This Article  • Full text  • PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on ISI (1)  • Contact me when this article is cited  Related Content  • Related article  • Similar articles in this journal  Topic Collections  • Amyotrophic Lateral Sclerosis  • Alert me on articles by topic

Arch Neurol. 2006;63:319-320.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Long considered to be a disorder restricted to the motor system, amyotrophic lateral sclerosis (ALS) is increasingly recognized to be syndromic, not only in its clinical manifestations but also in its biology. This comes as no surprise to neurogeneticists interested in ALS, long familiar with the concept of polygenic diseases, or with the newer field of toxicogenomics (neurotoxicology with a genetic bent to the rest of us). Nor is it a surprise to those interested in the hyperendemic foci of ALS in which the co-occurrence of ALS with dementia, and often parkinsonism, is well recognized. And to those familiar with the chromosome 17 linked ALS with frontotemporal dementia (FTD), with or with tau mutations, this again is of no surprise. The surprise to many is the extent to which cognitive impairment or dementia can be a feature of sporadic ALS.

On 2 levels, this creates controversy. First, there is the . . . [Full Text of this Article]

AUTHOR INFORMATION

Michael J. Strong, MD, FRCPC

RELATED ARTICLE

An Observational Study of Cognitive Impairment in Amyotrophic Lateral Sclerosis
Gregory A. Rippon, Nikolaos Scarmeas, Paul H. Gordon, Peregrine L. Murphy, Steven M. Albert, Hiroshi Mitsumoto, Karen Marder, Lewis P. Rowland, and Yaakov Stern
Arch Neurol. 2006;63(3):345-352.
ABSTRACT | FULL TEXT