Post-operative dysphagia following ventral cervical approach: complication or side-effect? Retrospective analysis and review of the literature.

OBJECTIVE: To ameliorate the clinical decision-making process when debating between a ventral or dorsal cervical approach by elucidating whether post-operative dysphagia be regarded as a complication or a transient side effect. METHODS: A literature review of studies comparing complication rates following ventral and dorsal cervical approaches was performed. A stratified complication rate excluding dysphagia was calculated and discussed. A retrospective cohort of patients operated for degenerative cervical myelopathy in a single institution comprising 665 patients was utilized to analyze complication rates using a uniform definition for dysphagia. RESULTS: Both the ventral and the dorsal approach groups exhibited comparable neurological improvement rates. Since transient dysphagia was not considered a complication, the dorsal approach was associated with higher level of overall complications. CONCLUSIONS AND RELEVANCE: Inconsistencies in the definition of dysphagia following ventral cervical surgery impedes the interpretation of trials comparing dorsal and ventral complication rates. A uniform definition for complications and side effects may enhance the validity of medical trials.

BCKDK regulates the TCA cycle through PDC in the absence of PDK family during embryonic development.

Pyruvate dehydrogenase kinases (PDK1-4) inhibit the TCA cycle by phosphorylating pyruvate dehydrogenase complex (PDC). Here, we show that PDK family is dispensable for murine embryonic development and that BCKDK serves as a compensatory mechanism by inactivating PDC. First, we knocked out all four Pdk genes one by one. Surprisingly, Pdk total KO embryos developed and were born in expected ratios but died by postnatal day 4 because of hypoglycemia or ketoacidosis. Moreover, PDC was phosphorylated in these embryos, suggesting that another kinase compensates for PDK family. Bioinformatic analysis implicated branched-chain ketoacid dehydrogenase kinase (Bckdk), a key regulator of branched-chain amino acids (BCAAs) catabolism. Indeed, knockout of Bckdk and Pdk family led to the loss of PDC phosphorylation, an increase in PDC activity and pyruvate entry into the TCA cycle, and embryonic lethality. These findings reveal a regulatory crosstalk hardwiring BCAA and glucose catabolic pathways, which feed the TCA cycle.