sudden unexplained nocturnal death syndrome symptoms

Then, the medication-induced SDS may appear. 2 the disease is termed "bangungut" in philippines, 1 "lai tai" in thailand, 2 (A) SSCP analysis demonstrates an abnormal conformer in the affected individual. Figure 1. To accurately define the cardiac abnormalities underlying SUNDS, 18 hearts collected from these SUNDS cases were reevaluated by Kirschner etal.20 They found that 17/18 had cardiac conduction system (CCS) anomalies and 14 hearts had persistent fetal dispersion of the atrial ventricular node within the central fibrous body of the atrial ventricular septum under microscopic examination. Impact of Obstructive Sleep Apnea On In-Hospital Outcomes in Patients With Atrial Fibrillation: A Retrospective Analysis of the National Inpatient Sample, Sudden cardiac death during nighttime hours, Sudden Unexplained Nocturnal Death Syndrome: Epidemiological and Morphological Characteristics in Thai Autopsy Cases, Nocturnal ventricular arrhythmias are associated with the severity of cardiovascular autonomic neuropathy in type 2 diabetes, Maladaptive Alterations of Autonomic Nerve System in Cardiovascular Disorders, Ethnic differences in patients with Brugada syndrome and arrhythmic events: New insights from Survey on Arrhythmic Events in Brugada Syndrome, Creative Commons AttributionNonCommercial, sudden unexplained nocturnal death syndrome, 2563y old SCD at night or during sleep You can learn more about how we ensure our content is accurate and current by reading our. A series of 44 autopsies performed on sudden unexplained nocturnal death syndrome victims in the northern region of Thailand showed variations in the time of death ranging from midnight to 6:00 AM. Both A735V and R1193Q, also observed in BrS, could cause reduced INa. If you need to go back and make any changes, you can always do so by going to our Privacy Policy page. An ambulance transported him to the hospital, and he was found to be in cardiac arrest. Association of common variants in NOS1AP gene with sudden unexplained nocturnal death syndrome in the southern Chinese Han population. Healthline Media does not provide medical advice, diagnosis, or treatment. Furthermore, most of these variants detected in SUNDS are not pathogenic in ClinVar interpretation while compound variants are detected in nearly 1/3 cases, suggesting that compound multigenic variations other than monogenic mutation might be the underlying genetic basis of SUNDS. SUNDS indicates sudden unexplained nocturnal death syndrome. In near-miss cases or in the related Brugada syndrome, anesthesia seems to be safe, but extra caution needs to be exercised when using propofol infusions. The dashed line 3 ms after the beginning of the pulse indicates the timing of peak transient outward current. (B and C) Current decay was fitted to a sum of two exponentials and the fast and slow time constants of each parameter were plotted against the membrane potential. The third mutation, R1193Q, located in DIII, accelerated the decay of INa. Sudden unexplained nocturnal death syndrome results in death. Many cases of SDS arent properly diagnosed, either. When fatal CCS abnormality was observed, we adopted a definite diagnosis, instead of SUNDS, as the cause of death. Nitric oxide synthase 1 adaptor protein (NOS1AP), a regulator of neuronal nitric oxide synthase, interacts with neuronal nitric oxide synthase or ion channels (especially potassium channels). However, patients enrolled in this study were more likely to be diagnosed as BrS. (C) DHPLC confirms an abnormal band migration in affected individuals. A case-control study of sudden unexplained nocturnal death syndrome in the southern Chinese Han population. Sudden unexplained nocturnal death syndrome has been identified in Southeast Asian male refugees, primarily the Hmong people, settling in the United States since 1975 and was the chief cause of death among these male refugees in the early 1980s, which was the peak time of Southeast Asian immigration to the United States (31). At 3.5years after migration, all of these symptoms improved, and so did the occurrence of SUNDS.40 Victims discovered in the night terrors are unarousable, and in the few successfully aroused patients, terrifying dreams were often experienced.40 In addition, frequent experiences of dab tsog (frightening night spirit pressing on chest), nightmares, sleep paralysis, and hypnogogic hallucinations still exist in Hmong after immigrating to the United States for decades, probably putting Hmong at high risk for SUNDS.41 The hypothesized mechanism is that night terrors cause sympathetic discharge, resulting in increased cardiac vulnerability to VA in patients with cardiac conduction defects.40, Nakajima etal observed elevated plasma remnant lipoprotein levels and narrowed circumferences of coronary arteries in PDS cases.2 They proposed the hypothesis that elevated plasma remnant lipoprotein levels might impair endotheliumdependent vasorelaxation in narrowed coronary arteries as an early event, and activated LOX1 receptor and Rhokinase pathway in smooth muscle cells then cause coronary artery vasospasm and cardiac arrest. Wu Q, Zhao Q, Yin K, Hu BJ, Cheng J. HCN4 gene variations in sudden unexplained nocturnal death syndrome in the southern Han Chinese population. Combining all these studies, we propose an assumption that SUNDS is a multigenic disorder and a subtype or early stage of cardiomyopathies. Pappone C, Santinelli V. Brugada syndrome: progress in diagnosis and management. However, no putative pathogenic mutations were found in SCN1BSCN4B, MOG1, or GPD1L, except for 2 rare nonsynonymous variants (V138I and T189M) on SCN1B and 1 (A195T) on SCN3B. Local Info The presence of syncopal episodes, a history of familial sudden death, or late potentials may increase its value. Seven forms of congenital long QT syndrome have been identified related to mutations in the ion channel. Customer Service On the other hand, a prospective multicenter registry proved that the clinical screening of the relatives of young subjects who died of sudden cardiac death due to general causes provided a diagnosis in 25% of the cases (19). Plakophilinshard work in the desmosome, recreation in the nucleus? Among these 33 genes, channelopathies and cardiomyopathiesassociated variants seem to share equal proportions in SUNDS. Currently there are 33 genes and nearly 100 variations and polymorphisms potentially associated with SUNDS. Epilepsy. Our website services, content, and products are for informational purposes only. Others risk factors, such as excessive vanadium intake, inhibition of Na, KATPase and H, KATPase activity,43 rapid eye movement bursts,14, 44 plasma testosterone,45 epilepsy,46, 47 diabetes mellitus,48 melioidosis bacteria,49 toxic shock,50 etc, may also be involved in the pathogenesis of SUNDS. Also, mutations of desmoplakin or the DSP gene seem to confer a higher risk for sudden unexplained nocturnal death syndrome in this population (29). Int J Cardiol 2017;226:87-92. et al. Although a mutation of SCN10A accounts for another 3% of sudden unexplained nocturnal death syndrome cases in this population, polymorphisms of the NOS1AP gene have also been associated with sudden unexplained nocturnal death syndrome among the Han Chinese, with some variations being protective and others conferring a higher risk for the condition (11; 28). In unexplained nocturnal death syndrome survivors and first-degree relatives, ECG with special right ventricular leads shows evidence of RSR' and ST elevation in leads V1 to V3, a pattern present in the genetically related Brugada syndrome. (, Bowles,K.R., Abraham,S.E., Brugada,R., Zintz,C., Comeaux,J., Sorajja,D., Tsubata,S., Li,H., Brandon,L., Gibbs,R.A. Current traces shown in (AD) were elicited by potential steps from 40 to +10 mV in 5 mV increments. This concept has become essential to explain the overlapping of 2 inherited diseases based on disturbance of the ID: arrhythmogenic cardiomyopathy (ACM) and BrS.71 ACM is considered to be a cardiac structural disease with monomorphic arrhythmias, whereas BrS is considered to be a typical electrical disorder without (or with only mild) structural abnormalities. Forensic Sci Int 2014;236:38-45. J Am Heart Assoc 2018;7(5). Currents were amplified by a Warner oocytes clamp (OC-725A), low-pass filtered at 3 kHz (3 dB, 4 pole Bessel filter, Wavetech, Model 432). However, doctors are torn about using treatment for SDS in a person who hasnt shown any symptoms. Considering the risk factors of SUNDS, they postulated that eating excessive carbohydrate or other physical and mental stress stimulated the shift of potassium into cells at night, thus resulting in a disturbance in potassium homoeostasis, which contributed to sudden VA death.27, 28, 29, From the above epidemiological studies, we can see that hypoxemia, caused by these respiratory signs (tachypnea, groan, gasping, and snoring), often appears before death. The final pathway of SUNDS is commonly accepted as lethal ventricular arrhythmia. The rapid depolarizing electrical impulse propagation is dependent on a highly specialized structure called intercalated disc (ID). Curr Opin Cardiol 2010;25(1):59-64. The variant I208I had a significantly lower MAF in the East Asian population than in SUNDS, suggesting that allele T of this SNP might be a SUNDS risk allele.84, Vinculin (VCL) is a membranecytoskeletal protein that connects integrin adhesion molecules to the actin cytoskeleton to form adhesion junctions at ID.85 Several mutations in VCL have been identified to be pathogenic for dilated cardiomyopathy or hypertrophic cardiomyopathy.86 We identified a rare variant M94I in 1/44 SUNDS cases39 and an East Asian common variant D841H in 8/120 SUNDS cases.87 Coexpression of Nav1.5 with M94IVCL showed a reduction in peak INa and a further reduction in acid conditions. SCN5A mutations have also been associated with more severe conduction abnormalities and higher risk for future cardiac events in Brugada Syndrome (26). American Academy of Sleep Medicine. Disruption of either action potential or propagation can result in potentially lethal arrhythmia.100 Hence, mutations in ion channels or structure proteins can cause SCD. Anyone at any age and in any state of health can have SDS. Soon after, van den Berg etal reported another SCN5A mutation (1795insD) in a large family characterized by nocturnal SCD. What should I do if I forget to take my anti-seizure drug? The authors are grateful to Melba Koegele, Yue-Sheng Wu, Stacy Scicchitano and Elena Burashnikov for expert technical assistance. Further studies are needed on the role of XIRP in sudden unexplained nocturnal death syndrome; however, rare variants of XIRP may be the reason behind many unexplained cases of sudden unexplained nocturnal death syndrome and Brugada syndrome (10). Figure 7. (, Wang,D.W., Makita,N., Kitabatake,A., Balser,J.R. Mutations of sodium channel resulting in decreased sodium current (INa) and increased or prolonged late sodium current (INaL) have been proven to be associated with BrS and long QT syndrome type 3, respectively.53, 54 Similar to SUNDS, both BrS and long QT syndrome type 3 tend to experience cardiac events at rest or during sleep. Dallas, TX 75231 Tomson T, Nashef L, Ryvlin P. Sudden unexpected death in epilepsy: current knowledge and future directions. SUNDS, then, is not identical to BrS in epidemiology, pathology, phenotype, and molecular genetics, but closely related with cardiomyopathy in genetics. However, current evidence cannot support or disprove our hypothesis. Two SNPs (11413C>A and C3269>T) of SCN5A showed significant differences in genotype or allele frequencies between SUNDS and controls.57 However, H558R and R1193Q, which were previously reported to be associated with BrS and SUNDS, did not have significant difference in this cohort.32, 58 We further conducted a targetcaptured nextgeneration sequencingbased (NGS) study on 44 consecutive individuals who had SUNDS to study 80 channelopathy and cardiomyopathyrelated genes, and a variant (V1340I) on SCN5A was detected in 1 case.25, Besides Nav1.5, another tetrodotoxinsensitive Na+ channel, Nav1.8, encoded by SCN10A, was also reported to be associated with BrS.59SCN10A, located adjacent to SCN5A, also has a structure and amino acid sequences similar to Nav1.5 (Figure2B).60 We detected 6 rare variations and 16 common SNPs on SCN10A in 105 SUNDS cases. 1 the syndrome is featured by predominance of healthy young males without significant medical history, who suddenly die during sleep. In addition to these risk factors, certain medical conditions can increase the risk of SDS, such as: Its important to note that despite these identified risk factors, they dont mean you have SDS. what to wear to moulin rouge broadway . For some people living with epilepsy, the risk of Sudden Unexpected Death in Epilepsy (SUDEP) is an important concern. Identification of rare variants of DSP gene in sudden unexplained nocturnal death syndrome in the southern Chinese Han population. In comparison, in a literature review conducted recently, sudden cardiac death in nighttime hours was more likely to be found among female patients (20). A 2sided P<0.05 was considered significant. Based on this strict criterion, we collected 148 consecutive SUNDS cases for 17years to investigate the pathological differences between SUNDS and controls. Familial SUNDS cases might carry ultrarare variants that confer them genetic susceptibility. Of the 6 rare variations, only 1 nonsense variant (R1263*) was novel. Menopause doesnt cause heart disease but it may increase your risk. Apparent sleep terrors have been reported to occur frequently in subsequent victims of sudden unexplained nocturnal death syndrome. It has been shown that recent exposure to carbon monoxide and nitrogen dioxide, even for a short term, was found to significantly increase the risk of SIDS in the postneonatal period; therefore, reducing the exposure of infants to pollutants may provide a new way to reduce the risk of SIDS (03). Childhood Degenerative & Metabolic Disorders, News releases, announcements, interviews and other supplemental content of neurologic interest, Featuring clinician-investigators who have made extraordinary contributions to neurology. These cookies perform functions like remembering presentation options or choices and, in some cases, delivery of web content that based on self-identified area of interests. Three of 10 families had identified SCN5A mutations, namely, R367H, A735V, and R1192Q (now termed R1193Q). Interestingly, V95ISCN5A and T189MSCN1B were detected in the same individual. et al. We screened 29 of the 105 coding exons on the RyR2 gene previously reported to be associated with catecholaminergic polymorphic ventricular tachycardia and arrhythmogenic right ventricular cardiomyopathy in 127 sporadic Chinese SUNDS cases. Because SDS is often misdiagnosed or not diagnosed at all, its unclear how many people have it. (B) Sequence analysis demonstrates a GA substitution nucleotide 3727, which results in substitution of arginine by glutamine at codon 1192 (R1192Q). and Wilde,A.A. Sudden cardiac death is a leading cause of mortality worldwide with an estimated 15% to 20% of all deaths and mostly occurs in older adults with acquired structural heart disease. Two rare missense variants (R14H and F386C) were predicted as likely pathogenic, while the remaining 3 (R817Q, T1181M, and P1683S) were benign. It is preferred that the dose be low and the duration short. Han Chinese have lower rates of SUNDS, likely because of our stricter inclusion criteria. A heterozygous mutation causing R1193Q polymorphism (amino acid substitution) has also been described (14). (, Dumaine,R., Wang,Q., Keating,M.T., Hartmann,H.A., Schwartz,P.J., Brown,A.M. Cookies used to make website functionality more relevant to you. Pyrogenic toxins of Staphylococcus aureus have also been implicated in some cases. First, SUNDS is mostly identified in people younger than 60years old, because structural changes caused by arrhythmogenic cardiomyopathy are more apparent in people over 60years old and can be diagnosed after routine postmortem autopsy. Cheng J, Kyle J, Lang D, et al. (, Rook,M.B., Alshinawi,C.B., Groenewegen,W.A., van Gelder,I.C., vanGinneken,A.C., Jongsma,H.J., Mannens,M.M. Last medically reviewed on June 13, 2019. Here, we focus on a specific SUD called sudden unexplained nocturnal death syndrome (SUNDS) and attempt to provide a comprehensive understanding of SUNDS. They can help you process the news and cope with changes in your medical status. (A) Current traces from WT and A735V during a test pulse to 30 mV were normalized to their respective maximal currents and superimposed. and Misaki,M. The total yields of variants in SUNDS cases was substantially higher than in East Asian (107.11% versus 13.68% or 14.37%), and the yield in SUNDS exceeds the value of 100% because of the compound variants in 1 case. Is sudden unexplained nocturnal death a breathing disorder? On the one hand, according to a postmortem study using whole-exome sequencing, screening for TTN mutations could improve the molecular diagnosis of this condition (22). Although silico prediction showed that A159T or G265E alone did not damage the function of PKP2, the effect of the compound mutation is still unknown. The word Lai in Laotian means a loud groan occurring during sleep or a loud noise made while frightened and Tai is a Thai word meaning death. Avoid seizure triggers, if these are known. JeffreyA.Towbin, MD is supported by the Texas Childrens Hospital Foundation Chair in Pediatric Cardiovascular Research. In Thailand, sudden unexplained nocturnal death syndrome is called Lai Tai ("sleep death"); and in the Philippines it is called Bangungut. Clinical yield of familial screening after sudden death in young subjects: The French experience. Cardiac channel molecular autopsy: insights from 173 consecutive cases of autopsy-negative sudden unexplained death referred for postmortem genetic testing. A study that included the largest sudden unexplained nocturnal death syndrome cohort to date has found a new possible factor, XIRP, in the pathogenesis of sudden unexplained nocturnal death syndrome (10). Perez-Riera AR, Barbosa-Barros R, Shenasa M. electrocardiographic markers of sudden cardiac death (including left ventricular hypertrophy). Currents were recorded at room temperature, and experiments in which the holding current was >200 nA at a holding potential of 90 mV were excluded from analysis. Specially trained cardiologists can look at the ECG results and identify possible problems, such as long QT syndrome, short QT syndrome, arrhythmia, cardiomyopathy, and more. All the variants detected in SUNDS cases are categorized as 3 major types: the novel mutations absent in all public databases; the rare variants with a minor allele frequency (MAF) 0.01 in the homologous population; and common single nucleotide polymorphisms (SNPs) with a MAF >0.01. Proteintoprotein interaction of the 33 genes responsible for SUNDS. implantable cardioverter defibrillator (ICD), rarediseases.org/rare-diseases/brugada-syndrome/, jems.com/articles/print/volume-40/issue-1/features/five-common-causes-sudden-unexpected-dea.html, nhlbi.nih.gov/health-topics/long-qt-syndrome, ghr.nlm.nih.gov/condition/short-qt-syndrome, heart.org/-/media/data-import/downloadables/pe-abh-what-is-arrhythmia-ucm_300290.pdf, Risk of Sudden Cardiac Death Nearly 3 Times Higher for Black Women, How Higher Intensity Exercise Can Improve Your Heart Health, What to Know About Menopause and the Risk of Heart Disease. (A)Currentvoltage relationship (IV) of WT (squares, n = 6) and A735V (circles, n = 8) obtained from current recordings as illustrated in Figure 5. Sudden cardiac death (SCD) is a leading cause of mortality worldwide with an estimated 15% to 20% of all deaths. In central China, the male to female ratio was 14 to 1 in the high-risk age group of 30 to 39 years of age, and overall it was 4 to 1 (04). We conducted a study with 123 sporadic SUNDS cases to screen SCN5A in the Han population of China. and Antzelevitch,C. Some types of heart block are minor, while other types are much more serious. Sudden unexplained nocturnal death syndrome predominantly affects previously healthy, young adult Southeast Asian males, who die suddenly during sleep. Refugee Resettlement Program. If the ECG isnt clear or the cardiologist would like additional confirmation, they may also request an echocardiogram. Others may be the result of irregularities within the electrical channels. Considering that BrS can cause SCD in nocturnal sleep, we postulate that the families included in SUNDS studies are most likely BrS patients. In epidemiology, only rare SUNDS cases have family history, while nearly 40% of BrS is familial,99 implying that there are different degrees of genetic and environmental contribution to the 2 disorders. Huang L, Tang S, Peng L, Chen Y, Cheng J. Molecular autopsy of desmosomal protein plakophilin-2 in sudden unexplained nocturnal death syndrome. Department of Forensic Pathology, Zhongshan School of Medicine, Sun Yatsen University, Guangzhou, China. Biophysical analysis in Xenopus oocytes showed that R367H mutation, located in the P loop between DIS5 and DIS6, did not express any inward current and the peak INa was thought to be decreased because of the loss of 1 functional allele. A genotyping result of the 4 LQTSsusceptibility genes was obtained by us, in which 14 rare genetic variants were identified but only 2 mutations were nonsynonymous: F54V in the KCNE1 gene, and a terminator codon mutation *124R of KCNE2 gene. (, Antzelevitch,C., Brugada,P., Brugada,J., Brugada,R., Nademanee,K. In addition, XIRP2 was associated with important cardiac ion channel components, Nav1.5 and Kv1.5. Sudden unexpected death in children: myth or reality? Therefore, altered sodium current caused by mutation on SCN5A or SCN1BSCN4B might explain some SUNDS. In this article, the authors discuss sudden unexplained nocturnal death syndrome. HCN4 variations could induce critical arrhythmias and contribute to the development of sudden unexplained nocturnal death syndrome. In (C), all values were statistically different (P < 0.01 except at 10 mV). Among these genes, DSP and SCN5A seem to be closely related with SUNDS with higher yields than others. Some people die as a result of it. A, Cardiac sodium channel comprises a poreforming ionconducting subunit Nav1.5 and ancillary subunits. You can review and change the way we collect information below. Only 2 novel synonymous but no nonsynonymous variants were identified.69 These results suggested that RyR2 may not be a key susceptible gene for Chinese SUNDS. There is a hypothesis that sudden unexplained nocturnal death syndrome will only occur if three factors present simultaneously during nocturnal sleep: a) carriers of genes that confer higher susceptibility of sudden unexplained nocturnal death syndrome, b) stressors caused by environmental or social factors, and c) disturbance in action potential production and propagation in nocturnal sleep (31). (, Dumaine,R., Towbin,J.A., Brugada,P., Vatta,M., Nesterenko,D.V., Nesterenko,V.V., Brugada,J., Brugada,R. Extensive studies are needed to prove or disprove our hypothesis. Released in 2014, The International Classification of Sleep Disorders, 3rd edition, no longer has diagnostic criteria for sudden unexplained nocturnal death syndrome (01). SCD during sleep or nap One individual merely carried a mutation of F1465L on CACNA1C, which was deleterious by Condel prediction and absent in all public databases, implying that the mutation was responsible for his death. The detected variant would decrease the expression of Conexin 43 (CX43) GJ channels, thus, very likely causing electrical coupling disorder of cardiac muscle cells and leading to sudden death (24). Leg Med (Tokyo) 2012;14(6):317-9. The variants severely damage the action potential production and propagation, and slight stressors can trigger lethal arrhythmia. Sudden unexpected death in epilepsy. The differential diagnosis includes: idiopathic ventricular fibrillation that occurs at night and without prodromal symptoms, death caused by REM sleep-related sinus arrest, REM sleep-related myocardial infarction, obstructive sleep apnea, sudden unexplained death in epilepsy that usually occurs in sleep, pulmonary hypertension in central sleep apnea, and Brugada syndrome, an inherited cardiac conduction defect that is genetically linked to both sudden unexplained nocturnal death syndrome and sudden infant death syndrome. In northeastern Thailand, the estimated annual rate of death from sudden unexplained nocturnal death syndrome among men 20 to 49 years of age was found to be 25.9 per 100,000 person-years in one study and 38 per 100,000 person-years in another study, indicating that sudden unexplained nocturnal death syndrome is one of the leading causes of death in young men in that region. On the other hand, a study in young, healthy Thai male university students demonstrated that individuals from rural (compared to urban) areas display decreased sympathetic and increased parasympathetic responses to cold and saline loading stressors. Figure 9. Chanavirut R, Tong-un T, Jirakulsomchok D, Wyss JM, Roysommuti S. Abnormal autonomic nervous system function in rural Thai men: A potential contributor to their high risk of sudden unexplained nocturnal death syndrome. As no pathogenic rare variants in 80 arrhythmiaassociated genes were found in the SCN10A variation carriers, R1263* was thought to be the putative pathogenic mutation. and Le Marec,H. SUNDS is a multifactorial disorder with racial and ethnic disparities in incidence, affected by susceptible variants and stressors caused by environmental and social factors. To better understand SUNDS, we conduct this comprehensive review and outline an academic history of SUNDS over the past 100years, including epidemiology, pathology, and pathogenetic hypotheses, particularly the molecular genetics of SUNDS. Deaths occurred more often during May and there were a few cases of respiratory difficulty, seizures, and urinary incontinence before death. Subtle cardiac structural changes (increased heart weight and enlarged heart size) may also be potential but unnecessary structure substrates for SUNDS. postmortem autopsy Negative, Choking, gurgling, gasping, or labored respirations, without wheezing or stridor, 2154y old In this review, we summarize the molecular genetic studies of SUNDS. and Kirsch,G.E. We conducted the first epidemiological survey of SUNDS in China in 2002 on peasantderived workers in Dongguan city.17 Since then, we have been collecting SUNDS cases and making a series of epidemiological reports on SUNDS.3, 13, 18, 19 Based on autopsy data collected in the city of Dongguan, and the Bao'an and Longgang Districts of the city of Shenzhen from 2001 to 2006, an incidence of 1/100000 was obtained for SUNDS3 and confirmed by our following study based on data collected from 2007 to 2013.13 These surveys demonstrate similar characteristics of SUNDS: (1) The highestrisk age was 30years old, and >80% of victims were 21 to 40years old; (2) More than 97% were bluecollar workers (poorly educated workers engaged in manual labor, such as construction workers); (3) The monthly distribution of SUNDS was positively correlated with monthly emergency fever cases with peak rates in April to June; (4)Family history of SUNDS was rarely observed; (5) Seventyfive percent of witnessed cases occurred with respiratory signs, abrupt tic, and other manifestations before death; (6) Seventy percent of witnessed cases died between 0:00 and 4:00am3, 13 (Table1). Figure 4. Saving Lives, Protecting People, Read SUDEP information for parents of children with epilepsy, National Center for Chronic Disease Prevention and Health Promotion, Sudden Unexpected Death in Epilepsy (SUDEP), Epilepsy Can Follow Traumatic Brain Injury, U.S. Department of Health & Human Services. Moreover, a few SUDs could be explained by the lethal CCS anomalies observed with this method.23 Since then, the examination of CCS has been incorporated in our routine postmortem examinations.

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