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1. Basal ganglia
By
Dr.Aparna.A

3. • An idea for a specific movement is translated
into detailed neural programs by basal ganglia,
premotor cortical areas, and the lateral
division of the cerebellum. These detailed
instructions for movement are then decoded
and executed by motor cortex. Sensory
receptors provide feedback about the actual
movement to various levels of the CNS, but
particularly the intermediate cerebellum,
which can compare this information with
information about the intended movement
and initiate a correction if necessary.

5. Organization of the Basal Ganglia
and Related Nuclei
• The basal ganglia include the caudate nucleus,
the putamen, and the globus pallidus .
• The term striatum - caudate nucleus and
putamen.
• The globus pallidus typically has two parts, an
external segment and an internal segment.
• Putamen and globus pallidus - lentiform
nucleus.

6. Associated nuclei
• Ventral anterior (VA) and ventral lateral (VL)
nuclei of thalamus.
• Subthalamic nucleus of the diencephalon
• Substantia nigra of the midbrain
• The substantia nigra further divided into pars
compacta and pars reticulata.

9. Connections of basal ganglia
Afferent connections-
- Corticostriatal projection- from frontal and
parietal cortex
- Thalamostriate fibers – from ventroant,
intalaminar and centromedian nuclei of
thalamus- glutamate

10. • Internuclear connections
-DOPAMINERGIC NIGROSTRAITAL PATHWAY –snc
to straitum
- GABAERGIC PROJECTIONS –from straitum to
gpi and gpe
- To pars reticulata
- GLUTAMINERGIC PROJECTIONS
- Gpe to stn
- Sub thalamic nucleus to gpe and gpi and vice
versa and substantia nigra

11. • Efferent connections- from GPI
- To prefrontal and premotor cortex from VL
and VA nuclei of thalamus.
- Via ansa lenticularis tract sends to SN, STN ,
RETICULAR FORMATION, RN-
EXTRAPYRAMIDAL SYSTEM.
- PR to superior colliculus

12. Connections and Operation of the
Basal Ganglia
• DIRECT PATHWAY- DECREASES GABA TO
THALAMUS
• INDIRECT PATHWAY- INCREASES GABA TO
THALAMUS

14. Direct pathway
• Straitum activated by cortex via glutamate.
• striatum send inhibitory GABA signals to Gpi
which itself is inhibitory, to the VA and VL
nuclei of the thalamus.
• Therefore, activation of the striatum causes
disinhibition of neurons of the VA and VL
nuclei.

15. • Thus, the disinhibition excites these neurons
and consequently excites their target neurons
in the motor areas of the cerebral cortex,

16. Indirect pathway
• In this pathway, pallidal neurons in the
external segment are inhibited by the GABA
released from striatal terminals .
• The external segment of the globus pallidus
normally releases GABA in the subthalamic
nucleus and thereby inhibits the subthalamic
neurons.

17. • Therefore, striatal inhibition of the external
segment of the globus pallidus results in the
disinhibition of neurons of the subthalamic
nucleus.
• When the neurons of the subthalamic nucleus
become more active because of disinhibition,
they release more glutamate in the internal
segment of the globus pallidus.

18. • This transmitter excites neurons in the internal
segment and consequently activates inhibitory
projections that affect the VA and VL thalamic
nuclei.
• The activity of the thalamic neurons
consequently decreases, as does the activity
of the cortical neurons that they influence.

19. Functions
• Helps in motor activities requiring a
pattern.eg- writing letters, shooting basketball
etc.
• Plays a role in cognitive control of Sequences
of motor Patterns.
• Plays a role in Changing the timing and
Scaling the Intensity of Movements

22. DISEASES OF BASAL GANGLIA
• Three distinct biochemical pathways in the
basal ganglia normally operate in a balanced
fashion: (1) the nigrostriatal dopaminergic
system, (2) the intrastriatal cholinergic system,
and (3) the GABAergic system, which projects
from the striatum to the globus pallidus and
substantia nigra.

23. • When one or more of these pathways become
dysfunctional, characteristic motor
abnormalities occur.
• Diseases of the basal ganglia lead to two
general types of disorders: hyperkinetic and
hypokinetic.

24. • The hyperkinetic conditions are those in which
movement is excessive and abnormal,
including chorea, athetosis, and ballism.
• Hypokinetic abnormalities include akinesia
and bradykinesia.

25. Parkinsons disease- paralysis agitans.
• Etiology-
1.idiopathic
2.autoimmune – antibodies against
dopaminergic neurons of nigrostriatal
pathway
3. neuroleptic drugs like phenothiazine
4.Injection of MTTP
5.Cerebral arteriosclerosis

26. • Complication of encephalitis.
• Neurodegenerative disease with depletion of
dopamine.

27. symptoms
• Hyperkinetic symptoms
• Cog wheel rigidity
• Rest tremor/pin rolling tremor

29. Hypokinetic features-
• Akinesia
• Bradykinesia
• Decreased associated movements
• Mask face
• Festinating gait
• micrographia

30. • Pathophysiology- when excitatory cholinergic
response increases more than inhibitory
dopaminergic effect hyperkinetic features are
seen.

31. • Dopamine secretion in the limbic system,
especially in the nucleus accumbens, is often
decreased along with its decrease in the basal
ganglia.
• It has been suggested that this might reduce
the psychic drive for motor activity so greatly
that akinesia results

32. • TREATMENT-Treatment with l-Dopa- Crosses
BBB there converted into dopamine
• Carbidopa is given alng with l-dopa to
prevent metabolism of l-dopa b liver

33. • Treatment with Transplanted Fetal Dopamine
Cells.
• Transplantation of dopamine-secreting cells
(cells obtained from the brains of aborted
fetuses) into the caudate nuclei and putamen
has been used with some short-term success
to treat Parkinson’s disease.
• However, the cells do not live for more than a
few months..

34. • If persistence could be achieved, perhaps this
would become the treatment of the future

35. Huntington's disease, autosomal dominant
disesase.
• The abnormal gene that causes Huntington’s
disease is many-times-repeating codon, CAG,
that codes for multiple extra glutamine amino
acids in the molecular structure of an
abnormal neuronal cell protein called
huntingtin.

36. • Leads to the loss of GABAergic ( chorea) and
cholinergic neurons (dementia) of the
striatum .
• Loss of inhibition of the external globus
pallidus presumably leads to diminished
activity of neurons in the subthalamic nucleus

37. • Hence, the excitation of neurons of the
internal segment of the globus pallidus would
be reduced.
• This will disinhibit neurons in the VA and VL
nuclei.
• The resulting enhancement of activity in
neurons in the motor areas of the cerebral
cortex may help explain the choreiform
movements of Huntington's disease.

39. • Chorea- caudate nucleus
• Athetosis- globus pallidus
• Hemiballismus- subthalamic nucleus