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Chronic Stages (chronic + stage)
Selected AbstractsActive Vegetations Can Be Differentiated from Chronic Vegetations by Visual Inspection of Standardized Two-Dimensional EchocardiogramsECHOCARDIOGRAPHY, Issue 2 2000PH.D., TAHIR TAK M.D. The ability to differentiate active from chronic valvular vegetations (VEGs) by digital image processing and by visual observation was evaluated in 18 patients with a clinical diagnosis of infective endocarditis (IE). Two-dimensional echocardiographic (2-DE) examinations were performed on all patients at diagnosis and after a mean period of 52 days. Two comparable images (active and chronic) from the same patient and in the same phase of the cardiac cycle were digitized, magnified, and displayed on a high resolution monitor. The mean pixel intensity (MPI) was 72 ± 14 in the active stage and 143 ± 23 in the chronic stage (P < 0.0001). The VEG size was 0.64 ± 0.15 cm2 in the active stage and decreased to 0.46 ± 0.17 cm2 in the chronic stage (P < 0.001). Two experienced echocar-diographers, who were blinded to the age of the VEGs, identified each echocardiographic image as active or chronic based on visual observation of density of the VEGs. The VEGs were correctly identified as active or chronic in 17 out of the 18 patients. In summary, although digital image processing of 2-DE may be useful, the density of VEGs assessed by visual inspection will help differentiate between active and chronic VEGs of IE. The standardization procedure at the time of the initial study and use of identical gain settings in subsequent studies are key factors in making this distinction. [source] Retrograde Wallerian degeneration of cranial corticospinal tracts in cervical spinal cord injury patients using diffusion tensor imagingJOURNAL OF NEUROSCIENCE RESEARCH, Issue 10 2008Saurabh Guleria Abstract Diffusion tensor imaging (DTI) has the potential to reveal disruption of white matter microstructure in chronically injured spinal cords. We quantified fractional anisotropy (FA) and mean diffusivity (MD) to demonstrate retrograde Wallerian degeneration (WD) of cranial corticospinal tract (CST) in cervical spinal cord injury (SCI). Twenty-two patients with complete cervical SCI in the chronic stage were studied with DTI along with 13 healthy controls. Mean FA and MD values were computed for midbrain, pons, medulla, posterior limb of internal capsule, and corona radiata. Significant reduction in the mean FA and increase in MD was observed in the cranial CST in patients with SCI compared with controls, suggesting retrograde WD. Statistically significant inverse FA and MD changes were noted in corona radiata, indicating some restoration of spared white matter tracts. Temporal changes in the DTI metrics suggest progressing degeneration in different regions of CST. These spatiotemporal changes in DTI metrics suggest continued WD in injured fibers along with simultaneous reorganization of spared white matter fibers, which may contribute to changing neurological status in chronic SCI patients. © 2008 Wiley-Liss, Inc. [source] Elevated Cerebrospinal Fluid Tau Protein Levels in Wernicke's EncephalopathyALCOHOLISM, Issue 6 2008Sachio Matsushita Objective:, Limited neuronal cell loss is seen in the neuropathology of Wernicke's encephalopathy (WE), but the extent of neuronal damage has not been well studied. Moreover, there is still a debate as to whether alcohol itself causes brain damage in humans. Although, it is difficult to examine the extent of neuronal damage in living patients, recent studies have revealed that total tau protein levels in the cerebrospinal fluid (CSF) reflect the rate of neuronal degeneration. Therefore, we hypothesized that the elevated CSF total tau in patients with WE was due to neuronal damage and thus we examined CSF total tau protein in patients with WE, as well as in those with alcohol withdrawal delirium (WD) and Korsakoff syndrome (KS). We also examined CSF total tau in nonalcohol dependent patients with Alzheimer's disease (AD) as a disease control. Methods:, CSF samples were obtained from 13 acute WE patients with alcohol dependence, 9 WD patients with alcohol dependence and 16 KS patients with alcohol dependence, and from 20 nonalcohol dependent AD patients. CSF was also obtained from 10 of the WE patients after their disease had progressed to the chronic stage. CSF tau protein levels in all samples were determined by sandwich enzyme-linked immunosorbent assay. Tau phosphorylated at threonine 181 (p-tau181) and amyloid ,-protein ending at amino acid 42 (A,42) in CSF were also determined for comparison between acute WE with AD. Results:, Total tau was significantly elevated in acute WE and decreased on long-term follow-up, but was not elevated in WD or KS. The patterns of p-tau181 and A,42 differed between acute WE and AD. Conclusions:, Intense neuronal cell death occurs transiently in WE, and the mechanism differs from that in AD. Neuronal damage is generally unaccompanied in WD. These results suggest that CSF total tau is a useful biological marker for WE. [source] Clinicopathological features of chronic hypersensitivity pneumonitisRESPIROLOGY, Issue 4 2002HIROSHI HAYAKAWA Objective: Only limited information exists concerning the clinical and pathological features of chronic hypersensitivity pneumonitis (HP) in Japan and elsewhere. We present data on clinicopathological features of chronic HP obtained through a Japanese nationwide survey. Methodology: We studied the clinical and pathological findings in 10 patients with chronic HP who underwent surgical lung biopsy or postmortem examination. Results: There were three types of clinical course: six of the 10 patients had persistent symptoms followed by repeated acute episodes; two showed a subacute onset with persistent symptoms; and two exhibited an insidious onset. Five patients made no attempt to avoid antigen exposure and they all had progressive disease. Pathological findings indicated that lesions were mainly centrilobular with or without epithelioid cell granulomas in specimens obtained during the acute or subacute stage. In contrast, most patients in the chronic stage predominantly showed interstitial fibrosis with a usual interstitial pneumonia pattern. Conclusions: The pathological findings of chronic HP depend on the stage of the disease at tissue sampling. [source] Serum VEGF levels in acute ischaemic strokes are correlated with long-term prognosisEUROPEAN JOURNAL OF NEUROLOGY, Issue 1 2010S.-C. Lee Background and purpose:, We investigated whether serum vascular endothelial growth factor (VEGF) levels in acute-stage ischaemic stroke patients with small vessel disease (SVD) or large vessel disease (LVD) are correlated with long-term prognoses, based on the difference in NIH Stroke Scale (NIHSS) scores between acute and chronic stages. Methods:, From March 2007 to May 2008, we evaluated patients who experienced an ischaemic stroke for the first time, defined as SVD (n = 89) or LVD (n = 91) using the TOAST classification. Serum samples were taken immediately after admission (within 24 h of stroke onset) to evaluate VEGF levels. After 3 months, follow-up NIHSS scores were collected for all patients. Results:, Serum VEGF levels in the acute stage (within 24 h of stroke onset) were higher in the LVD group than in the SVD group and were correlated with infarction volume. The increase in serum VEGF levels in the acute stage was proportional to an improved NIHSS score after 3 months. After adjustment for covariates, serum VEGF levels in the acute stage were still significantly correlated with the long-term prognosis of ischaemic stroke. Conclusion:, Serum VEGF levels are correlated with long-term prognoses in acute ischaemic stroke patients. [source] Joint capsule mast cells and neuropeptides are increased within four weeks of injury and remain elevated in chronic stages of posttraumatic contracturesJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 10 2008Kevin A. Hildebrand Abstract The purpose of this article was to determine mast cell and neuropeptide nerve fiber numbers in joint capsules in posttraumatic contractures, as elevated numbers have been implicated in other fibrotic and contracture conditions. Twelve skeletally mature rabbits had intraarticular cortical windows removed from the medial and lateral femoral condyles and the knee joint immobilized. The contralateral unoperated limb served as a control. Equal numbers of rabbits were sacrificed 4 weeks after surgery or 40 weeks after the first surgery that included 32 weeks of remobilization. Six patients with chronic posttraumatic elbow joint contractures and six age-matched organ donor controls free of elbow contractures were also studied. Joint capsule myofibroblast, mast cell, and neuropeptide containing nerve fiber numbers were assessed with immunohistochemistry. The numbers of myofibroblasts, mast cells, and neuropeptide containing nerve fibers expressed as a percentage of total cells were significantly greater in the contracture capsules when compared to the control capsules at all time points (p,<,0.0001). The range of percentages for the three components in the contracture capsules versus the controls were 41,48% versus 9,10%, 44,50% versus 11,13%, and 45,50% versus 10,12% for the acute and chronic stages of the rabbit model and the chronic stages in the human elbows, respectively. These data support the hypothesis that a myofibroblast,mast cell,neuropeptide fibrosis axis may underlie some of the pathologic changes in the joint capsule in posttraumatic contractures. Approaches designed to manipulate this axis, such as preventing degranulation of mast cells, warrant further investigation. © 2008 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 26:1313,1319, 2008 [source] Pathophysiology of spastic paresis.MUSCLE AND NERVE, Issue 5 2005II: Emergence of muscle overactivity Abstract In the subacute and chronic stages of spastic paresis, stretch-sensitive (spastic) muscle overactivity emerges as a third fundamental mechanism of motor impairment, along with paresis and soft tissue contracture. Part II of this review primarily addresses the pathophysiology of the various forms of spastic overactivity. It is argued that muscle contracture is one of the factors that cause excessive responsiveness to stretch, which in turn aggravates contracture. Excessive responsiveness to stretch also impedes voluntary motor neuron recruitment, a concept termed stretch-sensitive paresis. None of the three mechanisms of impairment (paresis, contracture, and spastic overactivity) is symmetrically distributed between agonists and antagonists, which generates torque imbalance around joints and limb deformities. Thus, each may be best treated focally on an individual muscle-by-muscle basis. Intensive motor training of the less overactive muscles should disrupt the cycle of paresis,disuse,paresis, and concomitant use of aggressive stretch and focal weakening agents in their more overactive and shortened antagonists should break the cycle of overactivity,contracture,overactivity. Muscle Nerve, 2005 [source] Cell death and apoptosis-related proteins in muscle biopsies of sporadic amyotrophic lateral sclerosis and polyneuropathyMUSCLE AND NERVE, Issue 8 2001Benedikt G.H. Schoser MD Abstract To investigate disease-related differences of cell death and apoptosis in human denervation atrophy, we studied DNA fragmentation by the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) method in 38 biopsies of clinically nonaffected and affected muscles from patients with sporadic amyotrophic lateral sclerosis (sALS), in 13 muscle biopsies from patients with chronic peripheral neuropathies, and in 8 biopsies from control subjects. In addition, expression of apoptosis-related proteins, bax, bcl-2, and Fas, was studied in 20 biopsies of sALS and 10 chronic peripheral neuropathies. We identified DNA cleavage in 10% of myofibers of patients and in up to 1.5% of control samples. In clinically affected muscles of ALS, a larger amount of TUNEL-positive myofibers (mean 10.5 ± 5.9%) was detected, similar to chronic peripheral neuropathies (mean 10.0 ± 7.4%). Atrophic myofibers were immunopositive for bax, bcl-2, and, to a weaker extent, for Fas. However, bax-, bcl-2-, or Fas-positive atrophic myofibers did not reveal consecutive DNA cleavage. Differences between sALS subgroups and chronic peripheral neuropathies were not found. In human denervation atrophy the bcl-2/bax and the FasL/Fas systems are apparently active independently of DNA fragmentation and apoptosis. DNA fragmentation thus displays an additional reaction that is not disease-specific at chronic stages of human denervation processes, probably recapitulating events like skeletal muscle fiber remodeling in embryonic skeletal tissue development. © 2001 John Wiley & Sons, Inc. Muscle Nerve 24: 1083,1089, 2001 [source] Clinical Application of Peroneal Nerve Stimulator System Using Percutaneous Intramuscular Electrodes for Correction of Foot Drop in Hemiplegic PatientsNEUROMODULATION, Issue 4 2006Yoichi Shimada MD Abstract Objective., To assess the orthotic effect of a functional electrical stimulation device (Akita Heel Sensor System; AHSS) in the treatment of hemiplegic gait with foot drop. Materials and Methods., In the AHSS, a heel sensor is attached to a small plastic heel brace, and the peroneal nerve is stimulated via percutaneous intramuscular electrodes. During the swing phase of the hemiplegic gait, the common peroneal nerve is stimulated by the AHSS. Eight patients in chronic stages of hemiplegia participated in this study. Walking speeds and step cadences on a 10-m course were compared between walking with stimulation and walking without stimulation. Results., Mean walking speed (± SD) was 0.50 ± 0.26 m/sec without stimulation and 0.64 ± 0.31 m/sec with stimulation. The mean percentage increase in walking speed with stimulation was 30.1%. Mean step cadence was 31 ± 7 steps/10 m without stimulation and 27 ± 7 steps/10 m with stimulation. By correcting foot drop, the AHSS significantly increased walking speed and decreased cadence (p < 0.05). Conclusion., The AHSS can significantly improve walking in hemiplegic patients with foot drop. [source] Role for CTLA-4 but not CD25+ T cells during Schistosoma mansoni infection of micePARASITE IMMUNOLOGY, Issue 6 2007C. M. WALSH SUMMARY Schistosoma mansoni infection of mice increases the frequency of cells that are CD4+CD25+ in the acute (4 and 8 weeks) and chronic (16 week) stages of infection. Depletion of > 85% of CD25+ cells in the acute or chronic stages of schistosome infection caused no overt changes in morbidity or immunological responses. The absence of effect in mice with CD25+ cells depleted may be due to the preferential expression of IL-4 and IL-10, two cytokines that are protective in schistosome infection, on CD25, CD4+ cells. We also assessed infection-induced changes of other regulatory markers, GITR, CD103 and CTLA-4 on CD4+ cells. We identified a marked expansion of CTLA-4+ population on CD25, CD4+ cells in acute and chronic infection. Blocking of CTLA-4 during acute, but not chronic infection, caused significant weight loss and altered the type 2 cytokine response of mice, with increased IL-4 and IL-5 production associated with significantly more Th2 cells and eosinophils in the liver granuloma. This study illustrates the complexity of regulation of T cells in schistosome infection and highlights a specific role for CTLA-4+, but not CD25+ cells, in the regulation of Th2 responses in helminth infection. [source] | |||||||||||||