Research Publications Spotlight

Bullock WM, Yalamuri SM, Gregory SH, Auyong DB, Grant SA. Ultrasound-Guided Suprainguinal Fascia Iliaca Technique Provides Benefit as an Analgesic Adjunct for Patients Undergoing Total Hip Arthroplasty. J Ultrasound Med. 2016 Dec 10. doi: 10.7863/ultra.16.03012. [Epub ahead of print]


Analgesia after total hip arthroplasty is often accomplished by the fascia iliaca compartment block, traditionally performed below the inguinal ligament, to anesthetize both femoral and lateral femoral cutaneous nerves. The course of the lateral femoral cutaneous nerve below the inguinal ligament is variable as opposed to consistent above the inguinal ligament in the pelvis. In this case series including 5 patients, we demonstrate that an ultrasound-guided suprainguinal fascia iliaca approach would consistently anesthetize the lateral femoral cutaneous nerve along with anterior cutaneous femoral nerve branches and provide cutaneous analgesia after total hip arthroplasty, as shown by decreased opioid consumption.

Low YH, Brudney CS, Pyati S. The Significance (Or the Insignificance) of Wide Pulse Pressure. Indian J Anaesth. 2016 Nov;60(11):864-866.

Han Q, Kim YH, Wang X, Liu D, Zhang ZJ, Bey AL, Lay M, Chang W, Berta T, Zhang Y, Jiang YH, Ji RR. SHANK3 Deficiency Impairs Heat Hyperalgesia and TRPV1 Signaling in Primary Sensory Neurons. Neuron. 2016 Nov 24. pii: S0896-6273(16)30845-5. [Epub ahead of print]


Abnormal pain sensitivity is commonly associated with autism spectrum disorders (ASDs) and affects the life quality of ASD individuals. SHANK3 deficiency was implicated in ASD and pain dysregulation. Here, we report functional expression of SHANK3 in mouse dorsal root ganglion (DRG) sensory neurons and spinal cord presynaptic terminals. Homozygous and heterozygous Shank3 complete knockout (Δe4-22) results in impaired heat hyperalgesia in inflammatory and neuropathic pain. Specific deletion of Shank3 in Nav1.8-expressing sensory neurons also impairs heat hyperalgesia in homozygous and heterozygous mice. SHANK3 interacts with transient receptor potential subtype V1 (TRPV1) via Proline-rich region and regulates TRPV1 surface expression. Furthermore, capsaicin-induced spontaneous pain, inward currents in DRG neurons, and synaptic currents in spinal cord neurons are all reduced after Shank3 haploinsufficiency. Finally, partial knockdown of SHANK3 expression in human DRG neurons abrogates TRPV1 function. Our findings reveal a peripheral mechanism of SHANK3, which may underlie pain deficits in SHANK3-related ASDs.