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While their efficacy in short-term ischemic events is limited, AEDs have shown promise in prolonged ischemia, suggesting their broader utility in neuroprotection. Further research continues to explore the role of AEDs in modulating energy stress, synaptic plasticity, and neurotransmission across various neurological conditions. | While their efficacy in short-term ischemic events is limited, AEDs have shown promise in prolonged ischemia, suggesting their broader utility in neuroprotection. Further research continues to explore the role of AEDs in modulating energy stress, synaptic plasticity, and neurotransmission across various neurological conditions. | ||
The use of antiepileptic drugs in conditions other than epilepsy has a relatively long history. As early as the mid-1960s, researchers like Campbell conducted the first clinical trials on the use of carbamazepine in the treatment of trigeminal neuralgia. The undesirable effects of first-generation antiepileptic drugs often limited their use. Today, efforts are being made to develop drugs (second-generation antiepileptic drugs) with fewer side effects that can be applied not only to epilepsy but also to conditions such as neuropathic pain and even as neuroprotective agents in stroke and neurodegenerative diseases. It is likely that the aforementioned conditions share common pathogenic mechanisms: numerous studies have hypothesized that neuronal hyperexcitability, increased excitatory glutamatergic tone (and a reduction of inhibitory tone), and long-term modification of synaptic transmission play a critical role in the pathogenesis of neuropathic pain, epilepsy, and cerebral ischemia. | '''Conclusion:''' The use of antiepileptic drugs in conditions other than epilepsy has a relatively long history. As early as the mid-1960s, researchers like Campbell conducted the first clinical trials on the use of carbamazepine in the treatment of trigeminal neuralgia. The undesirable effects of first-generation antiepileptic drugs often limited their use. Today, efforts are being made to develop drugs (second-generation antiepileptic drugs) with fewer side effects that can be applied not only to epilepsy but also to conditions such as neuropathic pain and even as neuroprotective agents in stroke and neurodegenerative diseases. It is likely that the aforementioned conditions share common pathogenic mechanisms: numerous studies have hypothesized that neuronal hyperexcitability, increased excitatory glutamatergic tone (and a reduction of inhibitory tone), and long-term modification of synaptic transmission play a critical role in the pathogenesis of neuropathic pain, epilepsy, and cerebral ischemia. | ||
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