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  1. This power point is made available as an educational resource or study aid for your use only. This presentation may not be duplicated for others and should not be redistributed or posted anywhere on the internet or on any personal websites. Your use of this resource is with the acknowledgment and acceptance of those restrictions.

  2. Basal GangliaMHD – Neuroanatomy ModuleFebruary 2, 2016 Gregory Gruener, MD, MBA Vice Dean for Education, SSOM Professor & Associate Chair, Department of Neurology LUHS/Trinity Health and Catholic Health East

  3. Anterolateral Lancet Neurol 2014; 13: 100–12

  4. Outcomes you need to be able to demonstrate • Define and identify the major divisions of the basal ganglia • Identify the basal ganglia on CT/MRI or brainstem sections • List the components of the basal ganglia functional “circuitry” and associated neurotransmitters • List the major basal ganglia functional loops and roles • Describe the direct and indirect motor pathways and relevance/role of the substantia nigra compacta

  5. General Terminology Striatum Caudate nucleus Nucleus accumbens Putamen Globus pallidus (pallidum) internal segment (GPi) external segment (GPe) Thalamus Subthalamic nucleus Substantia nigra compact part (SNc) reticular part (SNr) Nolte. Essentials of the human brain. Mosby, 2010

  6. Basal Ganglia

  7. Fitzgerald MJT, Gruener G, Mtui E. Clinical Neuroanatomy and related Neuroscience, 6th Ed., W. B. Saunders 2012

  8. Fitzgerald MJT, Gruener G, Mtui E. Clinical Neuroanatomy and related Neuroscience, 6th Ed., W. B. Saunders 2012

  9. Fitzgerald MJT, Gruener G, Mtui E. Clinical Neuroanatomy and related Neuroscience, 6th Ed., W. B. Saunders 2012

  10. Fitzgerald MJT, Gruener G, Mtui E. Clinical Neuroanatomy and related Neuroscience, 6th Ed., W. B. Saunders 2012

  11. Basal ganglia “circuitry” Nolte. Essentials of the human brain. Mosby, 2010 Fitzgerald MJT, Gruener G, Mtui E. Clinical Neuroanatomy and related Neuroscience, 6th Ed., W. B. Saunders 2012

  12. Basal ganglia “circuitry” Blumenfeld. Neuroanatomy through clinical cases. Sinauer Associates, 2002

  13. Basal ganglia “circuitry” • BG have no major outputs to LMNs • Influence LMNs via the cerebral cortex • Inputto striatum from cortex is excitatory • Glutamate is the neurotransmitter • Principaloutputfrom BG is via GPi + SNr • Output to thalamus, GABA is the neurotransmitter • Thalamocortical projections are excitatory • Concerned with motor “intention” • Balance of excitatory & inhibitory inputs to striatum, determine whether thalamus is suppressed

  14. BG circuits are parallel loops • Motor loop • Concerned with learned movements • Cognitive loop • Concerned with motor “intention” • Limbic loop • Emotional aspects of movements • Oculomotor loop • Concerned with voluntary saccades (fast eye-movements)

  15. BG circuits are in parallel loops Limbic Loop Cognitive Loop Motor Loop Obeso JA, Rodriguez-Oroz MC, tamelou M, et al. The expanding universe of disorders of the basal ganglia. Lancet 2014; 384: 523–31

  16. BG circuits are parallel loops Ventral pallidum Ventral striatum Ventral striatum – nucleus accumbens and adjacent putamen and caudate Ventral pallidum – small extension of the GPi under the anterior commissure Nolte. Essentials of the human brain. Mosby, 2010 Fitzgerald MJT, Gruener G, Mtui E. Clinical Neuroanatomy and related Neuroscience, 5th Ed., W. B. Saunders 2007

  17. Motor Circuit - Direct Pathway Purves D, et al. Neuroscience, 5th Ed., Sinauer Associates, 2012

  18. Motor Circuit - Direct Pathway Striatum inhibition on GPi is minimal Thalamic activity is decreased Cortex is “inhibited” Striatum inhibition on GPi is maximal Thalamic activity is increased Cortex is “excited”

  19. Motor Circuit - Indirect Pathway Purves D, et al. Neuroscience, 5th Ed., Sinauer Associates, 2012

  20. Motor Circuit - Indirect Pathway Striatum inhibition on GPi is minimal Thalamic activity is decreased Cortex is “inhibited”

  21. Parkinson Disease

  22. Parkinson Disease Purves D, et al. Neuroscience, 5th Ed., Sinauer Associates, 2012

  23. Huntington Disease • Autosomal dominant disorder • Chromosome 4 – Huntingtin gene • Abnormal trinucleotide repeat expansion • Onset age 30 - 50 years of age • Initial symptoms chorea and alternation of mood • Disease progression – dementia worsening personality changes

  24. Huntington Disease Purves D, et al. Neuroscience, 5th Ed., Sinauer Associates, 2012

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