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Spasticity
Management with a Focus on Rehabilitation
Spasticity has many causes and
Konstantina Petropoulou, MD, PhD
courses, so timing of therapy is
Member, International Neuromodulation Society
Head of 2nd PRM Department important
National Rehabilitation Center
Athens, Greece

Either injury to the brain or spinal cord can cause spasticity. The overactivity and expressions of generalized movement
condition develops gradually, reaching its maximum extent disorder. Their manifestation is sudden, unforeseeable, and
long after the initial injury occurs. Spasticity can cause pain and characterized by intense symptoms. The negative
abnormal posture, as well as difficulty with movement, self- phenomena are ‘‘phenomena of absence’’ that reflect an
care, and other activities of daily living. inability to move voluntarily (i.e. muscle hypoactivity), resist
treatment, and result in a more severe neurological disorder.
In spasticity, like a car with faulty brakes, nerves that control (3)
muscle tone and motor control no longer exert the same level
of inhibition that normally flows from the brainstem. As a Table 1 describes the positive and negative aspects of upper
result, muscles become hyperactive and reflexes are motor neurone Syndrome (UMNS).
exaggerated.
TABLE 1
Spasticity often occurs following spinal cord injury. Other The positive and negative findings of upper motor neuron
causes include stroke, traumatic brain injury, or multiple syndrome (UMNS)
sclerosis (MS). (1)
Positive findings Negative findings
In recent years, this medical classification has been Spasticity Loss of dexterity
systematically studied regarding its pathophysiological Spastic dystonia Atrophy
mechanism, the onset time after the injury, the severity of Dystonia Loss of coordination
occurrence, the impact on the individual's functioning and Clonus Loss of voluntary movement
therapeutic intervention. Athetosis Muscle weakness
Primary reflexes Fatigue
Following injury to the brain or spinal cord, a variety of clinical
Babinkski sign
manifestations may appear that are described as negative or
Rigidity
positive evidence of damage to the upper motor neuron. (2)
Synergias
An upper motor neuron (UMN) lesion is characterized by both Co-contractions
these positive and negative phenomena (Table 1), which differ Synkinesias
in their pathophysiological basis and respond variably to Associated contractions
treatment. The positive phenomena are ‘‘phenomena of Myelic automatisms
presence’’ of involuntary focal or generalized muscle

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Spasticity can be regarded as one of the positive features of nervous system (CNS) result in loss of descending
the upper motor neuron syndrome and should not be inhibitory commands, and in abnormal impulses. This
confused with other positive features like clonus, automatic disordered activity arises at several points along the
movement, etc. Every manifestation of upper motor neuron nervous system’s stretch reflex pathway. With loss of
syndrome may be independent of another finding of UNMS. descending inhibitory (reticulospinal) influences, there is
(4) exaggerated excitability of dynamic gamma neurons and
alpha motor neurons. Other spinal tracts such as the
Since there are many causes and courses for development of vestibulospinal and rubrospinal tracts become more active.
the disease, to provide a patient with the right treatment at Damage at more that one point in the central nervous
the right time, the medical provider will examine several system can lead to spasticity; essentially, spasticity can
things: (a) The nature of the spasticity, (b) how it differs result from injury to the cortex, basal ganglia, thalamus,
from other muscle tone disorders, (c) its development brainstem, cerebellum, central white matter, or spinal
related to the site and degree of injury, (d) its changes over cord. (8)
time, (e) its course throughout the day and during sleep, (f)
the presence of other symptoms such as pain, and (g) how Spasticity is not a static phenomenon but changes
the intensity changes due to touch or pressure, such as continuously throughout the day, even during sleep,
stroking a foot or having a full bladder. depending on the presence of pain or other irritants such
as inflammation, urinary stones, or infection, as well as
Spasticity Definition and Specific Traits general factors such as emotional states or a woman’s
menstrual period.
The definition of spasticity has varied over time based on
developments in laboratory and clinical investigations. Muscle overactivity can go beyond spasticity. One example
is upper motor neurone (UMN) syndrome, where spasticity
First, spasticity was described by neurologist James W. is present along with problems in normal movement,
Lance, MD in 1980 as a motor disorder with increased posture, and balance. The movement problems may
muscle tone and involuntary jerking of tendons (the flexible include repeated rhythmic contractions (clonus); excessive
cords that connect joints). In his words, "Spasticity is a muscle tone at rest that can lead to deformed joints and
motor disorder characterized by a velocity-dependent postures (spastic dystonia); exaggerated tendon reflexes;
increase in tonic stretch reflexes (muscle tone) with abnormal toe extension in response to touch; and muscle
exaggerated tendon jerks, resulting from hyper-excitability spasms. (9)
of the stretch reflex, as one component of the upper motor
neurone syndrome." (5) In its own right, spasticity is a chronic condition defined as
“disordered sensory-motor control, resulting from an
Nine years later, Robert R. Young, MD introduced the term upper motor neuron lesion, presenting as intermittent or
‘‘spastic paresis,’’ which includes weakness, loss of dexterity, sustained involuntary activation of muscles” with postural
and trouble controlling muscles. He termed it "a motor limb changes. (10)
disorder characterised by a velocity dependent increase in
tonic stretch reflexes that results from abnormal intra-spinal Even though spasticity should not be confused with
processing of primary afferent input". (6) movements that occur in upper motor neurone syndrome,
such as clonus, their presence interferes with attempts to
The European working group EUSPASM defined spasticity complete a normal motion. During a voluntary movement,
as “disordered sensorimotor control resulting from an upper unwanted spontaneous movements often appear, such as
motor neurone lesion, presenting as intermittent or spasmodic flexing or extending of a limb, muscle stiffness,
sustained involuntary activation of muscles.” (7) exaggerated movement, an unintended motion, and/or
associated reactions. These movements are stereotypical,
Since spasticity has sensory and motor aspects, the massive and irregular with no functional importance.
condition is a “sensorimotor” phenomenon in which
automatic movements appear in response to sensory input. As spasticity develops or increases, these “immature”
Muscle activity becomes overactive as the existing passive motor patterns tend to become activated, especially when
muscle stretch increases velocity. Changes occurring in the a patient attempts to move, and they negatively affect
spinal cord also play a role. Diffuse injuries in the central normal movement, posture, and torso balance.

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In injury to the central nervous system, there is a Spastic Dystonia
combination of involuntary muscle overactivity, i.e.,
“spasticity”, and the emergence of immature movements In contrast to what has been termed pure spasticity, when
leading to the so-called “pathological motor syndrome.” muscles at rest are overactive without any triggering factor,
parts of the body assume abnormal positions, which are a
Pure spasticity may be seen when an arm or leg appears to major cause of disfigurement and social handicap. (15) This
“catch” momentarily when a relaxed limb is quickly moved – condition was first described as “spastic dystonia” in the
there will be a stiffening and then relaxation so the motion 1960s by neurologist Derek Denny-Brown, MB, ChB. (16)
can be completed. Early in recovery from an injury to the
central nervous system, this temporary “catching” symptom In time, during spastic dystonia, there are changes in muscle
may appear as muscles gain tone and move from being composition, so the muscle becomes shortened and the
flaccid to spastic. The degree of spasticity is usually mild, range of motion limited. Muscles may reach a state of
and full range of motion is retained. (11) permanent contraction, or joints may become completely
immobile.
Stroke and Spasticity
Secondary Spasticity
In stroke, there are many abnormal pathological patterns in
the upper limb postures due to the spasticity of certain The shortening of soft tissues initiates chain reactions, such
muscle groups with respect to other muscle groups. as triggering a rhythmic contraction during walking, so the
In the initial stage of stroke, abnormal movements of the lower limbs bend or extend farther than necessary,
hemiplegic upper and lower limbs are formed, which are a disrupting normal gait. That occurrence is called “secondary
combination of muscles’ flexion and extension in the effort spasticity,” or hypertonia. It includes a nervous system
of movement. (12 –14) component triggered by spasticity, and a biomechanical
component arising from changes in the soft tissue.
When spasticity is present following a stroke, the abnormal
movements of the limbs are due to synergistic movements. The constant contraction of “spastic” muscles renders
They are characterized as primitive movements that opposing muscles inactive, and the latter grow weak due to
dominate reflex and voluntary effort. Their presence disuse.
interferes with coordinated voluntary movements such as
eating, dressing and walking. So, a vicious circle is created; in a typical example, when the
muscle that flexes the elbow is permanently contracted, the
In these cases, synergy patterns of muscle flexion in the arm inability to extend the elbow makes the opposing muscle
include scapular retraction, shoulder abduction and external become weak due to inactivity.
rotation, elbow flexion, forearm supination, and wrist and
finger flexion; in the leg, the patterns include hip flexion, Secondary spasticity in one or more muscles is the
adduction and external rotation, knee flexion, and ankle commonest condition we encounter in patients with
dorsiflexion. subacute spasticity – spasticity that lasts for a period of
time, rather than being short-lived or chronic.
Meanwhile, muscle extension synergy patterns in the arm
include scapular protraction, shoulder adduction and Hypertonia can be treated either with an injection of
internal rotation, elbow extension, forearm pronation, and botulinum toxin to temporarily paralyze the spastic muscle,
wrist and finger flexion; in the leg, extension patterns or an operation to lengthen or transfer tendons. The
include hip extension, adduction and internal rotation, knee decision will depend on which of the two components
extension, ankle plantar flexion and inversion, and toe (spasticity or tendon shortening) is prevalent and to what
flexion. degree. The coexistence of spasticity, either local or
generalized, must be taken into account. Usually the
The most common pattern in stroke patients is the “typical spasticity must be managed first.
arm posture” with characteristic antigravity postural
patterns with shoulder adduction, elbow and wrist flexion, As an example, a person who can flex their ankle up when
and the “typical leg posture” with hip adduction, knee the knee is bent, but not when the leg is straightened, will
extension, ankle plantar flexion, and foot inversion. be suspected of having spasticity in gastrocnemius muscles

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at the back of the shin. The problem is due to shrinkage of Co-contraction No co-contraction
the Achilles tendon.
Possible coexistence Possible coexistence
The Clinical Evaluation of Spasticity with extrapyramidal with peripheral nervous
damage system damage
The clinical signs of “spasticity” vary according to the injury
type (sudden or progressive), site and extent of lesion (brain Regional or focal Generalised spasticity
or spinal cord), and whether the spinal cord injury is spasticity
complete or incomplete.

In localized brain injury, such as stroke, or an incomplete Another important factor is duration of the condition. This is
spinal cord injury, spasticity creates varying degrees of because repeated abnormal movement over time leads to
excess tone or stiffness in different muscles. The opposing, the development of permanent contractions in adjacent
unaffected muscles also influence the position of the joint. normal muscles (dystonia). Normal muscles become
Taken together, those factors increase the risk the joint will involved in order to balance the body out in a motion that is
become deformed. safe, fast, and acceptable in appearance. (For instance,
when spasticity causes “tiptoe” walking, the quadriceps
In contrast, when the brain injury is diffuse or the spinal cord muscle in the thigh may be continually flexed as a result).
injury is complete, spasticity is much more even throughout
the body, causing relatively uniform muscle tone. There are four stages of clinical examination.

At the clinical level, there are similarities but also significant Stage 1: The clinician will note posture and motion as the
differences in the expression of spasticity due to whether patient enters the examination room, sits, and lies down.
the injury is complete or incomplete, whether sound Any muscle atrophy (weakness from disuse) and muscle
antagonist muscles are involved during the execution of a spasms will be noted.
movement, whether abnormal movement patterns are
present or absent, and whether there is any coexistent Stage 2: While the patient lies down, the clinician will test
damage of the peripheral nervous system or the the range of joint motion; note the degree of spasticity;
extrapyramidal system. observe the patient’s active movement; and test reflexes.
Motor control and muscle tone are noted.
Table 2 shows the differences in spasticity after a brain
lesion and after damage to the spinal cord, respectively. Stage 3: While the patient sits, the clinician will test upper-
body motor skills.
TABLE 2
Stage 4: Body balance is checked while the patient is in an
Clinical findings in Clinical findings in upright position and while the patient walks for a short and
spastic paralysis of spastic paralysis of longer distance. Whether the patient tires or not is
cerebral origin spinal origin considered of major importance.
Presence of spasticity Spinal shock. Late
very soon after injury appearance of Timing and Type of Treatment
spasticity
It is important to address the issue of proper timing of
Poor control of head and Massive automatic therapy to manage spasticity.
body movements – movements. Myelic
abnormal postures automatisms Early intervention with medication taken by mouth (oral
antispasm compounds baclofen and tizanidine or
Abnormal ‘‘models’’ of Diffuse distribution of dantrolene) is the method of choice. (17, 18)
movements. Presence of spasticity
primitive reflexes. Spasticity that is centered on one area or a region of the
Synergies and associated body may respond to treatment with botulinum toxin type A
reaction injected into stiff muscles to temporarily block the
contraction. This should be started early after spasticity
occurs and before soft tissues begin to shrink. (19, 20)

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At a later stage, and even at the chronic stage when A patient’s condition may move through several stages
abnormal motor patterns are established (such as the typical following an injury; the stages of spontaneous neurological
arm posture of an immobile upper limb), a medical provider “recovery” have been described for both cerebral and spinal
can inject botulinum toxin in selective “key muscles” to cord injuries, including transition from a flaccid to spastic
modify movements that amplify the disorder. (22) phase.

Botulinum toxin injections can be repeated after three Seven stages of recovery were described by the Swedish
months or more, as long as the injections serve a physical therapist Signe Brunnstrom in patients who had
predetermined goal each time. (23, 24) stroke-induced loss of movement on one side. In her model,
early spasticity management begins during the second
Repeated injections of the botulinum toxin type A, appear to stage, which is marked by several factors: “Spasticity
be safe for the patient if all the injection rules are appears. Basic synergy patterns appear. Minimal voluntary
maintained and the intervals between the new injection is movements may be present.” (29)
extended beyond three months (25)
In complete traumatic injury of the spinal cord, the
The time window (the time between the injury and the transition from spinal shock to spasticity includes four
beginning of spasticity treatment) and the time plateau stages, described by J. F. Ditunno, Jr., MD. Spasticity
(when the treatment will end) will be considered. develops during the 4th stage, 1-12 months after the injury,
when early management of spasticity will also begin. (30)
If spasticity throughout the body does not respond to
medication taken by mouth, or too many muscle groups are Any delays in treating the “spastic syndrome” create
involved to safely use botulinum toxin injection, then an problematic motor patterns as the brain and spinal cord
implanted catheter and pump are used to deliver baclofen to respond to an injury, thus increasing rehabilitation time and
the spinal cord. The medication is infused into the minimizing end results. The response could be called
intrathecal space around the spinal cord, so the treatment is maladaptive and pathological, since it creates problems that
called intrathecal baclofen or ITB. form the basis of a health condition.

ITB is a long-term treatment that offers continuous or Spasticity Treatment and Rehabilitation
programmable administration of medication to reduce
spasticity, especially in spinal injury and MS patients. Neurorehabilitation comprises four main categories of
spasticity management targets:
Several assessments precede a final pump implantation. For
instance, the patient may receive an injection (bolus test) in The first category involves nursing care: (a) Preventing or
the lower back, or be fitted with a temporary drug delivery treating deformation contractures, (b) preventing or
device. In the following 3-4 hours, the initial effectiveness treating a tendency to slump over, (c) proper positioning of
will be noted. The usually recommended first test dose is 50 the body on the bed/wheelchair, (d) easy catheterization of
micrograms in adults, with a maximum dose of 150 the bladder, (e) easy fitting of mechanical aids, such as a
micrograms that should be reached after three days. brace, (f) facilitating caregiver work, (g) pain relief, and (h)
improving sleep.
While it has been standard practice to wait a year after injury
for a pump to be implanted, there are cases when The second category centers on improving movement: (a)
implantation is recommended earlier, if advantages The unmasking of voluntary movements previously covered
outweigh disadvantages. (26) by significant spasticity in cases of incomplete lesions, (b)
accelerating the “spontaneous” recovery process, (c)
For example, for an incomplete spinal cord injury in which modifying the “immature” motor pattern, (d) using new
significant spasticity limits recovery of voluntary movement, recovery techniques to guide and encourage retraining of
waiting may have the adverse effect of delaying physical existing neural circuits, e.g. such as robotic, mechanized
therapy rehabilitation while other contractures develop. (27) aids, and (e) a new functional pattern in moving and
walking.
The time of intervention cannot be absolute, as it depends
on the patient’s clinical condition and overall therapeutic The third category includes daily life activities: transfers,
plan. (28) getting around, dressing, personal hygiene, driving, etc.

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living, and (b) social and professional reintegration. (18) methodological considerations in the measurement of
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