SEARCH · PubMed Health

Results for “Recovery”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources

PubMed1997

Differential effects of beta-blockers in patients after recovery from myocardial infarction and after recovery from unstable angina. Multicenter Myocardial Ischemia Research Group.

We examined the effect of beta-blockers on outcome in patients enrolled in the Multicenter Study of Myocardial Ischemia. We started prospective enrollment of patients after an acute coronary event (acute myocardial infarction [MI] or unstable angina) in North America, Israel, and Japan from mid-1988, and followed-up the 1042 patients for 6-43 months (average, 26 months); 47.2% of the patients were receiving beta-blockers at baseline. Overall, beta-blockers were associated with neutral effects on the chronic outcome: the cardiac event (cardiac death or recurrent nonfatal MI) rate was 6.8% for patients on beta-blockers and 7.5% for those who were not on beta-blockers (P = 0.72). However, a significant interaction (P = 0.018) was found between event type and the use of beta-blockers in regard to the cardiac event rate. That is, beta-blockers were associated with a lower risk of the cardiac event for patients whose index event type was MI (risk ratio, 0.59) in contrast to those whose index event was unstable angina (risk ratio, 1.92). The chronic use of beta-blockers in patients recovered from unstable angina may be associated with an increase in risk.

Adrenergic beta-Antagonists↗

PubMed1998

Attributions for positive life events predict recovery from depression among psychiatric inpatients: an investigation of the Needles and Abramson model of recovery from depression.

The authors investigated whether attributions for positive life events predict decreases in hopelessness and depressive symptoms among clinically depressed adults. Measures of attributional style, attributions for recent events, depressive symptoms, dysfunctional attitudes, hopelessness, and life events were administered to 52 depressed psychiatric inpatients treated with antidepressant medication; the measures were readministered 12 and 24 days later. Results indicated that (a) internal, stable, global attributions for recent positive events mediated a significant association between attributional style for positive life events and decreased hopelessness; (b) decreases in hopelessness mediated a significant association between internal, stable, global attributions for recent positive events and decreases in depressive symptom levels; and (c) depressotypic cognitions were not associated with decreases in either hopelessness or depressive symptom levels.

Adolescent↗

PubMed2002

Early dramatic recovery during intravenous tissue plasminogen activator infusion: clinical pattern and outcome in acute middle cerebral artery stroke.

BACKGROUND AND PURPOSE: Acute-stroke patients receiving standard intravenous tissue plasminogen activator (tPA) have been noted to experience early dramatic recoveries. The prevalence, clinical characteristics, and outcome of patients experiencing dramatic recovery is not well described. METHODS: We prospectively studied all patients presenting with acute middle cerebral artery (MCA) stroke syndromes and transcranial Doppler (TCD) evidence of an MCA obstruction. All patients received intravenous tPA per the National Institute of Neurological and Communicative Disorders and Stroke protocol, with serial National Institutes of Health Stroke Scale (NIHSS) scores and continuous TCD monitoring. Dramatic recovery was defined as an improvement of > or =10 NIHSS points or a decrease to an NIHSS score of < or =3 by the end of infusion. Outcome at the end of infusion, at 24 hours, and at long-term follow-up were obtained. The timing and pattern of deficit recovery during dramatic recovery was also studied. RESULTS: Dramatic recovery occurred in 22% of all patients. Compared with patients who did not experience dramatic recovery, those patients who did had significantly lower end-infusion NIHSS (median 2 and range 0 to 16 for dramatic-recovery patients versus median 17 and range 6 to 35 for non-dramatic-recovery patients, P<0.01) and 24-hour NIHSS (median 2 and range 0 to 16 for dramatic-recovery patients versus median 13 and range 2 to 35 for non-dramatic-recovery patients, P<0.01). A long-term modified Rankin Score benefit was noted (median 1 and range 0 to 6 for dramatic-recovery patients versus median 4 and range 0 to 6 for non-dramatic-recovery patients, P<0.01). Baseline clinical characteristics were similar. The only difference was improved TCD-determined flow values at the end of infusion (normal restoration of flow was 58% in dramatic-recovery patients versus 14% in non-dramatic-recovery patients, P<0.01). A characteristic pattern of recovery of deficit was noted. CONCLUSIONS: Early dramatic recovery in acute MCA stroke patients treated with intravenous tPA is relatively frequent. The benefit of dramatic recovery is maintained at 24 hours and over the long term. TCD monitoring suggests that dramatic recovery is a result of early restoration of MCA flow during the tPA infusion. The consistent pattern of early clinical recovery may help explain the mechanisms by which thrombolysis improves outcome and could suggest targets for enhancing the therapeutic effect of intravenous tPA.

Acute Disease↗

PubMed2006

Difference in recovery potential of peripheral nerves after graft repairs.

OBJECTIVE: To our knowledge, few studies have been published regarding differences in nerve recovery potentials. In this study, sensory and motor recovery potentials were compared between different nerves. METHODS: A prospective study of a homogenous group of 393 graft repairs of the median, ulnar, radial, tibial, peroneal, femoral, and musculocutaneous nerves, with the scoring of motor and sensory recoveries. Sensory and motor recovery potentials, defined on the basis of average scores and rates of useful recovery, were compared between the different nerves, and separately for high-, intermediate-, and low-level repairs. RESULTS: Sensory recovery potential was similar for all nerves tested (P > 0.05), but motor recovery potential differed significantly. After high-level repairs, motor recovery potential was significantly better for the radial and tibial nerves (useful recovery in 66.7 and 54.5% of patients, respectively), than for the ulnar and peroneal nerves (useful recovery in 15.4 and 13.8% of patients, respectively; P < 0.05). After intermediate-level repairs, motor recovery potential was better for the musculocutaneous, radial, and femoral nerves (useful recovery in 100, 98.3, and 87.5% of repairs, respectively), than for the tibial, median and ulnar nerves (useful recovery in 63.9, 52, and 43.6% of repairs, respectively; P < 0.05). In addition, motor recovery potential was significantly the worst with peroneal nerve repairs (useful recovery in 15.2% of patients; P < 0.05). After low-level repairs, motor recovery potential was similar for all nerves (useful recovery in the range of 88.9-100% of patients and in 56.3% of peroneal nerve repairs). CONCLUSION: Sensory recovery potential is similar for the median, ulnar, and tibial nerves. The expression of motor recovery potential depends on the repair level. With low- and high-level repairs, it does not stand out in an obvious way, but it is fully expressed with intermediate-level repairs, classifying nerves into three categories with excellent, moderate, and poor recovery potential.

Adult↗

PubMed1994

The kinetics of cellular recovery in exponential and plateau growth phase human glioma cells following gamma-irradiation.

PURPOSE: In this study the kinetics of recovery following irradiation was examined in a human glioma cell line. Specific objectives were: to determine whether recovery is mono- or biexponential in nature; to determine if recovery half-times are different in exponential and plateau growth phase cells; to compare recovery half-times as a function of dose or recovery levels; and finally, to compare the kinetics of sublethal damage recovery and potentially lethal damage recovery in plateau growth phase cells. METHODS AND MATERIALS: U-87MG cells were irradiated in exponential and plateau growth phases and then subjected to incubation at 37 degrees C for various periods of time following or between doses prior to assaying for survival. Survival recovery curves were fit to a sum of exponential terms. RESULTS: Potentially lethal damage recovery was monoexponential in both exponential and plateau growth phase cells and occurred at the same rate when isorecovery values were compared. Recovery half-times increased in an exponential manner within the observed dose range. Recovery between doses of radiation (sublethal damage recovery) proceeded at a slower rate than recovery following a single dose of radiation (potentially lethal damage recovery). CONCLUSIONS: This study suggests that potentially lethal damage recovery is a saturated process and that the recovery half-time may increase in a linear-quadratic exponential function of dose similar to the absolute recovery level. In addition, if iso-recovery levels are compared, the recovery half-time is similar in rapidly and slowly proliferating cell populations.

Cell Cycle↗

PubMed2000

Defining post-stroke recovery: implications for design and interpretation of drug trials.

Measurement of stroke recovery is complex because definition of successful recovery is highly variable across measures and cut-off points for defining successful outcomes vary. The purpose of this paper is to describe patterns of recovery in stroke patients of varying severity when different measures are used and when different cut-off points are selected. 459 individuals enrolled in a prospective cohort study were assessed within 14 days post stroke and re-evaluated at 1, 3, and 6 months. Recovery was assessed using the NIH Stroke Scale, the Fugl-Meyer Assessment of Motor Recovery, the Barthel Index of Activities of Daily Living, the Physical Function Index of the SF-36, and the Modified Rankin Outcome Scale. Subjects also defined their preference (utility) for their current health state with a time-trade off question. We compared patterns of recovery using the different measures and varying the cut-off points for defining successful recovery. The percentage of patients who are believed to have recovered depends on how recovery is defined. If recovery is defined at the disability level (Barthel > 90), the majority 57.3% of stroke survivors experience a full recovery. Fewer individuals are considered to be fully recovered if impairments are measured (NIH </= 1, 44.9% and Fugl-Meyer > 90, 36.8%. Less than 25% of stroke survivors are considered recovered if recovery is defined relative to reported prior function in higher levels of physical activity. Shifting the definition of recovery on the modified Rankin scale from </= 1 to </= 2 shifts the percentage of those deemed recovered from </= 25% to 53.8%. In designing drug trials the methods for defining stroke recovery should be carefully considered. If recovery is defined in terms of disability, a higher proportion of the placebo group will achieve the outcome than if impairments are used to define recovery. The benchmarks for recovery in minor strokes must include measures of higher functioning (e.g. the SF-36 physical functioning index or a Rankin 0 (no symptoms).

Activities of Daily Living↗

PubMed1999

The nature of spontaneous recovery from mivacurium-induced neuromuscular block.

UNLABELLED: The hypothesis of this study was that, in a given patient, recovery from a tracheal intubating dose of mivacurium would indicate the time course of spontaneous recovery after discontinuation of an infusion of mivacurium. Thirty-eight male patients consented to participate in the study. After induction of anesthesia and endotracheal intubation, the ulnar nerve was stimulated with train-of-four (TOF) stimuli at 12-s intervals. Patients received 0.3 mg/kg mivacurium in two evenly divided doses of 0.15 mg/kg each, separated by 30 s. Complete ablation of TOF responses occurred in most patients. Once the first twitch in the TOF (T ) had recovered to 25% of its baseline height, a mivacurium infusion was begun to maintain 95% suppression of T1. As surgery was nearing completion, the infusion was discontinued, and neuromuscular function was allowed to recover spontaneously. Data were analyzed for recovery intervals after the administration of the initial doses of mivacurium and after discontinuation of the infusion. Analysis of variance was used to determine the strength of correlation between the time from administration of the initial 0.3 mg/kg dose to 5% recovery of T1 and the times to recovery of TOF ratios of 70% and 90%. The 25%-75% recovery interval after discontinuation of the infusion ranged from 2.8 to 11.3 min. The time interval after administration of mivacurium 0.3 mg/kg to 5% recovery of T1 correlated with both the time to recovery of a TOF ratio of 70% and 90%. Recovery to a TOF of 90% after discontinuation of the infusion required approximately the same amount of time as recovery to 5% T1 after the administration of 0.3 mg/kg mivacurium. Each patient's recovery of neuromuscular function after discontinuation of a mivacurium infusion was related to his recovery after the administration of 0.3 mg/kg mivacurium. Therefore, the need for pharmacologic antagonism of block can be anticipated well before the end of an anesthetic. IMPLICATIONS: Mivacurium (0.3 mg/kg) was administered to 38 patients. As they began to recover muscle strength, a mivacurium infusion was begun and later discontinued as surgery was nearing completion. Each patient's early recovery (administration to 5% recovery of T1) after the initial dose of mivacurium correlated well with more complete recovery of muscle strength after discontinuation of an infusion. This relationship enables early prediction of recovery speed after a mivacurium infusion.

Adult↗

PubMed1993

Intracellular pH during reperfusion influences evoked potential recovery after complete cerebral ischemia.

BACKGROUND AND PURPOSE: Increasing ischemic duration delays recovery of intracellular pH and depresses recovery of somatosensory evoked potentials. We tested whether manipulation of the rate of pH recovery influences evoked potential recovery after complete ischemia. METHODS: Four groups of eight anesthetized dogs underwent 12 minutes of complete ischemia followed by 4 hours of reperfusion with either 1) normocapnia, 2) normocapnia and acetazolamide (25 mg/kg at reperfusion plus 12.5 mg/kg per hour, 3) hypocapnia, or 4) hypercapnia. Intracellular pH was measured by phosphorus magnetic resonance spectroscopy, and intracellular bicarbonate was calculated using sagittal sinus partial pressure of CO2 during reperfusion. RESULTS: In the normocapnic control group, intracellular pH decreased from 7.10 +/- 0.04 (+/- SEM) to 6.13 +/- 0.08 during ischemia and recovered to 6.90 +/- 0.08 by 30 minutes of reperfusion. Bicarbonate also largely recovered (9.9 +/- 1.6 mM). With acetazolamide pH (6.51 +/- 0.10) and estimated bicarbonate (4.8 +/- 1.3 mM) remained depressed at 30 minutes and did not fully recover until 60-75 minutes. However, percent recovery of somatosensory evoked potential amplitude at 4 hours of reperfusion was less with acetazolamide (23 +/- 4%) than in the control group (52 +/- 5%). With hypercapnic reperfusion, which delayed pH recovery but not bicarbonate recovery, evoked potential recovery was also depressed (27 +/- 5%). With hypocapnic reperfusion, which delayed bicarbonate recovery but not pH recovery, evoked potential recovery (52 +/- 6%) was not depressed compared with controls. Recovery of adenosine triphosphate and oxygen consumption was similar among groups. CONCLUSIONS: Delayed recovery of intracellular pH with or without delayed recovery of bicarbonate during reperfusion further impairs somatosensory evoked potential recovery independent of recovery of high-energy phosphates. Persistence of acidosis during reperfusion can contribute to postischemic electrophysiological deficit.

Acetazolamide↗

PubMed2003

The experience of recovery from schizophrenia: towards an empirically validated stage model.

OBJECTIVE: The consumer movement is advocating that rehabilitation services become recovery-orientated. The objectives of this study are to gain a better understanding of the concept of recovery by: (i) identifying a definition of recovery that reflects consumer accounts; and (ii) developing a conceptual model of recovery to guide research, training and inform clinical practice. METHOD: A review was conducted of published experiential accounts of recovery by people with schizophrenia or other serious mental illness, consumer articles on the concept of recovery, and qualitative research and theoretical literature on recovery. Meanings of recovery used by consumers were sought to identify a definition of recovery. Common themes identified in this literature were used to construct a conceptual model reflecting the personal experiences of consumers. RESULTS: The definition of recovery used by consumers was identified as psychological recovery from the consequences of the illness. Four key processes of recovery were identified: (i) finding hope; (ii) re-establishment of identity; (iii) finding meaning in life; and (iv) taking responsibility for recovery. Five stages were identified: (i) moratorium; (ii) awareness; (iii) preparation; (iv) rebuilding; and (v) growth. CONCLUSION: A five-stage model compatible with psychological recovery is proposed, which offers a way forward for attaining recovery-orientated outcomes. After further empirical investigation, a version of this model could be utilized in quantitative research, clinical training and consumer education.

Attitude↗

PubMed2003

Effect of anti-cytomegalovirus therapy on the incidence of immune recovery uveitis in AIDS patients with healed cytomegalovirus retinitis.

PURPOSE: To determine the association between anticytomegalovirus (CMV) maintenance therapy after immune recovery and immune recovery uveitis in acquired immunodeficiency syndrome (AIDS) patients on highly active antiretroviral therapy (HAART). DESIGN: Observational cohort study. METHODS: Data were obtained on AIDS patients with CMV retinitis followed up at the AIDS Ocular Research Unit of University of California San Diego from November 1995 to October 1999. Immune recovery was defined as CD4 count greater than 50 cells/microl for more than 3 months. Patients with immune recovery uveitis presented with vitritis, cystoid macular edema, or epiretinal membrane. Statistical analyses were conducted to determine the risk of continued use of anti-CMV therapy after immune recovery and the relationship of developing immune recovery uveitis with the type of anti-CMV therapy. RESULTS: Forty-three patients (64 eyes) had healed CMV retinitis and had achieved immune recovery. Thirty-one patients (48 eyes) received anti-CMV therapy after immune recovery, and 20 patients (29 eyes) developed immune recovery uveitis. Per-eye analyses revealed a 3.8-fold increase in the odds of developing immune recovery uveitis with anti-CMV therapy compared with no treatment (P =.02). If treated with cidofovir the odds were 3.3 greater than if treated with an alternative regimen (P =.04), 4.1 greater if treated intravenously (P =.01), and 5.2 greater than if not treated (P =.004). If not treated with cidofovir, a nonsignificant increase in the risk (2.4) of immune recovery uveitis was found (P =.15). Neither the potency nor the use of implants for noncidofovir treatment was related to the risk of recovery uveitis (P >.62). CONCLUSIONS: The use of cidofovir is a primary risk factor in the subsequent development of immune recovery uveitis. Ongoing treatment of healed CMV retinitis after immune recovery does not appear to protect against the development of immune recovery uveitis.

AIDS-Related Opportunistic Infections↗

PubMed2000

Prolonged recovery of cardiac output after maximal exercise in patients with chronic heart failure.

OBJECTIVES: The aim of this study was to characterize the kinetics of cardiac output during recovery from maximal exercise in patients with chronic heart failure (CHF). BACKGROUND: Recent studies have shown that oxygen uptake kinetics during recovery from exercise are delayed in patients with CHF. However, the kinetics of cardiac output during recovery from maximal exercise in CHF has not been examined. METHODS: Thirty patients with CHF performed maximal upright ergometer exercise with respiratory gas analysis. Kinetics of oxygen uptake (VO2) and carbon dioxide output (VCO2) during recovery were characterized by T1/2, the time to reach 50% of the peak values. Cardiac output was measured at 1-min intervals during exercise and recovery. Kinetics of cardiac output during recovery were characterized by the ratios of cardiac output during the first 4 min of recovery to cardiac output at peak exercise. Overshoot of cardiac output was defined as a further increase in cardiac output at 1 min of recovery above the cardiac output at peak exercise. RESULTS: Both T1/2 VO2 and T1/2 VCO2 increased as CHF worsened. The ratios of cardiac output during recovery to cardiac output at peak exercise were significantly correlated with T1/2 VO2 (r = 0.47 to 0.62, p < 0.05) and T1/2 VCO2 (r = 0.40 to 0.70, p < 0.05). There was a negative correlation between cardiac index at peak exercise and both T1/2 VO2 (r = -0.65, p < 0.001) and T1/2 VCO2 (r = -0.60, p < 0.001). Overshoot of cardiac output was recognized in 11 of 30 patients. Cardiac index at peak exercise was significantly lower in patients with overshoot (4.5 +/- 0.9 L/min/m2) than in those without overshoot (6.1 +/- 2.1 L/min/m2, p < 0.05). However, because of a continued increase in cardiac output at 1 min of recovery in patients with overshoot, there were no differences in cardiac index after the first minute of recovery. Heart rate at peak exercise and recovery of heart rate did not differ between these groups. Overshoot of cardiac output was caused by a rebound increase in stroke volume which was due to a reduction in systemic vascular resistance. CONCLUSIONS: Prolonged kinetics of VO2 or VCO2 during recovery from maximal exercise represent impairment of circulatory response to exercise and delayed recovery of cardiac output after exercise. Overshoot of cardiac output at 1 min of recovery was characteristic of severe CHF with poor cardiac output response to exercise.

Analysis of Variance↗

PubMed1995

Slowly recovering cardiac sodium current in rat ventricular myocytes: effects of conditioning duration and recovery potential.

INTRODUCTION: Recovery of the Na channel from inactivation is essential to the normal conduction and refractoriness of the myocardium. In addition to fast recovery, occurring within several milliseconds at hyperpolarized potentials, a component of the current exhibits slow recovery occurring over hundreds of milliseconds. Long conditioning depolarizations potentiate slow recovery. METHODS AND RESULTS: This study was designed to test conditioning durations (tc) between 0.25 and 4 seconds (s) as to whether recovery was slowed by an effect on the fast (tau f) and slow (tau s) time constants of recovery, the relative amplitude of the slow component (As), or both. We studied Na channel recovery at -150 mV from inactivation using whole cell voltage clamp of rat ventricular cells at 23 degrees C using a two-pulse recovery protocol. Longer conditioning durations dramatically increased A2 (from 12% for tc = 500 msec to 37% for tc = 4000 msec, P < 0.01). Neither tau f (6 vs 5 msec) nor tau s (115 vs 140 msec) were significantly affected. In a second set of experiments, the recovery potential was depolarized to a potential at which the sodium current was 70% available (approximately equal to - 105 mV). This recovery potential had no significant effect on A2, but both tau f and tau s were significantly slower (e.g., at tc = 2 s, tau s = 147 msec and As = 28% at Vr = - 150 mV, and tau s = 456 msec and As = 29% at Vr approximately equal to - 105 mV). In addition, a 1- to 2-msec lag in the onset of recovery was prominent at the depolarized recovery potentials. CONCLUSIONS: Our results support a model for slow recovery where conditioning duration determines entry into an inactivated state from which Na channels recover slowly, and recovery potential determines the rate of recovery from this state. A kinetic scheme with at least three inactivated states is proposed. These results also have implications for cardiac excitability under conditions, such as ischemia, where membranes are depolarized.

Animals↗

PubMed2002

Psychophysical recovery from pulse-train forward masking in electric hearing.

Psychophysical pulse-train forward-masking (PTFM) recovery functions were measured in fifteen subjects with the Nucleus mini-22 cochlear implant and six subjects with the Clarion cochlear implant. Masker and probe stimuli were 500-Hz trains of 200- or 77-micros/phase biphasic current pulses. Electrode configurations were bipolar for Nucleus subjects and monopolar for Clarion subjects. Masker duration was 320 ms. Probe duration was either 10 ms or 30 ms. Recovery functions were measured for a high-level masker on a middle electrode in all 21 subjects, on apical and basal electrodes in 7 of the Nucleus and 3 of the Clarion subjects, and for multiple masker levels on the middle electrode in 8 Nucleus subjects and 6 Clarion subjects. Recovery functions were described by an exponential process in which threshold shift (in microA) decreased exponentially with increasing time delay between the offset of the masker pulse train and the offset of the probe pulse train. All but 3 of the 21 subjects demonstrated recovery time constants on a middle electrode that were less than 95 ms. The mean time constant for these 18 subjects was 54 ms (s.d. 17 ms). Three other subjects tested on three electrodes exhibited time constants larger than 95 ms from an apical electrode only. Growth-of-masking slopes depended upon time delay, as expected from an exponential recovery process, i.e., progressively shallower slopes were observed at time delays of 10 ms and 50 ms. Recovery of threshold shift (in microA) for PTFM in electrical hearing behaves inthe same way as recovery of threshold shift (in dB) for pure-tone forward masking in acoustic hearing. This supports the concept that linear microamps are the electrical equivalent of acoustic decibels. Recovery from PTFM was not related to speech recognition in a simple manner. Three subjects with prolonged PTFM recovery demonstrated poor speech scores. The remaining subjects with apparently normal PTFM recovery demonstrated speech scores ranging from poor to excellent. Findings suggest that normal PTFM recovery is only one of several factors associated with good speech recognition in cochlear-implant listeners. Comparisons of recovery curves for 10- and 30-ms probe durations in two subjects showed little or no temporal integration at time delays less than 95 ms where recovery functions have steep slopes. The same subjects exhibited large amounts of temporal integration at longer time delays where recovery slopes are more gradual. This suggests that probe detection depends primarily on detection of the final pulses in the probe stimulus and supports the use of offset-to-offset time delays for characterizing PTFM recovery in electric hearing.

Adult↗

PubMed1991

Recovery of function after lesions in the superior temporal sulcus in the monkey.

1. Ibotenic acid lesions in the monkey's middle temporal area (MT) and the medial superior temporal area (MST) in the superior temporal sulcus (STS) have previously been shown to produce a deficit in initiation of smooth-pursuit eye movements to moving visual targets. The deficits, however, recovery within a few days. In the present experiments we investigated the factors that influence that recovery. 2. We tested two aspects of the monkey's ability to use motion information to acquire moving targets. We used eye-position error as a measure of the monkey's ability to make accurate initial saccades to the moving target. We measured eye speed within the first 100 ms after the saccade to evaluate the monkey's initial smooth pursuit. 3. We determined that pursuit recovery was not dependent specifically on the use of neurotoxic lesions. Although the rate of recovery was slightly altered by replacing the usual neurotoxin (ibotenic acid) with another neurotoxin [alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)] or with an electrolytic lesion, pursuit recovery still occurred within a period of days to weeks. 4. There was a relationship between the size and location of the lesion and the recovery time. The time to recovery for eye-position error and initial eye speed increased with the fraction of MT removed. Whether the rate of recovery and size of lesions within regions on the anterior bank were related was unresolved. 5. We found that a large AMPA lesion within the STS that removed all of MT and nearly all of MST drastically altered the rate of recovery. Recovery was incomplete more than 7 mo after the lesion. Even with this lesion, however, the monkey's ability to use motion information for pursuit was not completely eliminated. 6. The large lesion also included parts of areas V1, V2, V3, and V4, but analysis of the visual fields associated with this lesion indicated that these areas probably did not have a substantial effect on recovery. 7. We tested whether visual motion experience of the monkey after a lesion was necessary for recovery by limiting the monkey's experience either by using a mask or by using 4-Hz stroboscopic illumination. In one monkey the eye-position error component of pursuit was prolonged to greater than 2 wk, but recovery of eye speed was not. Reduced motion experience had little effect on recovery in the other two monkeys. These results suggest that such visual motion experience is not necessary for the recovery of pursuit.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2003

The McLean-Harvard First-Episode Mania Study: prediction of recovery and first recurrence.

OBJECTIVE: Since improved prediction of illness course early in bipolar disorder is required to guide treatment planning, the authors evaluated recovery, first recurrence, and new illness onset following first hospitalization for mania. METHOD: Bipolar disorder patients (N=166) were followed 2-4 years after their first hospitalization for a manic or mixed episode to assess timing and predictors of outcomes. Three aspects of recovery were measured: syndromal (DSM-IV criteria for disorder no longer met), symptomatic (Young Mania Rating Scale score </=5 and Hamilton Depression Rating Scale score </=8), and functional (regaining of premorbid occupational and residential status). Rates of remission (syndromal recovery sustained >/=8 weeks), switching (onset of new dissimilar illness before recovery), relapse (new episode of mania within 8 weeks of syndromal recovery), and recurrence (new episode postremission) were also assessed. RESULTS: By 2 years, most subjects achieved syndromal recovery (98%, with 50% achieving recovery by 5.4 weeks); 72% achieved symptomatic recovery. Factors associated with a shorter time to syndromal recovery for 50% of the subjects were female sex, shorter index hospitalization, and lower initial depression ratings. Only 43% achieved functional recovery; these subjects were more often older and had shorter index hospitalizations. Within 2 years of syndromal recovery, 40% experienced a new episode of mania (20%) or depression (20%), and 19% switched phases without recovery. Predictors of mania recurrence were initial mood-congruent psychosis, lower premorbid occupational status, and initial manic presentation. Predictors of depression onset were higher occupational status, initial mixed presentation, and any comorbidity. Antidepressant treatment was marginally related to longer time to recovery and earlier relapse. CONCLUSIONS: Within 2-4 years of first lifetime hospitalization for mania, all but 2% of patients experienced syndromal recovery, but 28% remained symptomatic, only 43% achieved functional recovery, and 57% switched or had new illness episodes. Risks of new manic and depressive episodes were similar but were predicted by contrasting factors.

Adolescent↗

PubMed1996

Autoregulation of body composition during weight recovery in human: the Minnesota Experiment revisited.

OBJECTIVES: To gain insights into the control systems underlying human variability in the regulation of body composition during weight recovery, as well as the disproportionate recovery of fat relative to lean tissue, the classical Minnesota Experiment conducted on 32 men subjected to long-term semi-starvation and refeeding was revisited with the following objectives: (1) to determine whether the control of energy-partitioning between lean and fat tissues during weight loss and weight recovery is an individual characteristic, and if a predictor can be statistically identified, (2) to determine whether the reduction in thermogenesis during weight loss persists during weight recovery, and underlies the disproportionate recovery of fat tissue and (3) to integrate the control of energy-partitioning and that of thermogenesis in order to explain the pattern of lean and fat tissue mobilisation and deposition during weight loss and weight recovery. METHODS: Individual data on body weight, body fat, fat-free-mass (FFM), and basal metabolic rate (BMR), assessed during the control baseline period (i.e. prior to weight loss), at the end of 24 weeks of semi-starvation, and at the end of a 12 week period of restricted refeeding, were used to calculate the following parameters: (i) a quantitative index of energy-partitioning, the P-ratio, defined as the proportion of body energy mobilised as protein during weight loss, or as the proportion of body energy deposited as protein during weight recovery, (ii) a quantitative index of changes in thermogenesis, defined as the change in BMR adjusted for FFM (or for both FFM and fat mass) and (iii) the degree of replenishment of fat and FFM compartments, defined as the recovery of body fat and FFM (during refeeding) as a percentage of that lost during semi-starvation. RESULTS: This re-analysis indicates the following: (i) a large inter-individual variability in P-ratio during both weight loss and weight recovery, but for a given individual, the P-ratio during refeeding is strongly correlated with the P-ratio during semi-starvation, (ii) body composition during the control period is the most important predictor of variability in P-ratio, such that the higher the initial % body fat, the lower the proportion of energy mobilised as protein, and hence the greater the propensity to mobilise fat during semi-starvation and to subsequently deposit fat during refeeding and (iii) at week 12 of refeeding, the change in adjusted BMR is found to be reduced by a magnitude which is inversely proportional to the degree of fat recovery, but is unrelated to the degree of FFM recovery. A quantitative relationship is derived between the P-ratio during refeeding, the % fat recovery, and the P-ratio during semi-starvation. CONCLUSIONS: Evidence is presented here suggesting that (i) human variability in the pattern of lean and fat tissue deposition during weight recovery is to a large extent determined by individual variations in the control of energy-partitioning, for which the initial % body fat is the most important predictor and (ii) the disproportionate gain in fat relative to lean tissue during weight recovery is contributed by a reduction in thermogenesis (i.e. increased efficiency of food utilization) for accelerating specifically the replenishment of the fat stores. These control systems, operating via energy-partitioning and thermogenesis, have been integrated into a compartmental model for the regulation of body composition during underfeeding/refeeding, and can be used to explain the individual pattern of lean and fat tissue deposition during weight recovery in situations ranging from the rehabilitation after malnutrition to the relapse of obesity.

Adipose Tissue↗

PubMed2006

Postoperative factors affecting neurological recovery after surgery for cervical spondylotic myelopathy.

OBJECT: Many prognostic factors associated with surgery for cervical spondylotic myelopathy (CSM) have been detailed in the literature. All of these factors, however, are defined preoperatively. If it is possible to clarify factors influencing surgical results that can be modulated after surgery, then the overall results of surgery may improve. The purpose of this study was to elucidate such postoperative factors affecting neurological recovery. METHODS: The authors assessed the surgical outcomes obtained in 183 patients with CSM who underwent expansive open-door laminoplasty between 1993 and 2004 and who underwent follow up for a minimum of 1 year. They classified the cases into two groups according to the degree of neurological recovery: an excellent recovery group, comprising patients in whom the recovery rates were greater than 75%, and a poor recovery group, composed of patients in whom the recovery rates were lower than 30%. Comparisons of various clinical and imaging parameters revealed that the mean age at surgery was significantly lower in patients in the excellent recovery group than that in the poor recovery group. Therefore, the authors repeated the same analyses after adjustment for age. Postoperative cervical range of motion (ROM) was significantly more reduced in the excellent recovery group than in the poor recovery group. There was a significant positive correlation between reduced cervical ROM and recovery rate in the poor recovery group. CONCLUSIONS: Dynamic stress may ameliorate functional recovery of the degenerated spinal cord even after sufficient decompression. Postoperative preservation of cervical ROM may not always be beneficial for neurological recovery in patients with CSM.

Age Distribution↗

PubMed1997

Factors influencing haematological recovery after allogeneic bone marrow transplantation in leukaemia patients treated with methotrexate-containing GVHD prophylaxis. A single-centre experience.

In the present single institution study of 66 leukaemia patients (28 AML, 23 ALL, 15 CML), the factors influencing haematological recovery after allogeneic bone marrow transplantation (alloBMT) were analysed retrospectively to identify the optimal conditions required for rapid haematological recovery after alloBMT. All patients received GVHD prophylaxis with cyclosporine A plus methotrexate. The mean number of days required to achieve a neutrophil count > or = 0.5 x 10(9)/l after alloBMT was 17 (range 9-27), 19 patients (28.8%) had rapid neutrophil recovery within 15 days after alloBMT. Haematological recovery was more rapid in the 38 patients without GVHD or with only grade I GVHD. Also, 50% and 40% of patients receiving 10 (n = 18) or 5 (n = 20) micrograms/kg G-CSF per day, respectively, had rapid neutrophil recovery within 15 days after alloBMT, as against only 7.1% of patients not receiving G-CSF after the transplant (n = 28); P < 0.001. The neutrophil recovery was similar in patients receiving either fresh or cryopreserved allografts and either a TBI-containing or a busulfan-containing conditioning regimen. A significant correlation was found between the neutrophil recovery and either the MNCs or CFU-GM contents of the allografts. The mean number of days required for neutrophil recovery was only 16 (range 9-24) in patients receiving allografts containing > 1 x 10(5) CFU-GM/kg (n = 28), as against 19 (range 13-27) in patients receiving allografts containing < or = 1 x 10(5) CFU-GM/kg (n = 35). Three patients receiving allografts containing < 0.5 x 10(5) CFU-GM/kg had primary neutrophil engraftment failure. The mean number of days required to achieve a platelet count > or = 20 x 10(9)/l was 21 (range 11-50), and 30 patients (46.9%) had platelet recovery within 20 days after alloBMT. The platelet recovery after alloBMT was not affected by the type of leukaemia, conditioning regimen, or G-CSF administration. The mean number of days required for platelet recovery after alloBMT was 20 in patients receiving allografts containing > 1.0 x 10(5) BFU-E/kg (n = 35), as against 23 days in patients receiving allografts containing < or = 1.0 x 10(5) BFU-E/kg (n = 24). Seven patients receiving allografts containing < 0.5 x 10(5) BFU-E/kg had primary platelet engraftment failure. The present study has identified the high number of progenitor cells in the allografts infused and the daily administration of G-CSF posttransplant as the optimal combination for rapid neutrophil recovery after alloBMT. More significantly, the number of BFU-E in allografts was the most significant determining factor in platelet recovery after alloBMT. The development of GVHD of grade II or more during the first weeks after alloBMT was associated with slower haematological recovery, a longer period of fever during neutropenia and longer hospitalization.

Adolescent↗