Visual evoked
potentials and serum magnesium levels in
juvenile migraine patients.
Aloisi P; Marrelli A; Porto C; Tozzi E;
Cerone G Servizio di Neurofisiopatologia,
University of L'Aquila, Italy.
Headache (United States) Jun 1997, 37 (6)
p383-5
Changes in visual evoked potentials and
decreased intracellular magnesium levels have
been separately described in patients affected
by migraine both during the attacks and in the
interictal periods. An inverse correlation
between increased P100 amplitude and lowered
serum magnesium levels was found in children
suffering from migraine with and without aura in
a headache-free period. A 20-day treatment with
oral magnesium pidolate seemed to normalize the
magnesium balance in 90% of patients. After
treatment, the reduced P100 amplitude confirmed
the inverse correlation with the serum magnesium
level. These data seem to suggest the hypothesis
that higher visual evoked potential amplitude
and low brain magnesium level can both be an
expression of neuronal hyperexcitability of the
visual pathways related to a lowered threshold
for migraine attacks.
Nocturnal plasma
melatonin profile and melatonin kinetics during
infusion in status migrainosus
Claustrat B.; Brun J.; Geoffriau M.; Zaidan
R.; Mallo C.; Chazot G. B. Claustrat, Serv.
Radiopharmacie/Radioanalyse, Hopital
Neurologique, 59 Boulevard Pinel, 69003 Lyon
France
Cephalalgia (Norway), 1997, 17/4
(511-517)
The plasma melatonin profile was
significantly disturbed (phase-shift of the
maximum melatonin level) in four out of six
female sufferers from status migrainosus,
compared with nine healthy controls. The number
of secretion peaks was similar in both groups. A
nocturnal 20 pg melatonin infusion (from 21.00
to 01.00 h) evoked plasma melatonin levels
slightly higher than a physiological secretion
peak. During infusion, the episodes of secretion
were reinforced and the endogenous plasma
profile was phase-advanced in two patients
displaying a phase-delay. These data suggest
impaired pineal function in migraine. In the
absence of side effects of melatonin infusion,
the relief of certain migraine symptoms
described by our patients might support a
controlled trial of melatonin in migraine.
Dentist Advocates
Cold Gel for Migraines 2002.
Feig, C.
CNN Medical Unit/CNN.com Health
(www.cnn.com/2002/HEALTH/conditions/02/11/migraine.treatment/index.html).
An extract of
Petasites hybridus is effective in the
prophylaxis of migraine.
Grossman W, Schmidramsl H. Department of
Neurology, Municipal Hospital,
Munchen-Harlaching, Germany.
Altern Med Rev 2001 Jun;6(3):303-10
OBJECTIVE: Migraine is still an unsolved
problem. This clinical trial investigates the
efficacy and tolerance of Petasites hybridus in
the prophylaxis of migraine.
METHODS: A randomized, group-parallel,
placebo-controlled, double-blind clinical study
was carried out with a special CO2 extract from
the rhizome of Petasites hybridus. Following a
four-week run-in phase, 60 patients received
either the special Petasites hybridus extract
Petadolex or placebo at a dosage of two capsules
(each capsule contains 25 mg) twice daily over
12 weeks. Outcome variables included the
frequency, intensity and duration of migraine
attacks as well as any accompanying
symptoms.
RESULTS: The frequency of migraine attacks
decreased by a maximum of 60 percent compared to
the baseline. This reduction in migraine attacks
with Petadolex was significant (p < 0.05)
compared to placebo. No adverse events were
reported. Petasites was exceptionally well
tolerated.
CONCLUSIONS: The results suggest that
migraine patients can benefit from prophylactic
treatment with this special extract. The
combination of high efficacy and excellent
tolerance emphasizes the particular value that
Petasites hybridus has for the prophylactic
treatment of migraine.
The results of
pycamilon therapy in patients with
hemicrania.
O A Kolosova, V I Osipova, T V Luniova,
All-Union Center of Vegetative Pathology of the
Ministry of Health of USSR, First Medical
Institute, 11, Rossolimo St., Moscow 119021,
USSR
Efficiency of pycamilon in patients with
hemicrania was studied. Indications for
pycamilon application in response to the
clinical form of hemicrania and to the course of
disease were defined more exactly. It was been
established that pycamilon has a pronounced
effect on painful hemicrania access both
decreasing its intensity and mitigating or
absolute ceasing of accompanying symptoms.
Pycamilon is most effective for simple forms of
hemicrania with preferential left sided
topoalgia in patients without pronounced
depressive hypochondria.
Results of a 5
years prospective study of estriol succinate
treatment in patients with climacteric
complaints.
Lauritzen C. Zentrum fur Gynakologie und
Geburtshilfe, Universitat Ulm, Germany.
Horm Metab Res 1987 Nov;19(11):579-84
In a prospective study 911 patients were
treated over a period of 5 years (M = 2.2) or a
total of 2007 treatment years with estriol
succinate oral (Synapause, 2-12 mg per day). The
treatment was very effective in the removal of
all typical climacteric complaints and of the
atrophic genital changes caused by estrogen
deficiency. Subjective side effects were seldom
seen and without practical importance for the
treatment. Objective, grave side effects were
only few: one superficial phlebo-thrombosis, 2
cases of thrombophlebitis, one carcinoma in situ
of the portio vaginalis uteri and 2 mammary
cancers were seen. The carcinoma had probably no
causal relationship to the treatment. Embolies,
myocardial infarctions, cerebrovascular and
liver-gall bladder complications did not occur
during treatment. The rate of uterine bleedings
was low. The incidence of all complications was
not increased by estriol succinate; but was even
lower than expected. Endometrial and ovarian
cancers were not seen. Estriol succinate is
accordingly a very effective and well tolerated
preparation against climacteric complaints,
exerting no significant side effects. It is
remarkable that it does not proliferate the
endometrium when given in one dose a day.
Estriol succinate can therefore be characterized
as the estrogen to be favoured for the treatment
of postclimacteric women, who do not want to
have uterine bleedings any longer.
Role of magnesium
in the pathogenesis and treatment of
migraines.
Mauskop A, Altura BM NY Headache Center, New
York, NY 10021, USA.
Clin Neurosci 1998;5(1):24-7
The importance of magnesium in the
pathogenesis of migraine headaches is clearly
established by a large number of clinical and
experimental studies. However, the precise role
of various effects of low magnesium levels in
the development of migraines remains to be
discovered. Magnesium concentration has an
effect on serotonin receptors, nitric oxide
synthesis and release, NMDA receptors, and a
variety of other migraine related receptors and
neurotransmitters. The available evidence
suggests that up to 50% of patients during an
acute migraine attack have lowered levels of
ionized magnesium. Infusion of magnesium results
in a rapid and sustained relief of an acute
migraine in such patients. Two double-blind
studies suggest that chronic oral magnesium
supplementation may also reduce the frequency of
migraine headaches. Because of an excellent
safety profile and low cost and despite the lack
of definitive studies, we feel that a trial of
oral magnesium supplementation can be
recommended to a majority of migraine sufferers.
Refractory patients can sometimes benefit from
intravenous infusions of magnesium sulfate.
[The new
cerebrovascular preparation
pikamilon]
Mirzoian RS; Gan'shina TS
Farmakol Toksikol (USSR) Jan Feb 1989, 52 (1)
p23 6,
Picamilon, a sodium salt of N nicotinoyl
gamma aminobutyric acid, was shown to induce a
significant increase of cerebral blood flow in
conscious cats. Picamilon was found to inhibit
neurogenic spasms of cerebral vessels that was
followed by suppression of tonic activity and
reflectory discharges in sympathetic nerves.
Picamilon led to restoration of the initial
condition of cerebral hemodynamics disturbed by
a previous administration of serotonin.
Randomised
double-blind placebo-controlled trial of
feverfew in migraine prevention.
Murphy JJ, Heptinstall S, Mitchell JR.
Department of Medicine, University Hospital,
Nottingham.
Lancet 1988 Jul 23;2(8604):189-92
The use of feverfew (Tanacetum parthenium)
for migraine prophylaxis was assessed in a
randomised, double-blind, placebo-controlled
crossover study. After a one-month single-blind
placebo run-in, 72 volunteers were randomly
allocated to receive either one capsule of dried
feverfew leaves a day or matching placebo for
four months and then transferred to the other
treatment limb for a further four months.
Frequency and severity of attacks were
determined from diary cards which were issued
every two months; efficacy of each treatment was
also assessed by visual analogue scores. 60
patients completed the study and full
information was available in 59. Treatment with
feverfew was associated with a reduction in the
mean number and severity of attacks in each
two-month period, and in the degree of vomiting;
duration of individual attacks was unaltered.
Visual analogue scores also indicated a
significant improvement with feverfew. There
were no serious side-effects.
Feverfew
(Tanacetum parthenium) as a prophylactic
treatment for migraine: A double-blind
placebo-controlled study
Palevitch D.; Earon G.; Carasso R. D.
Palevitch, Unit of Medicinal/Aromatic Plants,
Newe Yaar Research Center, P.O. Box 1021, Ramat
Yishay 30095 Israel
Phytotherapy Research (United Kingdom) 1997,
11/7 (508-511)
To assess the effectiveness of feverfew as a
prophylactic therapy for migraine, a
double-blind placebo controlled cross-over trial
was conducted for a period of 4 months. Fifty
seven patients who attended an outpatient pain
clinic were selected at random and divided into
two groups. Both groups were treated with
feverfew in the preliminary phase (phase 1),
which lasted 2 months, in the second and third
phases, which continued for an additional 2
months, a double-blind placebo controlled
cross-over study was conducted. The results
showed that feverfew caused a significant
reduction in pain intensity compared with the
placebo treatment. Moreover, a profound
reduction was recorded concerning the severity
of the typical symptoms that are usually linked
to migraine attacks, such as vomiting, nausea,
sensitivity to noise and sensitivity to light.
Transferring the feverfew -treated group to the
placebo treatment resulted in an augmentation of
the pain intensity as well as an increase in the
severity of the linked symptoms, in contrast,
shifting the placebo group to feverfew therapy
resulted in a reduction of the pain intensity as
well as in the severity of the linked
symptoms.
Open label trial
of coenzyme Q10 as a migraine
preventive.
Rozen TD, Oshinsky ML, Gebeline CA, Bradley
KC, Young WB, Shechter AL, Silberstein SD.
Jefferson Headache Center/Thomas Jefferson
University, Philadelphia, Pennsylvania, USA.
RozenT@ccf.org
Cephalalgia. 2002 Mar;22(2):137-41
The objective was to assess the efficacy of
coenzyme Q10 as a preventive treatment for
migraine headaches. Thirty-two patients (26
women, 6 men) with a history of episodic
migraine with or without aura were treated with
coenzyme Q10 at a dose of 150 mg per day.
Thirty-one of 32 patients completed the study;
61.3% of patients had a greater than 50%
reduction in number of days with migraine
headache. The average number of days with
migraine during the baseline period was 7.34 and
this decreased to 2.95 after 3 months of
therapy, which was a statistically significant
response (P < 0.0001). Mean reduction in
migraine frequency after 1 month of treatment
was 13.1% and this increased to 55.3% by the end
of 3 months. Mean migraine attack frequency was
4.85 during the baseline period and this
decreased to 2.81 attacks by the end of the
study period, which was a statistically
significant response (P < 0.001). There were
no side-effects noted with coenzyme Q10. From
this open label investigation coenzyme Q10
appears to be a good migraine preventive.
Placebo-controlled trials are now necessary to
determine the true efficacy of coenzyme Q10 in
migraine prevention.
Glucosamine for
migraine prophylaxis?
Russell AL, McCarty MF. Brampton Pain Clinic,
Bramalea, Ontario, Canada.
Med Hypotheses 2000 Sep;55(3):195-8
Following a fortuitous observation that
migraine headaches ceased in a patient receiving
glucosamine therapy for osteoarthritis, a
further ten patients with migraine or
migraine-like vascular headaches, refractory to
established preventive or abortive therapies,
have been treated with daily oral glucosamine.
After a lag of 4-6 weeks, a substantial
reduction in headache frequency and/or intensity
has been noted; in some cases, the benefit
appears to be dose-dependent. Since glucosamine
can be a rate-limiting precursor for
mucopolysaccharide synthesis, it is germane to
note previous reports that heparin and pentosan
polysulfate may have migraine-preventive
activity. There is reason to suspect that mast
cells are central mediators of the neurogenic
inflammation associated with migraine and
cluster headaches. The heparin produced by mast
cells may function to provide feedback
down-regulation of mast cell activation, and
exerts a range of other anti-inflammatory
effects. We postulate that supplemental
glucosamine can boost mast cell heparin
synthesis - perhaps correcting a functional
heparin deficiency - thereby preventing or
ameliorating the neurogenic inflammation that
mediates pain in vascular headache. Whether or
not this idea has validity, a controlled study
of glucosamine for migraine prophylaxis appears
to be warranted.
Prophylactic
treatment of migraine with beta-blockers and
riboflavin: differential effects on the
intensity dependence of auditory evoked cortical
potentials.
Sandor PS, Afra J, Ambrosini A, Schoenen J.
Neurology Department, CHR Citadelle, University
of Liege, Belgium.
Headache 2000 Jan;40(1):30-5
OBJECTIVE: To investigate the influence of
different pharmacological treatments on the
intensity dependence of auditory evoked cortical
potentials in migraineurs.
BACKGROUND: Between attacks, patients with
migraine show abnormalities in cortical
information processing and decreased brain
mitochondrial energy reserve. Both are most
probably relevant for migraine pathogenesis, and
they could be differentially modified by
prophylactic drug therapy. Design.-The intensity
dependence of the auditory evoked cortical
potentials is, on average, increased in
migraine. We have studied this intensity
dependence in 26 patients before and after a
4-month period of prophylaxis with beta-blockers
(n = 11, all migraine without aura; metoprolol
or bisoprolol) or riboflavin (n = 15, migraine
without aura: 13, migraine with aura: 2).
Recordings were performed at least 3 days before
or after an attack.
RESULTS: After the treatment with
beta-blockers, the intensity dependence of the
auditory evoked cortical potentials was
significantly decreased (before: 1.66+/-1.02
microV/10 dB; after: 0.79+/-1.06 microV/10 dB,
P=.02). The decrease in intensity dependence was
correlated significantly with clinical
improvement (r = .69, P = .02). There was no
change in intensity dependence after riboflavin
treatment (before: 1.80+/-0.81 microV/10 dB;
after: 1.56+/-0.83 microV/10 dB, P = .39),
although the majority of patients showed
improvement.
CONCLUSIONS: These results confirm that
beta-blockers and riboflavin act on two distinct
pathophysiological mechanisms. Combining both
treatments might enhance their efficacy without
increasing central nervous system side
effects.
High-dose
riboflavin as a prophylactic treatment of
migraine: Results of an open pilot
study
Schoenen J.; Lenaerts M.; Bastings E.
University Department of Neurology, CHR de la
Citadelle, Bd du 12 de Ligne 1, 4000 Liege
Belgium
Cephalalgia (Norway), 1994, 14/5
(328-329)
If the brain of migraineurs is characterized
between attacks by a reduction of mitochondrial
phosphorylation potential, riboflavin, which has
the potential of increasing mitochondrial energy
efficiency, might have prophylactic effects in
migraine. In this preliminary open pilot study,
49 patients suffering from migraine (45 without
aura, 4 with aura) were treated with 400 mg of
riboflavin as a single oral dose for at least 3
months. Twenty-three patients received in
addition 75 mg of aspirin. Mean global
improvement after therapy was 68.2% and there
was no difference between the two groups of
patients. With the exception of one patient in
the riboflavin plus aspirin group who withdrew
because of gastric intolerance, no drug-related
side effects were reported. High-dose riboflavin
could thus be an effective, low-cost
prophylactic treatment of migraine devoid of
short-term side effects. A placebo-controlled
trial of its efficacy seems worthwhile.
Pathogenesis of
migraine.
Welch KM Department of Neurology, Henry Ford
Hospital and Health Sciences Center, Detroit,
Michigan 48202, USA.
Semin Neurol (United States) 1997, 17 (4)
p335-41
Prevailing hypotheses for the mechanisms of
migraine are reviewed. Models of aura mechanisms
include transient cerebral ischemia and
spreading depression. Models of headache involve
trigeminovascular and brainstem mechanisms. The
ability to trigger an attack may depend on a
threshold of brain excitability. Mitochondrial
disorder, magnesium deficiency, and abnormality
of presynaptic calcium channels may be
responsible for neuronal hyperexcitability
between attacks. It remains to be determined
whether cortical or brainstem centers generate
the attack. (64 Refs.)
Suggested
Reading
Feverfew and
vascular smooth muscle: extracts from fresh and
dried plants show opposing pharmacological
profiles, dependent upon sesquiterpene lactone
content.
Barsby RW; Salan U; Knight DW; Hoult JR
Pharmacology Group, King's College London,
U.K.
Planta Med (Germany) Feb 1993, 59 (1)
p20-5
Preparations of fresh or dried feverfew
(Chrysanthemum parthenium) are widely consumed
in the U.K. as a remedy for arthritis and
migraine, but the pharmacological basis for this
has not been established. We have, therefore,
compared the properties of extracts of fresh
plants with those of dried powdered leaves
available commercially from health food shops.
The two extracts differed radically in their
content of alpha-methylbutyrolactones and in
their pharmacological profile when tested in
vitro on the rabbit aortic ring and rat
anococcygeus preparations. Extracts of fresh
leaves caused does- and time-dependent
inhibition of the contractile responses of
aortic rings to all receptor-acting agonists so
far tested; the effects were irreversible and
may represent a toxic modification of
post-receptor contractile function in the smooth
muscle. The presence of potentially -SH reactive
parthenolide and other sesquiterpene
alphamethylenebutyrolactones in these extracts,
and the close parallelism of the actions of pure
parthenolide, suggest that the inhibitory
effects are due to these compounds. In contrast,
chloroform extracts of dried powdered leaves
were not inhibitory but themselves elicited
potent and sustained contractions of aortic
smooth muscle that were not antagonised by
ketanserin (5-HT2 receptor antagonist). These
extracts did not contain parthenolide or
butyrolactones according to a chemical-HPLC
assay, We conclude that there are marked
differences in the pharmacological potency and
profiles between preparations from fresh and
dried feverfew and that this may relate to their
lactone content. As the effects of the lactones
are potentially toxic, it will be necessary to
compare the clinical profiles and side effects
of preparations obtained from the two
sources.
Inhibition of
5-lipoxygenase and cyclo-oxygenase in leukocytes
by feverfew. Involvement of sesquiterpene
lactones and other components.
Sumner H; Salan U; Knight DW; Hoult JR
Pharmacology Group, King's College London,
U.K.
Biochem Pharmacol (England) Jun 9 1992, 43
(11) p2313-20
Leaves or infusions of feverfew, Tanacetum
parthenium, have long been used as a folk remedy
for fever, arthritis and migraine, and derived
products are widely available in U.K. health
food shops. Previous reports have suggested
interactions with arachidonate metabolism. Crude
chloroform extracts of fresh feverfew leaves
(rich in sesquiterpene lactones) and of
commercially available powdered leaves
(lactone-free) produced dose-dependent
inhibition of the generation of thromboxane B2
(TXB2) and leukotriene B4 (LTB4) by ionophore-
and chemoattractant-stimulated rat peritoneal
leukocytes and human polymorphonuclear
leukocytes. Approximate IC50 values were in the
range 5-50 micrograms/mL, and inhibition of TXB2
and LTB4 occurred in parallel. Isolated lactones
(parthenolide, epoxyartemorin) treated with
cysteine (to neutralize reactive alpha-methylene
butyrolactone functions of the sesquiterpenes).
Inhibition of eicosanoid generation appeared to
be irreversible but not time-dependent. We
conclude that feverfew contains a complex
mixture of sesquiterpene lactone and
non-sesquiterpene lactone inhibitors of
eicosanoid synthesis of high potency, and that
these biochemical actions may be relevant to the
claimed therapeutic actions of the herb.
Efficacy of
feverfew as prophylactic treatment of
migraine.
Johnson ES; Kadam NP; Hylands DM; Hylands
PJ
Br Med J (Clin Res Ed) (England) Aug 31 1985,
291 (6495) p569-73
Seventeen patients who ate fresh leaves of
feverfew daily as prophylaxis against migraine
participated in a double blind placebo
controlled trial of the herb: eight patients
received capsules containing freeze dried
feverfew powder and nine placebo. Those who
received placebo had a significant increase in
the frequency and severity of headache, nausea,
and vomiting with the emergence of untoward
effects during the early months of treatment.
The group given capsules of feverfew showed no
change in the frequency or severity of symptoms
of migraine. This provides evidence that
feverfew taken prophylactically prevents attacks
of migraine, and confirmatory studies are now
indicated, preferably with a formulation
controlled for sesquiterpene lactone content, in
migraine sufferers who have never treated
themselves with this herb.
Herbal therapy
for migraine: An unconventional
approach
Diamond S. Inpatient Headache Unit at Louis
A. Weiss Memorial Hospital, Chicago, IL United
States
Postgraduate Medicine (United States) 1987,
82/1 (197-198)
A pilot study was conducted at the City of
London Migraine Clinic to establish whether
feverfew 's efficacy could be shown through
orthodox clinical evaluation and also to
demonstrate any adverse effects on cellular and
chemical elements of the blood. Because of
possible ethical objections, only patients who
had previously consumed feverfew leaves were
included in the study.
Platelet ionized
magnesium, cyclic AMP, and cyclic GMP levels in
migraine and tension-type headache.
Mishima K; Takeshima T; Shimomura T; Okada H;
Kitano A; Takahashi K; Nakashima K Division of
Neurology, Tottori University Faculty of
Medicine, Yonago, Japan.
Headache (United States) Oct 1997, 37 (9)
p561-4
Decreased serum and intracellular levels of
magnesium have been reported in patients with
migraine . It has been suggested that magnesium
may play an important role in the attacks and
pathogenesis of headaches. We measured ionized
magnesium, cyclic AMP (adenosine monophosphate),
and cyclic GMP (guanosine monophosphate) in
platelets of patients with migraine, in patients
with tension-type headache, and in healthy
controls. The platelet level of ionized
magnesium from patients with tension-type
headache was significantly lower than the levels
from the other two groups. The platelet level of
cyclic AMP from patients with migraine was
higher than those from the other groups. We
found no significant differences in the platelet
cyclic GMP levels among the three groups. It is
suggested that reduced platelet ionized
magnesium in patients with tension-type headache
is related to abnormal platelet function, and
that increased platelet cyclic AMP in patients
with migraine is related to alteration of
neurotransmitters in the platelet.
Omega- 3:
Essential for good health
Pelton R.
American Druggist (United States) 1997, 214/7
(52-53)
Supplements of omega -3 fatty acids may be
needed to maintain a careful balance with
omega-6 and regulate the production of
prostaglandins and their effects.
Pathophysiology
of the migraine aura
Cortelli P.; Pierangeli G.; Cevoli S.;
Montagna P. P. Cortelli, Clinica Neurologica,
Universita degli Studi, Bologna Italy
Bollettino - Lega Italiana contro l'Epilessia
(Italy) 1997, -/99 (359-362)
Modern techniques have improved our knowledge
of the pathophysiology of the migraine . In
general two approaches have been taken, modeling
the mechanisms of the attack and modeling the
true cause of migraine, in other word, the
mechanisms through which the attacks are
triggered. From animal experiments it is known
that there are two possible explanation for the
migraine aura. Aura symptoms could arise from
spreading depression or from the oligoemia due
to changes in diameter of small cerebral
vessels. Preliminary data obtained by functional
imaging techniques such as PET and f- MR
indicates that the spreading depression model
appears the most plausible to account for the
migraine aura. Neurophysiological, CBF and brain
metabolic measures have suggested neuronal and
neurovascular instability between migraine
attacks. A mitochondrial defect or a disturbance
in magnesium metabolism could account, alone or
in combination, for neuronal hyperexcitability
especially in the occipital cerebral cortex. In
families linked to chromosome 19, familial
hemiplegic migraine is caused by point mutations
in the CACNL1A4 gene coding for a P/Q type brain
specific a1 subunit calcium channel. This will
open a new window on the understanding the
pathophysiology of the migraine .
Food and
headache
Rose F.C. Dr. F.C. Rose, London Neurological
Centre, 110 Harley Street, London W1N 1AF United
Kingdom
Headache Quarterly (United States) 1997, 8/4
(319-329)
Objective: To review the significant
literature relating to food and headache. Data
sources study selection and data extraction:
Medline review and extraction. Synthesis was
done by selecting the more recant 'hard science'
articles.
Conclusion: Red wine can be a trigger for
migraine attacks in susceptible patients.
Susceptibility may be related to the low level
of phenosulphotransferase P, the enzyme that
detoxicates flavonoid phenols found in red wine.
Other types of alcohol drinks can also
precipitate migraine but their mechanism is
different. Chocolate may precipitate attacks
because of its phenolic content. Other dietary
triggers are probably multifactorial, ie they
trigger attacks only under certain
circumstances. Fasting is a wall- authenticated
trigger but not because of hypoglycemia . More
research needs to be done in this field as
dietary triggers can throw light on the
pathogenesis of headache.
Migraine
treatment
Young W.B.; Silberstein S.D.; Dayno J.M. Dr.
W.B. Young, Jefferson Headache Center, Thomas
Jefferson University Hospital, 111 S.11 St.,
Philadelphia, PA 19107 United States
Seminars in Neurology (United States) 1997,
17/4 (325-333)
Migraine is a primary headache disorder
characterized by recurring attacks of pain and
associated symptoms. Migraine sufferers require
a continuum of clinical care that depends on
their disability and response to treatment.
Treatment consists of: (1) prevention of attacks
by avoidance of triggers; (2) the use of
nonpharmacologic treatments; (3) treatment of
the acute attack; and (4) long-term prophylactic
therapy. Migraine is comorbid for affective
disorders, epilepsy, stroke, and mitral valve
prolapse. The therapy selected depends on the
headache severity and frequency, the pattern of
associated symptoms, comorbid illnesses, and the
patient's treatment response profile. Acute
treatment can be symptomatic or specific, using
drugs such as dihydroergotamine (DHE) or
sumatriptan. Preventive treatment can be
episodic, subacute, or chronic. The major drug
groups include beta- adrenergic blockers,
antidepressants, calcium channel blockers,
serotonin antagonists, anticonvulsants, and
nonsteroidal anti-inflammatory drugs (NSAIDs).
These can be divided into two major categories
and second-line choices.
In search of the
ideal treatment for migraine
headache.
Bic Z; Blix GG; Hopp HP; Leslie FM School of
Public Health, Loma Linda University, CA
92350-0001, USA.
Med Hypotheses (England) Jan 1998, 50 (1)
p1-7
Migraine headache is a common syndrome,
afflicting millions, that has so far defied a
definitive cure. Experimental research studies
of the syndrome tend to describe the triggering
factors separately. We propose a common
denominator--namely, high levels of blood lipids
and free fatty acids--as underlying factor in
the development of migraine headaches.
Biological states that may cause increases in
free fatty acids and blood lipids include: high
dietary fat intake, obesity, insulin resistance,
vigorous exercise, hunger, consumption of
alcohol, coffee, and other caffeinated
beverages, oral contraceptives, smoking, and
stress. Elevated blood lipids and free fatty
acids are associated with increased platelet
aggregability, decreased serotonin, and
heightened prostaglandin levels. These changes
lead to the vasodilatation that precedes
migraine headache. We suggest that migraine
headache should not be seen as an isolated
symptom, but as a first signal of potential
biochemical imbalances in the body, which can
lead to development of chronic disease. (69
Refs.)
Diet and
migraine
Leira R; Rodriguez R Servicio de Neurologia,
Hospital General de Galicia Clinico
Universitario, Santiago de Compostela.
Rev Neurol (Spain) May 1996, 24 (129)
p534-8
Some foods in our diet can spark off migraine
attacks in susceptible individuals. Some foods
can bring an attack on through an allergic
reaction. A certain number such as citrus
fruits, tea, coffee, pork, chocolate, milk,
nuts, vegetables and cola drinks have been cited
as possible allergens associated with migraine .
This mechanism has however been criticized: an
improvement in symptoms by eliminating some
food(s) from our diet does not necessarily mean
an immunologically based allergic reaction. The
high IgE incidence rate is not greater in such
patients than in the population at large. Other
allergic reactions unrelated to diet may also be
associated with migraine attacks. On the other
hand substances in food may be the cause of
modifications in vascular tone and bring
migraine on in those so prone. Among such
substances are tyramine, phenylalanine, phenolic
flavonoids, alcohol, food additives (sodium
nitrate, monosodium glutamate, aspartame) and
caffeine. Another recognized trigger for
migraine is hypoglycemia. Such foods as
chocolate, cheese, citrus fruits, bananas, nuts,
'cured' meats, dairy products, cereals, beans,
hot dogs, pizza, food additives (sodium nitrate,
monosodium glutamate in Chinese restaurant food,
aspartame as a sweetener), coffee, tea, cola
drinks, alcoholic drinks such as red wine, beer
or whisky distilled in copper stills, all may
bring on a migraine attack. For every patient we
have to assess which foodstuffs are involved in
the attack (not necessarily produced by
consuming the product concerned) in order to try
to avoid their consumptions as a means of
prophylaxis for migraine . (46 Refs.)
Dietary factors
in migraine precipitation: The physicians'
view
Blau J.N.; Diamond S. The National Hospital
for Nervous Diseases, City of London Migraine
Clinic, London United Kingdom
Headache (United States) 1985, 25/4
(184-187)
Five hundred and fifty questionnaires were
sent to members of the American Association for
the Study of Headache as well as to British
physicians with a known interest in migraine .
Of the 327 that replied, only 21% favored the
term 'dietary migraine '. To determine the
presence of food sensitivity in their patients
71% relied on information from the patient's
history alone. However, 21% employed special
tests in addition to the history. Estimates of
the percentage of patients in whom dietary
factors were operative ranged from 0-80%.
Seventy-four percent were in the 0-20% range
(some indicating an incidence nearer 1-5% or
less). Sixteen percent estimated the range of
their patients in whom diet provoked migraine
was between 20-40%, three percent estimated
40-60%, and two percent 60-80%. The foods most
commonly cited as triggering agents are
presented in descending rate of frequency:
chocolate, alcohol, cheese, monosodium
glutamate, nuts, citrus fruit, meat, coffee,
nitrates, fish, dairy products, onions, hot
dogs, pizza, wheat products, bananas, tomatoes,
apples, and various vegetables. Individual
comments invited on the questionnaire are
described. The consensus is that foods or
alcohol can provoke occasional attacks in some
patients. They conclude that the appropriate
term is 'dietary precipitated migraine'.
Pathogenesis of
posttraumatic headache and migraine: a common
headache pathway?
Packard RC; Ham LP Headache Management and
Neurology, Pensacola, FL 32503, USA.
Headache (United States) Mar 1997, 37 (3)
p142-52
In recent years, research implicating
biochemical abnormalities in various
pathological conditions has spiralled. Headache
is an area in which numerous research studies
have been conducted examining biochemical
alterations. We have noticed several
similarities in biochemical changes reported to
occur in migraine and in experimental traumatic
brain injury. The most common symptom in mild
head injury or mild traumatic brain injury is
headache which, in many instances, resembles
migraine but has a poorly understood
pathophysiology. Biochemical mechanisms believed
to be similar in both conditions include:
increased extracellular potassium and
intracellular sodium, calcium, and chloride;
excessive release of excitatory amino acids;
alterations in serotonin; abnormalities in
catecholamines and endogenous opioids; decline
in magnesium levels and increase in
intracellular calcium; impaired glucose
utilization; abnormalities in nitric oxide
formation and function; and alterations in
neuropeptides. In this paper, these proposed
biochemical alterations will be reviewed and
compared. Very similar alterations suggest
posttraumatic headache associated with mild head
injury and migraine may share a common headache
pathway. (114 Refs.)
[Migraine--diagnosis, differential
diagnosis and therapy]
Diener HC Klinik und Poliklinik fur
Neurologie, Universitat Essen.
Ther Umsch (Switzerland) Feb 1997, 54 (2)
p64-70
Migraine is caused by intermittent brain
dysfunction. Attacks result in severe unilateral
headache with nausea, vomiting, photophobia,
phonophobia and general weakness. The prevalence
of migraine is 12 to 20% in women and 8 to 12%
in man. Treatment of an acute attack is done by
antiemetics in combination with analgesics.
Severe migraine attacks are treated with
ergotamine or sumatriptan. Parenteral treatment
is performed most efficiently and safely with
i.v. ASA. Frequent and severe attacks require
prophylaxis. Drugs of first choice are
metoprolol, propranolol, flunarizine and
cyclandelate. Substances of second choice are
valproic acid, DHE, pizotifen, methysergide and
magnesium. Homeopathic remedies are not superior
to placebo. Nonpharmacological treatment
consists of sport therapy and muscle relaxation
techniques.
Magnesium
taurate and fish oil for prevention of
migraine.
McCarty MF Nutrition 21, San Diego, CA 92109,
USA.
Med Hypotheses (England) Dec 1996, 47 (6)
p461-6
Although the pathogenesis of migraine is
still poorly understood, various clinical
investigations, as well as consideration of the
characteristic activities of the wide range of
drugs known to reduce migraine incidence,
suggest that such phenomena as neuronal
hyperexcitation, cortical spreading depression,
vasospasm, platelet activation and sympathetic
hyperactivity often play a part in this
syndrome. Increased tissue levels of taurine, as
well as increased extracellular magnesium, could
be expected to dampen neuronal hyperexcitation,
counteract vasospasm, increase tolerance to
focal hypoxia and stabilize platelets; taurine
may also lessen sympathetic outflow. Thus it is
reasonable to speculate that supplemental
magnesium taurate will have preventive value in
the treatment of migraine. Fish oil, owing to
its platelet-stabilizing and antivasospastic
actions, may also be useful in this regard, as
suggested by a few clinical reports. Although
many drugs have value for migraine prophylaxis,
the two nutritional measures suggested here may
have particular merit owing to the versatility
of their actions, their safety and lack of
side-effects and their long-term favorable
impact on vascular health. (94 Refs.)
Prophylaxis of
migraine with oral magnesium: results from a
prospective, multi-center, placebo-controlled
and double-blind randomized study.
Peikert A; Wilimzig C; Kohne-Volland R
Department of Neurology and Clinical
Neurophysiology, Munich-Harlaching Clinic,
Germany.
Cephalalgia (Norway) Jun 1996, 16 (4)
p257-63
In order to evaluate the prophylactic effect
of oral magnesium, 81 patients aged 18-65 years
with migraine according to the International
Headache Society (IHS) criteria (mean attack
frequency 3.6 per month) were examined. After a
prospective baseline period of 4 weeks they
received oral 600 mg (24 mmol) magnesium
(trimagnesium dicitrate) daily for 12 weeks or
placebo. In weeks 9-12 the attack frequency was
reduced by 41.6% in the magnesium group and by
15.8% in the placebo group compared to the
baseline (p < 0.05). The number of days with
migraine and the drug consumption for
symptomatic treatment per patient also decreased
significantly in the magnesium group. Duration
and intensity of the attacks and the drug
consumption per attack also tended to decrease
compared to placebo but failed to be
significant. Adverse events were diarrhea
(18.6%) and gastric irritation (4.7%). High-dose
oral magnesium appears to be effective in
migraine prophylaxis.
Electromyographical ischemic test
and intracellular and extracellular magnesium
concentration in migraine and tension-type
headache patients.
Mazzotta G; Sarchielli P; Alberti A; Gallai V
Interuniversity (Perugia-Rome-Sassari-Bari)
Centre for the Study of Headache and
Neurotransmitter Disorders of the CNS,
Italy.
Headache (United States) Jun 1996, 36 (6)
p357-61
Headache has often been described in the
hyperexcitability syndrome which recognizes an
alteration of calcium and magnesium status in
its etiopathogenesis. Moreover, in migraine
patients magnesium has been shown to play an
important role as a regulator of neuronal
excitability and, therefore hypothetically, of
headache. The present research involves a
neurophysiological evaluation and magnesium
status assessment of a group of headache
patients. Nineteen patients (15 women and 4 men)
with episodic tension-type headache and 30
patients (27 women and 3 men) with migraine
without aura were examined. An ischemic test was
carried out on the right arm with
electromyographic (EMG) recording of motor unit
potential activity during the interictal period.
The determination of extracellular (serum and
saliva) and intracellular (red and mononuclear
blood cells) magnesium was also performed. The
EMG test was positive in 25 of 30 migraine
patients and in 2 of 19 tension-type headache
patients. Between the two patient groups, there
were no significant variations in the
concentration of extracellular and white blood
cell magnesium, while the red blood cell
concentration of this mineral in the group of
migraineurs was significantly reduced with
respect to that in the group of tension-type
headache patients (P < 0.05). The positive
EMG test was significantly associated with a low
concentration of red blood cell magnesium (P
< 0.0001). These results confirm previous
findings by demonstrating different
etiopathogenic mechanisms as the basis of
migraine and tension-type headache. Migraine
seems to be related to an altered magnesium
status, which manifests itself by a
neuromuscular hyperexcitability and a reduced
concentration in red blood cells.
Long-time
efficacy of cyclandelate and propranolol in
prophylaxis of migraine following four months of
treatment
Schellenberg R.; Schwarz A.; Niederberger U.;
Bolsche F.; Schindler M.; Gerber W.-D.; Wedekind
W.; Soyka D. Dr. R. Schellenberg, Talstrasse 29,
D-35625 Huttenberg Germany
Nervenheilkunde (Germany), 1997, 16/3
(183-187)
After a 4 months randomized double-blind
study with cyclandelate versus propranolol all
patients kept a miniaturized headache diary for
one more year. Both duration of migraine attacks
in hours and the number of additional analgetic
medication were recorded monthly. Reduction of
the duration of migraine attacks in the clinical
responders of the cyclandelate treated patients
remained nearly unchanged. In the propranolol
responders the duration of migraine attacks in
hours increased from the third month after
finishing the medication and reached values
comparable to those at the beginning of the
active treatment. Intake of additional analgetic
medication during the 1-year-follow-up was lower
in the cyclandelate responders than in the
propranolol-responders. Cyclandelate can be
described as an effective long-lasting drug in
migraine prophylaxis.
Nocturnal
melatonin excretion is decreased in patients
with migraine without aura attacks associated
with menses
Brun J.; Claustrat B.; Saddier P.; Chazot
G.
Cephalalgia (Norway), 1995, 15/2
(136-139)
Nocturnal melatonin excretion was studied
throughout a complete menstrual cycle in 10
women with migraine without aura attacks
associated with menses and 9 women controls.
Urine melatonin was determined by
radioimmunoassay. The mean nocturnal melatonin
excretion throughout the cycle was significantly
lower in the migraine patients than in controls.
In the control group, melatonin excretion
increased significantly from the follicular to
the luteal phase, whereas no difference was
observed in the migraine group. Results are
discussed in view of the role of the pineal
gland in the organization of biological rhythms
and homeostasis in relation to environmental
conditions.
Urinary
melatonin excretion throughout the ovarian cycle
in menstrually related migraine
Murialdo G.; Fonzi S.; Costelli P.; Solinas
G.P.; Parodi C.; Marabini S.; Fanciullacci M.;
Polleri A. Endocrinological/Metabol. Sci. Dept.,
Viale Benedetto XV, 6, I-16132 Genoa Italy
Cephalalgia 1994 Jun;14(3):205-9
Nocturnal urinary melatonin excretion was
significantly decreased throughout an ovarian
cycle in 12 migraine without aura patients
compared to 8 healthy controls. Normal increases
in urinary melatonin excretion during the luteal
phase was less pronounced in the migraine
patients. Melatonin excretion was further
decreased during headache. The data indicate
impaired pineal function in migraine.
Nocturnal plasma
melatonin levels in migraine: A preliminary
report
Claustrat B, Loisy C, Brun J, Beorchia S,
Arnaud JL, Chazot G
Headache (United States) Apr 1989, 29 (4)
p242-5
We determined by radioimmunoassay plasma
melatonin levels on blood samples drawn at 11
p.m. in migraine patients and control subjects.
Ninety-three cephalalgic outpatients (75
females, 18 males) were compared to a control
group (24 females, 22 males) matched according
to age. Patients were divided into subgroups
presenting common migraine (n = 38); ophthalmic
migraine (n = 12); and tension headache
associated with ophthalmic or common migraine (n
= 24), and associated depressive status (n =
19). Statistical analysis revealed a decrease in
plasma melatonin levels for the entire migraine
population, compared to the control one, and a
heterogeneity in both controls and patients;
this heterogeneity was found mainly in the
depressive and tension headache subgroups. When
the migraine population - from which the
depressive patients were excluded - was divided
into male and female subgroups, a decrease in
plasma melatonin levels was observed only for
the female subgroups. Results are discussed with
reference to the role of the pineal gland in the
synchronization of the organism with the
environmental conditions.
The influence of
the pineal gland on migraine and cluster
headaches and effects of treatment with
picoTesla magnetic fields.
Sandyk R
Int J Neurosci (England) Nov-Dec 1992, 67
(1-4) p145-71
For over half a century the generally
accepted views on the pathogenesis of migraine
were based on the theories of Harold Wolff
implicating changes in cerebral vascular tone in
the development of migraine. Recent studies,
which are based on Leao's concept of spreading
depression, favor primary neuronal injury with
secondary involvement of the cerebral
circulation. In contrast to migraine, the
pathogenesis of cluster headache (CH) remains
entirely elusive. Both migraine and CH are
cyclical disorders which are characterised by
spontaneous exacerbations and remissions,
seasonal variability of symptoms, and a
relationship to a variety of environmental
trigger factors. CH in particular has a strong
circadian and seasonal regularity. It is now
well established that the pineal gland is an
adaptive organ which maintains and regulates
cerebral homeostasis by "fine tuning" biological
rhythms through the mediation of melatonin.
Since migraine and CH reflect abnormal adaptive
responses to environmental influences resulting
in heightened neurovascular reactivity, I
propose that the pineal gland is a critical
mediator in their pathogenesis. This novel
hypothesis provides a framework for future
research and development of new therapeutic
modalities for these chronic headache syndromes.
The successful treatment of a patient with an
acute migraine attack with external magnetic
fields, which acutely inhibit melatonin
secretion in animals and humans, attests to the
importance of the pineal gland in the
pathogenesis of migraine headache. (242
Refs.)
Is migraine due
to a deficiency of pineal
melatonin?
Toglia JU
Ital J Neurol Sci (Italy) Jun 1986, 7 (3)
p319-23
Recent clinical observations favor the theory
that migraine is caused by a primary injury of
cerebral neurons with secondary involvement of
intracranial and extracranial blood vessels. The
primary injury is attributed to disruption of
cerebral neurotransmitters and particularly the
neuroadrenergic and serotonergic systems. These
theories have not explained the importance of
environmental factors, which so frequently
trigger migraine. The author suggests that the
pineal gland, which is outside the CNS
unprotected by blood brain barrier and sensitive
to external stimuli, could act as the
intermediate causative factor of migraine, via a
derangement of melatonin. (47 Refs.)
FEVERFEW
(Tanacetum pathenium):
Feverfew appears to work in the treatment and
prevention of migraine headaches by inhibiting
the release of blood vessel dilating substances
from platelets (serotonin and histamine),
inhibiting the production of inflammatory
substances (leukotrienes, serine proteases,
etc.), and re-establishing proper blood vessel
tone. Commercial sources providing assurance of
botanical identity and minimum required level of
parthenolides are needed (Awang DVC. Feverfew.
Car Pharm J 122:266-70, 1989).
In vitro Study: Feverfew was found to contain
a factor that inhibits prostaglandin synthesis,
but differs from salicylates by not inhibiting
cyclo-oxygenase by prostaglandin (PG) synthase.
"The ability of feverfew to inhibit PG
production may account for its effectiveness as
a herbal remedy in conditions responding to
acetylsalicylate and like-acting drugs" (Collier
HOJ, Butt NM, McDonald-Gibson WJ, Saeed SA.
Extract of feverfew inhibits prostaglandin
biosynthesis. Letter. lancet October 25,
1980).
The dosage of feverfew used in one
double-blind study was one capsule containing 25
mg of the freeze-dried pulverized leaves twice
daily; in another double-blind study it was one
capsule containing 82 mg of dried powdered
leaves once daily. While these low dosages may
be effective in preventing an attack, a higher
dose (I to 2 grams) may be necessary during an
acute attack.
Note: The efficacy of feverfew is dependent
upon adequate levels of parthenolide, the active
ingredient. (The preparations used in successful
clinical trials have a parthenolide content of
0.4-0.66%.)
Animal Ex vivo Study: Extracts of fresh
feverfew caused a dose- and time dependent,
irreversible inhibition of the contractile
response of rabbit aortic rings to all
receptor-acting agonists tested. The presence of
potentially SH reacting parthenolide and other
sesquiterpene alpha-methylenebutyrolactones in,
these extracts, and the close parallelism of
pure parthenolide, suggest that the inhibitory
effects are due to these compounds. Extracts of
the dry leaves were not inhibitory and actually
caused potent and sustained contractions of
aortic smooth muscle; these extracts were found
to be devoid or parthenolide or butyrolactones
(Barsby RWJ, Salan U, Knight BW, Hoult JRS.
Feverfew and vascular smooth muscle: Extracts
from fresh and dried plants show opposing
pharmacological profiles, dependent upon
sesquiterpene lactone content. Planta Medica
59:20-5, 1993).
Chemical Analysis: The parthenolide content
of over 35 different commercial preparations of
feverfew was determined by bioassay, 2 HPLC
methods, and NMR. The results indicate a wide
variation in the amts. of parthenolide in
commercial preparations. The majority of
products contained no parthenolide or only
traces (Heptinstall S et al. Parthenolide
content and bioactivity of feverfew (Tanacetum
parthenium (L.) Schultz-Bip.). Estimation of
commercial and authenticated feverfew products.
J Pharm Pharmaco1 44:391-5, 1992).
WARNING: No long-term toxicity studies have
been conducted. While feverfew is extremely
well-tolerated and no serious side effects have
ever been reported, chewing the leaves can
result in small ulcerations in the mouth and
swelling of the lips and tongue in about 10% of
users (Awang DVC. Feverfew. Can Pharml
122:266-70,
1989). |