Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The goal of this article is to review the idiosyncratic aspects of the epilepsy of Fyodor Dostoevsky, one of the greatest writers of all time. The onset of his seizures is controversial, with some evidence pointing to his childhood and other reports that would place the onset in his teens or his twenties. His life in prison in Siberia and then in the Russian army is reviewed. His lifestyle included many factors that exacerbated his epilepsy, especially stress and sleep deprivation. His compulsion for gambling played an important role in producing great stress in his life, as he tried to reverse his poverty in the casinos. The most idiosyncratic aspect of his epilepsy was his so-called ecstatic aura. The etiology of his seizures was probably inherited as revealed by the seizures of his father and the status epilepticus and death of his young son. This great writer died from lung hemorrhages in 1891. Discussed in this review is that he did not likely have an aura of ecstasy; only a few such possible cases can be found in the world literature. For those few cases, evidence from electrical self-stimulation studies in animals and humans, investigating "pleasure centers," can be found to involve the limbic system, especially the septal nucleus. Data from the human amygdala provide evidence why almost all auras are, in fact, unpleasant and not pleasant. A review of recent data on the risks to offspring of epileptic fathers confirms that the etiology of Dostoevsky's epilepsy was probably inherited and that he probably had an idiopathic generalized epilepsy with minor involvement of the temporal lobe. A relationship is seen between his severe obsession with gambling and his epilepsy. Finally, Fyodor Dostoevsky is an excellent example of the "temporal lobe personality."
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PMID:The idiosyncratic aspects of the epilepsy of Fyodor Dostoevsky. 1640 45

We report on the aggravation of absence seizures by lamotrigine leading to absence status epilepticus in a child. The patient is a 10-year-old girl with a history of absence seizures, learning disabilities, and hereditary neuropathy with liability to pressure palsies. Lamotrigine (up to 12 mg/kg/day) was prescribed after a brief course of valproate was associated with restlessness. Long-acting methylphenidate was also administered. The initial response to lamotrigine appeared to be excellent. The first episode of absence status epilepticus occurred during a febrile illness while lamotrigine was being gradually discontinued. Following this event, lamotrigine dose was increased to 10 mg/kg/day and methylphenidate was continued. Six weeks later, a second absence status epilepticus episode ensued without fever. Sulthiame and clonazepam were substituted for lamotrigine, whereas methylphenidate therapy was continued. A psychiatrist prescribed risperidone 1 month later owing to obsessive-compulsive behavior. Nine months later, she remained free of absence seizures. Whereas the first absence status epilepticus event could have been triggered by fever, the second episode occurred while the daily lamotrigine dose was being increased. Moreover, the patient is seizure free following lamotrigine discontinuation. Hence, it is quite possible that lamotrigine caused seizure aggravation and absence status epilepticus in this child.
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PMID:Recurrent absence status epilepticus (spike-and-wave stupor) associated with lamotrigine therapy. 1697 Aug 92