Zenobia Zaiwalla

Publications (7)15.63 Total impact

• Article: Paediatric video-telemetry safety survey.

  Charlotte Frances McAuley, Sarah Aylett, Colin Dunkley, Zenobia Zaiwalla, Tony McShane
  Archives of Disease in Childhood 01/2012; 97(3):298-9. · 2.88 Impact Factor
• Article: Video EEG outcome on children referred following a single unprovoked afebrile seizure.

  Geetha Anand, Anuruddha Padeniya, Rakesh Jain, Nadeem Hasan, Michael Pike, Sandeep Jayawant, Tony McShane, Zenobia Zaiwalla
  Archives of Disease in Childhood 01/2012; 97(1):90. · 2.88 Impact Factor
• Article: Electroclinical outcome of children referred with suspected absence seizures.

  Geetha Anand, Anuruddha Padeniya, Rakesh Jain, Nadeem Hasan, Sandeep Jayawant, Michael Pike, Tony McShane, Zenobia Zaiwalla
  Archives of Disease in Childhood 10/2011; 96(10):987-8. · 2.88 Impact Factor
• Article: Milder phenotypes of glucose transporter type 1 deficiency syndrome.

  Geetha Anand, Anuruddha Padeniya, Donncha Hanrahan, Hans Scheffer, Zenobia Zaiwalla, Debbie Cox, Nicholas Mann, John Hewertson, Sue Price, Andrea Nemeth, Todor Arsov, Ingrid Scheffer, Sandeep Jayawant, Michael Pike, Tony McShane
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  ABSTRACT: Glucose transporter type 1 deficiency syndrome (GLUT1DS) is a treatable condition resulting from impaired glucose transport into the brain. The classical presentation is with infantile-onset epilepsy and severe developmental delay. Non-classical phenotypes with movement disorders and early-onset absence epilepsy are increasingly recognized and the clinical spectrum is expanding. The hallmark is hypoglycorrhachia (cerebrospinal fluid [CSF] glucose<2.2 mmol/l) in the presence of normoglycaemia with a CSF/blood glucose ratio of less than 0.4. GLUT1DS is due to a mutation in the solute carrier family 2, member 1 gene (SLC2A1). We present five individuals (four males, one female), all of whom had a mild phenotype, highlighting the importance of considering this diagnosis in unexplained neurological disorders associated with mild learning difficulties, subtle motor delay, early-onset absence epilepsy, fluctuating gait disorders, and/or dystonia. The mean age at diagnosis was 8 years 8 months. This paper also shows phenotypical parallels between GLUT1DS and paroxysmal exertion-induced dyskinesia.
  Developmental Medicine & Child Neurology 07/2011; 53(7):664-8. · 2.92 Impact Factor
• Article: A novel ARX phenotype: rapid neurodegeneration with Ohtahara syndrome and a dyskinetic movement disorder.

  Michael Absoud, Jeremy R Parr, Dorothy Halliday, Pieter Pretorius, Zenobia Zaiwalla, Sandeep Jayawant
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  ABSTRACT: ARX mutations are associated with variable clinical phenotypes. We report a new neurodegenerative phenotype associated with a known ARX mutation and causing early abnormal neurodevelopment, a complex movement disorder, and early infantile epileptic encephalopathy with a suppression-burst pattern (Ohtahara syndrome). A male infant presented at age 5 months with a dyskinetic movement disorder, which was initially diagnosed as infantile spasms. Clinical deterioration was accompanied by progressive cortical atrophy with a reduction in white matter volume and resulting in death in the first year of life; such a rapidly progressive and severe phenotype has not previously been described. ARX mutation testing should be undertaken in children aged less than 1 year with Ohtahara syndrome and a movement disorder, and in infants with unexplained neurodegeneration, progressive white matter loss, and cortical atrophy.
  Developmental Medicine & Child Neurology 09/2009; 52(3):305-7. · 2.92 Impact Factor
• Article: Narcolepsy and excessive daytime sleepiness.

  Adam Zeman, Tom Britton, Neil Douglas, Andrew Hansen, Jane Hicks, Robin Howard, Andrew Meredith, Ian Smith, Gregory Stores, Sue Wilson, Zenobia Zaiwalla
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  ABSTRACT: Introduction Excessive daytime sleepiness is common,1 yet opportunities to learn about sleep medicine in medical school are rare; a survey in 1998 indicated that undergraduate courses devoted a median of five minutes to sleep and its disorders.2 In this review we provide an update on the biology, diagnosis, and management of narcolepsy—an important, yet often misdiagnosed, cause of sleepiness that has seen exciting recent advances. We also briefly outline the other principal causes of daytime sleepiness and aim to equip the general reader with a practical approach to the assessment of patients who complain of excessive daytime sleepiness. Sources and selection criteria This paper is based on a literature search conducted to produce evidence based guidelines on the diagnosis and management of narcolepsy in adults and children.3 We searched Medline, Embase, the Cochrane Collaboration, and two specialist sleep literature resources for abstracts with the key word “narcolepsy.” We read the full text of relevant papers and hand searched these for other relevant material. A multidisciplinary working party prepared the guidelines, and a group of 10 independent experts later reviewed them. These guidelines can be downloaded from the news section of http://www.sleeping.org.uk/ (accessed July 2004). Clinical features of narcolepsy Narcolepsy is a chronic neurological disorder affecting sleep regulation and causing excessive sleepiness and, in most cases, cataplexy (brief attacks of weakness on emotional arousal).3 4 The excessive sleepiness of narcolepsy comprises both a background feeling of sleepiness present much of the time and a strong, sometime irresistible, urge to sleep recurring at intervals through the day. This desire is heightened by conducive, monotonous circumstances, but naps at inappropriate times—such as during meals—are characteristic. The naps of narcolepsy usually last from minutes to an hour and occur a few times each day. Cataplexy refers to partial or generalised, almost invariably bilateral, loss of skeletal muscle tone and …
  BMJ (Clinical research ed.). 10/2004; 329(7468):724-8.
• Article: Parasomnias.

  Zenobia Zaiwalla
  Clinical medicine (London, England) 5(2):109-12. · 1.15 Impact Factor