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Anterior to the central cortical sulcus occupying
approximately the posterior one third of the frontal
Lobes. Divided into
 The primary motor cortex
 The pre motor area
 The supplementary motor cortex
Some other areas such as somatosensory
and parietal lobe association are also included in the
sensorimotor cortex.
view of the right side of
the brain showing the
supplementary
motor cortex, which lies
in the part of the
cerebral cortex that is
folded down between
the two cerebral
hemispheres. Other
cortical motor areas also
extend onto this area.
The premotor,
supplementary motor,
primary motor,
somatosensory, and
parietal-lobe association
cortices together make
up the
sensorimotor cortex.
SOMATOTOPIC
MAP
This is the projection
of the body surface
onto a brain area that
is responsible for our
sense of touch and
that is called the
somatosensory
cortex. This
projection connects
neurons of the cortex
with touch receptors
in the skin surface
such that
neighborhood
relations are
preserved.
 LOCATION
The primary motor cortex, or M1, is one of the principal brain
areas involved in motor function. M1 is located in the frontal
lobe of the brain, along a bump called the precentral gyrus .
It is the site of the primary motor cortex that in humans is
cytoarchitecturally (cytoarchitectonics, is the study of the
cellular composition of the central nervous system's tissues
under the microscope) defined as Brodmann area 4.
 FUNCTION
The role of the primary motor cortex is to generate neural
impulses that control the execution of movement.
.
 LOCATION
The premotor cortex is an area of motor cortex lying within
the frontal lobe of the brain just anterior to the primary
motor cortex.
 FUNCTION
The anterior part of the premotor area first develops a motor
image of total muscle movement that is to be performed.
Then, in the posterior premotor cortex, this image excites
each successive pattern of muscle activity required to achieve
the image.
The posterior part of the premotor cortex sends its signals
either directly to the primary motor cortex to excite specific
muscles or, often, by way of the basal ganglia and thalamus
back to primary motor cortex.
 LOCATION
It lies mainly in the longitudinal fissure but extends a
few centimeters onto the superior frontal cortex.
 FUNCTION
This area functions in concert with the premotor area to
provide body wide attitudinal movements, fixation
movements of the different body segments, positional
movements of head etc.
Association areas of the cerebral cortex also have other
functions in motor control. For example, neurons of the
parietal-lobe association cortex are important in the
visual control of reaching and grasping.
Imagine a glass of water sitting in front of you on your
desk—you could reach out and pick it up much more
smoothly with your eyes tracking your arm and hand
movements than you could with your eyes closed.
Subcortical and Brainstem
Nuclei
Numerous highly interconnected structures lie in the brainstem
and within the cerebrum beneath the cortex, where they interact
with the cortex to control movements.
These structures may play a minor role in motivation and
initiating movements, but they definitely are very important in
planning and monitoring them. Their role is to establish the
programs that determine the specific sequence of movements needed
to accomplish a desired action. Subcortical and brainstem nuclei
are also important in learning skilled movements

Prominent among the subcortical
nuclei are the paired basal
Nuclei. these structures are
often referred to as basal ganglia,
but their presence within the
central nervous system makes the
term nuclei more anatomically
correct. They form a link in some of
the looping parallel circuits
through which activity in the motor
system is transmitted from a
specific region of sensorimotor
cortex to the basal nuclei, from
there to the thalamus, and then
back to the cortical area where the
circuit started
Brain damage to subcortical
nuclei
 SYMPTOMS
Parkinson’s disease is characterized by a loss
or impairment of the power of voluntary
movement (akinesia), slowness of movements
(bradykinesia), muscular rigidity, and a
tremor at rest. Other motor and nonmotor
abnormalities may also be present. For
example, a common set of symptoms includes
a change in facial expression resulting in a
masklike, unemotional appearance, a
shuffling gait with loss of arm swing, and a
stooped and unstable posture.
CAUSES
In Parkinson’s disease, the input to the
basal nuclei is diminished, the interplay
of the facilitatory and inhibitory circuits
is unbalanced, and activation of the
motor cortex (via the basal nuclei–
thalamus limb of the circuit just
mentioned) is reduced.
inadequate functioning of the basal
nuclei, a major part of the initial defect
arises in neurons of the substantia nigra
SUBSTANTIA NIGRA
substantia nigra (“black substance”), a brainstem nucleus that gets its name
from the dark pigment in its cells. These neurons normally project to the basal
nuclei, where they release dopamine from their axon terminals
 The substantia nigra neurons degenerate
in Parkinson’s disease and the amount of
dopamine they deliver to the basal nuclei
is decreased. This decreases the
subsequent activation of the
sensorimotor cortex
 It is not known what causes the
degeneration of neurons of the substantia
nigra and the development of Parkinson’s
disease. there is evidence that it may have a
genetic cause, based on observed changes in
the function of genes associated with
mitochondrial function
 Scientists suspect that exposure to environmental toxins such as manganese,
carbon monoxide, and some pesticides may also be a contributing factor to
developing the disease. One chemical clearly linked to destruction of the substantia
nigra is MPTP (1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine). MPTP is an impurity
sometimes created in the manufacture of a synthetic heroin-like opioid drug, which
when injected leads to a Parkinson’s-like syndrome
Three main catagories of drugs
 agonists (stimulators) of dopamine receptors,
 inhibitors of the enzymes that metabolize dopamine at synapses,
 precursors of dopamine itself.
Levodopa (L-dopa) most widely prescribed drug
L-dopa enters the bloodstream, crosses the blood–brain barrier, and
is converted in neurons to dopamine. (Dopamine itself is not used
as medication because it cannot cross the blood–brain barrier and
it has too many systemic side effects.) The newly formed dopamine
activates receptors in the basal nuclei and improves the symptoms of
the disease Side effects sometimes occurring with L-dopa include
hallucinations, like those seen in individuals with schizophrenia who
have excessive dopamine activity
Deep Brain Stimulation lesioning (destruction) of overactive areas of
the basal nuclei by surgically implanting electrodes in regions of the basal
nuclei; the electrodes are connected to an electrical pulse generator
 LOCATION
The cerebrum is located in the upper part of the cranial cavity, which is a
space inside the top of the skull
 ROLE OF CEREBELLUM IN MOTOR CONTROL
 the planning of sequential movements
integrates information about the nature of an intended movement with the
surrounding space during the course of the movement, the cerebellum compares
information about what the muscles should be doing with information about what
they actually are doing. If a discrepancy develops between intended movement and
the actual one, the cerebellum sends an error signal to motor cortex and
subcortical centers to correct the ongoing program.
 timing function
provide timing signals to the cerebral cortex and spinal cord for precise
execution of the different phases of a motor program, in particular, the timing
of the agonist/antagonist components of a movement. It also helps coordinate
movements that involve several joints and stores the memories of these
movements so they are easily achieved the next time they are tried.
Symptoms of cerebellar diseases
 Intention tremor individuals with cerebellar disease cannot
perform limb or eye movements smoothly but move with a tremor so-
called intention tremor. People with cerebellar disease also cannot
combine the movements of several joints into a single, smooth,
coordinated motion
 Unstable and awkward posture are two other
symptoms characteristic of cerebellar disease. For example, people with
cerebellar damage walk with their feet wide apart, and they have such
difficulty maintaining balance that their gait is similar to that seen in
people who are intoxicated by ethanol gait
 Difficulty in learning new motor skills Individuals
with cerebellar disease find it hard to modify movements in response to
new situations.
The descending tracts are the pathways by
which motor signals are sent from the brain to
lower motor neurones. The lower motor
neurones then directly innervate muscles to
produce movements.
Functional classification
Pyramidal
tracts
Corticospinal
tracts
Corticobulbar
tracts
Extrapyramidal
tracts
Rubrospinal
tract
tectospinal
tract
Reticulospinal
tract
Vestibulospinal
tract
The pyramidal tracts derive their
name from the medullary pyramids
of the medulla oblongata, which
they pass through.
These pathways are responsible for
the voluntary control of the
musculature of the body and face.
Functionally, these tracts can be subdivided into two:
Corticospinal tracts – supplies the musculature
(the system or arrangement of muscles) of the body.
Corticobulbar tracts – supplies the musculature of
the head and neck.
The corticospinal tracts begin in the cerebral cortex, from which they receive a range of
inputs:
 Primary motor cortex
 Premotor cortex
 Supplementary motor area
They also receive nerve fibres from the somatosensory area, which play a role in regulating
the activity of the ascending tracts.
After originating from the cortex, the neurones converge, and descend through the internal
capsule (a white matter pathway, located between the thalamus and the basal ganglia). After
the internal capsule, the neurones pass through the crus cerebri of the midbrain, the pons and
into the medulla.
In the most inferior (caudal) part of the medulla, the tract divides into two:
 The fibres within the lateral corticospinal tract decussate (cross over to the other side
of the CNS). They then descend into the spinal cord, terminating in the ventral horn (at all
segmental levels). From the ventral horn, the lower motor neurones go on to supply the
muscles of the body.
 The anterior corticospinal tract remains ipsilateral, descending into the spinal cord.
They then decussate and terminate in the ventral horn of the cervical and upper thoracic
segmental levels.
The corticospinal tracts. Note the
area of decussation of the lateral
corticospinal tract in the
medulla.
cortex
internal capsule
crus cerebri and pons
medulla
Lateral anterior
Corticospinal Corticospinal
Tract Tract
Spinal cord
Muscles of upper thoracic
Body levels
The corticobulbar tracts arise from the lateral aspect of the primary motor cortex.
They receive the same inputs as the corticospinal tracts. The fibres converge and
pass through the internal capsule to the brainstem.
The neurones terminate on the motor nuclei of the cranial nerves. Here, they
synapse with lower motor neurones, which carry the motor signals to the muscles
of the face and neck.
IMPORTANCE
Clinically, it is important to understand the organisation of the corticobulbar
fibres. Many of these fibres innervate the motor neurones bilaterally. For example,
fibres from the left primary motor cortex act as upper motor neurones for the right
and left trochlear nerves. There are a few exceptions to this rule:
 Upper motor neurones for the facial nerve (CN VII) have a contralateral
innervation. This only affects the muscles in the lower quadrant of the face –
below the eyes. (The reasons for this are beyond the scope of this article)
 Upper motor neurons for the hypoglossal (CN XII) nerve only provide
contralateral innervation.
The extrapyramidal tracts originate in the brainstem, carrying motor fibres to the
spinal cord. They are responsible for the involuntary and automatic control of all
musculature, such as muscle tone, balance, posture and locomotion
On basis of
innervation to
supply nerves to.
Ipsilateral
innervation
Vestibulospinal
tract
Reticulospinal
tract
Contralateral
innervation
Tactospinal
tract
Rubrospinal
tract
Vestibulospinal Tracts
There are two vestibulospinal pathways; medial and lateral. They arise
from the vestibular nuclei, which receive input from the organs of balance.
The tracts convey this balance information to the spinal cord, where it
remains ipsilateral.
FUNCTION
Fibres in this pathway control balance and posture by innervating the
‘anti-gravity’ muscles (flexors of the arm, and extensors of the leg), via
lower motor neurones.
Reticulospinal Tracts
The two recticulospinal tracts have differing functions:
 The medial reticulospinal tract arises from the pons. It facilitates
voluntary movements, and increases muscle tone.
 The lateral reticulospinal tract arises from the medulla. It inhibits
voluntary movements, and reduces muscle tone.
Rubrospinal Tracts
The rubrospinal tract originates from the red nucleus, a midbrain
structure. As the fibres emerge, they decussate (cross over to the other
side of the CNS), and descend into the spinal cord. Thus, they have a
contralateral innervation.
FUNCTION
Its exact function is unclear, but it is thought to play a role in the fine
control of hand movements
Tectospinal Tracts
This pathway begins at the superior colliculus of the midbrain. The
superior colliculus is a structure that receives input from the optic nerves.
The neurones then quickly decussate, and enter the spinal cord. They
terminate at the cervical levels of the spinal cord.
FUNCTION
The tectospinal tract coordinates movements of the head in relation to
vision stimuli.
The brain motor centers and descending pathways
The brain motor centers and descending pathways

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The brain motor centers and descending pathways

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  • 5. Anterior to the central cortical sulcus occupying approximately the posterior one third of the frontal Lobes. Divided into  The primary motor cortex  The pre motor area  The supplementary motor cortex Some other areas such as somatosensory and parietal lobe association are also included in the sensorimotor cortex.
  • 6. view of the right side of the brain showing the supplementary motor cortex, which lies in the part of the cerebral cortex that is folded down between the two cerebral hemispheres. Other cortical motor areas also extend onto this area. The premotor, supplementary motor, primary motor, somatosensory, and parietal-lobe association cortices together make up the sensorimotor cortex.
  • 7. SOMATOTOPIC MAP This is the projection of the body surface onto a brain area that is responsible for our sense of touch and that is called the somatosensory cortex. This projection connects neurons of the cortex with touch receptors in the skin surface such that neighborhood relations are preserved.
  • 8.  LOCATION The primary motor cortex, or M1, is one of the principal brain areas involved in motor function. M1 is located in the frontal lobe of the brain, along a bump called the precentral gyrus . It is the site of the primary motor cortex that in humans is cytoarchitecturally (cytoarchitectonics, is the study of the cellular composition of the central nervous system's tissues under the microscope) defined as Brodmann area 4.  FUNCTION The role of the primary motor cortex is to generate neural impulses that control the execution of movement. .
  • 9.  LOCATION The premotor cortex is an area of motor cortex lying within the frontal lobe of the brain just anterior to the primary motor cortex.  FUNCTION The anterior part of the premotor area first develops a motor image of total muscle movement that is to be performed. Then, in the posterior premotor cortex, this image excites each successive pattern of muscle activity required to achieve the image. The posterior part of the premotor cortex sends its signals either directly to the primary motor cortex to excite specific muscles or, often, by way of the basal ganglia and thalamus back to primary motor cortex.
  • 10.  LOCATION It lies mainly in the longitudinal fissure but extends a few centimeters onto the superior frontal cortex.  FUNCTION This area functions in concert with the premotor area to provide body wide attitudinal movements, fixation movements of the different body segments, positional movements of head etc.
  • 11. Association areas of the cerebral cortex also have other functions in motor control. For example, neurons of the parietal-lobe association cortex are important in the visual control of reaching and grasping. Imagine a glass of water sitting in front of you on your desk—you could reach out and pick it up much more smoothly with your eyes tracking your arm and hand movements than you could with your eyes closed.
  • 12. Subcortical and Brainstem Nuclei Numerous highly interconnected structures lie in the brainstem and within the cerebrum beneath the cortex, where they interact with the cortex to control movements. These structures may play a minor role in motivation and initiating movements, but they definitely are very important in planning and monitoring them. Their role is to establish the programs that determine the specific sequence of movements needed to accomplish a desired action. Subcortical and brainstem nuclei are also important in learning skilled movements
  • 13.  Prominent among the subcortical nuclei are the paired basal Nuclei. these structures are often referred to as basal ganglia, but their presence within the central nervous system makes the term nuclei more anatomically correct. They form a link in some of the looping parallel circuits through which activity in the motor system is transmitted from a specific region of sensorimotor cortex to the basal nuclei, from there to the thalamus, and then back to the cortical area where the circuit started Brain damage to subcortical nuclei
  • 14.  SYMPTOMS Parkinson’s disease is characterized by a loss or impairment of the power of voluntary movement (akinesia), slowness of movements (bradykinesia), muscular rigidity, and a tremor at rest. Other motor and nonmotor abnormalities may also be present. For example, a common set of symptoms includes a change in facial expression resulting in a masklike, unemotional appearance, a shuffling gait with loss of arm swing, and a stooped and unstable posture. CAUSES In Parkinson’s disease, the input to the basal nuclei is diminished, the interplay of the facilitatory and inhibitory circuits is unbalanced, and activation of the motor cortex (via the basal nuclei– thalamus limb of the circuit just mentioned) is reduced. inadequate functioning of the basal nuclei, a major part of the initial defect arises in neurons of the substantia nigra SUBSTANTIA NIGRA substantia nigra (“black substance”), a brainstem nucleus that gets its name from the dark pigment in its cells. These neurons normally project to the basal nuclei, where they release dopamine from their axon terminals
  • 15.  The substantia nigra neurons degenerate in Parkinson’s disease and the amount of dopamine they deliver to the basal nuclei is decreased. This decreases the subsequent activation of the sensorimotor cortex  It is not known what causes the degeneration of neurons of the substantia nigra and the development of Parkinson’s disease. there is evidence that it may have a genetic cause, based on observed changes in the function of genes associated with mitochondrial function  Scientists suspect that exposure to environmental toxins such as manganese, carbon monoxide, and some pesticides may also be a contributing factor to developing the disease. One chemical clearly linked to destruction of the substantia nigra is MPTP (1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine). MPTP is an impurity sometimes created in the manufacture of a synthetic heroin-like opioid drug, which when injected leads to a Parkinson’s-like syndrome
  • 16. Three main catagories of drugs  agonists (stimulators) of dopamine receptors,  inhibitors of the enzymes that metabolize dopamine at synapses,  precursors of dopamine itself. Levodopa (L-dopa) most widely prescribed drug L-dopa enters the bloodstream, crosses the blood–brain barrier, and is converted in neurons to dopamine. (Dopamine itself is not used as medication because it cannot cross the blood–brain barrier and it has too many systemic side effects.) The newly formed dopamine activates receptors in the basal nuclei and improves the symptoms of the disease Side effects sometimes occurring with L-dopa include hallucinations, like those seen in individuals with schizophrenia who have excessive dopamine activity Deep Brain Stimulation lesioning (destruction) of overactive areas of the basal nuclei by surgically implanting electrodes in regions of the basal nuclei; the electrodes are connected to an electrical pulse generator
  • 17.  LOCATION The cerebrum is located in the upper part of the cranial cavity, which is a space inside the top of the skull  ROLE OF CEREBELLUM IN MOTOR CONTROL  the planning of sequential movements integrates information about the nature of an intended movement with the surrounding space during the course of the movement, the cerebellum compares information about what the muscles should be doing with information about what they actually are doing. If a discrepancy develops between intended movement and the actual one, the cerebellum sends an error signal to motor cortex and subcortical centers to correct the ongoing program.  timing function provide timing signals to the cerebral cortex and spinal cord for precise execution of the different phases of a motor program, in particular, the timing of the agonist/antagonist components of a movement. It also helps coordinate movements that involve several joints and stores the memories of these movements so they are easily achieved the next time they are tried.
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  • 19. Symptoms of cerebellar diseases  Intention tremor individuals with cerebellar disease cannot perform limb or eye movements smoothly but move with a tremor so- called intention tremor. People with cerebellar disease also cannot combine the movements of several joints into a single, smooth, coordinated motion  Unstable and awkward posture are two other symptoms characteristic of cerebellar disease. For example, people with cerebellar damage walk with their feet wide apart, and they have such difficulty maintaining balance that their gait is similar to that seen in people who are intoxicated by ethanol gait  Difficulty in learning new motor skills Individuals with cerebellar disease find it hard to modify movements in response to new situations.
  • 20. The descending tracts are the pathways by which motor signals are sent from the brain to lower motor neurones. The lower motor neurones then directly innervate muscles to produce movements.
  • 22. The pyramidal tracts derive their name from the medullary pyramids of the medulla oblongata, which they pass through. These pathways are responsible for the voluntary control of the musculature of the body and face. Functionally, these tracts can be subdivided into two: Corticospinal tracts – supplies the musculature (the system or arrangement of muscles) of the body. Corticobulbar tracts – supplies the musculature of the head and neck.
  • 23. The corticospinal tracts begin in the cerebral cortex, from which they receive a range of inputs:  Primary motor cortex  Premotor cortex  Supplementary motor area They also receive nerve fibres from the somatosensory area, which play a role in regulating the activity of the ascending tracts. After originating from the cortex, the neurones converge, and descend through the internal capsule (a white matter pathway, located between the thalamus and the basal ganglia). After the internal capsule, the neurones pass through the crus cerebri of the midbrain, the pons and into the medulla. In the most inferior (caudal) part of the medulla, the tract divides into two:  The fibres within the lateral corticospinal tract decussate (cross over to the other side of the CNS). They then descend into the spinal cord, terminating in the ventral horn (at all segmental levels). From the ventral horn, the lower motor neurones go on to supply the muscles of the body.  The anterior corticospinal tract remains ipsilateral, descending into the spinal cord. They then decussate and terminate in the ventral horn of the cervical and upper thoracic segmental levels.
  • 24. The corticospinal tracts. Note the area of decussation of the lateral corticospinal tract in the medulla. cortex internal capsule crus cerebri and pons medulla Lateral anterior Corticospinal Corticospinal Tract Tract Spinal cord Muscles of upper thoracic Body levels
  • 25. The corticobulbar tracts arise from the lateral aspect of the primary motor cortex. They receive the same inputs as the corticospinal tracts. The fibres converge and pass through the internal capsule to the brainstem. The neurones terminate on the motor nuclei of the cranial nerves. Here, they synapse with lower motor neurones, which carry the motor signals to the muscles of the face and neck. IMPORTANCE Clinically, it is important to understand the organisation of the corticobulbar fibres. Many of these fibres innervate the motor neurones bilaterally. For example, fibres from the left primary motor cortex act as upper motor neurones for the right and left trochlear nerves. There are a few exceptions to this rule:  Upper motor neurones for the facial nerve (CN VII) have a contralateral innervation. This only affects the muscles in the lower quadrant of the face – below the eyes. (The reasons for this are beyond the scope of this article)  Upper motor neurons for the hypoglossal (CN XII) nerve only provide contralateral innervation.
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  • 27. The extrapyramidal tracts originate in the brainstem, carrying motor fibres to the spinal cord. They are responsible for the involuntary and automatic control of all musculature, such as muscle tone, balance, posture and locomotion On basis of innervation to supply nerves to. Ipsilateral innervation Vestibulospinal tract Reticulospinal tract Contralateral innervation Tactospinal tract Rubrospinal tract
  • 28. Vestibulospinal Tracts There are two vestibulospinal pathways; medial and lateral. They arise from the vestibular nuclei, which receive input from the organs of balance. The tracts convey this balance information to the spinal cord, where it remains ipsilateral. FUNCTION Fibres in this pathway control balance and posture by innervating the ‘anti-gravity’ muscles (flexors of the arm, and extensors of the leg), via lower motor neurones. Reticulospinal Tracts The two recticulospinal tracts have differing functions:  The medial reticulospinal tract arises from the pons. It facilitates voluntary movements, and increases muscle tone.  The lateral reticulospinal tract arises from the medulla. It inhibits voluntary movements, and reduces muscle tone.
  • 29. Rubrospinal Tracts The rubrospinal tract originates from the red nucleus, a midbrain structure. As the fibres emerge, they decussate (cross over to the other side of the CNS), and descend into the spinal cord. Thus, they have a contralateral innervation. FUNCTION Its exact function is unclear, but it is thought to play a role in the fine control of hand movements Tectospinal Tracts This pathway begins at the superior colliculus of the midbrain. The superior colliculus is a structure that receives input from the optic nerves. The neurones then quickly decussate, and enter the spinal cord. They terminate at the cervical levels of the spinal cord. FUNCTION The tectospinal tract coordinates movements of the head in relation to vision stimuli.