The Underlying Mechanisms of Sleep Deprivation Exacerbating Neuropathic Pain

Zhu, Minli; Huang, Hao

doi:10.2147/nss.s414174

Cited by 3 publications

(1 citation statement)

References 140 publications

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“…Hypocretin interfaces with the central nervous system (CNS) and the peripheral nervous system (dorsal root ganglion). 23 Human narcolepsy type I is characterized by low levels of hypocretin-1 following loss of hypocretinergic cells in the lateral hypothalamus. 24 Authors demonstrate that hypocretin exhibits seasonal and circadian variations, with increased levels of CSF during periods of attention or physical activity.…”

Section: Hypocretin (Orexin)mentioning

confidence: 99%

Narcolepsy: an interface among neurology, immunology, sleep, and genetics

Coelho

2024

Arq Neuropsiquiatr

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Narcolepsy is a primary disorder of the central nervous system resulting from genetic, environmental, and immunological interactions defined as excessive daytime sleepiness plus cataplexy, hallucinations, sleep paralysis, and sleep fragmentation. The pathophysiology is not entirely known, but the interaction among genetic predisposition, environmental exposition, and immune component with consequent hypocretin-1 deficiency is the model to explain narcolepsy type I. The mechanism of narcolepsy type II is less understood. There is a delay of over ten years for the diagnosis of narcolepsy around the world. Patients with narcolepsy have many comorbidities with a negative impact on quality of life. The treatment of narcolepsy must contain an educational approach for the family, coworkers, and patients. Scheduled naps and sleep hygiene are essential to minimize the dose of medications. Much progress has been seen in the pharmacological treatment of narcolepsy with new stimulants, different presentations of oxybate, and recent studies with orexin agonists. Narcolepsy is a rare disease that needs to be more understood and highlighted to avoid delayed diagnosis and severe disabilities in patients.

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Section: Hypocretin (Orexin)mentioning

confidence: 99%

Narcolepsy: an interface among neurology, immunology, sleep, and genetics

Coelho

2024

Arq Neuropsiquiatr

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Nociplastic pain mechanisms and toll-like receptors as promising targets for its management

Rodríguez-Palma,

Huerta de la Cruz,

Islas-Espinoza

et al. 2024

PAIN

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Nociplastic pain, characterized by abnormal pain processing without an identifiable organic cause, affects a significant portion of the global population. Unfortunately, current pharmacological treatments for this condition often prove ineffective, prompting the need to explore new potential targets for inducing analgesic effects in patients with nociplastic pain. In this context, toll-like receptors (TLRs), known for their role in the immune response to infections, represent promising opportunities for pharmacological intervention because they play a relevant role in both the development and maintenance of pain. Although TLRs have been extensively studied in neuropathic and inflammatory pain, their specific contributions to nociplastic pain remain less clear, demanding further investigation. This review consolidates current evidence on the connection between TLRs and nociplastic pain, with a specific focus on prevalent conditions like fibromyalgia, stress-induced pain, sleep deprivation–related pain, and irritable bowel syndrome. In addition, we explore the association between nociplastic pain and psychiatric comorbidities, proposing that modulating TLRs can potentially alleviate both pain syndromes and related psychiatric disorders. Finally, we discuss the potential sex differences in TLR signaling, considering the higher prevalence of nociplastic pain among women. Altogether, this review aims to shed light on nociplastic pain, its underlying mechanisms, and its intriguing relationship with TLR signaling pathways, ultimately framing the potential therapeutic role of TLRs in addressing this challenging condition.

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The crucial role of locus coeruleus noradrenergic neurons in the interaction between acute sleep disturbance and headache

Li,

Cao,

Yuan

et al. 2024

J Headache Pain

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Background Both epidemiological and clinical studies have indicated that headache and sleep disturbances share a complex relationship. Although headache and sleep share common neurophysiological and anatomical foundations, the mechanism underlying their interaction remains poorly understood. The structures of the diencephalon and brainstem, particularly the locus coeruleus (LC), are the primary sites where the sleep and headache pathways intersect. To better understand the intricate nature of the relationship between headache and sleep, our study focused on investigating the role and function of noradrenergic neurons in the LC during acute headache and acute sleep disturbance. Method To explore the relationship between acute headache and acute sleep disturbance, we primarily employed nitroglycerin (NTG)-induced migraine-like headache and acute sleep deprivation (ASD) models. Initially, we conducted experiments to confirm that ASD enhances headache and that acute headache can lead to acute sleep disturbance. Subsequently, we examined the separate roles of the LC in sleep and headache. We observed the effects of drug-induced activation and inhibition and chemogenetic manipulation of LC noradrenergic neurons on ASD-induced headache facilitation and acute headache-related sleep disturbance. This approach enabled us to demonstrate the bidirectional function of LC noradrenergic neurons. Results Our findings indicate that ASD facilitated the development of NTG-induced migraine-like headache, while acute headache affected sleep quality. Furthermore, activating the LC reduced the headache threshold and increased sleep latency, whereas inhibiting the LC had the opposite effect. Additional investigations demonstrated that activating LC noradrenergic neurons further intensified pain facilitation from ASD, while inhibiting these neurons reduced this pain facilitation. Moreover, activating LC noradrenergic neurons exacerbated the impact of acute headache on sleep quality, while inhibiting them alleviated this influence. Conclusion The LC serves as a significant anatomical and functional region in the interaction between acute sleep disturbance and acute headache. The involvement of LC noradrenergic neurons is pivotal in facilitating headache triggered by ASD and influencing the effects of headache on sleep quality.

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The Underlying Mechanisms of Sleep Deprivation Exacerbating Neuropathic Pain

Cited by 3 publications

References 140 publications

Narcolepsy: an interface among neurology, immunology, sleep, and genetics

Narcolepsy: an interface among neurology, immunology, sleep, and genetics

Nociplastic pain mechanisms and toll-like receptors as promising targets for its management

The crucial role of locus coeruleus noradrenergic neurons in the interaction between acute sleep disturbance and headache

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