Lecture by
DR SHAIK ABDUL RAHIM
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Movements of our body are accomplished by
contraction of the skeletal muscles
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Flexion: contraction of a flexor muscle draws in a limb
Extension: contraction of extensor muscle
Skeletal muscle fibers have a striated appearance
Skeletal muscle is composed of two fiber types:
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Extrafusal: innervated by alpha-motoneurons from the
spinal cord: exert force
Intrafusal: sensory fibers that detect stretch of the muscle
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Afferent fibers: report length of intrafusal: when stretched, the
fibers stimulate the alpha-neuron that innervates the muscle fiber:
maintains muscle tone
Efferent fibers: contraction adjusts sensitivity of afferent fibers.
8.2
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Each muscle fiber consists
of a bundle of myofibrils
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Each myofibril is made
up of overlapping strands
of actin and myosin
During a muscle twitch,
the myosin filaments
move relative to the actin
filaments, thereby
shortening the muscle
fiber
8.3

The neuromuscular junction is the synapse formed
between an alpha motor neuron axon and a muscle
fiber
Each axon can form synapses with several muscle fibers
(forming a motor unit)
 The precision of muscle control is related to motor unit size

 Small: precise movements of the hand
 Large: movements of the leg

ACh is the neuromuscular junction neurotransmitter

Release of ACh produces a large endplate potential


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Voltage changes open CA++ channels
CA++ entry triggers myosin-actin interaction (rowing action)
Movement of myosin bridges shortens muscle fiber
8.4

Smooth muscle is controlled by the autonomic
nervous system

Multiunit smooth muscle is normally inactive


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Located in large arteries, around hair and in the eye
Responds to neural or hormonal stimulation
Single-unit smooth muscle exhibits rhythmic contraction
 Muscle fibers produce spontaneous pacemaker potentials that elicit

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action potentials in adjacent smooth muscle fibers
Single-unit muscle is found in gastrointestinal tract, uterus, small
blood vessels
Cardiac muscle fibers resemble striated muscle in
appearance, but exhibit rhythmic contractions like
that of single-unit smooth muscle
8.5

Striated muscle contraction is governed by sensory
feedback

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Intrafusal fibers are in parallel with extrafusal fibers
Intrafusal receptors fire when the extrafusal muscle fibers
lengthen (load on muscle)
 Intrafusal fibers activate agonist muscle fibers and inhibit antagonist
muscle fibers
 Extrafusal contraction eliminates intrafusal firing

Golgi tendon organ (GTO) receptors are located within
tendons
 Sense degree of stretch on muscle
 GTO activation inhibits the agonist muscle (via release of glycine

onto alpha-motoneuron
GTO receptors function to prevent over-contraction of striated
muscle
8.6

Spinal cord is organized
into dorsal and ventral
aspects


Dorsal horn receives
incoming sensory
information
Ventral horn issues
efferent fibers (alphamotoneurons) that
innervate extrafusal
fibers
Fig 3.23
8.7

Monosynaptic reflexes involve a single synapse between a
sensory fiber from a muscle and an alpha-motor neuron

Sensory fiber activation quickly activates the alpha motor neuron
which contracts muscle fibers
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

Patellar reflex
Monosynaptic stretch stretch (posture)
Polysynaptic reflexes involve multiple synapses between
sensory axons, interneurons, and motor neurons

Axons from the afferent muscle spindles can synapse onto


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Alpha motoneuron connected to the agonist muscle
An inhibitory interneuron connected to the antagonist muscle
Signals from the muscle spindle activate the agonist and inhibit the
antagonist muscle
8.8
8.9

Multiple motor systems control body movements


Walking, talking, postural, arm and finger movements
Primary motor cortex is located on the precentral
gyrus
Motor cortex is somatotopically organized (motor
homunculus)
 Motor cortex receives input from

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Premotor cortex
Supplemental motor area
Frontal association cortex
Primary somatosensory cortex
Planning of movements involves the premotor cortex and the
supplemental motor area which influence the primary motor
cortex
8.10
8.11
8.12

Axons from primary motor cortex descend to the
spinal cord via two groups

Lateral group: controls independent limb movements
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Corticospinal tract: hand/finger movements
Corticobulbar tract: movements of face, neck, tongue, eye
Rubrospinal tract: fore- and hind-limb muscles
Ventromedial group control gross limb movements
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Vestibulospinal tract: control of posture
Tectospinal tract: coordinate eye and head/trunk movements
Reticulospinal tract: walking, sneezing, muscle tone
Ventral corticospinal tract: muscles of upper leg/trunk
8.13

Neurons of the corticospinal tract terminate on
motor neurons within the gray matter of the spinal
cord
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Corticospinal tract starts in layer 5 of primary motor cortex
Passes through the cerebral peduncles of the midbrain
Corticospinal neurons decussate (crossover ) in the medulla


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80% become the lat. corticospinal tract
20% become the ventral corticospinal tract
Terminate onto internuncial neurons or alpha-motoneurons
of ventral horn
Corticospinal tracts control fine movements


Destruction: loss of muscle strength, reduced dexterity of hands
and fingers
No effect of corticospinal lesions on posture or use of limbs for
reaching
8.14

Apraxia refers to an inability to properly execute a
learned skilled movement following brain damage

Limb apraxia involves movement of the wrong portion of a
limb, incorrect movement of the correct limb part, or an
incorrect sequence of movements
 Callosal apraxia: person cannot perform movement of left hand to a
verbal request (anterior callosum interruption prevents information
from reaching right hemisphere)
 Sympathetic apraxia: damage to anterior left hemisphere causes
apraxia of the left arm (as well as paralysis of right arm and hand)
 Left parietal apraxia: difficulty in initiating movements to verbal
request

Constructional apraxia is caused by right parietal lobe damage
 Person has difficulty with drawing pictures or assembling objects
8.15
The Basal Ganglia

Basal ganglia consist of the caudate nucleus, the
putamen and the globus pallidus
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
Input to the basal ganglia is from the primary motor
cortex and the substantia nigra
Output of the basal ganglia is to
 Primary motor cortex, supplemental motor area, premotor cortex
 Brainstem motor nuclei (ventromedial pathways)

Cortical-basal ganglia loop
 Frontal, parietal, temporal cortex send axons to caudate/putamen
 Caudate/putamen projects to the globus pallidus
 Globus pallidus projects back to motor cortex via thalamic nuclei
8.17
Caudate Nucleus
•C shaped structure (“tail”)
•Lateral wall of lateral ventricle
•Head, body and tail
All regions of cerebral cortex project to the basal
ganglia, but output of basal ganglia is directed towards
the frontal lobe, particularly pre-motor and
supplementary motor cortex

Parkinson’s disease (PD) involves muscle rigidity,
resting tremor, slow movements


Parkinson’s results from damage to dopamine neurons
within the nigrostriatal bundle (projects to caudate and
putamen)
Slow movements and postural problems result from



Loss of excitatory input to the direct circuit (caudate-Gpi-VA/VL
thalamus-motor cortex)
Loss of output from the indirect circuit (which is overall an
excitatory circuit for motor behavior)
Neurological treatments for PD:


Transplants of dopamine-secreting neurons (fetal subtantia nigra
cells or cells from the carotid body)
Stereotaxic lesions of the globus pallidus (internal division)
alleviates some symptoms of Parkinson’s disease
8.20

Huntington’s disease (HD) involves uncontrollable,
jerky movements of the limbs
HD is caused by degeneration of the caudate nucleus and
putamen
 Cell loss involves GABA-secreting axons that innervate the
external division of the globus pallidus (GPe)
 The GPe cells increase their activity, which inhibits the activity
of the subthalamic nucleus, which reduces the activity level of
the GPi, resulting in excessive movements
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HD is a hereditary disorder caused by a dominant gene
on chromosome 4

This gene produces a faulty version of the protein huntingtin
8.21

Cerebellum consists of two hemispheres with
associated deep nuclei

Flocculonodular lobe is located at the caudal aspect of the
cerebellum
 This lobe has inputs and outputs to the vestibular system
 Involved in control of posture

Vermis is located on the midline of the cerebellum
 Receives auditory and visual information from the tectum and
cutaneous information from the spinal cord
 Vermis projects to the fastigial nucleus which in turn projects
to the vestibular nucleus and to brainstem motor nuclei
8.22
Cerebellum
Classifications
Classification by Phylogenetic and Ontogenic Development
Archicerebellum
Paleocerebllum
Neocerebellum
Classification by Afferent Connection
Vestibulocerebellum
Spinocerebellum
Pontocerebellum
Classification by Efferent Connection
Vermis
Paravermal Region
Cerebellar Hemisphere
Spinocerebellum
Pontocerebellum
Vestibulocerebellum
Cerebellum – little brain
 Two hemispheres with convoluted surfaces
 Responsible for maintenance of equilibrium, muscle tone
and posture.
 It plays a key role in accomplishing a smooth and
coordinated movements by means of its comparator
function.
 The cerebellum plays an important role in learning of
motor skills.
 Damage to the cerebellum generally results in
jerky, erratic and uncoordinated movements
Cerebellum
Function
 Maintenance of Equilibrium
- balance, posture, eye movement
 Coordination of half-automatic movement of
walking and posture maintenace
- posture, gait
 Adjustment of Muscle Tone
 Motor Leaning – Motor Skills
 Cognitive Function
Balance
Motor Skill
Pablo Casals
Cerebellum
Clinical
Syndromes
Ataxia: incoordination of movement
- decomposition of movement
- dysmetria, past-pointing
- dysdiadochokinesia
- rebound phenomenon of Holmes
- gait ataxia, truncal ataxia, titubation
Intention Tremor
Hypotonia, Nystagmus
Archicerebellar Lesion: medulloblastoma
Paleocerebellar Lesion: gait disturbance
Neocerebellar Lesion: hypotonia, ataxia, tremor
Posture
Gait – Ataxia
Tremor
a
d
b
c
Cerebellar
Ataxia
Ataxic gait and
position:
Left cerebellar tumor
a. Sways to the right in
standing position
b. Steady on the
right leg
c. Unsteady on the
left leg
d. ataxic gait
Cerebellar
Medulloblastoma
Cerebellar tumors on vermis
- Truncal Ataxia
- Frequent Falling
The child in this picture:
- would not try to stand
unsupported
- would not let go of the bed rail
if she was stood on the floor.
BG
CBLM
Courtesy of Stephen C. Voron, MD
BG
CBLM
Courtesy of Stephen C. Voron, MD
pyramidal cell
in the motor
homunculus
of the frontal
lobe
BG
CBLM
Courtesy of Stephen C. Voron, MD
corticospinal
tract
BG
CBLM
Courtesy of Stephen C. Voron, MD
BG
CBLM
decusation at
the pyramids
(spinomedullary
junction
Courtesy of Stephen C. Voron, MD
BG
thalamus:
AKA the
“gate keeper”
prevents
unwanted
movements
T
CBLM
Courtesy of Stephen C. Voron, MD
BASAL
GANGLIA
BG
consultant on
automatic
movements
T
CBLM
Courtesy of Stephen C. Voron, MD
provides
input into the
thalamus
Cerebellum:
consultant on
rapid
movements
BG
CBLM
Courtesy of Stephen C. Voron, MD
provides
input into the
thalamus
Basal Ganglia

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resting tremor
postural instability
festination
rigidity
masked facies
bradykinesia
dyskinesia
torticollis
chorea
athetosis
hemiballismus
akathisia
Cerebellum
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intention tremor
dysmetria
dysdiadochokinesia
hypotonia
heal to shin
finger to nose
rebound
ataxic gait
titubation
nystagmus
dysmetric saccades