scholarly journals Chronobiological features of primary headaches and the role of melatonin in the regulation of biological rhythms

2019 ◽  
pp. 33-38
Author(s):  
E. M. Evdokimova ◽  
M. G. Poluektov ◽  
G. R. Tabeyeva
Keyword(s):  
Circadian Rhythm ◽  
Cluster Headache ◽  
Suprachiasmatic Nucleus ◽  
Seasonal Pattern ◽  
Biological Rhythms ◽  
Primary Headaches ◽  
Melatonin Secretion ◽  
Clinical Observations

Frequency is considered as a key sign of the course of some forms of primary headaches (PH). One of the most prominent representatives is the hypnical and cluster headache, which predetermined their name. Clinical observations demonstrate a clear circadian rhythm and seasonal pattern of cluster headache (CH) and migraine (M) attacks. In accordance with modern concepts, the phenomenon of the periodicity of painful episodes of a number of forms of primary headaches is associated with dysfunction of the suprachiasmatic nucleus of the hypothalamus, the main pacemaker of biological rhythms. The connection of PH with chronopathology is confirmed by revealing the disturbances of melatonin secretion in CH and M. Melatonin has proven to be effective in treatment of these PH.

Hypothalamic Deep-Brain Stimulation: Target and Potential Mechanism for the Treatment of Cluster Headache

Cephalalgia ◽  
2008 ◽  
Vol 28 (7) ◽  
pp. 799-803 ◽  
Author(s):  
A May
Keyword(s):  
Deep Brain Stimulation ◽  
Cluster Headache ◽  
Brain Stimulation ◽  
Antinociceptive Effect ◽  
Primary Headaches ◽  
Imaging Data ◽  
Pain Transmission ◽  
Positron Emission ◽  
Deep Brain

Recently, functional imaging data have underscored the crucial role of the hypothalamus in trigemino-autonomic headaches, a group of severe primary headaches. This prompted the application of hypothalamic deep-brain stimulation (DBS), with the intention to preventing cluster headache (CH) attacks in selected severe therapy-refractory cases. To date, a total of 50 operated intractable CH patients, one patient with short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing and three with atypical facial pain, have been reported. However, it is not apparent why the spontaneous bursts of activation in the inferior posterior hypothalamus result in excruciating head pain, whereas continuous electrical stimulation of the identical area is able to prevent these attacks. Recently, this issue has been addressed by examining 10 operated chronic CH patients, using H215O-positron emission tomography and alternately switching the hypothalamic stimulator on and off. The stimulation-induced activation in the ipsilateral posterior inferior hypothalamic grey (the site of the stimulator tip) as well as activation and de-activation in several cerebral structures belonging to neuronal circuits usually activated in pain transmission. These data argue against an unspecific antinociceptive effect or pure inhibition of hypothalamic activity as the mode of action of hypothalamic DBS and suggest functional modulation of the pain-processing network.

scholarly journals Sleep disturbance management in patients with trigeminal autonomic cephalalgias

2021 ◽  
pp. 100-108
Author(s):  
N. V. Vashchenko ◽  
A. M. Uzhakhov ◽  
Ju. E. Azimova
Keyword(s):  
Cluster Headache ◽  
Vagus Nerve ◽  
Sleep Disturbances ◽  
Primary Headaches ◽  
Prophylactic Therapy ◽  
Trigeminal Autonomic Cephalalgias ◽  
Trigeminovascular System ◽  
Acute Therapy

Trigeminal autonomic cephalalgias (TACs) are rare but are the most intense primary headaches that severely limit patients’ ability to work and be socially active. This article reviews the modern classification of TACs, based on the International Classification of Headache Disorders-3, and the key differences between TAC types, as well as the pathophysiological mechanisms – the role of the trigeminovascular system, autonomic nervous system, hypothalamus and vagus nerve – and their relation to circadian rhythms. The sleep disturbances that can occur in patients with TACs, exacerbating the course of the disease, and the role of melatonin, hypothalamus and suprachiasmatic nucleus in these conditions are also discussed. In addition, current therapies for cluster headache are described, which include acute therapy and prophylactic therapy, with recommendations regarding the timing of prophylactic therapy discontinuation. The review also includes the available data on melatonin as well as new therapies such as CGRP monoclonal antibodies and neuromodulation, which includes the two most promising techniques: non-invasive vagus nerve stimulation and sphenopalatine ganglion microstimulation. Furthermore, the authors present the clinical case of a patient with chronic cluster headache, which was significantly reduced in frequency and intensity when melatonin was added to the therapy.

scholarly journals BMAL1 but not CLOCK is associated with monochromatic green light-induced circadian rhythm of melatonin in chick pinealocytes

2019 ◽  
Vol 8 (1) ◽  
pp. 57-68 ◽  
Author(s):  
Shuhui Ma ◽  
Zixu Wang ◽  
Jing Cao ◽  
Yulan Dong ◽  
Yaoxing Chen
Keyword(s):  
Circadian Rhythm ◽  
Circadian Rhythms ◽  
Pineal Gland ◽  
Clock Genes ◽  
Critical Role ◽  
Green Light ◽  
Circadian Oscillator ◽  
Melatonin Secretion ◽  
Expression Levels

The avian pineal gland, an independent circadian oscillator, receives external photic cues and translates them for the rhythmical synthesis of melatonin. Our previous study found that monochromatic green light could increase the secretion of melatonin and expression of CLOCK and BMAL1 in chick pinealocytes. This study further investigated the role of BMAL1 and CLOCK in monochromatic green light-induced melatonin secretion in chick pinealocytes using siRNAs interference and overexpression techniques. The results showed that si-BMAL1 destroyed the circadian rhythms of AANAT and melatonin, along with the disruption of the expression of all the seven clock genes, except CRY1. Furthermore, overexpression of BMAL1 also disturbed the circadian rhythms of AANAT and melatonin, in addition to causing arrhythmic expression of BMAL1 and CRY1/2, but had no effect on the circadian rhythms of CLOCK, BMAL2 and PER2/3. The knockdown or overexpression of CLOCK had no impact on the circadian rhythms of AANAT, melatonin, BMAL1 and PER2, but it significantly deregulated the circadian rhythms of CLOCK, BMAL2, CRY1/2 and PER3. These results suggested that BMAL1 rather than CLOCK plays a critical role in the regulation of monochromatic green light-induced melatonin rhythm synthesis in chicken pinealocytes. Moreover, both knockdown and overexpression of BMAL1 could change the expression levels of CRY2, it indicated CRY2 may be involved in the BMAL1 pathway by modulating the circadian rhythms of AANAT and melatonin.

scholarly journals The biological clock in cluster headache: A review and hypothesis

Cephalalgia ◽  
2019 ◽  
Vol 39 (14) ◽  
pp. 1855-1866 ◽  
Author(s):  
Willemijn C Naber ◽  
Rolf Fronczek ◽  
Joost Haan ◽  
Patty Doesborg ◽  
Christopher S Colwell ◽  
...  
Keyword(s):  
Cluster Headache ◽  
Sleep Stage ◽  
Seasonal Pattern ◽  
Biological Clock ◽  
Clear Correlation ◽  
Cluster Headache Attack ◽  
Autonomic Reflex ◽  
Role Of Light ◽  
Light Sleep

Objective To review and discuss the putative role of light, sleep, and the biological clock in cluster headache. Discussion Cluster headache attacks are believed to be modulated in the hypothalamus; moreover, the severe pain and typical autonomic cranial features associated with cluster headache are caused by abnormal activity of the trigeminal-autonomic reflex. The temporal pattern of cluster headache attacks suggests involvement of the biological clock, and the seasonal pattern is influenced by the number of daylight hours. Although sleep is often reported as a trigger for cluster headache attacks, to date no clear correlation has been established between these attacks and sleep stage. Conclusions We hypothesize that light, sleep, and the biological clock can change the brain’s state, thereby lowering the threshold for activating the trigeminal-autonomic reflex, resulting in a cluster headache attack. Understanding the mechanisms that contribute to the daily and seasonal fluctuations in cluster headache attacks may provide new therapeutic targets.

Knockdown of clock genes in the suprachiasmatic nucleus blocks prolactin surges and alters FRA expression in the locus coeruleus of female rats

2007 ◽  
Vol 293 (5) ◽  
pp. E1325-E1334 ◽  
Author(s):  
Maristela O. Poletini ◽  
De'Nise T. McKee ◽  
Jessica E. Kennett ◽  
Jamie Doster ◽  
Marc E. Freeman
Keyword(s):  
Circadian Rhythm ◽  
Locus Coeruleus ◽  
Suprachiasmatic Nucleus ◽  
Clock Genes ◽  
Random Sequence ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Gene Expressions ◽  
Circadian Time

The nature of the circadian signal from the suprachiasmatic nucleus (SCN) required for prolactin (PRL) surges is unknown. Because the SCN neuronal circadian rhythm is determined by a feedback loop of Period (Per) 1, Per2, and circadian locomotor output cycles kaput ( Clock) gene expressions, we investigated the effect of SCN rhythmicity on PRL surges by disrupting this loop. Because lesion of the locus coeruleus (LC) abolishes PRL surges and these neurons receive SCN projections, we investigated the role of SCN rhythmicity in the LC neuronal circadian rhythm as a possible component of the circadian mechanism regulating PRL surges. Cycling rats on proestrous day and estradiol-treated ovariectomized rats received injections of antisense or random-sequence deoxyoligonucleotide cocktails for clock genes ( Per1, Per2, and Clock) in the SCN, and blood samples were taken for PRL measurements. The percentage of tyrosine hydroxylase-positive neurons immunoreactive to Fos-related antigen (FRA) was determined in ovariectomized rats submitted to the cocktail injections and in a 12:12-h light:dark (LD) or constant dark (DD) environment. The antisense cocktail abolished both the proestrous and the estradiol-induced PRL surges observed in the afternoon and the increase of FRA expression in the LC neurons at Zeitgeber time 14 in LD and at circadian time 14 in DD. Because SCN afferents and efferents were probably preserved, the SCN rhythmicity is essential for the magnitude of daily PRL surges in female rats as well as for LC neuronal circadian rhythm. SCN neurons therefore determine PRL secretory surges, possibly by modulating LC circadian neuronal activity.

scholarly journals Cluster Headache: Evidence for a Disorder of Circadian Rhythm and Hypothalamic Function

2002 ◽  
Vol 29 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Tamara Pringsheim
Keyword(s):  
Circadian Rhythm ◽  
Cluster Headache ◽  
Suprachiasmatic Nucleus ◽  
Biological Clock ◽  
Primary Headache ◽  
Headache Disorder ◽  
Primary Headache Disorders ◽  
Hypothalamic Function ◽  
The Relationship ◽  
Further Development

This article reviews the literature for evidence of a disorder of circadian rhythm and hypothalamic function in cluster headache. Cluster headache exhibits diurnal and seasonal rhythmicity. While cluster headache has traditionally been thought of as a vascular headache disorder, its periodicity suggests involvement of the suprachiasmatic nucleus of the hypothalamus, the biological clock. Normal circadian function and seasonal changes occurring in the suprachiasmatic nucleus and pineal gland are correlated to the clinical features and abnormalities of circadian rhythm seen in cluster headache. Abnormalities in the secretion of melatonin and cortisol in patients with cluster headache, neuroimaging of cluster headache attacks, and the use of melatonin as preventative therapy in cluster headache are discussed in this review. While the majority of studies exploring the relationship between circadian rhythms and cluster headache are not new, we have entered a new diagnostic and therapeutic era in primary headache disorders. The time has come to use the evidence for a disorder of circadian rhythm in cluster headache to further development of chronobiotics in the treatment of this disorder.

Effect of suprachiasmatic nucleus lesion on circadian dentin increment in rats

2001 ◽  
Vol 280 (5) ◽  
pp. R1364-R1370 ◽  
Author(s):  
Mie Ohtsuka-Isoya ◽  
Haruhide Hayashi ◽  
Hisashi Shinoda
Keyword(s):  
Circadian Rhythm ◽  
Fourier Analysis ◽  
Suprachiasmatic Nucleus ◽  
Constant Light ◽  
Maxillary Incisors ◽  
The Brain

Mammalian dentin universally shows circadian increments. However, little is known about the mechanism of this phenomenon. The purpose of the present study was to investigate the role of the suprachiasmatic nucleus (SCN) in the generation of circadian rhythm in dentin increment. Rats underwent lesion of the SCN by electrodes and were maintained under constant light to examine whether the circadian increment free runs. The rats were injected with nitrilotriacetato lead to chronologically label the growing dentin. Two weeks after the operation, maxillary incisors and the locations of lesions in the brain were examined histologically. A harmonic (Fourier) analysis was performed to examine the densitometric pattern of the dentin increments to determine their periodicity. In rats with a completely lesioned SCN, ultradian increments, but no circadian increments, were observed in the dentin. Alternatively, in rats with an intact or only partially lesioned SCN, circadian increments persisted or were only temporarily disturbed. These results suggest that the SCN plays an important role in the generation of the circadian dentin increment in rats.

scholarly journals Propofol Anesthesia Significantly Alters Plasma Blood Levels of Melatonin in Rats

2010 ◽  
Vol 112 (2) ◽  
pp. 333-337 ◽  
Author(s):  
Garance Dispersyn ◽  
Laure Pain ◽  
Yvan Touitou
Keyword(s):  
Circadian Rhythm ◽  
Activity Rhythm ◽  
Blood Levels ◽  
Light Conditions ◽  
Melatonin Secretion ◽  
Blood Samples ◽  
Circadian Time ◽  
Normal Light ◽  
Rest Activity

Background General anesthesia combined with surgery has been shown to decrease the nocturnal peak of melatonin in patients. However, the role of anesthesia itself on melatonin secretion remains unknown. We previously showed that anesthesia induced by propofol modifies the circadian time structure in both rats and humans and phase advances the circadian rest-activity rhythm in rats. In this study, we examined the secretion of melatonin during 24 h after a 30-min propofol anesthesia in rats. Methods Rats were exposed to 12-h light/12-h dark alteration conditions and anesthetized with propofol (120 mg/kg intraperitoneally) around their peak of melatonin secretion (Zeitgeber time 16). Trunk blood samples were collected at seven subsequent Zeitgeber times to assess the effects of propofol on circadian melatonin secretion. Results Propofol modifies the peripheral melatonin by significantly decreasing its concentration ( approximately 22-28%) during the immediate 3 h after the wake up from anesthesia and then significantly increasing melatonin secretion 20 h after anesthesia ( approximately 38%). Cosinor analysis suggests that propofol induces a phase advance of the circadian secretion of peripheral melatonin. Conclusions The results demonstrate the disturbing effects of propofol anesthesia on the circadian rhythm of plasma melatonin in rats under normal light conditions. These results parallel the desynchronization of the circadian rhythms of locomotor activity and temperature previously observed after propofol anesthesia.

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