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Difference between revisions of "Neuronal Basis of Neuropathic Pain and Neuroprotective Mechanisms of Antiepileptic Drugs"
Neuronal Basis of Neuropathic Pain and Neuroprotective Mechanisms of Antiepileptic Drugs (view source)
Revision as of 17:35, 19 October 2024
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{{ArtBy|||autore=Domenico Tropepe|autore2=Diego Centonze|autore3=Paolo Calabrese}} | {{ArtBy|||autore=Domenico Tropepe|autore2=Diego Centonze|autore3=Paolo Calabrese}} | ||
'''Abstract:''' This article explores the use of antiepileptic drugs (AEDs) beyond their traditional role in treating epilepsy, particularly in managing neuropathic pain, trigeminal neuralgia, and as neuroprotective agents in conditions such as stroke and neurodegenerative diseases. These conditions often share pathophysiological mechanisms, including neuronal hyperexcitability, increased glutamatergic activity, and long-term synaptic changes, similar to epilepsy. | |||
Trigeminal neuralgia, a severe form of neuropathic pain, is linked to vascular compression and demyelination of the trigeminal nerve. AEDs are effective in managing neuropathic pain by modulating sodium and calcium channels, reducing glutamate release, and enhancing inhibitory GABAergic transmission. These mechanisms help reduce pain persistence and hyperalgesia. | |||
AEDs also show neuroprotective potential in experimental models of ischemia. Drugs like lamotrigine and remacemide have been found to reduce excitotoxicity—a major contributor to neuronal death in stroke and neurodegenerative diseases—by acting on NMDA receptors. Furthermore, AEDs may modulate pathological synaptic plasticity, offering therapeutic benefits for conditions such as Parkinson's, Huntington's, and Alzheimer's diseases. | |||
While the efficacy of AEDs in short-term ischemic events remains limited, they show promise in prolonged ischemia, suggesting broader applications in neuroprotection. Ongoing research continues to explore the role of AEDs in addressing energy stress, synaptic plasticity, and neurotransmission across various neurological disorders. | |||
Antiepileptic drugs (AEDs) have long been explored for uses beyond epilepsy, particularly in treating neuropathic pain, trigeminal neuralgia, and as neuroprotective agents in stroke and neurodegenerative diseases. The pathophysiology of these conditions often involves neuronal hyperexcitability, increased glutamatergic activity, and long-term synaptic changes, similar to epilepsy. Trigeminal neuralgia, a form of neuropathic pain, is linked to vascular compression and demyelination of the trigeminal nerve, leading to recurrent episodes of intense facial pain. | Antiepileptic drugs (AEDs) have long been explored for uses beyond epilepsy, particularly in treating neuropathic pain, trigeminal neuralgia, and as neuroprotective agents in stroke and neurodegenerative diseases. The pathophysiology of these conditions often involves neuronal hyperexcitability, increased glutamatergic activity, and long-term synaptic changes, similar to epilepsy. Trigeminal neuralgia, a form of neuropathic pain, is linked to vascular compression and demyelination of the trigeminal nerve, leading to recurrent episodes of intense facial pain. | ||