four patients). Although type 1 fiber atrophy was not a constant feature in nemaline myopathy and myotubular myopathy, all patients with these diseases had abnormal fiber type distribution which included type 1 fiber predominance both with and without type 2B fiber deficiency. Together with abnormal fiber type distribution, type 1 fiber atrophy was a common finding in childhood neuromuscular disorders, especially congenital myopathies.

Atrophy↗

PubMed1997

Longitudinal distribution of hippocampal atrophy in mesial temporal lobe epilepsy.

Patients with mesial temporal lobe epilepsy (MTLE) have asymmetric hippocampal volumes with atrophy that sometimes by visual inspection appears to favor different regions along the longitudinal axis of the affected hippocampus. Histological studies suggest that cell loss may affect the anterior hippocampus preferentially, and that hippocampal sclerosis (HS) limited to the anterior of the hippocampus may indicate better surgical outcome. We used volumetric magnetic resonance imaging (MRI): (1) to objectively describe the distribution of volume loss in HS; and (2) to relate this distribution to outcome of temporal lobectomy. Hippocampal volumes and anterior and posterior subvolumes (AHV, PHV) were measured from MP-RAGE MRI in 43 temporal lobectomy patients with MTLE determined by pathological findings of HS and compared to 23 age-matched controls. Atrophy was defined as 'anterior', 'diffuse', 'posterior', or 'normal' depending on position of AHV and PHV relative to the mean +/- 2 S.D. of regional volumes of control hippocampi. Anterior to posterior ratios (APR = AHV/PHV) were also calculated. Mean APR of hippocampi ipsilateral to lobectomy cannot be distinguished from hippocampi contralateral to lobectomy or from controls. AHV and PHV from hippocampi contralateral to temporal lobectomy were smaller than controls but larger than hippocampi ipsilateral to lobectomy. Surgical outcome was independent of longitudinal distribution of atrophy. We determined that overall volume loss in HS is diffuse, neither clearly favoring the head nor body-tail. Surgical outcome for MTLE is not related to the longitudinal distribution of atrophy revealed by volumetric MRI.

Adult↗

PubMedDate not supplied

The thymic epithelial reticulum and interdigitating cells in SIV-induced thymus atrophy and its comparison with other forms of thymus involution.

Alterations in the thymus were investigated in the early course of SIV infection of rhesus monkeys and compared with age-related and acute accidental thymus atrophy. The SIV-induced pathology was characterized by shrinkage of the thymic parenchyma and capsule, whereas in age-related thymus atrophy, the size of the capsule remained unaltered and the emerging space was filled by fatty tissue. Acute accidental thymus involution is characterized by massive cell death of the thymocytes, but there was no increase in pycnotic thymocytes either in SIV-induced or in age-related thymus atrophy. Ultrastructural analysis revealed no major differences between the juvenile control and the aged thymus. In contrast, SIV-induced thymus atrophy exhibited severe alterations of the epithelial cells of the cortex and the interdigitating dendritic cells, which were not found in the aged thymus nor in the juvenile control cortex.

Aging↗

PubMed1999

Visual assessment of medical temporal lobe atrophy in demented and healthy control subjects: correlation with volumetry.

The present study evaluated the validity of visual rating of medial temporal lobe atrophy on coronal magnetic resonance imaging scans in a population of demented and non-demented individuals. Medial temporal lobe atrophy in 194 subjects was visually rated from hard copies, using a 0-4 rating scale, and a comparison was made with the absolute volumes (ccm) of the medial temporal lobe as estimated with volumetry, using a stereological method. We found a highly significant correlation between the estimated and stereologically measured volumes. There was a 10-fold difference in time spent on rating medial temporal lobe atrophy (1-2 min) vs. time spent calculating the medial temporal lobe volume (10-12 min) on a single subject. The diagnostic accuracy of both methods showed that visual rating was more efficient than volumetry in differentiating Alzheimer's disease from control subjects, We conclude that visual rating is a reliable and fast method to estimate medial temporal lobe atrophy in demented subjects in a clinical setting.

Adult↗

PubMed1993

Role of microenvironmental deterioration of the bone marrow in the development of bone atrophy in magnesium silicate-treated rats.

The role of microenvironmental deterioration of the bone marrow in the development of bone atrophy was examined in rats with bone atrophy induced by magnesium silicate. In the tibial metaphyses, proliferation of myelocytic elements of haematopoietic tissue was prominent and caused narrowing of sinusoids, increased distance between sinusoids and trabecular bone and atrophy of trabecular bone. There was a significant correlation in volume percentage between haematopoietic cells and trabecular bone, between haematopoietic cells and sinusoids and between sinusoids and trabecular bone. These results imply that atrophy of trabecular bone is related to microenvironmental deterioration of the bone marrow, that is, a decrease in efficiency of exchange of nutrients and waste products between sinusoids and trabecular bone due to the proliferation of haematopoietic cells and a deficiency of nutrient supply to the bone marrow due to the narrowing of sinusoids.

Animals↗

PubMedDate not supplied

Patterns of muscle atrophy in the lower limbs in patients with Charcot-Marie-Tooth disease as measured by magnetic resonance imaging.

Intrinsic atrophy of the calf musculature is a common finding in Charcot-Marie-Tooth disease. Peroneal nerve atrophy leading to weakness in the anterior and lateral compartments is the most common clinical pattern, but considerable variability exists in the pattern of atrophy. Magnetic resonance imaging offers a valuable method for identifying the distribution and symmetry of muscle degeneration. Twenty-three patients with Charcot-Marie-Tooth disease had axial T-1 magnetic resonance images obtained at proximal, middle and distal calf muscle locations. Areas of fatty infiltration and muscle atrophy were measured in the four calf muscle compartments. The worst areas of involvement, on a scale of one to four, with four being worst, were in the lateral compartment in the mid calf (mean, 2.5) and in the anterior, posterior and lateral compartments of the distal calf (2.6, 2.8 and 2.5). Comparing right and left legs showed that there was visible asymmetry, which was not statistically significant. There was considerable variation in the pattern of involvement from patient to patient. The fact that all four calf muscle compartments may be involved asymmetrically and in varying degrees is important for treatment planning, including surgery. Not all patients have the classic symmetrical peroneal pattern of denervation.

Adolescent↗

PubMed2004

The IGF-1/PI3K/Akt pathway prevents expression of muscle atrophy-induced ubiquitin ligases by inhibiting FOXO transcription factors.

Skeletal muscle size depends upon a dynamic balance between anabolic (or hypertrophic) and catabolic (or atrophic) processes. Previously, no link between the molecular mediators of atrophy and hypertrophy had been reported. We demonstrate a hierarchy between the signals which mediate hypertrophy and those which mediate atrophy: the IGF-1/PI3K/Akt pathway, which has been shown to induce hypertrophy, prevents induction of requisite atrophy mediators, namely the muscle-specific ubiquitin ligases MAFbx and MuRF1. Moreover, the mechanism for this inhibition involves Akt-mediated inhibition of the FoxO family of transcription factors; a mutant form of FOXO1, which prevents Akt phosphorylation, thereby prevents Akt-mediated inhibition of MuRF1 and MAFbx upregulation. Our study thus defines a previously uncharacterized function for Akt, which has important therapeutic relevance: Akt is not only capable of activating prosynthetic pathways, as previously demonstrated, but is simultaneously and dominantly able to suppress catabolic pathways, allowing it to prevent glucocorticoid and denervation-induced muscle atrophy.

Animals↗

PubMed2006

Tracking atrophy progression in familial Alzheimer's disease: a serial MRI study.

BACKGROUND: Serial MRI scanning of autosomal dominant mutation carriers for Alzheimer's disease provides an opportunity to track changes that could predate symptoms or clinical diagnosis of the disease. We used hierarchical modelling to assess how hippocampal and whole-brain volumes change as familial Alzheimer's disease progresses from the presymptomatic stage through to diagnosis. METHODS: Nine mutation carriers had serial clinical assessments and volumetric MRI scans (41 scans: range 3-8 per patient) at different clinical stages (presymptomatic, mild cognitive impairment, or clinical Alzheimer's disease). 25 healthy controls had serial scanning (54 scans: range 2-4 per patient) for comparison. We measured whole brain and total hippocampal volumes using semi-automated techniques, and adjusted for total intracranial volume. Hierarchical models were developed to estimate differences in volume and atrophy rate between mutation carriers and controls in relation to when the disease was clinically diagnosed. FINDINGS: Mutation carriers had significantly increased hippocampal and whole-brain atrophy rates compared with controls and these differences increased with time. Differences in hippocampal and whole-brain atrophy rates between controls and mutation carriers were evident 5.5 and 3.5 years, respectively, before diagnosis of Alzheimer's disease. At a cross-sectional level, differences in mean hippocampal volume between mutation carriers and controls became significant 3 years before clinical diagnosis, whereas differences in mean brain volumes became significant only 1 year before diagnosis. INTERPRETATION: Structural changes can be seen on MRI scans that predate the clinical onset of familial Alzheimer's disease. Longitudinal measures of atrophy rates can identify differences between mutation carriers and controls 2-3 years earlier than cross-sectional volumetric measures.

Adult↗

PubMed2001

The prevalence of depression in relation to cerebral atrophy and cognitive performance in 70- and 74-year-old women in Gothenburg. The Women's Health Study.

BACKGROUND: Hospital-based studies report that depression in the elderly is associated with brain atrophy. This notion could not be confirmed in a population study on 85-year-olds. We aimed to assess depression in relation to brain atrophy and cognition in 70- and 74-year-old women. METHODS; A representative sample of 70- and 74-year-old women (N = 501) was examined with a psychiatric examination including the Mini-Mental State Examination (MMSE), measuring global cognitive function, and computerized tomography (CT) of the brain (N = 268). Depression was diagnosed according to DSM-III-R. Previous depression was diagnosed by history and by information from previous examinations in this 24-year longitudinal study. RESULTS: The prevalence of depression was 11.6%, including 8.4% with major depression (MDD). Among those who were currently mentally healthy, 43.0% had a history of previous depression. Women with current MDD had lower scores on the MMSE than the mentally healthy women. This association was only found in women with a lower level of education. Current depressives, previous depressives and mentally healthy women without a history of depression did not differ on CT with regard to brain atrophy or white matter lesions. The association between MDD and lower cognitive performance was independent of the association of cognitive performance with structural brain changes on CT. CONCLUSIONS: Brain atrophy on CT is not associated with depression in the general population, despite the fact that individuals with depression have a worse cognitive performance. The finding that cognitive performance was not decreased in individuals with previous depression suggests that cognitive dysfunction is a state phenomenon in depression.

Aged↗

PubMed2002

Prostatic atrophy: evidence for a possible role of local ischemia in its pathogenesis.

Prostatic atrophy may be histologically and at ultrasound similar to adenocarcinoma causing diagnostic confusion, its frequency increases with age but the etiopathogenesis is unknown. Based on a systematic study in autopsies previously done by one of us, ischemia due to local intense arteriosclerosis seems to be a potential factor for its pathogenesis. Absent blood flow in areas of prostatic atrophy might be a further evidence for a possible role of ischemia. From a total of 298 patients biopsied and studied by gray-scale and color Doppler transrectal ultrasound in the period 1998 to 2001, 33 patients had suspicious lesions (37 hypoechoic nodules and 3 heterogeneous lesions) showing prostatic atrophy as the only diagnosis on all these biopsied lesions. Adenocarcinoma, high-grade intraepithelial neoplasia or other atypical lesions were absent in all patients. On color Doppler the suspicious areas showed absent flow in 24/40 (60%), present flow in 12/40 (30%), and increased flow in 4/40 (10%) of the lesions. Absent flow in the majority of the lesions studied may be a further evidence for a possible role of local ischemia in the etiopathogenesis of prostatic atrophy.

Adult↗

PubMed2000

Hippocampal and temporal lobe atrophy and age-related decline in memory.

OBJECTIVES: To evaluate the relationship of memory decline that accompanies aging with structural changes in the medial temporal lobe, in healthy middle-aged and older subjects. MATERIAL AND METHODS: A sample of 35 neurologically non-diseased subjects, between 55 and 70 years of age, were examined in a 5-year follow-up study. Neuropsychological investigation included tests of learning, verbal memory, and visual memory. MRI was performed with a superconducting MRI system operating at 1.0 T, using coronal slices of T1-weighted images. Medial temporal lobe atrophy was rated separately in the neocortical, entorhinal and hippocampal regions. RESULTS: We did not find any statistically significant relationship between mild hippocampal or temporal atrophy and memory test performance. Nor did the longitudinal decline in memory show a relationship with temporal lobe atrophy. CONCLUSIONS: The main outcome of our study was that age-related memory decline was not related to mild temporal lobe atrophy in healthy subjects without mild cognitive impairment. There could be other factors influencing memory functions besides age-related structural changes in temporal lobes.

Aged↗

PubMed2003

Characterization of vigabatrin-associated optic atrophy.

AIMS: To report the discovery of a previously unknown form of optic atrophy associated with use of the anti-epileptic drug vigabatrin. METHODS: We conducted a retrospective analysis of digitally enhanced ocular fundus photographs, kinetic visual field maps and treatment parameters for 25 patients, who were selected to represent a large spectrum of visual field defects. RESULTS: In all, 21 patients (84%) evidenced subtle, diffuse atrophy of the retinal nerve fibre layer, in a pattern accessible to scoring. Atrophy scores correlated with visual field remains and cumulative vigabatrin doses. A pathophysiological model is proposed that involves the lengths of intraocular (unmyelinated) retinal ganglion cell axons. CONCLUSION: Optic atrophy attests to the irreversible nature of vigabatrin's visual toxicity. Ocular fundus imaging should prove useful for objectively monitoring vigabatrin-treated subjects for visual toxicity.

Anticonvulsants↗

PubMed1988

Regional correction of positron emission tomography data for the effects of cerebral atrophy.

Given the low spatial resolution of positron emission tomography (PET), regional measurements of neural tissue are often inaccurate because of the presence of non-neural elements and to mixtures of different tissue types within the volume of space influencing the measurements. These effects are significant in scans of brains both with and without atrophy, but are particularly significant when comparing measurements of brains with atrophy with those of normals, as is typically done in studies of aging and dementia. Previous attempts to correct for cerebral atrophy have been limited to global measurements. Using computer simulations, we illustrate the effects of atrophy and describe a method for correcting regional PET data to represent units of actual neural tissue volume.

Atrophy↗

PubMed2001

Mutations in the gene encoding immunoglobulin mu-binding protein 2 cause spinal muscular atrophy with respiratory distress type 1.

Classic spinal muscular atrophy (SMA) is caused by mutations in the telomeric copy of SMN1. Its product is involved in various cellular processes, including cytoplasmic assembly of spliceosomal small nuclear ribonucleoproteins, pre-mRNA processing and activation of transcription. Spinal muscular atrophy with respiratory distress (SMARD) is clinically and genetically distinct from SMA. Here we demonstrate that SMARD type 1 (SMARD1) results from mutations in the gene encoding immunoglobulin micro-binding protein 2 (IGHMBP2; on chromosome 11q13.2-q13.4). In six SMARD1 families, we detected three recessive missense mutations (exons 5, 11 and 12), two nonsense mutations (exons 2 and 5), one frameshift deletion (exon 5) and one splice donor-site mutation (intron 13). Mutations in mouse Ighmbp2 (ref. 14) have been shown to be responsible for spinal muscular atrophy in the neuromuscular degeneration (nmd) mouse, whose phenotype resembles the SMARD1 phenotype. Like the SMN1 product, IGHMBP2 colocalizes with the RNA-processing machinery in both the cytoplasm and the nucleus. Our results show that IGHMBP2 is the second gene found to be defective in spinal muscular atrophy, and indicate that IGHMBP2 and SMN share common functions important for motor neuron maintenance and integrity in mammals.

Amino Acid Sequence↗

PubMed2002

Inflammatory pigmented paravenous retinochoroidal atrophy.

PURPOSE: To describe an active inflammatory cause of pigmented paravenous retinochoroidal atrophy. METHODS: A 54-year-old female patient presented with complaints of worsening visual acuity and poor night vision was examined. Fundus examination was performed and color fundus photographs were taken. In addition to fluorescein angiography, visual field examinations and electroretinographic tests were performed. Macular evaluation was performed with optical coherence tomography. RESULTS: Both fundi showed circumscribed patches of retinochoroidal atrophy and pigmentation along the retinal veins. She had also marked vitreous cells with snow ball opacities and cystoid macular edema in both eyes. Fluorescein angiography confirmed the presence of a hyperfluorescence due to widespread paravenous retinal pigment epithelial defect while ICG angiography disclosed hypofluorescence in all phases. The electroretinogram showed reduced responses especially in the left eye. Visual field tests showed scotomas corresponding with areas of atrophy along the retinal veins. CONCLUSIONS: This is a report of the findings in pigmented paravenous retinochoroidal atrophy that is a nonspecific degenerative disease and may occur in association with systemic infections or inflammation. Ocular inflammation with cystoid macular edema is an unusual manifestation of the disease.

Atrophy↗

PubMed2006

Peripapillary atrophy in elderly Chinese in rural and urban Beijing.

PURPOSE: To determine peripapillary atrophy in elderly Chinese in an urban and rural regions of Beijing. METHODS: The Beijing Eye Study a population-based, cross-sectional cohort study, included 4,439 subjects out of 5,324 subjects who were asked to participate (response rate 83.4%). Mean age was 56.2+/-10.6 years (range, 40-101 years). Colour optic disc photographs (30 degrees ) were morphometrically examined. Peripapillary atrophy was divided into alpha zone and beta zone. RESULTS: Optic disc photographs were available for 4,027 (90.7%) subjects. Alpha zone and beta zone, respectively, were present in 2,867 (71.2%) subjects and 802 (19.9%) subjects, respectively, measuring 0.52+/-0.64 mm(2) and measuring 0.46+/-1.82 mm(2). Both zones were significantly widest and found significantly (P<0.001) most often in the temporal peripapillary region, followed by the temporal inferior region, the temporal superior region, and finally the nasal region. Size of both zones was significantly correlated with optic disc size (P<0.001), age (P<0.001), and myopic refractive error (P<0.001). Both zones increased significantly with decreasing uncorrected visual acuity (P<0.001) and decreasing best-corrected visual acuity (P<0.001). They did not vary significantly (P=0.10; and P=0.78) between male and female subjects. In multivariate analysis, the relationships between both zones and age, myopic refractive error, disc size, and uncorrected and best-corrected visual acuity remained statistically significant (P<0.001). CONCLUSIONS: Alpha zone and beta zone of peripapillary atrophy, respectively, occur in about 70 and 20%, respectively, of elderly Chinese. As peripapillary atrophy changes in glaucomatous optic neuropathy, these normative data may be helpful for glaucoma detection.

Adult↗