Difference between revisions of "Kindled seizures elevate blood pressure and induce cardiac arrhythmias"

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''Goodman JH, Homan RW, and Crawford IL(1990) Kindled seizures elevate blood pressure and induce cardiac arrhythmias. Epilepsia 31:5 489–95.''
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'''[http://onlinelibrary.wiley.com.ezp.welch.jhmi.edu/doi/10.1111/j.1528-1157.1990.tb06096.x/epdf Link to Article]'''
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'''Abstract:''' The effect of kindled seizures on the cardiovascular system was examined in amygdaloid kindled rats. The most prominent cardiovascular response during a generalized kindled seizure was an abrupt 50% increase in mean arterial pressure (MAP) lasting 20-30 s after initiation of the seizure. Superimposed on this change in blood pressure (BP) was a profound bradycardia characterized by a rate about half that recorded before stimulation. Changes in heart rate (HR) and BP observed during amygdaloid kindled seizures were similar to those observed during secondary spontaneous seizures. These effects apparently are independent of the kindling stimulus because stimulus-induced cardiovascular changes were not present at the beginning of the kindling process. These results suggest that the kindling seizure model is useful to study the underlying mechanisms of seizure-induced cardiac arrhythmias and possibly the clinical phenomenon of sudden unexplained death in epileptic patients.
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Goodman JH, Homan RW, and Crawford IL(1990) Kindled seizures elevate blood pressure and induce cardiac arrhythmias. Epilepsia 31:5 489–95.
  
'''Keywords:''' Convulsions, Neurologic models, Kindling, Amygdala, Blood  pressure, Hypertension, Arrhythmia
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http://onlinelibrary.wiley.com.ezp.welch.jhmi.edu/doi/10.1111/j.1528-1157.1990.tb06096.x/epdf
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The effect of kindled seizures on the cardiovascular system was examined in amygdaloid kindled rats. The most prominent cardiovascular response during a generalized kindled seizure was an abrupt 50% increase in mean arterial pressure (MAP) lasting 20-30 s after initiation of the seizure. Superimposed on this change in blood pressure (BP) was a profound bradycardia characterized by a rate about half that recorded before stimulation. Changes in heart rate (HR) and BP observed during amygdaloid kindled seizures were similar to those observed during secondary spontaneous seizures. These effects apparently are independent of the kindling stimulus because stimulus-induced cardiovascular changes were not present at the beginning of the kindling process. These results suggest that the kindling seizure model is useful to study the underlying mechanisms of seizure-induced cardiac arrhythmias and possibly the clinical phenomenon of sudden unexplained death in epileptic patients.
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Convulsions, Neurologic models, Kindling, Amygdala, Blood  pressure, Hypertension, Arrhythmia
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*Animal study in rat of effect of kindling on autonomic function finding that amygdalar seizures increased blood pressure and caused bradycardia with beat to beat fluctuations. Both changes occurred within 5-10 s of seizure onset and persisted for up to 30 s. Large fluctuations in blood pressure were also seen, like consistent with dropped ventricular beats observed on EKG. This model in rats has similar characteristics to studies in sheep with increase vascular pressure following seizure induction. See [https://sudepwiki.pathology.jhmi.edu/index.php/Epileptic_sudden_death:_Animal_models  R.P. Simon] and [https://sudepwiki.pathology.jhmi.edu/index.php/Central_apnea_and_acute_cardiac_ischemia_in_a_sheep_model_of_epileptic_sudden_death Johnston et al].
 
*Animal study in rat of effect of kindling on autonomic function finding that amygdalar seizures increased blood pressure and caused bradycardia with beat to beat fluctuations. Both changes occurred within 5-10 s of seizure onset and persisted for up to 30 s. Large fluctuations in blood pressure were also seen, like consistent with dropped ventricular beats observed on EKG. This model in rats has similar characteristics to studies in sheep with increase vascular pressure following seizure induction. See [https://sudepwiki.pathology.jhmi.edu/index.php/Epileptic_sudden_death:_Animal_models  R.P. Simon] and [https://sudepwiki.pathology.jhmi.edu/index.php/Central_apnea_and_acute_cardiac_ischemia_in_a_sheep_model_of_epileptic_sudden_death Johnston et al].
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Latest revision as of 13:39, 17 June 2019


Goodman JH, Homan RW, and Crawford IL(1990) Kindled seizures elevate blood pressure and induce cardiac arrhythmias. Epilepsia 31:5 489–95.

Link to Article

Abstract: The effect of kindled seizures on the cardiovascular system was examined in amygdaloid kindled rats. The most prominent cardiovascular response during a generalized kindled seizure was an abrupt 50% increase in mean arterial pressure (MAP) lasting 20-30 s after initiation of the seizure. Superimposed on this change in blood pressure (BP) was a profound bradycardia characterized by a rate about half that recorded before stimulation. Changes in heart rate (HR) and BP observed during amygdaloid kindled seizures were similar to those observed during secondary spontaneous seizures. These effects apparently are independent of the kindling stimulus because stimulus-induced cardiovascular changes were not present at the beginning of the kindling process. These results suggest that the kindling seizure model is useful to study the underlying mechanisms of seizure-induced cardiac arrhythmias and possibly the clinical phenomenon of sudden unexplained death in epileptic patients.

Keywords: Convulsions, Neurologic models, Kindling, Amygdala, Blood pressure, Hypertension, Arrhythmia

Context

  • Animal study in rat of effect of kindling on autonomic function finding that amygdalar seizures increased blood pressure and caused bradycardia with beat to beat fluctuations. Both changes occurred within 5-10 s of seizure onset and persisted for up to 30 s. Large fluctuations in blood pressure were also seen, like consistent with dropped ventricular beats observed on EKG. This model in rats has similar characteristics to studies in sheep with increase vascular pressure following seizure induction. See R.P. Simon and Johnston et al.

Comments

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