**4. Conclusion**

Inflammation plays an important role in the development of epilepsy and understanding this inflammatory process that happens during epileptogenesis could provide a strong basis for drug development and therapeutic approaches. We briefly highlighted the inflammatory response during epilepsy and some clinical correlation. Besides, we outlined the experimental findings in epilepsy research pertaining to inflammation and hope to clear the doubts as to whether inflammation is a cause or consequence of epilepsy. Evidently, inflammation can be both the cause as well as consequence of epilepsy. Inflammation due to hyperthermia or infection activates the release of inflammatory molecules which increases seizures susceptibility. On the other hand, BBB dysfunction and prolonged seizures cause an influx of inflammatory molecules which causes neuroinflammation to take place.

Anti-inflammatory drugs, such as acetaminophen, celecoxib or aspirin, along with other anti-inflammatory agents such as anti-MGB1 antibodies and COX-2 inhibitors have been shown to possess anti-convulsant properties [73]. Therefore, we suggest incorporating anti-inflammatory drugs into anti-epileptic treatments or therapy could be beneficial in the management of epilepsy and ameliorating comorbidities and side effects that could be exacerbated by neuroinflammation.

### **Acknowledgements**

The authors would like to thank Mr. Brandon Choo Kar Meng for proofreading the manuscript.

**27**

**Author details**

provided the original work is properly cited.

Vanessa Lin Lin Lee and Mohd. Farooq Shaikh\*

*Inflammation: Cause or Consequence of Epilepsy? DOI: http://dx.doi.org/10.5772/intechopen.83428*

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

Neuropharmacology Research Laboratory, Jeffrey Cheah School of Medicine and

Health Sciences, Monash University Malaysia, Bandar Sunway, Malaysia

\*Address all correspondence to: farooq.shaikh@monash.edu

## **Conflict of interest**

Authors declare no conflict of interest.

*Inflammation: Cause or Consequence of Epilepsy? DOI: http://dx.doi.org/10.5772/intechopen.83428*

*Epilepsy - Advances in Diagnosis and Therapy*

ficient to trigger spontaneous seizures.

**4. Conclusion**

**Acknowledgements**

**Conflict of interest**

Authors declare no conflict of interest.

the manuscript.

was found that albumin injection prominently increases IL-1β immunoreactivity in GFAP-positive astrocytes and the number of IL-1β immunopositive cells, indicating the presence of inflammation. Besides that, the production of rapid onset and transient spiking activity in the hippocampus can be found on the EEG analysis of rats injected with rat albumin. This means that the injection of albumin provokes the increase in neuronal excitability. Interestingly, rats presented a significant decline in seizure threshold 3 months after albumin injection. This suggests that acute tissue exposure to albumin induces a long-lasting increase in brain excitability [72].

In short, this model is able to show the pro-ictogenic effect of serum albumin in the brain, mimicking those attained after prolonged seizures and BBB dysfunction. Albumin induces the production of inflammatory molecules and together, they significantly increase brain excitability and seizure susceptibility although insuf-

Inflammation plays an important role in the development of epilepsy and under-

Anti-inflammatory drugs, such as acetaminophen, celecoxib or aspirin, along with other anti-inflammatory agents such as anti-MGB1 antibodies and COX-2 inhibitors have been shown to possess anti-convulsant properties [73]. Therefore, we suggest incorporating anti-inflammatory drugs into anti-epileptic treatments or therapy could be beneficial in the management of epilepsy and ameliorating comorbidities and side effects that could be exacerbated by neuroinflammation.

The authors would like to thank Mr. Brandon Choo Kar Meng for proofreading

standing this inflammatory process that happens during epileptogenesis could provide a strong basis for drug development and therapeutic approaches. We briefly highlighted the inflammatory response during epilepsy and some clinical correlation. Besides, we outlined the experimental findings in epilepsy research pertaining to inflammation and hope to clear the doubts as to whether inflammation is a cause or consequence of epilepsy. Evidently, inflammation can be both the cause as well as consequence of epilepsy. Inflammation due to hyperthermia or infection activates the release of inflammatory molecules which increases seizures susceptibility. On the other hand, BBB dysfunction and prolonged seizures cause an influx of inflam-

matory molecules which causes neuroinflammation to take place.

**26**
