Basal Ganglia

BASAL GANGLIA

  • Involved in motor system control.

  • Comprises upper and lower motor neurons and their tracts.

STRUCTURE OF BASAL GANGLIA

  • Components:

    • Lentiform Nucleus:

      • Putamen

      • Globus Pallidus (II and I)

    • Caudate Nucleus:

      • Head (lateral wall of anterior horn of lateral ventricle)

      • Body (floor of body of lateral ventricle)

      • Tail (roof of inferior horn of lateral ventricle, ends in the amygdala)

  • Other Structures:

    • Subthalamic Nucleus

    • Substantia Nigra

      • Pars Compacta

      • Pars Reticulata

    • Corpus Striatum:

      • Caudate Nucleus and Lentiform Nucleus

    • Ventral Striatum:

      • Head of Caudate Nucleus and Putamen

    • Nucleus Accumbens

DOPAMINERGIC PATHWAYS

  • Nigrostriatal: Substantia Nigra pars compacta to Basal Ganglia

  • Mesolimbic: Ventral Tegmental Area to Parahippocampal Gyrus and Nucleus Accumbens

  • Mesocortical: Substantia Nigra pars compacta and VTA to Prefrontal Cortex

BRAIN PATHWAYS TO AND FROM BASAL GANGLIA

  • Direct Pathway:

    • Cerebral cortex projects to striatum (caudate + putamen) with glutamatergic fibers.

    • Substantia Nigra pars compacta excites striatum via dopaminergic fibers.

    • Striatum uses acetylcholinergic interneurons; projects GABAergic neurons to GPI and SNr.

    • GPI inhibits thalamus less, thus thalamus gets excited, leading to motor cortex excitation and movement initiation.

  • Indirect Pathway:

    • Cortex excites striatum; dopaminergic fibers from SNpc inhibit.

    • Striatum projects GABAergic fibers to GPII.

    • GPII inhibits GABAergic fibers to Subthalamic Nucleus.

    • Excitation of GPI and SNpr inhibit thalamic nuclei (VA and VL), decreasing motor cortex activation and leading to movement inhibition.

BASAL GANGLIA DISORDERS

  • Hypokinetic Disorders:

    • Breakdown of the direct pathway

    • Symptoms: akinesia, bradykinesia

  • Hyperkinetic Disorders:

    • Breakdown of the indirect pathway

    • Symptoms: dyskinesias, chorea, ballismus, athetosis, dystonia

SPECIFIC DISORDERS

  • Parkinson’s Disease:

    • Caused by dopaminergic cell depletion in Substantia Nigra leading to nigrostriatal circuitry breakdown.

    • Symptoms: akinesia, bradykinesia, resting tremor, rigidity, flexed posture, shuffling gait, mask-like expression.

  • Treatment of Parkinson’s Disease:

    • L-DOPA administration; anticholinergic medications;

    • Human embryonic dopamine cell transplantation;

    • Surgical options like pallidotomy and thalamectomies for non-medicinal responders.

  • Huntington’s Disease:

    • Autosomal dominant disorder; degeneration of striatum neurons.

    • Symptoms: chorea, cognitive decline, psychiatric disturbances; life expectancy 15-20 years post onset.

  • Sydenham’s Chorea:

    • Transient childhood chorea related to rheumatic fever affecting the striatum.

  • Athetosis:

    • Degeneration of globus pallidus; characterized by slow, writhing movements.

  • Ballism:

    • Injury to the subthalamic nucleus; results in contralateral involuntary movements.

OTHER DISORDERS

  • Wilson’s Disease:

    • Autosomal recessive disorder impacting copper metabolism; leads to liver and basal ganglia degeneration.

    • Characterized by Kayser-Fleischer rings in corneas.

  • Dystonia Musculorum Deformans:

    • Rare hereditary condition linked to lentiform nucleus injury; causes muscle co-contraction.

  • Focal Dystonias:

    • Includes conditions like torticollis, blepharospasm, dysphonia, facial spasm, writer’s cramp.