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Angaben zur Quelle [Bearbeiten]

Autor     Ali Gorji
Titel    Spreading depression: a review of the clinical relevance
Zeitschrift    Brain Research Reviews
Verlag    Elsevier
Ausgabe    38
Jahr    2001
Seiten    33-60
URL    http://www.sciencedirect.com/science/article/pii/S0165017301000819

Literaturverz.   

yes
Fußnoten    yes
Fragmente    6


Fragmente der Quelle:
[1.] Aeh/Fragment 007 02 - Diskussion
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SD appears first at the stimulated site and spreads out in all directions at the velocity of 2–3 mm/min, so that increasingly distant areas undergo successively a similar temporary depression. A crucial manifestation of SD is a propagating negative potential with amplitude of 10–30 mV and duration of more than 30 sec, which may be preceded or succeeded by a positive fluctuation of variable amplitude and duration (Figure 1). Underlying this cellular depolarisation is a dramatic change in the distribution of micromilieu ions between extra- and intracellular compartments. Potassium and proton release from the cells, while sodium, calcium and chloride enter together with water causing cells to swell and the volume of the extracellular compartment to be decreased. SD is accompanied by an increase of glucose utilization and O2 consumption. Recovery of SD depends on energy metabolism.

SD has been studied in vivo and in vitro in brain slices and in retinal preparations under different experimental conditions. It has been also observed in human neocortical tissue in vitro and in human hippocampus as well as striatum and neocortex in vivo. SD can be regularly initiated if the tissue susceptibility is artificially raised. Hypoxia as well as hypoglycemia and changing the extracellular ionic concentrations by administration of solutions with increased K+, decreased NaCl or with the Cl of the latter replaced by certain other anions lower the threshold (Gorji, 2001).

It appears first at the stimulated site and spreads out in all directions at the velocity of 2–3 mm/min, so that increasingly distant areas undergo successively a similar temporary depression [243]. A necessary manifestation of SD is a propagating extracellular negative potential with an amplitude of 10-30 mV and a duration of more than 0.5-1 min, which may be preceded or succeeded by a positive deflection of variable amplitude and duration. Underlying this neuro-glial depolarization is a dramatic change in the distribution of ions between extra- and intracellular spaces. K+ and H+ release from the cells, while Na+, Ca2+ and Cl- enter together with water [152,166,222] causing cells to swell and the volume of the extracellular compartment to be reduced. SD is accompanied by an increase of glucose utilization and O2 consumption [47,283]. Recovery of SD depends on energy metabolism [47].

This phenomenon has been studied in vivo in several animal species and in vitro in brain slices and in retinal preparations under various experimental conditions [47]. It has been also observed in human neocortical tissue in vitro [16,17,149] and in human hippocampus as well as striatum [408] and neocortex [272] in vivo. [...]

SD can be regularly initiated if the tissue susceptibility is artificially raised. Hypoglycemia and hypoxia as well as changing the extracellular ionic micromilieu by applying solutions with increased K+, decreased NaCl or with the Cl- of the latter replaced by certain other anions lower the threshold.

Anmerkungen

The source is mentioned at the end, but it is not clear that the preceding two(!) paragraphs are taken from it.

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[2.] Aeh/Fragment 008 03 - Diskussion
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SD is also a well-known phenomenon in experimental epilepsy. SD has been observed in a variety of in vitro and in vivo epilepsy models in different animal species. Reduction of extracellular Mg2+ concentrations, activation of NMDA receptors, blocking of K+ channels, [e.g., by 4-aminopyridine, increased extracellular K+, blocking of Na+–K+ ATPase, e.g., by ouabain, blocking of Ca2+ channels, e.g., by NiCl2, blocking of GABA receptors, e.g., by picrotoxin, are the common pathways for eliciting epileptiform burst discharges and SD in experimental models.] SD is a well-known phenomenon in experimental epilepsy. SD has been observed in a variety of in vitro and in vivo epilepsy models in different animals [sic] species. Reduction of extracellular Mg2+ concentrations, activation of NMDA receptors, blocking of K+ channels, e.g., by 4-aminopyridine, increased extracellular K+ , blocking of Na+-K+ ATPase, e.g., by ouabain, blocking of Ca2+ channels, e.g., by NiCl2, blocking of GABA receptors, e.g., by picrotoxin, are the common pathways for eliciting epileptiform burst discharges and SD in experimental models [22,149,150,243,337,344,433].
Anmerkungen

The source is not mentioned.

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[3.] Aeh/Fragment 009 01 - Diskussion
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[SD has been observed in a variety of in vitro and in vivo epilepsy models in different animal species. Reduction of extracellular Mg2+ concentrations, activation of NMDA receptors, blocking of K+ channels,] e.g., by 4-aminopyridine, increased extracellular K+, blocking of Na+–K+ ATPase, e.g., by ouabain, blocking of Ca2+ channels, e.g., by NiCl2, blocking of GABA receptors, e.g., by picrotoxin, are the common pathways for eliciting epileptiform burst discharges and SD in experimental models. By all aforementioned mechanisms SD appears spontaneously between epileptiform ictal events. SD can be elicited in susceptible area by a single discharge of an epileptic focus (spike triggered SD). Epileptiform field potentials usually suppress during SD occurrence and reappear in few minutes. CSD penetration into the epileptic foci was established in different model of epilepsy. However, it should be noted that SD does not enter electrically or pharmacologically elicited foci of epileptic activity with high rates of interictal discharges which resulted in anomalous SD propagation. This abnormal SD conduction may account for periodic changes of ictal and interictal activity found in some types of focal epilepsy. SD has been observed in a variety of in vitro and in vivo epilepsy models in different animals [sic] species. Reduction of extracellular Mg2+ concentrations, activation of NMDA receptors, blocking of K+ channels, e.g., by 4-aminopyridine, increased extracellular K+ , blocking of Na+-K+ ATPase, e.g., by ouabain, blocking of Ca2+ channels, e.g., by NiCl2, blocking of GABA receptors, e.g., by picrotoxin, are the common pathways for eliciting epileptiform burst discharges and SD in experimental models [22,149,150,243,337,344,433]. By all aforemen-

[page 43]

tioned mechanisms SD appears spontaneously between epileptiform ictal events. SD can be elicited in susceptible area by a single discharge of an epileptic focus (spike triggered SD). Epileptiform field potentials usually suppress during SD occurrence and reappear in few minutes [150,217]. CSD penetration into epileptic foci established in different model of epilepsy. However, it should be noted that SD does not enter electrically or pharmacologically elicited foci of epileptic activity with high rates of interictal discharges which resulted in anomalous SD propagation. This abnormal SD conduction may account for periodic changes of ictal and interictal activity found in some types of focal epilepsy [50,215,217].


[...]

Anmerkungen

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[4.] Aeh/Fragment 017 17 - Diskussion
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It was postulated that the excitatory amino acid glutamate plays a role in the chain of events triggering SD (Bures et al., 1974). The neocortex releases excitatory amino acids including glutamate and aspartate, to the extracellular space during CSD (Van Harreveld and Kooiman, 1965). Subsequently it has been shown that the triggering of SD requires activation of the NMDA subtype of glutamate receptor in rat cerebral cortex (Bures et al., 1974), in chick retina (Seeling, 1993) and in human neocortical tissues (Gorji et al., 2001). Other glutamate subreceptor (AMPA, kainate and quisqualate) can induce SD but their initiation inhibited by [NMDA receptor antagonist (Lauritzen et al., 1988).]

Bures J., Buresova O., Krivanek J. In: The Mechanisms and Applications of Leao’s Spreading Depression of Electroencephalographic Activity, Academic Press, New York (1974).

Gorji A, Scheller D, Straub H, Tegtmeier F, Köhling R, Höhling JM, Tuxhorn I, Ebner A, Wolf P, Werner Panneck H, Oppel F, Speckmann EJ. Spreading depression in human neocortical slices. Brain Res. 2001;906:74-83.

Lauritzen M, Rice ME, Okada Y, Nicholson C. Quisqualate, kainate and NMDA can initiate spreading depression in the turtle cerebellum. Brain Res. 1988; 475:317–327.

Seelig MS, Interrelationship of magnesium and estrogen in cardiovascular and bone disorders, eclampsia, migraine and premenstrual syndrome. J. Am. Coll. Nutr. 1993;12:442–458.

Van Harreveld A, Kooiman M. Amino acid release from the cerebral cortex during spreading depression and asphyxiation. J. Neurochem. 1965;12:431–439.

It was postulated that the excitatory amino acid glutamate plays a role in the chain of events triggering SD [442,443]. The brain cortex releases excitatory amino acids including glutamate and aspartate, to the extracellular space during CSD [447]. Subsequently it has been shown that the triggering of SD requires activation of the NMDA subtype of glutamate receptor in rat cerebral cortex [147,261], in chick retina [380] and in human neocortical tissues [149]. Other glutamate receptor subtypes (AMPA, kainate and quisqualate) can induce SD but their effects inhibited by NMDA receptor antagonist [241,383].

[147] N.A. Gorelova, V.I. Koroleva, T. Amemori, V. Pavlik, J. Bures, Ketamine blockade of cortical spreading depression in rats, Electroencephalogr. Clin. Neurophysiol. 66 (1987) 440-447.

[149] A. Gorji, D. Scheller, H. Straub, F. Tegtmeier, A. Ebnen, P. Wolf, H.W. Panneck, F. Oppel, E.-J. Speckmann, R. Kohling, J. Hohling, I. Tuxhorn, Spreading depression in neocortical human slices, Brain Res. 906 (2001) 74-83.

[241] M. Lauritzen, M.E. Rice, Y. Okada, C. Nicholson, Quisqualate, kainate and NMDA can initiate spreading depression in the turtle cerebellum, Brain Res. 475 (1988) 317-327.

[261] R. Marrannes, R. Willems, E. De Prins, A. Wauquier, Evidence for a role of the N-metPyl-D-aspartate (NMDA) receptor in cortical spreading depression in the rat, Brain Res. 457 (1988) 226-240.

[380] M.S. Seelig, Interrelationship of magnesium and estrogen in cardiovascular and bone disorders, eclampsia, migraine and premenstrual syndrome, J. Am. Coll. Nutr. 12 (1993) 442-458.

[383] M.J. Sheardown, The triggering of spreading depression in the chicken retina: a pharmacological study, Brain Res. 607 (1993) 189-194.

[442] A. Van Harreveld, Compounds in brain extracts causing spreading depression of cerebral cortical activity and contraction of crustacean muscle, J. Neurochem. 3 (1959) 300-315.

[443] A. Van Harreveld, E. Fifkova, Glutamate release from the retina during spreading depression, J. Neurobiol. 2 (1970) 13-29.

[447] A. Van Harreveld, M. Kooiman, Amino acid release from the cerebral cortex during spreading depression and asphyxiation, J. Neurochem. 12 (1965) 431-439.

Anmerkungen

The source is not mentioned.

The correct Gorji et al. paper appears to have the title: "Spreading depression in human neocortical slices"; the other seems not to exist.

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[5.] Aeh/Fragment 018 01 - Diskussion
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This suggests that glutamate evokes SD via an action at NMDA receptors.

Migraine sufferers (notably with aura) have substantially higher plasma glutamate and aspartate levels than controls and tension headache patients between attacks. During migraine attacks, glutamate and to a lesser extent aspartate levels are even further increased which show a defective cellular reuptake mechanism for these excitatory amino acids in migraineurs (Ferrari et al., 1990). Another study showed that migraine patients during attacks had higher CSF concentrations of glutamic acid than in controls (Martinez et al., 1993). Aura symptoms cause severe disability over many hours to days in patients with familial hemiplegic migraine (FHM). Intranasal application of the NMDA antagonist ketamine reversibly reduced the severity and duration of neurological deficit in FHM (Kaube et al., 2000). Subcutaneous administration of ketamine produced a marked relief of pain both as an acute treatment and as a prophylactic therapy in migraineurs (Nicolodi and Sicuteri, 1995). In addition, it was suggested that NMDA-mediated transmission is involved in nociceptive trigeminovascular transmission within the trigeminocervical complex in cats (Goadsby and Classey, 2000). The NMDA receptor antagonist MK-801 reduces capsaicin-induced c-fos expression within rat trigeminal nucleus caudalis suggest that NMDA receptors provide a potential therapeutic target for cephalic pain (e.g., migraine) due to trigeminovascular activation from meningeal afferents (Mitsikostas et al., 1989).

5-HT1A receptor stimulation suppresses NMDA receptor-mediated synaptic excitation in the rat visual cortex (Edagawa et al., 1999). NMDA receptor blockade as well as activation of the 5-HT1A receptor attenuates the properties of KCl-induced SD in parietal cortical slices of adult rats (Kruger et al., 1999). Migraine patients have a greater cerebral 5-HT1A hypersensitivity and several anti-migraine agents exhibit marked 5-HT1A receptor activity (Leone et al., 1998).


Edagawa Y, Saito H, Abe K. Stimulation of the 5-HT1A receptor selectively suppresses NMDA receptor-mediated synaptic excitation in the rat visual cortex. Brain Res. 1999;827:225–228.

Ferrari MD, Odink J, Bos KD, Malessy MJ, Bruyn GW. Neuroexcitatory plasma amino acids are elevated in migraine. Neurology 1990; 40:1582–1586.

Goadsby PJ, Classey JD. Glutamatergic transmission in the trigeminal nucleus assessed with local blood flow. Brain Res. 2000;875:119–124.

Kaube H, Herzog J, Kaufer T, Dichgans M, Diener HC. Aura in some patients with familial hemiplegic migraine can be stopped by intranasal ketamine. Neurology 2000;55:139–141.

Kruger H, Heinemann U, Luhmann HJ. Effects of ionotropic glutamate receptor blockade and 5-HT1A receptor activation on spreading depression in rat neocortical slices. Neuroreport 1999;10:2651–2656.

Leone M, Attanasio A, Croci D, Ferraris A, D’Amico D, Grazzi L, Nespolo A,. Bussone G. 5- HT1A receptor hypersensitivity in migraine is suggested by the m-chlorophenylpiperazine test. Neuroreport 1998;9:2605–2608.

Martinez F, Castillo J, Rodriguez JR, Leira R, Noya M. Neuroexcitatory amino acid levels in plasma and cerebrospinal fluid during migraine attacks. Cephalalgia 1993;13:89–93.

Mitsikostas DD, Sanchez del Rio M, Waeber C, Moskowitz MA, Cutrer F. The NMDA receptor antagonist MK-801 reduces capsaicin-induced c-fos expression within rat trigeminal nucleus caudalis. Pain 1998;76:239–248.

Nicolodi M, Sicuteri F. Exploration of NMDA receptors in migraine: therapeutic and theoretic implications. Int. J. Clin. Pharmacol. Res. 1995; 15:181–189.

This suggests that glutamate evokes SD via an action at NMDA receptors.

Migraine sufferers (notably with aura) have substantially higher plasma glutamate and aspartate levels than controls and tension headache patients between attacks. During migraine attacks, glutamate and to a lesser extent aspartate levels are even further increased which show a defective cellular reuptake mechanism for these excitatory amino acids in migraineurs [125]. Another study showed that migraine patients during attacks had higher CSF concentrations of glutamic acid than in controls [263]. Aura symptoms cause severe disability over many hours to days in patients with familial hemiplegic migraine (FHM). Intranasal application of the NMDA antagonist ketamine reversibly reduced the severity and duration of neurological deficit in FHM [205]. Subcutaneous administration of ketamine produced a marked relief of pain both as an acute treatment and as a prophylactic therapy in migraineurs [307]. Furthermore, it was suggested that NMDA-mediated transmission is involved in nociceptive trigeminovascular transmission within the trigeminocervical complex in cats [140]. The NMDA receptor antagonist MK-801 reduces capsaicin-induced c-fos expression within rat trigeminal nucleus caudalis suggest that NMDA receptors provide a potential therapeutic target for cephalic pain (e.g., migraine) due to trigeminovascular activation from meningeal afferents [289].

As mentioned, migraineurs have a greater cerebral 5-HT1A hypersensitivity and several antimigraine agents exhibit marked 5-HT1A receptor activity [247,302]. 5-HT1A receptor stimulation suppresses NMDA receptor-mediated synaptic excitation in the rat visual cortex [116]. NMDA receptor blockade as well as activation of the 5-HT1A receptor attenuates the properties of KCl-induced SD in parietal cortical slices of adult rats [228].


[116] Y. Edagawa, H. Saito, K. Abe, Stimulation of the 5-HT1A receptor selectively suppresses NMDA receptor-mediated synaptic excitation in the rat visual cortex, Brain Res. 827 (1999) 225-228.

[125] M.D. Ferrari, J. Odink, K.D. Bos, M.J. Malessy, G.W. Bruyn, Neuroexcitatory plasma amino acids are elevated in migraine, Neurology 40 (1990) 1582-1586.

[140] PJ. Goadsby, J.D. Classey, Glutamatergic transmission in the trigeminal nucleus assessed with local blood flow, Brain Res. 875 (2000) 119-124.

[205] H. Kaube, J. Herzog, T. Kaufer, M. Dichgans, H.C. Diener, Aura in some patients with familial hemiplegic migraine can be stopped by intranasal ketamine, Neurology 55 (2000) 139-141.

[228] H. Kruger, U. Heinemann, H.J. Luhmann, Effects of ionotropic glutamate receptor blockade and 5-HT1A receptor activation on spreading depression in rat neocortical slices, Neuroreport 10 (1999) 2651-2656.

[247] M. Leone, A. Attanasio, D. Croci, A. Ferraris, D. D’Amico, L. Grazzi, A. Nespolo, G. Bussone, 5-HT1A receptor hypersensitivity in migraine is suggested by the m-chlorophenylpiperazine test, Neuroreport 9 (1998) 2605-2608.

[263] F. Martinez, J. Castillo, J.R. Rodriguez, R. Leira, M. Noya, Neuroexcitatory amino acid levels in plasma and cerebrospinal fluid during migraine attacks, Cephalalgia 13 (1993) 89-93.

[289] D.D. Mitsikostas, M. SancPez del Rio, C. Waeber, M.A. Moskowitz, F.M. Cutrer, The NMDA receptor antagonist MK-801 reduces capsaicin-induced c-fos expression within rat trigeminal nucleus caudalis, Pain 76 (1998) 239-248.

[302] A. Newman-Tancredi, C. Conte, C. Chaput, L. Verriele, V. Audinot- Bouchez, S. Lochon, G. Lavielle, M.J. Millan, Agonist activity of antimigraine drugs at recombinant human 5-HT1A receptors: potential implications for prophylactic and acute therapy, Naunyn Schmtrerbrrg’s ArcP. Pharmacol. 355 (1997) 682-688.

[307] M. Nicolodi, F. Sicuteri, Exploration of NMDA receptors in migraine: therapeutic and theoretic implications, Int. J. Clin. Pharmacol. Res. 15 (1995) 181-189.

Anmerkungen

The source is not mentioned.

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Magnesium is known to block the NMDA receptor. The available evidence suggests that up to 50% of patients during an acute migraine attack have lowered levels of ionized magnesium (Ramadan et al., 1999). Erythrocytes and lymphocytes magnesium concentrations are significantly lower in migraine patients as compared to controls (James et al., 2000). Infusion of magnesium results in a rapid and sustained relief of an acute migraine in such patients (Mauskop et al., 1995). However, it should be mentioned that magnesium concentration has an effect on serotonin receptors, nitric oxide synthesis and release, and a variety of other migraine-related receptors and neurotransmitters (Mauskop and Altura, 1998). It is well known that reduced magnesium facilitates the development of SD in animal models and human tissues (Mody et al., 1987). Intravenous magnesium as well as the NMDA receptor antagonist MK-801 significantly reduced the frequency of SD evoked by cortical KCl application in rats. On the other hand, SD affects magnesium metabolism in the central nervous system (van der Hel et al., 1998). The magnesium sulphate anesthesia was considerably shortened approximately four times by CSD in functional decorticated mice in comparison with control animals (Bohdanecky and Necina 1963).

Bohdanecky Z, Necina J. Course of some pharmacological tests in functionally decorticated animals. Physiol. Bohemoslov. 1963;12:55–61.

Mauskop A, Altura BM. Role of magnesium in the pathogenesis and treatment of migraines. Clin. Neurosci. 1998;5:24–27.

Mauskop A, Altura BT, Cracco RQ, Altura BM. Intravenous magnesium sulphate relieves migraine attacks in patients with low serum ionized magnesium levels: a pilot study. Clin. Sci. 1995;89:633–636.

Mody I, Lambert JD, Heinemann U. Low extracellular magnesium induces epileptiform activity and spreading depression in rat hippocampal slices. J. Neurophysiol. 1987;57:869– 888.

Ramadan NM, Halvorson H, Vande-Linde A, Levine SR, Helpern JA, Welch KM. Low brain magnesium in migraine. Headache 1989;29:590–593.

van der Hel WS, van den Bergh WM, Nicolay K, Tulleken KA, Dijkhuizen RM. Suppression of cortical spreading depressions after magnesium treatment in the rat. Neuroreport 1998;9:2179–2182.

Magnesium is known to block the NMDA receptor [271]. The available evidence suggests that up to 50% of patients during an acute migraine attack have lowered levels of ionized magnesium [348,455]. Erythrocytes and lymphocytes magnesium concentrations are significantly lower in migraine patients as compared to controls [426]. Infusion of magnesium results in a rapid and sustained relief of an acute migraine in such patients [270]. However, it should be mentioned that magnesium concentration has an effect on serotonin receptors, nitric oxide synthesis and release, and a variety of other migraine-related receptors and neurotransmitters [269]. It is well known that reduced magnesium facilitates the development of SD in animal models and human tissues [16,291]. Intravenous magnesium as well as the NMDA receptor antagonist MK-801 significantly reduced the frequency of SD evoked by cortical KCl application in rats [439]. On the other hand, SD affects magnesium metabolism in the central nervous system. The magnesium sulphate anesthesia was considerably shortened approximately four times by CSD in functional decorticated mice in comparison with control animals [35].

[16] M. Avoli, C. Drapeau, J. Louvel, R. Pumain, A. Olivier, J.G. Villemure, Epileptiform activity induced by low extracellular magnesium in the human cortex maintained in vitro, Ann. Neurol. 30 (1991) 589-596.

[35] Z. Bohdanecky, J. Necina, Course of some pharmacological tests in functionally decorticated animals, Physiol. Bohemoslov. 12 (1963) 55-61.

[269] A. Mauskop, B.M. Altura, Role of magnesium in the pathogenesis and treatment of migraines, Clin. Neurosci. 5 (1998) 24-27.

[270] A. Mauskop, B.T. Altura, R.Q. Cracco, B.M. Altura, Intravenous magnesium sulphate relieves migraine attacks in patients with low serum ionized magnesium levels: a pilot study, Clin. Sci. 89 (1995) 633-636.

[271] M.L. Mayer, G.L. Westbrook, PB. Guthrie, Voltage-dependent block by Mg21 of NMDA responses in spinal cord neurones, Nature 309 (1984) 261-263.

[291] I. Mody, J.D. Lambert, U. Heinemann, Low extracellular magnesium induces epileptiform activity and spreading depression in rat hippocampal slices, J. NeuropPysiol. 57 (1987) 869-888.

[348] N.M. Ramadan, H. Halvorson, A. Vande-Linde, S.R. Levine, J.A. Helpern, K.M. Welch, Low brain magnesium in migraine, Headache 29 (1989) 590-593.

[426] J. Thomas, J.M. Millot, S. Sebille et al., Free and total magnesium in lymphocytes of migraine patients: effect of magnesium-rich mineral water intake, Clin. Chim. Acta 295 (2000) 63-75.

[439] W.S. van der Hel, W.M. van den Bergh, K. Nicolay, K.A. Tulleken, R.M. Dijkhuizen, Suppression of cortical spreading depressions after magnesium treatment in the rat, Neuroreport 9 (1998) 2179-2182.

[455] K.M. Welch, G.L. Barkley, N. Tepley, N.M. Ramadan, Central neurogenic mechanisms of migraine, Neurology 43 (1993) S21- S25.

Anmerkungen

The source is not mentioned.

Note: there is no entry "James et al., 2000" in the bibliography.

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