Biomedical subjects

John R Østergaard

Publications and source records attributed to John R Østergaard.

6 recordsLinked to original sources

PubMed2006

[Neurological aspects of stuttering].

Stuttering is characterised by repetitions, prolongations and pausing while speaking. Researchers have looked for many explanations. However, the cause of stuttering remains unknown. In recent years, structural abnormalities in the speech-related structures of the central nervous system have been brought into focus as a cause of stuttering. Research has shown signs of a lateral hemisphere asymmetry, abnormalities in the basal ganglia, dysfunction in the supplementary motor area and/or a dysfunction in the coordination of the cerebellum. This article is a review of this part of the literature.

Brain↗

PubMed2004

Moyamoya angiopathy with dolichoectatic internal carotid arteries, patent ductus arteriosus and pupillary dysfunction: a new genetic syndrome?

We report on 2 children with moyamoya angiopathy and bilateral dolichoectatic internal carotid arteries in combination with iris hypoplasia with bilateral fixed dilated pupils and a history of patent ductus arteriosus. Both were symptomatic with moyamoya angiopathy and underwent bilateral extracranial-intracranial (EC-IC) bypass operations for cerebral revascularization. This is the first report on moyamoya angiopathy and bilateral dolichoectatic internal carotid arteries with simultaneous occurrence of ocular and cardiovascular malformations. There have been descriptions of cerebral vascular abnormalities in combination with either congenital heart disease or ocular abnormalities but not with both presenting together. The combination of these separate congenital developmental defects may not be purely coincidental: we propose that the 2 probands are affected with a not yet recognized clinical syndrome of probably genetic etiology.

Carotid Artery, Internal↗

PubMed2004

Aicardi-Goutières syndrome: neuroradiological findings after nine years of follow-up.

The main radiological features of Aicardi-Goutières syndrome include basal ganglia calcification, cerebral atrophy and white matter alterations. We present a case where progress of cerebral calcifications demonstrated on consecutive CT-scans later on was followed by a decrease. The MRI showed a progressive and significant loss of white matter and severe signal changes of the remaining myelin. The aetiology of the myelin changes and the transient worsening of the cerebral calcifications remains to be elucidated. It has previously been shown that the spinal fluid level of interferon-alpha decreases with age and we suggest that the biphasic course of the calcifications and the ventricular size as well as the clinical course shown in many patients with Aicardi-Goutières might favor a causal role of interferon-alpha in the disease leading to a transient microangiopathy.

Atrophy↗

PubMed2004

Reduced bone mineral density and increased bone turnover in Prader-Willi syndrome compared with controls matched for sex and body mass index--a cross-sectional study.

OBJECTIVES: To study bone mineral status, body composition, and biochemical markers of bone turnover in Prader-Willi syndrome (PWS). STUDY DESIGN: Eight subjects with PWS (three males, five females; mean age, 24 years [range 16-41]) were included. Each subject was compared with an age-, sex- and body mass index-matched control randomly drawn from the background population. Bone mineral density (BMD), lean body mass, and fat mass were measured. Plasma PINP, PIIINP, osteocalcin, total alkaline phosphatase, bone-specific alkaline phosphatase, C-terminal telopeptide of type I collagen, and urine cross-linked N-terminal telopeptide of type I collagen were measured as biochemical markers of bone and collagen turnover. RESULTS: The PWS patients had significantly lower whole-body BMD (mean +/- SD, 1.020 +/- 0.041 vs 1.237 +/- 0.118 g/cm(2); 2p <.01) than controls due to lower bone mineral content (BMC: 2291 +/- 607 vs 2825 +/- 409 g; 2p=.02). Resorptive and formative bone markers were significantly elevated in patients compared with controls. Plasma testosterone was low in male patients (3.50 +/- 4.97 vs 19.2 +/- 8.78 nmol/L, 2p=.05), whereas no difference in plasma estradiol was present. CONCLUSIONS: The patients had a low BMD due to a high bone turnover. This high turnover was probably linked to sex steroid deficiency.

Adolescent↗

PubMed2002

[Positional plagiocephaly].

INTRODUCTION: To prevent early sudden infant death syndrome, the health authorities recommend that newborn infants sleep on their back. This has led to an increase of positional plagiocephaly. The aim of this study was to describe this condition and to recommend a preventive treatment. MATERIAL AND METHODS: This is a retrospective registration of 133 children with positional plagiocephaly seen in the period from 1994 to 2000. RESULTS: The number of children with positional plagiocephaly increased from two in 1994 to a maximum of 43 in 1999. 83 were males and 50 were females. 84 were dextral and 49 were sinistral. In seven (14%) of the sinistral and three (4%) of the dextral, we found a physical explanation of the head turning. In 51 children, X-rays of the skull were performed, but no synostosis was found. DISCUSSION: The back-sleeping position of infants is a promotive factor to positional plagiocephaly which may be prevented by simple alternating head positioning. Otherwise early (< 6 months of age) corrective physiotherapy and positioning or an orthoplastic helmet must be considered. The diagnosis of positional plagiocephaly is based on clinical observations. There is a favourite head turning, an ipsilateral occipital flattening, an ipsilateral frontal bossing, and the ipsilateral ear is moved forward.

Craniosynostoses↗

PubMed2002

Risk factors for febrile convulsions.

BACKGROUND: Little is known about the relative importance of genes and early environment in the etiology of febrile convulsions. METHODS: We performed a follow-up study using data from two nationwide registers in Denmark, 1980-1998. The study population comprised 10,224 younger siblings of children who had had febrile convulsions, and 21,218 younger siblings of children who had never been hospitalized with febrile convulsions. RESULTS: The study provides three main findings. First, if a previous child had had a febrile convulsion, the risk was lower for the next child if either parent changed partners. Compared with full-siblings, the hazard ratio (HR) of febrile convulsions was 0.6 for paternal half-siblings and 0.7 for maternal half-siblings. In contrast, if there was no history of febrile convulsions in the previous child, a change in partner was associated with a slight increase in risk (1.2 among paternal half-siblings and 1.3 among maternal half-siblings). Secondly, the risk of febrile convulsion was strongly associated with the number of hospitalizations for febrile convulsions experienced by the older siblings, with a doubling of risk among those whose older sibling had had three or more hospitalizations. Thirdly, the risk of febrile convulsions increased with decreasing gestational age, birth weight, and birth weight ratio regardless of family history. CONCLUSIONS: Our data suggest that the etiology of febrile convulsions depends on a genetic susceptibility that can be transmitted through both parents, and corroborates the hypothesis that multiple febrile convulsions may constitute a separate etiological entity.

Birth Weight↗