Maxillary sinus cancer and metastatic compression of the cauda equina: report of two cases.

Maxillary sinus cancer with metastasis outside of the head and neck is a relatively rare occurrence. We describe two cases of carcinoma of the maxillary sinus that metastasized to the spine and compressed the cauda equina. In the first case, the neurological complication happened synchronously with the primary malignant neoplasm, while in the second instance, cauda equina compression occurred several months later. The treatment of metastatic compression of the cauda equina consisted mainly of radiotherapy, with palliation being achieved in one patient. Survival was expectedly short (3 months) for both individuals.

Effects of postoperative external beam irradiation after carotid artery stripping of nodal metastasis.

PURPOSE: The objective of this study was to determine the effects of postoperative external beam irradiation (PEBI) on patients after stripping the carotid vessel of nodal metastasis. PATIENTS AND METHODS: Of 245 patients who underwent radical neck dissection for cancer of the upper aerodigestive tract between 1981 and 1995, 13 patients with nodal metastasis adherent to the carotid artery (NMCA) received a full course of PEBI after the tumor was peeled off the carotid vessel. Patterns of treatment failure, survival, and serious morbidity were evaluated. RESULTS: At the time of last follow-up (range, 3 to 125 months), fewer than half of the patients (46%) were free of disease, and two patients (15%) had developed distant metastases. The estimated 2-year survival rate was 23%. There were no intraoperative, postoperative, or post-radiation therapy complications. CONCLUSION: PEBI after carotid artery stripping of tumor can achieve locoregional disease control in select patients without an increased risk of vessel rupture. However, if the prognosis for patients with NMCA is to improve, other effective management strategies need to be investigated.

Perineural invasion in skin cancer of the head and neck: a review of nine cases.

PURPOSE: To review the management and outcome of skin cancer of the head and neck with perineural invasion, a relatively uncommon and complex condition, in nine patients treated between 1965 and 1991. PATIENTS: Seven patients had skin cancers that were larger than 2 cm. All lesions were moderately or poorly differentiated. Curative surgery was performed in all nine cases, with or without radiotherapy. RESULTS: Local recurrence or regional disease appeared in three individuals; surgical salvage produced satisfactory results. At last follow-up (median, 45 months; range, 18 to 201 months), no one had developed intracranial or skull base metastasis; lung cancer was detected in one patient. The crude survival rate was 33% at 5 years and 22% at 10 years. The median survival was 25 months in patients who presented with neurologic symptoms and was 49 months in asymptomatic persons. CONCLUSION: Although the prognosis in patients with skin cancer of the head and neck complicated by perineural invasion is expectedly poor, long-term disease-free survival is attainable with the use of aggressive therapy.

Imidazoline desensitization of epinephrine responses in rat vas deferens.

Repeated exposure of the rat vas deferens to the imidazoline oxymetazoline (OXY) results in a progressive loss of response which can appear selective for imidazoline agonists. The present study tests the hypothesis that imidazolines produce desensitization through prolonged blockade or inactivation of alpha-1 adrenoreceptors. Repeated exposure to OXY, naphazoline (NPZ) or tetrahydrozoline (THZ) produces a concentration- and time-dependent rightward shift and depression of the (-)-epinephrine concentration-effect curve, suggesting a mechanism of prolonged receptor blockade or inactivation. (-)-Epinephrine Kd values were similar when estimated after either receptor inactivation with phenoxybenzamine or repeated exposure to imidazolines. The differences in the ability of individual imidazolines to produce desensitization (order of potency: OXY greater than NPZ greater than or equal to THZ) do not follow their intrinsic activity (NPZ approximately THZ approximately OXY) or affinity (OXY greater than or equal to NPZ greater than THZ). The ability of individual imidazoline and phenethylamine agonists to produce a response in imidazoline-desensitized rat vas deferens reflects agonist intrinsic efficacy. Desensitization by imidazoline exposure does not affect contraction produced by either KCl or neurokinin A. Imidazolines produce effects similar to receptor inactivation and their desensitization in vas deferens can be explained without invoking an imidazoline subtype of alpha-1 adrenoreceptor.

Destruction of cells in the midportion of the locus coeruleus by a dorsal bundle lesion in neonatal rats.

Although insult of the developing noradrenergic neuronal system in the brain has been associated with redistribution of noradrenergic fiber input to various target brain regions, few studies have investigated the effects of such insults on locus coeruleus cell survival. In the present study the dorsal noradrenergic bundle was transected by means of a midbrain knife cut in rats 3 days after birth, and the effects of this lesion were determined approximately 8-10 weeks later. By means of an immunofluorescent histochemical procedure, it was shown that tyrosine hydroxylase-containing fibers and dopamine beta-hydroxylase-containing fibers were markedly reduced in number in the neocortex and hippocampus--regions anterograde to the site of axonal transection. It was further demonstrated that the number of fluorescent fibers coursing through the dorsal bundle was similarly reduced. Sprouting of noradrenergic fibers in the brainstem and cerebellum accompanied the above alterations. When locus coeruleus cell number was determined by counting Cresyl violet-stained nucleoli in serial sections it was found that dorsal bundle transection produced a loss of 17% of the cells of the coeruleus. By dividing the counts for each nucleus into fifths, it was additionally found that approximately 20-25% of those cells comprising the midportion of the nucleus, along a rostrocaudal axis, were the ones destroyed by axonal transection. These findings indicate that a neonatal lesion of the dorsal bundle produces a loss of cells in the midportion of the nucleus locus coeruleus, and that this effect is associated with noradrenergic neuronal hyperinnervation of the brainstem and cerebellum.

Developmental localization of noradrenergic innervation to the rat cerebellum following neonatal 6-hydroxydopa and morphine treatment.

In order to demonstrate the influence of morphine on the developmental localization of regenerated noradrenergic fibers in rat cerebellum, a glyoxylic histofluorescent method and radiometric assay for norepinephrine (NE) were utilized. An initial reduction of NE in the cerebellum after 6-hydroxydopa [6-OHDOPA; 60 micrograms/g intraperitoneally (i.p.)] was followed by a return to control levels at 3 days, and an elevation above control levels at 7 days. The initial rates of recovery of NE in the cerebellum of the 6-OHDOPA group of rats and the group receiving morphine (20 micrograms/g i.p.) in combination with 6-OHDOPA were identical up to 7 days. However, by 14 days NE content was further elevated in the cerebellum of the morphine +6-OHDOPA group. Histofluorescent microscopic observations of the cerebellar cortex correlated with the biochemical findings. A reduction in cerebellar NE content at 3 days was associated with a reduction in the number of visible histofluorescent fibers in the cerebellar cortex. By 7 days the relative number of fibers in the 6-OHDOPA groups was similar to that seen in the control group, but by 9 days the relative number of fluorescent fibers in the cerebellar cortex was increased above control. By 13 days there was a further increase in the relative number of fluorescent fibers in the cerebellar cortex of the morphine +6-OHDOPA group, as compared to the group treated with 6-OHDOPA alone. These findings provide an anatomic correlate for recovery of noradrenergic fibers after 6-OHDOPA, and demonstrate an action of morphine in enhancing regenerative sprouting.

Opiate-enhanced toxicity and noradrenergic sprouting in rats treated with 6-hydroxydopa.

Because endorphin receptor activation alters the function of the central noradrenergic system, opiates may change the regenerative sprouting of neurons in response to adrenergic neurotoxins. To test this hypothesis, newborn rats were treated with several opioids and 6-hydroxydopa (6-OHDOPA) and the development of the noradrenergic system was evaluated. In combination with 6-OHDOPA morphine and naloxone potentiated the development of norepinephrine (NE) levels in the pons-medulla and cerebellum by four weeks of age, beta-Endorphin, Leu- and Met-enkephalin and d-Ala2-enkephalinamide produced a similar effect in the pons-medulla. The effect of morphine was partially attenuated by naloxone. Increased cerebellar noradrenergic histofluorescent staining was observed with the morphine + 6-OHDOPA and naloxone + 6-OHDOPA treatments. Both naloxone and morphine decreased NE levels in the pons-medulla of adult rats treated with 6-OHDOPA. These results suggest that opiates and endorphins may enhance sprouting of noradrenergic neurons following neonatal treatment with 6-OHDOPA, by increasing the toxicity of this neurotoxin.

Effect of corticosteroids on the production of superoxide and hydrogen peroxide and the appearance of chemiluminescence by phagocytosing polymorphonuclear leukocytes.

Human polymorphonuclear leukocytes were incubated with either methylprednisolone sodium succinate, hydrocortisone sodium succinate, or distilled water, and then latex spherules were added as target particles for phagocytosis. At low concentrations of these corticosteroids (0.04-0.22 mM), no effect was observed on O2-. production, H2O2 production, or chemiluminescence. At high concentrations of these steroids (2.7 mM), a significant inhibition was observed in both O2-. production and H2O2 production. At 2.7 mM, methylprednisolone sodium succinate significantly decreased chemiluminescence, whereas hydrocortisone sodium succinate was without effect on chemiluminescence.

Alar rim reconstruction by a dorsal nasal flap.

A method has been described to repair small to moderate full-thickness alar rim defects with a dorsal nasal flap. The flap is based inferiorly as a tiny axial pattern flap, and the dorsal nasal skin is rotated down and turned in on itself for lining. The donor site is closed with a full-thickness skin graft. The dog ear at the base re-forms the alar base.

MIF-I and postsynaptic receptor sites for dopamine.

In an attempt to determine the mechanism by which the tripeptide l-prolyl-l-leucyl-glycine amide (PLG, MIF-I) exerts its antiparkinsonian effect, the action of this substance on various postsynaptic components of striatal dopaminergic nerves was studied. It was shown that injection of rats with MIF-I (1 mg/kg, IPX5, 24 hr intervals) did not alter tyrosine hydroxylase, dopa decarboxylase, choline acetyltransferase and glutamic acid decarboxylase activities in the striatum under the conditions tested. The activities of adenylate cyclase, dopamine-stimulated adenylate cyclase, and guanylate cyclase were not altered in vitro by various concentrations of MIF-I (0.1 to 1000 micrometer), although VIP and neurotensin had some effect. Also the rate of uptake of 3H-dopamine by rat striatal synaptosomes was unchanged, as was the binding of 3H-dopamine and 3H-spiperone to beef caudate membranes. This series of studies indicates that MIF-I does not act directly on the striatal dopamine postsynaptic receptor under the conditions tested, although it is possible that MIF-I could act indirectly at this or another site in vivo by releasing or activating some other factor.

Monitoring the state of the human airways by analysis of respiratory sound.

A mechanism whereby sound is generated by the motion of vortices in the human lung is described. This mechanism is believed to be responsible for most of the sound which is generated both on inspiration and expiration in normal lungs. Mathematical expressions for the frequencies of sound generated, which depend only upon the axial flow velocity and diameters of the bronchi, are derived. This theory allows the location within the bronchial tree from which particular sounds emanate to be determined. Redistribution of pulmonary blood volume following transition from Earth gravity to the weightless state probably alters the caliber of certain airways and doubtless alters sound transmission properties of the lung. We believe that these changes can be monitored effectively and non-invasively by spectral analysis of pulmonary sound.

Source of hydrogen peroxide and of chemiluminescence observed in activated human platelet preparations.

Human platelet suspensions can be observed to produce small amounts of H2O2 (0.04 nmoles H2O2/min/2.5 X 10(5) cells/cu mm) and measurable chemiluminescence when exposed to target particles for phagocytosis, such as latex spherules. Both H2O2 production and chemiluminescence are characteristic of phagocytosing polymorphonuclear leukocytes (PMN) and analysis of the purified platelets indicates contamination by PMN at the level of 0.2%. The amount of H2O2 produced and the chemiluminescence observed can be duplicated by adding latex spheres to a preparation of PMN at a concentration equivalent to the contaminant in the platelet preparations. We conclude that the H2O2 produced and chemiluminescence observed from activated platelets is due to the presence of small amounts of contaminating PMN. These studies emphasize the importance of controlling for PMN contamination in studies of platelet biochemistry and physiology.