Lecture 31:
Spinal Cord Injury and Spasticity
Epidemiology:
 Approximately 450,000 people in the
United States live with SCI.
 There are about 10,000 new SCIs every
year; the majority of them (82%) involve
males between the ages of 16 and 30.
 Main causes: motor vehicle accidents
(36%), violence (28.9%), or falls (21.2%).
Spinal Cord Injury
 Paresis: partial loss of voluntary control of muscle
activity
 Plegia: total loss of voluntary motor control
 Para: two extremities are involved—forelimbs (arms)
or hindlimbs (legs)
 Hemi: half of the body (left or right) is involved
 Quadri: all four extremities are involved
 Spastic: with positive signs of spasticity (hyperreflexia)
 Flaccid: without positive signs of spasticity (areflexia)
Spinal Cord Injury
Level of SCI
Outcome
Supraspinal
Hemisyndromes
Cervical
Quadriparesis or quadriplegia
(spastic or flaccid)
Thoracic
Lower paraparesis or paraplegia
(likely spastic)
Lumbar
Lower paraparesis or paraplegia
(flaccid)
SCI: Cervical Injuries
 Commonly quadriplegia
 Above the C-4 level may require a ventilator
 C-5 injuries often result in shoulder and biceps
control, but no control at the wrist or hand
 C-6 injuries generally yield wrist control, but no
hand function
 C-7 and T-1 injuries: can straighten arms but
may have dexterity problems with the hand and
fingers
SCI: Thoracic-Lumbar Injuries
 Commonly paraplegia
 Hands not affected
 At T-1 to T-8, poor trunk control as the result
of lack of abdominal muscle control
 Lower T injuries (T-9 to T-12) allow good
trunk control and good abdominal muscle
control; sitting balance is very good
 Lumbar and sacral injuries yield decreasing
control of the hip flexors and legs
SCI: Stages
Minutes to hours:
 Spinal shock
 Depression of all reflexes; complete paralysis
Days to weeks or months:
 Development of typical consequences
 Spasticity; partial recovery of motor and
sensory functions
Months to years: therapy
SCI: Nonmotor Problems
 Chronic pain
 Loss of sensation
 Loss of bladder control
 Loss of control of other internal organs
SCI: Origin of Sensorimotor
Problems
 Damage to descending and ascending
spinal tracts
 Destruction of the spinal neuronal
apparatus
Spasticity
 James Lance: Velocity-dependent increase
in the spinal stretch reflex with exaggerated
tendon jerks
 Hughlings Jackson: Spasticity is a
combination of positive and negative signs.
They are relatively independent; treating
one group of signs should not be expected to
help the other group.
Spasticity: Positive and
Negative Signs
Positive signs:





flexor/extensor spasms
clonus
clasp-knife
Babinski reflex
exaggerated cutaneous
reflexes
 autonomic hyperreflexia
 dystonia
Negative signs:




paresis
lack of dexterity
fatigability
contractures
Spasticity: Possible Mechanisms
 Increase in the gain of the stretch reflex loop
 Change in the threshold of the tonic stretch reflex loop
 Lack of postsynaptic inhibition of alpha-motoneurons
(in particular, deficit in reciprocal inhibition, in Ib
inhibition, and in Renshaw cell action)
 Lack of presynaptic inhibition of inputs to alphamotoneurons
 Increased stiffness of peripheral structures
Spasticity: Babinski
Reflex
 A typical withdrawal
reaction induced by a
tactile stimulus to the
sole of the foot
 Imprecisely called the
Babinski reflex
Spasticity: Clonus
Typical clonus
induced by a quick
foot dorsiflexion.
Quantitative Assessment
of Spasticity
 Clinical scales (Ashworth, spasms)
 Functional scales (ADL)
 Monosynaptic reflexes
 Suppression of monosynaptic reflexes by
vibration (test of presynaptic inhibition)
 Wartenberg test
Spasticity: Lack of Presynaptic
Inhibition
EMG
M-response
A
H-reflex
St
M-response
St
M-response
H-reflex
St
EMG
B
EMG
H-reflex
vibration
EMG
M-response
St
H-reflex
vibration
In a healthy person, muscle vibration leads to a strong suppression
of the H-reflex (A). In a person with spasticity, the suppression
may be absent or even replaced with facilitation (B).
Spasticity: The Ashworth Scale
Score
Description of Muscle Tone
1
No increase in tone
2
Slight increase in tone, giving a “catch” when
affected segment is moved in flexion or extension
3
More marked increase in tone, but affected
segment is easily flexed and extended
4
Considerable increase in tone; passive movement
is difficult
5
Affected part is rigid in flexion or extension
Spasticity: The Spasm Scale
Score
Frequency of Spasms
0
No spasms
1
Mild spasms induced by stimulation
2
Infrequent full spasms occurring less frequently
than once per hour
3
Spasms occurring more frequently than once per
hour
4
Spasms occurring more frequently than ten times
per hour
Spasticity: Drug Therapies
 Baclofen (GABA agonist)
– oral
– intrathecal
 Clonidine and tizanidine (2 adrenergic agonists)
 Opioids (act on opioid receptors in dorsal horns)
Spasticity: A Scheme of Intrathecal
Delivery of Baclofen
Spine
Catheter
Pump
Computer
Spasticity: Intrathecal Baclofen
Effective suppression of reflexes:
 Elimination of monosynaptic reflexes
 Elimination of clonus
 Decrease of spasms
Unmasking of residual voluntary movements:
 No movement reversal by hyperactive reflexes
 Smoother trajectories
Danger of overdose, weakness, tolerance, etc.
IC Position in an Intact Muscle
In an intact
muscle, IC can
be shifted to
produce any
force at any
length.
Force
Length
1
2
Anatomical
Range
3
IC Position in a Spastic Muscle
Anatomical
Range
Force
sensory
signals
impossible to shift
the characteristic
voluntarily
Length
1
2
3
In a spastic
muscle, control
of the IC
position is
impaired, and
the muscle
cannot leave the
activation zone.
According to This View, a Decrease in Spastic Signs Can
Be Accompanied by Improved Voluntary Movements
Changes in ankle clonus
under intrathecal baclofen
Changes in Babinski resp.
under intrathecal baclofen
1000 SOL
100
SOL
2000 TA
100
TA
0
TIME
3000
0
TIME
2000
Intrathecal Baclofen Effects
on Voluntary Movement
Elbow extension
performed “as fast as
possible” before
(thin lines) and after
(thick lines) a dose of
baclofen.
0
Time (s)
2
Spasticity: Practical Issues
With Intrathecal Baclofen
 Infection; hardware malfunction; refills
 Dose adjustment within the 24-h cycle (sleep,
using extensor tone, avoiding atrophy)
 Drug holidays (tolerance, morphine or
diazepam)
Spasticity: Physical Therapy
 Stretching
 Inhibitory posturing
 Functional training
 Splinting
Treatment of Spasticity
Destructive chemical therapies:
 Botulinum toxin (blocks neuromuscular
transmission)
 Phenol/alcohol (damage nerve and weaken muscle)
Neurosurgical procedures:
 Selective dorsal rhizotomy
 DREZ-tomy (dorsal root entry zone lesions)
Treatment of Spasticity
 Orthopaedic surgery: tendon lengthening
 Functional electrical stimulation:
substitution for voluntary movement
Multiple Sclerosis
 Demyelination of axons within the CNS
 Epidemiology:
–
–
–
–
prevalence ranges from 10 to 100 per 1,000,000
peaks between 25 and 65 years
more frequent in females
strong genetic component (chance is 15 times
higher in a sibling of a patient)
– clustering in space and time (high-risk areas are
Northern Europe and North America)
Multiple Sclerosis:
Mechanism of Demyelination
 Role of immune system (suppressor T-cells)?
 Viral infection?
 Macrophages and mononuclear cells can strip
away myelin.
Multiple Sclerosis: Clinical Features
(Depending on Which Tract Is Affected)
Optic nerve:
 Sudden onset of blurred vision
 Dull ache in the eye
 Impaired acuity (rarely blindness)
Olfactory and auditory nerves: unilateral
deafness
Multiple Sclerosis: Clinical Features
(Depending on Which Tract Is Affected)
Brain stem pathways:
 Impairment of balance
 Intentional tremor
 Discoordination of limbs
 Dysarthria
 Facial weakness and numbness
 Unilateral ophthalmoplegia
Multiple Sclerosis: Clinical Features
(Depending on Which Tract Is Affected)
Spinal cord:
 Commonly high in posterior columns
 Tingling in hands and arms
 Discoordination (if spindle afferents are affected)
 Instability of stance (if lower limbs are affected)
Pyramidal tract:
 Heaviness
 Dragging of legs
 Weakness, even acute paraplegia
 Spasticity
Symptoms and Signs
of Multiple Sclerosis
Involved Structure
%
Posterior column
40
Pyramidal tract
37
Brain stem
30
Optic nerve
23
“Cerebellar”
17
Fatigue in Multiple Sclerosis
 Viewed as a very different feeling from
generic fatigue
 Disproportionate to the amount of effort
 Debilitating
 Loss of force has a clear central component
 Apparent neural component in the fatigue
Other Features
of Multiple Sclerosis
 Loss of control of bladder (urine retention)
 Transient dysarthria or ataxia
 Epilepsy
 Mental changes (such as euphoria, depression,
social disinhibition, and impaired memory)
Multiple Sclerosis: Lab Findings
 Delayed evoked potentials
 MRI can show plaques on affected tracts
Treatment of Multiple Sclerosis
 Spontaneous improvements are typical
 Hormone therapy (corticotropine, prednisolone)
 Modification of diet (polyunsaturated fatty acids)
 Hyperbaric oxygenation
 Immunosuppressive treatment
 Antispastic treatment
Prognosis for Multiple Sclerosis
 Very uncertain
 First episode may be followed by 20 years of no
symptoms, and then MS strikes again
 Older persons and males do worse
 Average duration: 25 to 30 years
 Average rate of clinical relapse: 1 per 2 years