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Biology Articles » Neurobiology » Update on the Neurobiology of Alcohol Withdrawal Seizures » Brain Substrates for Alcohol Withdrawal Seizures

Brain Substrates for Alcohol Withdrawal Seizures
- Update on the Neurobiology of Alcohol Withdrawal Seizures

Audiogenic seizures are the best-studied type of alcohol withdrawal seizures. These seizures are mediated largely in the brainstem, although the hippocampus may be invaded after seizure initiation (10). In rodents, the cortical EEG shows no sign of paroxysmal activity (1011). Similarly, in humans, epileptiform activity is rarely observed in the EEG between episodes of alcohol withdrawal–related tonic–clonic seizures (1213). Thus, alcohol withdrawal seizures are unlikely to be triggered in the neocortex. Indeed, electrophysiological studies have demonstrated a critical role for the inferior colliculus (IC) in the initiation of audiogenic seizures in rodents. Acute alcohol intoxication suppresses spontaneously and acoustically evoked neuronal firing in the IC central nucleus (14), whereas at the transition to seizure, sustained increases in firing persist during wild running, the initial phase of the seizure (15). The IC external cortex is believed to amplify and propagate neuronal activity originating in the IC central nucleus. Neurons within the deep layers of the superior colliculus (16) and the periaqueductal gray (17) also may play a role in the initiation of audiogenic seizures. It is hypothesized that seizure activity propagates from the IC to deep layers of the superior colliculus (a major output of the IC) to trigger the wild running phase of the audiogenic seizure. The deep layers of the superior colliculus send projections directly to the spinal cord via the pontine reticular formation and the periaqueductal gray. The periaqueductal gray is thought to trigger clonic seizures, whereas the pontine reticular formation is implicated in the generation of the tonic phase of audiogenic seizures (18). Some evidence suggests that the IC plays a role in alcohol withdrawal seizures in humans, as it does in rodents. Thus, humans with alcohol withdrawal seizures exhibit abnormalities in auditory-evoked potentials that are not observed in other settings, including increased latency to wave V (1920), whose major source is the IC (21).


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