The Neurology of Cerebral Palsy
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Cp-Research-News-2014-06-23
Monday 23 June 2014 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 www.cpresearch.org.au Professor Nadia Badawi Macquarie Group Foundation Chair of Cerebral Palsy PO Box 560, Darlinghurst, New South Wales 2010 Australia Subscribe at www.cpresearch.org/subscribe/researchnews Unsubscribe at www.cpresearch.org/unsubscribe Interventions and Management 1. Iran J Child Neurol. 2014 Spring;8(2):45-52. Associations between Manual Abilities, Gross Motor Function, Epilepsy, and Mental Capacity in Children with Cerebral Palsy. Gajewska E, Sobieska M, Samborski W. OBJECTIVE: This study aimed to evaluate gross motor function and hand function in children with cerebral palsy to explore their association with epilepsy and mental capacity. MATERIAL & METHODS: The research investigating the association between gross and fine motor function and the presence of epilepsy and/or mental impairment was conducted on a group of 83 children (45 girls, 38 boys). Among them, 41 were diagnosed with quadriplegia, 14 hemiplegia, 18 diplegia, 7 mixed form, and 3 athetosis. A neurologist assessed each child in terms of possible epilepsy and confirmed diagnosis in 35 children. A psychologist assessed the mental level (according to Wechsler) and found 13 children within intellectual norm, 3 children with mild mental impairment, 18 with moderate, 27 with severe, and 22 with profound. Children were then classified based on Gross Motor Function Classification System and Manual Ability Classification Scale. RESULTS: The gross motor function and manual performance were analysed in relation to mental impairment and the presence of epilepsy. -
Reframing Psychiatry for Precision Medicine
Reframing Psychiatry for Precision Medicine Elizabeth B Torres 1,2,3* 1 Rutgers University Department of Psychology; [email protected] 2 Rutgers University Center for Cognitive Science (RUCCS) 3 Rutgers University Computer Science, Center for Biomedicine Imaging and Modelling (CBIM) * Correspondence: [email protected]; Tel.: (011) +858-445-8909 (E.B.T) Supplementary Material Sample Psychological criteria that sidelines sensory motor issues in autism: The ADOS-2 manual [1, 2], under the “Guidelines for Selecting a Module” section states (emphasis added): “Note that the ADOS-2 was developed for and standardized using populations of children and adults without significant sensory and motor impairments. Standardized use of any ADOS-2 module presumes that the individual can walk independently and is free of visual or hearing impairments that could potentially interfere with use of the materials or participation in specific tasks.” Sample Psychiatric criteria from the DSM-5 [3] that does not include sensory-motor issues: A. Persistent deficits in social communication and social interaction across multiple contexts, as manifested by the following, currently or by history (examples are illustrative, not exhaustive, see text): 1. Deficits in social-emotional reciprocity, ranging, for example, from abnormal social approach and failure of normal back-and-forth conversation; to reduced sharing of interests, emotions, or affect; to failure to initiate or respond to social interactions. 2. Deficits in nonverbal communicative behaviors used for social interaction, ranging, for example, from poorly integrated verbal and nonverbal communication; to abnormalities in eye contact and body language or deficits in understanding and use of gestures; to a total lack of facial expressions and nonverbal communication. -
The Epidemiology of the Cerebral Palsies
Clinics in Developmental Medicine No. 87 The Epidemiology of the Cerebral Palsies Edited by FIONA STANLEY EVA ALBERMAN 1984 Spastics International Medical Publications OXFORD: Blackwell Scientific Publications Ltd. PHILADELPHIA: J. B. Lippincott Co. CHAPTER 11 Prenatal and Perinatal Risk Factors in a Survey of 681 Swedish Cases BENGT and GUDRUN HAGBERG I, that am curtail'd of this fair proportion, Cheated of feature by dissembling nature, , Deform'd, unfinish'd, sent before my time Into this breathing world, scarce half made up, And that so lamely and unfashionable That dogs bark at me, as I halt by them. Shakespeare, Richard III Introduction The aim of this chapter is to try and shed light on more specific aspects of the main groups of prenatal causes and risk factors for cerebral palsy, their mutual importance, and particularly their relationship to superimposed detrimental perinatal events. This survey is based on an investigation of 681 cases born in Sweden from 1959 to 1976. In our original retrospective analysis of causes of cerebral palsy (Hagberg et al. 1975a), it was found necessary to make certain generalisations about the aetiological groupings. Only the risk factor that was considered to be the predominating possible cause was used for classification. There is no doubt that this oversimplifies the issue as it neglects the complex network of different interacting detrimental risk factors that are present in the majority of cases, and in all probability underlie the development of brain lesions. Definitions For the purpose of the Swedish investigation, the following definition of cerebral palsy was used: a non-progressive 'disorder of movement and posture due to a defect or lesion of the immature brain' (Bax 1964). -
Focusing on the Re-Emergence of Primitive Reflexes Following Acquired Brain Injuries
33 Focusing on The Re-Emergence of Primitive Reflexes Following Acquired Brain Injuries Resiliency Through Reconnections - Reflex Integration Following Brain Injury Alex Andrich, OD, FCOVD Scottsdale, Arizona Patti Andrich, MA, OTR/L, COVT, CINPP September 19, 2019 Alex Andrich, OD, FCOVD Patti Andrich, MA, OTR/L, COVT, CINPP © 2019 Sensory Focus No Pictures or Videos of Patients The contents of this presentation are the property of Sensory Focus / The VISION Development Team and may not be reproduced or shared in any format without express written permission. Disclosure: BINOVI The patients shown today have given us permission to use their pictures and videos for educational purposes only. They would not want their images/videos distributed or shared. We are not receiving any financial compensation for mentioning any other device, equipment, or services that are mentioned during this presentation. Objectives – Advanced Course Objectives Detail what primitive reflexes (PR) are Learn how to effectively screen for the presence of PRs Why they re-emerge following a brain injury Learn how to reintegrate these reflexes to improve patient How they affect sensory-motor integration outcomes How integration techniques can be used in the treatment Current research regarding PR integration and brain of brain injuries injuries will be highlighted Cases will be presented Pioneers to Present Day Leaders Getting Back to Life After Brain Injury (BI) Descartes (1596-1650) What is Vision? Neuro-Optometric Testing Vision writes spatial equations -
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. -
Dystonia and Chorea in Acquired Systemic Disorders
J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.65.4.436 on 1 October 1998. Downloaded from 436 J Neurol Neurosurg Psychiatry 1998;65:436–445 NEUROLOGY AND MEDICINE Dystonia and chorea in acquired systemic disorders Jina L Janavs, Michael J AminoV Dystonia and chorea are uncommon abnormal Associated neurotransmitter abnormalities in- movements which can be seen in a wide array clude deficient striatal GABA-ergic function of disorders. One quarter of dystonias and and striatal cholinergic interneuron activity, essentially all choreas are symptomatic or and dopaminergic hyperactivity in the nigros- secondary, the underlying cause being an iden- triatal pathway. Dystonia has been correlated tifiable neurodegenerative disorder, hereditary with lesions of the contralateral putamen, metabolic defect, or acquired systemic medical external globus pallidus, posterior and poste- disorder. Dystonia and chorea associated with rior lateral thalamus, red nucleus, or subtha- neurodegenerative or heritable metabolic dis- lamic nucleus, or a combination of these struc- orders have been reviewed frequently.1 Here we tures. The result is decreased activity in the review the underlying pathogenesis of chorea pathways from the medial pallidus to the and dystonia in acquired general medical ventral anterior and ventrolateral thalamus, disorders (table 1), and discuss diagnostic and and from the substantia nigra reticulata to the therapeutic approaches. The most common brainstem, culminating in cortical disinhibi- aetiologies are hypoxia-ischaemia and tion. Altered sensory input from the periphery 2–4 may also produce cortical motor overactivity medications. Infections and autoimmune 8 and metabolic disorders are less frequent and dystonia in some cases. To date, the causes. Not uncommonly, a given systemic dis- changes found in striatal neurotransmitter order may induce more than one type of dyski- concentrations in dystonia include an increase nesia by more than one mechanism. -
Neuropathology of Dementia in Patients with Parkinson's Disease: a Systematic Review of Autopsy Studies
Neurodegeneration J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp-2019-321111 on 23 August 2019. Downloaded from REVIEW Neuropathology of dementia in patients with Parkinson’s disease: a systematic review of autopsy studies Callum Smith ,1 Naveed Malek,2 Katherine Grosset,1 Breda Cullen ,3 Steve Gentleman,4 Donald G Grosset1 ► Additional material is ABSTRact have other causes of cognitive impairment and published online only. To view Background Dementia is a common, debilitating dementia, such as comorbid Alzheimer’s disease please visit the journal online (http:// dx. doi. org/ 10. 1136/ feature of late Parkinson’s disease (PD). PD dementia (AD) or cerebrovascular disease. These pathologies jnnp- 2019- 321111). (PDD) is associated with α-synuclein propagation, but may be difficult to identify in vivo, as the clinical coexistent Alzheimer’s disease (AD) pathology may features often overlap with those of PDD, and there 1 Department of Neurology, coexist. Other pathologies (cerebrovascular, transactive are no definitive biomarkers. The differentiation Institute of Neurosciences, response DNA-binding protein 43 (TDP-43)) may of dementia type is an important consideration in Queen Elizabeth University Hospital, Glasgow, UK also influence cognition.W e aimed to describe the clinical research, as treatments under development 2Department of Neurology, neuropathology underlying dementia in PD. are specifically targeted against abnormal accumu- Ipswich Hospital NHS Trust, Methods Systematic review of autopsy studies lation of α-synuclein, which is the pathological Ipswich, UK 3 3 published in English involving PD cases with dementia. hallmark of PDD and DLB, or tau or amyloid-β, Institute of Health and 4 5 Wellbeing, College of Medical, Comparison groups included PD without dementia, AD, which underlie AD. -
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. -
Retained Neonatal Reflexes | the Chiropractic Office of Dr
Retained Neonatal Reflexes | The Chiropractic Office of Dr. Bob Apol 12/24/16, 1:56 PM Temper tantrums Hypersensitive to touch, sound, change in visual field Moro Reflex The Moro Reflex is present at 9-12 weeks after conception and is normally fully developed at birth. It is the baby’s “danger signal”. The baby is ill-equipped to determine whether a signal is threatening or not, and will undergo instantaneous arousal. This may be due to sudden unexpected occurrences such as change in head position, noise, sudden movement or change of light or even pain or temperature change. This activates the stress response system of “fight or flight”. If the Moro Reflex is present after 6 months of age, the following signs may be present: Reaction to foods Poor regulation of blood sugar Fatigues easily, if adrenalin stores have been depleted Anxiety Mood swings, tense muscles and tone, inability to accept criticism Hyperactivity Low self-esteem and insecurity Juvenile Suck Reflex This is active together with the “Rooting Reflex” which allows the baby to feed and suck. If this reflex is not sufficiently integrated, the baby will continue to thrust their tongue forward, pushing on the upper jaw and causing an overbite. This by nature affects the jaw and bite position. This may affect: Chewing Difficulties with solid foods Dribbling Rooting Reflex Light touch around the mouth and cheek causes the baby’s head to turn to the stimulation, the mouth to open and tongue extended in preparation for feeding. It is present from birth usually to 4 months. -
Understanding Cerebral Palsy
Understanding Cerebral Palsy Abstract Inclusion within sports, recreation, fitness and exercise is essential as every individual has the right to engage, participate in and have a choice of different sports, recreation, fitness and exercise activities. This is no different for individuals who have Cerebral Palsy. Although, in society, one of the main issues is how to make activities accessible and inclusive for individuals with disabilities. Additionally, within society there can be little understanding and appreciation of how different medical conditions can effect individuals and what this means when trying to engage in an activity. Therefore, the aim of this article is to give readers an understanding of Cerebral Palsy and how it can affect individuals. It will discuss the different types and forms of Cerebral Palsy, how it can affect individuals as well as the importance of recognising the individual even though they may have Cerebral Palsy. Keywords: Cerebral Palsy, Functional Implications of Cerebral Palsy, Cerebral Palsy and Impairment, Individuals with Cerebral Palsy Introduction CPISRA (Cerebral Palsy International Sports and Recreation Association) is extending its activities to facilitate and promote research into exercise, sport and recreation for individuals with Cerebral Palsy and related conditions. This is in response to the increasing interest in sports, recreation, fitness and exercise for individuals with Cerebral Palsy and a demand for further research. In embarking on this activity, we at CPISRA quickly became aware the need to increase awareness and understand various sport and recreation participation aspects relating to individuals with Cerebral Palsy. Before understanding these various aspects though, there is firstly the need to have a critical understanding of Cerebral Palsy. -
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. -
Psychiatry and Neurology
ensic For Ps f yc o h l a o l n o r g u y o J ISSN: 2475-319X Journal of Forensic Psychology Editorial Psychiatry and Neurology Carlos Roberto* Department of Psychology, La Sierra University, California, USA DESCRIPTION between neurological and psychiatric disorders. for instance , it's documented that a lot of patients with paralysis agitans and Psychiatry is that the medicine dedicated to the diagnosis, stroke manifest depression and, in some, dementia. Is there a prevention, and treatment of mental disorders. These include substantive difference between a toxic psychosis (psychiatry) and various maladaptation’s associated with mood, behavior, a metabolic encephalopathy with delirium (neurology) we've cognition, and perceptions. See glossary of psychiatry. known of those examples for several years? Never and dramatic evidence has come largely through functional resonance imaging Neurology is that the branch of drugs concerned with the study and positron emission tomography. Obsessive-compulsive and treatment of disorders of the system nervosum. The system a disorder is characterized by recurrent, unwanted, intrusive ideas, nervosum may be a complex, sophisticated system that regulates images, or impulses that appear silly, weird, nasty, or horrible and coordinates body activities. Its two major divisions: Central nervous system: the brain and medulla spinalis. (obsessions) and by urges to hold out an act (compulsions) which will lessen the discomfort thanks to the obsessions. Increasing the amount of brain serotonin with selective reuptake inhibitors DIFFERENCE BETWEEN PSYCHITARY may control the symptoms and signs of this disorder. Evidence AND NEUROLOGY of a genetic basis in some patients, structural abnormalities of the brain on resonance imaging in others, and abnormal brain For quite 2000 years within the West, neurology and psychiatry function on functional resonance imaging and positron were thought to be a part of one, unified branch of drugs, which emission tomography collectively suggest that schizophrenia may was often designated neuropsychiatry.