The association of serotonin reuptake inhibitors and benzodiazepines with ictal central apnea

Lacuey, Nuria; Martins, Renato; Vilella, Laura; Hampson, Johnson P.; Rani, M.R. Sandhya; Zaremba, Anita; Hampson, Jaison; Sainju, Rup K.; Friedman, Daniel; Nei, Maromi; Scott, Catherine; Gehlbach, Brian K.; Hupp, Norma J.; Schuele, Stephan; Ogren, Jennifer A.; Harper, Ronald M.; Allen, Luke; Diehl, Beate; Bateman, Lisa M.; Devinsky, Orrin; Lhatoo, Samden D.

doi:10.1016/j.yebeh.2019.06.029

Cited by 28 publications

(38 citation statements)

References 55 publications

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“…Risk of PIH is mostly associated with generalized convulsive seizures 8,9 and temporal lobe epilepsy 6–8 . However, a relation with molecular pathways involved in the regulation of breathing has also been reported, especially serotonin, 13,22,23 in line with data reporting alteration of these neuronal groups in the medulla of patients who died from SUDEP 12 . Using cross‐sectional analysis of data collected in patients suffering from drug‐resistant focal epilepsy undergoing long‐term EEG monitoring, we found a significant association between risk of PIH and coffee consumption.…”

Section: Discussionsupporting

confidence: 76%

Relation between coffee consumption and risk of seizure‐related respiratory dysfunction in patients with drug‐resistant focal epilepsy

et al. 2021

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Objective Caffeine is an antagonist of the adenosine pathway, which is involved in regulation of breathing. Extracellular concentrations of adenosine are increased in the immediate aftermath of a seizure. Seizure‐related overstimulation of adenosine receptors might promote peri‐ictal apnea. However, the relation between caffeine consumption and risk of seizure‐related respiratory dysfunction in patients with drug‐resistant focal epilepsy remains unknown. Methods We performed a cross‐sectional analysis of data collected in patients included in the SAVE study in Lyon's epilepsy monitoring unit at the Adult Epilepsy Department of the Lyon University Hospital between February 2016 and October 2018. The video‐electroencephalographic recordings of 156 patients with drug‐resistant focal epilepsy included in the study were reviewed to identify those with ≥1 focal seizure (FS), valid pulse oximetry (SpO2) measurement, and information about usual coffee consumption. This latter was collected at inclusion using a standardized self‐questionnaire and further classified into four groups: none, rare (≤3 cups/week), moderate (4 cups/week to 3 cups/day), and high (≥4 cups/day). Peri‐ictal hypoxemia (PIH) was defined as SpO2 < 90% for at least 5 s occurring during the ictal period, the post‐ictal period, or both. Results Ninety patients fulfilled inclusion criteria, and 323 seizures were analyzed. Both the level of usual coffee consumption (p = .033) and the level of antiepileptic drug withdrawal (p = .004) were independent risk factors for occurrence of PIH. In comparison with FS in patients with no coffee consumption, risk of PIH was four times lower in FS in patients with moderate consumption (odds ratio [OR] = .25, 95% confidence interval [CI] = .07–.91, p = .036) and six times lower in FS in patients with high coffee consumption (OR = .16, 95% CI = .04–.66, p = .011). However, when PIH occurred, its duration was longer in patients with moderate or high consumption than in those with no coffee consumption (p = .042). Significance Coffee consumption may be a protective factor for seizure‐related respiratory dysfunction, with a dose‐dependent effect.

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Section: Discussionsupporting

confidence: 76%

Relation between coffee consumption and risk of seizure‐related respiratory dysfunction in patients with drug‐resistant focal epilepsy

et al. 2021

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“…Likewise, duration of PGES was inversely correlated with interictal serotonin blood levels, prompting the hypothesis that blood serotonin levels play a role in shaping seizure features or may partly reflect serotonin levels in the CNS [51]. The hypothesis that serotonin levels have an impact on seizure features is further supported by the observation that patients taking SRIs display less frequently ICA, and patients on chronic treatment with benzodiazepines have shorter ICA and PGES durations [52,53]. Recently, possible associations between obstructive sleep apnea and SUDEP risk were also discussed [54].…”

Section: Seizure-related Respiratory Dysfunction and Deficits In Serotoninergic Signalingmentioning

confidence: 94%

Prevention of sudden unexpected death in epilepsy: current status and future perspectives

Pensel

Nass

Taubøll

et al. 2020

Expert Review of Neurotherapeutics

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Sudden unexpected death in epilepsy (SUDEP) affects about 1 in 1000 people with epilepsy, and even more in medically refractory epilepsy. As most people are between 20 and 40 years when dying suddenly, SUDEP leads to a considerable loss of potential life years. The most important risk factors are nocturnal and tonic-clonic seizures, underscoring that supervision and effective seizure control are key elements for SUDEP prevention. The question of whether specific antiepileptic drugs are linked to SUDEP is still controversially discussed. Knowledge and education about SUDEP among healthcare professionals, patients and relatives are of outstanding importance for preventive measures to be taken, but still poor and widely neglected.

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“…Regarding potential SUDEP risk factors, we found similar frequencies of GTCS, polytherapy, sex and ASM adherence in PWE and SUDEP cases, as previously reported. 5 , 7–9 The significantly younger age at death in SUDEP cases and positive correlation of age at death and epilepsy onset was reported. 5 We found a significant negative correlation of brain weight and epilepsy duration in SUDEP cases, that was present but not significant in PWE cases.…”

Section: Discussionmentioning

confidence: 91%

“… 1 , 10–14 After a GTCS, a prolonged postictal EEG suppression (PGES) may occur, in which many patients are unresponsive, have impaired respiration and autonomic function (e.g. postictal central apnea 15–17 and hypoxia 18 , 19 ), and diffusely attenuated EEG that reflects profound cerebral dysfunction. 20 , 21 Suppression of respiration and arousal during PGES, combined with a prone, face-down position increased SUDEP risk in some, 20 but not in all studies.…”

Section: Introductionmentioning

confidence: 99%

Neuropathology in the North American sudden unexpected death in epilepsy registry

Leitner

Faustin

Verducci³

et al. 2021

Brain Communications

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Sudden unexpected death in epilepsy is the leading category of epilepsy-related death and the underlying mechanisms are incompletely understood. Risk factors can include a recent history and high frequency of generalized tonic-clonic seizures, which can depress brain activity postictally, impairing respiration, arousal, and protective reflexes. Neuropathological findings in sudden unexpected death in epilepsy cases parallel those in other epilepsy patients, with no implication of novel structures or mechanisms in seizure-related deaths. Few large studies have comprehensively reviewed whole brain examination of such patients. We evaluated 92 North American Sudden unexpected death in epilepsy Registry cases with whole brain neuropathological examination by board-certified neuropathologists blinded to the adjudicated cause of death, with an average of 16 brain regions examined per case. The 92 cases included 61 sudden unexpected death in epilepsy (40 definite, 9 definite plus, 6 probable, 6 possible) and 31 people with epilepsy controls who died from other causes. The mean age at death was 34.4 years and 65.2% (60/92) were male. The average age of death was younger for sudden unexpected death in epilepsy cases than for epilepsy controls (30.0 versus 39.6 years; p = 0.006), and there was no difference in sex distribution respectively (67.3% male versus 64.5%, p = 0.8). Among sudden unexpected death in epilepsy cases, earlier age of epilepsy onset positively correlated with a younger age at death (p = 0.0005) and negatively correlated with epilepsy duration (p = 0.001). Neuropathological findings were identified in 83.7% of the cases in our cohort. The most common findings were dentate gyrus dysgenesis (sudden unexpected death in epilepsy 50.9%, epilepsy controls 54.8%) and focal cortical dysplasia (sudden unexpected death in epilepsy 41.8%, epilepsy controls 29.0%). The neuropathological findings in sudden unexpected death in epilepsy paralleled those in epilepsy controls, including the frequency of total neuropathological findings as well as the specific findings in the dentate gyrus, findings pertaining to neurodevelopment (e.g. focal cortical dysplasia, heterotopias), and findings in the brainstem (e.g. medullary arcuate or olivary dysgenesis). Thus, like prior studies, we found no neuropathological findings that were more common in sudden unexpected death in epilepsy cases. Future neuropathological studies evaluating larger sudden unexpected death in epilepsy and control cohorts would benefit from inclusion of different epilepsy syndromes with detailed phenotypic information, consensus among pathologists particularly for more subjective findings where observations can be inconsistent, and molecular approaches to identify markers of sudden unexpected death in epilepsy risk or pathogenesis.

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The association of serotonin reuptake inhibitors and benzodiazepines with ictal central apnea

Cited by 28 publications

References 55 publications

Relation between coffee consumption and risk of seizure‐related respiratory dysfunction in patients with drug‐resistant focal epilepsy

Relation between coffee consumption and risk of seizure‐related respiratory dysfunction in patients with drug‐resistant focal epilepsy

Prevention of sudden unexpected death in epilepsy: current status and future perspectives

Neuropathology in the North American sudden unexpected death in epilepsy registry

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