The basal ganglia are a group of subcortical nuclei that help regulate motor control and learning. They modulate movements through neuronal circuits and help produce purposeful movements while suppressing unwanted ones. Damage to different parts of the basal ganglia can result in either hypokinetic or hyperkinetic movement disorders. Parkinson's disease involves degeneration of dopaminergic neurons in the substantia nigra, leading to reduced excitation of motor cortex and hypokinesia. Other disorders like athetosis, hemiballism, chorea, and Wilson's disease each involve damage to specific basal ganglia structures and circuits.

1. BASAL GANGLIA
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2. Motor Cortex
+
Via Via
Thalamus Thalamus
Basal Ganglia Cerebellum
UMN
Motor neurons & Interneurons in
Spinal Cord
LMN
Skeletal Muscle
Modulation of motor activity by Basal Ganglia & Cerebellum
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3. Def:
• Large masses of grey
matter
• situated within the white
core of each cerebral
hemisphere
• Essential constituents of
the extra pyramidal system
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4. FUNCTIONS
Modulation of motor activities through neuronal
circuits:
– Production of movements
• Maintain purposeful motor activity while
suppressing unwanted or useless
movement
– Regulate muscle tone
• Inhibit muscle tone throughout the body
– proper muscle tone is maintained through a
balance of excitatory and inhibitory inputs
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5. – Monitor and coordinate slow, sustained
contractions related to posture and
support.
– Avoid abnormal involuntary movements
– Control group of movements for
emotional expretion
– Memory, emotion, and other cognitive
functions.
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6. Basal Ganglia - Components
Anatomical
Corpus striatum
Claustrum
Amygdaloid body
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9. Physiological/clinical
• Corpus striatum
• Subthalamic nu
• Substantia nigra
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11. • Phylogenetically:
– Neostriatum:
• Caudate nuc + Putamen
– Palaeostriatum:
• Globus Pallidus
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12. BASAL GANGLIA
• New classification
• Dorsal
• Dorsal striatum : Caudate Nu + Putamen
• Dorsal Pallidum : G Pallidus (Inner & outer segts)
• Ventral :
• Ventral striatum : Nu Acumbens & Olf tubercle
• Ventral pallidum : Loc below Ant commissure in Ant perf
substance
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13. CAUDATE NUCLEUS
• Comma shaped band of grey matter
• 3 Parts : Head, Body & Tail
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14. CAUDATE NUCLEUS :
• Lies in conformity with curvature of Lat ventricle
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15. HEAD of C Nucleus
Bulges into the floor of Ant horn of Lat V
Laterally : Ant limb of Int capsule & Lentiform Nu
(Ant limb)
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16. Relations of BODY:
Inferomedially :
• Floor of central part of Lat Ventricle
• Accompanied med by Stria terminalis & thalamostriate vein
Superolaterally : Corpus callosum, Fronto-occipital fasciculus
Lat ventricle (Central part)
Fronto-occipital Fasciculus
Body of caudate Nu
Thalamo-striate vein
Stria terminalis
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17. TAIL
Passes Dwn & Fwd along roof of Inf horn of Lat V
Tail of C N
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18. TAIL of C N : Caudate Nucleus
• Medially :
Lentiform Nu
- Str Terminalis
- Sublentiform part of IC &
Thalamus
• anterior: Amygdaloid body
Str Terminalis
• Above : Lentiform Nu Tail of C Nu
Inf horn of lat
ventricle
Substantia Nigra
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19. LENTIFORM NUCLEUS Caudate Nucleus
•Large & wedge shaped
Lentiform Nu
•Narrow part of wedge facing
medially
Ext Capsule
RELATIONS Claustrum
Str Terminalis
• Laterally : Tail of C Nu
• Ext capsule & Inf horn of
lat ventricle
Claustrum Substantia Nigra
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20. Caudate Nucleus
Lentiform Nu
• Medially :
Int Capsule
Thalamus
Ext Capsule
Head of Caudate Nu
Claustrum
Str Terminalis
Tail of C Nu
• Above : Corona radiata
Inf horn of
lat ventricle
Substantia Nigra
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21. Caudate Nucleus
• Below Lentiform Nu
•Ant Perf substance
•Inf horn of Lat V
•Sublentiform part of IC, Ext Capsule
Claustrum
•Tail of C Nu & Str Terminalis
•Stria terminalis Tail of C Nu
Inf horn of
lat ventricle
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22. Blood Supply
• Arterial
– Medial Striate Brs. -
MCA
– Lat. Striate Brs. – MCA
– Recurrent Br – ACA
– Ant. Choroidal Br -
MCA
• Venous
– Striate veins
– Int. cerebral vein
– Basal Vein
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23. CONNECTIONS
• Afferent- Caudate Nucleus & Putamen
• Efferent- Globus Pallidus
AFFERENTS
EFFERENTS
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24. CONNECTIONS : STRIATUM
AFFERENTS-
• Cortico-striate : from entire Neocortex
• Thalamo - striate : Centro-median nu of Thalamus
• Nigro- striate : From Pars compacta of S Nigra
Efferents
Strio-pallidal
Strio nigral (To Pars reticularis of S Nigra)
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25. 25

26. • Connections-
Striatum
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27. GLOBUS PALLIDUS :
AFFERENTS :
• Strio-pallidal : from CN & Putamen
• From Subthalamus
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28. GLOBUS PALLIDUS :
EFFERENTS : Pallido-fugal
• To Thalamus :
– Thru Ansa lenticularis & Fasciculus Lenticularis
– Join to form Fasciculus thalamicus
– End in VA, VL & CM nuclei
• To Subthalamus : From Outer Segt of GP
• To Reticular formation of MB
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29. • Connections -
Paleostriatum
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30. p.c.- pars compacta
p.r.- pars reticularis
Schematic Diagram showing connections of Basal Ganglia 30

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32. LEISIONS OF B G
Manifestations-
Two types.
• Hypokinetic, hypertonic :
– Increased tone & rigidity
– Eg : Parkinsonism
• Hyperkinetic hypotonic :
– Abnormal involuntary movements - dyskinesias
Eg : Athetosis, Chorea & Ballism
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33. • Organic basis of Parkinson’s disease:
– Degeneration of dopaminergic neurons from the
substantia nigra (Nigrostriate fibres)
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34. • The net effect is reduced
excitation of motor
cortex.
– loss of dopamine
producing neurons
– globus pallidus becomes
overactive
– inhibition of the VL
nucleus of the thalamus
– reduced excitation of the
cortex
hypokinesia
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35. PARKINSON’S DISEASE (Paralysis Agitans)
• Characterized by Rigidity
& tremors
• Rigidity – Caused by
increased muscle tone
– Due to increased
activity of static gama
fusiform fibers
• Affects all muscles, Cog-
wheel rigidity, Short
quick steps
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36. • Mask face : No emotional response
• Difficulty in taking initial steps & stopping movements
• Resting tremor – Pill rolling move of hands
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37. • Cause :
• Degenerative changes in
Globus Pallidus & S Nigra
• Marked reduction in Dopamine
• Treatment :
• Admn of L- Dopa
• Surgical destruction of GP /
VL Nu of Thalamus
• Striatal implants of dopamine
containing neurons of fetal
origin.
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38. ATHETOSIS
• Slow worm like
writhing
movements
affecting fingers &
wrist
• Due to damage of
Putamen – in birth
injury
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39. HEMIBALLISM
• Wild flail like movements of one arm
• Degeneration of Subthalamic nucleus of Opp side
• Damage to subthalamus decreases excitation of the globus
pallidus internal segment resulting in less inhibition of
thalamus causing hyperkinetic disorder.
• Common cause is lacunar infarct of subthalamic nucleus.
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40. CHOREA
• ”Dance like” movements
• Brisk, jerky, purposeless
movements in distal parts
of extremities asso with
twitching of face
• Two types :
– Sydenham’s Chorea
– Huntington’s chorea
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41. Sydenham’s Chorea :
• In childhood –
• A complication of Rheumatic (Streptococcal) fever
• Scattered minute hemorrhage & capillary emboli in
striatum
• Recover completely
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42. Huntington’s chorea :
• In middle age –
• Autosomal Dominant type
• Degeneration of Striatum & Cerebral cx
• Striatal neurons in caudate/Putamen degenerate leading
to decreased activity in the GP internal segment resulting
in less inhibition of thalamus causing a hyperkinetic
disorder.
• Mental deterioration
• Decreased level of GABA in Strio-nigral neurons
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43. WILSON’S DISEASE (Hepato-lenticular degeneration) :
• Genetic error of Copper metabolism
• Muscular rigidity, Tremor
• Impairment of movements
• Uncontrolled Laughing / Crying
• Degn & cavitation of Putamen, Cirrhosis of Liver
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