Sudden unexplained death in epilepsy: the role of the heart.

2007 ◽  
Vol 74 (Suppl_1) ◽  
pp. S121-S121 ◽  
Author(s):  
S. U Schuele ◽  
P. Widdess-Walsh ◽  
A. Bermeo ◽  
H. O Luders
Keyword(s):  
Sudden Unexplained Death ◽  
Unexplained Death

1. Sudden Unexplained Death in a Psychiatric Patient – A Case Report: The Role of Phenothiazines and Physical Restraint

1997 ◽  
Vol 37 (2) ◽  
pp. 170-175 ◽  
Author(s):  
Anil Kumar
Keyword(s):  
Case Report ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Psychiatric Patients ◽  
Physical Restraint ◽  
Unexpected Death ◽  
Sudden Unexplained Death ◽  
Unexplained Death ◽  
The Subject

Psychotropic drug use has long been associated with sudden unexplained and unexpected death in psychiatric patients despite controversies surrounding the issue. Physical restraint following violent episodes in psychiatric in-patients is also associated with neurally mediated sudden cardiac death. A case where these two mechanisms have jointly resulted in sudden death is reported. The literature on the subject is reviewed and the measures which may be useful in reducing the incidence of such deaths are discussed. The need for accurate and detailed reporting of such cases is emphasized.

Identifying the correct cause of death: The role of post-mortem computed tomography in sudden unexplained death

2014 ◽  
Vol 2 (4) ◽  
pp. 210-212
Author(s):  
Matthew Clarke ◽  
Angus McGregor ◽  
Claire Robinson ◽  
Jasmin Amoroso ◽  
Bruno Morgan ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Cause Of Death ◽  
Post Mortem ◽  
Sudden Unexplained Death ◽  
Unexplained Death

scholarly journals Cardiac Arrhythmia Following an Epileptic Seizure

2019 ◽  
Vol 3 (4) ◽  
pp. 354-356 ◽  
Author(s):  
Hani Kuttab ◽  
Elizabeth Harris ◽  
Katie Tataris ◽  
James Tao ◽  
David Beiser
Keyword(s):  
Ventricular Tachycardia ◽  
Status Epilepticus ◽  
High Risk ◽  
Cardiac Arrhythmia ◽  
Epileptic Seizure ◽  
Laboratory Data ◽  
Unique Case ◽  
Sudden Unexplained Death ◽  
Unexplained Death

Sudden unexplained death in epilepsy (SUDEP) refers to a death in a patient with epilepsy that is not due to trauma, drowning, status epilepticus, or another apparent cause. Although the pathophysiology of SUDEP is incompletely understood, growing evidence supports the role of seizure-associated arrhythmias as a potential etiology. We present a unique case of a patient presenting with ventricular tachycardia shortly following a seizure, along with corresponding laboratory data. Awareness of high risk arrhythmias in seizure patients could lead to advances in understanding pathophysiology and treatment of this complication of seizure disorder and ultimately prevention of SUDEP.

scholarly journals Sudden unexplained death syndrome – a new manifestation in melioidosis?

1991 ◽  
Vol 107 (3) ◽  
pp. 577-584 ◽  
Author(s):  
E. H. Yap ◽  
Y. C. Chan ◽  
K. T. Goh ◽  
T. C. Chao ◽  
B. H. Heng ◽  
...  
Keyword(s):  
Latent Infection ◽  
Immunofluorescence Assay ◽  
Construction Workers ◽  
Active Infection ◽  
Sudden Unexplained Death ◽  
Unexplained Death ◽  
Indirect Haemagglutination ◽  
Antibody Titres ◽  
Pseudomonas Pseudomallei

SUMMARYThe indirect haemagglutination (IHA) test using sensitized turkey erythrocytes and the indirect immunofluorescence assay (IgM-IFA) was confirmed to be sensitive in the detection of a recent or currentPseudomonas pseudomalleiinfection in 19 culture-confirmed Singapore melioidosis patients. All were found to have antibody titres from 4 to 32 768 in the IHA test and 10 to 320 in the IgM-IFA test. When these tests were employed on sera from 16 immigrant Thai construction workers who died of sudden unexplained death syndrome (SUDS) and 73 healthy Thai fellow workers, 93·8% and 68·8% of SUDS cases had IHA titre of ≥ 4 and IgM-IFA titre of ≥ 10 respectively, in contrast to 39·7% and 12·3% found among healthy Thai workers. These data indicate that at the time of death, most of the SUDS patients had an active infection withP. pseudomallei, possibly resulting from reactivation of a latent infection. The aetiological role ofP. pseudomalleias the major cause of SUDS is discussed.

scholarly journals Differential Methylation in the GSTT1 Regulatory Region in Sudden Unexplained Death and Sudden Unexpected Death in Epilepsy

2021 ◽  
Vol 22 (6) ◽  
pp. 2790
Author(s):  
Steffan Noe Christiansen ◽  
Stine Bøttcher Jacobsen ◽  
Jeppe Dyrberg Andersen ◽  
Marie-Louise Kampmann ◽  
Linea Christine Trudsø ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cardiac Tissue ◽  
Heart Diseases ◽  
Regulatory Region ◽  
Differential Methylation ◽  
Sudden Unexpected Death ◽  
Diagnostic Challenge ◽  
Unexpected Death ◽  
Sudden Unexplained Death ◽  
Unexplained Death

Sudden cardiac death (SCD) is a diagnostic challenge in forensic medicine. In a relatively large proportion of the SCDs, the deaths remain unexplained after autopsy. This challenge is likely caused by unknown disease mechanisms. Changes in DNA methylation have been associated with several heart diseases, but the role of DNA methylation in SCD is unknown. In this study, we investigated DNA methylation in two SCD subtypes, sudden unexplained death (SUD) and sudden unexpected death in epilepsy (SUDEP). We assessed DNA methylation of more than 850,000 positions in cardiac tissue from nine SUD and 14 SUDEP cases using the Illumina Infinium MethylationEPIC BeadChip. In total, six differently methylated regions (DMRs) between the SUD and SUDEP cases were identified. The DMRs were located in proximity to or overlapping genes encoding proteins that are a part of the glutathione S-transferase (GST) superfamily. Whole genome sequencing (WGS) showed that the DNA methylation alterations were not caused by genetic changes, while whole transcriptome sequencing (WTS) showed that DNA methylation was associated with expression levels of the GSTT1 gene. In conclusion, our results indicate that cardiac DNA methylation is similar in SUD and SUDEP, but with regional differential methylation in proximity to GST genes.

scholarly journals Re-evaluation of single nucleotide variants and identification of structural variants in a cohort of 45 sudden unexplained death cases

2021 ◽  
Author(s):  
Jacqueline Neubauer ◽  
Shouyu Wang ◽  
Giancarlo Russo ◽  
Cordula Haas
Keyword(s):  
Sudden Death ◽  
Cardiac Diseases ◽  
Structural Variants ◽  
Single Nucleotide Variants ◽  
Single Nucleotide ◽  
Sudden Unexplained Death ◽  
Unexplained Death ◽  
Pathogenic Variants ◽  
The Impact ◽  
Death Cases

AbstractSudden unexplained death (SUD) takes up a considerable part in overall sudden death cases, especially in adolescents and young adults. During the past decade, many channelopathy- and cardiomyopathy-associated single nucleotide variants (SNVs) have been identified in SUD studies by means of postmortem molecular autopsy, yet the number of cases that remain inconclusive is still high. Recent studies had suggested that structural variants (SVs) might play an important role in SUD, but there is no consensus on the impact of SVs on inherited cardiac diseases. In this study, we searched for potentially pathogenic SVs in 244 genes associated with cardiac diseases. Whole-exome sequencing and appropriate data analysis were performed in 45 SUD cases. Re-analysis of the exome data according to the current ACMG guidelines identified 14 pathogenic or likely pathogenic variants in 10 (22.2%) out of the 45 SUD cases, whereof 2 (4.4%) individuals had variants with likely functional effects in the channelopathy-associated genes SCN5A and TRDN and 1 (2.2%) individual in the cardiomyopathy-associated gene DTNA. In addition, 18 structural variants (SVs) were identified in 15 out of the 45 individuals. Two SVs with likely functional impairment were found in the coding regions of PDSS2 and TRPM4 in 2 SUD cases (4.4%). Both were identified as heterozygous deletions, which were confirmed by multiplex ligation-dependent probe amplification. In conclusion, our findings support that SVs could contribute to the pathology of the sudden death event in some of the cases and therefore should be investigated on a routine basis in suspected SUD cases.

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