The American journal of medicine
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Adenosine has recently become widely available for the treatment of paroxysmal supraventricular tachycardia. In order to evaluate its role in the management of arrhythmias, we have reviewed the literature on the cellular mechanisms, metabolism, potential for adverse effects, and clinical experience of the efficacy and safety of intravenous adenosine. Adenosine produces transient atrioventricular nodal block when injected as an intravenous bolus. ⋯ Immediate electrical cardioversion is indicated if the arrhythmia is associated with hemodynamic collapse. Adenosine is the preferred drug in those patients in whom verapamil has failed or may cause adverse effects, such as those with heart failure or wide-complex tachycardia. The safety profile of adenosine suggests that it should be the drug of first choice for the treatment of supraventricular tachycardia, but only limited comparative data to support this view are available at present.
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Case Reports
Optic neuropathy and central nervous system disease associated with primary Sjögren's syndrome.
Three cases of optic neuropathy associated with primary Sjögren's syndrome are reported. All three patients had clinical manifestations of primary Sjögren's syndrome, although two of the patients did not report sicca symptoms at initial examination. Two patients had focal neurologic signs in addition to optic neuropathy. ⋯ This diagnostic differentiation was facilitated by positive tests for xerophthalmia and findings of positive minor salivary gland biopsy. High titers of antinuclear antibody, anti-SSA(Ro), and anti-SSB(La), and the absence of antiphospholipid antibodies provided additional help in the differential diagnosis. In 5 years of observation, none of the patients developed symptoms of multiple sclerosis or additional connective tissue disorders.
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A stool guaiac test is often performed on newly hospitalized patients as part of the admission evaluation. However, little is known regarding the value of testing stool obtained by digital rectal examination. We sought to document the use of the admission stool guaiac test in a teaching hospital, to determine its diagnostic yield, and to assess its potential benefit to patients. ⋯ Like other commonly applied diagnostic tests, the stool guaiac test obtained during the admission physical examination is best reserved for patients whose clinical presentation provides a reason for testing. In patients without clinical indications, the test is of uncertain value and only infrequently leads to important diagnoses.
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Esophageal pain is transmitted via the sympathetic nervous system to the spinal cord, in which pain from visceral and somatic sources ascends to higher centers in the brain. Primary afferent neurons are bipolar, with the peripheral end specialized to be a sensory receptor. Nociceptors of somatosensory afferents are free nerve endings that can be activated by mechanical, thermal, or chemical stimuli. ⋯ Organ-specific pathways in the brain have yet to be defined, but neuroanatomic tracing techniques employing neurotropic viruses are being developed. The perception of pain can be influenced at multiple levels, such as the receptor in the esophagus, the synapses in the dorsal horn of the spinal cord or thalamus, or the cortex. A fundamental mechanism of modulating nociception is descending inhibition.(ABSTRACT TRUNCATED AT 400 WORDS)
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Severe hyponatremia is often associated with permanent brain damage. There has been substantial controversy about whether central pontine myelinolysis (CPM), a rare neurologic disorder of uncertain etiology, can complicate either hyponatremia or its therapy. This study was undertaken to determine how often hyponatremic patients with the clinical diagnosis of CPM actually have the disorder as an integral structural component of their encephalopathy. ⋯ These results suggest that: (1) Neither hyponatremic encephalopathy nor its therapy is commonly associated with CPM; (2) Patients with chronic alcoholism who also become hyponatremic can develop pontine demyelinating lesions; (3) Most patients with symptomatic hyponatremia who are diagnosed as having CPM in fact have diffuse cerebral demyelinating lesions with a normal pons; (4) The distribution of cerebral demyelinating lesions in patients with hyponatremic encephalopathy is compatible with hypoxic damage.