Cases reported "Status Epilepticus"

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1/2. status epilepticus after a massive intravenous N-acetylcysteine overdose leading to intracranial hypertension and death.

    Cases of N-acetylcysteine overdose have been reported before. In some cases, these overdoses have led to death if an anaphylactoid reaction was present. A healthy 30-month-old girl allegedly ingested acetaminophen at 418 mg/kg. Because the emergency physician feared the time of ingestion might not be accurate, he decided to start the 20.5-hour intravenous N-acetylcysteine protocol 8 hours after ingestion. He mistakenly prescribed the maximum milliliter-per-kilogram volume of the dextrose 5% diluent for the milliliter-per-kilogram volume of N-acetylcysteine 20% to be administered. Five hours after the error was detected (19.5 hours postingestion), the patient started developing myoclonus on the left side of her body, with left eye deviation. This condition persisted intermittently for 3 hours despite treatment with diazepam, lorazepam, and phenytoin. A first computed tomographic scan result was normal. A few hours later, she sustained shorter recurrences of the myoclonus. At 30 hours after ingestion, she started to have irregular breathing and became unresponsive to pain. A repeated computed tomographic scan showed diffuse cerebral edema. A postmortem examination showed the presence of acute anoxic encephalopathy with marked cerebral edema and the beginning of uncal herniation that confirmed the clinical diagnosis of intracranial hypertension and brain death. A cumulative intravenous dose of 2,450 mg/kg of N -acetylcysteine was associated with status epilepticus, intracranial hypertension, and death in a child.
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2/2. Combined partial temporal and secondary generalized status epilepticus. Report of a case with fear bouts followed by prolonged confusion.

    A right-handed 32-year-old woman had recurrent combined partial temporal and secondary generalized epileptic states almost constantly related to menstruations. During such more or less prolonged episodes sometimes the patient presented right adversive attacks with short postictal dysphasia. The catamenial status epilepticus observed in this cas was manifested in two clear-cut behavioral phases. The first phase was characterized by frequently recurrent left temporal epileptiform discharges without tendency to diffusion, progressively more prolonged and pseudorhythmic associated with a signalized feeling of intense fear without apparent impairment of consciousness or speech disturbances. The electroclinical features of the first phase suggest a depth origin of the paroxysms, probably due to a primary epileptogenic focus in the left amygdaloid-hippocampal complex. In the second phase the left temporal focal semirhythmic discharges associated with fear bouts became more frequent and prolonged and began to be followed by long-lasting generalized discharges resulting in a trance-like state with severe impairment of consciousness. The diffuse paroxysmal activity regularly preceded by the left temporal focal discharges was interpreted as a form of secondary bilateral synchrony constantly triggered from a focal pacemaker represented by the primary epileptogenic focus. During the very short transient periods of sudden cessation of the epileptiform activity the patient returned immediately to an apparent normal mental state. Good correlation could be established between different seizure patterns and predominant clinical signs. Intravenous diazepam rapidly decreased and then completely stopped the catamenial status epilepticus. Some problems related to the classification of these rare epileptic events are discussed.
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keywords = fear
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