The Experts below are selected from a list of 6183 Experts worldwide ranked by ideXlab platform
R M Goodman - One of the best experts on this subject based on the ideXlab platform.
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megalocornea macrocephaly mental and Motor Retardation mmmm
Clinical Genetics, 2008Co-Authors: Moshe Frydman, Michal Berkenstadt, A Raasrothschild, R M GoodmanAbstract:Two patients with macrocephaly, mild mental Retardation and megalocornea are reported. Hypotonia, poor coordination and swallowing difficulties were present. One patient was obese and the other had scoliosis. Both had large fleshy ears and long fingers. The spectrum of the mental Retardation megalocornea syndrome is not fully defined. These two patients resemble a previously reported case, and although there are distinct differences from patients with familial or sporadic Neuhauser syndrome, these cases may represent clinical variability of that syndrome.
Joel Ellwanger - One of the best experts on this subject based on the ideXlab platform.
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Motor and cognitive aspects of Motor Retardation in depression.
Journal of Affective Disorders, 2000Co-Authors: Michael P. Caligiuri, Joel EllwangerAbstract:Abstract Background: Motor Retardation is a common feature of major depressive disorder having potential prognostic and etiopathological significance. According to DSM-IV, depressed patients who meet criteria for psychoMotor Retardation, must exhibit Motor slowing of sufficient severity to be observed by others. However, overt presentations of Motor slowing cannot distinguish slowness due to cognitive factors from slowness due to neuroMotor disturbances. Methods: We examined cognitive and neuroMotor aspects of Motor slowing in 36 depressed patients to test the hypothesis that a significant proportion of patients exhibit Motor programming disturbances in addition to psychoMotor impairment. A novel instrumental technique was used to assess Motor programming in terms of the subject’s ability to program movement velocity as a function of movement distance. A traditional psychoMotor battery was combined with an instrumental measure of reaction time to assess the cognitive aspects of Motor Retardation. Results: The depressed patients exhibited significant impairment on the velocity scaling measure and longer reaction times compared with nondepressed controls. Approximately 40% of the patients demonstrated abnormal psychoMotor function as measured by the traditional battery; whereas over 60% exhibited some form of Motor slowing as measured by the instruments. Approximately 40% of the patients exhibited parkinsonian-like Motor programming deficits. A five-factor model consisting of Motor measures predicted diagnosis among bipolar and unipolar depressed patients with 100% accuracy. Limitations: The ability of Motor measures to discriminate bipolar from unipolar patients must be viewed with caution considering the relatively small sample size of bipolar patients. Conclusions: These findings suggest that a subgroup of depressed patients exhibit Motor Retardation that is behaviorally similar to parkinsonian bradykinesia and may stem from a similar disruption within the basal ganglia.
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Motor and cognitive aspects of Motor Retardation in depression.
Journal of affective disorders, 2000Co-Authors: Michael P. Caligiuri, Joel EllwangerAbstract:Motor Retardation is a common feature of major depressive disorder having potential prognostic and etiopathological significance. According to DSM-IV, depressed patients who meet criteria for psychoMotor Retardation, must exhibit Motor slowing of sufficient severity to be observed by others. However, overt presentations of Motor slowing cannot distinguish slowness due to cognitive factors from slowness due to neuroMotor disturbances. We examined cognitive and neuroMotor aspects of Motor slowing in 36 depressed patients to test the hypothesis that a significant proportion of patients exhibit Motor programming disturbances in addition to psychoMotor impairment. A novel instrumental technique was used to assess Motor programming in terms of the subject's ability to program movement velocity as a function of movement distance. A traditional psychoMotor battery was combined with an instrumental measure of reaction time to assess the cognitive aspects of Motor Retardation. The depressed patients exhibited significant impairment on the velocity scaling measure and longer reaction times compared with nondepressed controls. Approximately 40% of the patients demonstrated abnormal psychoMotor function as measured by the traditional battery; whereas over 60% exhibited some form of Motor slowing as measured by the instruments. Approximately 40% of the patients exhibited parkinsonian-like Motor programming deficits. A five-factor model consisting of Motor measures predicted diagnosis among bipolar and unipolar depressed patients with 100% accuracy. The ability of Motor measures to discriminate bipolar from unipolar patients must be viewed with caution considering the relatively small sample size of bipolar patients. These findings suggest that a subgroup of depressed patients exhibit Motor Retardation that is behaviorally similar to parkinsonian bradykinesia and may stem from a similar disruption within the basal ganglia.
F.g. Zitman - One of the best experts on this subject based on the ideXlab platform.
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Changes in fine Motor Retardation in depressed patients treated with fluoxetine.
Journal of affective disorders, 1996Co-Authors: Bernard Sabbe, Jacques J. M. Van Hoof, Wouter Hulstijn, F.g. ZitmanAbstract:Changes in psychoMotor slowing were studied in 21 inpatients with a Major Depressive Episode. Fine Motor Retardation was measured and analysed using computer-aided drawing and figure-copying tasks at T0 (the start of 6 weeks treatment with fluoxetine 20 mg/day) and 5 weeks later (T1). The differences in reaction time between the patients and a group of healthy, matched controls at T0 had disappeared at T1. The initial Motor deficit, expressed in longer movement times, had not improved at T1. These findings combined with the effect of manipulation of cognitive and Motor demands, suggested that only cognitive processes had accelerated.
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Fine Motor Retardation and depression
Journal of psychiatric research, 1996Co-Authors: Bernard Sabbe, Jacques J. M. Van Hoof, Wouter Hulstijn, F.g. ZitmanAbstract:New computerized techniques allow the precise measurement of psychoMotor Retardation in patients with a major depressive episode (MDE). One such technique is the analysis of writing and drawing behaviour during figure copying tasks. In the present study, 22 inpatients with an MDE were compared to 22 normal controls. Three tasks were used: the drawing of lines and simple figures, the copying of complex figures and a task in which figures had to be rotated. Objectives were to provide support for earlier findings that the patients were slower than the controls and to explore the cognitive and Motor processes involved. Two strategies were applied: analysis of the reaction time and movement time and their different components, and manipulation of the cognitive and Motor demands. Patients showed considerable Retardation with most of the kinematic variables. Motor deficits and cognitive slowing down contributed to this Retardation. Cognitive difficulties increased with increasing complexity of the task.
Müfit Arcasoy - One of the best experts on this subject based on the ideXlab platform.
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A case of Marden-Walker syndrome with Dandy-Walker malformation
Clinical genetics, 2008Co-Authors: Ferda Ozkinay, A. R. Özyürek, Ali Rahmi Bakiler, Nazmi Narin, H. Yüksel, Cihangir Ozkinay, Aytül Parlar, Müfit ArcasoyAbstract:A 5-month-old girl with Marden-Walker syndrome is presented. This is a rare autosomal recessive syndrome. So far, approximately 20 cases have been described in the literature. The patient was hospitalized because of difficulty in feeding and slow spontaneous movements. Her parents were first cousins. She was diagnosed with clinical findings of growth and Motor Retardation, typical facial appearance, congenital heart disease, arachnodactyly, joint contractures, and a Dandy-Walker malformation on magnetic resonance imaging.
Michael P. Caligiuri - One of the best experts on this subject based on the ideXlab platform.
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A quantitative neuroMotor predictor of antidepressant non-response in patients with major depression
Journal of affective disorders, 2003Co-Authors: Michael P. Caligiuri, Valentina Gentili, Sonja Eberson, John R. Kelsoe, Mark Hyman Rapaport, J. Christian GillinAbstract:Predicting response to antidepressant medication has been a challenge to clinicians and researchers for decades. Attention has been paid to the role of Motor Retardation as a putative indicator of treatment response, yet previous findings have been mixed. One reason for this inconsistency may be related to the subjective nature of Motor Retardation and how it is assessed. In the present study, we adopted a measure of Motor programming previously shown to characterize parkinsonian bradykinesia to test whether neuroMotor function could predict response to antidepressant treatment. Twenty-eight patients (14 males and 14 females with a mean age of 42.0 years) meeting DSM-IV criteria for a depressive disorder were randomized to receive 8 weeks of treatment with one of three antidepressant medications (sertraline, phenelzine, or bupropion). Treatment outcomes were assessed using the 17-item version of the Hamilton Rating Scale for Depression (HRSD). Patients were considered asymptomatic if their post-treatment HRSD total score was equal to or less than 7. Treatment responders (n=15) had significantly less baseline impairment (P=0.01) on the neuroMotor measure than non-responders (n=13). There was a significant relationship between amount of improvement on the HRSD and severity of baseline neuroMotor function (r=-0.51; P=0.006). No significant group effects were found for baseline psychoMotor slowing or clinical ratings of Motor Retardation. These results demonstrate that a quantitative measure of Motor programming may be a useful predictor of antidepressant non-response.
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Motor and cognitive aspects of Motor Retardation in depression.
Journal of Affective Disorders, 2000Co-Authors: Michael P. Caligiuri, Joel EllwangerAbstract:Abstract Background: Motor Retardation is a common feature of major depressive disorder having potential prognostic and etiopathological significance. According to DSM-IV, depressed patients who meet criteria for psychoMotor Retardation, must exhibit Motor slowing of sufficient severity to be observed by others. However, overt presentations of Motor slowing cannot distinguish slowness due to cognitive factors from slowness due to neuroMotor disturbances. Methods: We examined cognitive and neuroMotor aspects of Motor slowing in 36 depressed patients to test the hypothesis that a significant proportion of patients exhibit Motor programming disturbances in addition to psychoMotor impairment. A novel instrumental technique was used to assess Motor programming in terms of the subject’s ability to program movement velocity as a function of movement distance. A traditional psychoMotor battery was combined with an instrumental measure of reaction time to assess the cognitive aspects of Motor Retardation. Results: The depressed patients exhibited significant impairment on the velocity scaling measure and longer reaction times compared with nondepressed controls. Approximately 40% of the patients demonstrated abnormal psychoMotor function as measured by the traditional battery; whereas over 60% exhibited some form of Motor slowing as measured by the instruments. Approximately 40% of the patients exhibited parkinsonian-like Motor programming deficits. A five-factor model consisting of Motor measures predicted diagnosis among bipolar and unipolar depressed patients with 100% accuracy. Limitations: The ability of Motor measures to discriminate bipolar from unipolar patients must be viewed with caution considering the relatively small sample size of bipolar patients. Conclusions: These findings suggest that a subgroup of depressed patients exhibit Motor Retardation that is behaviorally similar to parkinsonian bradykinesia and may stem from a similar disruption within the basal ganglia.
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Motor and cognitive aspects of Motor Retardation in depression.
Journal of affective disorders, 2000Co-Authors: Michael P. Caligiuri, Joel EllwangerAbstract:Motor Retardation is a common feature of major depressive disorder having potential prognostic and etiopathological significance. According to DSM-IV, depressed patients who meet criteria for psychoMotor Retardation, must exhibit Motor slowing of sufficient severity to be observed by others. However, overt presentations of Motor slowing cannot distinguish slowness due to cognitive factors from slowness due to neuroMotor disturbances. We examined cognitive and neuroMotor aspects of Motor slowing in 36 depressed patients to test the hypothesis that a significant proportion of patients exhibit Motor programming disturbances in addition to psychoMotor impairment. A novel instrumental technique was used to assess Motor programming in terms of the subject's ability to program movement velocity as a function of movement distance. A traditional psychoMotor battery was combined with an instrumental measure of reaction time to assess the cognitive aspects of Motor Retardation. The depressed patients exhibited significant impairment on the velocity scaling measure and longer reaction times compared with nondepressed controls. Approximately 40% of the patients demonstrated abnormal psychoMotor function as measured by the traditional battery; whereas over 60% exhibited some form of Motor slowing as measured by the instruments. Approximately 40% of the patients exhibited parkinsonian-like Motor programming deficits. A five-factor model consisting of Motor measures predicted diagnosis among bipolar and unipolar depressed patients with 100% accuracy. The ability of Motor measures to discriminate bipolar from unipolar patients must be viewed with caution considering the relatively small sample size of bipolar patients. These findings suggest that a subgroup of depressed patients exhibit Motor Retardation that is behaviorally similar to parkinsonian bradykinesia and may stem from a similar disruption within the basal ganglia.