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At least 631 records · Page 35Linked to original sources

PubMed2006

Myostatin gene deletion prevents glucocorticoid-induced muscle atrophy.

Glucocorticoids mediate muscle atrophy in many catabolic states. Myostatin expression, a negative regulator of muscle growth, is increased by glucocorticoids and myostatin overexpression is associated with lower muscle mass. This suggests that myostatin is required for the catabolic effects of glucocorticoids. We therefore investigated whether myostatin gene disruption could prevent muscle atrophy caused by glucocorticoids. Male myostatin knockout (KO) and wild-type mice were subjected to dexamethasone treatment (1 mg/kg.d for 10 d or 5 mg/kg.d for 4 d). In wild-type mice, daily administration of low-dose dexamethasone for 10 d resulted in muscle atrophy (tibialis anterior: -15%; gastrocnemius: -13%; P < 0.01) due to 15% decrease in the muscle fiber cross-sectional area (1621 +/- 31 vs. 1918 +/- 64 microm(2), P < 0.01). In KO mice, there was no reduction of muscle mass nor fiber cross-sectional area after dexamethasone treatment. Muscle atrophy after 4 d of high-dose dexamethasone was associated with increased mRNA of enzymes involved in proteolytic pathways (atrogin-1, muscle ring finger 1, and cathepsin L) and increased chymotrypsin-like proteasomal activity. In contrast, the mRNA of these enzymes and the proteasomal activity were not significantly affected by dexamethasone in KO mice. Muscle IGF-I mRNA was paradoxically decreased in KO mice (-35%, P < 0.05); this was associated with a potentially compensatory increase of IGF-II expression in both saline and dexamethasone-treated KO mice (2-fold, P < 0.01). In conclusion, our results show that myostatin deletion prevents muscle atrophy in glucocorticoid-treated mice, by blunting the glucocorticoid-induced enhanced proteolysis, and suggest an important role of myostatin in muscle atrophy caused by glucocorticoids.

Animals↗

PubMed2003

Atrophy rates of entorhinal cortex in AD and normal aging.

OBJECTIVES: To explore the atrophy rate of entorhinal cortex (ERC) in AD and normal aging and assess the value of rate measurement of ERC atrophy for classifying subjects with AD from cognitively normal (CN) control subjects. METHODS: Twenty-one AD patients and 23 CN subjects had MRI scans and clinical evaluations twice within 1.8 +/- 0.6 years. ERC volumes were manually measured on volumetric T1-weighted MR images. RESULTS: Patients with AD had a greater annual percentage volume change of ERC than CN subjects on both sides (left: 6.8 +/- 4.3%/year for AD vs 1.4 +/- 2.5%/year for CN [F(1,42) = 25.6, p < 0.001]; right: 6.3 +/- 3.3%/year for AD vs 1.4 +/- 2.3%/year for CN [F(1,42) = 25.6, p < 0.001]). Furthermore, increased ERC atrophy rate was correlated (r = -0.56, p = 0.01) with decreased memory performance in AD. CN subjects had on average annual ERC atrophy rates greater than zero (p < 0.01). Baseline volume of ERC predicted atrophy rate of ERC (left: r = -0.53, p < 0.01; right: r = -0.42, p < 0.05) in CN subjects but not in AD subjects. Using ERC baseline volumes alone resulted in 77% overall correct classification (p < 0.01) between AD and CN subjects, with 76% sensitivity and 78% specificity and an area under receiver operator characteristic (ROC) curve of 0.83. Adding annual atrophy rate of ERC to the model accounted for most of the variance (p < 0.01), diminishing contributions from baseline volume and yielding 82% overall classification, with 76% sensitivity and 86% specificity and an area under the ROC curve of 0.93. CONCLUSION: ERC volume loss over time may be a better indicator for AD than cross-sectional measurements.

Aged↗

PubMed2003

Atrophy of superior cerebellar peduncle in progressive supranuclear palsy.

BACKGROUND: Pathologic changes in the superior cerebellar peduncles (SCP) are common in progressive supranuclear palsy (PSP), but atrophy of the SCP has never been systematically studied. OBJECTIVE: To investigate the SCP width in PSP cases and controls with morphometric methods. METHODS: The mean width of the SCP in transverse sections of the pons at the level of trigeminal nerve was determined in 48 PSP cases (29 men, 19 women; mean age 72.5 +/- 8.2 years) and 29 age-matched control subjects, many with neurodegenerative disorders that can be clinically mistaken for PSP. As the origin of the SCP is the cerebellar dentate nucleus, correlations were sought between SCP atrophy and severity of grumose degeneration in the dentate nucleus. RESULTS: The average width of the SCP was less in PSP (range 0.09 to 0.24 cm) than in controls (range 0.21 to 0.43 cm; Mann-Whitney U test, p < 0.001), including control cases that had been clinically misdiagnosed as PSP (range 0.26 to 0.41 cm). Severity of SCP atrophy normalized by brain weight correlated with disease duration (Spearman rank order correlation, r = 0.367, p = 0.028), suggesting that SCP atrophy is a relatively early feature of PSP. No correlation was found between grumose degeneration and SCP width. CONCLUSIONS: SCP atrophy is common in PSP and correlates with disease duration. Given that measurements of the SCP are within the resolution of MRI, it remains to be determined if SCP atrophy can be used as a diagnostic marker of PSP.

Adult↗

PubMed1981

Cerebral atrophy and functional deficits in alcoholics without clinically apparent liver disease.

Ninety-seven chronic alcoholics, both impaired and unimpaired, without clinically evident liver disease, showed significantly more cerebral atrophy on computed tomography than age-matched neurologic controls. Age was the variable most highly correlated with cerebral atrophy measurements, and it accounted for most of the correlations between atrophy and functional impairment, except in the Wernicke-amnesic group. Analysis of the slopes of atrophy scores versus age showed a more rapid "rate" of development of cerebral atrophy in alcoholics compared with controls. There were no correlations between liver biopsy scores (51 cases), drinking history (47 cases), or dietary intake (39 cases) and cerebral atrophy measurements.

Adult↗

PubMed1999

A longitudinal study of brain atrophy in relapsing multiple sclerosis. The Multiple Sclerosis Collaborative Research Group (MSCRG).

OBJECTIVE: To determine if progressive brain atrophy could be detected over 1- and 2-year intervals in relapsing MS, based on annual MR studies from the Multiple Sclerosis Collaborative Research Group (MSCRG) trial of interferon beta-1a (Avonex). METHODS: All subjects had mild to moderate disability, with baseline expanded disability status scores ranging from 1.0 to 3.5, and at least two relapses in the 3 years before study entry. Atrophy measures included third and lateral ventricle width, brain width, and corpus callosum area. RESULTS: Significant increases were detected in third ventricle width at year 2 and lateral ventricle width at 1 and 2 years. Significant decreases in corpus callosum area and brain width were also observed at 1 and 2 years. Multiple regression analyses suggested that the number of gadolinium-enhancing lesions at baseline was the single significant contributor to change in third ventricle width. Atrophy over 1 and 2 years as indicated by enlargement of the third and lateral ventricle and shrinkage of the corpus callosum was greater for patients entering the trial with enhancing lesions. Greater disability increments over 1 and 2 years were associated with more severe third ventricle enlargement. CONCLUSION: In patients with relapsing MS and only mild to moderate disability, significant cerebral atrophy is already developing that can be measured over periods of only 1 to 2 years. The course of cerebral atrophy in MS appears to be influenced by prior inflammatory disease activity as indicated by the presence of enhancing lesions. Brain atrophy measures are important markers of MS disease progression because they likely reflect destructive and irreversible pathologic processes.

Adjuvants, Immunologic↗

PubMed1999

Exocrine pancreatic atrophy in German Shepherd Dogs and Rough-coated Collies: an end result of lymphocytic pancreatitis.

Previously published studies of the pathology of canine exocrine pancreatic insufficiency (EPI) have been based on morphological findings during the clinical phase of the disease, when atrophy of acinar parenchyma occurs. Recently, low serum trypsinlike immunoreactivity (TLI) concentration has been shown to precede clinical signs, making it possible to diagnose EPI prior to onset of the clinical disease. This study presents histological and ultrastructural findings of pancreatic biopsies from 11 German Shepherd Dogs and 2 Rough-coated Collies with subclinical EPI (SEPI). These findings were compared with those from dogs with clinical EPI (n = 11) and healthy control dogs (n = 5). Biopsied tissue from dogs with SEPI typically contained both normal and atrophied acinar parenchyma. The most significant finding was the marked lymphocytic infiltration, which was most prevalent at the border zone of affected and nonaffected parenchyma but had spread into the normal acinar tissue. Numerous intraacinar lymphocytes were found. Most of the lymphocytes were positive by immunostaining for CD3. In more advanced stages of destruction, the findings were characteristic of pancreatic acinar atrophy. In the atrophied parenchyma, the inflammatory reaction, if present, was less prominent. Ultrastructural changes were in accordance with those of the histological study showing infiltration of lymphocytes both in affected acini and in acini that revealed no obvious ultrastructural changes. Progressive degenerative changes of acinar cells were considered a nonspecific finding. Apoptotic death of acinar cells was occasionally found. The inflammatory reaction was clearly shown to precede the pancreatic acinar atrophy, and the findings suggested that lymphocytic pancreatitis leads to atrophy of the pancreas. The possibility that EPI is an immune-mediated disease in German Shepherd Dogs and Rough-coated Collies is discussed.

Animals↗

PubMed1998

Molecular analysis and electromyoneurographic abnormalities in Croatian children with proximal spinal muscular atrophies.

Childhood onset proximal spinal muscular atrophy presents with considerable clinical variability. This study included 14 Croatian children aged 11 days to 8 years with spinal muscular atrophy types I-III verified clinically and electromyoneurographically. DNA of affected children was screened for deletions of exons 7 and 8 of the survival motor neuron gene and for deletion of exon 5 of the neuronal apoptosis inhibitor protein gene. Motor nerve conduction velocity and compound muscle action potential amplitude were decreased in children with spinal muscular atrophy type I and II. Deletions of exons 7 and 8 of the survival motor neuron gene and of exon 5 of the neuronal apoptosis inhibitor protein gene in children with spinal muscular atrophy type I-II suggested existence of more genetic abnormalities as compared to type III. A decrease in compound muscle action potential amplitude and motor nerve conduction velocity in children with spinal muscular atrophy correlated with the disease severity, probably as a result of axonal degeneration. Phenotypic severity in children onset spinal muscular atrophy is directly correlated with the extent of survival motor neuron and neuronal apoptosis inhibitor protein exon deletions.

Child↗

PubMed2001

Brain and spinal cord atrophy in multiple sclerosis: role as a surrogate measure of disease progression.

Magnetic resonance imaging (MRI) reveals that brain and spinal cord atrophy occur early in the course of multiple sclerosis (MS), far earlier than originally anticipated. This has important implications for the early treatment of patients with MS, as atrophy is thought to reflect destructive, irreversible pathology, and subclinical impairment if not overt disability. Several recent trials in MS have included atrophy as a secondary or exploratory measure of treatment efficacy. While measured cerebral volume or spinal cord area changes are small over 1 to 3 year intervals, they are sufficiently large that with current methodologies the atrophy measures should provide conclusive information as to the effectiveness of therapeutic interventions in halting progressive atrophy. Atrophy measures may also provide an important metric for the evaluation of disease in primary progressive MS, and in testing combined therapies and neuroprotective agents, where conventional MRI methodologies may be relatively weak.

Atrophy↗

PubMed1997

Hemispheric cerebral atrophy after traumatic extra-axial hematoma in adults.

The relationship between traumatic extra-axial hematomas and cerebral atrophy was investigated in 42 adult patients aged between 15 and 50 years who required removal of extra-axial hematomas. These patients were followed up by serial computed tomography for more than 6 months after head injury. Nine of these patients developed cerebral atrophy. Their Glasgow Coma Scale score on admission was 6.4 +/- 2.8 (mean +/- SD). The score of the patients without cerebral atrophy was 9.6 +/- 3.3 (p < 0.01). These patients had three extradural and six subdural hematomas. All patients with cerebral atrophy had cerebral swelling postoperatively, more prominent in the hemisphere ipsilateral to the hematoma in seven patients. This swelling was associated with global hypodensity and persisted for 10.4 +/- 2.9 days. The severity of cerebral atrophy was more prominent in the hemisphere ipsilateral to the hematoma in five of these seven patients. Extra-axial hematoma in patients with severe head injury can induce hemispheric cerebral atrophy in the underlying cerebral hemisphere.

Adolescent↗

PubMed2006

MRI in evaluating atrophy of the external anal sphincter in patients with fecal incontinence.

OBJECTIVE: External anal sphincter atrophy seen at endoanal MRI may predict poor outcome of surgical anal sphincter repair for an external anal sphincter defect. The purposes of this study were to compare external phased-array MRI to endoanal MRI for depicting external anal sphincter atrophy in patients with fecal incontinence and to evaluate observer reproducibility in detecting external anal sphincter atrophy with these techniques. SUBJECTS AND METHODS: Thirty patients with fecal incontinence (23 women, seven men; mean age, 58.7 years; age range, 37-78 years) underwent both endoanal and external phased-array MRI. Images were evaluated for external anal sphincter atrophy by three radiologists. Measures of differences and agreement between both MRI techniques and of interobserver and intraobserver agreement of both techniques were calculated. RESULTS: The MRI techniques did not significantly differ in their ability to depict external anal sphincter atrophy (p = 0.63) with good agreement (kappa = 0.72). Interobserver agreement was moderate (kappa = 0.53-0.56) for endoanal MRI and moderate to good (kappa = 0.55-0.8) for external phased-array MRI. Intraobserver agreement was moderate to very good (kappa = 0.57-0.86) for endoanal MRI and fair to very good (kappa = 0.31-0.86) for external phased-array MRI. CONCLUSION: External phased-array MRI is comparable to endoanal MRI in depicting external anal sphincter atrophy and, thereby, in selecting patients for anal sphincter repair. Because results among interpreters varied considerably depending on the experience level, both techniques can be recommended in the diagnostic workup of fecal incontinence only if sufficient experience is available.

Adult↗

PubMed1993

White matter lesions and cerebral atrophy on MR images in patients with and without AIDS dementia complex.

OBJECTIVE: The objective of this study was threefold: to determine if the frequency of deep white matter changes and cerebral atrophy seen on MR images is significantly different between patients with and without AIDS dementia complex, to determine if certain patterns of white matter changes are more closely associated with AIDS dementia complex, and to determine if focal lesions within the white matter of the splenium are more common in AIDS dementia complex. MATERIALS AND METHODS: Forty-five patients with AIDS were clinically examined for AIDS dementia complex. MR images from these patients were retrospectively reviewed without knowledge of the clinical results. The presence or absence of white matter abnormalities and cerebral atrophy was evaluated by using graded scales and correlated with the presence or absence of AIDS dementia complex. RESULTS: Ten patients met the criteria for AIDS dementia complex. Eight of 25 patients in whom MR images showed abnormal signal intensity in deep white matter had dementia compared with two of 20 in whom MR showed no changes in deep white matter. The presence of these deep white matter abnormalities was not significantly different between groups with and without dementia (p = .08), although higher grades of deep white matter abnormality were more likely to be associated with AIDS dementia complex. Nine of 19 patients in whom MR images showed atrophy had dementia compared with one of 26 in whom MR showed no atrophy. Atrophy was significantly associated with AIDS dementia complex (p = .001). Eight of 15 patients in whom MR images showed abnormal signal intensity within the white matter of the splenium had dementia compared with two of 30 in whom MR showed normal signal intensity in this area. The degree of abnormality in the splenium was weakly associated with AIDS dementia complex (Kendall's tau = .471, p = .001). CONCLUSION: MR findings of cerebral atrophy and abnormal signal intensity in the splenium are associated with AIDS dementia complex. The presence of generalized deep white matter abnormalities does not differ significantly between patients with and without dementia, although more severe grades of white matter abnormality are more likely to be seen in patients with AIDS dementia complex.

AIDS Dementia Complex↗

PubMed1991

The role of apoptosis in the development of renal cortical tubular atrophy associated with healed experimental renal papillary necrosis.

An animal model of chronic analgesic nephropathy, in which renal papillary necrosis was induced by the administration of a single injection of bromoethylamine 2-hydrobromide in male Sprague-Dawley rats, was used to investigate the pathogenesis of the atrophy of tubules that leads to cortical atrophy or 'scarring' in analgesic nephropathy. One of the major objectives was documentation of the participation of apoptosis, a distinctive mode of cell death, in the process of cortical tubular atrophy. Control and treated groups of animals were studied at 2 wks, and at subsequent monthly intervals up to 4 mths. At each time, light microscopy and ultrastructure were used to relate changes in cellular pathology to alterations in renal mass. Apoptosis was quantitated in paraffin sections, and autoradiographic identification of cells showing tritiated thymidine uptake was used as an indication of cell proliferation. In animals with total renal papillary necrosis (RPN), focal or diffuse cortical atrophy developed, the extent of which appeared to be proportional to the extent of the RPN. Renal mass was reduced only in those kidneys that developed extensive, diffuse lesions. Compensatory renal growth occurred in the areas of healthy tissue adjacent to the foci of atrophy, with both cellular hyperplasia and hypertrophy playing roles in its development. One of the prominent cellular events was the appearance of apoptotic cells and bodies, with invading intraepithelial macrophages involved in their phagocytosis and degradation. We propose that this form of cell death plays an important role in the pathogenesis of cortical atrophy. Current descriptions of the cortical lesions that occur in analgesic nephropathy refer to the changes as 'scars'. Although the focal lesions have a macroscopic appearance that resembles scars, the results of the present study indicate that usage of this terminology may be misleading, since scarring is often described after severe tissue injury or necrosis, which was not identified in the present study.

Animals↗

PubMed2001

Incidence and clinical profile of extra-medial-temporal epilepsy with hippocampal atrophy.

We tried to investigate the incidence and the clinical profile of intractable epilepsy with hippocampal atrophy and ictal onset zones located in areas other than the hippocampus (extra-medial-temporal epilepsy; EMTE). We included patients who had hippocampal atrophy confirmed by MRI but with extra-medial-temporal ictal onset zones as verified by invasive intracranial electrodes or video-EEG monitoring. The case histories, interictal EEG, ictal semiology, other MRI findings in addition to hippocampal atrophy, and results of ictal SPECT and PET scans were evaluated. Results were compared with those of surgically proven medial temporal lobe epilepsy with hippocampal atrophy recruited during the same period. 8.5% of the intractable epilepsy patients with hippocampal atrophy had extra-medial temporal epileptogenic zones. A history of encephalitis and hemiconvulsion-hemiparesis were significantly common in the EMTE group. Most of the interictal EEGs of EMTE patients showed extratemporal irritative zones. MRI, ictal SPECT, and FDG-PET seemed to be helpful at localizing the true epileptogenic zones. The predominant EMTE seizure type was focal motor seizure with secondary generalization. Some portion of intractable epilepsy patients with hippocampal atrophy had extra-medial-temporal epileptogenic foci and careful analysis of semiology and neuroimagings could yield clues to correct diagnosis.

Adult↗

PubMed2006

Isolated teres minor atrophy: manifestation of quadrilateral space syndrome or traction injury to the axillary nerve?

This article prospectively determines through magnetic resonance imaging (MRI) the incidence of isolated teres minor atrophy and its gender and age distribution, and documents associated findings related to the rotator cuff, labroligamentous complex, and quadrilateral space. Two hundred seventeen consecutive shoulder MRI examinations performed over a 3-month period were prospectively reviewed and evaluated for isolated teres minor atrophy. Twelve (5.5%) patients had non-compressive isolated teres minor atrophy. Ninety-two percent (n=11) of these patients had rotator cuff or labroligamentous complex tears. No patients had an associated mass within the quadrilateral space. The average patient age was 60 years and 11 of the 12 patients were male. Isolated teres minor atrophy on MRI is most commonly seen in older patients who do not fit the expected clinical presentation of quadrilateral space syndrome. The anatomical relationship of the teres minor nerve to the joint capsule and the frequency of associated shoulder injuries in these patients raises the possibility of an association between humeral decentering and teres minor atrophy. Quadrilateral space syndrome would appear to be a very rare cause of isolated teres minor atrophy.

Adult↗

PubMed2005

Optic disc morphometry with optical coherence tomography: comparison with planimetry of fundus photographs and influence of parapapillary atrophy and pigmentary conus.

PURPOSE: Optical coherence tomography (OCT) is an established method for visualising macular pathology and for measuring the thickness of parapapillary retinal nerve fibre layer. The purpose of the present study was to compare OCT measurements of the optic disc with those obtained by planimetry of fundus photographs and to investigate whether OCT measurements are influenced by the amount of parapapillary atrophy or pigmentary conus at the disc margin. MATERIALS AND METHODS: Eighty-two eyes of 41 randomly selected Asian-Indian subjects were included. The mean age was 44.2+/-14.3 years (mean+/-SD). All eyes underwent optic disc assessment by OCT (fast optical disc protocol) and digital 20 degree disc photos.. Planimetry of the discs were performed by outlining the disc and the cup. The amount of parapapillary atrophy (zone beta) was quantified as the number of clock-hours around the disc with adjacent parapapillary atrophy. The same procedure was performed to quantify the amount of pigmentary conus around the disc. RESULTS: Mean+/-SD disc size and mean+/-SD cup size in OCT measurements (2.37+/-0.51, 1.29+/-0.55) were significantly smaller than in photographic planimetry (2.83+/-0.62, 1.56+/-0.5: P<0.001, P<0.001). Optic discs with parapapillary atrophy (P=0.2) in their relative difference of disc sizes between OCT and planimetry. Similarly, optic discs with pigmentary conus (n=12) and discs without pigmentary conus (n=70) did not differ significantly (P=0.65). The relative difference in disc size between the two measurement modalities did not correlate with the amount of parapapillary atrophy (r=-0.17, P=0.29) or with the amount of pigmentary conus (r=-0.04, P=0.9). CONCLUSION: OCT analysis of the optic disc produces significantly smaller parameters, compared to the established method of optic disc planimetry. Neither presence, nor extent of parapapillary atrophy zone beta and pigmentary conus seems to produce a systematic error in measurements of disc size with the OCT.

Adolescent↗

PubMed2006

Grb2-associated binder 1 polymorphism was associated with the risk of Helicobactor pylori infection and gastric atrophy.

BACKGROUND: Various single nucleotide polymorphisms (SNPs) have explained the association between Helicobacter pylori (H. pylori) and gastric atrophy and cancer. This study investigated the associations of Grb2 associated binder 1 (Gab1) polymorphism and the combination of PTPN11 gene encoding src homology 2 domain-containing protein tyrosine phosphatase-2 (SHP2) and Gab1 gene with gastric cancer and gastric atrophy among H. pylori seropositive subjects. METHODS: A single nucleotide polymorphism at intron 2 of Gab1 (JST164345) was examined for 454 Japanese health checkup examinees (126 males and 328 females) aged 35 to 85 without a history of gastric cancer and 202 gastric cancer patients (134 males and 68 females) aged 33 to 94 with pathologically confirmed diagnosis of gastric adenocarcinoma. RESULTS: The decreased OR of the Gab1 A/A for H. pylori seropositivity was 0.25 (95% confidence interval (CI): 0.08-0.71). Among seropositive healthy controls, the OR of the Gab1 G/A+A/A for gastric atrophy was significant (OR=1.95, 95% CI: 1.12 -3.40). Seropositive individuals with PTPN11 G/G and Gab1 G/A+A/A demonstrated the highest risk of gastric atrophy with significance (OR=3.49, 95% CI: 1.54-7.90) relative to PTPN11 G/A+A/A and Gab1 G/G, the lowest risk combination, as a reference. However, the gene-gene interaction between PTPN11 and Gab1 was not observed (OR=1.39, 95% CI: 0.41-4.66). Compared to gastric cancer case, the Gab1 did not influence the step of atrophy/metaplasia-gastric cancer sequence. CONCLUSIONS: This study represents that the Gab1 polymorphism was associated with the low risk of H. pylori infection and the high risk of gastric atrophy among seropositive healthy controls, and that seropositive individuals with PTPN11 G/G and Gab1 G/A+G/G were associated with the greatest risk of gastric atrophy. These findings require confirmation in much larger studies.

Adaptor Proteins, Signal Transducing↗

PubMed1998

[Clinico-MRI study of hemispheric disorder in long-term follow-up cases of multiple system atrophy].

Twelve cases of multiple system atrophy (MSA) were studied for clinical and MRI findings of the cerebral hemispheric involvement. The subjects consisted of five olivopontocerebellar atrophy (OPCA) type and seven striatonigral degeneration (SND) type. The age at onset was 56.7 +/- 8.0 (M +/- SD) years, duration of illness at the first MRI study 3.2 +/- 1.1 years, duration of illness at the last study 8.1 +/- 2.2 years, and the following up duration 4.9 +/- 2.0 years. The grasping phenomenon was observed in 70% of the cases examined, snout reflex in 80%, slowness of verbal response in 88%, and decrease of spontaneous speech in 100%. Three cases finally fell into the state of mutism. Three out of ten cases were categorized as dementia by HDS-R (Hasegawa Dementia Scale-Revised) test. Besides the progression of the pontocerebellar atrophy and putaminal changes, MRI study revealed progressive frontal lobe atrophy in most cases. At six years after the onset, SND type showed significantly higher incidence of conspicuous frontal lobe atrophy and dilatatation of the Sylvian fissure than OPCA type. Cerebral ventricular dilatation was common feature, and atrophy of the temporal and occipital lobes were observed in several cases. We indicated the possible involvement of the cerebral hemisphere, especially the frontal lobe, and higher nervous function in MSA.

Adult↗

PubMedDate not supplied

[Cortical atrophy in computerized tomography of the brain and clinical characteristics of schizophrenia].

The aim of this paper was searching for correlates of cortical atrophy in schizophrenia. Schizophrenic patients with cortical prefrontal atrophy had more negative symptoms than patients with generalized cortical atrophy and patients without cortical atrophy (the difference was not statistically significant). They also had less positive symptoms than patients without atrophy (the difference was statistically significant) and patients with generalized cortical atrophy.

Adolescent↗