Parthasarathy D. Thirumala, MD

Clinical Associate Professor of Neurological Surgery & Neurology
Co-Director, Center of Clinical Neurophysiology


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412-648-2570

Biography

Parthasarathy D. Thirumala, MD, joined the Center of Clinical Neurophysiology in June 2008. Dr. Thirumala specializes in intraoperative neurophysiological monitoring to adult and pediatric neurosurgical, orthopedic, ENT, vascular and interventional neuroradiology procedures.

Dr. Thirumala completed his neurology residency and clinical neurophysiology fellowship training at the University of Pittsburgh Medical Center. He completed his internship in internal medicine training at Brookdale University Hospital and Medical Center in Brooklyn, NY. Prior to clinical training he completed his masters in biomedical engineering at the University of Illinois at Chicago. Dr. Thirumala completed his medical training in India at Stanley Medical College in Chennai, India.

Prior to joining the department, Dr. Thirumala was in private practice providing intraoperative neurophysiological monitoring services. His group was one of the largest physician groups in the country providing intraoperative neurophysiological to approximately 90 hospitals across 12 states in the United States.

His clinical and research interests include intraoperative neurophysiological monitoring during expanded endonasal approach, functional cortical mapping during awake craniotomies, ICU EEG.

He has published over 15 peer reviewed articles, book chapters, and invited articles in the journals including Neurosurgery, Journal of Neurosurgery, and Journal of Clinical Neurophysiology. He has given lectures both nationally and internationally on the value of intraoperative neurophysiological monitoring.

Dr. Thirumala's publications can be reviewed through the National Library of Medicine's publication database.

Board Certifications

American Board of Clinical Neurophysiology: Intraoperative Monitoring
American Board of Psychiatry and Neurology: Subspecialty Clinical Neurophysiology
American Board of Psychiatry and Neurology
American Board of Neuroimaging
American Board of Neurophysiologic Monitoring

Hospital Privileges

Children’s Hospital of Pittsburgh of UPMC
Jameson Hospital
Magee-Womens Hospital of UPMC
Mon Valley Hospital
UPMC Braddock
UPMC Horizon-Greenville
UPMC Mercy
UPMC Passavant
UPMC Presbyterian
UPMC St. Margaret
UPMC Shadyside

Professional Organization Membership

American Academy of Neurology
American Clinical Neurophysiology Society
American Medical Association
American Society of Neurophysiological Monitoring
American Society of Electroneurodiagnostic Technologists
American Telemedicine Association

Research Activities

1) The Role of Changes in Neurophysiologic Monitoring as a Predictor of Neurologic Deficit or Procedural Complication During the Endovascular Treatment of Cerebral Aneurysms

Endovascular management of cerebral aneurysms carries with it inherent risks of procedure related ischemia and hemorrhage. Few studies have examined the use and efficacy of neurophysiologic monitoring in predicting neurologic deficits or procedural complications. This study represents the largest published patient series investigating the use and value of neurophysiologic monitoring as an adjunct to endovascular cerebral aneurysm treatment.

Patients presenting between October 2000 and July 2010 (n=2016) who underwent endovascular treatment of cerebral aneurysms with neurophysiologic monitoring were included in this study. Neurophysiologic monitoring included somatosensory evoked potentials (SSEP), electroencephalography (EEG), and brainstem auditory evoked potentials (BAEP). Changes in SSEPs were characterized as significant change in responses (SCR), transient loss of responses (TLR) and complete loss of responses (CLR). Neurologic changes were defined as transient or permanent deficits not present prior to the procedure or rapid progression to death following a procedural complication. Procedural complications were defined as procedural rupture,embolic phenomenon, catheter related vasospasm and arterial dissection.

Neurologic changes were observed in 64 patients and procedural complications observed in 38 patients. Changes in neurophysiologic monitoring were observed in 123 patients. The sensitivity and specificity of changes in neurophysiologic monitoring were 0.62 and 0.93 respectively. The positive and negative predictive values of neurophysiologic changes were 0.41 and 0.97 respectively. When compared to the population with no changes in responses, odds ratios for neurologic changes or procedural complications were as follows: SCR 16.2 (95% CI 8.9- 29.1), TLR 55.1 (95% CI 18.3-164.8) and CLR 146.8 (29.8-721.7).

Neurophysiologic monitoring can be a powerful adjunct to the endovascular treatment of cerebral aneurysms. Proper characterization of the witnessed changes can increase the predictive value of a positive test result and potentially aid in the recognition of reversible neurologic deficits. 

2) Analysis of Wave III of Brain Stem Auditory Evoked Potential Durig Microvascular Decompression of Cranial Nerve VII for Hemifacial Spasm

Intraoperative monitoring (IOM) of brainstem auditory evoked potential (BAEP) during microvascular decompression (MVD) prevents hearing loss (HLS) in patients with hemifacial spasm. Previous studies have shown changes in wave III (wIII) is an early sign of auditory nerve injury.

Dr. Thirumala retrospectively analyzed the BAEP data of 156 patients who undergone MVD in our institute. HLS was classified by AAO-HNS criteria, based on changes in pure tone audiometry and speech discrimination score. Dr. Thirumala analyzed amplitude or latency of wIII at various time periods and compared it with baseline. He did one way ANOVA using mean, median and standard errors of wIII at different time periods to find its significance. A stepwise logistic regression was performed to assess the significant independent associations of BAEP parameters with HLS. 

Amplitude or latency of wIII were significant between groups (p<0.05) but regression analysis did not find wIII changes to increase the odds of HLS. wIII seems to be changed early (Dura open and change start I) in both amplitude and latency but none of them is statistically significant with one way ANOVA analysis. Correlation analysis did not find any positive relation between wIII and wV. 

Changes in wIII did not increase the odds of HLS in patients who underwent BAEPs during MVD. This information might be valuable to evaluate the value of wIII as alarm criteria during MVD to prevent HLS.