ARTICLE
Auteur(s) :, J
Durlach1,*, Nicole Pagès2, Pierre
Bac3, Michel Bara4, Andrée
Guiet-Bara4
1SDRM, Université Pierre et Marie Curie, Paris VI,
75252 Paris Cedex 05, France ;
2Laboratoire de toxicologie, Faculté de pharmacie,
Strasbourg, 67400 Illkirch-Grafenstaden, France ;
3Laboratoire de physiologie et pathologie, UPMC, 75252
Paris, Cedex 05, France ;
4Laboratoire de physiologie et pathologie, UPMC, 75252
Paris, Cedex 05, France
Patients complain of headache very often, since approximatively
70-75% of men and more than 80% of women are concerned. The great
majority of headaches are idiopathic in origin. Although they are
currently classified as Tension Type Headache (TTH) or Migraine
(M), this classification does not result in the delineation of
separate headache types. A clinical approach shows a continuum
ranging from mild to moderate then severe headaches, with clinical
symptoms, pathophysiological mechanisms and therapies similar in
both M and TTH. Clinicians and researchers alike may find it more
logical to use a continuum approach to primary headaches
[1-3].Headache patients often exhibit a hypersensitivity to light,
usually with photophobia – its clinical marker –, during and
between the algic attacks [4-17].Headache frequently appears as
related to magnesium deficit. Cephalalgia represents a symptom of
the nervous form of magnesium deficient balance and magnesium
depletion in particular may play a role in the pathophysiology of
migraine [3, 18, 19].The aim of this study was to stress the
importance of photosensitivity in headache; to analyze the place of
magnesium deficit in photosensitive cephalalgic patients; to
hypothesize a causality link between these factors with the
clinical and pathophysiological notion of « headache due to
photosensitive magnesium depletion »; to conclude with the
therapeutic consequences of this new concept, which encompasses a
large part of the so-called primary headaches.
Importance of the light sensitivity in headache patients
Clinical symptoms
Reported symptoms
In photosensitive headaches - of the migraine type - during algic
attacks (ictal period) but alsobetween episodes (interictal
period), light stimuli can trigger photophobia, the clinical
marker of light sensitivity and a common symptom in primary
headache. The term photophobia is derived from the Greek photo
(light) and phobia (fear or dread of) -hence « fear of
light ». This abnormal sensitivity to light may appear as pain
on exposure to light or an uncomfortable sense of glare. This
symptom is generally self-reported or diagnosed when questioning
patients. As early as the second century, A.D. Aretaei Cappadocis
had written (in liber IV) « fugiunt enim quodam modo lucem,
tenebrae aegritudinem solentur » (they avoid light by all
possible means and the dark subsides their feeling of sickness).
Today light intolerance is a well recognized symptom of primary
headache, and the patient may be improved by retreating into a dark
room [3-16].
Physical symptoms
The so-called « tinted glass sign » may be considered as
an indirect symptom of light hypersentivity. Photophobic patients
wear sunglasses in normal daylight. Frequent wearing of tinted
spectacles indoors is pathological. Though it may be a physical
sign of photosensibility, it may also be recorded as « a
marker of neurotic and hypochondrial personality » or « a
valid indicator of psychological distress ». All of these
various interpretations may be valid: photosensitivity may induce
anxiety, anxiety may be a precipitating factor of photosensitive
headache, the symptomatology may be increased by a neurotic
personality and by distress [20-23].
Paraclinical examinations
Objective paraclinical examinations involve: visual stress tests
which evaluate visual stress thresholds, in order to obtain
quantitative assessment of light induced-discomfort; electrical
photic response, studied through EEG tracings; circulating
photic response, studied through either Transcranial Doppler,
or Magnetic Resonance Imaging; visual Evoked Potentials.
Visual stress tests
Several types of exposure to light during interictal periods may
induce visual discomfort in cephalalgic patients such as certain
geometric patterns such as parallel lines of alternate light
and dark stripes, flicker, colors and fluorescent
light.
To sum up: photosensitive headache patients exhibit a
hyper-sensitivity to light during and between the attacks. Pain
thresholds are lower than in controls. Migraineurs are more
sensitive interictally to light stimuli than TTH patients during
attack and than controls [8, 12, 14, 15, 20-24].
ElectroEncephaloGram (EEG) photic response
In 1953, Mundy-Castle reported « considerably greater mean
response amplitude to photic stimulation » in headache
patients, during routine EEG.
Later Golla and Winter (1959) described persistance of photic
driving to 20 Hz flashes or above (the H response) in
headache patients.
Although many studies considered the H response as an EEG marker
of migraine, it is no longer considered as valid in routine
evaluation since « the sensitivity and specificity of the H
response are too low to change the probability of the presence of
migraine in a clinically significant way... », so « we do
not recommend the use of EEG instead of head cranial tomography or
magnetic resonance imaging in evaluating headache patients with
suspected intracranial pathology ». But a prominent photic
driving may identify clinical subsets of photosensitive headache
patients [29]. In addition a dynamic notion must be stressed since
photic driving power decreases (towards normal values) during the
headache phase [30, 31]. In any case there is a complete overlap of
the H response between the two main primary headache subgroups TTH
and M which agrees with the so-called continuum severity theory:
the lower limit of the continuum is TTH which progressively evolves
into migraine and finally into migraine with aura [30].
These various clinical forms of primary headache with abnormal
visual reactivity are compatible with the concept of
« photosensitive headache » [7, 10, 24-32].
Cerebrovascular photic responses
Circulatory responses have been studied through either TransCranial
Doppler (TCD), or Magnetic Resonance Imaging (MRI).
Changes in the cerebral perfusion were studied during repetitive
visual stimulation by functional TCD in the right posterior
cerebral artery and the left middle cerebral artery in interictal
migraineurs. They exhibited a steady increase in cerebral blood
flow velocity while normal subjects showed habituation. The lack
of habituation of the cerebrovascular response in migraineurs
was significantly more pronounced among patients with a high attack
frequency (at least 4 per month) compared with migraineurs with a
low attack frequency (less than 4 per month) [33]. These
cerebrovascular data, in accordance with neurophysiological
findings in migraineurs highlight the importance of the lack of
habituation in the pathophysiology of migraine.
Another study, using functional MRI, examined changes in resting
perfusion and in activation within the occipital cortex due to
photic stimulation in both controls and true menstrual migraine
patients. No difference in resting baseline perfusion was observed
between the two groups during either phase of the menstrual cycle.
But the results differed after photic stimulation. During the late
luteal phase, changes in perfusion within the occipital lobe were
similar for both groups. whereas it decreased in controls,
but significantly increased in menstrual migraine patients
during the mid-follicular phase.
A significant difference (p < 0.05) was observed in the mean
values for photic activation among the true menstrual
migraine patients compared to normals, after allowing for
effects of differences in cycle (late luteal phase versus
mid-follicular phase) [34].
Visual evoked potentials
Classical Visual Evoked Potentials (VEPs) concern the reactivity of
electrocortical activity to visual stimuli generated by either
transient flash (luminance stimulus) or checkerboard pattern
(contrast stimulus).
Stimulation produced surprising contradictory results since an
increased amplitude was often found in migraine, the typical form
of photoreactive headache.
Habituation has been studied after repetitive visual
stimuli. Visual stimuli were presented for example, as a
checkerboard pattern of 8 min of arc, black and white squares
(contrast 80%), at a reversal frequency of 3.1 Hz. Five
consecutive blocks of 50 responses averaging a total number of 250
responses were analyzed separately for latencies, peak to peak
amplitudes and areas under the components. Habituation was assessed
as the amplitude changes in blocks 2-5 compared to block 1.
Habituation was observed in healthy subjects. Migraine patients
were characterized by an amplitude increment (potentiation) of VEPs
components which reached their maximum value in the second to the
fourth blocks. Potentiation instead of habituation characterizes
VEPs in migraine patients between attacks [39]. Electrophysiologic
studies demonstrate that, the hallmark of migraine between
attack, is a deficient habituation.
Lack of habituation has been observed not only in migraineurs’
visual evoked potentials (and in related parents’), but also in
many other neurophysiologic data: other sensory and somato sensory
evoked potentials, event-evoked potentials (contingent negative
variation), cerebrovascular responses to visual stimuli [3-7,
35-60].
Habituation is a physiological phenomenon characterized
by a decrease in the responses to repetitive stimuli. It is
considered to be a protective mechanism against
overstimulation.
Dishabituation, by contrast, is a process that liberates
the nervous system from the habituation process. Dishabituation
stimuli act as sensitization or potentiation processes which
rely on a dysfunctioning of cortical information processing. The
dysfunction might result from the high level of cortical arousal
with increased energy demands and from hypofunction of the
subcortico-cortical pathways. Visual potentiation depends on the
type of visual subsystem which is preferentially activated, either
the magnocellular (luminance and motion sensitive) or the
parvocellular (contrast and colour sensitive) systems. The cortical
arousal level depends on the effects of various neurotransmitters
from the brainstem projecting to the cortex. Serotonin acts as a
gain control between a noradrenergic, unspecific, facilitating
system and a cholinergic, specific, inhibitory system.
Dishabituation may finally induce generalization when the
nervous alteration involves other stimuli or invades other
substrates. Generalization may concern various selective or global
targets such as hearing in particular (with phonophobia), smell
(with cacosmia), touch (with allodynia), diet (with alimentary
intolerance).
To sum up: there is an adaptative dysfunction to environmental
conditions in migraine [3, 9, 16, 24, 30, 41, 46-88].
Finally, the clinical and paraclinical data on the importance of
light sensitivity in primary headache demonstrate that: i) the
concept of photoreactive headache is fully justified. It may
correspond to a large number of the so-called primary
headaches, M and TTH particularly. Photosensitivity, as
well as its clinical marker photophobia, may be inherited or
acquired; ii) the interictal hallmark of such cephalalgic patients
is dishabituation with pathophysiologic potentiation (or
sensitization) instead of physiologic habituation; this
dishabituation is observed in all the studied types of repetitive
stimuli: sensory (i.e. auditory), cognitive (i.e. contingent
negative variation), painful (i.e. laser), sensory motor (i.e.
blink reflex), cerebrovascular (through TCD or MRI).
Photosensitive headache and magnesium status
Migraine may be considered as the paradigm for PhotoSensitive
Headache. An oral magnesium load test was performed to determine
whether migraineurs had a disorder of magnesium status. Two groups
of either migraineurs (n = 20) and to healthy volunteers (n = 20)
were given 3000 mg of magnesium lactate during a 24h period
(interictal for migraineurs. The 24h urinary magnesium excretions
were significantly lower (p = 0.0007) in migraineurs than in
controls after loading, suggesting a systemic magnesium deficit
[89].
A body of evidence has already stressed the difference between
two types of magnesium deficits:
- – deficiency linked to an insufficient intake
which may be corrected, through physiological nutritional oral
magnesium supplementation, over a long period of time;
- – depletion due to a dysregulation of the
magnesium status which cannot be corrected through nutritional
supplementation only, but requests the most specific control of the
dysregulation mechanism. There exist as many clinical forms of
magnesium depletion as numerous possibilities of dysregulation of
the magnesium status. But in both clinical and experimental
studies, the dysregulating mechanisms of magnesium depletion
associate a reduced magnesium intake with various types of stress.
Among them chronobiological dysrhythmias, such as hypofunction of
the biological clock (hBC) are often overlooked. Photosensitive
Headache is the main clinical form of photosensitive disorders due
to a secondary reactive response of the biological clock (BC) to
light neurostimulating effects through hBC [3, 81-83]( (figure 1) ).
In migraine, the typical form of photosensitive headache, the
nature of the magnesium deficit must be determined.
- – When chronic primary magnesium deficiency
coexists with migraine, it only constitutes a decompensatory factor
whose control with simple oral nutritional magnesium
supplementation should help in migraine therapy as an adjuvant
treatment since magnesium deficiency does not constitute the
cause for migraine per se [3, 18, 19];
- – Clinical studies on magnesium status in migraineurs
have shown heterogeneous and inconstant decreases in extra- or
intra-cellular, total or ionized magnesium concentrations in serum,
saliva, erythrocytes, mononuclear cells, thrombocyte and even in
brain. Positive therapeutic responses to oral physiological load
are unreliable. These data agree with magnesium depletion
corresponding to a magnesium deficit with dysregulation of the
magnesium status in migraine [3, 89-106].
The importance of magnesium deficit in the pathophysiology of
migraine should be stressed. Optokinetic stimulation may aggravate
clinical and paraclinical symptomatology of both primary magnesium
deficit [107] and migraine [108]; their MMPI patterns (with
elevation of neuroticism scales) are similar [19, 109, 110] and
nitric oxide is instrumental in the pathophysiology of these two
disorders [19, 31, 109-111].
To sum up: the aetiopathogenic mechanisms of photosensitive
headache associate hBC and magnesium depletion [3, 81-83,
89-107].
Headache due to photosensitive magnesium depletion
The coexistence of chronobiological stress and of magnesium deficit
does not necessarily involve a causality link between these two
factors but it does not, however, rule it out.
The inductive aetiopathogenic mechanism of magnesium depletion
with hBC may be due to the sum of nutritional magnesium deficiency
and of a stress: possibly a chronobiological stress such as hBC
through photosensitivity.
Chronic primary magnesium deficiency is frequent: about 20 per
cent of the population consumes less than two-thirds of the RDA for
magnesium [112]. In nutritionally magnesium deficient patients a
photosensitive chronobiological stress can induce a
photosensitive magnesium depletion whose main clinical form is
headache with photophobia (M and TTH particularly).
Comorbidity with other clinical forms of this photosensitive
pathology may concern the psychic, hypnic and neuromuscular
fields. Comorbidity with anxiety (panic attack or
generalized anxiety disorder) is frequent, but photosensitive
headache may also be associated with dyssomnias (i.e.
delayed sleep phase syndrome) or local or generalized
epilepsy.
To summarize: the new concept of headache due to
photosensitive magnesium depletion appears well founded and may
induce various therapeutic consequences [3, 19, 81, 112].
Treatment of headaches due to photosensitive magnesium
depletion
Classical medications used for the treatment of headaches: antalgic
drugs, anticonvulsivants, β-blockers, ergot derivatives,
triptans... although useful, will not to be considered in this
study.
The following therapeutic approach concerns only the treatment
of magnesium depletion due to light hypersensitivity: i) magnesium
depletion treatment, ii) photosensitivity treatment.
Treatment of magnesium depletion
Preventive treatment
Preventive treatment is more efficient than curative treatment.
Since magnesium depletion is usually due to both a primary chronic
magnesium deficiency and of a stress, the prophylactic treatment
must rely on a balanced magnesium status and the most
specific possible antistress treatment.
To insure a balanced magnesium status, in case of chronic
primary magnesium deficiency, atoxic nutritional magnesium
supplementation will be carried out via the diet or with
supplemental magnesium salts [112]. The dietetic supplement should
have a high magnesium density with the greatest availability.
Magnesium in drinking water is of particular interest as it
associates a high bioavailability with the lowest nutritional
density. The magnesium salt used would be hydrosoluble and the
properties of the anion should be considered [112-115]
No specific anti-photosensitive drug currently exists which
could be used as a preventive treatment of photosensitive magnesium
depletion.
Curative treatment
The aspecific treatments of magnesium depletion which are
available, such as pharmacological doses of parenteral
magnesium, may be used. Several studies have shown that 1 gram
of intravenous magnesium sulfate may be considered as efficient,
safe and well tolerated in migraine headache [116-120], but its
efficiency as an antalgic drug and as an anti-migraine treatment
remains controversial [121-124].
Pharmacological doses of magnesium salts may induce a
toxicity which varies according to the nature of anions. For
example, the effects of MgCl2 and MgSO4 on
the ionic transfer components through isolated amniotic membrane
were studied and revealed major differences. MgCl2
interacts with all the exchangers, whereas the effects of
MgSO4 are limited to paracellular components.
MgCl2 mainly increases the ionic flux ratio of this
asymmetric human membrane while MgSO4 decreases it, with
many deleterious fetal consequences.
It seems therefore necessary to determine the therapeutic
index (LD 50 / ED 50) of the various available magnesium
salts before pharmacological use. The selection of one magnesium
salt among others should take into account reliable pharmacological
and toxicological data and the comparative therapeutic index of
the various salts: the larger its value, the greater the safety
margin [125]. This logical prerequisite is lacking in most
protocols: MgSO4 is just routinely used without
justification.
Magnesium acetyltaurinate appeared as an efficient treatment in
another type of magnesium depletion: kainate magnesium
depletion experimentally induced by systemic kainic acid
injection in magnesium deficient rats [126]. But it is not possible
to extrapolate from the previous model concerning the efficiency of
this magnesium salt in photosensitive magnesium depletion [3, 81,
82, 112-126].
Treatment of photosensitivity (« darkness
therapy »)
The reactive response to photosensitivity induces a hBC. But, in
case of photosensitive headache, hBC is aggravated because the
repetitive stimulating effects of light induce potentiation
(sensitization) – sometimes with
generalization – instead of habituation [3].
Treatment of photosensitivity – the so-called
« darkness therapy » – mirrors
« phototherapy » the treatment of hyperfunction of the
biological clock.
Darkness therapy aims either at stimulating the BC, or at
palliating its hypofunction.
Stimulation of the biological clock may be obtained through
physiologic, psychotherapic, physiotherapic or pharmacologic
agents.
Palliative treatments of hBC are dependent on melatonin, its
analogs or its precursors.
Stimulating darkness therapies
a) Physiologic darkness therapies (Darkness therapy per
se)
The best physiologic stimulation of the BC is induced by light
deprivation.
It may be obtained by placing the patient in a closed room, in a
totally dark environment, with an eye mask on.
This genuine darkness therapy may be used in acute
indications, but should be of short duration. It is not compatible
with any activity and is frequently associated with induction of
bed rest, inactivity and sleep [3, 10, 81, 82, 127, 130].
Relative darkness therapy may be obtained by wearing dark
goggles or dark sun glasses but the number of lux passing through
is not negligible. This relative darkness therapy may be used as an
accessory treatment in the restoration of a light dark schedule: a
transition before a totally dark environment. A successful
double-blind study demonstrated a significant difference between
placebo and salicoside (salicin) in association with a
photoprotective mask in treating the two main clinical forms of
photosensitive headaches: M and TTH [128]. The good results of this
controlled clinical trial have not been confirmed [3, 81, 84, 128,
129].
Chromatotherapy uses a short exposure (4 min) to a
precise yellow wavelength, once a week for the treatment of hBC.
This method, even though successfully used in practice, has not
been validated yet [3, 81, 82].
Some studies have reported benefit from using colored filters in
headache patients: in childhood migraine particularly. A double
masked randomized controlled study with crossover design compared
the effectiveness of precision ophthalmic tints (optimal tint) or
glasses that provided a slightly different colour (control tint).
Using individually prescribed coloured filters selected by each
migraineur seems more helpful than the conventional practice of
using a neutral grey or sometimes brown tint, but the effect is
statistically marginal; it is suggestive rather than conclusive
[23, 24, 130].
b) Psychotherapic darkness therapies
Cognitive behavioral strategies have been efficient for the
treatment of photosensitivity. The treatment was to gradually
increase exposure to computer monitor and television screen
photostimulation. This desensitisation procedure resulted in
a complete removal of the patient’s phobic anxiety of
photo-stimulation and of avoidant behavior. This behavioral
therapy has been used in photo-sensitive epilepsy [131]. It is akin
to deconditioning techniques used as a non-pharmacological
approach to prevent photosensitive headache. For example: Variable
Frequency Photostimulation (VFP) goggles i.e. a portable
stroboscope using red Light Emitting Diodes (LED) to illuminate the
right and the left eye alternately were used with limited efficacy.
Various biofeedback treatments for migraine were disappointing
since a reduction in the number of migraine headaches was observed,
but with no change in the intensity, duration or disability of the
headaches [132-135].
The concept of headache due to photosensitive magnesium
depletion places this clinical form of headache among the
indications of psychological darkness therapies.
c) Physiotherapic darkness therapies
Magnetic fields may be used to stimulate the biological clock in a
variety of treatment methods using very weak (picotesla), extremely
low frequency (2 to 7 Hz) electromagnetic fields. Transcranial
treatment with alternative current pulsed electromagnetic fields of
picotesla flux density may stimulate various brain areas (the
hypothalamus particularly) and the pineal gland (which functions as
a magneto receptor). Several studies concern its use for treatment
of headaches. A double blind placebo controlled trial has shown
that this physiotherapy can alleviate symptoms of M but not of TTH.
Electromagnetic fields for at least three weeks may be considered
as an effective, short term intervention for migraine, although the
clinical effects were small [136-139].
d) Pharmacologic darkness therapies
Three agents may stimulate the biological clock: magnesium,
L-tryptophan and taurine.
- – Magnesium To stimulate the BC, it seems well
advised to facilitate the neural function of suprachiasmatic nuclei
(↗ SCN) and the hormonal pineal production (↗ MT). The deleterious
effects of light and those of magnesium deficiency are often found
together and may be partly palliated by a nutritional magnesium
supply (↗ Mg), providing the best possible link between photoperiod
and magnesium status. Palliative nutritional magnesium
supplementation is efficient and atoxic when magnesium deficiency
is present, but when there is a balanced magnesium status, it is
illogical and inefficient.Pharmacological use of magnesium (high
oral doses, or parenteral administration) is uncertain and
susceptible of inducing toxicity. Many data remain imprecise, such
as nature and doses of the magnesium salts, oral or parenteral
routes, association with magnesium fixing agents [3, 81, 82,
113].
- – L-tryptophan (or 5OH-tryptophan) may stimulate
the tryptophan pathway [140]. But they are unspecific as they not
only concern melatonin production, but also serotonin synthesis..
LTP supplementation may induce toxicity,
eosinophilia-myalgia syndrome particularly [141-145].
- – Taurine is a sulphonated aminoacid which is
present in the whole body in high concentrations, particularly in
the brain. It has multiple functions in cell homeostasis, such as
membrane stabilization, buffering, osmoregulation and antioxidant
activities together with effects on neurotransmitter release and
receptor modulation.
Taurine may act as a protective inhibitory neuromodulator which
participates in the functional quality of the neural apparatus and
in melatonin production and action. It plays a role in the
maintenance of homeostasis in the central nervous system,
particularly during central nervous hyperexcitability. Taurine, a
volume-regulating aminoacid, is released upon
excitotoxicity-induced cell swelling. It has an established
function as an osmolyte in the central nervous system [3, 18, 81,
82, 109, 122, 146-154].
In the course of magnesium deficit, the organism appears to
stimulate taurine mobilisation to play the role of
«a magnesium vicarious agent ». Usually, this
compensatory action is rather limited. However, it allows us to
observe the latent form of the least severe form of magnesium
deficiency[18, 109, 122, 148, 149]. During M, the typical form
of headache due to photosensitive magnesium depletion,
taurine mobilisation may be considered as a defensive reaction but
it is less effective than in case of magnesium deficiency
[155-160]( (figure
2) ).
To sum up, magnesium, tryptophan and taurine may be used to
stimulate the biological clock, but their efficiency seems
limited.
Palliative treatments of hypofunction of the biological clock
may be necessary.
« Substitutive darkness therapy » (darkness mimicking
agents)
a) Mechanisms of the action of darkness
The mechanisms of action of darkness appear to be the reverse of
those described with bright light, where direct cellular effects
(membraneous and redox) and neural mediated effects intervene.
Increased production of melatonin (↗ MT) constitutes the best
marker of darkness, but it is only an accessory mechanism in its
action.
The main central neural mechanisms of darkness therapy associate
decreased serotoninergy (↘ 5HT) -which could account for the
antimigraine effect- and stimulation of inhibitory neuromodulators
gamma-aminobutyric acid, taurine, kappa opiods (↗ GABA, ↗ TA, ↗ kO)
and stimulation of anti-inflammatory and antioxidative processes.
These effects may induce neural-hypoexcitability i.e. sedative and
anticonvulsant effects.
Humoral transduction may reinforce these last effects by
decreasing neuroactive gases (↘ CO, ↘ NO) through binding of CO
with hemoglobin (Hb) and by increasing melatonin, bilirubin and
biliverdin, three antioxidants which are able to quench NO.
Apart from the exception of decreased serotonergy, these effects
of darkness are similar to those of magnesium [3, 81, 82].
Substitutive darkness therapy should palliate all the mechanisms
of action of darkness. The only available darkness mimicking agents
are at present melatonin (its analogs and its precursors,
L-tryptophan, 5 hydroxytryptophan).
b) Melatonin: an accessory darkness mimicking agent
Melatonin is the prototype of darkness mimicking agents. But,
although its production is the best marker of photoperiod,
melatonin appears to be only an accessory factor among the
mechanisms of photoperiod actions. Most of the other mechanisms of
the effects of darkness have been overlooked, which may account for
the controversy around the therapeutic efficiency of MT. Its
posology varies from physiological doses (around 3 mg) to
pharmacological doses, usually 3 mg/per dose per day and even up to
300 mg as a contraceptive, which testifies to the weak toxicity of
the hormone. In case of chronopathology with decreased MT
production, MT constitutes a partial substitutive treatment
of its deficiency [3, 81, 82, 161-164].
To summarize: at the present time, substitutive darkness therapy
using melatonin as a partial substitutive treatment of hBC
is possible, though melatonin is only an accessory mechanism of the
action of darkness.
Conclusion
The treatment of headache due to photosensitive magnesium depletion
must, at present,associate:
- – the classical treatments of headache (antalgic
drugs, anticonvulsants, ergot derivatives, β-blockers,
triptans...)
- – a balanced magnesium status (through
nutritional or careful pharmacological magnesium
supplementation)
- – the control of hBC through physiologic,
psychotherapic, physiotherapic or pharmacologic
stimulation of the BC or through MT: partial darkness
mimicking agents.
Further research must study other agents with more efficient
darkness mimicking properties. A new model of photosensitive
magnesium depletion with potentiation is currently described [165].
This test should be a useful tool for discriminating the most
efficient darkness mimicking agent in photosensitive magnesium
depleted mice.
References
1 Featherstone HJ. Migraine and muscle contraction headaches:
a continuum. Headache 1995; 25: 194-8.
2 Marcus DA. Migraine and tension-type headaches: the
questionable validity of current classification systems. Clin J
Pain 1992; 8: 28-36.
3 Durlach J, Pages N, Bac P, Bara M,
Guiet-Bara A. Importance of magnesium depletion with
hypofunction of the biological clock in the pathophysiology of
headaches with photophobia, sudden infant death and some clinical
forms of multiple sclerosis. Magnes Res 2004; 17: 314-26.
4 Debney LM. Visual stimuli as migraine trigger factors.
In: Progress in Migraine. Res F Clifford Rose Ed., 1984: 30-54;
(ch. 4).
5 Drummond PD. A quantitative assessment of photophobia in
Migraine and Tension Headache. Headache 1986; 26: 465-9.
6 Rasmussen BK, Olesen J. Migraine with aura and
migraine without aura: an epidemiological study. Cephalalgia 1992;
12: 221-8.
7 Schoenen J. Clinical neurophysiology studies in headache:
a review of data and pathophysiological hints. Funct Neurol 1992;
7: 191-204.
8 Hay KM, Mortimer MJ, Barker DC, Debney LM,
Good PA. 1044 women with migraine: the effect of environmental
stimuli. Headache 1994; 34: 166-8.
9 Wray SH, Mijovic-Prelec D, Kosslyn SM. Visual
processing in migraineurs. Brain 1995; 118: 25-35.
10 Vingen JV, Sand T, Stovner LJ. Sensitivity to
various stimuli in primary headaches: a questionnaire study.
Headache 1999; 39: 552-8.
11 Martin PR, Teoh HJ. Effects of visual stimuli and
stressor on head pain. Headache 1999; 39: 705-15.
12 Main A, Vlachunikolis I, Dowson A. The
wavelenght of light causing photophobia in migraine and tension
type headache between attacks. Headache 2000; 40: 194-9.
13 Salvesen R, Bekkelund SI. Migraine, as compared to
other headaches, is worse during midnight-sun summer than during
polar night. A questionnaire study in an artic population. Headache
2000; 40: 824-9.
14 Mulleners WM, Aurora SK, Chronicle EP,
Stewart R, Gopal S, Koehler PJ. Self reported
photophobic symptoms in migraineurs and controls are reliable and
predict diagnostic category accurately. Headache 2001; 41:
31-9.
15 Kowacs PA, Piovesan EJ, Werneck LC,
Tatsui CE, Lange MC, Ribas LC, da Silva HP.
Influence of intense light stimulation on trigeminal and cervical
pain perception thresholds. Cephalalgia 2001; 21: 184-8.
16 Claustrat B, Brun J, Chiquet C, Chazot G,
Borson-Chazot F. Melatonin secretion is supersensitive to
light in migraine. Cephalalgia 2004; 24: 128-33.
17 Kowacs PA, Piovesan EJ, Werneck LC,
Fameli H, da Silva HP. Headache related to a specific
screen frequently band. Cephalalgie 2004; 24: 408-10.
18 Durlach J, Bac P, Durlach V, Bara M,
Guiet-Bara A. Neurotic, neuromuscular and autonomic nervous
form of magnesium imbalance. Magnes Res 1997; 10: 169-95.
19 Durlach J, Bara M. Le Magnésium en biologie et en
médecine. Paris: EMinter Tec et Doc, 2000; (403 p).
20 Marcus DA, Soso MJ. Migraine and stripe-induced
visual discomfort. Arch Neurol 1989; 46: 1129-32.
21 Coleston DM, Kennard C. Response to temporal visual
stimuli in migraine: the critical flicker fusion test. Cephalalgia
1995; 15: 396-8.
22 Vanagaite J, Pareja JA, Storen O,
White LR, Sand T, Stovner LJ. Light-induced
discomfort and pain in migraine. Cephalalgia 1997; 17: 733-41.
23 Wilkins AJ, Patel R, Adjamian P,
Evans BJW. Tinted spectacles and visually sensitive migraine.
Cephalalgia 2002; 22: 711-9.
24 Evans RW, Digre KB. Light sensitivity in
migraineurs. Headache 2003; 43: 917-20.
25 Mundy-Castle AC. The clinical significance of photic
stimulation. EEG Clin Neuro physiol 1953; 5: 187-202.
26 Golla EL, Winter AL. Analysis of cerebral responses
to flicker in patients complaining of episodic headache. EEG Clin
Neurophysiol 1959; 11: 539-49.
27 Simon RH, Zimmerman AW, Tasman A,
Hale MS. Spectral analysis of photic stimulation in migraine.
EEG Clin Neurophysiol 1982; 53: 270-6.
28 Scheuler W. Clinical significance of increased reaction
to photostimulation in the alpha frequency range. EEG EMG Z 1983;
14: 143-53.
29 Gronseth GS, Greenberg MK. The utility of the EEG
in the evaluation of patients presenting with headaches: a review
of litterature. Neurolgy 1995; 45: 1263-7.
30 de Tommaso M, Sciruicchio V, Bellotti R,
Guido M, Sasanelli G, Specchio LM, Puca F.
Photic driving response in primary headache: diagnostic value
tested by discriminant analysis and artificial neural network
classifiers. Ital J Neurol Sci 1999; 20: 23-8.
31 Sand T. Electroencephalography in migraine: a review
with focus on quantitative electroencephalography and the migraine
versus epilepsy relationship. Cephalalgia 2003; 23(Supp 1): 5-11;
(483).
32 Leniger T, Von den Driesch S, Isbruch K,
Diener HC, Hufnagel A. Clinical characteristics of
patients with comorbidity of migraine and epilepsy. Headache 2003;
43: 672-7.
33 Backer M, Sander D, Hammes MG, Funke D,
Deppe M, Conrad B, Tolle JR. Altered cerebrovascular
response pattern interictal migraine during visual stimulation.
Cephalalgia 2001; 21: 611-6.
34 Ances BM, Detre JA. Perfusion changes with photic
stimulation during two phases of the menstrual cycle: a pilot study
comparing controls and true menstrual migraine patients.
Cephalalgia 2003; 23: 907-13.
35 Thompson RF, Spencer WA. Habituation: a model
phenomenon for the study of neuronal substrates behaviour. Psychol
Rev 1966; 73: 16-43.
36 Monnier M, Boehmer A, Scholer A. Early
habituation, dishabituation and generalization induced in the
visual centres by colour stimuli. Vision Res 1976; 16:
1497-504.
37 Gawel M, Connoly JF, Clifford Rose F. Migraine
patients exhibit abnormalities in the Visual Evoked Potential.
Headache 1983; 23: 49-52.
38 Kropp P, Gerber WD. Is increased amplitude of
Contingent Negative Variation in migraine due to cortical
hyperactivity or to reduced habituation. Cephalalgia 1993; 13:
37-41.
39 Schoenen J, Wang W, Albert A,
Delwaide PJ. Potentiation instead of habituation characterizes
Visual Evoked Potentials in migraine patients between attacks. Eur
J Neurol 1995; 2: 115-22.
40 Wang W, Timsit-Berthier M, Schoenen J.
Intensity dependence of auditory evoked potentials is pronounced in
migraine: an indication of cortical potentiation and low
serotonergic neurotransmission? Neurology 1996; 46: 1404-9.
41 Schoenen J. The pathophysiology of migraine: a review
based on the litterature and on personal contributions. Func Neurol
1998; 13: 7-15.
42 Kropp P, Gerber WD. Prediction of migraine attacks
using a slow cortical potential, the Contingent Negative Variation.
Neurosc Lett 1998; 257: 73-6.
43 Oelkers R, Grosser K, Lang E,
Geisslinger G, Kobal G, Brure K, Lotsch J.
Visual Evoked Potentials in migraine patients: alterations depend
on pattern spatial frequency. Brain 1999; 122: 1147-55.
44 Judit A, Sandor PS, Schoenen J. Habituation of
visual and intensity dependence of auditory evoked cortical
potentials tend to normalyze just before and during the migraine
attacks. Cephalalgia 2000; 20: 714-9.
45 Afra J, Ambrosini A, Genicot R, Albert A,
Schoenen J. Influence of colors in patients with migraine with
aura and in healthy volunteers. Headache 2000; 36: 36-40.
46 Sand T, Vanagaite-Vingen J. Visual, long-latency
auditory and brainstem auditory evoked potentials in migraine:
relation to pattern size, stimulus intensity, sound and light
discomfort thresholds and pre-attack state. Cephalalgia 2000; 20:
804-20.
47 Bendtsen L. Central sensitization in tension-type
headache: possible pathophysiological mechanisms. Cephalalgia 2000;
20: 486-508.
48 Siniatchkin M, Kirsch E, Kropp P,
Stephani U, Gerber WD. Slow cortical potentials in
migraine families. Cephalalgia 2000; 20: 881-92.
49 Thomas E, Sandor PS, Ambrosini A,
Schoenen J. A neural network model of sensitization of evoked
cortical responses in migraine. Cephalalgia 2002; 22: 48-53.
50 Bendtsen L. Sensitization: its role in primary headache.
Curr Opin Investig Drugs 2002; 3: 449-53.
51 de Tommaso M, Stramaglia S, Schoffelen JM,
Guido M, Libro G, Losito L, Sciruicchio V,
Sardaro M, Pellicoro M, Puca FM. Study state visual
evoked potentials in the low frequency range in migraine: a study
of habituation and variability phenomena. Int J Psychophysiol 2003;
49: 165-74.
52 Sandrini G, Proietti Cecchini A, Milanov I,
Tassorelli C, Buzzi MG, Nappi G.
Electrophysiological evidence for trigeminal neuron sensitization
in patients with migraine. Neurosci Lett 2002; 317: 135-8.
53 Katsarava Z, Giffin N, Diener HC,
Kaube H. Abnormal habituation of nociceptive Blink Reflex in
migraine: evidence for increased excitability of trigeminal
nociception. Cephalalgia 2003; 23: 814-9.
54 Harter MC, Conway KP, Merikangas KR. Association between
anxiety disorders and physical illness. Eur Arch Psychiatry Clin
Neurosci 203;253:313–320.
55 Ambrosini A, Schoenen J. The electrophysiology of
migraine. Cur Opin Neurol 2003; 16: 327-31.
56 Bartsch T, Goadsby PJ. The trigemino-cervical
complex and migraine: current concepts and synthesis. Curr Pain
Headache Rep 2003; 7: 371-6.
57 Welch KM. Contemporary concepts of migraine
pathogenesis. Neurology 2003; 61: S2-S8.
58 Schoenen J, Ambrosini A, Sandor PS, Maertens
de Noordhout A. Evoked potentials and transcranial magnetic
stimulation in migraine: published data and viewpoint on their
pathophysiologic significance. Clin Neurophysiol 2003; 114:
955-72.
59 Siniatchkin M, Kropp P, Gerber WD. What kind
of habituation is impaired in migraine patients? Cephalalgia 2003;
23: 511-8.
60 de Tommaso M, Libro G, Guido M,
Difruscolo O, Losito L, Sardaro M, Cerbo R.
Nitroglycerin induced migraine headache and central sensitization
phenomena in patients with migraine without aura: a study of laser
evoked potentials. Neurosci Lett 2004; 363: 272-5.
61 Mathew NT, Kailasam J, Seifert T. Clinical
recognition of allodynia in migraine. Neurology 2004; 63:
848-52.
62 Sicuteri F. Migraine, a central biochemical
dysnociception. Headache 1976; 16: 145-59.
63 Solomon GD. Circadian rhythms and migraine. Cleve Czin J
Med 1992; 59: 326-9.
64 Jan JE, Groenveld M, Anderson DD. Photophobia
and cortical visual impairment. Developm Med Child Neurol 1993; 35:
473-7.
65 Drummond PD, Woodhouse A. Painful stimulation of
the forehead increases photophobia in migraine sufferers.
Cephalalgia 1993; 13: 321-4.
66 Brun J, Claustrat B, Saddier P, Chazot G.
Nocturnal melatonin secretion is decreased in patients with
migraine without aura attacks associated with menses. Cephalalgia
1995; 15: 136-9.
67 Takeshima T, Mishima T, Tabata M,
Burioka N, Nakashima K. Acrophase amplitude of ambulatory
blood pressure decreases in migraineurs. Headache 1997; 37:
577-82.
68 Murialdo G, Fonzi S, Costelli P,
Solinas GP, Parodi C, Marabini S,
Franczullacci M, Polleri A. Urinary melatonin excretion
throught the ovarian cycle in menstrually related migraine.
Cephalalgia 1994; 14: 205-9.
69 Zurak N. Role of the suprachiasmatic nucleus in the
pathogenesis of migraine attacks. Cephalalgia 1997; 17: 723-8.
70 Verri AP, Proietti Cecchini A, Galli F,
Sandrini G, Nappi G. Psychiatric comorbidity in chronic
daily headache. Cephalalgia 1998; 18(Suppl 21): 45-9.
71 Nategaal JE, Smits MG, Swart AC,
Kerkhof GA, van der Meer YG. Melatonin-responsive
headache in delayed sleep phase syndrome: preliminary observations.
Headache 1998; 38: 303-7.
72 Woodhouse A, Drummond PD. Mechanisms of increased
sensitivity to noise and light in migraine headache. Cephalalgia
1993; 13: 417-21.
73 Chronicle EP, Mulleners WM. Visual system
dysfunction in migraine: a review of clinical and psychological
findings. Cephalalgia 1995; 16: 525-35.
74 Drummond PD. Photophobia and autonomic responses to
facial pain in migraine. Brain 1997; 120: 1857-64.
75 Fox AW, Davis RL. Migraine chronobiology. Headache
1998; 38: 436-41.
76 Wang W, Wang GP, Ding XL, Wang YH.
Personality and response to repeated visual stimulation in migraine
and tension type headaches. Cephalalgia 1999; 19: 718-24.
77 Tabata M, Takeshima T, Burioka N,
Nomura T, Ishizaki K, Mori N, Kona H,
Nakashima K. Cosinor analysis of heart rate variability in
ambulatory migraineurs. Headache 2000; 40: 457-63.
78 Mick G. Physiopathologie de la crise migraineuse et
modes d’action des antimigraineux: dernières nouvelles du monde
animal. Pathol Biol 2000; 48: 593-607.
79 Peres MFP, Sanchez del Rio M, Scabra MLV,
Tufik S, Abucham J, Cipolla-Neto J,
Silberstein SD, Zukerman E. Hypothalamic involvement in
chronic migraine. J Neurol Neurosurg Psychiatry 2001; 71:
747-51.
80 Toglia JV. Melatonin: a significant contributor to the
pathogenesis of migraine. Med Hypotheses 2001; 57: 432-4.
81 Durlach J, Pagès N, Bac P, Bara M,
Guiet-Bara A. Biorhythms and possible central regulation of
magnesium status, phototherapy, darkness therapy and
chronopathological forms of magnesium depletion. Magnes Res 2002;
15: 49-66.
82 Durlach J, Pagès N, Bac P, Bara M,
Guiet-Bara A, Agrapart C. Chronopathological forms of
magnesium depletion with hypofunction or with hyperfunction of the
biological clock. Magnes Res 2002; 15: 263-8.
83 Pan JT, Li CS, Tang KC, Lin JY. Low
calcium high magnesium medium increases activities of hypothalamic
arcuate and suprachiasmatic neurons in brain tissue slices.
Neurosci Lett 1992; 144: 157-60.
84 de Tommaso M, Murasecco D, Libro G,
Guido M, Sciruicchio V, Specchio LM, Gallai V,
Puca F. Modulation of trigeminal reflex excitability in
migraine: effects of attention and habituation on the blink reflex.
Int J Psychophysiol 2002; 44: 239-49.
85 Valeriani M, de Tommaso M, Restuccia D, Le
Pera D, Guido M, Ianetti GD, Libro G,
Truini A, di Trapani G, Puca F, Tonali P,
Cruccu G. Reduced habituation to experimental pain in migraine
patients: a CO2 laser evoked potential study. Pain 2003; 105:
57-64.
86 Rogers KL, Lea RA, Griffiths LR. Molecular
mechanisms of migraine: prospects for pharmacogenomics. Am J
Pharmacogenomics 2003; 3: 329-43.
87 de Tommaso M, Guido M, Libro G, Losito L,
Difruscolo O, Sardaro M, Puca F. Interictal lack of
habituation of mismatch negativity in migraine. Cephalalgia 2004;
24: 663-6.
88 Nedeltchev K, Arnold M, Schwerzmann M, Nirkko A, Lagger F,
Mattle HP, Sturzenegger M. Cerebrovascular response to repetitive
visual stimulation in interictal migraine with aura. Cephalalgia
2004; 24: 700–706.
89 Trauninger A, Pfund Z, Koszegi T,
Czopf J. Oral magnesium load test in patients with migraine.
Headache 2002; 42: 114-9.
90 Ramadan NM, Halvorson H, Vandelinde A,
Levine S, Helpern JA, Welsh KMA. Low brain magnesium
in migraine. Headache 1989; 29: 590-3.
91 Schoenen J, Sianard-Gainko J, Lenaerts M.
Blood magnesium levels in migraine. Cephalalgia 1991; 11: 97-9.
92 Thomas J, Thomas E, Tomb E. Serum and
erythrocyte magnesium concentrations and migraine. Magnes Res 1992;
5: 127-30.
93 Gallai V, Sarchielli P, Costa G,
Firenze C, Mozucci P, Abbritti G. Serum and salivary
magnesium levels in migraine. Results in a group of juvenile
patients. Cephalalgia 1992; 32: 132-5.
94 Castelli S, Meossi C, Domenici R,
Fontana F, Stefani G. Il magnesio nella profilassi della
cefaleo primaria e di altri disturbi periodici del bambino. Ped Med
Chir 1993; 15: 481-8; (Med Surg Ped).
95 Mauskop A, Altura BT, Cracco RQ,
Altura BM. Deficiency in serum ionized magnesium but not total
magnesium in patients with migraines. Headache 1993; 33: 135-8.
96 Gallai V, Sarchielli P, Mozucci P,
Abbritti G. Red blood cell magnesium levels in migraine
patients. Cephalalgia 1993; 13: 74-81.
97 Soriani S, Arnaldi C, de Carlo L,
Arcudi D, Mazzotta D, Battistella PA,
Sartori S, Abbasciano V. Serum and red blood cell
magnesium levels in juvenile migraine patients. Headache 1995; 35:
14-6.
98 Pfaffenrath V, Weseley P, Meyer C,
Isler HR, Evers S, Grotemeyer KH, Taneri Z,
Soyka D, Gobel H, Fischer H. Magnesium in the
prophylaxis of migraine: a double blind placebo-controlled study.
Cephalalgia 1996; 16: 346.
99 Aloisi P, Marreli A, Porto C, Tozzi F,
Cerone G. Visual evoked potentials and serum magnesium levels
in juvenile migraine patients. Headache 1997; 37: 383-5.
100 Mishima K, Takeshima T, Shimomura T,
Okada H, Kitano A, Takahashi K, Nakashima K.
Platelet ionized magnesium, cyclic AMP and cyclic GMP levels in
migraine and tension-type headache. Headache 1997; 37: 561-4.
101 Mazzota G, Sarchielli P, Alberti A,
Gallai V. Intracellular Mg2+ concentration and
electromyographical ischemic test in juvenile headache. Cephalalgia
1999; 19: 802-9.
102 Lodi R, Iotti S, Cortelli P,
Pierangeli G, Cevoli S, Clementi V, Soriani S,
Montagna P, Barbiroli B. Deficient energy metabolism is
associated with low free magnesium in the brains of patients with
migraine and cluster headache. Brain Res Bull 2001; 54:
437-431.
103 Teppert JJ, Rapoport AM, Sheftell FD. The
pathophysiology of migraine. Neurology 2001; 7: 279-86.
104 Boska MD, Welch KM, Barker PB,
Nelson JA, Schultz L. Contrast in cortical magnesium,
phospholipid and energy metabolism between migraine syndromes.
Headache 2002; 42: 114-9.
105 Bigal ME, Rapoport AM, Sheftell FD,
Tepper SJ. New migraine preventive options: an update with
pathophysiological considerations. Rev Hosp Clin Fac Med Sao Paulo
2002; 57: 293-8.
106 Nechifor M. Magnesium involvement in neuropsychiatric
diseases. In: Nechifor M, Porr PJ, eds. Magnesium
involvements in biology and pharmacotherapy. Cluj-Napoca: Casa
Cartir de Stinta publ, 2003: 160-77.
107 Durlach J. Neurological manifestations of magnesium
imbalance. In: Vinken PJ, Bruyn GW, eds. Handbook of
Clinical Neurology. Amsterdam N.Y. Oxford: North Holland Publ C°,
1976: 545-79; (23).
108 Drummond PD. Motion sickness and migraine: optokinetic
stimulation increases scalp tenderness, pain sensitivity in the
fingers and photophobia. Cephalalgia 2002; 22: 117-24.
109 Durlach J. Magnesium in clinical practice. London: John
Libbey publ, 1988; (386p).
110 Ellertsen B, Klove H. MMPI patterns in chronic
muscle pain, tension headache and migraine. Cephalalgia 1987; 7:
65-71.
111 Thomsen LL, Olesen J. Nitric oxide in primary
headache. Curr Opin Neurol 2001; 14: 315-21.
112 Durlach J. Importance and clinical forms of chronic
primary magnesium deficiency in human beings. In: Mazur A,
Durlach J, eds. Advances in Magnesium Research: Nutrition and
Health. Y. Rayssignier, M. Bara and J. durlach, eds. John Libbey
& Company Ltd Publ, 2001: 13-21.
113 Durlach J, Durlach V, Bac P, Bara M,
Guiet-Bara A. Magnesium and therapeutics. Magnes Res 1994; 7:
313-28.
114 Facchinetti F, Sances G, Borella P,
Genazzani A, Nappi G. Magnesium prophylaxis of menstrual
migraine. Effects of intracellular magnesium. Headache 1991; 31:
298-301.
115 Silberstein SD. Hormone-related headache. Med Clin
North Am 2001; 85: 1017-35.
116 Opavsky J. Magnesium and its combination with
cinnarizine in the long term treatment of headache. Acta Univ
Palacki Olomuc Fac Med 1991; 131: 157-64.
117 Mauskop A, Altura BT, Craco RQ,
Altura BM. Intravenous MgSO4 rapidly alleviates headaches of
various types. Headache 1996; 36: 154-60.
118 Demirkaya S, Vural O, Dora B,
Topcuoglu MA. Efficacy of intravenous MgSO4 in the treatment
of acute migraine attacks. Headache 2001; 41: 171-7.
119 Bigal ME, Bordini CA, Tepper SJ,
Speciali JG. Intravenous magnesium sulphate in the acute
treatment of migraine without aura and migraine with aura. A
randomized double blind, placebo controlled studied. Cephalalgia
2002; 22: 345-53.
120 Rozen TD. Aborting a prolonged migrainous aura with
intravenous prochlorperazine and MgSO4. Headache 2003; 43:
901-3.
121 Crosby V, Wilcock A, Corcoran R. The safety
and efficacy of a single dose (500mg or 1g) of intravenous MgSO4 in
neuropathic pain poorly responsive to strong opioid analgesics in
patients with cancer. J Pain Symptom Manage 2000; 19: 35-9.
122 Durlach J, Bac P, Bara M, Guiet-Bara A.
Physiopathology of symptomatic and latent forms of central nervous
hyperexcitability due to magnesium deficiency: a current general
scheme. Magnes Res 2000; 13: 293-302.
123 Mikkelsen S, Dirks J, Fabricius P,
Petersen KL, Rowbotham MC, Dahl JB. Effect of
intravenous magnesium on pain and secondary hyperalgesia associated
with the heat capsaicin sensitization model in healthy volunteers.
Br J Anesth 2001; 86: 871-3.
124 Corbo J, Esses D, Bijur FE, Iamacone R,
Gallagher EJ. Randomized clinical trial of intravenous
magnesium sulphate as an adjunctive medication for emergency
department treatment of migraine headache. Ann Emerg Med 2001; 38:
621-327.
125 Durlach J, Bac P, Bara M, Guiet-Bara A.
Is the pharmacological use of intravenous magnesium before preterm
cerebroprotective or deleterious for premature infants? Possible
importance of the use of magnesium sulphate. Magnes Res 1998; 1:
323-5.
126 Bac P, Herrenknecht C, Pagès N,
Dupont C, Durlach J. Reversible model of magnesium
depletion induced by systemic kainic acid injection in
magnesium-deficient rats: I-Comparative study of various magnesium
salts. Magnes Res 1996; 9: 281-91.
127 Bruno C, Cuppini R, Cuppini C. Studio di
alcuni parametri elettrofisiologici nella giunzione neuromuscolare
di ratto in rapporto al ritmo luce-buio. Boll Soc It Biol Sper
1986; 32: 525-30.
128 Hyson ML. Anticephalic photosensitive premedicated
mask. A report of a successful double-blind placebo controlled
study of a new treatment for headaches with associated frontalis
pain and photophobia. Headache 1998; 38: 475-7.
129 Horowitz TS, Cade BE, Wolfe JM,
Czeisler CA. Efficacy of bright light and sleep darkness
scheduling in alleviating circadian maladaptation to night work. Am
J Physiol Endocrinol Metab 2001; 281: 384-91.
130 Good PA, Taylor RH, Mortimer MJ. The use of
tinted glasses in childhood migraine. Headache 1991; 31: 533-6.
131 Noeker M, Haverkamp F. Successful
cognitive-behavioral habituation training toward photophobia in
photogenic partial seizures. Epilepsia 2001; 42: 689-91.
132 Cohen MJ, McArthur DL, Rickles WH. Comparison
of four biofeedback treatments for migraine headache: physiological
and headache variables. Psychosom Med 1980; 42: 463-80.
133 Anderson DJ. The treatment of migraine with variable
frequency photostimulation. Headache 1989; 29: 154-5.
134 Noton D. Migraine and photic stimulation: report on a
survey of migraine using flickering light therapy. Complement Ther
Nurs Midwifery 2000; 6: 138-42.
135 Kowacs PA, Piovesan EJ, Werneck LC,
Tatsui CE, Lange MC, Ribas LC, da Silva HP.
Influence of intense light stimulation on trigeminal and cervical
pain perception thresholds. Cephalalgia 2001; 21: 184-8.
136 Mix E, Jensen HL, Lehmitz R, Lakner K,
Hitzschke B, Richter M, Heydenreich A. Effect of
pulsating electromagnetic field therapy on cell volume and
phagocytosis activity in multiple sclerosis and migraine. Psychiatr
Neurol Med Psychol (Leipz) 1990; 42: 457-66; (Leipzig).
137 Sandyk R. The influence of the pineal gland on migraine
and cluster headaches and effects of treatment with picotesla
magnetic fields. Int J Neurosci 1992; 67: 145-71.
138 Sherman RA, Robson L, Marden LA. Initial
exploring of pulsing electromagnetic fields for treatment of
migraine. Headache 1998; 38: 208-13.
139 Sherman RA, Acosta NM, Robson L. Treatment of
migraine with pulsing electromagnetic fields: a double blind,
placebo controlled study. Headache 1999; 39: 567-75.
140 Kangasniemi P, Falck B, Langvik V-A. Hygppä.
Levotryptophan treatment in migraine. Headache 1978; 18: 161-6.
141 Heiman-Patterson TD, Bird SJ, Parry GJ,
Varga J, Shy ME, Culligan NW, Edelson L,
Tatarian GT, Heyes MP, Garcia CA. Peripheral
neuropathy associated with eosinophilia-myalgia syndrome. An Neurol
1990; 28: 522-8.
142 Arnouts PJ, Colemont LJ, Van Outryve MJ, Van
Moer EM. L-tryptophan-induced eosinophilia-myalgia syndrome. J
Intern Med 1991; 230: 83-6.
143 Mayeno AN, Gleich GJ. Eosinophilia-myalgia
syndrome and tryptophan production: a cautionary tale. Trends
Biotechnol 1994; 12: 346-52.
144 Stenberg EM. Pathogenesis of L-tryptophan
eosinophilia-myalgia syndrome. Adv Exp Med Biol 1996; 398:
325-30.
145 Gros B, Ronen N, Honigman S, Livne E.
Tryptophan toxicity: time and dose response in rats. Adv Exp Med
Biol 1999; 467: 507-16.
146 Lopez-Colome A, Erlig D, Pasantes-Morales H.
Different effects of Ca flux blocking agents on light and K
stimulated release of taurine from retina. Brain Res 1976; 113:
527-34.
147 Pasantes-Morales H, Ademe RM, Quesada O.
Protective effects of taurine on the light induced disruption of
isolated frog rot outer segments. J Neurosci Res 1981; 6:
337-48.
148 Durlach J, Bara M, Guiet-Bara A,
Rinjard P. Taurine and magnesium homeostasis: new data and
recent advances. In: Altura BM, Durlach J,
Seelig MS, eds. Magnesium in cellular processes and medicine.
Basel: S Karger publ, 1987: 219-38.
149 Durlach J, Poenaru S, Rouhani S, Bara M,
Guiet-Bara A. The control of central neural hyperexcitability
in magnesium deficiency. In: Essman WB, ed. Nutrients in Brain
Function. Basel: S Karger publ, 1987: 48-71.
150 Sturman JA, Lu P, Xu YX, Imaki H. Feline
maternal taurine deficiency: effects on visual cortex of the
offspring. A morphometric and immunohistochemical study. In:
Huxtable R, Michalk DV, eds. Taurine in Health and
disease. New-York: Plenum Publ, 1994: 369-92; (Adv In Exp Med Biol:
359).
151 Stover JF, Pleines VE, Morganti-Kossman MC,
Kossman T, Lowitzch K, Kempski OS. Neurotransmitters
in cerebrospinal fluid reflect pathological activity. Eur J Clin
Invest 1997; 27: 1038-43.
152 Pasantes-Morales H, Quesada O, Moran J.
Taurine: an osmolyte in mammalian tissue. In: Schaffer S,
Lombardini JB, Huxtable RJ, eds. Taurine 3. New-York:
Plenum publ, 1998: 209-17; (Adv In Exp Med Biol: 442).
153 Labiner DM, Yan CC, Weinand ME,
Huxtable RJ. Disturbances of aminoacids from temporal lobe
synaptosomes in human complex partial epilepsy. Neurochem Res 1999;
24: 1379-83.
154 Husy N, Deleuze C, Bres V, Moos FC. New
role of taurine as an osmomediator between glial cells and neurons
in the rat supraoptic nucleus. In: Della, Corte L,
Huxtable RJ, Sgaragli G, Tipton KF, eds. Taurine 4.
New-York: Kluwer AC Plenum Publ, 2000: 227-37; (Adv In Exp Med
Biol: 483).
155 Dhopesh VP, Baskin SI. Change in platelet taurine
and migraine. Headache 1982; 22: 165-6.
156 Baskin SI, Finney CM. Factors that modify the
tissue concentration or metabolism of taurine. In:
Schaffer SW, Baskin SI, Kocsis JJ, eds. The effects
of taurine on excitable tissues. Jamaica, N.Y., US: Spectrum publ,
1981: 405-18; (Ch 28).
157 Rao A, Rao S. Urinary excretion of taurine in
migraine. Headache 1988; 28: 133-4.
158 Van Gelder NM. Neuronal discharge hypersynchrony and
the intracranial water balance in relation to glutamic acid and
taurine redistribution: migraine and epilepsy. In: Taurine:
Functional Neurochemistry, Physiology and Cardiology. Wiley-Liss
Inc, 1990: 1-20.
159 Martinez F, Castillo J, Leira R,
Prieto JM, Lema M, Nova M. Taurine levels in plasma
and cerebrospinal fluid in migraine patients. Headache 1993; 33:
324-7.
160 Rothrock JF, Mar KR, Yaksh TL,
Golbeck A, Moore AC. Cerebrospinal fluid analyses in
migraine patients and controls. Cephalalgia 1995; 15: 489-93.
161 Wetterberg L. Melatonin in humans: physiological and
clinical studies. J Neural Transm 1978(Suppl 13): 289-310.
162 Sanchez-Forte M, Moreno-Madrid F,
Munoz-Hoyos A, Molina-Carballo A,
Acuna-Castroviejo D, Molina-Font JA. The effect of
melatonin as anticonvulsant and neuron protector. Rev Neurol 1997;
25: 1229-34.
163 Gagnier JJ. The therapeutic potential of melatonin in
migraines and other headaches. Altern Med Rev 2001; 6: 383-9.
164 Musshoff U, Speckmann EJ. Diurnal actions of
melatonin on epileptic activity in hippocampal slices of rats. Life
Sci 2003; 73: 2603-10.
165 Bac P, Pagès N, Maurois P, Durlach J. A
new actimetry-based test of potentiation during iterative
photostimulation in a murine photosensitive magnesium depletion
model. Meth find. 2005; (in press).
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