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Iris atrophy, serous detachment of the ciliary body, and ocular hypotony in chronic phase of Vogt-Koyanagi-Harada disease.

PURPOSE: To describe iris atrophy, serous detachment of the ciliary body, and ocular hypotony in a patient with chronic phase of Vogt-Koyanagi-Harada (VKH) disease. METHODS: Ocular examination and follow-up including digital infrared transillumination imaging of the iris was done in a 52-year-old woman with chronic phase of VKH disease. RESULTS: Infrared transillumination imaging showed extensive atrophy of the iris stroma and occasional pigment clumps both in the pupillary and ciliary zones of the iris, and detachment of the ciliary body in both eyes. Conventional transpupillary transillumination using white light showed only minute patchy atrophy of the pigment epithelium in the pupillary zone. Treatment did not normalize bilateral shallow retinal detachment of the posterior pole, serous detachment of the ciliary body, or severe ocular hypotony. CONCLUSIONS: Severe atrophy of the iris stroma, retinal detachment of the posterior pole, serous detachment of the ciliary body, and ocular hypotony may occur in chronic phase of VKH disease.

Atrophy↗

PubMed2003

Effects of insulin-like growth factor-1/binding protein-3 complex on muscle atrophy in rats.

Muscle atrophy and wasting is a serious problem that occurs in patients with prolonged debilitating illness, burn injury, spinal injury, as well as with space flight. Current treatment for such atrophy, which often relies on nutritional supplementation and physical therapy, is of limited value in preventing the muscle wasting that occurs. Considerable recent attention has focused on the use of anabolic growth factors such as insulin-like growth factor (IGF-1) in preventing muscle atrophy during limb disuse or with various catabolic conditions. However, potential side effects such as hypoglycemia appear to be limiting factors in the usefulness of IGF-1 for clinical treatment of muscle wasting conditions. The formulation of IGF-1 used in this study (IGF-1/BP3) is already bound to its endogenous-binding protein (BP3) and, as a result, has a greater specificity of action and significantly less hypoglycemic effect. Using a rat model of hind limb suspension (HLS) for 10 days, we induced marked muscle atrophy that was accompanied by enhanced muscle proteolysis and reduced muscle protein content. When HLS rats were treated with IGF-1/BP3 (50 mg/kg, b.i.d.), they retained greater body and muscle mass. Muscle protein degradation was significantly reduced and muscle protein content was preserved. The rate of protein synthesis, although somewhat reduced in HLS muscle, was not significantly elevated by IGF-1/BP3 treatment. Volume density of HLS-treated muscles were increased compared to untreated HLS rats and the actual number of fibers per area of muscle was likewise increased. The results of the current study suggest that IGF-1/BP3 might be useful for inhibiting muscle proteolysis in catabolic conditions and thus preserving muscle protein content and mass.

Animals↗

PubMed2002

Brain atrophy in multiple sclerosis: impact of lesions and of damage of whole brain tissue.

INTRODUCTION: In multiple sclerosis (MS), brain atrophy measurement on magnetic resonance imaging (MRI) reflects overall tissue loss, especially demyelination and axonal loss. We studied which factor contributes most to the development of brain atrophy extent and severity of lesions or damage of whole brain issue (WBT). METHODS: Eighty-six patients with MS [32 primary progressive (PP), 32 secondary progressive (SP)] and 22 relapsing-remitting (RR) were studied MRI included T1- and T2-weighted imaging to obtain hypointense T1 lesion volume (T1LV) and two brain volume measurements: 1) the parenchymal fraction (PF; whole brain parenchymal volume/intracranial volume) as a marker of overall brain volume, and 2) the ventricular fraction (VF; ventricular volume/intracranial volume) as a marker of central atrophy. From magnetization transfer ratio (MTR) histograms, the relative peak height (rHp) was derived as an index of damage of WBT (a lower peak height reflects damage of WBT). RESULTS: Multiple linear regression analysis revealed that damage of WBT explains most of the variance of PF (standardized coeffcient beta = 0.59, p < 0.001 for WBT and beta = -0.19, p < 0.05 for T1LV). These findings are independent of disease phase; even in RR patients, damage of WBT plays a dominant role in explaining the variance in overall brain volume. By contrast the variance in VF is explained by both T1LV and damage of WBT (standardized coefficient beta = 0.43, p < 0.001 for T1LV and beta =-0.38, p < 0.001 for WBT). CONCLUSION: This study shows that overall brain volume (PF) is best explained by damage of WBT, supporting the significance of nonfocal pathology in MS in producing tissue loss. Central atrophy (VP) is determined by both lesion volume and damage of WBT. Our results underline the importance of nonfocal pathology even in the early (RR) phase of the disease.

Adult↗

PubMed1995

Brain atrophy in normal ageing and Alzheimer's disease. Volumetric discrimination and clinical correlations.

BACKGROUND: We examined the differences in volume of the ventricular and extracerebral cerebrospinal fluid spaces in normal ageing and in probable Alzheimer's disease (AD) and we tried to investigate the effects of the severity of illness on the morphometric differentiation of AD and ageing, the principal components underlying brain atrophy in both conditions, and the correlations of these measurements with clinical findings. METHOD: Forty patients with probable AD were matched with 40 non-demented elderly controls. Both groups underwent standardised clinical tests and unenhanced cranial computed tomography for post hoc volumetric analysis. RESULTS: The lateral and third ventricles and the anterior and lateral fissures were significantly larger in AD than in normal ageing. The volumes of the lateral ventricle and lateral fissure permitted a highly efficient differentiation between normal ageing and AD even at the mild stage of dementia, and this differentiation was improved further in the more severe stages of illness. We identified one principal component underlying brain atrophy in normal ageing and two components in AD: a 'grey matter' component accounting for sulcal and third ventricular enlargement, and a 'white matter' component for lateral ventricular enlargement. In AD, most of the volumetric measurements were significantly correlated with cognitive impairment, but in the group of non-demented elderly controls they were correlated with age. CONCLUSION. Volumetric indices of brain atrophy permit a highly efficient differentiation between normal ageing and AD even in the mild stages of illness and this demonstrates that substantial structural brain changes have developed in the preclinical phase of illness. We suggest that there is an uncoupling between lateral ventricular enlargement and cortical brain atrophy in AD.

Aging↗

PubMed2002

Chronic, treatment-resistant depression and right fronto-striatal atrophy.

BACKGROUND: Treatment-resistant depression (TRD) is relatively common but its neurobiological basis is poorly understood. Fronto-striatal structural brain changes have been reported in patients with depression but their association with treatment resistance and chronicity has not been established. METHOD: Magnetic resonance images of 20 patients with TRD were compared with images of 20 recovered patients and 20 healthy controls. Images were compared using a voxel-based analysis (VBA) method; the results were validated by conventional volumetric analysis. The clinical associations of magnetic resonance imaging (MRI) changes with illness duration and severity were examined by VBA. RESULTS: Only the TRD group exhibited right fronto-striatal atrophy, and subtle MRI changes in the left hippocampus on VBA. Atrophy was confirmed on volumetric analysis, the degree correlating with the cumulative number of electroconvulsive therapy (ECT) treatments received, suggesting an acquired deficit. CONCLUSIONS: This is the first study to demonstrate fronto-striatal atrophy in patients with depression with poor outcome; the atrophy is more marked in those with more severe illness.

Adult↗

PubMed2005

Relative atrophy of the flocculus and ocular motor dysfunction in SCA2 and SCA6.

Two hereditary ataxia syndromes show distinct profiles of region-specific atrophy and ocular motor deficits. Selective pontine atrophy is associated with slowed saccades in ataxin-2 mutations, and selective floccular atrophy is associated with impaired pursuit and gaze-holding abnormalities in Ca(V)2.1 mutations. Although the flocculus seems to be spared relative to the pons in ataxin-2 mutations, and pursuit and gaze-holding appear to be relatively normal, these can be difficult to assess at the bedside, as corrective saccades are also slow and hard to discern. Here, we show the presence of significant floccular atrophy compared with controls in both ataxin-2 and Ca(V)2.1 mutations, which raises the possibility that abnormalities of smooth pursuit or gaze-holding are present in both conditions.

Adult↗

PubMed2005

Inherited motor neuron disease in domestic cats: a model of spinal muscular atrophy.

Juvenile-onset spinal muscular atrophy was observed in an extended family of purebred domestic cats as a fully penetrant, simple autosomal recessive trait. Affected kittens exhibited tremor, proximal muscle weakness, and muscle atrophy beginning at ~4 mo of age. Apparent loss of function was rapid initially but progressed slowly after 7-8 mo of age, and variably disabled cats lived for at least 8 y. Electromyography and microscopic examination of muscle and nerve biopsies were consistent with denervation atrophy as a result of a central lesion. There was astrogliosis and dramatic loss of motor neurons in ventral but not dorsal horn gray matter of spinal cord and loss of axons in ventral horn nerve roots. These phenotypic findings were similar to mild forms (type III) of spinal muscular atrophy in humans caused by survival of motor neuron mutations, but molecular analysis excluded feline survival of motor neuron as the disease gene in this family. A breeding colony has been established for further investigation of this naturally occurring large-animal model of inherited motor neuron disease.

Age Factors↗

PubMed2003

Growth hormone receptor expression in atrophying muscle fibers of rats.

Biological actions of GH on muscle growth and metabolism are mediated through specific trans-membrane receptors. The aim of this study was to determine GH receptor (GHR) mRNA expression in muscle atrophy. GHR gene expression in the rat was investigated by in situ hybridization and RT-PCR in slow-twitch oxidative muscle [soleus (SOL)] and fast-twitch glycolytic muscle [extensor digitorum longus (EDL)] after 7 and 35 d of hindlimb unloading. In control rats, the RT-PCR mRNAs levels of GHR were greater (+34%) in EDL compared with SOL. At single fiber level, relative expression of GHR mRNA increases in the following order: IIb>IIa>I. After hindlimb unloading, GHR expression significantly increased in atrophied SOL muscle after 7 (+170%) and 35 (+220%) d, whereas no significant alterations appeared in the EDL muscle. At the individual fiber level, in situ hybridization demonstrated this increase was accounted for by an increase in type I fiber expression of GHR transcripts. This increase was also seen in the EDL, but the low content of type I fibers in EDL resulted in a nonsignificant increase in GHR transcript content. The present data suggest that muscle atrophy is associated with a muscle fiber type-specific GHR mRNA up-regulation mechanism that helps protect atrophying fibers in EDL but might be part of an attempt to repair in SOL.

Animals↗

PubMed1980

Disuse atrophy of skeletal muscle is associated with an increase in number of glucocorticoid receptors.

Atrophy of muscles due to disuse is similar in form to glucocorticoid atrophy of the general body musculature. Because of this similarity, a hypothesis was formed which attributed the selective muscle atrophy resulting from immobilization to an increase in glucocorticoid sensitivity. As an initial test of this hypothesis, the thermodynamic characteristics of 3H-dexamethasone binding were examined in cytosol prepared from immobilized and contralateral control gastrocnemius muscles. We report here an increase in numbers of glucocorticoid receptors in immobilized muscles relative to contralateral controls, with no change in binding affinity. These findings support the hypothesis that selective muscle atrophy is a result of changes in glucocorticoid sensitivity.

Animals↗

PubMed2006

Thyroid hormones, dementia, and atrophy of the medial temporal lobe.

CONTEXT: Thyroid function has been related to Alzheimer disease (AD), but it remains unclear whether thyroid dysfunction results from or contributes to developing AD. OBJECTIVE: The objective of the study was to determine the association between thyroid function and both medial temporal lobe atrophy on brain magnetic resonance imaging (MRI) as putative early sign of AD and risk of dementia. DESIGN AND PARTICIPANTS: This was a population-based cohort study among 1077 elderly subjects aged 60-90 yr and dementia free at baseline (1995-1996). MAIN OUTCOME MEASURES: Nonfasting serum levels of TSH, free T(4) (fT(4)), T(3), and rT(3) were available in 1025 subjects followed up for incident dementia until 2005. In a subset of 489 nondemented elderly, we assessed volumes of the hippocampus and amygdala on brain MRI. Subjects using thyroid medication were excluded. RESULTS: During 5657 person-years of follow-up (mean 5.5 yr), 63 subjects were diagnosed with dementia (46 with AD). TSH and thyroid hormones were not associated with risk of dementia or AD. TSH and T(3) were also not related to brain atrophy, whereas nondemented subjects with higher fT(4) levels had more hippocampal and amygdalar atrophy on MRI. Similar associations were found for rT(3). Excluding subjects with thyroid disorders or incipient AD did not change the results. CONCLUSION: In our study, TSH was related neither to risk of AD nor with early MRI markers thereof, arguing against an important role of thyroid function in the development of AD. Whether the association of higher fT(4) and rT(3) levels with brain atrophy on MRI has functional significance remains to be elucidated.

Aged↗

PubMed2003

Focal right inferotemporal atrophy in AD with disproportionate visual constructive impairment.

OBJECTIVE: To explore the structural neuroimaging correlates of visual constructive impairment in patients with mild to moderate Alzheimer disease (AD). BACKGROUND: There is considerable heterogeneity in the non-memory cognitive deficits associated with AD. Structural neuroimaging with MRI is an important diagnostic tool that is gaining acceptance as a surrogate measure of brain pathology in AD treatment trials. Most MRI measurements have focused on medial temporal lobe or global cortical atrophy, which may not reflect some important clinical features of AD. METHODS: Thirty-two patients with probable AD were stratified into two groups based on their relative performance on a visual constructive task, the copy of a modified Rey-Osterrieth figure (Rey). The two groups did not differ in basic demographic features or in neuropsychological performance, other than on the visual constructive task. MRI measurements of hippocampal volume, cortical gray matter volume, and focal cortical gray matter loss were performed in the patients and a group of 71 age-matched, normal controls. RESULTS: Both groups showed significant, bilateral hippocampal as well as cortical gray matter volume loss relative to controls. The more spatially impaired AD group (SAD) had more right than left cortical gray matter loss, whereas the opposite was true in the less spatially impaired group (NSAD). The SAD group had significantly less gray matter in the right inferior temporal gyrus relative to the NSAD group. Atrophy of this region was correlated with performance on the Rey task in all patients with AD. CONCLUSIONS: Right inferotemporal atrophy may serve as a neuroimaging marker of visual constructive impairment in mild to moderate AD. Heterogeneous cortical atrophy is a common feature of AD.

Aged↗

PubMed2004

Medial temporal lobe atrophy on MRI predicts dementia in patients with mild cognitive impairment.

BACKGROUND: Although detailed volumetric MRI assessment of medial temporal lobe atrophy (MTA) can predict dementia in patients with mild cognitive impairment (MCI), it is not easily applied to routine clinical practice. OBJECTIVE: To test the predictive accuracy of visually assessed MTA in MCI patients using a standardized visual rating scale. METHODS: Seventy-five MCI patients (mean age 63 years) underwent a coronal three-dimensional magnetization-prepared rapid gradient echo brain MRI sequence. MTA was rated visually using a 5-point rating scale. RESULTS: The mean follow-up period for the cohort was 34 months. At follow-up, 49% of the enrolled MCI patients fulfilled criteria for dementia. MTA assessed using a standardized visual rating scale was significantly associated with dementia at follow-up, with a hazard ratio of 1.5 for every point increase in atrophy score (p < 0.001) and of 3.1 for the presence of atrophy based on the dichotomized atrophy score (p = 0.003). The predictive accuracy of visually assessed MTA was independent of age, gender, education, Mini-Mental State Examination score, Clinical Dementia Rating Sum of Boxes score, Verbal Delayed Recall, and the presence of hypertension, depression, the APOE epsilon4 allele, and white matter hyperintensities. CONCLUSIONS: Visual assessment of MTA on brain MRI using a standardized rating scale is a powerful and independent predictor of conversion to dementia in relatively young MCI patients. As overlap existed in MTA scores between patients with and without dementia at follow-up, the results should be interpreted in the light of the odds for the individual patient.

Aged↗

PubMed2005

A voxel-based morphometry study of patterns of brain atrophy in ALS and ALS/FTLD.

OBJECTIVE: To investigate the patterns of MRI brain atrophy in patients with ALS with and without clinically evident frontotemporal lobar dementia (FTLD) using voxel-based morphometry (VBM). METHODS: Voxel-based morphometry was used to compare T1-weighted MRI images obtained from ten ALS patients with FTLD, ten ALS patients who were cognitively and behaviorally normal, and 22 control subjects. Images from patients and controls were spatially pre-processed using a study-specific, customized template and a priori images. A statistical threshold of p < 0.05 corrected for multiple comparisons determined significance. RESULTS: A common pattern of gray matter atrophy was seen in both ALS and ALS/FTLD patients when compared to controls that involved the bilateral motor/premotor cortices, the left middle and inferior frontal gyri, the anterior portion of the superior frontal gyri, the superior temporal gyri, the temporal poles and left posterior thalamus. Most of the frontal regions were significantly more atrophied in the ALS/FTLD group than in the ALS group. No significant differences were found in white matter volumes. CONCLUSIONS: Patients with ALS and ALS associated with frontotemporal lobar degeneration exhibit widespread gray matter atrophy in frontotemporal regions. This finding supports the idea of a clinical and anatomic continuum between ALS and frontotemporal lobar degeneration.

Adult↗

PubMed2005

Brain atrophy rates predict subsequent clinical conversion in normal elderly and amnestic MCI.

OBJECTIVE: To test the hypothesis that the atrophy rate measured from serial MRI studies is associated with time to subsequent clinical conversion to a more impaired state in both cognitively healthy elderly subjects and in subjects with amnestic mild cognitive impairment (MCI). METHODS: Ninety-one healthy elderly patients and 72 patients with amnestic MCI who met inclusion criteria were identified from the Mayo Alzheimer's Disease Research Center and Alzheimer's Disease Patient Registry. Atrophy rates of four different brain structures--hippocampus, entorhinal cortex, whole brain, and ventricle--were measured from a pair of MRI studies separated by 1 to 2 years. The time of the second scan marked the beginning of the clinical observation period. RESULTS: During follow-up, 13 healthy patients converted to MCI or Alzheimer disease (AD), whereas 39 MCI subjects converted to AD. Among those healthy at baseline, only larger ventricular annual percent volume change (APC) was associated with a higher risk of conversion (hazard ratio for a 1-SD increase 1.9, p = 0.03). Among MCI subjects, both greater ventricular volume APC (hazard ratio for a 1-SD increase 1.7, p < 0.001) and greater whole brain APC (hazard ratio for a 1-SD increase 1.4, p = 0.007) increased the risk of conversion to AD. Both ventricular APC (hazard ratio for a 1-SD increase 1.59, p = 0.001) and whole brain APC (hazard ratio for a 1-SD increase 1.32, p = 0.009) provided additional predictive information to covariate-adjusted cross-sectional hippocampal volume at baseline about the risk of converting from MCI to AD. DISCUSSION: Higher whole brain and ventricle atrophy rates 1 to 2 years before baseline are associated with an increased hazard of conversion to a more impaired state. Combining a measure of hippocampal volume at baseline with a measure of either whole brain or ventricle atrophy rates from serial MRI scans provides complimentary predictive information about the hazard of subsequent conversion from mild cognitive impairment to Alzheimer disease. However, overlap among those who did vs those who did not convert indicate that these measures are unlikely to provide absolute prognostic information for individual patients.

Age Factors↗

PubMed2006

Patterns of atrophy in pathologically confirmed FTLD with and without motor neuron degeneration.

The authors used voxel-based morphometry to compare the patterns of brain atrophy in two variants of pathologically confirmed frontotemporal lobar degeneration (FTLD): FTLD with motor neuron disease (FTLD-MND) and FTLD with ubiquitin-only-immunoreactive neuronal changes (FTLD-U). Patterns of atrophy were distinct and different from each other. A localized pattern of frontal lobe atrophy was found in FTLD-MND with a more widespread pattern of atrophy affecting the frontal and temporal lobes in FTLD-U.

Age Factors↗

PubMed2006

Brain atrophy after immunoablation and stem cell transplantation in multiple sclerosis.

The authors measured brain atrophy in nine patients undergoing immunoablation and autologous hematopoietic stem cell transplantation for multiple sclerosis. From baseline to 1 month after treatment, atrophy was 10 times faster than before treatment. A patient with non-CNS lymphoma showed comparable acute brain atrophy after analogous therapy. These observations suggest that brain atrophy after immunoablation may not be due entirely to the resolution of edema but may be related to chemotoxicity.

Adult↗

PubMed1979

Cortical atrophy, ventricular enlargement and intellectual impairment in the aged.

Fifty-nine subjects over age 60 had a computerized tomography (CT) scan and completed four neuropsychological tests. Measurements of ventricular size and sulcal enlargement were compared to test performance. Performance of the elderly subjects was also compared to that of subjects aged 16 to 40 years. Subjects over 60 years of age had significantly more brain atrophy and more impaired test performance than younger subjects. Subjects aged 80 to 99 had more atrophy and impaired performance than those 60 to 79 years. Our results suggest that, with aging, the brain atrophies and loses its abilities as measured by neuropsychological testing. However, CT evidence of atrophy only weakly predicts impaired mental function independently of age.

Adolescent↗

PubMed1993

MRI pallidal hyperintensity and brain atrophy in cirrhotic patients: two different MRI patterns of clinical deterioration?

In cirrhotic patients, even in a stable nonencephalopathic state, MRI may show cerebral atrophy and increased signal in globus pallidus on T1-weighted sequences. We investigated the relationship between cerebral atrophy and increased pallidal signal and the clinical status of 30 cirrhotic patients. We found a weak association between the two MRI findings. There were different patterns of clinical variables related to the imaging findings. Performance on motor tasks involving speed correlated with the pallidal signal and plasma ammonia levels but not with atrophy. Test results for memory and frontal-premotor function were associated with brain atrophy but not with the pallidal signal or with ammonia.

Aged↗