You are on page 1of 10

See discussions, stats, and author profiles for this publication at: https://www.researchgate.

net/publication/321112422

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


Palsy

Article  in  International Journal of Nutrition, Pharmacology, Neurological Diseases · October 2017


DOI: 10.4103/ijnpnd.ijnpnd_26_17

CITATION READS

1 495

5 authors, including:

Mahendra Rana Jyoti Upadhyay


Kumaun University University of Petroleum & Energy Studies
28 PUBLICATIONS   84 CITATIONS    22 PUBLICATIONS   40 CITATIONS   

SEE PROFILE SEE PROFILE

Sumit Durgapal Arvind Jantwal


Department of Pharmaceutical Sciences Bhimtal, Kumaun University Nainital Kumaun University
14 PUBLICATIONS   28 CITATIONS    11 PUBLICATIONS   24 CITATIONS   

SEE PROFILE SEE PROFILE

Some of the authors of this publication are also working on these related projects:

National Meicinal Plant Board funded project View project

NGS, Bacterial community and Phylogenetic Analysis View project

All content following this page was uploaded by Jyoti Upadhyay on 05 January 2018.

The user has requested enhancement of the downloaded file.


Vol 7 / Issue 4 / October-December 2017
Review Article

A Systematic Review on Etiology, Epidemiology, and


Treatment of Cerebral Palsy
Mahendra Rana, Jyoti Upadhyay, Amita Rana, Sumit Durgapal, Arvind Jantwal
Department of Pharmaceutical Sciences, Kumaun University, Campus Bhimtal, Bhimtal, Uttarakhand, India

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

INTRODUCTION (1) body movement or posture disorder, (2) static abnormality


in the brain, and (3) acquired brain disorder (early in life).
Cerebral palsy (CP) is a heterogenous permanent neurological
However, these characteristics do not specify (1) the severity of
disorder caused by nonprogressive damage to the developing
the movement disorders, (2) the static nature of the cerebral
brain. We all know that brain controls all the functions of our
abnormality, (3) age at which the abnormality occurs, and (4)
body like muscle movement. In this disorder, injury or
age before which CP was not detected. Postneonatal and
malformation occurs in the growing central nervous system
nonpostneonatal are the two widest distinctions in age of
that affects the development of motor function and body posture
acquiring cerebral abnormality.[5]
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 CLASSIFICATION OF CEREBRAL PALSY
weakness, shakiness, balance problems, and slow response, The topographic classification of CP involves (1) quadriplegia,
with symptoms ranging from mild to severe. In the case of (2) hemiplegia, (3) diplegia, (4) monoplegia, and (5) triplegia.
mild CP, the child may be heavy handed in one arm to some Monoplegia and triplegia are uncommon as there is substantial
extent, and this problem may be barely noticeable, whereas overlap of the affected areas. The most common form of
in severe CP, the child may have difficulties in performing CP in most of the studies is diplegia, which is the most
daily activities and maintaining movement, posture, and prevalent form (30–40%), followed by hemiplegia (20–30%)
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 Address for correspondence: Research Scholar, Jyoti Upadhyay, Department
its involvement distribution like hemiplegia and diplegia, of Pharmaceutical Sciences, Kumaun University, Campus Bhimtal, Bhimtal,
Uttarakhand, India.
and changes with age and surgery.[3,4] The exact definition
E-mail: jyotsna_pharma07@yahoo.co.in
of CP depends upon three common characteristics, which are
This is an open access article distributed under the terms of the Creative Commons
Access this article online Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix,
tweak, and build upon the work noncommercially, as long as the author is
Quick Response Code:
credited and the new creations are licensed under the identical terms.
Website:
www.ijnpnd.com For reprints contact: reprints@medknow.com

How to cite this article: Rana M, Upadhyay J, Rana A, Durgapal S,


DOI: Jantwal A. A Systematic Review on Etiology, Epidemiology, and
10.4103/ijnpnd.ijnpnd_26_17 Treatment of Cerebral Palsy. Int J Nutr Pharmacol Neurol Dis
2017;7:76-83.

76 © 2017 International Journal of Nutrition, Pharmacology, Neurological Diseases | Published by Wolters Kluwer - Medknow
Rana, et al.: Review on cerebral palsy

and quadriplegia (10–15%). A study of CP of 1000 cases functions. Monoplegic people are able to take care of
from India shows the highest percentage of cases with themselves. They perform their daily activities.[8]
spastic quadriplegia (61%) followed by diplegia (22%).[6]
Triplegic cerebral palsy
Quadriplegic cerebral palsy It is a form of paralysis involving three limbs, that is, paralysis
It is the most severe form and includes all four limbs; on one side of the body and of an arm or leg on the opposite
upper limbs are more severely affected than the lower limbs, side.[8,9]
related with acute hypoxic intrapartum asphyxia. Excessive
Based on the types of neuromuscular defects, CP is
cystic degeneration of the brain, which is polycystic
also classified as (1) spastic, (2) dyskinetic (including
encephalomalacia, polyporencephalon, and developmental
choreoathetoid and dystonic), (3) ataxic, (4) hypotonic, and
abnormalities (such as polymicrogyria and schizencephaly),
(5) mixed. The most common CP is spastic CP (70–75%),
is often revealed by neuroimaging. Very few voluntary
followed by dyskinetic (10–15%) and then ataxic (less than
movements are observed. Pseudobulbar signs are detected in
5% of cases).[8]
most children with recurrent aspiration of food material and
difficulty in swallowing. Optic atrophy and seizures are The CP disorder was classified according to Gross Motor
also observed in half of the patients. Severe intellectual Function Classification (GMFCS) and internationally used for
abnormality is reported in most of the cases.[7] research and clinical purposes. Researchers and therapist classify
the severity of CP using terms such as “mild,” “moderate,” and
Hemiplegic cerebral palsy “severe.” These classifications help validate the use of Gross
It is spastic unilateral hemiparesis wherein upper limbs are Motor Function Measure and evaluate children’s motor function.
affected more severely than the lower limbs. It is commonly This classification system has been extensively used and
observed in term infants (56%) and preterm infants (17%). internationally adopted. The major challenges for researchers
It has multifactorial pathogenesis. Impaired voluntary and clinicians in the classification of CP include generating and
movements are observed mostly affecting hand functions. validating similar classification for conditions like autism and
Other functions affected are pincer grasp of thumb, supination mental retardation.[9]
of the forearm, and extension of the wrist. Dorsiflexion and Another classification of CP called differential
aversion of foot are severely impaired in the lower limb. classification is based on etiology, pathology, and
Flexor tone is increased with hemiparetic posture. Affected clinical description. Classification of CP depends upon
limbs also have sensory abnormalities. Seizures occur in distribution and severity of motor impairments and
most children (>50%). Most common facial nerve palsies related (nonmotor) impairments. As some of the
are visual field defects, cranial nerve abnormalities, and terminologies are interpreted differently by clinicians
homonymous hemianopia.[7] from different disciplines, poor reliability of these
classification systems often ensues.[5]
Diplegic cerebral palsy
Prematurity and low birth weight are risk factors for spastic ETIOLOGY
diplegia. Neuroimaging study reveals cystic periventricular The etiology behind CP in infants remains unknown.
leukomalacia (PVL). The most common ischemic brain Complications like low birth weight, birth asphyxia,
injury is PVL in premature infants. This ischemia occurs premature separation of placenta, and abnormal fetal
in the white matter adjacent to the lateral ventricles.[7,8] position were associated with this disease. The associated
etiology for CP is given in Table 1. If a mother or infant
Monoplegic cerebral palsy suffer from any of these associated conditions, it does not
It is a form of paralysis affecting only one limb. Sometimes, mean this will result in CP, rather it means higher prevalence
the paralysis is limited only to a single muscle affecting body of CP.[10]

Table 1: Known etiology of cerebral palsy


S. No. Etiology References
1. Antenatal Causes Congenital brain malformations, and malformations of cortical developmentVascular events [11–14]
like middle cerebral artery occlusion Maternal infections during the first and second trimester of pregnancy
like rubella, cytomegalovirus, and toxoplasmosis. Metabolic disorders, maternal ingestion of toxins, and genetic syndromes
2. Perinatal care (during labor and delivery) Obstructed labor, cord prolapsed, antepartum hemorrhage causing [15]
hypoxia. Metabolic acidosis in fetal scalp (pH<7). Neonatal encephalopathy in infants (>34 weeks gestation)
results in cerebral palsy of Quadriplegic or dyskinetic type
3. Neonatal problems Severe hypoglycemia, jaundice, and neonatal infection [16]
4. Postneonatally acquired conditions Surgery for congenital malformations, Meningitis, septicemia, and other [16]
conditions like malaria

International Journal of Nutrition, Pharmacology, Neurological Diseases ¦ Volume 7 ¦ Issue 4 ¦ October-December 2017 77
Rana, et al.: Review on cerebral palsy

Several risk factors play a major role in the pathogenesis of Diagnosis of chorioamnionitis or endometritis was done
CP and may be present before or after pregnancy, during clinically and 14% of cases were observed as compared to
labor, and shortly after birth of the baby.[16] It is essential for 4% of controls. Other risk factors associated with CP are
us to distinguish between risk factors, associations, and maternal fever, maternal age more than 25 years, intrauterine
known etiology of CP. It was found in some cases that not growth restriction, prolonged rupture of membranes, and
a single event, but a series of events, is responsible for the nulliparity.[38]
damage of motor nerves which finally results in this
In some studies, investigation on the relationship between
condition.[17] The risk factors associated with CP are given
birth asphyxia and spastic CP was done, and data on children
in Table 2.
born with spastic CP (N = 183) were compared with matched
group of control children (N = 549) in Western Australia
Epidemiological studies on the possible risk factors between 1975 and 1980. Epidemiological methods were used
associated with cerebral palsy for collecting information on perinatal events for both CP
children and control group. It was found that there is a relation
A study at University of California, San Francisco, and Kaiser
between clinically observed signs of birth asphyxia and
Permanente Division of Research, Oakland, California, shows
spastic CP, and in only about 8% cases (15/183) of all the
the association between chorioamniontis and high risk of CP
children with spastic CP, the possible cause of brain injury
that was determined in term and near-term infants, and 109
was intrapartum asphyxia.[39]
children with CP were observed as compared to 218 controls.
Forty percent of the cases were hemiparetic, and 38% were Another study compared a 3-day course of dexamethasone
quadriparetic. Most common findings related to CP were white (N = 132) treatment with a control group given saline placebo
matter abnormalities, atrophy, and hypoxic–ischemic injury. (N = 116), administered shortly after birth, that is, from

Table 2: Cerebral palsy associated risk factors


S. No. Risk factors References
1. Before pregnancy i.e. maternal factors
Delay in menstrual cycle, irregular menstruation or long intermenstrual intervals [18]
Unusual long or short intervals between pregnancies [18,19]
Low social class [20,21]
Maternal medical conditions like intellectual disability, epilepsy, and thyroid disorders [22,23]
2. During pregnancy
Preeclampsia (results in preterm births) [24]
Maternal trauma in pregnancy [25]
Mother taking thyroid hormone or other estrogen during pregnancy [26]
Antepartum hemorrhage [27]
Multiple pregnancies [27]
3. During labor
A cause of perinatal asphyxia includes prolapsed cord, massive intrapartum hemorrhage, traumatic, [27]
or prolonged delivery due to cephalopelvic disproportion
Prolonged second stage of labor and ceserian section in emergency [28]
Premature separation of the placenta, abnormal fetal position [18]
Intrauterine exposure to infection like chorioamnionitis, in the latter stages of pregnancy and during labor [29–32]
Prolonged rupture of the membranes in infants of all gestation [26]
Presence of meconium-stained fluid [32]
Tight nuchal cord [33]

4. At birth
Premature children, decrease in length of gestation [27]
Low placental weight [18]
Low Apgar scores children with scores 0 to 3 at 5 min had an 81-fold increased risk of cerebral palsy [34,35]
5. Newborn period
Neonatal seizures [18,28]
Sepsis [36]
Respiratory disease [28]
Patient ductus arteriosus, hypotension, blood transfusion, prolonged ventilation, pneumothorax, sepsis, [37]
hyponatremia, total parenteral nutrition, seizures, and parenchymal damage with appreciable ventricular
dilatation detected by cerebral ultrasound
Neonatal seizures [18,37]

78 International Journal of Nutrition, Pharmacology, Neurological Diseases ¦ Volume 7 ¦ Issue 4 ¦ October-December 2017
Rana, et al.: Review on cerebral palsy

before 12 h of age in preterm infants ventilated for respiratory An epidemiological study of patients with CP determines the
distress syndrome. It was found that administration of demographical as well as clinical features of patients with CP
dexamethasone in the early stages of postnatal period attending various outpatient and inpatient clinics. This study
associated with high risk of CP and developmental delay.[40] included total 130 children. The known etiological risk
factors for CP were bleeding and threatened miscarriages
PREVALENCE OF CEREBRAL PALSY in prenatal period, birth asphyxia, premature baby and low
birth weight in the perinatal period, convulsions, and
Epidemiological studies on the prevalence of cerebral hyperbilirubinemia in the postnatal period. Types of CP
palsy included spastic quadriplegic, spastic diplegic, dyskinetic,
According to a study on the prevalence of CP and CP spastic hemiplegic, mixed type, and hypotonic or ataxic.
subtypes among children in three areas of the United Spastic quadriplegic was the most prevalent subtype of CP
States, a multisite collaboration shows that the average among children.[44]
prevalence of CP was 3.6 cases per 1000. The CP cases in
A study in Norway showed prevalence, subtypes, and severity
Wisconsin were 3.3 cases per 1000, Alabama 3.7 cases per
of CP. A total of 374 children born with CP were registered in
1000, and Georgia 3.8 cases per 1000. The prevalent cases of
the Cerebral Palsy Registry of Norway from January 1996 to
CP were highest in boys and black non-Hispanic children as
December 1998. This study shows the prevalence of CP 2.1
compared to girls and Hispanic children. It was also found
per 1000 live births. The percentage of subtypes of CP was
that prevalence among children living in low and middle-
spastic unilateral CP 33%, spastic bilateral 49%, dyskinetic
income neighborhoods was higher in comparison with high-
6%, ataxic 5%, and others 7% (not classified). A total of 5%
income neighborhoods. The most common subtype of CP
of impaired vision and 4% of hearing impairment cases were
among 77% of all cases was spastic CP; bilateral spastic CP
present and also 31% of mental retardation, 28% of active
was the most common type (70%) in the spastic group. These
epilepsy, and 28% of no speech cases were found in children.
findings added new knowledge in the epidemiological study
Children with low Apgar scores show severe impairment in
of CP.[41]
gross motor function, and children who had born in term, with
A study determined the birth-weight-specific trends in the normal birth weight and low Apgar scores, show severe
prevalence of CP. This study shows a modest increase in the impairment in fine motor function.[45]
prevalence pattern of congenital CP from 1.7 to 2.0 per 1000
Another study shows the risk factors for CP were very low
during the period from 1975 to 1991. The proportion of
birth weight (VLBW), that is, babies born, weighing
children having CP increased in normal birth weight
<1500 g, from multiple pregnancies than in infants having
infants from 17% in 1975 to 1977 to 39% in 1986 to
normal birth weight. A total of 1575 infants having VLBW
1991. Children weighing <1500 g, cases of spastic
are born with CP; out of which, 414 (26%) infants have birth
diplegic CP in these children were also increased overtime,
low weight (less than 1000 g) and 317 (20%) were from
that is, in the year 1975 to 1977 it was 7%, whereas 36% cases
multiple pregnancies. CP subtypes included spastic CP 1426
in the year 1985 to 1988 and 32% in the year 1986 to 1991.
(94%) which was unilateral, that is, hemiplegic in 336 (24%).
Low and very low birth weight infants show similar trends,
Decline in the prevalence of birth of VLBW infants was
whereas increase was seen in normal birth weight infant
reduced from 60.6 per 1000 live born in the year 1980 to 39.5
survivors.[38] A prospective descriptive study determining
per 1000 in 1996. This decline was due to reduction in the
the impact of health-related quality of life of CP patients
frequency of bilateral spastic CP among infants weighing
in their lives and families shows 11.1% patient’s quality of
1000 to 1499 g at the time of birth. In the group of birth weight
life was affected severely, 25.9% moderately, and 37%
between 1000 and 1499 g, the frequency of CP was found
mildly. Future studies can be done for measuring the
higher in male babies as compared to female babies. This
dynamics of this condition and also its influence on the
population-based study provides evidence that the prevalence
relationship between CP subtypes and quality of life.[42]
of CP in infants of birth weight less 1500 g has fallen,
A report provides information regarding the prevalence of CP especially of bilateral spastic CP, and has implications for
and its severity of the disability or comorbidity in England parents and healthcare services.[46]
and Scotland. The result of this report shows a total of
798,411 live births in between 1984 and 1989, with A pilot study in 53 Indian children with CP shows their oral
neonatal deaths 3651 (i.e., neonatal mortality 4.6 per 1000 health status and investigated various dental problems like
live births), and cases of CP were 1649, showing prevalence dental caries, plaque index, malocclusion, and drooling. A
of 2.1 per 1000 neonatal survivors, specified birth-weight- comparative study was done with the control group of same
related CP prevalence from 1.1 per 1000 neonatal survivors. age and sex of matched normal children. The result of this
No significant time trends in CP prevalence were observed in study shows a significant difference between cases and
any of the birth weight groups. As every one in five children controls for caries. It was found that maximum cases were
with CP suffers from severe multiple disabilities, the social in the age group of 6 to 8 years and quadriplegic and diaplegic
and clinical impacts must be addressed to provide continuous cases were highest among these children. Also one of the
care for these children.[43] significant findings of this study shows that those children

International Journal of Nutrition, Pharmacology, Neurological Diseases ¦ Volume 7 ¦ Issue 4 ¦ October-December 2017 79
Rana, et al.: Review on cerebral palsy

who were affected with drooling were not affected with dental In this condition, increased muscle tone is encountered at
carries.[47] A study in India shows trends of CP. This study the joint angle. Dystonia is also referred to as hypertonia
was conducted in Rajasthan, India. Diagnosed cases of spastic and decrease in the activity, whereas choreoathetosis is an
CP were observed from year 2010 to 2014. A total of 240 involuntary irregular spasmodic movement of the limbs or
children were included in this study; the male-to-female ratio facial muscles. Loss of order of muscle coordination occurs in
was found to be 2.3:1. Among these children, the cases of ataxic CP.[51]
diplegic CP were found maximum, that is, 52.92% followed
by quadriplegic CP which is 27.50 and 12.50% cases have Role of brain imaging
hemiplegic pattern. The most commonly associated dental Magnetic resonance imaging provides information about
problem was drooling. Prenatal asphyxia was found to be the adverse events timing, like cortical dysplasia’s date
major cause of CP.[48] during early pregnancy, that is, from 12th to 20th week
Subtypes of CP were studied using 2-deoxy-2(18F)fluoro-d- gestation, per ventricular leukomalacia between 28th and
glucose (FDG) and positron emission tomography (PET) in 34th week.[52]
23 children. The subtypes of CP included spastic quadriparesis
(N = 6), spastic diplegia (N = 4), infantile hemiplegia (N = 8), Treatment
and choreoathetosis (N = 5). Computed tomography or CP cannot be cured. As a result, various therapeutic
magnetic resonance imaging was used for correlating the interventions with interdisciplinary approaches have been
FDG–PET images. In spastic diplegic patients, PET shows used to manage CP. The main objective is to use a
focal areas of cortical hypometabolism, in which apparent combination of physical, developmental, medical, chemical,
structural abnormality was absent, whereas in choreoathetoid surgical, and technical procedures to treat patients. These
CP, normal pattern of cortical metabolism was observed instead procedures assist in preventing secondary impairments and
of hypometabolism in thalamus and nucleus of lenticular cells. improving child’s developmental capabilities.[53] Traditional
Symmetric cerebellar glucose metabolism with absence of physiotherapy and occupational therapy are broadly used
crossed cellular hypometabolism (diaschisis), FDT–PET measures and have shown benefit in the treatment of CP.
revealed symmetric cerebellar glucose metabolism in These therapeutic measures are found highly effective in
patients with infantile hemiplegia. FDG–PET may be useful improving the functional capabilities of the children with
in identifying CP patients.[49] CP.[54] For the treatment of inadequate muscle growth, the
following methods are used, that is, passive stretch, physical
TREATMENT OF CEREBRAL PALSY therapy, botulinum toxin injections, phenol injections,
Diagnosis of cerebral palsy orthopedic surgeries, and spasticity reduction. For the
CP diagnosed on the basis of clinical assessment. CP is a treatment of spasticity, selective dorsal rhizotomy (SDR)
permanent disorder of movement and posture development may be employed, whereas for mixed patterns and
that causes limitations in the activity, characterized by spasticity, selection criteria of SDR respond to intrathecal
nonprogressive disturbances occurring on the developing baclofen (ITB).[53]
brain of infant. This impairment in the movement and posture
Traditional physiotherapy
due to brain disorder is the invariant clinical manifestations.[50]
The GMFCS used by some researchers to include or exclude the It improves muscle strength, joint movement, and tolerance
cases of CP without functional impairment, in the Western to muscular movements. Traditional physiotherapy is a
Australian Cerebral Palsy Register. This register grades the routinely used interdisciplinary treatment approach for
severity of the cases. The diagnosis of CP, in clinical practice, school going children as it fulfills the requirement of
is generally based on observations of symptoms like sitting, cooperation and active participation of these children with
walking, pulling to stand evaluation of postures, deep tendon CP. Progressive resistance training program can help in
reflexes, and muscle tone. In premature infants, neurological progressively improving muscular strength. For improving
abnormalities observed in early months may resolve during the joint mobility, a range of motion exercises are carried out by
first 1 or 2 years of life. Such abnormality may or may not be physical therapists. Static and gentle stretches are performed
associated with motor impairment; one of these abnormalities on the patient joint for preventing joint contractions. Such
is transient dystonia, an abnormal neurological syndrome stretches performed within a pain-free joint range of
(e.g., hyperextension of the trunk) resolves after 1 year of age. movement. A group of healthcare providers, including
Severe CP can be seen in infants within first 12 months of birth. physical therapist, orthopedic surgeons, and orthotist, helps
The baby shows slow motor movement, floppy muscle tone, and in designing and implementing exercises, which improves
abnormal body posture. The diagnosis of CP is also based upon posture, balance control, gait, and mobility.[54]
its classification according to the nature of the movement
disorder, that is, spasticity, ataxia, dystonia, and athetosis and Physical/occupational therapy
also according to the topographic distribution of the motor The goal of this therapy is to improve infant–caregiver
abnormalities. Spasticity is the most predominant abnormality interaction, providing family support, parental education,
present among premature infants and analyzed clinically. and supplying resources. This therapy also promotes

80 International Journal of Nutrition, Pharmacology, Neurological Diseases ¦ Volume 7 ¦ Issue 4 ¦ October-December 2017
Rana, et al.: Review on cerebral palsy

developmental skills which are essential in performing very expensive and causes life-threatening complications, for
daily activities. These include self-care activities like example, neurological injuries due to dislodgement of
grooming, dressing, feeding, and fine motor tasks (like catheter tip. Both SDR and ITB act on lower limbs.[53]
painting and writing). Occupational therapy also directed
cognitive and noncognitive disabilities, particularly in the Phenol injection
visual motor area and adjustment of apparatus and seating to Neurolytic injection of phenol is used for motor nerves like
improve upper extremity use and to develop functional obturator nerve and musculocutaneous nerve. This phenol
independence. Some therapists use specialized techniques injection is rarely used because of the availability of
like neurodevelopmental treatment and sensory integration botulinum toxin.[58]
for achieving these goals, which are given below.
Botulinum toxin injection
Neurodevelopmental treatment
This injection causes a reversible chemodenervation of
In 1940, Berta and Karl Bobath developed this method of muscle, which is dose dependent. It is ineffective in the
treatment. The treatment approach is based on their personal case of lever arm disease. This treatment is useful in
observations from working with CP children. The main patients who are hypertonic either spastic or dystonic.[59]
objective of this treatment is to facilitate the normal motor
development and prevention of development of secondary
Antenatal magnesium sulfate
impairments caused by muscle contractions and limb
deformities.[55,56] 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
Sensory integration
infants less than 34 weeks of gestational age.[60]
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 Orthosis
processing difficulties. This model was designed to treat Newer light weight, made up of thermoplastic materials used
learning disabilities. The main hypothesis of this therapy below the knees. Articulated ankle foot orthosis and ground
is to develop and execute normal adaptive behavioral reaction articulated ankle foot orthosis are preferred over
response and to improve functional capabilities like ability solid articulated ankle foot orthosis in case of ambulatory
of the child to perform and integrate sensory network, children.[61]
including visual, auditory, perceptual, and others. Sensory
integration disorders include sensory modulation, sensory Hippotherapy
discrimination, and motor disorders (sensory based).[54,57] Also called as horseback riding therapy, it improves gross
motor function like tone, strength, balance, coordination, and
Oral muscle relaxants others in CP children. This therapy reduces the degree of
Diazepam, Baclofen, and dantrolene are muscle relaxants motor disability.[62]
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 CONCLUSION
have poor bioavailability because of their low lipid CP is a group of nonprogressive disorders affecting body
solubility.[53] 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
Selective dorsal rhizotomy
review paper, we summarize the risk factors associated
This neurosurgical operation includes laminoplasty of from CP, epidemiology as well as recent advances in its
L1 to S1 of the dorsal nerve roots. The inclusion criteria of treatment. The major risk factor for CP is preterm birth,
patients for this operation includes spasticity, selective and this risk increases with decreasing gestational age.
motor control, children aged 4 to 7 years, and spastic Better prenatal care and nutrition might reduce the chances
diplegia CP. Children who undergo this operation also of CP in children. A multidisciplinary, comprehensive, and
need orthopedic surgery after this. The ideal age for coordinated approach is needed in the care of children with
lower limb surgery is between 4 and 6 years, and 6 to 8 CP. Recent advances in the management of CP have
years for upper limb surgery.[53] increased. Implementation of new techniques like SDR,
ITB, and sensory integration helps in the treatment of CP.
Intrathecal baclofen Traditional physiotherapy and occupational therapy helps
A microprocessor-controlled pump containing small reduce spasticity. To minimize the cases of CP in children,
quantities of Baclofen administered into the subarachnoid additional research is required in understanding the etiology
space. It is used in severe spastic quadriplegia. This drug is of CP.

International Journal of Nutrition, Pharmacology, Neurological Diseases ¦ Volume 7 ¦ Issue 4 ¦ October-December 2017 81
Rana, et al.: Review on cerebral palsy

Financial support and sponsorship 22. Blair E, Stanley F. Aetiological pathways to spastic cerebral palsy.
Paediatr Perinat Epidemiol 1993;7:302-17.
Nil. 23. Collins M, Paneth N. Pre-eclampsia and cerebral palsy: Are they
related?. Dev Med Child Neurol 1988;40:207-11.
Conflicts of interest 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
There are no conflicts of interest. 1996;164:500-1
25. Nelson KB, Ellenberg JH. Predictors of low and very low birth-weight
REFERENCES 26.
and the relation of these to cerebral palsy. JAMA 1985;254:1473-9.
Stanley FJ, Blair E, Alberman E. Cerebral Palsies: Epidemiology and
1. Schimdt AA, Nordmark E, Czuba T, Westbom L. Stability of the Gross Causal Pathways. Clinics in Developmental Medicine (151). London:
Motor Function Classification System in children and adolescents with MacKeith Press; 2000.
cerebral palsy: A retrospective cohort registry study. Dev Med Child 27. Powell TG, Pharoah POD, Cooke RWI, Rosenbloom L. Cerebral palsy
Neurol 2017;59:641-46. in low birthweight infants. I. Spastic hemiplegia: Associations with
2. Wu CW, Huang SW, Lin JW, Liou TH, Chou LC, Lin HW. Risk of intrapartum stress. Dev Med Child Neurol 1988;30:11-8.
stroke among patients with cerebral palsy: A population-based cohort 28. Murphy DJ, Sellars S, MacKenzie IZ, Yudkin P, Johnson A. Case-
study. Dev Med Child Neurol 2017;59:52-6. control study of antenatal and intrapartum risk factors for cerebral palsy
3. Nelson KB. Can we prevent cerebral palsy?. N Engl J Med in very preterm singleton babies. Lancet 1995;346:1449-54.
2003;349:1765-69. 29. Nelson KB, Willoughby RE. Infection, inflammation and the risk of
4. Wren TA, Rethlefsen S, Kay RM. Prevalence of specific gait abnormalities cerebral palsy. Curr Opin Neurol 2000;13:133-9.
in children with cerebral palsy: Influence of cerebral palsy subtype, 30. Polivka BJ, Nickel JT, Wilkins JR. Urinary tract infection during
age, and previous surgery. J Pediatr Orthop 2005;25:79-83. pregnancy: A risk factor for cerebral palsy?. J Obstet Gynecol
5. Blair E, Watson L. Epidemiology of cerebral palsy. Semin Fetal Neonatal Nurs 1997;26:405-13.
Neonatal Med 2006;11:117-25. 31. Walstab J, Bell R, Reddihough D, Brennecke S, Bessell C, Beischer N.
6. Singhi PD, Ray M, Suri G. Clinical spectrum of cerebral palsy in North Antenatal and intrapartum antecedents of cerebral palsy—A case-
India—An analysis of 1000 cases. J Trop Pediatr 2002;48:162-6. control study. Aust N Z J Obstet Gynaecol 2002;42:138-46.
7. Menkes JH, Sarnat HB. Periuatal asphyxia and trauma. In: Menkes JH, 32. Nelson KB, Grether JK. Potentially asphyxiating conditions and spastic
Sarnat HB, editors. Child Neurology. Baltimore, United States: cerebral palsy in infants of normal birth weight. Am J Obstet Gynecol
Lippincott Williams & Wilkins; 2000. p. 427–36. 1998;179:507-13.
8. Sankar C, Mundkur N. Cerebral palsy-definition, classification, 33. Van de Riet JE, Vandenbussche FP, Le Cessie S, Keirse MJ. Newborn
etiology and early diagnosis. Indian J Pediatr 2005;72:865–8. assessment and long-term adverse outcome: A systematic review. Am J
9. Rosenbaum PL, Palisano RJ, Bartlett DJ, Galuppi BE, Russell DJ. Obstet Gynaecol 1999;180:1024-9.
Development of the Gross Motor Function Classification system for 34. Moster D, Lie R, Irgens L, Bjerkedal T, Markestad T. The association
cerebral palsy. Dev Med Child Neurol 2008;50:249-53. of Apgar score with subsequent death and cerebral palsy: A population-
10. Torfs CP, Von den berg BJ, Oechsli FW, Cummins S. Prenatal and based study in term infants. J Pediatr 2001;138:798-803.
perinatal factors in the etiology of cerebral palsy. J Pediatric 35. Blair E, Stanley F. When can cerebral palsy be prevented? The
1990;116:615. generation of causal hypotheses by multivariate analysis of a case-
11. Krageloh-Mann I, Petersen D, Hagberg G, Vollmer B, Hagberg B, control study. Paediatr Perinat Epidemiol 1993;7:272-301.
Michaelis R. Bilateral spastic cerebral palsy—MRI pathology and 36. Murphy DJ, Hope PL, Johnson A. Neonatal risk factors for cerebral
origin: Analysis from a representative series of 56 cases. Dev Med palsy in very preterm babies: Case-control study. BMJ 1997;314:404-
Child Neurol 1995;37:379-97. 8.
12. Steinlin M, Good M, Martin E, Banziger O, Largo RH, Boltshauser E. 37. Wu YW, Escobar GJ, Grether JK, Croen LA, Greene JD, Newman TB.
Congenital hemiplegia: Morphology of cerebral lesions and Chorioaamnionitis and cerebral palsy in term and near-term infants.
pathogenetic aspects from MRI. Neuropediatrics 1993;24:224-9. JAMA 2003;290:2677-84.
13. Truwit CL, Barkovich AJ, Koch TK, Ferriero DM. Cerebral palsy: MR 38. Blair E, Stanely FJ. Intrapartum asphyxia: A rare cause of cerebral
findings in 40 patients. Am J Neuroradiol 1992;13:67-78. palsy. J Pediatr 1988;112:515-9.
14. Reddihough DS, Collins KJ. The epidemiology and causes of cerebral 39. Shinwell ES, Karplus M, Reich D, Weintraub Z, Blazer S, Bader D,
palsy. Aust J Physiother 2003;49:7-12. et al. Early postnatal dexamethasone treatment and increased incidence
15. MacLennan A. A template for defining a causal relation between acute of cerebral palsy. Arch Dis Child Fetal Neonatal Ed 2000;83:F177-81.
intrapartum events and cerebral palsy: International consensus 40. Yeargin-Allsopp M, Braun KVN, Doernberg NS, Benedict RE, Kirby
statement. BMJ 1999;319:1054-9. RS, Durkin MS. Prevalence of cerebral palsy in 8-year-old children in
16. Stanley FJ, Blair E, Alberman E. Cerebral Palsies: Epidemiology and three areas of the United States in 2002: A multisite collaboration.
Causal Pathways. Clinics in Developmental Medicine (151). London: Pediatrics 2008;121:547.
MacKeith Press; 2000. 41. Winter S, Autry A, Boyle C, Yeargin-Allsopp M. Trends in the
17. Torfs CP, van den Berg BJ, Oechsil FW, Cummins S. Prenatal and prevalence of cerebral palsy in a population-based study. Pediatrics
perinatal factors in the etiology of cerebral palsy. J Pediatr 2002;110:122.
1990;116:615-9. 42. Seer Yee Lim M, Piau Wong C. Impact of cerebral palsy on the quality
18. Pinto-Martin JA, Cnaan A, Zhao H. Short interpregnancy interval and of life in patients and their families. Neurol Asia 2009;14:27-33.
the risk of disabling cerebral palsy in a low birth weight population. J 43. Pharoah PO, Cooke T, Johnson MA, King R, Mutch L. Epidemiology
Pediatr 1998;132:818-21. of cerebral palsy in England and Scotland, 1984–9. Arch Dis Child
19. Dolk H, Pattenden S, Johnson A. Cerebral palsy, low birthweight and Fetal Neonatal Ed 1998;79:F21-5.
socio-economic deprivation: Inequalities in a major cause of childhood 44. Fidan F, Baysal O. Epidemiologic characteristics of patients with
disability. Paediatr Perinat Epidemiol 2001;15:359-63. cerebral palsy. Open J Ther Rehabil 2014;2:126-32.
20. Dowding VM, Barry C. Cerebral palsy: Social class differences in 45. Andersen GL, Irgens LM, Hagaas I, Skranes JS, Meberg AE, Vik T.
prevalence in relation to birthweight and severity of disability. J Cerebral palsy in Norway: Prevalence, subtypes and severity. Eur J
Epidemiol Community Health 1990;44:191-5. Pediatr Neurol 2008;12:4–13.
21. Nelson KB, Ellenberg JH. Antecedents of cerebral palsy. Multivariate 46. Platt MJ, Cans C, Johnson A, Surman G, Topp M, Torrioli MG, et al.
analysis of risk factors. N Engl J Med 1986;315:81-6. Trends in cerebral palsy among infants of very low birthweight

82 International Journal of Nutrition, Pharmacology, Neurological Diseases ¦ Volume 7 ¦ Issue 4 ¦ October-December 2017
Rana, et al.: Review on cerebral palsy

(<1500 g) or born prematurely (<32 weeks) in 16 European centres: A 55. Mayston M. Physiotherapy management in cerebral palsy: An update
database study. Lancet 2007;369:43-50. on treatment approaches. Clin Dev Med 2004;161:147-60.
47. Nallegowda M, Mathur V, Singh U, Prakash H, Khanna M, Sachdev G, 56. Butler C, Darrah J. Effects of neurodevelopmental treatment (NDT) for
et al. Oral health status in Indian children with cerebral palsy—A pilot cerebral palsy: An AACPDM evidence report. Dev Med Child Neurol
study. IJPMR 2005;16:1-4. 2001;43:778-90.
48. Goel S, Ojha N. Trends of cerebral palsy in Rajasthan, India. Int J Adv 57. Schaaf R, Miller LJ. Occupational therapy using a sensory integrative
Ayurveda Yoga Unani Siddha Homeopath 2015;4:275-81. approach for children with developmental disabilities. Ment Retard
49. Kerrigan JF, Chugani HT, Phelps ME. Regional cerebral glucose Dev Disabil Res Rev 2005;11:143-8.
metabolism in clinical subtypes of cerebral palsy. Pediatr Neurol 58. Gormley ME Jr, Krach LE, Piccini L. Spasticity management of the
1991;7:415-25. child with spastic quadriplegia. Eur J Neurol 2001;5 Suppl 5:127-35.
50. Rosenbaum P, Paneth N, Leviton A, Goldstein M, Bax M, Damiano D, 59. Russman BS, Tilton A, Gormley ME Jr. Cerebral palsy: A rational
et al. A report: The definition and classification of cerebral palsy April approach to a treatment protocol and the role of botulinum toxin in
2006. Dev Med Child Neurol 2007;109:8-14. Erratum in: Dev Med treatment. Muscle Nerve 1997;20:S1-13.
Child Neurol 2007;49:480. 60. Conde-Agudelo A, Romero R. Antenatal magnesium sulfate for the
51. O’Shea TM. Diagnosis, treatment, and prevention of cerebral palsy in prevention of cerebral palsy in preterm infants less than 34 weeks’
near term/term infants. Clin Obstet Gynecol 2008;51:816-28. gestation: A systematic review and metaanalysis. Am J Obstet Gynecol
52. Barkovitch AJ, Truwit CL. Brain damage from perinatal asphyxia: 2009;200:595-609.
Correlation of MR findings with gestational age. Am J Neuroradiol 61. Romkes J, Brunner. Comparison of dynamic and hinged ankle foot
1990;11:1087-96. orthosis by gait analysis in patients with hemiplegic cerebral palsy. Gait
53. Sharan D. Recent advances in the management of cerebral palsy. Indian Posture 2002;15:18-24.
J Pediatr 2005;72:969-73. 62. Sterba JA, Rogers BT, France AP, Vokes DA. Horseback riding in
54. Patel DR. Therapeutic interventions in cerebral palsy. Indian J Pediatr children with cerebral palsy: Effect on gross motor function. Dev Med
2005;72:979-83. Child Neurol 2002;44:301-8.

International Journal of Nutrition, Pharmacology, Neurological Diseases ¦ Volume 7 ¦ Issue 4 ¦ October-December 2017 83

View publication stats

You might also like