Rascol and colleaguesArticle report that patients with advanced-stage Parkinson disease showed improvement on the Unified Parkinson Disease Rating Scale parts II and III, and in “off” time, when treated with tesofensine, a monoamine reuptake inhibitor. This was a pilot phase 2 randomized, double-blind, placebo-controlled parallel-group trial.
PleasureArticle provides a comprehensive and elegant review pointing out that autoantibodies against glutamate receptors, first reported in Rasmussen encephalitis, have now also been observed in other focal epilepsies, as well as in central nervous system ischemic infarcts, transient ischemic attacks, sporadic olivopontocerebellar atrophy, systemic lupus erythematosus, and paraneoplastic encephalopathies. The thesis proposed is that glutamate receptor autoantibodies can actively contribute to neurologic dysfunction and have diagnostic and pathogenic significance.
Trachtenberg and TrojanowskiArticle make the case for the elimination of the word dementia as a diagnostic term. They find it, as a generalization, to be pejorative and even harmful, based on historical and current patient, caregiver, and physician perspectives. Suggestions for more meaningful and nonstigmatizing terms are offered. Primary among these is the change from frontotemporal dementia to frontotemporal disease.
Berger and HouffArticle indicate in their highly informative discussion that the herpes viruses are clearly responsible for significant neurological morbidity. Importantly, 3 of the 8 human herpes viruses, herpes simplex virus type 1 (HSV-1), HSV-2, and varicella zoster virus, establish latency in the peripheral sensory ganglia and persist in the host throughout his or her lifetime. Clinical syndromes, diagnostic criteria, and current therapies are incisively reviewed. They emphasize that up to 45 million people in the United States have been infected with HSV-2, and the estimated incidence of new infection is 1 million annually. Their review provides an overview of the neurological complications of HSV-2.
Uyttenboogaart and colleaguesArticle have assessed whether prior use of antiplatelet drugs is related to outcome following intravenous tissue plasminogen activator therapy in patients with ischemic stroke. They report that, despite a higher incidence of symptomatic intracerebral hemorrhage, the net benefit of intravenous tissue plasminogen activator for acute ischemic stroke was greater in patients using antiplatelet drugs.
Anheim et alArticle studied patients with poor subthalamic nucleus stimulation (STN) results and suspected it was because of electrode misplacement. Through the use of imaging, they determined whether reimplantation of electrodes in the STN can effect improvement. Indeed, patients expressing a poor response to STN stimulation as a result of electrode misplacement did benefit from reimplantation of the electrodes closer to the theoretical target.
Correlation between the percentage improvement in the Unified Parkinson Disease Rating Scale (UPDRS) motor score under off-medication on-stimulation (ie, the patient is not receiving medication but receiving stimulation) condition compared with basal state (off-medication off-stimulation condition before reimplantation) and the mean distance in millimeters between the center of the electrode contact and the theoretical effective target (TET). Solid diamonds squares indicate results before reimplantation; open squares, results 1 year after reimplantation. On the x-axis, the distances from the center of the therapeutic contact to the TET are the sum of the left-side and right-side distances (*P =.02, Spearman rank correlation [diagonal line]).
Wang and colleaguesArticle provide data showing that at least 1 fiber parameter of each region of the injured brain showed diffuse axonal injury–associated alterations. Diffusion tensor tractography–based quantitative analysis of acute magnetic resonance imaging scans has the potential to serve as a valuable biomarker for diffuse axonal injury and to predict long-term outcome.
Pittock and LennonArticle put forward convincing evidence that aquaporin-4–specific IgG, in some cases, may reflect a paraneoplastic immune response. The clinical utility of this autoantibody as a cancer marker warrants prospective investigation.
Osteopontin, a proinflammatory cytokine, was found to be significantly elevated in the cerebrospinal fluid of patients with multiple sclerosis and other inflammatory neurological diseases, compared with those with noninflammatory neurological diseases, as reported by Braitch and colleaguesArticle. They conclude that osteopontin may play an important role in central nervous system inflammation.
Geser et alArticle show that pathological 43-kD, a transactivating response sequence DNA-binding protein (TDP-43), reported in amyotrophic lateral sclerosis and in frontotemporal lobar degeneration with ubiquitin-positive inclusions, with or without motor neuron disease, was present in multiple brain areas in patients with amyotrophic lateral sclerosis. Their findings support the view that amyotrophic lateral sclerosis does not selectively affect only the pyramidal motor system, but rather is a multisystem neurodegenerative TDP-43 proteinopathy.
Seshadri et alArticle have evaluated the relationship between plasma homocysteine level and brain magnetic resonance imaging in a community-based sample. They report that higher plasma homocysteine levels are associated with smaller brain volumes and presence of silent infarcts on magnetic resonance images, even in healthy, middle-aged adults.
Kuczynski and colleaguesArticle have elucidated how baseline cognitive function (episodic memory and executive function) and brain anatomy (white matter hyperintensities and hippocampal volume) are associated with baseline and longitudinal glucose metabolism, including normal cognition, cognitive impairment, and dementia. They conclude that low baseline episodic memory and hippocampal volume predict the metabolic alterations associated with Alzheimer disease. However, elevated baseline white matter hyperintensities predict a different pattern of metabolic decline that is plausibly associated with cerebrovascular disease.
This Month in Archives of Neurology. Arch Neurol. 2008;65(5):572-573. doi:10.1001/archneur.65.5.572