Clinicophysiologic Concepts of Spasticity and Motor Dysfunction in Adults with an Upper Motoneuron Lesion
Nathaniel H. Mayer, MD
MF Brin, MD, editor Muscle Nerve 1997; 20 (suppl 6):S1-S13.
Abstract: Spasticity is a disorder of the sensorimotor system characterized by a velocity-dependent increase in muscle tone with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex. It is one component of the upper motoneuron syndrome, along with released flexor reflexes, weakness, and loss of dexterity. Spasticity is an important "positive" diagnostic sign of the upper motoneuron syndrome, and when it restricts motion, disability may result. The "negative" signs–weakness and loss of dexterity–invariably alter patient function when they occur. In an upper motoneuron syndrome, the alpha motoneuron pool becomes hyperexcitable at the segmental level. This hyperexcitability is hypothesized to occur through a variety of mechanisms, not all of which have yet been demonstrated in humans. Spasticity caused by spinal cord lesions is often marked by a slow increase in excitation and overactivity of both flexors and extensors with reactions possibly occurring many segments away from the stimulus. Cerebral lesions often cause rapid build-up of excitation with a bias toward involvement of antigravity muscles. Chronic spasticity can lead to changes in the rheologic properties of the involved and neighboring muscles. Stiffness, contracture, atrophy, and fibrosis may interact with pathologic regulatory mechanisms to prevent normal control of limb position and movement. In the clinical exam, it is important to distinguish between the resistance due to spasticity and that due to rheologic changes, because the distinction has therapeutic implications. Diagnostic nerve or motor point blocks and dynamic or multichannel EMG are useful to distinguish the contributions of spasticity and stiffness to the clinical problem.
Alpha motoneuron hyperexcitability may be caused by reduced inhibitory input, denervation supersensitivity, shortening of motoneuron dendrites, or collateral sprouting of dorsal root afferents
As one component of the upper motoneuron syndrome, spasticity is a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex
Disorders which may lead to an upper motoneuron syndrome: cerebral palsy, multiple sclerosis, traumatic brain injury, stroke, spinal cord injury, neuro-degenerative diseases
The UMN syndrome includes the positive symptoms of spasticity and released flexor reflexes, and the negative symptoms of loss of dexterity and weakness
The negative symptoms are often more important to the function of the patient than the positive ones
Spasticity, spinal model:
- removal of inhibition on segmental polysynaptic pathways
- slow, progressive rise of excitatory state through cumulative excitation
- afferent activity from one segment may lead to muscle response many segments away
- flexors and extensors may be overexcited
Spasticity, cerebral model:
- enhanced excitability of monosynaptic pathways
- rapid build-up of reflex activity
- bias toward overactivity in the antigravity muscles and the development of hemiplegic posture
The clinical features of released flexor reflex are:
- big toe extension (principal component of Babinski's sign)
- ankle, knee, and hip flexion
- contraction of abdominals
Selective control of muscle groups may be replaced by mass synergies (obligatory patterns of movement)
Loss of finger and thumb dexterity often endures even after good proximal recovery in the upper limb
The rheologic properties of muscle–plasticity and visco-elasticity–also influence the control of muscle
Rheologic changes include stiffness, contracture, atrophy, and fibrosis
Rheologic changes and pathologic regulatory mechanisms interact to prevent normal control of limb position and movement
Resistance in recent-onset spasticity is reflex-induced, while resistance in chronically spastic muscle involves rheologic changes such as increased stiffness
The sources of resistance encountered in active movements can be difficult to interpret
Diagnostic nerve or motor point block and EMG are useful to distinguish the contributions of spasticity and stiffness to the clinical problem
When many muscles cross a joint, the behavior of each must be assessed when developing a treatment plan
Primary afferent Ia fibers surrounding intrafusal fibers of the muscle spindle are excited when a muscle is stretched. The Ia fiber makes a monosynaptic excitatory connection with alpha motoneurons of its muscle of origin, and it similarly connects with alpha motoneurons of synergistic muscles. The Ia fiber also monosynaptically connects with an inhibitory interneuron that projects directly to the alpha motoneurons of antagonist muscles. When a muscle is stretched, excitation of homonymous and synergistic motoneurons, combined with inhibition of antagonists, subserves the mechanism of reciprocal inhibition. There is evidence for impairment of this mechanism in the UMN syndrome.
Clinical Features of Movement Dysfunction in the Upper Motoneuron Syndrome
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
