Absence seizures (AS), presenting as short losses of consciousness with staring spells, are a common manifestation of childhood epilepsy that is associated with behavioral, emotional, and social impairments. It has also been suggested that patients with AS are more likely to suffer from mood disorders such as depression and anxiety. This systematic review and meta-analysis synthesizes human and animal models that investigated mood disorders and AS. Of the 1019 scientific publications identified, 35 articles met the inclusion criteria for this review. We found that patients with AS had greater odds of developing depression and anxiety when compared to controls (odds ratio = 4.93, 95% confidence interval = 2.91-8.35, p < .01). The included studies further suggest a strong correlation between AS and depression and anxiety in the form of a bidirectional relationship. The current literature emphasizes that these conditions likely share underlying mechanisms, such as genetic predisposition, neurophysiology, and anatomical pathways. Further research will clarify this relationship and ensure more effective treatment for AS and mood disorders.

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The enzyme glutamine synthetase (GS), also referred to as glutamate ammonia ligase, is abundant in astrocytes and catalyzes the conversion of ammonia and glutamate to glutamine. Deficiency or dysfunction of astrocytic GS in discrete brain regions have been associated with several types of epilepsy, including medically-intractable mesial temporal lobe epilepsy (MTLE), neocortical epilepsies, and glioblastoma-associated epilepsy. Moreover, experimental inhibition or deletion of GS in the entorhinal-hippocampal territory of laboratory animals causes an MTLE-like syndrome characterized by spontaneous, recurrent hippocampal-onset seizures, loss of hippocampal neurons, and in some cases comorbid depressive-like features. The goal of this review is to summarize and discuss the possible roles of astroglial GS in the pathogenesis of epilepsy.

Epilepsy is a neurological disorder affecting approximately 70 million people worldwide. It is characterized by seizures that are complex aberrant dynamical events typically treated with drugs and surgery. Unfortunately, not all patients become seizure-free, and there is an opportunity for novel approaches to treat epilepsy using a network view of the brain. The traditional seizure focus theory presumed that seizures originated within a discrete cortical area with subsequent recruitment of adjacent cortices with seizure progression. However, a more recent view challenges this concept, suggesting that epilepsy is a network disease, and both focal and generalized seizures arise from aberrant activity in a distributed network. Changes in the anatomical configuration or widespread neural activities spanning lobes and hemispheres could make the brain more susceptible to seizures. In this perspective paper, we summarize the current state of knowledge, address several important challenges that could further improve our understanding of the human brain in epilepsy, and invite novel studies addressing these challenges.

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