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Home , Neurosurgery, Restorative neurology, Spastic cerebral palsy, Spastic hemiplegia

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Spasticity in and the Selective Posterior Procedure Warwick J. Peacock and Loretta A. Staudt J Child Neurol 1990 5: 179 DOI: 10.1177/088307389000500303

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Downloaded from jcn.sagepub.com at UCLA on June 13, 2011 in Cerebral Palsy and the Selective Posterior Rhizotomy Procedure

Warwick J. Peacock, MD; Loretta A. Staudt, MS, PT

Abstract A review of the selective posterior rhizotomy procedure for reduction of spasticity in cerebral palsy is presented. The history of the procedure, selection of patients, operative technique, and results are described. The neurophysiologic basis for spasticity is considered, as well as the role of spasticity in the complex of cerebral palsy. Cerebral palsy is a multifaceted disorder of which spasticity is only one aspect. Reduction of spasticity can be effectively achieved using the current technique of selective posterior rhizotomy, but careful patient selection and establishment of realistic goals are vital to successful outcome. Postoperative physical and occupational are felt to be essential for regaining strength and improving motor function following the rhizotomy procedure. Further study in the areas of spasticity, cerebral palsy, and the effects of rhizotomy is expected to advance our treatment of spastic children. (J Child Neurol 1990;5:179-185).

’ posterior rhizotomy is a neurosurgi- History . Selectivecal procedure designed to reduce spasticity. Rhizotomy or &dquo;cutting roots&dquo; was originally per- Although the procedure was first used for this pur- formed on dorsal spinal roots for relief of pose almost 100 years ago/ it has recently become . Robert Abbe described his cases performed in repopularized for patients with spastic cerebral New York as early as 1888 and credited C. L. Dana palsy, due to refinements in technique. 2,3 The pro- with the original concept. 5 Abbe reported his own cedure today involves an L2 to L5 laminectomy, fol- four cases of upper extremity pain or pain plus lowed by the selective division of certain lumbo- spastic athetosis and also mentioned a slightly ear- sacral posterior spinal nerve rootlets, based on the lier case by Bennett in London who performed- electromyographic (EMG) responses to their electri- lumbosacral dorsal rhizotomy for lower extremity cal stimulation. It has been found to be beneficial in pain. carefully selected patients.3 In particular, spastic di- By 1908, Otfrid Foerster, a German neurosur- plegic patients with pure spasticity, no underlying geon, had used lumbosacral posterior rhizotomy to weakness or severe contractures, and the ability to relieve spasticity, although Munro is also credited walk have shown the most functional improvement with similar work as early as 1904.1,5 This followed from the procedure. Postoperative physical and oc- Sherrington’s neurophysiologic studies in the late’ cupational therapy were felt to be essential for suc- 1800s describing reduction of hypertonus following cessful surgical outcome. 3,4- division of afferent posterior nerve roots in decere- brate cats.6 Foerster described 159 cases in 1913, including 88 cases of &dquo;congenital spastic paraplegia.&dquo;’ He di- . vided the whole posterior nerve roots from L2 to S2, &dquo; either L4 or L5 to knee extensor From the Division of of California sparing preserve , University tone. Foerster used electrical stimulation Los Angeles, Los Angeles, CA. during the Address correspondence to Dr Warwick J. Peacock, Pediatric procedure to identify the nerve root associated with Neurosurgery, UCLA School of , 74-137 CHS, 10833 Le knee extension and to between anterior Conte Los CA distinguish Avenue, Angeles, 90024. and roots. He features Received Dec 21, 1989. Accepted for publication Dec 22, posterior emphasized many 1989. of patient selection and treatment that continue to

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Downloaded from jcn.sagepub.com at UCLA on June 13, 2011 be important today, such as identification of &dquo;real&dquo; bowel sphincters could be positively identified and spasticity and exclusion of cases with athetosis and spared. Thus, an L2-L5 laminectomy was used, and underlying . He reported better results in posterior nerve rootlets between L2 and S2 were those with lower extremity involvement and empha- each electrically stimulated and selectively divided, sized the benefit of motivation and intelligence to based on the EMG and visually observed muscular participate in a postoperative exercise program. responses. Foerster’s procedure fell from favor, presumably be- We now use 10 channels of EMG to simulta- cause of difficulties with sensory loss, particularly neously monitor activity in the hip adductors, quad- proprioception. 7 riceps femoris, anterior tibialis, hamstrings, and In the 1960s, Gros et al revised the procedure in gastrocnemius muscles bilaterally. The clinical pic- order to preserve sensation by cutting only a fraction ture of the child is taken into account in cases where of the posterior nerve rootlets that constitute the the EMG responses are equivocal. Follow-up for as posterior root.8 Gros had some difficulty with in- long as 7 years has shown maintenance of reduction complete relief of spasticity, as ivell as weakness, in and functional improvements in pa- and later adapted the procedure by attempting to tients with . Careful patient se- spare rootlets innervating functionally useful muscle lection and postoperative therapy are felt to be vital groups. Following exposure of the posterior roots at to successful surgical outcome. 3. the level of the conus, he used electrical stimulation of posterior nerve roots and EMG, working closely with a physiotherapist and neurophysiologist to Cerebral Palsy map out the rootlets innervating &dquo;useful&dquo; muscles, Cerebral palsy’ is a motor disorder resulting from such as the abdominal muscles, gluteus maximus, damage to the immature . Spastic ce- quadriceps femoris, and gastrocnemius. These root- rebral palsy is the most frequent type. 11,12 This is of- lets were spared, while rootlets innervating muscles ten associated with the sequelae of premature birth. deemed to have &dquo;handicapping&dquo; spasticity, such as The dyskinetic types of cerebral palsy have become the adductors and hip flexors, were CUt.7,9 .. less common presumably due to the reduced inci- In the 1970s, Fasano et al discovered that the re- dence of kernicterus from successful treatment of sponse to electrical stimulation was variable among neonatal jaundice. 13 Despite the marked reduction the posterior nerve rootlets in patients with spasti- in the incidence of dyskinesia, the overall incidence City.2 Some rootlets responded to a train of electrical of cerebral palsy has remained at about 2 per 1000

stimuli with a localized brief muscular contraction, live births. 14 This is probably due to improved sur- _ while others showed a continuous or prolonged re- vival of low-birth-weight infants who sustain hy- sponse that diffused to other muscle groups, includ- poxic brain or the damaging effects of ing the upper limb and trunk musculature. The intraventricular hemorrhage. - rootlets associated with the brief localized responses Cerebral palsy is a multifaceted disorder with a were spared, and the others were cut. This proce- range of types and severity. Individuals may present dure was found to relieve spasticity without signifi- with one or more tonal abnormalities, including cant recurrences or sensory disturbances. It was spasticity, rigidity, dystonia, and hypotonia. Persis- found to be most useful in spastic cerebral palsy, and tent and impairments of balance, improvement in function frequently accompanied re- strength, selective motor control, and coordination duction in spasticity. Children without dystonia who are usually present in varying degrees. Secondary had good underlying strength were identified as ap- joint contractures and deformities, including hip dis- propriate surgical candidates. Cooperation between location and scoliosis, often occur as a result of ab- the orthopedic and the neurosurgeon was normal tone and postures. Disorders of vision, Laitinen et al the of and emphasized. applied approach speech, hearing, , , ’. Fasano et al to a small group of adults with spinal learning may be associated with cerebral palsy. cord injury and , with positive re- These children may fail to thrive and may have sei- sults.10 zure disorders, , or other medical Peacock et al adapted the procedure of Fasano problems. ’ et al to allow for positive identification of the exact The selective posterior rhizotomy procedure is neuroanatomical level.~ By working at the level of aimed at improving function or care in children who the cauda equina rather than the conus, the lower have spasticity as their primary handicapping factor, sacral nerve roots that supply the bladder and although it must be realized that various other fea-

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Downloaded from jcn.sagepub.com at UCLA on June 13, 2011 tures of the disorder will continue to be and motor present power between these muscle groups in spas- interfere with function. tic patients is exaggerated further by intact inhibition of flexors and lack of reciprocal inhibition to exten- sors. Spasticity The role of other afferents, such as the Ib Golgi Spasticity has been defined as a velocity-dependent tendon organ fibers and type II fibers, in spasticity is increase in resistance to passive stretch associated not known.’6 In addition to the disinhibition or re- with hyperactivity of deep-tendon reflexes. 15 It iso tease phenomenon associated with spasticity, it has consequence of an upper motor neuron lesion at the also been proposed that sprouting of Ia afferents oc- spinal or cerebral level, along with other features curs in response to damage to descending motor such as weakness and loss of motor control and dex- tracts, thus increasing the hyperexcitability of the terity. motor neuron pools.21 The neurophysiologic mechanism behind spas- Although both adult-onset and cerebral ticity has long been debated. Among the theories palsy may result in spasticity, there is evidence have been fusimotor hyperactivity and deficient in- suggesting that the neurophysiologic mechanisms hibition of several types, including recurrent (Ren- and resultant functional disorders are different in shaw) inhibition, presynaptic inhibition, reciprocal individuals with cerebral palsy in whom the insult Ia inhibition, Golgi tendon organ inhibition, and occurred at an early stage of nervous system devel- 16’17 group II afferent inhibition. Although the hyper- opment. excitability of the gamma drive was once a popular Myklebust et al studied the EMG recordings in theory, it is no longer felt to be a tenable explana- response to ankle rotation in individuals with spastic tion. 16 The loss of inhibition to the motor neuron cerebral palsy, patients with adult-onset spasticity, pool at the spinal segmental level is an accepted and nonspastic subjects.22 On rapid dorsiflexion or view; however, the type of inhibition that is lacking stretching of the triceps surae, they found a pattern is not clearly defined and may vary in different pa- of &dquo;reciprocal excitation&dquo; or cocontraction in the pa- tient populations. tients with cerebral palsy, whereas the nonspastic The Renshaw cells are inhibitory interneurons in subjects and adult-onset spastic patients had a re- the that are activated by recurrent collat- sponse consistent with reciprocal inhibition. This led erals of the axon of the alpha motor neuron. They to the conclusion that the disorder in cerebral palsy inhibit the motor neuron pool from which they orig- is a developmental one that affects spinal cord cir- inally received stimulation and tend to reduce inhi- cuitry in addition to brain function. bition of antagonistic motor neuron pools. Katz and Further work by Myklebust et al revealed that Pierrot-Deseilligny studied recurrent inhibition in tendon jerk reflexes in normal neonates differed spastic patients and found evidence for increased re- from those of adults, with simultaneous activity of current inhibition at rest, although Renshaw cell ac- antagonistic muscles as a characteristic feature.23 tivity was reduced or absent in spastic adults during Thus, it was hypothesized that the reciprocal excita- activity.l8 tion in response to quick stretch seen in the child Decreased presynaptic inhibition of Ia afferents with cerebral palsy may be a persistence of an early has also been suggested as a possible contributing pattern or reflect lack of development of the mature mechanism in inhibition of of inhibition. spasticity. Presynaptic pattern reciprocal , . the Ia terminals in the spinal cord is mediated by Several authors have attempted to examine the )’-aminobutyric acid (GABA). 17 Morin et al have de- relationship between spasticity and the functional scribed a method to study presynaptic inhibition in motor disorder in individuals with upper motor new- - humans that may lead to further knowledge about ron lesions. 24-213 Sahrmann and Norton examined its role in spastic patients.l9 the upper extremities of individuals with adult-onset Reciprocal Ia inhibition refers to the disynaptic upper motor neuron lesions and found that impair- inhibition of antagonistic muscles via the Ia fiber of ment of movement was primarily related to poor ag- the agonist and the Ia inhibitory interneuron. onist control, rather than limitation of movement Tanaka et al studied this mechanism in adult pa- due to antagonistic stretch reflexes. 2’ Lee et al’simi- tients with , revealing that recip- larly concluded that stretch reflex enhancement was rocal inhibition from triceps surae to pretibial not responsible for stiffness of voluntarily activated muscles was intact, but the reverse was absent. 20 elbow muscles of adult spastic hemiplegic patients.25 Thus, the increased extensor tone and imbalance of Although impairment of voluntary motor power and

181

Downloaded from jcn.sagepub.com at UCLA on June 13, 2011 control is certainly a feature of cerebral palsy, it is muscle activity appears to be a dominant feature. doubtful that these findings in adult upper extremi- Successful outcome in surgical reduction of spas-’ ties can be applied to lower extremity spasticity in ticity is therefore dependent on the degree to which children with cerebral palsy. spasticity interferes with care and function, as well Knutsson and Martensson used isokinetic dyna- as the other features of the motor disability that re- mometry and EMG to look at spastic restraint during main, such as weakness, synergy patterns, abnor- active and passive lower extremity movements in mal timing of muscle activity, lack of balance, and adults with spastic paresis. 26 Antagonistic restraint contractures. was most commonly found during active motion at the fastest speeds. Holt demonstrated the complex nature of neuromuscular function in patients with Patient Selection cerebral palsy using EMG. 27 He noted phenomena Selection of patients for rhizotomy is performed by a such as cocontraction in response to stretch, and team including the pediatric neurosurgeon, physical variation between responses elicited during clinical therapist, and orthopedic surgeon. Neurologists, oc- examination and those seen during functional move- cupational therapists, physiatrists, nurses, psychol- ment, such as gait. ogists, and social workers also participate in the se- Nashner et al studied posture and equilibrium in lection process and refer patients for surgical consid- children with spastic cerebral palsy, using a movable eration. The patient’s history is taken, and the platform to perturb their balance under various con- diagnosis of cerebral palsy is confirmed. We have ditions of visual feedback .2’ Deficits in muscle coor- noted that children with a history of premature dination were primarily seen in three spastic birth seem more likely to be purely spastic, rather hemiplegic children, while problems related to sen- than having a mixed tonal picture. Veelken et al sory organization were found in three ataxic chil- found that spastic children who had a dren. Three children with had had fewer associated handicaps than various combinations of abnormal muscular coordi- those who were born at term.32 Neurologic exam- nation and/or sensory organization. The sequence of ination for evidence of spasticity, including velocity- muscle firing in spastic limbs was in a proximal to dependent increase in resistance to passive move- distal direction, which was reversed from the nor- ment, hyperactive stretch reflexes, limitation in range mal response. Cocontraction of antagonistic muscles of motion, and frequently, , is performed. was noted for spastic children and in young normal Other forms of abnormal tone and involuntary children in response to backward sway. 28,29 movement, such as athetosis, ataxia, dystonia, and Dietz investigated spinal reflexes during normal rigidity, must be ruled out. and impaired gait of children and adults, revealing The goal of is either to improve current that the presence of Ia mediated monosynaptic functional performance or to ease the daily care and stretch reflexes and the absence of polysynaptic handling of the child. It is also expected that reduc- reflexes is characteristic of very young children and tion of spasticity will help to prevent the continued of older children with cerebral palsy.3° The reverse formation of contractures and deformities. If func- is true for unaffected children over 5 years of age tional improvement is anticipated, the child must and adults. Cocontraction of antagonistic muscle have adequate strength, motor control, balance, and groups during the stance phase of gait and reduced freedom from fixed contractures to achieve this in amplitude of EMG were found in both spastic the absence of spasticity. If weakness is a factor, up- children and those with Duchenne muscular dystro- right motor function will be at risk. phy. The coactivation of muscles during stance Children with spastic diplegia who can walk in- phase of gait was seen as a persistence of an dependently without a device frequently have the immature pattern in individuals with motor dys- strength, motor control, and balance to benefit max-., function of early onset. imally from the procedure. Children with hemiple- Perry has attributed gait disorders in patients gia are not usually considered, due to their excellent with upper motor neuron lesions, including cerebral functional status and the tendency toward weakness palsy, to &dquo;spasticity, primitive locomotor patterns, and hypoplasia on their involved side. Quadriplegic impaired selective control and contracture forma- patients who are nonambulatory may be considered tion.&dquo;31 It is clear that spasticity alone is not the for the procedure if spasticity is interfering with po- causative factor in motor dysfunction in cerebral sitioning, sitting ability, or care. Children with mod- palsy but persistent cocontraction or antagonistic erate to severe involvement with some functional

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Downloaded from jcn.sagepub.com at UCLA on June 13, 2011 ability must be carefully evaluated to consider the spread proximally, distally, or contralaterally are risks and benefits of surgical reduction of spasticity. also considered to be abnormal. In equivocal cases, For example, a child who can walk for short dis- visual inspection and/or palpation of the muscular tances , with a walker may depend on spasticity for contraction are helpful. The pattern of rootlets previ- antigravity support, although his or her freedom of ously divided and the child’s clinical picture are also movement for sitting, dressing, and other activities taken into account. The use of muscle relaxants will may be improved through rhizotomy. The goals of disturb the procedure and the level of the procedure should be clearly defined based on may need to be adjusted if EMG re- the child’s current motor ability. sponses are generally excessive or hypoactive. During closure, the dura is filled with saline, and a Valsalva maneuver is used to ensure water- Operative Technique tightness. Following the procedure the patient is The surgical procedure is performed under general taken to the pediatric for 1 to 2 endotracheal anesthesia without long-acting muscle days, where medication, regular turning, and chest relaxants. The patient is placed prone on the operat- care are routinely given. Patients remain flat in bed ing table with bolsters under the chest and pelvis to for 5 days to prevent any potential dural leak. Phys- allow the abdominal wall to move freely. This pre- ical therapy begins on the third postoperative day vents epidural vein distension and reduces . for bed mobility, range of motion, and strengthen- The lumbosacral spinous processes are mapped out, ing. After the fifth day, sitting, transfers, and early using the posterior superior iliac spines as reference, weight bearing may begin. Children are discharged to the level of the L4 spine. A midline laminectomy from the on the eighth day and resume out- or is performed from L2 to L5. If a lami- patient on an intensive basis to im- nectomy is performed, a subperiosteal dissection is prove strength and functional motor skill. used to allow for continued bone formation from intact periosteum after closure. In cases where a laminotomy is used, the bone is sutured back in Results place. Reduction of spasticity and improvement in func- After exposure of the cauda equina, the nerve tion following rhizotomy have been noted by several root levels are confirmed using electrical stimulation authors over the years.1-3 The original series of 60 of the anterior roots of Sl (the largest root) and S2 patients reported by Peacock et al showed improve- and observing the muscular responses. The poste- ment in functional skills, such as sitting, standing, rior roots can be distinguished from anterior roots crawling, walking, upper extremity use, and speech.3 by position, size, shape, color, and threshold for Maximal benefit was seen in intelligent, spastic, di- _ muscular response on electrical stimulation. The plegic children with good trunk control (the ability posterior root is significantly larger and flatter than to side sit), no significant weakness, and the ability ’ the anterior root, which is rounder and has a to locomote. As no significant postoperative im- slightly darker color. The threshold for the anterior provement was found in four children with spastic roots is significantly lower than that of the posterior athetosis, the procedure is no longer used for pa- roots. tients with this diagnosis. The posterior nerve root of L2 is identified .and Long term follow-up for up to 7 years on 55 off electrically stimulated using specially insulated mi- these patients has revealed that reduction of. spasti- croneurosurgical blunt hook electrodes (Aesculap city and functional improvement have been main- Surgical Instruments, Burlingame, CA) to find a tained.4 Weakness continued to be present in 46 threshold voltage. Individual nerve rootlets consti- children, most notably in trunk flexors and exten- tuting that root are individually stimulated with sin- sors, hip extensors and abductors, and calf muscles. gle pulses to find the threshold and then with trains Several children required orthopedic procedures to of stimuli at a frequency of 50 Hz for 1 s. The rootlet address contractures and deformities that were not is either divided or spared, depending on the mus- affected by rhizotomy, although some children who cular response. Characteristic EMG patterns that are appeared to have contractures were able to improve associated with spared rootlets include decremental their range of motion without . and squared type responses. Rootlets associated Two-dimensional gait analysis of 14 of these chil- with incremental, clonic, multiphasic, or sustained dren revealed significant improvements in range of responses are generally divided. Responses that motion and stride length after rhizvtomy.33, ’

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Downloaded from jcn.sagepub.com at UCLA on June 13, 2011 Recent studies using instrumented gait analysis References of patients undergoing rhizotomy have shown simi- 1. Foerster O: On the indications and results of the excision of lar improvements in range of motion, stride length, posterior spinal nerve roots in men. Surg Gynecol Obstet and of In addition, EMG 1913;16:463-474. speed walking.~ analysis 2. Fasano VA, G, Barolat-Romana G, A: has revealed the of Broggi Sguazzi Surgical during gait persistence primitive treatment of spasticity in cerebral palsy. Childs Brain locomotor synergy patterns following rhizotomy. 1978;4:289-305. Evaluation of foot-floor contact patterns revealed a 3. Peacock WJ, Arens LJ, Berman B: Cerebral palsy spasticity: transition from primarily forefoot only at initial con- Selective posterior rhizotomy. Pediatr Neurosci 1987;13:61-66. 4. Arens LJ, Peacock WJ, Peter J: Selective tact to a heel or flatfoot position.35 Excessive knee posterior rhizotomy: A long term follow-up study. Childs Nerv Syst 1989;5:148-152. flexion related to calf weakness was noted in some 5. Abbe R: Resection of the posterior roots of spinal to re- patients, for which orthotic management was recom- lieve pain, pain reflex, athetosis and spastic paralysis— mended. Dana’s operation. Med Record (NY) 1911;79:377-381. Neurophysiologic studies of individuals with ce- 6. Sherrington CS: Decerebrate rigidity and reflex coordination rebral selective rhizot- of movements. J Physiol (Lond) 1898;22:319-337. palsy undergoing posterior 7. Gros C: and treat- have confirmed reduction of Spasticity—Clinical classification surgical omy spasticity, using ment. Adv Techn Stand Neurosurg 1979;6:55-97. the H reflex .36 Evaluation of somatosensory-evoked 8. Gros C, Ouknine G, Vlahovitch B, Frerebeau P: La radicoto- potentials has revealed spinal cord abnormalities mie selective posterieure dans le traitement neuro-chirurgical that were improved in some patients following de l’hypertonie pyramidale. Neurochirurgie 1967;13:505-518. 9. Privat Benezech Frerebeau P, Gros C: Sectorial of curves before JM, J, poste- rhizotomy.36 Comparison growth rior a new of treatment for and. after have been rhizotomy, technique surgical rhizotomy performed, revealing spasticity. Acta Neurochir 1976;35:181-195. improvement in 51% of 39 patients who had preop- 10. Laitinen LV, Nilsson S, Fugl-Meyer AR: Selective posterior erative weight below or equal to the 5th percentile rhizotomy for treatment of spasticity.J Neurosurg 1983; for their ages .31 Twenty-five percent of these chil- 58:895-899. 11. An of in dren to than the 5th for Stanley FJ: epidemiological study cerebral palsy improved greater percentile western Australia, 1956-1975. I: in total incidence of their The authors that Changes ages. speculated spasticity cerebral palsy and associated factors. Dev Med Child Neurol may diminish growth by increasing the energy re- 1979;21:701-713. quirements of these children. 12. Evans P, Elliott M, Alberman E, Evans S: Prevalence and dis- Continued investigation of various aspects of ce- abilities in 4 to 8 year olds with cerebral palsy. Arch Dis Child 1985;60:940-945. rebral spasticity, and the outcomes of the se- palsy, 13. Stanley F: Perinatal risk factors in the cerebral palsies. In lective are posterior rhizotomy procedure expected Stanley F, Alberman E (eds): The Epidemiology of Cerebral Palsy, to improve our ability to manage this disorder. in Developmental Medicine No. 87. Philadelphia, JB Lip- Treatment of spastic children has long been focused pincott, 1984, pp 98-115. on the need to reduce muscle tone in order to im- 14. Paneth N, Kiely J: The frequency of cerebral palsy: A review of studies in industrialised nations since 1950. In prove motor function. With the selective population posterior F, Alberman E (eds): The Epidemiology of the Cerebral we can now direct attention to Stanley rhizotomy procedure, Palsies. Clinics in Developmental Medicine No. 87. Philadelphia, the motor disorders associated with cere- remaining JB Lippincott, 1984, pp 35-45. bral palsy and develop programs to more effectively 15. Lance JW: Symposium synopsis. In Feldman RG, Young RR, evaluate and treat weakness, improper timing and Koella WP (eds): Spasticity: Disordered Motor Control. Chicago, coordination of muscle action, inadequate balance, Year Book Medical, 1980, p 45. 16. Burke D: as an to tract and other motor Further of Spasticity adaptation pyramidal injury. problems. exploration Adv Neurol 1988;47:401-423. the neurophysiologic dysfunction in cerebral palsy 17. Young RR, Wiegner AW: Spasticity. Clin Orthop 1987;219: should lead to new approaches for the comprehen- 50-62. sive management of these children, including fur- 18. Katz R, Peirrot-Deseilligny E: Recurrent inhibition of alpha- ther refinement and of motoneurons in patients with upper motor neuron lesions. development surgical Brain 1982;105:103-124. use of modalities such as electri- techniques, optimal 19. Morin C, Pierrot-Deseilligny E, Hultborn H: Evidence for pre- and EMG and cal stimulation biofeedback, develop- synaptic inhibition of muscle spindle Ia afferents in man. Neu- ment of new orthotic and technologic aides. The rosci Lett 1984;44:137-142. selective posterior rhizotomy procedure has given us 20. Tanaka R: Reciprocal Ia inhibitory pathway in normal man and in with motor disorders. In Desmedt Mo- a new tool for selected children with patients JE (ed): management tor Control Mechanisms in Health and Disease. New York, Raven cerebral and has the to palsy provided opportunity Press, 1983, pp 433-441. in more directly evaluate the effects of spasticity 21. McCouch GP. Austin GM, Liu CN, Liu CY: Sprouting as a children with cerebral palsy. cause of spasticity. J1958;21:205-216. Neurophysiol

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Downloaded from jcn.sagepub.com at UCLA on June 13, 2011 22. Myklebust BM, Gottlieb GL, Penn RD, Agarwal GC: Recipro- normal and impaired human gait. Rev Neurol (Paris) cal excitation of antagonistic muscles as a differentiating fea- 1987;143:241-254. ture in spasticity. Ann Neurol1982;12:367-374. 31. Perry J: Orthopedic surgery to reduce functional deficits fol- 23. Myklebust BM, Gottlieb GL, Agarwal GC: Stretch reflexes of lowing upper motor neuron lesions. In Eccles J, Dimitrijevic the normal infant. Dev Med Child Neurol 1986;28:440-449. M (eds): Recent Advances in Restorative Neurology (I. Upper Mo- 24. Sahrmann SA, Norton BJ: The relationship of voluntary tor Neuron Functions and Dysfunctions). Basel, Karger, 1985, pp movement to spasticity in the upper motor neuron syndrome. 114-127. Ann Neurol 1977;2:460-465. 32. Veelken N, Hagberg B, Hagberg G, Oloiv I: Diplegic cerebral 25. Lee WA, Boughton A, Rymer WZ: Absence of stretch reflex palsy in Swedish term and preterm children. Neuropediatrics gain enhancement in voluntarily activated spastic muscle. Exp 1983;14:20-28. Neurol1987;98:317-335. 33. Vaughan CL, Berman B, Staudt LA, Peacock WJ: Gait analysis 26. Knutsson E, Martensson A: Dynamic motor capacity in spas- of children with cerebral palsy before and after rhizotomy. Pe- tic paresis and its relation to prime mover dysfunction, spas- diatr Neurosci 1989;14:297-300. tic reflexes and antagonist co-activation. Scand J Rehabil Med 34. Cahan LD, Adams J, Perry J, Beeler L: Instrumented gait 1980;12:93-106. analysis following selective posterior rhizotomy, abstract. 27. Holt KS: Facts and fallacies about neuromuscular function in Phys Ther 1989;69:386. cerebral palsy as revealed by electromyography. Dev Med 35. Perry J, Adams, J, Cahan LD: Foot-floor contact patterns fol- Child Neurol 1966;8:255-268. lowing selective dorsal rhizotomy, abstract. Dev Med Child 28. Nashner LM, Shumway-Cook A, Marin O: Stance posture Neurol1989;31(Suppl 59):19-20. control in select groups of children with cerebral palsy: Defi- 36. Cahan LD, Kundi MS, McPherson D, et al: Electrophysiologic cits in sensory organization and muscular coordination. Exp studies in selective dorsal rhizotomy for spasticity in children Brain Res 1983;49:393-409. with cerebral palsy. Appl Neurophysiol 1987;50:459-460. 29. Forssberg H, Nashner LM: Ontogenetic development of pos- 37. Wilner LJ, Gaebler-Spira D: Growth parameters of cerebral tural control in man. Adaptation to altered support and visual palsy children: Status post selective posterior rhizotomy, ab- conditions during stance. J Neurosci 1982;2:545-552. stract. Arch Phys Med Rehabil 1989;70:A45-A46. 30. Dietz V: Role of peripheral afferents and spinal reflexes in

Vignette

A Psycic Analysis of the American Neurological Association by Milt Gross

This is a series of 16 cartoons depicting prominent early members of the American Neurological Association. The original is in the archives of the American Neurological Association, housed in the Coy C. Carpenter Library of the Boivman Gray School of Medicine of Wake Forest Univer- sity, and is reproduced with the kind assistance of Ms Sarah-Patsy Knight, Archivist, and Dr James F. Toole, Historian of the American Neurological Association.

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