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
2
3. Def:
• Large masses of grey
matter
• situated within the white
core of each cerebral
hemisphere
• Essential constituents of
the extra pyramidal system
3
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
4
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.
5
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)
15
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
17
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
19
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
20
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
21
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)
24
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
28
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
32
33. • Organic basis of Parkinson’s disease:
– Degeneration of dopaminergic neurons from the
substantia nigra (Nigrostriate fibres)
33
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
34
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
35
36. • Mask face : No emotional response
• Difficulty in taking initial steps & stopping movements
• Resting tremor – Pill rolling move of hands
36
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.
37
38. ATHETOSIS
• Slow worm like
writhing
movements
affecting fingers &
wrist
• Due to damage of
Putamen – in birth
injury
38
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.
39
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
40
41. Sydenham’s Chorea :
• In childhood –
• A complication of Rheumatic (Streptococcal) fever
• Scattered minute hemorrhage & capillary emboli in
striatum
• Recover completely
41
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
42
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
43