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Monday, September 1, 2014

Cluster Headaches and Teeth Grinding

Dan:     I have been diagnosed with Chronic Cluster Headaches. I also grind and clench my teeth at night. My pain is on the right side always.

Dr Shapira Response,

Good News, Neuromuscular Dentistry may help control or eliminate your cluster headaches.

Sorry to hear about your headaches.  While the causes of Cluster Headaches are not well understood they are unquestionably related to the Trigeminal Nerve, the same nerve responsible for TMJ disorders and headache, sinus pain, facial pain and related symptoms.

We know that 100% oxygen can relieve classic cluster headaches.  We also know that almost all nocturnal  clenching and grinding of the teeth is related to sleep disordered breathing that causes oxygen desaturation and disturbs hormonal systems.  The connection is critical.

Much of the literature on cluster headaches point to a hormonal link.  When sleep is disturbed most of the bodies hormonal systems go into malfunction.  Especially Growth hormone, melatonin, thyroid, sex hormones, insulin resistance and cortisol.

TMJ disorders and sleep disorders both upset the functions of our circadian clocks that are also implicated in cluster headaches.  

A thorough diagnosis by a trained Neuromuscular Dentist(ideally a Fellow or Master of ICCMO due to advanced  training and commitment to the science) would be an excellent first step.  The use of a Neurmucular Diagnostic Orthotic may by itself eliminate or greatly improve your symptoms. I would strongly suggest you take a broader approach and also seek out a Board certified Diplomat in Dental Sleep Medicine trained in treating sleep disordered breathing and sleep apnea.  Correcting sleep disordered breathing whether it is snoring or sleep apnea or anything between can have dramatic effects on your cluster headaches.

This will address the trigeminal nervous system which contributes over 50% of input to the brain after the reticular activating system.  The sleep treatment will eliminate or minimize circadian disruptions.  It will also allow hormonal systems to be properly regulated and will eliminate the oxidative stress of repeated hypoxias (drops in oxygen).

A doctor trained in Sphenopalatine Ganglion blocks and trigger point injections can offer additional methods of eliminating your cluster headaches.  Diplomats of the American Academy of Pain Management understand the complex nature of chronic pain.  Be wary of doctors who only "throw medications" at the problem because they often only treat the symptoms and not the underlying causes of the disorder.

Good Luck

Ira L Sahpira DDS, D,ABDSM, D,AAPM, FICCMO


This new abstract from PUBMED.gov explains how Trigeminal Nerves can be affected by reactive oxygen, exactly as created by sleep disordered breathing.



 2014 Mar;54(3):472-84. doi: 10.1111/head.12301. Epub 2014 Feb 11.

Reactive oxygen species induce procalcitonin expression in trigeminal ganglia glia.

Abstract

OBJECTIVE:

To examine calcitonin gene-related peptide (CGRP) gene expression under inflammatory conditions using trigeminal ganglia organ cultures as an experimental system. These cultures have increased proinflammatory signaling that may mimic neurogenic inflammation in the migraine state.

BACKGROUND:

The trigeminal nerve sends peripheral pain signals to the central nervous system during migraine. Understanding the dynamic processes that occur within the trigeminal nerve and ganglion may provide insights into events that contribute to migraine pain. A neuropeptide of particular interest is CGRP, which can be elevated and play a causal role in migraine. However, most studies have overlooked a second splice product of the Calca gene that encodes calcitonin (CT), a peptide hormone involved in calcium homeostasis. Importantly, a precursor form of CT called procalcitonin (proCT) can act as a partial agonist at the CGRP receptor and elevated proCT has recently been reported during migraine.

METHODS:

We used a trigeminal ganglion whole organ explant model, which has previously been demonstrated to induce pro-inflammatory agents in vitro. Quantitative polymerase chain reaction and immunohistochemistry were used to evaluate changes in messenger ribonucleic acid (mRNA) and protein levels of CGRP and proCT.

RESULTS:

Whole mouse trigeminal ganglia cultured for 24 hours showed a 10-fold increase in CT mRNA, with no change in CGRP mRNA. A similar effect was observed in ganglia from adult rats. ProCT immunoreactivity was localized in glial cells. Cutting the tissue blunted the increase in CT, suggesting that induction required the close environment of the intact ganglia. Consistent with this prediction, there were increased reactive oxygen species in the ganglia, and the elevated CT mRNA was reduced by antioxidant treatment. Surprisingly, reactive oxygen species were increased in neurons, not glia.

CONCLUSIONS:

These results demonstrate that reactive oxygen species can activate proCT expression from the CGRP gene in trigeminal glia by a paracrine regulatory mechanism. We propose that this glial recruitment pathway may occur following cortical spreading depression and neurogenic inflammation to increase CGRP nociceptive actions in migraine.
© 2014 American Headache Society.

KEYWORDS:

calcitonin gene-related peptide; migraine; procalcitonin; reactive oxygen species; trigeminal ganglion
PMID:
 
24512072
 
[PubMed - indexed for MEDLINE] 
PMCID:
 
PMC3947709
 [Available on 2015/3/1]

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posted by Dr Shapira at 6:17 AM

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