Surgery for Intractable Spasticity

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Chapter 122 Surgery for Intractable Spasticity

Spasticity is defined as a velocity-dependent resistance to passive movement of a joint and its associated musculature. It is characterized by hyperexcitability of the stretch reflex related to the loss of inhibition from descending supraspinal structures. Spasticity should not be treated just because it is present, as it may be useful for compensating for loss of motor power. Spasticity must only be treated when excess tone leads to functional losses, impairment of locomotion, or deformities. Functional neurosurgery should be considered when its harmful components cannot be controlled by physical therapy and medications.

Surgical procedures must be performed so that excess of tone be reduced without suppressing useful muscular tone or impairing any residual motor/sensory functions. In patients who retain some residual or masked voluntary motility, the aim is to re-equilibrate the balance between paretic agonist and spastic antagonist muscles so that surgery results in improvement in—or reappearance of—voluntary motor function. In patients with poor residual function, the aim is to stop evolving orthopedic deformities and to improve comfort.

Methods are classified according to whether their impact is general or focal and whether the effects are temporary or permanent (Fig. 122-1). They include intrathecal baclofen (ITB) therapy and botulinum toxin injections, along with lesioning operations aimed at peripheral nerves, dorsal roots, the spinal cord, and the dorsal root entry zone (DREZ).

Because spasticity features and their consequences differ from one patient to another, the first step is to define the objective or objectives of the treatment for every patient: improvement in function, prevention of deformities, alleviation of discomfort and pain—in other words, what can be gained and what will not be obtained by surgery. These issues must be explained to the patient, relatives, and caregivers within the frame of a multidisciplinary team.

The guidelines given in the present chapter have been built from personal surgical experience of more than 1000 adult patients and more than 150 children with cerebral palsy over the last 25 years. A strong anatomic–physiologic basis and knowledge of the history and evolution of concepts about surgery for spasticity are important prerequisites before starting to deal with these complex patients.14

Surgical Techniques

Intrathecal Baclofen Therapy

The placement of an intrathecal drug pump assures regional delivery of medications in the cerebrospinal fluid (CSF) surrounding the spinal cord for spasticity. Baclofen is a γ-aminobutyric acid B analogue, and direct delivery to the intrathecal CSF avoids the blood–brain barrier.5

ITB therapy can be preceded by a test to screen for adequate response to the medication. The common standard procedure is as follows: The patient receives a bolus of 25 to 50 μg of baclofen via lumbar puncture or via a temporary lumbar catheter connected to a subcutaneous access reservoir. In the absence of a positive response, indicated by a two-point reduction in the patient’s Ashworth score 4 to 8 hours following administration, the bolus dose is increased in 25-μg increments up to a maximum bolus of 100 μg. Once a positive response is observed without unacceptable loss of function, the patient is considered to be a candidate for pump implantation. However, the bolus dose response is a poor guide to the likely daily infusion rate that will be needed subsequently. The “bolus method” can be read as “false-negative responses” in the sense that it may produce a brutal or exaggerated loss of motor power and muscle tone, which might be interpreted by the patient as a decrease in functional status. This holds especially true for the patients with the ability to walk. Therefore, the bolus test should be replaced by a continuous infusion test, using an external automatic injection pump connected to a line implanted into a subcutaneous reservoir. The test should last several days so that functional capabilities can be reliably evaluated. The initial postimplantation infusion dose depends, in part, on the effective screening dose. Typically, the initial starting dose is double the effective screening dose. The dose is then increased daily by 10% to 30% until the desired effect is achieved. The most useful criterion for dose adjustment is effective suppression of the hyperactive reflexes, such as tendon jerk, clonus, spasms, cramps, and decrease of muscle tone. Once the effective dose has been stabilized, the administration of the drug can be fine-tuned. A programmable pump allowing cyclic dose adjustments makes it possible to provide levels that correlate with the daily variability of spastic symptoms. The Synchromed pump (Medtronic, Minneapolis, MN) is the most frequently used. A detailed and well-illustrated description of the surgical technique of implantation can be found in Penn and Kroin’s article.6

According to a literature review of the main published series, the ITB dosage varies between 167 and 462 μg/day (average 298 μg/day), with an Ashworth score decreasing from between 3 and 4 to between 0.5 and 1.8.

A serious risk of ITB therapy is overdose, which could be irreversible because of the lack of true baclofen antagonists; therefore, this technique requires great care. Other complications include mechanical catheter migration or occlusion and infection, which require revision or removal of the system, respectively. The advantage of the ITB method is reversibility of effects. However, high cost, necessity of periodic refilling and reprogramming the pump, and geographic dependence are limitations to this conservative method.

ITB is particularly indicated for patients with severe spasticity from a spinal cord origin, especially if painful spasms are present—such as in advanced multiple sclerosis or after spinal cord injury, when physical therapy and rehabilitation do not succeed in preventing the harmful components of spasticity from appearing. ITB may also be indicated for hyperspasticity due to brain stem lesions.

In recent years, ITB therapy has joined the neurosurgical armamentarium to treat cerebral palsy patients. Due to the large size of the available pump, ITB therapy cannot easily be performed in children under 6 years of age. Children with associated choreoathetosis, hypotonia of neck and trunk, obesity, poor motivation, and/or severe multiple deformities are poor candidates for ITB therapy. For cerebral palsy patients, adequate doses (i.e., ones effective on the excess of tone that do not produce motor weakness) are often difficult to establish.

Selective Peripheral Neurotomies

Peripheral neurotomies were introduced for treatment of the spastic foot in 1912 by Stoffel.7 Peripheral neurotomies were made more selective by using microsurgical dissection and mapping with intraoperative electric stimulation to better identify the function of individual nerve fascicles811 (Fig. 122-2). Neurotomies consist of partial sectioning of one or several motor fascicles corresponding to the muscle or muscles in which spasticity is considered excessive. They act by interrupting the segmental reflex arch on both its afferent and its efferent pathways. Neurotomies must not involve sensory nerve fibers; even their partial section could be responsible for paresthesias and deafferentation pain. Motor branches must be clearly isolated from the nerve trunk; motor fascicles have to be dissected and identified within the nerve trunk proximally to the formation of their corresponding identifiable branch. Empirically, it is agreed that to be effective, neurotomies should section around 50% to 80% of all motor fascicles to the targeted muscles.

Principles

Techniques

Surgery at the Lower Limb

Obturator Neurotomy for the Spastic Hip

Obturator neurotomy, which targets adductor muscles, should be proposed to diplegic children with cerebral palsy when walking is hampered by crossing of the lower limbs or to paraplegic patients to facilitate perineal toilet and self-catheterization.

The incision can be performed along the body of the adductor longus at the proximal part of the thigh or transversely at the hip flexion fold, centered on the prominence of the adductor longus tendon. In addition to its more aesthetic appearance, the later incision facilitates adductor longus tenotomy when necessary (Fig. 122-3A). To rapidly locate the anterior branch of the obturator nerve, which is the target, the dissection is conducted laterally to the adductor longus muscle body. The posterior branch, situated more deeply, should be spared to preserve the hip-stabilizing muscles (Fig. 122-3B).

Tibial Neurotomy for the Spastic Foot

Tibial neurotomy, the most frequently neurotomy used, is indicated for the treatment of varus spastic foot drop with or without claw of toes.10 It consists of exposing all motor branches of the tibial nerve at the popliteal fossa (i.e., the nerves to gastrocnemius and soleus, tibialis posterioris, flexor hallucis longus, and flexor digitorum longus). The soleus has usually been demonstrated to be almost fully responsible for the pathogenesis of spastic foot drop, allowing sparing of gastrocnemius.12 The incision can be vertical on either side of the popliteal fossa or transverse in the popliteal fossa. The latter gives a better aesthetic result and allows tenotomy of the gastrocnemius fascia insertion if necessary (Fig. 122-5A).

The first nerve encountered is the (sensory) medial cutaneous nerve of the leg; situated adjacent to the saphenous vein, it must be spared. More deeply, the tibial nerve trunk, from which the nerves to the gastrocnemius emerge, is easily identifiable. The superior soleus nerve is situated in the midline, just posterior to the tibial nerve. The effect of a soleus neurotomy is assessed by the immediate intraoperative disappearance of ankle clonus. Then by retracting the tibial nerve trunk medially, the other branches can be identified by electric stimulation as they emerge from the lateral edge of the tibial nerve trunk. The most lateral branch is the popliteal nerve, followed by the tibialis posterior nerve and finally by the inferior soleus nerve and the flexor digitorum longus nerves. Some fascicles, often larger, can give a toe flexion response via intrinsic toe flexors (Fig. 122-5B); however, neurotomy of these branches is not recommended if they cannot be clearly individualized at this level—the more so because they may be mixed with sensory fascicles.

Surgery at the Upper Limb

Pectoralis Major and Teres Major Neurotomies for the Spastic Shoulder

Neurotomy of collateral branches of the brachial plexus innervating the pectoralis major or the teres major are indicated for spasticity of the shoulder with internal rotation and adduction.13 For the pectoralis major, the skin incision is made at the innermost part of the deltopectoral sulcus and curves along the clavicular axis. Then the clavipectoralis fascia is opened and the upper border of the pectoralis major muscle is reflected downward. Close to the thoracoacromialis artery, the ansa of the pectoralis muscle is identified with the aid of a nerve stimulator. For teres major, the skin incision follows the inner border of teres major, from the lower border of the deltoid muscle posterior head to the lower extremity of the scapula. The lower border of the long portion of brachii triceps constitutes the upper limit of the approach. The dissection goes deeply between teres minor and major muscles. In the vicinity of the subscapularis artery, the nerve ending on teres major is identified. The nerve is surrounded by thick fat when approaching the anterior facet of the muscle body.

Median Neurotomy for Spastic Wrist and Fingers

Neurotomy of the median nerve needs to be selective to avoid functional losses and secondary painful phenomena.11,14,15 It is indicated for (1) spasticity of the forearm with pronation, depending on the pronator teres and quadratus muscle; (2) spasticity of the wrist with flexion, depending on the flexor carpi radialis and palmaris longus muscles; and (3) spasticity of the fingers with flexion, depending on the flexor digitorum superficialis (flexion of the proximal interphalangeal and metacarpophalangeal joints) and the flexor digitorum profondus muscle (flexion of the distal interphalangeal, proximal interphalangeal, and metacarpophalangeal joints).

Swan-neck deformation of the fingers, depending on the lumbrical and interosseous muscles, can be limited by a combined median/ulnar neurotomy, these muscles being innervated by both the median and the ulnar nerves.

Concerning the thumb, neurotomy of the median nerve is indicated for spasticity with flexion and adduction/flexion (thumb-in-palm deformity), depending on the flexor pollicis longus.

The skin incision begins 2 to 3 cm above the flexion line of the elbow, medial to the biceps brachii tendon; it passes through the elbow and curves toward the junction of the upper and middle thirds of the anterior forearm (the convexity of the curve turns laterally) (Fig. 122-8A). Thereafter, the median nerve is searched medially to the brachial artery and recognized at the elbow, deeply under the lacertus fibrosus, which is cut. Sharp dissection is used to separate the branches of the median nerve. The pronator teres belly with its two heads is retracted medially and distally so that its muscular branches can be inspected. Then this muscle is retracted up and laterally while the flexor carpi radialis is pulled down and medially. The muscular branches to the flexor carpi radialis and to the flexor digitorum superficialis can then be seen. Finally, the latter is retracted medially, uncovering the branches to the flexor digitorum profondus, the flexor pollicis longus, and the pronator quadratus. These latter muscular branches may be individualized as separate branches or remain together in the distal trunk of the anterior interosseous nerve. Sometimes, it may be useful to divide the fibrous arch of the flexor digitorum superficialis muscle to make the dissection easier (Fig. 122-8B).

Besides this approach, which has a “wide” configuration, a “minimal” approach can be performed. The different fascicles in the trunk of the median nerve, just medial to the brachial artery, are dissected. This latter approach provides a better cosmetic outcome (shorter incision). However, it has the inconvenience of offering a nerve exposure less propitious to identifying the various motor branches in the form of fascicles enclosed in the nerve sheath and mixed with the sensory ones. This entails the risk of sensory complications, especially of developing a complex regional pain syndrome.

Surgery in the Spinal Roots and Spinal Cord

On Sherrington’s experimental data,16 Foerster performed in 1913 the first dorsal rhizotomies, for lower limb spasticity in cerebral palsy patients.17 Sectioning was from L1 to S2—excluding L4, the root of the quadriceps.

To treat irreducible spasticities with severe spasms, Munro18 suggested sectioning lumbar ventral roots, on the rationale that such spastic phenomena are associated with spontaneous hyperactivity of the motor neurons. Such clinical manifestations are seen following anoxia. In such cases, sectioning dorsal roots was ineffective, whereas sectioning ventral root abolishes spasms.

Bischof described longitudinal myelotomy19 with the aim of interrupting the spinal reflex arch between the ventral and the dorsal horns by a vertical coronal incision performed laterally from one side of the spinal cord to the other, from L1 to S1. Indicated patients are totally paraplegic patients with triple flexion and severe sphincter disturbances.

Intrathecal chemical rhizotomies, originally introduced for the treatment of pain associated with cancerous lesions, were then used for the treatment of severe spasticity in bed-ridden patients; alcoholic solution was the first chemical agent used, followed by phenol, an hyperbaric solution.20 Percutaneous radiofrequency rhizotomies, also introduced to treat chronic pain, were then applied to certain spasticities. Indications are neurogenic detrusor hyperreflexia, for which the target is the sacral roots, or hip spasticity in flexion–adduction, for which the target is lumbar roots L2-L3.21

To reduce the incidence of harmful effects of dorsal rhizotomies on the postural tone, especially in patients with cerebral palsy capable of walking, a number of attempts were made to render dorsal rhizotomies more selective.2225

In 1972, Sindou observed that his technique of microsurgical lesioning of the ventrolateral part the DREZ, developed for treating pain,2628 led to marked hypotonia in the muscles corresponding to the operated spinal cord segments.29,30 Subsequently, the technique was applied not only to treat hyperspasticity in severely affected paraplegic patients30,31 but also to treat excess of spasticity in the upper limb of hemiplegic patients.32

Dorsal Rhizotomies

Surgical approaches for dorsal rhizotomies are significantly different from one team to another. The classical technique—the one described first by Fasano et al.25 and then by Peacock and Arens33 and Abbott et al.34—can be summarized as follows: The one piece laminotomy from L1 through S1 is performed using a power saw, which allows repositioning at end of the procedure. Bipolar electric stimulation (using the Nimbus i-Care neurostimulator) of the sensory roots is carried out using multichannel EMG recordings, in addition to palpation of the leg muscles for evidence of contraction. Roots that, when stimulated, cause either activity lasting after cessation of the stimulus or muscle activity outside of its myotome are deemed abnormal and are separated into their rootlets. The rootlets are in turn stimulated, and the same criteria are used to judge their normality. Abnormally responsive rootlets are candidates to be cut. Changes in excitability due to long exposure and extensive manipulation of the rootlets are major drawbacks of the method.

To limit the extent of the approach, we prefer to use a limited osteoplastic laminotomy from T11 to L135 (Fig. 122-11). Through this approach, L2 and L3 ventral (and corresponding dorsal) L1 roots can be identified by their muscular responses to electric stimulation performed intradurally just before entry into their respective dural sheaths. The dorsal lumbosacral rootlets can be identified at their entry into the dorsolateral sulcus at the conus medullaris. The landmark between S1 and S2 medullary segments is located approximately 30 mm from the exit of the tiny coccygeal root from the conus. The medullary segments S1, L5, and L4 can be identified by their evoked motor responses to stimulation (in triceps surae, dorsal flexors of the foot, and quadriceps, respectively). The roots for bladder (S2-S3) can be identified by monitoring vesical pressure, and those for the anal sphincter (S3-S4) can be identified by rectomanometry (or simply using a protected finger introduced into the anus canal) or EMG recordings.

To be effective, 60% of the dorsal rootlets must be cut, with a different-quantity cut according to the level and function of the roots involved and their implication in the harmful components of spasticity. To be safe, L4 (which predominantly gives innervation to the quadriceps femoris) is preserved in most cases.

To further reduce invasiveness, in 2001 we started using a “staged interlaminar (IL) approach,”35 the level or levels depending on the roots to be targeted (Fig. 122-12). The lumbar spine is approached posteriorly on the midline so that the preoperated selected IL spaces can be reached. The spinous processes, as well as interspinous ligaments, are preserved. After resecting the flavum ligament, the chosen IL spaces are enlarged by resecting the lower half of the upper lamina and the upper half of the lower laminae. Then the dura is opened in the midline over 2 cm.

L2 and L3 roots can be reached through the L1-L2 IL opening, L4 and L5 roots through the L3-L4 IL opening, and S1-S2 roots through the L5-S1 IL opening. The dorsal rootlets (average five per root) are easily identified under the microscope, as they are grouped posteriorly to the ventral root, separated from the latter by an arachnoid fold. Motor responses to stimulation (with a bipolar electric stimulator) are tested for the ventral and then the dorsal root (rootlets). The threshold for obtaining motor responses by stimulating the dorsal root is at least three times higher than the one of the corresponding ventral root (1-2 mA at 2 Hz for the latter). After identification of the dorsal rootlets, the appropriate number of them is divided, between one third and two thirds of the overall dorsal rootlets, according to the preoperative chart. Then the dural incision is sutured in a watertight fashion, and the dural suture line is covered with fat harvested subcutaneously.

Surgery in the DREZ

Microsurgical DREZotomy (MDT)26,27 aims at preferentially interrupting both the small-caliber (nociceptive) and the large-caliber (myotatic) fibers of the dorsal roots, both considered tonigenic and situated laterally and in the middle of the entry zone, respectively.

Surgical lesioning must at least partially preserve the medial bundle of large-caliber fibers that project to the dorsal horn and are located medially into the entry zone to reach the dorsal column. The surgical target also includes the dorsalmost layers of the dorsal horn, where the circuits and neurons, responsible for activation of the segmental circuitry of the spinal cord, are located (Fig. 122-13). The techniques for the cervical and the lumbosacral cord segments are detailed and illustrated in Figs. 122-14 and 122-15, respectively. In brief, the procedure consists of a 3-mm-deep microsurgical incision—at the level of the dorsolateral sulcus—with a 35-degree angle at the cervical level and a 45-degree angle at the lumbosacral level. Bipolar coagulations in a dotted fashion are performed ventrolaterally at the entrance of the rootlets into the dorsolateral sulcus and penetrate approximately of 3 mm inside the gray matter of the dorsal horn, along all the spinal cord segments selected for undergoing the operation. Each microcoagulation is performed under high magnification of the microscope. The intensity starts at the minimum of the bipolar coagulator and remains at a low value. The duration of each microcoagulation is 1 to 3 seconds. The degree and extent of the coagulation are controlled by vision. For performing MDT, special instruments have been designed by Sindou (Strycker-Leibinger, Freiburg, Germany), as indicated in the legend of Figs. 122-14 and 122-15).

image

FIGURE 122-13 Schematic representation of the DREZ and the target of MDT. A, Rexed lamination of the dorsal (and ventral) horn or horns. Transverse hemisection of the spinal cord (at the lower cervical level) with myelin stained by luxol–fuchsin, showing the myelinated rootlet afferents that reach the dorsal column (DC). The small arrow designates the pial ring (PR) of the dorsal rootlet (diameter = 1 mm). The two large arrows indicate the entry line of the incision for opening the dorsolateral sulcus to perform the MDT. B, Each rootlet can be divided (because of the transition of its glial support) into a peripheral and a central segment (upper part). The transition between the two segments is at the PR, which is located approximately 1 mm outside the penetration of the rootlet into the dorsolateral sulcus. Peripherally, the fibers are mixed together. As they reach the PR, the fine fibers (considered nociceptive) move toward the rootlet surfaces. In the central segment, they group in the ventrolateral portion of the DREZ and enter the DH through the tract of Lissauer (TL). The large myotatic fibers (myot.) are located in the center of the DREZ, whereas the large lemniscal fibers are located dorsomedially. Lower part, Schematic data on DH circuitry. Note the monosynaptic excitatory arc reflex, the lemniscal influence on a DH cell and an interneuron (IN), the fine fiber excitatory input onto the DH cells and the IN, the origins in layer I and layers IV to V of the anterolateral pathways (ALP), and the projection of the IN onto the motor neuron (MN). Rexed laminae are marked from I to VII. The MDT (arrowhead) targets most of the fine and myot. fibers and enters the medial (excitatory) portion of the LT, as well as the apex of the DH (four dorsalmost layers). It should preserve most lemniscal presynaptic fibers, the lateral (inhibitory) portion of TL and most of the DH. P, Pyramidal tract.

(From Sindou M. Anatomical study of the dorsal root entry zone (DREZ). Surgery in the DREZ for pain. MD Thesis, University of Lyon, 1972; Sindou M., Quoex C., Baleydier C. Fiber organization at the posterior spinal cord–rootlet junction in man. J Comp Neurol 153:14-26, 1974.)

image

FIGURE 122-15 MDT techniques at the lumbosacral level. A, Exposure of the conus medullaris through a T11 to L1 laminectomy. B, Approach of the dorsolateral sulcus on left side, as an example. For doing so, the dorsal rootlets of the selected roots are displaced dorsally and medially to obtain proper access to ventrolateral aspect of the DREZ. C, The selected dorsal roots are retracted dorsomedially and held with a ball-tip microsucker, used as a small hook (microsection tube, with a ball tip, of a diameter of 1.0 mm, with a length of 19.5 cm, from Strycker-Leibinger) to gain access to the ventrolateral part of the DREZ. After division of the fine arachnoidal filaments sticking the rootlets together with the pia mater with curved sharp microscissors (not shown), the main arteries running along the dorsolateral sulcus are dissected and preserved, while the smaller ones are coagulated with sharp bipolar microforceps (not shown). Then a continuous incision is performed using a microknife, made with a small piece of razor blade inserted within the striated jaws of a curved razor-blade holder (or a ophthalmologic microknife, not shown). The cut is—on average—at a 45-degree angle and to a depth of 2 mm. D, the surgical lesion is completed by doing microcoagulations under direct magnified vision, at a low intensity, inside the dorsolateral sulcomyelotomy down to the apex of the dorsal horn. These microcoagulations are made all along the segments of the cord selected to be operated on, by means of the special sharp bipolar forceps, insulated except at the tip over 5 mm and graduated every millimeter (bipolar coagulation forceps, from Stryker-Leibinger).

Decision Making in Adults

Generally, patients do not complain about spasticity; they are more likely to be aware of stiffness, deformity, and limitations in functional abilities. “Stiffness” is a useful term because it is widely understood by both clinicians and patients and does not imply a specific cause. After time, the patients have a mixture of spasticity and muscle shortening or contractures. In any discussion of management, an agreed terminology is important in recognizing two principal components of muscle stiffness: The first is “dynamic” shortening of muscles caused by spasticity; such patients exhibit hyperreflexia, clonus, and velocity-dependent resistance to passive joint motion. The second, “fixed” shortening of muscles, is described as contracture, which is much less velocity dependent and remains present under local blocks or anesthesia.

Spasticity should not be treated just because it is present; it should be treated because it is harmful to the patient. Patients may use spasticity in functional activities. An extensor pattern in lower limb or limbs may aid standing transfers. In this scenario, “successful” spasticity management, if measured by reduction in tone and improved range of motion, might reduce rather than enhance function. Hence, the primary goals of spasticity management must be to improve function and stop or prevent deformities. How to differentiate dynamic from fixed deformities is of prime importance before deciding any surgical treatment, whether neurosurgical, orthopedic, or both. The dynamic range of motion measures are useful starting points, supplemented with instrumented measures of spasticity and its effects on function, such as motion analysis.

Methods for control of spasticity can be classified according to whether they are focal or general in effect and whether the effects are permanent or temporary. Within this four-way matrix, practical clinical guidelines may be derived, as illustrated in Fig. 122-1.

Neuroablative Procedures

Focal spasticity, when harmful, should be treated first with botulinum toxin injections; only after this can ablative procedures be considered. They should be performed in a selective way so that excessive hypertonia is reduced without suppression of useful muscular tone or impairment of the residual motor and sensory functions.

Peripheral Neurotomies

Peripheral neurotomies are indicated when spasticity is localized to a few muscular groups, supplied by a single or a few peripheral nerves. To decide, a local anesthetic block of the nerve (with long-lasting bupivacaine) is useful and gives the patient an idea of what to expect from the operation. Botulinum toxin injections may also act as a “prolonged” test.

Neurotomies of the tibial nerve at the popliteal region for the so-called spastic foot and neurotomies of the obturator nerve just below the subpubic canal for spastic flexion–adduction deformity of the hip are the most common. Neurotomies can also be indicated for spasticity in the upper limb. A selective fascicular neurotomy can be performed in the musculocutaneous nerve for elbow in flexion. Median (and ulnar) neurotomies can be used for hyperflexion of the wrist and fingers. The procedure consists of sectioning the branches to the forearm pronators, wrist flexors, and extrinsic finger flexors. The aim is to open the hand and improve prehension.

Selective neurotomies are able not only to reduce excess of spasticity and prevent deformity but also to improve motor function by re-equilibrating the tonic balance between agonist and antagonist muscles. This is especially true for the spastic foot with equinovarus deformity, as shown in Fig. 122-10. With regard to the spastic hand, which is a difficult problem to deal with, a functional benefit in prehension can only be achieved if patients retain a residual motor function in the extensor and supinator muscles, together with a sufficient residual sensory function. If these conditions are not present, only better comfort and a better cosmetic aspect can be achieved.

Surgery in the DREZ

Surgery in the DREZ is preferred when severe spasticity affects an entire limb so as to render it functionally useless. For patients with paraplegia, the L2-S5 segments are approached through a T11-L2 laminectomy (Fig. 122-15). For the hemiplegic upper limb, a C4-C7 hemilaminectomy with conservation of the spinous processes is sufficient to reach the C5-T1 segments (Fig. 122-14). MDT is indicated in paraplegic patients, especially when they are bedridden as a result of disabling flexion spasms. In hemiplegic patients, MDT is indicated when the upper limb is affected with irreducible and/or painful hyperspasticity. MDT also can be applied to treat a neurogenic bladder with uninhibited detrusor contractions resulting in voiding around a catheter.

Decision Making in Children

Most indications in childhood are for children affected with cerebral palsy, a group of disorders that involves disorders of movement and/or of posture and motor function.

Spasticity in children, as in adults, can be useful to function or may increase disability. Indications for surgery are more difficult to define in children than in adults because the child is in constant development; thus, orthopedic status changes with increase of growth, in particular during puberty. For deciding which treatment to use for mitigating spasticity, when to propose it, and with which orthopedic procedure to combine it, the medical team has to project into the future, extrapolate the potential for musculoskeletal contractures and their harmful consequences, and extrapolate the positive functional evolution with spontaneous psychomotor development.37

The first stage for assessment is clinical observation to have a global idea of the child’s function. The second stage is measurement of the range of motion to detect contractures that would not be accessible to neurosurgical treatment. The third stage is quantification of the assessment of spasticity with the Ashworth scale or the Tardieu scale. The final stage is grading the child on the Gross Motor Function Measure (EMFG) and observing the child’s evolution with time (Fig. 122-17).38,39

There are several effective neurosurgical treatments for spasticity in children with cerebral palsy (Fig. 122-18). For diffuse spasticity of lower limbs, dorsal rhizotomy or ITB administration may be considered. For focal spasticity, botulinum toxin injection permits delay of surgery until the child is old enough to undergo a selective neurotomy or a dorsal rhizotomy (Fig. 122-19).

If spasticity in the two lower limbs is global, dorsal rhizotomy or ITB therapy can be considered. The latter imposes a visit every 6 months to fill the pump; thus, the child and family must be motivated to comply. The volume of the implanted pump is a major obstacle in young children. Dorsal rhizotomy is generally preferred before 6 years of age, especially when a definitive action is desired on certain and well-defined muscular groups.

If spasticity is focal and involves the gastrocnemius and soleus muscles, botulinum toxin can be proposed as a good complement to physiotherapy and a plaster cast. This approach enables neurosurgical treatment to be delayed until the child reaches the age for selective neurotomy. When spasticity is focal on the adductors, botulinum toxin is not always sufficient to avoid an obturator neurotomy, often coupled with a tenotomy of the adductors, to prevent dislocation of the hip.

For spasticity in the upper limb, the first stage of treatment is botulinum toxin injections. The muscles of the upper limbs are small. Even if quite a few must be injected, the maximum allowable dose is rarely too small to be insufficient. These injections can be considered a treatment and can be repeated every 6 to 12 months. However, the multiple visits required are a constraint. Also, patients may develop an immunoresistance that decreases the effectiveness of treatment with time. If so, botulinum injections, because they simulate the outcome of a selective neurotomy of the involved nerve, allow the patient and family to appreciate the potential benefit that could follow a selective neurotomy.

If spasticity involves the shoulder, elbow, wrist, and fingers, combined neurotomies or cervical DREZotomy can be indicated.

Dystonia is rarely directly improved by these treatments. However, neurotomies, by acting on the motor neurons, may decrease the amplitude and strength of the dystonic movement and improve the global cosmetic and functional aspects of the upper limb.

Conclusion

Neurosurgery for spasticity needs—by essence—to be practiced within the frame of a multidisciplinary approach.1,3,4 Teams dealing with “spastic patients” should at least have most of the technical modalities on hand to offer the best option to every patient.

Key References

Abbott A., Forem S.L., Johann M. Selective posterior rhizotomy for the treatment of spasticity. Childs Nerv Syst. 1989;5:337-346.

Bischof W. Die longitudinal myelotomie. Zbl. Neurochir. 1951;11:79-88.

Brunelli G., Brunelli F. Selective microsurgical denervation in spastic paralysis. Ann Chir Main. 1983;2:277-280.

Decq P., Filipetti P., Feve A., et al. Peripheral selective neurotomies of the brachial plexus branches for the spastic shoulder. Anatomical study and clinical results in 5 patients. J Neurosurg. 1997;86:648-653.

Decq P., Mertens P., et al. La neurochirurgie de la spasticité. Neurochirurgie. 2003;49:135-416.

Fasano V.A., Barolat-Romana G., Ivaldi A., Squazzi A. La radicotomie postérieure fonctionnelle dans le traitement de la spasticité cérébrale. Neurochirurgie. 1976;22:23-34.

Foerster O. On the indications and results of the excision of posterior spinal nerve roots in men. Surg Gynecol Obstet. 1913;16:463-474.

Fraioli B., Guidetti B. Posterior partial rootlet section in the treatment of spasticity. J Neurosurg. 1977;46:618-626.

Gros C.. Spasticity—Clinical classification and surgical treatment, Krayenbühl, editor, Advances and Technical Standards in Neurosurgery, Advances and Technical Standards in Neurosurgery, Wien, New York, Springer-Verlag, 1979;Vol 6:55-97.

Gros C., Ouaknine G., Vlahovitch B., Frerebeau P.H. La radicotomie sélective postérieure dans le traitement neurochirurgical de l’hypertonie pyramidale. Neurochirurgie. 1967;13:505-518.

Maarrawi J., Mertens P., Luaute J., et al. Long-term functional results of selective peripheral neurotomy for the treatment of spastic upper limb: prospective study in 31 patients. J. Neurosurg. 2006;104:215-225.

Munro D. The rehabilitation of patients totally paralysed below waist: anterior rhizotomy for spastic paraplegia. Engl J Med. 1945;233:456-461.

Nathan P.W. Intrathecal phenol to relieve spasticity in paraplegia. Lancet. 1959:1099-1102. ii

Peacock W.J., Arens L.J. Selective posterior rhizotomy for the relief of spasticity in cerebral palsy. S Afr Med J. 1982;62:119-124.

Penn R.D., Kroin J.S. Intrathecal baclofen alleviates spinal cord spasticity. Lancet. 1984;1:1078.

Privat J.M., Benezech J., Frerebeau P., Gros C. Sectorial posterior rhizotomy, a new technique of surgical treatment for spasticity. Acta Neurochir. 1976;35:181-195.

Sherrington C.S. Decerebrate rigidity and reflex coordination of movements. J Physiol. 1898;22:319-332.

Sindou M.. Neurosurgical Management of Disabling Spasticity, Spetzler R.F., editor, Operative Techniques in Neurosurgery, Operative Techniques in Neurosurgery, Philadelphia, Elsevier, 2004;Vol 7:95-174.

Sindou M., Jeanmonod D. Microsurgical DREZotomy for the treatment of spasticity and pain in the lower limbs. Neurosurgery. 1989;24:655-670.

Sindou M., Mertens P. Selective neurotomy of the tibial nerve for the treatment of the spastic foot. Neurosurgery. 1988;23:738-744.

Sindou M., Mifsud J.J., Boisson D., Goutelle A. Selective posterior rhizotomy in the dorsal root entry zone for treatment of hyperspasticity and pain in the hemiplegic upper limb. Neurosurgery. 1986;18:587-595.

Sindou M., Quoex C., Baleydier C. Fiber organization at the posterior spinal cord–rootlet junction in man. J Comp Neurol. 1974 (a);153:14-26.

Sindou M., Simon F., Mertens P., Decq P. Selective peripheral neurotomy for spasticity in childhood. Childs Nerv Syst. 2007;23:957-970. (contains 30 references for SNP)

Sindou M., Abbott A., Keravel Y. Neurosurgery for spasticity: A multidisciplinary Approach. Wien, New York: Springer-Verlag, 1991;218.

Stoffel A. The treatment of spastic contractures. Am J Orthop Surg. 1912;10:611-644.

Numbered references appear on Expert Consult.

References

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3. Decq P., Mertens P., et al. La Neurochirurgie de la Spasticité. Neurochirurgie. 2003;49:135-416.

4. Sindou M.. Neurosurgical Management of Disabling Spasticity, Spetzler R.F., editor, Operative Techniques in Neurosurgery, Operative Techniques in Neurosurgery, Philadelphia, Elsevier, 2004;Vol 7:95-174.

5. Penn R.D., Kroin J.S. Intrathecal baclofen alleviates spinal cord spasticity. Lancet. 1984;1:1078.

6. Penn R.D. Intrathecal baclofen therapy. Operative Techniques in Neurosurgery. 2004;vol:7:124-127.

7. Stoffel A. The treatment of spastic contractures. Am J Orthop Surg. 1912;10:611-644.

8. Gros C. La chirurgie de la spasticité. Neurochirurgie. 1972;23:316-388.

9. Gros C.. Spasticity—Clinical classification and surgical treatment, Krayenbühl, editor, Advances and Technical Standards in Neurosurgery, Advances and Technical Standards in Neurosurgery, Wien, New York, Springer-Verlag, 1979;Vol 6:55-97.

10. Sindou M., Mertens P. Selective neurotomy of the tibial nerve for the treatment of the spastic foot. Neurosurgery. 1988;23:738-744.

11. Mertens P., Sindou M. Selective peripheral neurotomies for the treatment of spasticity. In: Sindou M., Abbott R., Keravel Y. Neurosurgery for Spasticity. A Multidisciplinary Approach. Wien, New York: Springer-Verlag; 1991:119-132.

12. Decq P., Cuny E., Filipetti P., Keravel Y. Role of soleus muscle in spastic equinus foot. Lancet. 1998;11:118.

13. Decq P., Filipetti P., Feve A., et al. Peripheral selective neurotomies of the brachial plexus branches for the spastic shoulder. Anatomical study and clinical results in 5 patients. J Neurosurg. 1997;86:648-653.

14. Brunelli G., Brunelli F. Selective microsurgical denervation in spastic paralysis. Ann Chir Main. 1983;2:277-280.

15. Maarrawi J., Mertens P., Luaute J., et al. Long-term functional results of selective peripheral neurotomy for the treatment of spastic upper limb: prospective study in 31 patients. J Neurosurg. 2006;104:215-225.

16. Sherrington C.S. Decerebrate rigidity and reflex coordination of movements. J Physiol. 1898;22:319-332.

17. Foerster O. On the indications and results of the excision of posterior spinal nerve roots in men. Surg Gynecol Obstet. 1913;16:463-474.

18. Munro D. The rehabilitation of patients totally paralysed below waist: anterior rhizotomy for spastic paraplegia. Engl J Med. 1945;233:456-461.

19. Bischof W. Die longitudinal myelotomie. Zbl Neurochir. 1951;11:79-88.

20. Nathan P.W. Intrathecal phenol to relieve spasticity in paraplegia. Lancet. 1959:1099-1102. ii

21. Segnarbieux F., Frerebeau P.h. The different (open surgical, percutaneous thermal, and intrathecal chemical) rhizotomies for the treatment of spasticity. In: Sindou M., Abbott R., Keravel Y. Neurosurgery for spasticity: a multidisciplinary approach. Wien, New York: Springer-Verlag; 1991:133-139.

22. Gros C., Ouaknine G., Vlahovitch B., Frerebeau P.H. La radicotomie sélective postérieure dans le traitement neurochirurgical de l’hypertonie pyramidale. Neurochirurgie. 1967;13:505-518.

23. Privat J.M., Benezech J., Frerebeau P., Gros C. Sectorial posterior rhizotomy, a new technique of surgical treatment for spasticity. Acta Neurochir. 1976;35:181-195.

24. Fraioli B., Guidetti B. Posterior partial rootlet section in the treatment of spasticity. J Neurosurg. 1977;46:618-626.

25. Fasano V.A., Barolat-Romana G., Ivaldi A., Squazzi A. La radicotomie postérieure fonctionnelle dans le traitement de la spasticité cérébrale. Neurochirurgie. 1976;22:23-34.

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27. Sindou M., Quoex C., Baleydier C. Fiber organization at the posterior spinal cord–rootlet junction in man. J Comp Neurol. 1974 (a);153:14-26.

28. Sindou M., Fischer G., Goutelle A., Mansuy L. La radicellotomie postérieure sélective. Premiers résultats dans la chirurgie de la douleur. Neurochirurgie. 1974(b);20:391-408.

29. Sindou M., Fischer C., Gouttelle A., et al. La radicellotomie postérieure sélective dans le traitement des spasticités. Rev Neurol. 1974©;30:201-205.

30. Sindou M., Millet M.F., Mortamais J., Eyssette M. Results of selective posterior rhizotomy in the treatment of painful and spastic paraplegia secondary to multiple sclerosis. Appl Neurophysiol. 1982;45:335-340.

31. Sindou M., Jeanmonod D. Microsurgical DREZotomy for the treatment of spasticity and pain in the lower limbs. Neurosurgery. 1989;24:655-670.

32. Sindou M., Mifsud J.J., Boisson D., Goutelle A. Selective posterior rhizotomy in the dorsal root entry zone for treatment of hyperspasticity and pain in the hemiplegic upper limb. Neurosurgery. 1986;18:587-595.

33. Peacock W.J., Arens L.J. Selective posterior rhizotomy for the relief of spasticity in cerebral palsy. S Afr Med J. 1982;62:119-124.

34. Abbott A., Forem S.L., Johann M. Selective posterior rhizotomy for the treatment of spasticity. Childs Nerv Syst. 1989;5:337-346.

35. Sindou M. Radicotomies dorsales chez l’enfant. Neurochirurgie. 2003;49:312-323.

36. Sindou M., Mertens P. Decision-making for neurosurgical treatment of disabling spasticity in adults. Operative Techniques in Neurosurgery. 2004;vol. 7:113-118.

37. Hodgkinson I., Berard C. Assessment of spasticity in pediatric patients. Operative Techniques in Neurosurgery. 2004;vol. 7:109-111.

38. Hodgkinson I., Sindou M. Decision-making for treatment of disabling spasticity in children. Operative Techniques in Neurosurgery. 2004;vol. 7:120-123.

39. Sindou M., Simon F., Mertens P., Decq P. Selective peripheral neurotomy for spasticity in childhood. Childs Nerv Syst. 2007;23:957-970. (contains 30 references for SNP)

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