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Migraine And Blood Vessels – The Myth!


So You Have A Diagnosis Of Migraine – What Does It Mean Though?

My guess is that you have been told that there is a problem with the blood vessels in your head – that they dilate or expand excessively, or something similar.

Over 150 years ago, primarily because of the throbbing nature of headache, it was presumed that the major problem was (expansion or dilatation of) the blood vessels – and since any headache that was/is throbbing in nature was diagnosed as migraine and non-throbbing headaches were excluded from a diagnosis of migraine – the entity known as tension headache was born! (despite the lack of evidence, the cause of non-throbbing headaches was considered to be muscular and/or stress related; another assumption was made!)

Research has shown that:

- dilatation of intra (within) cranial (head) blood vessels does not occur in all migraine sufferers during a headache – if dilatation was the cause of pain one would expect to see dilatation in all migraineurs – but this is not the case;

- dilatation of intracranial blood vessels continue after head pain has subsided – if dilatation causes the pain one would expect ongoing pain in the presence of dilatation – but once again this is not the case;

- dilatation of blood vessels occurs in response to pain (in this experiment forehead pain was produced by injecting a pain producing substance) i.e. pain and then dilatation, not dilatation and then or leading to pain

A significant body of recent research has demonstrated that sensitisation or hyper excitability of the brainstem is the primary disorder in migraine sufferers and has led to the term ‘the migraine brain’… and that this sensitisation is present constantly i.e. even when migraine free – confused? But … don’t the ‘triptans’ (medication designed specifically to abort the migraine process)work by decreasing the dilatation of the blood vessels? Well initially this was thought (and largely assumed) to be the case, but experiments have shown that the triptans decrease the sensitisation of the brainstem.

Now what is this thing called the ‘Brainstem’. The brainstem is an area at the top of the spinal cord, which receives input from (activity of) structures inside the head (including blood vessels) and also from structures of the upper neck (ligaments, joints and there capsules, and muscles) which are supplied by the top three spinal nerves. The brainstem is also influenced by serotonin and a system known as the Diffuse Noxious Inhibitory Control system – don’t be overwhelmed by these terms – I will explain this elsewhere. Now all information or activity in relation to headache, head pain and migraine, passes through the brainstem to the higher brain centres where it is interpreted, where the decisions are made! The Brainstem is to headache what the black box is to the airplane – it is the final common pathway for all headache and migraine information.

One of the world’s leading authorities has suggested that migraine is a ‘sensory processing’ disorder i.e. one in which normal and minimal information or activity occurring within the head is misinterpreted (by the higher brain centers – where all the decisions are made) after having passed through a sensitised brainstem. This essentially means that the 9% (perhaps normal and/or minimal?) of dilatation of blood vessels inside the head that occurs in response to hormonal fluctuations, alcohol, additives in cheese, chocolate and other food triggers, is interpreted to be much higher, exceeding what is considered to be normal and the brain’s response is to create pain.

Is it reasonable to consider that there is a sea of activity occurring in and around intra cranial (within the head) structures (including blood vessels, teeth, gums, sinuses, meninges etc) in all of us, but the difference between the women suffering menstrual migraine from those who do not is that their brainstems are sensitised; from those in whom ½ a glass of red wine or a tiny piece of chocolate triggers a migraine, is that the normal and minimal activity is misinterpreted after having passed through a sensitised brainstem?

The overwhelming evidence has prompted a shift away from the maligned blood vessels as the cause of pain in migraine – now the question is “What is causing the sensitization of the brainstem – the ‘migraine brain’?”

Stay tuned …!

Dean

Dean H Watson

Consultant Headache & Migraine Physiotherapist; International Teacher; Director, The Headache Clinic & Watson Headache Institute; PhD Candidate Murdoch University, Western Australia; Adjunct Lecturer, Masters Program, Physiotherapy School, University of South Australia; MAppSc(Res) GradDipAdvManipTher

Experienced health practitioners trained in the Watson Headache Approach perform the examination and treatment techniques developed by Dean Watson. These techniques are based on his extensive experience of 7000 headache patients (21,000 hours) over 21 years and are now taught internationally.

For your nearest practitioner who has completed training in the ‘Watson Headache Approach’ please refer to the ‘Practitioner Directory’.

(Goadsby P. All in the mind. New Scientist. 2003: 36-39

Hoskin KL, Kaube H, Goadsby PJ. Sumatriptan can inhibit trigeminal afferents by an exclusively neural mechanism. Brain 1996; 119:1419-28

Katsavara Z, Giffin N, Diener HC, Kaube H. Abnormal habituation of ‘nociceptive’ blink reflex in migraine – evidence for increased excitability of trigeminal nociception. Cephalalgia 2003; 23:814-819

Katsavara Z, Lehnerdt G, Duda B, Ellrich J, Diener HC, Kaube H. Sensitization of trigeminal nociception specific for migraine but not pain of sinusitis. Neurology 2002; 59:1450-1453

Kaube H, Katasavara Z, Przywara S, Drepper J, Ellrich J, Diener HC. Acute migraine headache. Possible sensitization of neurons in the spinal trigeminal nucleus? Neurology 2002; 58:1234-1238

Nardone R et al Trigemino-Cervical Reflex Abnormalities in Patients with Migraine and Cluster Headache. Headache 2008; 48(4):578-585

Sandrini G, Cecchini AB, Milanov I, Tassorelli C, Buzzi MG, Nappi G. Electrophysiological evidence for trigeminal neuron sensitisation in patients with migraine. Neurosci Lett 2002; 317:135-138

Tegeler CH, Davidai G, Gengo FM, Knappertz VA,Troost BT, Gabriel H, Davis RL. Middle cerebral artery velocity correlates with nitroglcerin-induced headache onset. J Neuroimaging 1996; 6(2): 81-6

Thomsen LL, Iverson HK, Olesen J. Cerebral bloodflow velocities are reduced during attacks of unilateral migraine without aura. Cephalalgia 1995; 15(2): 109-116

Thomsen LL. Investigations into the role of nitric oxide and the large intracranial arteries in migraine headache. Cephalalgia 1997; 17:873-95)

© 2009 & Beyond. Watson Headache Institute, All Rights Reserved.

The information on this website is not intended or implied to be a substitute for professional medical advice, diagnosis or treatment.   Reading this article signifies your acceptance and understanding of the Terms and Conditions of YourHeadacheSolutions.co.uk.

Dean Watson

Dean Watson of YourHeadache Solutions, Consultant Headache and Migraine Physiotherapist; Adjunct Lecturer, Masters Program, School of Physiotherapy, University of South Australia; PhD Candidate, Murdoch University, Western Australia. On his site you can search all topics about headache migraine, headache treatment, migraine treatment, headache causes, migraine causes headache symptoms and more.

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