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Objective: We speculated that subarachnoid hemorrhage (SAH) induces ischemic lesions in the cranial parasympathetic nerves, which may decrease saliva secretion and lead to hyperthermia. We tested this hypothesis by examining histologic features of parotid glands and glossopharyngeal nerves (GPNs) in a rabbit model of SAH. Material and Methods: Rabbits (n = 25) were divided into control (n = 5), sham (n = 5), and SAH (n = 15) groups. Animals in the sham and SAH groups were examined over a 3week period before sacrifice. Salivation score (SC) was determined by measuring the mean wetted area of an orally inserted cotton ball. Sections of parotid glands and intracranial and intraparotideal branches of the GPNs were stained with hematoxylin and eosin and SAH-induced damage was analyzed by terminal deoxynucleotidyl transferase dUTP nick end labeling of apoptotic cells. Specimens were stereologically examined to determine saliva-filled total vesicle volume (TVV) per cubic meter; vasospasm index (VSI) based on wall/lumen ratio of parotid glands arteries, and degenerated neuron density (DND) of glossopharyngeal ganglia. Results: The mean oral temperature was 36.9°C. In the control group, mean values were as follows: SC, 46±8 mm2; DND, 19±4/mm3; VSI, 1.065±0.049; and TVV, (780±1187) × 106/μm3. In the sham group, mean values were as follows: SC, 31±6 mm2; DND, 98±23/mm3; VSI, 1.67±0.32; and TVV, (617±110) × 106/μm3. In the low hyperthermia SAH group, mean values were as follows: SC, 16±5 mm2; DND, 1520±261/mm3; VSI, 2.12±0.21, and TVV, (314±98) × 106/μm3. In the high hypothermia SAH group, mean values were as follows: SC, 9±2 mm2; DND, 3210±912/mm3; VSI, 3.18±0.30; and TVV, (432±99) × 106/μm3. Conclusions: Decreased salivary secretion due to secretory gland atrophy originated from ischemia-induced GPN network degeneration at the brainstem, which may be responsible for cranial hyperthermia following SAH.

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Cranial hyperthermia resulting from decreased parotid gland salivation induced by ischemic degeneration of glossopharyngeal network in subarachnoid hemorrhage