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PubMed1992

Somatofugal axonal atrophy precedes development of axonal degeneration in acrylamide neuropathy.

Somatofugal axonal atrophy is part of the neuronal perikaryal response to axonal injury (axon reaction). Chronic administration of acrylamide (AC) produces proximal atrophy in virtually all sensory fibers in lumbar dorsal root ganglion (DRG) despite the presence of many intact axons in the distal portion of the sciatic nerve. This suggests that the development of axonal atrophy in AC-intoxicated animals is not solely due to a toxic chemical-induced axonal degeneration (axotomy). In this study, we asked whether axonal atrophy arises before onset of axonal degeneration. Rats were given a single intraperitoneal (i.p.) high dose of AC (75 mg/kg), which blocks retrograde axonal transport, followed by daily intraperitoneal injections (30 mg/kg, for 4 days). At 5 days, sensory fibers in the L4 and L5 DRG appeared smaller in caliber and less circular in shape compared to fibers from age-matched normal animals. Axonal diameters of sensory fibers in the L5 dorsal root were significantly (p less than 0.05) reduced at distances up to 2 mm from the DRG. Quantitative electron microscopy demonstrated that the reduction in caliber was due to a decreased neurofilament (NF) content. Axonal degeneration was not present in the distal portion of both centrally (dorsal root) and peripherally (sciatic nerve) projecting sensory fibers at this time, although primary afferent terminals in muscles of the hindfeet were packed with NFs. The somatofugal progression of the atrophy was evident following more prolonged exposures (10-28 days). It is suggested that AC produces somatofugal axonal atrophy by inhibiting the delivery of a retrogradely transported target-derived "trophic" signal to the neuronal perikaryon.

Acrylamide↗

PubMed1997

Muscular atrophy in diabetic neuropathy: a stereological magnetic resonance imaging study.

Diabetic patients with polyneuropathy develop motor dysfunction. To establish whether motor dysfunction is associated with muscular atrophy the ankle dorsal and plantar flexors of the non-dominant leg were evaluated with magnetic resonance imaging in 8 patients with symptomatic neuropathy, in 8 non-neuropathic patients and in 16 individually matched control subjects. In the neuropathic patients the muscle strength of the ankle dorsal and plantar flexors was reduced by 41% as compared to the non-neuropathic patients (p < 0.005). Volume of the ankle dorsal and plantar flexors was estimated with stereological techniques from consecutive cross-sectional images of the lower leg. The neuropathic patients had a 32% reduction in volume as compared with the non-neuropathic patients (p < 0.005). To determine the regional distribution of atrophy cross-sectional magnetic resonance images were performed at predetermined levels of the lower leg in relation to bone landmarks. In the neuropathic patients there was an insignificant increase of 3% of muscle area at the proximal lower leg level, whereas the atrophy was 43% (p < 0.002) at the mid lower leg level and 65% (p < 0.002) distally. Analysis of individual muscles confirmed that the atrophy predominated distally. We conclude that muscular atrophy underlies motor weakness at the ankle in diabetic patients with polyneuropathy and that the atrophy is most pronounced in distal muscles of the lower leg indicating that a length dependent neuropathic process explains the motor dysfunction.

Adult↗

PubMed2005

Can three-dimensional endoanal ultrasonography detect external anal sphincter atrophy? A comparison with endoanal magnetic resonance imaging.

PURPOSE: Anal sphincter atrophy is associated with a poor clinical outcome of sphincter repair in patients with faecal incontinence. Preoperative assessment of the sphincters is therefore relevant. External anal sphincter (EAS) atrophy can be detected by endoanal magnetic resonance imaging (MRI), but not by conventional endoanal ultrasonography (EUS). Three-dimensional EUS allows multiplanar imaging of the anal sphincters and thus enables more reliable anal sphincter measurements. The aim of the present study was to establish whether 3D EUS measurements can be used to detect EAS atrophy. For this purpose 3D EUS measurements were compared with endoanal MRI measurements. METHODS: Patients with symptoms of faecal incontinence underwent 3D EUS and endoanal MRI. Internal anal sphincter (IAS) and EAS defects were assessed on 3D EUS and endoanal MRI. EAS atrophy was determined on endoanal MRI. The following measurements were performed: EAS length, thickness and area. Furthermore, EAS volume was determined on 3D EUS and compared with EAS thickness and area measured on endoanal MRI. RESULTS: Eighteen parous women (median age 56 years, range 32-80) with symptoms of faecal incontinence were included. Agreement between 3D EUS and endoanal MRI was 61% for IAS defects and 88% for EAS defects. EAS atrophy was seen in all patients on endoanal MRI. Correlation between the two methods for EAS thickness, length and area was poor. In addition, correlation was also poor for EAS volume determined on 3D EUS, and EAS thickness and area measured on endoanal MRI. CONCLUSION: Three-dimensional EUS and endoanal MRI are comparable for detecting EAS defects. However, correlation between the two methods for EAS thickness, length and area is poor. This is also the case for EAS volume determined on 3D EUS and EAS thickness and area measured on endoanal MRI. Three-dimensional EUS can be used for detecting EAS defects, but no 3D EUS measurements are suitable parameters for assessing EAS atrophy.

Adult↗

PubMed1999

Medial temporal lobe atrophy and memory dysfunction as predictors for dementia in subjects with mild cognitive impairment.

To determine whether the medial temporal lobe is atrophic in subjects with mild cognitive impairment, and whether atrophy of this structure is a better predictor of dementia than memory dysfunction. Forty-five noninstitutionalized subjects aged 65-85 years were randomly selected from a population based study to obtain a sample with Alzheimer's disease (AD; n = 7), and a clinically nondemented sample (n = 38). Twenty of the latter subjects displayed some cognitive impairment and fulfilled CAMDEX criteria for "minimal dementia." Coronal T1-weighted magnetic resonance imaging was used to visualize the medial temporal lobe. The volume of the parahippocampal gyrus and hippocampus was measured, and medial temporal lobe atrophy was assessed qualitatively. The memory subscore from the CAMCOG was used as a measure of memory functioning. The follow-up period was 3 years. Nine subjects who were diagnosed as being minimally demented at baseline met the criteria for AD during follow-up. At baseline the volume of the parahippocampal gyrus of these subjects was smaller than that of the other subjects with minimal dementia. The memory score was the best predictor of clinical outcome. All medial temporal lobe measures increased the accuracy of prediction compared with only the memory score, by reducing the number of false-negative classifications of dementia. Severe medial temporal lobe atrophy is present even in some subjects with mild cognitive impairment and is an indicator of subsequent AD. The absence of medial temporal lobe atrophy, however, does not exclude the development of dementia. In the majority of subjects memory impairment was a better predictor of dementia than atrophy of the medial temporal lobe. The combination of the two increased predictive accuracy. Nondemented subjects with severe atrophy of the medial temporal lobe could be enrolled in drug trials aimed at slowing the progression of AD.

Aged↗

PubMed2003

Concentric retinal pigment epithelium atrophy after a single photodynamic therapy.

PURPOSE: To report a case with concentric retinal pigment epithelium (RPE) atrophy after a single photodynamic therapy (PDT). METHODS: We report a case of a 33-year-old female patient who developed RPE atrophy after a single standard PDT for treatment of a juxtafoveal, predominantly classic choroidal neovascularization (CNV). RESULTS: After a single PDT treatment, visual acuity increased from 20/50 to 20/20. Six weeks after PDT, a concentric area of RPE atrophy was clearly visible on fluorescein angiogram. This circular area corresponded to the 3500 microm diameter of the laser spot used in the PDT treatment. The visual acuity and the RPE atrophy remained stable over the follow-up period of 3 years. CONCLUSIONS: We are unable to explain the exact mechanism of the observed RPE changes; however, they did not lead to loss of visual acuity. Different reasons for the RPE atrophy such as collateral damage of the choriocapillaris with a subsequent secondary RPE atrophy, a direct photochemical effect due to the early localization of the photosensitizer in the RPE, or a depigmentation or photobleaching of the RPE, which led to a window defect in the fluorescein angiogram without loss of the major functional properties of the RPE, are possible mechanisms involved in the development of the documented lesion.

Adult↗

PubMed1997

Attenuation of myosin light chain phosphorylation and posttetanic potentiation in atrophied skeletal muscle.

Previously we have demonstrated that the absence of staircase potentiation in atrophied rat gastrocnemius muscle is accompanied by a virtual absence of phosphorylation of the regulatory light chains (R-LC) of myosin. It was our purpose in the present study to determine if posttetanic potentiation and corresponding R-LC phosphorylation were also attenuated in disuse-atrophied muscles. Two weeks after a spinal hemisection (T12), twitch and tetanic contractile characteristics were measured in situ in control, sham-treated and atrophied (hemisected) muscles. Posttetanic potentiation 20 s after a 2 s tetanic contraction (200 Hz) was depressed in atrophied muscles (128.7 +/- 2.6%; mean +/- SEM) when compared to sham-treated (149.9 +/- 2.4%) and control (142.9 +/- 2. 7%) muscles. Atrophied muscles demonstrated a significant increase in R-LC phosphorylation from rest (0.05 +/- 0.04 moles of phosphate/mole of R-LC) to posttetanic conditions (0.21 +/- 0.03 moles of phosphate/mole of R-LC), and less phosphorylation than control and sham-treated muscles (0.43 +/- 0.06 and 0.49 +/- 0.03 moles of phosphate/mole of R-LC, respectively) after tetanic stimulation. The preservation of the potentiation-phosphorylation relationship in atrophied muscles is consistent with the hypothesis that R-LC phosphorylation may be the principal mechanism for twitch potentiation.

Animals↗

PubMed2005

Biological behavior of myoepithelial cells in the regeneration of rat atrophied sublingual glands following release from duct ligation.

The present study aimed to clarify how myoepithelial cells behave during regeneration of an atrophied sublingual gland by investigating cell proliferation and ultrastructure. Atrophy of rat sublingual glands was induced by unilateral ligation of the excretory duct near the hilum with metal clips, which were then removed after one week of ligation for regeneration. The sublingual glands 0-14 days after unligation were examined with single immunohistochemistry for actin as a marker of myoepithelial cells, double immunohistochemistry for actin and proliferating cell nuclear antigen (PCNA) as a marker of proliferating cells, and transmission electron microscopy (TEM). The single immunohistochemistry and TEM showed that myoepithelial cells surrounded residual ducts in the atrophied glands and immature and mature acini in the regenerating glands. Although PCNA-positive myoepithelial cells were identified during regeneration, PCNA labeling indices of myoepithelial cells were low at all time points except at day 7. Ultrastructurally, myoepithelial cells showing bizarre shaped structures in the atrophy changed with maturation of differentiating acinar cells and appeared normal in the regenerated glands. There was no differentiation of the remaining duct cells to myoepithelial cells. These observations suggest that proliferation of myoepithelial cells and differentiation to myoepithelial cells do not commonly participate in the regeneration of atrophied sublingual glands and that the bizarre shaped myoepithelial cells in the atrophied sublingual glands recover the original shapes with acinar cell regeneration.

Actins↗

PubMed1993

Cell kinetics of mucosal atrophy in rat stomach induced by long-term administration of ammonia.

BACKGROUND: Helicobacter pylori produces ammonia in the stomach from urea. The present study was undertaken to clarify whether ammonia has an etiological role in H. pylori-associated gastric mucosal atrophy. METHODS: Ammonia at 0.01% was administered as drinking water for 8 weeks and mucosal cell migration rate and cell proliferation were investigated in rat stomach. RESULTS: Long-term administration of 0.01% ammonia for 4-8 weeks decreased mucosal thickness in the antrum but not in the body. Acceleration of cell migration preceded the occurrence of mucosal atrophy. Labeling indices in both antral and body mucosa significantly increased in all ammonia-treated groups, compared with those of the control group. In the antrum, the proliferative zone was significantly enlarged as mucosal atrophy developed, whereas, in body mucosa, enlargement of the proliferative zone occurred despite the absence of mucosal atrophy. CONCLUSION: Ammonia at 0.01% accelerates epithelial migration, especially in the antrum, leading to mucosal atrophy. Acceleration of epithelial proliferation occurs during the development of mucosal atrophy.

Ammonia↗

PubMed1979

The significance of cerebral atrophy for the symptomatology of Parkinson's disease.

Hitherto published results on the impact of brain atrophy on the neurological and psychopathological sympion of this problem without risk of complications. We investigated 173 parkinsonian patients (89 men, 84 women) aged 37--83 years. Besides CT in all patients a standardized neurological and psychopathological investigation was carried out, including psychological tests, intelligence, personality structure, fine motor performance and visual reaction times. The investigations revealed pronounced correlations between CT-findings and more severe clinical symptomatology and a corresponding impairment in daily activities in the levodopa-treated and particularly in the untreated group, above all when there was a combination of cortical atrophy and ventricular enlargement. The same was true for fine motor performance and simple and complex reaction times. These functions were more impaired in patients with brain atrophy, irrespective of its localisation, whether cortical atrophy or ventricular enlargement. In contrast, no statistically significant relationship between the different parameters of brain atrophy and intelligence could be found. Considering cortical atrophy as a specific sign in Parkinson's disease -- our results are in favour of this assumption -- and ventricular enlargement more related to increasing age, parkinsonism is influenced by extranigral lesions inherent in the disease and dependent on increasing age.

Adult↗

PubMed1987

Brainstem auditory evoked responses and CT findings in multiple system atrophy.

Brainstem auditory evoked responses (BAERs) and CT findings were comparatively studied in 11 patients with Shy-Drager syndrome and 10 patients with olivopontocerebellar atrophy. The I-III interpeak latencies (IPLs) were prolonged in 6 patients with Shy-Drager syndrome and in 6 patients with olivopontocerebellar atrophy. Mean values of the I-III IPLs were 2.54 +/- 0.28 ms (Shy-Drager syndrome) and 2.62 +/- 0.15 ms (olivopontocerebellar atrophy). In each disease, the I-III IPLs correlated well with the degree of the pontine atrophy estimated from the CT scan. The patients with Shy-Drager syndrome could be clinically divided into two varieties. In addition to autonomic dysfunction, one variety (4 patients) was linked with parkinsonism, and the other (7 patients) with signs of multiple nervous systems involvement. Prolongation of I-III IPLs and pontine atrophy were noted in 6 out of the latters patients, whereas the former patients did not show such abnormalities. The combination of BAERs and CT scan provides useful clinical information on multiple system atrophy.

Adult↗

PubMed1992

Relationship between corpus callosum atrophy and cerebral metabolic asymmetries in multiple sclerosis.

Corpus callosum (CC) atrophy by magnetic resonance imaging (MRI) is a common finding in multiple sclerosis (MS). In order to examine the relationship between CC atrophy and cortical brain metabolism, we compared the cerebral metabolic rates for glucose (CMRglc), measured by positron emission tomography (PET), of 8 MS patients with evidence of CC atrophy on midsagittal MRI, 8 MS patients without CC atrophy and 10 healthy controls. Results showed no significant differences in supratentorial CMRglc absolute values between the three groups, although a slight metabolic reduction was observed in both MS groups compared with normal controls. By contrast, only patients with CC atrophy showed greater directional metabolic asymmetry than normals, the left frontal, temporal and parietal association cortices being significantly lower than the right. Predominant left hemispheric metabolic reductions were not accompanied by a corresponding left-sided predominance in the extent of MRI-detected demyelinating lesions. Therefore our data suggest that CC atrophy interfers more with left than with right metabolic function.

Adult↗

PubMed1995

Corpus callosum atrophy in amyotrophic lateral sclerosis.

Recent studies have suggested widespread involvement of the cerebral regions other than the primary motor cortex in amyotrophic lateral sclerosis. To investigate atrophy of the corpus callosum as a measure of cerebral pathology, we studied 25 right-handed patients with sporadic amyotrophic lateral sclerosis using magnetic resonance imaging. Five patients had cognitive decline or emotional and personality changes. The ratios of mid-sagittal corpus callosum areas to the midline internal skull surface area on T1-weighted images were analysed. Compared with 25 age- and sex-matched right-handed control subjects, the patients had significantly decreased callosal/skull area ratio, with anterior predominance of the degree of atrophy. The patients with cognitive decline or psychiatric symptoms had substantial atrophy of the anterior fourth of the corpus callosum. These findings suggest that atrophy of the corpus callosum, especially in the anterior half, is present in amyotrophic lateral sclerosis, and that severe atrophy in the anterior fourth is associated with cognitive decline and psychiatric symptoms. Callosal atrophy may reflect the widespread distribution of pathological changes in the cerebral cortex, which are accentuated in the frontal cortex.

Adult↗

PubMed1995

Stress-induced atrophy of apical dendrites of hippocampal CA3c neurons: involvement of glucocorticoid secretion and excitatory amino acid receptors.

Repeated restraint stress of rats for 21 days causes atrophy of apical dendrites of hippocampal CA3c pyramidal neurons. This effect is mimicked by daily corticosterone treatment for 21 days and is prevented y the anti-epileptic drug, phenytoin, known to interfere with excitatory amino acid release and action. The present study was designed to investigate the involvement of endogenous corticosterone secretion and excitatory amino acid receptors in the stress-induced hippocampal dendritic atrophy. Treatment of chronically stressed rats with the steroid synthesis blocker cyanoketone prevented stress-induced dendritic atrophy. Cyanoketone-treated animals showed an impaired corticosterone secretion in response to the stressor, while basal levels were maintained. Besides the involvement of endogenous corticosterone secretion, N-methyl-D-aspartate receptors also play a role, since the competitive receptor antagonist, CGP 43487, blocked stress-induced dendritic atrophy. In contrast, NBQX, a competitive inhibitor of the alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors, was ineffective at a dose that blocks ischemic damage. These results indicate that the reversible atrophy induced by 21 days of daily restraint stress requires corticosterone secretion and that excitatory mechanisms involving N-methyl-D-aspartate receptors play a major role in driving the atrophy.

2-Amino-5-phosphonovalerate↗

PubMed1982

Relation between central cerebral atrophy, memory defects and prolactin secretion.

Concentrations of prolactin in cerebrospinal fluid (CSF) and in serum were determined from 26 neurological patients with or without minor central cerebral atrophy. Neuropsychological memory tests also were performed on these patients. Twenty-eight neurological patients with peripheral nervous lesions and without endocrine dysfunctions served as controls for prolactin levels. Patients with central cerebral atrophy had significant loss of recall capacity, though they did not differ significantly from the normal population in their intellectual performances. CSF and serum prolactin levels in the patients with central cerebral atrophy and/or memory defects did not differ from the values obtained in the patients without cerebral atrophy. Thus, prolactin levels do not appear to reflect either central cerebral atrophy or memory dysfunctions, most likely due to the minor degree of neuronal atrophy around the third ventricle that occurs in patients with these findings.

Adult↗

PubMed1992

The relationship between apoptosis and atrophy in the irradiated lacrimal gland.

Atrophy is generally considered to be a true late effect of radiation. However, in serous glands, atrophy was thought to be a consequential late effect because serous cells die within hours of irradiation and the apparent effects of atrophy are observed contemporaneously with radiation treatment. Therefore, to determine the pathogenesis of atrophy in serous glands, it is necessary to differentiate between parenchymal loss as a result of direct radiation death of serous cells and parenchymal loss as a result of serous cell death that is secondary to fibrosis, vascular damage, or precursor cell death. The lacrimal glands of 62 rhesus monkeys have been irradiated to single doses of 2.5 to 20 Gy and examined at intervals of 4 hr to 112 days postirradiation. Serous cells (nuclei) and acini were counted in at least 30 high power fields per (dose, time) point. At each dose and time of sacrifice, the average number of nuclei per acinus and the average number of acini per high power field were calculated. Also at each dose and time, the distribution of the number of nuclei per acinus was examined to determine how the frequency of acinar sizes changed as a function of irradiation. The number of cells per acinus appears to rise initially, but this is likely a result of the degranulated cells being physically smaller, yielding an artificially higher count. Within 4 days after 12.5 Gy, the average number of nuclei per acinus approaches control values and remains within the range of controls for at least 112 days. The number of acini per high power field decreases steadily for 30 days after 12.5 Gy. From 30 to 112 days, there is some recovery of this number, but it remains well below control values. At 24 hr, the number of nuclei per acinus shows a distinct dose response up to 20 Gy. However, at 30 days there is no evidence of a dose response for this parameter. These results indicate that even though serous cells die in significant numbers within hours of irradiation, the atrophy of the lacrimal gland (and by extension, the parotid gland) is a result of the death of the serous stem cell or precursor. Consequently, protection of serous cells from radiation apoptosis will not diminish serous gland atrophy.

Animals↗

PubMedDate not supplied

Cerebral blood flow and brain atrophy correlated by xenon contrast CT scanning.

Correlations between cerebral blood flow (CBF) measured during stable xenon contrast CT scanning and standard CT indices of brain atrophy were investigated in the patients with senile dementia of Alzheimer type, multi-infarct dementia and idiopathic Parkinson's disease. Compared to age-matched normal volunteers, significant correlations were found in patients with idiopathic Parkinson's disease between cortical and subcortical gray matter blood flow and brain atrophy estimated by the ventricular body ratio, and mild to moderate brain atrophy were correlated with stepwise CBF reductions. However, in patients with senile dementia of Alzheimer type and multi-infarct dementia, brain atrophy was not associated with stepwise CBF reductions. Overall correlations between brain atrophy and reduced CBF were weak. Mild degrees of brain atrophy are not always associated with reduced CBF.

Aged↗

PubMed1990

The effect of focal cerebral atrophy in positron emission tomographic studies of aging and dementia.

We used x-ray computed tomographic (XCT) scans to measure the degree of cerebral atrophy in brain regions defined by a region of interest (ROI) anatomy atlas. The same atlas was employed for quantitation of local cerebral glucose metabolic rates (LCMRglc) by PET. PET data were obtained from 9 young controls, 7 healthy elderly controls, and 10 patients with dementia. Cerebrospinal fluid (CSF) in atrophic brain regions was assumed to be metabolically inert, and LCMRglc measurements were corrected for the degree of atrophy. Significantly greater atrophy was seen for 7 of 8 regions in comparisons between demented patients and age-matched controls. This atrophy was most pronounced in superior parietal (SP) regions. Decreases in parietal LCMRglc in dementia patients and SP LCMRglc in old controls were no longer significant after correction for atrophy. These results emphasize the need to consider focal atrophy effects in regional quantitative analyses of emission tomographic data.

Aged↗

PubMed2004

Dominant optic atrophy, sensorineural hearing loss, ptosis, and ophthalmoplegia: a syndrome caused by a missense mutation in OPA1.

PURPOSE: To describe the clinical features of and identify the disease-causing mutation in a large Utah family segregating a dominantly inherited syndrome of optic atrophy, sensorineural hearing loss, ptosis, and ophthalmoplegia. DESIGN: Observational case series. METHODS: Thirty individuals at risk for a syndrome of optic atrophy, sensorineural hearing loss, ptosis, and ophthalmoplegia in a single family underwent clinical examinations and venipuncture. Linkage analysis and mutation screening of the optic atrophy 1 gene (OPA1) were performed. RESULTS: Eighteen individuals demonstrated characteristics of the syndrome. Genetic analysis identified a G-->A substitution at nucleotide position 1334 in exon 14 of OPA1 causing an arginine-to-histidine change (R445H) in all affected members of the family. This change segregated with the disease phenotype in the study family with a LOD score of 7.02 at theta; = 0 and was not found in 200 normal control subjects. Analysis of an unrelated Belgian family with a similar phenotype revealed the same R445H mutation segregating with the disease phenotype. CONCLUSIONS: This study describes a mutation in OPA1 causing a unique syndrome of optic atrophy, sensorineural hearing loss, ptosis, and ophthalmoplegia. These results expand the spectrum of human disease associated with mutations of OPA1 and indicate that ophthalmologists caring for patients with optic atrophy should inquire about possible associated hearing loss. Although OPA1 is a nuclear gene, the gene product localizes to mitochondria, suggesting that mitochondrial dysfunction may be the final common pathway for many forms of syndromic and nonsyndromic optic atrophy, hearing loss, and external ophthalmoplegia.

Adolescent↗