Marra reviews the new epidemics of syphilis and human immunodeficiency virus (HIV). The new syphilis epidemic, as she points out, has been difficult to contain, and efforts to do so have resulted in political controversy. Although only through rigorous scientific research will syphilis and HIV be prevented, Dr Marra reminds us that this research effort will have to be broad enough to identify effective strategies in all risk groups, even those that make us uncomfortable.
Roos points out that the emergence of antimicrobial-resistant bacterial infections has changed the recommendations for the empirical therapy of community- and hospital-acquired meningitis. Inadequate empirical therapy is associated with increased mortality, but excessive antibiotic use promotes the emergence and spread of antibiotic-resistant pathogens. This vital and evolving area of infectious disease management is carefully and expertly reviewed in a clear and authoritative manner.
Intravenous immunoglobulin has been reported to reduce activity in patients with relapsing-remitting multiple sclerosis. Achiron and colleagues assessed the effect of intravenous immunoglobulin treatment in patients after the first neurological event suggestive of demyelinating disease in a randomized, double-blind, placebo-controlled trial. Of note, intravenous immunoglobulin treatment for the first year from onset of the first neurological event significantly lowered the incidence of the second attack and reduced disease activity as measured by brain magnetic resonance imaging.
Herpesvirus 6 has been the subject of intenseinterest as a causal agent for multiple sclerosis. Álvarez-Lafuente and colleagues report that herpesvirus 6 active infection was detected in 16.2% of patients with relapsing-remitting multiple sclerosis compared with 0% of healthy blood donors. Among patients with relapsing-remitting multiple sclerosis and herpesvirus 6 active replication, viral load was higher when they suffered from an acute attack than when they were in remission. Editorial perspective by Olaf Stüve, MD, Michael Racke, MD, and Bernhard Hemmer, MD.
Prins and colleagues have studied the association between white matter lesions in specific locations and the risk of dementia. Higher severity of periventricular white matter lesions increased the risk of dementia, whereas the association between subcortical white matter lesions and dementia was less prominent. Gustavo C. Román, MD,provides a comprehensive assessment in an accompanying editorial.
The Optic Neuritis Study Group studied and observed patients with monosymptomatic optic neuritis who manifest new brain lesions shown on magnetic resonance imaging without having developed clinically definite multiple sclerosis. Of note, a subset of patients manifest neither clinical signs nor magnetic resonance imaging evidence of demyelination after more than 10 years of follow-up. Other patients develop magnetic resonance imaging lesions without causing new clinical manifestations of multiple sclerosis. This study is useful in providing patients with counseling related to future risk of demyelinating disease after a first episode of optic neuritis.
Reed and colleagues have investigated the effects of subcortical lesions (lacunes and white matter lesions) on cortical function in the elderly, as reflected in glucose metabolism and cognitive function. They report that the metabolic effects of lacunes and white matter lesions are most apparent in dorsolateral frontal cortex, but the effects of white matter lesions are generalized and frontal hypometabolism correlates with memory and global cognitive impairment as well as executive function.
Human herpesviruses 2 and 1 have been recognized as causes of recurrent aseptic lymphocytic meningitis. Kupila and colleagues have evaluated the cause of recurrent aseptic lymphocytic meningitis in patients with at least 2 episodes of aseptic meningitis by using polymerase chain reaction detecting varicella zoster virus, cytomegalovirus, or human herpesvirus 6, in addition to herpes simplex virus, in the cerebrospinal fluid. Varicella zoster virus, cytomegalovirus, and human herpesvirus 6 were not identified in their cohort of patients with recurrent aseptic lymphocytic meningitis. Herpes simplex 2 was detected by polymerase chain reaction in the cerebrospinal fluid in the majority of patients.
Olanow and colleagues report that the catechol O-methyltransferase inhibitor entacapone, used as an adjunct to levodopa in patients with Parkinson disease who do not experience motor fluctuations, does not improve Unified Parkinson’s Disease Rating Scale motor scores but does improve avariety of quality-of-life measurements. Their study underscores the complexities of conducting clinical trials in levodopa-treated patients with mild Parkinson disease.
Martino and colleagues show that because of the low sensitivity of obtaining reliable family history data, there is a risk of definite error in determining the inherited basis of adult-onset dystonia. They conclude that the only valid means of ascertaining dystonia among relatives remains the neurological examination of at-risk subjects.
Josephs and colleagues studied whether apolipoprotein E ε4 influences the frequency of Alzheimer-type pathologic features in tauopathies, synucleinopathies, and frontotemporal degeneration and also whether the frequency of Alzheimer-type pathologic features in synucleinopathies is similar to the frequency of such features in tauopathies and frontotemporal degeneration. Of considerable interest, apolipoprotein E ε4 independent of older age and sex contributes to the co-occurrence of Alzheimer-type pathologic features in tauopathies, synucleinopathies, and frontotemporal degeneration but does not explain why Alzheimer-type pathologic features are significantly more likely to coexist with synucleinopathies than with tauopathies or frontotemporal degeneration. At the molecular level, this important finding implies an increased tendency for the α-synuclein protein and the Aβ protein to coexist. The authors postulate that other upstream genes or other genetic loci may help explain this increased association.
Prader-Willi syndrome is a genetic disorder usually caused by a deletion on the paternal chromosome 15 or by a maternal uniparental disomy 15. Patients may have findings indicative of involvement of the corticospinal motor system. Civardi and colleagues have studied patients with Prader-Willi syndrome with transcranial magnetic stimulation and have found hypo-excitability of the corresponding motor areas. Motor conduction time, central silent period, and F waves were normal. Motor threshold was higher compared with control subjects. Intracortical facilitation was significantly reduced. This study offers elegant genetic and neurophysiological correlations providing insight into the genetic basis for altered motor function in Prader-Willi syndrome.
The clinical features, response to therapy, and outcome of patients with traumatic benign paroxysmal positional vertigo were studied and compared with patients with the idiopathic form of this condition. Gordon and colleagues find that traumatic benign paroxysmal positional vertigo is more resistant to therapy and is more recurrent than the idiopathic form.
This Month in The Archives of Neurology. Arch Neurol. 2004;61(10):1494-1495. doi:10.1001/archneur.61.10.1494