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1. ? ? ? Basal Ganglia

2. Basal Ganglia Sub-cortical Masses of gray matter situated in the white core of each cerebral Hemisphere. Anatomical Classification: - Caudate Nucleus } Corpus Striatum - Lentiform Nucleus PutamenGlobusPallidus Claustrum Nucleus Accumbens Located at the base of striatum (D3 receptor)

3. Basal Ganglia Physiological Classification: • Caudate Nucleus • Putamen • GlobusPallidus • SubstantiaNigra • Subthalamus • Function –Accessory motor system work in association with Cerebral Cortex & Corticospinal system

4. Anatomical relationship of Basal Ganglia to other structures of the Cerebral Cortex

5. Anatomical relationship of Basal Ganglia to other structures of the Cerebral Cortex

6. Anatomical Position of Caudate Nucleus & Relation with Thalamus Comma shape Caudate N Extends in all lobes

7. Relation of Basal Ganglia circuit toCorticospinal – Cerebellar System for Control of Movement

8. Functional Circuits of Basal Ganglia • Putamen Circuit-Mainly Concerned with complexPattern of Motor Activity • Caudate Circuit – Concerned with Cognitivecontrol of sequence of motor Patterns

9. Putamen Circuit

10. Neural Connection of Putamen Circuit:For Learned Pattern of movement Primary Motor Cortex • Premotor , Supply. motor & Primary Sensory cortex Putamen Internal GlobusPallidus Vent. Ant & Ventro-Lat N of Thalamus

11. Putamen Circuit • Function in association with Corticospinal System to Control Complex Pattern of Motor Activity. • e.g. -Writing alphabet -Cutting paper with Scissors -Hammering nail -Skilled movements during different Games - Movements of Laryngeal & extra-ocular Muscles

12. Putamen: Additional Circuits Along with this Circuit, 3 other Circuits are: 1. PutamenExt.G.P Sub thalamus Thalamus Motor Cortex 2. Putamen G.P.E SubstantiaNigra Thalamus 3. Local Feedback from G.Pal. Ext. Sub thalamus

13. NeuralConnections -Caudate Circuit-Cognitive function- uses sensory information & stored memory for motor activity Pre frontal, Premotor & Supply Motor Cortex Caudate Nucleus receives input from association areas of Cerebral Cortex Caudate Nucleus Int. GlobusPallidus Ventro-Ant & Ventro Lat N Thalamus

14. Caudate Circuit. Impulses Finally returns to motor association areas which is concerned withputting together Sequence of movements & not individual muscles

15. Neural Pathways Secreting Different Types of neurotransmitters

16. Normal Vs Parkinsonism

17. Direct path: Dopamine(SNC) stimulate D1 receptors of (Putamen), > facilitate information flow by inhibitingGPi(GABA ergic) Dopamine Facilitate movement Indirect path: Dopamine(SNC) inhibit D2 receptors of (Putamen), which inhibit information flow, Via GPe > GPi > SubTh N Dopamine inhibit movement Dopaminergic control of striatum

18. Cortico-striatal-pallidal-thalamo-cortical loops • Direct path: cortex activates medium spiny neurons, which inhibit GPi neurons, decreasing the inhibition of thalamo-cortical neurons; net effect is disinhibition of the thalamus and facilitation of movement • Indirect path: cortex activates medium spiny neurons, > inhibition of GPe neurons, > inhibition of subthalamic neurons, which tonically activate neurons, which inhibit thalamo-cortical neurons; net effect is inhibition of thalamo-cortical neurons and inhibition of movement

19. Basal Ganglia Loop glutamate Motor Cortex Striatum Substantia Nigra DA GABA glutamate Motor Thalamus: VA GABA Pallidum

22. Direct pathway Disinhibits motor thalamus Thus activates thalamo-cortical neurons Activates motor cortex Facilitates movement Indirect pathway Inhibits motor thalamus Thus inhibits thalamo-cortical neurons Inhibits motor cortex Inhibits movement Direct and Indirect Pathways B A L A N C E

23. Clinical problems in basal ganglia • Movement disorders are one aspect; • Cognitive and memory impairments may also occur • Hypokinesias: Akinesia (difficulty in planning and initiating movements); Bradykinesia(reduction in velocity and amplitude of movement): inappropriate activity in antagonist muscles

24. Parkinsonison’s Disease (Paralysis Agitans) • Lesion- Substantia Nigra > • Nigrostriatal dopaminergic N degenerate • Fiber to Putamen are severely affected. • Symptoms appear when 60-80% nigrostriatal fibers are lost. • Also seen in patients taking Phenothiazines (D2 Receptor Blockers)

25. Parkinsonism Features: • Hypokinetic - Akinesia, Bradykinesia &Dyskinesia(Difficulty in planning & initiating movements) walks with Short steps & bending forward • Hyperkinetic- Rigidity- lead pipe or Cogwheel Rigidity Tremur- Tremur at rest(Pillrolling mevement) Loss of associated movements- e.g.Swinging of Arms during walking. Mask Shape Fcae

26. Treatments for Parkinson’s disease • Pharmacological • L-DOPA plus carbidopa to increase dopamine levels; usually initial improvements, but then progressive loss; D1 receptor agonists can induce tardive dyskinesia. • Deprinyl- Enzyme inhibitor • Neurosurgical • implantation of dopamine-producing cells: very controversial • lesions of thalamic or pallidal structures: blocks overactivity of pallido-thalamic projection • overstimulation of subthalamus to inhibit subthalamic activity: deep brain stimulation

27. Clinical problems in basal ganglia • Huntington’s chorea Genetic defect in gene called huntingtin • Loss of about 90% of striatal neurons, especially of indirect pathway: overactivity of direct pathway: uncontrolled movements • Progressive, untreatable, decreased function and dementia • Choreiform movements leading to severe impairment; death within 15 years

28. hyperkinesias • Choreiform movements: “dance-like movements – PutamenLesion • Ballismus and hemiballismus; Involuntary, flailing intense & violent movements – usually due to vascular lesions of contralateralsubthalamic nucleus • Athetoid movements: continual writhing movements of distal extremity- Lesion is in GlobusPallidus

29. Organization of motor System