What Is Cerebral Palsy?
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Common Medical Comorbidities Associated with Cerebral Palsy
Common Medical Comorbidities Associated with Cerebral Palsy a,b, a,b DavidW. Pruitt, MD *,TobiasTsai,MD KEYWORDS Cerebral palsy Seizures Gastroesophageal reflux Sleep Pain The 2004 International Workshop of Definition and Classification of Cerebral Palsy definition includes the following: ‘‘The motor disorders of cerebral palsy are often accompanied by disturbances of sensation, perception, cognition, communication, and behaviors, by epilepsy, and by secondary musculoskeletal problems.’’1 The Surveillance for Cerebral Palsy in Europe (SCPE) collaboration has reported that 31% of children with cerebral palsy (CP) have severe intellectual disability, 11% have severe visual disability, and 21% have epilepsy.2 Thus, although CP is primarily a disorder of movement, many children with this diagnosis have other impairments that may affect their function, quality of life, and life expectancy. Children with a diag- nosis of CP often have multiple medical issues that are best addressed by an interdis- ciplinary medical team, including a ‘‘medical home’’ with primary care physicians and additional assistance from multiple medical subspecialists. A comprehensive health plan implemented in the context of a well-defined ‘‘medical home’’ is a critical compo- nent to ensuring that the health needs of children with CP are adequately addressed.3,4 Management of the multisystem-associated comorbidities requires a careful review of systems. Cerebral palsy is defined as a nonprogressive neurologic condition; however, as the child grows and matures physically -
10Neurodevelopmental Effects of Childhood Exposure to Heavy
Neurodevelopmental E¤ects of Childhood Exposure to Heavy Metals: 10 Lessons from Pediatric Lead Poisoning Theodore I. Lidsky, Agnes T. Heaney, Jay S. Schneider, and John F. Rosen Increasing industrialization has led to increased exposure to neurotoxic metals. By far the most heavily studied of these metals is lead, a neurotoxin that is particularly dangerous to the developing nervous system of children. Awareness that lead poison- ing poses a special risk for children dates back over 100 years, and there has been increasing research on the developmental e¤ects of this poison over the past 60 years. Despite this research and growing public awareness of the dangers of lead to chil- dren, government regulation has lagged scientific knowledge; legislation has been in- e¤ectual in critical areas, and many new cases of poisoning occur each year. Lead, however, is not the only neurotoxic metal that presents a danger to children. Several other heavy metals, such as mercury and manganese, are also neurotoxic, have adverse e¤ects on the developing brain, and can be encountered by children. Al- though these other neurotoxic metals have not been as heavily studied as lead, there has been important research describing their e¤ects on the brain. The purpose of the present chapter is to review the neurotoxicology of lead poisoning as well as what is known concerning the neurtoxicology of mercury and manganese. The purpose of this review is to provide information that might be of some help in avoiding repeti- tion of the mistakes that were made in attempting to protect children from the dan- gers of lead poisoning. -
Child Neurology: Hereditary Spastic Paraplegia in Children S.T
RESIDENT & FELLOW SECTION Child Neurology: Section Editor Hereditary spastic paraplegia in children Mitchell S.V. Elkind, MD, MS S.T. de Bot, MD Because the medical literature on hereditary spastic clinical feature is progressive lower limb spasticity B.P.C. van de paraplegia (HSP) is dominated by descriptions of secondary to pyramidal tract dysfunction. HSP is Warrenburg, MD, adult case series, there is less emphasis on the genetic classified as pure if neurologic signs are limited to the PhD evaluation in suspected pediatric cases of HSP. The lower limbs (although urinary urgency and mild im- H.P.H. Kremer, differential diagnosis of progressive spastic paraplegia pairment of vibration perception in the distal lower MD, PhD strongly depends on the age at onset, as well as the ac- extremities may occur). In contrast, complicated M.A.A.P. Willemsen, companying clinical features, possible abnormalities on forms of HSP display additional neurologic and MRI abnormalities such as ataxia, more significant periph- MD, PhD MRI, and family history. In order to develop a rational eral neuropathy, mental retardation, or a thin corpus diagnostic strategy for pediatric HSP cases, we per- callosum. HSP may be inherited as an autosomal formed a literature search focusing on presenting signs Address correspondence and dominant, autosomal recessive, or X-linked disease. reprint requests to Dr. S.T. de and symptoms, age at onset, and genotype. We present Over 40 loci and nearly 20 genes have already been Bot, Radboud University a case of a young boy with a REEP1 (SPG31) mutation. Nijmegen Medical Centre, identified.1 Autosomal dominant transmission is ob- Department of Neurology, PO served in 70% to 80% of all cases and typically re- Box 9101, 6500 HB, Nijmegen, CASE REPORT A 4-year-old boy presented with 2 the Netherlands progressive walking difficulties from the time he sults in pure HSP. -
Accelerating Research. Empowering Families
RESEARCH STRATEGY AND MISSION We aggressively pursue research to identify treatments and a cure for Rett syndrome. New Mecp2 female mouse model developed AMO receives FDA Orphan Drug Designation 2018 + BEYOND With your support, we can Neuren begins plans for trofinetide Phase 3 continue to blaze a trail in Rett syndrome research and family 2017 14 clinics designated empowerment to transform lives. as Rett Syndrome Clinical Research First multi-site, Centers of Excellence multi-country clinical Join us in our mission: trial begins: sarizotan • Make a donation 2015 • Coordinate a Fundraiser Clinical trial for • Participate in an Event trofinetide begins • Advocate for Rett syndrome NIH funding of the NHS begins Visit www.rettsyndrome.org or Drug screening Scout program begins call 1.800.719.8214 2014 First multi-site clinical trial Rettsyndrome.org is a 501(c)3 organization in RTT begins: NNZ-2566 (trofinetide) Accelerating dedicated to accelerating research for treatments and a cure for Rett syndrome and related disorders, 2013 while providing family empowerment. As a Established stem Research. leading organization for Rett syndrome research, cell model for Rettsyndrome.org is committed to funding high- drug screening First clinical trial quality, peer-reviewed research grants and programs. in RTT supported by Rettsyndrome.org: IGF-1 Empowering Genetic manipulation 2010 and biochemical Families. intervention improve Rett-like symptoms in a mouse model 2007 4600 Devitt Drive Cincinnati, OH 45246-1104 ‘‘ (800) 818-7388 www.rettsyndrome.org I am very thankful that Rettsyndrome.org has taken such a strong leadership role /rettsyndrome /rettsyndrome /rettsyndromeorg with advancing research. Their progress to get trofinetide to market is very exciting as it could finally be an answer to relieving some of Jill’s daily struggles. -
Hereditary Spastic Paraparesis: a Review of New Developments
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.69.2.150 on 1 August 2000. Downloaded from 150 J Neurol Neurosurg Psychiatry 2000;69:150–160 REVIEW Hereditary spastic paraparesis: a review of new developments CJ McDermott, K White, K Bushby, PJ Shaw Hereditary spastic paraparesis (HSP) or the reditary spastic paraparesis will no doubt Strümpell-Lorrain syndrome is the name given provide a more useful and relevant classifi- to a heterogeneous group of inherited disorders cation. in which the main clinical feature is progressive lower limb spasticity. Before the advent of Epidemiology molecular genetic studies into these disorders, The prevalence of HSP varies in diVerent several classifications had been proposed, studies. Such variation is probably due to a based on the mode of inheritance, the age of combination of diVering diagnostic criteria, onset of symptoms, and the presence or other- variable epidemiological methodology, and wise of additional clinical features. Families geographical factors. Some studies in which with autosomal dominant, autosomal recessive, similar criteria and methods were employed and X-linked inheritance have been described. found the prevalance of HSP/100 000 to be 2.7 in Molise Italy, 4.3 in Valle d’Aosta Italy, and 10–12 Historical aspects 2.0 in Portugal. These studies employed the In 1880 Strümpell published what is consid- diagnostic criteria suggested by Harding and ered to be the first clear description of HSP.He utilised all health institutions and various reported a family in which two brothers were health care professionals in ascertaining cases aVected by spastic paraplegia. The father was from the specific region. -
Cerebral Palsy the ABC's of CP
Cerebral Palsy The ABC’s of CP Toni Benton, M.D. Continuum of Care Project UNM HSC School of Medicine April 20, 2006 Cerebral Palsy Outline I. Definition II. Incidence, Epidemiology and Distribution III. Etiology IV. Types V. Medical Management VI. Psychosocial Issues VII. Aging Cerebral Palsy-Definition Cerebral palsy is a symptom complex, (not a disease) that has multiple etiologies. CP is a disorder of tone, posture or movement due to a lesion in the developing brain. Lesion results in paralysis, weakness, incoordination or abnormal movement Not contagious, no cure. It is static, but it symptoms may change with maturation Cerebral Palsy Brain damage Occurs during developmental period Motor dysfunction Not Curable Non-progressive (static) Any regression or deterioration of motor or intellectual skills should prompt a search for a degenerative disease Therapy can help improve function Cerebral Palsy There are 2 major types of CP, depending on location of lesions: Pyramidal (Spastic) Extrapyramidal There is overlap of both symptoms and anatomic lesions. The pyramidal system carries the signal for muscle contraction. The extrapyramidal system provides regulatory influences on that contraction. Cerebral Palsy Types of brain damage Bleeding Brain malformation Trauma to brain Lack of oxygen Infection Toxins Unknown Epidemiology The overall prevalence of cerebral palsy ranges from 1.5 to 2.5 per 1000 live births. The overall prevalence of CP has remained stable since the 1960’s. Speculations that the increased survival of the VLBW preemies would cause a rise in the prevalence of CP have proven wrong. Likewise the expected decrease in CP as a result of C-section and fetal monitoring has not happened. -
CP Research News 2021
Monday 8 March 2021 Cerebral Palsy Alliance is delighted to bring you this free weekly bulletin of the latest published research into cerebral palsy. Our organisation is committed to supporting cerebral palsy research worldwide - through information, education, collaboration and funding. Find out more at cerebralpalsy.org.au/our-research Professor Nadia Badawi AM Macquarie Group Foundation Chair of Cerebral Palsy Subscribe to CP Research News Interventions and Management 1. Upper Extremity Strengthening for an Individual With Dyskinetic Cerebral Palsy: A Case Report Laura Graber, Claudia Senesac Pediatr Phys Ther. 2021 Feb 23. doi: 10.1097/PEP.0000000000000785. Online ahead of print. Purpose: The purpose of this case is to describe an exercise program designed for an individual with athetoid cerebral palsy who had difficulties with fine motor control and shoulder girdle stability. Summary of key points: ET is a 19-year-old man with dyskinetic-type cerebral palsy with rapidly fluctuating muscle tone and movements that preclude trunk and extremity control necessary for the effective performance of functional activities. The participant underwent a 6-week intense physical therapy program aimed at strength and stability at the shoulder girdle and fine motor movements of the hand. Conclusions: ET had improvements on the Performance of Upper Limb Scale, myometry, and from family report after 6 weeks. Recommendations: A progressive exercise program aimed at improving proximal stability and fine motor function might be an appropriate intervention -
Epilepsy and Cerebral Palsy*
Arch Dis Child: first published as 10.1136/adc.31.155.1 on 1 February 1956. Downloaded from EPILEPSY AND CEREBRAL PALSY* BY BRIAN H. KIRMAN From the Fountain Hospital, Tooting, London (RECEIVED FOR PUBLICATION SEPTEMBER 6, 1955) The two conditions epilepsy and palsy in its Frequency of Epilepsy as a Complication many forms are amongst the earliest syndromes of Cerebral Palsy recorded in history. The association between Brissaud and Souques (1904) attempted to confine epilepsy and cerebral palsy in childhood is a matter the term 'Little's disease' to those cases not com- of everyday experience, and this association is of plicated by fits or mental defect, but Little's (1861-2) scientific interest as throwing light on the nature of own description of 63 cases refers specifically to the cerebral palsy and, more particularly, of epilepsy. complication ofconvulsions. Kinnier Wilson (1940) It is also of practical importance in view of recent refers to Little's disease not as 'an ailment of a well efforts to make more adequate provision for those defined character but a mere syndrome and a rather children with cerebral palsy who are educable. wide-ranging one at that'. Since epilepsy is also The existence of the two conditions in one child not a disease but a symptom of cerebral dysfunction constitutes a double handicap. The present ten- it is understandable that cerebral palsy and epilepsy dency in our educational system is for ever-increasing should often be encountered in the same patient. copyright. subdivision of educational 'types', and any child Kinnier Wilson states that in his experience 30% of who is difficult to fit into one of the artificial cate- cases of cerebral diplegia have fits which may be gories thus constructed is in danger of remaining general or one-sided. -
Cerebral Palsy
Cerebral Palsy Cerebral palsy encompasses a group of non-progressive and non-contagious motor conditions that cause physical disability in various facets of body movement. Cerebral palsy is one of the most common crippling conditions of childhood, dating to events and brain injury before, during or soon after birth. Cerebral palsy is a debilitating condition in which the developing brain is irreversibly damaged, resulting in loss of motor function and sometimes also cognitive function. Despite the large increase in medical intervention during pregnancy and childbirth, the incidence of cerebral palsy has remained relatively stable for the last 60 years. In Australia, a baby is born with cerebral palsy about every 15 hours, equivalent to 1 in 400 births. Presently, there is no cure for cerebral palsy. Classification Cerebral palsy is divided into four major classifications to describe different movement impairments. Movements can be uncontrolled or unpredictable, muscles can be stiff or tight and in some cases people have shaky movements or tremors. These classifications also reflect the areas of the brain that are damaged. The four major classifications are: spastic, ataxic, athetoid/dyskinetic and mixed. In most cases of cerebral palsy, the exact cause is unknown. Suggested possible causes include developmental abnormalities of the brain, brain injury to the fetus caused by low oxygen levels (asphyxia) or poor circulation, preterm birth, infection, and trauma. Spastic cerebral palsy leads to increased muscle tone and inability for muscles to relax (hypertonic). The brain injury usually stems from upper motor neuron in the brain. Spastic cerebral palsy is classified depending on the region of the body affected; these include: spastic hemiplegia; one side being affected, spastic monoplegia; a single limb being affected, spastic triplegia; three limbs being affected, spastic quadriplegia; all four limbs more or less equally affected. -
The Cerebellum in Children with Spastic Cerebral Palsy: Volumetrics MRI Study
Prog Health Sci 2011, Vol 1 , No2 Cerebellum cerebral palsy volumetrics study The cerebellum in children with spastic cerebral palsy: Volumetrics MRI study Gościk E.1*, Kułak W.2, Gościk J.3, Gościk J.4, Okurowska-Zawada B.2, Tarasow E.5 1 Department of Children’s Radiology, Medical University of Bialystok, Poland 2 Department of Pediatric Rehabilitation, Medical University of Bialystok, Poland 3 Faculty of Computer Science, Bialystok University of Technology, Poland 4 Faculty of Mechanical Engineering, Bialystok University of Technology, Poland 5 Department of Radiology, Medical University of Bialystok, Poland ABSTRACT __________________________________________________________________________________________ Purpose: To determine the volume of the difference between the total cerebellar volume and cerebellum in children with spastic cerebral palsy gender in patients with CP was found. No (CP) in relation to risk factors and motor significant relationship between cerebellar volume development. and birth weight, Apgar score, gestational age, and Material and methods: The present study included Gross Motor Function Classification System 30 children with spastic CP, aged 2-17 years. The (GMFCS) level were noted. Positive correlations volume of the cerebellum was examined on sagittal between birth weight, Apgar score, gestational age, magnetic resonance images (MRI) of the CP and GMFCS level, between Apgar score and patients and on 33 healthy subjects. To estimate the gestational age, or between gestational age and total cerebellum volume of each subject we used GMFCS level were found. Analyze 10 Biomedical Imaging Software. Conclusion: Our results show that children with Results: Children with spastic CP (129726,2 ± spastic CP had smaller volumes of the cerebellum 26040,72 mm3) had a significantly smaller mean of as compared to controls. -
Cerebral Palsy: Critical Elements of Care
Cerebral Palsy CRITICAL ELEMENTS OF CARE Produced by The Center for Children with Special Needs Children's Hospital and Regional Medical Center, Seattle, WA Fourth Edition, Revised 2/2006 The Critical Elements of Care (CEC) consider care issues across the life span of the child. The intent of the document is to educate and support those caring for a child with Cerebral Palsy. The CEC is intended to assist the Primary Care Provider in the recognition of symptoms, diagnosis and care management related to a specific diagnosis. The document provides a framework for a consistent approach to manage- ment of these children. These guidelines were developed through a consensus process. The design team was multidisciplinary with state-wide representation involving primary and tertiary care providers, family members, and a represen- tative from a health plan. Original Consensus Team: Leslie Babbitt, RD, MS Jean Popalisky, RN, MN Barbara Boldrin, RN Diana Sandoval, MS, OTR/L Charles Cowan, MD Pat Trulson, PHN Betsey Denonville, RN Stephanie Underwood, Parent Kathy Mullin, RN William Walker, MD Chris Olson, MD Technical Assistance: John (Jeff) McLaughlin, MD Content reviewed and updated 2/06: William Walker, MD DISCLAIMER: Individual variations in the condition of the patient, status of patient and family, and the response to treatment, as well as other circumstances, mean that the optimal treatment outcome for some patients may be obtained from practices other than those recommended in this document. This consensus based document is not intended to replace sound clinical judgement or individualized consulta- tion with the responsible provider regarding patient care needs. © 1997, 2002, 2006 Children’s Hospital and Regional Medical Center, Seattle, Washington. -
Cerebral Hypotonia by Mihee Bay MD (Dr
Cerebral hypotonia By Mihee Bay MD (Dr. Bay of Kennedy Krieger Institute and Johns Hopkins School of Medicine has no relevant financial relationships to disclose.) Originally released July 12, 2006; last updated February 1, 2016; expires February 1, 2019 Introduction This article includes discussion of cerebral hypotonia, central hypotonia, essential hypotonia, benign congenital hypotonia, and floppy infant. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations. Overview Hypotonia is a clinical manifestation of numerous diseases affecting the central and/or peripheral motor nervous system. The key to accurate diagnosis involves integral steps of evaluation that include a detailed history, examination, and diagnostic tests. “Cerebral” (or central) hypotonia implies pathogenesis from abnormalities from the central nervous system, and related causal disorders include cerebral dysgenesis and genetic or metabolic disorders. Patients with central hypotonia generally have hypotonia without associated weakness, in contrast to the peripheral (lower motor neuron) causes, which typically produce both hypotonia and muscle weakness. Hypotonia is a clinical manifestation of over 500 genetic disorders; thus, a logical, stepwise approach to diagnosis is essential. With recent advances in the field of genetic testing, diagnostic yield will undoubtedly improve. There is no cure, but treatment includes supportive therapies, such as physical and occupational therapy, and diagnosis-specific management. Key points • Hypotonia is reduced tension or resistance of passive range of motion. • The first step in the evaluation of a child with hypotonia is localization to the central (“cerebral”) or peripheral nervous system, or both. • Central hypotonia is more likely to be noted axially with normal strength and hyperactive to normal deep tendon reflexes.