Pharyngeal diverticulum as a sequela of anterior cervical fusion.

A rarely diagnosed etiology of dysphagia is a pharyngeal diverticula occurring after anterior cervical fusion. Here we review 2 cases where patients developed pharyngeal diverticula following anterior cervical fusion. The first patient was a 28-year-old female who presented with regurgitation following C5 through C6 cervical fusion. She was diagnosed with a pharyngeal diverticulum and underwent open repair, but began to experience symptoms again a few months later. A barium swallow showed a recurrent pharyngeal diverticulum. Endoscopic repair was attempted; however, because of the thick scar band between the diverticulum and the esophagus, the operation had to be converted to an open repair with cricopharyngeal myotomy. The second case involved a 63-year-old male who presented with dysphagia and regurgitation 6 months after anterior cervical fusion. Esophagram demonstrated a small diverticulum at the right lateral border of the upper esophagus. Open repair of the diverticulum with cricopharyngeal myotomy was successfully performed. Pharyngeal diverticula after anterior cevical fusion have only been reported in 2 prior cases in the literature. Here we describe 2 additional cases at our institution, both requiring open repair. Radiographic studies demonstrate the diverticulum at the site of scarring from the cervical fusion. Because of the thick scar band and the atypical location of these diverticula, endoscopic repair with stapping (as done for Zenker's diverticula) may not be feasible. These cases highlight the importance of considering a diverticulum in the differential of posoperative patients presenting to the otolaryngologists with complaints of dysphagia following cevical spine surgery.

Cortical spreading depression produces long-term disruption of activity-related changes in cerebral blood volume and neurovascular coupling.

Cortical spreading depression (CSD) is a pronounced depolarization of neurons and glia that spreads slowly across the cortex followed by a period of depressed electrophysiological activity. The vascular changes associated with CSD are a large transient increase in blood flow followed by a prolonged decrease lasting greater than 1 h. Currently, the profile of functional vascular activity during this hypovolemic period has not been well characterized. Perfusion-based imaging techniques such as functional magnetic resonance imaging (fMRI) assume a tight coupling between changes in neuronal and vascular activity. Under normal conditions, these variables are well correlated. Characterizing the effect of CSD on this relationship is an important step to understand the impact acute pathophysiological events may have on neurovascular coupling. We examine the effect of CSD on functional changes in cerebral blood volume (CBV) evoked by cortical electrophysiological activity for 1 h following CSD induction. CBV signal amplitude, duration, and time to peak show little recovery at 60 min post-induction. Analysis of spontaneous vasomotor activity suggests a decrease in vascular reactivity may play a significant role in the disruption of normal functional CBV responses. Electrophysiological activity is also attenuated but to a lesser degree. CBV and evoked potentials are not well correlated following CSD, suggesting a breakdown of the neurovascular coupling relationship.

Multiwavelength optical intrinsic signal imaging of cortical spreading depression.

Cortical spreading depression (CSD) is an important disease model for migraine and cerebral ischemia. In this study, we exploit the high temporal and spatial resolution of optical imaging to characterize perfusion-dependent and -independent changes in response to CSD and to investigate the etiology of reflectance changes during CSD. In this experiment, we characterized the optical response to CSD at wavelengths that emphasize perfusion-related changes (610 and 550 nm), and we compared these results with 850 nm and blood volume data. Blood volume changes during CSD were recorded using an intravascular fluorescent dye, Texas Red dextran. We observed triphasic optical signals at 850 and 550 nm characterized by spreading waves of increased, decreased, then increased reflectance (Fig. 1) which expanded at a rate of approximately 3-5 mm/min. The signal at 610 nm had a similar initial phase, but the phase 2 response was slightly more complex, with a parenchymal decrease in reflectance but a vascular increase in reflectance. Reflectance values decreased in phase three. Blood volume signals were delayed relative to the optical intrinsic signals and corresponded temporally to phases 2 and 3. This is the first study to characterize optical imaging of intrinsic signal responses to CSD, in vivo, at multiple wavelengths. The data presented here suggest that changes in light scattering precede perfusion responses, the blood volume increase (phase 2) is accompanied by a reduction in deoxyhemoglobin, and the blood volume decrease (phase 3) is accompanied by an increase in deoxyhemoglobin. Previous studies have suggested the oligemia of spreading depression was a result of decreased metabolic demand. This study suggests that during the oligemic period there is a greater reduction in oxygen delivery than in demand.