Theresa Lii, M.D., currently holds the positions of Clinical Scholar and postdoctoral researcher at Stanford University, and is part of the Stanford Fellowship in Anesthesia Research (FARM) program. Her research interests include evaluating the effectiveness of non-opioid pharmacologic treatments for chronic pain, as well as exploring the impact of rapid-acting psychiatric interventions for patients with acute and chronic pain.

Clinical Focus

  • Pain Medicine
  • Pain Management

Professional Education

  • Board Certification: American Board of Anesthesiology, Pain Management (2022)
  • Board Certification: American Board of Anesthesiology, Anesthesiology (2022)
  • Fellowship: Stanford University Pain Management Fellowship (2021) CA
  • Residency: Stanford University Anesthesiology Residency (2020) CA
  • Internship: Santa Clara Valley Medical Center Dept of Medicine (2017) CA
  • Medical Education: Warren Alpert Medical School Brown University (2016) RI
  • Bachelor of Science, Brown University, Neuroscience (2012)

Current Research and Scholarly Interests

Ketamine for acute and chronic pain management

Research Projects

  • Intraoperative Ketamine Versus Saline in Depressed Patients Undergoing Anesthesia for Non-Cardiac Surgery

    Randomized clinical trial (NCT 03861988)


    Stanford, CA


    Stanford University

All Publications

  • Management of Postoperative Pain in Patients Following Spine Surgery: A Narrative Review. International journal of general medicine Prabhakar, N. K., Chadwick, A. L., Nwaneshiudu, C., Aggarwal, A., Salmasi, V., Lii, T. R., Hah, J. M. 2022; 15: 4535-4549


    Perioperative pain management is a unique challenge in patients undergoing spine surgery due to the increased incidence of both pre-existing chronic pain conditions and chronic postsurgical pain. Peri-operative planning and counseling in spine surgery should involve an interdisciplinary approach that includes consideration of patient-level risk factors, as well as pharmacologic and non-pharmacologic pain management techniques. Consideration of psychological factors and patient focused education as an adjunct to these measures is paramount in developing a personalized perioperative pain management plan. Understanding the currently available body of knowledge surrounding perioperative opioid management, management of opioid use disorder, regional/neuraxial anesthetic techniques, ketamine/lidocaine infusions, non-opioid oral analgesics, and behavioral interventions can be useful in developing a comprehensive, multi-modal treatment plan among patients undergoing spine surgery. Although many of these techniques have proved efficacious in the immediate postoperative period, long-term follow-up is needed to define the impact of such approaches on persistent pain and opioid use. Future techniques involving the use of precision medicine may help identify phenotypic and physiologic characteristics that can identify patients that are most at risk of developing persistent postoperative pain after spine surgery.

    View details for DOI 10.2147/IJGM.S292698

    View details for PubMedID 35528286

  • Comparison of intravenous lidocaine versus epidural anesthesia for traumatic rib fracture pain: a retrospective cohort study. Regional anesthesia and pain medicine Lii, T. R., Aggarwal, A. K. 2020


    BACKGROUND: Effective analgesia is essential in managing traumatic rib fractures. Intravenous lidocaine (IVL) is effective in treating perioperative pain, acute pain in the emergency department, cancer pain in hospice, and outpatient chronic neuropathic pain. Our study examined the associations between IVL versus epidural analgesia (EA) and pain for the treatment of acute rib fracture in the inpatient setting.METHODS: We performed a retrospective study involving adults admitted to an academic level I trauma center from June 1, 2011 to June 1, 2016 with consults to the pain service for acute rib fracture pain. Eighty-nine patients were included in the final analysis (54 IVL and 35 EA patients). Both groups had usual access to opioid medications. The primary outcome was absolute change in numeric pain scores during 0-24 and 24-48hours after initiating IVL or EA, compared with baseline. Secondary outcomes include opioid consumption, incentive spirometry, supplemental oxygens, pneumonia, endotracheal intubation and length of hospital stay.RESULTS: Numeric pain scores differed at baseline (mean 5.6 for IVL vs 4.5 for EA, p=0.01), while age, injury severity, and number of fractured ribs were similar. IVL and EA were associated with similar reductions in numeric pain scores within 0-24 and 24-48hours (mean -2.9 for IVL vs -2.3 for EA during both periods, p=0.19and p=0.17 respectively) . There was greater non-neuraxial opioid consumption with IVL compared with EA (98.6 vs 22.3 mg morphine equivalents (MME) at 0-24hours, p=0.0005; 105.6 vs 18.9 MME at 24-48hours, p<0.0001). When epidural opioids were analyzed, the EA group was exposed to higher total MME at 0-24hours (655.2 vs 98.6 MME, p<0.0001) and 24-48hours (586 vs 105.6 MME, p=0.0001), suggesting an opioid sparing effect of IVL.CONCLUSION: Our results suggest that IVL is similar to EA in numeric pain score reduction, and that IVL may have an opioid sparing effect when taking neuraxial opioids into account. IVL may be an effective alternative to epidurals for the treatment of rib fracture pain. It should be considered for patients who have contraindications to epidurals or are unable to receive an epidural in a timely manner.

    View details for DOI 10.1136/rapm-2019-101120

    View details for PubMedID 32503863

  • Electroencephalographic signatures of pain and analgesia in rats. Pain LeBlanc, B. W., Bowary, P. M., Chao, Y. C., Lii, T. R., Saab, C. Y. 2016; 157 (10): 2330–40


    Pain modulates rhythmic neuronal activity recorded by Electroencephalography (EEG) in humans. Our laboratory previously showed that rat models of acute and neuropathic pain manifest increased power in primary somatosensory cortex (S1) recorded by electrocorticography (ECoG). In this study, we hypothesized that pain increases EEG power and corticocortical coherence in different rat models of pain, whereas treatments with clinically effective analgesics reverse these changes. Our results show increased cortical power over S1 and prefrontal cortex (PFC) in awake, freely behaving rat models of acute, inflammatory and neuropathic pain. Coherence between PFC and S1 is increased at a late, but not early, time point during the development of neuropathic pain. Electroencephalography power is not affected by ibuprofen in the acute pain model. However, pregabalin and mexiletine reverse the changes in power and S1-PFC coherence in the inflammatory and neuropathic pain models. These data suggest that quantitative EEG might be a valuable predictor of pain and analgesia in rodents.

    View details for DOI 10.1097/j.pain.0000000000000652

    View details for PubMedID 27347647

  • T-type calcium channel blocker Z944 restores cortical synchrony and thalamocortical connectivity in a rat model of neuropathic pain. Pain LeBlanc, B. W., Lii, T. R., Huang, J. J., Chao, Y. C., Bowary, P. M., Cross, B. S., Lee, M. S., Vera-Portocarrero, L. P., Saab, C. Y. 2016; 157 (1): 255–63


    Oscillations are fundamental to communication between neuronal ensembles. We previously reported that pain in awake rats enhances synchrony in primary somatosensory cortex (S1) and attenuates coherence between S1 and ventral posterolateral (VPL) thalamus. Here, we asked whether similar changes occur in anesthetized rats and whether pain modulates phase-amplitude coupling between VPL and S1. We also hypothesized that the suppression of burst firing in VPL using Z944, a novel T-type calcium channel blocker, restores S1 synchrony and thalamocortical connectivity. Local field potentials were recorded from S1 and VPL in anesthetized rats 7 days after sciatic chronic constriction injury (CCI). In rats with CCI, low-frequency (4-12 Hz) synchrony in S1 was enhanced, whereas VPL-S1 coherence and theta-gamma phase-amplitude coupling were attenuated. Moreover, Granger causality showed decreased informational flow from VPL to S1. Systemic or intrathalamic delivery of Z944 to rats with CCI normalized these changes. Systemic Z944 also reversed thermal hyperalgesia and conditioned place preference. These data suggest that pain-induced cortical synchrony and thalamocortical disconnectivity are directly related to burst firing in VPL.

    View details for DOI 10.1097/j.pain.0000000000000362

    View details for PubMedID 26683108

  • Cortical theta is increased while thalamocortical coherence is decreased in rat models of acute and chronic pain. Pain Leblanc, B. W., Lii, T. R., Silverman, A. E., Alleyne, R. T., Saab, C. Y. 2014; 155 (4): 773–82


    Thalamocortical oscillations are critical for sensory perception. Although pain is known to disrupt synchrony in thalamocortical oscillations, evidence in the literature is controversial. Thalamocortical coherence has been reported to be increased in patients with neurogenic pain but decreased in a rat model of central pain. Moreover, theta (4 to 8 Hz) oscillations in primary somatosensory (S1) cortex are speculated to predict pain in humans. To date, the link between pain and network oscillations in animal models has been understudied. Thus, we tested the hypothesis that pain disrupts thalamocortical coherence and S1 theta power in two rat models of pain. We recorded electrocorticography (ECoG) waveforms over S1 and local field potentials (LFP) within ventral posterolateral thalamus in freely behaving rats under spontaneous (stimulus-independent) pain conditions. Rats received intradermal capsaicin injection (Cap) in the hindpaw, followed hours later by chronic constriction injury (CCI) of the sciatic nerve lasting several days. Our results show that pain decreases coherence between LFP and ECoG waveforms in the 2- to 30-Hz range, and increases ECoG power in the theta range. These changes are short-lasting after Cap and longer-lasting after CCI. These data might be particularly relevant to preclinical correlates of spontaneous pain-like behavior, with potential implications to clinical biomarkers of ongoing pain.

    View details for DOI 10.1016/j.pain.2014.01.013

    View details for PubMedID 24457192