Spasticity:
Spasticity is a disorder of the sensorimotor system characterized by a velocity-dependent increase in muscle tone withexaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex.
It is one component of the upper motor neuronsyndrome, along with released flexor reflexes, weakness, and loss of dexterity.
Spasticity is the hypertonicity in the muscle group. It can be defined as an initial catch or resistance felt by the examinerwhen rapid passive movements are performed.
In an upper motor neuron syndrome, the alpha motor neuron poolbecomes hyperexcitable at the segmental level.
Spasticity occurs because the inhibition normally provided by thesuppresser areas of the brain is not present.
Brain lesions disrupt the linkages and upset the balance betweensuppresser and facilitory areas of the brain.
The major consequence of the disruption of the balance is the excessfacilitation of gamma motor neurons resulting in hypersensitivemuscle spindles. This results in hyperactive phasic stretch reflexes,hyperactive tonic reflexes, and clonus.
Spasticity caused by spinal cord lesions is often marked by a slowincrease in excitation and over activity of both flexors and extensorswith reactions possibly occurring many segments away from thestimulus.
Cerebral lesions often cause rapid build-up of excitation with a biastoward involvement of antigravity muscles.
Chronic spasticity can lead to changes in the rheologic properties of the involved and neighboring muscles.
The abnormal joint positioning, postures, and unequal distribution of muscle activity imposed by spasticity can produce profound andlasting changes in joints and muscles.
Stiffness, contracture, atrophy, and fibrosis may interact withpathologic regulatory mechanisms to prevent normal control of limbposition and movement.
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Mechanism:
Primary afferent Ia fibers surrounding intrafusal fibers of themuscle spindle are excited when a muscle is stretched.
The Ia fiber makes a monosynaptic excitatory connection withalpha motor neurons of its muscle of origin, and it similarlyconnects with alpha motor neurons of synergistic muscles.
The Ia fiber also monosynaptically connects with an inhibitoryinterneuron that projects directly to the alpha motor neurons of antagonist muscles.
When a muscle is stretched, excitation of homonymous andsynergistic motor neurons, combined with inhibition of antagonists, subserves the mechanism of reciprocal inhibition.
There is evidence for impairment of this mechanism in the UMNsyndrome.
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Features:
Spasticity, spinal model:
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Removal of inhibition on segmental polysynaptic pathways
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Slow, progressive rise of excitatory state through cumulativeexcitation
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Afferent activity from one segment may lead to muscleresponse many segments away
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Flexors and extensors may be overexcited
Spasticity, cerebral model:
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Enhanced excitability of monosynaptic pathways
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Rapid build-up of reflex activity
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Bias toward over activity in the antigravity muscles and thedevelopment of hemiplegic posture
The clinical features of released flexor reflex are:
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Big toe extension (principal component of Babinski's sign)
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Ankle, knee, and hip flexion - contraction of abdominals
Clinical Features:
POSITIVE SYMPTOMS
Spasticity- Increased muscle tone- Exaggerated tendon jerks- Stretch reflex spread to extensors- Repetitive stretch reflex discharges; clonus
Released flexor reflexes- Babinski response- Mass synergy patterns
NEGATIVE SYMPTOMS
Loss of finger dexterity
Weakness- Inadequate force generation- Slow movements
Loss of selective control of muscles and limb segments
RHEOLOGIC CHANGES IN SPASTIC MUSCLE
Stiffness
Fibrosis
Contracture
Atrophy
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| Category: | Uncategorized. |
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| Upload Date: | 02/07/2009 |
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