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PubMed1988

Optic atrophy in children.

We reviewed the records of 218 children in whom a diagnosis of optic atrophy had been made between 1978 and 1987. A cause for the atrophy was determined for 195 patients (89%). Tumor, the most frequent cause, was found in 63 patients (29%). The most common tumor was a glioma of the anterior visual pathway; it was found in 27 patients (43% of tumors; 12% overall). The second most frequently encountered tumor, a craniopharyngioma, was found in 14 patients. Inflammation, the second most common cause of optic atrophy, occurred in 38 children (17%). Trauma caused optic atrophy in 24 patients (11%). No cause could be found for 23 patients (11%). Thirteen patients were less than 1 year of age at the time of diagnosis. Three of these patients had tumors. One was a cerebral glioblastoma, and the other two were optic gliomas. The diagnosis of optic atrophy in infancy does not imply a benign cause.

Adolescent↗

PubMed1978

Metabolic implications of distal atrophy. Carbohydrate metabolism in centronuclear myopathy.

Centronuclear myopathy, like myotonic dystrophy, is characterized by muscle wasting and type 1 fiber atrophy. To determine whether this disorder might include a derangement in carbohydrate metabolism similar to that in myotonic dystrophy, 3 comparably wasted patients with centronuclear myopathy, myotonic dystrophy, and neurogenic atrophy were investigated. The patient with centronuclear myopathy had mild glucose intolerance and hypoinsulinemia after oral glucose ingestion in bold contrast to the normal glucose tolerance and hyperinsulinemia observed in the myotonic dystrophy patient. No abnormality was seen in oral glucose tolerance in the patient with neurogenic atrophy, and all 3 patients had normal insulin tolerance. Forearm insulin infusion demonstrated normal stimulation of muscle glucose uptake in the patients with centronuclear myopathy and neurogenic atrophy in contrast to the markedly diminished response to insulin seen in the patient with myotonic dystrophy. These data indicate that neither distal wasting or type 1 fiber atrophy are responsible for the abnormalities in carbohydrate metabolism in myotonic dystrophy.

Adult↗

PubMed1995

Significance of type II fiber atrophy in chronic alcoholic myopathy.

To determine the significance of type II fiber atrophy in alcoholic myopathy and its relationship with ethanol-related diseases a prospective study was carried out in 100 chronic alcoholics who showed clinical suspicion of skeletal myopathy. Measurement of muscle strength, laboratory analysis, nutritional assessment and open biopsy of deltoid muscle were performed in each case, as well as electrophysiological testing for peripheral neuropathy. Hepatic ultrasonography and liver biopsy, echocardiography and radionuclide cardiac scanning were carried out in selected subjects. According to histomorphometric analysis, type II fiber atrophy was found in 33 cases (33%), being selective for type II B fiber in 23 (70%). Skeletal myopathy was diagnosed in 61 cases, alcoholic cardiomyopathy in 26, peripheral neuropathy in 23 and cirrhosis in 12. Patients with type II fiber atrophy had a significantly higher total lifetime dose of ethanol, presented a greater incidence of skeletal myopathy and peripheral neuropathy, and exhibited significantly lower values of percentage of ideal body weight and lean body mass than their counterparts. However, the only independent factors for developing type II fiber atrophy were the coexistence of caloric malnutrition (p = 0.004) and the presence of skeletal myopathy (p = 0.043). Selective type II fiber atrophy is a non-specific finding in alcohol-induced muscle damage appearing, overall, in the patients with caloric malnutrition as well as in those with histologic evidence of myopathy.

Adult↗

PubMed1985

Tumor growth in liver atrophy and growth. An experimental study in rats.

Despite vast knowledge on liver regeneration, little is known about the effect of active liver atrophy and regeneration on tumor growth. Ligation of a branch of the portal vein to the one or two anterior lobes was performed in inbred Wistar rats. This induces acute atrophy of the anterior and regeneration of the other lobes. During the same operation a tumor cell suspension (NGW1--adenocarcinoma) was inoculated in liver lobes undergoing atrophy and regeneration. Tumor volume and weight were measured and the histologic appearance was assessed. During the early and active phases the tumor growth was significantly accelerated in regenerating lobes and partially inhibited in rapidly atrophied segments. After the regeneration and atrophy was completed the normal pattern of growth was re-established in both parts of the liver. The results suggest that tumor growth is affected in proportion to regenerative response. They further suggest that portal branch ligation is of limited value in surgical palliation of liver tumors. The risk for further induction of growth of clinically undetected tumor foci in the remaining liver tissue appears to be small, although a significant, but short-lasting, stimulatory response was found.

Animals↗

PubMed1979

Elevated levels of a calcium-activated muscle protease in rapidly atrophying muscles from vitamin E-deficient rabbits.

A Ca2+-activated proteolytic enzyme that partially degrades myofibrils was isolated from hind limb muscles of normal rabbits and rabbits undergoing rapid muscle atrophy as a result of vitamin E deficiency. Extractable Ca2+-activated protease activity was 3.6 times higher in muscle tissue from vitamin E-deficient rabbits than from muscle tissue of control rabbits. Ultrastructural studies of muscle from vitamin E-deficient rabbits showed that the Z disk was the first myofibrillar structure to show degradative changes in atrophying muscle. Myofibrils prepared from muscles from vitamin E-deficient rabbits showed partial or complete loss of Z-disk density. Sodium dodecyl sulfate polyacrylamide gel electrophoresis showed that the amount of troponin-T (37 000 daltons) and alpha-actinin (96 000 daltons) was reduced in myofibrils from atrophying muscle as compared to myofibrils prepared from control muscle. In vitro treatment of purified myofibrils with purified Ca2+-activated proteolytic enzyme produced alterations in myofibrillar ultrastructure that were identical to the initial alterations occurring in myofibrils from atrophying muscle (i.e. weakening and subsequent removal of Z disks). Additonally the electrophoretic banding pattern of Ca2+-activated proteolytic enzyme-treated myofibrils is very similar to that of myofibrils prepared from muscles atrophying as a result of nutritional vitamin E deficiency. The possible role of Ca2+-activated proteolytic enzyme in disassembly and degradation of the myofibril is discussed.

Animals↗

PubMed1995

Stress-induced atrophy of apical dendrites of hippocampal CA3c neurons: comparison of stressors.

Repeated restraint stress induces an atrophy of apical dendrites of CA3c pyramidal neurons in the hippocampus, but the relationship between stress and adrenocortical activation has not been thoroughly investigated. In order to better understand the relationship between neural and non-neural indices of the severity of stress, we investigated the temporal relationship between CA3c dendritic atrophy and indices of adrenal steroid stress responsiveness. For this purpose, we used two different stress regimens: repeated restraint stress (6 h/day) and a chronic multiple stress paradigm (shaking, restraint and swimming, each day), differing in the degree of adrenal activation produced over 14 and 21 days. Atrophy of dendrites of CA3c neurons was found after 21 days of stress, but not after 14 days, and was of a similar magnitude for both stressors. However, non-neural measures differed between the two stress paradigms: (i) chronic restraint stress caused a significant habituation by day 21 in the corticosterone response to acute restraint, whereas chronic multiple stress exposure was not accompanied by habituation of the corticosterone response to restraint; (ii) chronic restraint stress caused neither adrenal hypertrophy nor thymus atrophy, but did reduce the rate of body weight gain throughout the 21 days, whereas chronic multiple stress caused a transient adrenal hypertrophy (on day 14), delayed suppression of thymus weight (on day 21) and transient reduction of body weight gain (on days 7 and 14, but not on day 21). Thus the non-neural indices of response to stress--although complex in their time course--suggest that the multiple stress regimen is a somewhat more potent chronic stressor for corticosterone and adrenal responses. Yet both stress regimens produced the same degree of apical dendritic atrophy in CA3c pyramidal neurons. These results are consistent with a model in which adrenocortical secretion plays a permissive role in enabling another agent, namely, excitatory amino acids, to produce the final effect.

Animals↗

PubMedDate not supplied

Cortical atrophy and cognitive performance in infantile nephropathic cystinosis.

A group of children and adolescents with infantile nephropathic cystinosis underwent cognitive testing and were examined for cortical atrophy using magnetic resonance imaging or computed tomography. Ten of 11 patients demonstrated cortical atrophy. A consistent pattern of lower cognitive performance was found in patients with greater atrophy; however, only the relationship between atrophy and short-term memory approached statistical significance. In addition, evidence for greater impairment of visual memory than of other cognitive functions was observed. This latter observation did not appear to be related to the degree of atrophy.

Adolescent↗

PubMed1995

Disparate circadian variations of blood pressure and body temperature in bedridden elderly patients with cerebral atrophy.

Twenty bedridden elderly patients with normal sleep-wake cycles were studied to evaluate the circadian variations of blood pressure, pulse rate, body core temperature, cortisol, and catecholamines with a focus on their relation to cerebral atrophy. Twenty-four-hour blood pressure (BP) and pulse rate monitorings were done with simultaneous measurement of urinary bladder temperature. Urine was also collected every 4 h to measure 17-hydroxycorticosterone and catecholamines. Based on the brain CT, frontal horn index (FHI: maximal distance between bilateral frontal horns/the corresponding width of the skull) was calculated as an index of cerebral atrophy. Analysis by the cosinor method revealed that the significant circadian rhythm with nocturnal decline was observed in only 9 patients (45%) for BP and in 13 patients (65%) for pulse rate. In contrast, 19 of 20 patients (95%) showed significant circadian rhythms of bladder temperature, with the nadirs appearing between 00:06 and 06:54. In the subgroup of mild cerebral atrophy (FHI < 0.30, n = 11), BP and pulse rate fell modestly but significantly during nighttime, whereas they did not fall in the subgroup of moderate to severe cerebral atrophy (FHI > or = 0.30, n = 9). The possibility could not be excluded that the sleep disturbance might result in the relatively high BP during nighttime. Bladder temperature, 17-hydroxycorticosteroids, and catecholamines showed significant nocturnal falls in both groups. In conclusion, nocturnal fall of BP disappeared in the bedridden elderly patients with cerebral atrophy, which cannot be explained by the change in the circadian variation of the sympathetic nervous system, cortisol, or body core temperature.

Aged↗

PubMedDate not supplied

Cortical atrophy in schizophrenia. Prevalence and associated features.

The degree of cortical atrophy as revealed by computed tomographic scans was assessed in 124 patients meeting the DSM III criteria for schizophrenia and in 45 age- and sex-matched healthy controls. 21 patients, i.e., 33% of the entire sample, showed moderate to severe atrophy. The presence of atrophy was not associated with such variables as patients' age, age at onset and duration of illness, diagnostic subtype of schizophrenia, family history of schizophrenia in first degree relatives, history of suicidal behavior, I.Q., employment status, clinical outcome on neuroleptic treatment and HLA antigens distribution. The only variables found to be associated with atrophy were: male sex and cerebral ventricular enlargement. The significance of the CT finding of cortical atrophy in schizophrenia is discussed in the light of these results.

Adolescent↗

PubMed2004

Optic atrophy and macular degeneration as initial presentations of subacute sclerosing panencephalitis.

PURPOSE: To report a case of subacute sclerosing panencephalitis in which the initial clinical presentations were optic atrophy and macular degeneration. DESIGN: Observational case report. METHODS: A 9-year-old boy with visual loss attributable to optic atrophy and macular degeneration had a diagnostic examination. RESULTS: The visual acuity levels of both eyes were light perception at presentation. Fundus examination revealed bilateral optic atrophy and macular degenerative changes including retinal pigment epithelial atrophy, macular scarring, and epiretinal membrane formation. The antimeasles IgG titers were high both in serum and cerebrospinal fluid samples. Neurologic symptoms of myoclonus, ataxia, motor, and mental disabilities occurred 4 months after the onset of first visual disturbances and 2 weeks after the patient applied to our clinic. CONCLUSION: Children with optic atrophy and macular degenerative lesions should be examined for sclerosing panencephalitis, even if the classical neurologic symptoms of this disease are not present.

Analgesics, Non-Narcotic↗

PubMed2005

Metaiodobenzylguanidine (MIBG) scintigraphy at various parts of the body in Parkinson's disease and multiple system atrophy.

We compared MIBG uptake at various parts of the body in controls and patients with Parkinson's disease and multiple system atrophy. In the heart, MIBG uptake in Parkinson's disease (early H/M: 1.668+/-0.325, late H/M: 1.500+/-0.402) was less than that in multiple system atrophy (early H/M: 2.395+/-0.186, late H/M: 2.530+/-0.391) and controls (early H/M: 2.635+/-0.508, late H/M: 2.575+/-0.635) (early: P<0.0001, late: P<0.0001). There were no significant differences in uptake by the lung, thyroid, or liver in the three groups. Only on early images, uptake in the shoulder in multiple system atrophy (early S/M: 0.473+/-0.78) and Parkinson's disease (early S/M: 0.470+/-0.710) was decreased compared to that in controls (early S/M: 0.560+/-0.118) (P=0.0252). MIBG is reported to be taken up in the terminal part of sympathetic nerves and demonstrates sympathetic nerve activity, especially on late images. The cause of differences between the heart and other parts of the body remains unknown. We consider the following possibilities: (a) differences in the sympathetic nervous system between Parkinson's disease and multiple system atrophy are more subtle in organs other than the heart; (b) the cause of MIBG uptake reduction by the heart in Parkinson's disease involves factors in addition to sympathetic nervous system damage; and (c) MIBG uptake by organs other than the heart involves not only the sympathetic nervous system but also non-neuronal components. In conclusion, MIBG uptake by organs other than the heart cannot differentiate Parkinson's disease from multiple system atrophy at present.

3-Iodobenzylguanidine↗

PubMed2006

Atrophy, hypertrophy, and hypoxemia induce transcriptional regulators of the ubiquitin proteasome system in the rat heart.

BACKGROUND: In skeletal muscle, transcript levels of proteins regulating the ubiquitin proteasome system (UPS) increase with atrophy and decrease with hypertrophy. Whether the same is true for heart muscle is not known. AIM OF THE STUDY: We set out to characterize the transcriptional profile of regulators of the UPS during atrophy-, hypertrophy-, and hypoxia-induced remodeling of the heart. METHODS AND RESULTS: Cardiac atrophy was induced by heterotopic transplantation of the rat heart. Left ventricular hypertrophy was induced by banding of the ascending aorta in rats. To study the effects of hypoxemia on the left ventricle, rats were exposed to hypobaric hypoxia. Transcript levels of six known regulators of the UPS, ubiquitin B (UbB), the ubiquitin conjugating enzymes UbcH2 and E2-14kDa, the ubiquitin ligases Mafbx/Atrogin-1 and MuRF-1, and the proteasomal subunit PSMB4 were measured using quantitative RT-PCR. Unloading-induced atrophy increased mRNA levels of UbB and decreased levels of both ubiquitin ligases. Transcript levels of all UPS genes investigated increased in the hypertrophied and hypoxic heart (with the exception of E2-14kDa). CONCLUSIONS: Cardiac atrophy, hypertrophy, and hypoxemia all increase myocardial UbB expression, suggesting that UbB is a transcriptional marker for load-induced and hypoxia-mediated cardiac remodeling.

Animals↗

PubMedDate not supplied

Fas and perforin are not required for thymus atrophy induced by Trypanosoma cruzi infection.

In the acute phase of Trypanosoma cruzi infection there is a prominent thymus atrophy, which is determined by massive loss of immature CD4/CD8 double positive cells. Recently, the involvement of a parasite transialidase, which is shed from the parasite cell membrane and the activation of P2X(7), a purinergic receptor, were stated as important pathways leading to thymus atrophy. In this work we evaluated the possible involvement of Fas- and perforin-based cytotoxic pathways in the thymus atrophy induced by T. cruzi infection using gld/gld and perforin (-/-) mice. We found similar kinetics of thymus atrophy in mice competent or deficient in both cytotoxic pathways, indicating that both molecules are not directly involved in the thymus atrophy, either inducing cellular death or as co-stimulatory molecules.

Animals↗

PubMed2006

Intraprostatic spermatozoa: zonal distribution and association with atrophy.

Intraprostatic spermatozoa (IS) have been demonstrated in only 2 articles in the literature reporting on postmortem prostates. Intraprostatic spermatozoa have not been previously described in radical prostatectomies. This is the first study that describes the presence of IS in radical prostatectomies with prostatic carcinoma (PC) and its association with atrophy. We examined whole mount sagittal sections from 69 consecutive radical prostatectomy cases for PC. A central section including the seminal vesicle ejaculatory duct urethra complex (SVEDU) from each case was stained with Berg's stain to identify spermatozoa and their location. The extent and the type of atrophy were assessed on the entire prostate by using a grid method. Eighteen cases (26.1%) revealed spermatozoa both in the SVEDU and in the prostate (IS) (group 1). Twenty-two cases (31.9%) showed spermatozoa exclusively in the SVEDU but not in the prostate (group 2). The remaining 29 cases (42.0%) had no spermatozoa in either site. Location of IS was 72.2% peripheral zone, 22.2% central zone, and 5.6% transitional zone. Intraprostatic spermatozoa were frequently seen accompanied by inflammatory infiltrate in the periglandular stroma. The extent of atrophy was greater in group 1 than in group 2 (25.7% versus 15.3%; P = .006). Postatrophic hyperplasia was seen more frequently in group 1 than in group 2 (72.2% versus 40.9%; P = .025). In conclusion, the frequency of IS is 26.1% when including all prostates and 45.0% when including prostates with evidence of residual ejaculate (spermatozoa in the SVEDU), more than previously reported. Intraprostatic spermatozoa are predominantly located in the peripheral zone similar to atrophy and PC. Prostates with IS have larger atrophic areas and increased frequency of postatrophic hyperplasia. The role of IS in the pathogenesis of prostate inflammation and atrophy should be investigated.

Adenocarcinoma↗

PubMed2006

Treatment of atrophic mandibular fractures based on the degree of atrophy--experience with different plating systems: a retrospective study.

PURPOSE: The aim of this retrospective study was to evaluate the clinical outcome of fractures of the atrophic mandible based on the degree of atrophy and treatment by different plating systems. PATIENTS AND METHODS: Thirty patients with 40 fractures of atrophic mandibles were treated by open reduction and internal fixation at our department between 1994 and 2001. Twelve fractures occurred in Class I (between 15- and 20-mm bone height), 10 fractures in Class II (between 10 and 15 mm), and 18 fractures in Class III atrophy (<10 mm). The profile heights of plating systems used for stabilization varied from 0.5 to 2.2 mm and were applied with an intraoral (n = 37) and extraoral (n = 3) approach. RESULTS: In 36 fractures, bone healing was uneventful. Major complications (loose hardware or nonunion) occurred in 4 fractures: 2 in Class II and 2 in Class III atrophy. Major complications were observed with 1.4-mm (n = 3) and 2.2-mm (n = 1) plates. Minor complications (infections or dehiscence) were observed in 6 fractures: 3 in Class II and 3 in Class III atrophy. Hypesthesia of the inferior alveolar nerve was present 1 week and 1 year postoperatively in 39 and 16 fractures, respectively. CONCLUSIONS: Treatment of atrophic mandible fractures should be based on the degree of atrophy. More rigid fixation may be necessary in mandibles with less than 15 mm bone height.

Adult↗

PubMed2004

Adeno-associated viral vector-mediated gene transfer of brain-derived neurotrophic factor reverses atrophy of rubrospinal neurons following both acute and chronic spinal cord injury.

Rubrospinal neurons (RSNs) undergo marked atrophy after cervical axotomy. This progressive atrophy may impair the regenerative capacity of RSNs in response to repair strategies that are targeted to promote rubrospinal tract regeneration. Here, we investigated whether we could achieve long-term rescue of RSNs from lesion-induced atrophy by adeno-associated viral (AAV) vector-mediated gene transfer of brain-derived neurotrophic factor (BDNF). We show for the first time that AAV vectors can be used for the persistent transduction of highly atrophic neurons in the red nucleus (RN) for up to 18 months after injury. Furthermore, BDNF gene transfer into the RN following spinal axotomy resulted in counteraction of atrophy in both the acute and chronic stage after injury. These novel findings demonstrate that a gene therapeutic approach can be used to reverse atrophy of lesioned CNS neurons for an extended period of time.

Acute Disease↗

PubMed2004

Differentiating AD from aging using semiautomated measurement of hippocampal atrophy rates.

Manual segmentation of the hippocampus is the gold standard in volumetric hippocampal magnetic resonance imaging (MRI) analysis; however, this is difficult to achieve reproducibly. This study explores whether application of local registration and calculation of the hippocampal boundary shift integral (HBSI) can reduce random variation compared with manual measures. Hippocampi were outlined on the baseline and registered-repeat MRIs of 32 clinically diagnosed Alzheimer's disease (AD) patients and 47 matched controls (37-86 years) with a wide range of scanning intervals (175-1173 days). The scans were globally registered using 9 degrees of freedom and subsequently locally registered using 6 degrees of freedom and HBSI was then calculated automatically. HBSI significantly reduced the mean rate (P < 0.01) and variation in controls (P < 0.001) and increased group separation between AD cases and controls. When comparing HBSI atrophy rates with manually derived atrophy rates at 90% sensitivity, specificities were 98% and 81%, respectively. From logistic regression models, a 1% increase in HBSI atrophy rates was associated with an 11-fold (CI 3, 36) increase in the odds of a diagnosis of AD. For manually derived atrophy rates, the equivalent odds ratio was 3 (CI 2,4). We conclude that HBSI-derived atrophy rates reduce operator time and error, and are at least as effective as the manual equivalent as a diagnostic marker and are a potential marker of progression in longitudinal studies and trials.

Aged↗

PubMed2005

Evidence for a direct association between cortical atrophy and cognitive impairment in relapsing-remitting MS.

Cognitive deficits affecting memory, attention and speed of information processing are common in multiple sclerosis (MS). The mechanisms of cognitive impairment remain unclear. Here, we examined the association between neuropsychological test performance and brain atrophy in a group of mildly disabled patients with relapsing-remitting MS. We applied voxel-based morphometry (SPM2) to investigate the distribution of brain atrophy in relation to cognitive performance. Patients had lower scores than control subjects on tests of memory and executive function, including the PASAT, Digit Span Backward and a test of short-term verbal memory (Memo). Among patients, but not healthy controls, performance on the PASAT, a comprehensive measure of cognitive function and reference task for the cognitive evaluation of MS-patients, correlated with global grey matter volume as well as with grey matter volume in regions associated with working memory and executive function, including bilateral prefrontal cortex, precentral gyrus and superior parietal cortex as well as right cerebellum. Compared to healthy subjects, patients showed a volume reduction in left temporal and prefrontal cortex, recently identified as areas predominantly affected by diffuse brain atrophy in MS. A comparison of low performers in the patient group with their matched control subjects showed more extensive and bilateral temporal and frontal volume reductions as well as bilateral parietal volume loss, compatible with the progression of atrophy found in more advanced MS-patients. These findings indicate that MS-related deficits in cognition are closely associated with cortical atrophy.

Adult↗