Aim As early intervention is important in cerebral palsy (CP), an early diagnosis is desirable. The aim of this study was to establish the median diagnostic age of CP and to identify predictors of an early diagnosis in a population‐based cohort. Method Using the Danish National Cerebral Palsy Registry (NCPR), we identified 1291 children with CP (764 males, 527 females) born between 1995 and 2003. The date of diagnosis was defined as the day the parents were told that their child was spastic or had CP. We calculated the age of diagnosis and analysed the following predictors: type of CP, degree of motor disability, cerebral ultrasonography results, epilepsy, gestational age, and degree of cognitive impairment. Results We found the overall median corrected diagnostic age of CP to be 11 months. Early diagnosis was associated with the type of CP, presence of epilepsy, a high degree of motor disability, and abnormalities in the cerebral ultrasonography. The gestational age was not associated with the diagnostic age. Interpretation The median diagnostic age implies that half of the Danish children with CP will be able to enter an early intervention program before 1 year of age. A late diagnosis was associated with less severe symptoms, and gestational age did not influence the diagnostic age.

Continuous glucose monitoring (CGM) is being explored using several types of glucose sensors. Some are designed for subcutaneous adipose tissue. It is important to determine to which extent these glucose fluctuations in different tissues reflect changes taking place in the central nervous system, where glucose sensing is thought to occur. We studied the ability of subcutaneous adipose interstitial fluid measurements to parallel glucose propagations in blood, muscle, and central nervous system (CNS) during hyper-and hypoglycemia. A subcutaneous CGM system was applied in the CNS, subcutaneous adipose tissue, and skeletal muscle of nine Vietnamese potbellied pigs, and data were compared with frequent sampling in blood. Alterations in glucose levels were induced with intravenous glucose and insulin. During hyperglycemia, no difference was detected in delay between blood and interstitial glucose levels in subcutaneous adipose tissue (18.0 ؎ 0.8 min), muscle (18.0 ؎ 0.9 min), and CNS (20.3 ؎ 1.2 min), respectively. During hypoglycemia, we found no time difference between interstitial parameters in the three tissues. However, the amplitude of glucose changes varied considerably, with a smaller magnitude of glucose change taking place in the brain. The timing of glucose excursions in subcutaneous adipose tissue and muscle reflect excursions in CNS. The reduced magnitude of glucose excursions in the brain suggests that different mechanisms of glucose transport are operative in CNS compared with subcutaneous adipose tissue and muscle.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is caused by mutations in the Notch3 gene on chromosome 19. The condition manifests itself clinically typically in the third to fifth decade with migraine and recurrent episodes of stroke or transient ischaemic attacks. We report the case of an 11‐year‐old male with CADASIL resulting in stroke with right hemiparesis and dysphasia. Acute magnetic resonance imaging suggested infarction in the left hemisphere; magnetic resonance angiography revealed calibre variation of the intracerebral arteries. The patient suffered from common migraine with five to six attacks per month for 3 years 6 months before the stroke. Attacks occurred early in the morning with severe one‐sided headache, photophobia, nausea, and vomiting. Antimigraine medications had no effect. The family history revealed more cases of CADASIL, with an autosomal dominant pattern. The diagnosis of CADASIL was confirmed by the finding of the known mutation of the Notch3 gene running in the family. With treatment in a neurorehabilitation centre the patient recovered most of his functions with only discrete fine‐motor and cognitive sequelae. Our case report highlights the need for paediatricians to consider CADASIL in childhood stroke as well as in migraine patients.

Aim To investigate the effect of zoledronate on bone mineral density (BMD) Z-scores in children with non-ambulant cerebral palsy in a randomized, controlled, double-blind trial. Method Five- to sixteen-year-old, non-ambulant children with cerebral palsy were randomized 1:1 to receive two doses of zoledronate or placebo at a 6-month interval. BMD Z-score changes at the lumbar spine and the lateral distal femur (LDF) were calculated from DXA scans. Monitoring included weight, bone age, pubertal staging, knee-heel length, adverse events, biochemical markers, and questionnaires. Results Twenty-four participants were randomized and all completed the study. Fourteen were assigned to zoledronate. The mean lumbar spine BMD Z-score increased (95% CIs) 0.8 SD (0.4; 1.2) in the zoledronate group, which was significant when compared to 0.0 SD (-0.3; 0.3) in the placebo group. Similarly, the LDF BMD Z-scores increased more in the zoledronate group. Severe acute phase symptoms affected 50% of the patients in the zoledronate group, but were reported exclusively after the first dose. Growth parameters were similar in both groups. Interpretation Zoledronate for twelve months increased BMD Z-scores significantly without affecting growth, but first-dose side-effects were common and considerable. Studies into lower first doses and long-term outcomes are needed.