Neurology
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Ischemic strokes occurring in patients with nonrheumatic atrial fibrillation are due to a variety of mechanisms, not exclusively to cardiogenic embolism. Without knowledge of antithrombotic therapy assignment, we categorized strokes in the Stroke Prevention in Atrial Fibrillation Study as presumed cardioembolic or noncardioembolic. We then compared patient clinical and echocardiographic variables, as well as the efficacy of aspirin prophylaxis, for each stroke type. ⋯ Patients developing noncardioembolic strokes, relative to cardioembolic strokes, were more commonly men (p = 0.005) and were more likely to have left ventricular wall motion abnormalities by two-dimensional echocardiography (p = 0.002). Aspirin reduced the occurrence of strokes categorized as noncardioembolic significantly more than it did those categorized as cardioembolic (p = 0.01). These results emphasize the value of considering stroke mechanisms in therapeutic trials of antithrombotic agents and suggest a differential effect of aspirin according to mechanism.
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We characterized postural stability in patients with Huntington's disease (HD) by examining their ability to use different sensory cues to maintain balance and by recording their automatic postural responses to externally applied perturbations. Our HD patients, like normal subjects, depended more on proprioceptive than on visual cues to maintain balance. ⋯ The onset of compensatory motor responses in the lower extremities following sudden translations of the support surface was delayed by 30 to 60 msec in HD patients as compared with normal subjects. HD patients also had more sway and falls during unexpected rotations of the support surface, although they could appropriately reduce their motor responses on the next trial.
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Comparative Study
Chronic inflammatory demyelinating polyradiculoneuropathy: comparison of patients with and without an associated monoclonal gammopathy.
We reviewed our data from patients with the clinical diagnosis of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Seventy patients had no demonstrable underlying disease to account for their polyneuropathy and were classified as idiopathic CIDP (CIDP-I). We detected a monoclonal gammopathy of uncertain significance (MGUS) in 30 patients who were classified as CIDP-MGUS; 17 had an IgG gammopathy, 12 an IgM gammopathy, and one an IgA gammopathy. ⋯ There were no significant differences in motor and sensory nerve conduction measures between CIDP-I and CIDP-MGUS patients, nor between CIDP-MGUS patients with IgM and those with IgG or IgA gammopathy. Strict electrodiagnostic criteria for primary demyelination were fulfilled by 54% of CIDP-I patients and 40% of CIDP-MGUS patients, but these were not significantly different. Our study suggests that (1) the demographic features and immunoglobulin class distribution of CIDP-MGUS patients largely reflect those of patients with an MGUS, but without polyneuropathy, (2) CIDP-MGUS patients as a group cannot be distinguished from CIDP-I patients on the basis of nerve conduction studies, and (3) IgM CIDP-MGUS patients cannot be distinguished from those with other immunoglobulin classes.
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In an atmosphere of escalating medical costs, clinical practice guidelines have been proposed as a viable means of achieving cost containment. The approaches to developing standards of practice have historically been varied, and new methods of development have been proposed to incorporate current scientific knowledge and patient preferences for achieving optimal health outcomes. We review the historical, governmental, and health organization approaches to achieve scientifically sound and clinically relevant parameters. ⋯ The Subcommittee has selected the term "practice parameter" in lieu of "practice policy" to be consistent with AMA terminology. Practice parameters may include one or more of the following types of recommendations: standards, guidelines, and options. These three terms reflect varying levels of clinical certainty as determined by the level of objective evidence.
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Review
Does selegiline monotherapy in Parkinson's disease act by symptomatic or protective mechanisms?
Selegiline monotherapy has been clearly demonstrated to delay the development of disability in early, otherwise untreated Parkinson's disease patients. It remains uncertain, however, whether this benefit is due to protective effects on residual neurons or to symptomatic effects that mask the detection of underlying disability. This paper examines the evidence and theory supporting the hypotheses that selegiline acts by protective or symptomatic mechanisms and considers what future studies might help clarify these issues.