Basal ganglia’sconnectionsPresented by IrmaSuntooROLL NUMBER 102
Table of content: Introduction. Components of Basal Ganglia. Connections. Functions. Disorders of Basal Ganglia. References.
Basal Ganglia Group of nuclei (masses of grey matter). Located at the base of forebrain and upper partof brain stem, in the telencephalon area.
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.
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.
Neurotransmitters: Inhibitory :(1) Dopamine.(2) GABA. Excitatory :(1) Acetylcholine(2) Glutamic acidThe direct pathway is excitatory.The indirect pathway is inhibitory.
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.
Disorders:Two types :(1) Hyperkinetic Excessive and abnormal movements.(2) Hypokinetic Difficulty in initiating movement. (Akinesia) Slowness of movement. (Bradykinesia)
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.
(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.
(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.
References: Class notes Ganong AK Jain Internet