Locked-in syndrome: A rare manifestation of pediatric stroke

Locked-in syndrome is characterized by upper motor neuron quadriplegia, paralysis of lower cranial nerves, bilateral horizontal gaze palsy and anarthria, with preserved consciousness. It is due to a ventral pontine lesion following a basilar artery occlusion. We report the first Indian case report of locked-in syndrome, a 10-year old girl in whom the syndome was preceded by a ‘herald hemiparesis’. Although the exact etiology for the basilar artery occlusion could not be determined, treatment with low molecular weight heparin and warfarin was followed by partial recovery.     

Selective sensitivity of synaptosomal membrane function to cerebral cortical hypoxia in newborn piglets

The effect of hypoxia on the structure and function of the synaptosomal membranes and myelin fraction (glial cells, neuronal cell bodies and axonal membranes) was investigated by measuring Na⁺,K⁺-ATPase activity and levels of lipid peroxidation products in cerebral cortical synaptosomal membranes and myelin fractions obtained from newborn piglets. Hypoxic hypoxia was induced and cerebral hypoxia was documented as a decrease in the ratio of phosphocreatine to inorganic phosphate (PCr/Oi) using³¹P-NMR spectroscopy. PCr/Pi decreased from baseline of2.93 ± 0.76to0.61 ± 0.36 during hypoxia. The synaptosomal membrane Na⁺,K⁺-ATPase activity decreased from a control value of56.6 ± 3.7to40.4 ± 6.0 μgmol Pi/mg protein/h during hypoxia. The level of conjugated dienes increased from zero (reference value) to4.5 ± 2.7 nmol/mg lipid and the level of fluorescent compounds increased from23.5 ± 2.2to92.6 ± 46.4 ng quinine sulfate/mg lipid in the synaptosomal membranes during hypoxia. No change in myelin fraction Na⁺,K⁺-ATPase activity or levels of lipid peroxidation products were noted. These data indicate that sunaptosomal membranes, rich in polyunsaturated fatty acids, are more susceptible to oxygen free radical mediated lipid peroxidative damage during hypoxia.     

Changes in Nurse Practitioners' Knowledge and Behaviors Following Brief Training on the Healthy Eating and Activity Together (HEAT) Guidelines

IntroductionPrimary care providers, particularly pediatric nurse practitioners, are an integral force involved in tackling the obesity epidemic among youth. The majority of nurse practitioners, however, report low proficiency regarding their ability to adequately prevent and treat pediatric overweight. In response, the National Association of Pediatric Nurse Practitioners (NAPNAP) developed the evidence-based Healthy Eating and Activity Together (HEAT) Clinical Practice Guideline (CPG) to improve provider behavior and efficacy.MethodThirty-five nurse practitioners attending the NAPNAP Annual Conference participated in an intensive 4-hour HEAT CPG training session. Pre-training and post-training data were collected on provider knowledge, practice behaviors, and barriers in relation to the prevention of overweight among youth.ResultsPost-training results revealed significant improvements in (a) practitioner knowledge (assessment of patient growth, family history, psychosocial functioning, nutrition, and physical activity); (b) practitioners' intent to improve behavior (i.e., increased intent to use behavior modification and counseling aimed at patient and family behavior change); and (c) practitioners' report of increased confidence in ability to address barriers.DiscussionStudy findings demonstrate preliminary support for the HEAT CPG as an effective tool aimed at helping providers to improve their ability to maintain patients' healthy weight. Future research is needed to verify the effects of HEAT CPG on long-term improvements in care.     

Which dyskinesia scale best detects treatment response?

Numerous scales assess dyskinesia in Parkinson's disease (PD), variably focusing on anatomical distribution, phenomenology, time, severity, and disability. No study has compared these scales and their relative ability to detect change related to an established treatment. We conducted a randomized placebo‐controlled trial of amantadine, assessing dyskinesia at baseline and at 4 and 8 weeks using the following scales: Unified Dyskinesia Rating Scale (UDysRS), Lang‐Fahn Activities of Daily Living Dyskinesia Rating Scale (LF), 26‐Item Parkinson's Disease Dyskinesia scale (PDD‐26), patient diaries, modified Abnormal Involuntary Movements Scale (AIMS), Rush Dyskinesia Rating Scale (RDRS), dyskinesia items from the Movement Disorder Society–sponsored revision of the Unified Parkinson's Disease Rating Scale (MDS‐UPDRS), and Clinical Global Impression (severity and change: CGI‐S, CGI‐C). Scale order was randomized at each visit, but raters were aware of each scale as it was administered. Sensitivity to treatment was assessed using effect size. Sixty‐one randomized dyskinetic PD subjects (31 amantadine, 30 placebo) completed the study. Four of the 8 scales (CGI‐C, LF, PDD‐26, and UDysRS) detected a significant treatment. The UDysRS Total Score showed the highest effect size (η² = 0.138) for detecting treatment‐related change, with all other scales having effect sizes < 0.1. No scale was resistant to placebo effects. This study resolves 2 major issues useful for future testing of new antidyskinesia treatments: among tested scales, the UDysRS, having both subjective and objective dyskinesia ratings, is superior for detecting treatment effects; and the magnitude of the UDysRS effect size from amantadine sets a clear standard for comparison for new agents. © 2012 Movement Disorder Society     

Saturable Leptin Transport Across the BBB Persists in EAE Mice

We have shown that mice with experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis, have upregulated leptin receptor expression in reactive astrocytes of the hippocampus, a region involved in sickness behavior. Leptin can exacerbate EAE when its serum concentration is high. Although leptin receptors in astrocytes modulate leptin transport across cultured endothelial cell monolayers, it is not known how leptin transport in EAE mice is regulated. Here, we determined brain and cervical spinal cord uptake of leptin in early and recovery stages of EAE, after either intravenous delivery or in situ brain perfusion of ¹²⁵I-leptin and the vascular marker ¹³¹I-albumin. While increased vascular space and general blood–brain barrier (BBB) permeability after EAE were expected, the specific saturable transport system for leptin crossing the BBB also persisted. Moreover, there was upregulation of leptin transport in hippocampus and cervical spinal cord in the early stage of EAE, shown by higher leptin uptake in these regions and by competitive inhibition with coadministered excess unlabeled leptin. We conclude that EAE induced a time- and region-specific increase of leptin transport. The results provide a link between circulating leptin and enhanced leptin signaling that may play a crucial role in disease progression.