B Hagberg

Uppsala University, Uppsala, Uppsala, Sweden

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Publications (122)278.71 Total impact

  • Bengt Hagberg
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    ABSTRACT: The clinical effect of pRÉSUMÉd minimal brain damage was studied in 26 apparently normal children and young adults who had suffered from a transient expansive hydrocephalus in infancy. Many of them had been late in motor and mental development, especially in their early years, and 5 had had convulsions. A dysplastic body build was present in 3 cases and 2 children had shown precocious püberty. Signs of ataxia were common (12 cases), but spastic pareses were only occasionally met with. Squint was found in 11 cases, and there were single cases of optic atrophy and nystagmus. Terman-Merrill tests showed variations in intelleétual capacity wider than would be expected in a healthy population. Behaviour déviations were common especially in the lower IQ groups and in children with neurological abnormalities. The minor neurological and mental déviations associated with slight early brain damage are often misunderstood.RÉSUMÉDommage minimum du cerveau dans l'hydrocéphalie enfantile arrêtée spontandmentL'effet clinique de l'atteinte présumée minime du cerveau a étéétudiié chez 26 enfants apparemment normaux et jeunes adultes connus pour avoir souffert d'une hydrocéphalie expansive transitoire pendant leur enfance. Beaucoup des cas étudié ont été retardés dans leur développement moteur et mental, surtout au cours de leurs premiéres années. On a recontré 3 cas de construction dysplastique du corps et 2 cas de püberté précoce. Les signes atactiques étaient communs (12 cas), tandis que les parésies spastiques n'étaient rencontrées qu'occasionnellement. On a compté 11 cas de strabisme. Atrophie optique et nystagmus ont été découverés, et 5 patients ont présenté des convulsions. Des tests de Terman-Merrill appliqués aux patients ont montré que les variations de leurs capacités intelleetuelles étaient plus grandes que chez une population en bonne santé. Les déviations de comportement étaient communes, rencontrées plus souvent dans les groupes à plus faible quotient d'intelligence et parmi les cas présentant des anomalies neurologiques et mentales.
    Developmental Medicine & Child Neurology 11/2008; 4(6):583 - 587. DOI:10.1111/j.1469-8749.1962.tb04149.x · 3.29 Impact Factor
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    ABSTRACT: This population-based study refers to 78 Swedish children with non-progressive ataxia from a total population of 3.1 million inhabitants. Inclusion criteria were ataxic gait without any signs of spasticity, dyssynergia, dysmetria and intention tremor. CT and/or MRI studies were available from 70 patients (90%). Infratentorial pathology was revealed in 27%. and findings were considered normal in 61%. If CT was normal, of recent date and of good quality, MRI did not add any new information. In half of the cases with pathological CT, however, MRI provided new information. The origin was considered prenatal in 45% (familial in 17%), perinatal in 4% and unclassifiable in 51%. 60% were mentally retarded; in the rest, cognitive development was near normal (18%) or normal (22%). Speech development was delayed in 88%, and 58% had visual dysfunction.RÉSUMÉAtaxie non évolutive. Olivine, pathologie cérébrate et handicaps chez 78 enfants suédoisCette etude de population porte sur 78 enfants suédois avec ataxie non évolutive, provenant ď unc population de 3.1 millions de habitants. Lcs critères ď appartenance comprcnaient une démarche ataxiquc avec ou sans signes de spasticité, une dyssynergie, une dysmétrie et un tremblement intcntionnel. Des scanners et/ou une imagerie IRM étaient présents pour 70 enfants (90%). Une pathologie sous-tentorielle fut trouvée dans 27% des cas, et les données étaient considérées comme normales dans 61% des cas. Si le scanner était normal, recent et de bonne qualityé, ITRM ne fournissait pas ď informations supplémentaires. Cependant dans la moitié des cas de scanners anormaux, ľ IRM apportait de nouvclles données. ľ origine a été considérée comme pré-natalc dans 45% des cas (17% des cas familiaux), 4% péri-natale et non classablc dans 51%. 60%étaient retardés mentaux; pour les autres, le développement cognitif était proche de la normale (18%) ou normal (22%). Le développement du langage était retardé dans 88% des cas. et il y avail une dysfonction visuelle dans 58% des cas.ZUSAMMENFASSUNGNicht progressive Ataxie. Ursacheit. Hirnpathologie mul Störungen bei 78 schwedischen KindernIm Rahmen dieser Populationsstudie wurden 78 schwedische Kinder mit einer nicht progressiven Ataxie aus einer Gesamtbevölkerung von 3.1 Millioncn untcrsucht. Die Kritericn für die Aufnahme in die Studie waren ataktischer Gang ohne Zeichen einer Spastik, Dyssynergie, Dysmetrie und Intcnsionstremor. CT - und/oder MRT Untcrsuchungen lagen bei 70 Patienten vor (90%). Bei 27% fand sich eine infratentorielle Patholgie und bei 61% waren die Befunde normal. War das CT normal, vor kurzem durchgefiihrt und qualitativ in Ordnung, ergaben sich aus dem MRT keine neuen Informationen. Bei der Hlfte der Flle mit pathologischem CT jedoch crgab das MRT neue Informationen. Die Ursache wurde in 45% (17% familir) als prnatal und in 4% als perinatal angesehen und war in 5% nicht einzuordncn. 60% waren gcistig retardicrt. die restlichen hatten einc nahezu normale (18%) bzw. normale (22%) kognitive Entwicklung. Die Sprachentwicklung war bei 80% vcrzögert und 58% hatten visuelle Störungen.RÉSUMÉAtaxia no progresiva. Origen, patología cerebral yalteraciones en 78 niños suecosEl estudio de población base se refiere a 78 niños suecos con ataxia no progresiva en una población total de 3.1 millones de habitantcs. Los criterios de inclusion fueron una marcha atáxica sin signos de espasticidad. dis-sinergia, dismctria y temblor intencional. En 70 pacientes (90%) se practiceó TAC o IRM. Se halló una patología infratentorial en el 27% y los hallazgosfueron eonsiderados normales en el 61%. Si la TAC era normal, realizada recientemente y de buena calidad. la IRM no proporcionó ninguna nueva información. Sin embargo, en la mitad de los casos con TAC patológica, la IRM proporcionó nueva información. Se consideró que el origen era prenatal en el 45% (familiar en el 17%). perinatal en el 4% y sin clasificaren el 51%. El 60% eran retrasados mentales; en el resto el desarrollo cognitivo era casi normal (18%) o normal (22%). El desarrollo del lenguaje estaba retrasado en el 88% y el 58% tenía una disfunción visual.
    Developmental Medicine & Child Neurology 11/2008; 38(4):285 - 296. DOI:10.1111/j.1469-8749.1996.tb12095.x · 3.29 Impact Factor
  • BENGT HAGBERG, ARNE HAMFELT, OLLE HANSSON
    Acta Paediatrica 01/2008; 55(4):371 - 384. DOI:10.1111/j.1651-2227.1966.tb08808.x · 1.84 Impact Factor
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    ABSTRACT: Lbid berg, U., Hagberg, B., Olsson, Y. and Sourander, P. (Department of Paediatrics II and Institute of Pathology, University of Göteborg, and Institute of Pathology, University of Uppsala, Sweden), Injury of the spinal cord at birth. A report of two cases. Acta Paediatr Scand, 64:546, 1975.–Spinal cord injury may occur as a severe complication to delivery. In the vast majority of such cases the injury results from a traumatic breech delivery, but cases of injuries after cephalic presentation and fetal malposition have also been described. Two cases are reported. One of the infants died at the age of 8 months and neuropathologies! examination of the brain and spinal cord was performed. The other child, now 6 years old, is still alive. Incidence, mechanism of injury, clinical and morphological features, and treatment are briefly discussed.
    Acta Paediatrica 01/2008; 64(3):546 - 550. DOI:10.1111/j.1651-2227.1975.tb03878.x · 1.84 Impact Factor
  • Acta Paediatrica 01/2008; 54(2):116 - 130. DOI:10.1111/j.1651-2227.1965.tb06353.x · 1.84 Impact Factor
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    ABSTRACT: Hagberg, B., Haltia, M., Sourander, P., Svennerholm, L. and Eeg-Olofsson, O. (Departments of Paediatrics II, Pathology I and Neurochemistry, University of Gothenburg, Sweden, and Pathology II, University of Helsinki, Finland). Poly-unsaturated fatty acid lipidosb—an infantile form of so-called neuronal ceroidlipo-fuscinosis. Acta Paediatr Scand, 63:753, 1974.—Clinical, histological and ultrastructural findings in three children of Finnish origin and with a severe progressive encephalopathy are reported. The main symptoms were rapid developmental regression from about one year of age, loss of speech, severe visual failure and pronounced secondary microcephaly. A decerebrated state was reached within 1–3 years. Laboratory tests revealed a successively decreasing CSF τ-fraction. The fatty acid composition of Serum lecithin showed an increased amount of arachidonic acid in the early stage of the disease, a pattern consistent with the biochemical changes in the brain.The morphological characteristics consisted of extreme cerebral and cerebellar atrophy, massive neuronal destruction associated with a pronounced macrophage and astrocytic reaction, and strongly PAS-reacting and autofluorescent granular deposits in the cytoplasm of the remaining cells. Electron microscopy revealed cytoplasmic osmiophilic deposits in the form of aggregates of globules with a uniform and finely granular ultra-structure.The condition was considered to be a nosological entity with a uniform clinical picture and characteristic ultrastructural changes in the brain. The evidence produced suggests that the disease described is identical with a progressive heredodegenerative disorder, known to have been diagnosed during recent years in more than 50 Finnish infants and small children and earlier described under the name of infantile type of so-called neuronal ceroidlipifuscinosis.
    Acta Paediatrica 01/2008; 63(5):753 - 763. DOI:10.1111/j.1651-2227.1974.tb17001.x · 1.84 Impact Factor
  • B. HAGBERG, G. HAGBERG, I. OLOW
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    ABSTRACT: Hagberg, B., Hagberg, G. and Olow, I. (Department of Paediatrics II, Children's Hospital and the Habilitation Unit of Bräcke-Östergård, Gothenburg, Sweden). The changing panorama of cerebral palsy in Sweden 1954–1970. II. Analysis of the various syndromes. Acta Paediatr Scand 64:193, 1975 From an unselected series of 560 Swedish cases of cerebral palsy, born 1954-70, various data of etiologic and pathogenetic interest were analysed in detail. Untraceable and prenatal factors were found to dominate within the group of spastic hemiplegia. Placental dysfunction in small-for-date babies and severe asphyxia were thought to be the two main pathogenetic factors among the patients with spastic tetraplegia. In spite of a significant decrease in the number of low birth weight children within the group of spastic diplegia, this syndrome was still very characteristic for the child born immature. Ataxic diplegic forms were found to have greater pathogenetic similarities to spastic diplegia than to simple ataxia. In two-thirds of the children the latter syndrome was characterized by normal pregnancy, delivery and birth weight and an untraceable (genetic?) factor. Oyskinetic syndromes were mostly encountered after perinatal asphyxia.
    Acta Paediatrica 01/2008; 64(2):193 - 200. DOI:10.1111/j.1651-2227.1975.tb03821.x · 1.84 Impact Factor
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    ABSTRACT: SummaryA case report is presented of a 6-year-old girl with a severe progressive encephalopathy of late infantile onset and with changes indicating marked disturbances in the metabolism of linolenic acid.
    Acta Paediatrica 01/2008; 57(6):495 - 499. DOI:10.1111/j.1651-2227.1968.tb06968.x · 1.84 Impact Factor
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    ABSTRACT: Lipid composition was studied on cerebral tissue from nine children who had died of a progressive encepha-lopathy called the infantile form of neuronal ceroid lipofus-cinosis (INCL) or polyunsaturated fatty acid lipidosis (PFAL). In the terminal stage of the disease, the concentrations of all lipid classes were found to be significantly reduced in the cerebral and cerebellar cortex and white matter. The concentration of gangliosides of the cerebral cortex was 15% and that of cerebrosides (galactosylceramide) in white matter 0.2–5% of the normal values for the children's ages. The reduction of gangliosides mainly affected those of the gangliotetraose series, particularly GDI a. The fatty acids of the linolenic acid series were strongly reduced in ethanolamine and serine phosphoglycerides. A very large increase up to 100-fold of oligoglycosphingolipids of the globo series and two fucose-containing lipids of the neo-lacto series was found in the forebrain of the three advanced cases examined. The brain tissue also contained very high concentrations of mono-, d -, and trisialogangliosides of the lacto and neolacto series, gangliosides with type 1 chain, dominating. The structures of the gangliosides were tentatively identified by gas chromatography-mass spectrometry and monoclonal antibodies with carefully determined epitope specificity. The gangliosides and neutral glycosphingolipids had very similar fatty acid composition, consisting of about 40% stearic acid and 40% C24-acids.
    Journal of Neurochemistry 10/2006; 49(6):1772 - 1783. DOI:10.1111/j.1471-4159.1987.tb02435.x · 4.24 Impact Factor
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    ABSTRACT: This is the ninth report from the western-Swedish study of the prevalence and origin of cerebral palsy. A population-based study covering the 88 371 live births in the area in 1995-1998. Birth characteristics, neuroimaging findings and risk factors in children with cerebral palsy were recorded, prevalence was calculated, and aetiology was analysed. The study comprised 170 children with cerebral palsy, i.e. a prevalence of 1.92 per 1000 live births. Excluding eight post-neonatally derived cases, the gestational age-specific prevalences were 77 per 1000 for children born before 28 wk of gestation, 40 for children born at 28-31 wk, 7 for children born at 32-36 wk and 1.1 for children born after 36 wk of gestation. Spastic hemiplegia, diplegia and tetraplegia accounted for 38%, 35% and 6%, respectively, dyskinetic cerebral palsy for 15%, and ataxia for 6%. For the first time, hemiplegia was now most common, due to the decline in preterm diplegia. There was a further increase in full-term dyskinetic cerebral palsy. The origin of cerebral palsy in children born at term was considered to be prenatal in 38%, peri/neonatal in 35% and unclassifiable in 27%, while in children born preterm it was 17%, 49% and 33%, respectively. The decreasing trend from the period 1991-1994 continued, both in children born at term and especially in those born preterm. However, the increase in dyskinetic cerebral palsy in children born at term was a matter of concern. In this group, a perinatal hypoxic ischaemic encephalopathy had been present in 71%.
    Acta Paediatrica 04/2005; 94(3):287-94. DOI:10.1111/j.1651-2227.2005.tb03071.x · 1.84 Impact Factor
  • American Journal of Obstetrics and Gynecology 12/2003; 189(6). DOI:10.1016/j.ajog.2003.10.338 · 3.97 Impact Factor
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    ABSTRACT: Previous studies have indicated that foetomaternal infection increases the risk of spastic cerebral palsy (CP) in term infants, whereas this association appears to be less evident in preterm infants. The aim of this study was to analyse infection-related risk factors for spastic CP in preterm infants. A population-based series of preterm infants with spastic CP, 91 very preterm (<32 wk) and 57 moderately preterm (32-36 wk), born in 1983-90, were included and matched with a control group (n = 296). In total, 154 maternal, antenatal and intrapartal variables were retrieved from obstetric records. In the entire group, histological chorioamnionitis/pyelonephritis, long interval between rupture of membranes and birth, admission-delivery interval <4 h and Apgar scores of <7 at 1 min just significantly increased the risk of CP, and Apgar scores of <7 at 5 and 10 min were strongly associated with an increased risk. Abruptio placentae, Apgar scores <7 at 1 min and pathological non-stress test (reason for delivery) were significant risk factors of CP only in the moderately preterm and hemiplegic groups, whereas fever before delivery was a significant risk factor in the very preterm and spastic diplegic groups. Antibiotics during pregnancy was associated with CP only in the spastic diplegic CP group. Conclusion: Antenatal infections marginally increased the risk of CP. Low Apgar score and abruptio placentae were associated with CP, especially in moderately preterm infants with hemiplegic CP.
    Acta Paediatrica 01/2002; 91(8):946-51. DOI:10.1080/080352502760148685 · 1.84 Impact Factor
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    ABSTRACT: Mutations in the MECP2 gene are known to be associated with Rett Syndrome (RTT) in the large majority of sporadic cases. Four Swedish families with a total of eight RTT patients (two in each family), were screened and found negative for MECP2 mutations. The series included females with both classical and forme fruste phenotypes. Rett syndrome thus might still be complex and genetically multifactorial.
    Neuropediatrics 09/2001; 32(4):217-8. DOI:10.1055/s-2001-17377 · 1.10 Impact Factor
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    ABSTRACT: Rett syndrome (RS) is a neurodevelopmental disorder almost exclusively affecting females. We have studied the mutation spectrum of the responsible gene MECP2, encoding methyl-CpG-binding protein 2 (MeCP2), in 16 sporadic classical RS females from Sweden. In 13 of 16 patients (81%) we detected nonsense or missense mutations in the coding parts of MECP2. This mutation rate is in agreement with other reports (65-80%). In all, 12 different mutations and one polymorphism were found; three of the mutations have not been reported previously. The missense mutations were restricted to highly conserved regions of the gene. None of the mutations was detected in parents; thus, they had probably arisen de novo. In contrast, two normal variants, one intron deletion and one silent mutation, were seen singly only in two patients' mothers; neither has been reported previously. One patient showed two different mutations closely located, i.e. 802C > T (R268W) together with 808C > T (R270X). Another patient had a mutation in the stop codon 1459T > C (X487R), leading to a gene product prolonged with 27 amino acids. In conclusion, our results indicate that the majority of Swedish RS patients (81%) have mutations in MECP2 that are sporadic cases with de novo mutations. Moreover, both missense and nonsense mutations occur, but in different parts of the gene, probably reflecting the function of the domains in MeCP2. This study has improved our ability to offer these families an early confirmation of Rett diagnoses.
    European Child & Adolescent Psychiatry 07/2001; 10(2):117-21. DOI:10.1007/s007870170034 · 3.55 Impact Factor
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    ABSTRACT: This 8th Swedish population-based cerebral palsy (CP) report comprises 241 children born 1991-94. The live birth prevalence was 2.12 per 1000. Excluding 7 postnatally-derived cases, the gestational age-specific prevalences were 86 for extremely preterm children, 60 for very preterm and 6 for moderately preterm, and 1.3 for term children per 1000. Spastic hemiplegic, diplegic and tetraplegic subtypes accounted for 33%, 44% and 6%, dyskinetic CP for 12% and simple ataxia for 4%. Neuroimaging had been performed in 90%. Probable aetiology was identified in 73% of preterm and 86% of term children. Among preterm children it was considered prenatal in 12%, peri/neonatal in 61% and unclassifiable in 27%, while it was 51%, 36% and 14% among term children. CONCLUSION: The live birth prevalence for CP in the birth year period 1991-94 continued to decrease slightly. Gestational age-specific prevalences increased marginally in extremely and very preterm births, continued to decrease in moderately preterm births and decreased slightly in term births. Probable aetiology and timing of the brain insult could be revealed in 81%, birth asphyxia being the likely cause in 28% of term children.
    Acta Paediatrica 04/2001; 90(3):271-7. DOI:10.1111/j.1651-2227.2001.tb00303.x · 1.84 Impact Factor
  • U Steffenburg, G Hagberg, B Hagberg
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    ABSTRACT: In a representative series of 53 females with Rett syndrome (RS), aged 5-55 y, a history of epilepsy was present in 50 (94%), 45 of whom had 5-y active epilepsy. Compared with severe mental retardation in general, the median age of seizure onset was significantly later (4 vs 0.8 y) and partial complex seizures were more frequent (54% vs 23%). Neonatal seizures had occurred in only one and infantile spasms in none compared with 26% and 12%. After teenage, the severity of epilepsy tended to decrease, i.e. lower seizure frequency and relatively more partial seizures. The rate of being seizure-free for 1 y was 8% after 10 y and 40% after 27 y of epilepsy duration. Frequent seizures were associated with smaller head circumference. CONCLUSION: This epilepsy profile could fit in with present-day knowledge of RS as a form of dendrito-synaptogenic developmental failure with mainly late postnatal consequences, as well as being a relatively stationary condition in adulthood.
    Acta Paediatrica 02/2001; 90(1):34-9. DOI:10.1111/j.1651-2227.2001.tb00252.x · 1.84 Impact Factor
  • B Hagberg, M Berg, U Steffenburg
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    ABSTRACT: Rett syndrome, a complicated neurodevelopmental disorder exclusively affecting girls in early childhood, is now known to be one of the major worldwide causes of severe mental retardation in females. Although internationally unknown until the mid-1980s, under another designation it had been observed in Sweden since the early 1960s. The article consists in a review of current clinical, neurobiological and genetic knowledge of the syndrome, and a systematic penetration of data collected from the follow-up of a west Swedish series of 54 female patients, 5-57 years of age. Mortality in the series was 17 percent, with a median age at death of 24 years. In most cases death was sudden and unexpected.
    Lakartidningen 01/2000; 96(49):5488-90.
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    ABSTRACT: A girl fulfilling four/five of six inclusion criteria and eight/nine of 11 supportive criteria for atypical Rett syndrome had a cytogenetic deletion of chromosome 3p, del(3)(pter-->3p25.1 approximately 25.2). The deletion was situated on the maternally derived chromosome and by molecular analysis the deletion breakpoint was shown to be between DNA markers D3S3589 and D3S1263.
    Journal of Medical Genetics 04/1999; 36(4):343-5. · 5.64 Impact Factor
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    ABSTRACT: Carbohydrate-deficient glycoprotein syndrome type 1 (CDGS-1) is an autosomal recessive hereditary metabolic disorder, the gene locus of which is chromosome 16p13. The disorder is characterised by genetic heterogeneity, and by decrease in the gene product, phosphomannomutase 2, though the heterogeneity is far less manifest in affected Swedish families. Its incidence is 1/80,000 live births, and the under-5 mortality rate over 30 per cent. The causes of death are liver failure, cardiac tamponade, haemorrhaging, and severe infection. The characteristic biochemical aberration is the occurrence of deficient carbohydrate chains in many but not all circulating glycoproteins, and the serum and blood concentrations of some glycoproteins may be above or below normal. These changes may improve over time, but never normalise. The clinical picture is generally more problematic during the first years of life when psychomotor retardation is complicated by failure to thrive, liver dysfunction, pericardial effusions, and stroke-like episodes. In addition, strabismus, lipocutaneous anomalies, and gluteal fat pads are always present, and muscular hypotonia and restricted joint mobility are common. Failure to thrive is common, with vomiting and diarrhoea and subsequent slow growth. Inflammation is a constant finding in the liver, and very common in the small bowel. Pancreatic function is also affected. Pericardial effusion has been reported in 50 per cent of the youngest children, requiring pericardectomy in 30 per cent of cases. Haemorrhaging and thromboembolic complications may occur, and the serum concentrations of several factors and inhibitors are low, particularly those of factors V and XI, protein C and antithrombin. Stroke-like episodes occur in about 30 per cent of cases, often following an infection, with coma lasting for hours to several days. Such sequelae as hemiplegia, blindness, and other focal neurological pathology have been observed transiently. Diagnosis is based on the serum carbohydrate-deficient transferrin level, verified by isoelectric focusing. Molecular genetic procedures enable point mutations to be identified and prenatal diagnosis to be performed in many families.
    Lakartidningen 01/1999; 95(50):5742-8.
  • Y Stenbom, B Tonnby, B Hagberg
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    ABSTRACT: This open pilot study was performed to evaluate the effect of Lamotrigine (LTG) in girls with Rett syndrome (RS) regarding seizure frequency, effect on gross motor dyspraxia and safety. Twelve girls with either the classical form of RS or the milder form fruste variants were included. The effect on epilepsy was evaluated as seizure frequency, motor performance (video comparison) and safety at clinical check up. The dosage of LTG was individualized and related to concomitant anti-epileptic drugs. Two of three girls with epilepsy responded relatively well to treatment, and for one of them even bad tantrums disappeared. LTG was useful in another four girls who became happier, more alert, more able to concentrate, and improved in contacting. Only mild adverse reactions as rash and tremor were seen. It is concluded that LTG could be worth trying as an adjunct in girls with RS, being aware of possible adverse reactions and no effect at all.
    European Child & Adolescent Psychiatry 04/1998; 7(1):49-52. DOI:10.1007/s007870050045 · 3.55 Impact Factor

Publication Stats

5k Citations
278.71 Total Impact Points

Institutions

  • 2008
    • Uppsala University
      Uppsala, Uppsala, Sweden
    • Uppsala University Hospital
      Uppsala, Uppsala, Sweden
  • 1973–2008
    • University of Gothenburg
      • • Department of Medical Biochemistry and Cell Biology
      • • Division of Paediatrics
      Goeteborg, Västra Götaland, Sweden
  • 1995–2001
    • Sahlgrenska University Hospital
      • Department of Cardiology
      Goeteborg, Västra Götaland, Sweden
    • Länssjukhuset Ryhov
      Jönköping, Jönköping, Sweden
  • 1993
    • Karolinska University Hospital
      • Department of Neurology
      Stockholm, Stockholm, Sweden
  • 1991
    • Universitair Ziekenhuis Leuven
      • Department of Pedriatrics
      Leuven, VLG, Belgium
  • 1977
    • Umeå University
      Umeå, Västerbotten, Sweden