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Copyright 1999 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.1999
Stangel and colleagues review concisely current evidence Article for the use of immunoglobulins in treating demyelinating diseases including Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy, multifocal motor neuropathy, and multiple sclerosis. Their comments are direct and provide guidance for the clinician.
Pulst provides a clear case for the precise and powerful use of genetic linkage analysis to detect the chromosomal location of diseased genes Article. His authoritative discussion describes the precision and value of this technique and its importance in defining the genetic basis of neurologic disease.
Andreasen and colleagues describe their experience in Sweden with CSF-β-amyloid(1-42) as a diagnostic marker of Alzheimer disease (AD) Article. They find high sensitivity for this marker with low CSF levels present as well in the early phases of dementia in AD. They concur that this type of analysis is of value in the clinical diagnosis of AD. These findings are also put into critical perspective in an accompanying editorial in this issue of the ARCHIVES by Douglas Galasko, MDArticle.
Díaz-Olavarrieta and colleagues provide critical evidence citing violent behavior suffered by female patients with neurologic disease Article. A modified version of The Abuse Assessment Screen was used to find that one third of female patients with chronic neurologic disease studied in Mexico were the victims of domestic violence. This pervasive problem in our society is placed in perspective in a most thoughtful editorial by Janice M. Massey, MDArticle.
Whitaker et al have measured levels of urine myelin basic proteinlike material (UMBPLM) in patients with multiple sclerosis (MS) treated with interferon beta-1b and have correlated their therapy with clinical changes Article. Importantly, they find that UMBPLM may allow the examination of treatment tested in the prevention of relapsing-remitting disease in becoming progressive. These observations are important in deciding on this form of therapy.
Sasaki and colleagues describe the clinical and genetic features of a family with paramyotonia congenita with a missense mutation in the SCN4A gene Article. This mutation results in substitution of a glutamic acid residue for a highly conserved glycine residue in the fourth transmembrane segment (S4) of domain IV. These elegant studies extend our knowledge of the clinical and molecular genetic associations in this disorder.
Beamer et al describe microalbuminuria as being prevalent in recent stroke patients compared with healthy elderly controls Article. It is an inexpensive and easily measured marker that needs further study.
Chamberlain and Kormanik have studied oral tamoxifen as a prospective phase 2 study in young patients with recurrent anaplastic astrocytomas Article. They found no toxic effects in this group of patients allowing clinical trials to be conducted.
Deletions in 2 genes on chromosome 5q, SMN, and NAIP have been identified in spinal muscular atrophy. These genes are implicated in the regulation of apoptosis Article. Parboosingh and colleagues have determined whether these mutations may be present in patients with non-SOD1 ALS.
Haroutunian and colleagues describe neurofibrillary tangles being present in most elderly individuals regardless of their cognitive status with an increase in their density in early dementia Article. It is a nice study documenting the natural history of this specific neuropathologic feature.
Hankey provides a Neurology and Public Health review Article describing his experience and recommendations about stroke as a major public health problem and how we need to deal with this looming epidemic of increasing proportion and magnitude.
This Month in Archives of Neurology. Arch Neurol. 1999;56(6):651–652. doi:10.1001/archneur.56.6.651