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Summary: Purpose:The recommended rate of administration of valproic acid injection is 20 mg/min. Drug delivery at this rate may be inadequate for expeditious control of seizures. The safety of rapid infusion of valproic acid has not been established, and this study was designed to explore the effects of rapid infusion in patients with acute seizures.Methods: Twenty patients with acute repetitive seizures received 20 mgkg loading doses of valproic acid. Infusion rates ranged from 33.3 to 555 mg/min (median, 200 rng/min). Sixteen patients had received previous or concomitant antiepileptic drugs, with inadequate seizure control. Heart rate, blood pressure, and respiratory rate were measured before infusion and at frequent intervals for 1 hour after infusion. Patients were also observed for changes in level of alertness and signs of local irritation. Results:No patient exhibited a decline in level of consciousness or respiratory function. Two patients with significant contributing factors exhibited declines in blood pressure requiring vasopressors. No significant local irritation was reported. AIthough efficacy was not a measured end point, seizures were abolished in all patients.Conclusions: Infusion of valproic acid at rates between 33 and 555 rng/min is well tolerated. No serious adverse effects attributable to the rapid infusion of valproic acid were encountered, although valproic acid, along with other factors, may have contributed to the hypotension in two patients. Intravenous valproic acid is an option for the control of acute seizures.
Summary: Purpose:The recommended rate of administration of valproic acid injection is 20 mg/min. Drug delivery at this rate may be inadequate for expeditious control of seizures. The safety of rapid infusion of valproic acid has not been established, and this study was designed to explore the effects of rapid infusion in patients with acute seizures.Methods: Twenty patients with acute repetitive seizures received 20 mgkg loading doses of valproic acid. Infusion rates ranged from 33.3 to 555 mg/min (median, 200 rng/min). Sixteen patients had received previous or concomitant antiepileptic drugs, with inadequate seizure control. Heart rate, blood pressure, and respiratory rate were measured before infusion and at frequent intervals for 1 hour after infusion. Patients were also observed for changes in level of alertness and signs of local irritation. Results:No patient exhibited a decline in level of consciousness or respiratory function. Two patients with significant contributing factors exhibited declines in blood pressure requiring vasopressors. No significant local irritation was reported. AIthough efficacy was not a measured end point, seizures were abolished in all patients.Conclusions: Infusion of valproic acid at rates between 33 and 555 rng/min is well tolerated. No serious adverse effects attributable to the rapid infusion of valproic acid were encountered, although valproic acid, along with other factors, may have contributed to the hypotension in two patients. Intravenous valproic acid is an option for the control of acute seizures.
Acute posthypoxic myoclonus portends a poor prognosis. Another form of posthypoxic myoclonus, Lance-Adams syndrome, is associated with a better outcome. Differentiating these two entities is important in prognostication and guiding further medical intervention. This can be difficult in the acute setting after hypoxic brain injury but the use of neurophysiologic studies may be helpful. In this article, we present a case of a patient who presented after pulseless electrical activity arrest, underwent targeted temperature management and subsequently developed Lance-Adams syndrome. The neurologic and electroencephalographic findings in Lance-Adams syndrome are discussed with an updated review.
Myoclonus is a movement disorder characterized by involuntary, sudden, brief muscle jerks caused by muscular contraction (positive myoclonus) or inhibition (negative myoclonus).1,2 Myoclonus is generally a medical sign and not a diagnosis. It can occur in multiple disorders. A short differential diagnosis list includes anoxic brain injury, multiple sclerosis, Parkinson's disease, subacute sclerosing panencephalitis, and Creutzfeldt-Jakob disease. One way to classify the etiologies is through review of the clinical presentation and comorbid conditions. This article presents a review of anoxic brain injury related myoclonus. Post-anoxic myoclonus (PAM) can develop in either acute or chronic phase. Acute PAM occurs within hours after hypoxic event; chronic PAM (Lance-Adams syndrome) develops in survivors several days to weeks after the episodes of brain hypoxia.
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