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1.
Psychiatr Prax ; 31 Suppl 1: S164-6, 2004 Nov.
Article in German | MEDLINE | ID: mdl-15570541

ABSTRACT

Schizophrenic disorders as well as neuroleptic treatment can affect locomotion. The study assessed the influence of neuroleptic treatment on externally triggered gait on a treadmill at three different velocities via ultrasonic topometric gait analysis. Spatial and temporal gait parameters were assessed in two groups of schizophrenic patients either under treatment with conventional neuroleptics (n = 12) or without neuroleptic treatment (n = 10) and re-assessed after treatment change to the atypical neuroleptic olanzapine in a repeated measures design. After switch from conventional neuroleptics to olanzapine patients showed an increase of step length and decrease of cadence at the low (p

Subject(s)
Antipsychotic Agents/adverse effects , Benzodiazepines/adverse effects , Exercise Test , Flupenthixol/adverse effects , Fluphenazine/adverse effects , Gait/drug effects , Haloperidol/adverse effects , Schizophrenia/drug therapy , Adult , Antipsychotic Agents/therapeutic use , Benzodiazepines/therapeutic use , Dose-Response Relationship, Drug , Exercise Test/drug effects , Female , Flupenthixol/therapeutic use , Fluphenazine/therapeutic use , Haloperidol/therapeutic use , Humans , Male , Middle Aged , Muscle Rigidity/chemically induced , Muscle Rigidity/diagnosis , Olanzapine
2.
Schizophr Res ; 69(2-3): 159-66, 2004 Aug 01.
Article in English | MEDLINE | ID: mdl-15469189

ABSTRACT

This study assessed the locomotor patterns of gait in schizophrenic patients and differentiated intrinsic effects of the illness from those caused by conventional and atypical neuroleptic treatment. Gait parameters of drug-naïve, conventionally and atypically treated patients as well as control subjects were evaluated. Differences in gait velocity and in stride length between the four investigated groups were highly significant (ANOVA: p<0.001). Mean gait velocities of all patient groups were significantly slower than those of controls, with the most striking difference observed between the control group and patients treated with conventional neuroleptics (p <0.001). Amongst the patient groups, significant differences were detected between patients treated with conventional neuroleptics and both patients treated with atypical neuroleptics and drug-naïve patients (p < 0.05), but not between untreated and atypically treated patients. In all patient groups the reduction of gait velocity was due to a smaller mean stride length, while the cadence (steps per minute) was not changed. These results indicate that schizophrenia causes a primary disturbance of stride length regulation. Conventional antipsychotic treatment intensifies this deficit, whereas atypical antipsychotic treatment does not cause any additional gait disturbances. In contrast to the spatial parameters, the temporal structure of schizophrenic gait is not affected either by antipsychotic treatment or schizophrenia itself.


Subject(s)
Gait Disorders, Neurologic/physiopathology , Locomotion/physiology , Schizophrenia/physiopathology , Spatial Behavior/physiology , Time Perception/physiology , Analysis of Variance , Antipsychotic Agents/adverse effects , Gait Disorders, Neurologic/chemically induced , Humans , Psychiatric Status Rating Scales , Schizophrenia/drug therapy , Walking
3.
Psychiatr Prax ; 30(Suppl 2): 110-114, 2003 May.
Article in German | MEDLINE | ID: mdl-13130352

ABSTRACT

Schizophrenic disorders as well as neuroleptic treatment can affect locomotion. The study assessed the influence of neuroleptic treatment on human gait via ultrasonic topometric gait analysis. In a control sample the test system proved high test-retest-reliability. Spatial and temporal gait parameters were assessed in schizophrenic patients without neuroleptic treatment (n = 12) and under treatment with conventional neuroleptics (n = 14) and re-assessed after treatment change to the atypical neuroleptic olanzapine in a repeated measures design. After switch from conventional neuroleptics to olanzapine patients showed an increase of gait velocity (p

4.
Psychiatr Prax ; 30 Suppl 2: S110-4, 2003 May.
Article in German | MEDLINE | ID: mdl-14509054

ABSTRACT

Schizophrenic disorders as well as neuroleptic treatment can affect locomotion. The study assessed the influence of neuroleptic treatment on human gait via ultrasonic topometric gait analysis. In a control sample the test system proved high test-retest-reliability. Spatial and temporal gait parameters were assessed in schizophrenic patients without neuroleptic treatment (n = 12) and under treatment with conventional neuroleptics (n = 14) and re-assessed after treatment change to the atypical neuroleptic olanzapine in a repeated measures design. After switch from conventional neuroleptics to olanzapine patients showed an increase of gait velocity (p < or = 0.01) and step length (p < or = 0.01) whereas the cadence remained stable. Significant differences between the untreated state and treatment with olanzapine were not detectable. We conclude that bipedal gait is affected by conventional neuroleptic treatment. The degree of impairment can be objectively measured by testing spatio-temporal and kinematic gait parameters via three-dimensional ultrasonic gait analysis.


Subject(s)
Antipsychotic Agents/adverse effects , Gait Disorders, Neurologic/chemically induced , Image Processing, Computer-Assisted/instrumentation , Imaging, Three-Dimensional/instrumentation , Pirenzepine/analogs & derivatives , Pirenzepine/adverse effects , Schizophrenia/drug therapy , Schizophrenic Psychology , Ultrasonography/instrumentation , Adult , Aged , Antipsychotic Agents/therapeutic use , Benzodiazepines , Equipment Design , Female , Gait Disorders, Neurologic/diagnostic imaging , Humans , Male , Middle Aged , Olanzapine , Pirenzepine/therapeutic use , Reference Values , Schizophrenia/diagnostic imaging , Sensitivity and Specificity , Software
5.
J Leukoc Biol ; 72(1): 35-42, 2002 Jul.
Article in English | MEDLINE | ID: mdl-12101260

ABSTRACT

CD137, a member of the TNF receptor family, and its ligand are expressed on T lymphocytes and antigen-presenting cells (APC), respectively. During interaction with APC, T lymphocytes receive a potent, costimulatory signal through CD137. Reverse signaling has been demonstrated for the CD137 ligand, which causes activation in monocytes. Here we show that B lymphocytes also receive costimulatory signals through the CD137 ligand. Immobilized CD137 augmented proliferation of preactivated B lymphocytes up to fivefold and immunoglobulin synthesis, up to threefold. CD137 had no effect on resting cells. Further, we show that CD137 is expressed in vivo by follicular dendritic cells (FDC) in germinal centers. Germinal centers form during humoral immune responses and are essential for B lymphocyte affinity maturation. These data imply that, similar to the CD40 receptor/ligand system, which mediates T lymphocyte help to B lymphocytes after the first antigen encounter, the CD137 receptor/ligand system may mediate costimulation of B lymphocytes by FDC during affinity maturation.


Subject(s)
B-Lymphocytes/immunology , Dendritic Cells, Follicular/immunology , Germinal Center/immunology , Lymphocyte Activation , Receptors, Nerve Growth Factor/metabolism , Receptors, Tumor Necrosis Factor/metabolism , Animals , Antigens, CD , Cells, Cultured , Humans , Hybrid Cells , Immunoglobulin M/biosynthesis , Mice , Models, Immunological , RNA, Messenger/biosynthesis , Receptors, Nerve Growth Factor/genetics , Receptors, Tumor Necrosis Factor/genetics , Transcription, Genetic , Tumor Necrosis Factor Receptor Superfamily, Member 9
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