4 Esquenazi

REHABILITATION I: TRANSDISCIPLINARY APPROACH TO GAIT DISORDERS

IN ACQUIRED AND CONGENITAL BRAIN INJURY

DYNAMIC POLYEMG, NEUROLYSIS AND CHEMODENERVATION

WITH BOTOX A

FOR ASSESSMENT AND TREATMENT OF GAIT DYSFUNCTION

Alberto Esquenazi, MD, Director, Gait and Motion Analysis Laboratory, MossRehab,

1200 W. Tabor Road, Philadelphia, PA 19141, 215-456-9470.

Nathaniel H. Mayer, MD, Director, Motor Control Analysis Laboratory, MossRehab,

1200 W. Tabor Road, Philadelphia, PA 19141, 215-456-9560.

Mary Ann Keenan, MD, Department of Orthopedics, Albert Einstein Medical Center,

5501 Old York Road, Philadelphia, PA 19141, 215-456-7900

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Problems of movement control and limb deformities are common consequences of the upper

motoneuron syndrome (UMN). The genesis of limb deformity is based, in large part, on the

concept that UMN features such as paresis, spasticity, and impaired motor control generate an

imbalance of muscular forces affecting joint position statically and joint movement dynamically.

Typical patterns of UMN deformities are diagnostically evaluated to identify which

muscles contribute dynamically and statically to the observed deformity and impaired motor

control. Dynamic EMG, gait, motion analysis and diagnostic nerve blocks frequently provide

the necessary detailed information about specific muscle groups that will guide decision making

for treatment. Based on such information, techniques to improve passive and active motion can

be carried out. These techniques frequently include the use of motor point blocks with phenol,

nerve blocks (primarily motor nerves) with phenol and chemodenervation with botulinum toxin

A (BOTOX). These interventions can be followed by rehabilitation techniques such as muscle

strengthening, stretching, retraining, EMG biofeedback, serial casting, and bracing. Not

infrequently, surgery will be necessary to achieve a more permanent correction of deforming

forces.

Prior to selecting interventions, the clinical team and the patient should explicitly develop

functional goals. Functional goals may be classified as passive or active in nature. Passive

function refers to the passive manipulation of limbs to achieve functional ends, typically

performed by caregivers, though patients may also manipulate their limbs passively with their

non-involved limbs. Active functions, on the other hand, refer to patient’s direct use of the limb

to carry out a functional activity. Identifying muscles with volitional capacity is important to the

achievement of this goal. Another requirement is behavioral compliance and the ability to

incorporate the newly gained increases in motion into the daily routine.

In broad terms, clinical evaluation focuses on the identification of three factors:

1) The clinical pattern of motor dysfunction. See previous chapter;

2) The patient’s ability to control muscles involved in the pattern of dysfunction and;

3) The role of rheologic properties of muscles, including contracture, as they relate to the

functional problem.

The treatment interventions suggested in this paper are usually muscle-specific and the

outcome of a detailed evaluation using dynamic EMG and other techniques available in the Gait

Laboratory is to identify muscle-specific motor behaviors that will be linked to specific

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interventions. This implies that the unit level of evaluation is typically a joint and individual

muscles affecting this joint.

Clinical examination is the mainstay of evaluation and seeks information about the following

questions: Is their selective voluntary control of a given muscle? Is the muscle activated

dyssynergically (i.e. as an antagonist in movement). Is the muscle resistive to passive stretch?

Does the muscle have fixed shortening (contracture)? The clinical examination alone may not be

sufficient to answer these questions and laboratory assessment, including dynamic polyEMG,

kinetic and kinematic studies, as well as nerve blocks, may be helpful. In the Gait Laboratory,

dynamic EMG is acquired and examined in reference to simultaneous measurements of joint

motion (kinematics) and ground reaction forces (kinetics) obtained from force platforms.

Kinetic, kinematic and dynamic EMG data augment the clinician’s ability to interpret whether

voluntary function is present in a given muscle and whether that muscle behavior is also out of

phase (dyssynergic). In addition, evaluation before and after temporary diagnostic nerve or

motor point blocks can help the clinician distinguish between obligatory and compensatory gait

patterns and postures.

Combined with clinical information, the laboratory measurements of muscle function

often provide the degree of detail and confidence necessary to optimize the rehabilitation

interventions.

The three main functional goals of human ambulation are to move from one place to

another, to move safely and to move efficiently. These three goals are frequently compromised

in the patient with residual effects of acquired or congenital brain injury. The great majority of

patients will be able to perform limited ambulation, but they will often have problems because of

inefficient movement strategies, the presence of pain due to abnormal limb postures and

decreased safety. Often, the compensatory movements necessary for ambulation produce

exaggerated displacements of the center of gravity, which result in increased energy expenditure.

Impaired balance, sensation and problems with limb clearance can contribute to the anxiety of

ambulation and may increase the frequency of loss of balance and falls.

Some generalizations can be made about the gait of a patient with residual effects of

acquired or congenital brain injury. These include a decrease in walking velocity with a

reduction in the duration of stance phase, impairment of weightbearing in the affected limb with

an increase in the duration of stance time of the less affected limb. Ochi et al reported on

differences in temporospatial parameters of locomotion among patients with residual stroke and

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traumatic brain injury. From a functional perspective, gait deficiencies can be categorized with

respect to the gait cycle. In the stance phase, an abnormal base of support can be caused by

equinovarus, toe flexion, or ankle valgus. Limb instability can occur due to knee buckling

(sudden flexion) or hyperextension, which may result in knee joint pain. This may make

walking unsafe, energy inefficient, and painful.

During the swing phase, inadequate limb clearance caused, for example, by a stiff knee

and inadequate limb advancement caused, for example, by limited hip flexion or knee extension

may interfere with the safety and energy efficiency of walking.

To focus more appropriately on the essence of multi-factorial gait dysfunction, formal

gait analysis in a laboratory may be required. Combining clinical evaluation with laboratory

measurements will increase the degree of information resolution needed to understand the

common patterns of gait dysfunction in the UMN.

EQUINOVARUS

Equinovarus deformity is the most common pathological posture seen in the lower limb

after central nervous system injuries. The foot and ankle are in a toe-down and turned in

position. Toe curling may coexist. The patient frequently will develop a painful bursa in the

lateral aspect of the foot, particularly in the area of the base of the fifth metatarsal. During

ambulation, initial contact of the foot with the ground occurs at the forefoot and weight is borne

primarily on the lateral border. Toe flexion is typically present. Equinovarus is frequently

maintained throughout stance phase and inversion may increase, causing ankle instability as

weightbearing is applied. Limited dorsiflexion during early and mid stance prevents the

appropriate forward advancement of the tibia over the stationary foot, which frequently promotes

knee hyperextension. Impairment in dorsiflexion range of motion in the late stance and preswing

phases interferes with push-off and forward propulsion, resulting in significant reduction in joint

power generation. During swing phase, equinus posture of the foot may result in a limb

clearance problem whereas the lack of adequate posture of the foot in stance phase may result in

instability of the body as a whole. Under these circumstances, correction of this problem is

essential even for limited ambulation.

Muscles that can potentially contribute to the equinovarus deformity include the tibiales anterior,

tibiales posterior, long toe flexors, gastrocnemius, soleus, extensor hallucis longus and the

peroneus longus. The dynamic polyelectromyographic (polyEMG) recordings of the above

mentioned muscles in combination with the clinical examination provide a more detailed

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understanding of the genesis of this deformity. Dynamic polyEMG recordings often demonstrate

prolonged activation of the gastrocnemius and soleus complex as well as the long toe flexors as

the commonest cause of plantar flexion. Occasionally, the gastrocnemius and soleus may activate

differentially and treatment interventions must take this into consideration. Inversion is the

result of the over-activation of the tibiales posterior and anterior in combination with the

gastrocnemius and soleus and, at times, the extensor hallucis longus. If the tibiales posterior and

anterior are both contributing to the varus deformity, a decision has to be made about which one

of the two muscles is the main contributor. Two approaches are possible. The first one is to use

the joint powers obtained as part of the kinematic data in routine gait analysis. The second

consideration is a diagnostic tibial nerve block with lidocaine. One has to be mindful that

reducing the activation of the gastrocnemius soleus complex will tend to increase dorsiflexion

and that tightness of the toe flexors usually becomes more apparent as a result of toe flexor

tenodesis brought on by the increased dorsiflexion. Plantar fasciitis may also become evident

after interventions to reduce ankle plantar flexor spasticity are carried out and the patient

increases his or her walking.

Based on dynamic polyEMG correlated with clinical findings, the treatment of choice is

injection of botulinum toxin into the tibiales posterior, gastrocnemius, soleus, and long toe

flexors. When a contracture is evident, surgical intervention needs to be considered.

VALGUS FOOT

The foot and ankle are turned outwards and the patient walks on the medial aspect of the

foot. The patient may develop callus over the navicular and may complain of pain over the

medial border of the foot. During walking, weightbearing occurs primarily on the medial aspect

of the foot. If present, limitation in ankle dorsiflexion will prevent the forward progression of

the tibia over the stationary foot and increase the valgus posture. This frequently is seen in

young individuals who sustain neurological injuries when skeletal maturation has not been

reached. Muscles that can potentially contribute to this deformity include peroneus longus,

peroneus brevis, gastrocnemius, soleus, the long toe flexors, and reduced activation or weakness

of the tibiales anterior and tibiales posterior. Dynamic polyEMG recordings obtained from the

above mentioned muscles in combination with clinical examination should provide detailed

information to formulate a hypothesis about the underlying deforming forces.

Electromyographic recordings may demonstrate prolonged activation of the peroneus longus

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and/or brevis, abnormal activation of the gastrocnemius and soleus. In some cases, lack of

activation of the tibiales anterior or posterior may also be encountered.

Occasionally, it is difficult to differentiate the contribution of peroneus longus from

peroneus brevis in the deformity. In those few instances, a lidocaine diagnostic motor point

block to one of the muscles can be used to ascertain the respective contributions.

BOTOX injected into the peroneus longus and/or brevis followed by aggressive

strengthening of the ankle invertors and stretching of the ankle evertors is pursued. The use of

motor point blocks with phenol to the peroneus brevis is possible. Motor point block of the

peroneus longus with phenol is not advisable because the motor points are close to the peroneal

nerve, a mixed sensorimotor nerve, and phenol may produce dysesthesia if it leaks onto nearby

sensory nerve fibers.

HYPEREXTENDED GREAT TOE

Sometimes referred to as striated toe or hitchhiker’s toe, the great toe is held in extension

throughout the gait cycle. Ankle equinus and varus may accompany this foot posture. At times,

lesser toe flexion is also noted. Dynamic polyEMG can elucidate the contribution of overactive

gastrocsoleus group or underactive tibiales anterior to this deformity as the extensor hallucis

longus (EHL) may be overactive in an effort to compensate for lack of dorsiflexion in swing

phase. A motor point block of the EHL with phenol or chemodenervation with BOTOX

following the recommended dose can easily be achieved. Stretching of the EHL into flexion and

strengthening of the tibiales anterior should follow this intervention.

STIFF KNEE

The knee is kept extended during preswing and initial swing, resulting in a reduction of

the arc of motion with its peak below 40 degrees (normal reference approximately 60 degrees).

In addition, there may be delay in the timing of flexion and a concomitant reduction in hip

flexion. Knee flexion during walking is generated by hip flexion. Reduced hip flexion moment

may result in decreased knee flexion in swing phase. This deviation may cause foot drag, for

which the patient attempts to compensate by circumduction, hip hiking, or contralateral vaulting

(early heel rise). Frequently, a reduction is noted in the activation of iliopsoas along with

excessive activation of the rectus femoris, vastus intermedius, vastus medialis, vastus lateralis

and, at times, excessive activation of the gluteus maximus. If an ankle equinus deformity is also

present, a reduction in joint power generation and plantarflexion moment may result in further

reduction of knee flexion.

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Based on clinical laboratory findings, phenolization of the motor branch of the femoral

nerve innervating the quadriceps mechanism or chemodenervation with botulinum toxin to

individual heads of the quadriceps may be considered. This should be followed by aggressive

stretching of the rectus femoris using the modified Ely technique. This technique requires that

the patient lie prone on a hard surface and that the knee be flexed as the hip is maintained in full

extension producing a stretch on the rectus femoris. Marching exercises and walking in water

are also beneficial in promoting hip flexor strength.

FLEXED KNEE

In this deviation, the knee is kept flexed in stance and swing. The patient does not

achieve full knee extension after the loading response in stance nor in terminal swing. This

deviation requires the patient to utilize compensatory mechanisms during stance phase,

particularly in the period of double support. The flexed knee deviation will result in a limitation

of step length because of the patient’s inability to extend the knee joint fully in the terminal part

of swing phase.

Dynamic polyEMG recordings obtained from medial and lateral hamstrings, quadriceps,

gastrocnemius and soleus should clarify the contribution of each of these muscles to the

deformity. Electromyographic recordings frequently demonstrate overactivation of the

hamstrings, medial more than lateral. Excessive activity in the gastrocnemius may also be

present, particularly during swing phase. Kinematic data demonstrate limited knee extension

and, frequently, accompanying hip flexion.

Interventions that may be considered to reduce spasticity of the hamstrings include

phenol neurolysis to the motor branches of the sciatic nerve, motor point blocks to the

hamstrings, or chemodenervation with BOTOX. Patients who have large muscle mass and

severe spasticity will require large doses of BOTOX and in these patients phenol may be more

appropriate. Gastrocnemius motor point blocks or chemodenervation with BOTOX can easily be

achieved.

ADDUCTED (SCISSORING) THIGH

This deformity is characterized by adduction of the hip during the swing phase of

locomotion. Adducted thigh results in a narrow base of support in stance phase with potential

impairment of balance. It also can interfere with limb clearance and advancement because the

adducting swing phase limb may collide with the stance limb.

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Dynamic polyEMG recordings will demonstrate overactivation of the hip adductors,

medial hamstrings, and pectineus. Weakness of the hip abductors and the iliopsoas may also

contribute to this deformity because the patient may be attempting to use the hip adductors

compensatorily to advance the limb forward in swing phase.

It is essential to ascertain if the deformity is obligatory (the result of adductor spasticity)

or compensatory (the result of weak hip flexors) since treatment will differ. Percutaneous

temporary diagnostic obturator nerve block can be used to differentiate the role of hip adduction

if the clinician is uncertain. Longer-term interventions, such as percutaneous phenol nerve

block, are easily carried out. After the intervention, aggressive stretching of the hip adductors,

strengthening of the hip flexors and abductors is pursued. Electrical stimulation to the hip

abductors may be beneficial for this purpose.

FLEXED HIP

This gait deviation is characterized by sustained hip flexion during the stance phase of

locomotion. This is particularly evident in mid to late stance when the hip is extending. A

shortening of contralateral step length is noted when this condition is unilateral.

Dynamic polyEMG recordings of iliopsoas, pectineus, gluteus maximus, rectus femoris,

and lumbar paraspinals should help in determining the contribution of the different muscles in

the gait cycle. Overactive iliopsoas, rectus femoris, hip adductors, or weakness of the hip

extensors and paraspinals may be evident. Interventions to reduce spasticity of the hip flexors

(iliopsoas and rectus femoris), particularly chemodenervation with BOTOX to the iliopsoas and

chemodenervation with BOTOX to the rectus femoris or the use of phenol motor branch block to

the rectus can be easily performed. This should be followed by aggressive stretching of the hip

flexors with the patient positioned in the modified Thomas test for the hip flexors and the Ely

test position for the rectus femoris. The Thomas test requires that the patient be in the supine

position on a hard surface. Both legs are flexed up towards the chest, stabilizing the pelvis and

preventing lumbar lordosis. One leg is allowed to extend and brought down to the examination

table resulting in stretching of the hip flexors. Strengthening of the hip extensors and paraspinals

should also be encouraged.

Gait dysfunction resulting from spasticity, contracture, and impaired motor control after

upper motor neuron injury can be quite complex. Kinematic, kinetic, and dynamic polyEMG

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analysis along with diagnostic selective temporary blocks can help optimize rehabilitation

planning and treatment interventions. It is important to clearly identify the muscles involved by a

combination of focused clinical examination supplemented by evaluation in the Gait and Motion

Analysis Laboratory. The imbalance of muscles can be improved by rehabilitation interventions

aided by the use of motor point and motor nerve blocks with phenol and chemodenervation with

BOTOX.

BOTULINUM TOXIN A:

Botulinum Toxin A (Botox®) has strong neuromuscular blocking properties that inhibit

the release of acetylcholine causing a flaccid paralysis. The clinical effect of the toxin is due

primarily to its action at the neuromuscular junction by inhibiting the release of acetylcholine.

Three steps are involved in the toxin mediated paralysis: 1) internalization, 2) disulfide reduction

and translocation and 3) inhibition of neurotransmitter release. The toxin must enter the nerve

ending to exert its effect. Botulinum toxin A injection is currently approved by the US FDA for

the treatment of blepharospasm, facial spasm, strabismus and torticolis. In Europe is also

approved for the management of spasticity 2nd to cerebral palsy and in Stroke.

The purpose of Botox® block is to reduce force produced by a contracting spastic muscle

or muscle group. A reduction in spastic tension can lead to improvement in passive and active

range of motion and allows for more successful stretching of tight musculature. More subtly, and

more importantly too, a patient's improved control over movement and posture may allow for

compensatory behaviors during functional activities (unmasking). A reduction in spastic activity

in one muscle or muscle group may have consequences for tone in other muscle groups of the

limb through a reduction in the overall effort required to perform movement and/or through

changes in sensory information going to the CNS from that limb. Finally, the application of

external devices such as braces, splints, casts, even shoes, can be facilitated by chemodenervation.

Botox® is injected directly into an offending muscle. The major advantages in its use are

the ease of application that permits its injection without anesthesia and its predictable effect. Most

common adverse effect is excessive weakness of injected muscles, but nausea, headache and

fatigue have also been reported. No effect on the sensory system is evident with Botox. Even

when the patient may have a strong response to the paralytic effect of the toxin with over

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weakening, strength will gradually return. No anaphylactic response has ever been reported due to

Botox injection.

Depending on the size of the muscle being injected, therapeutic doses have ranged

between 10 and 300 units (U). Extrapolation from animal studies would place the lethal dose to a

70 kg human at an estimated dose of 3200 u. In cases of accidental poisoning an antitoxin is

available. Due to the potential risk of migration out of the muscle and the possibility of antibody

formation, usually not more than 400 U are administered in a single treatment session. This may

be sufficient, however, to treat a number of muscles in that one session. Development of

resistance to BTX A therapy is an important clinical issue. To minimize the risk of immuno-

resistance use the smallest possible effective dose, extend the interval between treatments for at

least 3 months or longer if possible and avoid the use of booster injections in between treatment.

Careful documentation of muscle selection, dose and effects is encouraged so in the next

treatment cycle one may adjust the dose as necessary. In our practice we limit dose per treatment

to no more than 400 units of BTX-A and if multiple large muscles are to be injected try to

concentrate the available dose to a few muscles and consider using other interventions such as

phenol to other muscles or motor nerves to achieve a complete treatment strategy. With the

currently available information we recommend not injecting Botox to patients who are pregnant

or lactating.

Before using BTX-A in the clinical management of spasticity, the physician should be

knowledgeable about the diagnosis and medical management of the condition producing

spasticity. Should be proficient in the relevant anatomy and kinesiology. The physician should

have a clear understanding of the potential benefits of unmasking function and of the limitations

of this therapeutic intervention. Because there is a several days delay between injection of toxin

and onset of action, a patient may require several sessions to optimize the dose that seems to be

necessary for optimal treatment. Unlike the dystonias where voluntary capacity is not an issue,

spastic muscles may very well have voluntary capacity, which the clinician would like to

preserve, and, therefore, titration of the paralytic effect of the toxin becomes a much more critical

factor in its administration as unmasking of function may occur. The duration of toxin

effectiveness is usually ten weeks to four months but with the risk for development of antibodies,

injections should be spread at intervals of more than 3 months. In our experience patients have

received 300 to 400 u at 3 month intervals for more than 3 years, with out evidence of loss of

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effectiveness of the medication. It would seem that the toxin might be most effective as a

temporizing management in spasticity particularly in the period of expected neurological recovery

in which spasticity is changing as motor recovery occurs or as an effective tool to “simulate” the

effects of surgery, to the benefit of the surgeon and patient alike.

The strategy of performing a Botox injection is as follows: BTX-A is available worldwide

under the trade name Botox (Allergan) and in Europe Dysport (Speywood). Botox is available in

100 U vials that arrive frozen as a white powder in the vial. To prepare 100 units, it is to be

reconstituted with 1 to 3 cc of normal saline solution without preservative based on the desired

dilution. Gentle agitation of the vial is performed and the toxin is loaded to a syringe. The skin is

prepared by cleaning it with alcohol prior to insertion of the Teflon coated, 22 gauge stimulating

injecting needle. The electrically conductive inner core of the tip of the needle is used to pass

current to the tissues. After injection, muscle activation should be encouraged to increase the

uptake and internalization of the toxin. As the paralytic effect appears evident aggressive

stretching, muscle reeducation and functional training are performed.

Table # 1 SUGGESTED BOTOX® DOSING FOR ADULTS

Clinical Pattern Potential Muscles Involved Botox® Dose

Units/Visit

# of Injection

Sites

Flexed Hip iliacus

Psoas

Rectus femoris

50-150

50-200

100-200

2

2

3

Flexed Knee Medial hamstrings

Lateral hamstrings

Gastrocnemius (knee flexors)

50-150

50-150

100-200

3

3

4

Adducted Thighs Adductor brevis-longus-magnus 200-400 4 to 6

Stiff Knee Quadriceps

Gluteus maximus

100-300

200-300

6 to 8

4

Equinovarus Foot Gastrocnemius

Soleus

Tibiales posterior

Tibiales anterior

100-300

100-300

50-100

50-100

4

2

1

2

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Flexor dig. Longus

Ext. hallucis longus

20-75

30-100

1

2

Valgus Foot Peroneus longus

Peroneus brevis

50-150

50-100

2

1

Hyperextended

(Hitchhiker's) Great

Toe

Extensor Hallucis Longus 50-150 2

Phenol: This drug, a derivative of benzene is also known as carbolic acid, it denatures the

protein membrane of peripheral nerves in aqueous concentrations of 5% or more. When phenol

is injected in or near a nerve bundle, phenol’s neurolytic action on the myelin sheath or the cell

membrane of axons with which it makes contact serves to reduce neural traffic along the nerve

and hence, it’s usefulness in treating spasticity. The onset of the destructive process with higher

concentrations of phenol may begin to show effects several days after injection, but phenol also

has a local anesthetic feature that allows a clinician and the patient to see “partial results” shortly

after the phenol block is performed. The denaturing process induced by phenol extends

biologically on the order of weeks, perhaps months, but eventually regeneration occurs, so that a

phenol block clinically is used as a temporizing measure rather than a permanent intervention. In

our clinical experience and the experience of others, the effect of a phenol block typically lasts 3

- 5 months. Histologically it has been shown that phenol destroys axons of all sizes, probably is a

patchy distribution but more so on the outer aspect of the nerve bundle, onto which phenol is

dripped. In such a model, interior axons within a nerve bundle theoretically are more spared than

their sibling axons located more peripherally in a nerve bundle where phenol has access to them.

When phenol is injected percutaneously, it is extremely likely that the nerve block will be

incomplete. This is especially useful in situations where a spastic muscle also has volitional

capacity because under these circumstances it is desirable to reduce spasticity while still

preserving the volitional capacity of that muscle.

The technique of phenol injection is based on electrical stimulation. Except in few

circumstances we generally inject motor branches close to the offending muscle or muscle group

(motor point). Several texts are available that identify muscles and their motor points. A surface

stimulator is briefly used to approximate the percutaneous stimulation site in advance. The skin

is prepared with, alcohol and a local anesthetic can be injected or rubbed on to the skin. The

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purpose is to eliminate cutaneo motor reflexes that may cause the limb to jump when the

blocking needle is subsequently inserted. A 25 gauge Teflon ® coated hypodermic needle (which

is the same needle used for botulinum toxin injections) is advanced towards the motor nerve.

Depth of penetration and directional orientation of the needle tip require a steady hand, a

competent knowledge of anatomy and a good assistant. Electrical stimulation is adjusted by

noting whether muscle contraction of the desired muscle takes place. As one gets closer to the

motor nerve, less current intensity is required to produce a contractile response. The motor nerve

is injected when minimal current produces a visible or palpable contraction. We use a duo stim

electrical stimulator with pulse frequencies of 1 per second, we typically inject when the

milliamper reading on the unit reads less than 0.4 milliamps. We generally inject 3 - 7 cc of 5 or

7% aqueous solution of phenol. For longer effects, larger concentrations, larger volumes and

longer distances between the site of injection and the distance to the neuromuscular junction of

the muscle are used. The literature does report that phenol applied to sensory nerves may

produce a disesthesia that is troublesome. For this reason we do not recommend injection of

mixed peripheral nerves except in a patient who is vegetative and indifferent to any sensory

consequences. (Actually, sensory blockade may help reduce spasticity by reducing afferent input

to a hyperexcitable motor system). After the block, we recommend that ice be applied to the

injection site for 10 to 15 minutes every two hrs. in order to reduce any local irritation or

swelling. Because a certain amount of needling is required to find the best place for injecting the

motor nerve, we prefer not to use phenol in patients who are anticoagulated . The technique for

botulinum toxin injection (see above) may be preferable in this circumstance. As with any

injection, care needs to be taken not to inject into a blood vessel and this is done by aspirating

prior to the injection. We use the help of an assistant to perform the injection while the

physician holds the needle still. In contrast, injection with botulinum toxin is generally

performed by a physician alone. The literature has reported a range of injections between 1 and

10 ml of phenol in various concentrations, usually not exceeding 7%. The lethal range of phenol

that gets into the central nervous system is approximately 8.5 grams. 10 ml of a 7% solution of

phenol contains 0.7 grams of phenol. A tenfold factor of safety. We generally do not inject

more than 15 ml of 7% phenol in one session. If a phenol block seems ineffective after several

weeks, it may be repeated. With repeated phenol injections, an increase in fibrous tissue at the

site of injection may occur and this may make repeat injections more difficult Overall,

phenol is a very useful technique when pursuing the focal strategy of spasticity management

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during the period of motor recovery after brain injury. In clinically effective concentrations (5 -

7%), phenol causes peripheral nerve injury that reverses itself over the course of months

approximately proportional to the recovery rate of a motor nerve whose injury extends from the

site of phenol installation to the neuro muscular junction of that nerve, taking into account an

additional 3 - 4 weeks of Wallerian degeneration as well. Phenol injections are a good

temporizing measure during the period of motor recovery, and it facilitates serial casting, range

of motion exercises, passive activities of daily living, active movements and function. Phenol is

very inexpensive and its injection may be repeated fairly soon after it becomes clear that the

desired effect has not been obtained. In this sense it is a titratable drug.

14 Esquenazi

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2. Griffither, Bond MR, Miller JD editors. Rehabilitation of the Adult and Child with

Traumatic Brain Injury. 2nd ed. Philadelphia, PA. FA Davis, Co. 1990.

3. Lance JW. Symposium Synopsis in Feldman RG, Young RR, Koelia WP editors.

Spasticity: Disorder Motor Control. Chicago, IL, Yearbook Medical Publishers 1980.

4. Ochi F, Esquenazi A, Hirai B, Talaty M. Temporal-Spatial Features of Gait after

Traumatic Brain Injury. J. Head Trauma Rehabil. 14 (2): 1999, pp. 105-115.

5. Keenan MA, Mayer NH, Esquenazi A, Pelensky J. A Neuroorthopedic Approach to the

Management of Common Patterns of Upper Motor Neuron Dysfunction after Brain

Injury. Neuro Rehabilitation 12, 119-143, 1999.

6. Esquenazi A, Keenan MA. Gait Analysis in DeLisa J. et al. Editors. Rehabilitation

Medicine Principles and Practice. 2nd ed. Philadelphia, PA. J.P. Lippincott, 1993.

7. Mayer NH, Esquenazi A, Childress MK. Common Patterns of Clinical Motor

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