Physiology

1. Basal ganglia’s
connections
Presented by Irma
Suntoo
ROLL NUMBER 102

2. Table of content:
 Introduction.
 Components of Basal Ganglia.
 Connections.
 Functions.
 Disorders of Basal Ganglia.
 References.

3. Basal Ganglia
 Group of nuclei (masses of grey matter).
 Located at the base of forebrain and upper part
of brain stem, in the telencephalon area.

4. Components:
 (1) Caudate nucleus
 (2) Putamen
 (3)Globus pallidus
 (4) Subthalamic nucleus
 (5)Substantia Nigra
o The caudate nucleus and putamen are
together known as Corpus striatum.
o The putamen and globus pallidus are
together known as Lenticular Nucleus.

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.

7. Neurotransmitters:
 Inhibitory :
(1) Dopamine.
(2) GABA.
 Excitatory :
(1) Acetylcholine
(2) Glutamic acid
The direct pathway is excitatory.
The indirect pathway is inhibitory.

8. Connections:

9. Functions:
 Subthalamic nucleus is responsible for
planning and programming of movements.
 Caudate nucleus plays an important role in
cognitive processes.
 Globus pallidus provides appropriate muscle
tone for performance of skilled movements.
 Subs. Nigra is centre of coordination of those
impulses which are essential for skilled
movements.
 Basal ganglia is responsible for control of
normal auto. and associated movements
such as swinging of arms while walking.

10. Disorders:
Two types :
(1) Hyperkinetic
 Excessive and abnormal movements.
(2) Hypokinetic
 Difficulty in initiating movement. (Akinesia)
 Slowness of movement. (Bradykinesia)

11. 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.

13.  (2) Chorea.
 Hypokinetic.
 Interruption of inhibitory pathway via caudate to
thalamus.
 Rapid, irregular involuntary movements of short
duration.
 Decreased muscle tone& muscular weakness.
 (3)Athetosis
 Hypokinetic.
 Lesion of lenticular nucleus.
 Continuous slow twisting movement.

14.  (4) Huntington’s Disease
 Damage to GABA-ergic and cholinergic
neurons that project to the putamen.
 Damage to this inhibitory pathway results in
hyperkinetic features such as slurred speech
& dementia.
(5) Hemiballism
 Hyperkinetic.
 Damage to subthalamic nucleus.
 Haemorrhage within the nucleus.

15. References:
 Class notes
 Ganong
 AK Jain
 Internet