Modulatory effects of proinflammatory cytokines for action cascading processes - evidence from neurosarcoidosis.

Neurosarcoidosis is a rare central nervous system manifestation of sarcoidosis. T cell, T-helper cell and macrophage activation via the major histocompatibility complex (MHC) II-mediated pathway causes this disease. Little is known about the possible cognitive disturbances in this disease as most reported instances are case studies. Here, we provide the first in-depth analysis of psychomotor functions in a sample of 30 neurosarcoidosis patients. We investigated action control processes using a paradigm that is able to examine how different tasks are cascaded to achieve the task goal. We integrated electrophysiological (EEG) data with behavioural and neuroimmunological data. Our results show that there was no general cognitive decline in patients with neurosarcoidosis. Patients only presented deficits when two response options have to be prioritized. Patients apply an inefficient processing strategy where they try to processes different response options in parallel. The electrophysiological data show that the deficits are due to dysfunctions at the response selection stage. Behavioural and neurophysiological changes are predictable on the basis of soluble interleukin 2 receptor serum concentrations. The results show that neurosarcoidosis is not associated with nonspecific changes in cognitive functions but does lead to specific alterations in cognitive control that are strongly dependent on immunological parameters.