The document provides an overview of the basal ganglia. It discusses the physiological anatomy and components of the basal ganglia, including the caudate nucleus, putamen, globus pallidus, substantia nigra, and subthalamic nucleus. It describes the connections and functional neuronal circuits of the basal ganglia. The functions of the basal ganglia in motor control and disorders such as Parkinson's disease, chorea, athetosis, and Huntington's disease are summarized.
3. Physiological Anatomy.
Components.
Basal Ganglia ------ Group of
nuclei (mass of grey matter) in
the forebrain and
upper part of the brain stem
that have motor function of
great importance --
Head ganglia of Motor control.
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4. FIVE GREY NUCLEAR MASSESFIVE GREY NUCLEAR MASSES
At the base of the cerebral hemispheres.At the base of the cerebral hemispheres.
Caudate nucleusCaudate nucleus
Putamen (corpus striatum)Putamen (corpus striatum)
Globus pallidusGlobus pallidus
Substantia nigraSubstantia nigra
Sub-thalamic body of LuysSub-thalamic body of Luys
Red nucleusRed nucleus
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5. CORPUS STRIATUM.
Subcortical masses of
grey matter situated in
white core
Divided into 2 parts by
internal capsule.
Caudate nucleus
Lenticular nucleus.
Putamen
Globus pallidus.
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6. Salient Features of Nuclei of
Corpus Striatum.
Caudate nucleus.
Highly curved, comma
shaped band of grey
matter.
Consists of Head, body
& Tail
Separated from
lenticular nucleus by
internal capsule
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7. Lenticular Nucleus.
Biconvex lens.
Triangular in both
coronal & horizontal
sections.
Divided into 2 parts by
external lamina of
white matter.
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8. Putamen
Outer part of
lenticular nucleus.
Dark in colour
Quadrangular in
shape.
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9. Globus Pallidus.
Inner smaller part.
Paler.
Divided into 2 parts
External segment.
Internal segment.
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10. Sub Thalamic Nucleus.
Biconvex mass of grey
matter lateral to red
nucleus & dorsal to
substantia nigra.
Separated from
thalamus by Zona
inserta.
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11. Substantia Nigra.
Made up of small unpigmented &
large pigmented nerve cells.
Contains neuromelanin.
Divided into 2 parts
Pars compacta – contains
dopaminergic (75%) & cholinergic
(25%) neurons.
Pars reticularis contains GABA
ergic neurons.
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12. Connections.
Main input – Corpus Striatum ( Caudate
Nucleus & Putamen)
Main Output – Globus Pallidus.
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13. Afferent or Inputs to Striatum.
Corticostriate projections. – Glutamatergic.
Thalamostriate fibre. – from Centromedian N
Nigrostriate fibres.– Pars Compacta
(Dopaminergic)
Raphe striate fibres. – Raphe N. in reticular
formation (Serotoninergic)
Locus Coeruleus striate fibres. (Noradrenergic)
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14. Projections from striatum.
Striatum to Globus
pallidus. – GABAergic
inhibitory projections.
Striatum to
Substantia Nigra. –to
Pars Reticulata
(GABA-ergic inhibitary
impulses)
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15. Efferents or output from
Globus Pallidus.
Thalamus– thalamic
Fasiculus or Ansa
Fasicularis – to VA, VL and
centromedian N.– to
Prefrontal & Premotor
cortex.
Subthalamic nuclei – to
Substantia Nigra.
Red nucleus – rubrospinal
tract pathway.
Substantia nigra.
3 routes
Directly.
Via Subthalamic N.
Via Pedunculopontine
N.
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18. Functional neuronal circuits or
loops.
Corpus striatum does not have direct
connections to spinal cord.
GPi & SNpr behaves as a lateral & medial part
of single functional unit.
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19. Primary feedback loop or cortex
basal ganglia motor cortex circuit.
Cerebral cortex
(all parts)
Striatum
Globus Pallidus &
Substantia Nigra
Supplementary motor
cortex
Thalamus
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Provide Negative Feedback Loop to Control Motor Cortex
Activity
20. Caudate Loop
Supplementary motor area & motor sensory area.
Caudate Nucleus.
GPi SNPr
Caudal part caudal part
VL (Thalamus) Pars VL Oralis VL(Thalamus) Pars Medialis
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FUNCTION – Cognitive Control Of Motor Activity
-- Control Of EYE Movements
21. Putamen loop
Frontal Association Area.
Putamen Nucleus.
Gpi SNPr
VA (thalamus) VA (thalamus)
Parvocellular Magnocellular.
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FUNCTION – For Motor Control Of Body Movements
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Additional feedback loop.
Indirect Pathway via subthalamic N.
Cortex
Striatum
GPe
GPi SNPr
Subthalamic Nucleus
Supplementary Motor Cortex
Thalamus
23. Indirect Pathway Involving
Pars Compacta.
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Cortex Supplementary
Motor Cortex.
Thalamus
Striatum
Ach D2 Dopamine
Ach D1 Dopamine
GPi SNPr
SNPc
25. Functions of basal ganglia.
Control of voluntary motor activity.
Control of reflex muscular activity.
Control of muscle tone.
Role in arousal mechanism.
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26. Control of voluntary motor
activity.
Cognitive control of
motor activity.
Neural discharge in
Basal Ganglia begins
well before the
movement begins.
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27. Control of voluntary motor
activity.
Most of the motor actions
occur as a consequence of
thought process in mind.
So basal ganglia is involved
in planning &
programming of
movements.
It is executed through
functional neuronal
circuits.
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28. Timing & scaling of intensity of
movements.
How rapidly & how
much large the
movement should be.
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29. Subconscious execution of
some movements.
Swinging of arm while
walking.
Crude movements of
facial expressions with
emotions.
Movements of limbs
while swimming.
Importance – cortex can
be free to plan its
actions.
Pathway- Putamen
feedback circuits.
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30. Control of reflex muscular
activity.
Inhibitory effect on
spinal reflexes.
Regulate muscle
which maintains
posture.
Mainly visual &
Labyrinthine reflexes.
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31. Control of muscle tone.
Substantia Nigra of Basal
Ganglia control γ motor
neuron which maintain
muscle tone.
Pathway – cortical inhibitory
area- striatum-pallidum-
substantia nigra-reticular
formation- spinal cord.
Lesion – Lead pipe type
Rigidity in Parkinsonism.
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32. Role in arousal mechanism.
By connections of
Globus Pallidus & Red
Nucleus with Reticular
Formation.
Lesion – drowsiness ,
sleep.
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37. Clinical features.
Akinesia or Hypokinesia.
Unable to initiate
voluntary movements
or decreased
movements.
Causes – Due to
Hypertonicity of
Muscle.
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38. Clinical features
C/F – Bradykinesia,
mask like face,
prolonged reaction
time,
Absent associated
movements.
Shuffling or
Festinant type gait.
Retropulsion.
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39. Rigidity
Increased tone in the muscle.
Cause – increase discharge of
γ Efferents to muscle spindle.
Mechanism – striatum under
influence of both
Ach(excitatory) & Dopa
(Inhibitory)
Degeneration of neurons of
SN – less Dopa & more Ach
activity – hyperkinetic
features.
C/F – lead pipe & cog-
wheel type rigidity.
Hypertone in
protagonists &
antagonists muscle.
Statue like appearance.
Posture – flexion
attitude.
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40. Tremors
Involuntary rhythmic
oscillatory movements of
distal parts of limb & head.
Resting tremors.
Absent at sleep & increased
by stress & excitement.
4-6 times/sec.
Frill rolling movements.
Neural mechanism.
Due to pacemaker
activity in nucleus
ventralis intermedius of
thalamus.
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41. Treatment.
L-Dopa
As it crosses BBB.
With Carbidopa as it
prevents its conversion
to dopamine in liver.
Low dose – reduces
rigidity & high dose
reduces tremors.
Surgical Destruction.
Of Globus Pallidus or
VLN of thalamus.
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42. Chorea.
Rapid , jerky
involuntary
movements (dancing)
Due to damage to
caudate N.
Seen in children as a
complication of
Rheumatic fever.
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43. Athetosis.
Slow, rhythmic, twisting,
worm like , confluent
writhing movements of
the extremities
Mainly fingers & wrist.
Due to damage to
Putamen.
Seen in children after
birth injuries.
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44. Huntington’s disease.
Genetic disease.
Trinucleotide repeat
expansion.
Autosomal Dominant
disorder.
30-50 yrs of age.
Abnormal gene at
short arm of chr-4.
Lesion – damage to
GABAergic & cholinergic
neurons of striatum to
pallidum.
Hyperkinetic features.
C/F – hyperkinetic
chreiform movements,
Slurred speech, dementia,
jerky trajectory of hand.
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45. Hemiballism.
Cause – damage of
subthamic Nucleus
commonly haemorrhage.
So reduce output from
GPiSNpc to thalamus.
Disinhibition of thalamic
output – hyperkinetic
movements.
C/F – spontaneous
attack of flail-like,
intense violent
movements of whole
opp of body.
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46. Wilson’s disease.
Hepatolenticular
degeneration by Cu
toxicity due to
impaired biliary
excretion of Cu.
Changes more marked
in lenticular nucleus
mainly Putamen.
C/F – Parkinsonism,
Akinesia, muscle
rigidity & tremors.
Ceruloplasmin level
low & Cu content of
SN high.
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