Clinical Neuroscience

[Pneumococcal meningitis in children - 9 1/2-year-experience at Szent László hospital, Budapest, Hungary ]

IVÁDY Balázs, LIPTAI Zoltán, ÚJHELYI Enikő, BALÁZS György

DECEMBER 20, 2008

Clinical Neuroscience - 2008;61(11-12)

[Background and objective - No recent publications are available about pneumococcal meningitis in Hungarian children. The aim of this study was to collect data of epidemiological, clinical and prognostic features of pneumococcal meningitis in children treated at Szent László Hospital, Budapest, Hungary. Methods - We conducted a retrospective review of medical charts and follow-up records of patients aged 1 to 18 years admitted to our Pediatric and Pediatric Intensive Care Units due to pneumococcal meningitis between 1st Jan 1998 and 30th Jun 2007. Results - 31 children with 34 cases of pneumococcal meningitis were admitted to our hospital in the study period. Two children developed recurrent illness. The mean age was 6 years, 26% were under 1 year of age. The mean duration of hospital stay was 21 days, 97% required intensive care. Frequent clinical symptoms were fever (100%), nuchal rigidity and vomiting (78%), altered mental status (71%), Kernig's and Brudzinski's signs (58%) and seizures (41%). Otitis media, sinusitis, mastoiditis were present in 44%, 58%, 41%, respectively. Subdural effusion, parenchymal cerebral lesion and sinus thrombosis were documented in 5, 3 and 2 cases, respectively. One third of the patients recieved ceftriaxon, two thirds were administered ceftriaxon and vancomycin. Adjunctive therapy with dexamethason was given to 91% of the children. 70% of patients required mechanical ventillation. 9 patients (25%) required endoscopic sinus surgery. In 13 cases (38%) mastoidectomy, in 5 children (15%) neurosurgery was performed. The case fatality rate was 23.5%. 8 (23.5%) patients had mild or moderate, 1 child (3%) developed severe neurological sequelae. Conclusion - Pneumococcal meningitis in children remains a source of substantial morbidity and mortality in childhood. The long hospital stay, the frequent need for intensive care and severe neurologic sequelae emphasize the importance of early diagnosis, early treatment and prevention with pneumococcal conjugate vaccines.]

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Clinical Neuroscience

[Clinical and genetic diagnosis of dravet syndrome: report of 20 cases]

SIEGLER Zsuzsa, NEUWIRTH Magdolna, HEGYI Márta, PARAICZ Éva, PÁLMAFY Beatrix, TEGZES Andrea, BARSI Péter, KARCAGI Veronika, CLAES Lieve, DE Jonghe Peter, HERCZEGFALVI Ágnes, FOGARASI András

[Objective and background - Severe myoclonic epilepsy in infancy (SMEI; Dravet's syndrome) is a malignant epilepsy syndrome characterized by prolonged febrile hemiconvulsions or generalized seizures starting in the first year of life. Later on myoclonic, atypical absence, and complex partial seizures appear. When one of these seizure forms is lacking the syndrome of borderline SMEI (SMEB) is defined. Psychomotor delay resulting in mental retardation is observed during the second year of life. In most patients a de novo sodium channel alfa-1 subunit (SCN1A) mutation can be identified. By reviewing the clinical, laboratory, and neuroimaging data of our SMEI patients diagnosed between 2000 and 2008, we would like to share our experiences in this rare but challenging syndrome. Our results will facilitate the earlier and better diagnosis of Hungarian children with SMEI. Patients and methods - Clinical, EEG, MRI and DNA mutation data of 20 SMEI patients treated in the Bethesda Children’s Hospital (Budapest) were reviewed. Results - The first seizure appeared at age 6.3±3.0 months. At least one of the first two seizures were complex febrile seizures in 19/20 and unilateral seizures in 12/20 children. All children except for one showed hemiconvulsions at least once; all children had seizures lasting longer than 15 minutes. Eight of twenty patients had SMEB. DNA diagnostics identified an SCN1A mutation in 17 patients (6 missense, 4 nonsense, 4 frameshift, 2 splice site, 1 deletion) while 3 children had no mutation. Conclusion - Early diagnosis of SMEI is important for the avoiding unnecessary examinations and false therapies as well as for genetic counselling. Typical symptoms of SMEI are early and prolonged febrile hemiconvulsions with neurological symptoms, mental retardation and secondary seizure types later on. The presence of an SCN1A mutation supports the diagnosis. We propose the availability of molecular diagnostics and stiripentol therapy for SMEI children in Hungary.]

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[Authors summerized the etiology of convulsions in neonatal period and infancy (hypoxy, intracranial hemorrhage, infections of central nervous system, metabolic background, chromosomal abnormalities, brain developmental abnormalities, benign neonatal convulsions, benign neonatal familial convulsions, drug withdrawal, inborn error of metabolism). They suggest screening examinations after convulsion, summerized the basic princpile of tandem examination and review a proposal at suspicion of inborn error of enzym defects (aminoacidemias, defects of fatty acid oxydation, organic acidemias). They present case history of two patients suffered in extraordinary inborn error of enzym defect (SCO2 gene mutation, propionic acidemia). Diagnosis originated in Heim Pál Hospital (settlement Madarász Hospital) with a Hungarian and international cooperation.]

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[Recent medical genetic research has identified a number of novel, or previously known, but rare conditions, caused by private founder mutations. The Finnish and Ashkenazi Jew populations provide the best examples for identifying genes in unique genetic disorders. In these populations, research efforts and high-level medical services resulted in intense improvements of medical care and in organization of population- based screening programs. Hereditary disorders of the Roma populations are known for a long time. The genetic background of these diseases has been established by extensive molecular genetic studies. The Romas represent 6% of the Hungarian population and live under extremely bad health conditions. Therefore, our aim was to map the incidence of the hereditary neuromuscular disorders among the Hungarian Roma population. Moreover, we intended to provide proper information, genetic counseling and possible prevention strategies for the families at risk, which should represent a primer task in public health. Because of our experience in neuromuscular disorders, we choose six, frequent, autosomal recessive disorders for these clinical and genetic studies: hereditary motor and sensory neuropathy type Lom (HMSNL), hereditary motor and sensory neuropathy type Russe (HMSNR), congenital cataracts facial dysmorphism syndrome (CCFDN), Limb- Girdle muscular dystrophy 2C (LGMD2C), congenital myasthenic syndrome (CMS) and spinal muscular atrophy (SMA). Following identification of the founder mutations, the possibility of prenatal diagnosis and carrier screening for family members will contribute to the decrease of the recurrence risk for these severe, mostly untreatable disorders.]

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