The Motor System (Part 2)

Reported by: Cayyong, Juguilon | March 08, 2021

Trans by: Calaycay, Dumelod, Matila, Zingapan

OUTLINE 1. Vermis:
o fastigial nucleus (medial) and lateral vestibular
I. Cerebellar Control Circuit B. Anatomy
nucleus (lateral)
A. Overview C. Connectivity
B. Anatomy D. Intrinsic circuitry 2. Hemispheres:
C. Functional E. Physiology o Paravermis – emboliform and globose nuclei
Subdivisions F. Clinical correlations (interposed nuclei)
D. Inputs and Outputs III. Motor Examination o Lateral – dentate nucleus (largest)
E. Main Connections A. Strength
F. Basic Intrinsic B. Muscle tone
Cerebellar Circuit C. Muscle Bulk
G. Physiology D. Reflexes
H. Clinical correlations E. Coordination
II. Basal Ganglia Control F. Gait and Station
Circuit G. Abnormal
A. Overview Movements

I. CEREBELLAR CONTROL CIRCUIT

A. OVERVIEW
• Essential for learning, planning, initiating, executing, and
adapting movements and postures.
• The cerebellum controls the initiation, speed , amplitude, and
termination of movement by providing timing signals to motor
areasIt acts as a comparator between the central motor
commands and the sensory consequences of execution
• Provides correction signals for appropriate movement
execution.
Figure 2: Horizontal section showing the main functional subdivisions of the
• It controls eye movement, speech, posture, gait, and cerebellum and their output nuclei. A, Functional subdivisions of the cerebellar
coordination of the ipsilateral limbs. cortex. B, Cerebellar output nuclei. The flocculonodular lobe corresponds to the
vestibulocerebellum and has direct reciprocal connections with the vestibular
nuclei, controlling ocular movements. The vermis acts through the fastigial nucleus
B. ANATOMY to control trunk movement and gait. The cerebella hemispheres include an
intermediate region (paravermis) that by way of the globose and emboliform nuclei
controls movements of the ipsilateral limbs. The lateral portion of the hemispheres,
through the dentate nucleus, controls ipsilateral limb movement and cognitive
function.[MayoClinic]

C. FUNCTIONAL SUBDIVISIONS
1. Flocculonodular lobe – vestibulocerebellum, controls ocular
movements and balance.
2. Vermis – control trunk movement and gait.
3. Paravermis – controls movement of ipsilateral limbs.
4. Lateral hemisphere – controls ipsilateral limb movement and
cognitive function, including sequencing of movements, timing,
and coordination.

Figure 1: Gross anatomy of the cerebellum. The body of the cerebellum includes
a medially located vermis and the expanded lateral hemispheres. The primary
fissure divides the dorsal portion of the cerebellum into an anterior lobe and
posterior lobe. The cerebellum consists of a flocculonodular lobe and a body,
which consists of the anterior and posterior lobes. Most of the body of the
cerebellum corresponds to the cerebellar hemispheres (posterior lobe).

• 2 Main components:
1. Flocculonodular lobe
2. Body of the cerebellum
a. Anterior Lobe
b. Posterior Lobe
→ Each lobe is divided into several lobules, each
consisting of leaflet like folia.
Figure 3: superior view of cerebellum
→ Primary fissure
→ Posterolateral fissure D. INPUTS AND OUTPUTS
• The grey mater consists of the: cortex and deep cerebellar • Travel through the cerebellar peduncles
nuclei (receive afferents to the cerebellum) • Inputs
• The cerebellar cortex projects to the deep cerebellar nuclei.
• Sagittal zones of the cerebellum
Trans # 3 THE MOTOR SYSTEM 1 of 8
 → Inferior cerebellar peduncle (ICP) – input from spinal 1. Mossy fibers
cord and medulla → axons from the ipsilateral spinal cord, contralateral
→ Middle cerebellar peduncle (MCP) – input from pontine nuclei, and ipsilateral labyrinth, vestibular
contralateral pons nuclei, and reticular formation.
• Outputs → glutaminergic and synapse on the granule cells of
→ Superior cerebellar peduncle (SCP) – output of deep the cerebellar cortex.
cerebellar nuclei, including projections to the contralateral 2. Climbing fibers
midbrain and thalamus and ones that descend to the pons → solely from the contralateral inferior olivary nucleus.
and midbrain → provide a powerful, direct excitatory glutamatergic
input to both the deep cerebellar nuclei and Purkinje
E. MAIN CONNECTIONS cells (1:1 or 1:2).
• Inputs:
→ Corticopontocerebellar pathway
→ Spinocerebellar pathway (dorsal and ventral)
→ Vestibulocerebellar tract
→ Reticulocerebellar tract
→ Olivo-cerebellar tract
• Output:
→ Cerebellothalamocortical pathway
→ and allows for detection of degree of stretch.

Figure 4: Basic Cerebellar Circuit

G. PHYSIOLOGY

1. CONTROL OF EYE MOVEMENTS

• Mediated by the Flocculonodular lobe aka the
Vestibulocerebellum (most primitive)
• Primary function is control of eye movement through the
vestibular system.
• Input: the labyrinth, vestibular nuclei, and neurons in the
parieto-occipital cortex (via the pontine nuclei) when
activated by the visual perception of object movement.
• It receives input from the brainstem areas involved in the
control of eye movement and its main output is to the medial
and superior vestibular nuclei.
• The vestibular nuclei innervate the ocular motor neurons
mediating vestibulo-ocular reflexes, allowing a person to
maintain visual fixation, smooth visual pursuit, and
Figure 4: The main connections of the cerebellum. The cerebellum receives input
from the contralateral cerebral cortex via the pontine nuclei, which project to the
maintenance of gaze in the excentric position.
cerebellum through the middle cerebellar peduncle (MCP). The cerebellum also • Through projections to the fastigial nucleus, the dorsal vermis
receives input from the ipsilateral spinal cord via the spinocerebellar tracts and controls the amplitude, direction, and velocity of fast (saccadic)
input from the vestibular nuclei and reticular formation. All these inputs end as eye movements to changes in target location.
mossy fibers. The cerebellum also receives input from the contralateral inferior
olivary nucleus, whose axons end as climbing fibers. Dorsal spinocerebellar,
vestibulocerebellar, reticulocerebellar, and olivocerebellar pathways reach the
cerebellum through the inferior cerebellar peduncle (ICP). All cerebellar inputs
are excitatory and reach the Purkinje cells of the cerebellar cortex and the
cerebellar nuclei. The Purkinje cells inhibit the deep cerebellar nuclei, which are
the source of the output of the cerebellum and project through the superior
cerebellar peduncle (SCP). This peduncle decussates at the level of the lower
midbrain and provides excitatory inputs, through a relay in contralateral thalamus,
to motor areas of the cerebral cortex. Other cerebellar outputs (not shown) end in
brainstem motor nuclei and inferior olivary nucleus. Vim, ventral intermedius
thalamic nucleus; VL, ventral lateral thalamic nucleus.

F. BASIC INTRINSIC CEREBELLAR CIRCUIT

• The cortex consists of layers:
1. Molecular layer
2. Purkinje cell layer and Figure 5: Connections of the Flocculonodular Lobe
3. Granular layer
• Both Purkinje cells and deep cerebellar nuclei receive 2. CONTROL OF POSTURE AND GAIT
excitatory input from mossy and climbing fibers. • The vermis and paravermis receive information from:
→ Spinocerebellar tracts.
Trans # 3 THE MOTOR SYSTEM 2 of 8
 → Corticopontocerebellar pathway
→ Reticular formation and vestibular nuclei.
• Dorsal spinocerebellar tract
→ originates in Clarke column
→ provides proprioceptive and exteroceptive input from the
ipsilateral lower extremity
• Ventral spinocerebellar tract
→ Originates from interneurons in the lateral portion of the
ventral horn.
→ The axons ascend contralaterally in the spinal cord and
then cross again in the superior cerebellar peduncle to
terminate in the ipsilateral vermis and paravermis.
→ Provides the cerebellum with information about the activity
of the inhibitory interneurons and the descending motor
pathways.
• Vermis
→ Input: spinocerebellar tract (from the trunk and proximal
portion of the extremities, particularly the lower limbs)
→ Projects: medially, to the reticular formation and laterally
to the lateral vestibular nucleus
→ Function: controls postural reflexes of the head and trunk
and proximal limb movements involved in locomotion.
3. CONTROL OF LIMB MOVEMENTS
• The cerebellar hemispheres, including the intermediate
(paravermis) and the large lateral portions, control
movement of the ipsilateral limbs.
• Paravermis
→ Input: contralateral motor cortex and ipsilateral spinal
cord
→ It projects to the globose and emboliform nuclei
→ which in turn sends axons to the contralateral thalamus
and magnicellular portion of the red nucleus.
→ The thalamus then projects to the motor cortex.
→ Function: controls the activity of the crossed lateral motor
pathways that control movement of the limbs.
→ The cerebellum provides continuous feedback for
monitoring and correcting motor commands that
activate agonist and antagonist muscles of the ipsilateral
arm and leg.
• Lateral cerebellar hemispheres
→ Input: the pontine nuclei, various areas of the cerebral
cortex, including the premotor, motor, and prefrontal
cortices.
→ Projects to: the dentate nucleus
→ Sends axons to the contralateral thalamus, specifically to
the ventral lateral or ventral intermedius nucleus.
→ Thalamic nucleus projects to primary motor cortex and
lateral premotor cortex
4. CEREBELLO-OLIVARY INTERACTION, ERROR
CORRECTON, AND MOTOR LEARNING
• The inferior olivary nucleus
→ Input: projections from all brain regions that provide input
to the cerebellum.
• Pathway:
→ Inferior olives > (inferior cerebellar peduncles) >
contralateral cerebellar cortex (climbing fibers)
• Activity of the inferior olives is regulated by:
→ Monosynaptic inhibitory input from the contralateral
dentate nucleus
→ The direct GABAergic dentato-olivary pathway
→ Disynaptic excitatory input from the parvicellular portion of
the red nucleus
5. COGNITIVE FUNCTION OF THE CEREBELLUM
• The cerebropontocerebellar path provides the cerebellum
→ Prefrontal cortex - executive functions
Trans # 3 THE MOTOR SYSTEM
→ Anterior cingulate cortex - initiation of movement,
motivation, and goal-oriented behaviors
→ Posterior cingulate and medial temporal cortices - spatial
and declarative memory
→ Posterior parietal cortex – visuospatial processing
• The cerebellar output to these non-motor areas of the cerebral
cortex is from the ventral portion of the dentate nucleus.
G. CLINICAL CORRELATIONS
1. DISTURBANCE IN OCULAR MOTOR CONTROL
• Nystagmus
→ caused by lesions that affect the flocculonodular lobe
→ Repetitive to-and-fro eye movements initiated by a slow
drift, or slow phase in one direction, followed by a fast
corrective movement in the opposite direction
→ The inability to perform smooth pursuit (tracking) eye
movements
2. DISTURBANCE IN POSTURE, EQUILIBRIUM, AND GAIT
• Gait ataxia
→ lesions of the caudal vermis cause postural ataxia of the
head and trunk during sitting, standing, and walking
→ Characterized by a broad-based gait, with the tendency of
the person to veer toward either side.
→ Tandem gait is impaired.
→ instability of the trunk.
→ apparent with the eyes open. The Romberg sign is not
present in cerebellar ataxia.
3. LIMB ATAXIA
• Lesions of the cerebellar hemisphere lead to errors in the
timing, direction, and the extent of movement of the ipsilateral
limb.
• Inaccuracy and poor coordination of multijoint movements.
• Dysmetria
→ involvement of the paravermis of the hemisphere disrupts
the accuracy of reaching movements.
→ loss of the ability to measure the range of motion.
• Intention tremor
→ inability to coordinate the contraction of agonist and
antagonist muscles that act on a particular joint
• Dyssynergy
→ lesions of the lateral cerebellum and dentate nucleus
→ delays in the initiation of movement and irregularities in
the timing of the components of a movement.
→ inability to perform rapid repetitive movements.
• Dysdiadochokinesia
→ combination of abnormalities in timing, velocity, and
acceleration produces an irregularity in the rate of
alternate movements.
4. ATAXIC DYSARTHRIA
• motor disorder that affects the production of speech.
• lesions are associated with irregularities in articulation,
loudness, and rhythm of speech.
• speech is slow, with excessive stress on some words or
syllables and random breakdown of articulation.
II. BASAL GANGLIA CONTROL CIRCUIT
A. OVERVIEW
• What is the Basal ganglia?
→ Collection of gray matter (nuclei) located deep within the
brain.
→ Essential subcortical components of circuits involved in
motor, ocular motor, cognitive and affective functions.
3 of 8
• Function in motor control (Triple role)
1. To facilitate the automatic execution of selected
sequential programs while simultaneously suppressing
all other potentially competing and interfering motor
programs.
2. To interrupt ongoing motor behavior in response to a
novel, behaviorally significant stimulus.
3. To scale the amplitude and duration of postures and
movements during execution of a motor plan.
B. ANATOMY
• Location: Inferior part of cerebral hemispheres, lateral to the
thalamus
• Basal ganglia circuit has 2 core structures: STRIATUM
(composed of Caudate nucleus and Putamen) & GLOBUS
PALLIDUS
• Lenticular Nucleus: Putamen & Globus Pallidus (Lens-shaped) Figure 7&8: Connectivity of The Basal Ganglia[MayoClinic]
• 2 other critical components are the substantia nigra (midbrain)
and subthalamic nucleus.
• Stratium
→ Putamen
→ Caudate nucleus
→ Nucleus accumbens (limbic striatum)
• Caudate nucleus
→ forms the lateral wall of the lateral ventricle.
→ separated from the putamen by the anterior limb of the
internal capsule.
• Globus pallidus
→ has an external segment and internal segment.
• The main neurons of the striatum and globus pallidus are
inhibitory GABAergic neurons. • Basal ganglia circuit is a fronto-striato-pallido-thalamocortical
• Substantia nigra circuit
→ Parallel circuit
→ Pars reticulata- homologous to the internal pallidal
→ Controls motor, ocular motor, cognitive and affective
segment
functions
→ Pars compacta- contains dopaminergic neurons. 1. Motor circuit
→ Subthalamic nucleus- contains glutaminergic excitatory
neurons.

2. Ocular motor circuit

Figure 6: The main nuclei and connections of the basal ganglia circuit. The basal
ganglia include the striatum (putamen, caudate nucleus, and accumbens nucleus
[not shown]), globus pallidus (including external and internal segments),
subthalamic nucleus, and substantia nigra (including pars reticulata [not shown] 3. Cognitive circuit
and pars compacta). A, Coronal section. B, Horizontal section.

C. CONNECTIVITY OF BASAL GANGLIA CIRCUITRY

• Comprises of different circuits involved in different functions.
• It controls motor, ocular motor, cognitive and affective
functions.
• 1. Cerebral cortex (Frontal lobe) → 2. Striatum, Subthalamic
nucleus, Substantia Nigra pars compacta → 3. Globus pallidus
internal & Substantia nigra pars reticulata → 4. Thalamus 4. Emotional (Limbic circuit)

Trans # 3 THE MOTOR SYSTEM 4 of 8

 D. INTRINSIC CIRCUITRY
• Several general principles of organization of the basal ganglia.
• Mediated by the internal pallidal segment and substantia nigra
pars reticulata, tonically inhibits targets involved in the initiation
of motor programs, including those related to voluntary and
automatic movements, locomotion, and saccadic eye
movements.
The basal ganglia exert a dual control on the initiation and
execution of movement:
a. They facilitate the initiation of a particular motor program
by transiently interrupting the output of the internal
pallidal segment and substantia nigra pars reticulata to a
target thalamic or brainstem neuron.
b. They inhibit the initiation of competing motor programs
by increasing the tonic inhibitory output of the internal
pallidal segment and substantia nigra pars reticulata to
all other targets.
• Dual effect of the basal ganglia circuit arises from:
→ output of the internal pallidal segment
→ substantia nigra pars reticulata
→ being regulated by two opposing influences: tonic
excitation by the subthalamic nucleus and transient
(phasic) inhibition by the striatum
• The dual functions of the basal ganglia (facilitation of one motor
program and inhibition of all others).
These pathways are triggered by inputs from the cerebral cortex and
regulated by dopaminergic input to the striatum.
1. Direct pathway
→ consists of excitatory input from the cerebral cortex to a
group of neurons in the striatum that send GABAergic
inhibitory input to the internal pallidal segment and
substantia nigra pars reticulate
→ cortical activation of this direct pathway results in a net
inhibition of the internal pallidal segment and disinhibition
of its target, facilitating the initiation of a particular motor
program
Trans # 3 THE MOTOR SYSTEM
2. Indirect pathway
→ involves excitatory input from the cerebral cortex to a
group of striatal neurons that send GABAergic inhibitory
input to the external pallidal segment
→ Because this pallidal segment inhibits both the
subthalamic nucleus (which excites the internal pallidal
segment and substantia nigra pars reticulata) and the
internal pallidal segment and substantia nigra pars
reticulata, activation of the indirect pathway increases the
activity of the internal pallidal segment and substantia
nigra pars reticulata, thus increased inhibition of their
target, preventing the initiation of a motor program.
3. Hyperdirect pathway
→ consists of excitatory input from the cerebral cortex to the
subthalamic nucleus
→ Because this nucleus activates the internal pallidal
segment and substantia nigra pars reticulata,the
hyperdirect pathway also increases the inhibitory output of
the basal ganglia
E. PHYSIOLOGY
1. CONTROL OF THE ACTIVITY OF THE STRIATUM
• Striatal output neurons (medium spiny GABAergic neurons)
have intrinsic electrophysiologic properties so they have very
low activity at rest. (INACTIVE or “off-state”)
• ACTIVE OR “on-state”
→ Occurs only when activated by powerful, converging
excitatory glutamatergic input from the cerebral
cortex, in which these neurons fire a burst of action
potentials that phasically inhibit the internal or
external pallidal segment.
→ Modulated by dopaminergic input from neurons in the
substantia nigra pars compacta which specifically
discharge in response to a reward signal from the
environment or in anticipation of a reward signal and
facilitate the initiation of a specific, behaviorally
relevant motor program.
• DOPAMINE
→ has a dual role in the striatum, mediated by D1 and
D2 receptors.
→ When striatal cells are in the “off-state,” dopamine
maintains this state, thus preventing spurious
activation by weak cortical stimuli.
→ In contrast, if a behaviorally significant, powerful
cortical input brings the striatal neurons to the “on-
state,” dopamine acts on D1 receptors and facilitates
firing of the neurons.
→ Thus, dopamine increases the signal-to-noise ratio in
the striatum
→ The activity of the medium spiny GABAergic neurons
is regulated also by acetylcholine released from
tonically active local neurons in the striatum.
→ In general, striatal acetylcholine, acting on muscarinic
receptors, opposes the effects of dopamine.
2. DUAL CONTROL OF THE BASAL GANGLIA OUTPUT
• The GABAergic neurons of the GPi and Substantia nigra pars
reticulata fire tonically at high frequency because of tonic
excitatory input from the STN.
• In the resting state, the initiation of motor programs is tonically
inhibited at the level of the cerebral cortex (supplementary
motor area), superior colliculus, and pedunculopontine
nucleus.
• Initiation of a specific motor program requires a powerful
cortical input to the medium (spiny) striatal GABAergic neurons
of the direct pathway, which transiently inhibits the internal
5 of 8
 pallidal segment and substantia nigra pars reticulata, and thus
disinhibits its targets.
• At the same time, the cerebral cortex inhibits the initiation of
potentially competing motor programs mediated by the
hyperdirect pathway to the subthalamic nucleus and by the
indirect pathway from the striatum to the external pallidal
segment.
• Dopamine has a net excitatory effect on the striatal neurons of
the direct pathway (contains more D1 receptors than D2
receptors) that disinhibit the motor programs
• It has net inhibitory effect on striatal neurons of the indirect
pathway (contain more D2 receptors than D1 receptors) that
inhibit motor programs.
• Because the discharge of dopaminergic neurons provides a
reward signal, these neurons allow the context-dependent
initiation of selected motor programs in response to
behaviorally significant stimuli.
3. Potential for Oscillatory Activity in the basal ganglia
circuitry
• The reciprocal interconnections between the excitatory
glutamatergic neurons of the subthalamic nucleus and the
GABAergic inhibitory neurons of the external pallidal segment
form a network that supports the oscillatory activity in the basal
ganglia circuits that influences the output of the internal pallidal
segment and substantia nigra pars reticulata.
• The cerebral cortex influences this network by its direct
monosynaptic projections to the subthalamic nucleus.
• By increasing the signal-to-noise ratio in the basal ganglia
circuits, dopamine prevents synchronized oscillatory output of
this circuit, which could degrade motor performance.
F. CLINICAL CORRELATIONS
1. Pathophysiology of Movement Disorders
• shifts in the balance between the activity in the direct and
indirect pathways underlies several movement d/o.
• Decrease in dopaminergic transmission in the striatum
decreases the activity in the direct pathway and increases that
in the indirect pathway.
• The net effect is excessive activity in the subthalamic nucleus
and in the output from the internal pallidal segment and
substantia nigra pars reticulata causing exaggerated inhibition
of the thalamic neurons and the inability to interrupt this
inhibition when attempting to initiate a motor program results in
the akinetic/rigid syndrome of parkinsonism.
Trans # 3 THE MOTOR SYSTEM
• In contrast, decreased activity in the subthalamic nucleus (and
thus the internal pallidal segment) gives rise to hyperkinetic
movement Disorders.
2. Hypokinetic-Rigid Syndromes
• Characterized by akinesia (or hypokinesia),bradykinesia,
muscle rigidity, and postural instability
a. Parkinson disease
→ degenerative disorder due to loss of
dopaminergic neurons in the substantia nigra
pars compacta
→ primary treatment is dopamine replacement
therapy.
→ Administration of levodopa, a precursor of
dopamine, together with carbidopa, a drug that
prevents the peripheral decarboxylation of the
precursor.
In patients with severe disease or disease of long duration, levodopa may
have a short-duration effect and cause excessive movements (levodopa-
induced dyskinesias). In this situation, reducing the dose of levodopa and
prescribing drugs that activate dopamine receptors (direct dopamine
agonists) are beneficial.
b. Hypokinesia/akinesia
→ global paucity of spontaneous or associated
movements (e.g., eye blinking and arm swing)
c. Bradykinesia
→ slowness in the initiation and performance of
voluntary or automatic acts
d. Rigidity
→ an increase in muscle tone
e. Tremor
→ typically occurs at rest and diminishes with
voluntary activity
3. Hyperkinetic Movement Disorders
• There are several types of hyperkinetic movement disorders,
and their pathologic substrate varies.
a. Chorea
→ Irregular, writhing, involuntary movements that flow from
one part of the body to another and interfere with the
execution of motor acts
→ generally, but not always, is associated with lesions in the
caudate nucleus
→ A typical example is Huntington disease, an autosomal
dominant neurodegenerative disorder characterized by
chorea, cognitive deterioration, and affective and
psychiatric symptoms from severe involvement of the
caudate nucleus
Figure11. Coronal section of the brain of a normal control (A) and an age-matched
patient with Huntington disease (B). In the latter, note the severe atrophy of the
caudate nucleus, which produces a bat-wing shape or ballooning of the lateral
ventricles.
b. Athetosis
→ Slow writhing movements of the fingers commonly
associated with chorea
c. Dystonia
6 of 8
 → Sustained muscle contraction that leads to abnormal fixed A. STRENGTH
postures and intermittent twisting movements • Evaluates the power of muscle groups in performing specific
→ may be local or generalized actions.
→ typical manifestation of basal ganglia disease but the • Depends on:
pathophysiologic mechanism is heterogeneous. 1. Age
→ It may occur from a lesion involving the putamen or it may 2. Occupation
occur without a recognizable lesion. 3. Physical activity
4. Muscular development
d. Hemiballismus
• Decreased in patients with:
→ Cause by lesions in the subthalamic nucleus → Bone deformity
→ Produces involuntary, often violent, predominantly → Pain
proximal movements of the contralateral limb. → Lack of understanding of the test

All these hyperkinetic movement disorders may also occur • The object of strength testing is to detect disease of the
as a manifestation of overdosage of levodopa in patients with neuromuscular system, these extraneous factors must be
Parkinson disease or as a toxic manifestation of some drugs, excluded.
including cocaine and amphetamine, that increase dopamine • Strength cannot be graded as abnormal on the basis of an
levels. absolute measure of force.
3. Other Movement Disorders • Each muscle group should be tested in the position that best
• TREMOR isolates its function and puts it at a relative mechanical
→ An oscillating movement that affects one or more disadvantage.
body parts, particularly the limbs SYSTEM FOR GRADING STRENGTH:
→ It also affects the neck, orofacial muscles,and vocal
cords. 1. Normal: level of strength expected for that person
→ Tremor is usually rhythmic and regular and due to 2. Mild weakness: level of strength less than expected but not
alternate or simultaneous contraction of agonist and sufficient to impair any daily function
antagonist muscles. 3. Severe weakness: strength sufficient to activate the muscle and
move it against gravity but not against any added resistance
TYPES OF TREMOR 4. Complete paralysis: no detectable movement
→ Resting Tremor -occur when the muscle is at rest; typical
of parkinsonism. • The muscle groups that are tested as part of the general
→ Essential tremor- Tremor during muscle contraction; may neurologic examination:
occur with posture-holding against gravity (e.g.,with the → Facial muscles
arms extended in front of the body → Neck muscles
→ Cerebellar (Intention tremor)- Seen with intention → Arm abductors
maneuvers (e.g., bringing the finger to touch the nose) → Elbow flexors and extensors
→ Wrist extensors
• TICS → Finger flexors
→ are abnormal movements (motor tics) or sounds (vocal → Trunk flexors
tics) that are involuntary, paroxysmal movements that can → Hip flexors
be simple jerks (such as eye-blinking or shoulder shrug) → Hip extensors
or complex coordinated sequential movements.
→ Knee flexors
• Tourette Syndrome
→ Knee extensors
→ The combination of simple and complex motor and vocal
→ Ankle plantar flexors
tics is typical
→ Ankle dorsiflexors
• Myoclonus
→ Motor jerks consisting of sudden, brief, shock-like muscle
B. MUSCLE TONE
contractions that can be rhythmic or arrhythmic and may
or may not be provoked by sensory stimuli • The elbows, wrists, and knees are passively flexed and
extended with the patient completely relaxed.
→ It may occur with lesions of the cerebral cortex, brainstem,
or spinal cord • There should be only minimal smooth resistance to the
movement.
Deep brain stimulation of the subthalamic nucleus or internal C. MUSCLE BULK
segment of the globus pallidus improves the symptoms of
• All major muscle groups should be examined for signs of
parkinsonism and hyperkinetic movement disorders.
focal atrophy.
• The circumference of the extremities may be measured and
compared with each other.
III. MOTOR EXAMINATION
D. REFLEXES
• Movement - the simultaneous, coordinated activities of all the • Muscle stretch reflexes and superficial (cutaneous) reflexes
major divisions of the motor system. Therefore, these are • Depend on:
tested together in the neurologic examination.
→ rapid, brisk stretch of the muscle
→ uncomfortable stimulus to the skin
The examination is best organized into separate evaluations of:
1. Strength → Correct positioning and application of the stimulus
2. Reflexes (Stretch and Cutaneous) (extremely important in eliciting reflexes)
3. Coordination • Stretch reflex
4. Gait In testing all these reflexes, the patient must be completely
5. Tone relaxed.
6. Muscle bulk → Jaw jerk
7. Observation for abnormal movements → Biceps jerk

Trans # 3 THE MOTOR SYSTEM 7 of 8

 → Triceps jerk
→ Knee jerk
→ Ankle jerk
• Cutaneous reflex
Includes the:
→ Abdominal reflexes
→ Plantar response
→ Cremasteric reflex
→ Anal reflex

E. COORDINATION
• Ability to coordinate the movements of multiple muscle groups
can be observed during ordinary activity, such as shaking
hands, talking, dressing, and writing.

Specific tests allow the assessment of coordination in localized

areas.
1. Finger-to-nose testing
→ the patient is asked to touch alternately his or her own
nose and the examiner’s finger with the tip of his or
her own index finger
2. Heel-to-shin testing
→ the patient places the heel carefully on the opposite
knee and slides it slowly along the edge of the tibia to
the ankle and back up to the knee again
3. Rapid alternating testing
→ the patient pats each hand or foot as rapidly and
regularly as possible against a firm surface
→ A more difficult variation requires alternately patting
the front and back of the hand on the knee as rapidly
and regularly as possible

F. GAIT AND STATION

• Tests of gait and station involve all areas of the motor system.
• Various patterns of gait abnormality occur with different
disorders.
• The test of gait and station is perhaps the single most useful
motor system test and should be observed in all patients.

GAIT: the patient walks normally back and forth at a moderate rate
and then walks on the heels and toes and tandem along a straight
line, touching heel to toe; the patient then hops on each leg.

STATION: the patient is asked to stand with the feet together, first
with the eyes open and then with the eyes closed. There should be
little or no sway.

G. ABNORMAL MOVEMENTS
• Motor disorders are manifested as abnormal involuntary
movements, the patient should be examined when he or she is
undressed, both sitting and supine, and

V. REFERENCES
• Lecture of reporters from Section B
• Benarroch EE, Daube JR, Flemming KD, Westmoreland BF. 2008.
Mayo Clinic Medical Neurosciences Organized by Neurologic
Systems and Levels Fifth Edition. Rochester, MN: Mayo Clinic
Scientific Press.

Trans # 3 THE MOTOR SYSTEM 8 of 8