Epileptic Seizure, Cataract, and Tongue Atrophy during the 8 Years after Electrical Brain Injury

Kuwabara, Takeo; Fukushima, Takao; Makino, Kunihiko; Kondo, Hiroshi

doi:10.2169/internalmedicine.48.2008

Cited by 7 publications

(3 citation statements)

References 11 publications

(14 reference statements)

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“…Various epidemiological studies indicate the associations between cataract prevalence and epilepsy is equivalent to association of cataract with aging, diabetes, arterial hypertension and smoking (Hanhart et al, 2010; Isaac et al, 1991; Kato et al, 1990; Kinoshita et al, 2004; Kuwabara et al, 2009; Mathers et al, 1987). The onset of epilepsy is due to over-synchronous firing of brain neurons (Kerr et al, 2013) and these firing patterns are modulated by a major excitatory neurotransmitter, glutamate, through the family of glutamate receptors (Kim et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Valproic acid suppresses Nrf2/Keap1 dependent antioxidant protection through induction of endoplasmic reticulum stress and Keap1 promoter DNA demethylation in human lens epithelial cells

Periyasamy

Bidasee

Shinohara

2014

Experimental Eye Research

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Recent epidemiological studies confirm the prevalence of cataract in epileptic patients. Similarly, the drugs used to treat epilepsy also show the connection with increased cataract formation. In this present study, we investigated the suppression of Nrf2/Keap1 dependent antioxidant protection through induction of endoplasmic (ER) stress and Keap1 promoter DNA demethylation in human lens epithelial cells (HLECs) treated with valproic acid (VPA), an antiepileptic drug. 20 mM VPA induces ER stress and activates the unfolded protein response (UPR) within 4 h by phosphorylating the ER stress sensor proteins, such as PERK, IRE1α, and ATF6 in HLECs. Consequently, the integrated ER stress signals, such as eIF2α, ATF4, BiP, and CHOP are altered accordingly to induce ER-Ca2+ release, reactive oxygen species (ROS) overproduction, and cell death in HLECs treated with VPA. VPA also suppresses the Nrf2, catalase, and glutathione reductase expressions with significant increases in Keap1 protein. Bisulphite genomic DNA sequencing reveals the promoter DNA demethylation in the Keap1 promoter, which results in the overexpression of Keap1 mRNA and protein in HLECs treated with 20 mM VPA. VPA also alters the expression profiles of passive DNA demethylation pathway enzymes such Dnmt1, Dnmt3a, Dnmt3b, and active DNA demethylation pathway enzyme, TET1 leading to DNA demethylation in the Keap1 promoter of HLECs. Overexpressed Keap1 decreases the Nrf2 level, thereby abolishing the Nrf2 dependent antioxidant protection. This might be responsible for lenticular proteins oxidation and cataract formation.

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Section: Introductionmentioning

confidence: 99%

Valproic acid suppresses Nrf2/Keap1 dependent antioxidant protection through induction of endoplasmic reticulum stress and Keap1 promoter DNA demethylation in human lens epithelial cells

Periyasamy

Bidasee

Shinohara

2014

Experimental Eye Research

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“…Any part of the lens structures such as lens capsule, anterior subcapsular cortex and posterior cortex may be affected by electrical injury. 5,6 There are only a few case reports in the literature regarding electric shock maculopathy (ESM). The most commonly reported form of ESM is characterized by defect in retina pigment epithelium (RPE) and outer retinal layers progressing to form outer lamellar hole with an intact ILM over the bare RPE, with or without associated cystic changes noted on OCT. [7][8][9] Fullthickness macular holes which are associated with more severe injuries are reported less frequently.…”

Section: Discussionmentioning

confidence: 99%

Simultaneous Cataract, Maculopathy and Optic Atrophy Secondary to High-Voltage Electrical Shock Injury

Korkmaz

Kartı

Zengin

et al. 2018

Neuro-Ophthalmology

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A 32-year-old man presented to our clinic with complaint of vision loss in both eyes (oculus utro; OU). Past medical history revealed that he had been exposed to high-voltage electrical current that passed through the temporal region of the head 2 months ago. Slit-lamp examination demonstrated cortico-nuclear cataract and mature cataract in his right eye (oculus dexter; OD) and left eye (oculus sinister; OS), respectively. On fundus examination, a macular hole was observed in OD. Optic atrophy and foveal atrophy were observed in the left fundus examination after cataract surgery. Simultaneous cataract, maculopathy and optic atrophy may occur after high-voltage electrical current injury. Therefore, clinicians should perform detailed anterior and posterior segment examinations in such patients.

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“…Similar to other extensive burn injuries, abnormal temperature sensation, sensory loss, and pruritis may continue for several years after the injury [9,10]. In addition, other complications, such as epilepsy, cataracts, tongue atrophy, and paraplegia, may also have an insidious onset [11,12]. Limb loss, a common complication of electrical burn injuries, substantially affects the lives of affected individuals [13].…”

Section: Introductionmentioning

confidence: 99%

Outcomes of Patients with Amputation following Electrical Burn Injuries

Kim,

Wan,

Solis-Beach

et al. 2023

EBJ

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This study aimed to examine patients who sustained amputation as a result of electrical burns and to evaluate their long-term health outcomes compared to non-electrical burn patients with amputation. A retrospective analysis was conducted on burn patients from 1993 to 2021, utilizing the Burn Model System National Database, which includes the Veterans RAND 12-Item Health Survey and the Patient-Reported Outcomes Measurement Information System 29. The data was collected at discharge, 6 months, and 12 months after the burns occurred. The findings revealed that the rate of amputation was significantly higher in electrical burn patients (30.3%) compared to non-electrical burn patients (6.6%) (p < 0.0001). At the time of discharge, electrical burn patients with amputation exhibited significantly lower physical component scores (PCS = 34.00 ± 8.98) than electrical burn patients without amputation (PCS = 44.66 ± 9.90) (p < 0.05). However, there were no significant differences in mental component scores observed between patients, regardless of the burn type or amputation. Among all patient groups, non-electrical burn survivors with amputation faced the greatest challenges in terms of physical and social well-being, likely due to larger total body surface area burns. This study emphasizes the importance of early rehabilitation for electrical burn patients with amputation and highlights the need for ongoing support, both physically and socially, for non-electrical burn survivors with amputation. These findings, consistent with previous studies, underscore the necessity of providing psychological support to all burn survivors.

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Epileptic Seizure, Cataract, and Tongue Atrophy during the 8 Years after Electrical Brain Injury

Abstract: As a delayed neurologic complication following a high-voltage electrical injury

Cited by 7 publications

References 11 publications

Valproic acid suppresses Nrf2/Keap1 dependent antioxidant protection through induction of endoplasmic reticulum stress and Keap1 promoter DNA demethylation in human lens epithelial cells

Valproic acid suppresses Nrf2/Keap1 dependent antioxidant protection through induction of endoplasmic reticulum stress and Keap1 promoter DNA demethylation in human lens epithelial cells

Simultaneous Cataract, Maculopathy and Optic Atrophy Secondary to High-Voltage Electrical Shock Injury

Outcomes of Patients with Amputation following Electrical Burn Injuries

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