Basal ganglia
The basal ganglia are formed of:
1-Caudate nucleus.
2-Lenticular nucleus
Corpus
formed oF:
striatum
Putamen (Laterally)
Globus pallidus (medially)
3-Related nuclei.
Subthalamus
Substantia nigra.
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Basal ganglia
Caudate
Putamen
Globus pallidus
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Lateral view
Anterior view
Basal ganglia
Caudate
Input: Nucleus
striatum
Putamen
Globus pallidus
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Subthalamus:
It controls the normal pattern of
forward walking.
Substantia nigra:
It sends inhibitory impulses to
corpus striatum the fibers
secrete dopamine.
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Connections
of the basal ganglia:
The
afferent connections to the
basal ganglia terminate mainly in
the striatum (Caudate N. &
Putamen).
While the efferent connections
(outputs) originate mainly from the
Globus pallidus.
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The
basal ganglia are
connected with:
1- Cerebral cortex by two
closed circuits.
2- The basal ganglia.
3- The brain stem.
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1- Connection
with the cerebral cortex:
A- Caudate circuit:
 Cortex
(from association areas) to
Caudate nucleus to globus pallidus to
thalamus to Cortex (Premotor and
supplementary motor areas).
 It is cortico- striato- pallido- thalamocortical circuit
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Caudate circuit
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It
has a role in:
Cognitive control of
voluntary movements
(sequence).
Control of timing and the
intensity of movement.
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B- Putamen circuit:
Cortex (motor, premotor,
supplementary motor and
sensory areas I and II) to
putamen to globus pallidus
to thalamus to cortex
(primary motor area).
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Putamen circuit
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Fibers
from cerebral cortex
secrete acetyl choline
(excitatory transmitter) to
the corpus striatum.
It has a role in execution
(production) of motor
activity.
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2- Connections
within the basal ganglia:
A- Nigro-striatal dopaminergic
pathway:
From
substantia nigra to the
striatum (caudate N. and
putamen) and secrete the
inhibitory neurotransmitter
Dopamine.
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It
maintain certain
degree of inhibition of the
striatum.
Lesion of this pathway
leads to parkinsonism.
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Connections within basal ganglia
Dopamine
Nigrostriatal
Dopaminergic
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pathway
 B-
Striato-nigral and striato-pallidal
GABA-ergic pathway:
 Fibers from the striatum to substantia
nigra and globus pallidus secrete the
inhibitory neurotransmitter GABA.
 It maintain certain degree of inhibition
of substantia nigra and globus
pallidus.
 Lesion in this pathway leads to
Huntington’s chorea.
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Chemical transmission in basal ganglia
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3-Connections
with the brain stem:
Fibers
from the brain
stem to basal ganglia
secrete noradrenalin,
serotonin &
enkephalin.
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Output
tracts from basal
ganglia to brain stem :
Arise from globus pallidus then
pass either through
subthalamus or substantia
nigra and then project to
reticular formation, red nucleus,
vestibular nucleus & inferior
olivary nucleus
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from
them reticulospinal,
rubrospinal,vestibulospinal
& olivospinal tracts arise
and pass to the spinal
cord (Constitute a part of
extra pyramidal system).
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N.B.:
The
proper function of the
basal ganglia depends on the
balance between the excitatory
transmitter (acetylcholine and
Noradrenalin) and the inhibitory
transmitter (dopamine and
GABA).
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Functions of basal ganglia
 The
basal ganglia of one side are
related to the opposite side of the
body.
 1-Cognitive control of voluntary
movements: subconscious thinking
of the brain that precedes the
voluntary movements to determine
which movement will be done and in
what sequence.
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when a person sees a lion approaching,
he responds automatically by:
a- Turning away from the lion.
b- Beginning to run.
c- Even attempting to climb a tree.
 Without this cognitive function the
person is not able to respond quickly.
 This function is exerted through the
caudate circuit.
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2-Control of timing (rapidity)
& intensity (size) of movement:
 This
means that the basal ganglia
control:
a-How rapid the movement will be
(control of timing).
b-How large the movement will be
(control of intensity).
 This function is exerted through the
caudate circuit.
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 thus
the movement is performed
with a fixed scale regarding rapidity
and size .
 A person write a letter (a) slowly or
rapidly, also he may write a small
(a) on a piece of paper or a large
(a) on a board.
 The proportional characteristics
remain the same.
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3- Execution (production)
of voluntary movements
(control of skilled movements):
Basal
ganglia function in
association with the corticospinal system to control skilled
movements e.g. writing,
hammering nails, passing a
foot ball & cutting with cissor.
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In
serious damage of basal
ganglia, the performance of
these movements become
crude, as if he was learning
for the first time how to do it.
It is a function of putamen
circuit.
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4- Control of muscle tone:
Caudate N.: Stimulate muscle
tone.
Lentiform N. & other parts:
inhibit muscle tone.
N.B.: The net effect of basal
ganglia is inhibition of muscle
tone.
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Disorders of Basal Ganglia
1-Chorea (Sydenham’s chorea):
 It
is due to lesion in caudate nucleus.
 It occur as a complication of rheumatic
fever in children.
 Usually is a self –limiting disease.
 Characterized by:
 1- Involuntary rapid purposeless
dancing movements.
 2- Hypotonia.
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2-Huntington’s disease
(Huntington’s chorea):
 Causes:
 Loss
of intrastriatal GABA-secreting
neurons leading to decreased GABA
in the globus pallidus and substantia
nigra.
 Inherited as an autosomal dominant
disorder and its onset is between age
30 – 50 years.
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 Manifestations:
 a-
Chorea movements that usually
increase until they incapacitate the
patient & hypotonia.
 b- progressive dementia followed by
death within 10 – 15 years.
 Treatment:
 There is no effective treatment and
the disease is fatal.
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Chorea
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3-Athetosis:
It
is due to a lesion in lentiform
nucleus.
It is characterized by:
a- Involuntary spasmodic slow
twisting movements affecting
mainly the upper limbs.
b- High degree of hypertonia.
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Athetosis
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4-Hemiballismus:
It
is due to a lesion in
subthalamic nuclei.
Characterized by violent
spasmodic movements
affecting the opposite side of
the body.
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Left hemiballismus
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5- Wilson’s disease:
Low
ceruloplasmin (cupper
binding protein).
Increase free cupper in plasma.
Deposition of cupper in liver &
basal ganglia specially the
lentiform nucleus causing
hepato-lenticular degeneration.
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6-Parkinsonism
(paralysis agitans):
Causes: Lesion or
degeneration of nigro-striatal
dopaminergic pathway
leading to decrease or absence
of dopamine in the striatum
leading to over activity of acetyl
choline pathway to the striatum.
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 This
may result from:
a- Aging (idiopathic parkinsonism):
there is a steady loss of dopamine
and dopamine receptors with age.
b- As a complication of treatment
with phenothiazine group of
tranquilizers and other drugs that
block D2 dopaminergic receptors.
c- After encephalitis.
d- After head trauma.
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Manifestations:
(A R T)
I- Akinesia:
 It
means poverty of movements.
 It leads to:
1-Difficulty in initiating the voluntary
movements.
2-Shuffling gait: The patient walks in short
steps without lifting his legs from the
ground.
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Left hypokinesia
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Oro-facial dyskinesia
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Shuffling gait
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3-Dysartheria: in the form of
slow monotonous speech.
4-Loss of facial expression
(mask face).
5-Loss of swinging the arms
during walking.
6-Loss of blinking of the eyes.
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Mask face
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II- Rigidity:
There
is increased muscle tone
all over the body with the
following characters:
1- Affects both flexors and
extensors but more in flexors
leading to flexion attitude.
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2- Lead pipe rigidity (as bending a
pipe of lead) when tremors are
absent or cog wheel when
tremors are present.
The rigidity is due to increased
discharge of impulses to the
alpha motor neurons along the
corticospinal tract.
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Rigidity (cogwheel resistance)
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III-Tremors:
 Due
to regular alternating contractions of
agonistic & antagonistic muscle.
 It has the following characters:
1- Appear during rest and disappear during
voluntary movements (static tremors).
2-Affects small distal joints e.g.
metacarpo-phalangeal and
interphalangeal joints.
3-Pill-rolling or cigarette rolling form.
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Static tremor
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Treatment:
A- Medical treatment:
 In
parkinsonism there is decreased
dopamine and increased acetylcholine in
the striatum.
1- Administration of anticholinergic drugs .
2- Administration of L-dopa because
dopamine can’t cross the blood brain
barrier while L-dopa crosses it and is
converted to dopamine by the brain
tissues.
3- Use of dopamine agonists e.g.
bromocryptin.
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Striatal dopaminergic synapse
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B- Surgical treatment:
1-
Implantation of fetal substantia
nigra into the striatum, the cells
persist only for few months.
2-Destruction of VLNT & VANT by
electro-coagulation to block the
feedback circuits to the cortex
which are the cause of
abnormalities.
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