Basal Ganglia (brain) Physiology, Parkinsonism

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Basal Ganglia (brain) Physiology, Parkinsonism

  1. 1. Basal ganglia’sconnectionsPresented by IrmaSuntooROLL NUMBER 102
  2. 2. Table of content: Introduction. Components of Basal Ganglia. Connections. Functions. Disorders of Basal Ganglia. References.
  3. 3. Basal Ganglia Group of nuclei (masses of grey matter). Located at the base of forebrain and upper partof brain stem, in the telencephalon area.
  4. 4. Components: (1) Caudate nucleus (2) Putamen (3)Globus pallidus (4) Subthalamic nucleus (5)Substantia Nigrao The caudate nucleus and putamen aretogether known as Corpus striatum.o The putamen and globus pallidus aretogether known as Lenticular Nucleus.
  5. 5.  Substantia nigra is divided into :(1) dorsomedial pars compacta.(2)ventrolateral pars reticulata. Globus pallidus is divided into:(1) globus pallidus internal.(2) gobus pallidus external.
  6. 6. Neurotransmitters: Inhibitory :(1) Dopamine.(2) GABA. Excitatory :(1) Acetylcholine(2) Glutamic acidThe direct pathway is excitatory.The indirect pathway is inhibitory.
  7. 7. Connections:
  8. 8. Functions: Subthalamic nucleus is responsible forplanning and programming of movements. Caudate nucleus plays an important role incognitive processes. Globus pallidus provides appropriate muscletone for performance of skilled movements. Subs. Nigra is centre of coordination of thoseimpulses which are essential for skilledmovements. Basal ganglia is responsible for control ofnormal auto. and associated movementssuch as swinging of arms while walking.
  9. 9. Disorders:Two types :(1) Hyperkinetic Excessive and abnormal movements.(2) Hypokinetic Difficulty in initiating movement. (Akinesia) Slowness of movement. (Bradykinesia)
  10. 10. Disorders of Basal ganglia (1) Parkinson’s disease: Both hypokinetic and hyperkinetic. Degeneration of D1 fibres of Subs. Nigra. Tremor,rigidity,festinant gait, mask-like face.
  11. 11.  (2) Chorea. Hypokinetic. Interruption of inhibitory pathway via caudate tothalamus. Rapid, irregular involuntary movements of shortduration. Decreased muscle tone& muscular weakness. (3)Athetosis Hypokinetic. Lesion of lenticular nucleus. Continuous slow twisting movement.
  12. 12.  (4) Huntington’s Disease Damage to GABA-ergic and cholinergicneurons that project to the putamen. Damage to this inhibitory pathway results inhyperkinetic features such as slurred speech& dementia.(5) Hemiballism Hyperkinetic. Damage to subthalamic nucleus. Haemorrhage within the nucleus.
  13. 13. References: Class notes Ganong AK Jain Internet

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