Globus Pallidus

Anatomy

• The medial part of the lentiform nucleus; divided by the medial medullary lamina into external (GPe) and internal (GPi) segments.
• Together with the substantia nigra pars reticulata, the GPi is the main output nucleus of the basal ganglia.
• Ventral pallidum: part of the reward and motivation circuit.
• Blood supply: anterior choroidal artery (GPi), lenticulostriate arteries.

Substructures

2 substructures; each has its own page.

• Globus Pallidus, External Segment GPeThe relay station of the indirect pathway: tunes the suppression of unwanted movements by braking the subthalamic nucleus.
• Globus Pallidus, Internal Segment GPiThe main output nucleus of the basal ganglia: brakes the thalamus; a deep brain stimulation target in dystonia and refractory Tourette syndrome.

Functions

• Direct pathway (striatum → GPi): disinhibition of the thalamus → release of the wanted movement.
• Indirect pathway (striatum → GPe → STN → GPi): suppression of unwanted movements.
• Regulation of movement amplitude and speed.
• Ventral pallidum: hedonic “liking” and motivation.

Connections and chemistry

• Striatum (input)
• Subthalamic nucleus (indirect and hyperdirect pathways)
• Thalamus VA/VL (GABAergic output)
• Pedunculopontine nucleus
• GABA, enkephalin, substance P

Development

Developmental course through childhood and adolescence.

• Kernicterus (neonatal hyperbilirubinemia) selectively affects the globus pallidus.
• Basal ganglia–thalamus pattern of injury in perinatal hypoxia-ischemia.

Clinical

• Kernicterus → dyskinetic cerebral palsy (choreoathetosis).
• Dystonia: GPi DBS is effective in children (especially DYT1).
• Tourette syndrome: GPi as a DBS target in refractory cases (late adolescence and adults).
• PKAN (pantothenate kinase-associated neurodegeneration): the “eye of the tiger” sign on MRI.
• Carbon monoxide poisoning: bilateral pallidal necrosis.

Treatment

This region from the perspective of medication, psychotherapy and neuromodulation. Letter badges are evidence levels.

• Primary generalized dystonia (especially DYT1): bilateral GPi deep brain stimulation markedly reduced movement disorder and disability in controlled trials (Vidailhet et al., 2005; Kupsch et al., 2006, sham-controlled). Earlier treatment in children is associated with better outcomes. B
• In Tourette syndrome, the anterior GPi is the most frequent deep brain stimulation target after the centromedian thalamus; details on the thalamus card (Martinez-Ramirez et al., 2018). C
• Preventing kernicterus: phototherapy guided by risk curves in neonatal jaundice and exchange transfusion if needed; pallidal damage is permanent. A

Assessment

Neuropsychological tasks and measures that probe this region's function.

• Movement disorder scales: YGTSS (tics), AIMS (tardive dyskinesia), Simpson-Angus (EPS)
• Neurological examination: dystonia, chorea, bradykinesia

Lesions and damage

Clinical findings expected with damage or dysfunction.

• Bilateral pallidal lesions: apathy, abulia (“psychic akinesia”), parkinsonism or dystonia.

In the model

How this structure is defined in the 3D model, and the data source.

CerebrA pallidum label (external and internal segments together). When selected, GPe and GPi from CIT168 appear inside.

References

Full citations for the card; links go to the paper (DOI) or a PubMed search.

1. Vidailhet M et al. Bilateral deep-brain stimulation of the globus pallidus in primary generalized dystonia. N Engl J Med 2005;352:459–467. Search PubMed
2. Kupsch A et al. Pallidal deep-brain stimulation in primary generalized or segmental dystonia. N Engl J Med 2006. Search PubMed