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PubMed1998

Potentially asphyxiating conditions and spastic cerebral palsy in infants of normal birth weight.

OBJECTIVE: Our purpose was to examine the association of cerebral palsy with conditions that can interrupt oxygen supply to the fetus as a primary pathogenetic event. STUDY DESIGN: A population-based case-control study was performed in four California counties, 1983 through 1985, comparing birth records of 46 children with disabling spastic cerebral palsy without recognized prenatal brain lesions and 378 randomly selected control children weighing > or = 2500 g at birth and surviving to age 3 years. RESULTS: Eight of 46 children with otherwise unexplained spastic cerebral palsy, all eight with quadriplegic cerebral palsy, and 15 of 378 controls had births complicated by tight nuchal cord (odds ratio for quadriplegia 18, 95% confidence interval 6.2 to 48). Other potentially asphyxiating conditions were uncommon and none was associated with spastic diplegia or hemiplegia. Level of care, oxytocin for augmentation of labor, and surgical delivery did not alter the association of potentially asphyxiating conditions with spastic quadriplegia. Intrapartum indicators of fetal stress, including meconium in amniotic fluid and fetal monitoring abnormalities, were common and did not distinguish children with quadriplegia who had potentially asphyxiating conditions from controls with such conditions. CONCLUSION: Potentially asphyxiating conditions, chiefly tight nuchal cord, were associated with an appreciable proportion of unexplained spastic quadriplegia but not with diplegia or hemiplegia. Intrapartum abnormalities were common both in children with cerebral palsy and controls and did not distinguish between them.

Apgar Score↗
PubMed1997

Differences in the retinal GABA system among control, spastic mutant and retinal degeneration mutant mice.

Immunocytochemical methods were used to compare the GABA system in control mice and two mutant strains: spastic which has reduced glycine receptors and retinal degeneration mutant in which the photoreceptors degenerate and reportedly have increased GABA and GAD levels. We found that the spastic mutant retina had reduced GABA-immunoreactivity (IR) in the proximal retina, reduced staining for GAD-1440 in the OPL, and reduced GABAA receptor staining in the OPL, compared to control. The retinal degeneration mutant retinas had enhanced GABA-IR throughout the retina, particularly in Müller cells, bipolar cells and IPL, and enhancement of GABAA receptor staining in the OPL, compared to control. The distributions of GABA-IR, GAD-1440-IR and GABAA receptor-IR in retinas of spastic mutant mice that also expressed the retinal degeneration phenotype resembled those found in retinas of mice that expressed only the retinal degeneration phenotype rather than those that expressed only the spastic mutation. No differences were observed among the conditions for GAD-65, GAD-67 or GABA-T. Our results with the spastic and retinal degeneration mutant mice demonstrate that attenuation in the glycinergic system and photoreceptor degeneration, respectively, is accompanied by alterations in different aspects of the GABA system, giving impetus for caution in the interpretation of experiments involving genetic manipulation of complex phenotypes.

Animals↗
PubMed1998

Muscle activation characteristics of stance balance control in children with spastic cerebral palsy.

Two studies were conducted to investigate muscle recruitment of children with spastic cerebral palsy in response to unexpected perturbation of balance in stance. The aim of the studies was to investigate neural and non-neural mechanical contributions to muscle responses differences these children display when maintaining balance. In the first study, muscle responses of children with spastic diplegia were compared to typically developing children with similar levels of walking experience. Each child stood on a moveable platform that was displaced backward. Electromyographic recordings of posterior agonist and anterior antagonist muscles of the legs and trunk were analyzed and compared to those of normal children who had obtained a similar developmental levels of mobility. Children with spastic cerebral palsy were found to have an increase in antagonist recruitment and decreased trunk activation when compared to typically developing children at the same level of walking experience. Developmental trends were noted to be similar in all children with or without pathology. As children gained independent walking skills, they demonstrated shorter onset latencies in leg and thigh muscles. In the second study, older children with no pathology were perturbed in crouch stance, simulating the posture of their matched children with cerebral palsy. Changes in their muscle responses were observed to more clearly approximate the muscle onset latency organization of children with spastic diplegia. Results of these studies suggest that muscle recruitment differences for balance control in children with spasticity are due to CNS deficits as well as mechanical changes in posture. Copyright 1998 Elsevier Science B.V.

Journal Article↗
PubMed2000

Regulation of stretch reflex threshold in elbow flexors in children with cerebral palsy: a new measure of spasticity.

The tonic stretch reflex threshold in children with cerebral palsy (CP) was measured to determine its test-retest reliability and its concurrent validity as a potential measure of spasticity. Fourteen children with spastic CP aged 6 to 18 years were tested on three separate occasions for clinical spasticity and stretch reflex thresholds of affected elbow flexors. Electromyographic (EMG) recordings were obtained by surface electrodes for elbow flexors and extensors during mechanical displacements of the passive joint towards extension. Displacements were produced by a torque motor at seven velocities which randomly varied from trial to trial. EMG activity was measured in the stretched flexor muscles to determine threshold angles and velocities for each velocity of stretch. These were plotted on a velocity-angle-phase diagram and regression analysis was used to determine the static stretch reflex threshold for each participant. The measure showed good test-retest reliability for the group (ICC 0.73, p<0.001) whereas a significant correlation between the measure and the clinical spasticity scale was not found. This technique is a potential outcome variable for measuring the efficacy of treatments aimed at decreasing spasticity in children with CP.

Adolescent↗
PubMed2002

Wartenberg pendulum test: objective quantification of muscle tone in children with spastic diplegia undergoing selective dorsal rhizotomy.

The aim of this study was to investigate the reliability and sensitivity of the Wartenberg pendulum test for quantification of muscle tone in young children with spastic diplegia undergoing selective dorsal rhizotomy (SDR). Fourteen nondisabled children (mean age of 5.5 years, age range 2.3 to 8.8 years, one female and one male in each year) were tested twice. Twenty children with spastic diplegia (12 males, eight females; mean age of 4.3 years, age range 2.5 to 6.3 years) consecutively selected for SDR, were assessed before and 6 months after SDR. Parameters of the pendulum test: R2, R1, maximal velocity, and swing time were correlated with clinical assessments for spasticity (modified Ashworth scale, quadriceps reflex) and measurements of gross motor function: the Gross Motor Function Classification System and the Gross Motor Function Measure. The Wartenberg pendulum test was found to be an objective and sensitive method for quantifying spasticity in knee extensor muscles in children as young as 2.5 years old. The method was responsive to changes after SDR. The only correlation with clinical measurements of spasticity was between the R2 ratio and the quadriceps reflex. Swing time was the most reliable and sensitive variable; it showed a weak correlation with measurements for gross motor function.

Cerebral Palsy↗
PubMed1975

Decorticate spasticity: a re-examination using quantitative assessment in the primate.

Decorticate spasticity in the squirrel monkey was chosen as a convenient laboratory model of spasticity capable of quantitative assessment upon which to evaluate various currently popular clinical spasmolytic measures. The effects of a wide variety of cortical lesions were studied involving primary and supplementary motor, premotor and parietal cortex unilaterally and bilaterally, measuring muscle tone with the evoked integrated E.M.G. technique. Measurable spasticity resulted only if primary motor cortex was ablated bilaterally usually but not always preferentially involving biceps brachii and quadriceps. Resulting postures were variable offering no justification for the term "decorticate posture". The integrated evoked E.M.G. was proportional to rate of stretch and chiefly phasic in type as in hemiplegic man. Stereotactic dentatectomy resulted in profound ipsilateral reduction in this spasticity, but was without effect in intercollicular or anemic decerebrate cats. The mechanism of the spasticity and of the cerebellar effects are discussed.

Animals↗
PubMed2001

Management of the upper limb with botulinum toxin type A in children with spastic type cerebral palsy and acquired brain injury: clinical implications.

The aim of this article is to describe our clinical experience in treating muscle imbalance in 49 children with spastic upper extremity involvement. We discuss four cohorts of children treated with botulinum toxin type A (BTX-A), each with different treatment objectives. In the first group, 27 children were treated for functional improvement and, of these, 23 had a positive effect, while four had no objective benefit. In the second group, eight children were treated for purposes of presurgical planning; of these, four were referred for surgery, three continued with serial treatment and one child did not benefit from injection. The third group comprised six children who were treated to improve posture and care: in this group, four children demonstrated clear benefit and two children lost some function subsequent to injection. Finally, a fourth group of seven children were treated after acquired brain injury (three with severe tetraplegia, four with hemiplegia). In this group, all children experienced spasticity relaxation and two children with hemiplegia also gained functional benefit. In terms of adverse events, deterioration of upper extremity function was poorly tolerated but limited to the first 1--3 weeks postinjection. Grip strength or thumb grip were diminished if too high doses were used. Overall, our results with BTX-A were rewarding in children with no fixed contracture, good motor learning capacity and high motivation to train. Additionally, BTX-A treatment has proven valuable for counteracting spasticity in children with acquired brain injury. This treatment modality may not, however, be an appropriate treatment option for all children with severe upper extremity spasticity, due to the shorter duration of effect and the potential reduction in functional abilities seen in this cohort. In all cases, the selection of muscles to be treated needs careful clinical assessment. Dynamic EMG analysis should be performed whenever required to aid muscle selection, especially in children with spasticity combined with dystonia. Evaluation of M-responses suggests that for the forearm muscles, doses of BTX-A above 1.5 U/kg/muscle should not be used.

Adolescent↗
PubMed2004

Treatment of childhood spasticity of cerebral origin with intrathecal baclofen: a series of 52 cases.

Continuous intrathecal baclofen infusion (CIBI) for spasticity of spinal and cerebral origin has been practised for over two decades. More recently, it has been used for severe spasticity of cerebral origin in children. Intrathecal baclofen (ITB) appears most beneficial in severe spastic tetraparetics or tetraplegics, but the evaluation of the outcome of ITB and the benefit of the treatment are largely subjective. The evidence base for this treatment has been questioned, in particular for ambulant children, mainly because of the lack of objective outcome measures. Fifty-two spastic tetraparetic children have been treated by this method in Nottingham, from 1998 to 2003. This represents a large homogeneous series of CIBI in children with severe spasticity of cerebral origin. We carried out a prospective audit of our experience, morbidity and observations during that period. We identified that the lack of a suitable scoring system for the evaluation of effectiveness and benefit is a drawback. As a result of these observations a multicentre randomized controlled trial on ITB in tetraplegia-paresis and ambulant children is advocated.

Adolescent↗
PubMed1990

Disorders of the inhibitory glycine receptor: the spastic mouse.

The mutant mouse spastic suffers from a motor disorder of autosomal recessive inheritance which is characterized by tremor, myoclonic episodes, and a disturbed righting response. The most prominent alteration in the mutant is a substantial deficit of postsynaptic glycine receptor channels resulting in a dramatic reduction of glycinergic synaptic inhibition. Function and structure of the glycine receptor protein appear unaffected, which argues for a regulatory rather than a structural effect of the spastic mutation. It appears that other alterations in the spastic mouse are secondary to this fundamental disturbance in the balance of excitatory and inhibitory impulses. In particular, a significant increase in GABAA receptors of the lower parts of the CNS may serve a compensatory function, counteracting in part losses of glycinergic inhibition. Pharmacological experiments indeed show that facilitation of GABAA receptor-mediated inhibition alleviates symptoms of the spastic motor disorder. The recent cDNA cloning of glycine receptor subunits should help define the molecular mechanism by which the spastic gene causes the glycine receptor deficit.

Animals↗
PubMed2000

Endocannabinoids control spasticity in a multiple sclerosis model.

Spasticity is a complicating sign in multiple sclerosis that also develops in a model of chronic relapsing experimental autoimmune encephalomyelitis (CREAE) in mice. In areas associated with nerve damage, increased levels of the endocannabinoids, anandamide (arachidonoylethanolamide, AEA) and 2-arachidonoyl glycerol (2-AG), and of the AEA congener, palmitoylethanolamide (PEA), were detected here, whereas comparable levels of these compounds were found in normal and non-spastic CREAE mice. While exogenously administered endocannabinoids and PEA ameliorate spasticity, selective inhibitors of endocannabinoid re-uptake and hydrolysis-probably through the enhancement of endogenous levels of AEA, and, possibly, 2-arachidonoyl glycerol-significantly ameliorated spasticity to an extent comparable with that observed previously with potent cannabinoid receptor agonists. These studies provide definitive evidence for the tonic control of spasticity by the endocannabinoid system and open new horizons to therapy of multiple sclerosis, and other neuromuscular diseases, based on agents modulating endocannabinoid levels and action, which exhibit little psychotropic activity.

Amides↗
PubMed2004

Spastic diplegia and other motor disturbances in infants receiving interferon-alpha.

OBJECTIVE: To determine how frequently the use of -interferon (-IFN) is associated with the development of spastic diplegia. STUDY DESIGN AND METHODS: Meta-analysis of 600 English manuscripts published January 1991 to June 2002 reporting -IFN use in infants/children. We identified 3,113 children 18 years of age or younger and an estimated 3,055 children 12 years of age or younger who received -IFN therapy. Sixty-nine percent were treated for chronic hepatitis and 14% for vascular neoplasms. OUTCOME MEASURE: Neurologic examination to confirm spastic diplegia or a motor developmental disturbance other than spastic diplegia such as hyperactive deep tendon reflexes, gait disturbances, or impaired fine motor control. RESULTS: Including our index case, 11 of 441 children with vascular lesions developed spastic diplegia and an additional 16 of 441 developed a motor developmental disturbance. All of these children were less than 1 year of age at initiation of therapy. Mean age of initiation and duration of -IFN therapy were not significantly different between groups (P >.05); however, motor developmental disturbances improved with cessation of therapy, whereas spastic diplegia did not. No child receiving treatment for chronic hepatitis developed neurologic complications; however, only 49 children were less than 1 year of age at initiation of therapy. CONCLUSION: -IFN should not be used in infants under 1 year of age unless life-threatening conditions do not respond to any other form of treatment. If -IFN must be used, children should have monthly neurologic examinations. If a motor developmental disturbance is detected and -IFN therapy can be discontinued, it should be.

Adolescent↗
PubMed2001

Deficits in eccentric versus concentric torque in children with spastic cerebral palsy.

PURPOSE: The purposes of this study were to determine whether ambulatory children with spastic cerebral palsy (CP) had abnormal isokinetic eccentric peak torque values at the knee and ankle, and to gain further insights on the influence of spasticity on voluntary force production in this population. METHODS: Twenty-four children with spastic CP (mean = 11.1+/-2.6 yr) and twenty children of comparable age with no neuromotor pathology (mean = 10.3+/-2.6 yr) participated in an isokinetic testing protocol on a Biodex dynamometer that measured eccentric and concentric peak torques of the knee extensors, knee flexors, ankle dorsiflexors, and ankle plantarflexors. Angular velocity of the eccentric trials was 30 degrees x s(-1) and of the concentric trials was 30 degrees x s(-1), 60 degrees x s(-1), and 120 degrees x s(-1). Peak torque values were normalized by body weight and compared across groups by using ANOVA procedures. Eccentric to concentric (E/C) peak torque ratios at 30 degrees x s(-1) were computed for each muscle and compared across groups. The torque values in CP were also expressed as a percent of the mean normalized value of the comparison group and compared across conditions using repeated measures ANOVA (P < 0.05). RESULTS: Children with CP demonstrated decreased eccentric and concentric peak torques for all muscle groups tested. The relative deficit in eccentric torque was less than the concentric torque and the decrement in concentric torque across speeds was greater in CP for all muscle groups except the ankle dorsiflexors. The E/C ratios for the knee extensors and flexors were also greater in CP. CONCLUSIONS: Children with CP have diminished eccentric as well as concentric peak torques at the knee and ankle. The influence of spasticity on voluntary force production can be inferred from the bias toward greater eccentric torque and the greater decrement in concentric torque across speeds in children with spastic CP.

Adolescent↗
PubMed2003

The effects of a neuromuscular electrical stimulation home program on impairments and functional skills of a child with spastic diplegic cerebral palsy: a case report.

PURPOSE: To examine the effects of neuromuscular electrical stimulation (NMES) on impairments and functional skills of a 13-year-old child with spastic diplegic cerebral palsy (CP). METHODS: NMES was administered to the right quadriceps muscles every other day for six weeks. Pre- and posttesting included assessment of strength using a hand-held dynamometer, spasticity using a KinCom isokinetic dynamometer, gait spatiotemporal parameters using GAITRite, and functional motor performance with the use of the Pediatric Evaluation of Disability Inventory (PEDI). RESULTS: After intervention, right quadriceps strength increased from 16.3 +/- 3.06 to 41.7 +/- 4.2 Newtons. Right hamstring spasticity decreased at three tested velocities. In the untreated left lower extremity, strength remained unchanged but spasticity increased. The PEDI showed development of new skills, including the ability to climb stairs with less assistance. CONCLUSION: These findings indicate that NMES was an effective therapeutic technique to improve strength and motor function of a child with spastic diplegic CP.

Journal Article↗
PubMedDate not supplied

The morphology of spastic intracerebral arterioles.

Pial and parenchymatous vessels of cat cerebral cortex were subjected to electrical stimulation by direct current by the application of a silver gel electrode to the vessel wall. A current of small intensity (5V, 10mA, 2s) was sufficient to produce spastic constriction of the pial arteries. Arterial spasm was always segmental and lasted up to 20 min. Intracerebral vessels were stimulated by applying a DC of 20 to 100 V, 20 to 150 mA for 30 s to the brain. Intracerebral muscular vessels showed varying diameters and spastic segments in frozen sections and by electron microscopy. The lumen of spastic vessels was collapsed. The vessel wall convoluted, indicating that the factors causing spastic constriction are different from those responsible for physiological vessel wall constriction. In many cases the perivascular tissue of moderately constricted or spastic arterial vessels was destroyed while the tissue around capillaries always remained intact. It is suggested that periarterial tissue destruction is the result of the sudden and powerful constriction in muscular arteries.

Animals↗
PubMed2004

Spinal implantation of hNT neurons and neuronal precursors: graft survival and functional effects in rats with ischemic spastic paraplegia.

Transient spinal ischemia, a complication associated with aortic cross-clamp may lead to spastic paraplegia. Once fully developed this deficit is permanent. Quantitative histopathological assessments and pharmacological studies show that the ischemic spasticity is secondary to the loss of lumbar GABA and glycinergic inhibitory interneurons. In the present study, we investigated whether human hNT neurons or committed Sprague-Dawley rat spinal neuronal precursors (SNPs) when grafted into previously ischemic spinal segments depleted of inhibitory neurons would restore local inhibitory tone and ameliorate spasticity. Rats with functionally and electrophysiologically defined spasticity that received spinal graft of hNT neurons or neuronal precursors and immunosuppressive treatment displayed a progressive recovery of motor function that correlated with the improvement of otherwise exacerbated peripheral motor response evoked by stimulation of motor cortex. In contrast, in control, medium-injected or oligodendrocyte-grafted animals no significant therapeutic effect was seen. Stereological quantification of grafted neurons revealed 1-2% survival at three months after transplantation. These surviving neurons displayed a robust axo-dendritic sprouting and expression of markers typical of mature neurons including NSE, NeuN and synaptophysin. In both treatment groups a subpopulation of grafted neurons developed GABA immunoreactivity. These data provide evidence that a region specific grafting of hNT neurons or other neuronally committed cells, which have a potential to develop inhibitory neurotransmitter phenotype, represent an effective treatment modality to modulate ischemia-induced spastic paraplegia.

Animals↗
PubMed1998

Lower-extremity strength profiles in spastic cerebral palsy.

Although weakness has been identified in cerebral palsy (CP) in isolated muscle groups, the magnitude of weakness in multiple muscles and the patterns of weakness across joints have not been documented. The maximum voluntary contraction of eight muscle groups in the lower extremities of 15 children with spastic diplegia, 15 with spastic hemiplegia, and 16 age-matched peers was determined using a hand-held dynamometer. Children with spastic diplegia were shown to be weaker than age-matched peers in all muscles tested, as were the children with hemiplegia on the involved side, with strength differences also noted on the uninvolved side. Weakness was more pronounced distally in the groups with CP, and the hip flexors and ankle plantarflexors in spastic CP tended to be relatively stronger than their antagonists as compared with the strength ratios of the comparison group. In conclusion, children with spastic CP demonstrate quantifiable lower-extremity weakness and muscle imbalance across joints.

Cerebral Palsy↗
PubMed2001

Facilitation of transmission in heteronymous group II pathways in spastic hemiplegic patients.

OBJECTIVE: A potent heteronymous group II excitation of quadriceps motor neurons has been recently demonstrated in normal subjects. The present study was undertaken to investigate whether this heteronymous group II excitation also contributes to spasticity in hemiplegic patients. METHOD: The early and late facilitations of the quadriceps H reflex elicited by a conditioning volley to the common peroneal nerve at three times motor threshold, attributed to non-monosynaptic group I and group II excitations respectively, were investigated. The comparison was drawn between results obtained in 20 patients after stroke, with hemiplegia due to a vascular lesion in the territory of the middle cerebral artery, and 20 age and sex matched normal subjects. RESULTS: A significant increase in the group I as well as in the group II common peroneal nerve induced facilitation of the quadriceps H reflex was seen on the spastic side of the patients (group I: 159 (SEM 10)% of control H reflex; group II: 165 (SEM 8)%) compared with their unaffected side (group I: 126 (SEM 4)%; group II: 128 (SEM 5)%) (Wilcoxon signed rank test, p<0. 01), or to the right (group I: 132 (SEM 4)%; group II: 131 (SEM 5)%) or left (group I: 130 (SEM 3)%; group II: 135 (SEM 6)%) side of controls (Mann-Whitney U test, p<0.01). No significant correlation (Spearman rank test) was found between the degree of group I and group II induced facilitations on the spastic side of the patients and the degree of clinically assessed spasticity (Ashworth scale). CONCLUSION: These results reflect a facilitation of the transmission in the interneuronal pathway coactivated by group I and group II afferents, probably resulting from a change in their descending control in spastic hemiplegic patients.

Adult↗
PubMed1995

Bradykinin-induced vasodilation is impaired at the atherosclerotic site but is preserved at the spastic site of human coronary arteries in vivo.

BACKGROUND: Bradykinin causes endothelium-dependent vasodilation of isolated human coronary arteries in vitro. However, the effect of bradykinin on vasomotion of human coronary arteries in vivo has not been studied. The aim of this study was to examine whether bradykinin-induced vasodilation is altered at the atherosclerotic or spastic site of human coronary arteries in vivo. METHODS AND RESULTS: The effect of bradykinin on vasomotion of epicardial coronary arteries was evaluated in 8 patients with normal coronary arteries (control group), 14 patients with organic coronary stenosis (coronary artery disease [CAD] group), and 8 patients with vasospastic angina (VSA group). Changes in the diameter of epicardial coronary artery were assessed by quantitative coronary arteriography. Intracoronary administration of bradykinin at graded doses (60, 200, and 600 ng) dilated epicardial coronary arteries without altering arterial pressure or heart rate in all patients of either group. In the control group, vasomotor responses of the site where acetylcholine caused dilation were compared with the responses of the site where acetylcholine caused constriction. The magnitudes of bradykinin-induced dilation at the site with acetylcholine-induced dilation (mean +/- SD: 6 +/- 6%, 11 +/- 9%, and 15 +/- 9%) were comparable to that (3 +/- 6%, 8 +/- 8%, and 13 +/- 9%) at the site with acetylcholine-induced constriction. In the CAD group, vasomotor responses of the stenotic site (% diameter stenosis, 15% to 50%) and nonstenotic site were examined. The bradykinin-induced dilation at the stenotic site (0 +/- 4%, 3 +/- 8%, and 5 +/- 9%) was significantly less (P < .01) than at the nonstenotic site (3 +/- 4%, 8 +/- 6%, and 16 +/- 11%) and in the control group. Coronary vasodilation with nitrate at the stenotic site (20 +/- 11%) was comparable to that at the nonstenotic site (22 +/- 16%) and in the control group (21 +/- 10%). In the VSA group, vasomotor responses of the site with acetylcholine-induced spasm and the site without spasm were examined. The bradykinin-induced vasodilation at the spastic site (5 +/- 5%, 16 +/- 15%, and 33 +/- 17%) was comparable to that at the nonspastic site (4 +/- 8%, 12 +/- 14%, and 21 +/- 9%). Nitrate-induced dilation was comparable at the spastic site (51 +/- 19%) and the nonspastic site (32 +/- 13%). The ratio of bradykinin-induced vasodilation to nitrate-induced vasodilation at the spastic site was comparable to the control group. CONCLUSIONS: These results suggest that bradykinin causes vasodilation of human epicardial coronary arteries in vivo and that bradykinin-induced endothelium-dependent vasodilation is impaired at the stenotic site but is preserved at the angiographically normal site where endothelium-dependent vasodilation by acetylcholine is impaired and at the spastic site.

Acetylcholine↗