Transcript THE BASAL GANGLIA - Selam Higher Clinic

THE MAJOR
NEURONAL CIRCUITS
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THE MOTOR CORTEX
The anatomical region of the brain known as
Area 4 is the primary motor cortex (PMC)

Focal stimulations elicited muscle contractions
 Is organized somatotopically
 The surface area varies.
 Is proportional to the precision of the movements
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The motor cortex also includes Area 6,
 Which lies rostrally to Area 4 Divided into



Premotor area or premotor cortex(PMA)
Supplementary motor area. (SMA)
The PMA is believed to help


Regulates posture by dictating an optimal position to
the motor cortex for any given movement.
The SMA, for its part, seems to influence
• The planning and initiation of movements
• On the basis of past experience

The mere anticipation of a movement triggers neural
transmissions in the SMA
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4

Somatotopic representations in the motor cortex
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The posterior parietal cortex (PPC)
Also plays a role in voluntary movements

The parietal cortex receives:
• Somatosensory
• Proprioreceptive
• Visual inputs

Assesses the context in which they are being made.
Based on which determines such things as
•
•
•
•
The positions of the body
And the target in space.
Produces internal models of the mov’ts to be made.
Before the premotor & motor cortices are involved
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Within the PPC, two particular areas

Area 5 & Area 7

Area 5 receives information from
• Somatosensory areas 1, 2, & 3 of the cortex.

Area 7 further integrates
• The already highly integrated signals from the visual
areas of the cortex, such as MT and V5.
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The parietal lobes are themselves closely

interconnected with the prefrontal areas.

The two regions represent the highest level of
integration in the motor control hierarchy.

Decisions are made about what action to take.
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 The
PP & PFA send their axons to Area 6
 Which,
once it has been informed about the
kind of action to take
 Helps
to determine the characteristics of the
appropriate movement for this purpose
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 These
 Have
two elongated regions face each other
the same somatotopic organization
 MC
& in the SSC, the scale of this map is not
constant.
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In the somatosensory cortex, it varies with:

Each body part's sensitivity to sensory
information.
In the motor cortex, it varies with:
 The
precision of the movements controlled in
the body part in question.
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AXONS ENTERING AND LEAVING THE MOTOR CORTEX

Receive inputs from PMA & SMA
 The pyramidal neurons of the PMC receive
information directly from:

Somatosensory areas 3, 1, & 2.
Axons mainly from the thalamus,
Caudal ventrolateral nucleus ( VLc)


Relays information from the cerebellum.
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The PMC projects its axons mainly to the
Corticospinal tract,
which is composed of the
1.
Lateral
2.
Ventromedial systems.
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The lateral system has two main neural pathways
 The Lateral Corticospinal tract. (The larger)


Arising mainly in Areas 4 and 6 of the frontal lobe,
which together constitute the motor cortex,

Is the longest neural pathway

One of the largest in terms of the number of axons containing 1 milion
The other axons in this tract arise mainly in the
somatosensory areas and the parietal lobe.
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
Axons cross internal capsule, midbrain& pons
 They join together at the medulla oblongata to form a dense
bundle of nerve fibers.
 Shaped like a pyramid (pyramidal tract)
 Extends along the ventral surface of the medulla,
 Just before entering the spinal cord, the pyramidal tract
decussates.
 They ultimately synapse on the

motor neurons and interneurons of the dorsolateral portion of the
ventral horn of the spinal cord.
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
The lateral system
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Rubrospinal tract the 2nd in the lateral system.

Arising from the neurons of the red nucleus, in the
midbrain.

This nucleus receives information from the frontal cortex.

Which also projects massively to the corticospinal tract.
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The other major descending pathway, is the
Ventromedial system


Is composed of four tracts that originate in various
areas of the brainstem
Contribute chiefly to:
 postural control

certain reflex movements.
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
The originating neurons of these tracts receive
sensory information related to:



Balance
Body position
And the visual environment
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1.

The Vestibulospinal tract
Originates in the vestibular nuclei.

Maintains the head in position in relation to the
shoulder

Which is essential for continuing to look in a given
direction while the body is moving
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2. The Tectospinal tract

Arises in the superior colliculus in the midbrain.

The superior colliculus receives:

some visual information directly from the retina

somatosensory and auditory information

the tectospinal tract contributes to visual orientation
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3. Pontine (medial) and
4. Medullary (lateral) Reticulospinal tracts

Arise from the reticular formation nuclei in two main parts of the
brainstem:
 The pons & the medulla oblongata.

The reticular formation receives inputs from many sources

Extends the entire length of the brainstem, from the pons to the
medulla.
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
These two tracts help to maintain posture.

Pontine axons enhance the spinal antigravity
reflexes.

The medullary have the opposite effect,
releasing the muscles

Thus facilitating other movements
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ventromedial system
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THE BASAL GANGLIA
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The basal ganglia and its connections

No input from ascending sensory path way

No direct spinal projection


Cortico-striato-pallido-thalamo-cortical loop
Cortical projections of to the basal ganglia are
directed mainly to the striatum and subthalamic
nucleus (STN)
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
The striatum receives inputs from all areas of the
cerebral neocortex

Cortical inputs to the subthalamus come mainly from
the frontal lobe

The striatum sends GABAergic inhibitory projections:
 Globus pallidus externa GPe
 Globus pallidus interna GPi
 Substantia nigra pars reticulata SNr
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
GPe sends GABAergic inhibitory projections to:

GPi / SNr & STN

STN sends excitatory Glutamergic fibers to GPe
and GPi/ SNr

Thus there are to types of path ways
Direct :
1.
a. Striatum-Gpi/SNr
2.
Indirect:
a. Striatum-GPe-STN-GPi / SNr
b. Striatum-Gpe-Gpi/SNr
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ASSOCIATIVE
LIMBIC
SENSORY MOTOR
G
L G
O L
DORSAL
B O
B
Anterior putamen ASSOCIATIVE
U U
Most of caudate
S S
P
ROSTRO
A P
N. Accumbens
A
MEDIAL
L
Olfactory tubercle
L
LIMBIC
Ventral putamen
L L
Ventral caudate
I I
D
D U
VENTRO
P.Comm. Putamen S.MOTOR LATERAL U S
S (I)
D.lat. head of caudate
(E)
S
U
B
S
T
A
N
T
I
A
MD
LIMBIC
N
I
G
R
A
VL/VA
SENMOTOR
ASS
VA
MD
®
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LIMBIC
Accumbens
Olfactory tubercle
Ventral putamen
Ventral caudate
ASSOCIATIVE
Anterior putamen
Most of caudate
SENSORY MOTOR
Postcommissural
DorsolateralHead of caudate
DORSAL
VENTROLATERAL
ROSTROMEDIAL
INTERNAL AND EXTERNA L PALLIDAL SEGMENTS
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Thalamic Nucleii
OCCULO MOTOR
SUP.
COLLICULUS
LIMBIC
ASSOCIATIVE
MD
SENSORY
MOTOR
VL
MD
VA
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GLUTAMATE
Excitatory
MD
STRIATUM
D1 GABA/P
D2GABA/E
RET
CM/PF
D1GABA/P
VA/VL
SNc
DA
INDIRECT PATH
DIRECT PATH
GABA
Globus Pallidus Extrna
INDIRECT PATH 2
GABA
INDIRECT PATH 1
GABA
Gpi/SNr
GABA
GABA
Glu
STN
PPN/MEA
Ach/GlU
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
1.
2.
3.
Parkinsonism
Rest tremor upper or lower extrimities
Rigidity,akinesia and bradykinesia
Incapacitating type of action tremor UL
Loss of dopamine in the nigrostriatal pathway
 Facilitates the direct path way
 Inhibits the indirect path way
 Net result is increased and abnormally
phasic activity in STN and GPi/SNr
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Tremor
 Multiple sites neuronal oscillations have been observed
 Neurons in the cortex,thalamus (VL),Gpi, STN
 No clear cut specific source of tremor
 Rather collective oscillation
Akinesia
 Large cholinergic interneurons b/n striosomes &matrisomes
 Give burst-pause-burst signal could be “GO” signal for mov’t
 Its absence in Dopa depleted neurons.? reason for akinesia
 Loss Dopa & NA inputs in the cortex
Start hesitation and freezing
 Inhibition of the brainstem via GPi/SNr to PPN/MEA
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Chorea
 Destructive lesions of STN
 Gives hemiballismus and hemichorea
 Slow writhing mov’t of athetosis- in conjunction with chorea
 Is probably due to reduced STN inhibitory output on GPi/SNr
 But pallidal lesion doesn’t cause hemiballismus or chorea
IN HUNTINGTON DISEASE
 Loss of GABAE earlier than GABAP
 Loss of inhibition of the indirect pathway
 Chorea appears
In addition the striatal striosomes(caudate & putamen)
 Loss of inhibitory input to SNc
 Gives enhanced dopaminergic state leading to chorea
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Dystonia
An abnormal cocontraction of antagonistic muscles
 In reduced inhibition of VL thalamic neurons by Gpi
 Hence dystonia is a hyplerkinetic disorder
 Hence thalmotomy for treatment
Tics
Brief coordinated sterotyped movements and vocalizations
 Most are suppressed for short period
 Which might cause anxiety
 The limbic pathway in the BG play a role in pathogenesis
 Effectiveness of D2 antagonists
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THE CEREBELLUM
The pathologies of the cerebellum have long
revealed that this part of the brain is
involved in motor co-ordination
The cerebellum is divided into three regions,
each of which is connected to a specific
structure in the brain and involved in a
specific function
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1,The archicerebellum (vestibulocerebellum)
First appeared in fish.
 It is connected to the vestibule of the inner ear
 And is involved in balance.

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2,The Palaeocerebellum (Spinocerebellum)

Consists mainly of the vermis.

Is connected to the spinal cord

Controls postural muscle activity by influencing
muscle tonus.

The cerebellum therefore controls muscle tension at
all times

while releasing those muscles required to execute
movements.
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3,Nneocerebellum (Cerebrocerebellum)
 It
is more voluminous in primates and
especially so in humans.

It consists of the Cerebellar hemispheres,
 Is
connected to the cortex, and contributes to
the co-ordination of voluntary movements.
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Cerebellum schema
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 The
cerebellar grey matter organized like the
cerebral grey matter

A cortex forming the grey matter at the
surface,
 Deep
nuclei that serve as relays for the
efferent pathways leaving this cortex .
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
There are four cerebellar nuclei on either
side of the median line:
1.
Fastigial nuclei for the archicerebellum
Emboliform for the palaeocerebellum
Globose nuclei for thepalaeocerebellu
Dentate nuclei for the neocerebellum
2.
3.
4.
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
Provides control over the timing of the
body's movements.
 Via
loop circuit that connects it to the MC
 Modulates
the signals that the motor
cortex sends to the motor neurons
 Analyzes
the visual signals associated
with movement
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 Signals
 Or

from the movement of objects
from moving body segments themselves.
Calculate the speed of these movements and
adjust the motor commands accordingly.
 Errors
in such calculations largely account for
the poor motor control
 Participates
in language, attention, memory,
and emotions
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 The
Purkinje cells are the most characteristic
type of neurons in the cerebellum.
 The
axons of the Purkinje cells synapse on the
neurons of the Dentate Nuclei of the
Cerebellum.
 These
nuclei relay the information to the
thalamus
 Which
then projects to the cortex and the
Striatum.
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
Cellular organization of the cerebellum
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 The
dendrite branches of each Purkinje cell
receive synapses from of a single afferent
Climbing Fiber.
 This
fiber is the axon of a neuron in the inferior
olive, a nucleus in the medulla oblongata.
 The
inferior olive integrates the information from
the muscle proprioceptors.
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 Each
climbing fiber winds closely around
the dendrites of its corresponding Purkinje
cell
 So
that the activation of this fiber will
cause a massive excitation of this cell.
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
Mossy Fibers, act in a highly diffuse fashion
 Are
the axons of neurons in the pontine nuclei
 They
receive information from the cerebral
cortex.

They carry this information to synapses with
the small granular cells in the deep layer of
the cerebellum.
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 The
axons of these granular cells ascend into
the surface layer of the cerebellum
 where
they branch into T shapes to form the
parallel fibres.
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 The
parallel fibers then run perpendicular to
the Purkinje cell dendrite fans,
 Thus
crossing many Purkinje cells and
connecting them into a single contact.
 Each
parallel fiber makes only one contact
with each Purkinje cell that it crosses,.
 Likewise,
each Purkinje cell receives over
100 000 synapses from 100 000 different
parallel fibers.
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Schematic representations of cells in the cerebellum
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Neuronal connections in
the cerebellum
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Pontine n.
 Biggest source of mossy fibers
 Premotor ,suplementary motor,primay
motor,somatosensory, posterior
parietalextrasriataal visual and cingulate
corteces and auditory cortex
Reticular n.
 Inputs mainly from sensory motor cortex
 Mosssy fiber input from dorsal an ventral
spinocerbellar pathways
 From vestibulocerebellar patway
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Cerebellar nuclei project to






The brainstem nuclei and ventrolateral thalamus
containing N. Ventralis intermedius
Sources are mainly from Dentae, Globoce and
Emboliform nucleii
Fastigium mainly gives to the ventromedial
thalamus and also to VL
It also project to Red N., Reticular formation, inferior
olive, lateral vestibular n.
Dentate n. receives input from lateral cerebellar
cortex (no direct somatosensory input)
Activated during cognitive and sensory processing
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
Interposed nucleii receive input from the paramedian
cerebellar cortex
 Receive abundant input from the SMC
 Involved in the control of muscle antagonists
 Inactivation causes ipsilateral dysmetria and intention
tremor

Fastigum receives input from the cerebellar vermis
and floculonodular lobe
 Participate in control of vestibulo-occular control and
locomotion
 Inactivation causes severe truncal disequilibrium, gait
ataxia falls to the side of the lesion
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Comparison of the basal ganglia and cerebellar control circuits
Features
Basal ganglia
Cerebellum
Cortical inputs
Wide spread (predominantly
frontal lobe)
Wide spread
Receptive components
Striatum( caudate& Putamen)
Subthalamic nuclei
Cerebellar cortex Purkinje
cells
Effectors component
Globus pallidus internal
component
Cerebellar Nucleii
Regulatory component
Substantia Nigra C
inferior Olivary nucleus
Thalamic nucleus
Ventral anterior & others
Ventral lateral)
Motor cortex target
Supplementary & Premotor
cortices
Primary motor cortex
(supplementary & premotor)
Brainstem target
Pedenculopontine nucleus,
Superior colliculus
Red nucleus, Vestibular nuclei
Reticular formation
Direct spinal input
No
Yes
Function
Selection of motor programs
Initiation an execution of
motor acts
Clinical correlates
Hypokinesis, rigidity, tremor at
rest abnormal mov’t
Hyperkinesis
Disequilibrium Incoordination,
ataxia, action tremor
Localization of clinical
findings
Contralateral to te lesion
Ipsilatral to lesion
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Cerebellar control circuit
 Schematic
presentation
MOTOR
CORTEX
THALAMUS
RED
NUCLEUS
PONTINE
NUCLEUS
CEREBELLUM
VESTIBULAR N.
RETICULAR
FORMATION
INFERIOR
OLIVARY
NUCLEUS
SPINAL
CORD
MUSCLE
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