Herpes simplex encephalitis with relapse.

Pike, Michael; Kennedy, Colin; Neville, Brian; Levin, M J

doi:10.1136/adc.66.10.1242

Cited by 38 publications

(26 citation statements)

References 6 publications

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“…A few cases of relapsing H S E after acyclovir treatment have also been reported and were attributed either to post-infectious encephalopathy of u n k n o w n mechanism [1,4] or to failure of the drug to eradicate the virus completely [4,5]. In our patient the time of relapse and the favourable response to the second course of acyclovir treatment strongly suggest that the first course of the 10-day treatment was not adequate for complete eradication of H S V infection.…”

Section: Fig 2 Brain Ct After Enhancement the Anterior Temporal Armentioning

confidence: 46%

“…R e l a p s e of H S E has b e e n r e p o r t e d after v i d a r a b i n e therapy [3]. F u r t h e r m o r e , in recent years a few cases of relapses following 8 [2] -1 0 [1,4,5] days of acyclovir therapy have also b e e n r e p o r t e d . W e r e p o r t a new case of clinical relapse of H S E following a 10-day course of therapy with acyclovir which r e s p o n d e d c o m p l e t e l y to a second 10-day course with the same drug.…”

Section: Introductionmentioning

confidence: 97%

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Relapse of herpes simplex encephalitis after acyclovir therapy

et al. 1993

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A case of herpes simplex encephalitis in a previously healthy 17-month-old girl relapsing 1 week after completion of a 10-day acyclovir therapy is described. The child responded favourably to a second 10-day course with acyclovir. The time of relapse and the satisfactory response to a second course of acyclovir treatment indicate that the first course of therapy was inadequate for eradication of herpes simplex virus infection.

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Section: Fig 2 Brain Ct After Enhancement the Anterior Temporal Armentioning

confidence: 46%

Section: Introductionmentioning

confidence: 97%

Relapse of herpes simplex encephalitis after acyclovir therapy

et al. 1993

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“…These include attention deficit hyperactivity disorder (ADHD), autism spectrum and Obsessive-Compulsive Disorder (OCD). 1 Neuro-biological mechanisms of these conditions are unknown. Due to the high heritability, gene discovery in large families will provide insight into aetiology.…”

Section: Sessionmentioning

confidence: 99%

Session 4: Thursday 24 January

2013

Develop Med Child Neuro

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fied by WES followed by nine additional patients by Sanger sequencing, ranging in severity from Walker Warburg syndrome to limb girdle muscular dystrophy; (ii) two genes are responsible for a congenital form of spinal muscular atrophy affecting the lower limbs (three cases mutated for one gene and two cases for a second gene); (iii) one gene is responsible for a core myopathy/King Demborough phenotype in a large consanguineous family.Conclusions: New generation sequencing allows the identification of novel genes much more effectively than previous techniques. The level of genetic heterogeneity of neuromuscular disorders exceeds recent estimations and it is realistic to expect that we will at least double the number of genes involved in neuromuscular conditions in the next few years.This brings significant challenges; firstly the necessity to clearly define the phenotype of patients; secondly the need to be involved in collaborative studies to access other patients affected by these often exceedingly rare conditions; finally the demonstration of pathogeneicity of putative mutations in novel genes.These challenges can be addressed by deep phenotyping, access to international collaboration networks and biobanked material, and multidisciplinary collaborations.Acknowledgements: The Wellcome Trust Sanger Institute; affected families; the Muscular Dystrophy Campaign; the GOSH Charity; and colleagues from the Dubowitz neuromuscular centre; the DNA laboratory at Guy's Hospital.

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“…Insofern kann immunhistochemisch ein unterschiedlicher inflammatorischer Prozess vermutet werden: Bei der HSE ist die Persistenz aktivierter T-Lymphozyten und Makrophagen verantwortlich, bei der SSPE werden dagegen virale Glykoproteine auf den infizierten Wirtszellen exprimiert und somit eine Immunantwort mit vorwiegender humoraler B-Zell-Aktivierung induziert. Aufgrund dieser lang anhaltenden immunogenen Aktivierung empfiehlt die Arbeitsgruppe von Pike et al [13] sogar eine mindestens 2-malig negative PCR im Liquor zur Dokumentation einer effektiven antiviralen Therapie.…”

Section: Introductionunclassified