Pathophysiology, Functional Implications
and Management of Spasticity in Stroke – A
review
Akosile, C. O. , Fabunmi, A.A.1 2
Department of Medical Rehabilitation, Faculty of Health Sciences and Technology, Nnamdi Azikiwe University,1
Awka, Nnewi Campus, Nnewi, Anambra State
Department of Physiotherapy, College of Medicine, University of Ibadan and University College Hospital, Ibadan2
Correspondence
Dr. C.O. Akosile, Department of Medican Rehabilitation, Faculty of Health Sciences and Technology, Nnamdi
Azikiwe University, Awka, Nnewi Campus, Nnewi, Anambra State, Nigeria • E-mail coakosile@yahoo.com
SUMMARY
The management of spasticity in stroke requires a multidisciplinary approach but more importantly, an
understanding of the pathophysiology of its consequences. This paper reviews different definitions from
neurophysiology and medical literature which try to place spasticity in stroke in its proper context and describes
the current understanding of its pathophysiology and resultant functional implications. It also highlights the
current medical, surgical and physical therapy available for its management. It seems spasticity in stroke is best
managed using a combination of physiotherapy and Botulinum Toxin- Type A injection, as this is the current
trend in research and practice.
KEY WORDS: Spasticity, stroke
INTRODUCTION
Spasticity is a major cause of disability in stroke survivors,
causing pain, significant functional problems and likely to
lead to complications such as muscle contracture if
untreated or badly treated (Barnes, 2001). The term
spasticity is used synonymously in medical and physical
therapy literature to refer to both the severe hypertonus
emerging immediately after a head injury and the slowly-
evolving hypertonus following a more focal lesion-like
stroke. It has been defined as a motor disorder
characterised by velocity-dependent increase in tonic
stretch reflexes (muscle tone) with exaggerated tendon
jerks, resulting from the hyperexcitability of the stretch
reflex (Brown, 1994; Ivanhoe and Reistetter, 2004).
Bakhta (2000) opined that while this definition is
useful for diagnostic purposes, it is rather restrictive in
terms of understanding and managing the consequence of
inappropriate muscle activity found after stroke. It could
not account for the abnormal posture and mass pattern
seen or the inappropriate muscle co-contraction and
involuntary limb movement associated with exaggerated
cutaneous reflexes or efforts (associated reactions), in
addition to stretch reflex hyperexcitability which ought to
be considered together for success in antispasticity
treatment.
True spasticity is apparent when the relaxed spastic
muscle is stretched (Rothwell, 1994) and is dependent upon
afferent information from feedback following movement
of the stretched muscle (Young, 1994). On the other hand,
the abnormal posture which is a consequence of increased
tonic muscle contraction in the absence of movement is
referred to as spastic dystonia (Young, 1994). This is
exemplified by the abnormal posture of upper limb flexion
and lower limb extension seen in hemiplegia (Young,
1994). It is considered as a form of sustained efferent
muscular hyperactivity, dependent upon continuous
supraspinal drive to the alpha motor neurone (Sheean,
1998).
AJPARS Vol. 3, No. 1, June 2011, pp. 6-12 • doi: http://dx.doi.org/10.4314/ajprs.v3i1.26
Pathophysiology, Functional Implications and Management of Spasticity in Stroke
PATHOPHYSIOLOGY OF SPASTICITY
Neural Components
The balance interaction between parapyramidal tracts
arising in the brainstem is responsible for the supraspinal
control of muscle tone. The major tracts are the dorsal
reticulospinal tract (DRT), the medial reticulospinal tract
(MRT), and the vestibulospinal tract (VST), which are
descending pathways synapsing upon the inter-neural
network within the spinal cord to exert this influence
(Edward, 2002). The DRT has an inhibitory influence,
while the MRT and VST have a facilitatory influence on
extensor tone. The three together inhibit flexor reflex
afferent responsible for flexor spasm (Brown, 1994;
Sheean, 1998).
The DRT, unlike the others, is under direct cortical
control from the premotor and supplementary motor areas
via corticoreticular neurones descending through the
internal capsule (Brown, 1994). In stroke, there is damage
to this cortical drive due to internal capsule lesion which
reduces the activity of the DRT such that the facilitatory
effects of MRT and VST become relatively unopposed
(Sheean, 1998; Edward, 2002). These impaired modulation
of monosynaptic input from primary afferent (Ia) fibres
(segmental myotactic reflex), polysynaptic afferent input
from cutaneous receptors and golgi tendon organs
contribute to alpha motor neurone hyperexcitability of
flexor muscles in the upper limb and extensor muscles in
the lower limb.
Post-stroke patients often demonstrate an initial
flaccidity or hypertonia for a variable period of time before
the emergence of hypertonia and excess reflex activity.
During this period of shock, the muscles may become
toneless and areflexic (Edward, 2002). The delayed
appearance of hypertonus is presumed to involve some
functional or structural rearrangement within the central
nervous system (CNS) (Edward, 2002). These are plastic
changes, for which increased receptor activity and
collateral sprouting have been implicated.
Nociceptive and motor pathways have also been
reported to have considerable influence on each other,
emphasizing the clinical importance of pain management
in treating spasticity (Barnes, 2001).
Non-neural Components
Some authors have suggested that an increase in the
mechanical stiffness of the muscle is responsible for spastic
hypertonia (Dietz, 1992; Brown 1994; Ada et al, 1998). It is
thought that the stiffness is mediated by permanent
structural changes in the mechanical properties of muscle
or connective tissues which may be variable in character
(Katz and Rymer, 1989; Carey and Burghardt, 1993). It is
important to note that this mechanical contribution to
hypertonia would not arise without the damage to the
central nervous system (CNS), producing the reduced
activity and/or stereotypical postures associated with upper
motor neurone lesions (Brown, 1994).
Disuse atrophy is another phenomenon occurring in
patients with hypertonus, even in the presence of sustained
muscle activity. This is due to the disruption of central and
segmental synaptic drive onto spinal inter-neurones
(Rothwell, 1994; Gordon and Mao, 1994). Patients who are
unable to sustain muscle activity against gravity will be
unable to maintain the muscle characteristics associated
with postural control. Atrophy of the slow twitch fibres
responsible for function then results with a consequent
increase in the dominance of fast twitch fibres (Edward,
2002). In stroke and in the presence of hypertonia, there
can be a gradual change in fibre-type composition with
increased numbers of slow muscle fibres (Dietz, 1992),
which may be the result of a muscle fibre transformation
following continuous activity in hypertonus (Dattola et al,
1993). Slow-twitch fibres develop larger forces at lower
firing rates and are recruited first. An increase in their
proportion may thus contribute to a gradual increase in
hypertonia. This selective atrophy of fast twitch muscle
fibres is also assumed to contribute to a reduction in
voluntary power in hemiparesis (Vrbova et al., 1995).
F U N C T I O N A L I M P L I C A T I O N O F
SPASTICITY
Certain pathological activities associated with hypertonus
will help in discussing the functional implication of
spasticity. These are:
Positive Support Reaction: This rigid extension of the leg
with subsequent inability to balance with normal alignment
of the trunk and pelvis (Edward, 2002) is thought to be due
to a proprioceptive stimulus evoked by the stretch of the
intrinsic muscle of the foot and an exteroceptive stimulus
evoked by the contact of the pad of the foot with the
ground (Bobath, 1990). Clinically, plantarflexor hypertonia
associated with the inversion of the foot is a primary
feature of this reaction. There is also a shortening of the
intrinsic foot musculature due to the inability to transfer
weight across the full surface of the foot and loss of range
in the plantar fascia. Shortening of the tricep surae may
also result due to the inability to attain a plantigrade
during the stance phase of walking, which further
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Akosile, Fabunmi
exacerbates the inability to transfer weight or to adapt to
irregularities in ground surface (Dietz, 1992).
Consequently, the post-stroke individual tries to
maintain balance by a compensatory hip flexion with a
retraction of the pelvis, due to the backward displacement
of weight by the pressure from the ball of the foot
(Edward, 2002). The knee extension obtained with this is
not due to appropriate quadriceps activity as the
quadriceps may even be wasting. Hyperextension of the
knee may occur due to the abnormal alignment of the
pelvis over the foot, an impaired interaction between the
hamstrings and quadriceps muscle groups and a shortening
of the gastrocnemius (Edward, 2002). The hip flexors,
adductors and medial rotators may be shortened as a result
of the flexed, retracted position of the hip and pelvis,
invariably producing a mechanical obstruction to correct
hip alignment in the stance phase (Edward, 2002). The
knee is prevented from being released by the pressure
exerted by the foot pushing into plantarflexion. The
extended leg is hitched forward in order to step through in
moving the foot away from the floor (Dietz, 1992). This
compensatory strategy coupled with associated flexion
reaction of the upper limb is responsible for the typical
hemiplegic gait. The described lower limb activity demands
greater effort, particularly from the latissimus dorsi,
resulting in the shortening of the trunk side flexors and
hypertonicity of the upper limb flexors (Dvir et al, 1996).
The ability to stand up and sit down is also affected.
The stiff extended leg prevents the post-stroke individual
from standing, pushing him back into the chair. The
inability to flex the knee also makes the attempt at sitting
largely unsuccessful and the individual ends up falling into
the chair. Hemiplegics tend to stand up and sit down on
their sound leg due to the inability to support their weight
on their paretic leg (Edward, 2002).
Complications like contracture at the ankle affects
function. For example, an equinus deformity will interfere
with donning footwear and the use of a wheelchair
footplate.
Associated Reaction: These are thought to be pathological
movements indicating a potential for hypertonus
development or accentuating prevailing spastic synergy
(Bobath, 1990). They are initiated with attempted
movement or at the preparatory stage of movement
(Dickstein et al, 1995) and may also occur with involuntary
action such as yawning, coughing and sneezing or when
dysphasic patients try to communicate (Edward, 2002). The
appearance and severity of the associated reactions with
hypertonia may be due to underlying low tone or lack of
stability of proximal key points. Sustained associated
reactions may lead to decreasing functional level in that
movement. For example, repeated flexion of the arm may
lead to a gradual loss of range and ultimately contracture
(Davies, 1990; Dvir and Panturin, 1993). The involuntary
elbow flexion (accompanying the stepping through attempt
at the lower limb in some patients) is thought to interfere
with walking and standing balance (Bhakta, 2000).
Inappropriate co-activation of agonist and antagonist
muscles: This can impede normal limb movement and
function. For example, the coactivation of the triceps and
biceps may affect placement function, while the co-
contraction of the forearm flexor and extensor muscles
may prevent voluntary finger extension and relaxation of
grip (Bhakta, 2000).
Inappropriate muscular activity: This may lead to painful
deformity and interference with function. For example,
painful toe flexion and difficulty with walking and running
may result from the inappropriate activity of the intrinsic
foot muscles and long toe flexors. Extensor hallucis longus
overactivity may cause involuntary big toe hyperextension
and difficulty in donning footwear (Bhakta, 2000).
MEDICAL MANAGEMENT OF SPASTICITY
The available drugs for spasticity management are either
systemic or focal in the nature of their administration.
They are:
Oral baclofen: The most widely-used anti-spastic agent. It
is a structural analogue of gamma-amino butyric acid
(GABA) and binds at the Gaba B-receptor. Its
recommended dosage is around 40 -100mg daily, given in
divided doses due to its relatively short half-life. Significant
side effects include drowsiness, fatigability and muscle
weakness (even of the unaffected muscles), which may
increase disability. The side effects limit the role of oral
baclofen in stroke and it is not advisable as a first line anti-
spasticity (Bhakta, 2000; Barnes, 2001). Headache, ataxia,
insomnia and sudden withdrawal, seizures, hallucinations
and psychosis are other side effects (Terrence and Fromn,
1981).
Tizanidine: A central a-2 adrenergic agonist with similar
side effects (drowsiness, fatigability and muscle weakness)
to baclofen, though to a lower extent (Barnes, 2001). Its
effects are thought to be mediated via neurones in the
locus ceruleons and inhibitory spinal inter-neorones. It
appears that tizanidine also has an anti-nociceptive effect.
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Pathophysiology, Functional Implications and Management of Spasticity in Stroke
It is however not recommended for routine use in stroke
due to limited evidence of its effectiveness (Bhakta, 2000).
Monitoring of liver function is essential as it leads to
incidence of abnormal liver function. (Barnes, 2001).
Dantrolen Sodium: This acts peripherally and probably
suppresses the release of calcium ions from the
sarcoplasmic reticulum producing a dissociation of
excitation/ contraction and coupling. Side effects are
similar to those of baclofen. It also causes abnormality of
liver function.
Diazepam: An effective anti-spastic agent with very limited
clinical implications. Anti-spastic dosages produce
significant drowsiness and fatigue. Diazepam affects
walking and increases the risk of cognitive dysfunction and
should not be used for the routine management of
spasticity in stroke (Bhakta, 2000; Barnes, 2001).
FOCAL TREATMENT
Intrathecal Baclofen Infusion: This is done via pumps and
is effective in refractory lower limb spasticity where several
muscle groups in both legs are affected (Bhakta, 2000).
There is a need to exercise caution in its use in stroke due
to the risk of weakening muscles on the normal side.
Meythaler et al (1999) reported tone reduction on the
affected side and muscle strength preservation on the
normal side with continuous intrathecal baclofen infusion.
Francisco and Boake (2003) also reported improvement in
subjects’ walking speed, functional mobility rating, and
spasticity with 9 months of combined physical therapy and
intrathecal baclofen.
Nerve Blocks: This refers to the blockade of percutaneous
nerves and/ or motor points using phenol or alcohol.
Phenol nerve blocks have been found effective in managing
abnormal arm and leg posture in hemiparesis over 6
months. In equinovarous, deformity and inappropriate
knee flexion, lasting from a few months to several years
have also been reported (Petrilla and Knoploch, 1988). The
risk of painful and persistent dysaesthesia following the
injection of mixed motor and sensory nerves exists (Skeil
and Barnes, 1994). Phenol nerve block is no longer
recommended, though the risk of sensory disturbance may
be reduced by phenol motor point block ((Bhakta, 2000;
Skeil and Barnes, 1994). Fifty per cent alcohol has been
used as an alternative to phenol but has been less effective.
Botulinum Toxin Type A (BT-A): Injection of BT-A into
spastic muscles produced chemodenervation by preventing
the release of acetylcholine at the neuromuscular junction.
BT-A acts peripherally to reduce muscle contraction
caused by the hyperexcitable alpha motor neuron pool.
The relaxation period lasts about 3 months with loss of
effects occurring through axonal sprouting proximal to the
affected nerve terminal and the formation of
neuromuscular junctions (Bhakta, 2000). The advantage of
BT-A over other anti-spasticity drug treatments includes
the ability to target specific muscle groups, lack of sensory
disturbance, patient tolerability, and ease of
administration. Muscles have to be properly chosen and
BT-A doses individualised for an optimal functional
outcome (Cardoso et al, 2007). A medium BT-A dosage
(320 UI spread over 2-5 muscles) have been found to be
both safe and effective in producing long-lasting
improvement of spastic foot dysfunction in post-stroke
individuals (Mancini et al, 2005). Different authors have
advocated combining BT-A injection with physical therapy
modalities such as exercise therapy, functional
neuromuscular stimulation or robotic training for a more
potent effect (Bhakta 2000; Cardoso et al, 2007; Levy et al,
2007).
SURGICAL TREATMENT
This includes procedures that interfere with the neuronal
pathways and procedures that correct musculoskeletal
deformity (Bhakta, 2000). Selective tibial neurotomy
improves a range of active ankle dorsiflexion in patients
with calf spasticity. Surgical intervention can be divided
into peripheral ablative procedures such as rhizotomy or
peripheral neurotomy or more central ablative procedures
such as cordectomy, myelotomy, and stereotactic
procedures. Other techniques include cerebellar or spinal
stimulators (Smyth and Peacock, 2000; Barnes, 2001).
Surgical sectioning of tendons and muscles combined with
post-operative serial splintage is done for patients with
persistent deformity (Achilles tendon lengthening for
equines deformity at the ankle), functional lengthening of
forearm finger flexors, elbow flexor release and tenodesis
facilitate arm placement and grip in patients with a
potential for functional voluntary movement.
PHYSIOTHERAPY TREATMENT
Physiotherapy treatments of hypertonus are based on many
assumptions and beliefs which are largely unsubstantiated
(Edward, 2002). The general aim however is to improve
motor performance and functional ability (Bhakta, 2000).
The treatments target both the neural and non-neural
components of spasticity. Functionally-based therapies
integrate the repetition of everyday tasks. Basically,
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Akosile, Fabunmi
physiotherapy modalities attempt to normalize the
spasticity as much as possible through retraining,
reproducing, patterning or positioning the muscles or
groups of muscles to mimic normal movements. These
techniques attempt to bring the muscle to a state of normal
stretch without causing the stretch reflex to react
abnormally or co-contraction of agonist muscles.
Contentious issues in what should be the major
therapy focus include whether weakness is apparent or
real, aerobic or resisted exercises are beneficial or
deleterious in spastic hemiplegics and if tone should be
compromised for function or vice-versa (Bhakta, 2000).
Reports from different authors have shown that muscle
weakness truly exists in upper motor neurone lesions with
other features like loss of dexterity, muscle atrophy and
potential for contracture development (Rothwell, 1994;
Gordon and Mao, 1994; Young, 1994, Edward 2002)