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Apolipoprotein E and Neuromuscular Disease
Apolipoprotein E (apoE) is an established risk factor for Alzheimer disease. Now, Bedlack and colleaguesArticle review the association of apoE with neuromuscular disease. APOE4 appears to be associated with an increased risk for developing diabetic neuropathy and human immunodeficiency virus neuropathy. It may also be associated with a faster progression of some neuromuscular diseases, including diabetic neuropathy and possibly motor neuron disease. APOE2 appears to confer protection against certain neuromuscular diseases, including the amyotrophic lateral sclerosis/parkinsonism/dementia complex of Guam. APOE2 is also associated with a better prognosis for motor neuron disease. Thus, apoE has far-reaching influence on the expression of both central and peripheral neurological disorders.
The Human Genome Project and Neurology
Grodin and LaurieArticle provide a timely review of what the human genome project holds for the genetic expression of neurological functions and specific neurological diseases. The legal and ethical implications of applying information derived from an individual's genome are reviewed and practical lessons are offered. As the authors point out, "it is imperative that the disciplines of medicine, science, ethics, and law work together to find solutions" to implement the information that will soon be descending upon us from the deciphering of the human genome.
Increased Risk for Alzheimer Disease
Finckh et alArticle report that homozygosity for the B haplotype of the cystatin C gene confers increased risk for developing AD late in life and is thus of considerable importance. They offer new insight into the mechanisms of disease pathogenesis and potential specific genomic therapy for at-risk persons.
Treating Alzheimer Disease
Broe and colleaguesArticle have studied nonsteroidal anti-inflammatory drugs and aspirin and their effect on the progression on Alzheimer disease. Low-dose administration of these drugs is sufficient to have beneficial effects, and their mechanisms of action are reviewed.
Measuring the Severity of Myasthenia Gravis
Romi and colleaguesArticle report that the combination of titin, citric acid antigen, and ryanodine receptor antibodies occurred significantly more often in patients with severe myasthenia gravis (MG) than in patients with less severe disease. Furthermore, changes in MG severity correlated with changes in titin antibody titer in the individual patient. Titin antibodies showed a better longitudinal correlation with disease severity than the standard acetylcholine receptor antibodies. Thus, this study shows that specific antibodies can serve as important prognostic markers in MG irrespective of the presence of thymoma.
Human Immunodeficiency Virus Type 1–Associated Motor Deficits
Von Giesen and colleaguesArticle have studied human immunodeficiency virus–positive patients and show that such patients have significant hypermetabolism in the basal ganglia as measured by positron emission tomography. Other patients also show a significant frontomesial hypometabolism. Altered motor function correlates with basal ganglia hypometabolism and progresses coordinately. Thus, positron emission tomography does provide a progressive correlation of altered motor function and reduced metabolic activity in the basal ganglia in this selected group of patients.
Diaz-Arrastia and colleaguesArticle have studied a series of patients with intractable epilepsy after a traumatic brain injury. Of 23 patients studied, 8 had mesial temporal lobe epilepsy. Two of these patients underwent anterior temporal lobectomies. Two other patients were not treated surgically because of bilateral temporal lobe dysfunction noted on intracarotid amobarbital testing. Eleven patients had neocortical epilepsy; 1 of these patients had primary generalized epilepsy, and in 3 cases, the site of seizure onset was not localized. Thus, mesial temporal lobe epilepsy can result from traumatic brain injury in adolescents and adults as well as in children and can often be bilateral.
Seizures After Stroke
Bladin and colleaguesArticle describe a large series of patients with acute stroke and their subsequent incidence of developing seizures. Overall, seizures occurred in 168 (8.9%) of their 1897 stroke patients, including 28 (10.6%) of 265 with hemorrhagic stroke and 140 (8.6%) of 1632 with ischemic stroke. Patients with a disabling cortical infarct or cortical hemorrhage were more likely to have seizures after stroke, and those with late-onset seizures were at greater risk for epilepsy.
Alazzaz and colleaguesArticle describe their experience with percutaneous transluminal angiography for patients with arteriosclerotic stenosis of the carotid and vertebral arteries. This approach is an attractive alternative for patients with significant stenotic disease of the major vessels and can be performed with relatively low risk and good clinical outcome.
This Month in Archives of Neurology. Arch Neurol. 2000;57(11):1557–1558. doi:10.1001/archneur.57.11.1557
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