Bilateral absence of the musculocutaneous nerve: implications for humerus fracture and atypical median nerve palsy.

The absence of the musculocutaneous nerve represents a failure of the nerve to depart from the median nerve during early development. During a routine dissection of a 66-year-old white female cadaver, a bilateral absence of the musculocutaneous nerve was observed in the upper limbs. Muscles of the anterior flexor compartments of the arms including biceps brachii and brachialis were supplied by branches of the median nerve.

Clinical Implications of the Submental and Sublingual Arteries in Relation to the Mylohyoid Boutonnière.

Objective: Mylohyoid musculature may be included in the submental artery flap to protect perforators. However, blood vessels may pass through the mylohyoid muscle and therefore cause bleeding and risk to pedicle or perforator injury when a mylohyoid-containing flap is lifted. The objectives of this study were to identify the prevalence of the submental and sublingual arteries that traverse the mylohyoid and to assess relationships between vasculature transmitted through mylohyoid muscles and mylohyoid boutonnières.

Ozone exposure initiates a sequential signaling cascade in airways involving interleukin-1beta release, nerve growth factor secretion, and substance P upregulation.

Previous studies demonstrated that interleukin-1β (IL-1β) and nerve growth factor (NGF) increase synthesis of substance P (SP) in airway neurons both after ozone (O3) exposure and by direct application. It was postulated that NGF mediates O3-induced IL-1β effects on SP. The current study specifically focused on the influence of O3 on IL-1β, NGF, and SP levels in mice bronchoalveolar lavage fluid (BALF) and whether these mediators may be linked in an inflammatory-neuronal cascade in vivo.

Early Postnatal Ozone Exposure Alters Rat Nodose and Jugular Sensory Neuron Development.

Sensory neurons originating in nodose and jugular ganglia that innervate airway epithelium (airway neurons) play a role in inflammation observed following exposure to inhaled environmental irritants such as ozone (O(3)). Airway neurons can mediate airway inflammation through release of the neuropeptide substance P (SP). While susceptibility to airway irritants is increased in early life, the developmental dynamics of afferent airway neurons are not well characterized.

Role of nerve growth factor in ozone-induced neural responses in early postnatal airway development.

Airway neural plasticity contributes to the process of airway remodeling in response to airway irritants. However, the mechanisms of neural remodeling in the airways during the early postnatal period, when responses to airway irritation may be most sensitive, have not been characterized. This study used a rat model to examine a possible mechanism of ozone (O(3))-induced neural hyperresponsiveness during a critical period of developmental, postnatal day (PD) 6, that may be mediated by the neurotrophin nerve growth factor (NGF), resulting in an enhanced release of inflammatory neuropeptide substance P (SP) from airway nerves.

Sensory neural responses to ozone exposure during early postnatal development in rat airways.

Airway infections or irritant exposures during early postnatal periods may contribute to the onset of childhood asthma. The purpose of this study was to examine critical periods of postnatal airway development during which ozone (O(3)) exposure leads to heightened neural responses. Rats were exposed to O(3) (2 ppm) or filtered air for 1 hour on specific postnatal days (PDs) between PD1 and PD29, and killed 24 hours after exposure.

Prenatal and early, but not late, postnatal exposure of mice to sidestream tobacco smoke increases airway hyperresponsiveness later in life.

Background: Cigarette smoke exposure in utero and during early postnatal development increases the incidence of asthma and airway hyperresponsiveness (AHR) later in life, suggesting that a possible critical period of developmental sensitivity exists in the prenatal and early postnatal periods.

Objective: We investigated mechanisms of susceptibility during critical developmental periods to sidestream smoke (SS) exposure and evaluated the possible effects of SS on neural responses.

Methods: We exposed three different age groups of mice to either SS or filtered air (FA) for 10 consecutive days beginning on gestation day (GD) 7 by maternal exposure or beginning on postnatal day (PND) 2 or PND21 by direct inhalation.

Allergen-induced substance P synthesis in large-diameter sensory neurons innervating the lungs.

Background: Tachykinins such as substance P are localized in unmyelinated slow-conducting C fibers that can be activated by noxious stimuli and tissue inflammation. Substance P is seldom expressed in fast-conducting large-diameter (A-fiber) vagal sensory neurons. We have previously found that allergic inflammation causes a phenotypic change in tachykinergic innervation of the trachea such that the production of substance P is induced in large-diameter sensory neurons projecting mechanosensitive A fibers to the trachea.

Expression of tachykinins in nonnociceptive vagal afferent neurons during respiratory viral infection in guinea pigs.

Immunohistochemistry was combined with retrograde labeling to characterize the effect of respiratory infection with Sendai virus on the number of Substance P/Neurokinin A-containing vagal afferent neurons whose cell bodies resided in the nodose ganglia and whose receptive fields were located in guinea pig trachea. Of the neurons labeled from the trachea of vehicle-inoculated guinea pigs, few stained positively for Substance P/Neurokinin A (approximately 3% of total labeled neurons). These neurons had small diameter cell bodies (mode = 16-20 microm), a feature of nociceptive-like C-fibers.