All patients with cluster headaches that have onset during sleep should be evaluated for sleep apnea. Sleep apnea causes hypoxia (drop in oxygen) and a rise in CO2. Oxygen therapy is a recognized and effective treatment for sleep apnea. Prevention of many cluster headaches can be addressed by correcting sleep problems.
During apneic events the patients quit breathing oxygen drops followed by hypercapnia or a rise in carbon dioxide levels. This can cause acidosis that could trigger cluster headaches. This leads to an awakening and patients gasping and is associated with adrenaline release or fight or flight reflex. Repetition throughout the night can also be the trigger.
Patients with untreated sleep apnea have abnormal cortisol levels and this disturbs the ability to cope with normal life stresses. There is also an increase in insulin resistance and changes in blood sugar can also be a cluster headache trigger. The article
Timing patterns of cluster headaches and association with symptoms of obstructive sleep apnea." from Sleep Res Online. 2000;3(3):107-12 concludes that "in some patients, physiological consequences of OSA may trigger CH during the first few hours of sleep and thereby influence the timing of subsequent daytime headaches."
The National Heart Lung and Blood Institute (NHLBI) considers sleep apnea to be a Temporomandibular Disorder. The NHLBI report "CARDIOVASCULAR AND SLEEP-RELATED CONSEQUENCES OF TEMPOROMANDIBULAR DISORDERS" discusses effects of sleep apnea in detail. Learn more about the dangers of sleep apnea and oral appliance treatment at http://www.ihatecpap.com
A section of the report titled The Craniofacial Complex and its Impact on Control of Upper Airway Resistance and Cardiopulmonary Function- Jaw Biomechanics and Function" discusses sexual dimorphism and may explain why cluster headaches are more common in men. Part of that report follows: "These compartments are activated differently during the production of different oral behaviors, suggesting that they function as output elements used in different combinations by the nervous system. These muscles are complex and unique, containing fibers of phenotypes not found in limb muscles. They are smaller, and express myosin heavy chain isoforms found only in limb muscles during development. The cardiac alpha-myosin heavy chain isoforms of the masseter and temporalis muscles are unique to skeletal muscle and resemble heart muscle. Considerable sexual dimorphism has been identified in these muscles with regard to the slow and fast fibers types of the masseter. Males have predominately fast fiber types while females predominately slow fiber types. These sex differences arise in response to androgens in males but persist even in the absence of androgens."
It is widely accepted that the Trigeminal Nervous system that controls the jaws teeth and associate dental structures is implicated in the majority of all headaches including cluster headache.
Control of the upper airway often decrease or fails during sleep as seen in this excerpt: "Control of Upper Airway Collapsibility During Sleep
The upper pharyngeal airway in humans has relatively little bony or rigid support. Since there is variability in soft tissue and bony structures of the head and neck, there must be mechanisms in place that enable the pharyngeal dilator muscles to adjust for these anatomic differences. Animal and human studies indicate that there are at least three mechanisms to control the activity of the genioglossus muscle. First, negative pressure has substantial impact on this muscle and a clear linear relationship exists between negative pressure in the airway and genioglossal activation. Second, there is pre-motor neuron input to these muscles from respiratory pattern generating circuits as shown by the pre-activation of these muscles that occurs prior to the development of negative pressure in the airway. Third, tonic activity in the muscle is consistently evident, although the mechanisms that determine the level of this activity have not been studied. During sleep, the mechanisms that control upper airway resistance are importantly impacted. Specifically, tonic activity drops markedly and the negative pressure reflex is substantially attenuated or completely lost. These findings have important implications in the pathophysiology of SDB." They probably also have important implications in the physiology and pathology of cluster headaches.
The report also discusses physiological pain processes and central sensitization found in TMJD patients that is similar to findings in cluster and headache patients in this excerpt: "Craniofacial/Deep Tissue Persistent Pain and Relationships to Cardiovascular and Pulmonary Function and Disease.
Injury to peripheral tissues following trauma or surgery often results in hyperalgesia that is characterized by increased sensitivity to painful stimuli. This is a common problem in patients with TMD. Until recently, it was thought that the increase in pain was due to changes at the site of injury but it is now known that it involves central nervous system hyper-excitability leading to long-term changes in the nervous system. Animal models of hyperalgesia produced by inflammation or nerve injury that mimic persistent pain conditions have shown that an increased neuronal barrage into the central nervous system (CNS) leads to central sensitization involving activation of excitatory amino acid transmitters and their receptors. The activation of N-methyl- D-aspartate (NMDA) receptors leads to influx of calcium into neurons, the activation of protein kinases, and phosphorylation of receptors. The net effect of these responses is increased gene expression of NMDA receptors, an alteration in the sensitivity of receptors, increased excitability, and an amplification of pain. These responses appear to be most robust in response to deep tissue injury such as occurs in TMD patients.
Modulation by descending pathways from the CNS importantly influences these events. Under normal conditions, the net effect of the descending neural projections from the brain stem to the spinal cord is to inhibit or counterbalance the hyper-excitability produced by tissue injury. It is now understood that this balance can shift to a net excitatory effect whereby descending modulation results in more hyper-excitability and more pain after injury. This central sensitization appears to be a prominent component in patients suffering from deep pain conditions such as TMD and fibromyalgia. It is believed that the diffuse nature and amplification of pain is in part due to this imbalance and that these findings have important functional implications relevant to the survival of the organism in response to the presence of persistent tissue injury. It is therefore now believed that persistent pain can be attacked both at the site of injury and where it is elaborated in the nervous system."
The report also documents connections with autonomic system derangements that are normally found in headaches, migraines and cluster headaches. These autonomic symptoms are the ones that Sphenopalatine Ganglion Blocks can relieve or eliminate. The relevant section is excerpted below:
" Alteration in Baroreceptor Activity - Impact on Pain, Autonomic Function, Motor Output, and Sleep":
"Evidence has emerged that several regions of the CNS interact in complex ways to integrate sensory perception, autonomic function, motor output, and sleep architecture. The outcomes of a number of recent studies also suggest that several of the signs and symptoms associated with TMD may result, at least in part, from impairments in neural networks that coordinate the interplay between sensory systems, autonomic function, motor output, and sleep architecture. Many of the central pathways that are critically involved with the integration of these systems are regulated by visceral afferent input, including input from cardiopulmonary, carotid sinus, and aortic arch baroreceptors. In addition, abnormalities in the function and central integration of baroreceptor afferent information has been associated with abnormalities in pain perception, autonomic function, motor output, and sleep architecture, and thus may contribute to the development and maintenance of TMD and other related disorders (e.g., fibromyalgia). There is a need for additional studies that systematically examine whether abnormal baroreceptor function contributes to the pathogenesis of TMD."
Several relevant studies on TMD and Sleep Apnea are included below:
Cranio. 1997 Jan;15(1):89-93.
Cluster-like signs and symptoms respond to myofascial/craniomandibular treatment: a report of two cases.
Vargo CP, Hickman DM.
Raleigh Regional Center for Head, Neck and Facial Pain in Beckley, West Virginia, Morgantown, USA.
Abstract
Two cases with pain profiles characteristic of cluster-like headache, both within and outside the trigeminal system, are reported. One male patient would typically awaken from sleep with severe unilateral temporal head pain and autonomic signs of ipsilateral lacrimation and nasal congestion. A female patient exhibited severe unilateral boring temporal and suboccipital head pain with associated ipsilateral lacrimation and rhinorrhea. In addition, both patients presented with signs and symptoms of masticatory and/or cervical disorders. These two cases illustrate possible treatment alternatives, as well as possible influences from cervical and masticatory structures in the development of cluster or cluster-like headache.
PMID: 9586493 [PubMed - indexed for MEDLINE]
Cranio. 1995 Jul;13(3):177-81.
Sphenopalatine ganglion block: a safe and easy method for the management of orofacial pain.
Peterson JN, Schames J, Schames M, King E.
Headache and Pain Center, Hollywood Community Hospital, Los Angeles, CA 90028, USA.
Abstract
The sphenopalatine ganglion (SPG) block is a safe, easy method for the control of acute or chronic pain in any pain management office. It takes only a few moments to implement, and the patient can be safely taught to effectively perform this pain control procedure at home with good expectations and results. Indications for the SPG blocks include pain of musculoskeletal origin, vascular origin and neurogenic origin. It has been used effectively in the management of temporomandibular joint (TMJ) pain, cluster headaches, tic douloureux, dysmenorrhea, trigeminal neuralgia, bronchospasm and chronic hiccup.
PMID: 8949858 [PubMed - indexed for MEDLINE]
Ned Tijdschr Tandheelkd. 2006 Nov;113(11):474-7.
[Spontaneous pain attacks: neuralgic pain]
[Article in Dutch]
de Bont LG.
Universitair Medisch Centrum, Groningen. l.g.m.de.bont@kchir.umcg.nl
Abstract
Paroxysmal orofacial pains can cause diagnostic problems, especially when different clinical pictures occur simultaneously. Pain due to pulpitis, for example, may show the same characteristics as pain due to trigeminal neuralgia would. Moreover, the trigger point of trigeminal neuralgia can either be located in a healthy tooth or in the temporomandibular joint. Neuralgic pain is distinguished into trigeminal neuralgia, glossopharyngeal neuralgia, Horton's neuralgia, cluster headache and paroxysmal hemicrania. In 2 cases trigeminal neuralgia is successfully managed with a neurosurgical microvascular decompression procedure according to Jannetta. Characteristic pain attacks resembling neuralgic pain result from well understood pathophysiological mechanisms. Consequently, adequate therapy, such as a Janetta procedure and specific pharmacological therapy, is available.
PMID: 17147031 [PubMed - indexed for MEDLINE]
Sleep Res Online. 2000;3(3):107-12.
Timing patterns of cluster headaches and association with symptoms of obstructive sleep apnea.
Chervin RD, Zallek SN, Lin X, Hall JM, Sharma N, Hedger KM.
Sleep Disorders Center, Department of Neurology, University of Michigan, Ann Harbor, Michigan, USA. chervin@umich.edu
Abstract
Cluster headaches (CH) frequently recur at the same point in the circadian cycle, often during sleep. They may, in some cases, represent a susceptible individual's response to hypoxemia or other physiological changes induced by obstructive sleep apnea (OSA). If and when this mechanism exists, timing of CH close to the onset of sleep-and therefore OSA-might be expected. We questioned 36 subjects with CH about the times at which their CH usually occurred and about several symptoms known to be predictive of OSA, including habitual snoring, loud snoring, observed apneas and excessive daytime sleepiness. We then used logistic regression to determine whether occurrence of CH in each of six time periods was associated with OSA symptoms. The 23 subjects (64%) who reported CH in the first half of a typical night's sleep also tended to report headaches during the midday/afternoon period. Symptoms of OSA, and in particular habitual snoring, were predictive of both first-half-of-the-night and midday/afternoon CH (p<.05). Thirty-one subjects (86%) reported that their CH were sleep-related, usually occurring during any part of the night or on awakening, but symptoms of OSA were not predictive of this timing pattern. In short, several OSA symptoms showed an association with CH occurrence in the first half of the night but not with sleep-related CH in general. These findings suggest that in some patients, physiological consequences of OSA may trigger CH during the first few hours of sleep and thereby influence the timing of subsequent daytime headaches.
PMID: 11382908 [PubMed - indexed for MEDLINE]
