GyRL

847-570-2622

2650 Ridge Ave
Evanston, IL 60201
USA

©2019 GyRL

KEVIN (KALMAN) HELLMAN, PHD

Assistant Professor (Part Time),
Dept of Obstetrics & Gynecology
University of Chicago

I study mechanisms and treatments for dysmenorrhea, the leading cause of school/work absence and foremost risk factor for chronic visceral pain in reproductive age women. Our NIH (3 separate grants) and institutionally funded laboratory has developed new animal models, investigated novel diagnostic methods, and conducted treatment studies. Seven of our eleven recent manuscripts on dysmenorrhea or related gynecological pain issues are published in the American Journal of Obstetrics & Gynecology, the most cited journal in gynecology. My goal is to systematically define the pathophysiology of dysmenorrhea and develop new treatments, while simultaneously training a cadre of future investigators to revolutionize the study of visceral pain. Our research is essential because there are few other laboratories dedicated to eradicating dysmenorrhea, one of the most frequent causes of suffering and gender disparity worldwide.

 
 

SELECTED PUBLICATIONS

For a full list of publications see pubmed

or research gate

 
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CINE MRI DURING SPONTANEOUS CRAMPS IN WOMEN WITH MENSTRUAL PAIN

We developed novel MRI and pain testing methods for clarifying pathophysiological mechanisms responsible for dysmenorrhea in humans.  I recognized a key gap in the dysmenorrhea research field was a lack of attention to the temporal relationship between myometrial activity and pain. Improving on these study design limitations was a key focus, as spontaneous cramps are the primary phenomenon reported by dysmenorrhea sufferers. Discerning the temporal relationship between the perception of pain and uterine physiological changes is also essential for establishing causality. To clarify whether myometrial contractile-induced ischemia is responsible for cramping symptoms, I developed a real-time method for monitoring spontaneous pain with fMRI. In this paradigm, participants were instructed to squeeze a bulb every time they felt a severe menstrual cramp. Simultaneously, acquired pelvic MRI signals demonstrated that decreases in myometrial signal occurred either coincident with pain report or 30-70 seconds before. The location and directionality of signal change and its temporal relationship to pain onset lead me to hypothesize that cramping pain results from a combination of uterine pressure and hemodynamic dysfunction. My study is unique in demonstrating the underlying physiology in an internal pelvic organ, time-locked to the report of spontaneous pain. Thus, as a new technical method it holds promise as a technique for identifying the cause of pelvic pain and other visceral pain disorders that are amenable to fMRI interrogation.  

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ABDOMINAL SKELETAL MUSCLE ACTIVITY PRECEDES SPONTANEOUS MENSTRUAL CRAMPING PAIN IN PRIMARY DYSMENORRHEA.

We developed a method of studying spontaneous cramping to identify neurological mechanisms responsible for referred pelvic pain, which could allow for clinical phenotyping of dysmenorrhea. By evaluating the relationship between abdominal muscle activity and spontaneous pain, I was able to provide evidence linking distinct abdominal muscle activity to reported spontaneous cramps in primary dysmenorrhea.  In contrast, women with chronic pelvic pain were less likely to have abdominal muscle activity preceding cramping pain, had widespread mechanical hypersensitivity and responded poorly to naproxen. The phenotyping methods described in this manuscript provide a strategy for characterizing nociceptive mechanisms in cyclical uterine pain and may ultimately predict treatment responsiveness

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THE ASSOCIATION OF DYSMENORRHEA WITH NONCYCLIC PELVIC PAIN ACCOUNTING FOR PSYCHOLOGICAL FACTORS

Our analysis of over 1000 adult women found that the severity of dysmenorrhea along with self-report of sensory sensitivity predict nearly 75% of the participants who experience high levels of overall pelvic pain (odds ratio 13).  Depression and anxiety may be secondary effects.

THE EFFECTS OF PLATELET-ACTIVATING FACTOR ON UTERINE CONTRACTILITY, PERFUSION, HYPOXIA, AND PAIN IN MICE

I developed an in vivo mouse model to clarify the pathophysiological mechanisms responsible for dysmenorrhea and to allow for the testing of new therapeutics. My model allowed us to characterize the effects of candidate molecules while simultaneously using novel optical methods to monitor uterine perfusion and oxygenation. Our model demonstrated that prostaglandin and Platelet Activating Factor (PAF) could directly elicit visceral pain and pelvic hyperalgesia via uterine hypercontractility and uterine ischemia. These results challenged the dogma that uterine ischemia never occurs. Furthermore, since PAF is not inhibited by NSAIDS it represents a new potential druggable target for NSAID-resistant dysmenorrhea. This animal model provided the fundamental conceptual foundation for the mechanisms (inflammation, contractility and ischemic pain) underlying menstrual pain that I subsequently tested in humans as described above.

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IDENTIFICATION OF EXPERIMENTAL BLADDER SENSITIVITY AMONG DYSMENORRHEA SUFFERERS

Since treatments for chronic pelvic pain have low efficacy, it is critical to develop prevention methods. A first step would be to identify at-risk women for prevention trials.  The prior use of invasive visceral tasks (such as colorectal distension) had greatly limited research because it deterred participation and was vulnerable to fear-related factors. Therefore, we developed a noninvasive task in which women are asked to promote diuresis by drinking water, followed by structured measurement of their level of bladder pain as their bladder fills, with serial monitoring of this process with ultrasonography. Together, we performed additional experiments, and I performed the necessary analyses for validation of these findings to confirm my hypothesis that women with dysmenorrhea are more likely to have bladder sensitivity. We have confirmed our original novel finding that a subset of women with severe dysmenorrhea (~25%) have significant bladder pain (even off menses) without having any symptomatology resembling chronic pelvic pain. We have also validated our task and shown that it is less confounded by psychological factors than even questionnaire methods. The development and validation of this bladder task has led to its use as a tool for identifying preventable factors responsible for the transition from episodic menstrual pain to chronic pelvic pain. This task serves as the foundation for our NIH-funded chronic pelvic pain prevention program.

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OVERVIEW OF COURSES

Knowledge for Every Level

NEUROSCIENCE OF PAIN AND OPIOIDS

The prevalence and impact of chronic pain and the resulting complications stemming from opioid treatment, including addiction and overdose, are well known in contemporary medical practice. Understanding the mechanisms of both pain and opioids are an important foundation for those who prescribe these medications as well as physician-scientists that wish to develop better options for the future. This course is designed to be a guided tour through the primary opioid and pain literature focused on teaching how to critically evaluate scientific papers while simultaneously learning about the scientific basis for opioid use in modern pain medicine. The experience of going through the primary literature will provide a foundation for students that wish to educate themselves and their patients on the frontiers of pain research. We will examine the most clinically relevant scientific articles, review articles, and policy statements on the mechanisms of pain and opioid analgesia/addiction (see tentative class schedule below for details) We will also discuss case studies relevant to the selected articles.

PRITZKER SCHOLASTIC RESEARCH

My main contribution has been towards mentorship of undergraduate, graduate, and postdoctoral research projects—both within my laboratory and other laboratories. Since 2013, I have been very active in the Pritzker Scholarship & Discovery and Summer Research Program, serving as a mentor, a cluster group leader, and paper judge. Although multiple group leaders are assigned to each section, clinical responsibility of the other leaders has often resulted in me being a sole facilitator at weekly sessions. Between these weekly sessions, I have helped the students with their statistical analyses and manuscript writing. Most importantly, I have provided strong encouragement for them to continue their projects which has led to their own publications. Cumulatively, I have read and commented on over 100 papers written by students in the Summer Research Program. The Summer Research Program is a critical transformative experience for medical students and it requires significant time commitment among many faculty members to ensure its success.

GLOBAL YEAR FOR EXCELLENCE IN PAIN EDUCATION WEBINAR: ABDOMINAL AND PELVIC PAIN: SCIENTIFIC PROGRESS VIS-À-VIS CLINICAL EVALUATION AND MANAGEMENT

This is an online webinar.

The goal of this webinar is to provide clinical pearls on Abdominal and Pelvic Pain over a backdrop of current basic research. I present the current scientific framework for mechanisms underlying common abdominopelvic pain conditions, including Irritable Bowel Syndrome, Bladder Pain Syndrome and Chronic Pelvic Pain. Novel fMRI research methods for clarifying the causes of menstrual pain to develop better treatment strategies are highlighted.

 

 ACADEMIC AFFILIATIONS AND TRAINING

 

ASSISTANT PROFESSOR
(PART TIME)

2011-

Department of Obstetrics and Gynecology, University of Chicago

RESEARCH ASSOCIATE
(ASSISTANT PROFESSOR)

2009-2010

Department of Neurobiology, University of Chicago

POSTDOCTORAL SCHOLAR

2004 - 2009

Department of Neurobiology, University of Chicago

PHD IN NEUROSCIENCE

1998-2004

The University of Pennsylvania

B.S. IN COMPUTER SCIENCE

1998-2004

University of Wisconsin-Madison

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FIND OUT MORE

We are located in Evanston Hospital, NorthShore University HealthSystem.

To find out about participating fill out the form or call us 847-570-2622

2650 Ridge Ave
Evanston, IL 60201
USA