Effects of haloperidol and atypical neuroleptics on psychomotor performance and driving ability in schizophrenic patients - Results from an experimental study

The influence of antipsychotic treatment on the neuropsychological and psychomotor performance of schizophrenic patients is still a subject of investigation. The present study was designed to evaluate the effects of atypical neuroleptics in comparison with a conventional dopamine antagonist neuroleptic (haloperidol) on several dimensions of psychomotor performance (visual perception, attention, reaction time, and sensorimotor performance) considered to be of relevance in evaluating driving fitness. Psychomotor performance was assessed by means of the ART 90, a computerized Act and React Test which is generally used in diagnosis of psychomotor performance. The 49 participating patients were examined at discharge following psychopathological stabilisation; 20 received haloperidol, 29 received an atypical neuroleptic. Our findings demonstrate a remarkably reduced psychomotor performance in the haloperidol-treated group of schizophrenic patients compared with patients treated with atypical neuroleptics. Only 1 (5%) subject passed all subtests without major failures and could be regarded as competent to drive. Among patients with atypical neuroleptics, 7 patients (24%) passed all test parameters without major failures. Copyright (C) 2003 S. Karger AG, Basel

Effects of haloperidol and atypical neuroleptics on psychomotor performance and driving ability in schizophrenic patients - Results from an experimental study

The influence of antipsychotic treatment on the neuropsychological and psychomotor performance of schizophrenic patients is still a subject of investigation. The present study was designed to evaluate the effects of atypical neuroleptics in comparison with a conventional dopamine antagonist neuroleptic (haloperidol) on several dimensions of psychomotor performance (visual perception, attention, reaction time, and sensorimotor performance) considered to be of relevance in evaluating driving fitness. Psychomotor performance was assessed by means of the ART 90, a computerized Act and React Test which is generally used in diagnosis of psychomotor performance. The 49 participating patients were examined at discharge following psychopathological stabilisation; 20 received haloperidol, 29 received an atypical neuroleptic. Our findings demonstrate a remarkably reduced psychomotor performance in the haloperidol-treated group of schizophrenic patients compared with patients treated with atypical neuroleptics. Only 1 (5%) subject passed all subtests without major failures and could be regarded as competent to drive. Among patients with atypical neuroleptics, 7 patients (24%) passed all test parameters without major failures. Copyright (C) 2003 S. Karger AG, Basel

Synaptogenic gene therapy with FGF22 improves circuit plasticity and functional recovery following spinal cord injury

Functional recovery following incomplete spinal cord injury (SCI) depends on the rewiring of motor circuits during which supraspinal connections form new contacts onto spinal relay neurons. We have recently identified a critical role of the presynaptic organizer FGF22 for the formation of new synapses in the remodeling spinal cord. Here, we now explore whether and how targeted overexpression of FGF22 can be used to mitigate the severe functional consequences of SCI. By targeting FGF22 expression to either long propriospinal neurons, excitatory interneurons, or a broader population of interneurons, we establish that FGF22 can enhance neuronal rewiring both in a circuit‐specific and comprehensive way. We can further demonstrate that the latter approach can restore functional recovery when applied either on the day of the lesion or within 24 h. Our study thus establishes viral gene transfer of FGF22 as a new synaptogenic treatment for SCI and defines a critical therapeutic window for its application

Magnetic relaxation measurements of exchange biased (Pt/Co) multilayers with perpendicular anisotropy

Magnetic relaxation measurements were carried out by magneto-optical Kerr effect on exchange biased (Pt/Co)5/Pt/FeMn multilayers with perpendicular anisotropy. In these films the coercivity and the exchange bias field vary with Pt spacer thickness, and have a maximum for 0.2 nm. Hysteresis loops do not reveal important differences between the reversal for ascending and descending fields. Relaxation measurements were fitted using Fatuzzo's model, which assumes that reversal occurs by domain nucleation and domain wall propagation. For 2 nm thick Pt spacer (no exchange bias) the reversal is dominated by domain wall propagation starting from a few nucleation centers. For 0.2 nm Pt spacer (maximum exchange bias) the reversal is strongly dominated by nucleation, and no differences between the behaviour of the ascending and descending branches can be observed. For 0.4 nm Pt spacer (weaker exchange bias) the nucleation density becomes less important, and the measurements reveal a much stronger density of nucleation centers in the descending branch.Comment: Europhysical Journal B, in print DOI: 10.1140/epjb/e2005-00053-

Synaptogenic gene therapy with FGF22 improves circuit plasticity and functional recovery following spinal cord injury

Functional recovery following incomplete spinal cord injury (SCI) depends on the rewiring of motor circuits during which supraspinal connections form new contacts onto spinal relay neurons. We have recently identified a critical role of the presynaptic organizer FGF22 for the formation of new synapses in the remodeling spinal cord. Here, we now explore whether and how targeted overexpression of FGF22 can be used to mitigate the severe functional consequences of SCI. By targeting FGF22 expression to either long propriospinal neurons, excitatory interneurons, or a broader population of interneurons, we establish that FGF22 can enhance neuronal rewiring both in a circuit-specific and comprehensive way. We can further demonstrate that the latter approach can restore functional recovery when applied either on the day of the lesion or within 24 h. Our study thus establishes viral gene transfer of FGF22 as a new synaptogenic treatment for SCI and defines a critical therapeutic window for its application