title: One-year follow-up of tick-borne central nervous system infections in childhood.
abstract: BACKGROUND
  Neurologic sequelae, including cognitive deficits, after childhood tick-borne encephalitis (TBE) and neuroborreliosis (NB) are not well-characterized. These infections are among the most common affecting the central nervous system in children and can be difficult to diagnose due to vague symptomatology. The aim of this study was to investigate long-term (>1 year) consequences of pediatric TBE and NB as well as the value of markers for brain damage and genetic susceptibility.
  
  
  METHODS
  From a previous prospective study, children diagnosed with TBE (n = 8) and NB (n = 12) as well as pediatric controls (n = 15) were followed up by clinical examination, semistructured interview and screening for cognitive dysfunction by the Five-to-Fifteen Questionnaire. The follow-up also included detection of serum autoantibodies against the neural proteins; glial fibrillary acidic protein and myelin basic protein, as well as genotyping of a 32 basepair deletion in the chemokine receptor type 5 gene.
  
  
  RESULTS
  Children diagnosed with TBE displayed significantly more long-term subjective complaints (ie, fatigue, headache and irritability) compared with the NB and control groups. Significantly higher frequency of disabilities was also detected by the Five-to-Fifteen Questionnaire in the TBE group. Both TBE and NB cause consequences (eg, prolonged convalescence, worries and financial loss) for the families. Markers for genetic susceptibility and brain damage had no prognostic values in this cohort.
  
  
  CONCLUSIONS
  Pediatric TBE results in long-lasting residual symptoms and neurologic deficits affecting daily life. Vigilance for TBE-related morbidity among pediatricians and long-term clinical follow-up with assessment of cognitive dysfunctions and appropriate interventions seems reasonable for these children.
authors.affiliation: Division of Pediatrics, Department of Clinical Science, Intervention and Technology, Karolinska Institutet at Karolinska University Hospital Huddinge, Sweden.
authors.forename: Mona-Lisa
authors.initials: ML
authors.lastname: Engman
authors.forename: Katarina
authors.initials: K
authors.lastname: Lindström
authors.forename: Marie
authors.initials: M
authors.lastname: Sallamba
authors.forename: Carl
authors.initials: C
authors.lastname: Hertz
authors.forename: Berit
authors.initials: B
authors.lastname: Sundberg
authors.forename: Magnus E A
authors.initials: ME
authors.lastname: Hansson
authors.forename: Lars
authors.initials: L
authors.lastname: Lindquist
authors.forename: Claes
authors.initials: C
authors.lastname: Orvell
authors.forename: Karl-Johan
authors.initials: KJ
authors.lastname: Lidefelt
authors.forename: Mikael
authors.initials: M
authors.lastname: Sundin
mesh_terms: D000293:Adolescent; D000818:Animals; D001323:Autoantibodies / Q000097:blood; D001327:Autoimmune Diseases / Q000453:epidemiology*; D002648:Child; D002675:Child, Preschool; D003072:Cognition Disorders / Q000453:epidemiology*; D004675:Encephalitis, Tick-Borne / Q000150:complications*; D005260:Female; D005500:Follow-Up Studies; D005904:Glial Fibrillary Acidic Protein / Q000276:immunology; D006801:Humans; D020852:Lyme Neuroborreliosis / Q000150:complications*; D008297:Male; D004676:Myelin Basic Protein / Q000276:immunology; D009414:Nerve Growth Factors / Q000276:immunology; D019713:Receptors, CCR5 / Q000235:genetics; D011795:Surveys and Questionnaires
chemical_list: D001323:Autoantibodies; D005904:Glial Fibrillary Acidic Protein; D004676:Myelin Basic Protein; D009414:Nerve Growth Factors; D019713:Receptors, CCR5