Epilepsy after head injury: The impact of impact

Lowenstein, Daniel H.

doi:10.1002/ana.10090

Cited by 4 publications

(2 citation statements)

References 14 publications

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“…Na + channels initiate/propagate the action potentials, K + channels repolarize the action potentials, and ATPases maintain the ionic gradients across plasma membranes. Hence, decreased functionality of these channels disrupts the ionic homeostasis, leading to decreased posttraumatic axonal conductance and epilepsy (Lowenstein, 2001).…”

Section: Discussionmentioning

confidence: 99%

Traumatic brain injury‐induced acute gene expression changes in rat cerebral cortex identified by GeneChip analysis

Rao

Dhodda

Song

et al. 2002

J of Neuroscience Research

126

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Proper CNS function depends on concerted expression of thousands of genes in a controlled and timely manner. Traumatic brain injury (TBI) in mammals results in neuronal death and neurological dysfunction, which might be mediated by altered expression of several genes. By employing a CNS-specific GeneChip and real-time polymerase chain reaction (PCR), the present study analyzed the gene expression changes in adult rat cerebral cortex in the first 24 hr after a controlled cortical impact injury. Many functional families of genes not previously implicated in TBI-induced brain damage are altered in the injured cortex. These include up-regulated transcription factors (SOCS-3, JAK-2, STAT-3, CREM, IRF-1, SMN, silencer factor-B, ANIA-3, ANIA-4, and HES-1) and signal transduction pathways (cpg21, Narp, and CRBP) and down-regulated transmitter release mechanisms (CITRON, synaptojanin II, ras-related rab3, neurexin-1beta, and SNAP25A and -B), kinases (IP-3-kinase, Pak1, Ca(2+)/CaM-dependent protein kinases), and ion channels (K(+) channels TWIK, RK5, X62839, and Na(+) channel I). In addition, several genes previously shown to play a role in TBI pathophysiology, including proinflammatory genes, proapoptotic genes, heat shock proteins, immediate early genes, neuropeptides, and glutamate receptor subunits, were also observed to be altered in the injured cortex. Real-time PCR analysis confirmed the GeneChip data for many of these transcripts. The novel physiologically relevant gene expression changes observed here might explain some of the molecular mechanisms of TBI-induced neuronal damage.

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Section: Discussionmentioning

confidence: 99%

Traumatic brain injury‐induced acute gene expression changes in rat cerebral cortex identified by GeneChip analysis

Rao

Dhodda

Song

et al. 2002

J of Neuroscience Research

126

View full text Add to dashboard Cite

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“…This finding is not surprising. Epileptogenesis after TBI appears to be a very complex and still unclear process; a wide spectrum of factors possibly involved is under investigation at macroscopic, microscopic, and molecular levels (30)(31)(32)(33)(34)(35). Although the cohort studied was initially selected with regard to risk factors for epilepsy, individual factors that might play a role cannot be excluded.…”

Section: Discussionmentioning

confidence: 99%

Predicting Posttraumatic Epilepsy with MRI: Prospective Longitudinal Morphologic Study in Adults

et al. 2005

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Summary:Purpose: Evaluation of morphologic risk factors for posttraumatic epilepsy (PTE) by using brain magnetic resonance imaging (MRI) in serial assessments ≤2 years after traumatic brain injury (TBI).Methods: Brain MRI hyperintense (gliosis) or hypointense (hemosiderin) areas or both were assessed in the images of 135 adult TBI inpatients who completed a 2-year clinical, EEG, and MRI study protocol. Overall clinical follow-up for the development of PTE was 5-10 years (median, 102 months). Morphologic risk factors for PTE were evaluated by using Kaplan-Meier curves and Cox regression analysis.Results: In 20 patients, PTE developed. Kaplan-Meier curves showed that gliomesenchymal sequelae of focal brain lesions (subdural hematomas/contusions) that required surgical treatment (sSDH-C) were a PTE risk factor (p < 0.001), as were sequelae of nonsurgical hemorrhagic contusions with gliosis wall incompletely surrounding hemosiderin dregs (IW) (p = 0.039) and mainly those with time-related changes from incomplete to complete gliosis wall around hemosiderin (I/CW) (p = 0.005); those with early hemosiderin completely surrounded by gliosis (CW) were not (p = 0.821). Cox regression analysis showed that for patients with sequelae of sSDH-C, the PTE risk was 4.38 (p = 0.023) times higher than for those who did not require surgical treatment or underwent surgery because of purely extradural hematoma; for those with IW and I/CW lesions, considered pooled, it was 6.61 times higher (p = 0.014) than for those with CW lesions.Conclusions: MRI follow-up examination in the early chronic stage can differentiate among low-, intermediate-, and high-risk sequelae of TBI. These findings yield new evidence for, but do not resolve, the debate on posttraumatic epileptogenesis. Key Words: Posttraumatic epilepsy-Brain MRI-HemosiderinGliosis.Risk factors for posttraumatic epilepsy (PTE) are still debated; however, the extensive use of computed tomography (CT) scanning in patients with traumatic brain injury (TBI) has confirmed the important role of documented focal brain lesions not only in military, but also in civilian TBI (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). This means that a precise neuroradiologic diagnosis is of paramount value in determining the individual PTE risk.Magnetic resonance imaging (MRI) has become the imaging method of choice for evaluation of TBI patients in the chronic stage because of its exquisite capability in showing posttraumatic brain abnormalities, provided that the appropriate pulse sequences are used. However, the relation between PTE and brain damage as revealed by MRI has not been established (18). A few years ago, our group participated in a joint prospective longitudinal study to evaluate risk factors for PTE in adults by using clini-

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Neurobiology and neuropathology underlie the neuropsychological deficits associated with traumatic brain injury

Bigler

2003

Archives of Clinical Neuropsychology

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The neurobiological and neuropathological bases that underlie the neuropsychological deficits associated with traumatic brain injury (TBI), including mild TBI, are further reviewed. The article provides an update on neuroimaging methods and findings in the study of TBI since the author's published address of the 1999 Distinguished Neuropsychologist Award of the National Academy of Neuropsychology (see Bigler, 2001a). The review addresses and answers criticisms raised about the interface of neuroimaging abnormalities and neuropsychological deficits, particularly in mild TBI. The article provides further guidelines in making the link between neuroimaging findings and neuropsychological outcome in the clinical practice of neuropsychology. The article also opines on the future role and importance that neuroimaging will play in neuropsychological practice, particularly functional neuroimaging methods.

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Epilepsy after head injury: The impact of impact

Cited by 4 publications

References 14 publications

Traumatic brain injury‐induced acute gene expression changes in rat cerebral cortex identified by GeneChip analysis

Traumatic brain injury‐induced acute gene expression changes in rat cerebral cortex identified by GeneChip analysis

Predicting Posttraumatic Epilepsy with MRI: Prospective Longitudinal Morphologic Study in Adults

Neurobiology and neuropathology underlie the neuropsychological deficits associated with traumatic brain injury

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