The purpose of this study was to investigate the existence and extent of cognitive impairment in type 1 diabetic children with episodes of recurrent severe hypoglycemia, using meta-analysis to synthesize data across studies. The meta-analysis sample included: 441 children with diabetes and recurrent severe hypoglycemia, 560 children with diabetes and without recurrent severe hypoglycemia. Overall, children with type 1 diabetes and recurrent severe hypoglycemia had slightly lower performance than diabetic children without severe hypoglycemia, only in some cognitive domains: intelligence, memory, learning, and verbal fluency/language. Greater impairment was found in memory and learning. No impairment was found for motor speed. Our results seem to confirm the hypothesis that recurrent severe hypoglycemia has a selective negative effect on the children's cognitive functions. However, these results must be considered with caution taking into account factors such as small sample sizes, the different definitions of severe hypoglycemia, and the variety of neuropsychological tests used.

Afebrile seizures in children usually necessitate investigations in order to determine the etiology and estimate the prognosis. Recently, convulsions that are described as benign but afebrile have been documented in children, in association with diarrhea, and are now recognized as a distinct entity. Benign afebrile seizures with mild gastroenteritis are defined as convulsions accompanying symptoms of mild diarrhea without dehydration or electrolyte derangement and without fever before and after the seizures in healthy children without meningitis, encephalitis or encephalopathy. The convulsions are short, symmetrical, generalized tonic-clonic seizures, occurring in clusters. Laboratory studies (full blood count, blood glucose, creatinine, serum electrolytes, cerebrospinal fluid, bacterial and viral cultures) are usually normal, and other investigations (neuroimaging and electroencephalogram) are not necessary. Prognosis is always favorable (normal psychomotor development, no recurrences of seizures), and anticonvulsant therapy is not warranted. Recognition of this benign infantile convulsion avoids extensive evaluation and long-term anticonvulsant therapy; physicians may reassure the parents regarding the lack of long-term sequelae. In conclusion, this type of seizure seems to be a new entity, but it awaits a correct place in the large group of infantile convulsion disorders.

In these patients, a relatively low incidence of SH was recorded, without pronounced association with lower HbA1c or multiple daily injection insulin therapy. SH seems to be mainly related to management of diabetes. We believe that the main path to SH prevention is through patient and family education in the management of T1DM.

Visual dysfunction has been reported in patients diagnosed with epilepsy. Some of these visual disturbances may be attributable to either the disease process, or the anticonvulsant therapy prescribed to control the seizures. The aims of our study were to evaluate whether color vision and macular function are impaired in epileptic adolescents, to study if the monotherapy with valproic acid (VPA) and carbamazepine (CBZ) can affect color vision and macular function and to determine the possible relationship between color vision, retinal function and antiepileptic drugs (AEDs) dosage and their serum concentrations. We examined 45 (16 male and 29 female, mean age +/- SD, 15.71 +/- 2.01 years) Caucasian epileptic patients suffering from various types of cryptogenic epilepsy before the beginning of therapy and after 1 year of VPA or CBZ monotherapy and 40 sex- and age-matched healthy controls. Color vision was assessed by Farnsworth Munsell (FM) 100-hue test and total error score (TES) was evaluated. This test consists of colored caps: the testee has to arrange the caps according to their colors macular function was assessed by nyctometry evaluating initial recovery time (IRT) and summation method (SM). This test evaluates visual acuity after a period of intense illumination of macula. Analysis of variance was used to evaluate the difference between controls and patients; moreover, Pearson's correlation test have been performed. Before the beginning of therapy, there were no differences in color vision and macular function between controls and epileptic patients. After 1 year, the patients, treated with VPA or CBZ, showed a deficit in FM 100-hue test. At nyctometry, all patients showed no significant variation of macular function between baseline evaluation and second evaluation at end of the follow-up. Our study demonstrates that, in our group of epileptic patients, epilepsy per se does not affect color vision and retinal function. In contrast, after 1 years of therapy with VPA and CBZ these patients showed a deficit in FM 100-hue test although nyctometry evaluation continued to be normal allowing to exclude an impairment in macular function. Further investigations are required to determine the pathophysiological alteration(s) that are at the basis of color perception defects.

We report a rare case of monozygotic (MZ) twins who developed simultaneous onset of type 1 diabetes mellitus (T1DM). Laboratory fi nding showed similar values of blood sugar, pH, glycosylated hemoglobin, and C-peptide. Urinary sugar and ketones were detected in both. Endocrine and immunological assessment showed similar results. No evidence (clinical or serological) of recent viral or bacterial infection was found. In the 4 years of follow-up, the twins also showed a similar course of disease. Concordance rates for T1DM are high in MZ twins; nevertheless, a simultaneous onset and a similar course of disease are unusual, as well as the HLA allelic variants of our patients. This extraordinary concordance in a pair of MZ twins could be the consequence of a greater environmental similarity or the role of genetic factors other than HLA genes in our twins.