Abstract
The spinal cord injured population is a group that has a high incidence of spasticity. Though their spasms can occur spontaneously, they are often aggravated by internal and external stimuli. Functional activities, including those elicited by FES, can therefore be affected. This paper reports on a paraplegic that uses FES for standing, but whose quality of stand is complicated by an interesting pattern of flexor spasms. These occur after a period of spasm free standing and repeat at regular intervals, getting progressively worse. Whether this effect is dependent upon the stimulation, as EMG recordings suggest, but as yet not proven, or upon the varied and complex nature of spasticity, it conjures up issues both in identifying more robust controllers to deal with spasticity patterns and in selecting appropriate individuals.
1.
Introduction
Spasticity
has been defined as ‘a motor disorder characterised by a velocity dependent
increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks,
resulting from hyperexcitability of the stretch reflex, as one component of the
upper motor neuron syndrome’ [1]. From a clinical perspective, spasticity is an
important factor in the rehabilitation of patients with neurological conditions
and, if severe, can significantly affect the individual’s quality of life by
interfering with functional activities and behaviour. Spinal cord injured (SCI)
persons have a high incidence of spasticity. Though they can occur spontaneously,
spasms are often aggravated by internal and external stimuli; such as an
infection, anxiety, temperature and touch. However, in our experience most SCI
individuals have an understanding of the triggers for their spasms.
Standing
is encouraged in paraplegics for physiological and psychological benefits and
can be used to reduce flexor tone and encourage extensor activity [2]. One
approach to assist in standing is electrical stimulation of the paralysed
quadriceps muscles thereby generating knee extension to allow weight bearing
through the legs. This technique has been successful, but to provide safe
standing issues around the maintenance of balance, including during spasms,
need to be addressed. Closed-loop controllers that respond to changes in the stand
have therefore been advocated (see [3]). We are also interested in the types of
disturbances that will be encountered.
This
paper reports on a paraplegic who has achieved competent FES-assisted standing,
but whose quality of stand is complicated by an interesting pattern of spasms.
Spasms occur at the beginning of each stand, but these soon diminish allowing a
spasm free stand. This in itself is not uncommon, because changes in muscle
lengths, such as in standing up, can initiate responses [4]. The interesting
observation is that within two minutes, flexor spasms occur that repeat at
regular intervals of several seconds and in the absence of any known noxious
stimuli. These spasms are found to get progressively worse and limit standing
times to just a few minutes. This paper discusses these observed patterns.
2.
Methods
2.1. Participant
Details
The
individual sustained a crush injury in 1994 resulting in a complete spinal cord
lesion (T10 right, T11 left). Following rehabilitation, he achieved competent
standing in calipers and in a standing frame, with minimal spasm activity on
sit-to-stand. In 1996 he received an implanted sacral root bladder stimulator
[5] – trapping bilateral anterior roots S2-S4 in intrathecal electrodes,
accompanied by a bilateral posterior rhizotomy of roots S2-S5. Immediately
following this procedure there was a marked increase in the severity of spasms
and the number of triggers. Their effect was to cause him to discontinue using
calipers. Baclofen is used to reduce lower limb and abdominal muscle spasms.
While
participating on a FES-assisted standing programme [6], he demonstrated the
ability to stand competently and to balance using a single arm for support.
However, during these stands he experiences a series of spasms that are remarkably
consistent. Following a period of approximately two minutes standing with no
spasms, hip and trunk flexion spasms subsequently occur, figure 1, and repeat
every 16 seconds.
Fig. 1; Standing in the
presence of flexor spasms
2.2. Measurement
Methods
The
approach taken to investigate the observed spastic patterns and their
implications to the biomechanics in standing has been to measure the kinematics
and reaction vectors, at the floor and handles, while recording EMG. During
each test, the individual stands on a pair of Kistler force plates (Kistler Instruments AG Winterthur,
Switzerland) and uses instrumented handles [7] for support. A dynamic position
measuring system, Selspot (Selspot
AB, Sweden), is used to record the individual’s posture in 3D space. Data is
sampled at 50 Hz and analysed using MATLAB
(The Math Works Inc, Natick, Mass., U.S.A.). EMG signals are recorded from
quadriceps, hamstrings, gastrocnemius and tibialis anterior, and sampled at 1
kHz.
3.
Results
Anecdotal
evidence from the participant suggests that he is aware of the impending spasm
before it has a resulting effect on his posture. This is supported by the video
record that illustrates him “bracing himself”, extending his elbows and taking
increased weight through his arms. In the periods between spasms, the arms are
only used for balance and carry a small force, estimated to be approximately
equal to the mass of the arms.
During
a spasm, figure 2, the reaction forces demonstrate the increased proportion of
the body weight (approximately 70%) taken through the arms. The ground reaction
vector, in this case, passes significantly behind the knee and in front of the
hip - both resulting in flexion moments. He attempts to correct this by
applying a lateral downward push to maintain standing and to assist in
correcting the hip flexion.
Fig.
2; Snapshot of biomechanical data during a spasm
Regarding
each occasion where the individual flexes at the waist as a single spasm, the
rhythmic nature has a period of approximately 16 seconds, figure 3. These
continue for the rest of stand. Between spasms, the knee and hip angles remain
relatively stable and the forces are taken again predominantly through the
legs. This supports the clinical observation that an upright standing posture
can be regained.
Fig.
3; Reaction forces and EMG recorded during FES-assisted standing
From
the EMG recordings, there is a clear increase in activity in non-stimulated
muscles, for example the hamstrings, for the duration of the clinically
observed spasm, figure 3. In the stimulated quadriceps muscle, EMG recordings
indicate a short latency reflex component that starts as the spasm is elicited,
but outlasts the clinically observed spasm, figure 4.
Fig.
4; M-wave and reflex in quadriceps for a single spasm.
4.
Discussion
This
individual demonstrates a peculiar result in his rhythmic pattern of flexor
spasms while standing. At present we cannot determine if the SARSI procedure had a direct effect on
the rhythmic pattern, or why it resulted in such a dramatic alteration in
spasms. An increase in spasms following SARSI
has been reported elsewhere [5], but these are not usually as severe as
reported here.
It is
not unusual for spasms to be generated in relation to noxious stimuli. With the
same individual, the same pattern of flexor spasms was observed while palpating
the metatarsal heads, an effect described elsewhere [4]; with S1 nociceptive
stimulation of the foot generating L5 knee flexor, L2 hip flexor and T10
abdominal muscle contraction in a paraplegic. It is possible that in standing
the same responses could be triggered by some stimulus, but from video the
spasm occurrence is not correlated with any observed change in posture. It is
also unusual that the spasms occur mid stand, after a minute or two of spasm free
standing, and have an inter-spasm interval of approximately 16 seconds. The
cause is not known, but the effect from applying a train of electrical impulses
to stimulate the muscle could be acting to influence remaining neural circuits.
From
an engineering perspective, these spasms present a difficulty in applying a
suitable controller to assist in standing. From clinical experience [6],
optimising a controller can be time-consuming and empirical, particularly in
the presence of complex and varied spasticity. Generally, spasms result in fast
transients in joint angles and using a controller to respond, by altering
stimulation levels, may initiate further spasms resulting in instability and
increased fatigue, particularly if the levels are caused to change too fast.
The design of clinically more robust controllers should therefore try and
accommodate for the often varied and complex nature of spasms and spasticity.
5.
Conclusion
It is
interesting to note that this individual continues to stand at home by FES. It
is unknown as to whether we can improve his quality of standing, but we
consider that an increased emphasis should be attached to identifying more
robust controllers to deal with spasms. This may however, be complicated by its
varied nature and complexity, raising issues not only in defining controllers,
but also in selecting appropriate individuals and neuroprostheses. In addition
and perhaps with this, a better understanding of the functional capacity of the
residual nervous system and the effects of stimulation upon it is required.
Acknowledgment
The
authors wish to thank the individual who participated during this investigation
and Drs Donaldson (University College London) and Cole (University of
Southampton) for their advice. Financial support was from the Wellcome Trust
and the U.K. Medical Research Council. Norton is supported by a UCL Graduate
School Research Scholarship.
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