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PubMed2003

Atrophying tinea versicolor: a clinical and histological study of 12 patients.

BACKGROUND: We describe 12 patients with an atrophying dermatitis in whom the biopsy findings were compatible with tinea versicolor. DESIGN: We encountered 12 skin biopsies from 12 patients in whom a clinically atrophying dermatosis was associated with light microscopic (LM) evidence of atrophy and epidermal colonization by Pityrosporum sp. Formalin-fixed, paraffin-embedded tissue sections were cut at 5 microns and stained with H&E, alcian blue-PAS and PAS-diastase preparations. RESULTS: Five men and seven women aged 17-73 years in whom lesions characterized as atrophic plaques, patches or macules prompted clinical differential diagnoses including parapsoriasis or mycosis fungoides (MF), anetoderma, lupus erythematosus, and steroid atrophy. A LM examination showed epidermal colonization with pityrosporum hyphae and spores accompanied by variable epidermal and dermal atrophy characterized by rete-ridge effacement, subepidermal fibroplasia, pigment incontinence and elastolysis. CONCLUSIONS: Atrophying cutaneous lesions comprise part of the clinical spectrum of tinea versicolor for which we propose the term 'atrophying tinea versicolor'. The pathogenetic basis is unclear but could be the sequela of delayed type hypersensitivity and the release by T-helper lymphocytes of leukotrienes which perturb collagen metabolism and/or keratinocyte growth. Lesions may be mistaken clinically for MF or other atrophying dermatoses.

Adolescent↗

PubMed1995

Bilateral hippocampal atrophy in medial temporal lobe epilepsy.

Quantitative evidence of hippocampal atrophy has been correlated with site of seizure onset, hippocampal neuronal loss, and seizure relief after resection. Most studies have quantified hippocampal atrophy using ratios or differences between right and left hippocampal values. However, bilateral hippocampal atrophy may remain undetected by these techniques. To assess the frequency and implications of bilateral hippocampal atrophy, we studied absolute hippocampal volumes in 53 temporal lobectomy patients who had undergone intracranial electroencephalogram recordings preoperatively. Coronal images were constructed perpendicular to the longitudinal axis of the hippocampus. Atrophy was defined as > 2 SD below control values in the volume of the posterior 1.5 cm of the hippocampus. Five of 53 patients (9%) had bilateral hippocampal atrophy; four of these cases were undetected by ratios. Surgery was performed on the side of ictal onset in all five patients; four have been seizure-free for > 2 years. These results suggest that (a) mesial temporal sclerosis can be present bilaterally and may go undetected by hippocampal ratio or difference measures; (b) absolute hippocampal volume values as well as ratios are needed to detect all patients with bilateral hippocampal atrophy; and (c) temporal lobectomy is not contraindicated in patients with bilateral hippocampal atrophy, but success depends on electroencephalographic documentation of the side of predominant ictal onset.

Atrophy↗

PubMed1996

Association of restriction fragment-length polymorphisms in the alcohol dehydrogenase 2 gene with alcoholic brain atrophy.

Alcohol abuse can induce brain atrophy, but it only occurs in some alcoholics. To investigate whether genetic polymorphism of alcohol-metabolizing enzymes [including alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH)] was related to alcoholic brain atrophy, we determined restriction fragment-length polymorphisms of the ADH2 and ALDH2 genes in 77 male alcoholics. Computed tomography was used to determine the severity of brain atrophy. Digestion with MaeIII and MboII after polymerase chain reaction amplification showed that the ADH2(1) gene frequency was significantly higher in patients with brain atrophy than in those without brain atrophy (chi 2 = 9.274, p < 0.01), whereas no significant association was observed between brain atrophy and the ALDH2 gene Multivariate analysis (including age, total alcohol intake, liver cirrhosis, and ADH2 genotype) showed that the ADH2(1)/ADH2(1) genotype was associated with alcoholic brain atrophy. These findings suggest that the ADH2(1) allele may be associated with alcoholic brain atrophy.

Adult↗

PubMed2001

Regional brain atrophy is associated with physical disability in multiple sclerosis: semiquantitative magnetic resonance imaging and relationship to clinical findings.

OBJECTIVE: Brain atrophy may occur early in the course of multiple sclerosis (MS) and may be associated with disability. Brain magnetic resonance imaging (MRI) of 114 MS patients (group A) were analyzed for regional atrophy (vs age-/gender-matched controls) and T1 and T2 lesions using 4-point rating systems. Thirty-five separate patients (group B) were analyzed for cortical atrophy (ordinal scale), third ventricular width, and total T2 hyperintense lesion volume (computer assisted). In group A, regression modeling indicated that inferior frontal atrophy (P = .0003) and T2 lesions in the pons (P = .02) predicted physical disability (Expanded Disability Status Scale [EDSS] score). Secondary progressive (SP) versus relapsing patients were predicted by inferior parietal (P = .002), superior parietal (P = .006), temporal (P = .008), inferior frontal (P = .01), superior frontal (P = .01), cerebellum (P = .01), occipital (P = .01), and midbrain (P = .02) atrophy. SP patients were also predicted by total atrophy (P = .01) and third ventricular enlargement (P = .03) but not T1 or T2 lesions. In group B, the regression model predicting EDSS score included only superior frontal atrophy (r = 0.515, P = .002). Mean kappa coefficients of ordinal ratings were 0.9 (intraobserver) and 0.8 (interobserver). Ordinal ratings correlated well with quantitative assessments. The authors conclude that brain atrophy is closely associated with physical disability and clinical course in MS patients and can be appreciated using a semiquantitative MRI regional rating system.

Adult↗

PubMed1975

Statistical correlations of diffuse cerebral atrophy, with special reference to diagnostic and aetiological clues.

To evaluate diagnostic and aetiological clues for diffuse cerebral atrophy, the statistical correlations between 35 pneumoencephalographic and 97 clinical variables in 268 patients were analysed. Each case of diffuce cerebral atrophy was originally of unknown cause, and all had pneumoencephalography. Ventricular diffuse atrophy correlated positively with psychic and co-ordinative impairment and dysarthria, and cortical diffuse cerebral atrophy with psychic impairment (P smaller than 0.01 to 0.001). There was a close correlation (P smaller than 0.001) of cortical diffuse cerebral atrophy with use of vibrating tools at work. Psychic impairment combined with co-ordinative dysfunction and dysarthria is an unspecific syndrome, but should make one think of diffuse cerebral atrophy, Arteriosclerosis, abuse of alcohol, and vibrating tools at work appear to have aetiological significance for some types of diffuse cerebral atrophy. Thus the number of patients with idiopathic diffuse cerebral atrophy may rapidly decline.

Age Factors↗

PubMed1996

Biochemical and clinical study of muscle atrophy at thenar and hypothenar eminences in patients with cirrhosis.

The results of various biochemical examinations in 14 patients with cirrhosis (6 males and 8 females) with muscle atrophy at the thenar and hypothenar eminence (muscle atrophy group; mAG) were compared with those in 13 patients (8 males and 5 females) with cirrhosis without muscle atrophy at these sites (non-muscle atrophy group; NmAG). All patients were elderly men and women (mAG and NmAG, mean age, 69 +/- 3 years and 60 +/- 7, respectively). In most mAG patients, muscle atrophy was accompanied by palmar erythema. Muscle atrophy was histologically demonstrated by biopsy. Furthermore, electromyography and magnetic resonance study of the cervical spinal cord revealed that the atrophy was of myogenic rather than neurogenic origin. The Child-Pugh score, body mass index and sex hormone level in urine (total 24 h) in the two groups were compared along with the biochemical results. There were no significant differences between the two groups in urine estrogen and testosterone levels. The urinary creatinine excretion was significantly reduced in mAG. The creatine phosphokinese, lactate dehydrogenase isoenzyme and aldolase levels in serum did not differ significantly in the two groups, whereas the serum albumin level was significantly increased in NmAG. Significant differences were observed only for the serum albumin level, age and body mass index. Thus, we consider that palmar muscle atrophy in patients with cirrhosis is not due to hormonal excess in serum, but may be attributable to advanced age and diminished physical strength.

Aged↗

PubMed2001

Identification of ubiquitin ligases required for skeletal muscle atrophy.

Skeletal muscle adapts to decreases in activity and load by undergoing atrophy. To identify candidate molecular mediators of muscle atrophy, we performed transcript profiling. Although many genes were up-regulated in a single rat model of atrophy, only a small subset was universal in all atrophy models. Two of these genes encode ubiquitin ligases: Muscle RING Finger 1 (MuRF1), and a gene we designate Muscle Atrophy F-box (MAFbx), the latter being a member of the SCF family of E3 ubiquitin ligases. Overexpression of MAFbx in myotubes produced atrophy, whereas mice deficient in either MAFbx or MuRF1 were found to be resistant to atrophy. These proteins are potential drug targets for the treatment of muscle atrophy.

Amino Acid Sequence↗

PubMed2006

Hippocampal atrophy in systemic lupus erythematosus.

OBJECTIVES: To determine the frequency and progression of hippocampal atrophy in systemic lupus erythematosus (SLE) and the clinical, laboratory and treatment features associated with its occurrence. METHODS: 150 patients with SLE and 40 healthy volunteers were enrolled in our study. A complete clinical, laboratory and neurological evaluation was performed. Magnetic resonance imaging was carried out using a 2T scanner (Elscint Prestige) and coronal T1-weighted images were used for manual volumetric measurements. Atrophy was defined as values <2 standard deviations from the means of controls. RESULTS: At entry into the study, the mean right and left hippocampal volumes of patients were significantly smaller than the hippocampal volumes of controls (p<0.001). After the follow-up magnetic resonance imaging, a significant progression of reduction in right and left hippocampal volumes in patients was observed (p<0.001). At entry, atrophy was identified in 43.9% and at follow-up in 66.7% of patients with SLE. Hippocampal atrophy was related to disease duration (p<0.001) total corticosteroid dose (p = 0.01) and history of central nervous system (CNS) manifestations (p = 0.01). Progression of atrophy was associated with cumulative corticosteroid dose (p = 0.01) and number of CNS events (p = 0.01). Patients with cognitive impairment had more severe hippocampal atrophy than those without. CONCLUSION: Disease duration, total corticosteroid dose and greater number of CNS manifestations were associated with hippocampal atrophy in patients with SLE. A significant progression of hippocampal atrophy related to total corticosteroid dose and number of CNS events was observed. Further studies are necessary to confirm these findings.

Adolescent↗

PubMed1997

Cerebellar atrophy and prognosis after temporal lobe resection.

OBJECTIVE: Experimental data indicate inhibitory effects of the cerebellum on seizure activity. Structural damage such as cerebellar atrophy, which is a common finding in patients with chronic epilepsy, may reduce these effects. METHODS: Outcome after temporal lobectomy was studied in 78 consecutive patients, with or without cerebellar atrophy diagnosed by MRI. RESULTS: Thirty five patients (45%) showed cerebellar atrophy. At a mean follow up of 14.6 (range, 6-40) months, 50 patients (64%) had no postoperative seizures. In these patients, the frequency of cerebellar atrophy was significantly lower (34%) than in patients who relapsed (64%, p < 0.01). Occurrence of generalised tonic-clonic seizures (GTCS) within two years before surgery, occurrence of GTCS at any time preoperatively, long duration of epilepsy, and older age at surgery were also associated with recurrence of seizures. Multiple logistic regression analysis suggested occurrence of GTCS within two years before surgery and cerebellar atrophy as the main predictive indicators. When both factors were present, the percentage of patients remaining seizure free since surgery fell to 30%, compared with 60% when only GTCS were present, 78.6% when only cerebellar atrophy was present, and 87.5% when both factors were absent. CONCLUSIONS: Cerebellar atrophy shown by MRI was a frequent finding in surgically treated patients with temporal lobe epilepsy. The presence of cerebellar atrophy seems to worsen the prognosis after temporal lobe resection.

Adolescent↗

PubMed2004

Skeletal muscle atrophy leads to loss and dysfunction of muscle precursor cells.

Atrophy of skeletal muscle leads to decreases in myofiber size and nuclear number; however, the effects of atrophic conditions on muscle precursor cells (MPC) are largely unknown. MPC lie outside myofibers and represent the main source of additional myonuclei necessary for muscle growth and repair. In the present study, we examined the properties of MPC after hindlimb suspension (HS)-induced atrophy and subsequent recovery of the mouse hindlimb muscles. We demonstrated that the number of MPC in atrophied muscles was decreased. RT-PCR analysis of cells isolated from atrophied muscles indicated that several mRNA characteristic of the myogenic program in MPC were absent. Cells isolated from atrophied muscles failed to properly proliferate and undergo differentiation into multinucleated myotubes. Thus atrophy led to a decrease in MPC and caused dysfunction in those MPC that remained. Upon regrowth of the atrophied muscles, these deleterious effects were reversed. Our data suggest that preventing loss or dysfunction of MPC may be a new pharmacological target during muscle atrophy.

Animals↗

PubMed2006

Microarray gene expression analysis in atrophying rainbow trout muscle: a unique nonmammalian muscle degradation model.

Muscle atrophy is a physiological response to diverse physiological and pathological conditions that trigger muscle deterioration through specific cellular mechanisms. Despite different signals, the biochemical changes in atrophying muscle share many common cascades. Muscle deterioration as a physiological response to the energetic demands of fish vitellogenesis represents a unique model for studying the mechanisms of muscle degradation in non-mammalian animals. A salmonid microarray, containing 16,006 cDNAs, was used to study the transcriptome response to atrophy of fast-switch muscles from gravid rainbow trout compared with sterile fish. Eighty-two unique transcripts were upregulated and 120 transcripts were downregulated in atrophying muscles. Transcripts having gene ontology identifiers were grouped according to their functions. Muscle deterioration was associated with elevated expression of genes involved in the catheptic and collagenase proteolytic pathways; the aerobic production, buffering, and utilization of ATP; and growth arrest; whereas atrophying muscle showed downregulation of genes encoding a serine proteinase inhibitor, enzymes of anaerobic respiration, muscle proteins as well as genes required for RNA and protein biosynthesis/processing. Therefore, gene transcription of the trout muscle atrophy changed in a manner similar to mammalian muscle atrophy. These changes result in an arrest of normal cell growth, protein degradation, and decreased glycolytic cellular respiration that is characteristic of the fast-switch muscle. For the first time, other changes/mechanisms unique to fish were discussed including genes associated with muscle atrophy.

Animals↗

PubMed2004

Measurement of whole-brain atrophy in multiple sclerosis.

Brain atrophy reflects the net result of irreversible and destructive pathological processes in multiple sclerosis (MS). The gross morphological changes can be accurately quantified using standard magnetic resonance imaging (MRI) acquisitions and various image analysis tools. The current methods used to assess whole-brain atrophy in patients with MS can be classified into 2 groups based on their reliance on segmentation and registration. Segmentation-based methods employed to measure whole-brain atrophy in MS include the brain parenchymal fraction, the index of brain atrophy, the whole-brain ratio, the brain to intracranial capacity ratio, fuzzy connectedness/Udupa's method, 3DVIEWNIX, the Alfano method, and SIENAX. Current registration-based methods used to measure whole-brain atrophy in MS include the brain boundary shift integral, SIENA, statistical parametric mapping, template-driven seg mentation, and voxel-based morphometry. Most of the methods presented here are sensitive to subtle changes in brain structures and have been successfully applied to MS as measures of whole-brain atrophy. Yet comparative studies of these methods are limited and are complicated by the lack of a gold standard for image acquisition, a segmentation algorithm, an image analysis method, or a reproducibility measure. Overall, the measure of whole-brain atrophy from MRI contributes to an appreciation of the dynamics of MS pathology and its relationship to the clinical course of MS. Determination of the relative reproducibility, precision, sensitivity, and validity of these methods will promote the use of whole-brain atrophy measures as components of comprehensive MRI-based outcome assessment in MS clinical trials.

Atrophy↗

PubMed2005

Measurement of brain and spinal cord atrophy by magnetic resonance imaging as a tool to monitor multiple sclerosis.

Evaluation of brain and spinal cord atrophy by magnetic resonance imaging (MRI) has become an increasingly important component of understanding the multiple sclerosis (MS) disease process. These destructive aspects of the disease develop early in the disease course. A growing body of data links brain and spinal cord atrophy to clinical impairment more closely than can be linked with conventional measures of overt lesions. Thus, irreversible tissue damage may be a key factor leading to disease progression. In this review, the authors present the proposed mechanisms leading to central nervous system (CNS) atrophy. They describe the available MRI-based techniques to measure regional and global atrophy of the brain and spinal cord. They compare the rate of atrophy among MS phenotypes and summarize the emerging data linking atrophy to neurological and neuropsychological impairment. Finally, they discuss the effect of disease-modifying immunotherapies on the rate of CNS atrophy in patients with MS. Future research to clarify the etiology and pathophysiology of brain and spinal cord atrophy should provide new targets for therapeutic development.

Atrophy↗

PubMed2005

Microglial imaging with positron emission tomography and atrophy measurements with magnetic resonance imaging in multiple sclerosis: a correlative study.

OBJECTIVE: The objectives of the present study were to assess brain atrophy in multiple sclerosis (MS) patients during different disease stages and to investigate by PET and [11C]PK11195, a marker of microglial activation, the relationship between inflammation, atrophy and clinically relevant measures. METHODS: Eight healthy subjects and 22 MS patients were included. Semiquantitative [11C]PK11195 uptake values, with normalization on cortical grey matter, were measured for magnetic resonance imaging T2- and T1-lesions and normal appearing white matter (NAWM). As atrophy index we used the ratio of the amount of white and grey matter divided by the ventricular size, using an optimized a priori based segmentation algorithm (SPM99). RESULTS: Atrophy was significantly greater in MS patients compared to age-matched controls. A significant correlation was found between brain atrophy and both disease duration and disability, as measured with the Expanded Disability Status Scale. For NAWM, [11C]PK11195 uptake increased with the amount of atrophy, while T2-lesional [11C]PK11195 uptake values decreased according to increasing brain atrophy. CONCLUSIONS: The present study suggests that brain atrophy, correlating with disease duration and disability, is directly related to NAWM and T2-lesional inflammation as measured by microglial activation.

Adult↗

PubMed2004

Higher atrophy rate of entorhinal cortex than hippocampus in AD.

OBJECTIVES: To determine if atrophy rates were higher for entorhinal cortex (ERC) than for hippocampus in Alzheimer disease (AD), to determine the relationship between hippocampal atrophy rate and memory impairment, and to compare atrophy rates of ERC and hippocampus in differentiating between patients with AD and cognitively normal (CN) controls. METHODS: Twenty patients with AD and 25 CN subjects had MRI scans and clinical evaluations twice approximately 1.9 years apart. ERC volumes were measured manually and hippocampal volumes were measured semiautomatically on volumetric T1-weighted MR images. RESULTS: In AD, the atrophy rate of ERC (7.1 +/- 3.2%/year) was higher (p < 0.02) than that of hippocampus (5.9 +/- 2.4%/year). Furthermore, memory deficit in mild AD, measured with the Delayed List Verbal Recall test, correlated significantly with atrophy rates of both ERC (r = -0.61) and hippocampus (r = -0.59). Atrophy rates of ERC and hippocampus were comparable in differentiating between AD and CN. Using atrophy rates of ERC or hippocampus to detect a 20% treatment effect with 90% power (p < 0.05) would require about 100 completed patients per arm in a 2-year study. CONCLUSION: The finding in AD that the atrophy rate in the entorhinal cortex is higher than in the hippocampus is consistent with the view that AD pathology begins in the entorhinal cortex.

Aged↗

PubMed2004

Onset and rate of striatal atrophy in preclinical Huntington disease.

BACKGROUND: Huntington disease (HD) is characterized by striatal atrophy that begins long before the onset of motor symptoms. OBJECTIVE: To determine when striatal atrophy begins, the extent and rate of atrophy before diagnosis of motor symptoms, and whether striatal atrophy can predict when symptom onset will occur. METHODS: Caudate and putamen volumes were measured on MRI scans of 19 preclinical subjects with the HD gene expansion who were very far (9 to 20 years) from estimated onset, and on serial scans from 17 preclinical subjects, six of whom were diagnosed with HD within 5 years after the initial scan. RESULTS: Striatal volumes were significantly smaller for the subjects who were very far from estimated onset than for age-matched control subjects. Statistical models fit to the longitudinal data suggest that rate of caudate atrophy becomes significant when subjects are approximately 11 years from estimated onset and rate of putamen atrophy becomes significant approximately 9 years prior to onset. In the six incident cases, caudate and putamen were approximately one-third to one-half of normal volume at diagnosis, and caudate volume alone was able to predict with 100% accuracy those subjects who would be diagnosed within 2 years of imaging. CONCLUSIONS: Striatal atrophy begins many years prior to diagnosable HD, and assessment of atrophy on MRI may be very useful in both predicting HD onset and in tracking progression in future therapeutic trials in preclinical subjects.

Adult↗

PubMed2004

A 24-year follow-up of body mass index and cerebral atrophy.

OBJECTIVE: To investigate the longitudinal relationship between body mass index (BMI), a major vascular risk factor, and cerebral atrophy, a marker of neurodegeneration, in a population-based sample of middle-aged women. METHODS: A representative sample of 290 women born in 1908, 1914, 1918, and 1922 was examined in 1968 to 1969, 1974 to 1975, 1980 to 1981, and 1992 to 1993 as part of the Population Study of Women in Göteborg, Sweden. At each examination, women completed a survey on a variety of health and lifestyle factors and underwent anthropometric, clinical, and neuropsychiatric assessments and blood collection. Atrophy of the temporal, frontal, occipital, and parietal lobes was measured on CT in 1992 when participants were age 70 to 84. Univariate and multivariate regression analyses were used to assess the relationship between BMI and brain measures. RESULTS: Women with atrophy of the temporal lobe were, on average, 1.1 to 1.5 kg/m2 higher in BMI at all examinations than women without temporal atrophy (p < 0.05). Multivariate analyses showed that age and BMI were the only significant predictors of temporal atrophy. Risk of temporal atrophy increased 13 to 16% per 1.0-kg/m2 increase in BMI (p < 0.05). There were no associations between BMI and atrophy measured at three other brain locations. CONCLUSION: Overweight and obesity throughout adult life may contribute to the development of temporal atrophy in women.

Adult↗

PubMed1992

Patterns of cerebral atrophy in HIV-1-infected individuals: results of a quantitative MRI analysis.

Cerebral atrophy is a common radiologic manifestation of HIV dementia. To evaluate the relationship between cognitive impairment and cerebral atrophy, adjusting for age and immune status, we used standardized planimetry to measure the ventricle-brain ratio (VBR) and the bifrontal (BFR) and bicaudate (BCR) ratios, three measures of cerebral atrophy. We analyzed cranial MRIs of 23 HIV-1-seronegative controls (SN) and 116 HIV-1-infected individuals. Of the HIV-1-seropositive individuals, 37 had HIV dementia (DM group), 40 had neurologic or neuropsychological abnormalities insufficient for HIV dementia (NP+ group), and 39 were neurologically normal (NML group). We performed comparisons using analysis of covariance with correction for multiple comparisons. Both the VBR, a general measure of overall cerebral atrophy, and the BCR, a measure of atrophy in the region of the caudate nucleus, are significantly associated with dementia. The association is stronger for BCR enlargement than for VBR enlargement, suggesting that selective caudate region atrophy is associated with HIV dementia. These results indicate that overall cerebral atrophy and prominent caudate region atrophy are important radiographic features of HIV dementia.

AIDS Dementia Complex↗