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REVIEW ARTICLE
Year : 2017  |  Volume : 7  |  Issue : 4  |  Page : 76-83

A Systematic Review on Etiology, Epidemiology, and Treatment of Cerebral Palsy


Department of Pharmaceutical Sciences, Kumaun University, Campus Bhimtal, Bhimtal, Uttarakhand, India

Date of Web Publication6-Nov-2017

Correspondence Address:
Jyoti Upadhyay
Department of Pharmaceutical Sciences, Kumaun University, Campus Bhimtal, Bhimtal, Uttarakhand
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijnpnd.ijnpnd_26_17

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   Abstract 

The most common physical disability in childhood is cerebral palsy (CP). It is difficult to assess and clarify the risk factors associated with this disorder. The aim of this article is to review the recent literature relating to etiology, epidemiology, and advances in the treatment of CP. A systematic search for peer-reviewed articles with keywords “cerebral palsy” and “neurodisability” since 1980 was performed. An investigational research on CP offers an excellent opportunity in understanding the risk factors associated with this disorder as well as its incidences and prevalence. Various new techniques have evolved in the management of CP, such as traditional physiotherapy, occupational therapy, selective dorsal rhizotomy, sensory integration, botulinum toxin injection, and intrathecal baclofen. The care and management of CP in an individual is a very complex process. Although a number of therapeutic interventions have been used by healthcare professionals, but the efficacy of only few has been established by scientific research. To prevent the chances of CP, we need to understand the causes as well as risk factors associated with this disorder.

Keywords: Cerebral palsy, diplegia, hemiplegia, quadriplegia, spasticity


How to cite this article:
Rana M, Upadhyay J, Rana A, Durgapal S, Jantwal A. A Systematic Review on Etiology, Epidemiology, and Treatment of Cerebral Palsy. Int J Nutr Pharmacol Neurol Dis 2017;7:76-83

How to cite this URL:
Rana M, Upadhyay J, Rana A, Durgapal S, Jantwal A. A Systematic Review on Etiology, Epidemiology, and Treatment of Cerebral Palsy. Int J Nutr Pharmacol Neurol Dis [serial online] 2017 [cited 2017 Nov 18];7:76-83. Available from: http://www.ijnpnd.com/text.asp?2017/7/4/76/217552


   Introduction Top


Cerebral palsy (CP) is a heterogenous permanent neurological disorder caused by nonprogressive damage to the developing brain. We all know that brain controls all the functions of our body like muscle movement. In this disorder, injury or malformation occurs in the growing central nervous system that affects the development of motor function and body posture before, during, or shortly after birth.[1] The term “Cerebral” refers to the brain and “Palsy” means lack of control in muscles. The problem associated with CP in children involves muscle weakness, shakiness, balance problems, and slow response, with symptoms ranging from mild to severe. In the case of mild CP, the child may be heavy handed in one arm to some extent, and this problem may be barely noticeable, whereas in severe CP, the child may have difficulties in performing daily activities and maintaining movement, posture, and neuromuscular control, resulting in epilepsy, osteoporosis, and dysphagia.[2] The prevalence of CP occurs in 2.5% per 1000 live births globally, and this abnormality varies with its involvement distribution like hemiplegia and diplegia, and changes with age and surgery.[3],[4] The exact definition of CP depends upon three common characteristics, which are (1) body movement or posture disorder, (2) static abnormality in the brain, and (3) acquired brain disorder (early in life). However, these characteristics do not specify (1) the severity of the movement disorders, (2) the static nature of the cerebral abnormality, (3) age at which the abnormality occurs, and (4) age before which CP was not detected. Postneonatal and nonpostneonatal are the two widest distinctions in age of acquiring cerebral abnormality.[5]


   Classification of Cerebral Palsy Top


The topographic classification of CP involves (1) quadriplegia, (2) hemiplegia, (3) diplegia, (4) monoplegia, and (5) triplegia. Monoplegia and triplegia are uncommon as there is substantial overlap of the affected areas. The most common form of CP in most of the studies is diplegia, which is the most prevalent form (30–40%), followed by hemiplegia (20–30%) and quadriplegia (10–15%). A study of CP of 1000 cases from India shows the highest percentage of cases with spastic quadriplegia (61%) followed by diplegia (22%).[6]

Quadriplegic cerebral palsy

It is the most severe form and includes all four limbs; upper limbs are more severely affected than the lower limbs, related with acute hypoxic intrapartum asphyxia. Excessive cystic degeneration of the brain, which is polycystic encephalomalacia, polyporencephalon, and developmental abnormalities (such as polymicrogyria and schizencephaly), is often revealed by neuroimaging. Very few voluntary movements are observed. Pseudobulbar signs are detected in most children with recurrent aspiration of food material and difficulty in swallowing. Optic atrophy and seizures are also observed in half of the patients. Severe intellectual abnormality is reported in most of the cases.[7]

Hemiplegic cerebral palsy

It is spastic unilateral hemiparesis wherein upper limbs are affected more severely than the lower limbs. It is commonly observed in term infants (56%) and preterm infants (17%). It has multifactorial pathogenesis. Impaired voluntary movements are observed mostly affecting hand functions. Other functions affected are pincer grasp of thumb, supination of the forearm, and extension of the wrist. Dorsiflexion and aversion of foot are severely impaired in the lower limb. Flexor tone is increased with hemiparetic posture. Affected limbs also have sensory abnormalities. Seizures occur in most children (>50%). Most common facial nerve palsies are visual field defects, cranial nerve abnormalities, and homonymous hemianopia.[7]

Diplegic cerebral palsy

Prematurity and low birth weight are risk factors for spastic diplegia. Neuroimaging study reveals cystic periventricular leukomalacia (PVL). The most common ischemic brain injury is PVL in premature infants. This ischemia occurs in the white matter adjacent to the lateral ventricles.[7],[8]

Monoplegic cerebral palsy

It is a form of paralysis affecting only one limb. Sometimes, the paralysis is limited only to a single muscle affecting body functions. Monoplegic people are able to take care of themselves. They perform their daily activities.[8]

Triplegic cerebral palsy

It is a form of paralysis involving three limbs, that is, paralysis on one side of the body and of an arm or leg on the opposite side.[8],[9]

Based on the types of neuromuscular defects, CP is also classified as (1) spastic, (2) dyskinetic (including choreoathetoid and dystonic), (3) ataxic, (4) hypotonic, and (5) mixed. The most common CP is spastic CP (70–75%), followed by dyskinetic (10–15%) and then ataxic (less than 5% of cases).[8]

The CP disorder was classified according to Gross Motor Function Classification (GMFCS) and internationally used for research and clinical purposes. Researchers and therapist classify the severity of CP using terms such as “mild,” “moderate,” and “severe.” These classifications help validate the use of Gross Motor Function Measure and evaluate children’s motor function. This classification system has been extensively used and internationally adopted. The major challenges for researchers and clinicians in the classification of CP include generating and validating similar classification for conditions like autism and mental retardation.[9]

Another classification of CP called differential classification is based on etiology, pathology, and clinical description. Classification of CP depends upon distribution and severity of motor impairments and related (nonmotor) impairments. As some of the terminologies are interpreted differently by clinicians from different disciplines, poor reliability of these classification systems often ensues.[5]


   Etiology Top


The etiology behind CP in infants remains unknown. Complications like low birth weight, birth asphyxia, premature separation of placenta, and abnormal fetal position were associated with this disease. The associated etiology for CP is given in [Table 1]. If a mother or infant suffer from any of these associated conditions, it does not mean this will result in CP, rather it means higher prevalence of CP.[10]
Table 1: Known etiology of cerebral palsy

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Several risk factors play a major role in the pathogenesis of CP and may be present before or after pregnancy, during labor, and shortly after birth of the baby.[16] It is essential for us to distinguish between risk factors, associations, and known etiology of CP. It was found in some cases that not a single event, but a series of events, is responsible for the damage of motor nerves which finally results in this condition.[17] The risk factors associated with CP are given in [Table 2].
Table 2: Cerebral palsy associated risk factors

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Epidemiological studies on the possible risk factors associated with cerebral palsy

A study at University of California, San Francisco, and Kaiser Permanente Division of Research, Oakland, California, shows the association between chorioamniontis and high risk of CP that was determined in term and near-term infants, and 109 children with CP were observed as compared to 218 controls. Forty percent of the cases were hemiparetic, and 38% were quadriparetic. Most common findings related to CP were white matter abnormalities, atrophy, and hypoxic–ischemic injury. Diagnosis of chorioamnionitis or endometritis was done clinically and 14% of cases were observed as compared to 4% of controls. Other risk factors associated with CP are maternal fever, maternal age more than 25 years, intrauterine growth restriction, prolonged rupture of membranes, and nulliparity.[38]

In some studies, investigation on the relationship between birth asphyxia and spastic CP was done, and data on children born with spastic CP (N = 183) were compared with matched group of control children (N = 549) in Western Australia between 1975 and 1980. Epidemiological methods were used for collecting information on perinatal events for both CP children and control group. It was found that there is a relation between clinically observed signs of birth asphyxia and spastic CP, and in only about 8% cases (15/183) of all the children with spastic CP, the possible cause of brain injury was intrapartum asphyxia.[39]

Another study compared a 3-day course of dexamethasone (N = 132) treatment with a control group given saline placebo (N = 116), administered shortly after birth, that is, from before 12 h of age in preterm infants ventilated for respiratory distress syndrome. It was found that administration of dexamethasone in the early stages of postnatal period associated with high risk of CP and developmental delay.[40]


   Prevalence of Cerebral Palsy Top


Epidemiological studies on the prevalence of cerebral palsy

According to a study on the prevalence of CP and CP subtypes among children in three areas of the United States, a multisite collaboration shows that the average prevalence of CP was 3.6 cases per 1000. The CP cases in Wisconsin were 3.3 cases per 1000, Alabama 3.7 cases per 1000, and Georgia 3.8 cases per 1000. The prevalent cases of CP were highest in boys and black non-Hispanic children as compared to girls and Hispanic children. It was also found that prevalence among children living in low and middle-income neighborhoods was higher in comparison with high-income neighborhoods. The most common subtype of CP among 77% of all cases was spastic CP; bilateral spastic CP was the most common type (70%) in the spastic group. These findings added new knowledge in the epidemiological study of CP.[41]

A study determined the birth-weight-specific trends in the prevalence of CP. This study shows a modest increase in the prevalence pattern of congenital CP from 1.7 to 2.0 per 1000 during the period from 1975 to 1991. The proportion of children having CP increased in normal birth weight infants from 17% in 1975 to 1977 to 39% in 1986 to 1991. Children weighing <1500 g, cases of spastic diplegic CP in these children were also increased overtime, that is, in the year 1975 to 1977 it was 7%, whereas 36% cases in the year 1985 to 1988 and 32% in the year 1986 to 1991. Low and very low birth weight infants show similar trends, whereas increase was seen in normal birth weight infant survivors.[38] A prospective descriptive study determining the impact of health-related quality of life of CP patients in their lives and families shows 11.1% patient’s quality of life was affected severely, 25.9% moderately, and 37% mildly. Future studies can be done for measuring the dynamics of this condition and also its influence on the relationship between CP subtypes and quality of life.[42]

A report provides information regarding the prevalence of CP and its severity of the disability or comorbidity in England and Scotland. The result of this report shows a total of 798,411 live births in between 1984 and 1989, with neonatal deaths 3651 (i.e., neonatal mortality 4.6 per 1000 live births), and cases of CP were 1649, showing prevalence of 2.1 per 1000 neonatal survivors, specified birth-weight-related CP prevalence from 1.1 per 1000 neonatal survivors. No significant time trends in CP prevalence were observed in any of the birth weight groups. As every one in five children with CP suffers from severe multiple disabilities, the social and clinical impacts must be addressed to provide continuous care for these children.[43]

An epidemiological study of patients with CP determines the demographical as well as clinical features of patients with CP attending various outpatient and inpatient clinics. This study included total 130 children. The known etiological risk factors for CP were bleeding and threatened miscarriages in prenatal period, birth asphyxia, premature baby and low birth weight in the perinatal period, convulsions, and hyperbilirubinemia in the postnatal period. Types of CP included spastic quadriplegic, spastic diplegic, dyskinetic, spastic hemiplegic, mixed type, and hypotonic or ataxic. Spastic quadriplegic was the most prevalent subtype of CP among children.[44]

A study in Norway showed prevalence, subtypes, and severity of CP. A total of 374 children born with CP were registered in the Cerebral Palsy Registry of Norway from January 1996 to December 1998. This study shows the prevalence of CP 2.1 per 1000 live births. The percentage of subtypes of CP was spastic unilateral CP 33%, spastic bilateral 49%, dyskinetic 6%, ataxic 5%, and others 7% (not classified). A total of 5% of impaired vision and 4% of hearing impairment cases were present and also 31% of mental retardation, 28% of active epilepsy, and 28% of no speech cases were found in children. Children with low Apgar scores show severe impairment in gross motor function, and children who had born in term, with normal birth weight and low Apgar scores, show severe impairment in fine motor function.[45]

Another study shows the risk factors for CP were very low birth weight (VLBW), that is, babies born, weighing <1500 g, from multiple pregnancies than in infants having normal birth weight. A total of 1575 infants having VLBW are born with CP; out of which, 414 (26%) infants have birth low weight (less than 1000 g) and 317 (20%) were from multiple pregnancies. CP subtypes included spastic CP 1426 (94%) which was unilateral, that is, hemiplegic in 336 (24%). Decline in the prevalence of birth of VLBW infants was reduced from 60.6 per 1000 live born in the year 1980 to 39.5 per 1000 in 1996. This decline was due to reduction in the frequency of bilateral spastic CP among infants weighing 1000 to 1499 g at the time of birth. In the group of birth weight between 1000 and 1499 g, the frequency of CP was found higher in male babies as compared to female babies. This population-based study provides evidence that the prevalence of CP in infants of birth weight less 1500 g has fallen, especially of bilateral spastic CP, and has implications for parents and healthcare services.[46]

A pilot study in 53 Indian children with CP shows their oral health status and investigated various dental problems like dental caries, plaque index, malocclusion, and drooling. A comparative study was done with the control group of same age and sex of matched normal children. The result of this study shows a significant difference between cases and controls for caries. It was found that maximum cases were in the age group of 6 to 8 years and quadriplegic and diaplegic cases were highest among these children. Also one of the significant findings of this study shows that those children who were affected with drooling were not affected with dental carries.[47] A study in India shows trends of CP. This study was conducted in Rajasthan, India. Diagnosed cases of spastic CP were observed from year 2010 to 2014. A total of 240 children were included in this study; the male-to-female ratio was found to be 2.3:1. Among these children, the cases of diplegic CP were found maximum, that is, 52.92% followed by quadriplegic CP which is 27.50 and 12.50% cases have hemiplegic pattern. The most commonly associated dental problem was drooling. Prenatal asphyxia was found to be major cause of CP.[48]

Subtypes of CP were studied using 2-deoxy-2(18F)fluoro-d-glucose (FDG) and positron emission tomography (PET) in 23 children. The subtypes of CP included spastic quadriparesis (N = 6), spastic diplegia (N = 4), infantile hemiplegia (N = 8), and choreoathetosis (N = 5). Computed tomography or magnetic resonance imaging was used for correlating the FDG–PET images. In spastic diplegic patients, PET shows focal areas of cortical hypometabolism, in which apparent structural abnormality was absent, whereas in choreoathetoid CP, normal pattern of cortical metabolism was observed instead of hypometabolism in thalamus and nucleus of lenticular cells. Symmetric cerebellar glucose metabolism with absence of crossed cellular hypometabolism (diaschisis), FDT–PET revealed symmetric cerebellar glucose metabolism in patients with infantile hemiplegia. FDG–PET may be useful in identifying CP patients.[49]


   Treatment of Cerebral Palsy Top


Diagnosis of cerebral palsy

CP diagnosed on the basis of clinical assessment. CP is a permanent disorder of movement and posture development that causes limitations in the activity, characterized by nonprogressive disturbances occurring on the developing brain of infant. This impairment in the movement and posture due to brain disorder is the invariant clinical manifestations.[50] The GMFCS used by some researchers to include or exclude the cases of CP without functional impairment, in the Western Australian Cerebral Palsy Register. This register grades the severity of the cases. The diagnosis of CP, in clinical practice, is generally based on observations of symptoms like sitting, walking, pulling to stand evaluation of postures, deep tendon reflexes, and muscle tone. In premature infants, neurological abnormalities observed in early months may resolve during the first 1 or 2 years of life. Such abnormality may or may not be associated with motor impairment; one of these abnormalities is transient dystonia, an abnormal neurological syndrome (e.g., hyperextension of the trunk) resolves after 1 year of age. Severe CP can be seen in infants within first 12 months of birth. The baby shows slow motor movement, floppy muscle tone, and abnormal body posture. The diagnosis of CP is also based upon its classification according to the nature of the movement disorder, that is, spasticity, ataxia, dystonia, and athetosis and also according to the topographic distribution of the motor abnormalities. Spasticity is the most predominant abnormality present among premature infants and analyzed clinically. In this condition, increased muscle tone is encountered at the joint angle. Dystonia is also referred to as hypertonia and decrease in the activity, whereas choreoathetosis is an involuntary irregular spasmodic movement of the limbs or facial muscles. Loss of order of muscle coordination occurs in ataxic CP.[51]

Role of brain imaging

Magnetic resonance imaging provides information about the adverse events timing, like cortical dysplasia’s date during early pregnancy, that is, from 12th to 20th week gestation, per ventricular leukomalacia between 28th and 34th week.[52]

Treatment

CP cannot be cured. As a result, various therapeutic interventions with interdisciplinary approaches have been used to manage CP. The main objective is to use a combination of physical, developmental, medical, chemical, surgical, and technical procedures to treat patients. These procedures assist in preventing secondary impairments and improving child’s developmental capabilities.[53] Traditional physiotherapy and occupational therapy are broadly used measures and have shown benefit in the treatment of CP. These therapeutic measures are found highly effective in improving the functional capabilities of the children with CP.[54] For the treatment of inadequate muscle growth, the following methods are used, that is, passive stretch, physical therapy, botulinum toxin injections, phenol injections, orthopedic surgeries, and spasticity reduction. For the treatment of spasticity, selective dorsal rhizotomy (SDR) may be employed, whereas for mixed patterns and spasticity, selection criteria of SDR respond to intrathecal baclofen (ITB).[53]

Traditional physiotherapy

It improves muscle strength, joint movement, and tolerance to muscular movements. Traditional physiotherapy is a routinely used interdisciplinary treatment approach for school going children as it fulfills the requirement of cooperation and active participation of these children with CP. Progressive resistance training program can help in progressively improving muscular strength. For improving joint mobility, a range of motion exercises are carried out by physical therapists. Static and gentle stretches are performed on the patient joint for preventing joint contractions. Such stretches performed within a pain-free joint range of movement. A group of healthcare providers, including physical therapist, orthopedic surgeons, and orthotist, helps in designing and implementing exercises, which improves posture, balance control, gait, and mobility.[54]

Physical/occupational therapy

The goal of this therapy is to improve infant–caregiver interaction, providing family support, parental education, and supplying resources. This therapy also promotes developmental skills which are essential in performing daily activities. These include self-care activities like grooming, dressing, feeding, and fine motor tasks (like painting and writing). Occupational therapy also directed cognitive and noncognitive disabilities, particularly in the visual motor area and adjustment of apparatus and seating to improve upper extremity use and to develop functional independence. Some therapists use specialized techniques like neurodevelopmental treatment and sensory integration for achieving these goals, which are given below.

Neurodevelopmental treatment

In 1940, Berta and Karl Bobath developed this method of treatment. The treatment approach is based on their personal observations from working with CP children. The main objective of this treatment is to facilitate the normal motor development and prevention of development of secondary impairments caused by muscle contractions and limb deformities.[55],[56]

Sensory integration

The theory of this treatment was developed by A. Jean Ayres in 1970. This occupational therapy develops treatment pathway for children with CP having sensory processing difficulties. This model was designed to treat learning disabilities. The main hypothesis of this therapy is to develop and execute normal adaptive behavioral response and to improve functional capabilities like ability of the child to perform and integrate sensory network, including visual, auditory, perceptual, and others. Sensory integration disorders include sensory modulation, sensory discrimination, and motor disorders (sensory based).[54],[57]

Oral muscle relaxants

Diazepam, Baclofen, and dantrolene are muscle relaxants used in the cases of CP, but their use is limited because of the side effects caused by them like lethargy, impaired cognitive skills, and others when given orally. They also have poor bioavailability because of their low lipid solubility.[53]

Selective dorsal rhizotomy

This neurosurgical operation includes laminoplasty of from L1 to S1 of the dorsal nerve roots. The inclusion criteria of patients for this operation includes spasticity, selective motor control, children aged 4 to 7 years, and spastic diplegia CP. Children who undergo this operation also need orthopedic surgery after this. The ideal age for lower limb surgery is between 4 and 6 years, and 6 to 8 years for upper limb surgery.[53]

Intrathecal baclofen

A microprocessor-controlled pump containing small quantities of Baclofen administered into the subarachnoid space. It is used in severe spastic quadriplegia. This drug is very expensive and causes life-threatening complications, for example, neurological injuries due to dislodgement of catheter tip. Both SDR and ITB act on lower limbs.[53]

Phenol injection

Neurolytic injection of phenol is used for motor nerves like obturator nerve and musculocutaneous nerve. This phenol injection is rarely used because of the availability of botulinum toxin.[58]

Botulinum toxin injection

This injection causes a reversible chemodenervation of muscle, which is dose dependent. It is ineffective in the case of lever arm disease. This treatment is useful in patients who are hypertonic either spastic or dystonic.[59]

Antenatal magnesium sulfate

Administration of antenatal magnesium sulfate alone can prevent all cases of this illness in preterm infants. This drug could be used for the prevention of CP in preterm infants less than 34 weeks of gestational age.[60]

Orthosis

Newer light weight, made up of thermoplastic materials used below the knees. Articulated ankle foot orthosis and ground reaction articulated ankle foot orthosis are preferred over solid articulated ankle foot orthosis in case of ambulatory children.[61]

Hippotherapy

Also called as horseback riding therapy, it improves gross motor function like tone, strength, balance, coordination, and others in CP children. This therapy reduces the degree of motor disability.[62]


   Conclusion Top


CP is a group of nonprogressive disorders affecting body movement and posture. This condition is permanent and occurs during fetal development or infancy. Different treatment options are available for patients with CP. In this review paper, we summarize the risk factors associated CP, epidemiology as well as recent advances in its treatment. The major risk factor for CP is preterm birth, and this risk increases with decreasing gestational age. Better prenatal care and nutrition might reduce the chances of CP in children. A multidisciplinary, comprehensive, and coordinated approach is needed in the care of children with CP. Recent advances in the management of CP have increased. Implementation of new techniques like SDR, ITB, and sensory integration helps in the treatment of CP. Traditional physiotherapy and occupational therapy helps reduce spasticity. To minimize the cases of CP in children, additional research is required in understanding the etiology of CP.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Schimdt AA, Nordmark E, Czuba T, Westbom L. Stability of the Gross Motor Function Classification System in children and adolescents with cerebral palsy: A retrospective cohort registry study. Dev Med Child Neurol 2017;59:641-46.  Back to cited text no. 1
    
2.
Wu CW, Huang SW, Lin JW, Liou TH, Chou LC, Lin HW. Risk of stroke among patients with cerebral palsy: A population-based cohort study. Dev Med Child Neurol 2017;59:52-6.  Back to cited text no. 2
    
3.
Nelson KB. Can we prevent cerebral palsy?. N Engl J Med 2003;349:1765-69.  Back to cited text no. 3
    
4.
Wren TA, Rethlefsen S, Kay RM. Prevalence of specific gait abnormalities in children with cerebral palsy: Influence of cerebral palsy subtype, age, and previous surgery. J Pediatr Orthop 2005;25:79-83.  Back to cited text no. 4
    
5.
Blair E, Watson L. Epidemiology of cerebral palsy. Semin Fetal Neonatal Med 2006;11:117-25.  Back to cited text no. 5
    
6.
Singhi PD, Ray M, Suri G. Clinical spectrum of cerebral palsy in North India—An analysis of 1000 cases. J Trop Pediatr 2002;48:162-6.  Back to cited text no. 6
    
7.
Menkes JH, Sarnat HB. Periuatal asphyxia and trauma. In: Menkes JH, Sarnat HB, editors. Child Neurology. Baltimore, United States: Lippincott Williams & Wilkins; 2000. p. 427–36.  Back to cited text no. 7
    
8.
Sankar C, Mundkur N. Cerebral palsy-definition, classification, etiology and early diagnosis. Indian J Pediatr 2005;72:865–8.  Back to cited text no. 8
    
9.
Rosenbaum PL, Palisano RJ, Bartlett DJ, Galuppi BE, Russell DJ. Development of the Gross Motor Function Classification system for cerebral palsy. Dev Med Child Neurol 2008;50:249-53.  Back to cited text no. 9
    
10.
Torfs CP, Von den berg BJ, Oechsli FW, Cummins S. Prenatal and perinatal factors in the etiology of cerebral palsy. J Pediatric 1990;116:615.  Back to cited text no. 10
    
11.
Krageloh-Mann I, Petersen D, Hagberg G, Vollmer B, Hagberg B, Michaelis R. Bilateral spastic cerebral palsy—MRI pathology and origin: Analysis from a representative series of 56 cases. Dev Med Child Neurol 1995;37:379-97.  Back to cited text no. 11
    
12.
Steinlin M, Good M, Martin E, Banziger O, Largo RH, Boltshauser E. Congenital hemiplegia: Morphology of cerebral lesions and pathogenetic aspects from MRI. Neuropediatrics 1993;24:224-9.  Back to cited text no. 12
    
13.
Truwit CL, Barkovich AJ, Koch TK, Ferriero DM. Cerebral palsy: MR findings in 40 patients. Am J Neuroradiol 1992;13:67-78.  Back to cited text no. 13
    
14.
Reddihough DS, Collins KJ. The epidemiology and causes of cerebral palsy. Aust J Physiother 2003;49:7-12.  Back to cited text no. 14
    
15.
MacLennan A. A template for defining a causal relation between acute intrapartum events and cerebral palsy: International consensus statement. BMJ 1999;319:1054-9.  Back to cited text no. 15
    
16.
Stanley FJ, Blair E, Alberman E. Cerebral Palsies: Epidemiology and Causal Pathways. Clinics in Developmental Medicine (151). London: MacKeith Press; 2000.  Back to cited text no. 16
    
17.
Torfs CP, van den Berg BJ, Oechsil FW, Cummins S. Prenatal and perinatal factors in the etiology of cerebral palsy. J Pediatr 1990;116:615-9.  Back to cited text no. 17
    
18.
Pinto-Martin JA, Cnaan A, Zhao H. Short interpregnancy interval and the risk of disabling cerebral palsy in a low birth weight population. J Pediatr 1998;132:818-21.  Back to cited text no. 18
    
19.
Dolk H, Pattenden S, Johnson A. Cerebral palsy, low birthweight and socio-economic deprivation: Inequalities in a major cause of childhood disability. Paediatr Perinat Epidemiol 2001;15:359-63.  Back to cited text no. 19
    
20.
Dowding VM, Barry C. Cerebral palsy: Social class differences in prevalence in relation to birthweight and severity of disability. J Epidemiol Community Health 1990;44:191-5.  Back to cited text no. 20
    
21.
Nelson KB, Ellenberg JH. Antecedents of cerebral palsy. Multivariate analysis of risk factors. N Engl J Med 1986;315:81-6.  Back to cited text no. 21
    
22.
Blair E, Stanley F. Aetiological pathways to spastic cerebral palsy. Paediatr Perinat Epidemiol 1993;7:302-17.  Back to cited text no. 22
    
23.
Collins M, Paneth N. Pre-eclampsia and cerebral palsy: Are they related?. Dev Med Child Neurol 1988;40:207-11.  Back to cited text no. 23
    
24.
Gilles MT, Blair E, Watson L, Badawi N, Alessandri L, Dawes V et al. Trauma in pregnancy and cerebral palsy: Is there a link? Med J Aust 1996;164:500-1  Back to cited text no. 24
    
25.
Nelson KB, Ellenberg JH. Predictors of low and very low birth-weight and the relation of these to cerebral palsy. JAMA 1985;254:1473-9.  Back to cited text no. 25
    
26.
Stanley FJ, Blair E, Alberman E. Cerebral Palsies: Epidemiology and Causal Pathways. Clinics in Developmental Medicine (151). London: MacKeith Press; 2000.  Back to cited text no. 26
    
27.
Powell TG, Pharoah POD, Cooke RWI, Rosenbloom L. Cerebral palsy in low birthweight infants. I. Spastic hemiplegia: Associations with intrapartum stress. Dev Med Child Neurol 1988;30:11-8.  Back to cited text no. 27
    
28.
Murphy DJ, Sellars S, MacKenzie IZ, Yudkin P, Johnson A. Case-control study of antenatal and intrapartum risk factors for cerebral palsy in very preterm singleton babies. Lancet 1995;346:1449-54.  Back to cited text no. 28
    
29.
Nelson KB, Willoughby RE. Infection, inflammation and the risk of cerebral palsy. Curr Opin Neurol 2000;13:133-9.  Back to cited text no. 29
    
30.
Polivka BJ, Nickel JT, Wilkins JR. Urinary tract infection during pregnancy: A risk factor for cerebral palsy?. J Obstet Gynecol Neonatal Nurs 1997;26:405-13.  Back to cited text no. 30
    
31.
Walstab J, Bell R, Reddihough D, Brennecke S, Bessell C, Beischer N. Antenatal and intrapartum antecedents of cerebral palsy—A case-control study. Aust N Z J Obstet Gynaecol 2002;42:138-46.  Back to cited text no. 31
    
32.
Nelson KB, Grether JK. Potentially asphyxiating conditions and spastic cerebral palsy in infants of normal birth weight. Am J Obstet Gynecol 1998;179:507-13.  Back to cited text no. 32
    
33.
Van de Riet JE, Vandenbussche FP, Le Cessie S, Keirse MJ. Newborn assessment and long-term adverse outcome: A systematic review. Am J Obstet Gynaecol 1999;180:1024-9.  Back to cited text no. 33
    
34.
Moster D, Lie R, Irgens L, Bjerkedal T, Markestad T. The association of Apgar score with subsequent death and cerebral palsy: A population-based study in term infants. J Pediatr 2001;138:798-803.  Back to cited text no. 34
    
35.
Blair E, Stanley F. When can cerebral palsy be prevented? The generation of causal hypotheses by multivariate analysis of a case-control study. Paediatr Perinat Epidemiol 1993;7:272-301.  Back to cited text no. 35
    
36.
Murphy DJ, Hope PL, Johnson A. Neonatal risk factors for cerebral palsy in very preterm babies: Case-control study. BMJ 1997;314:404-8.  Back to cited text no. 36
    
37.
Wu YW, Escobar GJ, Grether JK, Croen LA, Greene JD, Newman TB. Chorioaamnionitis and cerebral palsy in term and near-term infants. JAMA 2003;290:2677-84.  Back to cited text no. 37
    
38.
Blair E, Stanely FJ. Intrapartum asphyxia: A rare cause of cerebral palsy. J Pediatr 1988;112:515-9.  Back to cited text no. 38
    
39.
Shinwell ES, Karplus M, Reich D, Weintraub Z, Blazer S, Bader D et al. Early postnatal dexamethasone treatment and increased incidence of cerebral palsy. Arch Dis Child Fetal Neonatal Ed 2000;83:F177-81.  Back to cited text no. 39
    
40.
Yeargin-Allsopp M, Braun KVN, Doernberg NS, Benedict RE, Kirby RS, Durkin MS. Prevalence of cerebral palsy in 8-year-old children in three areas of the United States in 2002: A multisite collaboration. Pediatrics 2008;121:547.  Back to cited text no. 40
    
41.
Winter S, Autry A, Boyle C, Yeargin-Allsopp M. Trends in the prevalence of cerebral palsy in a population-based study. Pediatrics 2002;110:122.  Back to cited text no. 41
    
42.
Seer Yee Lim M, Piau Wong C. Impact of cerebral palsy on the quality of life in patients and their families. Neurol Asia 2009;14:27-33.  Back to cited text no. 42
    
43.
Pharoah PO, Cooke T, Johnson MA, King R, Mutch L. Epidemiology of cerebral palsy in England and Scotland, 1984–9. Arch Dis Child Fetal Neonatal Ed 1998;79:F21-5.  Back to cited text no. 43
    
44.
Fidan F, Baysal O. Epidemiologic characteristics of patients with cerebral palsy. Open J Ther Rehabil 2014;2:126-32.  Back to cited text no. 44
    
45.
Andersen GL, Irgens LM, Hagaas I, Skranes JS, Meberg AE, Vik T. Cerebral palsy in Norway: Prevalence, subtypes and severity. Eur J Pediatr Neurol 2008;12:4–13.  Back to cited text no. 45
    
46.
Platt MJ, Cans C, Johnson A, Surman G, Topp M, Torrioli MG et al. Trends in cerebral palsy among infants of very low birthweight (<1500 g) or born prematurely (<32 weeks) in 16 European centres: A database study. Lancet 2007;369:43-50.  Back to cited text no. 46
    
47.
Nallegowda M, Mathur V, Singh U, Prakash H, Khanna M, Sachdev G et al. Oral health status in Indian children with cerebral palsy—A pilot study. IJPMR 2005;16:1-4.  Back to cited text no. 47
    
48.
Goel S, Ojha N. Trends of cerebral palsy in Rajasthan, India. Int J Adv Ayurveda Yoga Unani Siddha Homeopath 2015;4:275-81.  Back to cited text no. 48
    
49.
Kerrigan JF, Chugani HT, Phelps ME. Regional cerebral glucose metabolism in clinical subtypes of cerebral palsy. Pediatr Neurol 1991;7:415-25.  Back to cited text no. 49
    
50.
Rosenbaum P, Paneth N, Leviton A, Goldstein M, Bax M, Damiano D et al. A report: The definition and classification of cerebral palsy April 2006. Dev Med Child Neurol 2007;109:8-14. Erratum in: Dev Med Child Neurol 2007;49:480.  Back to cited text no. 50
    
51.
O’Shea TM. Diagnosis, treatment, and prevention of cerebral palsy in near term/term infants. Clin Obstet Gynecol 2008;51:816-28.  Back to cited text no. 51
    
52.
Barkovitch AJ, Truwit CL. Brain damage from perinatal asphyxia: Correlation of MR findings with gestational age. Am J Neuroradiol 1990;11:1087-96.  Back to cited text no. 52
    
53.
Sharan D. Recent advances in the management of cerebral palsy. Indian J Pediatr 2005;72:969-73.  Back to cited text no. 53
    
54.
Patel DR. Therapeutic interventions in cerebral palsy. Indian J Pediatr 2005;72:979-83.  Back to cited text no. 54
    
55.
Mayston M. Physiotherapy management in cerebral palsy: An update on treatment approaches. Clin Dev Med 2004;161:147-60.  Back to cited text no. 55
    
56.
Butler C, Darrah J. Effects of neurodevelopmental treatment (NDT) for cerebral palsy: An AACPDM evidence report. Dev Med Child Neurol 2001;43:778-90.  Back to cited text no. 56
    
57.
Schaaf R, Miller LJ. Occupational therapy using a sensory integrative approach for children with developmental disabilities. Ment Retard Dev Disabil Res Rev 2005;11:143-8.  Back to cited text no. 57
    
58.
Gormley ME Jr, Krach LE, Piccini L. Spasticity management of the child with spastic quadriplegia. Eur J Neurol 2001;5 Suppl 5:127-35.  Back to cited text no. 58
    
59.
Russman BS, Tilton A, Gormley ME Jr. Cerebral palsy: A rational approach to a treatment protocol and the role of botulinum toxin in treatment. Muscle Nerve 1997;20:S1-13.  Back to cited text no. 59
    
60.
Conde-Agudelo A, Romero R. Antenatal magnesium sulfate for the prevention of cerebral palsy in preterm infants less than 34 weeks’ gestation: A systematic review and metaanalysis. Am J Obstet Gynecol 2009;200:595-609.  Back to cited text no. 60
    
61.
Romkes J, Brunner. Comparison of dynamic and hinged ankle foot orthosis by gait analysis in patients with hemiplegic cerebral palsy. Gait Posture 2002;15:18-24.  Back to cited text no. 61
    
62.
Sterba JA, Rogers BT, France AP, Vokes DA. Horseback riding in children with cerebral palsy: Effect on gross motor function. Dev Med Child Neurol 2002;44:301-8.  Back to cited text no. 62
    



 
 
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