Download Hyperstiffness

Corticospinal tract
myelination
Signs of motor neuron lesions
•
•
•
•
•
•
•
Paresis and paralysis
Muscle atrophy
Involuntary muscle contractions
Abnormal muscle tone
Abnormal reflexes
Muscle hyperstiffness
Distrurbances of movements efficiency and
speed
• Impaired postural control
Paresis & paralysis
• Common consequences of motor neuron
lesion:
– Paresis & paralysis
– decreased ability to generate muscle force and a
decrease in muscle bulk
• Decreased muscle strength:
– hemiplegia, paraplegia, tetraplegia
• Stroke
– Retain some voluntary control of hand movement
via the lateral reticulospinal & tectospinal tracts.
Atrophy
• The loss of muscle bulk :
– disuse atrophy : muscle atrophy resulting from
lack of use
– neurologic atrophy : muscle atrophy resulting from
damage to the nervous system
• In UMN lesions,
– skeletal muscle continues to receive stimulation
from the intact LMNs, and the rate of atrophy is
slower than in LMN lesions.
Involuntary muscle contractions
• Muscle spasms:
– sudden, involuntary contractions of muscle
• Cramps:
– particularly severe and painful muscle spasms
• Fasciculations:
– quick twitches of muscle fibers of a single motor unit that
are visible on the surface of the skin.
• Myoclonus:
– Involuntary contractions of a muscle or group of muscles.
• Fibrillations:
– brief contractions of single muscle fibers not visible on the
surface of the skin.
• Abnormal movements generated by dysfunctional
basal ganglia
Abnormal muscle tone
• Muscle tone:
– Is defined as the stiffness (resistance to stretch) in
resting muscle
• Hypotonia(flaccidity) or abnormally low
resistance to passive stretch:
– Lower motor neuron lesions
– Temporarily following an acute upper motor neuron
lesion
– Developmental disorders, Intracranial hemorrhage
• Hypertonia or abnormally strong resistance to
passive stretch:
- Chronic upper motor neuron lesions
- Some basal ganglia disorder
• Spastic:
– amount of resistance to passive movement
depends on the velocity of movements
• Rigidity:
– resistance to passive movement remains constant,
regardless of the speed of force application
– Decerebrate rigidity:
• Severe midbrain lesions
• rigid extension of the limbs and trunk, internal rotation of
the upper limbs, plantar flexion
– Decorticate rigidity:
• Severe lesions superior to the midbrain
• upper limbs are flexed and the lower limbs are extended
• Spinal or cerebral shock:
– when descending motor commands are
interrupted by an acute upper motor neuron lesion,
the lower motor neurons affected become
temporarily inactive
Disorders of lower motor neurons
• Lower motor neurons innervate muscle fibers
– Trauma, infection (poliomyelitis), degenerative or vascular
disorders, tumors can damage LMNs.
• Interrupting LMN signals to muscle:
– decrease or prevents muscle contraction
• If the lower motor neuron cell bodies/or axons are
destroyed:
–
–
–
–
Loss of reflexes
Atrophy
Flaccid paralysis
Fibrillations
• Post-polio syndrome:
– increasing muscle weakness, joint and muscle pain, fatigue,
breathing problems
Poliomyelitis: an acute infection of
the anterior horn of the spinal cord
Effects of polio on alpha motor neurons
Healthy motor units with
Normal innervation
Acute polio
recovery
Late post-polio
LMN Syndrome - Muscular Atrophy
Upper motor neuron syndrome
• Neurons whose axons descend from the
cerebrum and brain stem to synapse on lower
motor neuron (alpha and gamma)
– loss of blood supply to part of the brain, spinal
cord injury, cerebral palsy, multiple sclerosis,
trauma
• UMLs can produce several changes:
–
–
–
–
–
Paresis
Loss of fractionation of movement
Abnormal reflexes
Muscle hyperstiffness
Cocontraction & abnormal muscle synergies
Paresis
• Paresis:
– consequence of inadequate recruitment of LMNs.
• Stroke do not lack muscle power on the affected
side weakness post stroke was due to antagonist
m. contraction opposing agonist m. activity (bobath).
• Decreased agonist activity was associated with
inability to perform the tasks; no evidence for
excessive antagonist activation was found : post
stroke
• Paresis following UMN lesions leads to muscle disuse,
causing secondary changes in muscles and the
nervous system.
Loss of Fractionation of Movement
• Fractionation is the ability to activate
individual muscles independently of
other muscles.
• Interruption of lateral corticospinal
signals prevents fractionation,
profoundly affecting the ability to use
the hand.
Abnormal reflexes
Changes in cutaneous reflexs
Include Babinski’s sign and
muscle spasm in response to
normally innocuous stimuli
Babinski’s test
In infants until about 7months of age,
Babinski’s sign is normal because the
corticospinal tracts are not adequately
myelinated.
Muscle stretch hyperreflexia
• Absence of the moderating influence of
UMNs onto the LMNs cause an
excessive response to muscle spindle
input.
• The result is excessive muscle
contraction when spindles are stretched,
due to the excessive firing of LMNs.
• Page 203, figure 9-16.
Clonus
• Involuntary, repeating, rhythmic muscle
contractions are called clonus.
• Sustained clonus is always pathologic.
Clasp-knife response
• Clasp-knife response:
– when a paretic muscle is slowly & passively
stretched, resistance drops at a specific
point in the range of motion.
Muscle Hyperstiffness
• Myo-plasticity:
– ability of skeletal muscle to adapt structually and
functionally in response to changes in activity level
and to prolonged positioning
• Hyperstiffness:
– excessive resistance to muscle stretch (both
passive and active muscle stretch)
• Post stroke, paretic muscle exert excessive
resistance to muscle stretch
– loss of sarcomeres
– increased weak binding of actin and myosin
– atrophy of muscle fibers
Myo-plastic Hyperstiffness Post
stroke
• Contracture
– Sarcomeres are lost in muscles that are
maintained in a shortened position, even when the
nerveous system is intact
– muscle shortening
• Post stroke paretic muscle
– Stretched, the initial, stronger resistance to stretch
is produced by weak actin-myosin bonds.
– The later resistence, as the stretch continues, is
produced by titin.
Spasticity
• 2 definitions
– Research definition
• Increase in muscle tone due to hyper excitability
of the tonic stretch reflex, characterized by a
velocity-dependent increase in phasic stretch
reflexes.
– Clinical definition
• Paresis, myoplastic hyperstiffness,
cocontraction, and hyperreflexia are not
distinguished. Therefore, the term spasticity is
enigmatic.
Cause of excessive m. stiffness
• Myoplastic hyperstiffness
– Denotes contracture, excess weak actin-myosin
binding, and selective muscle fiber atrophy.
• Hyperreflexia
– Refers to muscle spindle stretch leading to
overactivity in the LMNs and resulting in active
muscle contraction.
• Muscle overactivity
– Is excessive muscle contraction caused by
excessive UMN activity.
Evaluation of movement impairments in
chronic upper motor neuron lesions
• Contracture:
– decreased PROM without increased EMG output
• Cocontraction:
– temporal overlap of EMG activity in antagonist
muscle
• Hyperreflexia:
– EMG activity occuring at a specific latency after
the initiation of muscle stretch
• Excessive upper motor neuron activity:
– excessive EMG activity
Abnormal timing of muscle activation
• Disrupted timing of muscle activation also
contributes to the movement problems in
people with upper motor neuron syndrome
–
–
–
–
Initiation of movement : delayed
The rate of force development : slowed
Muscle contraction time : prolonged
The timing of activation of antagonists relative to
agonist : disrupted
• EMG : evaluate movements
Types of upper motor neuron
•
•
•
•
•
•
Spinal cord injury
Stroke
Congenital lesions (cerebral palsy)
Head trauma
Tumors
And M.S.
Spinal cord injury
• In complete SCI
– Stretch reflexes are hyperactive during passive
movements yet during active movements stretch
reflexes are the same as in people with intact
nervous system
• iSCI
– Sig. correlation between contracture and
resistance to muscle stretch.
– Predominance of type 2b m. and reduction in
type1 m.
– Excessive stretch reflexes in the quadriceps m.
during the swing phase of gait.
Stroke
Typical posture
-of an adult who has
sustained a left middle cerebral artery
Stroke.
Emotional lability
-also called pseudobulbar affect
-because emotional expression is less
controlled by the corticobulbar neurons
than normally
Spastic Cerebral Palsy
• Abnormal supraspinal influences
– Failure of normal neuronal selection
– Consequent aberrant muscle development
lead to movement dysfunction.
– Motor disorders
• Paresis
• Abnormal tonic stretch reflexes both at rest and
during movement
• Reflex irradiation
• Lack of postural preparation prior to movement
Common sings of UMN lesions
•
•
•
•
•
Paresis
Abnormal cutaneous reflexes
Abnormal timing of muscle activity
Myoplastic hyperstiffness
Hyperreflexia of the phasic stretch reflex
– Clonus
– Clasp-knife phenomenon
Interventions for impairments secondary
to upper motor neuron lesions
• Improvement in function post stroke
– constraint-induced movement
• Timing and extent of forced use are important
–
–
–
–
movements against resistance
bicycling with high workloads
partial body weight support gait training
botulinum toxin
• Treatment of hyperreflexia post SCI
– Baclofen : produce inhibition in stretch reflex
pathways
Body weight support gait training.
A harness, mounted overhead, supports
part of the person’s weight while the
individual walks on a treadmill.
Degeneration of the voluntary motor system
• Amyotrophic lateral sclerosis(ALS) :
– destroys only the lateral activating tracts
and anterior horn cells in the spinal cord,
resulting in both upper and lower motor
neuron signs
– Paresis, myoplastic hyperstiffenss,
hyperreflexia, Babinski’s sign, atrophy,
fasciculations, fibrillations
• Death : respiratory complication
Amyotrophic Lateral Sclerosis
1. corticospinal
tract (UMN)
2. lower motor
neuron (LMN)
*
*
*
* *
*