Read this and other papers by leistad rb et al.

it is suggested that ANS disturbation is correlated with migraine. the parasympathic impulsed also maybe the source of trigger of trigeminovascular system in the migraine without aura. please look at below papers:

Migraine and autonomic nervous system function

Apopulation-based,case-controlstudy

Aaron Shechter, BA; Walter F. Stewart, PhD, MPH; Stephen D. Silberstein, MD; and Richard B. Lipton, MD,NEUROLOGY 2002;58:422–427

Origin of pain in migraine: evidence for peripheral sensitisation

Jes Olesen, Rami Burstein, Messoud Ashina, Peer Tfelt-Hansen, Lancet Neurol2009; 8: 679–90

Migraine and cardiovascular disease: systematic review and meta-analysis

Markus Schu¨rks, instructor,

Pamela M Rist, doctoral student,

Marcelo E Bigal, director,

Julie E Buring,

professor,

Richard B Lipton, professor,

Tobias Kurth, senior researcher, BMJ2009;339:b3914

I think to begin to answer this question, and it is an interesting one, it is necessary to take two steps back and look at the picture from a wider perspective, for it asks the question whether one can see the ANS as a separate isolated entity to the sentient elements of the CNS.

The historical neurological perspective is to divide migraines into many sub-categories based on ether symptoms or effective treatments. The problem is that neither is useful since preventive treatments are given on a suck-it-and-see basis. If propranolol doesn't work lets try antidepressants, or antiepileptics, or....

To my mind migraines are a CNS disorder akin to a faulty, oversentitive fire alarm panel connected to a series of peripheral sensors akin to smoke detectors that can also be faulty. Migraines are very common - 20% of women suffer from them and the trigger factors are very different for different individuals.

Treatment can be directed at the CNS panel (propranolol etc) or to reduce the periperal nocciceptive influences. These are very varied, from oestrogen levels in pure menstrual migraines (uncommon in their pure form) to nocciceptive afferents mediated through unmyelinated c fibres from free nerve endings back to the trigemino-cervical tract where the pain centres of the ophthalmic branch of the trigeminal nerve overlap with those of the C2 Greater Occipital nerve.

Variations of migraines are so common that the osteopaths say "I know the cause" while dentists label the main cause as Temporo-mandibular dysfunction. They are all right, but not exclusively so.

Botox is interesting because it works to varying degrees in many but not all migraines, and while it is not agreed how, one route is by blocking nocciceptive afferents from the free nerve endings by blocking the release of locally active neurotransmitter substance p. Botox blocks this by the same route as it blocks the neurotransmitter release at the neuro-muscular synapse, thus breaking the cascade that starts the migraine up to 24 hours before the acute attack with headache starts

So to get back to the sympathetic pathways, migraines can be seen as having a sympathetic symptomatology (compared to cluster headaches which are parasympathetic), but the interesting idea for me is to integrate the CNS and the ANS. Nocciceptive afferents via the c fibres are generally seen as separate to the the ANS but I question this. One can view the ANS as an earlier, more primitive system which has been overlaid with, but importantly not superceded by the higher centres where the non-localised pain from c fibres is related to the ANS and it makes sense that they should be integrated.

Chris , it seems interesting your comment. Please , may you consider the attached scheme as reference for your comments?

Chris , it seems interesting your comment. Please , may you consider the attached scheme as reference for your comments?

Dear Boshra, I am unable to find the paper you signed. Please, may you send me a pdf at [email protected]? Thank you

Hi Elio

Although I can't speak Italian I think I get the point of your chart, which is to interrelate the different parts of the autonomic nervous system

I see the ANS as a primitive element of the CNS (this is NOT to say simple at all!). This is hardly an original thought but the important part for me is a reminder of how there is an integration of many different afferents from a wide area which is then influencing other wide areas. A good example of this is the control of blood pressure and how this is linked to controlling /diverting blood to the gut after food (while still maintaining cerebral blood flow). The sympathetic thoracic and abdominal paravertebral plexuses are a bit like cloud computing and by comparison some of the higher functions like initiation of voluntary movement and localised sensation are quite simple servants of our higher intellectual functions

The interesting thing for me is to keep this wider view in mind. Bodruk said some 20 years ago that the subdivisions of migraines was of limited use, and he expounded the importance of the neuroanatomy of the trigemino-cervical nucleus.

I agree with you on the integrated manner to see the matter. Thank you for your comments.

Sorry,I forgot . In the light og my previous scheme.. what do you expect when onvestigating... an increased or decreased sympathetic modiulation in migraine case? Obviously this is a comment that I request to all not only to Chris.

Sorry,I forgot and I did so much errors . In the light of my previous scheme.. what do you expect when investigating... ......an increased or decreased sympathetic modulation in migraine case? Obviously this is a comment that I request to all not only to Chris. Sorry , once again.