Annals of neurology
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Annals of neurology · Apr 2010
Treatment-induced diabetic neuropathy: a reversible painful autonomic neuropathy.
To describe the natural history, clinical, neurophysiological, and histological features, and outcomes of diabetic patients presenting with acute painful neuropathy associated with glycemic control, also referred to as insulin neuritis. ⋯ Treatment-induced neuropathy is characterized by acute, severe pain, peripheral nerve degeneration, and autonomic dysfunction after intensive glycemic control. The neuropathy occurred in parallel with worsening diabetic retinopathy, suggesting a common underlying pathophysiological mechanism. Clinical features and objective measures of small myelinated and unmyelinated nerve fibers can improve in these diabetic patients despite a prolonged history of poor glucose control, with greater improvement seen in patients with type 1 diabetes.
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Annals of neurology · Apr 2010
How neurologists think: A cognitive psychology perspective on missed diagnoses.
Physicians use heuristics or shortcuts in their decision making to help them sort through complex clinical information and formulate diagnoses efficiently. Practice would come to a halt without them. However, there are pitfalls to the use of certain heuristics, the same ones to which humans are prone in everyday life. ⋯ Articulation of the errors inherent in certain common heuristics alerts clinicians to their weaknesses as diagnosticians and should be beneficial to practice. Analysis of cases with missed diagnoses in teaching conferences might proceed along formal lines that identify the type of heuristic used and of inherent potential cognitive errors. Addressing these cognitive errors by becoming conscious of them is a useful tool in neurologic education and should facilitate a career-long process of continuous self-improvement.
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Annals of neurology · Mar 2010
Effect of apolipoprotein E on biomarkers of amyloid load and neuronal pathology in Alzheimer disease.
To study the effect of apolipoprotein E epsilon4 status on biomarkers of neurodegeneration (atrophy on magnetic resonance imaging [MRI]), neuronal injury (cerebrospinal fluid [CSF] t-tau), and brain Abeta amyloid load (CSF Abeta(1-42)) in cognitively normal subjects (CN), amnestic subjects with mild cognitive impairment (aMCI), and patients with Alzheimer disease (AD). ⋯ Low CSF Abeta(1-42) (surrogate for Abeta amyloid load) is more closely linked to the presence of APOE epsilon4 than to clinical status. In contrast, MRI atrophy (surrogate for neurodegeneration) is closely linked with cognitive impairment, whereas its association with APOE epsilon4 is weaker. The data in this paper support a model of AD in which CSF Abeta(1-42) is the earliest of the 3 biomarkers examined to become abnormal in both APOE carriers and noncarriers.
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Annals of neurology · Mar 2010
Comment Letter Case ReportsPredicted pathogenic missense mutation of PGRN found in a normal control.