1958
DOI: 10.1152/jn.1958.21.5.430
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Electroclinical Features of Convulsions Induced by Stimulation of Brain Stem

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Cited by 142 publications
(66 citation statements)
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“…Whereas generalized clonic seizures require the integrity of forebrain structures for their expression (Browning and Nelson, 1986;Magistris et al, 1988;Browning et al, 1993), brainstem circuitry is both necessary and sufficient for the expression of running/bouncing and tonic motor manifestations (Kreindler et al, 1958;Browning and Nelson, 1986). Thus, the progression of flurothyl-induced seizure behaviors seen after exposure to our paradigm appears to be the result of an initial activation of the forebrain system followed rapidly by activation of the brainstem seizure system.…”
Section: Changes In Seizure Behaviormentioning
confidence: 92%
See 1 more Smart Citation
“…Whereas generalized clonic seizures require the integrity of forebrain structures for their expression (Browning and Nelson, 1986;Magistris et al, 1988;Browning et al, 1993), brainstem circuitry is both necessary and sufficient for the expression of running/bouncing and tonic motor manifestations (Kreindler et al, 1958;Browning and Nelson, 1986). Thus, the progression of flurothyl-induced seizure behaviors seen after exposure to our paradigm appears to be the result of an initial activation of the forebrain system followed rapidly by activation of the brainstem seizure system.…”
Section: Changes In Seizure Behaviormentioning
confidence: 92%
“…Because running / bouncing seizures and generalized tonic seizure manifestations can be elicited in the absence of forebrain connections (Kreindler et al, 1958;Browning and Nelson, 1986), these seizure behaviors have been collectively referred to as "brainstem seizures." Therefore, generalized seizures featuring any of the motor behaviors defined above as grades 3-7 are designated "brainstem seizures."…”
Section: Behavioral Rating Of Flurothyl-induced Seizuresmentioning
confidence: 99%
“…Although the functional anatomy of this convulsive process is yet unclear, substantial evidence suggests that subcortical brain regions, through their widespread cortical connections, play a major role in the propagation and perhaps initiation of these attacks. Early studies demonstrated numerous facilitatory and inhibitory influences on seizure activity in both the brain stem and diencephalon (Morison and Dempsey, 1942;Jasper and Droogleever-Fortuyn, 1946;Hunter and Jasper, 1949;Ingvar, 1955a, b;Ralston and Ajmone-Marsan, 1956;Kriendler et al, 1958;Andy and Mukawa, 1959;Bergman et al, 1963;Guerrero-Figueroa et al, 1963;Weir, 1964) and suggested important roles for diffusely organized regions such as the reticular formations of the pons, mesencephalon, and thalamus. Specific areas of the subcortex have also been associated with seizure mechanisms, including the hypothalamus (Murphy and Gellhorn, 1945;Jasper and Droogleever-Fortuyn, 1946;Green and Morin, 1953;Gellhorn et al, 1959) fields of Fore1 (Jinnai, 1966;Jinnai et al, 1969;Jinnai and Mukawa, 1970), substantia nigra (Iadarola and Gale, 1982;Garant and Gale, 1983;Gonzalez and Hettinger, 1984;McNamara et al, 1983McNamara et al, , 1984, and several thalamic nuclei (Mullen et al, 1967;Jinnai et al, 1969;Feeney and Gullotta, 1972;Kusske et al, 1972;Van Straaten, 1975;Quesney et al, 1977).…”
mentioning
confidence: 99%
“…As we previously reported (3), TE seizure induced by maximal electroshock was closely related with potent muscle contraction, and neither the duration nor magnitude of EMG seizures induced by maximal electroshock was inhibited by ethosuximide, even at a dose of 1000 mg/ kg. Kreindler et al (17) and Bergmann et al (18) demonstrated that the mesencephalic reticular formation is responsible for the occurrence of TE seizure in rats and rabbits. As shown in the present data, ethosuximide caused no inhibition of TE seizure because the action site of ethosuximide was the thalamus and cortex as reported by Pellegrini et al (19).…”
Section: Discussionmentioning
confidence: 99%