Neurologic clinics
-
Data from randomized therapeutic trials often provide little relevant evidence for therapeutic decisions physicians make daily. By illustrating the nuances of these four complex cases involving cerebrovascular disease, the authors stress the importance of more time spent by specialists at the bed-side, exploring patients' symptoms and learning their thoughts, fears, biases, and wishes.
-
In this series of clinical vignettes, the authors have attempted to provide a "feel" for the varied causes of syncope. The neurologist should be able to diagnose most causes of syncope using a simple algorithmic approach. Initial evaluation includes detailed clinical history, physical examination, and 12-lead ECG. ⋯ Patients with heart disease will need the most comprehensive evaluations, possibly including exercise testing, cardiac electrophysiology, and tilt-table testing. As better understanding of pathophysiology and epidemiology emerge, under-standing of the diagnosis and treatment of syncope will improve. In the meantime, there is no substitute for astute clinical acumen.
-
Electrophysiologic testing continues to play an important role in injury stratification and prognostication in patients who are comatose after cardiac arrest. As discussed previously, however, the adage about treating whole patients, not just the numbers, is relevant in this situation. EEG and SSEP can offer high specificity for discerning poor prognosis as long as they are applied to appropriate patient populations. ⋯ Aside from prognostication, electrophysiologic testing holds great promise in defining the basic anatomy and physiology of coma emergence after cardiac arrest. In addition, quantitative EEG and automated evoked potentials have the potential to render these tools less subjective and arcane and more applicable for monitoring patients in the period during and immediately after resuscitation. Quantitative EEG also has great potential asa tool to define the time window for neuroprotective intervention and the means to track the response to such therapies in real time.
-
It is difficult to predict precisely the final neurologic outcome from cardiac arrest and accompanying cerebral hypoxia. Although rare, several movement disorders may arise as a consequence of hypoxic injury, including myoclonus, dystonia, akinetic-rigid syndromes, tremor, and chorea. ⋯ Many outstanding questions remain, however. What factors promote susceptibility to the development of posthypoxic movement disorders? Why do patients who have similar clinical hypoxic insults develop markedly dis-similar movement disorders? Why are the basal ganglia especially vulnerable to cerebral hypoxia? Why do some movement disorders occur in delayed fashion and progress for years after the hypoxic insult? Is the pathogenesis of progressive posthypoxic movement disorders related to that of neurodegenerative diseases? What are the most effective medications for the various posthypoxic movement disorders? Is there a role for deep brain stimulation in the treatment of posthypoxic movement disorders? We anticipate that current and future research in the area of posthypoxic movement disorders will reveal answers to some of these important questions.
-
Less than 3% of all patients who have out-of-hospital cardiac arrests have return of spontaneous circulation (ROSC), survive the hospitalization, and have a reasonable functional recovery. The fact that many patients who have ROSC ultimately die or fail to have favorable neurologic recovery suggests that processes that occur after hospitalization, especially in the ICU, have an impact on survival and neurologic recovery. This article addresses the acute care, with emphasis on the cardiac and neurologic aspects,that patients who have post cardiac arrest are provided in the cardiac ICU.