A New Neuropathologic Mechanism of Blood pH Irregularities After Neck Trauma: Importance of Carotid Body-Glossopharyngeal Nerve Network Degeneration.

OBJECTIVE: We created a neck trauma model by injecting blood into the sheath of rabbits' carotid bodies (CBs). Then we determined the relationship between neuronal degeneration of the CB due to hemorrhage of this organ and its clinical effects such as blood pH and heart rhythm. METHODS: The present study included 24 adult male New Zealand rabbits. The animals were divided into 3 groups: control (n = 5); sham (0.5 mL saline injected into CBs; n = 5); and study (CB trauma model; n = 14). pH values and heart rhythms were recorded before the experiment to determine the values under normal conditions, and measurements were repeated thrice in the days following the experiment. The number of normal and degenerated neuron density of CBs was counted. The relationship between the blood pH values, heart rhythms, and degenerated neuron densities was analyzed. RESULTS: Heart rhythms were 218 ± 20 in the control group, 197 ± 16 in the sham group (P = 0.09), and 167 ± 13 in the study group (P < 0.0005). pH values were 7.40 ± 0.041 in the control group, 7.321 ± 0.062 in the sham group (P = 0.203), and 7.23 ± 0.02 in study group (P < 0.0005). Degenerated neuron densities were 12 ± 4/mm3 in the control group, 430 ± 74/mm3 in the sham group (P < 0.005), and 7434 ± 810/mm3 in the study group (P < 0.0001). CONCLUSIONS: A high degenerate neuron density in the CB can decrease blood pH and hearth rhythm after neck trauma, and there might be a close relationship between the number of degenerated neurons and clinical findings (such as heart rhythm and blood pH). This relationship suggests that injury to the glossopharyngeal nerve-CB network can cause acidosis by disturbing the breathing-circulating reflex and results in respiratory acidosis.

Vernet's syndrome after carotid endarterectomy.

Unilateral paresis of cranial nerves IX to XI is defined as Vernet's syndrome. We retrospectively assessed cranial nerve symptoms from the clinical records of 143 carotid endarterectomy patients. A flexible nasolaryngoscope was used to examine vocal fold movements in 73 patients. If vocal fold paresis (VFP) was confirmed, the patient also underwent magnifying laryngoscopy (for correct diagnosis of injury to the glossopharyngeal and vagus nerves). It was found from clinical records that 8 patients (6%) were confirmed to have cranial nerve symptoms corresponding to Vernet's syndrome; 7 patients (9 %) had VFP on nasolaryngoscopy. In 2 patients, magnifying laryngoscopy confirmed ipsilateral VFP, pharyngeal paresis, pharyngeal wall hypesthesia, and ipsilateral pharyngeal wall swelling. These 2 patients also had symptoms of injury to the accessory nerve. Damage to cranial nerves IX to XI probably occurred in the parapharyngeal space, based on the existence of posterior pharyngeal wall edema or swelling after carotid endarterectomy.