Neurologic sequelae of domoic acid intoxication due to the ingestion of contaminated mussels

Article Abstract:

In late 1987, an outbreak of gastrointestinal symptoms occurred in Canada which was traced to the ingestion of mussels from Prince Edward Island. One hundred seven cases were clearly identified, though the actual number of cases was probably larger. Four patients died and several had serious neurological complications. Mice injected with extract from the suspected mussels developed neurological symptoms and died within an hour. The syndrome was found to be a result of the neurotoxic amino acid domoic acid, which is similar in chemical structure to glutamic acid and kainic acid. To determine the precise nature of the neurological effects of domoic acid intoxication, 14 patients with neurologic symptoms were investigated with neuropsychological testing and positron-emission tomography, an imaging technique. In addition, the brain tissues from four patients who died within four months of eating the mussels were examined microscopically. All patients were confused and disoriented within the first two days of eating the mussels. The oldest patient, a man of 87, developed global intellectual impairment, and one patient returned to normal. The remaining twelve had memory disturbances which spared other cognitive functions. The impairment was generally anterograde amnesia, which means that the patients had immediate recall, and could remember past experiences, but had difficulty remembering new experiences or learning new tasks. A few of the more severely affected patients also had retrograde amnesia, their ability to recall past experiences was impaired. Histological studies revealed that the amygdala and the hippocampus were the areas of the brain most severely affected; the hippocampus is thought to play an important role in consolidating new memories. Among the living patients, positron-emission tomography revealed a decrease in metabolism in these same areas of the brain. (Consumer Summary produced by Reliance Medical Information, Inc.)

Case studies, Memory, Disorders of, Memory disorders, Hippocampus (Brain), Amnesia, Amygdala (Brain)

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An outbreak of toxic encephalopathy caused by eating mussels contaminated with domoic acid

Article Abstract:

In late 1987, an outbreak of illness occurred in Canada in which the patients developed gastrointestinal symptoms, sometimes with neurological complications. The only feature all the patients had in common was that they had eaten mussels from Prince Edward Island. A total of 107 cases were clearly identified, though the number of actual cases is almost certainly larger. Some patients experienced severe neurological complications, which included apparently irreversible damage to the mechanisms of short-term memory; these neurological complications are the subject of a companion article in the June 21, 1990 issue of The New England Journal of Medicine. Three patients died. Many organisms concentrate substances in their bodies which can pose problems for the larger creatures who eat them, and mussels are capable of concentrating a variety of environmental toxins in their bodies. However, in this case, the only poisonous compound which could be identified was domoic acid. Domoic acid is an amino acid which can excite nervous tissue, like the biochemically similar compounds glutamic acid and kainic acid. The source of the domoic acid in the mussels appears to be the microscopic creature Nitzschia pungens, which biologists refer to as a pennate phytoplanktonic diatom. The tiny creatures were eaten by the mussels, which concentrated the poisonous domoic acid in their tissues. Steps have now been taken in Canada to monitor the level of domoic acid in mussels prior to their commercial distribution. (Consumer Summary produced by Reliance Medical Information, Inc.)

Demographic aspects, Diatoms, Marine phytoplankton

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Efficacy of felbamate in childhood epileptic encephalopathy (Lennox-Gastaut syndrome)

Article Abstract:

The antiepileptic drug felbamate may be useful in treating patients with Lennox-Gastaut syndrome. This syndrome is a severe form of epilepsy characterized by the childhood onset of many types of seizures and progressive mental retardation. In a two-phase study, 73 patients with Lennox-Gastaut syndrome took their regular antiepileptic drugs for 28 days. In the second phase, 37 patients took felbamate in addition to their regular treatment and 36 took a placebo and their regular treatment. There was a 34% decrease of atonic seizures (that cause a fall) among patients taking felbamate compared with only a 9% decrease among patients taking placebo. The total frequency of seizures as reported by the parents dropped 19% among patients taking felbamate, but rose 4% among patients taking placebo. Furthermore, parents of patients taking felbamate gave higher quality-of-life ratings for their children than did parents of patients taking placebo. The side effects experienced were similar in both groups and not severe.

Drug therapy, Anticonvulsants, Encephalopathy, Epilepsy in children, Pediatric epilepsy

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