Generalized Seizures Induced by an Epileptic Focus in the Mesencephalic Reticular Formation: Impact on the Understanding of the Generalizing Mechanism

Hashizume, Kazuyoshi; Tanaka, Tatsuya; Fujita, Tsutomu; Tanaka, Shigeya

doi:10.1159/000056474

Cited by 7 publications

(4 citation statements)

References 15 publications

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“…Among the motor reactivities involved in the deep SC/ DpMe are defensive reactions (Dean et al, 1988;Redgrave et al, 1996;Niemi-Junkola et al, 1997;Brandao et al, 2003), startle response modulation (Meloni and Davis, 2000), convulsions (Garcia-Rill et al, 1985;Hashizume et al, 2000;Ishimoto et al, 2000), and locomotor activity (Sinnamon and Stopford, 1987;Sinnamon, 1993;Jordan, 1998). The specificity of NBQX infused into this area on fear-potentiated startle compared with baseline startle suggests that amygdala terminals may release glutamate into the deep SC/DpMe when activated by a CS.…”

Section: Discussionmentioning

confidence: 99%

Fear-Potentiated Startle in Rats Is Mediated by Neurons in the Deep Layers of the Superior Colliculus/Deep Mesencephalic Nucleus of the Rostral Midbrain through the Glutamate Non-NMDA Receptors

Zhao¹,

Davis²

2004

J. Neurosci.

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The amygdala sends heavy and broad projections to the rostral midbrain including the periaqueductal gray (PAG), the deep layers of the superior colliculus/deep mesencephalic nucleus (deep SC/DpMe), and the lateral mesencephalic reticular formation (MRF) that in turn project to the nucleus reticularis pontis caudalis (PnC), an obligatory relay in the primary acoustic startle circuit. Chemical lesions or inactivation of these areas blocked fear-potentiated startle, suggesting that these areas serve as a relay between the amygdala and the PnC. In the present study, we tried to determine more precisely which of these sites were critical for fear-potentiated startle and the role of glutamate receptors in this site in mediating fear-potentiated startle. Local infusion of the non-NMDA receptor antagonist 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(F)-quinoxaline (NBQX) dose-dependently blocked fear-potentiated startle when infused into the deep SC/ DpMe before testing but had no effect on baseline startle amplitude. NBQX did not block fear-potentiated startle when infused before training. The same dose of NBQX infused into the dorsal/lateral PAG, the lateral MRF, or the superficial layers of the SC did not affect fear-potentiated startle. However, NBQX tended to reduce contextual freezing when infused into the dorsal/lateral PAG. These findings suggest that the deep SC/DpMe is the site that serves as a critical output relay between the amygdala and the PnC in mediating fearpotentiated startle and that glutamatergic transmission is required for this action.

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Section: Discussionmentioning

confidence: 99%

Fear-Potentiated Startle in Rats Is Mediated by Neurons in the Deep Layers of the Superior Colliculus/Deep Mesencephalic Nucleus of the Rostral Midbrain through the Glutamate Non-NMDA Receptors

Zhao¹,

Davis²

2004

J. Neurosci.

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“…Nonetheless, convulsive seizures can be induced by electrical or chemical stimulation of the brainstem tegmentum. 41 - 43 The observation that convulsive seizures induced by stimulation of the mesencephalic reticular formation attenuate with pontine tegmentum lesions but are barely affected by precollicular transection suggest that the mesencephalic reticular formation plays a crucial role in the generation of convulsive seizures, perhaps by directly activating the descending reticular formation. 44 We also pointed out that Zhang et al recorded epileptic discharges from the brainstem, but not from the hippocampi or neocortex, during MCAO-induced convulsive seizures.…”

Section: Discussionmentioning

confidence: 99%

Stroke-Onset Seizures During Midbrain Infarction in a Patient With Top of the Basilar Syndrome

Mader

Losada

Baity

et al. 2020

Journal of Investigative Medicine High Impact Case Reports

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Risk factors for early-onset seizures in acute ischemic stroke include anterior circulation stroke, infarction of the cerebral cortex, large infarct size, and ischemic-to-hemorrhagic transformation. We define stroke-onset seizures as seizures occurring within 2 hours of stroke onset. A 64-year-old woman presented with top of the basilar artery syndrome—thalamic infarction occurred first and midbrain infarction 12 days later. She manifested stroke-onset seizures during midbrain infarction, which was heralded by stupor. Within 2 hours of the onset of stupor, she had a clonic seizure of the lower extremities, electroencephalography (EEG) revealed nonconvulsive status epilepticus, and an episode of convulsive movements of all extremities was recorded on video and on EEG. Continuous EEG recording showed epileptiform discharges that would appear, disappear, and reappear over a 3-week period. It took 3 weeks and 4 antiepileptic drugs to fully suppress cortical hyperexcitability, perhaps because injury to some midbrain structures resulted in global lowering of the seizure threshold. The most important risk factor for stroke-onset seizures appears to be posterior circulation stroke, particularly brainstem infarction. The difference in risk profile between stroke-onset seizures and other forms of early-onset seizures suggest that their pathophysiology is not exactly the same. Focusing some of the research spotlight on stroke-onset seizures can help us better understand their unique clinical, electrographic, radiologic, and pathophysiologic features.

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“…Penfield suggested this system functioned as a causative center of seizures [8]. In addition, animal experimental studies have suggested that electrolytic lessoning of reticular formation (RF) also can cause seizure [9]. So the infarct lesions of Bithalamic, which are part of the centrencephalic system and the reticular formation, can induce seizure as well as unconsciousness.…”

Section: Discussionmentioning

confidence: 99%

Bilateral Paramedian Thalamic Infarction Initially Presenting as a Convulsive Seizure

Wang

Jiang

et al. 2013

Case Reports in Neurological Medicine

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Bithalamic infarctions initially presenting as a convulsive seizure are rarely reported and, to our best knowledge, have never been reported in China. Here, we present a patient with convulsive seizure at the onset of bilateral paramedian thalamic infarction. The diffusion-weighted imaging revealed that the infarct area is supplied by Percheron artery. Associated with the relationship between seizure and centrencephalic system and reticular formation as previously reported, we suggest that seizure could be the onset symptom of paramedian thalamic infarction. Physicians should recognize this condition, because both seizure control and early ischemic stroke management are required.

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Generalized Seizures Induced by an Epileptic Focus in the Mesencephalic Reticular Formation: Impact on the Understanding of the Generalizing Mechanism

Cited by 7 publications

References 15 publications

Fear-Potentiated Startle in Rats Is Mediated by Neurons in the Deep Layers of the Superior Colliculus/Deep Mesencephalic Nucleus of the Rostral Midbrain through the Glutamate Non-NMDA Receptors

Fear-Potentiated Startle in Rats Is Mediated by Neurons in the Deep Layers of the Superior Colliculus/Deep Mesencephalic Nucleus of the Rostral Midbrain through the Glutamate Non-NMDA Receptors

Stroke-Onset Seizures During Midbrain Infarction in a Patient With Top of the Basilar Syndrome

Bilateral Paramedian Thalamic Infarction Initially Presenting as a Convulsive Seizure

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