• Medical hypotheses · Apr 2009

    The subthalamic nucleus is a key-structure of limbic basal ganglia functions.

    • Claire Haegelen, Tiphaine Rouaud, Pierre Darnault, and Xavier Morandi.
    • Department of Neurosurgery, CHRU Pontchaillou, Rue Henri Le Guilloux, 35033 Rennes, Cedex 2, France. Claire.HAEGELEN@chu-rennes.fr
    • Med. Hypotheses. 2009 Apr 1; 72 (4): 421-6.

    AbstractAmong the basal ganglia nuclei, the subthalamic nucleus has a major function in the motor cortico-basal ganglia-thalamo-cortical circuit and is a target site for neurosurgical treatment such as parkinsonian patients with long-term motor fluctuations and dyskinesia. According to animal and human studies, the motor functions of the subthalamic nucleus have been well documented whereas its implication on limbic functions is still less well understood and is only partially explained by anatomical and functional theories of basal ganglia organisation. After chronic subthalamic nucleus stimulation in patients with Parkinson's disease, many studies showed executive impairments, apathy, depression, hypomania, and impairment of recognition of negative facial emotions. The medial tip of the subthalamic nucleus represents its limbic part. This part receives inputs from the anterior cingulate cortex, the medial prefrontal cortex, the limbic part of the striatum (nucleus accumbens), the ventral tegmental area and the limbic ventral pallidum. The medial tip of the subthalamic nucleus projects to the limbic part of the substantia nigra and the ventral tegmental area. We propose a new function scheme of the limbic system, establishing connections between limbic cortical structures (medial prefrontal cortex, amygdala and hippocampus) and the limbic part of the basal ganglia. This new circuit could be composed of a minor part based on the model of cortico-basal ganglia-thalamo-cortical loop, and of a major part linking the subthalamic nucleus with the mesolimbic dopaminergic pathway via the ventral tegmental area and the nucleus accumbens, and with limbic cortical structures. This scheme could explain limbic impairments after subthalamic nucleus stimulation by disruption of limbic information inside the subthalamic nucleus and the ventral tegmental area.

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