Changes in Intracortical Excitability After Transient Ischemic Attack Are Associated With ABCD2 Score

Background and Purpose— A transient ischemic attack (TIA) is a brief ischemic episode characterized by rapid clinical resolution and not associated with permanent cerebral infarction. Whether changes in intracortical excitability persist and are related to clinical predictors of stroke risk after TIA remains unknown. Methods— Participants were individuals with clinically resolved motor TIA with no structural lesions and healthy age-matched control participants. Single and paired-pulse transcranial magnetic stimulation was used to measure intracortical excitability. Recruitment curves for percent inhibition and facilitation were used to derive excitability thresholds. Correlations between threshold asymmetries and ABCD2 score were performed. Results— Results showed a significant 3-way interaction with reduced inhibition and enhanced facilitation in the affected compared with unaffected hemisphere after TIA. No significant differences were present in healthy participants. Asymmetries in intracortical inhibition and facilitation were significantly correlated with ABCD2 score. Conclusions— The present study is the first, to our knowledge, to demonstrate altered intracortical inhibition and facilitation in the affected hemisphere after TIA. These changes occurred on average 2 weeks after clinical signs of TIA resolved and in the absence of structural lesions and were not present in healthy age-matched control participants. Furthermore, this study is the first, to our knowledge, to report that changes in intracortical excitability after TIA are associated with ABCD2 score.

[1]  K. Werhahn,et al.  Recruitment of motor cortex inhibition differentiates between generalized and focal epilepsy , 2009, Epilepsy Research.

[2]  G. Zanette,et al.  Motor Cortical Disinhibition During Early and Late Recovery After Stroke , 2008, Neurorehabilitation and neural repair.

[3]  J. Rothwell,et al.  Stages of Motor Output Reorganization after Hemispheric Stroke Suggested by Longitudinal Studies of Cortical Physiology , 2008, Cerebral cortex.

[4]  S. Johnston,et al.  Short-term prognosis after a TIA: a simple score predicts risk. , 2007, Cleveland Clinic journal of medicine.

[5]  D. Centonze,et al.  Endocannabinoids limit metabotropic glutamate 5 receptor-mediated synaptic inhibition of striatal principal neurons , 2007, Molecular and Cellular Neuroscience.

[6]  G. Tsivgoulis,et al.  Validation of the ABCD Score in Identifying Individuals at High Early Risk of Stroke After a Transient Ischemic Attack: A Hospital-Based Case Series Study , 2006, Stroke.

[7]  John W Krakauer,et al.  Hypoperfusion without stroke alters motor activation in the opposite hemisphere , 2004, Annals of neurology.

[8]  W. Byblow,et al.  Elevated threshold for intracortical inhibition in focal hand dystonia , 2004, Movement disorders : official journal of the Movement Disorder Society.

[9]  W. Byblow,et al.  Impaired modulation of corticospinal excitability following subthreshold rTMS in focal hand dystonia. , 2004, Human movement science.

[10]  H. Meinck,et al.  Long-lasting motor cortex disinhibition after short transient ischemic attacks (TIAs) in humans , 2004, Neuroscience Letters.

[11]  J. Rothwell,et al.  The variability of intracortical inhibition and facilitation , 2003, Clinical Neurophysiology.

[12]  Volker Hömberg,et al.  Remote changes in cortical excitability after stroke. , 2003, Brain : a journal of neurology.

[13]  P. Rossini,et al.  Motor cortical disinhibition in the unaffected hemisphere after unilateral cortical stroke. , 2002, Brain : a journal of neurology.

[14]  E. Wassermann.  Variation in the response to transcranial magnetic brain stimulation in the general population , 2002, Clinical Neurophysiology.

[15]  P. Manganotti,et al.  Motor disinhibition in affected and unaffected hemisphere in the early period of recovery after stroke , 2002, Clinical Neurophysiology.

[16]  Ichiro Kanazawa,et al.  Mechanisms of intracortical I‐wave facilitation elicited with paired‐pulse magnetic stimulation in humans , 2002, The Journal of physiology.

[17]  J. Liepert,et al.  Motor cortex disinhibition of the unaffected hemisphere after acute stroke , 2000, Muscle & nerve.

[18]  J. Liepert,et al.  Motor cortex disinhibition in acute stroke , 2000, Clinical Neurophysiology.

[19]  F Di Salle,et al.  Diffusion MRI in patients with transient ischemic attacks. , 1999, Stroke.

[20]  T. Neumann-Haefelin,et al.  Upregulation of GABAA-receptor α1- and α2-subunit mRNAs following ischemic cortical lesions in rats , 1999, Brain Research.

[21]  M Hallett,et al.  Dextromethorphan decreases the excitability of the human motor cortex , 1998, Neurology.

[22]  K. Zilles,et al.  Long-term cellular dysfunction after focal cerebral ischemia: in vitro analyses , 1998, Neuroscience.

[23]  A. Schleicher,et al.  Long-term changes of ionotropic glutamate and GABA receptors after unilateral permanent focal cerebral ischemia in the mouse brain , 1998, Neuroscience.

[24]  O. Witte,et al.  Systemically administered cycloheximide reduces inhibition in rat neocortical slice preparation , 1996, Brain Research.

[25]  Babak Boroojerdi,et al.  Transcallosal inhibition in cortical and subcortical cerebral vascular lesions , 1996, Journal of the Neurological Sciences.

[26]  J. Rothwell,et al.  Interaction between intracortical inhibition and facilitation in human motor cortex. , 1996, The Journal of physiology.

[27]  Walter Paulus,et al.  The effect of lorazepam on the motor cortical excitability in man , 1996, Experimental Brain Research.

[28]  C. Marsden,et al.  Corticocortical inhibition in human motor cortex. , 1993, The Journal of physiology.

[29]  David Lee Gordon,et al.  Classification of Subtype of Acute Ischemic Stroke: Definitions for Use in a Multicenter Clinical Trial , 1993, Stroke.

[30]  M. Tegenthoff,et al.  The glutamate antagonist Riluzole suppresses intracortical facilitation , 2005, Journal of Neural Transmission.

[31]  T. Neumann-Haefelin,et al.  Upregulation of GABAA-receptor alpha1- and alpha2-subunit mRNAs following ischemic cortical lesions in rats. , 1999, Brain research.