| Internal globus pallidus | |
|---|---|
 Internal globus pallidus (GPi) is seen in the 2nd image from the left | |
| Details | |
| Part of | Globus pallidus |
| Identifiers | |
| Latin | globus pallidus internus, globus pallidus medialis |
| Acronym | GPi |
| NeuroNames | 233 |
| NeuroLex ID | birnlex_1555 |
| TA98 | A14.1.09.511 |
| TA2 | 5572 |
| FMA | 61840 |
| Anatomical terms of neuroanatomy | |
Theinternal globus pallidus (GPi ormedial globus pallidus) is one of the twosubcorticalnuclei that provides inhibitoryoutput in thebasal ganglia, the other being thesubstantia nigrapars reticulata. Together with theexternal globus pallidus (GPe), it makes up one of the two segments of theglobus pallidus, a structure that can decay with certain neurodegenerative disorders and is a target for medical and neurosurgical therapies. The GPi, along with thesubstantia nigra pars reticulata, comprise the primary output of the basal ganglia, with its outgoingGABAergic neurons having an inhibitory function in the thalamus, the centromedian complex and the pedunculopontine complex.[1]
The efferent bundle is constituted first of theansa andlenticular fasciculus, then crosses theinternal capsule within and in parallel to the Edinger's comb system then arrives at the laterosuperior corner of thesubthalamic nucleus and constitutes thefield H2 of Forel, then H, and suddenly changes its direction to formfield H1 that goes to the inferior part of the thalamus. The distribution of axonal islands is widespread in the lateral region of the thalamus. The innervation of the central region is done by collaterals.[2]
The GPi has outgoingGABAergic neurons that connect to theventral anterior nucleus (VA) and theventral lateral nucleus (VL) in the dorsalthalamus, to thecentromedian complex, and to thepedunculopontine complex.[3]
The GPi acts to tonically inhibit theventral lateral nucleus andventral anterior nucleus of thethalamus. As these two nuclei are needed for movement planning, this inhibition restricts movement initiation and prevents unwanted movements.
The GPi receives inhibitoryGABAergic signals from thestriatum by way ofstriatopallidal fibres, when a movement requirement is signaled from thecerebral cortex. As the GPi is one of the direct output centers of thebasal ganglia, this causes disinhibition of thethalamus, increasing overall ease of initiating and maintaining movement. As this pathway only contains onesynapse (from the striatum to the internal globus pallidus), it is known as thedirect pathway.[4]
The direct pathway is modulated by stimulation of the GPi by theexternal globus pallidus andsubthalamic nucleus, via theindirect pathway.[5]
Dysfunction of the internal globus pallidus has been correlated toParkinson's disease,[6]Tourette syndrome,[7] andtardive dyskinesia.[8]
The internal globus pallidus is the target ofdeep brain stimulation (DBS) for these diseases. Deep brain stimulation sends regulated electrical pulses to the target. In patients with tardive dyskinesia treated with DBS, most people reported more than a 50% improvement in symptoms.[8] Tourette syndrome patients have also benefited from this treatment, showing over 50% improvement intic severity (compulsive disabling motor tics are symptoms of Tourette patients).[7] The GPi is also considered a "highly effective target for neuromodulation" when using deep brain stimulation on Parkinson's disease patients.[6]There is seen to be only some involvement inHuntington's disease[9] with mostly theexternal globus pallidus being affected.[10]
Inrodents its homologue is known as theentopeduncular nucleus.[11]
