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• HIDDEN DANGEROUS HEADACHES
  CELIO LEVYMAN,MD,MSc
  Published on: 15 September 2004
• Migraine following haemorrhage in brain stem cavernous angioma: pathophysiological considerations.
  Vinod K Gupta
  Published on: 23 June 2003

• Published on: 15 September 2004

  HIDDEN DANGEROUS HEADACHES

  • CELIO LEVYMAN,MD,MSc, Senior Neurologist

  Dear Editor,

  This paper from Prof. Goadsby is very useful to put certain things in focus. Migraine or other benign head pains could perpass as nothing, and an investigation could show an organic pathology, like the AV malformation.

  The careful medical history, with special topics related to pain and head pain, is fundamental, and the same must be applied to clinical and neurological examination.

  G...

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  Dear Editor,

  This paper from Prof. Goadsby is very useful to put certain things in focus. Migraine or other benign head pains could perpass as nothing, and an investigation could show an organic pathology, like the AV malformation.

  The careful medical history, with special topics related to pain and head pain, is fundamental, and the same must be applied to clinical and neurological examination.

  Guidelines, such as from IHS are useful, but must be followed with care: spend little money in a CT scan or MRI could make an enormous difference. That is the thin line to the neurologist consultation a headache suffer patient, and the always present doubt about whether or not to perform a scan.

  Years ago, I saw a woman with three kinds of pain in the same side of the head, with features of trigeminal and glossopharyngeal neuralgia, and cluster headache. But a careful propedeutics showed cranial nervesabnormalities and the scan showed a mass in cerebello-pontine angle after the surgery, the pathology examination proved that we have an epydermoid tumour,and the resection returned the patient to a non-headache sufferer until today [1].

  Reference

  1) Levyman C, Dagua Filho A dos S, Volpato MM, Settanni FA, de Lima WC. Epidermoid tumour of the posterior fossa causing multiple facial pain- -a case report.Cephalalgia. 1991 Feb;11(1):33-6.

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  Conflict of Interest:
  None declared.

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• Published on: 23 June 2003

  Migraine following haemorrhage in brain stem cavernous angioma: pathophysiological considerations.

  • Vinod K Gupta, Physician

  Dear Editor

  Afridi and Goadsby present a case of new onset migraine in a patient who developed a pontine bleeding episode from a cavernous angioma.[1] These authors believe that the pontine bleed triggered the migraine attacks in this patient and seek a parallel with the headaches observed following implantation of stimulating electrodes [2] into the periaqueductal gray matter (PAG).

  Structural changes fol...

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  Dear Editor

  Afridi and Goadsby present a case of new onset migraine in a patient who developed a pontine bleeding episode from a cavernous angioma.[1] These authors believe that the pontine bleed triggered the migraine attacks in this patient and seek a parallel with the headaches observed following implantation of stimulating electrodes [2] into the periaqueductal gray matter (PAG).

  Structural changes following pontine bleed are unlikely to predispose to an intermittent disorder such as migraine and are more likely to lead to a persistent dysfunction, negative or positive. In 15 out of 175 patients undergoing brain electrode transplantation, significant headache was observed.[2] Of these 15 patients, 13 had PAG electrodes implanted (with four of these also receiving thalamic electrodes) while two patients had thalamic electrodes only. Unlike the present case,1 headache was continuous at onset in 14 of 15 patients.[2] Reserpine produced dramatic initial resolution of headache,[2] whereas it causes a typical headache in most migraine patients.[3,4] No migraine prophylactic agent offered any benefit.[2] There is, thus, little pathophysiological similarity between this case1 and the headaches following implantation of electrodes in the PAG.[2]

  Lateralization of migraine headache is one of its most characteristic features. Simply because the physico-chemical substrate / idiosyncracy responsible for unilateral headache has not yet been detected, it does not mean that it is unimportant; what is immeasurable might be more important than what is measurable.[5] If peripheral frontotemporal application of nitroglycerine can precipitate ipsilateral headache [6] without any primary involvement of the PAG in the afferent limb of headache, the relevance of brain stem neuronal interconnections to lateralization of migraine headache is limited. Secondly, generalisation is essential to the process of theorizing.[7] Explaining laterality of headache of migraine (in patients with bilateral headache) by neuronal interconnections at the pontine level [1] will create significant conceptual pathophysiological limitations for strictly unilateral headache in migraine patients as well for other primary headaches that are strictly unilateral, such as cluster headache (CH) and chronic paroxysmal hemicrania (CPH). In other words, if crossover of experimental inhibitory PAG input [8] is indeed clinically relevant, why does persistently unilateral headache occur at all in migraine or CH or CPH? Furthermore, while stimulation of the ventrolateral PAG produces inhibition of nociceptive signals experimentally,[8] PAG stimulation did not affect headaches in patients.[2] On the contrary, in one patient the headache was intensified ipsilaterally.[2] Finally, atenolol and nadolol are effective migraine prophylactic agents that modulate primary pathophysiological aberrations but do not readily cross the blood-brain barrier, and, therefore, cannot affect brain function either at the level of the cortex or the brain stem, including nociceptive mechanisms.[9]

  Migraine has not been linked previously to pontine bleeding. Stress is a common precipitant of migraine.[7] As expected following a neurological episode with fear of loss of function,[10] this patient1 noted that stress precipitated her headaches. It is important to consider, in the first instance, as with other theories of migraine,[11] why antinociception should be spontaneously altered during remissions and exacerbations of migraine. Equally important, there is no clinical evidence of impaired nociception in migraine. The acute phase of migraine attacks (with or without aura) is associated with substantial increases in plasma methionine-enkephalin (analgesia mediating opiate peptide) which return to baseline only slowly in the pain-free period.[12] Also, peripheral pain threshold to low- intensity stimulation was greater or unchanged during headache than during the headache-free interval, and pressure-pain threshold was not correlated to the tenderness scores obtained by manual palpation, thereby eliminating the possibility of both a general ictal increase in sensitivity to pain as well as focal dysfunction in the antinociceptive system.[13,14] Activation of vasopressin related adaptive systems also enhances antinociception during migraine attacks, the process beginning in the pre-prodromal and prodromal phases.[15] The onset of migraine in this patient following haemorrhage in brain stem cavernous angioma1 is a rare coincidence that offers no support to theories of migraine pathogenesis involving brain stem nociceptive dysfunction.

  References

  (1) Afridi S, Goadsby PJ. New onset migraine with a brain stem cavernous angioma. J Neurol Neurosurg Psychiatry 2003;74:680-683.

  (2) Raskin NH, Hosobuchi Y, Lamb S. Headache may arise from perturbation of brain. Headache 1987;27:416-20.

  (3) Kimball RW, Friedman AP, Vallejo E. Effect of serotonin in migraine patients. Neurology 1960;10:107-111.

  (4) Anthony MA, Hinterberger H, Lance JW. Plasma serotonin in migraine and stress. Arch Neurol 1967;16:544-554.

  (5) Gupta VK. Regional cerebral blood flow patterns in migraine: what is the contribution to insight into disease mechanisms? Eur J Neurol 1995;2:586-587.

  (6) Bonuso S, Marano E, Stasio ED, Sorge F, Barbieri F, Ullucci E. Source of pain and primitive dysfunction in migraine: an identical site? J Neurol Neurosurg Psychiatry 1989;52:1351-1354.

  (7) Blau JN. Migraine: theories of pathogenesis. Lancet 1992;339:1202-1207.

  (8) Knight YE, Goadsby PJ. The periaqueductal grey matter modulates trigeminovascular input: a role in migraine? Neuroscience 2001;106:793- 800.

  (9) Gupta VK. Nitric oxide and migraine: another systemic influence postulated to explain a lateralizing disorder. Eur J Neurol 1996;3:172- 173.

  (10) Spierings ELH, Reinders MJ, Hoogduin CAL. The migraine aura as a cause of avoidance behaviour. Headache 1989;29:254-255.

  (11) Blau JN. The challenge of unexplained disease: migraine. J R Soc Med 1993;86:245-246.

  (12) Mosnaim AD, Diamond S, Wolf ME, Puente J, Freitag FG. Endogenous opioid-like peptides in headache. An overview. Headache 1989; 29:368-372.

  (13) Drummond, P.D. Scalp tenderness and sensitivity to pain in migraine and tension headache. Headache 1987; 27: 45-50.

  (14) Jensen K, Tuxen C, Olesen J. Pericranial muscle tenderness and pressure-pain threshold in the temporal region during common migraine. Pain 1988;35:65-70.

  (15) Gupta VK. A clinical review of the adaptive role of vasopressin in migraine. Cephalalgia 1997;17:561-569.

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  Conflict of Interest:
  None declared.

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