Posttraumatic Epilepsy: The Roles of Synaptic Plasticity

Acute cerebral cortical trauma often leads to paroxysmal activities that terminate in a few hours, but several months later, patients can develop epilepsy. The process occurring between the initial acute triggered seizures and the onset of spontaneous unprovoked seizures is termed epileptogenesis. Here the authors summarize recent morphological, electrophysiological, and computational studies demonstrating that partial cortical isolation increases the number and duration of silent states in the cortical network, boosting neuronal connectivity and network excitability. These changes develop progressively, and after several weeks their synergetic action leads to epilepsy.

[1]  Igor Timofeev,et al.  Increased propensity to seizures after chronic cortical deafferentation in vivo. , 2006, Journal of neurophysiology.

[2]  Igor Timofeev,et al.  Modulation of synaptic transmission in neocortex by network activities , 2005, The European journal of neuroscience.

[3]  Niraj S. Desai,et al.  Activity-dependent scaling of quantal amplitude in neocortical neurons , 1998, Nature.

[4]  G. Turrigiano Homeostatic plasticity in neuronal networks: the more things change, the more they stay the same , 1999, Trends in Neurosciences.

[5]  M. Steriade,et al.  Waking-sleep modulation of paroxysmal activities induced by partial cortical deafferentation. , 2006, Cerebral cortex.

[6]  P A Salin,et al.  Chronic neocortical epileptogenesis in vitro. , 1994, Journal of neurophysiology.

[7]  T. Sejnowski,et al.  Homeostatic synaptic plasticity can explain post-traumatic epileptogenesis in chronically isolated neocortex. , 2005, Cerebral cortex.

[8]  T. Sejnowski,et al.  Origin of slow cortical oscillations in deafferented cortical slabs. , 2000, Cerebral cortex.

[9]  Paul Antoine Salin,et al.  Axonal sprouting in layer V pyramidal neurons of chronically injured cerebral cortex , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[10]  M Steriade,et al.  Disfacilitation and active inhibition in the neocortex during the natural sleep-wake cycle: an intracellular study. , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[11]  Jordan Grafman,et al.  Epilepsy after penetrating head injury. I. Clinical correlates , 1985, Neurology.

[12]  T. Schikorski,et al.  Inactivity Produces Increases in Neurotransmitter Release and Synapse Size , 2001, Neuron.

[13]  Ivan Soltesz,et al.  Homeostatic Plasticity Studied Using In Vivo Hippocampal Activity-Blockade: Synaptic Scaling, Intrinsic Plasticity and Age-Dependence , 2007, PloS one.

[14]  I. Timofeev,et al.  Synaptic Strength Modulation after Cortical Trauma: A Role in Epileptogenesis , 2008, The Journal of Neuroscience.

[15]  M. Steriade,et al.  Neocortical seizures: initiation, development and cessation , 2004, Neuroscience.

[16]  Anita E Bandrowski,et al.  Cortical injury affects short-term plasticity of evoked excitatory synaptic currents. , 2005, Journal of neurophysiology.

[17]  J. Zoll,et al.  Paroxysmal high voltage discharges from isolated and partially isolated human and animal cerebral cortex. , 1952, Electroencephalography and clinical neurophysiology.

[18]  I. Timofeev,et al.  Neocortical post-traumatic epileptogenesis is associated with loss of GABAergic neurons. , 2009, Journal of neurotrauma.

[19]  Maxim Bazhenov,et al.  Focal Generation of Paroxysmal Fast Runs during Electrographic Seizures 2008 International League against Epilepsy , 2022 .

[20]  Bernard S. Chang,et al.  Practice parameter: Antiepileptic drug prophylaxis in severe traumatic brain injury , 2003, Neurology.

[21]  D. Prince,et al.  Synaptic activity in chronically injured, epileptogenic sensory-motor neocortex. , 2002, Journal of neurophysiology.

[22]  Maxim Bazhenov,et al.  Pathological Effect of Homeostatic Synaptic Scaling on Network Dynamics in Diseases of the Cortex , 2008, The Journal of Neuroscience.

[23]  Igor Timofeev,et al.  Partial cortical deafferentation promotes development of paroxysmal activity. , 2003, Cerebral cortex.

[24]  M. Marcikić,et al.  Management of war penetrating craniocerebral injuries during the war in Croatia. , 1998, Injury.

[25]  Maxim Volgushev,et al.  Precise Long-Range Synchronization of Activity and Silence in Neocortical Neurons during Slow-Wave Sleep , 2006, The Journal of Neuroscience.

[26]  Niraj S. Desai,et al.  Critical periods for experience-dependent synaptic scaling in visual cortex , 2002, Nature Neuroscience.

[27]  J SZENTAGOTHAI,et al.  THE USE OF DEGENERATION METHODS IN THE INVESTIGATION OF SHORT NEURONAL CONNEXIONS. , 1965, Progress in brain research.

[28]  W. Regehr,et al.  Short-term synaptic plasticity. , 2002, Annual review of physiology.

[29]  Xiaoming Jin,et al.  Enhanced Excitatory Synaptic Connectivity in Layer V Pyramidal Neurons of Chronically Injured Epileptogenic Neocortex in Rats , 2006, The Journal of Neuroscience.

[30]  A. Walker POSTTRAUMATIC EPILEPSY. , 1965, Journal of the Medical Association of the State of Alabama.

[31]  D. Prince,et al.  Epileptogenesis in chronically injured cortex: in vitro studies. , 1993, Journal of neurophysiology.