SPASTIC HIP IN CEREBRAL PALSY

LILIANA PADURE CIOBANU CONSTANTINANDRADA MIREA MIHAELA AXENTEMIHAI DUMANGIU FLORIN DRĂGANALBERT BICLINERU CONSTANTIN FELICIAN IONVERONICA MORCOV GEORGETA PETREMIRUNA CARDOS

ABSTRACT Walking initiative corresponds to a “fall” due to posture inhibition. First, the gravity center is moving on one leg, permitting the other to straggle from the floor. Gravity center is placed above and the body switch the boost point onto the advanced leg. Muscular contrac-tions are permanently redistributed on the postural muscles, which reestablish the balance at any time. All these disordered spasticity mechanisms through the limbs extensors hypertonia (anti-gravitational muscles) generate walking dif-ficulties and joints modifications in cerebral palsy (CP) affected children. By this paper, we proposed spastic hip joint modifications tracking for the child who achieved walking, because surgery interventions, on these joints in early childhood with chronologic and motric age, block the correct rehabilitation program continuity. Our follow up lot with CP affected children comprises 44 inpatients (88 hip joints), between February and July 2009.The child must be analyzed by clinical methods, video recordings, complex gait analysis, for evaluating the most appropriate surgery moment (when cerebral maturation is complete – the brain being ready for the anesthetic shock) and achieving the best decision.

Key-words: cerebral palsy, spastic hip joint. 1. INTRODUCTIONIn the beginning of autonomous gait, normal child do not reach to adapt himself to the postural perturbations produced by unfriendly soil or by visible obstacles. Usually, at about 2 years old, the child is anticipating perturbations from the obstacle. Sutherland is estimating that scarcely at 6-7 years of age the child’s gait has the adult electromyographical, kinematical and kinetic feature. At the age of one year, before the firsts steps, the child has the body tilted forward, lower limbs in triple flexion, arms in abduction and variable flexion, elbows flexed. Alternated displacements of upper and lower limbs are absent. Anterior foot is establishing initial contact, ankle is in plantar flexion. Hips are in external rotation. Sustaining on heel duration is short; the child being in anterior un balance, such as him or her would try to reach his or her gravity center.In the swing phase, hip flexion, pelvic ante version and his right – left rotation are important. At one year and a half of age, plantar flexion is diminishing at the swing end phase, and so, the foot is positioned for an initial contact made with the heel: the child begins to “attack” with the heel. At about 2 and a half years of age the hip passes in internal rotation and in abduction during phase of sustaining on one foot. The pelvis has a little ante-version and in consequence pelvic flexion is reducing at the end of sustentation. Stride length and speed are enough to provoke the belts’ alternative rotation, inducing arm swing at about 75% of children. For the rest of 25%, alternative rotation and arm swing will be acquired at about 3 and a half years of age. If posture and locomotion are apart “systems”, they are converging concurrently on motor neurons, being coordinated by central interactions needed by biped walking. Coordination between posture and locomotion is appearing from the gait beginning. balance is more complex because it is associating more divergent obstacles: postural dynamic stability in time dynamic conditions while the body is propelled forward with a variable sustaining mono or bipedal function of locomotor’s cycle phase. Loco motor activity is installing Loco motor when cortical activity has a sufficient level. Locomotion depends on both cortical and sub cortical activity, being also on the strong influence of the gravity. Gait initiation is corresponding to a real falling, due to the posture inhibition. In a first moment, the gravity centre is displacing laterally, allowing to the other limb to rise. Then, the gravity centre is displacing, allowing to the body to pass to the front foot. At last, contraction is redistributed to the postural muscles, which are reestablishing balance. If until there we have expressed some short data about the connection of the elements witch are concurring to the gait acquisition, it is because the practitioner is obliged to take account about the phase subtlety in this process at the child with cerebral palsy (CP).All SNC lesions are producing subjacent partial de-enervated structures reorganization where there are appearing architectural changes of the peripheral nervous system and also collateral agglomeration of the intact neural fiber, or the apparition of both new motor plates and neural synapses. Reorganization of spinal segmental reflexes which are interfering in somatic motility explains spasticity appearance. Direct and inverse miotatic reflexes are disinhibited and are appearing both a tonus lost and a modification of a balance between agonists and antagonists by diminishing reciprocal inhibition. Spasticity can became excessive, perturbing posture or residual motility. Beside deficit of muscular voluntary strength in various degrees (paresis, palsy), spasticity is associated to motor deficit because of their proximal neural paths. Spasticity prevails on postural muscles, on extensor muscles on lower limbs (flexing of upper limbs) and has some features:Is dependent of strength speed – reflex activity subsides in rest in case of spasticity, regardless other causes of muscular hyper tone.;

spasticity subsides at prolonged elongation (blade of knife switch phenomena). While elongation amplitude is increasing, reflex contraction is reducing on the extensor muscle, which is due to: Golgi receptors, secondary fusal afferences , inhibiting effect of the reflex afferences in flexion (recent findings conclude that reflex in flexion is absent in upper limb)Fatigue – reflex activity is diminishing when is repeating muscular elongation at time durations incompatible with the activation of presynaptic inhibition – this is translate as a excessive progressive myotatic hyperexcitability depletion (synaptic depletion) in neuromediator. Spasticity is variable at the same child, in time, but also because of different parameters: temperature, unfriendly environment considered by the child, vigilance state, position, cutaneous stimulation, vegetative afferentions, and constipation. It is regrettable that those pathophysiological mechanisms, and also different therapeutic approach possibilities of cerebral palsy are unknown or ignored by many clinicians, which are looking strictly from an anatomic point of view at the motor and cerebral infirm child’s lower limbs.Although we had to consider that lesions in cerebral palsy as non progressive, us, who are treating those children, are conscious that unfortunately, we are in the presence of a progressive pathology along the growth phase, when are struggling for our patients not to shut down in “triple flexion”. In a direct observation, in a multidisciplinary team, we had to analyze motricity and clinical findings of children with CP:Primary expression of the neuronal lesions (observed on cranial CT, MRI) with both muscular tone, balance and segmental muscular strength perturbations;Clinical consequences secondary to growth which is faster for bone, and then primary problems, generated by muscular retractions and osseous deformities.Tertiary problems, represented by walking compensatory postural mechanisms.In the child with CP assessment is always taking into account:Functional level of neuropsychomotor developmentFast enough physical development especially between 1 and 7 years of age, when child waist is slurring. “Mature” gait acquisition (autonomous, reliable, most esthetical possible)After those considerations, therapeutic protocol has to be coherent function of the assembly of items discussed previously. Intervention against hypertonia has to be earlier to prevent onset of secondary disturbances. (retractions, vicious postures, osseous deformities).At the lower limb level, we take care of particular details of each patient linked to an inactive or less active muscle, to the voluntary contraction, but excessively active in a synergic movement. For example: anterior calf muscle can be inactive in dorsal analytical foot flexion, bat very active in hip flexion, and also having only one phase of inactivity in the course of a normal gait and being permanently active in accelerated gait. In diplegics with motor deficit symmetrically apparent, patterns right-left are often lightly different such as hipertonia is more accentuate on hemi-case hemi-body.Hip adductors are unjustly considered the only responsible of hip adduction. Attitude in adduction is a kinematical consequence of combination of hip flexion and internal rotation.Attenion, to the intern right muscle, which differentiating itself from internal ischiohamstrings, can participate at knee flexion ant at hip adduction and internal rotation. Taking into account of these considerations, smart surgical intervention is avoiding adductors and also intervention with botulinum toxin is not made on adductors, but on internal right muscle. When internal rotation is combined with hip flexion, foot is laterally deviated. During sustaining flexion, on deviated lower limb, lateral shoulder swing on the sustaining limb, do not mean week lateral stabilizers but a necessary adaptation to bring gravity center nearest to the sustaining lower limb. Equinuus dynamic leg (without retraction of triceps sural muscle components) is the consequence of a shorter activity of the rising limb muscles, followed by a premature activation of gastrocnemius (most often) and soleus muscles.Propulsion phase is hidden because triceps has low activity. Our insistence on the muscular activity intimacy explain the necessity to adapt to each child both kinetic patterns and electrical, thermal or biochemical interventions(with botulinum toxin) and , most of all, o careful analysis about the surgical decisions of the spastic patient: tendinous transpositions, muscular stretching. To reduce hypertonia a therapy has to be :a. selective because more hypertonic muscle affects child motricityb. reversible, not to create prejudice to a muscle, muscle group and implicitly to the osseousc. segments which are forming a joint where there is a growing cartilage.Reliable, correct doses of electricity, shock waves, of botulinum toxin.

2. EXPERIMENTAL

2.1. Used materialsFor our team, The National Children’ Neuropsychomotor Rehabilitation Medical Centre „Dr. Nicolae Robanescu”, botulinum toxin, by its local action of chemical neuroctomy, reversible, local and lasting (between 3 and 6 month) has the endorsement to be the most required treatment for plurifocal spasticity, especially at young children, until 5-6 years of age.

2.2. Work methodologyWe are practicing:1. A rigorous multidimensional both clinical (Ashworth academy) and video assessment

multi site injections in the frame of judicious sagital realignment 2. an adapted and sustained kinetic therapy whose functional benefits we are maintaining in specific orthoses. Short recall – botulinum toxin of A type is acting at the neuromuscular junction level where inhibits acetylcholine release generating a local hypotonia, the muscle is recovering strength after 8-24 weeks, recovering morphologically completely. We know today that the neuromuscular junction blockage it is not reversible, that it is appearing a new neuromuscular junction like a help for the blocked one, which is degrading itself when the primarily blocked neuromuscular junction is recovering. Rehabilitation after injection with botulinum toxin is hence complete, with the recovery of a normal function of the neuromuscular junction. The therapeutic action by choosing muscle to be injected is made in the multidisciplinary team (physician, kinetic therapist, ergo therapist, psychologist), with the knowledge of biomechanics of both hip, knee and ankle (and in gait, when it is acquired) and discussing the child as a whole: relationship between both body and pelvis, hip, knee, ankle, foot.

2.3. CharacterizationsWe are targeting to the muscles really involved in the therapeutic goals, applying the following principles:Necessity to maintain continuity in neuropsychomotor development action to improve both kinesthetic image and motor pattern of the child with cerebral palsyObtaining of precise functional benefits, expected in a clinic good sense logic of the child development.Realizing a multi site strategy to obtain a functional gain expected by a correct assignment of doses by areas located in a kinematical chain to deliver to the muscle the appropriate quantity of toxin (avoiding waste in little dose and on many sites – many muscles). Our major goals, in the future, in CP treatment, are:Re-alignment in sagital plane to ameliorate stability on the floor (sustaining on all sole, by bringing the heel on the floor) – this in the case of predominant distal motor deficit;The goal to stabilize the heel on the floor and to give to the child support on the whole sole, has the role both to limit supraiacent compensations, to offer a proximal motricity and to diminish both knee and hip deformation, for getting out from the logic of the falling down in flexion (of hip, knee) of the spastic patient. This is a goal which is often achieved. Soleus muscle is week, the descent of the heel and sole stabilization is reducing often falls of the child. Both foot orthosis earlier, so in time, and adequate kinetic therapy use are making from this goal a success on short term. On medium and long time, knee and hip are progressively hard to ameliorate – hypertonia, orhoses barely accepted are making the goal hard to achieve. Frontal balance – can be obtained only by preventing rotation disturbances, by seeking to maintain a symmetric support, by injection with botulinum toxin of both intern right and posterior tibial muscles, by the conservation of the gain in correct manufactured orthoses. It is a continuous struggle of both physician, kinetic therapist and mother to limit rotational disturbance structuration which is an aggravating factor of the child’s functional level. Improvement will be progressive, objectified by the multidisciplinary team, warned by anterior experiences and will be registered in distance by:Child’s functional stability in all of his or her acquisitionsSurgical interventions on tendon diminishing at young child until 5-6 years of age.A limitation of surgical gesture in osseous area.We are making an example by observing in time a sample of 44 children with cerebral palsy, which are walking. We are choosing to look and analyze one joint, the hip, because in our experience, we have lived the drama of come children with an unexpected surgical intervention at this level. The 44 children are walking, we have:1. their videotapes before and after injection with botulinum toxin.2. Hip radiographies 3. Recordings of clinical observations

3. RESULTS AND DISCUTIONS:Observed changes showed that spastic patient can have at the age of walk acquisition hip unmodified or with the following deficiencies presented unilaterally or bilaterally (even 2 types of modifications):1. Hip dislocation – 1%2. Coxa magna breva – 1%3. Hip dislocation treated by surgery – 3%4. Bilateral dysplasia – 4%5. Coxa recta unilateral – 5%6.Coxa recta bilateral – 7%7. Coxa valga unilateral – 13%8. Coxa valga bilateral – 16%9. Normal hip– 50%One of the patients has coxa valga bilateral and subluxation

4. CONCLUSIONS:Insufficient, short surgical examination of a complex neuromuscular pathology of central origin which needs direct and long term observation, is generating errors which are aggravating ulterior state of spastic child.The child has to be analyzed by clinical methods video records, complex assessments of gait, to make an adequate

decision for the case and to make the surgical intervention when cerebral maturation is accomplished (the brain can sustain the total anesthetic shock) and when motric potential asks for it.

BIBLIOGRAPHY

[1]. Viel, E., La marche humaine, Elsevier Massons, 2008[2]. Padure, L., Managementul spasticitatii la copil, Ed. Universitara, 2007

Authors:Conf.Dr.LILIANA PADURE,

Dr. CONSTANTIN CIOBANUKt. MIHAI DUMANGIU,Kt FLORIN DRAGAN,

Kt. ALBERT BICLINERU,Dr.MIHAELA AXENTE,Kt. C.FELICIAN ION

Psih.VERONICA MORCOVAs. Med.GEORGETA PETRE,

Trad. MIRUNA CARDOS“Dr. N. Robanescu” RehabilitationMedicalCenter for Children

40 Dumitru Minca St, 041408Bucharest,Romania

E-mail: info@recuperarecopii.ro; Tel: +40 021 4600232

Dr. ANDRADA MIREA”Carol Davila” University of Medicine and Pharmacy

Dionisie Lupu No. 37 Street, 020021 Bucharest, RomaniaE-mail: andrada.mirea@gmail.com

Tel.: +40 0213343025