Copyright 2006 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.2006
Höke proposes a theory and offers data in support of neuroprotective therapies directed at distal axonal degeneration of the peripheral nervous system—an early event that may be amenable to treatment. Axon injury induces nitric oxide production within neurons, which stimulates erythropoietin production by neighboring Schwann cells. The Schwann cell–derived erythropoietin results in activation of an “axonoprotective” pathway via erythropoietin receptor ligation on neurons. This new and enterprising concept is generating great interest.
Langer-Gould and colleagues identified clinical and demographic factors associated with long-term disability in patients with relapsing-remitting multiple sclerosis. Of considerable interest, after searching multiple computerized databases and reference lists of retrieved articles, they found that the most robust predictors of long-term physical disability in relapsing-remitting multiple sclerosis are sphincter symptoms at onset and early disease course outcomes.
Kinoshita et al point out that proteomics represents the comprehensive study of cellular proteins and is aimed at analyzing their structure, function, expression interactions, and localization in complex biological systems. Proteomics using these same study approaches is now able to promote a better understanding of neurological diseases and foster the identification of therapeutic agents by comparing proteomes of normal and diseased samples.
An investigation of the relationship between muscle and blood mitochondrial DNA load and phenotype was conducted by Jeppesen and colleagues. They report a close relationship between muscle mutation load and phenotype in persons carrying the 3243A>G mutation. There is, however, a lack of correlation between mutation load in blood and symptoms from other tissues. They emphasize the importance of assessing phenotype-genotype correlations in the same tissue in mitochondrial disease. Their results indicate that the threshold of muscle mutation load at which oxidative impairment occurs can be as low as 50%, which is up to 40% lower than suggested by in vitro studies. These findings are put into perspective in an insightful editorial by Salvatore DiMauro, MD, and Michio Hirano, MD.
Scarmeas and colleagues comprehensively examined the association between the Mediterranean diet and Alzheimer disease. They report that higher adherence to the Mediterranean diet is associated with a reduced risk for Alzheimer disease. The biological mechanisms involved in this effect were thoroughly examined and analyzed.
Odds ratios and 95% confidence intervals (bars) for subjects with Alzheimer disease vs nondemented subjects for each Mediterranean diet (MeDi) adherence tertile based on logistic regression models that adjusted for cohort, age, sex, ethnicity, education, apolipoprotein E genotype, caloric intake, smoking, comorbidity index, and body mass index (calculated as weight in kilograms divided by height in meters squared).
This report is directed at studying the role of the nigrostriatal system for parkinsonism in patients with amyotrophic lateral sclerosis (ALS). Positron emission tomographic (PET) and single-photon emission computed tomographic (SPECT) studies were conducted by Hideyama et al on 5 patients with ALS manifesting overt parkinsonism. They report that the PET studies indicated normal nigrostriatal function, but the SPECT data demonstrated decreased blood flow in the frontotemporal cortices. They conclude that parkinsonism in ALS is the result of cortical lesions rather than nigrostriatal dysfunction and, further, that both symptoms are the clinical manifestation of frontotemporal dementia with motor neuron diseases, including classic ALS.
Tong and colleagues found that dopamine loss in Parkinson disease was inversely correlated with normal noradrenaline levels. Regions rich in noradrenaline were relatively spared from dopamine loss. They conclude that these data are consistent with the view that noradrenaline might influence neuron loss in Parkinson disease and could be protective.
Whether ischemic lesion recurrence on magnetic resonance imaging predicts subsequent clinical events was studied by Kang et al. They found that both early and late silent lesion recurrences on magnetic resonance imaging independently predicted clinical recurrent ischemic stroke, transient ischemic attack, or vascular deaths. Thus, these data suggest that silent ischemic lesion recurrence on magnetic resonance imaging may be a potential surrogate marker of clinical recurrence.
Lee and colleagues compared clinical and angiographic characteristics and stroke patterns between spontaneous intracranial vertebral artery dissection and vertebral large artery disease (ie, atherosclerosis). They found that diffusion-weighted imaging on magnetic resonance imaging and noninvasive vascular studies provide a means in addition to the clinical features to differentiate between vertebral artery dissection and atherosclerosis.
Cavaliere et al studied the factors that contribute to the development of status epilepticus in patients with a brain neoplasm. Status epilepticus in this setting is responsive to therapy. A thorough workup is indicated because coexistent conditions contributing to the development of status epilepticus may be present. In those with a known brain neoplasm, brain imaging should be preformed because status epilepticus occurs in a setting of tumor progression or new metastases.
Jette and colleagues determined the incidence, predictors, and timing of nonconvulsive seizures during continuous electroencephalographic(cEEG) monitoring in critically ill children. They found that seizures, the majority being nonconvulsive seizures, are common during cEEG in critically ill children (44%). They show the importance of prolonged cEEG for critically ill children in detecting nonconvulsive seizures.
Factors associated with the development of motor fluctuations and dyskinesias in patients with Parkinson disease was studied by Hauser and colleagues. They conclude that higher cumulative levodopa dosages and higher cumulative levodopa-equivalent dosages (levodopa plus pramipexole) were associated with the earlier occurrence of motor complications. Motor fluctuations and dyskinesias appear to be interrelated as the presence of one is associated with the earlier development of the other.
Aggarwal et al found that a person with impaired lower limb performance of parkinsonian gait (score at the 10th percentile) was 2 to 3 times more likely to develop Alzheimer disease than a person with good lower limb function (score at the 90th percentile). Thus, persons with mild cognitive impairment may also have impaired motor function, and the degree of impairment in the lower extremity is related to the risk of developing Alzheimer disease.
Sabbagh and colleagues assessed nicotinic receptor binding and pathological differences in clinically and pathologically described nondemented controls, subjects with mild cognitive impairment (MCI), and subjects with Alzheimer disease (AD). They report that, in general, subjects with MCI were pathologically intermediate between normal controls and subjects with AD. However, binding for nicotinic acetylcholine receptors did not differ between normal controls and subjects with MCI but was significantly less in subjects with AD.
This Month in Archives of Neurology. Arch Neurol. 2006;63(12):1676-1677. doi:10.1001/archneur.63.12.1676