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PubMed1998

Peripapillary atrophy in normal and primary open-angle glaucoma.

This study was undertaken in order to determine the value of measuring peripapillary atrophy for the diagnosis and follow-up of patients with glaucoma, and to evaluate how closely peripapillary atrophy is related to structural and functional optic nerve damage in glaucoma. Magnification-corrected morphometry of photographs using a computer graphic program and automated static threshold perimetry were performed in 234 eyes of 141 patients with primary open-angle glaucoma and 139 eyes of 86 normal subjects. The groups were not significantly different in age, refractive error or disc area. Zones alpha and beta were significantly larger, total peripapillary atrophy was significantly more extensive, and zone beta occurred more often in the glaucoma group than in the normal group. The frequency of zone beta increased with advancing glaucoma stage. The areas of zones alpha and beta and total peripapillary atrophy increased significantly with decreasing rim/disc area ratio, rim area, and mean deviation, and with increasing vertical and horizontal cup-to-disc ratios and cup area. Correlation coefficients were generally higher for zone beta than for zone alpha. Peripapillary atrophy was greater in a sector in which the neuroretinal rim loss was more marked. These findings suggest that increases in the extent of peripapillary atrophy are related to the severity of glaucomatous optic nerve damage and visual field defects, and that peripapillary atrophy is useful for the diagnosis and progression of glaucomatous nerve damage.

Chi-Square Distribution↗

PubMed1999

[Effect of gravitation loading and retabolil on development of atrophy in muscles and bones of rats due to suspension].

In a 3-wk experiment with tail-suspended rats histological and histomorphometric methods were used to determine the effects of graded gravitational loading (GGL) and anabolic steroid retabolil (nortestosterone decanoate) on the course of atrophy in soleus m. (SM), gastrocnemius m. (GM), tibia and humerus, and functioning of somatotrophic hormones (STH) of the pituitary and thyrocytes of the thyroid. Suspension was found to produce atrophy in SM and, to a less degree, in GM, partial transformation of SM slow fibers into the fast ones, suppression of the tibial longitudinal growth, demineralization of the tibial and humeral spongious metaphyses; besides, functional activities of STH-cells and thyrocytes were inhibited. Graded gravitational loading of rats by intermittence of suspension for 2 hrs slowed down atrophy in both muscles and osteopenia in tibia, stimulated the synthetic and secretory functions of STH-cells without any marked effect on thyrocytes or humeral osteopenia. GGL failed to influence the slow-to-fast transformation of SM fibers. Two injections of retabolil at the total dose of 3 mg/kg of the body mass somewhat interfered with the SM atrophy and humoral osteopenia, and were favorable to the synthetic but not secretory activity of STH-cells. Neither SM and tibial atrophies nor thyroid activity of the gland were improved. The prophylactic action of GGL upon the SM and humeral atrophies was significantly higher when combined with retabolil, whereas GM and tibia were not noticeably cured by retabolil. Inhibition of the SM atrophy and humeral osteopenia in rats treated with GGL and retabolil concurred with elevated activities of STH-cells and thyrocytes indirectly suggesting their more intensive production of the growth hormone and thyroid hormones, respectively.

Anabolic Agents↗

PubMed2000

[Dynamics of human muscle fibers atrophy during long-term head-down hypokinesia].

The dynamics of atrophy in the muscles-extensors of the leg and thigh during long-term hypokinesia was studied with the model of head-down tilt (HDT -6 degrees) in a series of two experiments (120 and 60 days in duration) with participation of men and women. Dynamics of the cross-sectional area of human muscular fibers was characterized by similar atrophy of the fast and slow fibers on the first stage of HDT. Later on, the size of fast fibers in m. soleus and m. gastrocnemius lateralis reached plateau whereas the size of slow fibers continued to diminish. These were only fast fibers that underwent further atrophy in locomotor m. vastus lateralis. A supposition can be made that the controversy between literature data on the character of atrophy of muscular fibers in experiments with human subjects and rodents is primarily linked with different rates of atrophy developed by muscles in various species; besides, investigators describe different stages of one process. Analysis of the benefit from preventive exercises for the muscular atrophy control during HDT indicated that locomotor (with loading restraint belts) and resistive exercises can preclude slow fibers atrophy under the conditions of hypokinesia.

Adaptation, Physiological↗

PubMed2001

[Etiological diagnosis of villous atrophy].

Villous atrophy may have various etiologies. The diagnosis of villous atrophy relies on an intestinal biopsy which necessitates a perfect histological technique to assert the villous atrophy and its degree. The most frequent etiology is coeliac disease. Villous atrophy regresses with gluten free diet. The failure of a strict gluten free diet implies to exclude a refractory sprue thought to be the earliest form of enteropathy associated T cell lymphoma. The other etiologies of villous atrophy are unusual and could be observed in alpha chain disease, inflammatory and infectious diseases, immune disorders, and primitive ileal villous atrophy. Other etiologies characterize villous atrophy in children as cow milk allergy and epithelial abnormalities.

Atrophy↗

PubMed2001

[Transition of soleus troponin I isoforms and atrophy of testis in tail-suspended rats].

Objective. To observe the transition time of soleus I (TnI) isoforms and to elucidate the relationship between soleus TnI transition and atrophy; and to analyze the time course between testis atrophy and soleus atrophy. Method. Eight groups of male rats were suspended for 3, 4, 5, 7, 14, 21, 28 and 42 d, respectively. Besides, three groups of female rats were suspended for 3, 4 and 5 d respectively. Wet and relative weights (wet weight/body weight) of testis and soleus were measured. The expression of TnI was observed by Western blot. Result. The relative weight of soleus of tail-suspended male rats decreased significantly after 4 d of suspension as compared with control. The degree of rats soleus atrophy in the first 14 d of suspension was greater than that after 14 d. The relative weight of testis showed the same change as that of soleus. There was no significant change in the relative weight of soleus in 4 d of tail-suspended female rats. The significant decrease in the relative weight of tail-suspended female rats began on the 5th day. The Western blot showed that the transition from slow skeletal TnI (ssTnI) to fast skeletal TnI (fsTnI) in the soleus occurred in 14 d of tail-suspension. Conclusion. The overt atrophy of tail-suspended male rats occurs on the 4th day. The soleus TnI transition from ssTnI to fsTnI is on the 14th day. It is suggested that the TnI is not the sensitive protein to gravity. The overt atrophy of female tail-suspended rats occurs at the 5th day. This indicated that the decrease in testosterone level may accelerate the atrophy of the soleus.

Animals↗

PubMed1992

[A case of progressive hemiatrophy with type 2 muscle atrophy in muscle biopsy].

We reported a case of progressive hemiatrophy, whose skeletal muscle biopsy revealed type 2 fiber atrophy. This patient, a 40-year-old woman, noticed left leg atrophy at the age of 39. She had a history of minor trauma of the left thigh at the age of 30. On admission, physical examination revealed atrophy of various parts of her left side of body, predominantly in the left leg. There was no dermatological or neurological abnormalities except these atrophies. Hematological and biochemical examinations were normal. EEG, EMG, nerve conduction studies and autonomic function tests were normal in either side of the body. MRI study showed reduced muscle bulk as well as subcutaneous fatty tissue especially in her left leg. Skeletal muscle biopsy of her left quadriceps femoris muscle revealed type 2 fiber atrophy and type 1 fiber predominance. However, no abnormality was found in the intramuscular nerves. We considered that type 2 muscle fiber atrophy was one of the cause of atrophy of this case.

Adult↗

PubMed1991

Distribution of atrophy in the nasal ventral conchae of piglets infected experimentally with Bordetella bronchiseptica.

The distribution and extent of atrophy caused by Bordetella bronchiseptica in the nasal ventral conchae were investigated by intranasally infecting piglets at day 4 of life. Experimental and control piglets were killed at one, two, three, four, five and six weeks of age. Serial transverse 80 microns thick nondecalcified sections were cut throughout the entire length of the nasal ventral conchae, and microradiographed. It was observed that the distribution and extent of atrophy was not uniform along the ventral conchae. The articular and transverse laminae as well as the connecting zone were not atrophied, except at their rostral extremity. The entire dorsal scroll was atrophied. This atrophy was moderate, except at the rostral and caudal extremities of the dorsal scroll, where its size was less than half that of the controls. The ventral scroll was less atrophied than the dorsal scroll, although a marked atrophy was present at its rostral extremity. From these observations, it is suggested that two transverse sections should be made through the nose of pigs in order to establish a diagnosis of atrophic rhinitis at slaughter: one section at the level of the first-second premolar tooth and one more rostral section, at the level of the canine tooth.

Animals↗

PubMed1990

Fiber-type discrimination in disuse and glucocorticoid-induced atrophy.

Data are presented which demonstrate that phasic/glycolytic muscles atrophy more than tonic/oxidative muscles in response to exogenously introduced glucocorticoids. Data are also presented demonstrating that immobilization makes a muscle unusually sensitive to glucocorticoid-induced atrophy and that remobilization of a previously immobilized muscle protects a muscle from glucocorticoid-induced atrophy. These observations are discussed within the context of the role of mechanical activity in the acquisition and maintenance of fiber-type characteristics. In addition, the available data on the glucocorticoid receptor population in skeletal muscles of various types and circumstance are reviewed within the context of the recent observations concerning the glucocorticoid induction of the enzyme glutamine synthetase in skeletal muscle. It is proposed here that atrophy is not necessarily the response of skeletal muscle to glucocorticoids. Rather, atrophy is a possible consequence of the glucocorticoid-induced increase in export of amino acid carbon from the muscle. Whether such export causes a muscle to atrophy or perhaps even hypertrophy will depend on the capacity of the muscle to sustain its free amino acid pools. Mechanical activity greatly promotes the uptake of free amino acids in skeletal muscle. Such promotion takes the form of both contraction-induced uptake and increased insulin sensitivity. Within this perspective, it is suggested that tonic muscles and remobilized muscles are protected from atrophy by exogenous glucocorticoids because their high level of mechanical activity allows them to maintain their free amino acid pools.

Animals↗

PubMed1989

Histochemical study on the atrophy of the quadriceps femoris muscle caused by knee joint injuries of rats.

Atrophy developing in the quadriceps femoris muscle following knee injury is one of the serious problems not only in the field of orthopedics but also of rehabilitation. However the pathogenesis of this atrophy has not yet been elucidated. The author therefore produced a complex ligament injury model using the knee joints of rats in order to study the pathogenesis of this atrophy. After severing the anterior cruciate ligament, the medial collateral ligament and tibial insertion of the medial meniscus of rats, these animals were sacrificed at 4, 8 and 12 weeks. After removing the vastus lateralis muscle, vastus medialis muscle, and rectus femoris muscle, specimens of these muscles were stained for ATPase. The transection area of the muscle fibers was measured and the fiber type composition was determined. At 4 weeks the vastus medialis muscle and at 12 weeks the vastus lateralis muscle showed marked atrophy. The rectus femoris muscle exhibited the least atrophy throughout the entire observation period. In examining the atrophy of the quadriceps femoris muscle by muscle fiber type, the degree of atrophy was found to differ among the venters and even the same venter showed a different reaction depending on the elapsed time after sustaining the injury. Neither changes in the fiber type composition not neurogenic findings could be observed.

Adenosine Triphosphatases↗

PubMed1985

Cerebral atrophy in patients on long-term regular hemodialysis treatment.

The presence of Cerebral Atrophy in the form of cortical damage (Cortical Atrophy) or subcortical damage (enlargement of ventricular cavities) was explored by computed tomography (CT) scans in 30 patients maintained on regular hemodialysis treatment (RDT) for not less than 10 years, and less than 50 years of age. Whereas a group of 50 normal subjects of the same age, used as control, gave no evidence of cerebral atrophy, 46.6% of the patients maintained on RDT showed cortical atrophy, evenly diffuse in half the cases and predominantly frontal in the other half. In addition 16.6% of the patients showed subcortical atrophy, even in the absence of evident central neurologic or neuropsychic symptoms. In a search for the possible causes of this high incidence of cerebral atrophy in chronic hemodialysis patients we reviewed the last five years' profiles of clinical and blood biochemistry parameters known or suspected to produce brain damage when altered, as stored in a computer system available to our Hemodialysis Unit: these were mean blood pressure before and after hemodialysis, blood cholesterol and triglyceride assays, and mean daily oral intake of A1(OH)3. The status of arterial blood vessels in terms of vascular calcification in soft tissue roentgenograms was also defined; then we correlated these clinical and biochemical indices with the findings of cerebral CT scans by the Fisher test and Discriminant Analysis. The Fisher test revealed a decreasing correlation of cerebral atrophy with mean blood pressure, A1(OH)3 intake, blood cholesterol content, arterial calcifications and blood trygliceride assay in that order.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMedDate not supplied

Cerebral atrophy in systemic lupus erythematosus: steroid- or disease-induced phenomenon?

Thirty-two patients with systemic lupus erythematosus were evaluated clinically and with computed tomography in order to determine whether the occurrence of cerebral atrophy in systemic lupus erythematosus was due to the steroid therapy or the cerebral manifestations of the disease itself. Of these patients, 14 had central nervous system manifestations of the disease (lupus cerebritis) and 12 of the 14 were on long-term steroid therapy. Eighteen patients had no clinical evidence of lupus cerebritis and all were on long-term steroids. Of the 14 lupus cerebritis patients, 10 showed moderate cerebral atrophy, four minimal atrophy, and none were normal. Of the 18 patients without lupus cerebritis, none had moderate atrophy, six (33%) showed minimal atrophy, and 12 (67%) had normal CT scans. This data suggest that it is the lupus cerebritis rather than the steroid therapy that is responsible for the moderate cerebral atrophy. In patients suspected of lupus cerebritis, steroids should not be withheld because of concern for steroid-induced atrophy. Rather, the dose may need to be increased.

Adolescent↗

PubMed1976

Facial atrophy.

The author's personal experience with 84 patients demonstrating varying degrees of facial atrophy is reported. Of these, 59 patients had forms of progressive hemifacial atrophy. Hemifacial atrophy seems best classified into two groups: those who demonstrate inflammatory changes during the course of the disease as opposed to the more benign or noninflammatory types. The inflammatory type of hemifacial atrophy is usually associated with skin and ophthalmic pathology. It is suggested that it is often difficult, if not impossible, to distinguish between Romberg's disease and hemifacial atrophy from scleroderma; therefore, these terms might best be eliminated in classifying hemifacial atrophy. The etiology of facial atrophy remains unknown in the overwhelming majority of cases.

Adolescent↗

PubMed1993

[Cerebellar atrophy and phenytoin poisoning. An MR study].

Phenytoin has been considered a possible cause of cerebellar degeneration, especially after clinical intoxication. Magnetic resonance provides the diagnosis of anatomical structures in the posterior fossa without the limitation of beam hardening artefacts. The aim of this study was to evaluate the relationship of phenytoin medication and cerebellar atrophy in 11 patients with increased serum levels (21.4 micrograms/ml-95.6 micrograms/ml). Five patients had normal cerebellar structures, although three of them had a history of clinical intoxication and all had at least one episode of increased serum level of DPH. The remaining six patients had moderate severe cerebellar atrophy (n = 4) and atrophy of the vermis cerebelli (n = 5). Two of them had never experienced clinical intoxication. There was no correlation between the degree of atrophy and severity of clinical symptoms and evaluation of serum DPH levels (up to four times normal values). There was also no correlation between cerebellar atrophy, duration of epilepsy and frequency of seizures. We conclude that phenytoin overdosage does not necessarily result in cerebellar atrophy and it is unlikely that phenytoin medication was the only cause of cerebellar atrophy in the remaining patients.

Adult↗

PubMedDate not supplied

Gyrate atrophy of the choroid and retina.

Gyrate atrophy of the choroid and retina is characterized by autosomal recessive inheritance, progressive chorioretinal atrophy beginning in late childhood, and hyperornithinemia with ornithinuria caused by deficient ornithine aminotransferase activity. In this paper, four patients with gyrate atrophy are described. All patients had visual impairment, mental retardation, hyperornithinemia, hypolysinemia, ornithinuria and lysinuria. The first case had hypermetropic astigmatism in contrast to other reported gyrate atrophies. These are the first reported cases from Turkey, but gyrate atrophy may not be rare in Turkey since the frequency of some other metabolic disorders has also been reported to be high. It is suggested that gyrate atrophy must be considered in all patients with chorioretinal atrophy.

Adolescent↗

PubMed1997

[Neurological CPC.57. An 80-year-old woman with four years history of muscle atrophy involving lower extremities predominantly on the right side].

We report an 80-year-old woman with progressive muscular atrophy predominantly involving her right lower extremity. She was well until 1992 (75 years of age) when she noted an onset of weakness in her right leg which had got progressively worse. She was admitted to our service in July 1994. On admission, general physical examination was unremarkable. She was alert and well oriented without dementia. Higher cerebral functions were normal. Cranial nerves also appeared intact. She dragged her right leg in walking. Mild to moderate weakness (2/5 to 4/5) was noted in muscles in her right lower extremity more in the distal part. Deep tendon reflexes were within normal limits, and the plantar response was flexor bilaterally. Sensation was intact. Laboratory examinations were also unremarkable except for slight increase in CK which was 470 IU/l. CSF was also normal. EMG revealed neurogenic changes in the lower extremities. She was admitted to Aoki Hospital on October 21, 1994, by that time, her weakness in the right lower extremity had gotten worse in that the muscle strength of the right extensor hallucis longus was 0 and tibialis anterior 2; muscle atrophy was also prominent in her right leg; the right ankle jerk could not be elicited. In the subsequent course, weakness and atrophy appeared in her left lower extremity, however, upper extremities and cranial nerves had never been affected. Babinski sign was always negative. In February 1996, she developed delusional ideation of self persecution, and showed difficulty in communication with medical staffs. She developed fever of 38.7 degrees C on June 13, 1996 expired on the next day. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had a form of spinal muscular atrophy. Opinions were divided between ALS and spinal muscular atrophy. Post-mortem examination revealed marked loss of anterior horn neurons in the lumbar area with astrogliosis. Bunina bodies were seen in some of the remaining neurons. No myelin pallor was noted in the pyramidal tracts, however, atrophy and loss of Betz cells were noted in the motor cortex. Other cortical areas were unremarkable. The neuropathologist arrived at the conclusion that the patient had ALS. This patient was unique in that she had asymmetric atrophy and weakness limited to the lower extremities. This is quite unusual as ALS of four years duration. In addition, the patient developed some mental change which was thought to represent dementia by some participants. But no clear morphologic changes were seen to account for her mental change.

Aged↗

PubMed2006

Association between gastric atrophy and Helicobacter pylori infection in Japanese children: a retrospective multicenter study.

The purpose of this study was to determine whether Helicobacter pylori infection and mucosal inflammation result in gastric atrophy in Japanese children. A total of 196 patients ages 1-16 years were retrospectively studied: 131 patients were infected with H. pylori and 65 patients were uninfected. Antral (n = 196) and corpus biopsy specimens (n = 70) were investigated based on the Updated Sydney system. In both the antrum and corpus, H. pylori-infected patients showed significantly higher degrees of inflammation and activity of gastritis, compared with noninfected patients. The prevalence of grade 2 or 3 atrophy in the antrum was 10.7% in H. pylori-infected patients and 0% in the noninfected patients (P < .01) and in corpus 4.3% and 0%, respectively (P = .20). The frequency of intestinal metaplasia in the 2 study groups was 4.6% and 4.6% in the antrum and 0% and 4.2% in the corpus, respectively. Among H. pylori-infected patients, the antrum showed significantly higher degrees of H. pylori density, inflammation and activity of gastritis, and atrophy than the corpus. In the antrum, atrophy was significantly correlated with activity, whereas in the corpus, atrophy correlated with H. pylori density, inflammation, and activity. H. pylori-induced gastric inflammation can cause atrophy in Japanese children, predominantly in the antrum. It remains to be determined whether H. pylori-infected children with gastric atrophy are at increased risk for gastric cancer.

Adolescent↗

PubMed1997

Disuse muscle atrophy of lower limbs in hemiplegic patients.

OBJECTIVE: To clarify the histopathologic findings from lower limb muscles in hemiplegic patients and determine whether the findings are related to the severity of paralysis or daily physical activity. DESIGN: Nonrandomized control trial. SETTING: Referral center. PATIENTS: Eight patients were selected from 21 hemiplegic persons who underwent a muscle biopsy, and the controls were four men who had no abnormal findings in their histopathology. MAIN OUTCOME MEASURES: Morphometric evaluations of bilateral vastus lateralis muscles on the involved (I-VL) and non-involved (N-VL) sides in eight hemiplegic subjects, five flexor hallucis longus muscles on the involved side (I-FHL), and vastus lateralis muscles of four controls (C-VL) were performed. Muscle fiber diameters were measured with an image analyzer, and atrophy factors, hypertrophy factors, and fiber type proportions were calculated based on the data. RESULTS: The morphometric measurements revealed that the hemiplegic patients had type 2 fiber atrophy, type 2B fiber atrophy, and type 2 fiber atrophy with type 1 fiber hypertrophy in the I-VL, N-VL, and I-FHL, respectively, and that the controls had no muscle fiber atrophy or hypertrophy. The muscle fiber atrophy in the hemiplegic patients was not related to the period after the onset, the severity of paralysis, or activities of daily living score but was related to daily physical activity. CONCLUSIONS: Although the hemiplegic patients had undergone rehabilitative treatments, which did not include muscle strengthening exercises, in a hospital without a board-certified doctor of rehabilitation medicine, a considerable amount of muscle atrophy was found characteristic of changes seen in disuse.

Aged↗

PubMed2002

Juvenile dentatorubral-pallidoluysian atrophy: new clinical features.

Dentatorubral-pallidoluysian atrophy is a rare autosomal-dominant neurodegenerative disorder caused by an expansion of a CAG repeat in the atrophin-1 gene on chromosome 12. Dentatorubral-pallidoluysian atrophy is characterized clinically by prominent anticipation and a wide variety of symptoms that depend on age of onset and number of trinucleotide repeats. The juvenile type of dentatorubral-pallidoluysian atrophy, like Huntington's disease, is most commonly inherited via paternal transmission of the gene and most frequently presents with early-onset progressive myoclonus epilepsy with mental retardation and ataxia. We present six affected individuals with dentatorubral-pallidoluysian atrophy from a black family living in North America. This pedigree includes two severe juvenile-onset cases, one of maternal transmission and the other of paternal transmission. Both cases of juvenile-onset disease presented with autistic features and seizures. Interestingly, cranial magnetic resonance imaging performed on the more affected child revealed only mild cerebellar atrophy. The present family expands the clinical description of juvenile-onset dentatorubral-pallidoluysian atrophy and emphasizes the importance of considering dentatorubral-pallidoluysian atrophy in children with progressive myoclonus epilepsy.

Adolescent↗