Autoimmune encephalitis is an increasingly recognised cause for a combination of symptoms of seizures, disturbance of memory, behaviour and cognition. Other manifestations include acute onset movement disorders, unexplained encephalopathy and refractory status epilepticus. N-methyl aspartate (NMDA) encephalitis and voltage gated potassium channel mediated (VGKC) limbic encephalitis are the two commonest causes of autoimmune encephalitis. These children initially present to general paediatricians therefore it is vital to consider this in the differential diagnosis of infective encephalitis as prompt recognition, investigation and immune therapy determines longterm outcome. Early recognition and treatment can potentially halt temporal lobe atrophy and improve outcome. We report a 14 year old girl who presented with symptomatic, intermittent memory loss, behaviour disturbance, fatigue and cognitive change with limbic encephalitis. Initial investigations revealed negative PCR for HSV, EBV. Brain imaging detected mesial right temporal high signal area in FLAIR sequences. EEG showed epileptic inter-ictal focal abnormality over right frontal mesial temporal region. NMDA, VGKC, Anti GAD, Hu, Ma, CV2, CRMP5 and thyroid antibodies were negative. Screening for tumour with baseline abdominal ultrasound and CXR were negative. Baseline WISC testing prior to starting medications revealed her immediate memory for verbal information was in the low average range (verbal immediate index score:82,12th percentile) and her time delayed recall verbal information was in the impaired range (verbal delayed index score:72, 3rd percentile). She was treated with iv methylprednisolone followed by tapering dose of oral prednisolone. Repeat WISC assessment is due in 6 months. Limbic encephalitis should be considered in children with prominent neuropsychiatric manifestation of encephalitis. Her future MRI reports will determine the 3 month and 6 month outcome for this teenager. Longterm surveillance for tumour detection is recommended in autoimmune encephalitis.

Introduction Boys with Duchenne muscular dystrophy (DMD) have low bone density. Although corticosteroids improve muscle strength and function in boys with DMD, potential adverse effects include osteoporosis and vertebral fractures. Bianchi et al1 reported low Vitamin D levels in a small cohort of boys with DMD. The optimal 25-OH vitamin D levels in children have been redefined by Misra et al2 with the recommendation that serum 25-OH vitamin D level <37.5 nmol/litre constitutes vitamin D deficiency and a level greater than 50 nmol/l is indicative of sufficiency. In the UK there are no large studies to establish vitamin D levels in children with DMD. Objectives To establish the prevalence of vitamin D deficiency in boys with DMD. Methodology The North Star neuromuscular network consensus is to check vitamin D levels prior to starting corticosteroid therapy. Data on vitamin D levels was retrospectively collected from the case records through the north star neuromuscular database. Results 25-OH vitamin D levels were available in 157 boys with DMD. The mean age at checking vitamin D level was 6.9 years (1.5–15.5). Vitamin D levels ranged from 4–155 mol/litre. Alkaline phosphatase was low or normal in all. Clinical rickets was not diagnosed in any of these boys. Among those with levels > 50 nmol/L, at least 2/28 were on supplements. Conclusion 78% of boys who were tested had inadequate vitamin D levels according to current standards and 15% had severe deficiency. These data have important implications for optimising bone health and for corticosteroid treatment in DMD.

Introduction Boys with Duchenne muscular dystrophy (DMD) have low bone density. Although corticosteroids improve muscle strength and function in boys with DMD, potential adverse effects include osteoporosis and vertebral fractures. Bianchi et al1 reported low Vitamin D levels in a small cohort of boys with DMD. The optimal 25-OH vitamin D levels in children have been redefined by Misra et al2 with the recommendation that serum 25-OH vitamin D level <37.5 nmol/litre constitutes vitamin D deficiency and a level greater than 50 nmol/l is indicative of sufficiency. In the UK there are no large studies to establish vitamin D levels in children with DMD. Objectives To establish the prevalence of vitamin D deficiency in boys with DMD. Methodology The North Star neuromuscular network consensus is to check vitamin D levels prior to starting corticosteroid therapy. Data on vitamin D levels was retrospectively collected from the case records through the north star neuromuscular database. Results 25-OH vitamin D levels were available in 157 boys with DMD. The mean age at checking vitamin D level was 6.9 years (1.5–15.5). Vitamin D levels ranged from 4–155 mol/litre. Alkaline phosphatase was low or normal in all. Clinical rickets was not diagnosed in any of these boys. Among those with levels > 50 nmol/L, at least 2/28 were on supplements. Conclusion 78% of boys who were tested had inadequate vitamin D levels according to current standards and 15% had severe deficiency. These data have important implications for optimising bone health and for corticosteroid treatment in DMD. Abstract G6 Table 1 Range Degree of deficiency Number of boys with DMD Percentage <17.5 nmol/litre Severe 24 15 17.5–37.5 nmol/litre Deficiency 67 43 37.5–50 nmol/litre Insufficient 31 20 >50 nmol/litre Adequate 35 22