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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
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
Years ago, I saw a woman with three
kinds of pain in the same side of the head, with features of trigeminal and
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) 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.
Afridi and Goadsby present a case of new onset migraine in a patient who developed a pontine bleeding episode from a cavernous angioma. 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  into the periaqueductal gray
Structural changes fol...
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. 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. Reserpine produced dramatic
initial resolution of headache, whereas it causes a typical headache in
most migraine patients.[3,4] No migraine prophylactic agent offered any
benefit. There is, thus, little pathophysiological similarity between
this case1 and the headaches following implantation of electrodes in the
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. If peripheral frontotemporal application of
nitroglycerine can precipitate ipsilateral headache  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. Explaining laterality of headache of migraine (in patients
with bilateral headache) by neuronal interconnections at the pontine
level  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  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, PAG stimulation did not
affect headaches in patients. On the contrary, in one patient the
headache was intensified ipsilaterally. 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.
Migraine has not been linked previously to pontine bleeding. Stress
is a common precipitant of migraine. As expected following a neurological
episode with fear of loss of function, this patient1 noted that stress
precipitated her headaches. It is important to consider, in the first
instance, as with other theories of migraine, 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. 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. 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.
(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
(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-
(9) Gupta VK. Nitric oxide and migraine: another systemic influence
postulated to explain a lateralizing disorder. Eur J Neurol 1996;3:172-
(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
(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.
(15) Gupta VK. A clinical review of the adaptive role of vasopressin in
migraine. Cephalalgia 1997;17:561-569.