Electrical Stimulation for Modulation of Spasticityin Hemiplegic and Spinal Cord Injury Subjects

Vittorio Alfieri, MD

Department of Physical Therapy and Rehabilitation, University of Milan, and General Hospital,Monza, Italy

KEY WORDS: electrical stimulation, hemiplegia, spas- tients. I applied the stimulation on the antagoniststicity, spinal cord injury. of the spastic muscles.

In 1977, after more than four years of experience,Since the early 1960s (and in the ensuing years), inI published the results of ES in 250 hemiplegic pa-Italy the application of electricity for human pathol-tients(1). ES was employed with the following aims:ogy was considered detrimental or very dangerousa) to inhibit the spastic muscles through reciprocal(except for some few particular cases, such as theinhibition; b) to counteract the atrophy by disuse;heart pacemaker). I began a bibliographic researchc) to preserve or, possibly, to regain the possibleon the subject in 1970.most correct sensation of the limb; and d) to supplyI was encouraged to pursue electrical stimulationfacilitating impulses to the inhibited muscles to give(ES) research because of my clinical experience thatback afferential balance of facilitation and inhibitionyear with a woman affected by a minor spastic rightto the neuromotor unit(5).hemiparesis who was under treatment in the hospi-

I observed that in cases in which ES was effectivetal where I was working. Her paretic hand was acci-in reducing spasticity, the effect became longer last-dentally shocked by a domestic electrical device ating after a certain number of applications. This num-her home. She told me that for about two days sheber was variable from case to case, requiring afelt her paretic hand was no longer ‘‘hard’’ but ‘‘moreminimum of 20 sessions to a maximum of 50 ses-movable’’.sions and sometimes more than 50. It was crucialThis fact induced me to think about the possiblethat the sessions were held every day and if possiblecauses of her response, and I concluded that hertwice a day. A cycle of ES was applied to each patientimprovement was linked in some way to reciprocalat least once every eight to ten months. Accordinginhibition. In 1972, when I became Head Physicianto my own experience, long-lasting reduction ofin the Rehabilitation Department of the main hospi-spasticity was possible in 30 to 65% of the patients.tal in Monza, I began to use ES on paretic or paralyticThis large variability is mainly due to the age andextremities of cerebral vascular accident (CVA) pa-general conditions of the patients. The best modula-tion of spasticity occurred in patients under 60 yearsAddress correspondence and reprint requests to Vittorio Alfieri, MD, via

Robecco 30, 20092 Cinisello-Balsamo, Milano, Italy. of age who were in good general health.This lecture was presented at the 5th Annual Conference of the Interna- Although there have been reports of successfultional Functional Electrical Stimulation Society, Aalborg University, Aalb-

modulation of spasticity by stimulating the spasticorg, Denmark, 18th–20th June 2000.

muscle to contract and by using a submotor intensityof stimulation over the dermatome corresponding

� 2001 International Neuromodulation Society, 1094–7159/00/$15.00/0Neuromodulation, Volume 4, Number 2, 2001 85–92 to the myotomal innervation of the spastic mus-

86 � ALFIERI

cle(2–6), I have applied ES to the antagonists of thespastic muscles and found this to be most successful.After careful location of the motor points, I userelatively small cutaneous electrodes (2.5 by 2.5, or4 � 4, or 4 � 6 cm) and square impulses between0.5 and 1 ms, at a frequency between 25 and 50 Hzwith a 1-s ramp-up and 0.5-s ramp down.

I suggest starting ES as soon as possible, two tothree weeks after CVA. The paralyzed muscles rap-idly become hypotrophic because of central andperipheral inhibition. For example, our data indicatethat flaccid shoulder muscles atrophy in up to 21%of the cases within one month after CVA in patients

Figure 1. The original MRI, Muscle Restraint Indicator, a firstover 60 years of age(7). Another reason to begin ESkind lever connected to a computer. This is endowed with aas soon as possible is to reduce the risk of retractionprogram suitable for giving in 1/100 degrees the shift in exten-

in ligaments, fasciae, tendons, and connective tis-sion of the wrist every 1/100 sec for 2 sec, and then every

sue. When these tissues develop an increased num- 3/100 sec for another 2 seconds. The movement is given byber of collagen crosslinks, they resist passive means of a load (not applied in the photograph) of 1 Nm.

elongation.The Ashworth scale is generally used to assess

is possible by means of a linear potentiometer of 5spasticity, but it is not objective and is exposed toKohms and a A/D converter transmitting the move-subjective influences by the examiner. In 1991 Iment data to an IBM PC. Each test was repeated threepresented at a Congress of the Italian section of thetimes. During each test the computer produced: a)International Society of Electrophysiological Kinesi-the times in hundredths of second and the averageology in Pisa a new instrumental measurement ofvalues of the angles with the standard deviation; b)spasticity developed in collaboration with Professora graphic representation of the movement curvesEvert Knutsson, Director of the Department of Clini-(Fig. 2); c) the time taken to reach the first peak;cal Neurophysiology, Karolinska Institute, Stock-and d) the velocity of the movement.holm University(8). We called the instrument,

‘‘Stretch Reflex Indicator’’, because the measure-ment was based upon a mechanical stretch of thespastic muscles. Later, we called it ‘‘Muscle RestraintIndicator’’ because the resistance of the muscles torapid elongation is due not only to spasticity butalso, and some times almost exclusively, to the al-terations of muscles, fasciae, ligaments, and otherstructures. The Muscle Restraint Indicator was aug-mented with surface electromyography, H reflex re-cruitment curves, and the Hmax/Mmax ratio.

The Muscle Restraint Indicator (Fig. 1), adaptedfor the upper limbs, is based upon a first kind lever(fulcrum is located between the resistance and thepower), setting the wrist in motion from flexion toextension by means of a drop load, to rapidly stretchthe flexor muscles of wrist and fingers. After manytests, I established the load to be Kg 2.5 and theradius of the pulley 41 mm, in order to give to the

Figure 2. Graphic representation of the rapid passive move-movement a load of 1Nm.ment from flexion to extension of a paretic patient. Bold line,

In this way it is possible to record the angles mean values in degrees of the movement; thin line, SD; ROMreached by the hand, the velocity, and the pattern 1, range of motion at first peak; ROM 2, range of motion at the

end of the test; VOM, velocity of motion to the first peak.of the movement every hundredth of a second. This

ES in Cerebral Vascular Accidents � 87

Figure 3 illustrates a summary of the course of In addition to spasticity, there are a number ofother sequelae of the loss of voluntary movementsspasticity in a young woman affected with left hemi-

plegia. ROM 1 refers to the initial range of motion that can be counteracted by electrically stimulatedmuscle contraction. These benefits may be realizedand ROM 2 refers to the range of motion at the

end of the test. The velocity of motion (VOM) is by the use of ES to control completely paralyzedmuscles or the use of ES to augment volitional con-represented for the initial measurement as is the

course of voluntary extension of the hand after 10 traction.It is well known that muscle contraction mobi-weeks of treatment.

Unfortunately not all the patients respond in the lizes a considerable amount of blood and lymph,thus preventing circulatory stasis, edema, and othersame way regarding spasticity. Figure 4 describes

the course of a 62-year-old, left hemiplegic patient functional, biochemical and histologic impairments.The heart stroke volume of a healthy adult, bothwho started with more severe spasticity. After more

than 24 weeks of treatment, there was little change sedentary and trained, is approximately 5 L/min.During maximal exercise, in a sedentary young man,in his spasticity, according to our measurements.

This man was older and more disabled than the stroke volume increases to 20–22 L, or an increaseof 4–4.5 times. In a young athlete, stroke volumeyoung woman described in Fig. 3.increases to 35–40 L, or an increase of 7–8 times.

Blood volume is distributed to the active organsin different proportions at rest and during exercise.At rest the muscles receive about one liter of oxygen-ated blood, or 20% of the stroke volume (9).

During exercise the stroke volume is differentiallydistributed according to the type of exercise, theambient conditions, and the level of fatigue. Theactive muscles receive the majority of the strokevolume during exercise, with approximately 88%going, at maximal effort, to the muscles, resultingin an increase in perfusion of 22 times greater thanat rest.

The contracting muscles exert a compressionforce on the blood vessels and there is a restrictionof blood flow at about 50% of maximal voluntary

Figure 3. Summary of the course of spasticity of a hemiplegiceffort. It is therefore the active contraction followedyoung woman. ES, electrical stimulation; PhTh, physical ther-by the relaxation that produces the muscle pump.apy.Without this muscle pump, the circulation of bloodand lymph is severely compromised. For example,exercise increases the oxidative capacity of the mito-chondrion fraction of the muscle by about 55% be-cause of the increase in mitochondrial enzymes(cytochrome C and suxinate-dehydrogenase), whichare the markers of mitochondrion respiratory chain.The active exercise stimulates the exocyanasis andglycogen synthetasis activities; increases muscle gly-cogen concentration; raises mitochondrion volume;and stimulates the activities of the mitochondrionmembrane components as well as the mitochon-drion respiratory enzymes.

It is therefore clear that the only mechanism ableto achieve the aforesaid aims in the healthy individ-Figure 4. Course of resistance to rapid elongation (spasticityual, and thus preserve muscle integrity and function,of flexor muscles of wrist and fingers in a patient with a high

grade of spasticity. is the active contraction of the muscle. In paralyzed

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or paretic muscles, electrical stimulation is the only nected with other cortical areas and going back toperipheral motoneurons along the pyramidal sys-available means of contracting the muscle, aug-

menting its contraction, and maintaining reasonable tem(16–18). The spino-cervical, spino-reticular,spino-cerebellar, and spino-thalamic tracts carry themuscle integrity for functional use.

Modulation of spasticity is the underlying theme afferent information. These group II proprioceptiveafferents are known as strong evocators of responsesto improving motor performance in patients with

central nervous system disorders such as stroke and from neurons in the motor cortex(19,20), and theirinfluence is more prevalent than the Ia spindle affer-spinal cord injury. For that reason it is worthwhile

to consider the physiologic basis for the improve- ents, which also reach the cortex but in a verylow measure. In 1979, Zarzecki and Asanuma(21)ment in spasticity after ES. When ES is applied to

the antagonists of the spastic muscles, inhibition is demonstrated that the group II afferent from boththe skin and the muscles of an anterior limb of anearly immediate and quite transient. This prompt

but fleeting inhibition is attributed to stimulation cat reach the motor cortex through a direct thalamo-motorcortical path.of the Ia fibers and may be extinguished by volitional

effort exerted by some parts of the body. In addition, So, it appears reasonable to think that this controlmechanism, the long loop transcortical reflex mech-it has been demonstrated by myself and others(10)

that in some cases the inhibition of spasticity be- anism, by Wiesendanger, has two main functions:a) to enhance conscious awareness of the sensationcomes long-lasting, including reduction of both the

stretch reflex and the tonic irradiation(11). We hy- of muscle contraction, of movement, and of thereciprocal position of the limb segments; b) to subtlypothesize that this very likely means that other pro-

cesses with more complex integration, besides the regulate the movement with modulation at the cor-tical level. This fine movement regulation impliesreciprocal inhibition, are primed by ES, and are able

to condition the start of a new stable inhibiting the presence of a significant amount of inhibitoryactivity.circuits.

If this hypothesis is true, as I think it is, particular Thus, it appears correct to hypothesize that thelong-lasting antispastic effect obtained by ES shouldattention should be dedicated to the activity of

group II fibers coming from the secondary spindle be mainly ascribed to the excitation of the II groupspindle fibers. This excitation primes a complexendings which are primarily inserted on the intrafu-

sal fibers with chain nuclei. There are eight to ten inhibitory mechanism able to involve the corticalcenters, the reticular substance, the rubro-spinalof these fibers in the spindle, while there are only

two to four Ia afferent fibers coming from the nu- tract, and whatever residual pyramidal system re-mains after central nervous system (CNS) insult. Thisclear bag fibers. It is well known that the intrafusal

fibers with chain nuclei are found in greater num- inhibitory mechanism, after some number of repeti-tions, allows an automatic process of muscle regula-bers in the hand muscles where fine motor control

is required. tion(1,22).The response to electrical stimulation is obviouslyThe group II afferent fibers take part in complex

polysynaptic circuits involved in coordinate limb correlated with the residual integrity of the centralnervous system. Cody et al.(23) studied the reflexmovements. In the awake condition, the secondary

endings are continuously exited, with a discharge contribution of group Ia and group II muscle affer-ents to the reaction to stretch and to vibration infrequency proportional to the elongation degree of

the muscle. For that reason the intraspindle fibers normal subjects as well as in patients affected withdifferent kinds of upper motoneurons lesions. Allon which the secondary endings are inserted are

called ‘‘length measuring fibers.’’ So, the group II of the patients demonstrated flexor spasticity of theupper limb. Stretching at different velocities re-fibers coming from them continuously monitor

length and contraction status of the muscle and vealed that in normal subjects the short and longlatency responses to stretch increased as the velocitytherefore the instant position of the body segments

between themselves and in the space(12–15). The of stretch increased, and in spastic patients only theshort latency responses increased while the longinformation from the group II fibers is integrated

in a long and very complex reflex control circuit, latency responses remained low or absent. The longlatency response to stretch was present in 19 of 23passing through three and four cortical areas, con-

ES in Cerebral Vascular Accidents � 89

subjects. So, in about 80% of the controlled patients of movement, was partially preserved. Therefore, itcan be proposed that at least a partial recovery ofthe circuit covered by the muscle proprioceptive

afferents, the basis of a refined cortical modulation inhibitory system by electrical stimulation may bepossible.

Table 1. H Latencies and Hmax/Mmax Ratios in 10Normal Young Adults

FES IN SPINAL CORD INJURED SUBJECTS:H lat H lat H/M A NEW PERSPECTIVENo. Sex Age ms predicted max

I would now like to discuss my point of view regard-1 F 26 27.5 34.3 0.492 F 21 28.2 30.0 0.19 ing the presentation of spasticity in spinal cord in-3 F 21 29.5 29.5 0.18 jury (SCI) and to reflect upon the prognosis and4 F 20 28.4 28.5 0.49

therapeutic management of the different subgroups5 F 20 29.7 28.5 0.106 M 39 H reflex not perceivable of spastic SCI patients. My collaborators and I have7 M 37 29.2 30.6 0.16 already presented the following considerations in8 M 22 28.8 29.4 0.21

1996 at the First Mediterranean Congress of Physical9 M 21 27.5 28.7 0.24Medicine and Rehabilitation held in Herzliya, Israel,10 M 23 31.3 29.8 0.18

and published in 1997(24).Total (averages) 28.9�1.13 0.25�0.13 The spontaneous muscle contractions in SCI pa-Females (av.) 25 0.29�0.16Males (av.) 0.19�0.03 tients, usually called ‘‘spastic,’’ appear in different

Table 2. Hmax/Mmax Ratio of 29 SCI Subjects

Time from injuryLevel of injury & ASIA (years) Clinical severity

Patient Age grade (m � months) of contractions H/M

1 43 C4-C 1 moderate 0.712 65 C5-B 4 m moderate 0.583 23 C5-C 6 moderate 0.604 33 C5-A 4 severe 1.045 22 C5-D 10 moderate 0.566 29 C5-D 10 moderate 0.337 53 C6-A 5 severe 0.898 63 C6-A 3.5 moderate 0.289 24 C6-B 1 moderate 0.3210 29 C6-D 9 moderate 0.7711 22 C7-C 2 m moderate 0.4212 33 C7-A 3 m moderate 0.2913 21 C7-C 3 severe 0.5214 21 T4-A 3 mild 0.2215 31 T4-A 6 m moderate 0.2716 29 T5-A 1 moderate 0.4117 39 T5-A 13.5 no contractions 0.1818 58 T6-A 3.5 moderate 0.4519 46 T7-A 6 moderate 0.3520 27 T7-B 2 mild 0.3421 44 T7-B 8 m absent not measurable22 40 T8-A 1 moderate 0.2723 30 T9-A 1 moderate 0.6024 35 T10-A 5 m no contractions 0.1525 29 L1-C 6 m mild not perceivable26 51 L1-C 6 m severe 1.227 45 L2-D 3 m no contractions 0.1628 40 encephalomyelitis-D 4 mild 0.4129 48 T10-A (gas embolism) 3 m moderate 0.13

90 � ALFIERI

forms and different intensities according to the level but this was not proven by the measurements wemade.and severity of injury. I have employed electromyog-

raphy, H reflex recruitment curves, Hmax/Mmax Based upon our measurements, we distinguishedthree forms of involuntary muscle contractions, oramplitude ratio, and the results of electrical stimula-

tion to distinguish three or four types or subgroups spasticity. The first form may be subdivided intotwo groups.of spastic or ‘‘spastic-like’’ involuntary contractions

in 29 SCI subjects. This number is not sufficient to The first form was observed in thoracic paraple-gic patients who demonstrated clonus in their lowerget statistical data, but I think that it is enough to

give a realistic view and to promote new research limbs musculature. In these patients, the spontane-ous contractions could be expected to increase ason this subject.

During the first two or three months after SCI, muscle atrophy increased(26) and then to decreaseover the ensuing years. In this group of patients,spasticity is very variable, but it later becomes more

stable(25). It also must be recognized that the H ES to the spastic muscles reduced the number andintensity of contractions. The H/M ratio was normalreflex and the H/M amplitude ratio is variable within

a day and between days in normal healthy subjects or even at the lowest levels of normal in these sub-jects (Fig. 5).as well as in hemiplegic or SCI subjects. I propose

that the variability, after three months, is not great In my opinion, the clonic contractions observedin this group are due to a train of stretch reflexes,enough to significantly alter the results of our study.

The H/M amplitude ratios of 10 normal young subsequent to a first sudden elongation of the mus-cle.adults (0.10–0.49) are given in Table 1. The H/M

amplitude ratios of 29 SCI subjects are summarized Other thoracic paraplegic patients in this groupdemonstrated an H/M ratio greater than normal inin Table 2.

Ten of the 29 SCI subjects had an H/M ratio of the spastic muscles. We designated these subjectsas a group (second form). Some subjects in thisless than 0.50. I expected that all of the spastic SCI

patients would have a high H/M ratio (i.e., > 0.5), group did not respond positively to ES. Figure 6

Figure 5. Male, age 22. Post-trau-matic tetraplegia from 115 days, levelC5-C6, ASIA A. Tonic and clonic con-tractions, sharp tendon reflexes, bilat-eral inexhaustible clonus at Achillestendon. H/M ratio, 0.41.

ES in Cerebral Vascular Accidents � 91

not evaluate the efficacy of sensory level (i.e., sub-motor) ES in this study.

In summary, it is important to recognize that pat-terns of spasticity and responses to treatment, in-cluding electrical stimulation, may vary from onepatient to another. While many patients benefit fromES-induced modulation of spasticity and the im-provement in metabolic as well as mechanical per-formance of muscle, there is a need for furtherresearch into the clinical presentation and neuro-physiologic basis for the various patterns of spas-ticity.

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