To compare optical coherence tomography measurements; central macular thickness, ganglion cell complex, and retinal nerve fiber layer thickness in patients with epilepsy versus healthy controls.
Methods:
We evaluated 28 eyes of 28 patients with epilepsy and 34 eyes of 34 healthy subjects. Central macular thickness, ganglion cell complex, and retinal nerve fiber layer thickness measurements were performed by spectral-domain optical coherence tomography.
Results:
Superior and superotemporal quadrant ganglion cell complex, average, and superior quadrant retinal nerve fiber layer thickness measurements were significantly lower in epilepsy group compared to healthy control subjects. Central macular thickness was significantly lower in polytherapy group compared to monotherapy group. Ganglion cell complex and retinal nerve fiber layer thickness measurements were not significantly different between polytherapy and monotherapy groups.
Conclusion:
The present study shows that epileptic patients taking antiepileptic drugs have reduced ganglion cell complex and retinal nerve fiber layer thickness compared to healthy controls. This can be related to the epileptic process in the brain. Optical coherence tomography may be a useful tool for showing the neurodegeneration in patients with epilepsy.
BayerAUThielHJZrennerE, et al. Color vision tests for early detection of antiepileptic drug toxicity. Neurology1997; 48(5): 1394–1397.
7.
MecarelliORinalduzziSAccorneroN.Changes in color vision after a single dose of vigabatrin or carbamazepine in healthy volunteers. Clin Neuropharmacol2001; 24: 23–26.
8.
DurnianJMClearkinLG.Retinal nerve fibre layer characteristics with vigabatrin-associated visual field loss—could scanning laser polarimetry aid diagnosis. Eye (Lond)2008; 22(4): 559–563.
9.
HuiACLiuDTWongKK, et al. Vigabatrin-induced visual dysfunction in Chinese patients with refractory epilepsy. Eur J Ophthalmol2008; 18(4): 624–627.
10.
LobefaloLRapineseMAltobelliE, et al. Retinal nerve fiber layer and macular thickness in adolescents with epilepsy treated with valproate and carbamazepine. Epilepsia2006; 47(4): 717–719.
11.
DereciSKocaTAkcamM, et al. An evaluation of peripapillary retinal nerve fiber layer thickness in children with epilepsy receiving treatment of valproic acid. Pediatr Neurol2015; 53(1): 53–57.
12.
BalestriniSClaytonLMBartmannAP, et al. Retinal nerve fibre layer thinning is associated with drug resistance in epilepsy. J Neurol Neurosurg Psychiatry2016; 87(4): 396–401.
13.
LiuRSLemieuxLBellGS, et al. Cerebral damage in epilepsy: a population-based longitudinal quantitative MRI study. Epilepsia2005; 46(9): 1482–1494.
14.
LiuRSLemieuxLBellGS, et al. Progressive neocortical damage in epilepsy. Ann Neurol2003; 53(3): 312–324.
15.
WhelanCDAltmannABotiaJA, et al. Structural brain abnormalities in the common epilepsies assessed in a worldwide ENIGMA study. Brain2018; 141(2): 391–408.
16.
CaciagliLBernhardtBCHongSJ, et al. Functional network alterations and their structural substrate in drug-resistant epilepsy. Front Neurosci2014; 8: 411.
17.
BernhardtBCBernasconiNKimH, et al. Mapping thalamocortical network pathology in temporal lobe epilepsy. Neurology2012; 78(2): 129–136.
18.
VaughanDNRaynerGTailbyC, et al. MRI-negative temporal lobe epilepsy: a network disorder of neocortical connectivity. Neurology2016; 87(18): 1934–1942.
19.
CretinBPhilippiNDibitontoL, et al. Epilepsy at the prodromal stages of neurodegenerative diseases. Geriatr Psychol Neuropsychiatr Vieil2017; 15(1): 75–82.
20.
SpillantiniMGGoedertM.Tau pathology and neurodegeneration. Lancet Neurol2013; 12: 609–622.
21.
TaiXYKoeppMDuncanJS, et al. Hyperphosphorylated tau in patients with refractory epilepsy correlates with cognitive decline: a study of temporal lobe resections. Brain2016; 139(Pt. 9): 2441–2455.
22.
CascinoGD.Temporal lobe epilepsy is a progressive neurologic disorder: time means neurons!Neurology2009; 72: 1718–1719.
23.
RobersonEDScearce-LevieKPalopJJ, et al. Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer’s disease mouse model. Science2007; 316(5825): 750–754.
24.
LondonABenharISchwartzM.The retina as a window to the brain—from eye research to CNS disorders. Nat Rev Neurol2013; 9(1): 44–53.
25.
RatchfordJNQuiggMECongerA, et al. Optical coherence tomography helps differentiate neuromyelitis optica and MS optic neuropathies. Neurology2009; 73(4): 302–308.
26.
HajeeMEMarchWFLazzaroDR, et al. Inner retinal layer thinning in Parkinson disease. Arch Ophthalmol2009; 127(6): 737–741.
27.
LeeWWTajunisahISharmillaK, et al. Retinal nerve fiber layer structure abnormalities in schizophrenia and its relationship to disease state: evidence from optical coherence tomography. Invest Ophthalmol Vis Sci2013; 54(12): 7785–7792.
28.
FisherJBJacobsDAMarkowitzCE, et al. Relation of visual function to retinal nerve fiber layer thickness in multiple sclerosis. Ophthalmology2006; 113(2): 324–332.
29.
PulickenMGordon-LipkinEBalcerLJ, et al. Optical coherence tomography and disease subtype in multiple sclerosis. Neurology2007; 69(22): 2085–2092.
30.
BerishaFFekeGTTrempeCL, et al. Retinal abnormalities in early Alzheimer’s disease. Invest Ophthalmol Visual Sci2007; 48: 2285–2289.
31.
KwonJYYangJHHanJS, et al. Analysis of the retinal nerve fiber layer thickness in Alzheimer disease and mild cognitive impairment. Korean J Ophthalmol2017; 31(6): 548–556.
32.
OberwahrenbrockTSchipplingSRingelsteinM, et al. Retinal damage in multiple sclerosis disease subtypes measured by high-resolution optical coherence tomography. Mult Scler Int2012; 2012: 530305.
33.
HarwerthRSCarter-DawsonLShenF, et al. Ganglion cell losses underlying visual field defects from experimental glaucoma. Invest Ophthalmol Vis Sci1999; 40(10): 2242–2250.
34.
CurcioCAAllenKA.Topography of ganglion cells in human retina. J Compar Neurol1990; 300: 5–25.
35.
ZeimerRAsraniSZouS, et al. Quantitative detection of glaucomatous damage at the posterior pole by retinal thickness mapping. Ophthalmology1998; 105(2): 224–231.
36.
SeongMSungKRChoiEH, et al. Macular and peripapillary retinal nerve fiber layer measurements by spectral domain optical coherence tomography in normal-tension glaucoma. Invest Ophthalmol Vis Sci2010; 51(3): 1446–1452.
37.
NakataniYHigashideTOhkuboS, et al. Evaluation of macular thickness and peripapillary retinal nerve fiber layer thickness for detection of early glaucoma using spectral domain optical coherence tomography. J Glaucoma2011; 20(4): 252–259.
38.
RogawskiMALoscherW.The neurobiology of antiepileptic drugs. Nat Rev Neurosci2004; 5: 553–564.
39.
O’DonnellTRotzingerSNakashimaTT, et al. Chronic lithium and sodium valproate both decrease the concentration of myo-inositol and increase the concentration of inositol monophosphates in rat brain. Brain Res2000; 880(1–2): 84–91.
40.
VadenDLDingDPetersonB, et al. Lithium and valproate decrease inositol mass and increase expression of the yeast INO1 and INO2 genes for inositol biosynthesis. J Biol Chem2001; 276(18): 15466–15471.
41.
VerrottiALobefaloLPrioloT, et al. Color vision in epileptic adolescents treated with valproate and carbamazepine. Seizure2004; 13: 411–417.
42.
AktasZCansuAErdoganD, et al. Retinal ganglion cell toxicity due to oxcarbazepine and valproic acid treatment in rat. Seizure2009; 18(6): 396–399.
43.
IseriPKAltinasOTokayT, et al. Relationship between cognitive impairment and retinal morphological and visual functional abnormalities in Alzheimer disease. J Neuroophthalmol2006; 26(1): 18–24.
44.
Han SongMLeeSHanHJ, et al. A case report of occipital lobe epilepsy and related optical coherence tomography findings. J Korean Ophthalmol Soc2017; 58(3): 367–371.
