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PubMed2003

Inflammatory atrophy of the prostate. Prevalence and significance.

CONTEXT: Recently, prostatic atrophy associated with chronic inflammation has been linked to carcinoma either directly or indirectly by first developing into high-grade prostatic intraepithelial neoplasia. OBJECTIVE: The purpose of our study was to test this hypothesis in autopsies. DESIGN: A step section method was used to cut the posterior lobe in coronal planes at intervals of 0.3 to 0.5 cm in 100 consecutive autopsies of men older than 40 years. Prostatic atrophy was classified as simple, hyperplastic (or postatrophic hyperplasia), and sclerotic and was analyzed for the presence of chronic inflammation. Prostatic atrophy without (group A) and with inflammation (group B) was correlated with the following variables: age, race, histologic (incidental) carcinoma, high-grade prostatic intraepithelial neoplasia, and extent of both these lesions. RESULTS: Of the 100 prostates examined, 12%, 22% and 66%, respectively, had no atrophy, atrophy without inflammation (group A), and atrophy with inflammation (group B). There was no statistically significant difference between groups A and B for age (P =.55), race (P =.89), presence of histologic (incidental) carcinoma (P =.89), extensive carcinoma (P =.43), presence of high-grade prostatic intraepithelial neoplasia (P =.65), extensive high-grade intraepithelial neoplasia (P =.30), or subtypes of prostatic atrophy. Neither a topographical relation nor a morphologic transition was seen between prostatic atrophy and histologic carcinoma or high-grade intraepithelial neoplasia. Sclerotic atrophy either alone or combined with other subtypes was more frequent in the group with inflammation. A striking morphologic finding was a topographical relation of focal inflammation with sclerotic atrophy in areas with erosion of the epithelium. CONCLUSIONS: Inflammatory prostatic atrophy does not appear to be associated with histologic (incidental) carcinoma or high-grade intraepithelial neoplasia. One possible cause of inflammatory infiltrate associated with prostatic atrophy may be the extravasated prostatic secretions, which were noted in areas of eroded epithelium, a common finding in the sclerotic type of prostatic atrophy.

Atrophy↗

PubMedDate not supplied

[Clinical symptomatology of primary brain atrophy].

A group of 185 patients with brain atrophy found in CT is presented. The purpose of the study was to call attention to the the significance, frequency and clinical signs of brain atrophy. All patients were divided into two groups: 78 cases with secondary brain atrophy associated with other diseases of central nervous system and 107 cases of "primary" brain atrophy. The last one was an only finding without any other pathological lesions in the brain. Depending on the localisation, three groups of brain atrophy were isolated: generalized, subcortical and cortical. The clinical picture was analysed in the group of "primary" brain atrophy. In the studied group the most frequent cause of hospitalisation were epileptic seizures, the next one: headache, one-side hemiparesis or hemihypaesthesia, dizziness and incoordination. Neurological examination showed that one-side signs were observed very often in generalized brain atrophy. In the group of patients with cortical brain atrophy most patients were without any neurological signs. The analysis of the relationship between the clinical examination and "primary" brain atrophy found in CT, showed lack of characteristic, typical signs, which could be connected with brain atrophy. The problem of difficulty in the diagnosis of brain atrophy is stressed aesthesia. The definition and the significance of brain atrophy should be verified in diagnosis and the conclusions after finding brain atrophy have to be very careful.

Adult↗

PubMed1992

[Quantitative evaluation of tongue atrophy on midsagittal magnetic resonance images (MRIs)].

This study was undertaken mainly to establish the quantitative parameter to evaluate the tongue atrophy on midsagittal MRIs and to show the clinical usefulness of such quantitative evaluation. Midsagittal MRIs of the tongue of consecutive 103 patients were analyzed. They were classified into 67 patients showing normal size (group without atrophy), 11 patients showing atrophy (group with atrophy) and 25 patients showing unsatisfactory MRIs with artefacts based on the routine evaluation. The patients in the group without atrophy did not show any pathologic processes to produce tongue atrophy on clinical findings. The area and perimeter of tongue and oral cavity, and the ratio of tongue area to oral cavity area and the ratio of tongue perimeter to oral cavity perimeter on midsagittal MRIs were obtained in each patient of groups with and without atrophy by using quantitative image analysis system. In the group without atrophy, regression analysis of the data on age was made and the 95% confidence interval of the data for age was obtained. No evidence that the tongue becomes atrophic with aging was obtained in the group without atrophy. Patients in the group with atrophy were best separated from those in the group without atrophy statistically when the ratio of tongue area to oral cavity area was regressed on age. Among 11 patients in the group with atrophy, 6 patients were not regarded as having tongue atrophy on clinical neurological examinations. Therefore, the evaluation of midsagittal MRIs is clinically useful.

Adolescent↗

PubMedDate not supplied

Effect of activities of daily living on fiber type atrophy of the vastus lateralis muscle in patients with joint disorders.

The histopathologic study was performed to elucidate whether the fiber type atrophy of the vastus lateralis muscle in patients with hip or knee joint disorders is related to the activities of daily living (ADL) or habitual physical activity. Subjects were 16 female patients, 52.4 +/- 16.0 yr of age (mean +/- standard deviation), who underwent a vastus lateralis muscle biopsy at the time of total hip or knee replacement. At the time of referral to the rehabilitation center, the Functional Independence Measure (FIM) motor score and habitual physical activity at home were evaluated, and the diameter and atrophy factor for each muscle fiber type were measured on the histopathologic preparations of the biopsied muscles. The data were analyzed using ttest, one-way analysis of variance (ANOVA), Kruskal-Wallis one-way ANOVA, Spearman's correlation coefficient, and partial correlation coefficient. The patients showed muscle fiber atrophy and small angular fibers, and the atrophy factor was significantly increased in type 1, 2A, and 2B fibers, in that order (one-way ANOVA, P < 0.05). The patterns of the fiber type atrophy, consisting of normal, type 2B atrophy, type 2AB atrophy, and type 1 and 2AB atrophy, had a significant relationship with the fiber type atrophy (Spearman's correlation coefficient; rho = 0.834, P < 0.001). The FIM motor score showed a significant correlation with the atrophy factor (r = -0.584, P < 0.05), and significant differences were recognized among the four patterns of the fiber type atrophy (Kruskal-Wallis one-way ANOVA, P < 0.05). In conclusion, the muscle atrophy and patterns of the fiber type atrophy of the vastus lateralis muscle in patients with joint disorders may be related to changes in the FIM motor score.

Activities of Daily Living↗

PubMed2001

Rapid quantitative assessment of gastric corpus atrophy in tissue sections.

BACKGROUND/AIMS: Grading of Helicobacter pylori induced atrophic gastritis using the updated Sydney system is severely limited by high interobserver variability. The aim of this study was to set up a quantitative test of gastric corpus mucosal atrophy in tissue sections and test its reproducibility and correlation with the Sydney scores of atrophy. METHOD: Mucosal atrophy was assessed in 124 haematoxylin and eosin stained corpus biopsy specimens by two experienced gastrointestinal pathologists (EB, JL) according to the updated Sydney system as none (n = 33), mild (n = 33), moderate (n = 33), or pronounced (n = 25). In each specimen, the proportions of glands, stroma, infiltrate, and intestinal metaplasia in the glandular zone were measured as volume percentages using a point counting method. The optimal point sample size, intra-observer and interobserver reproducibility, discriminative power for degrees of atrophy, and correlations with H pylori status were evaluated. RESULTS: Counting 400 points in 200 fields of vision provided the smallest sample size that still had excellent intra-observer and interobserver reproducibility (r > or = 0.96). Overall, the volume percentage of glands (VPGL), infiltrate (VPI), and stroma (VPS) correlated well with the Sydney scores for atrophy (p < or = 0.003). However, no differences were found between non-atrophic mucosa and mild atrophy. No correlation was found between age and either the Sydney grade of atrophy or the VPGL or VPS. In non-atrophic mucosa and mild atrophy, H pylori positive cases showed a significantly higher VPI than did H pylori negative cases. A lower VPGL was seen in H pylori positive cases than in H pylori negative cases in the mild atrophy group. VPS did not correlate with H pylori status within each grade of atrophy. CONCLUSION: Point counting is a powerful and reproducible tool for the quantitative analysis of mucosal corpus atrophy in tissue sections. These data favour the combination of "none" and "mild" atrophy into one category, resulting in a three class grading system for corpus atrophy, when using the updated Sydney system.

Adult↗

PubMed1992

[Oligodendroglial inclusions, a marker of multisystemic atrophies].

Nine cases of multiple system atrophy and 1 case of autosomal dominant olivopontocerebellar atrophy (neuropathological diagnosis) were retrospectively examined for the presence of oligodendroglial inclusions. Clinical diagnosis in the first 9 cases had been: olivopontocerebellar atrophy (3 cases), atypical Parkinson's disease (2 cases), Shy-Drager syndrome (2 cases) and multiple system atrophy (1 case); one of the patients could not be included in any of the above mentioned groups. The oligodendroglial inclusions were argyrophilic and located in the cytoplasm around the nucleus. They were revealed by Bodian's method in all cases of multiple system atrophy. They were not found in the case of autosomal dominant olivopontocerebellar atrophy. They were labelled by anti-ubiquitin antibodies, and were negative with anti-tau antibodies. At electron microscopy, they consisted of rectilinear profiles coated with a fuzzy material (diameter: 20-33 nm); this aspect was compatible with microtubules. Oligodendroglial inclusions were prominent in regions selectively vulnerable in multiple system atrophy (tegmentum pontis, putamen, inferior olives, substantia nigra and cerebellar white matter), even in those areas where neuronal loss or fascicular atrophy were minimal or absent. They were also observed in regions considered to be spared in multiple system atrophy, such as the motor cortex and the corpus callosum. Argyrophilic oligodendroglial inclusions are an early and specific marker of multiple system atrophy. It is suggested that autosomal dominant olivopontocerebellar atrophy lacking oligodendroglial inclusions does not belong to multiple system atrophy.

Adult↗

PubMed2001

Interrelations of myogenic response, progressive atrophy of muscle fibers, and cell death in denervated skeletal muscle.

Little is known concerning the time-course and structural dynamics of reactivation of compensatory myogenesis in denervated muscle, its initiating cellular mechanisms, and the relationship between this process and the progression of postdenervation atrophy. The purpose of this study was to investigate the interrelations between temporal and spatial patterns of the myogenic response in denervated muscle and progressive atrophy of muscle fibers. Another objective was to study whether reactivation of myogenesis correlates with destabilization of the differentiated state and death of denervated muscle cells. It has remained unclear whether muscle fiber atrophy was the primary factor activating the myogenic response, what levels of cellular atrophy were associated with its activation, and whether the initiation and intensity of myogenesis depended on the local and individual heterogeneity of atrophic changes among fibers. For this reason, our objective was also to identify the levels of atrophic and degenerative changes in denervated muscle fibers that are correlated with activation of the myogenic response. We found that the reactivation of myogenesis in the tibialis anterior and extensor digitorum longus muscles of the rat starts between days 10-21 following nerve transection, before atrophy has attained advanced level, long before dead cells are found in the tissue. Formation of new muscle fibers reaches its maximum between 2 and 4 months following denervation and gradually decreases with progressive postdenervation atrophy. The myogenic response is biphasic and includes two distinct processes. The first process resembles the formation of secondary and tertiary generations of myotubes during normal muscle development and dominates during the first 2 months of denervation. During this period, activated satellite cells form new myotubes on live differentiated muscle fibers. Most of the daughter myotubes in 1- and 2-month denervated muscle develop on the surface of fast type parent muscle fibers, and some of the newly formed muscle fibers express slow myosin. Some fast type parent fibers are weakly or, more rarely, moderately immunopositive for embryonic isomyosin. This indicates that reactivation of myogenesis may also depend on the fiber type. The level of atrophy, destabilization of the differentiated myofiber phenotype, and degenerative changes of individual fibers in denervated muscle are very heterogeneous. The myogenic response of the first type is associated predominantly with fibers of average and higher than average levels of atrophy. Muscle cells that undergo a lesser degree of atrophy also form daughter fibers, although with a lower incidence. We did not find any correlation between the size of newly formed fibers and the level of atrophy of parent fibers. The topographical distribution of new myotubes both in the peripheral and central areas of the mid-belly equatorial sections at the early stages following nerve transection indicates that myogenesis of the first type represents a systemic reaction of muscle to the loss of neural control. These data indicate that activation of the myogenic response does not depend on cell death and degenerative processes per se. The second type of myogenesis is a typical regenerative reaction that occurs mainly within the spaces surrounded by the basal laminae of dead muscle fibers. Myocytes of different sizes are susceptible to degeneration and death, which indicates that cell death in denervated muscle does not correlate with levels of muscle cell atrophy. The regenerative process frequently results in development of abnormal muscle cells that branch or form small clusters. Replacement of lost fibers becomes activated between 2 and 4 months following nerve transection, i.e., mainly at advanced stages of postdenervation atrophy, when cell death becomes a contributing factor of the atrophic process. In long-term denervated muscle, the first and second types of myogenesisoccur concurrently, and the topographical distribution of the myogenic response becomes more heterogeneous than during the first weeks following denervation. Thus, our data demonstrate differential temporal and spatial expression of two patterns of myogenesis in denervated muscle that appear to be controlled by different regulatory mechanisms during the postdenervation period. (c) 2001 Wiley-Liss, Inc.

Animals↗

PubMed1999

Peripapillary atrophy in primary angle-closure glaucoma: a comparative study with primary open-angle glaucoma.

PURPOSE: To investigate the characteristics of peripapillary atrophy in primary angle-closure glaucoma and to compare peripapillary atrophy in primary angle-closure glaucoma with that in primary open-angle glaucoma. METHODS: Twenty-one eyes (of 21 patients) with chronic primary angle-closure glaucoma that had no evidence of an acute attack or combined-mechanism glaucoma and 31 eyes (31 patients) with primary open-angle glaucoma were enrolled in this study. The cup-to-disk area ratio and the visual field mean deviation were matched in both groups. The prevalence of peripapillary atrophy and peripapillary atrophy-to-disk area ratio of eyes with primary angle-closure glaucoma and eyes with primary open-angle glaucoma were compared. The correlation between the peripapillary atrophy area and the cup-to-disk area ratio or the mean deviation was also evaluated. RESULTS: Eight (38%) of 21 eyes with primary angle-closure glaucoma and 21 (68%) of 31 eyes with primary open-angle glaucoma had peripapillary atrophy. The peripapillary atrophy-to-disk area ratio averaged 0.16 in primary angle-closure glaucoma and 0.41 in primary open-angle glaucoma. There were statistically significant differences regarding the prevalence of peripapillary atrophy (P = .048) and peripapillary atrophy-to-disk area ratio (P = .005) between the two groups. There was no significant correlation between the peripapillary atrophy area and the cup-to-disk area ratio or the mean deviation in primary angle-closure glaucoma. In contrast, the peripapillary atrophy-to-disk area ratio significantly correlated with the cup-to-disk area ratio (P = .003) and the mean deviation (P = .0001) in primary open-angle glaucoma. CONCLUSIONS: The peripapillary atrophy in primary angle-closure glaucoma has a different relationship to the structural and functional optic disk changes than that in primary open-angle glaucoma. Different mechanisms seem to be involved in the development of the optic disk damage in the two types of glaucoma.

Adult↗

PubMed2003

Corpus callosum atrophy, white matter lesions, and frontal executive dysfunction in normal aging and Alzheimer's disease. A community-based study: the Tajiri Project.

BACKGROUND AND OBJECTIVES: Cerebral MRIs of normal aging and Alzheimer's disease (AD) frequently reveal corpus callosum (CC) atrophy, white matter hyperintensity (WMH), and hippocampal atrophy. However, their relationship or the relationship between these findings and cognitive function has not been fully studied. We investigated the relationship between CC atrophy, WMH, and hippocampal atrophy, together with frontal executive dysfunction in both normal aging and AD. METHOD: We examined 170 randomly selected residents from a designated community: 99 Clinical Dementia Rating (CDR) 0 (healthy, control group, HC) participants, 54 CDR 0.5 (very mild AD) patients, and 17 CDR 1 & 2 (probable AD) patients. By means of MRI, WMH and CC atrophy were visually rated. Four portions of the CC and the hippocampal width were measured. A Mini-Mental State Examination and Cognitive Abilities Screening Instrument (CASI) were performed to assess global function. For the frontal function, the CASI subitems of attention and word fluency, letter-based fluency, the Digit Symbol test of the WAIS-R, and Trail Making Tests were performed. RESULTS: Those patients with CDR 1 & 2 had both hippocampal and CC atrophy, whereas the CDR 0.5 patients had only hippocampal atrophy. Frontal executive dysfunction was associated with CC atrophy in both the HC and AD groups. Significant Spearman correlations were noted between CC atrophy and WMH in both groups. The combined effect of CC atrophy and WMH was noted only in the verbal fluency test in the HC group. CONCLUSION: In both groups, CC atrophy was associated with frontal executive dysfunction. The combined effect of CC atrophy and WMH in normal aging was probably due to subclinical ischemic conditions.

Aged↗

PubMed2003

[Prevalence of optic atrophy and associated ocular and systemic diseases in a department of paediatric ophthalmology].

BACKGROUND: Optic atrophy is one of the most common causes of severe visual impairment in children. So far an analysis of ocular and systemic findings comparing patients with and without optic atrophy has not performed. PATIENTS AND METHODS: Ocular and systemic findings of a total of 1042 patients (examination of all patients in May 1995 [N = 485] and May 2001 [N = 557]) of the department of paediatric ophthalmology in Homburg/Saar were retrospectively evaluated and diagnoses of patients with and without optic atrophy were compared. Optic atrophy was diagnosed ophthalmoscopically and in 1/3rd of the patients by VEP as well. RESULTS: 18 % of all patients (N = 188; 87.2 % [N = 164] were children) had optic atrophy. Nearly half of these children were prematurely born (46.7 %). 53.2 % of patients with optic atrophy (N = 88) showed nystagmus (without atrophy: 10.7 %), especially sensory defect nystagmus. Median of visual acuity level was 0.2 with optic atrophy and 0.8 without. Albinism and buphthalmia were common findings. 69.5 % of all patients with optic atrophy suffered from systemic diseases (without atrophy: 25.2 %), especially mental retardation, neurologic findings and oculocutaneous albinism. In 10.4 % more than two systemic diagnoses could be found. 55.3 % of all the patients with optic atrophy were disabled, 31.9 % multiply disabled. CONCLUSIONS: Sequelae of prematurity, peripartal asphyxia and congenital brain damages are the main findings in patients with optic nerve atrophy. Such children are worst-case patients of any paediatric ophthalmology department with a high prevalence of severe visual impairment, mental retardation and multiple disability. Treatment in a specialised center is therefore necessary for an efficient therapy. In addition, the statistical survey shows that in children who survived the critical phases of prematurity secondary damages can lead to persistent impairment and to alterations of visual and general development.

Adolescent↗

PubMed1997

Elevated nerve growth factor levels in cerebrospinal fluid associated with progressive cortical atrophy.

Using a two-site enzyme-linked immunosorbent assay, we measured nerve growth factor (NGF) levels in cerebrospinal fluid (CSF) from 40 patients with or without brain atrophy due to various neurologic disorders. White matter and cortical atrophies were assessed by frontal horn index (FHI) and subarachnoid space area/inner skull space area (SSA/ISSA) ratio, respectively. CT findings of 40 patients were classified into 4 grades: normal (< mean + 2SD), grade I (mean + 2SD < or = or < mean + 4SD), grade II (mean + 4SD < or = < mean + 8SD), and grade III (mean + 8SD < or =). NGF levels in CSF were significantly elevated in 3 of 6 patients with grade III cortical atrophy and normal in 2 with grade II atrophy, 4 with grade I atrophy and 28 without atrophy. Cortical atrophy was progressive in the 3 with NGF elevation in CSF. With respect to white matter atrophy, NGF elevation was observed in none of 3 with grade III white matter atrophy, two of 4 with grade II atrophy, none of 3 with grade I atrophy and one of 30 without atrophy. The symptoms of the two of three with NGF elevation were progressive at the time of obtaining the CSF samples, while those of other patients without NGF elevation were non-progressive. The present study suggests that NGF elevation in CSF may reflect extensive cortical degenerative change.

Adolescent↗

PubMed1998

Histology and cellular kinetics of prostatic atrophy.

This study addresses two issues regarding prostatic atrophy: (1) the histologic features of atrophy as seen on needle biopsy results and how they affect the diagnosis of atrophy and (2) the cellular kinetics of atrophy and what it suggests about the mechanism of atrophy. We reviewed hematoxylin and eosin sections for 103 prostate needle biopsy specimens with atrophy. Each biopsy specimen was classified as either simple atrophy (large atrophic glands without crowding: 53 cases) or postatrophic hyperplasia (PAH) (crowded focus of small atrophic acini: 50 cases). Cell proliferation in both the atrophic and benign glands was evaluated in 103 cases by immunohistochemistry using antibodies against MIB-1. The TdT-mediated dUTP-biotin nick-end labeling technique was performed on 61 cases to quantitate apoptosis in atrophic and benign glands. Thirty-two percent of cases showed chronic inflammation, 21% showed acute inflammation, 14% showed nucleoli, and 1% showed mitoses. In comparison to simple atrophy, PAH contained more frequent prominent nucleoli (p < 0.0001) and acute inflammation (p < 0.0001), yet not chronic inflammation. In a multivariate analysis, acute inflammation and PAH pattern influenced the presence of prominent nucleoli. Staining for MIB-1 was greater in atrophic (27.5 cells/1000 cells) than in benign glands (3.5 cells/1000 cells), greater in PAH than in simple atrophy (p = 0.0015), and greater with acute (p = 0.05) but not chronic inflammation. In a multivariate analysis, only the pattern of atrophy and not acute inflammation was found to influence MIB-1. The rate of apoptosis was negligible in both the benign and atrophic glands, did not vary with pattern of atrophy, and did not correlate with MIB-1. Despite the atrophic appearance, atrophic glands in PAH show more proliferative activity than benign, nonatrophic glands and show no evidence of active involution, justifying the term "postatrophic hyperplasia" for this pattern of atrophy. Prominent nucleoli are seen more frequently in postatrophic hyperplasia, even in the absence of acute inflammation. To avoid a potential erroneous diagnosis of cancer, a constellation of features suggestive of malignancy should be considered, rather than relying on prominent nucleoli as the sole criteria for the diagnosis of prostate cancer.

Antigens, Nuclear↗

PubMed2005

Clinical implications of peripapillary atrophy in glaucoma.

PURPOSE OF REVIEW: To elucidate peripapillary atrophy in glaucomatous optic neuropathy; its ranking in the morphologic diagnosis of the glaucoma, and its value for the differentiation of various types of chronic open-angle glaucoma, for the separation of glaucomatous eyes from nonglaucomatous eyes, and for the detection of progression of glaucoma. RECENT FINDINGS: Recent studies showed an association of peripapillary atrophy with glaucoma and the eventual development of glaucomatous disc hemorrhages independent of a small neuroretinal rim area, and an association between increasing peripapillary atrophy and progressive glaucoma. A ranking of optic disc parameters to detect glaucomatous damage revealed that the alpha and beta zones of peripapillary atrophy, compared with neuroretinal rim parameters, are less useful. Pseudoexfoliation syndrome without glaucoma is not a risk factor for peripapillary atrophy. In arteritic anterior ischemic optic neuropathy, peripapillary atrophy does not enlarge. Peripapillary atrophy does not differ markedly between Europeans and South Indians. In contrast to the position of the central retinal vessel trunk, the presence and position of cilioretinal arteries do not markedly influence the progression of peripapillary atrophy in glaucoma. SUMMARY: Peripapillary chorioretinal atrophy is one among several morphologic variables to detect glaucomatous abnormalities. Ranking optic disc variables for the detection of glaucomatous optic nerve damage, peripapillary atrophy is a variable of second order. It is useful for the differentiation of various types of chronic open-angle glaucomas. In contrast to glaucomatous eyes, eyes with nonglaucomatous optic nerve atrophy, including eyes after arteritic anterior ischemic optic neuropathy, do not show an enlarged peripapillary atrophy.

Animals↗

PubMed2004

Hippocampal and prefrontal atrophy in patients with early non-demented Parkinson's disease is related to cognitive impairment.

BACKGROUND: Early stage patients with Parkinson's disease (PD) show cognitive impairment in frontal lobe functions and memory tests. Hippocampal atrophy is seen in medicated patients with advanced PD. OBJECTIVES: To examine whether prefrontal or hippocampal atrophy are already present in early stage PD, and whether such atrophy is associated with cognitive impairment. METHODS: Twenty non-medicated, non-demented patients with early stage PD and 22 neurologically healthy age matched controls were studied. All subjects underwent magnetic resonance imaging to study hippocampal and prefrontal atrophy. Atrophy was evaluated by a neuroradiologist using a five point scale. In addition, the patients underwent a neuropsychological test battery sensitive to frontal lobe functions and memory. RESULTS: Patients with PD had atrophy in the right and the left prefrontal cortex. In the right hippocampus, the mean atrophy score was 1.15 in PD and 0.45 in controls. Corresponding figures for the left hippocampus were 1.05 for PD and 0.64 for controls. In PD, the left hippocampus atrophy correlated with verbal memory and prefrontal atrophy correlated with impaired performance in a test measuring vigilance. CONCLUSIONS: Non-medicated, non-demented patients with early stage PD show hippocampal and prefrontal atrophy. Impaired memory is related to hippocampal atrophy, whereas sustained attention is related to prefrontal atrophy.

Aged↗

PubMed2004

Central nervous system atrophy and clinical status in multiple sclerosis.

In this review, the authors focus on clinical aspects of central nervous system (CNS) atrophy in multiple sclerosis (MS), including the relationship between atrophy and disability, disease course, disease duration, quality of life, and fatigue. Cross-sectional studies have demonstrated a moderate but significant correlation between brain or spinal cord atrophy and physical disability in patients with MS. Longitudinal studies (>/= 5 years) have shown that CNS atrophy is a significant predictor of subsequent long-term neurologic deterioration. The clinical relevance of CNS atrophy is reinforced by studies showing that atrophy accounts for more variance than conventional lesion measures in predicting disability. Impaired quality of life and both urodynamic and sexual dysfunction, but not fatigue, are associated with brain atrophy. It is likely that once the level of CNS atrophy reaches a critical threshold, patients begin to suffer clinical impairment and disease progression. Longitudinal studies suggest that CNS atrophy may occur in patients with clinically isolated demyelinating syndromes who are at high risk for developing clinically definite MS. Longitudinal natural history studies in relapsing-remitting, secondary progressive, and primary progressive MS have suggested that patients develop CNS atrophy at a faster rate in the first few years of disease than later in the disease course. Similarly, long-term follow-up studies have shown a poor relationship between disease duration and the rate of brain atrophy. The authors conclude that measurement of atrophy of the CNS is emerging as a clinically relevant biomarker of the MS disease process.

Atrophy↗

PubMed2006

[Efficacy of intravenous immunoglobulin for slowly progressive cerebellar atrophy].

In slowly progressive cerebellar atrophy, it has been difficult to suppress the progression of cerebellar symptoms because no effective therapeutic agents are available when the diagnosis of secondary cerebellar atrophy, such as drug-induced cerebellar atrophy or paraneoplastic syndrome, is denied. However, amongst the different forms of slowly progressive cerebellar atrophy, some may be associated with treatable immune abnormalities. Therefore, we investigated the therapeutic efficacy of intravenous immunoglobulin (IVIg) in 9 patients with slowly progressive cerebellar atrophy (4 sporadic atrophy; 5 hereditary atrophy). The results were as follows. With regard to the 4 cases of sporadic atrophy, gait ataxia and imbalance were markedly improved in 1 patient who had positive anti-GAD antibody. Moderate improvement was seen in 1 patient and slight improvement in 2. With regard to the 5 cases of hereditary atrophy, gait ataxia and imbalance were moderately improved in 2 patients with SCA3, although there were 3 non-responders. In conclusion, our study results suggested that not only patients with sporadic atrophy but also some with hereditary atrophy may respond to therapy. In cases of slowly progressive cerebellar atrophy in which the cause may be due to immune abnormality, we should consider instituting active immunotherapy when a pathological state caused by immune abnormality is suspected after extensive evaluations of autoantibodies, including anti-GAD, anti-thyroid and anti-gliadin antibody, malignancy, and so on.

Aged↗

PubMed1993

Effect of age, Helicobacter pylori infection, and gastritis with atrophy on serum gastrin and gastric acid secretion in healthy men.

Gastric acid secretion has been considered to decline with increasing age but this view is being re-evaluated as the importance of Helicobacter pylori infection emerges. This study aimed to determine the effect of age, H pylori, and gastritis with atrophy on the serum gastrin concentration, gastric secretory volumes, and acid output in healthy, asymptomatic men. Young men (mean (SD) age 22.9 (0.6) years; n = 22) were compared with old men (72.9 (1.2) years; n = 28) in respect of basal serum gastrin and basal, sham fed, pentagastrin stimulated maximal and peak acid secretion. Antral, corpus, and fundal biopsy specimens were taken for histology and H pylori status (histology, culture, and rapid urease test). H pylori associated gastritis was present in three of 22 young (13.6%) and 16 of 28 old (57.1%) men. Gastritis with atrophy was present in 11 old subjects, 10 of whom were H pylori positive. These subjects had higher mean (SD) serum gastrin concentrations than old subjects without atrophy and young subjects (61.8 (9.2); 40.0 (2.9); 36.8 (2.3) pmol/l respectively; p < 0.001). H pylori infected subjects had higher gastrin values than uninfected subjects, overall (55.3 (5.9); 36.0 (1.8) pmol/l; p < 0.001) and in subjects without atrophy (45.3 (4.2); 36.0 (1.8) pmol/l; p < 0.03). In subjects without H pylori infection, gastrin values did not differ with age (old 37.1 (1.7); young 35.4 (2.1) pmol/l). The maximal gastric secretory volume was lower in old subjects with atrophy. Acid output (mmol/h) in subjects with atrophy was lower than in subjects with no atrophy (basal: 3.0(1.1); 5.1(0.7); p=NS; sham led: 5.4 (1.4); 9.3 (0.8); p<0.02; maximal: 18.9 (4.0); 31.4(1.8); p<0.002; peak: 25.1(5.3); 43.4(2.7); p<0.003). However, acid secretion in old subjects without atrophy was not different to that in young subjects, irrespective of H pylori status. These results did not differ when acid output was expressed as mmol/h/kg lean body mass or mmol/h/kg fat free body weight. Using multiple linear regression analysis, gastritis with atrophy was the only factor that had an independent negative effect on acid secretion. In healthy men without atrophy, gastric acid secretion is preserved with ageing and is independent of H pylori status. Atrophy, which is closely related to H pylori infection, is associated with a decline in acid secretion. Increased basal serum gastrin is related to both atrophy and H pylori infection but not to ageing per se.

Adolescent↗

PubMed1988

Multiple sclerosis and corpus callosum atrophy: relationship of MRI findings to clinical data.

Among 110 patients (45 men, 65 women), aged 15 to 66, with clinical and/or biological diagnosis of multiple sclerosis (MS), severe to moderate corpus callosum (CC) atrophy was observed in 67 (60%) patients. Correlation between CC atrophy, brain atrophy, duration and severity of clinical symptoms, and high signal white matter areas, was carried out in 90 patients. Mean age was 46 years for patients with severe CC atrophy, and 33 years for those without atrophy. Mean duration of the disease was 14 years in patients with severe atrophy, and 5 years in patients without atrophy. Severity of clinical symptoms is more pronounced in patients with severe CC atrophy. Numerous or large white matter high signal areas are observed in patients with severe CC atrophy on T2-weighted images. CC atrophy appears earlier than brain atrophy in the course of MS.

Adolescent↗