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Thursday, April 7, 2011

Can Dentists Prevent Migraines? The Answer Is Yes According To New Research Out Of Germany.

The Journal of Neuroscience (J Neurosci. 2011 Feb 9;31(6):1937-43) recently published an article titled "Trigeminal nociceptive transmission in migraineurs predicts migraine attacks"

I have long advocated that the majority of Migraines and Tension-Type headaches are actually input-output errors. Nociceptive information entering the Trigeminovascular system are the pathology that triggers migraines and other headaches.

This study looked at fMRI or functional MRI studies of the brain.

They found that predicting migraine by trigeminal nociceptive activity could predict migraines.

Whers does most nociceptive trigeminal input arise?

In the Jaw Muscles, Muscle Spindles, Golgi Tendon Organs and periodontal ligaments of the teeth.

Neuromuscular Dentistry is very effective in eliminating and preventing migraines and muscular tension-type headaches. The majority of "sinus headaches" are actually referred muscle pain. The reason for the success of Neuromuscular Dentistry is the ability to eliminate nociceptive input.

Input/output errors are often described in computer lingo as Garbage In / Garbage Out.

The neurofeedback loops from periodontal ligaments , muscles, muscle spindles etc send nociceptive input (ie Garbage in) into the trigeminovascular system.

Migraines and other headaches are the "Garbage Out " part of the equation.
The article states that:
"Remarkably, the distance to the next headache attack was predictable by the height of the signal intensities in the spinal nuclei. Migraine patients scanned during the acute spontaneous migraine attack showed significantly lower signal intensities in the trigeminal nuclei compared with controls, demonstrating activity levels similar to interictal patients. Additionally we found-for the first time using fMRI-that migraineurs showed a significant increase in activation of dorsal parts of the pons, previously coined "migraine generator." Unlike the dorsal pons activation usually linked to migraine attacks, the gradient-like activity following nociceptive stimulation in the spinal trigeminal neurons likely reflects a raise in susceptibility of the brain to generate the next attack, as these areas increase their activity long before headache starts. This oscillating behavior may be a key player in the generation of migraine headache, whereas attack-specific pons activations are most likely a secondary event."

Another article in Neurology. 2011 Jan 18;76(3):206-7 states "Photophobia is an abnormal sensitivity to light experienced by migraineurs during attacks. The pathophysiology of photophobia is poorly understood. Nevertheless, 2 facts appear to have a link with photophobia: visual cortex hyperexcitability on the one hand and interactions between visual pathway and trigeminal nociception on the other."

The photophobia or sensitivity to light during a migraine attack is also due, in part to trigeminal nociception (Garbage in. The nociceptive input from the teeth,jaws, periodontal ligaments are the "garbage in" and the migraines and photophobia are the Garbage out".

Experimental studies on rats "J Neurosci. 2010 Oct 27;30(43):14420-9.
Changes of meningeal excitability mediated by corticotrigeminal networks: a link for the endogenous modulation of migraine pain." confirm the effect of trigeminanl nociception on meningeal migraines. The Trigeminovascular system is always paramount in migraine. The Trigeminal nerve controls the blood flow to the anterior 2/3 of the meninges of the brain.

Primary Stabbing Headaches are also trigeminally innervated as reported in"
J Headache Pain. 2011 Jan 6. [Epub ahead of print]
Incidence and influence on referral of primary stabbing headache in an outpatient headache clinic." The article states that "Primary stabbing headache (PSH) is a pain, as brief, sharp, jabbing stabs, predominantly felt in the first division of trigeminal nerve." The trigeminal nerve you will remember is the Dentist's nerve.


PubMed Abstract below:

J Neurosci. 2011 Feb 9;31(6):1937-43.
Trigeminal nociceptive transmission in migraineurs predicts migraine attacks.

Stankewitz A, Aderjan D, Eippert F, May A.

Department of Systems Neuroscience, University Medical Center Hamburg-Eppendorf, D-20246 Hamburg, Germany.
Abstract

Several lines of evidence suggest a major role of the trigeminovascular system in the pathogenesis of migraine. Using functional magnetic resonance imaging (fMRI), we compared brain responses during trigeminal pain processing in migraine patients with those of healthy control subjects. The main finding is that the activity of the spinal trigeminal nuclei in response to nociceptive stimulation showed a cycling behavior over the migraine interval. Although interictal (i.e., outside of attack) migraine patients revealed lower activations in the spinal trigeminal nuclei compared with controls, preictal (i.e., shortly before attack) patients showed activity similar to controls, which demonstrates that the trigeminal activation level increases over the pain-free migraine interval. Remarkably, the distance to the next headache attack was predictable by the height of the signal intensities in the spinal nuclei. Migraine patients scanned during the acute spontaneous migraine attack showed significantly lower signal intensities in the trigeminal nuclei compared with controls, demonstrating activity levels similar to interictal patients. Additionally we found-for the first time using fMRI-that migraineurs showed a significant increase in activation of dorsal parts of the pons, previously coined "migraine generator." Unlike the dorsal pons activation usually linked to migraine attacks, the gradient-like activity following nociceptive stimulation in the spinal trigeminal neurons likely reflects a raise in susceptibility of the brain to generate the next attack, as these areas increase their activity long before headache starts. This oscillating behavior may be a key player in the generation of migraine headache, whereas attack-specific pons activations are most likely a secondary event.

PMID: 21307231 [PubMed - indexed for MEDLINE]


Neurology. 2011 Jan 18;76(3):213-8. Epub 2010 Dec 9.
A PET study of photophobia during spontaneous migraine attacks.

Denuelle M, Boulloche N, Payoux P, Fabre N, Trotter Y, Géraud G.

Service de Neurologie et Explorations Fonctionnelles du Système Nerveux, CHU Rangueil, Toulouse, France. denuelle.m@chu-toulouse.fr

Comment in:

* Neurology. 2011 Jan 18;76(3):206-7.

Abstract

BACKGROUND: Photophobia is an abnormal sensitivity to light experienced by migraineurs during attacks. The pathophysiology of photophobia is poorly understood. Nevertheless, 2 facts appear to have a link with photophobia: visual cortex hyperexcitability on the one hand and interactions between visual pathway and trigeminal nociception on the other.

METHODS: We used H(2)(15)O PET to study photophobia induced by continuous luminous stimulation covering the whole visual field in 8 migraineurs during spontaneous migraine attacks, after headache relief by sumatriptan and during attack-free interval. The intensity of the luminous stimulation provoking photophobia with subsequent headache enhancement was specifically determined for each patient.

RESULTS: We found that low luminous stimulation (median of 240 Cd/m(2)) activated the visual cortex during migraine attacks and after headache relief but not during the attack-free interval. The visual cortex activation was statistically stronger during migraine headache than after pain relief.

CONCLUSION: These findings suggest that ictal photophobia is linked with a visual cortex hyperexcitability. The mechanism of this cortical hyperexcitability could not be explained only by trigeminal nociception because it persisted after headache relief. We hypothesize that modulation of cortical excitability during migraine attack could be under brainstem nuclei control.

PMID: 21148120 [PubMed - indexed for MEDLINE]

J Neurosci. 2010 Oct 27;30(43):14420-9.
Changes of meningeal excitability mediated by corticotrigeminal networks: a link for the endogenous modulation of migraine pain.

Noseda R, Constandil L, Bourgeais L, Chalus M, Villanueva L.

Department of Anesthesia, Critical Care, and Pain Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA.
Abstract

Alterations in cortical excitability are implicated in the pathophysiology of migraine. However, the relationship between cortical spreading depression (CSD) and headache has not been fully elucidated. We aimed to identify the corticofugal networks that directly influence meningeal nociception in the brainstem trigeminocervical complex (Sp5C) of the rat. Cortical areas projecting to the brainstem were first identified by retrograde tracing from Sp5C areas that receive direct meningeal inputs. Anterograde tracers were then injected into these cortical areas to determine the precise pattern of descending axonal terminal fields in the Sp5C. Descending cortical projections to brainstem areas innervated by the ophthalmic branch of the trigeminal nerve originate contralaterally from insular (Ins) and primary somatosensory (S1) cortices and terminate in laminae I-II and III-V of the Sp5C, respectively. In another set of experiments, electrophysiological recordings were simultaneously performed in Ins, S1 or primary visual cortex (V1), and Sp5C neurons. KCl was microinjected into such cortical areas to test the effects of CSD on meningeal nociception. CSD initiated in Ins and S1 induced facilitation and inhibition of meningeal-evoked responses, respectively. CSD triggered in V1 affects differently Ins and S1 cortices, enhancing or inhibiting meningeal-evoked responses of Sp5C, without affecting cutaneous-evoked nociceptive responses. Our data suggest that "top-down" influences from lateralized areas within Ins and S1 selectively affect interoceptive (meningeal) over exteroceptive (cutaneous) nociceptive inputs onto Sp5C. Such corticofugal influences could contribute to the development of migraine pain in terms of both topographic localization and pain tuning during an attack.

J Headache Pain. 2011 Jan 6. [Epub ahead of print]
Incidence and influence on referral of primary stabbing headache in an outpatient headache clinic.

Guerrero AL, Herrero S, Peñas ML, Cortijo E, Rojo E, Mulero P, Fernández R.

Neurology Department, Hospital Clínico Universitario, Avda Ramón y Cajal 3, 47005, Valladolid, Spain, gueneurol@gmail.com.
Abstract

Primary stabbing headache (PSH) is a pain, as brief, sharp, jabbing stabs, predominantly felt in the first division of trigeminal nerve. Population studies have shown that PSH is a common headache. However, most people suffer attacks of low frequency or intensity and seldom seek for medical assistance. There are few clinic-based studies of PSH, and its real influence as a primary cause for referral to neurology outpatient offices is to be determined. We aim to investigate the burden of PSH as main complaint in an outpatient headache clinic. We reviewed all patients with PSH (ICHD-II criteria), attended in an outpatient headache clinic in a tertiary hospital during a 2.5-year period (January 2008-June 2010). We considered demographic and nosological characteristics and if PSH was main cause of submission. 36 patients (26 females, 10 males) out of 725 (5%) were diagnosed of PSH. Mean age at onset 34.1 ± 2.9 years (range 10-72). Mean time from onset to diagnosis 68.8 ± 18.3 months. Twenty-four patients fulfilled ICHD-II criteria for other headaches (14 migraine, 6 tension-type headache, 2 hemicrania continua, 1 primary cough headache and 1 primary exertional headache). 77.7% of patients were submitted from primary care. In 14 patients (39%), PSH was main reason for submission, its intensity or frequency in 5 (35.7%) and fear of malignancy in 9 (74.3%). Only two patients of those who associated other headaches were submitted due to PSH. In conclusion, PSH is not an uncommon diagnosis in an outpatient headache office. However, and according to our data, it is not usually the main cause of submission to a headache clinic.

PMID: 21210176 [PubMed - as supplied by publisher]

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posted by Dr Shapira at 7:54 PM

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