Basal ganglia

Dr. Mohamed Alzain

The basal ganglia of all the
following, except:
• a) Amygdaloid nucleus
• b) Claustrum
• c) Uncus
• d) Caudate nucleus
• e) Lentiform nucleus
The corpus striatum is referred to as
a) Caudate nucleus and putamen
b) Caudate nucleus and globus
pallidus
c) Caudate nucleus and lentiform
nucleus
d) Amygdaloid body and lentiform
nucleus
e) Amygdaloid body and putamen
• The basal ganglia are a group of nuclei origin
in the brains of vertebrates situated at the
base of the forebrain on both sides of the
thalamus.
 Unlike the cerebellum,
the basal ganglia do
not receive input from
the spinal cord, but
they do receive direct
input from the cerebral
cortex.
 The main action of
basal ganglia is on the
motor areas of the
cortex by way of the
 In addition to their role
in motor control, the
basal ganglia
contribute to affective
and cognitive
functions.
 Lesions of the basal
ganglia produce
abnormal movement
and posture.
 Nucleus of basal ganglia
 The caudate nucleus.
 The lentiform nucleus;
Consist of two;
 Putamen [outer part].
 Globus pallidus [inner ].
 Thesubthalamic nucleus
 Substantia nigra
 Caudate and putamen[striatum]
 The term striatum, derived from the striated
appearance of these nuclei.
 The striations are produced by the fiber
bundles formed by the anterior limb of the
internal capsule as it separates the caudate
nucleus and putamen.
Subdivision of Striatum

o striosomes .
o matrix.
 N hjhn jgykfd;d;;

 Striosomes (an area with little

acetylcholinesterase).
 Matrix (an area high in acetylcholinesterase).
 The neurons of the corticostriate projection
that originate in the deep portion of layer V of
the cortex terminate in the patches,
 whereas the neurons that originate in layers II
and III and the superficial part of layer V end
primarily in the matrix.
 Substantia nigra
The substantia divided into.
 SNr (reticulata) .
 SNc (compacta).
 SNr often works with GPi, and the SNr-GPi
complex inhibits the thalamus.
 Substantia nigra pars compacta (SNc) however,
produces the neurotransmitter dopamine, which
is very significant in maintaining balance in the
striatal pathway.
 Subthalamic nucleus

o The subthalamic (STN) is a diencephalic gray

matter portion of the basal ganglia, and the
only nucleus that actually produces an
excitatory neurotransmitter, glutamate.
o The role of the subthalamic nucleus is to
stimulate the SNr-GPi complex and it is part of
the indirect pathway.
Basal Ganglia connections

• Input Portion

• STRIATUM (Caudate Nucleus and Putamen)

• Output Portion

• Globus palidus.
 Connections of basal ganglia
It has three
connections;
• Cortical connection
• Intreconnections
• Brainstem connections
 [a]Cortical connection
Neurons of the striatum begin to discharge
before movement occurs.
This sequence suggests that these neurons
help select the movement that is to be made.
Activity in the putamen is related to the
occurrence of movement of the body,
whereas activity in the caudate nucleus is
related to eye movement.
Cortical connection
 most regions of the cerebral cortex project to
the striatum.
 The corticostriatal projection arises from
neurons in the cortex.
 The neurons appear to use glutamate as their
excitatory neurotransmitter.
 The striatum then influences in the thalamus by
two pathways, direct and indirect.
The thalamic neurons in turn excite neurons of the
motor areas of the cerebral cortex.
Direct pathway,
cortical cells project excitatory inputs to the striatum, which in turn
projects inhibitory neurons into the cells of the SNr-GPi complex.
 The SNr-GPi complex projects directly onto the thalamus through
the inhibitory pathway.
 The striatal inhibition of the SNr-GPi complex coupled with SNr-GPi
inhibition of the thalamus therefore results in a net reduction of
inhibition of the thalamus via the striatum.
 The thalamus projects excitatory glutamatergic neurons to the
cortex itself.
 The direct pathway, therefore, results in the excitation of the motor
cortex by the thalamus. Once stimulated, the cortex projects its own
excitatory outputs to the brain stem and ultimately muscle fibers via
the lateral corticospinal tract.
• Cortex (stimulates) → Striatum (inhibits)
→ "SNr-GPi" complex (less inhibition of
thalamus) → Thalamus (stimulates) →
Cortex (stimulates) → Muscles, etc. →
(hyperkinetic state).
 Indirect pathway
 also starts from neurons in the striatum.
 Once stimulated by the cortex, striatal neurons in
the indirect pathway project inhibitory axons onto
the cells of the globus pallidus externa (GPe), which
tonically inhibits the subthalamic nucleus (STN).
 This inhibition (by the striatum) of the inhibitory
projections of the GPe, results in the net reduction
of inhibition of the STN.
o The STN, in turn, projects excitatory inputs to
the SNr-GPi complex (which inhibits the
thalamus).
o The end-result is inhibition of the thalamus
and, therefore, decreased stimulation of the
motor cortex by the thalamus and reduced
muscle activity.
o The direct and indirect pathways are therefore
antagonist in their functions.
• Cortex (stimulates) → Striatum (inhibits) →
GPe (less inhibition of STN) → STN (stimulates)
→ "SNr-GPi" complex (inhibits) → Thalamus
(is stimulating less) → Cortex (is stimulating
less) → Muscles, etc. → (hypokinetic state).
 [b]Interconnections
Pathways from neostriatum to the [SN] to the
[GP] ,release [GABA].
From the [SN] to the neostriatum and to
ventrolatral of the thalamus release dopamine.
and from the raphe nuclei to the neostriatum
release serotonin.
Neostriatum also receive glutamate and [Ach]
from cerebral cortex.
 [C]Brainstem connections:[efferent pathway]

• The principal output from the basal ganglia is

from the internal segment of the globus
pallidus which it is fibers project to;
• Reticular formation.
• Red nucleus.
• Vestibular nucleus.
• Inferior olivary nucleus.
 Functions of Specific Neurotransmitter
Substances in the Basal Ganglial System
specific neurotransmitters that are known to
function within the basal ganglia, showing;
(1) dopamine pathways from the substantia nigra
to the caudate nucleus and putamen,[it is an
inhibitary transmitter]
(2) gamma-aminobutyric acid (GABA) pathways
from the caudate nucleus and putamen to the
globus pallidus and substantia nigra,[it is an
inhibitary transmetter].
• (3) acetylcholine pathways from the cortex
to the caudate nucleus and putamen, and[it
is an excitatory transmettr]
• (4) multiple general pathways from the brain
stem that secrete norepinephrine, serotonin,
enkephalin, and several other
neurotransmitters in the basal ganglia.
• glutamate pathways provide most of
the excitatory signals that balance out
the large numbers of inhibitory signals
transmitted especially by the dopamine,
GABA, and serotonin inhibitory
transmitters.
 Functions of basal ganglia
• Planning and programming of voluntary
movement.
• Initiation of voluntary movement.
• Associated movements[swinging the upper
limbs while waking]
• Inhibition of muscle tone.
• Cognitive function
 Diseases of the Basal :

 disease processes affecting these ganglia in

humans produce marked and characteristic
abnormalities of motor function.
 Disorders of movement associated with diseases
of the basal ganglia in humans are of two general
types:
• 1-hyperkinetic .
• 2-hypokinetic.
 The hyperkinetic conditions:
o those in which movement is excessive and abnormal,
include;
o Chorea: is characterized by rapid, involuntary "dancing"
movements (putamen).
o Athetosis is characterized by continuous, slow writhing
movements (GP).
o In ballism, involuntary flailing, intense, and violent
movements occur.
Hypokinetic abnormalities include:
- Akinesia; is difficulty in initiating movement and
decreased spontaneous movement.
 -Bradykinesia; is slowness of movement.
• Parkinsonism
• Dopamine is both inhibitory and excitatory in
the basal ganglia on which receptor acts
• 1- Dopamine D1 receptor in the basal ganglia
is excitatory
• 2- Dopamine, D2, receptor in the basal ganglia
is inhibitor
• Deficiency of dopamine in the basal ganglia
• Result in two features’
• A- The hypokinetic features of Parkinson's
disease ;
• 1- Bradykinesia (slow movement)
• 2- Akinesia (no movement) small steps,
difficulty in initiation and stop of movement
• B- hyperkinetic of Parkinson's disease
• 1 Rigidity (lead pipe rigidity. ,cogwheel rigidity).
• 2- Involuntary movements ( tremor at
rest ).
• C- Other features.
• Mask face , Loss of swinging of the upper
limb during walking.
Treatment
2- AdministraDrugs .

1- Administration of anticholinergic drugs.

2-Asdministration of dopamine precursor L-dopa (levodopa)

drug
Surgical.
1- Making lesions in the basal ganglia helps to restore the output
balance toward normal

2- Implantation of dopamine-secreting tissue in or near the basal

ganglia.
Chorea ( dance)
• Chorea is due to damage of corpus striatum
(putamen).
• It is characterized by the following features:
• A- dancing movements that occur suddenly during
rest & may superimpose on voluntary movements.
• -it results due to GABA deficiency,which allows
spontaneous discharge of excitatory signals to the
cortical motor area.
B- hypotonia ;
- due to loss of facilitatory effect on the stretch
reflex.
C- dementia (decrease memory & cognitive
function)
- this is because in chorea, there is also
degeneration of the cholinergic neurons in the BG
& cerebral cortex.
 Chorea
• They are two types of chorea;
• Huntington.
• Sydenhams
Huntington's Disease
damage to medium spiny neurons in the caudate
and putamen.
 An early sign is a jerky trajectory of the hand
when reaching to touch a spot, especially toward the
end of the reach.
 Speech becomes slurred and then
incomprehensible, and a progressive dementia is
followed by death.
Huntington's disease is inherited as an
autosomal dominant disorder,
 onset is usually between the ages of 30
and 50.
The abnormal gene is located near the
end of the short arm of chromosome 4.
 no effective treatment is clinically
available, and the disease is uniformly
fatal.
Sydenham,s chorea:
 -this occurs in young ages(5-15 years).
 - more commonly in females.
 -often as a complication of rheumatic fever.
Hemiballismus
• Due to damage of subthalamic nucleus.
• It is characterized by:
- hypertonia.
- sudden,violet, rapid spasmodic
involuntary movements,e.g. sudden flexion
of the lower limb.(fall during walking)
- if bilateral it is may fatal due to spasm of
resp. muscles.
 Athetosis
• It is due to damage of the globus pallidus.
• It is characterized by:
• -hypertonia.
• -involuntary spasmodic slow writhing movements
(twisting snake like movement) .
• - e.g.pronation of with flexion followed by
supination with extention.
• - the result in mobile spasm(abnormal postures
that are not kept at a fixed position.
 .

•Thanks