Primary percutaneous coronary intervention of native chronic total occlusions to treat ST elevation myocardial infarction secondary to acute vein graft occlusion

Primary percutaneous coronary intervention (PCI) is the treatment modality of choice in patients presenting with ST elevation myocardial infarction (STEMI). Clinical outcomes have dramatically improved with the wide adoption of primary PCI in patients with STEMI because of acute thrombotic native coronary artery occlusion. However, patients with prior coronary artery bypass graft (CABG) surgery who present with STEMI because of acute saphenous vein graft (SVG) occlusion continue to have worse outcomes because of poor acute and long‐term results of SVG stenting. Therefore, it may be preferable to treat the native coronary artery supplied by the occluded graft although this can be challenging if the native vessel is a chronic total occlusion (CTO). Recent advances in technology and techniques in CTO PCI have significantly improved the success rate and efficiency of CTO procedures. At our institution we have developed a high volume CTO programme with high success rates. We present three cases of acute inferior STEMI because of SVG occlusion which were treated with successful retrograde PCI of the native vessel CTO, utilising the occluded graft as a retrograde channel in two cases and native septal collaterals in the other. Thrombolysis In Myocardial Infarction (TIMI) 3 flow in the native coronary artery was achieved in all three cases with good acute outcomes. Our case series highlights the benefits of a high volume CTO programme. With recent advances in CTO techniques, acute PCI to native vessel CTO is feasible and may be the treatment of choice in selected cases of acute SVG failure. © 2017 Wiley Periodicals, Inc.     

Neuropsychological profile of children with subcortical band heterotopia

Aim  Subcortical band heterotopia (SBH) or 'double cortex' is a malformation of cortical development resulting from impaired neuronal migration. So far, research has focused on the neurological, neuroimaging, and genetic correlates of SBH. More recently, clinical reports and small sample studies have documented neuropsychological dysfunction in patients with this malformation. This study aimed to characterize further the phenotype of patients with SBH by describing the neuropsychological profiles of children.
Method  Seven children (six females) aged 4 to 15 years were assessed for cognitive functioning (intellectual ability, processing speed, attention, working memory) and academic achievement (reading, spelling, arithmetic). Parents completed questionnaires examining their child's social skills and problem behaviours. Magnetic resonance images (MRI) conducted for routine clinical follow-up were coded by a paediatric neurologist. Genetic and seizure history were obtained from medical records.
Results  There was variation in the neurological, neuroimaging, and genetic presentation of children in the sample. Impairments were observed in all areas of neuropsychological functioning examined. Intellectual ability was generally within the 'extremely low' range (full-scale IQ 44–74; performance IQ 45–72; verbal IQ 57–80). Generalized impairments in cognitive skills were typical, with severe impairments (scores greater than 2SD below the test mean) reported in processing speed, working memory, and arithmetic. Impairments in academic, social, and behavioural functioning were less generalized. No clear relationship between neuroimaging and neuropsychological impairments was found.
Interpretation  Children with SBH demonstrate cognitive, academic, social, and behavioural problems, with the greatest difficulties in processing speed and complex cognitive skills.     

Electrophysiological signs of supplementary-motor-area deficits in high-functioning autism but not Asperger syndrome: an examination of internally cued movement-related potentials

Aims  Motor dysfunction is common to both autism and Asperger syndrome, but the underlying neurophysiological impairments are unclear. Neurophysiological examinations of motor dysfunction can provide information about likely sites of functional impairment and can contribute to the debate about whether autism and Asperger syndrome are variants of the same disorder or fundamentally distinct neurodevelopmental conditions. We investigated the neurophysiology of internally determined motor activity in autism and Asperger syndrome via examination of movement-related potentials (MRPs).
Method  We used electroencephalography to investigate MRPs, via an internally cued movement paradigm, in the following three groups: (1) individuals with high-functioning autism (14 males, one female; mean age 13y 1mo, SD 4y 2mo, range 7y 8mo to 20y 9mo; mean Full-scale IQ 93.40, SD 20.72); (2) individuals with Asperger syndrome (10 males, two females; mean age 13y 7mo, SD 3y 9mo, range 8y 11mo to 20y 4mo; mean Full-scale IQ 103.25, SD 19.37), and (3) a healthy control group (13 males, seven females; mean age 14y 0mo, SD 3y 11mo; range 8y 4mo to 21y 0mo; mean Full-scale IQ 114.25, SD 11.29).
Results  Abnormal MRPs can reflect disruption of motor-related neural networks involving the basal ganglia, thalamus, and supplementary motor area. There was evidence for abnormal MRPs in autism (e.g. increased post-movement cortical activity, abnormal peak time) but not in Asperger syndrome.
Interpretation  The results support basal ganglia, thalamus, and supplementary motor area involvement as a likely source of motor dysfunction in autism, and provide further evidence for the neurobiological separateness of autism and Asperger syndrome.     

BLADDER DEFORMITY A Sign of Major Inferior Venous Obstruction. Two Case Reports and a Review.

Urinary bladder deformity is a sign of major inferior venous occlusion. This deformity is characteristic and different from that due to more common bladder deforming lesions e.g. pelvic haematoma. This intravenous urographic (IVU) Fmding is not rare, especially in the population being in vestigated for possible renal carcinoma.