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May Highlights

This issue contains two articles and an accompanying editorial dealing with biologic markers in AD. Hulstaert et al. (p. 1555) provide evidence that the combined measure of CSF beta-amyloid 1-42 and tau may be useful in discriminating AD from normal aging and specific neurologic disorders. Fox et al. (p. 1687), in their Brief Communication, describe the results of their volumetric MRI assessments involving patients with AD and normal controls. They determined that the rate of global cerebral volume loss was highly correlated with rate of change in Mini-Mental State Examination scores. In her accompanying editorial, Black (p. 1533) discusses the work of these authors in the context of a broader overview of biologic markers in AD. She provides an update on marker development to date, describes the attributes ideal diagnostic and progression markers should possess, and predicts how and when the optimum techniques will be useful in diagnosis and monitoring of responses to AD treatment.

Epilepsy

Two articles in this issue discuss the use and toxicity of vigabatrin in children. Cossette et al. (p. 1691) performed a retrospective study in which they compared vigabatrin with ACTH for the treatment of infantile spasms. They conclude that vigabatrin is as effective and better tolerated. Vanhatalo and Pääkkönen (p. 1713) report two cases of children who developed visual field constriction that appeared to be attributable to vigabatrin. Sankar and Wasterlain (p. 1537), in their accompanying editorial, discuss both articles in the context of the challenging issue of risks versus benefits of pharmacotherapies for epilepsy.Four articles and an accompanying editorial by Meador and Loring (p. 1535) are devoted to new data and thoughts about the intracarotid amobarbital, or Wada, test. Using SPECT imaging and bilateral intrahippocampal depth electrodes to monitor the electrophysiologic effects of amobarbital, Urbach et al. (p. 1596) determined that the drug can affect posterior hippocampal function during the test without direct perfusion of these brain areas. Rihs et al. (p. 1591) prospectively performed functional transcranial Doppler sonography (fTCD) and Wada tests in 14 patients with various diseases. They determined that fTCD seems to be able to assess hemispheric dominance and suggest that it might become an alternative noninvasive or complementary tool to the Wada test. Glosser et al. (p. 1583) evaluated level of arousal and memory in epilepsy patients undergoing intracarotid amobarbital testing. They found a hemispheric asymmetry in arousal and an impact of arousal on memory, which they suggest should be considered when using these test results to select patients for temporal lobectomy. Grote et al. (p. 1577) reviewed the records of patients who received two intracarotid amobarbital injections and found that depending on the laterality and order of injections, failure to consider the interaction between testing could lead to erroneous predictions about postsurgical memory loss.

Stroke

Anzola et al. (p. 1622) performed TCD on consecutively referred migraine patients with and without aura. Age-matched controls were similarly evaluated. The authors found that patency of the foramen ovale is associated with migraine with aura. The authors suggest that the increased risk of stroke in patients who experience migraines with aura may be explained by an increased propensity to paradoxical cerebral embolism.

HIV

Blumenthal et al. (p. 1648) report a series of HIV-infected patients with intracranial tumors not usually considered to be associated with immunodeficiency. They suggest that gliomas may be occurring at a higher rate than in the general population.Sacktor et al. (p. 1640) compared longitudinal neuropsychological test results among different treatment groups of HIV-positive homosexual men and determined that combination antiretroviral regimens with and without protease inhibitors are associated with improved psychomotor speed performance.

Multiple sclerosis

Borràs et al. (p. 1636) evaluated patients with relapsing-remitting MS for the presence of depressive symptoms at the onset of treatment with interferon beta-1b and again at 12 or 24 months. They conclude that this drug does not increase depression or anxiety in this group of patients with MS during the first and second years of treatment.Brassat et al. (p. 1632) identified 87 sibling pairs diagnosed with MS. The study revealed a concordance for disease severity, which the authors suggest might reflect the influence of familial factors (environmental or genetic).

Irene H. Richard, MD

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