OBJECTIVE – To study the different lesions in the brain in children with clinically diagnosed cerebral palsy and correlation of the findings on MRI brain with type of cerebral palsy.

METHODS– 60 diagnosed cases of cerebral palsy were evaluated with history and clinical examination. Cerebral Palsy children were investigated by performing neuroimaging (MRI). The MRI scans were conducted on a GE Sigma 1.5 Scanner. Routinely, the scans obtained were T1 Weighted, T2 Weighted and FLAIR (axial, corona and sagittal) sequences. In each patient, the images were assessed for: Any abnormal signal in the brain parenchyma, myelination of brain as per age of the baby and size of the ventricle.

RESULTS – It was found that maximum number of children (28.33%) were from the age group 3-5 years followed by (20%) in the age group of 1-12months and 5-7 years. Out of 60 patients 56.67% were males and 43.33% females. The majority of patients were delivered pre-term (68.33%) followed by term delivery (31.67%). The majority of patients had Spastic quadriplegia type of Cerebral Palsy. The unspecified form of Cerebral palsy was seen in 14 (23.33%) while mixed form of Cerebral palsy was observed in 12 (20%) patients. The malformations were seen in 5 (8.33%) patients while miscellaneous lesions were observed in 2 (3.33%) patients. The distribution of patients according to brain malformation in Cerebral palsy showed out of total 5 patients with malformation, Pachygyria was observed in 2 (40%) patients followed by Lissencephaly (40%). The corpus callosum agenesis was seen in 1 (20%) patient.

CONCLUSION– The MRI scans help to reveal the pathologic causes leading to the condition with the MRI brain findings having a strong correlation with the clinical findings. The relationship between the locality of brain lesions, the structure and clinical functions in children with CP point to further workup as they are important prerequisites for questioning reorganization and plasticity.

INTRODUCTION

One of the most common form of severe disability of childhood is cerebral palsy which has a special relationship to preterm birth. Prevalence of cerebral palsy is around 2 per 1000 live births with increase in prevalence in very low birth weight children and those born preterm to around 40 to 100 per 1000 live births (1) (2). Cerebral palsy presents with a wide variety of clinical symptoms which include difficulty in language, learning, epilepsy, hearing as well as vision impairment (3). The basis of definition of cerebral palsy is usually phenomenological in origin; which implies that cause of cerebral palsy is related to any lesion within the brain, any interference and abnormality in brain development.

The term cerebral Palsy is a broad term used to describe a spectrum of non-progressive motor disabilities, resulting from brain damage at or around birth. Cerebral Palsy presents with muscle spasticity with involuntary movements, impaired mobility, seizures etc. The four major types of cerebral palsy are: spastic, ataxic, athetoid/ dyskinetic and mixed. Currently, there is no cure for cerebral palsy and symptomatic management with rehabilitation is the mainstay of treatment (4) (5).

All cases of cerebral palsy especially of unknown origin should undergo neuroimaging as recommended by The American Academy of Neurology. The recommendation is still controversial as there is not enough supporting evidence to the adequacy of the same. Abnormal neuroradiological findings are seen in many cases of cerebral palsy, around 70-80% with the most common abnormality being white matter damage. In children with hemiplegia combined gray and white matter abnormalities are more common; in children with athetosis or bilateral spasticity and ataxia, the most common abnormality is isolated white matter damage and in children; with the least common finding being isolated gray matter damage. Brain malformations attribute to about 10% of causes cerebral palsy and no imaging abnormality is detectable in around 17% of cerebral palsy cases (4) (5) (6).

The timing and the nature of brain lesions can be well depicted on Magnetic resonance imaging. It is being increasingly used in the workup of children with cerebral palsy but it is still important to determine how much it can assist in pointing towards the etiology of cerebral palsy being an expensive procedure. Also a general anesthetic may also be required in young children (6).

Previous studies have shown the relationship between the degree of motor impairment and the neuroimaging findings with less severe motor impairment showed an association with focal periventricular white-matter lesions or focal cortical/subcortical lesions, and children with severe motor impairment showed a more diffuse encephalopathy and lesions also in basal ganglia. (3) (4) (5).

Many risk factors have now come into play with a better survival rate presently as compared to earlier birth cohorts. Now, more children born extremely preterm also survive. Despite the revolution, several neonatal morbidities are still seen in preterm children for example periventricular white-matter lesions and intraventricular haemorrhage that will lead to cerebral palsy. Children with brain malformation, perinatal asphyxia, and other severe conditions who would not have survived 10 years ago do so today because of improved neonatal intensive care (7).

The potential benefits of neuroimaging and currently used techniques help in improving the understanding of etiology of cerebral palsy. Understanding the etiology and pathogenesis of cerebral palsy is the main contribution of neuroimaging, which also helps us to rule in or out the conditions implicated for genetic counselling for example brain malformations (7).

Thus, this study was carried out to define the etiology of cerebral palsy in correlation with neuroimaging findings.

MATERIALS AND METHODS

STUDY DESIGN:

The study was cross sectional study undertaken to study magnetic resonance imaging (MRI) of brain in children with cerebral palsy

STUDY PERIOD:

The study period was 24 months.

STUDY POPULATION:

The study population was children from 1 month to 14 years of age with Cerebral palsy.

SAMPLE SIZE:

In the present study a total sample size of 60 children fulfilling inclusion and exclusion criteria were included. Inclusion criteria was children with clinical diagnosis of cerebral palsy, 1 month to 14 years of age. The patients not undertaken for neuroimaging were the critically ill patients and those noted willing to undergo neuroimaging.

ETHICAL CONSIDERATION:

The study was approved by the Ethical Committee of the institute and taken permission from appropriate authority.

MRI IMAGING:

The MRI scans were conducted on a GE Sigma 1.5 Scanner. Routinely, the scans obtained were T1 Weighted, T2 Weighted and FLAIR (axial, corona and sagittal) sequences. In each patient, the images were assessed for: Any abnormal signal in the brain parenchyma, myelination of brain as per age of the baby and size of the ventricle. Congenital anomalies were also looked for.

STATISTICAL ANALYSIS:

O SPSS Version 17 was used for both database entry and statistical analysis.

O The baseline characteristics were recorded. Simple descriptive statistics were used throughout.

O Possible statistical associations between categorical variables were evaluated using Pearson x2 analysis. The statistical significance was attained when P value <0.05.

REFERENCE CITING:

Vancouver system of listing and citing of references is used. As per this system, the references are numbered and listed consecutively in the order in which they are first cited in the text.

OBSERVATIONS AND RESULTS

Table I: Distribution according to age

Age group	No. of Patients	Percentage
1-12 months	12	20.00
1-3 years	09	15.00
3-5 years	17	28.33
5-7 years	12	20.00
7-9 years	05	08.33
9-12 years	03	05.00
12-14 years	02	03.33
Total	60	100

Table no 1 shows the distribution of study population (n=60) according to the age group. It was found that maximum number of children (28.33%) were from the age group 3-5 years followed by (20%) in the age group of 1-12months and 5-7 years.

Table II: Distribution according to sex

Sex	No. of Patients	Percentage
Male	37	61.6
Female	23	38.33
Total	60	100

The table 2 shows distribution of patients according to their sex and respective percentage. Out of 60 patients 61.6% were males and 38.33% females.

Table III: Distribution according to delivery by weeks of gestation

Gestation	No. of Patients	Percentage
Preterm	41	68.33
Term	19	31.67
Total	60	100

The above table no. 3 shows the distribution of patients according to delivery by weeks of gestation. The majority of patients were delivered pre-term (68.33%) followed by term delivery (31.67%)

Table IV: Distribution according to type of delivery

Type of delivery	No. of Patients	Percentage
Vaginal	46	76.67
Assisted	09	15.00
LSCS	05	08.33
Total	60	100

The above table no. 4 shows number of patients according to type of delivery. The majority of patients were delivered vaginally (76.67%) followed by assisted delivery (15%) and LSCS (8.33%)

Table V: Distribution according to birth weight

Birth weight (grams)	No. of Patients	Percentage
<2000	06	10.00
2000- 2500	33	55.00
>2500	21	35.00
Total	60	100

The above table no. 5 shows the distribution of patients according to birth weight. The majority of patients were with birth weight 2000-2500 grams (55%) The patients with birth weight >2500 grams were 21 (35%) while with birth weight <2000 grams were 6 (10%)

Table VI: Distribution according to plurality of delivery

Plurality	No. of Patients	Percentage
Singleton	55	91.67
Twin	04	06.67
Triplet	01	01.66
Total	60	100

The distribution of patients according to plurality of delivery showed that majority of patients were with born singleton (91.67%) The patients born twins were 04 (6.67%) and triplet 1 (1.66%)

Table VII: Distribution according to APGAR score

APGAR score	No. of Patients	Percentage
<4	14	23.33
5-7	42	70.00
>7	04	06.67
Total	60	100

The above table no. 7 shows the distribution of patients according APGAR score. The majority of patients were with APGAR score 5-7 (70%) followed by APGAR score of <4 in 14 (23.33%) patients. The APGAR score of >7 was observed only in 4 (6.67%) patients.

Table VIII: Distribution according to clinical classification of cerebral palsy

Classification of Cerebral palsy	No. of Patients	Percentage
Spastic quadriplegia	18	30.00
Spastic hemiplegia	09	15.00
Spastic diplegia	04	06.67
Dyskinetic form	02	03.33
Ataxic form	01	01.67
Mixed form	12	20.00
Unspecified form	14	23.33
Total	60	100.00

The above table no. 8 shows the number of patients according to clinical classification of Cerebral Palsy. The majority of patients had Spastic quadriplegia. The unspecified forms were seen in 14 (23.33%) while mixed form of Cerebral palsy was observed in 12 (20%) patients.

Table IX: Distribution according to Gross motor function classification

GMFC	No. of Patients	Percentage
I	12	20.00
II	18	30.00
III	28	46.67
IV	07	11.67
V	05	08.33
Total	60	100.00

The distribution of patients according to Gross Motor Function Classification (GMFC) type of Cerebral Palsy observed that the majority of patients belonged to category III (46.67%) followed by category II (30%). The category V form of Cerebral palsy was seen in 5 (8.33%) patients.

Table X: Distribution according to spectrum of MRI findings

MRI findings	No. of Patients (n=60)	Percentage
White matter leukomalacia – periventricular in location	28	46.67
Abnormalities in deep grey matter	21	35.00
Brain malformations	05	08.33
Miscellaneous lesions	02	03.33

The above table no. 10 shows the distribution of patients according to MRI findings among Cerebral Palsy patients. The majority of patients had Periventricular white matter abnormalities (46.67%) (Figure 1) followed by deep grey matter abnormalities among 21 (35%) patients. The malformations were seen in 5 (8.33%) patients while miscellaneous lesions were observed in 2 (3.33%) patients.

Table XI: Distribution according to brain Malformation in cerebral palsy

Malformations	No. of Patients	Percentage
Pachygyria	02	40.00
Lissencephaly	02	40.00
Corpus callosum agenesis	01	20.00
Total	05	100

The distribution of patients according to brain malformation in Cerebral palsy showed out of total 5 patients with malformation, Pachygyria was observed in 2 (40%) patients followed by Lissencephaly (40%). The corpus callosum agenesis was seen in 1 (20%) patient.

Table XII: Distribution according to Corpus callosum MRI Findings in cerebral palsy

Corpus callosum MRI Findings	No. of Patients	Percentage
Mild Diffuse Thinning	07	11.67
Severe Diffuse Thinning	02	03.33
Thinned Posteriorly	01	01.67
Thinned Body	03	05.00
Agenesis	01	01.67
Normal	46	76.67
Total	60	100

The above table no. 12 shows the distribution of patients according to Corpus Callosum MRI findings among Cerebral Palsy patients. In majority of patients observed mild diffuse thinning (11.67%) (Figure 2) followed by thinned body of Corpus Callosum in 3 (5%) patients. The Corpus Callosum agenesis was seen in 1 (1.67%) patient (Figure 3) while 46 (76.67%) patients had normal MRI findings related to Corpus Callosum.

Fig 2: In a 18 months old child, MRI brain revealed supraventricular hyperintensities and diffuse thinning of corpus callosum on axial T2WI (a) and sagittal T2WI (b) respectively

Fig 3: In a 2 month old baby, MRI brain reveals (a) in axial T2W MR image, parallel configuration of the lateral ventricles. (b) Coronal T2W MR image reveals the viking helmet appearance which refers to the appearance of lateral ventricles in coronal projection where the cingulate gyrus is everted into narrowed and elongated frontal horns. (c) Sagittal T2W MR image reveals completely absent corpus callosum, absent cingulate sulcus with the sulci of medial hemisphere seen reaching in a radial fashion onto the third ventricle. (d) Axial T2W MR image reveals a dilated high riding third ventricle

Table XIII: Distribution according to abnormalities among patients

Abnormalities	No. of Patients (n=60)	Percentage
Developmental Delay	56	93.33
Abnormal Muscle Tone	35	58.33
Seizures	17	28.33
Mental Retardation	13	21.67
Ophthalmic Impairment	03	05.00

The distribution of patients according to abnormalities showed out of total 60 patients with developmental delay was observed in 56 (93.33%) patients followed by abnormal muscle tone (58.33%). Seizures were seen 17 (28.33%) patients while Mental retardation among 13 (21.67%) patients. Among 3 (5%) patients ophthalmic impairment was seen.

Table XIV: Correlation of clinical classification of cerebral palsy and MRI findings

Classification of Cerebral palsy	MRI Findings		Total (%)
Classification of Cerebral palsy	Abnormal (%)	Normal (%)	Total (%)
Spastic quadriplegia	14 (77.78)	04 (22.22)	18 (100)
Spastic hemiplegia	07 (77.78)	02 (22.22)	09 (100)
Spastic diplegia	03 (75.00)	01 (25.00)	04 (100)
Dyskinetic form	02 (100)	00 (00)	02 (100)
Ataxic form	01 (100)	00 (00)	01 (100)
Mixed form	10 (83.33)	02 (16.67)	12 (100)
Unspecified form	10 (71.43)	04 (28.57)	14 (100)
Total	47 (78.33)	13 (21.67)	60 (100)

The above table showed correlation of clinical type of cerebral palsy and MRI findings among patients. It was observe that out of 60 patients, 47 (78.33%) had abnormal MRI findings.

Table XV: Distribution according to abnormalities in ventricles

Abnormalities	No. of Patients (n=60)	Percentage
Irregularity of lateral ventricles	23	38.33
Hydrocephalus	13	21.66
Cysts	04	06.67
Others	02	03.33

The above table showed abnormalities in ventricles of cerebral palsy patients. It was observe that out of 60 patients, 9 (15%) had irregularity of lateral ventricles. It was also observed that 4 (6.67%) patients showed hydrocephalus and one patient had cyst in the lateral ventricle.

Table XVI: Distribution according to Severity of hydrocephalus

Severity	No. of Patients	Percentage
Mild	06	46.16
Moderate	05	38.46
Severe	02	15.38
Total	13	100

For example in figure 4, MRI brain axial sections (T2WI) in a 9 month old preterm boy reveals severely dilated lateral and third ventricles with irregularity of the ventricular system and periventricular hyper intensities suggestive of periventricular leukomalacia

Table XVII: Relation of ventricular abnormality and birth weight

Birth weight (grams)	Ventricular abnormality		Total
Birth weight (grams)	Present	Absent	Total
VLBW (<2000)	03	03	06
LBW (2000- 2500)	11	22	33
Normal (>2500)	09	12	21
Total	23	37	60

Table XVIII: Relation of severity of hydrocephalus and birth weight

Birth weight (grams)	Severity of Hydrocephalus			Total
Birth weight (grams)	Mild	Moderate	Severe	Total
VLBW (<2000)	01	02	01	04
LBW (2000- 2500)	03	02	01	06
Normal (>2500)	02	01	00	03
Total	06	05	02	13

For example in figure 5 in a 6 month old pre-term boy, very low both weight with history of birth asphyxia MRI brain study reveals communicating hydrocephalous

Table XIX: Distribution according to leukodystrohies among patients

Leukodystrophies	No. of Patients (n=60)	Percentage
Present	03	05.00
Absent	57	95.00
Total	60	100

The distribution of patients according to leukodystrophies showed out of total 60 patients leukodystrophies were observed in 03 (5%). Among all the patients one patient with metachromatic leukodystrophy (MLD), one case of adrenoleukodystrophy (ALD) (Figure 6) and one case of cystic leukodystrophy (Figure 7) was observed.

DISCUSSION

The study conducted was a cross sectional study which was undertaken to study the magnetic resonance imaging (MRI) findings of brain in children with clinically diagnosed cerebral palsy.

All the patients attending radiology department with clinically diagnosed Cerebral Palsy was recruited for the study. A total sample size of 60 children was included in the study. The critically ill patients with Cerebral palsy and parents not willing to undergo neuroimaging were excluded from the study.

The neuroimaging in all the children was done after a proper parental consent who reported for follow up at the time allotted. Clearance from the ethical committee of the institute was obtained before the initiation of the study.

The data collection was done by using predesigned pretested questionnaire. All the children with diagnosed case of cerebral palsy were evaluated with history and clinical examination. A detailed review of the obstetric and medical records of the mother as well as the child’s neonatal history, medical, and rehabilitation history if any present was recorded. A history of consanguinity was asked for. Family history of congenital malformations was also taken. Mother was asked for her history during the antenatal period regarding alcohol intake, any drug abuse, tobacco intake, smoking, history of previous abortions and diabetic history. Cerebral Palsy children were investigated by performing Neuroimaging study (MRI).

In the present study the distribution of study population (n=60) showed that maximum number of children (28.33%) were from the age group 3-5 years followed by (20%) in the age group of 1-12 months and 5-7 years.

Similar findings were seen in a study done by Moifo B et al (8) to determine and describe common brain lesions of cerebral palsy patients observed that the mean age of the study population was 42 months with 77.4% aged 0 to 60 months.

The findings in study done by Kolawole T. et al (9) also observed that the average period for clinical diagnosis and the establishment of a possible prognosis was 1 to 5 years. At 1 year, the brain structure is well developed to permit more precise clinical manifestations and diagnosis and at 1.5 years a notion on the evolution of the condition can be obtained and consequently on the outcome or prognosis. However, diagnosis of cerebral palsy is usually not possible until after 1 year of age when the baby fails to achieve the milestones acceptable to that particular age.

In the present study the distribution of patients according to their sex and respective percentage showed that out of 60 patients 56.67% were males and 43.33% females.

The findings were in accordance to study done by Mbonda et al(10), Karumuna and Mgone (11) found a sex ratio of 1.3 in favour of males, while Ndiaye et al(12)found a sex ratio of 1.44 in favour of males.

In the study done by Stanley et al(1)suggested that male sex may contribute to the cause of cerebral palsy, thus appearing as a risk factor

Similarly, in a study done by Aggarwal A. et al (13) among the 98 children studied for Cerebral palsy, 80.5% were males.

The findings by Johnston and Hagberg (14) suggested that sex hormones seem to protect the female fetal brain from anoxia and ischemia and hence would be less predisposed to cerebral palsy compared to the males.

The findings were in contrast to present study done by Moifo B et al (8) were among 120 patients, 66 were females with sex-ratio of 0.8.

The distribution of patients according to delivery by weeks of gestation showed that majority of patients were delivered pre-term (68.33%) followed by term delivery (31.67%). The incidence of cerebral palsy was more in children born prematurely than those born at term. The number of children born preterm in the study were also more in number.

The findings were in contrast to study done by Aggarwal A. et al (13) where out of 98 children diagnosed with Cerebral Palsy at a tertiary centre observed that only around 22.2% of children out of total 98 were premature.

In a study done by Martin Bax et al (15) to investigate the correlates of cerebral palsy observed that among 585 children with cerebral palsy, children born at term were 235 (54%) while those born preterm (<28 weeks) were 47 (10.9%) in number.

The distribution of patients according to type of delivery showed that majority of patients were delivered vaginally (76.67%) followed by assisted delivery (15%) and LSCS (8.33%)

Similar findings were seen in study done by Aggarwal A. et al (13) for clinico-radiological profile of children diagnosed as Cerebral Palsy observed that vaginal delivery was conducted in 88.5% patients.

In the present study the distribution of patients according to birth weight showed that the majority of patients were with birth weight 2000-2500 grams (55%) The patients with birth weight >2500 grams were 21 (35%) while with birth weight <2000 grams were 6 (10%)The distribution of patients according to plurality of delivery showed that majority of patients were with born singleton (91.67%) The patients born twins were 04 (6.67%) and triplet 1 (1.66%)

In a study done by Martin Bax et al (15) to investigate the correlates of cerebral palsy observed that among children with cerebral palsy, children from a multiple pregnancy were around 51 in number corresponding to 12%, while those from a twin pregnancy were 48 corresponding to 9.90% of the total sample and those from a triplet pregnancy were only 3 corresponding to around 2.1% of the total sample size.

In the study, the distribution of patients according APGAR score showed that the majority of patients were with APGAR score 5-7 (70%) followed by APGAR score of <4 in 14 (23.33%) patients. The APGAR score of >7 was observed only in 4 (6.67%) patients.

The distribution of patients according to clinical classification of Cerebral Palsy showed that the majority of patients had Spastic quadriplegia. The unspecified form was seen in 14 (23.33%) while mixed form of Cerebral palsy was observed in 12 (20%) patients.

Similar findings were seen in study done by Aggarwal A. et al (13) where the most frequent clinical type of Cerebral palsy was spastic (75.83%), followed by hypotonic (1.67%), dystonic (1.67%) and the least common being the mixed (2.5%). Among spastic classification, most cases had involvement of upper and lower limb bilaterally.

Similar findings observed by Taylor F et al (16) from National Institute of Neurological Disorders and Stroke (U.S.) that the most common Cerebral Palsy was Spastic quadriplegic. 10 to 20% of patients clinically presented with the athetoid or dyskinetic subtype of cerebral palsy which was characterized clinically by writhing, abnormal, and slow movements of upper and lower limbs which increase in frequency during stress periods and are not seen during sleep. Around 5-10% of patients are affected by ataxic subtype which is very rare and baby presents with impaired balance and haphazard behavior.

The higher frequency of spastic forms may be due to the fact that the clinical type of cerebral palsy was not specified in 23.33% cases in the study.

In Mbonda et al (10) study, spastic forms accounted for 57.8% while 38.1% of cases were mixed cases, and in Ndiaye et al (12) study, accounted for 49% with 26.5% spastic quadriplegia. Spastic cerebral palsy is characterized by spasticity which refers to increase in the tone of muscles which is dependent on velocity, exaggerated reflexes, clonus, and a positive Babinski reflex.

The distribution of patients according to classification of gross motor functions (GMFC) observed that the majority of patients belonged to category III (46.67%) followed by category II (30%). The category V form of Cerebral palsy was seen in 5 (8.33%) patients.

In a study done by Aggarwal A. et al (13) to compare the clinical and radiological findings in children diagnosed with Cerebral palsy observed that as per classification of the gross motor function in cerebral palsy, 17.5% cases were in category I, 14.16% in category II, 19.16% in category III, and around 30.83% cases in category IV.

The distribution of patients according to MRI findings among Cerebral Palsy patients showed that the majority of patients had Periventricular white matter abnormalities (46.67%) followed by deep grey matter abnormalities among 21 (35%) patients. The malformations were seen in 5 (8.33%) patients while miscellaneous lesions were observed in 2 (3.33%) patients.

In case of PVL, the MRI findings show white matter cavitations and loss along with gliosis but overlying cortex is somewhat unaffected. Secondary manifestations include corpus callosum thinning along with lateral ventricular enlargement and irregularities.

Injury to the cortico-spinal tracts that travel along the angle of lateral ventricle dorso-laterally result for the spasticity seen in children with periventricular leukomalacia. These tracts innervate preferentially the lower extremities. Extensive white matter loss is seen in severe cases of periventricular leukomalacia leading to involvement of upper and lower extremities bilaterally.

There is greater magnitude of involvement of visuo-motor ability and abilities of perception rather than the ability of verbal commands as cognitive impairment in children with periventricular leukomalacia.

In a study done by Aggarwal A. et al (13) in among 98 children with neuroimaging, around 94 (95.92%) children had abnormal findings. The findings included abnormalities in white matter periventricular in location (34%), malformations in brain (11.7%), abnormalities in deep grey matter (47.8%) and other miscellaneous lesions (6.5%).

In a study done by Martin Bax et al (15) the MRI scans showed that the most common finding was damage to the white matter caused by immaturity (WMDI, including PVL) seen in around 42.5% of patients, followed by lesions in the basal ganglia seen in around 12.8% of patients, lesions in the cortical/subcortical region seen in 9.4% of patients, malformations in brain in around 9.1% of patients. Around 7.4% patients shoed infarcts focally and 7.1% patients had miscellaneous lesions. 11.7% of patients had normal brain MRI.

In a study done by Krageloh-Mann I et al (17) abnormalities in gray matter and periventricular changes were equally seen irrespective of gestational age as compared to the western studies where a higher incidence of similar changes were seen in preterm babies.

The distribution of patients according to brain malformation in Cerebral palsy showed out of total 5 patients with malformation, Pachygyria was observed in 2 (40%) patients belonged followed by Lissencephaly (40%). The corpus callosum agenesis was seen in 1 (20%) patient.

In a study done by Aggarwal A. et al (13) the various brain malformations seen in children with cerebral palsy were focal cortical dysplasia and lissencephaly both seen in around 27% of patients, cranio-vertebral anomalies, arachnoid cyst and pachygyria both seen in around 9% of patients and colpocephaly seen in around 18% patients.

The distribution of patients according to Corpus Callosum MRI findings among Cerebral Palsy patients showed that in majority of patients observed mild diffuse thinning (11.67%) followed by thinned body of Corpus Callosum in 3 (5%) patients. The Corpus Callosum agenesis was seen in 1 (1.67%) patient while 46 (76.67%) patients had normal MRI findings related to Corpus Callosum.

In a study done by Moifo B et al (8) the most frequent associated clinical signs were language impairment (45.6%), mental retardation (40.2%) and epilepsy (37.8%).

The correlation of clinical type of cerebral palsy and MRI findings among patients showed that out of 60 patients, 47 (78.33%) had abnormal MRI findings with no correlation. (P>0.05)

In the present study, it was observe that out of 60 patients, 23 (38.33%) had irregularity of lateral ventricles. It was also observed that 13 (21.66%) patients showed hydrocephalus and 04 (6.67%) patients had cyst in the lateral ventricle.

Numerous cysts replaced the white matter in periventricular location due to deficiency of the same in periventricular region and also in centrum semiovale. The cyst integrity with the ventricle is lost with the destruction of the ependyma between the two. Ventricle appears irregular in shape with jagged edges and expansion locally or passively (15). It presents as suffocation and is commonly observed in children born preterm or at term.

In the present study, ventricular abnormalities were irregular ventricular contour and ventricular enlargement, reflecting incorporation of parenchymal cysts or white matter hypoplasia,), with ventricular enlargement alone. The ventricular trigones were slightly rounded. All had abnormal ventricles with irregular contour indicating the presence of periventricular cysts.

It was observe that patients with VLBW had more ventricular abnormality as compared to normal weight patients with cerebral palsy. The relation of ventricular abnormality and birth weight among cerebral palsy patients showed no statistical significance. (P>0.05)

Similar findings were seen in study by Charles L. Truwit et al (18) where ventricular abnormalities were apparent in 20patients born at term, including 12 (41%) with an irregular ventricular contour and ventricular enlargement, seven (24%) with ventricular enlargement alone and one with hydranencephaly.

It was observed that, out of total 60 patients, 13 (21.67%) showed hydrocephalus. It was observed that among 13 patients with hydrocephalus 06 (46.16%) patients had mild hydrocephalus, 05 (38.46%) had moderate hydrocephalus and 02 (15.38%) had severe hydrocephalus. Among all the patients with hydrocephalus, ten had communicating and three had non-communicating hydrocephalus.

It was observe that patients with VLBW had more severity of hydrocephalus as compared to normal weight patients with cerebral palsy. The relation of severity of hydrocephalus and birth weight among cerebral palsy patients showed no statistical significance. (P>0.05)

In a study done by Judith Rankin et al (19) on congenital anomalies seen in children diagnosed with cerebral palsy observed that congenital hydrocephalus was present in 17.3% of cerebral palsy patients. Hydrocephalous was more commonly seen in children born at term than those born prematurely.

Chromosome and gene abnormalities also contribute to pathogenesis of cerebral anomalies in limited cases. Other causes include infections, deficiency of nutrients, environmental factors and teratogens. The precise etiology however remains unknown in most cases and is likely considered multifactorial in origin, including environmental and genetic causes. It has been postulated that in a multiple gestation early fetal loss may be attributed to prenatal origin of cerebral palsy

The distribution of patients according to leukodystrophies showed out of total 60 patients leukodystrophies were observed in 03 (5%). Among patients two patients with metachromatic leukodystrophy (MLD) and one case of adrenoleukodystrophy (ALD) was observed. Patients who clinically presented with regression of development and pyramidal dysfunction with metachromatic leukodystrophy (MLD) were evaluated. MRI revealed diffuse hyper-intensities in periventricular region bilaterally. Long standing disease was suggested by hypointensity on T2 weighted images in the thalamus and cerebral atrophy.

Similar findings were observed in study done by B. N. Lakhkar et al (20), leukodystrophies constituted only 7.5%.

Metachromatic leukodystrophy results in a butterfly configuration caused by extensive white matter demyelination in periventricular and subcortical region symmetrically. The subcortical U fibres and basal ganglia and initially spared. Late in the course of disease there is involvement of arcuate fibres and white matter in the cerebellum resulting in cortical atrophy. Also in late stages a hypointense basal gnalia is seen due to hemosiderin deposition. Basal ganglia hypointensities were seen in both cases in the study implicating a disease which is long standing. There are 3 types of metachromatic leukodystrophy categorized according to age at onset in the patient: late infantile, juvenile, and adult. Late infantile metachromatic leukodystrophy is the most common type, manifesting in children usually between 12 and 18 months of age. It clinically presents as deterioration in speech, intellect and coordination and also motor signs of peripheral neuropathy (21).

At around 4-8 years of age adrenoleukodystrophy presents clinically with dementia, changes in behavior, auditory and visual disturbances. It may be accompanied by the symptoms of addison’s disease. The classic appearance on MRI is demyelination of occipital lobes, bilaterally and symmetrically, and splenium of corpus callosum. On contrast administration, the inflammatory edge of demyelination enhances. Parietal and occipital regions may show calcification (22).

Pelizaeus-Merzbacher disease present mostly in younger age group as leukodystrophy with mixed pyramidal and extrapyramidal symptoms clinically such as spastic quadreparesis, choreoathetosis and nystagmus. Microcephaly is also seen (22).

Globoid cell leukodystrophy also known as Krabbe disease, is an autosomal recessive disorder which is caused by deficiency of galactocerebroside β-galactosidase. This enzyme causes degradation of cerebroside which is a normal constituent of myelin. 4 forms of krabbe disease are recognized which present differently clinically. The four forms are infantile, late infantile, juvenile, and adult forms. Progression of disease is indicated by a decline in the cognitive functions, nystagmus, myoclonus and opisthotonus. Krabbe disease progresses rapidly and is fatal (23).

Alexander disease also known as fibrinoid leukodystrophy usually presents clinically between 2^nd -7^th decades of life and is characterized pathologically by Rosenthal fiber deposition in the subpial, subependymal and perivascular locaations (24).

Cystic leukodystrophy was present as multiple variable sized cysts following CSF signal on all sequences noted throughout the brain parenchyma in periventricular and subcortical region in bilateral parietal region (21).

Canavan disease is a rare type of leukodystrophy which shows an autosomal recessive pattern on inheritance. It is caused by a mutation in the ASPA gene. Aspartoacylase is encoded by this gene which is responsible for metabolism of N-acetyl-L-aspartate (NAA). A deficiency of aspartoacyclase is caused by this mutation. Formation of lipids is the main function of NAA. Excess levels of NAA are seen which lead to demyeoination (25).

Another leukodystrophy where peroxismal ATP binding cassette mutation occus is the X-linked adrenoleukodystrophy (X-ALD). Myelin destabilization results which causes inflammatory demyelination in the cerebrum. Corpus callosum is the first to get involved. Progression outwards is then seen towards hemispheres bilaterally. Also, these patients show increased quantities of very long chain fatty acid (VLCFA) followed by accumulation into fluids and body tissue. This later leads to incorporation into complex lipids where they normally are not seen. This is directly involved with cerebral inflammation. Destabilization of myelin sheath occurs due to the above described pathological processes which eventually leads to demyelination (26).

Not only the conditions pathological basis is revealed by MRI scans but also a strong clinical correlation is seen with the findings. The nature of the child’s condition can be better understood with better prediction of their future needs, thus helping parents, clinicians and other people to care better for the child.

CONCLUSION

The study conducted was a cross sectional study which was undertaken to study the magnetic resonance imaging (MRI) findings of brain in children with clinically diagnosed cerebral palsy.

In the study maximum number of children was in the age group 3-5 years with male dominance. The majority of patients were delivered pre-term and vaginally. The patients were with APGAR score 5-7 were maximum.

Spastic quadriplegia type of Cerebral Palsy was observed in majority of children. While type III of classification of Gross Motor Functions was most commonly seen in children with cerebral palsy.

MRI findings showed that Periventricular white matter abnormalities were maximum followed by deep grey matter abnormalities among patients. The brain malformation in Cerebral palsy patients were Pachygyria, Lissencephaly and corpus callosum agenesis. In Corpus Callosum MRI findings among Cerebral Palsy patients majority of patients observed mild diffuse thinning followed by thinned body of Corpus Callosum. The developmental delay was observed in mostly all patients followed by abnormal muscle tone. The correlation of clinical type of cerebral palsy and MRI findings among patients showed that no correlation.

Not only the pathological basis of the condition is better understood with MRI scans but also the strong clinical correlations of the findings are also documented. The relationship between the locality of brain lesions, the structure and clinical functions in children with CP point to further workup as they are important prerequisites for questioning reorganization and plasticity.

Bibliography

1.	Stanley F, Blair E, Alberman E. Cerebal Palsies: Epidemiology and CausalPathways London, United Kingdom: MacKeith Press; 2000.
2.	Himmelmann K, Hagberg G, Beckung E, Hagberg B, Uvebrant P. The changing panorama of cerebral palsy in Sweden IX. Prevalence and origin in the birth-year period 1995–1998. ActaPaediatr. 2005; 94: p. 287–294.
3.	Bax M, Goldstein M, Rosenbaum P, Paneth B, Dan B, Jacobsson B, et al. Proposed definition and classification of cerebral palsy. Dev Med Child Neurol. 2005; 47: p. 571–576.
4.	Kuban K, Leviton A. Cerebral palsy. N Engl J Med. 1994; 330: p. 188-95.
5.	Towsley K, Shevell M, Dagenais L. Population-based study of neuroimaging findings in children with cerebral palsy. Eur J PaediatrNeurol. 2011; 15: p. 29-35.
6.	Korzeniewski S, Birbeck G, Delano M, Potchen M, Paneth N. A systematicreview of neuroimaging for cerebral palsy. J Child Neurol. 2008; 23: p. 216-27.
7.	Yoshida S, Hayakawa K, Oishi K, Mori S, Kanda T, Yamori Y, et al. Athetoticand spastic cerebral palsy: anatomic characterization based ondiffusion-tensor imaging. Radiology. 2011; 260: p. 511-20.
8.	Moifo B, Nguefack S, Zeh O, Obi F, Tambe J, Mah E, et al. Computed Tomography Findings In Cerebral Palsy In Yaounde-Cameroon. J AfrImag Med. 2013; 5(3): p. 134-142.
9.	Kolawole T, Patel P, Mahdi A. Computedtomographic (CT) scans in cerebral palsy. Pediatric Radiology. 1989; 7: p. 20-23.
10.	Mbonda E, Nguefack S, Chiabi A, Djampou N, Pondy O, Mbassi A, et al. Epilepsie chez les Enfants Atteintesd’ InfirmitéMotrice Cérébrale: à propos de 412 Observations à Yaoundé. Clinics in Mother and Child Health. 2011; 8: p. 1–5.
11.	Karumuna J, Mgone C. Cerebral Palsy inDar Es Salaam. CentrAfr J Med. 1990; 36: p. 8-10.
12.	Ndiaye M, Tall I, Basse A, Touré K, Seck L, Sene M, et al. Infirmité motriced’ origine cérébrale : uneseries énégalaise. AJNS. 2012; 31(1): p. 15-22.
13.	Aggarwal A, Mittal H, Debnath S, Rai A. Neuroimaging inCerebral Palsy – Report from North India. Iran Child NeurolJ. 2013; 7(4): p. 41-6.
14.	Johnston M, Hagberg H. Sex and thepathogenesis of cerebral palsy. Dev Med Child Neurol. 2007; 49: p. 74–8.
15.	Martin Bax D, Tydeman C, Flodmark O. Clinical and MRI Correlates of Cerebral Palsy: The European Cerebral Palsy Study. JAMA. 2006; Vol 296(13).
16.	Taylor F. Cerebral Palsy: Hope Through Research London: NINDS; 2013.
17.	Krageloh-Mann I, Petersen D, Hagberg G, Vollmer B, Hagberg B, Michaelis R. Bilateral spastic CP—MRIpathology and origin: analysis from a representativeseries of 56 cases. Dev Med Child Neurol. 1995; 37: p. 379-397.
18.	Truwit CL, Barkovich JA, Koch TK, Ferriero DM. Cerebral Palsy: MR Findings in 40 Patients. AJNR. 1992; 13: p. 67-78.
19.	J R, C C, E G. Congenital anomalies inchildren with cerebral palsy: a population-based record linkage study. Developmental Medicine and Child Neurology. 2010; 52(4): p. 345–351.
20.	Aggarwal M, John J, Lakhkar B. MRI in white matter diseases – clinico radiological correlation. Indian Journal of Radiology and Imaging. 2002; 12(2): p. 43-50.
21.	Barboura I, Ferchichi S, Dandana A, Jaidane Z, Ben Khelifa S, Chahed H, et al. Metachromatic leucodystrophy. Clinical, biological, and therapeutic aspects. Annales de Biologie Clinique. 2010; 68(4): p. 64-72.
22.	Gieselman V, Krageloh-Mann I. Metachromatic Leukodystrophy – An Update. Neuropediatrics. 2010; 41(1): p. 412-16.
23.	Szymanska K, Lugowska A, Laure-Kamionowska M, Gieruszczak-Bialek D, Musielak M, Eichler S, et al. Diagnostic difficulties in Krabbe disesase: a report of two cases and review of literature. Folia Neuropathol. 2012; 50(4): p. 346–356.
24.	Singh N, Bixby C, Etienne D, Tubbs RS, Loukas M. Alexander’s disease: reassessment of a neonatal form. Child’s Nervous System. 2012; 28(12): p. 2029–2031.
25.	United Leukodystrophy Foundation. Canavan Disease.
26.	Berger J, Forss-Petter S, Eichler FS. Pathophysiology of X-Linked Adrenoleukodystrophy. Biochimie. 2014; 98: p. 135–142.
27.	Hagberg G, Beckung E, Hagberg B, Uvebrant P, Himmelmann K. The changing panorama of cerebral palsy in Sweden IX. Prevalence and origin in the birth-year period. ActaPaediatr2005. 1995–1998; 94: p. 287–294.

Cerebral Palsy and Brain Lesions Analysis

Cerebral Palsy and Brain Lesions Analysis

List of Figures

List of Tables

Abstract and Keywords

INTRODUCTION

MATERIALS AND METHODS

STUDY DESIGN:

STUDY PERIOD:

STUDY POPULATION:

SAMPLE SIZE:

ETHICAL CONSIDERATION:

MRI IMAGING:

STATISTICAL ANALYSIS:

REFERENCE CITING:

OBSERVATIONS AND RESULTS

DISCUSSION

CONCLUSION

Bibliography

study

http://au.freedissertation.com

Leave a Reply
Cancel reply

Leave a Reply

Cerebral Palsy and Brain Lesions Analysis

List of Figures

List of Tables

Abstract and Keywords

INTRODUCTION

MATERIALS AND METHODS

STUDY DESIGN:

STUDY PERIOD:

STUDY POPULATION:

SAMPLE SIZE:

ETHICAL CONSIDERATION:

MRI IMAGING:

STATISTICAL ANALYSIS:

REFERENCE CITING:

OBSERVATIONS AND RESULTS

DISCUSSION

CONCLUSION

Bibliography

study

http://au.freedissertation.com

Leave a Reply Cancel reply

Leave a Reply

Leave a Reply
Cancel reply