Substantia nigra lesions in mercaptopropionic acid induced status epilepticus: a light and electron microscopic study

Towfighi, Javad; Kofke, W. Andrew; O'Connell, Bridget; Housman, Cathy; Graybeal, J. M.

doi:10.1007/bf00687889

Cited by 10 publications

(4 citation statements)

References 27 publications

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“…inhibitor 3-mercaptopropionic acid (OConnell et al, 1988;Towfighi et al, 1989) in rats. The challenge facing contemporary investigators is to demonstrate what contribution, if any, systemic physiologic alterations make to the neuropathologic sequelae seen following SE.…”

Section: Systemic Effects Of Status Epilepticus S55mentioning

confidence: 99%

Systemic Effects of Generalized Convulsive Status Epilepticus

Walton¹

1993

Epilepsia

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Generalized convulsive status epilepticus (GCSE) is accompanied by a marked increase in plasma catecholamines. This produces a number of changes in general systemic physiology including hypertension, tachycardia, cardiac arrhythmias, hyperglycemia, acidosis, and hyperpyrexia. If SE is stopped quickly, these changes are self-correcting and do not produce an increased risk of neuropathology. However, if seizures continue, many of the early physiologic changes reverse, and late status epilepticus is marked by hypotension, hypoglycemia, pulmonary edema and a continued acidosis and elevation of body temperature. Prevention of serious hypoglycemia, maintenance of adequate systemic blood pressure to provide adequate cerebral perfusion, and normalizing the body temperature will minimize or prevent neuropathologic sequelae to SE of extended duration.

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Section: Systemic Effects Of Status Epilepticus S55mentioning

confidence: 99%

Systemic Effects of Generalized Convulsive Status Epilepticus

Walton¹

1993

Epilepsia

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“…Only 20.7% of patients with RSE will return to baseline clinical conditions compared to 62.6% of those with nonrefractory SE [71]. These clinical epidemiologic data are supported by preclinical [72][73][74][75][76] and clinical [77] studies. The management of SE is thus aimed to rapidly control seizure, provide an element of neuroprotection, and avoid complications.…”

Section: Refractory Status Epilepticus (Rse)mentioning

confidence: 81%

Toxicity of inhaled agents after prolonged administration

Manatpon

Kofke

2017

J Clin Monit Comput

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Inhaled anesthetics have been utilized mostly for general anesthesia in the operating room and oftentimes for sedation and for treatment of refractory status epilepticus and status asthmaticus in the intensive care unit. These contexts in the ICU setting are related to potential for prolonged administration wherein potential organ toxicity is a concern. Over the last decade, several clinical and animal studies of neurotoxicity attributable to inhaled anesthetics have been emerging, particularly in extremes of age. This review overviews potential for and potential mechanisms of neurotoxicity and systemic toxicity of prolonged inhaled anesthesia and clinical scenarios where inhaled anesthesia has been used in order to assess safety of possible prolonged use for sedation. High dose inhaled agents are associated with postoperative cognitive dysfunction (POCD) and other situations. However, thus far no strong indication of problematic neuro or organ toxicity has been demonstrated after prolonged use of low dose volatile anesthesia.

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“…It is known that MP administration induces damage in different brain areas, a condition that augments with the duration of the seizure activity [30]. Interestingly, substantia nigra, a brain area that represents an endogenous seizure suppressing target [31], shows a significant damage as consequence of MP-induced seizures [32]. It is possible that the high expression of status epilepticus after repetitive MP-induced seizures results from the significant damage of substantia nigra [33] and other brain areas.…”

Section: Discussionmentioning

confidence: 99%