Cough and paradoxical vocal fold motion

OBJECTIVES: The differential diagnosis and treatment of patients with chronic cough, paradoxical vocal fold motion, and disordered breathing can be a challenge to most practicing otolaryngologists. Tracheobronchial (ie, asthma, bronchitis, and tracheal stenosis), laryngeal (ie, vocal fold paralysis and neoplasms), and rhinologic (ie, allergies and rhinosinusitis) etiologies are commonly diagnosed and treated effectively. However, occasionally one is faced with patients who are refractory to medical treatment and have no obvious rhinologic, laryngeal or pulmonary cause. STUDY DESIGN AND SETTING: We conducted a review of the literature. METHODS: We present a thorough review of the current medical literature exploring the complex neurologic mechanisms involved in the production of cough and the relationship between gastroesophageal reflux disease, vagal neurapathy, and paradoxical vocal fold motion. RESULTS: The diagnosis and successful treatment of chronic cough can be complex. It requires a thorough understanding of the neurologic mechanisms behind cough excitation and suppression. Successful treatment strategies include aggressive management of the patient's reactive airway disease, gastroesophageal reflux disease, and, in select cases, paradoxical vocal fold motion. This may involve a well-coordinated effort among pulmonologists, otolaryngologists, gastroenterologists, and speech pathologists. CONCLUSION: Gastroesophageal reflux disease, vagal neuropathy, and paradoxical vocal fold motion are additional causes of chronic cough and disordered breathing that need to be considered, in the absence of obvious laryngotracheal and/or rhinologic pathology. A high index of suspicion is essential in making the diagnosis and formulating an effective multidisciplinary treatment plan for these patients.     

Leptin, lipid and lipid metabolism-related hormones in chronic renal failure in Arabia

SUMMARY: In patients with chronic renal failure (CRF), hyperleptinaemia has been widely reported, but the exact mechanisms leading to elevated leptin levels are unclear. Impaired renal clearance of leptin and the influence of other hormones may be important. In this study, we measured serum leptin levels in 150 patients on haemodialysis, peritoneal dialysis or in the predialysis phase of CRF. Furthermore, we measured plasma levels of insulin, growth hormone (GH) and insulin-like growth factor 1 (IGF-1), as well as plasma levels of triacylglycerols and total low density lipoprotein (LDL)- and high density lipoprotein (HDL)-cholesterol. We observed significantly elevated levels of leptin, particularly in female patients, and leptin was shown to correlate significantly with insulin, total and LDL-cholesterol and log triacylglycerols. Leptin was inversely correlated with GH concentrations, but was not correlated with IGF-1 levels. Despite the multiple correlations established between leptin levels and other variables, only hyperinsulinaemia in CRF seems to be important as a determinator of leptin levels.     

Antipeptide antibodies against the 5-HT1A receptor.

The availability of the primary amino acid sequence for a large number of molecules provides a fruitful opportunity for their cellular localization by utilizing the procedure of antipeptide antibody formation. This procedure permits a synthetic peptide sequence to be attached to a carrier molecule for the purpose of inoculating an animal to raise specific antibodies against the selected protein sequence. In this report we describe a number of steps that can be taken to increase the likelihood that the selected peptide sequence will be specific and antigenic. In addition, we describe how the peptides are synthesized, purified and coupled to keyhold limpet hemocyanin. The preparation of the antibody and its characterization are also presented in this method report. The immunocytochemical staining at both the light and ultrastructural level with serotonin (5-HT1A) receptor antipeptide antibodies is discussed. The advantages and disadvantages of this procedure are summarized.     

Prenatal cocaine exposure disrupts the development of the serotonergic system.

Prenatal cocaine exposure has been found to result in a number of neurobehavioral abnormalities in both clinical and laboratory studies. We have previously shown that cocaine inhibits the growth of developing serotonin neurons in culture. This study examines the effects of cocaine on the developing serotonin system in vivo. Pregnant rats were injected with cocaine (40 mg/kg s.c.) from gestational day 13 to parturition. One group of rats was additionally injected on postnatal days 1-5 with cocaine (10 mg/kg s.c.). [3H]Paroxetine, a selective ligand for the serotonin uptake carrier, was used to quantify serotonin terminal fiber density at one day, one week, and four weeks postnatal. Cocaine exposure was found to significantly decrease [3H]paroxetine-labelled sites and thus the density of serotonin fibers in the cortex and hippocampus at one day and one week postnatal. By four weeks postnatal, no significant effect was observed, indicating that a recovery had occurred. Serotonin immunocytochemistry performed at one month revealed normal fiber distribution in the cortex but a loss of fibers in the CA1 and CA2 hippocampal fields. Postnatal treatment alleviated the effects of prenatal cocaine exposure, resulting in [3H]paroxetine binding levels at one week which were comparable to and, in the cortex, even higher than those of saline controls. We conclude that cocaine delays the maturation of the serotonin system when administered prenatally but may accelerate maturation when administered both pre- and postnatally.     

Preoperative risk stratification using gated myocardial perfusion studies in patients with cancer.

Cancer patients frequently have anemia or an altered coagulation state that may affect their risk stratification for perioperative cardiac events. We performed this study to investigate the incidence of perioperative cardiac events in cancer patients who had abnormal stress myocardial perfusion imaging (MPI) results versus cancer patients with normal MPI results. METHODS: We included 394 consecutive cancer patients with normal (n = 201) or abnormal (n = 193) results on MPI studies performed for preoperative risk stratification. MPI was performed within 6 mo before each patient's scheduled operation. All the patients had surgical procedures requiring general anesthesia, except for 18 who had endoscopic or colonoscopic procedures. We retrospectively reviewed their data for the incidence of major cardiac events intraoperatively and for 1 mo postoperatively. We collected data on their cancer type, risk factors for coronary artery disease, MPI findings, risk of operation, and intraoperative or postoperative major cardiac events, which included death, myocardial infarction (MI), and congestive heart failure (CHF). RESULTS: The patients with abnormal MPI results included 97 with ischemia, 80 with scarring, and 16 with mixed scarring and ischemia. The mean left ventricular ejection fraction and end-diastolic volume were 63.8% +/- 9.8% and 82.0 +/- 53.5 mL in the normal MPI group versus 52.1% +/- 13.1% and 118.1 +/- 53.4 mL in the abnormal-MPI group (P < 0.001). There were 9 major intraoperative or postoperative cardiac events (4.7%) in the patients with abnormal MPI results and none in the patients with normal MPI results (P = 0.001). These major events consisted of 3 deaths, 2 acute MIs, 1 non-Q-wave MI, and 3 cases of CHF. Four of these patients had only scarring on their MPI studies, 3 had ischemia, and 2 had scarring and ischemia. CONCLUSION: Normal MPI results have a high negative predictive value for perioperative cardiac events in cancer patients. Abnormal MPI results, whether demonstrating scarring or ischemia, should prompt appropriate perioperative management in patients with cancer to minimize major cardiac events.