Paroxysmal arousal in epilepsy associated with cingulate hyperperfusion

Vetrugno, Roberto; Mascalchi, Mario; Vella, Alessandra; Nave, Riccardo Della; Provini, Federica; Plazzi, Giuseppe; Volterrani, Duccio; Bertelli, Paolo; Vattimo, A; Lugaresi, E; Montagna, Pasquale

doi:10.1212/01.wnl.0000149530.07703.fa

Cited by 32 publications

(16 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Additional [18F]-fluoro-deoxyglucose PET detected hypometabolism in the area of the orbitofrontal cortex in these patients. The unexpected nAChR density increase in the mesencephalon was considered relevant to the pathophysiology of ADNFLE because of the role of the brainstem ascending cholinergic systems in arousal [43], while the involvement of the frontal cortex was in line with the very concept of frontal lobe epilepsy and with several previous functional imaging studies implicating activation of the mesial cingulate regions during NPD [52] and PA attacks [61]. The involvement of the mesencephalon in ADNFLE demonstrated by PET imaging is also remarkably in agreement with the histological distribution of the Ach channel subunits in the monkey [17].…”

Section: Somnologie 1 2008mentioning

confidence: 54%

Nocturnal epileptic seizures versus the arousal parasomnias

et al. 2008

View full text Add to dashboard Cite

Section: Somnologie 1 2008mentioning

confidence: 54%

Nocturnal epileptic seizures versus the arousal parasomnias

et al. 2008

View full text Add to dashboard Cite

“…12 Ictal single-photon emissioncomputed tomography in patients with nocturnal frontal epilepsy has demonstrated increased blood flow in the cingulate gyrus and cerebellar cortex, suggesting a direct connection between these regions. 13 Disruption of these connections may also have partially contributed to the patient's astasia.…”

Section: Discussionmentioning

confidence: 99%

Novel Representation of Astasia Associated With Posterior Cingulate Infarction

Kataoka

Sugie

Kohara

et al. 2006

Stroke

View full text Add to dashboard Cite

Background and Purpose-The representation elicited in the cingulate motor area has been demonstrated in animals, but remains unclear in humans. In particular, the representation and pathogenic mechanisms of the posterior cingulate cortex are poorly understood, especially in humans. We describe a case of posterior cingulate infarction associated with contralateral astasia. Case Description-A 67-year-old right-handed man with a 10-year history of hypertension suddenly presented with right-sided pulsion on attempting to stand or sit. On the following day, he could not maintain a sitting position. The patient immediately fell to the floor because of instability, characterized by marked right-sided pulsion despite no muscle weakness, sensorial deficits, or cerebellar ataxia. Magnetic resolution imaging of the brain showed abnormal intensity in the posterior parts of the cingulate, with no other clinically significant lesions. Conclusions-Because the cingulate motor area is connected to the vestibulocerebellar system through the thalamic nuclei, disruption of this connection by posterior cingulate infarction may result in astasia. (Stroke. 2006;37:e3-e5.)

show abstract

“…These clinical signs—which are the hallmark of seizures affecting area 24—have been described by Bancaud and Talairach (1992) as part of the epileptic syndromes of frontal origin. ACC hyperactivity has also been reported in patients with nocturnal frontal lobe epilepsy, a disorder characterized by paroxysmal arousals with motor and autonomic manifestations along with psychiatric disorders (Vetrugno et al., 2005).…”

mentioning

confidence: 99%

Epileptiform synchronization in the cingulate cortex

Panuccio

Curia

Colosimo³

et al. 2009

Epilepsia

View full text Add to dashboard Cite

SUMMARYPurpose: The anterior cingulate cortex (ACC)-which plays a role in pain, emotions and behaviorcan generate epileptic seizures. To date, little is known on the neuronal mechanisms leading to epileptiform synchronization in this structure. Therefore, we investigated the role of excitatory and inhibitory synaptic transmission in epileptiform activity in this cortical area. In addition, since the ACC presents with a high density of opioid receptors, we studied the effect of opioid agonism on epileptiform synchronization in this brain region. Methods: We used field and intracellular recordings in conjunction with pharmacological manipulations to characterize the epileptiform activity generated by the rat ACC in a brain slice preparation. Results: Bath-application of the convulsant 4-aminopyridine (4AP, 50 lM) induced both brief and prolonged periods of epileptiform synchronization resembling interictal-and ictal-like discharges, respectively. Interictal events could occur more frequently before the onset of ictal activity that was contributed by N-methyl-D-aspartate (NMDA) receptors. Mu-opioid receptor activation abolished 4AP-induced ictal events and markedly reduced the occurrence of the pharmacologically isolated GABAergic synchronous potentials. Ictal discharges were replaced by interictal events during GABAergic antagonism; this GABA-independent activity was influenced by subsequent mu-opioid agonist application. Conclusions: Our results indicate that both glutamatergic and GABAergic signaling contribute to epileptiform synchronization leading to the generation of electrographic ictal events in the ACC. In addition, mu-opioid receptors appear to modulate both excitatory and inhibitory mechanisms, thus influencing epileptiform synchronization in the ACC.

show abstract

Paroxysmal arousal in epilepsy associated with cingulate hyperperfusion

Cited by 32 publications

References 8 publications

Nocturnal epileptic seizures versus the arousal parasomnias

Nocturnal epileptic seizures versus the arousal parasomnias

Novel Representation of Astasia Associated With Posterior Cingulate Infarction

Epileptiform synchronization in the cingulate cortex

Contact Info

Product

Resources

About