In this study, brain atrophy was the most important imaging abnormalities in children with cerebral palsy, occurring in 18 of the 29 patients in this study. Other brain imaging abnormalities include periventricular leukomalacia, arachnoid cyst, and cerebellar atrophy/cerebellar hypoplasia. Van Bogaert et al (1992) reported 3 children with cerebral palsy who had normal brain CT-scans, but MRI revealed some CT-scan undetectable white matter abnormalities. The two patients with spastic diplegia showed bilateral abnormalities either in the subcortical regions or in the occipital periventricular areas. The patient with congenital hemiplegia exhibited unilateral abnormalities in the periventricular area. van Bogaert et al suggested that MRI is probably more useful than CT-scan for the assessment of cerebral palsy [16]. In our study, isolated periventricular leukomalacia occurred in one patient with spastic cerebral palsy, and occurred with evidence of brain atrophy in an other two patients who also had spastic cerebral palsy.

In our study, polymicrogyri was observed on MRI in association with brain atrophy and dilatation of the basal cisterns in one patient with spastic cerebral palsy. Truwit et al (1992) from the USA reported the MRI findings of 40 patients (aged 1 month to 41 years) with cerebral palsy. In 82% of the 11 patients who had been born before term, MRI showed periventricular white matter damage suggestive of hypoxic-ischemic brain injury. MRI findings in the remaining 29 patients who had been born at term included gyral abnormalities such as polymicrogyria, isolated periventricular leukomalacia, and watershed cortical or deep gray nuclear damage. In 16 (55%) of 29 patients born at term, MRI included intrauterine brain damage including developmental abnormalities [17].

In our study, imaging abnormalities in the three patients who had ataxic cerebral palsy included generalized cerebral atrophy, cerebellar atrophy with absence of the inferior vermis, and cerebellar hypoplasia, vermian hypoplasia with retro-cerebellar hypoplasia.

Imamura et al (1992) from Japan reported the MRI abnormalities in 5 patients with ataxic cerebral palsy which included generalized atrophy of cerebellum (particularly in the anterior superior region) and slight atrophy of pons in a patient with inherited disorder. The second patient also had cerebellar atrophy especially in anterior superior region. In the third patient, CT and MRI showed generalized spino-ponto-cerebellar atrophy, and the patient received a diagnosis of Marinesco-Sjörgren syndrome. CT and MRI of the fourth patient showed generalized spino-ponto-cerebellar atrophy. The MRI of the fifth patient showed cranium bifida and agenesis of anterior medullar velum [18].

Campistol Plana et al (1996) from Barcelona reported the CT-scan findings in 90 children with spastic cerebral palsy of the diplegic type. 51 of them had typical evidence of residual periventricular leukomalacia. Six of the 51 children were recognized in early in life by brain ultrasound. Campistol Plana et al suggested that the CT-scan evidence of residual periventricular leukomalacia include slight ventricular dilation, subcortical atrophy or periventricular heterotopia [19].

In our study, imaging abnormalities in the two patients with hemiplegic cerebral palsy included large right sided temporo-parietal gliotic changes with large communicating porencephaly cyst in one patient, and arachnoid cyst in the left sphenoid observed in association with periventricular leukodystrophy-like changes of signal abnormalities in the occipital area, in the second patient.

Gururaj et al (2002) reported brain imaging findings in 65 children (41 term-born and 24 preterm-born) patients with cerebral palsy from the United Arab Emirates. 23 patients had spastic diplegia, with 57% of them had marked periventricular leukomalacia, which occurred more in preterm-born patients. In 13 with hemiplegia, 12 had unilateral abnormalities on brain imaging. Patients with spastic tetraplegia had extensive, bilateral, diffuse brain damage. Extra-pyramidal cerebral palsy was much commoner in term-born patients and 80 % of them had marked abnormalities in the basal ganglia. Ataxic cerebral palsy was not associated with important correlation between the clinical manifestations and abnormalities on brain imaging [20].

The study of Gururaj et al suggested that brain imaging findings were closely related to the type of cerebral palsy and the clinical abnormalities except in ataxic cerebral palsy [20].

Wu et al (2006) from California University reported the brain imaging abnormalities in 78 infants with congenital hemiparetic cerebral palsy (55 had an MRI and 23 patients had a CT-scan). Perinatal arterial infarction was the most common brain imaging abnormalities occurring in 30% of term infants. Infants with right hemiparesis or moderate to severe weakness were more likely to show a perinatal arterial infarction on imaging studies. Periventricular white matter abnormalities occurred more in preterm infants. Brain malformations occurred in 14 patients, and included polymicrogyria, heterotopia, and schizencephaly. 14 patients who didn’t have abnormalities on imaging study showed more likelihood to outgrow hemiparesis by the age of three years than patients who had abnormalities on an image study [21].

In our study, one patient has cerebral palsy occurring as a complication of meningitis during early infancy.

Tillberg and colleagues (2008) reported the occurrence of CNS infection during life in 13 children which resulted in the development of hemiplegic cerebral palsy [22].

Therefore, the pattern of brain imaging abnormalities was rather different from the pattern reported from other countries such as USA, Spain, Japan, and United Arab Emirates.