Thalamus
The thalamus plays critical roles in brain function that QEEG brain mapping can assess. Neurofeedback protocols can target activity in thalamus-related circuits, training toward improved regulation and function. Explore our 2 research papers covering this topic.
Research Papers
Involvement of the Red Nucleus in the Compensation of Parkinsonism may Explain why Primates can develop Stable Parkinson's Disease
Neurological compensatory mechanisms help our brain to adjust to neurodegeneration as in Parkinson's disease. It is suggested that the compensation of the damaged striato-thalamo-cortical circuit is focused on the intact thalamo-rubro-cerebellar pathway as seen during presymptomatic Parkinson, paradoxical movement and sensorimotor rhythm (SMR). Indeed, the size of the red nucleus, connecting the cerebellum with the cerebral cortex, is larger in Parkinson's disease patients suggesting an increased activation of this brain area. Therefore, the red nucleus was examined in MPTP-induced parkinsonian marmoset monkeys during the presymptomatic stage and after SMR activation by neurofeedback training. We found a reverse significant correlation between the early expression of parkinsonian signs and the size of the parvocellular part of the red nucleus, which is predominantly present in human and non-human primates. In quadrupedal animals it consists mainly of the magnocellular part. Furthermore, SMR activation, that mitigated parkinsonian signs, further increased the size of the red nucleus in the marmoset monkey. This plasticity of the brain helps to compensate for dysfunctional movement control and can be a promising target for compensatory treatment with neurofeedback technology, vibrotactile stimulation or DBS in order to improve the quality of life for Parkinson's disease patients.
View Full Paper →Neural dynamics necessary and sufficient for transition into pre-sleep induced by EEG NeuroFeedback
The transition from being fully awake to pre-sleep occurs daily just before falling asleep; thus its disturbance might be detrimental. Yet, the neuronal correlates of the transition remain unclear, mainly due to the difficulty in capturing its inherent dynamics. We used an EEG theta/alpha neurofeedback to rapidly induce the transition into pre-sleep and simultaneous fMRI to reveal state-dependent neural activity. The relaxed mental state was verified by the corresponding enhancement in the parasympathetic response. Neurofeedback sessions were categorized as successful or unsuccessful, based on the known EEG signature of theta power increases over alpha, temporally marked as a distinct “crossover” point. The fMRI activation was considered before and after this point. During successful transition into pre-sleep the period before the crossover was signified by alpha modulation that corresponded to decreased fMRI activity mainly in sensory gating related regions (e.g. medial thalamus). In parallel, although not sufficient for the transition, theta modulation corresponded with increased activity in limbic and autonomic control regions (e.g. hippocampus, cerebellum vermis, respectively). The post-crossover period was designated by alpha modulation further corresponding to reduced fMRI activity within the anterior salience network (e.g. anterior cingulate cortex, anterior insula), and in contrast theta modulation corresponded to the increased variance in the posterior salience network (e.g. posterior insula, posterior cingulate cortex). Our findings portray multi-level neural dynamics underlying the mental transition from awake to pre-sleep. To initiate the transition, decreased activity was required in external monitoring regions, and to sustain the transition, opposition between the anterior and posterior parts of the salience network was needed, reflecting shifting from extra- to intrapersonal based processing, respectively.
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