Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Gary Abrams is active.

Publication


Featured researches published by Gary Abrams.


Neurorehabilitation and Neural Repair | 2003

Effectiveness of Sensory and Motor Rehabilitation of the Upper Limb Following the Principles of Neuroplasticity: Patients Stable Poststroke:

Nancy N. Byl; Jennifer Roderick; Olfat Mohamed; Monica Hanny; Josh Kotler; Amy Smith; Molly Tang; Gary Abrams

Based on the principles of neuroplasticity, the purpose of this crossover study was to determine if improvement in upper extremity (UE) function and independence could be achieved in patients 6 months to 7 years poststroke following an outpatient rehabilitation program (supervised 1.5 hours per week for 8 weeks reinforced with home gloving unaffected side and attended, graded, repetitive sensory and motor training activities). Twenty-one subjects (right or left hemiparesis; able to walk 100 feet with or without a cane; partially opened and closed the hand; partially elevated the shoulder and elbow against gravity) were randomly assigned to Group A (sensory training 4 weeks, motor training 4 weeks) or Group B (motor training 4 weeks, sensory training 4 weeks). Greater than 20% (P <0.01) improvement was measured in functional independence and UE function (fine motor, sensory discrimination, and musculoskeletal performance). Gains were hemispheric and training specific and maintained over 3 months. This study provides evidence documenting significant improvement in function in the late poststroke recovery period following 12 hours of supervised learning based sensory motor training.


Journal of Clinical Investigation | 1973

Triiodothyronine and Thyroxine in the Serum and Thyroid Glands of Iodine-Deficient Rats

Gary Abrams; P. R. Larsen

Triiodothyronine (T(3)) and thyroxine (T(4)) were measured by immunoassay in the serum and thyroid hydrolysates of control (group A), mildly iodine-deficient (group B), and severely iodine-deficient rats (group C). These results were correlated with changes in thyroidal weight, (131)I uptake and (127)I content as well as with the distribution of (131)I in Pronase digests of the thyroid. There was a progressive increase in thyroid weight and (131)I uptake at 24 h with decrease in iodine intake. The (127)I content of the thyroids of the group B animals was 44% and that of the group C animals 2% of that in group A. The mean labeled monoiodotyrosine/diiodotyrosine (MIT/DIT) and T(3)/T(4) ratios in group A were 0.42+/-0.07 (SD) and 0.12+/-0.01, 0.59+/-0.06 and 0.11+/-0.03 in group B, and 2.0+/-0.3 and 1.8+/-0.9 in the group thyroid digests.Mean serum T(4) concentration in the control rats was 4.2+/-0.6 (SD) mug T(4)/100 ml, 4.5+/-0.3 mug/100 ml in group B animals, and undectectable (<0.5 mu(4)/100 ml) in group C animals. There was no effect of iodine deficiency on serum T(3) concentrations, which were 44+/-9 (Mean+/-SD) ng/100 ml in A animals, 48+/-6 ng/100 ml n B animals, and 43+/-6 ng/100 ml in the C group. Thyroidal digest T(3) and T(4) concentrations were 39 and 400 ng/mg in group A animals and were reduced to 5 and 1% of this, respectively, in group C. The molar ratio of T(3)/T(4) in the thyroid digests of the groups A and B animals was identical to the ratio of labeled T(3)/T(4) and was slightly less (1.0+/-0.9) than the labeled T(3)/T(4) ratio in the group C animals. The mean ratio of labeled T(4) to labeled T(3) in the serum of the severely iodine-deficient animals 24 h after isotope injection was 11+/-1 (SEM). With previously published values, it was possible to correlate the ratio of labeled T(4)/T(3) in the thyroid digest with the labeled T(4)/T(3) ratio in the serum of each iodine-deficient animal. This analysis suggested that the labeled thyroid hormones in the severely iodine-deficient rat were secreted in the ratio in which they are present in the gland. Kinetic analysis of total iodothyronine turnover indicated that two-thirds of the T(3) utilized per day by the iodine-sufficient rat arises from T(4). If the T(4)-T(3) conversion ratio remains the same in iodine deficiency, then the analysis suggests that about 90% of the T(3) arises directly from the thyroid. Therefore, it would appear that absolute T(3) secretion by the thyroid increases severalfold during iodine deficiency. The fact that serum T(3) remains constant and T(4) decreases to extremely low levels, combined with previous observations that iodine-deficient animals appear to be euthyroid, is compatible with the hypothesis that T(4) in the normal rat serves primarily as a precursor of T(3).


Neurology | 1982

Neurosecretion and Brain Peptides

Gary Abrams

The major purpose of this book is to give readers a “multidisciplinary approach to the problem of ‘brain damage’ and ‘brain dysfunction’ . . .” In a very brief introduction, Dr. Black tries to arrive a t a consensus concerning the nature of the clinical problem, indicating “the shared clinical feature-with or without structural brain involvemeneis some degree of disability in the realm of behavior, intellect, or learning.” Since every insult that involves the brain can produce one or more of the above disabilities, this is a license to write a mini textbook of neurology. Indeed, that is the major problem with this book. It is really two books, one of which deals with the etiology of brain dysfunction consisting of brief paragraphs about single diseases, or lists of diseases that may result in brain dysfunction under the heading of Metabolic Disorders, Congential Malformations, Perinatal Brain Damage, Central Nervous System Infections, Malnutrition, and Head Trauma. These brief comments about disease often are not helpful to either the student or the neurologist, and are probably too technical for educators, therapists or psychologists who provide handicapped children with medical services. Clinical pathophysiology is often overlooked with the exception of that written by Dr. Towbin on Neuropathologic Aspects of Perinatal Brain Damage and Its Sequels, which is interesting although controversial. The chapter by Drs. Kleiman and Carver on central nervous system infections resulting in brain damage and dysfunction is an excellent reference source. All of the chapters that deal with etiology have excellent bibliographies. The second half of the book is clearly more valuable for physicians and for others who provide care to brain damaged children. This section of the text is very heavily weighted toward problems concerned with “minimal brain dysfunction.” There are interesting chapters on classifications of syndromes, educational therapy, drug therapy, physical therapy, and recreational therapy for some of these children. There is an informed discussion about patterning that is well worth reading. Problems that exist in providing and evaluating various forms of occupational and physical therapy are not discussed at any great length, nor is behavioral management, other than by drug therapy. These are serious shortcomings. However, the chapter on education of the learning-disabled child suspected of minimal brain dysfunction is as excellent a review of this subject as I have read. Another chapter on sociologic perspectives emphasizes the relationship of outcomes to parents’ expectations, and how those expectations may be influenced by professionals. It is written with great insight. The book concludes with an epilogue by Dr. Black which summarizes a revised classification of brain dysfunction, the BELIND classification, which has been developed to discuss behavioral and emotional traits; learning; intellect; and neurologic dysfunction. It is a very functional approach which gives an idea of a child’s immediate problems, without having to assign a specific etiology to, or a structural cause for, the child’s disabilities. The BELIND system is an extension of multiple focused classifications that are popular in psychiatry today. They do not enhance our understanding of the brain’s structure and its function, but they do have the advantage of describing what is wrong with the patient without using misleading labels. This is a difficult book to classify, as it includes sections that are worth reading, but many chapters will be of little or no use to the pediatric or adult neurologist. The book should be available through hospital or medical school libraries, where neurologists may read those sections that interest them.


Health Psychology | 2011

Identification of distinct depressive symptom trajectories in women following surgery for breast cancer.

Laura B. Dunn; Bruce A. Cooper; John Neuhaus; Claudia West; Steven M. Paul; Bradley E. Aouizerat; Gary Abrams; Janet Edrington; Debby Hamolsky; Christine Miaskowski

OBJECTIVE Depressive symptoms, common in breast cancer patients, may increase, decrease, or remain stable over the course of treatment. Most longitudinal studies have reported mean symptom scores that tend to obscure interindividual heterogeneity in the symptom experience. The identification of different trajectories of depressive symptoms may help identify patients who require an intervention. This study aimed to identify distinct subgroups of breast cancer patients with different trajectories of depressive symptoms in the first six months after surgery. METHOD Among 398 patients with breast cancer, growth mixture modeling was used to identify latent classes of patients with distinct depressive symptom profiles. These profiles were identified based on Center for Epidemiological Studies-Depression (CES-D) scale scores completed just prior to surgery, and 1, 2, 3, 4, 5, and 6 months after surgery. RESULTS Four latent classes of breast cancer patients with distinct depressive symptom trajectories were identified: Low Decelerating (38.9%), Intermediate (45.2%), Late Accelerating (11.3%), and Parabolic (4.5%) classes. Patients in the Intermediate class were younger, on average, than those in the Low Decelerating class. The Intermediate, Late Accelerating, and Parabolic classes had higher mean baseline anxiety scores compared to the Low Decelerating class. CONCLUSIONS Breast cancer patients experience different trajectories of depressive symptoms after surgery. Of note, over 60% of these women were classified into one of three distinct subgroups with clinically significant levels of depressive symptoms. Identification of phenotypic and genotypic predictors of these depressive symptom trajectories after cancer treatment warrants additional investigation.


The Journal of Pain | 2012

Identification of patient subgroups and risk factors for persistent breast pain following breast cancer surgery.

Christine Miaskowski; Bruce A. Cooper; Steven M. Paul; Claudia West; Dale J. Langford; Jon D. Levine; Gary Abrams; Deborah Hamolsky; Laura B. Dunn; Marylin Dodd; John Neuhaus; Christina Baggott; Anand Dhruva; Brian L. Schmidt; Janine K. Cataldo; John D. Merriman; Bradley E. Aouizerat

UNLABELLED Study purposes were to determine the prevalence of persistent pain in the breast; characterize distinct persistent pain classes using growth mixture modeling; and evaluate for differences among these pain classes in demographic, preoperative, intraoperative, and postoperative characteristics. In addition, differences in the severity of common symptoms and quality of life outcomes measured prior to surgery, among the pain classes, were evaluated. Patients (n = 398) were recruited prior to surgery and followed for 6 months. Using growth mixture modeling, patients were classified into no (31.7%), mild (43.4%), moderate (13.3%), and severe (11.6%) pain groups based on ratings of worst breast pain. Differences in a number of demographic, preoperative, intraoperative, and postoperative characteristics differentiated among the pain classes. In addition, patients in the moderate and severe pain classes reported higher preoperative levels of depression, anxiety, and sleep disturbance than the no pain class. Findings suggest that approximately 25% of women experience significant and persistent levels of breast pain in the first 6 months following breast cancer surgery. PERSPECTIVE Persistent pain is a significant problem for 25% of women following surgery for breast cancer. Severe breast pain is associated with clinically meaningful decrements in functional status and quality of life.


Brain | 2011

Training of goal-directed attention regulation enhances control over neural processing for individuals with brain injury

Anthony J.-W. Chen; Tatjana Novakovic-Agopian; Terrence J. Nycum; Shawn Song; Gary R. Turner; Nancy K. Hills; Scott Rome; Gary Abrams; Mark D’Esposito

Deficits in attention and executive control are some of the most common, debilitating and persistent consequences of brain injuries. Understanding neural mechanisms that support clinically significant improvements, when they do occur, may help advance treatment development. Intervening via rehabilitation provides an opportunity to probe such mechanisms. Our objective was to identify neural mechanisms that underlie improvements in attention and executive control with rehabilitation training. We tested the hypothesis that intensive training enhances modulatory control of neural processing of perceptual information in patients with acquired brain injuries. Patients (n=12) participated either in standardized training designed to target goal-directed attention regulation, or a comparison condition (brief education). Training resulted in significant improvements on behavioural measures of attention and executive control. Functional magnetic resonance imaging methods adapted for testing the effects of intervention for patients with varied injury pathology were used to index modulatory control of neural processing. Pattern classification was utilized to decode individual functional magnetic resonance imaging data acquired during a visual selective attention task. Results showed that modulation of neural processing in extrastriate cortex was significantly enhanced by attention regulation training. Neural changes in prefrontal cortex, a candidate mediator for attention regulation, appeared to depend on individual baseline state. These behavioural and neural effects did not occur with the comparison condition. These results suggest that enhanced modulatory control over visual processing and a rebalancing of prefrontal functioning may underlie improvements in attention and executive control.


Journal of Head Trauma Rehabilitation | 2011

Rehabilitation of executive functioning with training in attention regulation applied to individually defined goals: a pilot study bridging theory, assessment, and treatment.

Tatjana Novakovic-Agopian; Anthony J.-W. Chen; Scott Rome; Gary Abrams; Holli Castelli; Annemarie Rossi; Ryan McKim; Nancy K. Hills; Mark DʼEsposito

Objective:To assess feasibility and effects of training in goal-oriented attentional self-regulation for patients with brain injury and chronic executive dysfunction. Participants:Sixteen individuals with chronic brain injury and mild to moderate executive dysfunction. Design:Participants were divided into 2 groups: one group completed goal-oriented attentional self-regulation training during the first 5 weeks, followed by a brief (2-hour) educational instruction session as a control midway through the second 5 weeks; the other group participated in reverse order. Measures:Neuropsychological and functional performance assessed at baseline and at weeks 5 and 10. Results:Participants found training in goal-oriented attentional self-regulation engaging, incorporated some trained strategies into daily life, and reported subjective improvements in personal functioning. At week 5, participants who completed goals training significantly improved on tests of attention and executive function and had fewer functional task failures, while performance did not change after educational instruction. At week 10, participants who crossed over from educational instruction to goals training also significantly improved on attention and executive function tests. Participants who crossed from goals training to educational instruction maintained their week 5 gains. Conclusions:Training in goal-oriented attentional self-regulation is theoretically driven and feasible in a research setting. Pilot results suggest improvements in cognitive and functional domains targeted by the intervention.


IEEE Transactions on Neural Systems and Rehabilitation Engineering | 2013

Kinematic Data Analysis for Post-Stroke Patients Following Bilateral Versus Unilateral Rehabilitation With an Upper Limb Wearable Robotic System

Hyunchul Kim; Levi Makaio Miller; Irina Fedulow; Matt Simkins; Gary Abrams; Nancy N. Byl; Jacob Rosen

Robot-assisted stroke rehabilitation has become popular as one approach to helping patients recover function post-stroke. Robotic rehabilitation requires four important elements to match the robot to the patient: realistic biomechanical robotic elements, an assistive control scheme enabled through the human-robot interface, a task oriented rehabilitation program based on the principles of plasticity, and objective assessment tools to monitor change. This paper reports on a randomized clinical trial utilizing a complete robot-assisted rehabilitation system for the recovery of upper limb function in patients post-stroke. In this study, a seven degree-of-freedom (DOF) upper limb exoskeleton robot (UL-EXO7) is applied in a rehabilitation clinical trial for patients stable post-stroke (greater than six months). Patients had a Fugl-Meyer Score between 16-39, were mentally alert (19 on the VA Mini Mental Status Exam) and were between 27 and 70 years of age. Patients were randomly assigned to three groups: bilateral robotic training, unilateral robotic training, and usual care. This study is concerned with the changes in kinematics in the two robotic groups. Both patient groups played eight therapeutic video games over 12 sessions (90 min, two times a week). In each session, patients intensively played the different combination of video games that directly interacted with UL-EXO7 under the supervision of research assistant. At each session, all of the joint angle data was recorded for the evaluation of therapeutic effects. A new assessment metric is reported along with conventional metrics. The experimental result shows that both groups of patients showed consistent improvement with respect to the proposed and conventional metrics.


Neuroendocrinology | 1980

Neonatal Monosodium Glutamate

Richard J. Bodnar; Gary Abrams; Earl A. Zimmerman; T Dorothy Krieger.; Gayle Nicholson; John S. Kizer

Neonatal administration of monosodium glutamate (MSG) produces neurotoxic degeneration of the retina and medial-basal hypothalamus, including the arcuate nucleus. Since this hypothalamic area contains the only neuronal cell bodies in brain which contain adrenocorticotrophic hormone (ACTH) and beta-lipotropin (beta-LPH) and beta-endorphin, destruction of these cells by MSG may interfere with pain responses mediated by nerve fibers arising from these perikarya. The present study examined whether MSG-treated rats, as compared to littermate controls, exhibited concomitant changes in the immunocytochemical distribution of ACTH and beta-LPH, and their reactivity to several analgesia-inducing manipulations. Although MSG-treated rats did not differ from control rats in their baseline reactivity to electric shock, they displayed an inability to exhibit analgesia following acute exposure to cold-water swim stress. In addition, MSG-treated rats showed an attenuated analgesic response following morphine administration. However, the analgesia elicited by either abrupt food deprivation, or the glucoprivic stress of 2-deoxy-D-glucose, was unaffected by neonatal MSG treatment. Concomitant with these selective analgesic deficits, MSG-treated rats displayed a marked immunocytochemical reduction in ACTH/beta-LPH perikarya and terminals in brain, but not pituitary. These data indicate that multiple pain-inhibitory systems exist, and that some rely upon an intact medial-basal hypothalamus to produce analgesia.


Neurorehabilitation and Neural Repair | 2013

Effect of a Foot-Drop Stimulator and Ankle–Foot Orthosis on Walking Performance After Stroke A Multicenter Randomized Controlled Trial

Dirk G. Everaert; Richard B. Stein; Gary Abrams; Alexander W. Dromerick; Gerard E. Francisco; Brian J. Hafner; Thy Huskey; Michael C. Munin; Karen J. Nolan; Conrad Kufta

Background. Studies have demonstrated the efficacy of functional electrical stimulation in the management of foot drop after stroke. Objective. To compare changes in walking performance with the WalkAide (WA) foot-drop stimulator and a conventional ankle–foot orthosis (AFO). Methods. Individuals with stroke within the previous 12 months and residual foot drop were enrolled in a multicenter, randomized controlled, crossover trial. Subjects were assigned to 1 of 3 parallel arms for 12 weeks (6 weeks/device): arm 1 (WA–AFO), n = 38; arm 2 (AFO–WA), n = 31; arm 3 (AFO–AFO), n = 24. Primary outcomes were walking speed and Physiological Cost Index for the Figure-of-8 walking test. Secondary measures included 10-m walking speed and perceived safety during this test, general mobility, and device preference for arms 1 and 2 for continued use. Walking tests were performed with (On) and without a device (Off) at 0, 3, 6, 9, and 12 weeks. Results. Both WA and AFO had significant orthotic (On–Off difference), therapeutic (change over time when Off), and combined (change over time On vs baseline Off) effects on walking speed. An AFO also had a significant orthotic effect on Physiological Cost Index. The WA had a higher, but not significantly different therapeutic effect on speed than an AFO, whereas an AFO had a greater orthotic effect than the WA (significant at 12 weeks). Combined effects on speed after 6 weeks did not differ between devices. Users felt as safe with the WA as with an AFO, but significantly more users preferred the WA. Conclusions. Both devices produce equivalent functional gains.

Collaboration


Dive into the Gary Abrams's collaboration.

Top Co-Authors

Avatar
Top Co-Authors

Avatar

Steven M. Paul

University of California

View shared research outputs
Top Co-Authors

Avatar

Jon D. Levine

University of California

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Kord M. Kober

University of California

View shared research outputs
Top Co-Authors

Avatar

Claudia West

University of California

View shared research outputs
Top Co-Authors

Avatar

Nancy N. Byl

University of California

View shared research outputs
Top Co-Authors

Avatar

Betty Smoot

University of California

View shared research outputs
Top Co-Authors

Avatar

Charles Elboim

University of California

View shared research outputs
Researchain Logo
Decentralizing Knowledge