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Morphometric approaches to perifascicular atrophy in muscle biopsy: do they help to diagnose polymyositis?

The sizes of muscle fibres in the peripheral and central parts of fascicles were compared in biopsies from patients with polymyositis/dermatomyositis, patients with slowly progressing muscular dystrophies and normal controls. Of three quantitative parameters tested, perifascicular atrophy factor gave the best discrimination between the patient groups. This factor is obtained by subtracting the atrophy factor of the peripheral fibres from that of the central ones. In polymyositis, the values tend to be negative as a result of atrophy affecting selectively the peripheral fibres, whereas in dystrophies the values are usually close to zero or positive. For the comparison between polymyositis and muscular dystrophy, the test based on perifascicular atrophy factor has an estimated sensitivity of 83% and a specificity of 65%. This quantitative method is thus able to increase sensitivity of the diagnosis of polymyositis over that attained by the subjective evaluation, even at the cost of a sizeable false-positive rate.

Adolescent↗

PubMed1989

Spinal muscular atrophy in Brown Swiss calves.

Nineteen Brown Swiss calves affected with spinal muscular atrophy were described. Weakness of the rear legs was the first sign observed at 3 to 4 weeks of age. Terminal stages were characterized by severe muscular atrophy, quadriparesis, and sternal recumbency. Bronchopneumonia was a frequent complicating disease. Microscopic changes consisted mainly of degeneration and loss of motor neurons in the ventral horns of the spinal cord. Neurogenic atrophy of muscles was a constant finding. Electron microscopy revealed accumulation of neurofilaments and mitochondria in affected neurons. The disease shares many features with Werdnig-Hoffmann disease in man and the spinal muscular atrophies of other animals.

Animals↗

PubMed1991

Hyperplasia of somatostatin and pancreatic polypeptide immunoreactive cells in dogs with idiopathic atrophy of the exocrine pancreas.

The pancreatic tissue from 25 dogs with idiopathic atrophy of the exocrine pancreas, and from 6 control dogs, was studied histologically and immunohistometrically. Cells producing insulin (B), glucagon (A), somatostatin (D), and pancreatic polypeptide (PP) were identified using specific antisera and the ABC technique. Histometrical quantitation revealed differences in the distribution of these cell types between the right and left pancreatic lobe. Initial stages of atrophy showed little changes concerning the relative proportions of the four cell types examined. In more advanced stages of atrophy, however, there was significant increase in the percentage of the D cells in the cell population of the left lobe. B and A cells showed no significant changes. In final stages, only tiny tissue spots were considered a secondary and regenerative phenomenon, but an endocrine dysregulation cannot be excluded. Atrophy accompanied by diabetes mellitus and a lack of B cells seem to be due to a deficiency of insulin.

Animals↗

PubMed1994

3-Methylglutaconic aciduria in the Iraqi-Jewish 'optic atrophy plus' (Costeff) syndrome.

Eleven new patients of Iraqi-Jewish origin with bilateral optic atrophy, neurological abnormalities ('optic atrophy plus' syndrome) and 3-methylglutaconic aciduria (type III) are described. Clinical abnormalities in decreasing order of frequency were bilateral optic atrophy, extrapyramidal signs, spasticity, ataxia, dysarthria and cognitive deficit. An association with age was found only for spasticity. Spasticity, extrapyramidal signs and optic atrophy frequently led to major disability, in contrast to ataxia, dysarthria and cognitive deficit. The combined excretion of 3-methylglutaconic and 3-methylglutaric acid ranged between 9 and 187 mmol/mol creatinine. The primary enzymatic defect possibly may reside in the mitochondrial respiratory chain.

Adolescent↗

PubMed1994

Inhibition of glucocorticoid-induced epidermal and dermal atrophy with KH 1060--a potent 20-epi analogue of 1,25-dihydroxyvitamin D3.

1. The possibility of preventing and treating glucocorticoid-induced skin atrophy with KH 1060 (the potent 20-epi-22-oxa-24a-homo-26,27-dimethyl analogue of 1,25-dihydroxyvitamin D3) was examined in a hairless mouse model. 2. KH 1060 (0.625-6.25 pmol cm-2 of skin) applied topically for 7 days together with 2.5 nmol cm-2 betamethasone-17-valerate prevented, in a concentration-dependent manner, the development of epidermal, dermal and total skin thinning caused by the glucocorticoid. The effect of KH 1060 on the epidermis occurred at a lower dose than on the dermis, and at doses above 1.25 pmol cm-2 KH 1060 caused epidermal hyperplasia. 3. KH 1060 (2.5 pmol cm-2) prevented the development of betamethasone-associated skin atrophy in mice during a long-term (4 weeks) treatment, and reversed established cutaneous glucocorticoid atrophy. 4. Radiolabelling experiments with [35S]-sulphate and [3H]-proline in vivo revealed that KH 1060 stimulated the synthesis of sulphated glycosaminoglycans and hydroxyproline in skin treated with betamethasone. 5. These findings strongly suggest that KH 1060 prevents and reverses glucocorticoid-induced skin atrophy by stimulating epidermal proliferation and enhancing synthesis of extracellular matrix in the dermis.

Animals↗

PubMed1977

Cerebellar atrophy in phenytoin-treated mentally retarded epileptics.

The relationship among the serum concentration of phenytoin, pneumoencephalographic measurements describing, in particular, cerebellar atrophy, and various other clinical variables was analyzed statistically in a series of 131 phenytoin-treated mentally retarded epileptics. Phenytoin intoxication was diagnosed retrospectively in 73 patients (56%), of whom 18 had persistent loss of locomotion. The mean duration of phenytoin intoxication until locomotion was lost was 22.8 +/- 23.6 months. There was a temporal relationship between the high serum level of phenytoin and the loss of locomotion. The degree of brain atrophy in the posterior fossa was most severe in these 18 patients with severe phenytoin intoxication. The frequency of cerebellar and/or brain stem atrophy in the present series was 28%, the same as in mentally retarded epileptics without phenytoin treatment from the same institution. That phenytoin levels in serum correlated significantly with the heights of the fourth ventricle suggests that an overdosage of phenytoin or an underlying disease, or both, were the probable causes of cerebellar impairment and atrophy. Thus brain-damaged mentally retarded epileptics appear to be unusually susceptible to the side effects of phenytoin. This antiepiliptic drug is therefore not recommended for patients with no locomotor ability or with marked cerebellar signs and symptoms. To prevent phenytoin intoxication in susceptible patients, careful observation of the patients and routine monitoring of phenytoin levels in blood are stressed.

Adolescent↗

PubMed1997

Volumetric magnetic resonance imaging evidence of bilateral hippocampal atrophy in mesial temporal lobe epilepsy.

PURPOSE: We measured absolute volumes and volume differences of hippocampi in patients with mesial temporal lobe epilepsy (MTLE) using volumetric magnetic resonance imaging (MRI) to determine the extent of bilateral atrophy in MTLE and to relate hippocampal volumes (HV) to outcome of temporal lobectomy. METHODS: HV and hippocampal differences (HD) were measured in 40 patients with MTLE determined by pathology of hippocampal sclerosis (HS) and compared with those of age-matched controls. Results were matched with surgical outcome. RESULTS: Hippocampi contralateral to lobectomy (right hippocampi 2.96 +/- 0.49 cm3, left 3.14 +/- 0.51 cm3) were significantly smaller than those of controls (right hippocampi 3.73 +/- 0.52 cm3, left 3.60 +/- 0.51 cm3) but were significantly larger than hippocampi ipsilateral to lobectomy (right hippocampi 2.63 +/- 0.61 cm3, 2.18 cm3) as compared across groups by analysis of variance (ANOVA: F = 27.2, p < 0.0001). The smaller hippocampus was ipsilateral to lobectomy in 39 of 40 cases. Seven of 40 MTLE patients (18%) had bilateral atrophy, defined by volumes of each hippocampi 2 SD lower than control means. Surgical outcome was independent of hippocampal asymmetry and bilateral atrophy measured by chi-square and Fisher's exact tests. CONCLUSIONS: We determined that most patients with MTLE have some degree of bilateral, asymmetric hippocampal pathology. However, asymmetry and bilateral atrophy have no clear relation to surgical outcome.

Adult↗

PubMed1997

Development of hippocampal atrophy: a serial magnetic resonance imaging study in a patient who developed epilepsy after generalized status epilepticus.

PURPOSE: To investigate changes in hippocampal volume. METHODS: We used serial magnetic resonance imaging (MRI) in a patient who developed chronic epilepsy after having generalized tonic-clonic status epilepticus (SE). Five MRI investigations were performed during SE and a 58-month follow-up period. Hippocampal volumetric measurements and coregistration of scans were performed to detect hippocampal atrophy. RESULTS: During status both mesiotemporal regions returned a high signal on T2-weighted images. Two months after the onset of SE, bilateral hippocampal atrophy was detected. Further progressive hippocampal atrophy was detected in the subsequent 58 months by both hippocampal volumetric measurements and coregistration of scans. CONCLUSIONS: Our findings suggest that hippocampal atrophy is a process that may continue after the end of the SE.

Adult↗

PubMed1995

Brain atrophy and cognitive function in older abstinent alcoholic men.

We used computer-aided magnetic resonance image analysis and an age-normed battery of neuropsychological tests to measure brain atrophy and cognitive function in 14 older abstinent alcoholic men and 11 older controls in the expectation that these subject groups would show the greatest and most persistent cerebral effects consequent to chronic alcoholism. The abstinent alcoholics exhibited cognitive impairments (primarily in memory and visual-spatial-motor skills) compared with the controls. In contrast, we found no difference in global cerebral atrophy between the groups, although two alcoholics had extensive atrophy compared with all other subjects. However, there was a stronger association between age and ventricular dilation in the alcoholic sample compared with controls. We conclude that a substrate other than magnetic resonance imaging-detectable global atrophy must underlie the persistent cognitive impairments evident in the sampled alcoholics. Furthermore, if there are global atrophic changes in the brain associated with chronic alcoholism, these effects are not ubiquitous and/or may be reversible in most patients with sufficient abstinence.

Aged↗

PubMed1982

Sex difference in brain atrophy during aging; a quantitative study with computed tomography.

Brain atrophy in 154 men and 147 women without neurologic deficits was quantitatively studied by means of computed tomography. The ages ranged from 20 to 79 years. The volume percentage of brain to cranial cavity (Craniocerebral Index, or CCI) was calculated by means of computer programs available in CT systems. The mean CCI in the 20-39 age group was constant at 98.4 per cent in men and 98.7 in women, and this was considered the standard for the CCI in subjects with nonatrophied brains. The percentage of each subject's CCI in relation to this standard in both sexes (Brain Volume Index, or BVI) was calculated as the indicator of brain atrophy. The normal value for BVI was therefore 100 per cent in both sexes. A clear difference was observed between men and women in the process of brain atrophy with increasing age. In men a significant reduction in BVI began in the sixth decade of life (P less than 0.01); thereafter, the decline was gradual and steady through the eighth decade (P less than 0.05). In women, a significant reduction in BVI began in the fifth decade (P less than 0.01) and remained relatively constant during the fifth and sixth decades but declined significantly again in the seventh and eighth decades. In both sexes, remarkable individual differences in brain atrophy were characteristic.

Adult↗

PubMed1984

Brain atrophy during aging: a quantitative study using computed tomography.

Using computed tomography, the authors studied brain atrophy during aging in 483 males and 497 females with no neurologic disturbances, ranging in age from 10 to 88 years. They measured cerebrospinal fluid (CSF) space volume and cranial cavity volume above the level of the tentorium cerebelli and calculated a brain atrophy index (BAI):BAI (%) = 100% X (CSF space volume/cranial cavity volume). Both CSF space volume and the BAI started to increase significantly after the thirties in both men and women (P less than 0.001). While the rate with which the brain atrophied accelerated constantly during aging in females, the rate of atrophy in men in their thirties and forties was more than twice that of women of the same age; the rate then declined in men in their forties and fifties. Both CSF space volume and the BAI increased exponentially with increasing age after the thirties, continuing to increase until the eighties in both men and women.

Adolescent↗

PubMed1996

Atrophy of the corpus callosum in Alzheimer's disease versus healthy aging.

OBJECTIVE: To investigate the specificity of atrophic changes in the corpus callosum (CC) compared with the cerebellum and pons in patients with Alzheimer Disease (AD), healthy elderly subjects (HE), and a sample of prospectively studied subjects who have developed cognitive decline or "incipient dementia" (ID). DESIGN: Cross-sectional comparison by age using quantitative MRI. SETTING: Ambulatory research unit. PARTICIPANTS: Sixty HE subjects (mean age 78.2 years; range 66-95), 20 ID subjects (mean age 88.1 years; range 78-98) and 39 AD subjects (mean age 72.2 years; range 52-91) were enrolled in longitudinal studies of healthy aging or AD. The population was selected for optimal health; all were examined to exclude medical, neurological and psychiatric illness. MEASUREMENTS: Brain atrophy by quantitative MRI. RESULTS: AD subjects had smaller CC than HE or ID subjects, who did not differ from each other. All three sectors of the CC were smaller in AD than in HE or ID subjects. The cross sectional area of the cerebellum and pons did not differ between groups. HE and ID subjects showed a significant decline in CC size with age. No age-related decline was found for AD subjects. The regional atrophy of the CC in AD subjects was significantly related to cognitive function but not to disease duration. CONCLUSIONS: Atrophy of the CC differentiates HE and ID from AD subjects and tracks the cognitive decline of this disease. In addition, optimally healthy subjects show an age-related decline in callosum size. The atrophy is specific to the CC, a cortical projection system, and does not occur in cerebellum or pons.

Aged↗

PubMed2001

Quantitative assessment of gastric corpus atrophy in subjects using omeprazole: a randomized follow-up study.

OBJECTIVES: Atrophy of the gastric mucosa most frequently results from chronic Helicobacter pylori infection and is a risk factor for the development of gastric cancer. Profound acid suppression has been suggested to accelerate the onset of gastric mucosal atrophy. The aim of the present study was to evaluate the effects of H. pylori eradication and acid inhibition by omeprazole on gastric atrophy by means of quantitative analysis of tissue morphology. METHODS: Corpus biopsy specimens were obtained during endoscopy in 71 gastroesophageal reflux disease (GERD) patients at baseline and after 3 and 12 months. A total of 48 subjects were H. pylori positive and 23 were H. pylori negative. All subjects received omeprazole 40 mg once daily after the first endoscopy for 12 months. After randomization, 27 of the 48 H. pylori-positive patients also received eradication therapy. In hematoxylin and eosin-stained slides the volume percentages of glands (VPGL), volume percentages of stroma (VPS), and volume percentages of infiltrate (VPI) were measured in the glandular zone of the mucosa. The results were evaluated by computerized morphometric analysis. RESULTS: In the eradication group, the mean VPGL increased from 63.0% to 67.7% and 71.5% after 3 and 12 months (p < 0.001), respectively. The mean VPS and VPI decreased from 33.1% and 4.0% to 29.3% and 3.0% and to 26.4% and 2.1% (p < 0.001 and p = 0.04), respectively. Patients with the lowest VPGL at baseline showed the largest increases of VPGL after eradication treatment as compared to patients with high a VPGL at baseline. In the H. pylori-persistent group the VPI showed a significant increase (p = 0.01), and in the H. pylori-negative group VPGL increased significantly from 71.9% to 75.2% (p = 0.03) after 12 months. CONCLUSIONS: Eradication of H. pylori leads to restitution of the volume percentage of glandular epithelium to normal levels, even during treatment with proton pump inhibitors. Whether this effect can also be seen in patients with marked atrophy needs further investigation.

Adult↗

PubMed2001

Morphometric evaluation of gastric antral atrophy: improvement after cure of Helicobacter pylori infection.

OBJECTIVE: Our purpose was to find out if morphometric techniques can document long term changes in gastric antral atrophy after curing Helicobacter pylori infection with or without dietary supplementation with antioxidant micronutrients. METHODS: Study subjects were 132 adult volunteers from a Colombian region with high gastric cancer rates. Participants were randomly assigned to ascorbic acid, beta-carotene, and anti-H. pylori treatment, following a factorial design. Gastric biopsies were obtained at baseline and after 72 months of intervention. Atrophy was evaluated by a standard visual analog scale and by morphometry. RESULTS: Statistically significant changes in antral atrophy were detected with morphometric techniques after intervention in subjects who received anti-H. pylori treatment. A nonsignificant trend was also observed with visual scores. This effect was greater among those who were free of infection at the end of the trial. After accounting for the effect of anti-H. pylori treatment, no significant effect was noted for dietary supplementation with ascorbic acid and/or beta-carotene. CONCLUSIONS: We conclude that gastric atrophy improves significantly after long term control of H. pylori infection. This effect can be demonstrated both by conventional histological grading and by morphometry.

Adult↗

PubMed1975

Pneumoencephalographic and clinical characteristics of diffuse cerebral atrophy.

The clinical features in 268 patients with diffuse cerebral atrophy of initially unknown origin have been analysed. Pneumoencephalography showed supratentorial ventricular atrophy in 87 per cent (cortical in 71 per cent), and brain stem and/or cerebellar atrophy in 17 per cent of the patients. Epileptic seizures, dizziness and clumsiness were the most frequent initial symptoms. Vibration in work, psychic impairment, gait difficulties, co-ordinative dysfunction, excessive use of alcohol, and arterial hypertension dominated the clinical picture. Serum cholesterol and triglycerides, and beta-globulins in the cerebrospinal fluid protein electrophoresis were normal. Diffuse cerebral atrophy without defined cause appears to affect all parts of the brain, with particular predilection for the frontotemporal area and the left side, and to have diffuse and unspecific clinical characteristics.

Adolescent↗

PubMed1993

Effect of advanced brain atrophy and vitamin deficiency on cognitive functions in non-demented subjects.

The relationship between the cognitive functions, structural changes of the brain and vitamin levels was evaluated in 36 non-demented subjects with advanced brain atrophy, and 57 age- and sex-matched healthy controls. In the control subjects ageing was associated with mild decline of cognitive skills, but the cognitive changes were not linked to the structural changes of the brain. In contrast, advanced brain atrophy and vitamin deficiency was related to the decline of complex cognitive functions in the atrophy group. Our results indicate that there are limits of normal age-related changes of the brain structure, and advanced brain atrophy on CT scans increase the probability of mild deficits of the cognitive skills.

Aged↗

PubMed1994

A study of parkinsonism in multiple system atrophy: clinical and MRI correlation.

We investigated clinical and MRI correlation in 18 patients with clinically-diagnosed multiple system atrophy (MSA) and 16 age-matched controls, using 1.5 T magnetic resonance imaging (MRI). We evaluated the severity of parkinsonism in each MSA patient. In assessing the MRI findings, we examined three parameters quantitatively: width of the pars compacta of the substantia nigra (SNc); putaminal hypointensity on T2-weighted images; and putaminal atrophy. As in previous studies, SNc width was narrowed and the putaminal signal intensity was decreased in patients with MSA compared with controls. The clinical severity of parkinsonism did not correlate significantly with the SNc width or the score of putaminal hypointensity in MSA. However, not only did putaminal atrophy occur, but correlated well with the severity of parkinsonism in MSA. A significant correlation could not be established between narrowing of SNc and shrinkage of the putamen. These findings suggest that putaminal atrophy is associated with the clinical manifestations of parkinsonism and do not support the hypothesis that transsynaptic degeneration occurs in MSA.

Adult↗

PubMed2006

Atrophy and hypertrophy of skeletal muscles: structural and functional aspects.

This review summarizes current information on structural and functional changes that occur during muscle atrophy and hypertrophy. Most published studies consider an increase in total mass of a muscle as hypertrophy, whereas a decrease in total mass of a muscle is referred to as atrophy. In hypertrophy, the rate of synthesis is much higher than the rate of degradation of muscle contractile proteins, leading to an increase in the size or volume of an organ due to enlargement of existing cells. When a muscle remains in disuse for a long period, the rate of degradation of contractile proteins becomes greater than the rate of replacement, resulting in muscle atrophy. This defect may occur as a result of lack of nutrition, loss of nerve supply, micro-gravity, ageing, systemic disease, prolonged immobilization or disuse. An understanding of the specific modifications that occur during muscle atrophy and hypertrophy may facilitate the development of novel techniques, as well as new therapies for affected muscles.

Animals↗