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PubMed2000

Cerebral ischemia as a causative mechanism for rapid progression of brain atrophy in chronic hemodialysis patients.

BACKGROUND: It has been found that brain atrophy develops more rapidly in patients with end-stage renal failure after initiation of dialysis therapy. The present study was designed to analyze the relationship between brain atrophy and asymptomatic ischemic brain lesions. PATIENTS AND METHODS: Magnetic resonance imaging (MRI) was performed for the evaluation of brain atrophy and ischemic lesions. Brain atrophy was assessed by the ventricular-brain ratio (VBR), calculated as the ratio of the ventricular area to the whole brain area on the maximum MRI slice. The severity of periventricular hyperintensity (PVH) and the number of lacunae were also regarded as ischemic brain lesions. Fifty-five patients undergoing maintenance hemodialysis (HD) without clinically overt neurological signs and symptoms, with a mean age of 52 +/- 11 (SD) years and a mean HD duration of 7 +/- 6 (SD) years were subjected. VBR and its relationship to ischemic brain lesion data were compared to those in 35 non-HD patients (controls), with a mean age of 42 +/- 14 (SD) years. RESULTS: The VBR, the number of lacunae and the severity of PVH tended to increase with age in HD. The VBRs at all age groups were significantly higher in HD than in controls (7.0 vs 3.7% at the 4th decade, p < 0.05; 8.4 vs 5. 9% at the 5th decade, p < 0.05; 9.6 vs 5.4% at the 6th decade, p < 0.05; and 11.6 vs 6.3% at the 7th decade, p < 0.05). HD patients had significantly higher number of lacunae and had more advanced PVH than did controls. Both the number of lacunae and the severity of PVH were significantly correlated to VBR in HD. CONCLUSION: In conclusion, the rapid progression of brain atrophy was related to the asymptomatic ischemic brain lesions in our HD patients. Such data indicated that cerebral ischemia might be a causative mechanism of brain atrophy in chronic hemodialysis patients.

Atrophy↗

PubMed2002

Prenatal diagnosis for risk of spinal muscular atrophy.

OBJECTIVES: Prenatal diagnosis of spinal muscular atrophy is usually performed in high risk couples by detection of a homozygous deletion in the survival motor neurone gene (SMN1). However, other relatives at risk of being carriers very often request genetic counselling and the possibility of prenatal diagnosis. The aim of this study was to validate a SMN1 gene quantitative test to help the couples formed by one spinal muscular atrophy carrier and a partner of the general population (1/200 potential risk) to achieve a less ambiguous risk result for the pregnancy. DESIGN: Spinal muscular atrophy carrier studies in at-risk individuals. SETTING: Department of Genetics and Gynaecology and Obstetrics in a large university hospital. POPULATION: Seventy-nine obligate carriers (more than one affected child with deletion in the offspring) and 58 non-carriers (relatives of spinal muscular atrophy families defined by marker studies) were tested to set up a quantitative analysis. The method was applied in different situations in 126 members from 34 families with spinal muscular atrophy patients. METHODS: DNA studies of the SMNI gene by marker analysis and quantitative assay. MAIN OUTCOME MEASURES: To determine double (non-carrier) or single dose (carrier) of exon 7 of the SMN1 gene in relatives of spinal muscular atrophy patients. Bayesian calculation of risk. RESULTS: The sensitivity and specificity of the method were 96% and 100%, respectively. Studies on different couples with an a priori risk of 1/200 allowed us to reduce the final risk to 1/5000 or to increase it to 1/4. CONCLUSIONS: The quantitative method can be used to achieve a less ambiguous risk in pregnancies with a 1/200 risk and in families where no sample is available to study the index case. Screening of gamete donors when the recipient is a known carrier should also be considered.

Cyclic AMP Response Element-Binding Protein↗

PubMed1977

Do hormonal (stress) and vascular (ischaemia) factors contribute to reflex muscle atrophy induced by chronic nociceptive stimulation in rats?

1. Reflex muscle atrophy was induced in rats by fracturing the metatarsal bones of one hind paw and injecting 0.02 ml turpentine oil into the planta under shortlasting ether anaesthesia. The atrophy thus evoked in the soleus and extensor digitorum longus (EDL) was compared with the contralateral muscles. 2. There was a twelvefold increase of plasma corticosteroid levels one hour after application of the above nociceptive stimulus and the levels were still somewhat enhanced at 3 days. Neither bilateral adrenalectomy nor administration of corticosteroid hormones or cold stress affected the development of reflex atrophy. 3. Restriction of the arterial blood supply (ligature of the common iliac artery) led to a slowly progressing atrophy with a maximum 10 days after the ligature. Reflex atrophy introduced at different times after ligature was not enhanced. 4. These results are interpreted as evidence that neither general stress (and the effect of catabolic hormones) nor local restriction of muscle blood flow (by reflex vasospasm, for example) are likely to play any appreciable role in the mechanism of reflex muscle atrophy.

Adrenal Cortex Hormones↗

PubMed2004

[MRI findings in schizophrenic patient with frontal lobe atrophy].

In schizophrenic patients, cognitive and behavioral deficits are often associated with frontal lobe dysfunction. By functional neuroimaging studies, abnormalities of the frontal lobe (especially the prefrontal lobe) have been detected in schizophrenic patients. As for morphological changes on neuroimaging, lateral lobe atrophy and enlargement of the lateral ventricles or third ventricle are often reported, but there is no consensus as to whether frontal lobe atrophy is seen more frequently in schizophrenic patients compared with normal controls. The reasons for this disagreement include variations in the precision of measurement on MRI, differences in the methods of MRI among studies, and biases in the subjects being evaluated. Here we present a patient with schizophrenia and frontal lobe atrophy, which was clearly recognized on MRI and showed no progress in the 2 years following its detection. The patient was a 26-year-old woman with a 4.5-year history of schizophrenia when she was referred to us for the treatment of persistent auditory hallucinations and delusions. She showed no neurological findings apart from her psychiatric symptoms. Head MRI showed mild atrophy of the frontal lobe, and the extent of atrophy did not change over the following two years. On resting SPECT 99mTc-HMPAO, hypoperfusion of the bilateral frontal regions was demonstrated. There were no significant findings in the temporal lobe on either MRI or SPECT. She achieved low scores in neuropsychological tests of intelligence, memory, and frontal lobe-associated functions, and showed almost the same degrees of impairment in all of the tests in 2 years of follow-up. The possibility of degenerative diseases, such as young-onset frontotemporal dementia, was ruled out. She had a low intelligence quotient in the WAIS-R and her answers showed the specific pattern which is commonly seen in schizophrenic patients. There is a possibility that hypoperfusion on resting SPECT reflected not only frontal lobe atrophy, but also frontal lobe dysfunction in this patient. Frontal lobe dysfunction in schizophrenics is generally considered to be a secondary effect of meso-limbic system pathology. In this patient, however, the dysfunction seemed to arise from an intrinsic disorder of the frontal lobe, because frontal lobe abnormalities were conspicuous, whereas the temporal lobe was almost normal on both MRI and SPECT.

Adult↗

PubMedDate not supplied

Cerebellar vermian atrophy after neonatal hypoxic-ischemic encephalopathy.

BACKGROUND AND PURPOSE: Although pathologic evidence of cerebellar injury due to birth asphyxia is well described, neuroimaging evidence is sparse. The primary purpose of this retrospective study was to evaluate the early and late imaging findings in the cerebellum of patients who had neonatal hypoxic-ischemic encephalopathy with thalamic edema shown by neonatal CT. The secondary aims were to validate thalamic edema shown by neonatal CT as a marker of thalamic injury and to assess the late cerebral cortical abnormalities associated with neonatal thalamic edema. METHODS: Fifty-five neonates with thalamic edema shown by CT performed when patients were 3 days old were identified from a cohort of full-term neonates with hypoxic-ischemic encephalopathy. Twenty-six of the 55 underwent follow-up neuroimaging. All sonograms, CT scans, and MR images of the brains of the 55 neonates were retrospectively reviewed by two pediatric neuroradiologists. The examinations were reviewed for evidence of hemorrhage, edema, atrophy, and CT attenuation or MR signal intensity abnormalities in the cerebellum, basal ganglia, and cerebral cortex. The neonatal autopsy findings in four cases were reviewed separately by a pediatric neuropathologist. RESULTS: Of the 55 neonates with thalamic edema shown by neonatal CT, 28 (51%) had thalamic edema with diffuse cerebral cortical edema, and 27 (49%) had thalamic edema without diffuse cortical edema. The cerebellar vermes appeared normal on all neonatal sonograms, CT scans, and MR images. However, atrophy of the cerebellar vermis was found in 12 (46%) of 26 patients by use of follow-up studies (95% CI, 27-65%). One of the 12 patients also had cerebellar hemispheric atrophy. Cerebellar vermian atrophy was shown at follow-up in eight (67%) of 12 patients who had neonatal thalamic edema with cortical sparing, compared with four (29%) of 14 patients who had thalamic edema with diffuse cortical edema. The difference did not reach statistical significance. The thalami appeared abnormal on follow-up neuroimages in 25 of 26 cases. Different patterns of cortical atrophy were observed on the images of patients who had thalamic edema with cortical sparing compared with those obtained in patients who had thalamic edema with cortical involvement. CONCLUSION: Cerebellar vermian atrophy is a frequent finding on follow-up images of patients in whom neonatal CT showed hypoxic-ischemic encephalopathy with abnormal thalami.

Atrophy↗

PubMedDate not supplied

Cell death does not herald epithelial involution ("atrophy") in oral sub mucous fibrosis: a TEM study.

The disease progression in oral submucous fibrosis (OSF) seems to be in a biphasic manner, along both fibroblastic and keratinocytic lineages. The epithelial malignancy is considered to be a sequel of connective tissue changes. "Atrophy" of epithelium makes it amenable to the effect of oral carcinogens. This concept looks rather simplistic in the light of the current understanding of epithelial cell biology. So the concept of epithelial "atrophy" needs redressal against the backdrop of recent investigations. 12 cases of clinically and histologically advanced OSF cases (M:F = 4:8) who were habitual areca-quid chewers comprise the study group. 5 (M:F=1:4) non-OSF, non-areca-nut chewing healthy volunteers, constituted the control group. Biopsy was done and the sections were processed for light and electron microscopy. Cell countings were made based on established criteria for apoptosis and necrosis under the high resolution of a TEM and electron micrographs were taken. The Apoptotic Index (A1) calculated for the diseased mucosa was 3.0 +/- 1.3 and for the control was 2.1 +/- 1.5 (X2 = 1.21, df= 1, p>0.05). The necrotic indices (NI) were respectively, 2.5 +/- 0.6 and 2.0 +/- 1.3 (X2 = 0.24, df = 1, p>0.05). The Absolute Cell death Index (ACI), which is the cumulative figure of apoptosis and necrosis indices, was 5.5 and 4.2 respectively for diseased and normal samples (X2 = 1.8, df = 1, p>0.05). The inability to compute an increased ACI in OSF epithelium, when compared to normal, goes against the concept of epithelial "atrophy". Atrophy envisages an increased apoptotic cell death of keratinocytes, induced by the same signals that caused atrophy and this may contribute to loss of cell of an entire organ. This basic concept in pathology seems to be unfounded with disease. This prompted us for an alternative concept in favour of a reduced proliferation index of the adult stem cell compartment of the oral epithelium. So this study favours the concept of epithelial hypoplasia, rather than atrophy, which causes thinning of surface epithelium in advanced OSF.

Adult↗

PubMed2006

[Optic nerve atrophy after vitrectomy for diabetic retinopathy: its systemic and local risk factors].

PURPOSE: To evaluate the incidence and risk factors of optic nerve atrophy after vitrectomy for diabetic retinopathy. SUBJECTS AND METHODS: Clinical charts of 48 eyes of 40 patients who underwent vitrectomy for diabetic retinopathy were retrospectively reviewed. The relationship between postoperative optic nerve atrophy and patients' physical condition was statistically analyzed. RESULT: Postoperative optic nerve atrophy, distinct from glaucomatous optic nerve atrophy, occurred in 5 eyes (10.4%). Its incidence was correlated with higher plasma creatinine concentration (p=0.001), proliferative diabetic retinopathy (p= 0.046), and retinal white vessel formation (p= 0.007). Maintenance of the best postoperative visual acuity was difficult in the patients with optic nerve atrophy. CONCLUSION: Patients with proliferative diabetic retinopathy accompanied by renal dysfunction were at high risk of optic nerve atrophy after vitrectomy.

Adult↗

PubMed1991

Parapapillary atrophy and retinal vessel diameter in nonglaucomatous optic nerve damage.

Parapapillary chorioretinal atrophy and decreased retinal vessel diameter occur in glaucomatous eyes. To evaluate the frequency and degree of these signs in nonglaucomatous optic neuropathy, the authors evaluated morphometrically and compared 47 patients with nonglaucomatous optic nerve atrophy from extraocular causes with 292 patients with primary open-angle glaucoma and 179 normal subjects. Eyes with anterior ischemic optic neuropathy were excluded. The parapapillary atrophy was differentiated into a central zone (beta) with sclera and large choroidal vessels visible by ophthalmoscopy and a peripheral zone (alpha) with irregular pigmentation. Both zones did not differ significantly in the eyes with nonglaucomatous optic neuropathy and the normal eyes. In the glaucomatous eyes, they were significantly larger and occurred more frequently. The retinal vessel diameter was significantly smaller in both groups with optic nerve atrophy than in the normal group. It was concluded that decreased retinal vessel diameters unspecifically suggest optic nerve atrophy. Evaluation of parapapillary chorioretinal atrophy can be helpful in differentiating nonglaucomatous from glaucomatous optic neuropathy.

Adolescent↗

PubMed1991

Pathologic and hemodynamic sequelae of unilobar biliary obstruction and associated liver atrophy.

A patient is presented with unilobar biliary obstruction associated with marked liver atrophy and compensatory hypertrophy. Characteristically she was not jaundiced and had no portal hypertension. Quantitative measurements of the degree of hepatocyte hyperplasia showed that over 50% of cells in the hypertrophied lobe were hyperplastic. Surprisingly, a similar percentage of cells in the atrophied lobe were also hyperplastic. No difference was found in the size of hepatocytes between the two lobes or among the hepatocyte subpopulations in the atrophied lobe. The findings in this case suggest (1) lobar atrophy induces a hyperplastic response in more than one half of the cells of the contralateral lobe; (2) the development of atrophy consequent on biliary obstruction is likely the result of destruction of whole cells rather than cytoplasmic loss; (3) the development of a hyperplastic response within the atrophied lobe is a new finding and is consistent with the hormonal theory of hepatic regeneration; and (4) striking compensatory hypertrophy of the liver is associated with normal portal venous pressure.

Atrophy↗

PubMedDate not supplied

Asymmetrical cerebral atrophy in Alzheimer's disease.

In most Alzheimer patients brain atrophy seems to be symmetrical. Recent neuropsychological and brain imaging investigations suggest, however, that in some patients one hemisphere is more severely affected from the onset of symptoms. We have observed four Alzheimer patients with grossly asymmetrical cerebral atrophy at autopsy, in whom the topography of the most severe atrophy was consistent with the earliest clinical signs of focal brain damage. In the three patients who at onset had relevant language disorders, atrophy of the brain was more severe in the association areas surrounding the left sylvian fissure. In the fourth patient, who first complained of visuospatial troubles, the right, nondominant hemisphere was more affected. These clinical and pathological findings suggest that association areas of one hemisphere were involved quite early in the evolution of the disease, conceivably at the same time as the hippocampus and related limbic structures. In these patients, a morphometric analysis of cortical changes in homologous areas of the cortex (area 22) was carried out in order to investigate the effect of the evolution of the disease upon cortical changes. This analysis showed that the numerical densities of nerve cells and tangle-bearing neurons were lower on the more atrophied side and suggested that the severity of cortical atrophy might have affected the size, but not the density, of senile plaques.

Aged↗

PubMed1990

[Para-papillary chorioretinal atrophy in eyes with shallow glaucomatous optic disk cupping].

Parapapillary chorioretinal atrophy is present in some, but not all glaucomatous eyes. We examined whether eyes with shallow or with deep optic cupping showed more pronounced parapapillary atrophy. To this end, we analyzed 15 degree color stereo optic disc photographs of 141 eyes of 95 normal subjects and 211 eyes of 120 patients suffering from chronic open-angle glaucoma morphometrically. Optic cup depth was semiquantitatively estimated in a relative score ranging from 0 to 5. It increased significantly with increasing glaucoma damage indicated by smaller neuroretinal rim area, higher visual field loss, decreased retinal nerve fiber layer index and more advanced morphological glaucoma stage. Conversely, optic cup depth was inversely correlated with parapapillary atrophy. It decreased significantly with increasing glaucomatous parapapillary atrophy. When two subgroups of eyes with deep and eyes with shallow cups, were formed, matched for neuroretinal rim area, perimetric defects and retinal nerve fiber layer index, the parapapillary atrophy was found to be significantly more pronounced in the subgroup with shallow optic cups than in the subgroup with deep cupping. We conclude that there is a correlation between shallow optic disc cupping and pronounced parapapillary chorioretinal atrophy. This may indicate a common element in their pathogenesis.

Adolescent↗

PubMedDate not supplied

Spinocerebellar degeneration: qualitative and quantitative MR analysis of atrophy.

Magnetic resonance imaging at 1.5 T was performed in 27 patients with either the cerebellar or spinocerebellar form of spinocerebellar degeneration and in 10 control subjects. Neither T1- nor T2-weighted images (T1WIs and T2WIs) of the patients showed any abnormal intensity areas within the cerebellum or in any other structures of the brain. The T2WIs delineated normal configurations of symmetrical dentate and red nuclei. On T1WIs two patterns of atrophy were detected: (a) moderate to severe shrinkage of the basis pontis and the middle cerebellar peduncles associated with atrophy of the cerebellum, and (b) moderate atrophy of the cerebellum with a preserved basis pontis. The former morphological changes are consistent with the pathology of pontocerebellar atrophy (PCA) and the latter with those of cerebellar cortical degeneration (CCD). In 11 patients, only after a quantitative analysis of the images were we able to classify them in one of the two morphological categories (PCA or CCD). There was a significant correlation between atrophy of the cerebellum and atrophy of the basis pontis. Furthermore, in the PCA group the anterior portion of the body of the corpus callosum was significantly smaller in comparison with the control subjects.

Adult↗

PubMedDate not supplied

Testicular atrophy and impaired spermatogenesis in rats fed high levels of the methylxanthines caffeine, theobromine, or theophylline.

Experiments were designed to determine the effects of feeding the methylxanthines caffeine, theobromine, or theophylline to 4- to 6-week-old males rats at a dietary level of 0.5 percent for periods ranging from 14 to 75 weeks. In the first two experiments, Osborne-Mendel rats were fed the test substances alone or in combination with sodium nitrite to test the hypothesis that these amines might nitrosate in vivo to produce toxic nitrosamine compounds. The compounds failed to produce neoplastic or preneoplastic lesions, but a significant positive finding was the occurrence of severe bilateral testicular atrophy with aspermatogenesis or oligospermatogenesis in 85-100 percent of the rats fed caffeine or theobromine. In a third experiment the methylxanthines were fed to Holtzman rats for 19 weeks to determine whether testicular atrophy would be induced in a second strain of rat. The testicular effects were similar to those in Experiments I and II but were more pronounced. Caffeine and theobromine induced testicular injury in nearly all rats. Theophylline induced severe testicular atrophy in 14 percent of the rats, mild to moderate atrophy in 71 percent, and had no effect in 15 percent. The relative testicular toxicity of the methylxanthines was caffeine, most potent; theobromine, slightly less potent; and theophylline, considerably less potent. Somewhat variable atrophic changes of the accessory sexual organs (epididymis, prostate, and seminal vesicles) accompanied the testicular changes. Cytogenetic analysis of testes from caffeine- or theophylline-treated rats revealed a significantly reduced number of mitotic cells in the caffeine-treated group. Plasma testosterone concentrations were significantly elevated in the theobromine group and somewhat elevated in the caffeine-treated group; this correlated morphologically with an apparent hyperplasia of interstitial cells in severely atrophied testes in these groups. Plasma cholesterol concentrations were significantly increased in the caffeine and theobromine groups. Possible sites and mechanisms of action of the methylxanthines in the induction of testicular atrophy and impaired spermatogenesis are discussed.

Animals↗

PubMed1982

[Hereditary features of progressive retinal atrophy (PRA) and its consequences in dog-breeding (author's transl)].

Progressive retinal atrophy (PRA) is a collective term comprising a group of hereditary degenerative lesions of the retina. A central and a generalized form can be differentiated. The central form (day blindness, hemeralopia) is characterized by accumulations of pigment in the layer of pigmented epithelium of the retina, atrophy of the cones and subsequent atrophy of the rods, eventually terminating in blindness. The generalized form (night blindness, nycteralopia) is marked by dysplasia of the rods and or cones, followed later by atrophy of the rods and cones, or it may be marked solely by atrophy of the rods and cones. Blindness occurs between the first and seventh years of life, varying with the breed and form. Hereditary transmission of the generalized form is recessive. Detection of patients is essential in controlling the disease. The number of carriers can be estimated on the basis of this detection, part of the carriers can be identified and the likelihood of an animal being a carrier can be calculated. The condition may be controlled by test matings to determine the genetic patterns of breeding dogs where progressive retinal atrophy is concerned.

Animals↗

PubMed1982

[Scleroderma with progressive facial hemiatrophy and atrophy of the other side of the body].

The authors report the case of a 28 year old woman suffering from a chronic polyarthritis with a linear sclerodermia and presenting a crossed atrophy involving the left side of the body and the right side of the face and neck. The polyarthritis began at age 6, with signs of systemic illness, resulting early in important joint disability and proceeding with exacerbations and remissions. From the onset of this polyarthritis the patient experienced in the left side of the body highly painful and frequent muscular cramps which became rarer with the occurrence and progression of atrophy on the same side. At age 15, the patient experienced similar cramps in the right face, followed by progressive right hemiatrophy. At age 28, examination showed crossed atrophy involving the left side of the body and the right side of the face, tongue and neck, associated in these territories with several atrophic plaques on the skin, circumscribed alopecia, as well as numerous joint sequella. The laboratory date yielded immunologic abnormalities. On the CT scan the brain was normal but the right facial hemiatrophy involving orbital region and pharynx was visible. On the muscular biopsy there were inflammatory changes in the atrophic territory. Skin biopsies were consistent with sclerodermia. Two clinical points should be emphasized. Firstly, the remarkably crossed topography of the atrophy: the upper limit of the left body atrophy corresponded with the lower limit of the right face and neck atrophy; secondly, the unusual features of the muscular cramps. The relationship between sclerodermic facial hemiatrophy and Parry Romberg syndrome are then discussed: the study of this case and the literature do not provide sufficient criteria to allow description of two separate entities. Finally, the pathogenesis of localized sclerodermia is considered; in this case the association with the immunologic abnormalities and chronic polyarthritis is in favor of the hypothesis of a systemic disorder.

Adult↗

PubMedDate not supplied

Testicular atrophy and impaired spermatogenesis in rats fed high levels of the methylxanthines caffeine, theobromine, or theophylline.

Experiments were designed to determine the effects of feeding the methylxanthines caffeine, theobromine, or theophylline to 4- to 6-week-old male rats at a dietary level of 0.5 percent for periods ranging from 14 to 75 weeks. In the first two experiments, Osborne-Mendel rats were fed the test substances alone or in combination with sodium nitrite to test the hypothesis that these amines might nitrosate in vivo to produce toxic nitrosamine compounds. The compounds failed to produce neoplastic or preneoplastic lesions, but a significant positive finding was the occurrence of severe bilateral testicular atrophy with aspermatogenesis or oligospermatogenesis in 85-100 percent of the rats fed caffeine or theobromine. In a third experiment the methylxanthines were fed to Holtzman rats for 19 weeks to determine whether testicular atrophy would be induced in a second strain of rat. The testicular effects were similar to those in Experiments I and II but were more pronounced. Caffeine and theobromine induced testicular injury in nearly all rats. Theophylline induced severe testicular atrophy in 14 percent of the rats, mild to moderate atrophy in 71 percent, and had no effect in 15 percent. The relative testicular toxicity of the methylxanthines was caffeine, most potent; theobromine, slightly less potent; and theophylline, considerably less potent. Somewhat variable atrophic changes of the accessory sexual organs (epididymis, prostate, and seminal vesicles) accompanied the testicular changes. Cytogenetic analysis of testes from caffeine- or theophylline-treated rats revealed a significantly reduced number of mitotic cells in the caffeine-treated group. Plasma testosterone concentrations were significantly elevated in the theobromine group and somewhat elevated in the caffeine-treated group; this correlated morphologically with an apparent hyperplasia of interstitial cells in severely atrophied testes in these groups. Plasma cholesterol concentrations were significantly increased in the caffeine and theobromine groups. Possible sites and mechanisms of actions of the methylxanthines in the induction of testicular atrophy and impaired spermatogenesis are discussed.

Animals↗

PubMed1993

Quantitative analysis of PET and MRI data in normal aging and Alzheimer's disease: atrophy weighted total brain metabolism and absolute whole brain metabolism as reliable discriminators.

Average whole brain metabolic rates, when corrected for brain atrophy, are similar between patients with Alzheimer's disease (AD) and age-matched controls. To elucidate the relationship between reduced cognitive function and cerebral metabolism in patients with AD, we hypothesized that the absolute amount of glucose used by the entire brain may prove to be a more reliable indicator of the disease than metabolic rates calculated for a unit of brain weight. Twenty patients with the probable diagnosis of AD and 17 similarly aged controls underwent 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) studies as well as magnetic resonance imaging (MRI) within a few days of each other. Average metabolic rates, when corrected for atrophy, were 3.91 +/- 1.02 and 4.43 +/- 0.87 (mg of glucose per 100 cc brain tissue per min +/- s.d.) respectively for AD patients and controls. Two other indices were determined, atrophy weighted total brain metabolism (calculated by multiplying the brain volume, determined by MR analysis, by the average metabolic rate) and absolute whole brain metabolism (calculated by multiplying the brain volume by the average metabolic rate corrected for atrophy). The former showed a very significant difference between the two groups (29.96 +/- 7.90 for AD patients compared to 39.1 +/- 7.0 for controls, p < 0.001). Atrophy weighted total brain metabolism also correlated very well with mini mental status exam (MMSE) scores (r = 0.59, p < 0.01). Absolute whole brain metabolism was significantly different between AD and control groups and correlated well with MMSE. These data demonstrate that although the metabolic rate per unit weight of the brain is unchanged in AD compared to controls, atrophy weighted total brain metabolism and absolute whole brain metabolism are significantly affected. Both indices may prove to be a sensitive correlate for cognitive dysfunction in AD.

Aged↗

PubMed1993

Magnetic resonance imaging in the diagnosis of dominantly inherited cerebello-olivary atrophy: a clinicopathologic study.

To facilitate the study of cerebellar degenerative disorders, improved clinical diagnosis is needed. Cerebello-olivary atrophy is pathologically distinct, but until now its diagnosis has been thought to require postmortem examination. This condition was considered as a possible diagnosis in two patients from different families with dominantly inherited ataxia. The affected members of each family demonstrated a stereotyped, progressive, "pure" cerebellar syndrome, which began with gait ataxia followed years later by dysarthria and limb ataxia. The autopsy findings for the first patient's father revealed paleocerebellar and olivary atrophy, characteristic of cerebello-olivary atrophy. Magnetic resonance imaging (MRI) of the brain of both patients revealed medullary, vermian and, to a lesser extent, cerebellar hemispheric atrophy but a normal pons. Dominantly inherited cerebello-olivary atrophy was diagnosed in both patients. Characteristic clinical and MRI features thus permit a confident clinical diagnosis of dominantly inherited cerebello-olivary atrophy. Recognition of this entity during life should advance the classification of cerebellar degenerative disorders.

Brain↗