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Wandinger et al. (p. 178) studied antibodies to Epstein–Barr virus (EBV), cytomegalovirus, and herpes simplex virus in 108 patients with MS and healthy controls. They found evidence for EBV reactivation in the majority of MS patients with exacerbations.
In the accompanying Editorial, Hunter and Hafler (p. 164) discuss the various common pathogens that could trigger an autoimmune cause of MS: EBV, Chlamydia pneumoniae, and human herpesvirus 6, and point out that it remains unclear whether EBV "reactivation" is the cause or effect of MS exacerbations. Koch’s postulates have not been satisfied for any pathogen, although each could exacerbate MS through one or more of several mechanisms: molecular mimicry, inflammatory cytokine release, adjuvant action, or as a Trojan horse (with a pathogen entering the CNS via inflammatory cells).
MRI outcome measures in MS: T1 hypointense lesions
Simon et al. (p. 185) studied T1 hypointense lesion volume in patients with relapsing MS (80 on placebo and 80 on interferon ß–1a [IFNß-1a]). In both groups disability correlated with lesion volume. Lesion volume increased more in the placebo (29.2%) than in the IFNß-1a (11.8%) treated patients.
What is the prevalence of AD?
Hy and Keller (p. 198) reviewed data from 21 European and North American studies. A single study (East Boston) reported a US prevalence in 1996 of 4.0 million. This study is an outlier: the combined analysis of the other 20 studies suggests a figure of 1.7 million. They point to the use of a different case definition as the basis for the higher estimate in the outlier study.
In the accompanying Editorial, Albert and Drachman (p. 166) consider the criteria for definitive AD and how they affect prevalence figures, as well as the importance of accurate prevalence figures.
Seizures in paroxysmal kinesigenic dyskinesia (PKD)
Swoboda et al. (p. 224) studied 11 families (44 affected subjects) with PKD. Infantile convulsions were common (9 of 11 families). The disorder was linked to chromosome 16.
The accompanying Editorial by Berkovic (p. 169) reviews the evolution in thinking about PKD—initially considered a seizure disorder, then a nonepileptiform movement disorder, and now both. Noting that other inherited seizure and paroxysmal movement disorders are channelopathies, Berkovic postulates that PKD/convulsions results from channel dysfunction in different areas of the brain.
Hippocampal atrophy after surgery: Progressive memory loss
Do postoperative changes add to preoperative state and surgical factors to influence memory loss? Baxendale et al. (p. 243) performed volumetric MRI and neuropsychological assessments preoperatively and 3 months postoperatively in 17 adults with temporal lobe epilepsy. Hippocampus shrinkage was noted in 16 of 17 patients and the extent of shrinkage correlated with postoperative memory loss.
Cell death genes in epileptic surgery brain
Henshall et al. (p. 250) studied genes of the bcl-2 and caspase families in temporal lobe tissue taken from 19 patients undergoing epilepsy surgery. Both glia and neurons showed evidence for activation of genes that influence apoptosis (cell death). Some specimens showed DNA fragmentation evidence of apoptosis. The authors speculate that cell death may be ongoing in epilepsy and may be a target for therapy.
Seizures after subarachnoid hemorrhage (SAH)
Rhoney et al. (p. 258) reviewed 95 patients with aneurysmal SAH for seizures and factors contributing to seizures as well as antiepileptic drug (AED) use. Definite or possible seizures occurred prehospital in 25% and in hospital in 4%. Posthospital seizures occurred in 8%. Only CT evidence of cisternal blood was a predictor of seizures. The authors emphasize that issues of AED treatment merit prospective study.
Stroke
Kamran et al. (p. 265) studied MRI of 304 patients with stroke. They focused on fluid-attenuated inversion recovery MRI and noted that a hyperintense vessel was present in 10% of patients and that subsequent angiography and other techniques as well as follow-up MRI suggest that hyperintense vessels indicate impaired blood flow and early ischemia.
Lamy et al. (p. 269) obtained 5-year follow-up on 441 women who had a stroke during a pregnancy. Recurrent stroke was uncommon during subsequent pregnancy and pregnancy outcome was normal.
Shorthand publications of Gowers
Tyler et al. (p. 289) challenge the conclusion of MacDonald Critchley that Gowers’ articles in Pitman shorthand are "buried in obscurity and locked up in code" by translating his nearly 100 papers. The authors survey the work and make accessible these papers by one of neurology’s greatest figures.
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