Refractory epilepsy and obstructive sleep apnea: is there an association?

Rashed, H.; Tork, Mohamad A.; Elnabil, L.; Ahmed, Nahed S.; Abdelhady, Salem; Abdulghani, Khaled O.; Abdul‐Ghani, Mohammad

doi:10.1186/s41983-019-0072-0

Cited by 5 publications

(3 citation statements)

References 29 publications

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“…There is also increasing evidence that treatment of OSA leads to better seizure control among patients with DRE ( Rashed et al, 2019 ). However, this has not been specifically addressed for TLE.…”

Section: Resultsmentioning

confidence: 99%

Sleep and Temporal Lobe Epilepsy – Associations, Mechanisms and Treatment Implications

Garg

Charlesworth

Shukla

2022

Front. Hum. Neurosci.

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In this systematic review, we aim to describe the association between temporal lobe epilepsy (TLE) and sleep, with bidirectional links in mechanisms and therapeutic aspects. Sleep stages may variably impact seizure occurrence, secondary generalization and the development, frequency and distribution of interictal epileptiform discharges. Conversely, epilepsy affects sleep micro- and macroarchitecture. TLE, the most frequent form of drug resistant epilepsy (DRE), shares an enduring relationship with sleep, with some intriguing potential mechanisms specific to anatomic localization, linking the two. Sleep characteristics of TLE may also inform localizing properties in persons with DRE, since seizures arising from the temporal lobe seem to be more common during wakefulness, compared to seizures of extratemporal origin. Polysomnographic studies indicate that persons with TLE may experience excessive daytime somnolence, disrupted sleep architecture, increased wake after sleep onset, frequent shifts in sleep stages, lower sleep efficiency, decreased rapid eye movement (REM) sleep, and possibly, increased incidence of sleep apnea. Limited literature suggests that effective epilepsy surgery may remedy many of these objective and subjective sleep-related concerns, via multipronged effects, apart from reduced seizure frequency. Additionally, sleep abnormalities also seem to influence memory, language and cognitive-executive function in both medically controlled and refractory TLE. Another aspect of the relationship pertains to anti-seizure medications (ASMs), which may contribute significantly to sleep characteristics and abnormalities in persons with TLE. Literature focused on specific aspects of TLE and sleep is limited, and heterogeneous. Future investigations are essential to understand the pathogenetic mechanisms linking sleep abnormalities on epilepsy outcomes in the important sub-population of TLE.

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Section: Resultsmentioning

confidence: 99%

Sleep and Temporal Lobe Epilepsy – Associations, Mechanisms and Treatment Implications

Garg

Charlesworth

Shukla

2022

Front. Hum. Neurosci.

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“…In addition, we think that up-state dependent synaptic potentiation in cortical neurons during NREM sleep contributes to underlying cellular mechanisms 41 for this operational mechanism leading to sleep-related epilepsy incidence in animal models and human patients. As the subcortical POA functions as the sleep switch 2 , this operational mechanism can underlie sleep-related epilepsy incidence in refractory epilepsy 14,61,62 . Beyond this, this mechanism suggests the translational implication in epilepsy field.…”

Section: Discussionmentioning

confidence: 99%

Preoptic area controls sleep-related seizure onset in a genetic epilepsy mouse model

Potesta,

Cargile,

Yan

et al. 2023

Preprint

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In genetic and refractory epileptic patients, seizure activity exhibits sleep-related modulation/regulation and sleep and seizure are intermingled. In this study, by using one hetGabrg2Q390XKI mice as a genetic epilepsy model and optogenetic methodin vivo, we found that subcortical POA neurons were active within epileptic network from the hetGabrg2Q390XKI mice and the POA activity preceded epileptic (poly)spike-wave discharges(SWD/PSDs) in the hetGabrg2Q390XKI mice. Meanwhile, as expected, the manipulating of the POA activity relatively altered NREM sleep and wake periods in both wt and the hetGabrg2Q390XKI mice. Most importantly, the short activation of epileptic cortical neurons alone did not effectively trigger seizure activity in the hetGabrg2Q390XKI mice. In contrast, compared to the wt mice, combined the POA nucleus activation and short activation of the epileptic cortical neurons effectively triggered or suppressed epileptic activity in the hetGabrg2Q390XKI mice, indicating that the POA activity can control the brain state to trigger seizure incidence in the hetGabrg2Q390XKI micein vivo.In addition, the suppression of POA nucleus activity decreased myoclonic jerks in theGabrg2Q390XKI mice. Overall, this study discloses an operational mechanism for sleep-dependent seizure incidence in the genetic epilepsy model with the implications for refractory epilepsy. This operational mechanism also underlies myoclonic jerk generation, further with translational implications in seizure treatment for genetic/refractory epileptic patients and with contribution to memory/cognitive deficits in epileptic patients.

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“…Another study of 60 adult PWE demonstrated that older patients and those with a longer epilepsy duration tend to have a higher AHI. 30 Those authors suggested that age and the duration of epilepsy play a role in the pathogenesis of worsened OSA, because the BMI was not higher in PWE with a higher AHI than in nonapneic patients. DRE patients who participated in this study were taking a mean of 4.4 AEDs (range: 3–7 AEDs) at baseline, and taking multiple AEDs is associated with weight gain, which potentially exacerbates or increases the risk of OSA.…”

Section: Discussionmentioning

confidence: 99%

Effects of Vagus Nerve Stimulation on Sleep-Disordered Breathing, Daytime Sleepiness, and Sleep Quality in Patients With Drug-Resistant Epilepsy

et al. 2022

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Background and Purpose This study aimed to determine the long-term effects of vagus nerve stimulation (VNS) on sleep-disordered breathing (SDB), daytime sleepiness, and sleep quality in patients with drug-resistant epilepsy (DRE). It also investigated the relationships among these main effects, clinical characteristics, and VNS parameters. Methods Twenty-four patients were recruited. Paired t -tests and multiple linear regression analyses were performed to determine how the demographic and clinical characteristics of the patients influenced the variables that changed significantly after VNS treatment. Results After VNS, the patients showed significant increases in the apnea-hypopnea index (AHI), respiratory disturbance index (RDI), apnea index, hypopnea index, and oxygen desaturation index (ODI), as well as a significant decrease in the lowest arterial oxygen saturation (SaO 2 nadir) ( p <0.05). The multiple linear regression analyses demonstrated that the predictor of larger increases in AHI and RDI was being older at baseline, and that the predictor of a larger increase in apnea index was a longer epilepsy duration. The strongest predictor of a larger increase in ODI was a higher frequency of aura episodes at baseline, followed by a longer epilepsy duration. The strongest predictor of a larger decrease in SaO 2 nadir was a higher frequency of aura episodes at baseline, followed by a longer epilepsy duration. Conclusions This study has confirmed that VNS improves seizure control in patients with DRE, whereas it increases obstructive sleep apnea (OSA). Furthermore, the increase in OSA is affected by age and the duration of epilepsy. Therefore, careful observation and monitoring of SDB is recommended in patients who undergo VNS.

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Refractory epilepsy and obstructive sleep apnea: is there an association?

Cited by 5 publications

References 29 publications

Sleep and Temporal Lobe Epilepsy – Associations, Mechanisms and Treatment Implications

Sleep and Temporal Lobe Epilepsy – Associations, Mechanisms and Treatment Implications

Preoptic area controls sleep-related seizure onset in a genetic epilepsy mouse model

Effects of Vagus Nerve Stimulation on Sleep-Disordered Breathing, Daytime Sleepiness, and Sleep Quality in Patients With Drug-Resistant Epilepsy

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