SPECT studies
In a study by Joo et al., the researchers performed interictal studies, meaning they scanned the patients brain between attacks to find an underlying abnormality, rather than ictal scans, which look at the abnormalities that present themselves during an attack. The researchers found interictally decreased cerebral blood flow in the posterior parts of the bilateral caudate nucleus. However, the literature does state that although this could be a cause of PKD, it could also be a result of PKD. Another SPECT study showed an increase in the cerebral blood flow in the left posterior thalamus in a PKD patient during an attack. The researchers also subtracted the ictal from the postictal scans, and saw increased blood flow in the thalamus. They ultimately suggested that hyperactive blood flow in this area could be causing the pathophysiology of PKD. This study, however, was only performed on one patient, and would need to be replicated many more times in order to be generalized to the population of PKD patients. Other SPECT studies have been cited showing hyperactivity in the basal ganglia. fMRI studies
In a study by Zhou et al., the researchers performed fMRI studies on PKD patients, and analyzed the differences between the amplitude low frequency fluctuations (ALFF) of the patients. They found that the left postcentral gyrus and the bilateral putamen had increased ALFF in PKD patients. The researchers concluded that the hyperactivity in these regions suggested that there is a dysfunction in the basal ganglia-thalamo-cortical circuit in PKD.
Microliths could possibly form reservoirs, thus allowing infection to ascend further towards the glands but this could not be confirmed due to the liths and microliths being distinct in this study. However, many glands did show only very minimal variations, which could allow the opportunity for more conservative treatment instead of the surgical removal of the affected gland in the future. Histopathology
Initial stage of acute bacterial sialadenitis involves the accumulation of bacteria, neutrophils and inspissated fluid in lumen of ductal structures. Damage to ductal epithelium results in sialodochitis (periductal inflammation), accumulation of neutrophils in glandular stroma, followed by acini necrosis with microabscesses formation. Recurrent episodes results in chronic stage, which involves the establishment of periductal lymph follicles and further destruction of salivary acini. Infective sialadenitis
Generally, in acute bacterial and viral sialadenitis cases, the lobular architecture of the gland is maintained or may be slightly expanded. Areas of liquefaction, indicating presence of abscess, may also be seen microscopically. In Acute bacterial sialadenitis, acinar destruction with interstitial neutrophil infiltrates is observed. Small abscesses with necrosis are common.