RESUMO
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 = 0.01) and the intermediately low treadmill velocity (p = 0.05), whereas the parameters remained stable at the normal gait velocity. Significant differences between the untreated state and treatment with olanzapine were not detectable. We conclude that conventional neuroleptic treatment impairs the regulation of gait parameters and that this effect can be reversed at slow gait velocities by external stimulation via treadmill walking.
Assuntos
Antipsicóticos/efeitos adversos , Benzodiazepinas/efeitos adversos , Teste de Esforço , Flupentixol/efeitos adversos , Flufenazina/efeitos adversos , Marcha/efeitos dos fármacos , Haloperidol/efeitos adversos , Esquizofrenia/tratamento farmacológico , Adulto , Antipsicóticos/uso terapêutico , Benzodiazepinas/uso terapêutico , Relação Dose-Resposta a Droga , Teste de Esforço/efeitos dos fármacos , Feminino , Flupentixol/uso terapêutico , Flufenazina/uso terapêutico , Haloperidol/uso terapêutico , Humanos , Masculino , Pessoa de Meia-Idade , Rigidez Muscular/induzido quimicamente , Rigidez Muscular/diagnóstico , OlanzapinaRESUMO
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.
Assuntos
Transtornos Neurológicos da Marcha/fisiopatologia , Locomoção/fisiologia , Esquizofrenia/fisiopatologia , Comportamento Espacial/fisiologia , Percepção do Tempo/fisiologia , Análise de Variância , Antipsicóticos/efeitos adversos , Transtornos Neurológicos da Marcha/induzido quimicamente , Humanos , Escalas de Graduação Psiquiátrica , Esquizofrenia/tratamento farmacológico , CaminhadaRESUMO
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 = 0.01) and step length (p = 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.
RESUMO
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.
Assuntos
Antipsicóticos/efeitos adversos , Transtornos Neurológicos da Marcha/induzido quimicamente , Processamento de Imagem Assistida por Computador/instrumentação , Imageamento Tridimensional/instrumentação , Pirenzepina/análogos & derivados , Pirenzepina/efeitos adversos , Esquizofrenia/tratamento farmacológico , Psicologia do Esquizofrênico , Ultrassonografia/instrumentação , Adulto , Idoso , Antipsicóticos/uso terapêutico , Benzodiazepinas , Desenho de Equipamento , Feminino , Transtornos Neurológicos da Marcha/diagnóstico por imagem , Humanos , Masculino , Pessoa de Meia-Idade , Olanzapina , Pirenzepina/uso terapêutico , Valores de Referência , Esquizofrenia/diagnóstico por imagem , Sensibilidade e Especificidade , SoftwareRESUMO
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.