Posttraumatic Epilepsy and Neurorehabilitation

Author(s):  
Theresa Hernández ◽  
Paul Levisohn ◽  
Dean Naritoku
2017 ◽  
Vol 48 (S 01) ◽  
pp. S1-S45
Author(s):  
S. Schubert-Bast

Epilepsia ◽  
2015 ◽  
Vol 56 (8) ◽  
pp. 1198-1206 ◽  
Author(s):  
Matthew L. Diamond ◽  
Anne C. Ritter ◽  
Edwin K. Jackson ◽  
Yvette P. Conley ◽  
Patrick M. Kochanek ◽  
...  

2003 ◽  
Vol 56 (2-3) ◽  
pp. 165-173 ◽  
Author(s):  
Carolina Samuelsson ◽  
Eva Kumlien ◽  
Åse Elfving ◽  
Dan Lindholm ◽  
Elisabeth Ronne-Engström

Epilepsia ◽  
1978 ◽  
Vol 19 (2) ◽  
pp. 177-183 ◽  
Author(s):  
Sureyya Dikmen ◽  
Ralph M. Reitan

Author(s):  
Daniel Luciano ◽  
Kenneth Alper ◽  
Siddhartha Nadkarni

2018 ◽  
Vol 38 (06) ◽  
pp. 619-626 ◽  
Author(s):  
Brigid Dwyer

AbstractPosttraumatic headaches are among the most challenging complaints after mild traumatic brain injury (mTBI). They are a debilitating problem experienced by patients after TBI of all severities. Up to 90% of mild TBI patients experience headache, particularly if female and with a premorbid history of primary headache. Tension headache has classically been the most common subtype, but in military populations migraine has dominated. Posttraumatic headache encompasses a spectrum of headache types that overlap heavily with common primary headache disorders, but also autonomic cephalgias as well as several secondary headache conditions. It is important to understand the evolution of postconcussion syndrome as a concept, and the challenges associated with diagnosing and treating multidomain drivers effectively. The first-line treatments for posttraumatic headache are typically the same as those used in nontraumatic headache, with additional considerations for cognitive side effects, posttraumatic epilepsy, and coexisting injuries resulting in neuropathic pain or medication overuse.


2010 ◽  
Vol 103 (3) ◽  
pp. 1490-1500 ◽  
Author(s):  
Robert F. Hunt ◽  
Stephen W. Scheff ◽  
Bret N. Smith

Posttraumatic epilepsy is a frequent consequence of brain trauma, but relatively little is known about how neuronal circuits are chronically altered after closed head injury. We examined whether local recurrent excitatory synaptic connections form between dentate granule cells in mice 8–12 wk after cortical contusion injury. Mice were monitored for behavioral seizures shortly after brain injury and ≤10 wk postinjury. Injury-induced seizures were observed in 15% of mice, and spontaneous seizures were observed weeks later in 40% of mice. Timm's staining revealed mossy fiber sprouting into the inner molecular layer of the dorsal dentate gyrus ipsilateral to the injury in 95% of mice but not contralateral to the injury or in uninjured controls. Whole cell patch-clamp recordings were made from granule cells in isolated hippocampal brain slices. Cells in slices with posttraumatic mossy fiber sprouting had an increased excitatory postsynaptic current (EPSC) frequency compared with cells in slices without sprouting from injured and control animals ( P < 0.001). When perfused with Mg2+-free artificial cerebrospinal fluid containing 100 μM picrotoxin, these cells had spontaneous bursts of EPSCs and action potentials. Focal glutamate photostimulation of the granule cell layer evoked a burst of EPSCs and action potentials indicative of recurrent excitatory connections in granule cells of slices with mossy fiber sprouting. In granule cells of slices without sprouting from injured animals and controls, spontaneous or photostimulation-evoked epileptiform activity was never observed. These results suggest that a new regionally localized excitatory network forms between dentate granule cells near the injury site within weeks after cortical contusion head injury.


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