CEREBRAL PALSY, SPASTICITY,AND SELECTIVE DORSAL RHIZOTOMY

Cerebral Palsy (CP)

• A static neurological disorder characterized by abnormalities of movement and posture.
• Leading cause of developmental disability in children, occurring in 1 in 500 live births and affecting > 500,000 individuals in the United States (12, 25).
• Incidence is increasing due to improved survival in very-low-birth-weight infants (12).
• Classified by the predominant motor impairment (spasticity, rigidity, dystonia, hypotonia, athetosis, ataxia, or mixed) and limb involvement (monoplegia, diplegia, hemiplegia, quadriplegia).

• Spastic CP is the most common subtype of cerebral palsy.
• Spastic diplegia and spastic quadriplegia affect approximately 60% of patients. Coexists with dyskinesia and ataxia in mixed subtypes of CP.
• Spasticity affects ~80% of all patients with CP (21, 44).
• The prevalence of spastic diplegia increases with decreasing gestational age and birth weight (6, 24). This relationship does not exist in other subtypes of the disease, such as athetoid and dyskinetic CP.
• Periventricular leukomalacia (PVL-ischemic necrosis of the periventricular and subcortical white matter) is the most common MRI finding in these children and may represent the neuropathological substrate for spastic CP (31, 34). White matter projection fibers descending from the motor homunculus and leg fibers traverse the white matter closer to the ventricle than do the arm fibers.

• The neural pathways involved in CP spasticity remain speculative
• Spinal cord ventral horn alpha motor neuron output is a primary determinant of muscle tone. The activity of alpha motor neurons is modulated by excitatory influences (e.g., Ia fibers from muscle spindles) and inhibitory influences (eg descending GABA-ergic pathways from the cerebellum and basal ganglia; aberrant Renshaw cell pathways).
• Spasticity results from an imbalance of excitatory and inhibitory influences.
• Excessive alpha motor neuron activity of target muscles, coupled with decreased inhibition of antagonistic muscles, may result in co-contraction of agonist and antagonist muscle groups.
• Clinically, spasticity is characterized by a velocity-dependent, increased resistance to passive stretch. Clinical signs include hyperactive deep tendon reflexes, the Babinski sign, ankle clonus, and reduced range of joint motion.

• CP spasticity has significant harmful effects on growing children by inhibiting motor activity and voluntary movements and thus requires optimal treatment at an early age.
• Normal muscle growth proceeds as sarcomeres are added to the ends of muscle fibers The greatest increase in sarcomere numbers occurs at an early age and is induced primarily by the amount of tension on the muscle (15, 18). When muscles are immobilized, atrophy of the existing sarcomeres occurs and compounds the slowed muscle growth Ultimately, abnormally shortened muscles, long tendons, and “muscle contracture” (i.e., increased resistance of the muscle to passive stretch in the absence of muscle contraction), result. Muscle contractures typically worsen as a child grows and produce various bone and joint deformities in the extremities (23).

Treatment of Spastic Cerebral Palsy

• Commonly used oral medications:
• GABAB receptor agonist Baclofen (Lioresal)
• benzodiazepines such as diazepam (Valium)
• the anticholinergic trihexylphenidyl
• other agents such as dantrolene, and tizanidine (Zanaflex) (38, 46).
• oral medications are moderately effective in treating spasticity and may have significant adverse effects (sedation, confusion, dependence).
• Intramuscular (IM) injections for “chemodenervation” have been performed for many years with alcohol and phenol. The introduction of IM injection of botulinum toxin A (Botox) was a major advance in the treatment of CP spasticity, with predictable benefits and fewer adverse effects. Botox is injected directly into the affected muscle, and relaxation is generally seen within several days. Maximal benefit occurs approximately 4 weeks after injection, and the effect declines requiring repeat injection in ~3-4 months.

• Intrathecal adminstration of baclofen offers the benefit of delivering the medication directly to the CNS without systemic side effects. Chronic intrathecal baclofen infusion (CIBI) is discussed in detail in Chapter 24 (3, 4, 17, 48).
• SDR reduces spasticity and increase range of motion (27, 28, 39, 41, 49). Physical therapy+SDR produces significant improvements in gross motor function and gait.
• Stereotactic ablative procedures such as thalamotomy and dentatotomy may offer some benefit in patients with unilateral dystonia (9, 20, 47). Deep brain stimulation of the internal globus pallidus and thalamus have been performed in children with dystonia and tremor, respectively (2). The role for these procedures in CP spasticity has not been investigated.

Selective Dorsal Rhizotomy (32, 33)

• Spastic diplegics derive the greatest benefit from SDR. Spastic quadriplegic gain significant functional improvements.
• Patients should have sufficient motor function to potentially become ambulators, either assisted or independent.

• Optimal age for SDR is 2 to 6 years. Early treatment is recommended to reduce the chance of severe orthopedic deformities of the lower extremities.
• SDR should not be considered for children under the age of 2 years. 30% of children who are diagnosed with CP at the age of 1 year subsequently became free of symptoms (6).

• CP associated with severe congenital hydrocephalus or intrauterine CNS infection
• Mixed CP with predominant dystonia, rigidity, athetosis, or ataxia
• Spastic hemiplegia
• CP due to widespread neuronal migration disorder
• schizencephaly of sensorimotor cortex causing spastic diplegia is not a contraindication.
• Severe head injury or hypoxic encephalopathy (e.g., near-drowning)
• Familial spastic paraplegia and other progressive neurological disorders
• Severe basal ganglia damage in children younger than 5 years
• Dystonia manifests itself during the first 5 years of age (28). After the age of 5 years, SDR may be considered even in the presence of demonstrable basal ganglia damage if spasticity is severe.
• Severe thoracolumbar scoliosis or lumbar lordosis
• Profound motor impairment with no head control
• Multiple prior muscle and tendon releases
• Lack of commitment to carry out postoperative therapy

• Review of a perinatal history, including gestational age, birth weight, twin birth, hypoxic/ischemic event, intraventricular hemorrhage, neonatal infection, seizures.
• Course of motor impairment: Does it date back to infancy? Has there been steady improvement or progressive deterioration?
• If the child had a period of normal motor development followed by signs of motor impairment, one should consider a neoplasm or neurological disorder rather than CP.
• Prior treatments for spasticity
• If a child received intramuscular injection of botulinum A toxin (Botox) or intrathecal baclofen infusion, the extent of improvements following the treatments can help assess the effect of spasticity on a child’s motor function and thus may be predictive of outcome following SDR.

• Signs of spasticity include increased muscle tone, hyperactive deep tendon reflexes, and ankle clonus. Spasticity increases as the child rapidly repeats movements. Thus an easy way to elicit spasticity in a young child is to instruct the child to walk, stand, crawl, and sit. The attempted movements increase not only muscle tone but also abnormal postures. The presence of concomitant ataxia, athetosis, and dystonia is also ascertained.
• Motor strength can be determined by testing individual muscles. In young children, past motor milestones, speed of movement, and ability to isolate joint movements are reliable indices of motor strength. Crawling or walking in a walker and making rapid transitions between positions are signs of good motor function. Isolated joint movements in the lower extremities are predictive of gait outcome in children under the age of 3-4 years (18).
• Assessment of orthopedic deformities and their effects on motor performance. Determination of muscle weakness caused by prior muscle releases and the effects on walking and posture. Common problems include excessive foot dorsiflexion and consequent crouch gait following heel cord release, genu recurvatum following hamstring release, and excessive hip abduction and valgus deformities of the foot following adductor release. These problems are in general refractory to any treatment modality.

• Includes measurements of gross motor function and an assessment of orthopedic deformities. Function also should be assessed with the aid of appropriate braces. Videotaping is useful for gross motor function measurements but also to record changes in the child’s condition over time.

• X-rays of the thoracolumbar spine may demonstrate the presence of lumbar hyperlordosis, scoliosis, spondylolysis, spondylolisthesis, or congenital anomalies. Hip radiographs may reveal hip subluxation or dislocation, both of which may influence the timing of surgical intervention. Routine head or spine MRI is unnecessary; however, in specific cases, these studies may be helpful in identifying cases in which SDR is contraindicated (see above).

• Gait analysis with dynamic electromyography (EMG) helps to confirm the presence of spasticity prior to SDR and also serves as a tool to assess postoperative changes in motor performance.

• Induction and intubation is performed with thiopental, halothane, and nitrous oxide. Short-lasting muscle relaxants (e.g., atracurium or vecuronium) sometimes are used to facilitate intubation. The patient is maintained on fentanyl (10 µg/kg), 1% halothane, and 70% nitrous oxide throughout the case.
• Propofol is avoided because it greatly alters EMG.
• Intravenous antibiotics are administered prior to skin incision.

• The patient is positioned prone on gel bolsters. The operating table is maintained in a position of slight Trendelenburg to minimize CSF loss. Needle electrodes are placed bilaterally in the adductor longus, vastus lateralis, anterior tibialis, peroneus, medial hamstring, and medial gastrocnemius muscles in preparation for intraoperative EMG examination.

• In children, the spinous process of the L1 vertebra is estimated by counting the lumbar spinous processes from the level of the iliac crest. The level of the conus medullaris is then identified transcutaneously using ultrasound.
• Once the level has been localized, the lower thoracic and entire lumbar regions are prepared and included in the draped operative field. The paraspinal muscles at the presumed L1-2 segments then are injected with saline solution containing 1:400,000 epinephrine.

• An incision is made based on the ultrasonographic localization. Electrocautery is used to expose the spinous process and lamina. ultrasound isused to examine the intradural structures through the exposed interlaminar space. In older children, a keyhole laminotomy may be performed to improve visualization with the ultrasound (Figure 1).
• The conus is easily distinguished from the cauda equina using ultrasound (Figure 1). Sagittal views show the conus as a hypodense triangle tapering caudally, while the cauda equina appears hyperdense. On axial views, the conus appears as a hypodense circular structure centered within the dural sac. A narrow gap between the dorsal and ventral spinal roots, lateral to the conus, also can be appreciated on the axial view. In general, axial views localize the conus more reliably than do sagittal views.
• A single-level laminectomy is performed to visualize 5-10 mm of the caudal conus, providing adequate exposure to safely separate the dorsal roots from the ventral roots later in the operation. The laminectomy may be extended to include a portion of the lamina above or below to obtain this exposure.
• The location of the conus is confirmed with ultrasoundbefore opening the dura. A midline durotomy then is made and the dural edges are tacked back with sutures.

• Saline irrigation is not used after the dura is opened because it alters EMG responses. An operating microscope is used. The operating table is rotated slightly away from the surgeon as the contralateral spinal roots are dissected. The arachnoid is removed by sharp dissection, and the filum terminale is identified. The L1-2 spinal roots are identified at the neural foramen, and the dorsal root is separated from the ventral root (Figure 2). The L2 ventral and dorsal roots are traced back to the conus until the cleft between the ventral and dorsal roots is identified. The L2 and adjacent dorsal roots are gently retracted medially, and a cotton patty is placed over the ventral roots. The L1 root is left untouched at this point. The conus and the filum terminale are examined, and the S2-5 sacral roots exiting the conus are identified. The S2 dorsal root can be bulky, especially in patients with postfixed lumbosacral plexus, but there is always an abrupt and marked decrease in its size. The individual S3-5 spinal roots appear as thin threads. The dorsal and ventral roots at this level are close together without intervening space, so all of the S3-5 spinal roots are left intact. The lower sacral roots can be identified best by gently lifting the dorsal roots from the entry zone on the dorsal aspect of the conus. Whenever the surgeon is unsure of the exact identification of the S3-5, it is prudent to spare the S2 dorsal root. Direct electrical stimulation of the dorsal roots does not help identify the sacral nerve roots (30).
• Once the L2-S2 dorsal roots are identified, a 5-mm-wide blue silastic sheet is placed around all of the ipsilateral dorsal roots distant from the conus and ventral lower sacral roots (Figure 2). To ensure that no ventral root or lower sacral root is over the silastic material, examine three structures prior to EMG testing: the L2 foraminal exit, the cleft lateral to the conus between the ventral and dorsal roots, and the S3-5 roots.
• Identification of individual dorsal roots: A shortcoming of this particular dorsal rhizotomy procedure is a difficulty in identifying individual dorsal roots with certainty. However, precise identification of the dorsal roots is not critical for following reasons: 1) the dorsal roots project to multiple segments within the spinal cord, 2) all major muscles of the lower extremities of children with spastic CP receive motor innervation from several segments (37), 3) somatotopic organization occurs in the spinal cord and brain following deafferentation (7).
• The L2 dorsal root is readily identified at the neural foramen. The L3-S2 are roughly identified in the following manner. First, the dorsal roots are spread on top of the silastic sheet. The L3 and L4 dorsal roots, which are located medial to the L2 root, are identified; each of the roots consists of two and three naturally separated rootlets. The L5 and S1 roots are medial to the L4 root and largest of all the lumbosacral roots. The L5 and S1 dorsal roots consist of three or four rootlets with natural demarcation. The S2 root has a single fascicle. Second, an innervation pattern of each root is examined by EMG testing. An individual dorsal root is placed over two hooks of the rhizotomy probes (Aesculap Instrument Co., Burlingame, CA), and responses to electrical stimulation with a threshold voltage are recorded from the lower extremity muscles. The entire dorsal root is tested at each level immediately before subdividing the dorsal root into rootlets.

• Once stimulated, the root is sharply subdivided with a Scheer needle (Storz, St. Louis MO) into four to seven smaller rootlet fascicles of equal size . The rootlet fascicles are suspended over two hooks of the rhizotomy probes. Single constant square wave pulses of 0.1 msec duration are applied to the rootlet at a rate of 0.5 Hz. The stimulus intensity is increased stepwise until a reflex response appears from the ipsilateral muscles. After the reflex threshold is determined, a 50-Hz train of tetanic stimulation for 1 second is applied to the rootlet. The reflex response is then graded according to the criteria detailed in Table 1. Rootlets produce 1+ to 4+ responses. The rootlets that produce a response of 0 are left intact. The rootlets producing 3+ and 4+ responses are cut, and those producing 1+ and 2+ responses are spared. If only 1+ and 2+ responses are detected, then rootlets with the most active responses are cut. At least one rootlet is left, irrespective of EMG responses, to avoid postoperative sensory loss. The dorsal rootlets spared from sectioning are placed behind the silastic sheet and kept separated from rootlets yet to be tested. The procedure is carried out in sequence on the remaining L3-S2 dorsal roots. Between 50% and 75 % of the rootlets examined are sectioned. The L1 dorsal root is identified at the neural foramen, and half of the root is cut without EMG testing. EMG testing of the L1 root is unreliable. The sectioning of the L1 dorsal root is necessary to further reduce spasticity in hip flexors, especially in patients with a large L1 root associated with prefixed lumbosacral plexus. Repeat above for the contralateral side.
  
  Table I
  Grade:EMG Reponse
  0:Unsustained or single discharge to a stimulus train
  1+: Sustained discharges from muscles innervated by the stimulated segment
  2+: Sustained discharges from muscles innervated by the stimulated and immediately adjacent segments
  3+: Sustained discharges from segmentally innervated muscles and muscles innervated through segments distant from the stimulated segment
  4+: Sustained discharges from contralateral muscles with or without sustained discharges from the ipsilateral muscles

• The intradural space then is irrigated with saline solution. Bipolar is seldom needed to control bleeding from the cut ends of fascicles. Clonidine (2 μg/kg in children up to 7 years of age and 1 μg/kg in those ≥ 8 years) with 15 μg/kg morphine is injected prior to dural closure. The dura is closed in a running fashion with 4-0 monofilament nylon. The wound is closed with nonabsorbable sutures in the muscle and fascial layers and absorbable sutures in the subdermal tissue. Tissue adhesive is used to close the incision.

• One night in the PICU.
• Medications: Continuous fentanyl infusion at a dose of 0.5-2.0 µg/kg/hr and Diazepam intravenously at 2 mg/kg IV every 4 hours for 48 hours.
• Transfer to floor POD 1.
• Flat X 48 hours.
• POD 2, stop IV meds. Allow to sit. Light physical therapy is initiated with an emphasis on stretching exercises.
• Aggressive physical therapy is begun on postoperative days 3 and 4
• Discharged POD 5.
• Mandatory outpatient physical therapy from local therapists at home. Postoperative in-patient rehabilitation is not recommended.

• Immediate reduction of spasticity. Complain of numbness, tingling, and a feeling of heaviness in the lower extremities for 5 to 10 days. Voluntary urination is regained within 72 hours.
• Independent walkers walk with assistance by the 5th postoperative day and resume full independent walking by the 14th day. Patients who walk with aids preoperatively take a slower postoperative course; it often takes over 6 weeks for their motor performance to reach preoperative levels.

• CSF leak, meningitis, neurogenic bladder, sensory loss, ileus, bronchospasm, pneumonia, and urinary tract infection (1).
• None of our patients developed neurological complications, but a small number experienced bronchospasm, pneumonia, or urinary tract infection.

• Sensory loss of clinical significance did not occur. Several patients have reported numbness in discrete areas in the upper lumbar dermatomes with hypesthesia confirmed on examination.
• Dysesthesias typically involve hypersensitivity of the foot. May be severe enough to hinder walking for the first few months but generally improves or resolves in several months. No report of new-onset sexual dysfunction following SDR. Male reported erectile dysfunction or impairment of ejaculation.
• Spinal deformities (i.e., spondylosis, spondylolisthesis) (36), lumbar spinal stenosis (19), and lumbar hyperlordosis (14) in SDR through a multilevel lumbosacral laminectomy or laminotomy. Highlights the importance of limited laminectomy in SDR. Although some claim that osteoplastic laminotomy may reduce the risk of spinal deformities, convincing evidence for the claim remains to be demonstrated.

• Reduction of spasticity in nearly all with spastic diplegia and in with spastic quadriplegia (16, 28, 40, 41, 49). The marked reduction of spasticity is apparent shortly after the operation as a decrease in muscle tone, knee and ankle jerk reflexes, and the absence of ankle clonus. Months to years postoperatively, muscle tone may increase to a minor degree but remains lower than preoperative levels.
• There is a significant risk of failure in spastic quadriplegics. Reason for this is unclear
• The highest failure rate for SDR is seen among nonambulatory and severely involved quadriplegics in whom SDR is performed to improve hygiene care and sitting. Spasticity increases progressively over 6 weeks, reaching preoperative levels of severity by 2 years after the operation.

• When spasticity is reduced or eliminated, motor weakness underlying the spasticity surfaces. When SDR is performed through a multilevel laminectomy, a transient motor weakness may be observed immediately postoperatively. SDR does not produce lasting motor weakness. Strength in CP patients was less than that in able-bodied children, but 6 months after the SDR, strength had increased over pre-rhizotomy levels (16).

• Three controlled trials have evaluated the effect of SDR combined with physical therapy on changes in gross motor function measure (GMFM) scores (28, 41, 49). Two studies found the SDR group to have significantly higher GMFM scores at 9 months and 12 months than the group receiving physical therapy alone (41, 49). However, the third study found no beneficial effect of SDR on GMFM scores assessed at 12 and 24 months postoperatively (28).

• To predict gait outcome: consider the type of spasticity, the level of motor development, and the ability to dorsiflex the foot.
• Virtually all children who can dorsiflex the foot bilaterally without associated simultaneous movements of other joints, either before or after SDR, become independent walkers. If the dorsiflexion of the foot is lacking bilaterally, independent walking after SDR is impossible, and a walker or crutches will be needed for assistance.
• Children who can sit alone at years will either walk independently or use assistive devices (29).
• Computerized gait analysis evaluating cadence, velocity, and other parameters has been used to assess gait outcome following SDR (8, 10, 45). Early changes in the assessed gait parameters are frequently predictive of sustained improvements in gait lasting as long as 10 years postoperatively (42).

• SDR performed between 2 and 4 years of age reduced the need for orthopedic surgery for heel cord, hamstring, and adductor releases (11). It is rare to encounter the need for late orthopedic surgery in diplegic children 2-4 years of age who walk unaided after SDR (T.S.P., personal observation). In contrast, children who walk with assistive devices or cannot walk at all often need orthopedic surgery.

• Hip subluxation and dislocation occur in approximately 35% of CP patients (26). Spasticity in the hip adductor and iliopsoas muscles, combined with lack of normal weight-bearing, play an important role in hip development. SDR may prevent progressive hip subluxation (22, 35).

• Some children show marked improvements in their attention, language, temperament, mood, and interpersonal interactions after SDR. The improvements may result in part from relief of spasticity-associated physical discomfort or from intensified therapy following SDR. The improvements also may be related to “suprasegmental effects” of SDR on neural circuits beyond the operated lumbosacral segments (13).

• Improvements in upper extremity function are manifested primarily as increased range of motion (10).
• Spastic quadriplegic children who have some upper extremity movement are likely to show improvement after SDR.
• Fine motor skills are generally not affected by SDR.

• We have observed improvements in bladder function in spastic diplegics following SDR(43). No such improvement has been noted in spastic quadriplegics following SDR.
• Long-term outcome
• Long-term outcomes following benefits observed after SDR were durable and sustained over time (5, 42). Spasticity remained reduced in all patients, and motor function continued to improve in 80% of patients. Repeat gait analysis 10 years after SDR in children with spastic diplegia demonstrated sustained improvement in hip and knee ranges of motion, step length, and velocity of gait (42).

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