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PubMed1995

Gastric atrophy and regional variation in upper gastrointestinal disease.

OBJECTIVE: To compare the upper gastrointestinal disease profiles of Helicobacter pylori-infected patients drawn from two distinct regions of China, one with a low incidence of gastric cancer (Guangzhou) and the other with a high incidence of gastric cancer (Lanzhou). The age-standardized prevalence of H. pylori within the populations of these two cities was similar (approximately 56%). In these patient groups, the prevalence of different gastrointestinal disease states and the occurrence and severity of gastritis, gastric atrophy, and intestinal metaplasia were compared. METHODS: This study was based on consecutive patients: 265 from Guangzhou and 275 from Lanzhou. The grading of gastritis and the detection of H. pylori was determined by histology using the "Sydney System". RESULTS: The ratio of cases of duodenal to gastric ulceration for the two cities was: Guangzhou 14:1 and Lanzhou 3:1. Gastric cancer was more prevalent in the patients from Lanzhou (9.8%) than from Guangzhou (3%). In nonulcer dyspepsia patients from Guangzhou, gastritis was predominantly antral, whereas, in Lanzhou, gastritis was predominantly uniform. The amount and severity of atrophy was significantly greater in Lanzhou compared with Guangzhou. CONCLUSIONS: The prevalence of atrophy, rather than age of acquisition and prevalence of H. pylori infection, appears to be a marker of the major upper gastrointestinal disease profiles of a region. Development of atrophy, although apparently related to H. pylori infection, may be a multifactorial condition. Differences in diet, as seen between Guangzhou and Lanzhou, may be important in this regard. Understanding the factors leading to the development of atrophy may enhance our understanding of processes leading to gastric malignancy.

Atrophy↗

PubMed1994

Topographic investigation of brain atrophy in parkinsonism-dementia complex of Guam: a comparison with Alzheimer's disease and progressive supranuclear palsy.

The topographic distribution of brain atrophy in nine patients with parkinsonism-dementia complex of Guam (Guam PDC) was evaluated quantitatively, and compared with that in six Japanese patients with Alzheimer's disease or senile dementia of Alzheimer type (AD), five Japanese patients with progressive supranuclear palsy (PSP), and nine Japanese control subjects. Characteristic features of Guam PDC were as follows: (1) severe atrophy of the frontal and temporal cortex with relative preservation of the white matter; (2) atrophy of the tectum, tegmentum and cerebral peduncle of the midbrain, and (3) atrophy of the tegmentum and base of the upper pons. In contrast, sectional areas of the tectum and cerebral peduncle of the midbrain were relatively well preserved in PSP, while in AD there was no significant atrophy in the brain stem.

Aged↗

PubMed1994

Effects of the beta-adrenergic agonist cimaterol on chicken muscle atrophy induced by stretch-release.

Thirty-eight White Leghorn chickens, 5 weeks of age, were used to investigate the effect of cimaterol on patagialis muscle (PAT) atrophy due to release of passive-stretch. Cimaterol (CIM) was mixed in a standard commercial chicken diet at 0.5 ppm. Passive-stretch of PAT for 7 days significantly (P < 0.01) increased muscle weight (43%), fiber cross-sectional area (40%) and DNA unit size (34%) compared with unstretched control muscle. In birds fed the standard diet, stretch-release (SR) resulted in immediate and rapid atrophy and by 5 days the stretch-released muscle reached the size of control muscles. In the CIM-fed birds, the atrophy was delayed for 5 days after SR, at which time muscle atrophy at a rate similar to the birds fed the standard diet occurred. It was concluded that cimaterol retarded muscle atrophy induced by stretch-release but the effect was transient and limited to the first 5 days of treatment.

Adrenergic beta-Agonists↗

PubMed1994

[Cortical atrophy and higher cortical dysfunction in systemic lupus erythematosus].

The relationships between cortical atrophy and higher cortical dysfunction in systemic lupus erythematosus (SLE) were investigated. The subjects were 27 females, right-handed patients with SLE. None of them had a history of cerebro-vascular disorders. The CT index of cortical atrophy included Huckman number, Evans' ratio, Ventricular index, and Cella-media index calculated from the brain CT. As controls, 27 age- and sex- matched, healthy subjects were studied and compared with the SLE group. All underwent the following neuropsychological examinations: intelligence and mental state, linguistic function, and recognition and praxis. As a result, Huckman number and Evans' ratio were significantly higher in the SLE group than in controls, clearly showing evidence of cortical atrophy. With regard to the relationships between cortical atrophy and neuropsychological tests, there were significant relationships between digit span and Huckman number and Evans' ratio, and between word fluency and Evans' ratio. These findings suggested that the atrophy of frontal lobe was characteristic in SLE, being associated with dysfunction of frontal lobe.

Adolescent↗

PubMed1993

[Atrophy of the gastric mucosa and Helicobacter pylori].

The authors investigated the prevalence of Helicobacter pylori (H. p.) in atrophic gastritis in the antrum and/or in the corpus of the stomach (groups I-IV), as compared with mucosae without atrophy. Criteria for elimination were age under 50 years, a case-history of the use of antibiotics during the last 6 months and chronic ingestion of alcoholic beverages. Group IV was formed by probands with pernicious anaemia who were divided into sub-group IVa with atrophy of the corpus and sub-group IVb with atrophy of the corpus and antrum. It was revealed that in probands with pernicious anaemia the presence of H. p. is significantly reduced (p < 0.01) when atrophy was present not only in the corpus but also in the antrum. The authors concluded that atrophic changes in the corpus only do not have a significant effect on the presence of H. p. in the antrum. The presence of H. p. is significantly influenced in a negative sense only when atrophic changes, in particular total atrophy, affect the antral mucosa.

Aged↗

PubMed1993

Bone fracture induces reflex muscle atrophy which is sex-dependent.

Longlasting nociceptive stimulation is known to cause atrophy of adjacent muscles. The aim of this study was to determine further the possible mechanisms of this pathological phenomenon. Unilateral fracture of the paw was performed under pentobarbital anaesthesia in several experimental groups (n = 8-11) of female and male rats. Dry muscle weights of the soleus (SOL), extensor digitorum longus (EDL), gastrocnemius (GA) and tibialis anterior (TA) were determined 7 days following the bone fracture and compared to the weight of contralateral control muscles. To demonstrate the reflex origin of this atrophy, deafferentation of the paw by dorsal root section (L4-6) was performed before or after unilateral fracture of hindlimb metatarsal bones. In female rats, the fracture resulted in a significant loss of muscle weight in all the four muscles examined. When the hindlimb was deafferented prior to the fracture, no muscle atrophy developed, and neither did deafferentation itself cause any appreciable change in muscle weight except in male rats. This supports the concept that this type of atrophy is reflex in origin. Deafferentation, when performed after the fracture, did not prevent the weight loss in extensor muscles (SOL, GA), while the flexors (EDL, TA) did not in general lose any weight. The results in male rats had a similar trend as in female rats, although the weight loss was significantly smaller. Our results showed that the mechanism of reflex muscle atrophy following metatarsal bone fracture involves a component which is dependent on afferent information from the injured paw.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗

PubMed1993

[A case of hereditary motor and sensory neuropathy type I with optic atrophy, neural deafness and pyramidal tract signs].

A case of hereditary motor and sensory neuropathy (HMSN) type I with optic atrophy, neural deafness and pyramidal tract signs was described. The patient was a 53-year-old man who had suffered from difficulty in walking, decreased visual acuity since age 16 years. These symptoms were slowly progressive. At the age of 37, he was pointed out optic atrophy, positive pyramidal tract signs. Distal muscle weakness with atrophy of four limbs was prominent at the age of 50. Since then, he noticed progressive hearing loss with blindness. His elder sister was diagnosed Charcot-Marie-Tooth disease. On neurological examination, he showed to have optic atrophy without retinitis pigmentosa and neural deafness. Also he showed mild degree of muscle weakness and atrophy in four limbs, severe in the distal part of lower limbs. Deep tendon reflexes were absent in all limbs with right Babinski sign. Superficial sensation was decreased slightly in the distal parts of four limbs. Deep sensation was markedly decreased in the leg. There were no cerebellar signs. Audiometric examination revealed bilateral neural hearing loss. There were no findings of spinal cord compression on spinal MRI. On the nerve conduction studies, sensory nerve action potential was not elicited in all nerves tested. Motor nerve conduction velocity of the right median was 41.1 M/sec, also ulnar nerve 44.7 M/sec, but M-wave was not elicited with the electrical stimulation of other tested nerves. On sural nerve biopsy, the density of myelinated fibers was severely decreased. Well-myelinated axon surrounded by onion bulb formation was observed in electron microscopic examination.(ABSTRACT TRUNCATED AT 250 WORDS)

Charcot-Marie-Tooth Disease↗

PubMed1993

[A case of flexion myelopathy presenting with reversible muscular weakness and atrophy of the unilateral proximal upper limb].

A 16-year-old man visited our clinic because of right-sided weakness of shoulder abduction and elbow flexion. He was well until about three weeks previously. Neurological examination revealed only that he had severe weakness together with mild atrophy of the muscles innervated by the C5 and C6 segments (the deltoid, biceps brachii, brachioradialis), slight hypesthesia on the thumb, and loss of deep reflexes of the biceps brachii on the right. No pyramidal signs were found in the lower extremities. EMG showed neurogenic changes of the atrophied muscles. Neuroradiological studies revealed right-sided atrophy of the spinal cord at C4-5 disk level, anterior shift of the posterior cervical dura mater and congestion of the internal vertebral venous plexus mainly at C4 and C5 vertebral level with his neck flexed. Conservative physiotherapy provided a good recovery within a few months. The clinical and neuroradiological findings of this case resemble those of juvenile type of distal and segmental muscular atrophy of upper extremities excluding distribution of involved muscles because of the different level of the spinal cord lesion. Pathomechanism of this case is considered to be the same as that of juvenile type of distal and segmental muscular atrophy of upper extremities.

Adolescent↗

PubMed1995

[Familial posterior cortical atrophy with visual agnosia and Bálint's syndrome].

We report a patient of posterior cortical atrophy with progressive visual agnosia, Bálint's syndrome and dementia in which posterior cortical atrophy with similar characteristics on CT and progressive dementia were found in a sister. The patient was a 75-year-old woman who noted the onset of a progressive visual disorder at the age of 70, and whose family first noticed disoriented behavior at around the same period. Ophthalmologic examinations revealed mild cataract but no evidence of peripheral optic nerve or retinal lesions. Neuropsychological examination showed right homonymous hemianopia, visual agnosia, Bálint's syndrome, mild transcortical sensory aphasia, Gerstmann's syndrome, constructional apraxia, mild ideomotor apraxia and memory disorder. MRI showed marked dilatation of both lateral ventricles, especially the posterior horns, and severe atrophy of the occipital lobes, hippocampus, and the parahippocampal gyrus. Assessment of regional cerebral blood flow by IMP-SPECT revealed a generalized decrease in the temporo-parieto-occipital region bilaterally. The patient's sister began to show evidence of progressive dementia at 80 years of age and CT of the brain revealed marked atrophy, predominantly in the occipital lobes, similar to that of the patient. We believe this to be the first report of posterior cortical atrophy with a positive family history, suggesting the possibility of a hereditary syndrome.

Aged↗

PubMed1996

Stereological analysis of cerebral atrophy in human immunodeficiency virus-associated dementia.

Brain atrophy is a common finding in patients with AIDS, but the relationship of atrophy to HIV-associated dementia is unclear. We used unbiased, stereological methods on postmortem brain specimens to estimate volumes of different brain regions in patients prospectively diagnosed with and without HIV-associated dementia. Thirty HIV-seropositive (9 without AIDS/without dementia, 6 with AIDS/without dementia, 15 with AIDS/with dementia) and 7 HIV-seronegative controls were studied using the technique of point counting and Cavalieri's principle of volume estimation. There was a significant reduction in the mean neocortical volume (15%, p = 0.032) in the group with AIDS when compared to the seronegative controls, and this difference was accentuated when comparing only the group with HIV-associated dementia to the seronegatives (neocortex: 18%, p = 0.020). There were no significant differences between the AIDS groups with and without HIV-associated dementia, although there was a trend for smaller volumes in the most severely demented patients. There were no differences in white matter volumes between groups. In conclusion, patients dying with AIDS and particularly those with HIV-associated dementia, show significant neocortical atrophy when compared to seronegative controls. The lack of a significant difference in cerebral atrophy between HIV-seropositive patients with and without dementia suggests that atrophy may be a more generalized phenomenon of AIDS as opposed to a specific marker for HIV-associated dementia.

AIDS Dementia Complex↗

PubMedDate not supplied

[Cortical atrophy in MRI, mental status and neuroleptic treatment effect in schizophrenia].

MR imaging of the head was performed in forty schizophrenics (DSM-IV). Mental status was evaluated before and during 8-weeks of neuroleptic treatment. Cortical atrophy in frontal and temporal regions was found in 40% of subjects. They were older, had longer history of schizophrenia, were less active professionally and were more frequently hospitalized. Patients with and without cortical atrophy in MRI did not differ in the severity of schizophrenic psychopathology at baseline. During neuroleptic treatment negative schizophrenia symptoms were significantly better diminished in patients without cortical atrophy than in subjects with cortical atrophy in MRI; this regarded specially the severity of emotional blunting. Clinical improvement after 8-weeks of neuroleptic administration was less favorable in patients with cortical atrophy.

Adult↗

PubMed1998

Prostatic atrophy: an autopsy study of a histologic mimic of adenocarcinoma.

Prostatic atrophy (PA) is one of the most frequent mimics of prostatic adenocarcinoma. It occurs almost exclusively in the peripheral zone of the gland and gained importance with the increasing use of needle biopsies for the detection of prostatic carcinoma The etiopathogenesis is unknown, and there is controversy related to the potential of PA as a precancerous lesion. The frequency increases with age. Compressions caused by hyperplastic nodules, inflammation, hormones, nutritional deficiency, or systemic or local ischemia, are all possible factors in the pathogenesis of PA. The peripheral zone of the prostate was step-sectioned and totally embedded from the bodies of 100 consecutively autopsied men more than 40 years of age. The fragments were microscopically studied for presence of PA, latent (histologic) carcinoma, high-grade prostatic intraepithelial neoplasia, local arteriosclerosis, and prostatitis. The prostates were macroscopically examined for the presence of nodular prostatic hyperplasia. The autopsy reports provided information concerning the presence of generalized atherosclerosis and benign or malignant nephrosclerosis. PA was seen in 85 of the 100 prostates examined and histologically was subtyped into simple, hyperplastic, and sclerotic atrophy. In 65 (76.47%) of 85 cases, the histologic subtypes were combined. In 33 (50.76%) of these 65 cases, the three subtypes were seen concomitantly, favoring the hypothesis that they represent a morphologic continuum of only one lesion. Fibrosis of the stroma may or may not be present in simple and hyperplastic atrophy. Hyperplastic atrophy associated with fibrosis of the stroma is the histologic subtype that most frequently mimics adenocarcinoma Sclerotic atrophy always presents fibrosis of the stroma. PA increases with age, and, in our study, ischemia caused by local intense arteriosclerosis seems to be a potential factor for its etiopathogenesis. Because there was no relation to latent (histologic) carcinoma or high-grade prostatic intraepithelial neoplasia, PA is probably not a premalignant lesion.

Adenocarcinoma↗

PubMed1997

[Evaluation of visual evoked potentials in partial optic nerve atrophy].

PURPOSE: Parameters of visual evoked potentials in partial optic nerve atrophy in different aetiology were studied. MATERIALS AND METHODS: The study involved 48 patients (68 eyes) with partial optic nerve atrophy from neuritis, toxic, arteriosclerosis and trauma. The tests of visual evoked potentials were performed by the use of UTAS E-1000 computer system in all patients with the use of pattern and flash stimulation. RESULTS: Amplitude of all waves were reduced in 74% patients using "pattern" and in 61% patients using "flash" stimulation. Latency of wave P2 was delayed in all patients with optic nerve atrophy from arteriosclerosis. Latency of P100 wave and N1 wave were not delayed in patients with optic nerve atrophy from toxic neuropathy. CONCLUSIONS: Estimation of latency of the VEP may be useful in diagnosis of the partial optic nerve atrophy. Variety of records of VEP indicate different degree of disturbances of nerve conduction.

Adult↗

PubMed1998

Measures of brain and spinal cord atrophy in multiple sclerosis.

Although conventional magnetic resonance imaging (MRI) has greatly increased the understanding of the pathophysiology of multiple sclerosis, its relation to the development of disability is complex. More pathologically specific imaging markers have therefore been sought to try and understand the underlying process that is responsible for the progressive disability that so commonly occurs in multiple sclerosis. Of these the most simple to understand conceptually is the measurement of atrophy, which most probably represents axonal loss. Several recent studies have shown that atrophy is a process closely linked with the progressive phase of multiple sclerosis and worsening disability. Furthermore it has also been shown that atrophy may evolve despite the absence of inflammatory activity as judged by gadolinium enhanced MRI and thus its measurement gives information in addition to that obtained from conventional MRI. Because of new developments in imaging we are now able to measure atrophy reliably and reproducibly. Hence the measurement of atrophy now provides objective markers by which to evaluate putative treatment aimed at preventing disability in multiple sclerosis.

Atrophy↗

PubMed2004

Prediction of neuropsychological impairment in multiple sclerosis: comparison of conventional magnetic resonance imaging measures of atrophy and lesion burden.

BACKGROUND: Cognition and magnetic resonance imaging correlations are well established in patients with multiple sclerosis (MS), but it is unclear whether lesion burden or atrophy accounts for most of the predictive variance. These indices have been directly compared in only a few studies. No such study included measurement of the third ventricle, which was strongly predictive of neuropsychological competence in the early literature. Furthermore, few studies accounted for the influence of age, premorbid intelligence, or depression. OBJECTIVE: To determine if conventional measures of lesion burden or atrophy predict cognitive dysfunction in MS while accounting for age, premorbid intelligence, and depression. METHODS: We studied 37 patients with MS and 27 controls matched according to demographic variables. Correlations between neuropsychological tests and the following magnetic resonance imaging indices were considered: T1 hypointense lesion volume, fluid-attenuated inversion recovery hyperintense lesion volume, third ventricle width, bicaudate ratio, and brain parenchymal fraction. Regression models predicting neuropsychological performance controlled for the effects of age, premorbid intelligence, and depression. We included only those tests discriminating patients with MS from controls. RESULTS: In each regression model, third ventricle width was the sole magnetic resonance imaging measure retained. When this variable was removed from consideration, brain parenchymal fraction was retained in all analyses. CONCLUSIONS: Brain atrophy accounts for more variance than lesion burden in predicting cognitive impairment in MS, and central atrophy in particular is strongly associated with neuropsychological morbidity. This finding may be explained in part by atrophy of the thalamus, a deep gray matter structure that mediates cognitive function via cortical and subcortical pathways. Enthusiasm for the clinical utility of third ventricle width is tempered by modest intraobserver and interobserver reliability.

Adult↗

PubMed2005

Prediction of longitudinal brain atrophy in multiple sclerosis by gray matter magnetic resonance imaging T2 hypointensity.

BACKGROUND: Gray matter magnetic resonance imaging T2 hypointensity, a marker of iron deposition, is associated with clinical impairment and brain atrophy in cross-sectional studies of multiple sclerosis. Treatment with intramuscular interferon beta-1a limits brain atrophy in the second year of treatment. OBJECTIVE: To test whether T2 hypointensity predicts brain atrophy and whether interferon affects this relationship. DESIGN: Post hoc analysis. SETTING: A multicenter treatment trial conducted at tertiary care comprehensive multiple sclerosis centers. Patients Patients with multiple sclerosis who took part in a 2-year clinical trial in which they received intramuscular interferon beta-1a (30 mug/wk) or placebo. MAIN OUTCOME MEASURES: Deep gray matter T2 hypointensity, brain parenchymal fraction (BPF), and total T2, gadolinium-enhancing, and T1 lesion volumes. RESULTS: T2 hypointensity in various gray matter areas correlated with baseline BPF (r = 0.19-0.39; P = .001-.03). In placebo-treated patients (n = 68), baseline T2 hypointensity predicted the change in BPF in the first year and throughout 2 years (r = 0.26-0.42; P<.001-.03). T2 hypointensity was chosen in regression modeling as the best predictor of BPF change at the 1-year (R(2) = 0.23; P = .002) and 2-year (R(2) = 0.33; P<.001) time points after accounting for all magnetic resonance imaging variables. In the interferon group (n = 65), no relationship existed between baseline T2 hypointensity and BPF change. CONCLUSIONS: Gray matter T2 hypointensity predicts the progression of brain atrophy in placebo- but not interferon beta-1a-treated patients. This predictive effect is seen as early as the first year. We hypothesize that interferon beta may exert its effect on brain atrophy in part by reducing a cascade of events that involve iron deposition as a mediator of neurotoxicity or as a disease epiphenomenon.

Adult↗

PubMed1996

Wolfram syndrome: hereditary diabetes mellitus with brainstem and optic atrophy.

Wolfram syndrome was originally described as a combination of familial juvenile-onset diabetes mellitus and optic atrophy. Other neurological features subsequently emerged, and "DIDMOAD" (diabetes insipidus, diabetes mellitus, optic atrophy, and deafness) became a commonly accepted acronym. Here, we describe 4 further cases from 2 families, in whom there occurred previously unrecognized neurological features, central apnea and neurogenic upper airway collapse, together precipitating primary respiratory failure (fatal in 1 case), startle myoclonus (in 2 unrelated cases), axial rigidity, and Parinaud's syndrome. Magnetic resonance images revealed striking brainstem atrophy affecting, in particular, the pons and midbrain. The mitochondrial DNA from 3 cases (and relatives) showed no evidence of any of the previously reported abnormalities. These neurological and neuroradiological features, in conjunction with (1) analyses showing the neurodegenerative origin of optic atrophy, deafness, diabetes insipidus, and incontinence, (2) other previously reported neurological complications (including anosmia, ataxia, epilepsy, and neuropsychiatric and cognitive abnormalities), and (3) the very small number of published postmortem studies, indicate that Wolfram syndrome should be reemphasized as a unique hereditary neurodegenerative disorder with prominent optic atrophy and diabetes mellitus.

Adolescent↗

PubMed2002

Skeletal muscle hypertrophy and anti-atrophy effects of clenbuterol are mediated by the beta2-adrenergic receptor.

Analyses were performed to evaluate the roles of the beta1- and beta2-adrenergic receptors in the skeletal muscle hypertrophy and anti-atrophy response to the beta-adrenergic agonist, clenbuterol. Treatment of wild-type mice with clenbuterol resulted in statistically significant hypertrophy of the innervated tibialis anterior and medial gastrocnemius muscles and inhibition of denervation-induced atrophy of these muscles. Treatment of beta1-adrenergic receptor knockout mice with clenbuterol also resulted in statistically significant hypertrophy of the innervated tibialis anterior and medial gastrocnemius muscles and inhibition of denervation-induced atrophy of these muscles. In contrast, in beta2-adrenergic receptor knockout mice and in mice lacking both the beta1- and beta2-adrenergic receptors, clenbuterol treatment did not result in hypertrophy of the innervated tibialis anterior and medial gastrocnemius muscles, nor did it inhibit denervation-induced atrophy in these muscles. Together these data demonstrate that the beta2-adrenergic receptor is responsible for both the skeletal muscle hypertrophy and anti-atrophy effects of the beta-adrenergic agonist clenbuterol.

Adrenergic beta-Agonists↗