Neurosurgery in cerebral palsy

Stereotaxic subthalamotomy of 55 patients with cerebral palsy gave a good result in 65% of the selected cases. The result was uncertain in 15 and poor in 20%. An independent socio-medical follow-up study confirmed the clinical finding. The more rapid the involuntary movements, the better was the effect of subthalamotomy. Intention tremor was the most suitable symptom for stereotaxic treatment. Rigidospasticity was alleviated in the distal muscles only. Speech and gait were often improved. Good results were obtained in patients with normal intelligence, while feeble-minded patients did not benefit from the operation. Subthalamotomy was followed by transitory side-effects in 20%, of which increased involuntary movements on the ipsilateral side and mental restlessness were the most frequent. The operation had no mortality. Spinal longitudinal myelotomy effectively relieved the spasticity of the lower limbs in the three patients operated upon.     

Scoliosis in cerebral palsy

Spinal deformity is a common musculoskeletal problem for individuals with cerebral palsy. Severe scoliosis may impair physical function and may be a source of pain. Spine braces and carefully constructed seating arrangements may moderate the behavior of these deformities but do not seem capable of stopping progression, which often continues in adulthood. Spine fusion surgery can produce a stable, durable trunk shape that improves sitting and positioning but the process of surgery is arduous and outcomes can be compromised by numerous serious complications. Despite complications, many families and caregivers express satisfaction with the results of surgery. Careful patient evaluation, studious attention to surgical planning and performance, and a good relationship with patients, family members, and other providers is essential.     

Spontaneous remission of cerebral palsy

Among 2100 children with a diagnosis of cerebral palsy (CP) twenty carried the diagnosis: Previous CP, now normalized. Seventeen patients could be traced and were reevaluated. Cerebral palsy was diagnosed in these seventeen children (ten boys, seven girls) between the ages of three months and three years (average eleven months). They were found to be normal when reexamined between the ages of one year and five years (average two years two months). Two patients had tetraplegia, three diplegia, nine paraplegia ("paraplegia" were cases of diplegia with minimal affection of the upper limbs - now called "diplegia type I"), and one hemiplegia. One patient had atactic diplegia, and one was athetotic. The records of these seventeen patients were evaluated with respect to aetiology and symptomatology. Upon reexamination seven patients were found to be completely normal. Five patients had no motor symptoms but showed signs of specific neuropsychological difficulties. Two patients were intellectually retarded without motor symptoms. One showed signs of neuropathy, and one had fetal alcohol syndrome. Signs consistent with CP could be demonstrated in one patient only. This study shows that signs of CP may in rare cases disappear altogether.     

显微神经外科手术治疗脑性瘫痪

脑性瘫痪(cerebral palsy,CP)是指出生前到出生后1个月内由各种原因引起的脑损伤或发育缺陷所致的运动障碍及姿势异常[1],可分为痉挛型、不随意运动型、共济失调型、肌张力低下型和混合型。自2002年2月至2005年2月,我们对25例脑性瘫痪患者施行了选择性脊神经后根切断术(selectiveposterior rhizotomy,SPR),现报告如下。一、对象与方法1.一般资料:本组男17例,女8例;年龄5~16岁。智力正常或接近正常者21例(84%),智障较重者4例(16%)。痉挛型20例(80%),以痉挛为主的混合型5例(20%)。2.临床表现:瘫痪仅累及单侧者4例,累及双侧者21例,共计46侧肢…     

Genetic mimics of cerebral palsy

The term “cerebral palsy mimic” is used to describe a number of neurogenetic disorders that may present with motor symptoms in early childhood, resulting in a misdiagnosis of cerebral palsy. Cerebral palsy describes a heterogeneous group of neurodevelopmental disorders characterized by onset in infancy or early childhood of motor symptoms (including hypotonia, spasticity, dystonia, and chorea), often accompanied by developmental delay. The primary etiology of a cerebral palsy syndrome should always be identified if possible. This is particularly important in the case of genetic or metabolic disorders that have specific disease‐modifying treatment. In this article, we discuss clinical features that should alert the clinician to the possibility of a cerebral palsy mimic, provide a practical framework for selecting and interpreting neuroimaging, biochemical, and genetic investigations, and highlight selected conditions that may present with predominant spasticity, dystonia/chorea, and ataxia. Making a precise diagnosis of a genetic disorder has important implications for treatment, and for advising the family regarding prognosis and genetic counseling. © 2019 International Parkinson and Movement Disorder Society     

The origins of cerebral palsy

PURPOSE OF REVIEW: Cerebral palsy is the most common and visible motor disability of childhood. Its aetiology remains a topic of hot debate between those who see it as a reflection of medical mismanagement of an avoidable complication and those who see its origins in the development of the fetal brain affected at many points along a causal pathway to damage. This review outlines the themes of research publications over the year 2004/2005. RECENT FINDINGS: The review looks at recent findings relating to epidemiology, infection and inflammation, prematurity, multiple pregnancy, thrombophilias, genetics, placenta, neuroimaging and rescue therapies in cerebral palsy. SUMMARY: Papers this year have helped clarify risk groups and identify some areas (e.g. the management of thrombophilias and the potential of induced hypothermia) with the potential to be rapidly introduced into clinical practice. In this enigmatic and multifactorial condition, however, progress remains slow. New tools such as magnetic resonance imaging are providing valuable insights into the lesions that result in cerebral palsy but the pathways to injury remain unclear. The future of cerebral palsy research lies in understanding the complex interactions of multiple factors on the road to cerebral palsy or in looking for final common pathways such as inflammation which may be amenable to manipulation.     

Neuropathologic substrate of cerebral palsy

Animal models have assisted in understanding the mechanisms of brain injury underlying cerebral palsy. Nevertheless, no such models replicate every aspect of the human disease. This review summarizes the classic and more recent studies of the neuropathology of human perinatal brain injury most commonly associated with cerebral palsy, for use by researchers and clinicians alike who need to analyze published animal models with respect to their fidelity to the human disorder. The neuropathology underlying cerebral palsy includes white-matter injury, known as periventricular leukomalacia, as well as germinal matrix hemorrhage with intraventricular extension, and injury to the cortex, basal ganglia, and thalamus. Each has distinctive features while sharing some risk factors, such as prematurity and/or hypoxia-ischemia in the perinatal period. Periventricular leukomalacia consists of diffuse injury of deep cerebral white matter, with or without focal necrosis. Recent work directly in human postmortem tissue has focused on the role of free radical injury, cytokine toxicity (especially in light of the epidemiologic association of periventricular leukomalacia with maternofetal infection), and excitotoxicity in the development of periventricular leukomalacia. Premyelinating oligodendrocytes, which predominate in periventricular regions during the window of vulnerability to periventricular leukomalacia (24-34 postconceptional weeks), are the targets of free radical injury, as determined by immunocytochemical markers of lipid peroxidation and protein nitration. This maturational susceptibility can be attributed in part to a relative deficiency of superoxide dismutases in developing white matter. Microglia, which respond to cytokines and to bacterial products such as lipopolysaccharide via Toll-like receptors, are increased in periventricular leukomalacia white matter and can contribute to cellular damage. Indeed, several cytokines, including tumor necrosis factor-a and interleukins 2 and 6, as well as interferon-g, have been demonstrated in periventricular leukomalacia. Preliminary work suggests a role for glutamate receptors and glutamate transporters in periventricular leukomalacia based on expression in human developing oligodendrocytes. Germinal matrix hemorrhage, with or without intraventricular hemorrhage, occurs in premature infants and can coexist with periventricular leukomalacia. Studies in human germinal matrix tissue have focused on maturation-based vascular factors, such as morphometry and expression of molecules related to the structure of the blood-brain barrier. Gray-matter injury, seen more commonly in term infants, includes cortical infarcts and status marmoratus. Subtle cortical injury overlying periventricular leukomalacia is the subject of current interest as a possible substrate for the cognitive difficulties seen in patients with cerebral palsy. In summary, it is hoped that work in human tissue, in conjunction with experimental animal models, will lead to eventual therapeutic or preventive strategies for the perinatal brain injury underlying cerebral palsy.     

Reciprocal inhibition in cerebral palsy

We studied reciprocal inhibition by recording the changes in firing probability of single motor units of the tibialis anterior muscle following stimulation of low-threshold afferents in the posterior tibial nerve. In 15 patients with cerebral palsy, the inhibition was as great or greater than normal. We found no evidence that group I afferents produce "reciprocal facilitation" in cerebral palsy.