Cerebral palsy in Jordan: clinical and neuroimaging characteristics

To evaluate the diagnostic findings of neuroimaging in patients with cerebral palsy and if there is any specific finding correlated to certain types of Cerebral Palsy. Case records of 158 patients diagnosed to have cerebral palsy attending the pediatric neurology and neurodevelopmental clinics at King Hussein Medical Center and King Abdullah University Hospital over 2 years period, 2006 and 2007, were studied retrospectively with reference to their clinical characteristics and their correlation to the neuroimaging [MRI and CT scan] findings. A total of 158 cases with cerebral palsy were included in the study, 84 [53%] males, 74 [47%] females, 41 [26%] preterm and 117 [74%] full- term babies. Spastic cerebral palsy was seen in 112[70.8%] with spastic quadriplegia being the commonest seen in 63[40%]. Hypotonic ataxic type present in 22[14%], dyskinetic 15[9.4%] and mixed cerebral palsy in 9[5.6%]. Abnormal neuroimaging findings were seen on MRI in 125[79%], while in CT scan in 113[71%]. Specific neuroimaging findings were seen suggesting brain asphyxia in 40[25%], congenital brain anomaly in 22[14%], intracranial hemorrhage in 10[6%], vascular and infectious causes in 29[18.5%], unknown/Isolated brain atrophy in 26[16.5%], and periventricular leukomalacia in 31[20%]. The most common single etiology identified was birth asphyxia 40[25%], and the second is periventricular leukomalacia which was identified in 31 patients [20%]. Nonspecific brain atrophy was considered as nonspecific finding, that was found most often in patients with dyskinetic CP 5/15[33%], and in patients with spastic quadriplegia 15/63[24%] as compared to other groups. The principle contribution of imaging is to the understanding of etiology and pathogenesis, including ruling in or out conditions that may have implicated a genetic counseling, such as malformations. MRI is a more sensitive test than CT in detecting brain abnormalities

Febrile seizures: Review article

Demographic, Genetic and clinical profiles Febrile seizures are broadly defined as seizures' occurring in the presence of fever, but in the absence of central nervous system infection. They occur in children aging from 6 months to 5 years with a mean age of onset of 18-24 months and they occur slightly more commonly in boys than in girls. 1 It is the most common reason for convulsions in children less than 6 years of age, and they occur in 2 to 5% of all children, although it has been reported to be more frequent in Asian countries. In Japan, the rate has been reported to be 7% and in Jordan 6.5%.2 It is thought that the rates in these areas are higher because some of the common infections of childhood may occur earlier in life when children are most susceptible to febrile seizures. 3 Febrile seizures can be divided into two types: simple and complex. Simple febrile seizures are characterized by the following: duration less than 15 minutes generally, and it occurs in normal children neurologically and developmentally. Complex febrile seizures have the following features: duration greater than 15 minutes, multiple within 24 hours, and/or focal. [2] The risk of recurrence after the first febrile seizure is about 33%. The risk factors for recurrence are: occurrence of the first febrile seizure at a young age; family history of febrile seizures; short duration of fever before the seizure; relatively low fever at the time of the initial seizure; and possibly a family history of an afebrile seizure. It has been observed that the time of recurrence is usually within the first year of onset. Although complex febrile seizures are not usually associated with an increased risk of recurrent febrile seizures, they may be a risk factor for epilepsy later in life. Febrile seizures seem to run in families, but their mode of inheritance is unknown. The risk for other siblings developing febrile seizures is about 10-20%, but may be higher if the parents also have a history of febrile seizures themselves. 4 In large families, the FS susceptibility trait is inherited by autosomal dominant pattern with a reduced penetrance. It has long been recognized that there is a significant genetic component for susceptibility to this type of seizure and this may be caused by a mutation in several genes.[2] In the presence of cases of FS and epilepsy in the same family one study the concept of a genetic epilepsy syndrome termed Generalized Epilepsy with FC plus [GEFS+]. GEFS has a spectrum of phenotypes including FC, and FC plus.[2]. Febrile seizures usually occur in the first 24 hours of the onset of fever. It has been suggested that it is the rapid rise in the child's temperature, which causes a febrile seizure rather than the actual height of the fever itself; however, there is no substantial proof to support this suggestion. The seizures are usually generalized and tonic-clonic, but other types may be present as well. There may be variations to this such as staring without stiffness, jerking movements without prior stiffening, and localized stiffness or jerking