Basal Ganglia: Anatomy, Function, and Pathways

Overview

• Focus: Anatomy, pathways (direct, indirect, nigrostriatal), and clinical relevance of basal ganglia lesions.
• Functions: Starting, stopping, and modulating motor movements.

Anatomy of Basal Ganglia

Basic Components

1. Caudate Nucleus
2. Putamen
   • Together with Caudate Nucleus, forms the Striatum.
3. Globus Pallidus
   • Internal part (Globus Pallidus Internus)
   • External part (Globus Pallidus Externus)
   • Together with Putamen, forms the Lentiform Nucleus.
4. Thalamus
   • Specifically, the Ventral Anterior (VA) Nucleus and Ventral Lateral (VL) Nucleus.
5. Subthalamic Nucleus
6. Substantia Nigra
   • Zona Compacta (dopaminergic neurons)
   • Zona Reticularis

Function of Basal Ganglia

• Primary Role: Motor function coordination in conjunction with the cerebral cortex.
• Cerebral Cortex Involvement:
  • Primary Motor Cortex
  • Premotor Cortex
  • Primary Somatosensory Cortex

Pathways

Direct Pathway

• Function: Increase/stimulate motor activity (initiate motor movements).
• Pathway Steps:
  1. Cortex → Striatum (via Glutaminergic fibers; Glutamate = stimulatory).
  2. Striatum → Globus Pallidus Internus (via GABAergic fibers; GABA = inhibitory).
  3. Globus Pallidus Internus → Thalamus (less GABA = less inhibition = stimulation).
  4. Thalamus → Cortex (increased motor activity).

Indirect Pathway

• Function: Decrease/inhibit motor activity (prevent unwanted motor movements).
• Pathway Steps:
  1. Cortex → Striatum (via Glutaminergic fibers; Glutamate = stimulatory).
  2. Striatum → Globus Pallidus Externus (via GABAergic fibers; GABA = inhibitory).
  3. Globus Pallidus Externus → Subthalamic Nucleus (less GABA = less inhibition = stimulation).
  4. Subthalamic Nucleus → Globus Pallidus Internus (via Glutaminergic fibers; Glutamate = stimulatory).
  5. Globus Pallidus Internus → Thalamus (via GABAergic fibers; GABA = inhibitory).
  6. Thalamus → Cortex (decreased motor activity).

Nigrostriatal Pathway

• Function: Modulate direct and indirect pathways, amplify motor activity.
• Direct Pathway Modulation (via D1 receptors):
  • Dopamine from Substantia Nigra (Zona Compacta) to Striatum → stimulates striatal neurons.
  • Increased inhibition of Globus Pallidus Internus → less inhibition of Thalamus → increased motor activity.
• Indirect Pathway Modulation (via D2 receptors):
  • Dopamine from Substantia Nigra (Zona Compacta) to Striatum → inhibits striatal neurons.
  • Decreased inhibition of Globus Pallidus Externus → increasing inhibition of Subthalamic Nucleus → less stimulation of Globus Pallidus Internus → increased motor activity.

Neurotransmitters

GABA (Gamma-Aminobutyric Acid)

• Type: Inhibitory neurotransmitter.
• Mechanism:
  • Binding opens ligand-gated ion channels → Kᐩ exits or Cl⁻ enters → hyperpolarization (IPSP).

Glutamate

• Type: Stimulatory neurotransmitter.
• Mechanism:
  • Binding opens ligand-gated ion channels → Naᐩ/Ca²ᐩ enters → depolarization (EPSP).

Dopamine Receptors

• D1 Receptor (stimulatory): G-stimulatory protein → increased cAMP → increased protein kinases → depolarization.
• D2 Receptor (inhibitory): G-inhibitory protein → decreased cAMP → decreased protein kinases → hyperpolarization.

Clinical Relevance

Disorders Associated with Basal Ganglia Lesions:

• Parkinson’s Disease:
  • Damage to direct pathway and nigrostriatal pathway.
  • Symptoms: Difficulty initiating and maintaining movement.
• Huntington’s Disease:
  • Damage to indirect pathway.
  • Symptoms: Unwanted motor movements.
• Wilson’s Disease:
  • Copper buildup affects liver and CNS.
  • Symptoms: Mixed motor symptoms.
• Syndenham’s Chorea:
  • Autoimmune attack on basal ganglia post-rheumatic fever.
• Extrapyramidal Syndrome:
  • Drug-induced movement disorders (e.g., first-generation antipsychotics).
  • Symptoms: Tardive dyskinesia, akathisia, dystonic reactions.

Conclusion

• Basal ganglia play a crucial role in motor control through their involvement in the direct, indirect, and nigrostriatal pathways.
• Understanding these pathways aids in diagnosing and managing basal ganglia-related disorders.