Dr. Barad joined the Pain Medicine faculty in 2008. Dr. Barad is a board-certified Neurologist, Headache and Pain physician. Her primary focus is helping patients with head and facial pain or pain related to other neurologic conditions such as Parkinson’s Disease, Multiple Sclerosis, and peripheral neuropathy. She has collaborated in creating a cross-disciplinary headache center, so that headache sufferers can benefit from the Pain Center’s comprehensive approach. She is also the Director of the Stanford Orofacial Pain Program.
Originally from Colorado, Dr. Barad completed her undergraduate studies in biology and honors liberal arts at the University of Texas, Austin, TX. She earned her medical degree from Stanford University School of Medicine and completed her internship at Santa Clara Valley Medical Center in San Jose, CA. She completed her Neurology residency and Pain Medicine fellowship at Stanford Hospital. Then she pursued a two-year research training fellowship studying neuroimaging and pain in the lab of Dr. Sean Mackey at Stanford. This research involved using functional magnetic resonance imaging (fMRI) to image the brain activation of a patient in chronic pain and train the patient to modify both the activation and experience of pain. In addition to seeing patients and developing the headache center, she helps train anesthesia residents and pain fellows and headache fellows and runs their educational lecture series.

Clinical Focus

  • Pain Management
  • Headache Disorders
  • Orofacial Pain
  • Pain Medicine

Academic Appointments

Administrative Appointments

  • Director Orofacial Pain Program, Stanford Hospital and Clinics (2014 - Present)

Professional Education

  • Internship:Santa Clara Valley Medical Center Radiology Residency (2004) CA
  • Board Certification: Headache Medicine, United Council for Neurologic Subspecialties (2012)
  • Board Certification, United Council for Neurologic Subspecialites, Headache (2012)
  • Residency:Stanford University School of Medicine (2007) CA
  • Medical Education:Stanford University School of Medicine (2003) CA
  • Board Certification: Pain Medicine, American Board of Psychiatry and Neurology (2009)
  • Board Certification: Neurology, American Board of Psychiatry and Neurology (2008)
  • Fellowship:Stanford Hospital and Clinics - Pain Mgmt (2008) CA

Community and International Work

  • National Take Back Day, Redwood City


    Return of unused medications

    Partnering Organization(s)

    Redwood City Police Departmet

    Populations Served

    Redwood City community


    Bay Area

    Ongoing Project


    Opportunities for Student Involvement


Research & Scholarship

Current Research and Scholarly Interests

My current research interests involve novel treatment paradigms for challenging pain problems such as orofacial pain, trigeminal neuralgia and low pressure headaches. I am also interested in migraine and trigeminal autonomic cephalgias. Finally I amI interested in the intersection between chronic pain and headache.

Clinical Trials

  • Sphenopalatine Ganglion Stimulation for the Treatment of Chronic Cluster Headache Recruiting

    The primary objective of the study is to demonstrate the safety and efficacy of SPG stimulation with the ATI Neurostimulation System when used to treat acute cluster attacks in chronic cluster headache patients.

    View full details


Graduate and Fellowship Programs

  • Pain Management (Fellowship Program)


All Publications

  • Complex regional pain syndrome is associated with structural abnormalities in pain-related regions of the human brain. journal of pain Barad, M. J., Ueno, T., Younger, J., Chatterjee, N., Mackey, S. 2014; 15 (2): 197-203


    Complex regional pain syndrome (CRPS) is a chronic condition that involves significant hyperalgesia of the affected limb, typically accompanied by localized autonomic abnormalities and frequently by motor dysfunction. Although central brain systems are thought to play a role in the development and maintenance of CRPS, these systems have not been well characterized. In this study, we used structural magnetic resonance imaging to characterize differences in gray matter volume between patients with right upper extremity CRPS and matched controls. Analyses were carried out using a whole brain voxel-based morphometry approach. The CRPS group showed decreased gray matter volume in several pain-affect regions, including the dorsal insula, left orbitofrontal cortex, and several aspects of the cingulate cortex. Greater gray matter volume in CRPS patients was seen in the bilateral dorsal putamen and right hypothalamus. Correlation analyses with self-reported pain were then performed on the CRPS group. Pain duration was associated with decreased gray matter in the left dorsolateral prefrontal cortex. Pain intensity was positively correlated with volume in the left posterior hippocampus and left amygdala, and negatively correlated with the bilateral dorsolateral prefrontal cortex. Our findings demonstrate that CRPS is associated with abnormal brain system morphology, particularly pain-related sensory, affect, motor, and autonomic systems.This paper presents structural changes in the brains of patients with CRPS, helping us differentiate CRPS from other chronic pain syndromes and furthering our understanding of this challenging disease.

    View details for DOI 10.1016/j.jpain.2013.10.011

    View details for PubMedID 24212070

  • Human Response to Unintended Intrathecal Injection of Botulinum Toxin PAIN MEDICINE Carroll, I., Fischbein, N., Barad, M., Mackey, S. 2011; 12 (7): 1094-1097


    Describe the first reported human intrathecal (IT) botulinum toxin injection.Case report.We report here the sequelae to an unintended IT injection of botulinum toxin type B (BTB) in a 60-year-old woman with chronic back pain.Following the IT administration of BTB, the patient experienced the onset of symmetric ascending stocking distribution painful dysesthesias, which persisted for approximately 6 months before receding. Objective neurologic deficits were not appreciated, and analgesic effects were prominently absent.Analgesic actions of botulinum toxins in animals and in humans have led to speculation that IT botulinum toxin might exert significant analgesic effects. The unusual and unexpected subsequent clinical course, neurologic sequelae, dysesthesias, and absence of analgesia suggest that botulinum toxin will not be a therapeutic modality to treat pain as proposed by those studying botulinum toxin in animal models.

    View details for DOI 10.1111/j.1526-4637.2011.01135.x

    View details for Web of Science ID 000292697100016

    View details for PubMedID 21627762

  • Serratus muscle stimulation effectively treats notalgia paresthetica caused by long thoracic nerve dysfunction: a case series. Journal of brachial plexus and peripheral nerve injury Wang, C. K., Gowda, A., Barad, M., Mackey, S. C., Carroll, I. R. 2009; 4: 17-?


    Currently, notalgia paresthetica (NP) is a poorly-understood condition diagnosed on the basis of pruritus, pain, or both, in the area medial to the scapula and lateral to the thoracic spine. It has been proposed that NP is caused by degenerative changes to the T2-T6 vertebrae, genetic disposition, or nerve entrapment of the posterior rami of spinal nerves arising at T2-T6. Despite considerable research, the etiology of NP remains unclear, and a multitude of different treatment modalities have correspondingly met with varying degrees of success. Here we demonstrate that NP can be caused by long thoracic nerve injury leading to serratus anterior dysfunction, and that electrical muscle stimulation (EMS) of the serratus anterior can successfully and conservatively treat NP. In four cases of NP with known injury to the long thoracic nerve we performed transcutaneous EMS to the serratus anterior in an area far lateral to the site of pain and pruritus, resulting in significant and rapid pain relief. These findings are the first to identify long thoracic nerve injury as a cause for notalgia paresthetica and electrical muscle stimulation of the serratus anterior as a possible treatment, and we discuss the implications of these findings on better diagnosing and treating notalgia paresthetica.

    View details for DOI 10.1186/1749-7221-4-17

    View details for PubMedID 19772656