Congestive heart failure (CHF) is characterized by reduced heart rate variability. Although various methods to achieve parasympathetic withdrawal and sympathetic activation have been documented, stimulation of the vagal nerve (that is, vagal maneuvers) has not often been used to assess the autonomic impairment associated with disease progression in veterinary species. In this study, we investigated cardiac autonomic control in a naturally occurring canine model of mitral insufficiency by means of individual responses to oculocardiac reflex. Indices of heart rate variability were calculated from 5-min ECG tracings obtained before and after ocular compression. After compression, significant increases in the standard deviation of RR intervals, root mean square of the successive differences in RR intervals, and vasovagal tonus index were documented in healthy control animals. In addition, these indices were increased in asymptomatic dogs with remodeled hearts, but no variation occurred in symptomatic animals. Although only the percentage change in vasovagal tonus index differed significantly between controls and diseased dogs, all other parameters showed a tendency to behave the opposite way in the symptomatic group as in the control and asymptomatic groups. Our results document CHF-dependent autonomic dysfunction in a canine model of valve insufficiency.

Triple A (Allgrove) syndrome, an autosomal recessive disease is characterized by achalasia, alacrimia and ACTH-resistant adrenal failure with progressive neurological syndrome including central, peripheral and autonomic nervous system impairment, and mild mental retardation. The triple A syndrome gene, designated AAAS, localized on chromosome 12q 13 encodes for a 546 amino acid protein called ALADIN (Alacrimia-Achlasia-Adrenal Insufficiency and Neurologic disorder). This report relates to two sisters, aged 8 and 12 years, who had vomiting, muscle weakness, alacrimia, excessive fatigue and dysphagia. Abdominal sonography, esophago-gastroduodenoscopy, barium swallow, esophageal manometry, CT scan abdomen and brain, biochemical profiles, as well as neurologic and ophthalmic evaluations were consistent with Allgrove's syndrome. Management consisted of pneumatic balloon dilatation for achalasia and initiation of cortisone therapy with successful resolution of dysphagia and other symptoms.

Pediatric aspiration is a multifactorial process that is often complex to manage. Recurrent laryngeal nerve (RLN) injury can cause glottic insufficiency and aspiration. We describe three cases of unilateral vocal fold paralysis resulting in aspiration and the successful use of the RLN reinnervation for its treatment. The theory for utilizing the reinnervation procedure is that when glottic closure improves and a less breathy vocalization occurs, then the larynx is better equipped to protect the lower airway and avoid aspiration. Our cases demonstrate stronger voice and improved swallow function, with normalization of modified barium swallow evaluation, at approximately 6-months post reinnervation.

The pathologic consequences of sodium retention in the CKD population can lead to hypertension, edema, and progressive disease. Sodium excess is responsible for increases in oxidative stress, which alters kidney vasculature. As progression of CKD occurs, hyperfiltration by remaining nephrons compensates for an overall decrease in the filtered load of sodium. In the later stages of CKD, compensatory mechanisms are overcome and volume overload ensues. Nephrotic syndrome as it relates to sodium handling involves a different pathophysiology despite a common phenotype. Extrarenal sodium buffering is also examined as it has significant implications in the setting of advanced CKD.