Week 3 HUBS - Basal Ganglia

Components of Basal Ganglia

• Five main nuclei: caudate nucleus, putamen, globus pallidus (internal & external segments), subthalamic nucleus, substantia nigra (pars compacta & pars reticulata)
• Additional related areas: nucleus accumbens (ventral striatum), claustrum, thalamic VA/VL complex, internal capsule
• Nomenclature summary
  • Corpus striatum = caudate + putamen + globus pallidus
  • Striatum / neostriatum = caudate + putamen (principal cortical input zone)
  • Lentiform nucleus = putamen + globus pallidus

Anatomical Identification (coronal & horizontal)

• Caudate: medial to internal capsule; head anterior, body superior to thalamus, tail curves into temporal lobe
• Putamen: lateral to internal capsule, separated from caudate by capsule
• Globus pallidus: medial to putamen; internal (medial) & external (lateral) segments identified by medullary laminae
• Substantia nigra: ventral midbrain (compact = dorsal, reticular = ventral)
• Subthalamic nucleus: inferior to thalamus, medial to internal capsule
• Internal capsule: white-matter tract between caudate (medial) & putamen/GP (lateral); limbs & genu visible on axial images

Functional Pathways

• Two major motor pathways
  • Direct pathway: striatum → GPi/SNr → thalamus → cortex → promotes movement
  • Indirect pathway: striatum → GPe → STN → GPi/SNr → thalamus → cortex → inhibits movement
• Dopamine from SNc modulates striatum
  • $D1$ receptors facilitate direct pathway
  • $D2$ receptors suppress indirect pathway → overall facilitation of movement
• Output nuclei provide tonic inhibition to thalamus; pathway balance adjusts cortical excitation of upper motor neurons

Basal Ganglia Circuits

1. Skeletomotor loop – facial, limb, trunk control (primary & premotor cortex ↔ putamen)
2. Oculomotor loop – saccadic eye movements (frontal eye fields ↔ caudate body)
3. Prefrontal (associative) loop – cognition & executive functions (dorsolateral prefrontal cortex ↔ caudate head)
4. Limbic loop – motivation & emotion (orbitofrontal/anterior cingulate ↔ ventral striatum)

Basal Ganglia Disorders

• Parkinson’s disease (hypokinetic)
  • Degeneration of SNc → ↓ dopamine
  • ↓ direct & ↑ indirect pathway activity → ↑ tonic inhibition of thalamus
  • Clinical: hypokinesia, bradykinesia, rigidity, resting tremor
• Huntington’s disease (hyperkinetic)
  • Autosomal dominant loss of striatal $\text{GABA/ACh}$ neurons, esp. indirect pathway
  • ↓ inhibition → thalamic disinhibition → choreiform movements, dementia
• Ballism/Hemiballism
  • Lesion of subthalamic nucleus → loss of indirect pathway drive → violent flinging movements
• Tardive dyskinesia
  • Chronic antipsychotic (D2 blockade) side effect → repetitive choreic movements

Quick Recap

• Direct = Go | Indirect = Stop
• Dopamine biases to Go via $D1$ (+) & $D2$ (–) effects
• Movement disorders arise from imbalance between these pathways or degeneration of specific nuclei