The role of inflammation in epilepsy
Open accessAbstract
Epilepsy is the third most common chronic brain disorder, and is characterized by an enduring predisposition to generate seizures. Despite progress in pharmacological and surgical treatments of epilepsy, relatively little is known about the processes leading to the generation of individual seizures, and about the mechanisms whereby a healthy brain is rendered epileptic. These gaps in our knowledge hamper the development of better preventive treatments and cures for the approximately 30% of epilepsy cases that prove resistant to current therapies. Here, we focus on the rapidly growing body of evidence that supports the involvement of inflammatory mediators-released by brain cells and peripheral immune cells-in both the origin of individual seizures and the epileptogenic process. We first describe aspects of brain inflammation and immunity, before exploring the evidence from clinical and experimental studies for a relationship between inflammation and epilepsy. Subsequently, we discuss how seizures cause inflammation, and whether such inflammation, in turn, influences the occurrence and severity of seizures, and seizure-related neuronal death. Further insight into the complex role of inflammation in the generation and exacerbation of epilepsy should yield new molecular targets for the design of antiepileptic drugs, which might not only inhibit the symptoms of this disorder, but also prevent or abrogate disease pathogenesis.
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Blood-brain barrier breakdown caused by traumatic brain injury and underlying inflammatory reactions can trigger epilepsy.
“BBB breakdown caused by TBI and underlying inflammatory reactions can trigger epilepsy (204, 618).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [618]
In “Does inflammation cause cell loss?” (page unavailable), the review says TBI causes tissue inflammation that seems to contribute to long-term hyperexcitability and describes injury-related inflammation as a possible contributor to epilepsy in adult rodents. It also reports BBB breakdown alongside vascular inflammation in epilepsy models, but the passages do not establish that TBI-caused BBB breakdown triggers epilepsy. (LLM, conf=0.83)
Experimental — accuracy not yet measuredThe cells of the NVU, especially glial cells, have an overwhelming importance in epileptogenesis.
“Taking all the recent data into consideration, we can suggest that the cells of the NVU, specially glial cells, have an overwhelming importance in epileptogenesis.”
From The impact of microglial activation on blood-brain barrier in brain diseases (2014) · cites this paper as Vezzani et al., 2011
Inflammatory pathways activated by microglial cells induce BBB dysfunction, which contributes to epileptogenesis.
“These current findings show the increasing importance of the inflammatory pathways activated by microglial cells in inducing BBB dysfunction, which contributes to epileptogenesis.”
From The impact of microglial activation on blood-brain barrier in brain diseases (2014) · cites this paper as Vezzani et al., 2011
In epilepsy, chronic seizures lead to excitotoxicity and neuronal apoptosis with associated gliosis.
“In epilepsy, chronic seizures lead to excitotoxicity and neuronal apoptosis with associated gliosis [188].”
From Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation (2019) · cites this paper as [188]
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Seizure-induced brain-borne inflammation sustains seizure recurrence and blood-brain barrier damage
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Self-citationNeurons under T Cell Attack Coordinate Phagocyte-Mediated Synaptic Stripping
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Cyclooxygenase-2 (COX-2) inhibitors: future therapeutic strategies for epilepsy management
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Dysfunction of ABC transporters at the blood-brain barrier: Role in neurological disorders
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Joint single-cell measurements of nuclear proteins and RNA in vivo
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Levetiracetam Mechanisms of Action: From Molecules to Systems
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Rapamycin reverses status epilepticus-induced memory deficits and dendritic damage
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- Authors
- Vezzani, A., French, J., Bartfai, T., & Baram, T. Z.
- Affiliations
- Mario Negri Institute for Pharmacological Research (IT)
- NYU Langone Health (US)
- University of California, Irvine (US)
- Corresponding author
- Vezzani, Annamaria
- Venue
- Nature Reviews Neurology
- Published
- 2010-12-07
- Volume
- 7
- Issue
- 1
- Pages
- 31-40
- ISSN
- 1759-4758 (ISSN-L)
- 1759-4766
- PMC
- PMC3378051
- OpenAlex
- W2022981588
- Cited by
- 1,876
- References
- 181
- Citations by year
- 2026: 135 · 2025: 145 · 2024: 153 · 2023: 144 · 2022: 136 · 2021: 170 · 2020: 130 · 2019: 118 · 2018: 106 · 2017: 124 · 2016: 106 · 2015: 87 · 2014: 111 · 2013: 86 · 2012: 83
- FWCI
- 9.37
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Neurology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by)
- Funders
- American Epilepsy Society
- Parents Against Childhood Epilepsy
- Fondazione Cariplo
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (R37NS035439, R37 NS 35439, R01NS035439)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Vagus Nerve Stimulation Research
- Keywords
- epilepsy, neuroinflammation, inflammatory mediators, seizures, epileptogenesis, peripheral immune cells, seizure-induced neuronal death, antiepileptic drug targets
- MeSH terms
- Animals, Encephalitis, Epilepsy, Humans, Immunity, Innate, Adaptive Immunity
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