Category Archives: Clinical

Chaos, Migraine, and Evolution

Lawrence Robbins, MD

 INTRODUCTION

Migraine often results in disability and diminished quality of life. Despite this, our species remains particularly vulnerable to migraine. Why is this so?  Evolution may provide answers. The study of evolution and disease is not simply an academic exercise. In studying the history of our species, and those that preceded us, we may be able to develop safer and more effective treatments. We ignore evolution at our peril.

Chaos theory is a subset of nonlinear dynamics. Nature has been able to utilize chaotic dynamics in the brain, heart, and elsewhere (Korn, & Faure, 2003). Chaotic dynamics provide advantages over stochastic (random) or reductive (simple, linear) systems. Neurons and neuron clusters effectively utilize chaos. One hallmark of chaos is the extreme sensitivity to initial conditions (Bird, 2003). This leads to the classic butterfly effect, where a tiny perturbation in the beginning results in enormous changes down the line. Initial conditions played a significant role in the development of Homo sapiens (Bird, 2003). If we travelled back in time, and changed even the tiniest initial traits, today’s human would appear significantly different. 

Chaotic dynamics may play several roles in migraine pathophysiology. For instance, a tiny initial change in blood flow, such as occurs due to a patent foramen ovale (PFO), could eventually lead to the initiation of a migraine. The complex electrical wiring of the brain involves chaotic dynamics (Korn et al., 2003).  Chaos, migraine, and evolution are intimately interwoven. This paper outlines some of their connections. 

CHAOS AND THE NERVOUS SYSTEM

Chaos is a math-based subset of non-linear dynamics. Chaos improves the adaptability, efficiency, and versatility of neuronal systems.  A number of biological systems are governed somewhat by chaotic dynamics.  These systems include the ion flow and electrical activity of the brain, the beating of the heart, blood glucose levels, and glycolysis. Several studies have demonstrated chaos at the cellular level in the brain (Schweighofer, Doya, et al., 2004). By evaluating the flow of ions through the energy barriers of the channel protein, maps reveal the chaotic controls. Algorithms and numerical solutions have been constructed revealing when the transition to chaotic dynamics occurs (Landau, Sompolinsky, 2018). Characteristics of chaotic systems include, most importantly, an exquisite sensitivity to initial conditions.  Chaos is deterministic and predictable solely from one point to the next, but not beyond that point. The initial conditions are then reset after each point.

When compared to reductive or stochastic systems, chaotic systems save energy and are more adaptable.  Chaotic dynamics are involved in governing cortical spreading depression (CSD) (Pietrobon, Moskowitz, 2014). Chaos has been demonstrated to play a role in K+, Ca+, and Na+ movements. The flow of ions about the cell has been determined to be a combination of randomness, reductive(linear) movements, and chaotic processes. A small initial change in K+ efflux, or Ca+ influx, will result in a large effect downstream. Clusters of neurons, as well as single neurons, fire in a variety of patterns. These range from regular oscillating patterns to bursts, and everything in between. Neuronal systems undergo transitions that carry them between diverse states (Vreeswijk, Sompolinsky, 1998). Chaotic dynamics partially govern both individual neurons, as well as groups of neurons.

CHAOS AND MIGRAINE

Tiny CNS perturbations may be brought about by the usual migraine triggers such as weather, stress, or hormonal changes. Through chaotic dynamics this may result in plasma protein extravasation (PPE) and cortical spreading depression, both of which are vital processes in the pathophysiology of migraine (Kernick, 2005). Medications affecting CSD may influence the neuronal membrane through chaotic controls. A small number of patients with patent foramen ovale (PFO) have experienced resolution of their migraines after PFO closure. The usual explanation for the PFO induction of migraine is via microemboli. It is also possible that chaotic dynamics play a role.  A small change in blood flow downstream (the heart) may induce a significant change in CNS dynamics upstream.

Chronic migraine pathophysiology involves wind-up and central sensitization(CS) . These are possibly controlled by chaotic dynamics. Thalamic recruitment involved in expansion of the pain area is likely governed by chaotic dynamics. Thalamic-cortical circuits involve chaotic dynamics. The pathological shift of homeostasis observed in chronic CS, with a loss of brainstem inhibition, may actually reflect a loss of chaotic control (Vreeswijk,et al.,1998). This is similar to the loss of control in the heart, resulting in arrhythmia.  The brainstem periaqueductal grey (PAG)—important in migraine—has been shown to be under chaotic control thru P/Q- type Ca+ channels. Migraine physiology incorporates a combination of genetic and environmental factors.  Trigger factors that affect migraine include stress, weather, and hormonal   changes.   These may affect the delicate balance between interneuronal nonlinear, reductive, and stochastic dynamics.  This may lead to chronic migraine. When a system is forced or stressed, nonlinear dynamics may be affected. 

New onset daily persistent headache (NDPH) may result from a perturbation of neuronal dynamics. Emotional, infectious, or other stresses may influence the delicate balance between nonlinear dynamics and stochastic or reductive dynamics. This could lead to chronic head pain.

Calcium and sodium efflux occur with CSD. Potassium and P/Q calcium channels are also involved. This complex system is unlikely to be governed primarily by random or linear kinetics. Chaotic controls have been demonstrated to be involved with these ionic movements (Pietrobon, et al., 2014). Chaotic dynamics could explain some of the properties of CSD. The initiation of CSD may be brought about by a miniscule change in potassium levels. This tiny effect may activate receptors and result in a large change downstream. The result is CSD and oligemia. With the potassium efflux partially under chaotic control, the chaos probably helps to regulate the increased cortical hyperactivity inherent in the brain of some migraineurs.

The trigeminal nucleus caudalis, vital in migraine pathophysiology, may be activated by a tiny initial stimulus. Through chaotic dynamics, this may result in the release of pro-inflammatory peptides and a release of glutamate. CSD leads to increased plasma protein extravasation. Only chaotic dynamics may explain how this may be possible. The medications that affect CSD (amitriptyline, topiramate, sodium valproate) may influence chaotic dynamics via membrane effects. When nonlinear dynamics are involved, it possibly takes less drug to produce an effect. The periaqueductal gray matter is involved in a number of CNS processes, including migraine. There is evidence that the periaqueductal gray is partially controlled by chaotic dynamics (Schweighofer, et al., 2004).

The loss of chaotic dynamics may lead to a pathological shift of homeostasis. The loss of brainstem inhibitory activity may actually reflect a lessening of chaotic control, eventually leading to a migraine. Similar loss of chaotic dynamics may explain certain arrhythmias and epileptic seizures.

The primary excitatory neurotransmitter in the brain is glutamate.  Along with calcium, glutamate is crucial in the feedback process. Glutamate is directly involved in bi-directional communications between neurons and astrocytes. It is likely that glutamate feedback processes are critical in the generation of complex bursting oscillations in astrocytes. These glutamate-mediated events are involved in migraine, epilepsy, and memory storage. The control of this feedback process may be partially enacted through chaotic dynamics. The cascade of magnesium binding to N-methyl-D-aspartate (NMDA) in the periphery about the brain, with subsequent calcium influx, is very sensitive to minute initial changes (Kernick, 2005).  This cascade is important in peripheral sensitization, which leads to migraine attacks. These magnesium and NMDA effects may be under chaotic control.

Brain-derived neurotrophic factor (BDNF) is a neurotropin that modulates neuronal membrane excitability. BDNF was used in one study to affect hippocampal neurons (Fujisawa, Yamada, Nishiyama, Ikegaya, 2004). Chaotic dynamics partially govern patterns of electrical activity in hippocampal neurons. The hippocampal electrical system is a deterministic one with a few degrees of freedom. Neuronal chaos may be sensitive to change by the application of small amounts of materials, such as BDNF, that influence temporal spiking. The application of BDNF to cultured hippocampal neurons enhanced spike timing and resulted in stereotyped firing patterns. It was felt that BDNF influenced chaos through effects on membrane levels of sodium (Fujisawa, et al., 2004).  BDNF enhanced membrane conductance and thus stabilized the membrane. The application of BDNF affected the switching between periodic and aperiodic neuronal oscillations. BDNF has been linked to modulation of neuroplasticity. The BDNF application decreased irregularity of firing patterns by modulating neuronal outputs as well as inputs. The result was a BDNF-induced chaos stabilization. This was the first experiment to demonstrate a pharmacological stabilization of chaos at the neuronal level (Fujisawa, et al., 2004).

CHAOS AND EVOLUTION

Chaos and evolution are intimately interconnected. There is a chaotic (non-linear) connection between phenotype and genotype. This complex relationship is constantly in flux. A single mutation may be inconsequential, or it may result in enormous changes that are unpredictable. This is typical for a non-linear system. With these unpredictable mutations, iterations over thousands of generations will usually result in evolutionary changes (McKee, 2000). It is debatable as to how much the environment plays a role, versus genetic changes that are generated internally.

The unpredictability of evolution is typical of non-linear systems. Most discussions of evolution predictors focus on random, stochastic processes (mutations, genetic drift, random environmental changes). A reductive system would behave in a much more orderly, predictable manner. However, these fixed reductive systems are limited, and non-linear dynamics allows for enhanced evolutionary adaptability. The behavior of evolutionary systems is extremely sensitive to initial conditions. This was demonstrated during the quaternary period. At the beginning of each interglacial, the initial circumstances determined the outcome of that period. Between interglacials there were differences that were unpredictable, due to the non-linear nature of the system (Bird, 2003).

Non-linear dynamics lead to a system that is not scaled. The tree of life is fractal, and follows non-linear dynamics. The branches of the tree are continuously being split, resulting in evolutionary changes.  If we travelled back 5 million years, and re-started the human evolutionary process, the result would be dramatically different. This is the nature of a non-linear system. A simpler stochastic reductive system would be predictable but limited. It has been demonstrated that, when many traits interact, chaotic dynamics may govern phenotypic evolution.   Ancient species in human evolution, such as Australopithecus and Homo habilis, may have diverged due to chaotic dynamics (McCann, Yodzis, 1994).

Natural selection utilizes chaotic dynamics, chance, and coincidence (McKee, 2000). Natural selection does not invent, it tends to mosey along and tinker. The chance mutation must be coincidentally beneficial because of some environmental change.  For instance, if our ancestors needed robust teeth due to changing climactic conditions, those who happened to have larger teeth would have prevailed. Chaotic dynamics oversees chance and coincidence in the evolutionary process.

 EVOLUTION AND MIGRAINE

 Examining evolutionary systems in relation to disease is much more than an academic exercise. The evolutionary history will give us a complete picture of a disease. Understanding the evolutionary foundation may help us in developing safe and effective treatments.

Illness can be considered through two frameworks: 1. a proximate view, and 2. an evolutionary lens. The proximate view considers the nuts and bolts of a disease: pathophysiology, treatment, biochemistry, etc. It’s vitally important to also consider the disease process using an evolutionary viewpoint (Perlman, 2013). One essential question is: “why have migraines persisted, and why are humans still so susceptible to migraine?” The proximate lens says that migraine is a physical trait that involves multiple physiologic systems. The evolutionary framework begs the question: “why does our DNA code for migraine?”

There are physiological trade-offs that permeate evolution. While sickle cell disease is devastating, the sickle cell gene does also protect against malaria. Cystic fibrosis also involves serious trade-offs. Heterozygotes for cystic fibrosis were less likely to suffer dehydration from illnesses such as cholera. Genes exist to propagate themselves, sometimes to the detriment of the organism (the “selfish gene”)(Dawkins, 2013). This is also the story of migraine. Evolutionary benefits from migraine are possible (Loder, 2002).  It is also possible that our species simply continues to be vulnerable to migraine, and the evolutionary benefits are few. There are multiple genes involved in migraine, and evolution does not easily remove “bad genes”(Loder, 2002).

 It’s likely that migraines in humans increased as a result of our migration to more northern latitudes (Vigano, Manica, Di Piero, Leonardi, 2019).  Low vitamin D levels may help explain the increase in prevalence of migraine farther north (Prakash, 2010). The TRPM8 gene involves a receptor that plays a part in cold sensation and thermoregulation. TRPM8 (the “T” variation) is also linked to an increased risk for migraine (Dussor, Cao, 2016).  People who carry the “T” variation are better adapted to cold environments, and this adaptation likely improved their survival and reproductive success. Migraine may have been a negative consequence from this cold adaptation: another trade-off. The TRPM8 and latitudinal studies were the first to link migraine, evolution, natural selection, and geography (Vigano, et al., 2019).

The reasons why migraine persists are varied. While there is no epidemiological data from past millenia, the prevalence of migraine may be increasing. An increased sensitivity to light, smells, and sound could be beneficial under certain conditions. Migraine may be advantageous in combating certain infections (Loder, 2002). This may occur through an enhanced immune response, or by an increase in blood flow. Only a small percentage of people never experience headache (7% of men, and 1% of women), signaling that there may be some evolutionary advantage of headache.

Certain genes that result in harmless “quirks” in one environment can have deadly outcomes in other venues. Our modern environment certainly contributes to migraine frequency. The environment has radically changed, after millions of years of evolution (Cochran, Harpending, 2009).  For the vast majority of human history, we were primarily hunting and gathering. Recently, only 10 to 12 thousand years ago, societies in Southwest Asia (the fertile crescent) began to cultivate plants and domesticate animals. Many factors may contribute to increased migraine frequency: changes in culture, living circumstances, agriculture and diet, environmental toxins, densely packed populations, infections (particularly viral), harsh indoor lighting, loud speakers, poor sleep, and increased stress (Loder, 2002).  When modern hunter-gatherer societies switch to our “western diet,” they suffer from heart disease and an increase in cancer (Milton, 2000).  One of many examples where a changing environment has an impact on disease involves the genes for heart disease. These genes may not have been particularly detrimental for Stone Age humans, due to short lifespans. But as lifespans have been significantly lengthened, these genes have become threatening. Phenotypic and adaptive plasticity are significant factors in humans adapting to the changing environment (Perlman, 2013).

While migraine is three times more common in women than in men, the evolutionary explanation for this is unclear. Men generally did most of the hunting and gathering, for which migraine could pose disadvantages. For child care, food preparation, and homekeeping, migraine may possibly offer small evolutionary advantages. Migraine commonly decreases during pregnancy, providing an evolutionary incentive for more pregnancies.

It’s likely that migraine only afflicts the human species. Our ancient human brainstem has obstacles in coping with a cortex that is recently enlarged. With excessive afferent input, our brainstem may be overwhelmed. Having higher cortical functions not found in other primates may contribute to our continued vulnerability to migraine.   

Migraine may function as a defense mechanism against excessive stress, noise, or light (Loder, 2002).  The elevated sense of smell may serve as a defense from toxins or viruses entering the CNS. Vomiting may help to remove toxins. Women migraineurs probably have a lower prevalence of type 2 diabetes, compared to those without migraine (Fagherazzi, El Fatouhi, Fournier, et al., 2019).  An activation of the trigeminal nuclear complex could be protective (Loder, 2002).  If migraine offers protections for an individual, then that individual’s genes may be propagated more successfully. If an ancestral human experienced 100 migraines during a year, and just one of those migraines protected the person from harm, the trade-off would have been worthwhile. In an evolutionary framework, the cost of migraine may be inexpensive.

There is a difference between a defense and a defect. Coughing is a defense, but becoming blue from hypoxia is not. We want to retain our natural defenses. The calcitonin gene-related peptide (CGRP) associated with migraine may be advantageous under stress (Kee, 2018). CGRP has existed in a variety of species for hundreds of millions of years. CGRP plays various roles in the body, some positive, some harmful (Kee, Kodji, Brain, 2018). Under stress, CGRP is beneficial for our cerebrovascular and cardiovascular systems. Disrupting this natural defense, as happens with our CGRP monoclonal antibodies that prevent migraine, may be harmful.  The CGRP story is one example of the danger in ignoring the evolutionary importance of a compound.       

Natural selection is dependent on reproduction. After the reproductive years, a particular trait could very well become detrimental, but that does not affect gene propagation. In order to understand a trait (or disease) such as migraine, we must consider all of the evolutionary processes. These include genetic drift, mutations, migration, non-random mating, and natural selection (Perlman, 2013). Sometimes, natural selection produces opposing effects, resulting in a heightened vulnerability to disease.

 It’s imperative to not only view individuals through an evolutionary lens, but to also consider the phylogeny of the species (Perlman, 2013). The relationships between humans have morphed in the past 12,000 years (Cochran, et al., 2009).  One primary factor driving phylogenetic changes is the increase in population density, resulting in most humans living in significantly smaller spaces. Culture, which influences our state of disease or health, may also contribute to an increase in headache prevalence.

Headache and pain are adaptive responses. Being still, or in bed, may help repair damaged tissues. Incomplete or inadequate natural selection is often cited as the cause for our flaws or disease, but it is more likely that many illnesses are the result of compromises and/or design flaws (Nesse, Williams, 2012).  For example, our esophagus crosses our trachea. Because of this, our airway must inconveniently be closed every time that we swallow, to prevent choking. Allergies, atherosclerosis, nearsightedness, and nausea in pregnancy are similar examples stemming from evolutionary compromises and design flaws (Nesse, 2005, 2012).

Another important evolutionary concept to consider is intrinsic vulnerability (Nesse, 2011). Different species have various levels of vulnerability to certain diseases. Humans mature rather slowly, with infrequent reproduction. This is a factor regarding enhanced vulnerability of our species to certain diseases. It’s difficult for us to rid ourselves of genes that cause harm. Migraine involves a multitude of factors and genes, and it’s not likely that natural selection would be capable of eliminating migraine.

To more wholly understand migraine, we should venture beyond the proximate and physiologic processes. The evolutionary foundations of migraine are vitally important to study. Examining migraine under an evolutionary lens may help us in evaluating the safety of new treatments, such as the CGRP monoclonal antibodies. We must pay attention to evolution.

CONCLUSION

Chaos, migraine, and evolution are intertwined. Chaotic dynamics are vital within the central nervous system. Chaos is important at the ionic, neuronal, and neuronal cluster levels. Chaos may be involved in the generation of CSD. Sensitization and wind-up, crucial components of migraine, probably incorporate chaotic dynamics.

Evolution and natural selection involve chaos, chance, and coincidence. The evolutionary result of thousands of generations depends exquisitely upon initial conditions, characteristic of chaotic dynamics.

For myriad reasons, our species remains remarkably vulnerable to migraine. To understand migraine, we have to look farther than simple physiologic and proximate processes. We cannot truly understand migraine without examining the evolutionary underpinnings. The safety of new migraine treatments should be evaluated under an evolutionary lens.

                                                               REFERENCES

Bird, R. (2003). Chaos and Life: complexity and order in evolution and thought. NY,NY: Columbia University Press.

Cochran G, Harpending H (2009). The 10,000 Year Explosion: How civilization accelerated human evolution. NY,NY: Basic Books.

Dawkins,R.  (2016). The Selfish Gene. Oxford, UK: Oxford University Press.

Dussor G, Cao,Y-Q. (2016). TRPM8 and migraine. Headache, 56, 1406-1417.

Fagherazzi G, El Fatouhi D, Fournier A. (2019). Associations between migraine and type 2 diabetes in women: findings from the E3N cohort study. JAMA, 76, 257-263.

Fujisawa S, Yamada M, Nishiyama N, Ikegaya N. (2004). BDNF boosts spike fidelity in chaotic neural oscillations. Biophysics J, 86, 1820-1828.

Kee Z, Kodji X, Brain SD. (2018). The role of calcitonin gene related peptide (CGRP) in neurogenic vasodilation and its cardioprotective effects. Frontiers in Physiology, 9, 1249.

Kernick D. (2005). Migraine—new perspectives from chaos theory. Cephalalgia, 25, 561-566.

Korn H, Faure P. (2003). Is there chaos in the brain? C.R. Biologies, 326, 787-840.

Landau ID, Sompolinsky H. (2018). Coherent chaos in a recurrent neural network with structured connectivity. Computational Biology, Retrieved May 20, 2020 from https://doi.org/10.1371/journal.pcbi.1006309

Loder E. (2002). What is the evolutionary advantage of migraine? Cephalalgia, 22, 624-632.

McCann K, Yodzis P. (1994). Non-linear dynamics and population disappearances. The American Naturalist, 144, 873-879.

McKee, J (2000). The Riddled Chain: chance, coincidence, and chaos in human evolution. Piscataway,NJ: Rutgers University Press.

Milton K. (2000). Hunter-gatherer diets: a different perspective. The American Journal of Clinical Nutrition, 71, 665-667.

Nesse,RM. (2005). Maladaptation and natural selection. The Quarterly Review of Biology, 80, 62-70.

Nesse,RM. (2011). Ten questions for evolutionary studies of disease vulnerability. Evolution Applications, 4, 264-277.

Nesse,RM, Williams GC. (2012). Why We Get Sick: the new science of Darwinian medicine. New York, New York: Vintage Books.

Perlman R. (2013). Evolution and Medicine. Oxford, UK: Oxford University Press.

Pietrobon D, Moskowitz MA. (2014). Chaos and commotion in the wake of cortical spreading depression and spreading depolarizations. Nature Review Neuroscience, 15, 379-393.

Schweighofer N, Doya K, et al. (2004). Chaos may enhance transmission in the inferior olive. Proceedings of the National Academy of Science, 101, 4655-4660.

Vigano A, Manica A, Di Piero V, Leonardi M. (2019). Did going north give us migraine? An evolutionary approach on understanding latitudinal differences in migraine epidemiology. Headache, 59, 632-634.

Vreeswijk C, Sompolinsky H. (1998). Chaos in neuronal networks with balanced excitatory and inhibitory activity. Science, 274, 1724-1726.

Update on Gepants: New Abortives for Migraine

Lawrence Robbins,M.D.

Gepants are small molecule calcitonin gene-related peptide (CGRP) receptor antagonists. The preventive CGRP monoclonal antibodies(Aimovig, Emgality, Ajovy) are large molecules, delivered once per month as a SQ injection. Seven gepants have been developed since 2004. (1) Telcagepant was extensively studied, but withdrawn due to hepatotoxicity concerns. CGRP has many effects throughout the body. CGRP triggers a cascade of inflammatory mediators that feed into the trigeminovascular system. By blocking CGRP, the gepants stop the process prior to inflammation.

Regarding migraine, CGRP is an inflammatory compound. They will initially be utilized as migraine abortives, but eventually they will also be used to prevent migraine. The gepants may be helpful for 3 groups of migraineurs. They will be prescribed for a number of patients who found triptans (sumatriptan, rizatriptan, zolmitriptan, etc.) to be ineffective. In addition, gepants will be used for certain patients who cannot tolerate triptans. Finally, for those patients with significant cardiac or cerebrovascular risk factors, the gepants may be relatively safe, since they do not constrict cardiac or cranial arteries. While efficacy is modest, these are well tolerated medications.

The first gepant to come to market will be ubrogepant. Almost 2,700 patients participated in the ubrogepant ACHIEVE studies. (2,3) The doses have ranged from 25mg to 100mg. The t-max is 0.7 to 1.5 hours. Approximately 20% of patients who used the 50mg dose were pain free after 2 hours. While 25mg and 100mg tablets of ubrogepant were evaluated, it is likely that 50mg will be the primary dose. Ubrogepant was well tolerated, with 2% to 5% of patients reporting nausea, somnolence, dry mouth, dizziness, or upper respiratory tract infections. No serious adverse events were reported. The safety and tolerability were also explored in a 52 week extension study. Few adverse events, and no hepatotoxicity was reported. The effect of ubrogepant on the patient’s most bothersome migraine symptom was evaluated 2 hours post-dose. 39% of those treated with ubrogepant reported that their worst migraine symptom was resolved. The therapeutic gain for ubrogegepant (active drug vs. placebo) is relatively low, 6.4%-9.4%. In comparison, the therapeutic gain for sumatriptan is 16%-21%.

Rimegepant is another gepant, in development for abortive and preventive use. The dose is 75mg, with a t-max of 2 hours. In the 2 main trials, 19.4% of patients achieved pain freedom at 2 hours. (4) 37% of patients reported freedom from their most bothersome symptom. As with ubrogepant, no significant liver toxicity was reported. Adverse events were low, with nausea being reported by 1.4% of patients. The therapeutic gain for rimegepant is 5% to 7.6%.

A third gepant, atogepant, is currently being studied.

The gepants will be a useful alternative to triptans. Many patients find triptans to be ineffective. Some migraineurs cannot tolerate the adverse effects of the triptans. For certain patients with cardiovascular risk factors, triptans may not be completely safe. Gepants will be considered in these clinical settings. The initial (2 hour) efficacy rates are fairly low, but it appears that gepants may become more effective over 2 to 8 hours. During the trials, these were fairly well tolerated medications. It will take at least several years before we are able to accurately assess the true adverse effect profile of the gepants.

References

1. Olesen J, Diener H-C, Husstedt IW et al Calcitonin gene-related peptide receptor antagonist BIBN 4096 BS for the acute treatment of migraine. 2004. N Eng J Med 350:1104-1110.

2. Allergan Announces Positive Top Line Phase 3 Clinical Trial for Ubrogepant- an Oral CGRP Receptor Antagonist for the Acute Treatment of Migraine. Available at http://www.allergan.com/news/news/thomson-reuters/allergan-announces-positive-phase-3-resul.

3. Allergan Announces Second Positive Phase 3 Clinical Trial for Ubrogepant- an Oral CGRP Receptor Antagonist for the Acute Treatment of Migraine. Available at http://www.allergan.com/News/News/Thomson-Reuters/Allergan-Announces-Second-Positive-Phase-3-Clinica.

4. Biohaven Announces Successful Achievement of Both Co-Primary regulatory Endpoints in Two Pivotal Phase 3 Trials of Rimegepant an Oral CGRP Receptor Antagonist for the Acute Treatment of Migraine Available at https://biohavenpharma.com/wp-content/uploads/2018/03/CONFIDENTIAL-BIOHAVEN-PRESS-RELEASE-FINAL-v2.pdf.

Reducing Harm from Opioids – Lessons Learned

Lisa Edgerton, PharmD, BCPS, CPP, Olivia Herndon, MA, and Joseph Pino, MD, MHA

Wilmington is a community in southeastern North Carolina known for its beautiful beaches, historic river-walk district, and the largest domestic television and movie production facility outside of California. In April of 2016, this city also became recognized for something else.

In 2016, Castlight Health released a report titled “The Opioid Crisis in America’s Workforce.” The study noted those who abused opioids are more likely to live in the rural south with 22 of the top 25 cities in Southern states. Furthermore, it named Wilmington, NC as the city with the highest abuse rate in the United States. In response, our medical community mobilized and recruited partners from disciplines outside of healthcare to reduce harm from opioids in our region.

Through a “call to action” where more than 100 regional stakeholders and leaders, the Community Partners Coalition (CPC) was born. This CPC aims to improve collaboration and coordination between those who provide care to individuals seeking access to mental health and substance use services by aligning efforts in the region. A primary focus of the CPC was to improve safe medication disposal options in our region by expanding medication take-back events and permanent drop boxes.

The first medication take-back event was held at New Hanover Regional Medical Center (NHRMC) in March 2009. This event was held at one location on our hospital’s main campus in New Hanover county. NHRMC partnered with the Wilmington Sheriffs office and collected 140 pounds of medication at that event. This solo event continued biannually however, dates were chosen based upon availability of volunteer coordinators and coinciding community events. NHRMC continued to host this single site medication take-back event biannually through the Spring of 2017.

Through the support of the CPC, in the Fall of 2017, this event was expanded to 9 locations within 4 counties and collected 3,680 pounds of medication and 29,675 needles or sharps. This biannual medication take-back event has continued to grow now hosting 19 locations spanning 6 counties in our region.

In October 2019, we collected almost 6,000 pounds of medication, 43,000 needles or sharps and 178 medications, valued at $55,000, that were donated to a local clinic serving those without resources for re-dispensing. Expanding our medication take-back event to 19 locations did present some challenges along the way.

To expand our reach, leaders of the takeback event needed to engage in detailed planning and consider logistical challenges. We aligned our event dates to the Drug Enforcement Administrations (DEA) National Prescription Drug Take Back Day. Aligning with the DEA allowed us to plan for future events as these dates are standardized on the last Saturdays in April and October. Alignment also enabled law enforcement to register event locations in their national website. This site is searchable and provides a map of locations nearest to search area. Alignment with the DEA also connected us to our regional State Bureau of Investigation (SBI). This partnership enabled us to receive support including standard boxes used to collect medications at each take-back location. The SBI supplied NHRMC with 250 evidence boxes that were distributed to site leaders at each take-back location.

When planning to staff each of our sites, federal rules indicate that law enforcement must be present at each medication take-back location. When planning for our Fall 2017 expansion, we discovered that our hospital law enforcement officers could staff all NHRMC and affiliate locations. At the Fall 2017 event, we were able to utilize NHRMC police for 5 of the 9 locations. This allowed us to extend our partnership with local sheriff’s offices and expand to additional sites. We continue to collaborate with our regional county sheriff departments who provide an additional 1-2 law enforcement officers for each location.
NHRMC company police have been instrumental in not only staffing these events but also coordinating with regional law enforcement agencies. They collect and store the medication until the “burn day”. This often occurs 2-3 days after the takeback event. Our event has become so large that NHRMC law enforcement transports over 100 boxes of medication. As a result of our success, we have outgrown the transport capacity of our standard vehicles. We now either have to rent commercial trucks or borrow large box trucks from another department in our hospital.

In addition to organizing law enforcement to be present at each site, we decided we would accept needles or sharps at each of the 19 drop off locations. This became an issue for sites that were not affiliated with a health system because they did not have sharps containers at their locations. Prior to each event, NHRMC now donates sharps containers to each of these sites. Following the event, we now also coordinate with either law enforcement or a volunteer at the site to collect the sharps bins.

To raise awareness of this multi-county, multi-site drug takeback event, we approached our hospital’s marketing department to help us by advertising this event. They created a universal flyer listing each drop off location by county. This flyer is printed in a variety of sizes and is posted across our health system and to each of our drop-off location partners. We also advertise in advance of this event on social media, radio stations and local newspapers as well as media outlets on the day of the event. We also created a NHRMC webpage dedicated to medication disposal where we post our upcoming flyer and list locations of all area permanent drop boxes. Through this effort, we also learned that funeral homes, hospice care centers, veterinarian offices and churches are effective locations to advertise these events and added these sites to our marketing locations for future events. We also realized that we needed to create a Spanish-version of our flyer to appeal to other segments of our community and plan to do so for our next event.

We also discovered that we needed to develop a standard process to enable us to repurpose unused medication. Medication take-back locations staffed with NHRMC volunteers may collect any unused medications and can donate them to a charitable clinic. These medications must meet North Carolina repository rules and regulations to qualify for donation. Following the event, each unused medication collected is visually inspected by a pharmacist to ensure it meets all applicable federal guidelines for donated medications. By following this process, we could donate $ 55,000 of medication to one of our local, charitable clinics.

During our medication take-back expansion in 2017, NHRMC also installed three permanent medication drop boxes across several sites within our health system. Medication drop boxes were installed on the main campus within our Outpatient Pharmacy, at our free-standing emergency department located off campus, and at our critical access hospital located in a neighboring county. It was anticipated that the drop boxes would need to be emptied once a month. When first installed, the permanent drop box in our main hospital, which holds roughly 55 pounds of medication, needed to be emptied every 9-10 days. This was not anticipated. We now collect 1,600 pounds of medication in our 3 permanent medication boxes annually.

Like other communities across the country, Wilmington and our surrounding area have been significantly impacted by the opioid crisis. Through the development of the CPC and the leadership of NHRMC, we expanded our drug takeback events to multiple sites in multiple counties in our region. As a consequence of our success, we also discovered we needed to coordinate law enforcement at each location, establish safe storage, rent large trucks to transport thousands of pounds of medication collected at each event, develop a process to reclaim medication and manage high volume disposal of medication in permanently installed drop boxes across our health system. We are fortunate to have such an engaged community to collectively work to reduce harm from medication. Hopefully, these lessons learned will help you do the same.

Personality and Pain: Which Came First?

James N. Weisberg, PhD

This article is adapted from a chapter in a soon to be published text:
Weisberg, J.N., Paul, C. & Twyner, C. Personality and Personality Disorders in Chronic Pain.  In Incayawar, M., Clark, M. & Maldonado-Bouchard, S. (Eds.). Overlapping Pain and Psychiatric Syndromes-Global Perspectives. New York, NY: Oxford University Press

Chronic pain is a significant health care issue at epidemic proportions in the United States1 and there is a high incidence of both clinical psychiatric disorders2,3 and personality disorders (PD) in the chronic pain population.4 This article will briefly summarize some of the important points pertaining to the prevalence and interplay between personality disorders and chronic pain.

Personality and Pain

The relationship between personality and pain can easily be traced to ancient Greece. More recently, in the late 19th century psychodynamic theorists discussed the connection between emotional factors and the experience of chronic pain.5 George Engel maintained that, while physical pain may result from underlying pathophysiology, the interpretation of pain is a psychological phenomenon and also noted that certain diagnoses, including Depression, Hysteria and Hypochondriasis were relatively common in people experiencing chronic pain.6 In an attempt to further characterize personality characteristics, the use of Minnesota Multiphasic Personality Inventory (MMPI)7 and its successors (MMPI-2, MMPI-2-RF) led to a plethora of research seeking to use psychometric tests quantify these early theorists, help predict treatment outcome from multidisciplinary treatment8, spine surgery9, spinal cord  stimulators10as well as  and pain-related disability11.  However, despite the hundreds of studies using the MMPI and its successors, there continues to be controversy regarding the applicability and appropriateness of in the chronic pain population.12,13

A number of other psychological inventories have been used in an attempt to describe and characterize individuals with chronic pain and to predict treatment outcomes. Some, but not all of these measures include the NEO Personality Inventory (Neuroticism-Extroversion-Openness Personality Inventory-NEO-PI) and its revisions,14-16 the Millon Clinical Multiaxial Inventory and subsequent revisions (MCMI; MCMI-IV)17,18 and the Temperament and Character Inventory (TCI).19

While psychological inventories have investigated different personality characteristics as they relate to pain, relatively few studies have investigated personality disorders in chronic pain. 

Personality Disorders and Chronic Pain

Whereas personality refers to the constellation of non-pathological characteristics in an individual’s patterns of thought, emotion, and behavior the DSM defines a personality disorder as “an enduring pattern of inner experience and behavior that deviates markedly from the expectations of the individual’s culture, is pervasive and inflexible, has an onset in adolescence or early adulthood, is stable over time, and leads to distress or impairment.”20 Thus, the essential difference between a trait and disorder is the degree of distress and disruption caused.

Personality and personality disorders are likely the combination of biological, developmental, and environmental factors that become impacted by state-dependent variables such as mood and anxiety. The Diathesis-Stress model purports that individuals have underlying genetic vulnerabilities and possibly early life experiences that interact with stressors the individual encounters later in life.21  Depending on the nature of the stressors and the individual’s ability to cope with such stressors, the underlying vulnerability may or may not become expressed as a disease process. The diathesis-stress model was first applied to explain schizophrenia21 and depression.22  It has also been applied to the development of chronic back pain23 and the development of depression in chronic pain patients.2 Similarly, this model has been proposed to apply to personality disorders in chronic pain patients.24 Thus, combined with underlying traits and situational stressors brought on by chronic pain, an individual’s underlying personality traits and characteristics may become magnified to the extent the individual meets criteria for a personality disorder.

Epidemiology of Personality Disorders:

In its most recent edition, the American Psychiatric Association cites data from a national epidemiologic survey suggesting approximately 15% of US adults meet criteria for at least one personality disorder.25 A large epidemiological study found prevalence estimates for the different clusters suggest 5.7% for disorders in Cluster A (Paranoid, Schizotypal and Schizoid Personality Disorder), 1.5% for disorders in Cluster B (Histrionic, Narcissistic and Borderline Personality disorders),  6.0% for disorders in Cluster C (Avoidant, Dependent, Obsessive-Compulsive Personality Disorders), and 9.1% for any personality disorder, indicating frequent co-occurrence of disorders from different clusters.26

To date, approximately 15 studies have investigated the prevalence of personality disorders in chronic pain.  Some of the more seminal studies are highlighted here.  The first published study using a semi-structured interview to diagnose DSM-III personality disorders in chronic pain found 37% of their sample met criteria for at least one personality disorder with the most common diagnoses being histrionic PD (14%), dependent PD (12%) and borderline PD  (7%).27  Fishbain et al,28 using a semi-structured interview to diagnosis both DSM-III axis I and Axis II disorders, found 59% of their chronic pain sample met criteria for a personality disorder with most common diagnoses being dependent PD (17%), Passive-Aggressive PD (15%) and histrionic PD (12%).   Weisberg et al29 used a combination of clinical interview, treatment notes and both patient and family self-report measures to assess personality disorders in 55 chronic pain patients who were evaluated and treated at a comprehensive outpatient pain management program. They found that 31% met criteria for at least one PD and an additional 27% met criteria for PD-NOS which is used when an individual meets incomplete criteria for two or more personality disorders.  Similar to other studies, the most common diagnoses were borderline PD (13%) and dependent PD (11%).  These researchers suggest that obtaining longitudinal information from both the patient and an individual with a longstanding relationship with the patient might provide a more thorough assessment of the impact of state factors such as mood, anxiety, and stress on the presentation of personality.29 More recently, Conrad et al30 found that 41% of their chronic pain sample met criteria for a personality disorder diagnoses compared to 7% of their control group.  Most common were Borderline PD (11%) and paranoid PD (12%). The authors found clinical disorders, such as depression at a equally high rate, lending more credence to the importance of assessing personality in context of state factors.

In summary, the relatively few studies that have investigated personality disorders in various samples of patiens with  chronic pain have found prevalence rates from 31% to over 80%. However, as has been noted by previous researchers, due to a variety of factors including state-dependent variables, stressors unique to chronic pain, genetic and developmental influences and other known and unknown factors, significant caution must be used when making a personality disorder diagnosis in the individuals with chronic pain.  In addition, knowing premorbid functioning is crucial in understanding the multifactorial nature of the observed behavior.  Nontheless, the presence of a personality disorder increases the liklihood of co-morbid conditions, such as substance misuse and abuse and makes treatment of chronic pain that much more challenging to the pain clinician.

The Nexus of Personality Disorders in Chronic Pain and Substance Use Disorders:

There has also been a paucity of research on the interaction between personality disorders and substance use disorders in chronic pain.  One study investigated psychological comorbidities, including personality disorders, in chronic pain sufferers presenting to either a university emergency department or an urgent care clinic requesting opioids.31 Pertinent results demonstrated 18% likely had a personality disorder diagnosis and found that personality disorder was significantly related to opioid abuse.31 A recent study found the incidence of personality disorders to be 52% in those with co-occurring chronic pain and substance use disorders.32 The most common personality disorder was antisocial PD (22%) followed by avoidant PD (19%) and paranoid PD (16%). Although there is little literature on this topic, both of these studies suggest that personality disorders may be a moderating variable in the incidence of substance use disorders in persons with chronic pain.                                                                                                                                         

Treatment of Personality Disorders in Chronic Pain

While working with people living with either chronic pain or personality disorders can prove to be daunting to the clinician separately, working with those with the co-morbid diagnoses of both personality disorders and chronic pain can pose unique challenges and opportunities in regard to treatment. Although maladaptive behaviors are, by definition, problematic in a variety of settings, legitimate concerns may be disregarded as secondary to the manifestations of personality disorders or simply attributed to being “difficult.”

The need for the pain clinician to screen for personality disorders is rooted in the understanding that the manifestations of a personality disorder in a person living with chronic pain can be exacerbated or unmasked by the individual’s pain condition according to the diathesis-stress model.24  In addition, the need for vigilance and awareness with these conditions is considerable as these patients are at higher risk for various adverse outcomes, including substance use disorders. 31 Attempting to detangle the personality disorder from the chronic pain state with the goal of treating one or the other may be difficult at best.

Cognitive-Behavioral Therapy for chronic pain (CBT-CP) has been well documented in the literature to be one of the most effective treatments for chronic pain.33-35 Acceptance and Commitment Therapy (ACT)36, has been shown to benefit patients with personality disorders that had failed in previous treatment with significant improvements in personality pathology and quality of life.37 ACT for chronic pain has also been effective at decreasing pain intensity, anxiety, and disability38 The use of CBT-CP and ACT may be a potential avenue for treatment, but research designed to investigate these interventions among people with coexisting chronic pain and personality disorders is lacking.

Dialectical Behavior Therapy (DBT), a current mainstay of treatment of borderline personality disorder, focuses on the development of coping skills with the ultimate goal of improving emotional regulation and control.39 However, as with other therapeutic modalities, there is minimal evidence for treatment for DBT in those with chronic pain and comorbid personality disorders.

Given the common elements between Cognitive-Behavioral Therapy and Dialectical Behavior Therapy, it stands to reason that a hybrid model combining elements of both CBT-CP with DBT might be a highly successful approach to maximizing treatment potential in patients with co-morbid chronic pain and personality disorders, especially borderline personality disorder.

Summary: 

In summary, it is important to assess patients not just for depression, anxiety and other clinical psychiatric disorders, but for personality traits and disorders in order to better understand the impact personality may have on the expression of their pain perception, medication use and coping styles.  Understanding the role personality disorders may play in the complexities of chronic pain should result in the tailoring of multimodal treatments for chronic pain that emphasize non-opioid medical management, cognitive-behavioral and physical therapies.

References

  1. Institute of Medicine. Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research. Washington (DC)2011.
  2. Banks SM, Kerns RD. Explaining the high rates of depression in chronic pain: A diathesis-stress framework. Psychological bulletin. 1996;119(1):95-110.
  3. McWilliams LA, Cox BJ, Enns MW. Mood and anxiety disorders associated with chronic pain: an examination in a nationally representative sample. Pain. 2003;106(1-2):127-133.
  4. Weisberg JN. Personality and personality disorders in chronic pain. Curr Rev Pain. 2000;4(1):60-70.
  5. Breuer J, Freud S. Studies on hysteria. Original work published 1893-1895 ed. New York, NY: Basic Books; 1957.
  6. Engel GL. Psychogenic pain and pain-prone patient. Am J Med. 1959;26(6):899-918.
  7. Hathaway SR, McKinley J. Minnesota Multiphasic Personality Inventory. Minneapolis, MN: University of Minnesota Press; 1943.
  8. Kleinke CL, Spangler AS, Jr. Predicting treatment outcome of chronic back pain patients in a multidisciplinary pain clinic: methodological issues and treatment implications. Pain. 1988;33(1):41-48.
  9. Block AR, Ohnmeiss DD, Guyer RD, Rashbaum RF, Hochschuler SH. The use of presurgical psychological screening to predict the outcome of spine surgery. The Spine Journal. 2001;1(4):274-282.
  10. Block AR, Marek RJ, Ben-Porath YS, Kukal D. Associations Between Pre-Implant Psychosocial Factors and Spinal Cord Stimulation Outcome: Evaluation Using the MMPI-2-RF. Assessment. 2017;24(1):60-70.
  11. Gatchel RJ, Polatin PB, Mayer TG. The dominant role of psychosocial risk factors in the development of chronic low back pain disability. Spine. 1995;20(24):2702-2709.
  12. Fishbain D, Cole B, Cutler R, Lewis J, Rosomoff H, Rosomoff R. Chronic pain and the measurement of personality: Do states influence traits? Pain Medicine. 2006;7(6):509-529.
  13. Turk DC, Fernandez E. Personality assessment and the minnesota multiphasic personality inventory in chronic pain: underdeveloped and overexposed. Pain Forum. 1995;4(2):104-107.
  14. Costa PT, McCrae RR. The NEO Personality Inventory Manual. Orlando, FL: Psychological Assessment Resources; 1985.
  15. Costa PT, McCrae RR. Revised NEO Personality Inventory (NEO–PI–R) and NEO Five-Factor Inventory (NEO–FFI) professional manual. Odessa, FL: Psychological Assessment Resources; 1992.
  16. McCrae RR, Costa PT, Jr., Martin TA. The NEO-PI-3: a more readable revised NEO Personality Inventory. J Pers Assess. 2005;84(3):261-270.
  17. Millon T. Millon Clinical Multiaxial Inventory. Minneapolis, MN: National Computer Systems; 1977.
  18. Millon T, Grossman S, Millon C. Millon Clinical Multiaxial Inventory-IV: MCMI-IV. Bloomington: NCS Pearson; 2015.
  19. Cloninger C, Svrakic, DM., Przybeck, TR. A psychobiological model of temperment and character. Archives of general psychiatry. 1993;50:975-990.
  20. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders: DSM-5. 5th ed. Washington, D.C.: Author; 2013.
  21. Meehl PE. Schizotaxia, schizotypy, schizophrenia. American Psychologist. 1962;17:827-838.
  22. Monroe SM, Simons AD. Diathesis-stress theories in the context of life stress research: implications for the depressive disorders. Psychological bulletin. 1991;110(3):406-425.
  23. Flor H, Turk DC. Etiological theories and treatments for chronic back pain. I. Somatic models and interventions. Pain. 1984;19(2):105-121.
  24. Weisberg JN, Keefe FJ. Personality disorders in the chronic pain population: Basic concepts, empirical findings, and clinical implications. Pain Forum. 1997;6(1):1-9.
  25. Grant BF, Hasin DS, Stinson FS, et al. Prevalence, correlates, and disability of personality disorders in the United States: results from the national epidemiologic survey on alcohol and related conditions. J Clin Psychiatry. 2004;65(7):948-958.
  26. Lenzenweger MF, Lane MC, Loranger AW, Kessler RC. DSM-IV personality disorders in the National Comorbidity Survey Replication. Biological psychiatry. 2007;62(6):553-564.
  27. Reich J, Tupin JP, Abramowitz SI. Psychiatric diagnosis of chronic pain patients. Am J Psychiatry. 1983;140(11):1495-1498.
  28. Fishbain DA, Goldberg M, Meagher BR, Steele R, Rosomoff H. Male and female chronic pain patients categorized by DSM-III psychiatric diagnostic criteria. Pain. 1986;26(2):181-197.
  29. Weisberg JN, Gallagher RM, Gorin A. Personality disorder in chronic pain: A longitudinal approach to validation of diagnosis. Paper presented at: 15th Annual Scientific Meeting of the American Pain Society; November 1996, 1996; Washington, DC.
  30. Conrad R, Schilling G, Bausch C, et al. Temperament and character personality profiles and personality disorders in chronic pain patients. Pain. 2007;133(1-3):197-209.
  31. Wilsey BL, Fishman SM, Tsodikov A, Ogden C, Symreng I, Ernst A. Psychological comorbidities predicting prescription opioid abuse among patients in chronic pain presenting to the emergency department. Pain Medicine. 2008;9(8):1107-1117.
  32. Barry DT, Cutter CJ, Beitel M, Kerns RD, Liong C, Schottenfeld RS. Psychiatric Disorders Among Patients Seeking Treatment for Co-Occurring Chronic Pain and Opioid Use Disorder. J Clin Psychiatry. 2016;77(10):1413-1419.
  33. Majeed MH, Sudak DM. Cognitive Behavioral Therapy for Chronic Pain-One Therapeutic Approach for the Opioid Epidemic. J Psychiatr Pract. 2017;23(6):409-414.
  34. Ehde DM, Dillworth TM, Turner JA. Cognitive-behavioral therapy for individuals with chronic pain: efficacy, innovations, and directions for research. Am Psychol. 2014;69(2):153-166.
  35. Knoerl R, Lavoie Smith EM, Weisberg J. Chronic Pain and Cognitive Behavioral Therapy: An Integrative Review. West J Nurs Res. 2016;38(5):596-628.
  36. Cederberg JT, Cernvall M, Dahl J, von Essen L, Ljungman G. Acceptance as a Mediator for Change in Acceptance and Commitment Therapy for Persons with Chronic Pain? Int J Behav Med. 2016;23(1):21-29.
  37. Chakhssi F, Janssen W, Pol SM, van Dreumel M, Westerhof GJ. Acceptance and commitment therapy group-treatment for non-responsive patients with personality disorders: An exploratory study. Personality and mental health. 2015;9(4):345-356.
  38. McCracken LM. Learning to live with the pain: Acceptance of pain predicts adjustment in persons with chronic pain. Pain. 1998;74(1):21-27.
  39. Wilks CR, Korslund KE, Harned MS, Linehan MM. Dialectical behavior therapy and domains of functioning over two years. Behaviour research and therapy. 2016;77:162-169.

 

 

Hypnotically Enhanced Addictions Treatment

Joseph Tramontana, Ph.D.

As a member of the Board of Directors of the Southern Pain Society, I want to share with the membership a recent workshop I presented to the Canadian Federation of Clinical Hypnosis in Banff, Canada.  The workshop was titled “Hypnotically Enhanced Addictions Treatment: Drug Abuse, Alcoholism and Alcohol Abuse, Gambling Addiction, Smoking Cessation, and Obesity, with a Focus on Drug Dependence during this Opioid Crisis.”

The 2-day workshop was presented by invitation to a group of 19 advanced hypnosis practitioners, including MDs, Psychologists, Licensed Clinical Social Workers, and Licensed Counselors.

While the title was lengthy, a number of problem behaviors were addressed. Dealing with pain patients, was a major focus. For example, if a patient came in experiencing pain at a “7,” (on a 10-point scale)  and after the first hypnosis session he/she reported it was down to a “3,” the change was not only significant, but interpreted to them as “probably as much relief as you get from a pain pill, but it’s natural.” More importantly, the patient is taught self-hypnotic techniques to use at home as a coping skill. The goal is to use hypnotic relaxation when hurting instead of instinctively reaching for the pill bottle. 

Another technique is having the patient, while in trance, imagine the sensation of pain medication, but replicating the relief without the actual medicine.

These techniques fit well with psychoeducation interpretations to patients about the “Mind-body connection.”

Cognitive Behavioral Therapy for Chronic Pain

James L. McAbee, Ph.D.

Individuals living with chronic pain often present with myriad complaints and a decrease in quality of life driven, in many cases, by a lack of adaptive coping skills. Frequently, patients apply conventional wisdom, opting to reduce their activity levels and “resting” as a response to their pain and, in doing so, further reduce their functional capacity and involvement in daily life. These changes in behavior increase the likelihood of time spent ruminating over and brooding about their pain- “will this ever get better?”, “this might get worse”, “nothing seems to help me or my pain”, “I can’t do anything anymore”. Such thought patterns are known in the psychological literature as “Pain Catastrophizing” (Gatchel, 2017; Leung, 2012; Quartana, 2009), and are driven by fears associated with pain and a sense of helplessness/hopelessness when faced with demands to manage pain. This form of thinking leads to increased negative emotions such as anxiety and depression, which can also be influenced by decreased socialization and increased isolation. Patients can then experience physical deconditioning from inactivity and once they engage in some form of activity again they often misinterpret an increase in pain, any experience of new pain, or activity-related soreness as confirmation that that activity is “dangerous”, thus reinforcing the cycle of negative thinking and behaviors. Over time, if left untreated, this cycle leads to less time spent tending to the important territories of life, the boundaries of life shrink inward, and pain overshadows the land.

Cognitive Behavioral Therapy (CBT) is the most efficacious therapeutic intervention utilized by clinical psychologists and has been researched and validated across a multitude of diagnostic categories. CBT is a collaborative, problem-focused intervention that is intended to be delivered in a time-limited format, and which challenges the problematic thoughts/beliefs and behaviors which contribute to and/or maintain the patient’s presenting concern and negative emotions. A therapy session in this approach is more active than traditional psychotherapies and challenges the patient to make changes in both behavioral and cognitive patterns. In CBT the focus is on ‘doing’ things, not just ‘talking’ about things. CBT for Chronic Pain (CBT-CP) can help patients to break free from the chronic pain cycle, and evidence suggests that this modality of psychological intervention improves patients’ functioning and quality of life (Hoffman, Papas, Chatkoff, &Kerns, 2007; Morley, Williams, & Eccleston, 1999; Turner, Mancl, & Aaron, 2006).

As one can see in the cycle of chronic pain described above there are various entry points for intervention from a psychological perspective. In my clinical practice, the initial meeting with a patient is focused on normalizing the patient’s experience, reassuring them that they are not “crazy” nor are they meeting with a psychologist because their pain is “all in their head”, common concerns of patients referred to a pain psychologist. The information gathered via the clinical interview and the patient’s responses to screening instruments and questionnaires, their self-report of current difficulties and observations of their behavior permit more comprehensive feedback regarding the conceptualization of their situation and the opportunity to educate them about the rationale for how CBT-CP can be helpful. I find that when I reflect back to the patient my understanding of their condition (in their own words) paired with printed materials depicting the relationships of how chronic pain impacts their thoughts, feelings, and behaviors, and the cycle of chronic pain, patients are able to relate to the information, understand these connections and “see” problem areas in their lives, thus demystifying the process of treatment.

The overarching goals of CBT-CP are to promote adaptive coping by increasing self-efficacy in the management of pain, reduce avoidant behaviors, reduce “catastrophizing”, reduce negative or unhelpful beliefs about their pain, reduce negative mood symptoms, increase physical activity, to shift the perspective from pain to improved functioning, and to increase general quality of life despite having chronic pain. The intervention itself works toward achieving these goals through liberal use of psychoeducation about factors that perpetuate chronic pain and those which reduce the experience of chronic pain through the acquisition and development of adaptive coping skills. In essence, the goal of CBT-CP is to help patients reclaim the lost territories in their lives, and to have a life worth living despite chronic pain.

CBT-CP sessions are highly structured with the provider setting an agenda of important topics and specific skills to be introduced and developed during a session; however, assisting patients in the development of their own behavioral goals is equally, if not more, important. After all, the goal of CBT is to promote self-efficacy. Printed materials are always given in my practice to allow visual integration of the topics covered in session. Doing so allows patients to leave with information in hand which they can review between sessions. I find that this approach allows patients to remain connected to the material in their everyday environment and to return to the next session with any questions to be clarified. CBT-CP sessions are initially focused on increasing general activities to promote behavioral activation and increase functioning. The use of psychoeducation about how to properly pace activities without overexerting oneself (and possibly a few gentle reminders of the perils of inactivity) allow for development of specific, measurable, achievable, relevant, and time-limited goals (SMART Goals). Integration of scheduling pleasurable activities is also conducted in these early phases of treatment. In addition to increasing general activity, these “new” behaviors begin to inconspicuously challenge patients’ assumptions of “I can’t do anything”, and also begin to improve negative mood symptoms. As one patient eloquently stated, “I’m learning that I can do nothing and hurt, or I can hurt and do some things I enjoy”.

Of course, CBT would simply not be CBT without the “C”. Assisting patients to identify problematic, maladaptive, and unhelpful cognitive patterns is a critical component of the intervention. Providing patients with psychoeducation about the powerful influence thinking has on their behaviors and emotions helps to ground them in their own internal experiences and in their everyday lives. Normalizing problematic thinking can be a validating experience for patients. I always tell patients when reviewing a list of the 12 most common cognitive errors, “If you identify with these, congratulations, you have a normal brain!”. As we review the list together many patients will say, “oh yeah, I do that” and will frequently provide a recent example from their lives. However, simply identifying problematic thoughts is not enough for change to occur, it is essential to “do” something about it. The use of thought logs allows patients to identify their thoughts and beliefs about their pain in relation to a triggering event and their emotional, physical, and behavioral reactions. Once we have a “map” of this process, together the patient and provider can begin to collaboratively examine how thoughts and behaviors influence emotions and outcomes of the situation in question, and to decide what to “do” about it. Cognitive restructuring is the process of developing more balanced, adaptive, and helpful thought patterns which lead to more adaptive behaviors, reduction in negative emotions, and greater desired outcomes. Patients are then encouraged to experiment with these new patterns of thinking and behaviors to determine whether this change was effective. CBT-CP trains patients to become behavioral scientists in their own right- continuously positing hypotheses and testing new behaviors to (dis)confirm the null hypothesis.

Like any other field of healthcare, pain psychology is also concerned with significant and reliable change. In order to determine whether or not the intervention is effective, we must have a system of objective measurement. Therefore, empirical assessments of symptoms are given on an ongoing basis to track patients’ progress and to better inform treatment. Not only is CBT-CP an evidence-based practice, we generate our own practice-based evidence! These data can be utilized for various purposes in the context of treatment. For example, data can be used to challenge patients’ maladaptive beliefs that they are “not getting any better” when subjective reports of difficulties remain high despite the evidence of lower scores compared to the baseline. Equally important, it is quite validating for patients to witness positive change in their objective measures and enhances motivation for sustained behavioral change, particularly in cases where their pain scores remain unchanged, but their function and quality of life is improved.

CBT-CP is an effective intervention to complement a comprehensive approach to pain management. If you are a non-psychologist pain provider, you might find yourself asking, “how do I know that my patients are receiving ‘good’ CBT”. Aside from witnessing a change in your patients’ behaviors (i.e. increased behavioral activities, decreased “catastrophizing” talk, increased self-efficacy, improved mood), ‘good’ CBT is informed by ongoing assessment. It is important for clinicians to ask about patients’ experiences with their pain psychologist to determine the topics discussed and skills developed and ask them directly if they are routinely completing brief assessment measures and receiving feedback in treatment. I personally welcome collaboration with pain providers and encourage patients to sign release of information forms so that I can communicate with other members of the pain management team. This open communication allows for other providers to see what the patient and I are doing, and to provide them with practice-based evidence of patients’ progress. Moreover, it is helpful to hear other potential concerns that have developed over the course of treatment outside the initial referral or the patients’ reports which ought to be addressed in treatment. Speak with the psychologists to whom you refer routinely about how patients are progressing, although we “CBTer’s” are “doers”, we also enjoy talking with other providers.

References:

Gatchel, R. J., & Neblett, R. (2017). Pain Catastrophizing: What clinicians need to know. Practical Pain Management, 15(6). Retrieved from: https://www.practicalpainmanagement.com/pain/other/co-morbidities/pain-catastrophizing-what-clinicians-need-know

Hoffman, B.M., Papas, R.K., Chatkoff, D.K., & Kerns, R.D. (2007). Meta-analysis of psychological interventions for chronic low-back pain. Health Psychology, 26(1), 1-9. doi: 10.1037/0278-6133.26.1.1

Leung, L. (2012). Pain Catastrophizing: An updated review. Indian Journal of Psychological Medicine, 34(3), 204–217. http://doi.org/10.4103/0253-7176.106012

Morley, S., Eccleston, C., & Williams, A. (1999). Systematic review and meta-analysis of randomized controlled trials of cognitive behavior therapy and behavior therapy for chronic pain in adults, excluding headache. Pain, 80(1-2), 1-13. http://dx.doi.org/10.1016/S0304-3959(98)00255-3

Quartana, P. J., Campbell, C. M., & Edwards, R. R. (2009). Pain catastrophizing: a critical review. Expert Review of Neurotherapeutics, 9(5), 745–758. http://doi.org/10.1586/ERN.09.34

Sullivan, M. J. L., Bishop, S. R., & Pivik, J. (1995). The Pain Catastrophizing Scale: Development and validation. Psychol. Assess., 7: 524–532.

Turner, J.A., Mancl, L., & Aaron, L.A. (2006). Short- and long-term efficacy of brief cognitive-behavioral therapy for patients with chronic temporomandibular disorder pain: A randomized, controlled trial. Pain, 121(3). 181-194.

Catastrophizing and the Meaning of Pain: Why It Matters

by David Gavel, PhD

Consider this situation: A 51-year-old pipe-welder and father of 3 was in your office this morning to hear the results of an MRI related to complaints of progressively worsening back pain. He sits down and anxiously awaits your feedback as he writhes in pain. You inform him that imaging showed the presence of degenerative disc disease and briefly explain that his condition is present in some form with more than 90% of men over the age of 50 [1], many of whom are asymptomatic [2]. Before he even asks, you explain a variety of non-invasive treatment options for managing the pain and recommend that he consider limiting or altering activities that may speed up the “wear and tear” of his back. He expresses his understanding and heads home to inform his wife that “the doc said my back is disintegrating and I’ll never be able to work again. I don’t know how we’ll survive if I can’t work.”

Notice how the news received by the wife seems to be drastically different than the words you expressed in the office. In this scenario, during your conversation with him there was no conversation about employment, specific worsening of symptoms, or any direct orders to cease and desist all meaningful activity. So, what happened? How did your objective diagnosis and empirically supported recommendations turn into a convoluted message to the wife as if it was a game of telephone at a 7-year-old slumber party? The answer is catastrophizing, and it is explained by the cognitive model.

The cognitive model [3] is a widely accepted and well published framework for understanding the crucial role that internal thoughts and attitudes play in the daily experience of emotion and behavior. More specifically, the model proposes that over the course of our lifetime, we all develop patterns of thought that influence our understanding of the world around us and the meaning we place on events in our lives. Unfortunately, these thought patterns do not always work in our favor and certain dysfunctional thinking patterns tend to underline many of our most undesirable experiences. Among these dysfunctional patterns is the aforementioned catastrophizing. In a nut shell, catastrophizing is the tendency to draw erroneous and often irrational conclusions about the severity of a current situation or to believe that a future situation will end in the worst possible way. For example, after a seven-week romantic relationship ends, a 15-year-old screams “I’ll be alone forever in a house full of cats for the rest of my life!”. Or a middle-aged employee recklessly speeds through rush hour traffic with the thought “If I’m late, I’ll be fired, and we’ll be out on the street for sure.” In both examples, the individual expresses emotions and behaviors that seem unreasonable given the reality of the situation. But that reality is distorted by the worst-case scenario (i.e., belief) that keeps running through their mind (i.e., thought). And the result is a series of undesirable emotions and behaviors.

In the management of chronic pain, catastrophizing is linked to a host of negative physical [4] and psychological outcomes [5] and is a common reason why patients sit in my office and describe how their depression began after a medical provider said “Your back is the worst I’ve ever seen,” “You’ll just have to learn to live with the pain,” or “You will never be able to…(work, play, walk, run, function)…again.” Now to be clear, I have no way of knowing whether quotes like these are the exact words used by the treating medical provider or not. In fact, it is quite likely they are not, and I would like to go on believing that way. But when a patient sits in my office for a psychological evaluation after 8 years of chronic pain that nearly ended with a recent suicide attempt, it is almost irrelevant whether these exact words were ever spoken or not. What matters most is that the patient carrying these burdensome thoughts interpreted that meaning from the situation: “life as I know it, is over.” And like a church bell clanging through the empty halls of a cathedral, this sentiment rings loud and clear inside the mind of the patient and influences every aspect of life for the worse.

Fortunately, there are a number of very effective forms of mental health treatment of chronic pain (e.g. cognitive behavioral therapy for pain) but one does not have to be a psychologist or other mental health provider to help offset some of this influence with patients. In a brief informational blog post entitled “What’s in a Word? The Power of Language in Chronic Pain Treatment,” [6] physiotherapist Carol Miller discusses the influence of language in the assessment and treatment of pain. Ms. Miller encourages providers to use language to explore and understand the patients’ subjective beliefs about pain, expectations for their treatment, and goals for the future. Asking open ended questions or using norm-referenced pain screeners (e.g., Pain Catastrophizing Scale) are two effective and brief methods for eliciting thoughtful information about the patient experience. Furthermore, she offers the idea that understanding our own beliefs about chronic pain and how those beliefs are reflected in our language can lead to more effective patient encounters. Regarding catastrophizing, Ms. Miller’s recommendations for intentional focus on language can lead to invaluable opportunities for providers to clarify any erroneous conclusions a patient may have drawn about the implications of their condition. George Orwell once remarked that “if thought corrupts language, language can also corrupt thought.” If we accept that our spoken words are the outward expression of internal thought, then we must also accept that our words carry weight that bears meaning for the thoughts and lives of our patients.

[1] Teraguchi M, Yoshimura N, Hashizume H, et al. Prevalence and distribution of intervertebral disc degeneration over the entire spine in a population-based cohort: the Wakayama Spine Study. Osteoarthritis And Cartilage. 2014;22(1):104-110. doi:10.1016/j.joca.2013.10.019.

[2] Brinjikji W, Luetmer PH, Comstock B, et al. Systematic Literature Review of Imaging Features of Spinal Degeneration in Asymptomatic Populations. AJNR American journal of neuroradiology. 2015;36(4):811-816. doi:10.3174/ajnr.A4173.

[3] Beck, J. S. (2011). Cognitive behavior therapy: Basics and beyond (2nd ed.). New York, NY, US: Guilford Press.

[4] Talaei KM, Fischerauer SF, Lee S, Ring D, Vranceanu A. Pain Catastrophizing Mediates the Effect of Psychological Inflexibility on Pain Intensity and Upper Extremity Physical Function in Patients with Upper Extremity Illness. Pain Practice. 2017;17(1):129-140. doi:10.1111/papr.12494.

[5] Shim E, Song Y, Park S-H, Lee K-M, Go D, Hahm B-J. Examining the Relationship Between Pain Catastrophizing and Suicide Risk in Patients with Rheumatic Disease: the Mediating Role of Depression, Perceived Social Support, and Perceived Burdensomeness. International Journal of Behavioral Medicine. 2017;24(4):501-512. http://lynx.lib.usm.edu/login?url=http://search.ebscohost.com/login.aspx? direct=true&db=s3h&AN=124131574&site=ehost-live. Accessed October 10, 2018.
[6] https://ignitephysio.ca/blog/whats-in-a-word-the-power-of-language-in-chronic-pain-treatment/

The Homebound Adolescent Headache Patient

Larry Robbins, MD and Alison Alford, MD

Introduction: Which Adolescents Should Be On Homebound?

It is not uncommon for adolescents with severe headaches to be absent from school for long periods of time. Each child is unique, with multiple variables that include: frequency and severity of headaches, response to medication, psychological make-up, history of abuse, resilience and functioning, catastrophizing, stresses and response to stress, family and friends support system, and school support. In addition, family dynamics plays a role. The parents’ psychological condition is also an important factor.  

Traditional schooling is not for every child. Many adolescents with chronic headaches function significantly better at home. They do not have to contend with a stressful, noisy, bright environment throughout the day. The goal of finishing high school, one way or another, is sometimes easier through homebound. The downsides of homebound include: the patient is at risk for isolation (as social interactions are limited), and learning high school material can be more challenging at home. The decision to go on homebound is a complex and difficult one. There are some children on homebound that should be in school. Many adolescents require a tough love approach and must be pushed to go to school. Others do best with home schooling, or primarily online education. A modified school program, with very limited hours in school, works for some. In our experience, for most on homebound, it has been the correct decision.

Frequency and Severity of The Headaches

The nature of the headaches is important. NDPH (New Onset Daily Persistent Headache) is often more difficult to treat than is transformed migraine. Pain severity is only one contributing factor towards disability (along with catastrophizing, fear of pain, psychological make-up, resilience, etc). Daily headaches are more likely to lead to homebound than are episodic migraines. Family history may provide clues. If headaches are prevalent on both sides of the family, then it is more likely that frequent or daily headaches will occur in the child.  Most homebound adolescents with headaches suffer from chronic migraine.

Medications

When the preventive medications are effective, functioning is usually improved. For many with frequent or daily migraines, preventives are not effective over the long-term. They may work reasonably well for 3 to 6 months, but the dropout rate from 6 to 12 months is significant. Side effects often limit use. Even onabotulinum toxin A (Botox) may not provide adequate relief. It helps if abortive medications are effective, but the headache patient cannot “chase” the pain all day, every day.

Choosing medications is highly individualized. Algorithms do not work. We assess previous response and side effects to medications. Family history of medication response is helpful as well. For instance, if mom brings in her daughter, Heather, and we suggest topiramate, mom may say, “Yes, topiramate was a miracle for me!” Topiramate would then be a reasonable medication for Heather, because of genetic response to medications, and also the “placebo by proxy” factor. If the mom says, “No, topiramate was horrible, it almost killed me!” then it would not be a good choice. With that response, we may incur the “nocebo by proxy” response to topiramate.

Weight issues play a role in determining medication choice, as does energy level. Fatigue is often present among those with daily headaches, and we don’t want to exacerbate tiredness with our medication.       Comorbidites drive where we go with treatment. Medical comorbidities in adolescents include various GI issues, low blood pressure, tachycardia, asthma, and others. Psychiatric comorbidities help to determine our medication choices. For anxiety and depression, the SNRIs, such as duloxetine or venlafaxine, may help both headaches and moods (assuming mild bipolar is not present). Insomnia is commonly encountered in this population, and the older tricyclics are often helpful. Certain muscle relaxants may improve insomnia and pain. SSRIs may help with moods, but usually are ineffective for headache prevention.  

Cost may be an issue with certain medications. For instance, onabotulinum toxin A (Botox) is only officially indicated age 18 and up. However, many adolescents receive Botox (off label) for chronic migraine, but it is costly. Patient preferences play a major role in choosing therapies; many patients (and their parents) want only “natural” treatments, or do not wish to take daily preventives.

Psychological Conditions

Anxiety and/or depression are conditions commonly seen in homebound adolescents. Psychotherapy is our most valuable therapy for many of the patients.  Stresses and family dynamics need to be explored. For adolescents with significant depression, the mild end of the bipolar spectrum should be considered. We do not want to prescribe antidepressants prior to assessing for the soft signs of bipolar. Soft signs of bipolarity include: early depression, positive family history, persistent agitation and anger, mild hypomanias, poor or opposite response to antidepressants (and certain other medications), mind racing, hypersomnia (insomnia may occur but is less frequent), and other traits. The family history may include severe depression, hospitalization, mania, opposite reaction to certain drugs (such as antidepressants), and abuse of drugs or alcohol. The quality of the mind racing is helpful to determine. With anxiety, minds will race with worries. The patient in the bipolar spectrum often will simply have racing thoughts, regardless of worry or anxiety. Bipolar I with manic episodes is usually easily diagnosed; it is the softer end of the bipolar spectrum that is frequently missed.

A history of abuse (physical, emotional, or sexual) as a child predisposes to chronic severe pain. A stressful childhood may influence the sensitive, developing brain chemistry. This may also predispose to psychiatric conditions as well.

Personality disorders, or personality disorder characteristics, may be diagnosed prior to age 18. For those diagnosed with personality disorders at age 16, at least 1/3 of the patients will be significantly improved by age 30. Most with personality disorders have a spectrum of traits. These include: splitting and inability to see “greys” (black and white thinking), poor sense of self, abandonment issues, anger, irritability, thin-skinned (families are “walking on eggshells”), impulsivity, self-harm, suicidal thoughts, ultra-rapid cycling of moods, lack of empathy, narcissism, drama, chaos, severe loneliness, constant spending, and other traits. We would only diagnose a probable personality disorder in an adolescent if these behaviors were moderate to severe, persistent, and pervasive. Certainly, many of these personality traits coincide with typical adolescent behaviors, but it is the severity and persistence of the behaviors that raises the possibility of a personality disorder.

Factitious disorders occasionally are encountered among homebound adolescents. True conversion disorder occurs, but is rare. Neurologic symptoms may take various forms, such as: headache, weakness or paralysis, non-epileptic seizures, motor tics, and tremors.

The psychiatric health of the parents is important.  The most difficult situations occur when a parent has a personality disorder. Mild factitious disorder by proxy (“factitious disorder imposed on another”) is occasionally present. With the mild form, the parent (usually the mother) is not actually directly poisoning the adolescent. She will drag the child to various healthcare providers, with a variety of medical complaints, including headache. The parent almost always has a personality disorder, usually borderline.  When confronted by the physician, the parent (and adolescent in tow) usually flees the office, never to be seen again. When the factitious disorder by proxy (“factitious disorder imposed on another”) is mild, a non-confrontational “dialectical by proxy” approach sometimes is effective. After high school, if we can achieve a separation of adolescent from parents, headaches and behaviors usually improve. The major problem that occurs is when both the parent and child have a personality disorder. In those situations, the patient is likely to continue living at home in a dysfunctional state, even into adulthood.

Catastrophizing and Acceptance

Catastrophizing is often a major contributor towards disability. We can, as physicians, therapists, and parents, work on “dialing down the catastrophizing dial.”  We often see “catastrophizing by proxy,” where the parent makes statements such as, “My child has severe daily headaches, nobody has pain like this, he can’t possibly go on like this…” Fear of pain, and passive (vs. active) coping, are also important contributors toward disability.

Acceptance is also an important concept. We try and work towards “acceptance, but not resignation.” Lack of acceptance by the parent (“lack of acceptance by proxy”) is frequently encountered. As with any chronic pain condition, accepting that there is not a miracle “aha moment cure” is important. Lack of acceptance leads to a constant search for the magic cure, and can result in visits to many various types of providers. The road to acceptance may take various pathways. Along with acceptance, we also emphasize that the headaches are very treatable, and may improve or resolve naturally.

Resilience and Coping

Resilience often has an underlying genetic basis. The serotonin transporter gene has 2 “arms,” short or long. Each person has 2 “arms.” Two long arms predicts a tendency towards higher resilience. Two short arms often leads to a lower level of resilience. Tests for long arm-short arm of this gene are commercially available. The genetic basis for resilience has been studied mostly in the setting of moderate to severe childhood stress or abuse. Various psychological conditions also play a major role in resilience. In addition, modeling of resilience (or lack thereof) by the parents is important.  

Resilience and coping vary widely among adolescents. One patient may have severe stress at home, severe 24/7 headaches, and never miss a day of school. The next person may have mild pain, and be out of school for years. We don’t want to “punish” adolescents for their lack of resilience or coping. However, improving coping is always a major goal. We usually need to have the patient, physicians, therapists, teachers, and parents all working together. As with adults on disability, improving coping is not easily accomplished.

Active coping is a key, along with improving self-efficacy. We must encourage coping strategies outside of simply taking medication. These include seeing therapists, exercise, meditation, etc.

It Takes A Village

While medications may be important, it’s also important that we take a multidisciplinary approach. Individual psychotherapy is often our most effective tool for helping the adolescent patient. Therapists may help with the usual adolescent stresses, coping, insomnia, and family issues. Parents and siblings are profoundly affected by the adolescent with chronic pain. Family therapy may be beneficial. Not all adolescents, or parents, are ready for psychotherapy. Sometimes it takes repeated efforts to convince the family of the benefits of therapy.

Physical therapists can be helpful with posterior head pain, or with associated neck or back pain. Working on posture, stretching, and exercise is important.

Biofeedback is time intensive and expensive, but may be very helpful. Meditation is easier to learn, and may be more accessible for patients than biofeedback. For the patient with sleep issues, working on “sleep rules” and improving sleep may benefit mood and headache.

We are not simply treating one child in isolation. Along with the family, we are also working with the school. Teachers and school staff are important “villagers” in our multidisciplinary approach. 

Returning To School

When a homebound child returns to school, it is helpful to ease back slowly. Late starts, shortened days and no gym(or limited physical activity) may help. Extra time on exams may be appropriate. If the adolescent is at least willing to return to school part time, we will do our part and help to facilitate the return.  A 504 medical plan may help.  Permission to leave class early may minimize exposure to loud noise. Eating lunch in an alternative location may minimize the loud noises. Some students find sunglasses, usually a mild tint, to be very beneficial.  For students on homebound, some communities offer select classes off-site, with a small group of students. This small setting may also work for science lab classes. It may take a combination of home schooling, part time regular high school, and summer classes as well.  The primary goal is to achieve a high school degree, either through the local high school, or via the GED.

Conclusion

 Our approach with refractory adolescent headache patients has evolved over time. While the “tough love” approach is best for a minority of patients, many adolescents do well with partial or full homebound programs. It “takes a village,” and we favor a multidisciplinary approach. Once high school is finished, most adolescent headache patients improve and do fairly well.

Author’s Bio:  Lawrence Robbins, M.D. is the author of 5 headache books. The latest is “Advanced Headache Therapy.” He has had 320 articles/abstracts published. Dr. Robbins is in private headache practice in Riverwoods, Ill.  Web:  Chicagoheadacheclinic.com

Alison Alford, M.D. is a board certified pediatric headache specialist in Richmond, VA. She has co-authored a chapter in Pediatric Epilepsy (subject=felbamate) by Pellock, et al.   Dr. Alford is in private practice at the Pediatric Headache Center of Richmond. Pediatricheadachecenter.com

Resources

  1. Agoston, A., Gray, L., Logan, D. Pain in school: Patterns of pain-related school impairment among adolescents with primary pain conditions, juvenile idiopathic arthritis pain, and pain-free peers.  Published online (2016) November 30, MDPI.com.  doi: 10.3390/children3040039.
  2. Chann, E., Piira, T, Betts, G. The school functioning of children with chronic and recurrent pain. Pain Lett. (2005), 7, 11-14.
  3. Logan, D.E., Simons, L.E., Stein, M.J., Chastain, L. School impairment in adolescents with chronic pain. Pain (2008), 9, 407-416.
  4. Konijnenberg, A.Y, Uiterwaal, C.S., Kimpen, J.L., van der Hoeven, J., Buitelaar, J.K., de Graeff-Meeder, E.R. Children with unexplained chronic pain: Substantial impairment in everyday life. Dis. Child (2005), 90, 680-686.
  5. Roth-Isigkeit, A., Thyen, U., Stoven, H., Schwarzenberger, J., Schmucker, P. pain among children ad adolescents: Restrictions in daily living and triggering factors. Pediatrics (2005), 115, e152-e152-e162.
  6. Logan, D.E., Curran, J.A., Adolescent chronic pain problems in the school setting: Exploring the experiences and beliefs of selected school personnel through focus group methodology. Adolesc. Health (2005), 37, 281-288.
  1. Logan, D.E., Coakley, R.M., Scharff, L. Teachers’ perceptions of and responses to adolescents with chronic pain syndromes. Pediatr. Psychol. (2007), 32, 139-149.
  2. Lewandowski, A.S., Palermo, T.M., Kirchner, H.L., Drotar, D. Comparing diary and retrospective reports of pain and activity restriction in children and adolescents with chronic pain conditions. J. Pain (2009), 25, 299-306.
  1. Sturge, C., Garralda, M.E., Boissin, M., Dore, C.J., Woo, P. School attendance and juvenile chronic arthritis. J. Rheumatol. (1997), 36, 1218-1223.
  1. Kashikar-Zuck, S., Lynch, A.M., Graham, T.B., Swain, N.F., Mullen, S.M., Noll, R.B. Social functioning and peer relationships of adolescents with juvenile fibromyalgia syndrome. Arthritis Rheum. (2007), 57, 474-480.
  1. Walker, L.S. Helping the child with recurrent abdominal pain to return to school. Ann. (2004), 33, 128-136.
  1. Hunfeld, J.A., Perquin, C., Duivenvoorden, H.J. , Hazebroek-Kampschreur, A., Passchier, J., van Suijlekom-Smit, L., van der Wouden, J. Chronic pain and its impact on quality of life in adolescents and their families. Pediatr. Psychol. (2001), 26, 145-153.
  1. Brna, P., Gordon, K., Dooley, J. Canadian adolescents with migraines: Impaired health-related quality of life. Child Neurol. (2008), 15, 39-43.
  1. Fuh, J.L., Wang, S.J., Lu, S.R., Liao, Y.C., Chen, S.P., Yang, C.Y. Headache disability among adolescents: A student population-based study. Headache (2010), 15, 210-218 doi: 10.1111/j.1526-4610.2009.01531.x.
  1. Just U., Oelkers, R., Bender, S., Parzer, P., Ebinger, F., Weisbrod, M., Resch, F. Emotional and behavioral problems in children and adolescents with primary headache. Cephalalgia (2003), 15, 206-213. doi: 10.1046/j.1468-2982.2003.00486.x.
  1. Milde-Busch, A., Boneberger, A., Heinrich, S., Thomas, S., Kuhnlein, A., Radon, K., Straube, A., von Kries, R. Higher prevalence of psychopathological symptoms in adolescents with headache. A population-based cross-sectional study. Headache (2010), 15:738-748. doi: 10.1111/j.1526-4610.2009.01605.x.
  1. Bellini, B., Arruda, M., Cescut, A., Saulle, C., Persico, A., Carotenuto, M. … Guidetti, V. Headache and comorbidity in children and adolescents. Headache Pain (2013), 14, 79. doi: 10.1186/1129-2377-14-79.
  1. Arruda, M.A., Bigal, M.E. Behavioral and emotional symptoms and primary headaches in children: A population-based study. Cephalalgia (2012), 14, 1093-1100. doi: 10.1177/0333102412454226.
  1. Bruijin, J., Locher, H., Passchier, J., Dijkstra, N., Arts, W.F. Psychopathology in children and adolescents with migraine in clinical studies: A systemic review. Pediatrics (2010), 14, 323-332. doi: 10.1542/peds.2009-3293.
  1. Brazelon, E. A question of resilience. New York Times Magazine, April 30, 2006.

Is Compassion Fatigue the Adversary of Compassionate Pain Management?

Ann Quinlan-Colwell, PhD, RNC, AHNBC, DAAPM

In the last newsletter, compassion was discussed as the possible ghost of pain management.  Intrinsic in that possible relationship is the potential ingredient known as compassion fatigue which is described by Sinclair and colleagues (2017) as “a work-related stress response in healthcare providers that is considered a ‘cost of caring’ and a key contributor to the loss of compassion in healthcare.”   The stress response involved in compassion fatigue is believed to evolve while caring for patients, clinicians repeatedly experience, in a secondary manner, the traumatic events and/or suffering of patients.  Although, there is no identified theoretical basis, empirical validation or measurement, there is general consensus that compassion fatigue is real and does clinically exist internationally (Sinclair et al, 2017).  It is certain that for a clinician to experience compassion fatigue, the clinician must first have compassion and experience compassion with patients. Ironically, the terminal result of compassion fatigue is that such an originally compassionate caregiver, no longer feels empathic or nurturing toward others, and no longer feels energetic or enthusiastic about the profession once so loved.

The term was first used in 1992 by a nurse educator, C. Joinson, who coined the term compassion fatigue to describe the burnout she observed among healthcare providers.  Today, although compassion fatigue is at times considered a branch of burnout (Sabo, 2011), it is generally considered different from burnout (Lanier, 2017).  In 1995, Dr. Charles Figley (Tulane University) described compassion fatigue occurring as the result of secondary traumatic stress occurring among caregivers when caring for people who are suffering as a result of a traumatic event.  He described the secondary traumatic stress/compassion fatigue as being similar to the post traumatic stress disorder (PTSD) experienced by the traumatized person.  In fact, the symptoms attributed to PTSD and compassion fatigue are remarkably similar (See Table 1). 

Table 1

Post Traumatic Stress Disorder Symptoms

Compassion Fatigue Symptoms

   

Upsetting thoughts

Intrusive thoughts

Irritable

Irritability

Flashbacks

Traumatic memories

Upset by memories

Anger

Trouble sleeping

Insomnia or difficulty sleeping

Nightmares

Nightmares

Concentration difficulties

Difficulty concentrating or focusing

Jumpy

Startle reactions

Overly careful

Hypervigilant

Emotional distance

Patient/client avoidance

Overly careful

Self-doubt and questioning self

Loss of interest

Depressed mood

Avoid activities

Isolating self

Memory difficulties

 

Taken from:

Foa, Johnson, Feeny, & Treadwell, (2001).

Taken from:

Fidley, 1995; Fidley, 2002; Sabo, 2011; Sinclair, et al, 2017

Figley defined compassion fatigue “as a state of tension and preoccupation with the traumatized patients by re-experiencing the traumatic events, avoidance/numbing of reminders persistent arousal (e.g. anxiety) associated with the patients … a function of bearing witness to the suffering of others”  (Figley, 2002, p. 1435).  The Compassion Fatigue Self Test of Psychotherapists was developed by Figley and later adapted by others with one version adapted with the permission of Figley available via http://www.community-networks.ca/wp-content/uploads/2015/07/Self-Assessment-Tools-Compassion-Fatigue-Feb-22-2010.pdf   In his Compassion Stress and Fatigue Model, Figley (1995, 1997, 2002) described ten variables which combine to result in compassion fatigue and which can be modified to avoid or mediate the development or experience.  The ten variables are listed in Table 2 along with a brief description of each one.

Table 2 Variables of Figley Compassion Stress and Fatigue Model

Model Variable

Description  of variable

Empathic ability

The ability to appreciate pain in another person.

Empathic concern

The impetus to respond to the pain of another person.

Exposure to the patient

Directly being exposed to and experiencing the emotional energy of the suffering person.

Empathic Response

Using insight to share the perspective of the suffering person in an effort to ease the pain and suffering of the person.

Compassion Stress

The effect of the energy expending during the empathic response which can result in negative effects on the well- being of the caregiver.

Sense of Achievement

The satisfaction with compassionate efforts that are experienced by the caregiver who has clear boundaries and concepts of responsibility. 

This variable is protective against compassion fatigue and promotes compassion satisfaction.

Disengagement

The ability, between encounters, to put space between self and the suffering patient and let go of the qualities associated with the suffering experience.  It also involves the clinician in fully engaging in his or her own life. 

When utilized this variable also is protective against compassion fatigue. 

Prolonged Exposure

Over time the persistent belief of responsibility for the person and the associated suffering.  The more intense the exposure with limited interruptions the greater the compassion fatigue.

Traumatic Recollections

These are memories of other experiences or the experiences of other patients which trigger emotional and stressful reactions (i.e. anxiety or depression).

Life Disruption

The unanticipated events that necessitate change in routine or schedule which normally occur in life.  However, when combined with the other variables, the likelihood of compassion fatigue developing increases.

 

Taken from: Figley, 2002, pp. 1436 – 1438.

Although the concept descriptor, compassion fatigue, was only coined 25 years ago, compassion fatigue is now considered an occupational hazard of health care workers (Mathieu, 2012).  Estimates of prevalence range as high as 40% in Intensive Care Units (van Mol, Kompanje, Benoit, Bakker, & Nijkamp, 2015).  Not only is it a general occupational hazard, but among clinicians who strive not only to do well, but to at all times to do their best,  Figley noted it is a “disorder that affects those who do their work well” (Figley, 1995, p. 5).  Traumatologist Eric Gentry proposed that many who enter caregiving professions suffer from compassion fatigued prior to even starting their profession because they previously learned to care for others rather than learning to care for self (Lanier, 2017).

Equipped with this knowledge, it seems reasonable to conclude there is an ethical responsibility to educate those who are at greatest risk (i.e. all clinicians) to be able to empathically and compassionately care for patients while promoting compassionate satisfaction and preventing compassion fatigue.  As a first step in addressing this responsibility, the next segment of this series will address the concept of self-compassion and the final segment will discuss restoring compassion in the work of pain management.  Now that you have read about the dilemma, hopefully, you will return to read about viable resolutions.

 

References

Abendroth, M., (Jan 31, 2011) “Overview and Summary: Compassion Fatigue: Caregivers at Risk” OJIN: The Online Journal of Issues in Nursing Vol. 16, No. 1, Overview and Summary. DOI: 10.3912/OJIN.Vol16No01OS01

Figley, C. (1995). Compassion fatigue: Coping with secondary traumatic stress disorder in those who treat the traumatized. New York, NY: Brunner-Routledge.

Figley, C.R. (1997). Burnout in families: The systemic costs of caring. Boca Raton: CRC Press

Figley, C. (2002). Compassion fatigue: Psychotherapists’ chronic lack of self care. Psychotherapy in Practice, 58(11), 1433-1441.

Foa, E. B., Johnson, K. M., Feeny, N. C., & Treadwell, K. R. (2001). The Child PTSD Symptom Scale: A preliminary examination of its psychometric properties. Journal of Clinical Child Psychology, 30(3), 376-384.

Gentry, J. E..  Baranowsky, A. & Dunning,   (1997).  Compassion Fatigue Article: Accelerated Recovery Program (ARP) for compassion fatigue.  Traumatology Institute. Online Training for Trauma Professionals.

Joinson, C. (1992). Coping with compassion fatigue. Nursing 22(4), 116-122.

Lanier, J. (2017).  Running on empty: Compassion fatigue in nurses and non-professional caregivers. The Bulletin Indiana State Nurses Association, 44(1), 10-14.

Mathieu, F. (2012). The Compassion Fatigue Workbook. NY, NY: Taylor and Francis Group.

Sabo, B., (Jan 31, 2011) “Reflecting on the Concept of Compassion Fatigue” OJIN: The Online Journal of Issues in Nursing Vol. 16, No. 1, Manuscript 1. DOI: 10.3912/OJIN.Vol16No01Man01

Sinclair, S., Raffin-Bouchal, S., Venturato, L., Mijovic-Kondejewski, J., & Smith-MacDonald, L. (2017). Compassion fatigue: A meta-narrative review of the healthcare literature. International Journal of Nursing Studies, 69, 9-24.

Todaro-Franceschi V.  (2013). Compassion Fatigue and Burnout in Nursing New York, NY: Springer Publishing Company.  ISBN: 978-0826109774

van Mol, M. M., Kompanje, E. J., Benoit, D. D., Bakker, J., & Nijkamp, M. D. (2015). The prevalence of compassion fatigue and burnout among healthcare professionals in intensive care units: a systematic review. PloS one, 10(8), e0136955.

Personality Disorders: Recognition and Management in a Pain Clinic

by Larry Robins, MD

Introduction

Patients with moderate-to-severe personality disorders (PD) Are frequently seen in medical practices. It is increasingly important to recognize, limit and manage those with aggressive types of PD.  Likewise, it is crucial to recognize those who fit the bipolar spectrum. In particular, the mild end of the spectrum is often missed. The clinical stakes for missing bipolar are enormous, as these patients tend to bounce from antidepressant to antidepressant, with predictably poor results.  This article delves into recognition and management of patients whose pain treatment is complicated by psychological concerns.

Personality Disorders at a Clinic

Consider the following scenario: a 28 year old man, Bill, presents to the pain clinic with severe low back pain.  He seems angry on the first visit and is very demanding with the front office staff.  Bill tells the staff he is mistrustful of physicians.  He openly states to the doctor, “I will go back to work when you give me the right amount of drugs that help take away my pain.” Bill is upset with his last two health providers.

Over the next few months, the clinic staff bends over backwards for Bill, even though at times he is verbally abusive to the staff with a sense of entitlement.  This is demonstrated in instances such as when he calls and tells the staff: “I want to talk to Dr. Smith NOW, put me through!”  The staff, out of fear, jumps and does what he orders.  His behavior is manipulative. The physician feels as though he is in a subservient position, trying to appease Bill and end the confrontations.

When the physician recommends that Bill be evaluated by a psychotherapist, Bill laughs at the idea and refuses. Suddenly, after nine months of treatment, Bill is suddenly blaming the physician and clinic for all of his difficulties including his pain, obesity, and sexual dysfunction.  Bill threatens to sue the clinic and reports the doctor to the state regulatory office.  What happened here?

Bill was subsequently diagnosed with a paranoid personality disorder.  The clinic employees did not recognize him as having that diagnosis and failed to set limits on Bill’s behavior.  The disruptions in the usual activities of the clinic, the increased stress on the staff, and the monopolization of clinician time are difficult to quantify.  In the remainder of this article features of personality disorders that should help with identification are discussed. Optimal care and management of the disorder begins with recognition.

Approximately 10-12% of people in the general population have features of a personality disorder.1 There are a number of personality disorders, and some are more serious and difficult to treat than others.  In general, characteristics of personality disorders include: lack of insight, poor response to psychotherapy or other therapeutic interventions, difficulty with attachments and trust, a sense of entitlement, and chaotic relationships and distress with family, friends and co-workers.  Comorbid personality disorder with substance abuse is common.

Personality disorders range from mild to very severe and patients with such disorders may take on different roles, including victim, rescuer or persecutor.  When the persecutor role is assumed, the person who is the target may be in danger. Seeing a therapist for a long period of time, perhaps 5-7 years, can help to some degree.  However, goals and expectations must be limited.  Considering the plasticity of the brain is important, as some people can improve naturally over time, particularly among younger patients.   The following section describes some of the more severe personality disorder types.  However, many people do not fit neatly into any of these single categories, because they have features of two or three different personality disorders.

Paranoid Personality Disorder.  People who are diagnosed with paranoid personality disorder tends to be non-trusting, suspicious, related to seeing the world as dangerous. They may seem secretive and reluctant to confide in others.  In relationships, they view themselves as being constantly mistreated, doubt the loyalty of everybody around them, and believe they are being exploited or harmed.  Patients diagnosed with this disorder bear severe grudges against others, often, become angry easily and have a sense of entitlement.  People with paranoid personality disorders can become violent and dangerous, with many spree killers being diagnosed with paranoid personalities.  Several notorious world leaders, including Joseph Stalin and Saddam Hussein, were most likely paranoid personalities.2

Antisocial Personality Disorder.  People diagnosed with antisocial personality disorder characteristically have no regard for the rights of others.  In demeanor, they tend to be irritable, impulsive, and exploitative.  They tend to, see themselves as better or superior, and can be very opportunistic in getting what they want.  People with this disorder   have characteristics of being deceitful, stealing from people around them, and often having trouble with the law.  They frequently engage in fraudulent activities and may be successful as scam artists.  For example, a person with this disorder may take on the role of financial savior for a church, then end up stealing everything from the church.  Generally, people with this disorder have no remorse for their actions. Conduct disorder in a child often morphs into antisocial personality disorder.  Examples include fictional character Tony Soprano on the television show, and, in real life, the mafia’s “Dapper Don,” John Gotti.2

Borderline Personality Disorder (BPD).  Characteristics of people with borderline personality disorder are instability of mood, poor self-image, pervasive abandonment fears, identity disturbance and major boundary issues.  People with borderline personality disorders usually demonstrate impulsiveness, and very quick shifts from depression to anxiety to irritability.  They usually have chronic feelings of emptiness or severe loneliness, plus anger volatile tempers and even suicidal behavior. Under stress, they can become somewhat paranoid.  Coexisting problems with substance abuse or other addictive behaviors may occur, as well as sleep disorders with severe insomnia.  People with severe borderline personality disorders will react with high drama and create chaos for everybody around them.  They tend to have a split world view, which is, they see people as wonderful or terrible, with nothing in between. Borderline personality disorders can vary from mild to severe, nd become better or worse over time. Suicide becomes more likely as patients age into their upper twenties and thirties.3 Suicide is also more common within a week of discharge from a psychiatric unit. Examples of people reportedly diagnosed with borderline personality disorder include Adolph Hitler, Marilyn Monroe, and Glenn Close’s character Alex, in the movie, “Fatal Attraction.” 

Narcissistic Personality Disorder.  Narcissistic personality disorder is less common than those previously discussed and is typified by a personality in which the person sees him or herself as superior to others.  People with this personality have characteristics of grandiosity, being vain, requiring admiration, lacking empathy, having a deep sense of entitlement, having strong belief of self-importance and acting to support those feelings of self-importance.  They characteristically have behaviors which are envious, arrogant, exploitative, and can be very angry.  Examples might include General George Patton, Nicole Kidman’s character in the movie, “To Die For,” Michael Douglas’ character, Gordon Gekko, in the movie, “Wall Street.”2

There are a number of other personality disorders which are not as dangerous for the people around them or for health care providers.  Even though PD characteristics may seem extreme, they are often overlooked, and health care clinics may react by reacting to and treating these patients in a dysfunctional manner.  The difficulties begin with not recognizing the personality disorder.

Pain and Personality Disorders

One  study on people with borderline personality (BPD) concluded that BPD comorbidity with migraine is associated with increased disability from the headaches.4  In addition, in that study  those people diagnosed with BPD, were more severely affected by headaches; more inclined to be refractory to treatment; had increase in medication overuse headache; headaches were more pervasive; there was a higher degree of depression; , more unscheduled visits for acute headache treatment; and less chance of adequate response of headache medications..4

Another study indicated the incidence of BPD was increased in migraineurs.5 My recent study of 1000 migraineurs indicated that 5.5% of patients had a moderate or severe personality disorder.6 There is ample evidence that transformed migraine is associated with more prevalent psychopathology, including personality disorder, than is episodic migraine.  BPD can be considered the mental health equivalent of chronic pain.  In my experience, the two most important prognostic indicators for those with PD are impulsivity and substance abuse.

Treatment for those with PD necessitates a caring, but stern, approach.  Limits must be set on clinician contact, including telephone calls. Abuse of staff should not be tolerated.  Referral to other health care providers, particularly mental health professionals, should be suggested.  Psychotherapists and psychiatrists who are experienced with this population are vital if the patient is to be adequately managed.  Many of the PD patients do not do well with traditional, insight-oriented therapy treatment, but are better managed long-term with dialectical behavioral approach.  For a therapy to be beneficial, it must be consistent and long-term.  A psychoeducational approach may also help.  Unfortunately, even with encouragement and support many PD patients will not continue in therapy. Therapeutic goals for the PD patient are relatively modest.

It is easy to become drawn into the drama surrounding patients with PDs, particularly those with BPD.  The patient with BPD may grant the clinician power, but then subvert the therapy.  An example of this would be, “Doctor, you are the greatest, only you can help me.  These headaches ruin my life, ….and I know that nothing is going to work!”  Some clinicians are able to manage working with these patients without becoming involved in the drama and countertransference, but most do not do well working with them.  If there are signs of a dangerous PD (i.e. abuse and anger being demonstrated), during the first visit or phone call to the clinic), rather than becoming enmeshed in the relationship, is better to refer the patient to someone experienced in working with patients with PD.

There are risks inherent in caring for people who are diagnosed with personality disorders. As compared to the general population, those with BPD are at increased risk for suicide, particularly as they progress into middle age.  Identifiable risk factors for suicide among BPD patients include repeated hospitalizations (i.e. five or more), a recent psychiatric hospitalization, and, among adolescents, birth trauma.3 Certain types of PD (i.e. paranoid, narcissistic, antisocial and borderline) are more likely to become angry and vengeful with health care providers working with them; resorting to lawsuits or writing letters to the departments of regulation.  Violence may be threatened.  A patient with PD often presents as a victim, and then rapidly flips into the role of persecutor.  Anger among these patients becomes intently focused, creating a stressful environment for healthcare workers.  Setting limits and keeping careful documentation are important in these situations.

It does take a village to help a patient with a personality disorder, just as it does to adequately treat those with severe pain. It is important to recruit other clinicians, such as mental health providers, physical therapists, biofeedback therapists, etc., to aid in the treatment.

While there are no specific medications indicated for those with PD, the Axis I symptoms are more amenable to pharmacotherapy. Medications, though limited, may be beneficial for the impulsivity, aggression, self-mutilation, anxiety and depression components of PD.7   Antidepressants, mood stabilizers, and antipsychotics may ameliorate symptoms.  Some of these medications may also lessen headache pain as well.  PD patients with severe, chronic pain present additional challenges for treatment. It is important to limit and closely monitor addictive medications.  Particularly with BPD, opioids and benzodiazepines are best avoided.  The diagnosis of a moderate or severe personality disorder alters both goals and approach for pain management.

Conclusion

For patient care, it has become increasingly important to recognize those patients whose psychiatric problems complicate their treatment in a pain clinic. Patients with a personality disorder are more likely to abuse drugs, file lawsuits, or display abusive behavior toward the staff.  With personality disorders, setting limits is vital. 

Treating patients with chronic pain can be complex and challenging enough.  When their patients who live with chronic pain also have psychological comorbidities, it is vital that the psychopathology be effectively attended to, as well as the pain. 

References

  1. Lester G. Personality Disorders in Social Work and Health Care. Nashville: Cross Country University Press; 2002:28-79.
  2. Lester G. Borderline Personality Disorder. Treatment and Management That Works. Nashville: Cross Country University Press; 2005:24-25.
  3. Lester G. Borderline Personality Disorder. Treatment and Management That Works. Nashville: Cross Country University Press; 2005:15-19.
  4. Rothrock J, et al. Borderline Personality Disorder and Migraine. Headache. 2007; 47:22-26.
  5. Hegarty AM. The prevalence of migraine in borderline personality disorder. Headache.1993;33:271.
  6. Robbins L. The prevalence of personality in migraineurs. US Neurological Disease, 2007, Vol.4, Issue I.
  7. Lester G. Borderline Personality Disorder. Treatment and Management That Works. Nashville: Cross Country University Press; 2005:88-91.
  8. American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4th edition. Washington D.C. American Psychiatric Association: 1994.
  9. Akiskal HS. Classification, diagnosis and boundaries of bipolar disorders. Bipolar Disorder.  Edited by Maj M, Akiskal H, Lopez-Ibor J et al.  London, Wiley, 2002, pp 1-52.
  10. Merikangas KR, et al. Comorbidity of migraine and psychiatric disorders.  Neurol Clin. 1997;15:115-123
  11. Baskin SM, et al. Mood and anxiety disorders in chronic headache. Headache. 2006;46(suppl 3):S76-S87.
  12. Robbins L. Bipolar spectrum in Migraine, Cluster and Chronic Tension Headache. US Neurological Disease, 2007, Vol. 3, Issue II.
  13. McIntyre RS, et al. The prevalence and impact of migraine headache in bipolar disorder: Results from the Canadian community health survey. Headache. 2006;46:973-982.
  14. Low NC, et al. Prevalence, clinical correlates and treatment of migraine in bipolar disorder. Headache. 2003;64:53-59.
  15. El-Mallakh, et al. Antidepressants in bipolar depression, in El-Mallakh R, Ghaem S. Bipolar Depression. Washington DC, American Psychiatric Publishing, Inc.; pp149-153.
  16. Calabrese J, et al. A randomized, double-blind, placebo-controlled trail of quetiapine in the treatment of bipolar I or II depression. AM J Psychiatry. 2005;162:1351-1360.

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