Effect of inhibition of nitric oxide synthase on chronic tension-type headache: a randomised crossover trial

@article{Ashina1999EffectOI,
  title={Effect of inhibition of nitric oxide synthase on chronic tension-type headache: a randomised crossover trial},
  author={Messoud Ashina and L. H. Lassen and Lars Bendtsen and R A Jensen and Jes Olesen},
  journal={The Lancet},
  year={1999},
  volume={353},
  pages={287-289}
}

Possible mechanisms of action of nitric oxide synthase inhibitors in chronic tension-type headache.

TLDR
It is suggested that the decrease in muscle hardness following treatment with L-NMMA may be caused by reduction of central sensitization, which may reflect sensitization of second order neurons due to prolonged nociceptive input from myofascial tissues.

Nitric oxide synthase inhibitors for the treatment of chronic tension-type headache

  • M. Ashina
  • Biology
    Expert opinion on pharmacotherapy
  • 2002
TLDR
The analgesic effect of nitric oxide synthase inhibition in patients with chronic tension-type headache is probably due to a reduction in central sensitisation at the level of the spinal dorsal horn, trigeminal nucleus or both, and inhibition of nitrics oxide synthases may become a novel principle in the future treatment of chronic headache.

Glyceryl Trinitrate may Trigger Endogenous Nitric Oxide Production in Patients with Chronic Tension-Type Headache

TLDR
It is suggested that GTN administration may trigger endogenous production of NO in patients with chronic tension-type headache resulting in activation of perivascular sensory afferents.

Possible Mechanisms of Glyceryl-Trinitrate-Induced Immediate Headache in Patients With Chronic Tension-Type Headache

TLDR
The unchanged sensitivity of pericranial myofascial pain pathways indicates that peripheral and central sensitization is not involved in the mechanisms of GTN-induced immediate headache.

Chronic headache and nitric oxide inhibitors

TLDR
It is suggested that the analgesic effect of NOS inhibition in patients with chronic tension-type headache is most likely due to reduction of central sensitization at the level of the spinal dorsal horn or trigeminal nucleus, or both, and inhibition of Nos may become a novel means of future treatment of chronic headache.

Nitric oxide in primary headaches

TLDR
The most relevant evidence for an increased response to exogenous NO in all primary headaches emerges from the experimental model of nitroglycerin-induced headache and the effectiveness of non-selective NO synthase inhibitor L-N-monomethylarginine further supports the involvement of NO in migraine and chronic tension-type headache.

Nitric oxide-related drag targets in headache

  • J. Olesen
  • Medicine, Biology
    Neurotherapeutics
  • 2011

Nitric oxide in primary headaches

TLDR
Evidence suggests that the release of nitric oxide from blood vessels, perivascular nerve endings or from brain tissue is an important molecular trigger mechanism in spontaneous headache pain.

Calcitonin gene‐related peptide levels during nitric oxide‐induced headache in patients with chronic tension‐type headache

TLDR
The present study indicates that NO‐induced immediate headache is not associated with release of CGRP and plasma levels of C GRP during headache induced by the NO donor glyceryl trinitrate (GTN) in 16 patients with chronic tension‐type headache and 16 healthy controls.
...

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Inhibition of nitric oxide synthesis increases blood pressure in healthy humans.

TLDR
Basal generation of nitric oxide influences total peripheral resistance and blood pressure in healthy humans and the natriuresis induced by L-NMMA may be related to the increase in blood pressure, or arise from inhibition of the intrarenal actions of Nitric oxide.

Flunarizine in Prophylaxis of Childhood Migraine: A Double-Blind, Placebo-Controlled, Crossover Study

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It is concluded that flunarizine is an effective drug for the treatment of childhood migraine and in a study of this length no serious side effects were discovered.

Nitric oxide evokes pain at nociceptors of the paravascular tissue and veins in humans.

TLDR
Pain intensity‐NO concentration relations were congruent, indicating that the respective nociceptive systems are equally sensitive to NO, consistent with the hypothesis that NO is a chemical link in peripheral nocICEption.