Common and unusual diseases of the nipple-areolar complex.

The nipple-areolar complex is often best evaluated as a separate region of the breast. Because of the intricacy of the anatomic structures and their superficial position, the diagnostic techniques required for optimal evaluation of the nipple-areolar complex differ from those routinely used to evaluate the whole breast. Although clinical examination and screening mammography are still of central importance, the adjunct use of multiple imaging modalities (ultrasonography, contrast material-enhanced magnetic resonance imaging, or both) as well as nonstandard mammographic views is often necessary to differentiate benign abnormalities from malignant ones. For accurate diagnosis, familiarity with a wide range of appearances of the normal anatomy, including congenital anomalies (eg, supernumerary nipples), is necessary, as is a thorough knowledge of the features of the benign and malignant processes that commonly occur in the nipple-areolar complex. Benign abnormalities may include mammary duct ectasia, nipple calcifications, cutaneous horn of the nipple, abscess of the Montgomery gland, and nipple adenoma. Malignant abnormalities may include Paget disease and primary lymphoma as well as carcinoma of the breast. Some conditions, such as nipple retraction and inversion, may have either a benign or a malignant cause. In such cases, a thorough radiologic assessment is especially important.

Subthreshold sodium current from rapidly inactivating sodium channels drives spontaneous firing of tuberomammillary neurons.

A role for "persistent," subthreshold, TTX-sensitive sodium current in driving the pacemaking of many central neurons has been proposed, but this has been impossible to test pharmacologically. Using isolated tuberomammillary neurons, we assessed the role of subthreshold sodium current in pacemaking by performing voltage-clamp experiments using a cell's own pacemaking cycle as voltage command. TTX-sensitive sodium current flows throughout the pacemaking cycle, even at voltages as negative as -70 mV, and this current is sufficient to drive spontaneous firing. When sodium channels underlying transient current were driven into slow inactivation by rapid stimulation, persistent current decreased in parallel, suggesting that persistent sodium current originates from subthreshold gating of the same sodium channels that underlie the phasic sodium current. This behavior of sodium channels may endow all neurons with an intrinsic propensity for rhythmic, spontaneous firing.