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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).
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