Home About us Contact
|
Home About us Contact | ||
|
|
||
Motor Disability (motor + disability)
Selected AbstractsPatterns of motor disability in very preterm childrenDEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 4 2002Melanie Bracewell Abstract Motor development in very preterm children differs in several important ways from that of children born at full term. Variability is common, although the anatomic and physiologic bases for that variability are often poorly understood. Motor patterns over the first postnatal year may depend on behaviours learned during often long periods of neonatal intensive care. The normal pattern of development may be modified by disturbances of brain function caused both by the interruption of normal brain maturation ex-utero and the superimposition of focal brain injuries following very preterm birth. Abnormal patterns of development over the first year may evolve into clear neuromotor patterns of cerebral palsy or resolve, as "transient dystonias." Cerebral palsy is associated with identified patterns of brain injury secondary to ischaemic or haemorrhagic lesions, perhaps modified by activation of inflammatory cytokines. Cerebral palsy rates have not fallen as might be expected over the past 10 years as survival has improved, perhaps because of increasing survival at low gestations, which is associated with the highest prevalence of cerebral palsy. Children who escape cerebral palsy are also at risk of motor impairments during the school years. The relationship of these impairments to perinatal factors or to neurological progress over the first postnatal year is debated. Neuromotor abnormalities are the most frequent of the "hidden disabilities" among ex-preterm children and are thus frequently associated with poorer cognitive ability and attention deficit disorders. Interventions to prevent cerebral palsy or to reduce these late disabilities in very preterm children are needed. MRDD Research Reviews 2002;8:241,248. © 2002 Wiley-Liss, Inc. [source] Ataxia, autism, and the cerebellum: a clinical study of 32 individuals with congenital ataxiaDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 3 2005Ingegerd Åhsgren MD The suggested link between autism and cerebellar dysfunction formed the background for a Swedish clinical study in 2001. Thirty-two children (17 females, 15 males; mean age 12y, SD 3y 10mo; range 6 to 21y) with a clinical suspicion of non-progressive congenital ataxia were examined, and parents were interviewed about the presence of neuropsychiatric problems in the child. Twelve children had simple ataxia, eight had ataxic diplegia, and 12 had,borderline'ataxia. All but one of the 32 children had a mild to moderate gross motor disability according to Gross Motor Function Classification System (15 were categorized as level I,16 as level II, and one child as level IV). Neuroimaging and neuropsychological testing were achieved in most cases. There was a strong association between learning disability* and autism spectrum disorder (often combined with hyperactivity disorder) on the one hand, and both simple and borderline,ataxia'on the other, but a weaker link between ataxic diplegia and neuropsychiatric disorders. A correlation between cerebellar macropathology on neuroimaging and neuropsychiatric disorders was not supported. Congenital ataxia might not be a clear-cut syndrome of cerebellar disease, but one of many signs of prenatal events or syndromes, leading to a complex neurodevelopmental disorder including autism and learning disability. [source] Health status of children with moderate to severe cerebral palsyDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 6 2001Gregory S Liptak MD MPH The aim of the study was to evaluate the health of children with cerebral palsy (CP) using a global assessment of quality of life, condition-specific measures, and assessments of health care use. A multicenter population-based cross-sectional survey of 235 children, aged 2 to 18 years, with moderate to severe impairment, was carried out using Gross Motor Function Classification System (GMFCS) levels III (n= 56), IV (n=55), and V (n=122). This study group scored significantly below the mean on the Child Health Questionnaire (CHQ) for Pain, General Health, Physical Functioning, and Impact on Parents. These children used more medications than children without CP from a national sample. Fifty-nine children used feeding tubes. Children in GMFCS level V who used a feeding tube had the lowest estimate of mental age, required the most health care resources, used the most medications, had the most respiratory problems, and had the lowest Global Health scores. Children with the most severe motor disability who have feeding tubes are an especially frail group who require numerous health-related resources and treatments. Also, there is a relationship among measures of health status such as the CHQ, functional abilities, use of resources, and mental age, but each appears to measure different aspects of health and well-being and should be used in combination to reflect children's overall health status. [source] Assessment of corticodiaphragmatic pathway and pulmonary function in acute ischemic stroke patientsEUROPEAN JOURNAL OF NEUROLOGY, Issue 3 2000E. M. Khedr This study investigates the effect of stroke on the corticodiaphragmatic pathway and attempts to clarify the relationship between neurophysiological data and degree of motor disability, site of infarction in computerized tomography (CT) scan, diaphragmatic excursion, blood gases and pulmonary function in stroke patients. Using magnetic stimulation of the scalp sites and cervical roots, an assessment of corticodiaphragmatic pathway was made. The study included 34 sequentially selected patients from a total of 250 patients with acute ischemic stroke. Twenty-five (age- and sex-matched) volunteers served as controls. Sixteen patients had cortical infarction, 13 had subcortical infarction and five had both cortical and subcortical infarction. The mean according to the Scandinavian Stroke Scale was 32.2. Decreased diaphragmatic excursion was observed in 41% of the patients. Twenty-four patients (70.5%) had abnormal magnetic evoked potentials (MEPs) in the affected hemisphere. In five patients MEPs could not be elicited from the affected hemisphere; the remaining 19 patients had abnormal values of both cortical latency and central conduction time (CCT). Cortical latency, CCT, amplitude of compound muscle action potentials (CMAPs) and excitability threshold of the affected hemisphere were significantly altered compared with both the unaffected hemisphere and the control group. Those patients with hemiplegia had a greater degree of hypoxia, hypocapnia and decreased serum bicarbonate level compared with the control group. Also, hemiplegic patients had different degree of respiratory dysfunction. A statistically significant association was found between neurophysiological data and disability score, diaphragmatic excursion, site of infarction in CT scan and degree of respiratory dysfunction. Central diaphragmatic impairment may occur in acute stroke and could contribute to the occurence of hypoxia in those patients. [source] Study of the regulation of the endocannabinoid system in a virus model of multiple sclerosis reveals a therapeutic effect of palmitoylethanolamideEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2008Frida Loría Abstract Cannabinoids have recently been approved as a treatment for pain in multiple sclerosis (MS). Increasing evidence from animal studies suggests that this class of compounds could also prove efficient to fight neurodegeneration, demyelination, inflammation and autoimmune processes occurring in this pathology. However, the use of cannabinoids is limited by their psychoactive effects. In this context, potentiation of the endogenous cannabinoid signalling could represent a substitute to the use of exogenously administrated cannabinoid ligands. Here, we studied the expression of different elements of the endocannabinoid system in a chronic model of MS in mice. We first studied the expression of the two cannabinoid receptors, CB1 and CB2, as well as the putative intracellular cannabinoid receptor peroxisome proliferator-activated receptor-,. We observed an upregulation of CB2, correlated to the production of proinflammatory cytokines, at 60 days after the onset of the MS model. At this time, the levels of the endocannabinoid, 2-arachidonoylglycerol, and of the anti-inflammatory anandamide congener, palmithoylethanolamide, were enhanced, without changes in the levels of anandamide. These changes were not due to differences in the expression of the degradation enzymes, fatty acid amide hydrolase and monoacylglycerol lipase, or of biosynthetic enzymes, diacylglycerol lipase-, and N -acylphosphatidylethanolamine phospholipase-D at this time (60 days). Finally, the exogenous administration of palmitoylethanolamide resulted in a reduction of motor disability in the animals subjected to this model of MS, accompanied by an anti-inflammatory effect. This study overall highlights the potential therapeutic effects of endocannabinoids in MS. [source] A modified MPTP treatment regime produces reproducible partial nigrostriatal lesions in common marmosetsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2005Mahmoud M. Iravani Abstract Standard MPTP treatment regimens in primates result in >,85% destruction of nigral dopaminergic neurons and the onset of marked motor deficits that respond to known symptomatic treatments for Parkinson's disease (PD). The extent of nigral degeneration reflects the late stages of PD rather than events occurring at its onset. We report on a modified MPTP treatment regimen that causes nigral dopaminergic degeneration in common marmosets equivalent to that occurring at the time of initiation of motor symptoms in man. Subcutaneous administration of MPTP 1 mg/kg for 3 consecutive days caused a reproducible 60% loss of nigral tyrosine hydroxylase (TH)-positive cells, which occurred mainly in the calbindin-D28k -poor nigrosomes with a similar loss of TH-immunoreactivity (TH-ir) in the caudate nucleus and the putamen. The animals showed obvious motor abnormalities with reduced bursts of activity and the onset of motor disability. However, the loss of striatal terminals did not reflect early PD because a greater loss of TH-ir occurred in the caudate nucleus than in the putamen and a marked reduction in TH-ir occurred in striatal patches compared to the matrix. Examination of striatal fibres following a partial MPTP lesion showed a conspicuous increase in the number and the diameter of large branching fibres in the putaminal and to some extent caudatal matrix, pointing to a possible compensatory sprouting of dopaminergic terminals. In addition, these partially lesioned animals did not respond to acute treatment with L-DOPA. This primate partial lesions model may be useful for examining potential neuroprotective or neurorestorative agents for PD. [source] Cellular and behavioural effects of the adenosine A2a receptor antagonist KW-6002 in a rat model of l -DOPA-induced dyskinesiaJOURNAL OF NEUROCHEMISTRY, Issue 6 2003M. Lundblad Abstract We have examined the ability of KW-6002, an adenosine A2a antagonist, to modulate the dyskinetic effects of l -DOPA in 6-hydroxydopamine-lesioned rats. In animals rendered dyskinetic by a previous course of l -DOPA treatment, KW-6002 did not elicit any abnormal involuntary movements on its own, but failed to reduce the severity of dyskinesia when coadministered with l -DOPA. A second experiment was undertaken in order to study the effects of KW-6002 in l -DOPA-naive rats. Thirty-five animals were allotted to four groups to receive a 21-day treatment with: (i) KW-6002 (10 mg/kg/day); (ii) l -DOPA (6 mg/kg/day) i.p.; (iii) KW-6002 plus l -DOPA (same doses as above) or (iv) vehicle. Chronic treatment with KW-6002-only produced a significant relief of motor disability in the rotarod test in the absence of any abnormal involuntary movements. Combined treatment with l -DOPA and KW-6002 improved rotarod performance to a significantly higher degree than did each of the two drugs alone. However, this combined treatment induced dyskinesia to about the same degree as did l -DOPA alone. In situ hybridization histochemistry showed that KW-6002 treatment alone caused an approximately 20% reduction in the striatal levels of preproenkephalin mRNA, whereas neither the coadministration of KW-6002 and l -DOPA nor l -DOPA alone significantly altered the expression of this transcript in the dopamine-denervated striatum. Either alone or in combination with l -DOPA, KW-6002 did not have any modulatory effect on prodynorphin mRNA expression or FosB/,FosB-like immunoreactivity in the dopamine-denervated striatum. These results show that monotreatment with an adenosine A2a receptor antagonist can relieve motor disability without inducing behavioural and cellular signs of dyskinesia in rats with 6-hydroxydopamine lesions. Cotreatment with KW-6002 and l -DOPA potentiates the therapeutic effect but not the dyskinesiogenic potential of the latter drug. [source] Addiction in Parkinson's disease: Impact of subthalamic nucleus deep brain stimulationMOVEMENT DISORDERS, Issue 8 2005Tatiana Witjas MD Abstract In Parkinson's disease, dopamine dysregulation syndrome (DDS) is characterized by severe dopamine addiction and behavioral disorders such as manic psychosis, hypersexuality, pathological gambling, and mood swings. Here, we describe the case of 2 young parkinsonian patients suffering from disabling motor fluctuations and dyskinesia associated with severe DDS. In addition to alleviating the motor disability in both patients, subthalamic nucleus (STN) deep brain stimulation greatly reduced the behavioral disorders as well as completely abolished the addiction to dopaminergic treatment. Dopaminergic addiction in patients with Parkinson's disease, therefore, does not constitute an obstacle to high-frequency STN stimulation, and this treatment may even cure the addiction. © 2005 Movement Disorder Society [source] Treatment of post-stroke dysphagia with repetitive transcranial magnetic stimulationACTA NEUROLOGICA SCANDINAVICA, Issue 3 2009E. M. Khedr Background,,, Up to one-third of patients experience swallowing problems in the period immediately after a stroke. Objective,,, To investigate the therapeutic effect of repetitive transcranial magnetic stimulation (rTMS) on post-stroke dysphagia. Materials and methods,,, Twenty-six patients with post-stroke dysphagia due to monohemispheric stroke were randomly allocated to receive real (n = 14) or sham (n = 12) rTMS of the affected motor cortex. Each patient received a total of 300 rTMS pulses at an intensity of 120% hand motor threshold for five consecutive days. Clinical ratings of dysphagia and motor disability were assessed before and immediately after the last session and then again after 1 and 2 months. The amplitude of the motor-evoked potential (MEP) evoked by single-pulse TMS was also assessed before and at 1 month in 16 of the patients. Results,,, There were no significant differences between patients who received real rTMS and the sham group in age, hand grip strength, Barthel Index or degree of dysphagia at the baseline assessment. Real rTMS led to a significantly greater improvement compared with sham in dysphagia and motor disability that was maintained over 2 months of follow-up. This was accompanied by a significant increase in the amplitude of the oesophageal MEP evoked from either the stroke or non-stroke hemisphere. Conclusion,,, rTMS may be a useful adjunct to conventional therapy for dysphagia after stroke. [source] Insufficient energy and nutrient intake in children with motor disabilityACTA PAEDIATRICA, Issue 8 2009P Kilpinen-Loisa Abstract Aim:, Children with motor disabilities are at increased risk of compromised bone health due to impaired weight bearing. Poor nutritional status may be an additional risk factor. The aim of this study was to evaluate energy and nutrient intakes in children with motor disability. Patients and Methods:, Fifty-four children with motor disability (cerebral palsy in 59%) were included. Three-day food diaries were collected and analysed. The results were compared with recommended dietary allowances for age and sex. Results:, The median age was 10.9 years. The median energy intake was 76% of the recommendation and <80% in 57% of children. Of the total energy, 17% was from protein, 32% from fat and 50% from carbohydrates. The medians were for calcium intake 142% and for vitamin D intake 76% of the recommendation; serum 25-hydroxy-vitamin D concentrations were low (median 46 nmol/L). Children with low energy intake were shorter and lighter and had more severe motor disability than children with sufficient energy intake. Conclusion: Insufficient energy and nutrient intake is common in children with motor disability. This may have adverse health effects especially when associated with low vitamin D intake. Energy and vitamin D supplements should be considered. [source] | |||||||||||||