Literature DB >> 22903242

Establishing baseline rod electroretinogram values in achromatopsia and cone dystrophy.

Isaac Wang1, Naheed W Khan2, Kari Branham2, B Wissinger3, Susanne Kohl3, J R Heckenlively4.   

Abstract

PURPOSE: To establish the normal range of values for rod-isolated b-wave amplitudes in achromatopsia and cone dystrophies.
METHODS: We reviewed charts of 112 patients with various types of cone dystrophy, and compared their standardized electroretinographic rod b-wave amplitudes with age-matched normal controls. Twenty-six patients had known mutations in achromatopsia and cone dystrophy genes, while 53 were characterized by their inheritance pattern since they had yet to have their gene identified. Visual acuity information and scotomata were documented.
RESULTS: We found that patients with achromatopsia and cone dystrophy had rod b-wave amplitudes that were significantly lower than age-matched controls, but found no evidence of rod amplitude progression nor loss of peripheral visual fields in the study group.
CONCLUSIONS: We found that cone dystrophy patients of all types had depressed rod-isolated ERGs across the board. If typical diagnostic criteria are used, these patients might be considered to have "abnormal" rod-isolated electroretinographic values, and might be called "cone-rod dystrophy", even though the waveforms are stable for years. Patients with cone-rod dysfunction patterns on ERG can be better understood by also performing kinetic (Goldmann) visual fields, which will help to distinguish cone dystrophies from progressive cone-rod dystrophies by central scotomata size and progression over time in many forms of cone-rod dystrophy.

Entities:  

Keywords:  Achromatopsia; Central scotomata; Cone dystrophy; Cone-rod interaction; Rod electroretinogram

Mesh:

Substances:

Year:  2012        PMID: 22903242     DOI: 10.1007/s10633-012-9350-1

Source DB:  PubMed          Journal:  Doc Ophthalmol        ISSN: 0012-4486            Impact factor:   2.379


  8 in total

1.  Achromatopsia caused by novel mutations in both CNGA3 and CNGB3.

Authors:  S Johnson; M Michaelides; I A Aligianis; J R Ainsworth; J D Mollon; E R Maher; A T Moore; D M Hunt
Journal:  J Med Genet       Date:  2004-02       Impact factor: 6.318

2.  CNGB3 achromatopsia with progressive loss of residual cone function and impaired rod-mediated function.

Authors:  Naheed Wali Khan; Bernd Wissinger; Susanne Kohl; Paul A Sieving
Journal:  Invest Ophthalmol Vis Sci       Date:  2007-08       Impact factor: 4.799

3.  Cone and rod function in cone degenerations.

Authors:  B Sadowski; E Zrenner
Journal:  Vision Res       Date:  1997-08       Impact factor: 1.886

4.  CNGA3 deficiency affects cone synaptic terminal structure and function and leads to secondary rod dysfunction and degeneration.

Authors:  Jianhua Xu; Lynsie M Morris; Stylianos Michalakis; Martin Biel; Steven J Fliesler; David M Sherry; Xi-Qin Ding
Journal:  Invest Ophthalmol Vis Sci       Date:  2012-03-01       Impact factor: 4.799

5.  Mutations in the gene KCNV2 encoding a voltage-gated potassium channel subunit cause "cone dystrophy with supernormal rod electroretinogram" in humans.

Authors:  Huimin Wu; Jill A Cowing; Michel Michaelides; Susan E Wilkie; Glen Jeffery; Sharon A Jenkins; Viktoria Mester; Alan C Bird; Anthony G Robson; Graham E Holder; Anthony T Moore; David M Hunt; Andrew R Webster
Journal:  Am J Hum Genet       Date:  2006-07-24       Impact factor: 11.025

6.  Novel mutations in the KCNV2 gene in patients with cone dystrophy and a supernormal rod electroretinogram.

Authors:  Sureka Thiagalingam; Terri L McGee; Richard G Weleber; Michael A Sandberg; Karmen M Trzupek; Eliot L Berson; Thaddeus P Dryja
Journal:  Ophthalmic Genet       Date:  2007-09       Impact factor: 1.803

7.  Mutations in CNGA3 impair trafficking or function of cone cyclic nucleotide-gated channels, resulting in achromatopsia.

Authors:  Peggy Reuter; Katja Koeppen; Thomas Ladewig; Susanne Kohl; Britta Baumann; Bernd Wissinger
Journal:  Hum Mutat       Date:  2008-10       Impact factor: 4.878

8.  Novel KCNV2 mutations in cone dystrophy with supernormal rod electroretinogram.

Authors:  Safouane Ben Salah; Satomi Kamei; Audrey Sénéćhal; Séverine Lopez; Christian Bazalgette; Cécile Bazalgette; Claudie Malrieu Eliaou; Xavier Zanlonghi; Christian P Hamel
Journal:  Am J Ophthalmol       Date:  2008-04-09       Impact factor: 5.258

  8 in total
  3 in total

1.  Differences in ocular findings in two siblings: one with complete and other with incomplete achromatopsia.

Authors:  Shinji Ueno; Ayami Nakanishi; Akira Sayo; Taro Kominami; Yasuki Ito; Takaaki Hayashi; Kazushige Tsunoda; Takeshi Iwata; Hiroko Terasaki
Journal:  Doc Ophthalmol       Date:  2017-02-14       Impact factor: 2.379

2.  Disease progression in autosomal dominant cone-rod dystrophy caused by a novel mutation (D100G) in the GUCA1A gene.

Authors:  Eva Nong; Winston Lee; Joanna E Merriam; Rando Allikmets; Stephen H Tsang
Journal:  Doc Ophthalmol       Date:  2013-12-19       Impact factor: 2.379

3.  The morphology of human rod ERGs obtained by silent substitution stimulation.

Authors:  J Maguire; N R A Parry; J Kremers; I J Murray; D McKeefry
Journal:  Doc Ophthalmol       Date:  2017-01-13       Impact factor: 2.379

  3 in total

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