Seropositivity of Toxoplasma gondii and Toxocara spp. in Children with Cryptogenic Epilepsy, Benha, Egypt

The present study aimed to investigate the possible association of Toxoplasma gondii and Toxocara spp. infections with cryptogenic epilepsy in children. The study was carried out between June 2014 and March 2015. Total 90 children (40 with cryptogenic epilepsy, 30 with non-cryptogenic epilepsy, and 20 healthy control children) were evaluated to determine the anti-Toxocara and anti-T. gondii IgG seropositivity using ELISA kits. Epileptic cases were selected from those attending the pediatrics outpatient clinic of Benha University Hospital, Pediatrics Neurology Unit, and from Benha Specialized Hospital of children. The results showed that the level of anti-T. gondii IgG seropositivity was significantly higher among children with cryptogenic epilepsy (20%) than among children with non-cryptogenic children (0%). In healthy controls (10%), there was no association between toxocariasis seropositivity and cryptogenic epilepsy (only 5.7%; 4 out of 70 cases) among cases and 10% (2 out of 20) among controls. Among toxocariasis IgG positive cases, 3 (7.5%) were cryptogenic, and only 1 (3.3%) was non-cryptogenic. These statistically significant results support the association between T. gondii infection and cryptogenic epilepsy while deny this association with toxocariasis.

Serum non-protein bound Iron:a useful prognostic marker of neonatal asphyxia

Four million infants suffer from birth asphyxia allover the world each year; of them, one million dies and a similar number will develop serious sequelae; including hypoxic ischemia encephalopathy [HIE]. A better understanding of the pathogenesis of this event and its early identification is highly required. The role of non-protein bound iron [NPBI], lactate, and other laboratory and clinical criteria as diagnostic and prognostic markers were studied. This study included 25 asphyxiated neonates and 25 healthy matched neonates as a control group. Both groups were subjected to clinical assessment, routine laboratory tests, serum lactate and NPBI measurements. Clinical follow-up was done every three months till the age of 1 year. Developmental screening test was done every six months using Denver Developmental Screening Test [DDST]. Serum lactate levels were found to be significantly higher in the HIE group compared to the control group [t = 15.13, P < 0.001].HIE group [were divided into mild [10], moderate [7] and severe [8]] according to sarnat classification and there was a significant elevation in serum lactate levels in severe HIE in comparison to mild cases [P< 0.05]. Statistical analysis of serum NPBI levels in control group and HIE group revealed that there was a significant increase of NPBI in HIE group in comparison to control group [t= 7.02 P < 0.001, t= 9.89 P < 0.001, t= 13.3 P < 0.001 for mild, moderate, and severe subgroups respectively]. One way anova test revealed a significant elevation of the level of NPBI with the increase of severity in the studied subgroups [mild, moderate and severe] indicating that there is a correlation between the level of NPBI and the severity of the clinical presentation of HIE [F= 52.37, P < 0.001]. ROC curve was used to test the performance and clinical value of NPBI for predicting neurodevelopment outcome, and it indicated reliable performance for NPBI [ROC area under curve was 0.95]. We found a significant negative correlation coefficient between the level of NPBI and pH [r = -0.5794, P< 0.001], Na[+][r = -0.06084, P< 0.05], Ca[++[r = -0.7511, P < 0.001], Apgar score at 1 minute [r = -0.5766, P < 0.001], Apgar score at 5 minute,[r = -0.5248, P < 0.001] and pO-2[--] [r = -0.2668, P < 0.05]. A positive correlation coefficient was found between the level NPBI and HCO3 [r = 0.3568, P < 0.05], urea [r = 0.2681, P < 0.05], creatinine [r = 0.5552, P < 0.001], p[co][2] [r = 0.6053, P < 0.001], lactate [r = 0.5927, P < 0.001], and K[+] [r = 0.0855, P < 0.05]. All HIE cases devoid of neurological complications [manifested by seizures] had a normal development m contrast to HIE cases which complained from seizures [75%, 9 of 12 cases] after 6 months, and [81.8%, 9 of 11 cases] after 12 months had developmental delay tested by DDST. All of neurologically complicated cases [presented with seizures] had a significant elevation of the serum level of NPBI [P < 0.001. Serum NPBI assay may be a reliable early indicator of infra and extra-uterine oxidative stress and brain injury, with a prognostic value regarding HIE. use of free iron scavengers may be indicated of those cases with increased NPBI and eventual threat of HIE occurrence with its catastrophic complications

Study of neurometabolic disorders in Egyptian children

Background: Metabolic brain diseases usually present with a complex neurological picture so they are often overlooked. This prospective study was undertaken to focus on the clinical aspects, biochemical abnormalities and neuroimaging of the brain in children suffering from neurometabolic disorders

Patients and methods: This study was carried out on 130 patients suspected clinically of having metabolic brain diseases and presented to the neuropediatric clinic, neonatal intensive care unit in Benha faculty of medicine and the neurometabolic specialized clinic in Abu El-Reesh hospital. The diagnosis of neurometabolic disorders was confirmed in 29 children [22%]. They were 19 males and 10 females, their age ranged from 5 days to 10 yrs with mean age 3.61 +/- 2.2 years. They presented with clinical manifestations suggestive of metabolic brain diseases. They were subjected to thorough history, clinical examination, investigations in the form of serum ammonia, serum lactate ,blood glucose, blood gases assessment, ketone bodies in urine, CPK [creatine phosphokinase],urine organic acids, plasma aminogram, enzymatic assay, EMG [Electromyography],EEG[electroencephalography], muscle biopsy, CT and MRI of the brain

Results: Patients were classified according to their clinical presentations, biochemical and radiological findings into 5 groups, Group I, Organic acidemia 10 cases [34.5%], including, Methyl malonic acidemia [4 cases], Biotinidase deficiency [3 cases], Glutaric Aciduria type 1 [2 cases] and Maple syrup urine disease [one case]. Group II, Mitochondrial disorders 9 cases [31%] including, Leigh syndrome [4 cases], Pyruvate dehydrogenase deficiency [2 cases], mitochondrial encephalomyopathy [2 cases] and MELAS syndrome[mitochondrial encephalopathy, lactic acidosis and stroke] [one case]. Group III, Urea cycle abnormalities 5 cases [17.2 %]. Group IV Aminoacidopathy 3 cases [10.4 %]in the form of Phenylketonuria. Group V Fatty acid oxidation defect 2 cases [6.9%]. The main neurological manifestations were global developmental delay [93.1%], seizures [89.7%], hypertonia [65.5%] and microcephaly [55.2%]. Biochemical abnormalities were: Group I: had acidosis in 9 cases[90%] [ketoacidosis in [4 cases],lactic acidosis in[3 cases],acidosis without ketosis in [2 cases]], ketosis only in one case [10%] and hyperammonemia in 7 cases [70%] of cases. GroupII: had mainly lactic acidosis 5 cases [55.6%] and mild hyperammonemia [11.1%]. GroupIII: had isolated hyperammonemia [100%]. Group IV: had hyperphenylalaninemia in [100%] of cases with phenylketonuria. Group V: had lactic acidosis,mild hyperammonemia, hypoglycemia and absent ketosis in [100%]of cases. Neuroimaging showed abnormal findings in the form of basal ganglia abnormalities [41.4%], brain atrophy [27.5%], diffuse demeylination and focal demeylination [6.9%]each and normal findings in [17.3%]

Conclusion: Presence of unexplained neurological symptoms whose severity is out of proportion to the inciting illness should arouse suspicion of a metabolic disease. Screening tests like blood gas analysis, blood levels of lactate, glucose and ammonia, urine examination for ketones and neuroimaging provide valuable clues to the presence of an underlying metabolic disease