A recent study in Sleep Med on altered Cortical Excitability in sleep apnea concluded that " This TMS-based study suggests that untreated severe OSAS patients have imbalanced cortical excitabilities that enhanced inhibition or decreased brain excitability when awake during the day."
This may be a major cause of chronic headaches or migraines or other biochemical imbalances leading to stress disorders ofr depression. Many patients do not reach the clinical definition of sleep apnea but have UARS (upper respiratory resistance syndrome). This has been implicated in fibromyalgia and central sensitization as well.
I have included a few relevant pubmed articles below.
Sleep apne is the result of a TMJ disorder (http://www.nhlbi.nih.gov/meetings/workshops/tmj_wksp.pdf)
Neuromuscular Dentistry can help reduce incresed corticl activity, Treatment of sleep apnea can do the same.
Patients with sleep apnea have a smaller airway 24/7 that collapses at night. Correction of apnea and daytime jaw position may be ideal for all patients with chronic pain and sleep apnea.
Sleep Med. 2010 Oct;11(9):857-61.
Altered cortical excitability in patients with untreated obstructive sleep apnea syndrome.
Joo EY, Kim HJ, Lim YH, Koo DL, Hong SB.
Sleep Center, Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Comment in:
Sleep Med. 2010 Oct;11(9):820-1.
Abstract
OBJECTIVE: To investigate cortical excitability in patients with obstructive sleep apnea syndrome (OSAS) during wakefulness.
METHODS: The authors recruited 45 untreated severe OSAS (all males, mean age 47.2 years, mean apnea-hypopnea index=44.6h(-1)) patients and 44 age-matched healthy male volunteers (mean apnea-hypopnea index=3.4h(-1)). The TMS parameters measured were resting motor threshold (RMT), motor evoked potential (MEP) amplitude, cortical silent period (CSP), and short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF). These parameters were measured in the morning (9-10 am) more than 2h after arising and the parameters of patients and controls were compared. The Epworth Sleepiness Scale (ESS) and the Stanford Sleepiness Scale (SSS) were also measured before the TMS study.
RESULTS: OSAS patients had a significantly higher RMT and a longer CSP duration (t-test, p<0.001) compared to healthy volunteers. No significant difference was observed between MEP amplitudes at any stimulus intensity or between the SICI (2, 3, 5ms) and ICF (10, 15, 20ms) values of OSAS patients and healthy volunteers (p>0.05).
CONCLUSIONS: This TMS-based study suggests that untreated severe OSAS patients have imbalanced cortical excitabilities that enhanced inhibition or decreased brain excitability when awake during the day.
PMID: 20817550 [PubMed - in process]
Handb Clin Neurol. 2010;97:73-83.
Biological science of headache channels.
Pietrobon D.
Abstract
Several episodic neurological diseases, including familial hemiplegic migraine (FHM) and different types of epilepsy, are caused by mutations in ion channels, and hence classified as channelopathies. The classification of FHM as a channelopathy has introduced a new perspective in headache research and has strengthened the idea of migraine as a disorder of neural excitability. Here we review recent studies of the functional consequences of mutations in the CACNA1A and SCNA1A genes (encoding the pore-forming subunit of Ca(V)2.1 and Na(V)1.1 channels) and the ATPA1A2 gene (encoding the alpha(2) subunit of the Na(+)/K(+) pump), responsible for FHM1, FHM3, and FHM2, respectively. These studies show that: (1) FHM1 mutations produce gain-of-function of the Ca(V)2.1 channel and, as a consequence, increased glutamate release at cortical synapses and facilitation of induction and propagation of cortical spreading depression (CSD); (2) FHM2 mutations produce loss-of-function of the alpha(2) Na(+)/K(+)-ATPase; and (3) the FHM3 mutation accelerates recovery from fast inactivation of Na(V)1.5 channels. These findings are consistent with the hypothesis that FHM mutations share the ability to render the brain more susceptible to CSD, by causing excessive synaptic glutamate release (FHM1) or decreased removal of K(+) and glutamate from the synaptic cleft (FHM2) or excessive extracellular K(+) (FHM3).
PMID: 20816411 [PubMed - in pr
Handb Clin Neurol. 2010;97:47-71.
Pharmacology.
Bolay H, Durham P.
Department of Neurology, Gazi Hospital and Neuropsychiatry Centre, Gazi University, Besevler, Ankara, Turkey.
Abstract
Headache treatment has been based primarily on experiences with non-specific drugs such as analgesics, non-steroidal anti-inflammatory drugs, or drugs that were originally developed to treat other diseases, such as beta-blockers and anticonvulsant medications. A better understanding of the basic pathophysiological mechanisms of migraine and other types of headache has led to the development over the past two decades of more target-specific drugs. Since activation of the trigeminovascular system and neurogenic inflammation are thought to play important roles in migraine pathophysiology, experimental studies modeling those events successfully predicted targets for selective development of pharmacological agents to treat migraine. Basically, there are two fundamental strategies for the treatment of migraine, abortive or preventive, based to a large degree on the frequency of attacks. The triptans, which exhibit potency towards selective serotonin (5-hydroxytryptamine, 5-HT) receptors expressed on trigeminal nerves, remain the most effective drugs for the abortive treatment of migraine. However, numerous preventive medications are currently available that modulate the excitability of the nervous system, particularly the cerebral cortex. In this chapter, the pharmacology of commercially available medications as well as drugs in development that prevent or abort headache attacks will be discussed.
PMID: 20816410 [PubMed - in process]
Cephalalgia. 2010 Sep;30(9):1101-9. Epub 2010 Mar 19.
Cortical hyperexcitability and mechanism of medication-overuse headache.
Supornsilpchai W, le Grand SM, Srikiatkhachorn A.
Department of Physiology, Faculty of Medicine, Chulalongkorn University, Patumwan, Bangkok, Thailand.
Abstract
The present study was conducted to determine the effect of acute (1 h) and chronic (daily dose for 30 days) paracetamol administration on the development of cortical spreading depression (CSD), CSD-evoked cortical hyperaemia and CSD-induced Fos expression in cerebral cortex and trigeminal nucleus caudalis (TNC). Paracetamol (200 mg/kg body weight, intraperitonealy) was administered to Wistar rats. CSD was elicited by topical application of solid KCl. Electrocorticogram and cortical blood flow were recorded. Results revealed that acute paracetamol administration substantially decreased the number of Fos-immunoreactive cells in the parietal cortex and TNC without causing change in CSD frequency. On the other hand, chronic paracetamol administration led to an increase in CSD frequency as well as CSD-evoked Fos expression in parietal cortex and TNC, indicating an increase in cortical excitability and facilitation of trigeminal nociception. Alteration of cortical excitability which leads to an increased susceptibility of CSD development can be a possible mechanism underlying medication-overuse headache.
PMID: 20713560 [PubMed - in process]
