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PubMed2006

Asymmetrical extra-hippocampal grey matter loss related to hippocampal atrophy in patients with medial temporal lobe epilepsy.

BACKGROUND: Structural neuroimaging studies have consistently shown a pattern of extra-hippocampal atrophy in patients with left and right drug-refractory medial temporal lobe epilepsy (MTLE). However, it is not yet completely understood how extra-hippocampal atrophy is related to hippocampal atrophy. Moreover, patients with left MTLE often exhibit more intense cognitive impairment, and subtle brain asymmetries have been reported in patients with left MTLE versus right MTLE but have not been explored in a controlled study. OBJECTIVES: To investigate the association between extra-hippocampal and hippocampal atrophy in patients with MTLE, and the effect of side of hippocampal atrophy on extra-hippocampal atrophy. METHODS: Voxel-based morphometry analyses of magnetic resonance images of the brain were performed to determine the correlation between regional extra-hippocampal grey matter volume and hippocampal grey matter volume. The results from 36 patients with right and left MTLE were compared, and results from the two groups were compared with those from 49 healthy controls. RESULTS: Compared with controls, patients with MTLE showed a more intense correlation between hippocampal grey matter volume and regional grey matter volume in locations such as the contralateral hippocampus, bilateral parahippocampal gyri and frontal and parietal areas. Compared with right MTLE, patients with left MTLE exhibited a wider area of atrophy related to hippocampal grey matter loss, encompassing both the contralateral and ipsilateral hemispheres, particularly affecting the contralateral hippocampus. CONCLUSIONS: Our results suggest that left hippocampal atrophy is associated with a larger degree of extra-hippocampal atrophy. This may help to explain the more intense cognitive impairment usually observed in these patients.

Adolescent↗

PubMed2003

Transient ischaemic attacks are associated with increased rates of global cerebral atrophy.

OBJECTIVES: To determine whether patients presenting with a first transient ischaemic attack (TIA) subsequently show increased rates of brain atrophy compared with age matched controls; and to assess potential risk factors for brain atrophy in this group. METHODS: 60 patients with a first, isolated TIA and 26 age and sex matched controls were recruited. None had evidence of cognitive impairment. Vascular risk factors were treated appropriately. All subjects had volumetric imaging at the start of the study and one year later, when they were clinically reassessed. TIA patients also had serial dual echo brain imaging. Rates of whole brain atrophy were calculated from the registered volumetric scans, as was the incidence of new ischaemic lesions. In the TIA group, the degree of white matter disease was assessed. Atrophy rates and blood pressure were compared between patients and controls. RESULTS: 22 patients (37%) developed new "clinically silent" infarcts during follow up. The mean (SD) annualised percentage atrophy rate in the TIA group was significantly higher than in the controls, at 0.82 (0.39)% v 0.33 (0.3)% (p < 0.0001). In the TIA group, diastolic blood pressure (p = 0.004) and white matter disease severity (p < 0.001) were correlated with cerebral atrophy rate. Increased white matter disease was found in patients in whom new ischaemic lesions developed (p < 0.001). CONCLUSIONS: Patients presenting with a first TIA have excess global brain atrophy compared with age matched controls over the subsequent year. Increased atrophy rates following a TIA may be directly or indirectly related to increasing white matter disease and diastolic hypertension. Future studies should assess whether this atrophy inevitably leads to cognitive decline, and whether aggressive treatment of risk factors for cerebrovascular disease (particularly hypertension) after a TIA can influence outcome.

Aged↗

PubMed2005

Fatty atrophy of supraspinatus and infraspinatus muscles: accuracy of US.

PURPOSE: To prospectively evaluate the accuracy of ultrasonography (US) in depicting fatty atrophy of the supraspinatus (SSP) and infraspinatus (ISP) muscles, with magnetic resonance (MR) imaging as the reference standard. MATERIALS AND METHODS: Institutional review board approval and informed consent were obtained. SSP and ISP muscles of 65 consecutive patients (27 women, 38 men; mean age, 53.1 years; range, 28-83 years) with possible rotator cuff tears were evaluated with US in two planes. Visibility of muscle contour, pennate pattern, the central tendon, and muscle echogenicity was assessed by two radiologists. On the basis of these findings, diagnosis of substantial fatty atrophy was made at US. Accuracy, sensitivity, specificity, proportion of over- and underestimations, and interobserver agreement in diagnosis of substantial (grade 2 or greater) muscle atrophy were determined. Fatty atrophy was graded at MR imaging as follows: score of 0 = no intramuscular fat, score of 1 = some fatty streaks, score of 2 = fat evident but less extensive than muscle, score of 3 = fat equal to muscle, and score of 4 = fat more extensive than muscle. RESULTS: For readers 1 and 2, the accuracy of US in depicting fatty atrophy of SSP muscle was 75% (49 of 65) and 72% (47 of 65), sensitivity was 89% (eight of nine) and 100% (nine of nine), and specificity was 73% (41 of 56) and 68% (38 of 56), respectively. For readers 1 and 2, the accuracy of US in depicting fatty atrophy of ISP muscle was 85% (55 of 65) and 80% (52 of 65), sensitivity was 58% (11 of 19) and 63% (12 of 19), and specificity was 96% (44 of 46) and 87% (40 of 46), respectively. Overestimation of SSP muscle atrophy was more common (23% [15 of 65] for reader 1 and 28% [18 of 65] for reader 2) than underestimation (2% [one of 65] for reader 1 and 0% [0 of 65] for reader 2). For readers 1 and 2, overestimation of ISP muscle atrophy was 3% (two of 65) and 9% (six of 65) and underestimation was 12% (eight of 65) and 9% (seven of 65), respectively. Interobserver agreement was moderate for SSP (kappa = 0.55) and substantial for ISP (kappa = 0.71) muscles. CONCLUSION: US is moderately accurate in the diagnosis of substantial fatty atrophy of the SSP or ISP muscle.

Adipose Tissue↗

PubMed2004

The molecular basis of skeletal muscle atrophy.

Skeletal muscle atrophy attributable to muscular inactivity has significant adverse functional consequences. While the initiating physiological event leading to atrophy seems to be the loss of muscle tension and a good deal of the physiology of muscle atrophy has been characterized, little is known about the triggers or the molecular signaling events underlying this process. Decreases in protein synthesis and increases in protein degradation both have been shown to contribute to muscle protein loss due to disuse, and recent work has delineated elements of both synthetic and proteolytic processes underlying muscle atrophy. It is also becoming evident that interactions among known proteolytic pathways (ubiquitin-proteasome, lysosomal, and calpain) are involved in muscle proteolysis during atrophy. Factors such as TNF-alpha, glucocorticoids, myostatin, and reactive oxygen species can induce muscle protein loss under specified conditions. Also, it is now apparent that the transcription factor NF-kappaB is a key intracellular signal transducer in disuse atrophy. Transcriptional profiles of atrophying muscle show both up- and downregulation of various genes over time, thus providing further evidence that there are multiple concurrent processes involved in muscle atrophy. The purpose of this review is to synthesize our current understanding of the molecular regulation of muscle atrophy. We also discuss how ongoing work should uncover more about the molecular underpinnings of muscle wasting, particularly that due to disuse.

Gene Expression↗

PubMed2004

Correlating brain atrophy with cognitive dysfunction, mood disturbances, and personality disorder in multiple sclerosis.

Neuropsychological impairment is a common feature of multiple sclerosis. Affected patients often have deficits in information-processing speed and memory and exhibit psychopathological states such as depression. A minority of patients have rarer affect/mood disorders such as euphoria sclerotica and pathological laughter/crying. Neuropsychological impairment is a major predictor of low quality of life, unemployment, and caregiver distress. Studies evaluating correlations between neuropsychological impairment and findings on magnetic resonance imaging show that neuropsychological dysfunction is associated with lesion burden and diffuse disease in normal-appearing brain tissue. However, measures of tissue atrophy including whole-brain and central atrophy are especially well correlated with and predictive of cognitive impairment. Moreover, recent studies have shown that conventional measures of brain atrophy explain more variance in neuropsychological dysfunction than do measures of lesion burden. In particular, neuropsychological outcomes correspond highly with linear measures of subcortical atrophy such as ventricle enlargement. Within the domain of emotional dysfunction, both lesion burden and atrophy are related to major depressive disorder. Brain atrophy also predicts euphoria and disinhibition. The preliminary data suggest that although lesion burden primarily predicts depressive disorder, both lesion burden and atrophy predict the presence of euphoria. Euphoria and disinhibition likely represent personality change associated with worsening cognition as the disease progresses. Taken together, this growing body of data on magnetic resonance imaging to neuropsychological correlations supports the clinical relevance and validity of brain atrophy as a measure of disease progression in multiple sclerosis. Continuing research focuses on the possible relationship between measures of regional brain atrophy and cognitive and emotional impairment.

Atrophy↗

PubMed1976

The clinical significance of pneumographic cerebellar atrophy.

The clinical significance of apparent pneumographic cerebellar atrophy has been studied in a group of 44 otherwise unselected patients found to have cerebellar atrophy, according to previously suggested criteria, at pneumoencephalography. Lateral and postero-anterior tomography of the posterior fossa was performed in all these cases. In each case the width of two or more sulci in the cerebellar vermis exceeded 2 mm. We have concluded that: (1) There is a relationship between the severity of pneumographic cerebellar atrophy and the severity of clinical signs of cerebellar disease (p = 0.03). (2) Severe or moderate atrophy of the vermis, whether generalized or focal, is usually associated with clinical signs of cerebellar disease, but mild atrophy of the vermis, equivalent to the "moderate" atrophy of previous studies, has no apparent diagnostic significance. (3) Atrophy of the cerebellar hemispheres, in the absence of atrophy of the vermis, is very unusual and it cannot, by itself, be correlated with clinical signs of cerebellar disease. (4) In individual cases, assessment of the significance of pneumographic cerebellar atrophy cannot be made without adequate clinical information.

Adult↗

PubMed1995

CT findings of atrophy of chest wall muscle after thoracotomy: relationship between muscles involved and type of surgery.

OBJECTIVE: Postthoracotomy atrophy of chest wall muscles results from nerve injury during surgery. After encountering patients with different patterns of chest wall muscular atrophy postthoracotomy, we performed this study to determine the relationship between type of thoracotomy and atrophic muscles as seen on CT scans. MATERIALS AND METHODS: CT scans of 58 patients who had previously undergone unilateral thoracotomy were reviewed. Forty patients had a posterolateral thoracotomy, and 18 had an anterolateral thoracotomy. In two cases, the incision extended posteriorly. Atrophy seen on CT scans was defined as a marked decrease in size or thickness of a muscle compared with the muscle on the other side. RESULTS: Atrophy of the latissimus dorsi muscle and of the inferior portion of the serratus anterior muscle was detected on CT scans in 40 patients. No atrophy was found in 16 patients. The remaining two displayed atrophy only in the serratus anterior muscle. Atrophy of the latissimus dorsi muscle and of the inferior portion of the serratus anterior muscle developed in all patients who had a posterolateral thoracotomy. Atrophy developed in only two of the 18 patients who had an anterolateral thoracotomy, and in these two, the incision had been extended posteriorly. CONCLUSION: A direct correlation was found between type of thoracotomy and site of atrophy of the chest wall muscles seen on CT scans. This finding may account for different CT appearances of the thoracic wall in patients who have had thoracic surgery.

Aged↗

PubMed1991

The relationship of pineal calcification to cortical atrophy in schizophrenia.

Several recent computed tomographic (CT) studies have provided evidence for structural cerebral abnormalities in schizophrenia. CT scan findings included enlargement of the lateral cerebral ventricles, cortical atrophy, third ventricular dilatation, ventricular asymmetry, and cerebellar atrophy. In addition, there is increasing data to suggest that abnormal pineal melatonin functions are associated with the pathophysiology of schizophrenia. To explore further the relationship of the pineal gland to the pathophysiology of schizophrenia and its specific association with structural abnormalities, we investigated: (a) the relationship of pineal calcification (PC) to computerized tomographic (CT) scan measurements of cortical and subcortical atrophy in 41 chronic schizophrenic patients, and (b) the relationship of PC size to CT scan measurements and cortical and subcortical atrophy in 51 chronic schizophrenic patients. Results of the first study revealed that the presence of PC was significantly associated with measurements of prefrontal cortical atrophy (p less than .01), while there was no association with measurements of parieto-occipital atrophy, sulcal prominence, or ventricular brain ratio (VBR). These findings support the notion that the various structural brain abnormalities in schizophrenia may reflect different pathological processes and that abnormal pineal melatonin functions may be associated with the pathophysiology of prefrontal cortical atrophy. In addition, since some clinical facets of schizophrenia covary with frontal lobe dysfunction, our findings highlight the significance of abnormal pineal functions for the pathophysiology of schizophrenia. In the second study we found a significantly higher prevalence of pathologically enlarged PC (i.e., greater than 1 cm in diameter) in schizophrenia as compared to controls of similar age. In addition, we found a significant association between CT scan measurements of cortical atrophy and pathologically enlarged PC size (p less than .05). By contrast, PC size was unrelated to VBR. These findings demonstrate a specific association between pathologically enlarged PC and cortical atrophy in schizophrenia. The implications of these findings to the pathophysiology of schizophrenia and, specifically, to the morphological abnormalities that accompany the disease are discussed.

Adult↗

PubMed1992

Relationship between condylar atrophy and tooth loss in craniomandibular disorders.

In order to investigate the relationship between condylar atrophy and tooth loss in craniomandibular disorders, we examined 37 patients with condylar atrophy (atrophy (+) group) and 109 patients without condylar atrophy (atrophy (-) group). No significant difference in the number of missing teeth between the atrophy (+) group and atrophy (-) group was observed. However, a significant relationship between condylar atrophy and loss of the lower first molars was found. And individuals in the atrophy (+) group had a tendency to lose one or both lower first molars and left them without any prosthetic restorations in the growth period of the TMJ components.

Adolescent↗

PubMedDate not supplied

Comparisons between global and focal brain atrophy rates in normal aging and Alzheimer disease: Boundary Shift Integral versus tracing of the entorhinal cortex and hippocampus.

The objectives of this study were to (1) compare atrophy rates associated with normal aging and Alzheimer disease (AD) using the semi-automated Boundary Shift Integral (BSI) method and manual tracing of the entorhinal cortex (ERC) and hippocampus and (2) calculate power of BSI vs. ERC and hippocampal volume changes for clinical trials in AD. We quantified whole brain and ventricular BSI atrophy rates and ERC and hippocampal atrophy rates from longitudinal MRI data in 20 AD patients and 22 age-matched healthy controls. All methods revealed significant brain atrophy in controls and AD patients. AD patients had approximately 2.5 times greater whole brain BSI atrophy rates and more than 5 times greater ERC and hippocampal atrophy rates than controls. ERC and hippocampal atrophy rates were higher in both groups than whole brain BSI atrophy rates, but lower than ventricular BSI atrophy rates. Effect size and power calculations suggest that ERC and hippocampal measurements may be more sensitive than ventricular or whole brain BSI for detecting AD progression and the potential effects of disease modifying agents. Logistic regression analysis revealed that combined rates of ERC and ventricular BSI were the best explanatory variables for classifying AD from controls.

Aged↗

PubMed1989

[Evaluation of bone atrophy by microdensitometry and effect of active vitamin D3 (1 alpha-OH-D3) administration in patients receiving anticonvulsants].

Attention has been paid to bone atrophy caused by oral anticonvulsants. Bone atrophy has been judged on X-ray picture in combination with measuring bio-chemical parameters such as serum calcium (Ca), phosphorus (P) and alkaline phosphatase (Alp), and assessing X-ray findings such as bone density and morphological findings of bone. However, the conventional techniques based on these parameters and findings do not always permit diagnosing the disease. Microdensitometric (MD) method, recently developed by Inoue et al. as a method to assess the grades of severity of bone atrophy on X-ray picture of the metacarpal bone II, has been improved in its exactitude and widely applied in clinical practice for diagnosis of bone atrophy. In 174 patients receiving anticonvulsants, the severity of bone atrophy was quantitatively assessed by the MD method. 1 microgram/day of active vitamin D3 (1 alpha-OH-D3) was administered to patients presenting abnormal MD findings indicative of bone atrophy, and the results were as follows: 1. Bone atrophy of grades initial to III was noted in 46 patients (26.4%). There was no sex-difference in incidence of bone atrophy. 2. In patients receiving valproic acid (VPA) for two years or longer, there was no correlation between the duration of VPA treatment and the severity of the disease as assessed by MD method or its incidence, nor between the mean blood level of VPA and the severity. 3. Bone atrophy was found in 25 (29.1%) of the patients receiving anticonvulsants even for less then two years. Five of these 25 patients were alcoholism , and 9 patients received steroids.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorptiometry, Photon↗

PubMed1995

Crossed cerebellar atrophy in children: a neurologic sequela of extreme prematurity.

Unilateral atrophy of a cerebellar hemisphere occurring as a sequela of ischemic or destructive injury of the contralateral cerebral hemisphere is uncommon in children. We reviewed our experience with this phenomenon and found an unexpected association with extreme prematurity and a complicated perinatal course with a poor subsequent neurologic outcome. We retrospectively identified eight children, aged 8 months to 13 years, in whom cerebellar atrophy associated with cerebral injury was diagnosed on MR or CT, and reviewed their past medical history, neurologic findings, and neuroimaging studies. Seven patients were born extremely premature, EGA 25-28 weeks, and had severe perinatal intracranial hemorrhage. Neurologic problems include severe developmental delay in seven, spastic paresis in six, and seizures in five. Neuroimaging showed severe unilateral holohemispheric atrophy in four, bilateral asymmetric holohemispheric atrophy in two, and left temporoparietal atrophy in one. Cerebellar atrophy was unilateral in five and bilateral but asymmetric in two. Gliosis of the atrophic cerebellum occurred in one patient. Sequential neuroimaging in one patient showed evolution of crossed cerebellar atrophy at 8 months of age. The final patient, a term infant, had an idiopathic perinatal left cerebral infarct. In our experience, crossed cerebellar atrophy was an uncommon manifestation of extreme prematurity complicated by severe intracranial hemorrhage and/or ischemic necrosis of white matter. The cerebellar atrophy is most often a secondary degenerative phenomenon rather than a result of direct cerebellar injury.

Atrophy↗

PubMed1994

Dexamethasone, beta-estradiol, and 2,3,7,8-tetrachlorodibenzo-p-dioxin elicit thymic atrophy through different cellular targets.

The effects of single doses of dexamethasone (DEX), beta-estradiol-17-valerate (E2), and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the kinetics of thymic atrophy and related bone marrow and thymocyte phenotype alterations were examined. The results imply differences in the mechanisms by which these compounds act. Of the three compounds, DEX induced maximal atrophy by 3 days with complete recovery by Day 12. At the point of maximal atrophy, the RAG-1+TdT+CD4+8+3int thymocyte population was proportionately the most depleted. In contrast, TCDD and E2 caused maximal thymic atrophy by Day 12. E2 treatment, like DEX, resulted in a preferential decrease in the RAG-1+TdT+CD4+8+3int population, but unlike DEX, this decrease persisted. TCDD-induced thymic atrophy resulted from a proportional loss of all classes of thymocytes. There was no significant relative reduction of TdT+RAG-1+ cells by TCDD in the thymus. A slow and persistent reduction of TdT and RAG-1 in bone marrow by both TCDD and E2 contrasted with the rapid reduction and quick recovery of these markers in marrow from DEX-treated animals. Additional studies showed that only DEX-induced atrophy was accompanied by the induction of thymocyte apoptosis, as detected by multiple nucleosomal length DNA fragments within the first 24 hr. The different kinetics and proportions of subsets in the atrophied thymuses, as well as the distinct patterns of alterations of RAG and TdT expression, and the presence or the absence of apoptosis provide evidence for different mechanisms of thymic atrophy by these agents. The slow induction and longer persistence of thymic atrophy induced by E2 and TCDD, as well as their effects on bone marrow stem cell markers, suggest that bone marrow thymocyte precursors are major targets for these agents.

Animals↗

PubMed2006

Rapid disuse and denervation atrophy involve transcriptional changes similar to those of muscle wasting during systemic diseases.

We previously identified a common set of genes, termed atrogenes, whose expression is coordinately induced or suppressed in muscle during systemic wasting states (fasting, cancer cachexia, renal failure, diabetes). To determine whether this transcriptional program also functions during atrophy resulting from loss of contractile activity and whether atrogene expression correlates with the rate of muscle weight loss, we used cDNA microarrays and RT-polymerase chain reaction to analyze changes in mRNA from rat gastrocnemius during disuse atrophy induced by denervation or spinal cord isolation. Three days after Den or SI, the rate of muscle weight loss was greatest, and 78% of the atrogenes identified during systemic catabolic states were induced or repressed. Of particular interest were the large inductions of key ubiquitin ligases, atrogin-1 (35- to 44-fold) and MuRF1 (12- to 22-fold), and the suppression of PGC-1alpha and PGC-1beta coactivators (15-fold). When atrophy slowed (day 14), the expression of 92% of these atrogenes returned toward basal levels. At 28 days, the atrophy-inducing transcription factor, FoxO1, was still induced and may be important in maintaining the "atrophied" state. Thus, 1) the atrophy associated with systemic catabolic states and following disuse involves similar transcriptional adaptations; and 2) disuse atrophy proceeds through multiple phases corresponding to rapidly atrophying and atrophied muscles that involve distinct transcriptional patterns.

Animals↗

PubMed2006

Iris atrophy in patients with newly diagnosed multibacillary leprosy: at diagnosis, during and after completion of multidrug treatment.

AIM: To describe the prevalence and incidence of iris atrophy in patients with multibacillary (MB) leprosy. METHODS AND PATIENTS: Prospective longitudinal cohort study. 301 newly diagnosed patients with MB leprosy were followed up during the 2 years of treatment with multidrug therapy (MDT) and for a further 5 years with biannual ocular examinations. Incidence of iris atrophy was calculated as the number of patients with iris atrophy per person-year (PY) of follow-up among those who did not have iris atrophy at baseline. Stepwise multiple regression confirmed the presence of specific associations of demographic and clinical characteristics (p<0.05) with iris atrophy, detected by univariate analysis. RESULTS: Iris atrophy was present in 6 (2%) patients at enrolment. During MDT, with 445 PYs of follow-up, 9 patients developed iris atrophy (IR 0.02, 95% CI 0.01 to 0.04) that was associated with cataract (HR 15.13, 95% CI 3.71 to 61.79, p<0.001) and corneal opacities (HR 6.83, 95% CI 1.62 to 28.8, p = 0.009). After MDT, with 2005 PYs of follow-up, 60 patients developed iris atrophy (IR 0.03, 95% CI 0.023 to 0.039) that was associated with age (per decade; HR 1.40, 95% CI 1.10 to 1.78, p = 0.006), skin smear positivity (HR 3.50, 95% CI 1.33 to 9.24, p = 0.011), cataract (HR 3.66, 95% CI 1.85 to 7.25, p<0.001), keratic precipitates (HR 2.76, 95% CI 1.02 to 7.47, p = 0.046) and corneal opacity (HR 3.95, 95% CI 1.86 to 8.38, p<0.001). CONCLUSIONS: Iris atrophy continues to develop in 3% of patients with MB leprosy every year after they complete a 2-year course of MDT, and is associated with age, increasing loads of mycobacteria, subclinical inflammation, cataract and corneal opacity.

Adolescent↗

PubMed1997

Muscle fatigue in spinal muscular atrophy.

We previously reported that patients with spinal muscular atrophy do not lose muscle strength over time as measured quantitatively. However, we noted that many patients with spinal muscular atrophy suffer from what they call fatigue. We wondered if we could measure fatigue during a single maximal voluntary contraction, whether fatigue might increase with time, independent of muscle strength, and whether increasing fatigue might correlate with loss of function in some patients. We measured fatigue during a single maximal voluntary contraction in a cohort of patients having spinal muscular atrophy using quantitative strength testing. We included only patients with spinal muscular atrophy aged 5 years or older, so they could follow instructions regarding muscle contraction, and who were followed for at least 2 years. Seventy-six children with spinal muscular atrophy and 24 untrained individuals, aged 5 to 57 years (mean, 16.8 years), were studied. There was no discernible abnormal fatigue in patients with spinal muscular atrophy compared to untrained controls using our methodology. Thus, spinal muscular atrophy may not be associated with fatiguability. Moreover, spinal muscular atrophy does not appear to cause progressive muscle fatigue with age or loss of function. It is possible that fatigue was undetectable by our methods. An alternative explanation is that what patients describe as fatigue may be caused by factors outside the neuromuscular system. Such factors may include chronic respiratory insufficiency with hypoventilation and carbon dioxide retention as well as chronic malnutrition and negative nitrogen balance.

Adolescent↗

PubMed2002

Longitudinal brain volume measurement in multiple sclerosis: rate of brain atrophy is independent of the disease subtype.

BACKGROUND: In multiple sclerosis (MS), brain atrophy depicted by magnetic resonance imaging reflects overall tissue loss, including axonal loss. OBJECTIVE: To determine the course of atrophy by studying the rate of development of brain atrophy in patients who have different subtypes of MS. METHODS: Eighty-three patients with MS (42 with relapsing-remitting, 21 with secondary progressive, and 20 with primary progressive) were studied longitudinally, with an interval of 2 to 4 years. Magnetic resonance imaging included T1- and T2-weighted images to obtain 2 brain volume measurements: (1) the parenchymal fraction as a marker of global brain atrophy and (2) the ventricular fraction as a marker of central atrophy. The annualized rate of global and central brain atrophy was compared between those with different subtypes of MS and related to clinical characteristics, including sex, age, disease duration, and disability. RESULTS: There was a significant decrease of the parenchymal fraction (-0.7% per year; SEM, 0.11% per year) and a significant increase of ventricular fraction (3.7% per year; SEM, 0.54% per year) in the total group. Significant tissue loss was also seen in all 3 subtypes of MS; the decrease in parenchymal fraction was not different between subtypes, whereas the increase in ventricular fraction tended to be larger in patients with secondary progressive MS compared with patients with primary progressive MS. Marginal associations were found between clinical determinants and the rate of brain atrophy. Annualized increase in the ventricular fraction was correlated with age (r = -0.26) and duration of symptoms (r = -0.22): younger patients (mainly patients with relapsing-remitting MS who have a limited disability) displayed a larger increase in ventricular fraction compared with older patients. CONCLUSIONS: The rate of development of brain atrophy is largely independent of the course of the disease and other clinical characteristics. The relentless loss of tissue occurring in MS is not restricted to later (progressive) phases of the disease, thereby stressing the need for early neuroprotective treatment in MS.

Adult↗

PubMed2002

Proteomic analysis of rat soleus muscle undergoing hindlimb suspension-induced atrophy and reweighting hypertrophy.

A proteomic analysis was performed comparing normal rat soleus muscle to soleus muscle that had undergone either 0.5, 1, 2, 4, 7, 10 and 14 days of hindlimb suspension-induced atrophy or hindlimb suspension-induced atrophied soleus muscle that had undergone 1 hour, 8 hour, 1 day, 2 day, 4 day and 7 days of reweighting-induced hypertrophy. Muscle mass measurements demonstrated continual loss of soleus mass occurred throughout the 21 days of hindlimb suspension; following reweighting, atrophied soleus muscle mass increased dramatically between 8 hours and 1 day post reweighting. Proteomic analysis of normal and atrophied soleus muscle demonstrated statistically significant changes in the relative levels of 29 soleus proteins. Reweighting following atrophy demonstrated statistically significant changes in the relative levels of 15 soleus proteins. Protein identification using mass spectrometry was attempted for all differentially regulated proteins from both atrophied and hypertrophied soleus muscle. Five differentially regulated proteins from the hindlimb suspended atrophied soleus muscle were identified while five proteins were identified in the reweighting-induced hypertrophied soleus muscles. The identified proteins could be generally grouped together as metabolic proteins, chaperone proteins and contractile apparatus proteins. Together these data demonstrate that coordinated temporally regulated changes in the skeletal muscle proteome occur during disuse-induced soleus muscle atrophy and reweighting hypertrophy.

Amino Acid Sequence↗