A Neural Network Model of Sensitization of Evoked Cortical Responses in Migraine

Migraine patients show abnormalities of cerebral electrophysiology that manifest themselves mainly during the attack interval. Cortical-evoked potentials of migraineurs fail to habituate to repetitive presentations of visual stimuli, and the amplitude of components of their auditory cortical-evoked potentials have a higher dependence on the stimulus intensities than in healthy subjects. A computer model of a neural network has been developed that is able to reproduce both these neurophysiological dysfunctions. It predicts a positive correlation between the magnitudes of both these dysfunctions. The model also offers an explanation of why mutations in the same ion channel gene with opposite consequences on channel function, e.g. P/Q Ca2+ channels in migraine, may lead to similar electrophysiological abnormalities.

[1]  R. Ophoff,et al.  Familial hemiplegic migraine locus on 19p13 is involved in the common forms of migraine with and without aura , 1995, Human Genetics.

[2]  R. Kraus,et al.  Familial Hemiplegic Migraine Mutations Change α1ACa2+ Channel Kinetics* , 1998, The Journal of Biological Chemistry.

[3]  A. Koschak,et al.  Three New Familial Hemiplegic Migraine Mutants Affect P/Q-type Ca2+ Channel Kinetics* , 2000, The Journal of Biological Chemistry.

[4]  P J Delwaide,et al.  Potentiation instead of habituation characterizes visual evoked potentials in migraine patients between attacks , 1995, European journal of neurology.

[5]  Georg Juckel,et al.  Intensity dependence of auditory evoked potentials as an indicator of central serotonergic neurotransmission: A new hypothesis , 1993, Biological Psychiatry.

[6]  S. Evers,et al.  Cognitive Processing in Primary Headache , 1997, Neurology.

[7]  M. Timsit-Berthier,et al.  Contingent Negative Variation (CNV) as a Diagnostic and Physiopathologic Tool in Headache Patients , 1985 .

[8]  P. Montagna,et al.  Molecular Genetics of Migraine Headaches: A Review , 2000, Cephalalgia : an international journal of headache.

[9]  U. Stephani,et al.  Intensity dependence of auditory evoked cortical potentials in migraine families , 2000, Pain.

[10]  J. Schoenen,et al.  Impairment of neuromuscular transmission in a subgroup of migraine patients , 1999, Neuroscience Letters.

[11]  K. Stauderman,et al.  Functional Consequences of Mutations in the Human α1A Calcium Channel Subunit Linked to Familial Hemiplegic Migraine , 1999, The Journal of Neuroscience.

[12]  J. Schoenen,et al.  Deficient habituation of evoked cortical potentials in migraine: a link between brain biology, behavior and trigeminovascular activation? , 1996, Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie.

[13]  M. Timsit-Berthier,et al.  Intensity dependence of auditory evoked potentials is pronounced in migraine , 1996, Neurology.

[14]  Michael A. Arbib,et al.  The handbook of brain theory and neural networks , 1995, A Bradford book.

[15]  Dennis E Bulman,et al.  Familial Hemiplegic Migraine and Episodic Ataxia Type-2 Are Caused by Mutations in the Ca2+ Channel Gene CACNL1A4 , 1996, Cell.

[16]  J. C. Stanley Computer simulation of a model of habituation , 1976, Nature.

[17]  T. Sejnowski,et al.  Ionic mechanisms underlying synchronized oscillations and propagating waves in a model of ferret thalamic slices. , 1996, Journal of neurophysiology.

[18]  J. Schoenen,et al.  Habituation of Visual and Intensity Dependence of Auditory Evoked Cortical Potentials Tends to Normalize Just Before and During the Migraine Attack , 2000 .

[19]  R. Ophoff,et al.  Involvement of the CACNA1A gene containing region on 19p13 in migraine with and without aura , 2001, Neurology.

[20]  R. F. Thompson,et al.  Habituation: a model phenomenon for the study of neuronal substrates of behavior. , 1966, Psychological review.

[21]  Elizabeth Thomas,et al.  Increased Synchrony with Increase of a Low-Threshold Calcium Conductance in a Model Thalamic Network: A Phase-Shift Mechanism , 2000, Neural Computation.

[22]  P. Kropp,et al.  Contingent Negative Variation During Migraine Attack and Interval: Evidence for Normalization of Slow Cortical Potentials During the Attack , 1995, Cephalalgia : an international journal of headache.

[23]  J. Schoenen,et al.  Visual evoked potentials during long periods of pattern-reversal stimulation in migraine. , 1998, Brain : a journal of neurology.

[24]  G. Fein,et al.  Effect of Photic Stimulation on Human Visual Cortex Lactate and Phosphates Using 1H and 31P Magnetic Resonance Spectroscopy , 1992, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[25]  M. Alexander,et al.  Principles of Neural Science , 1981 .

[26]  D. Nyholt,et al.  Familial typical migraine , 1998, Neurology.

[27]  J. Schoenen,et al.  Repeatability of the Intensity Dependence of Cortical Auditory Evoked Potentials in the Assessment of Cortical Information Processing , 1999, Cephalalgia : an international journal of headache.

[28]  W. Lytton,et al.  Computer model of antiepileptic effects mediated by alterations in GABAA‐mediated inhibition , 1998, Neuroreport.

[29]  J. Schoenen,et al.  Subclinical cerebellar impairment in the common types of migraine: A three‐dimensional analysis of reaching movements , 2001, Annals of neurology.

[30]  G. Augustine,et al.  Exocytosis: proteins and perturbations. , 1996, Annual review of pharmacology and toxicology.