6 research outputs found
Comparação de inibições medulares entre indivĂduos com doença de Parkinson e saudáveis
O objetivo do presente estudo foi comparar os nĂveis de inibição prĂ©-sináptica (IPS) e inibição recĂproca (IR) entre indivĂduos com Doença de Parkinson e saudáveis e, a correlação entre essas inibições e a rigidez muscular e a severidade clĂnica de indivĂduos com Doença de Parkinson (avaliadas atravĂ©s da Escala Unificada de Avaliação da Doença de Parkinson). Foram avaliados 11 indivĂduos nos estágios 2 e 3 da doença e 13 indivĂduos saudáveis pareados pela idade. A IPS foi menor em indivĂduos com Doença de Parkinson (31,6%) do que em saudáveis (67,1%) (p = 0,02). A IR nĂŁo diferiu entre indivĂduos com Doença de Parkinson (26,9%) e saudáveis (27,6%) (p = 0,91). Adicionalmente, nĂŁo foram detectadas correlações entre os nĂveis de IPS com a rigidez e a severidade clĂnica (p >; 0,05). Portanto, mecanismos inibitĂłrios nĂŁo explicam totalmente a rigidez muscular e a severidade clinica da doença. Alterações entre ativação de mĂşsculos agonistas e antagonistas parecem estar relacionadas a influĂŞncias supraespinhais anormais nos mecanismos espinhais decorrentes da doença.The purposes of the present study were to compare presynaptic inhibition (PI) and disynaptic reciprocal inhibition (DRI) levels between parkinsonians and healthy individuals and to verify the correlation of such inhibitions with muscle rigidity and clinical severity (assessed by the Unified Parkinson Disease Rating Scale). We evaluated 11 parkinsonians in stages 2 and 3 of the disease and 13 healthy individuals matched for age. The PI was significant lower in parkinsonians (31.6%) than in healthy individuals (67.1%) (p = 0.02). The DRI did not differ between parkinsonians (26.9%) and healthy individuals (27.6%) (p = 0.91). Furthermore, no significant correlation was observed between PI with muscle rigidity and clinical severity (p >; 0.05). Therefore, inhibitory mechanisms do not fully explain the cause of muscle rigidity and clinical severity of parkinsonians. Changes between the activation of agonist and antagonist muscles seem to be caused by abnormal supraspinal influence on spinal mechanisms
Mesencephalic Locomotor Region and Presynaptic Inhibition during Anticipatory Postural Adjustments in People with Parkinson’s Disease
Individuals with Parkinson’s disease (PD) and freezing of gait (FOG) have a loss of presynaptic inhibition (PSI) during anticipatory postural adjustments (APAs) for step initiation. The mesencephalic locomotor region (MLR) has connections to the reticulospinal tract that mediates inhibitory interneurons responsible for modulating PSI and APAs. Here, we hypothesized that MLR activity during step initiation would explain the loss of PSI during APAs for step initiation in FOG (freezers). Freezers (n = 34) were assessed in the ON-medication state. We assessed the beta of blood oxygenation level-dependent signal change of areas known to initiate and pace gait (e.g., MLR) during a functional magnetic resonance imaging protocol of an APA task. In addition, we assessed the PSI of the soleus muscle during APA for step initiation, and clinical (e.g., disease duration) and behavioral (e.g., FOG severity and APA amplitude for step initiation) variables. A linear multiple regression model showed that MLR activity (R2 = 0.32, p = 0.0006) and APA amplitude (R2 = 0.13, p = 0.0097) explained together 45% of the loss of PSI during step initiation in freezers. Decreased MLR activity during a simulated APA task is related to a higher loss of PSI during APA for step initiation. Deficits in central and spinal inhibitions during APA may be related to FOG pathophysiology