Acute otitis media

A 3-year-old girl is brought to your office by her mother because she has a fever and complains that her ear hurts. She has no significant medical history. The child is not pleased to be in the physician's office and has been crying. Her mother explains that she developed a cold about 3 days ago with sniffles. Her temperature is 37.8 degreesC (100 degreesF), and the rest of the physical examination is completed with some difficulty. The only abnormalities are slight redness of the throat. a nose full of thick green mucus, and injected tympanic membranes. You wonder what findings other than red tympanic membranes should lead you to diagnose otitis media and also consider the recent controversy about whether to treat acute otitis media (AOM) with antibiotics.

Should watchful waiting be used more often for acute otitis media?

RECENT ANXIETY about the treatment of acute otitis media has been precipitated by a resistance to antibiotics by the common pathogens that can cause this infection.1, 2 The medical profession is facing an increasingly impotent option in the form of antibiotics, prompting physicians around the world to consider alternatives. In this issue of the ARCHIVES, Pichichero and Poole3 have undertaken a comprehensive study involving pediatricians and otorhinologists. The objectives were to assess their recognition of the physical findings of acute otitis media and their ability to perform myringotomy. The principal issue is the safety of performing myringotomy in children with acute otitis media. Because this is an office procedure in which a general anesthetic is not administered, the child is strapped to a papoose board and held down. Myringotomy is not without potential serious complications. The superior part of the middle ear cavity contains the ossicles and the chorda tympani branch . . . [Full Text of this Article]

Selective down-regulation of the astrocyte glutamate transporters GLT-1 and GLAST within the medial thalamus in experimental wernicke's encephalopathy

Although earlier studies on thiamine deficiency have reported increases in extracellular glutamate concentration in the thalamus, a vulnerable region of the brain in this disorder, the mechanism by which this occurs has remained unresolved. Treatment with pyrithiamine, a central thiamine antagonist, resulted in a 71 and 55% decrease in protein levels of the astrocyte glutamate transporters GLT-1 and GLAST, respectively, by immunoblotting in the medial thalamus of day 14 symptomatic rats at loss of righting reflexes. These changes occurred prior to the onset of convulsions and pannecrosis. Loss of both GLT-1 and GLAST transporter sites was also confirmed in this region of the thalamus at the symptomatic stage using immunohistochemical methods. In contrast, no change in either transporter protein was detected in the non-vulnerable frontal parietal cortex. These effects are selective; protein levels of the astrocyte GABA transporter GAT-3 were unaffected in the medial thalamus. In addition, astrocyte-specific glial fibrillary acidic protein (GFAP) content was unchanged in this brain region, suggesting that astrocytes are spared in this disorder. Loss of GLT-1 or GLAST protein was not observed on day 12 of treatment, indicating that down-regulation of these transporters occurs within 48 h prior to loss of righting reflexes. Finally, GLT-1 content was positively correlated with levels of the neurofilament protein alpha -internexin, suggesting that early neuronal drop-out may contribute to the down-regulation of this glutamate transporter and subsequent pannecrosis. A selective, focal loss of GLT-1 and GLAST transporter proteins provides a rational explanation for the increase in interstitial glutamate levels, and may play a major role in the selective vulnerability of thalamic structures to thiamine deficiency-induced cell death.