Lawson R. Wulsin, MD

Treating depression in the context of any other medical disorders can challenge our usual approaches and frustrate our efforts to reach good outcomes. Not surprisingly, this is especially true for patients with depression and 

 (CHD). For example, how should we screen for CHD risks in our patients with recurrent depression? Does it matter which came first, the depression or the heart disease? What is next for patients who do not respond to the second or third antidepressant trial? How does relapse prevention for depression in patients with CHD differ from relapse prevention in those with depression alone?

Psychiatric epidemiology over the past 10 years has given us some useful guideposts for approaching patients with comorbid depression and CHD.

Psychosocial factors, especially recurrent depressive symptoms, severe mental illness, and high numbers of adverse childhood experiences, contribute substantially to both the onset and progression of CHD.

 is as strong as that of the traditional CHD risk factors, such as 

 Since there is no single cause of CHD, it is helpful to consider psychosocial risk factors among the many contributing influences that determine the course of CHD. The more effectively these psychosocial factors are managed, the fewer hurdles patients will face.

 for CHD represent the many faces of autonomic imbalance, hypothalamic-pituitary-adrenal axis dysregulation, and/or low grade inflammation.

 Each of these pathways reflects chronic dysregulation of the stress response system.

 High risk health behaviors common in depression, such as smoking, physical inactivity, and high-carbohydrate diets, add to this dysregulation process.

 Effective treatment of depression in patients at risk for CHD includes reducing these early indicators of metabolic syndrome.

Patients with depression and elevated cardiac risk factors can often be identified in their 30s and 40s, a prime opportunity for 

 in the context of depression treatment and relapse prevention.

 For patients with recurrent depression, psychiatrists can play an essential role, offering both 

 of CHD risks and behavioral interventions for CHD risk reduction.

The most robust psychosocial interventions for CHD are intensive lifestyle medicine programs.

 Psychiatrists can motivate patients with depression to engage in and sustain these behavior changes.

 summarizes the pathways by which depression leads to adverse cardiac outcomes, and it suggests a framework for approaching common dilemmas in assessment and treatment.

Figure. Mechanisms by Which Depression May Impact Cardiac Outcomes and Possible Targets for Psychiatric Interventions

“Norma,” a 34-year-old single Black woman comes to see you after her third panic attack on the job as a high school history teacher. She is most concerned about the cat calls and notes passed around by 3 senior athletes insinuating she is gay, which she finds threatening and humiliating. She scores 18 on the Patient Health Questionnaire-9 (PHQ 9). Her history reveals at least 2 other episodes of depression lasting several months at ages 18 and 23, both of which resolved without treatment.

Psychiatrists should consider these important questions as they move forward with such a case (

 More digging may illuminate underlying and complicating issues that need to be considered to develop a successful treatment plan.

 The interrelationship and how one disorder impacts the other is an important consideration in understanding the issues at hand and implementing a treatment plan.

 The preceding questions should lead to this important query. Based on the issues uncovered, it should become obvious which cardiac and depressive symptoms should be monitored to ensure a successful outcome.

Table. Guiding Questions When Treating Comorbid CHD and Depression

Do we keep treatment simple, ie, treat her with sertraline, and see what happens? Or do we dig and look for potential complications? Norma’s blood pressure is 135/90, and her resting heart rate is 88, both of which she attributes to her being nervous about the appointment. Further probing reveals she has had high blood pressure readings at 2 gynecology visits for birth control pills in the past 2 years, but it has never been addressed. Her BMI is 29, and her mother developed 

 at age 46. A metabolic panel ordered at your first visit confirms she has high low-density lipoprotein and, therefore, metabolic syndrome (3 of 5 risk factors for CHD).

On her second visit, you press Norma to return to her gynecologist or establish a relationship with a primary care clinician. In addition to a trial of sertraline, you devote some of each monthly appointment to helping her understand how untreated depression accelerates the development of common risk factors for heart disease. At first, she is alarmed. But eventually Norma is motivated to walk to work instead of riding the bus and give up sweetened drinks, 2 behavior changes that are good for her limbic system as well as her heart.

In most individuals the age of onset for 

 appears to precede the age of onset for CHD by about 30 years. But Norma’s case reminds us that the underlying processes for each illness may begin much closer in time for many individuals. These 2 illnesses, recurrent depression and CHD, may be driven by shared genetic vulnerabilities to stress.

 The bidirectional relationship between depression and CHD—each illness raises the risks for the other—means that we should always suspect that in a given patient the occurrence of 1 illness may accelerate the development of the other. It is also safe to assume that effective treatment of either illness facilitates the treatment or prevention of the other illness. For psychiatrists, this translates into the necessity of effective collaborations with primary care clinicians and cardiologists. It is easier to reverse the course of cardiac risk factors when 

, compared to reversing them after the first heart attack.

Systematic symptom monitoring for depression is especially helpful in the context of physical illnesses symptoms that overlap with depressive symptoms. Serial assessments of depressive symptoms with a PHQ-9 or similar measure improves the efficiency of antidepressant treatment trials. It also charts the relationship between depressive symptoms and the target physical measures of CHD. For example, effective treatment of Norma’s panic attacks and depression may reduce her resting heart rate and her need for antihypertensive medication, or it may not. Serial monitoring of both targets is the most efficient way to establish the relationship between these dimensions of the 2 illnesses.

Choosing a treatment option can be guided by a few considerations, such as previous responses, side effects, and genetic drug metabolism profiles. In the absence of any evidence pointing to or from a specific strategy, the serotonin reuptake inhibitors (SSRIs) sertraline and citalopram have the broadest

from clinical trials of antidepressants in patients with CHD, are well tolerated, and have the fewest clinically relevant drug interactions.

 There is also some evidence that SSRIs may provide a protective anti-inflammatory effect in patients with 

 Serotonin-norepinephrine reuptake inhibitors (SNRIs) are second tier choices only because of their smaller research base. The atypical antidepressant mirtazapine carries a heavier risk for metabolic burden, while bupropion may be a first choice for patients who smoke or those who need to avoid potential sexual side effects. Tricyclic antidepressants, because of their lethality in overdose, should be reserved for patients with malabsorption, since blood levels in tricyclics follow a linear dose-response relationship. Their use requires attention to the 

 of arrhythmias and postural hypotension.

Two areas of drug interactions between antidepressants and CHD medications deserve consideration for special monitoring: anticoagulation and arrhythmias. In some patients, SSRIs may augment the effects of anticoagulants in a clinically significant way. International Normalized Ratio (INR) monitoring provides the best way to adjust the proper doses of both sets of medications. In a similar way, SSRIs may prolong the QT-interval (QTc) in a clinically significant way for some patients on antiarrhythmic medications. Citalopram carries a black box warning about its potential for QTc prolongation. Regular electrocardiogram monitoring provides the standard measure for adjusting these doses or determining when a medication switch is necessary.

Studies of response rates to standard antidepressant treatment trials of both medications and psychotherapies have shown mixed results.

 Psychiatrists can expect to see a disproportionate number of nonresponders and partial responders referred by primary care physicians and cardiologists. Here is where a familiarity with standard approaches to treatment-resistant depression can serve us well. After revisiting the accuracy of our 2 primary diagnoses (major depression and CHD), it helps to scour the terrain for any missed comorbid diagnoses, medical or psychiatric, that could undermine the current treatment efforts. On the psychiatric side of the street, the most commonly missed comorbid conditions include attention-deficit/hyperactivity disorder, anxiety disorders, and substance use disorders. On the medical side, unrecognized or inadequately managed chronic pain and sleep disorders are common disrupters of treatment efforts. Effective management of these comorbid conditions often turns a partial responder into a full responder to antidepressant treatments.

The role of daily self-management plans in the treatment of complex comorbid disorders is often overlooked by psychiatrists. For example, exercise has been shown to be as 

 for the treatment of major depression as cognitive beahvioral therapy and pharmacotherapy,

 yet formal exercise regimens are not a common element of treatment plans for patients with depression. Careful attention to structured, daily self-management plans that address both the depression and the CHD can often turn a partial responder into a responder within months. The intensity of the self-management plan needed to achieve a remission of the depression may require a care manager or a health coach in the early stages of exploring what works and sustaining the habit of practicing the plan.

For almost all patients with complex comorbid chronic disorders, many of whom only partially respond to initial treatments, combined treatment plans that include a course of psychotherapy, care management, and stepped care focused on achieving remission from depression is an investment that brings returns for many years.

The relief and sense of emancipation that comes with recovery from depression invites patient and psychiatrist alike to count our victories and overlook the risks for relapse. Although we have achieved our primary goal of relieving suffering, it is also important to prevent future suffering, and there is no better time to prevent relapse than in the wake of a depressive episode. Given that the risks of recurrence for depression are magnified by CHD, and the consequences of a recurrence are more severe when the management of CHD is undermined by a depressive episode, the stakes are high to prevent a relapse in the months and years that follow a recovery from depression. Relapse prevention plans are essential, not extra, especially for patients with comorbid CHD.

Effective relapse prevention plans should include a list of maintenance treatment plans, early warning signs, a monitoring measure, and predetermined early steps to respond to warning signs. This information should be shared in writing with the patient and relevant clinicians, and documented in the patient’s chart. Periodic check-ins, if only through brief phone appointments at 6- or 12-month intervals, can verify which plans are working, and which are not.

Treating depression in people with CHD can be tricky and pose complicated dilemmas. It is reassuring to remember that, in spite of all the dilemmas, guidelines to treat these patients boil down to a simple maxim: what is good for the brain is good for the heart.

is professor emeritus of psychiatry and family medicine in the Department of Psychiatry and Behavioral Neuroscience and Department of Family and Community Medicine at the University of Cincinnati.

is a research fellow in psychiatry in the Department of Psychiatry at Massachusetts General Hospital.

1. Rosengren A, Hawken S, Ounpuu S, et al. Association of psychosocial risk factors with risk of acute myocardial infarction in 11119 cases and 13648 controls from 52 countries (the INTERHEART study): case-control study. 

2. Galatzer-Levy IR, Bonanno GA. Optimism and death: predicting the course and consequences of depression trajectories in response to heart attack. 

3. Thayer JF, Yamamoto SS, Brosschot JF. The relationship of autonomic imbalance, heart rate variability and cardiovascular disease risk factors. 

4. Wulsin L, Herman J, Thayer JF. Stress, autonomic imbalance, and the prediction of metabolic risk: a model and a proposal for research. 

5. Huffman JC, Celano CM, Beach SR, et al. Depression and cardiac disease: epidemiology, mechanisms, and diagnosis. 

6. Dong M, Giles WH, Felitti VJ, et al. Insights into causal pathways for ischemic heart disease: adverse childhood experiences study. 

7. Brown DW, Balluz LS, Heath GW, et al. Associations between recommended levels of physical activity and health-related quality of life. Findings from the 2001 Behavioral Risk Factor Surveillance System (BRFSS) survey. 

8. Weissman MM, Pilowsky DJ, Wickramaratne PJ, et al. Remissions in maternal depression and child psychopathology: a STAR*D-child report. 

9. Jagannathan R, Patel SA, Ali MK, Narayan KMV. Global updates on cardiovascular disease mortality trends and attribution of traditional risk factors. 

10. Silberman A, Banthia R, Estay IS, et al. The effectiveness and efficacy of an intensive cardiac rehabilitation program in 24 sites. 

11. Razavi M, Fournier S, Shepard DS, et al. Effects of lifestyle modification programs on cardiac risk factors. 

12. McCaffery JM, Frasure-Smith N, Dubé MP, et al. Common genetic vulnerability to depressive symptoms and coronary artery disease: a review and development of candidate genes related to inflammation and serotonin. 

13. Sun Q, Townsend MK, Okereke OI, et al. Physical activity at midlife in relation to successful survival in women at age 70 years or older. 

14. Lachman ME, Teshale S, Agrigoroaei S. Midlife as a pivotal period in the life course: balancing growth and decline at the crossroads of youth and old age. 

15. Zambrano J, Celano CM, Januzzi JL, et al. Psychiatric and psychological interventions for depression in patients with heart disease: a scoping review. 

16. Wang L, Wang R, Liu L, et al. Effects of SSRIs on peripheral inflammatory markers in patients with major depressive disorder: a systematic review and meta-analysis. 

17. Marshall JB, Forker AD. Cardiovascular effects of tricyclic antidepressant drugs: therapeutic usage, overdose, and management of complications. 

18. Blumenthal JA, Smith PJ, Hoffman BM. Is exercise a viable treatment for depression? 

Articles

Does it matter which came first, the depression or the heart disease?

Clinical Dilemmas: What’s Good for the Brain Is Good for the Heart

Treating depression in the context of any other medical disorder can challenge our usual approaches and frustrate our efforts to reach good outcomes. Not surprisingly, this is especially true for patients with depression and 

Exploring Integrated and Collaborative Care


Special Report Chair, Michelle Riba, MD, MS

Positivism and Heart Health: Issues for Psychiatrists


Christopher M. Celano, MD, and Jeff C. Huffman, MD

The ABCs of Cardiac Screening and Electrocardiography


Margo C. Funk, MD, MA, and Theodore A. Stern, MD

The Cardiovascular Consequences of Drug Use

Craig J. Beavers, PharmD, FACC, FAHA, FCCP, BCCP, BCPS-AQ Cardiology, CACP


Margo C. Funk, MD, MA, and Junyang Lou, MD, PhD

Treatment Dilemmas in Depression and Coronary Heart Disease


Lawson Wulsin, MD, and Juliana Zambrano, MD

 Psychosocial factors, especially recurrent depressive symptoms, severe mental illness, and high numbers of adverse childhood experiences, contribute substantially to both the onset and progression of CHD.

The large number of psychosocial risk factors for CHD represent the 

 of autonomic imbalance, hypothalamic-pituitary-adrenal axis dysregulation, and/or low grade inflammation.

 High risk health behaviors common in depression, such as 

, physical inactivity, and high-carbohydrate diets, add to this dysregulation process.

Patients with depression and elevated cardiac risk factors can often be 

 in their 30s and 40s, a prime opportunity for preventive interventions in the context of depression treatment and relapse prevention.

, psychiatrists can play an essential role, offering both early identification of CHD risks and behavioral interventions for CHD risk reduction.

The most robust psychosocial interventions for CHD are intensive lifestyle medicine programs

summarizes the pathways by which depression leads to adverse cardiac outcomes, and it suggests a framework for approaching common dilemmas in assessment and treatment.

 More digging may illuminate underlying and complicating issues that need to be consider to develop a successful treatment plan.

The preceding questions should lead to this important query. Based on the issues uncovered, it should become obvious which 

 symptoms should be monitored to ensure a successful outcome.

On her second visit, you press Norma to return to her gynecologist or establish a relationship with a primary care clinician. In addition to a trial of 

, you devote some of each monthly appointment to helping her understand how untreated depression accelerates the development of common risk factors for heart disease. At first, she is alarmed. But eventually Norma is motivated to walk to work instead of riding the bus and give up sweetened drinks, 2 behavior changes that are good for her limbic system as well as her heart.

In most individuals the age of onset for depression appears to precede the age of onset for CHD by about 30 years. But Norma’s case reminds us that the underlying processes for each illness may begin much closer in time for many individuals. These 2 illnesses, recurrent depression and CHD, may be 

 by shared genetic vulnerabilities to stress.

 The bidirectional relationship between depression and CHD—each illness raises the risks for the other—means that we should always suspect that in a given patient the occurrence of 1 illness may accelerate the development of the other. It is also safe to assume that effective treatment of either illness facilitates the treatment or prevention of the other illness. For psychiatrists, this translates into the necessity of effective collaborations with primary care clinicians and cardiologists. It is easier to reverse the course of cardiac risk factors when treated early, compared to reversing them after the first heart attack.

Choosing a treatment option can be guided by a few considerations, such as previous responses, side effects, and genetic drug 

 profiles. In the absence of any evidence pointing to or from a specific strategy, the serotonin reuptake inhibitors (SSRIs) sertraline and 

 have the broadest research base from clinical trials of antidepressants in patients with CHD, are well tolerated, and have the fewest clinically relevant drug interactions.

 There is also some evidence that SSRIs may provide a protective anti-inflammatory effect in patients with major depression.

 Serotonin-norepinephrine reuptake inhibitors (

) are second tier choices only because of their smaller research base. The atypical antidepressant mirtazapine carries a heavier risk for metabolic burden, while bupropion may be a first choice for patients who smoke or those who need to avoid potential sexual side effects. Tricyclic antidepressants, because of their lethality in overdose, should be reserved for patients with malabsorption, since blood levels in tricyclics follow a linear dose-response relationship. Their use requires attention to the potential risks of arrhythmias and postural hypotension.

Two areas of drug interactions between antidepressants and CHD medications deserve consideration for special monitoring: anticoagulation and arrhythmias. In some patients, SSRIs may augment the effects of anticoagulants in a clinically significant way. International Normalized Ratio (INR) monitoring provides the best way to adjust the proper doses of both sets of medications. In a similar way, SSRIs may prolong the 

 (QTc) in a clinically significant way for some patients on antiarrhythmic medications. Citalopram carries a black box warning about its potential for QTc prolongation. Regular electrocardiogram monitoring provides the standard measure for adjusting these doses or determining when a medication switch is necessary.

Studies of response rates to standard antidepressant treatment trials of both medications and psychotherapies have shown mixed results.15 Psychiatrists can expect to see a disproportionate number of nonresponders and partial responders referred by primary care physicians and cardiologists. Here is where a familiarity with standard approaches to 

 can serve us well. After revisiting the accuracy of our 2 primary diagnoses (major depression and CHD), it helps to scour the terrain for any missed comorbid diagnoses, medical or psychiatric, that could undermine the current treatment efforts. On the psychiatric side of the street, the most commonly missed comorbid conditions include attention-deficit/hyperactivity disorder, anxiety disorders, and substance use disorders. On the medical side, unrecognized or inadequately managed chronic pain and sleep disorders are common disrupters of treatment efforts. Effective management of these comorbid conditions often turns a partial responder into a full responder to antidepressant treatments.

The role of daily self-management plans in the treatment of complex comorbid disorders is often overlooked by psychiatrists. For example, exercise has been shown to be as effective for the treatment of major depression as 

The relief and sense of emancipation that comes with 

 invites patient and psychiatrist alike to count our victories and overlook the risks for relapse. Although we have achieved our primary goal of relieving suffering, it is also important to prevent future suffering, and there is no better time to prevent relapse than in the wake of a depressive episode. Given that the risks of recurrence for depression are magnified by CHD, and the consequences of a recurrence are more severe when the management of CHD is undermined by a depressive episode, the stakes are high to prevent a relapse in the months and years that follow a recovery from depression. Relapse prevention plans are essential, not extra, especially for patients with comorbid CHD.

Effective relapse prevention plans should include a list of maintenance treatment plans,

, a monitoring measure, and predetermined early steps to respond to warning signs. This information should be shared in writing with the patient and the relevant clinicians, and documented in the patient’s chart. Periodic check-ins, if only through brief phone appointments at 6- or 12-month intervals, can verify those plans that are working, and identify those that are not.

1. Rosengren A, Hawken S, Ounpuu S, et al. 

Association of psychosocial risk factors with risk of acute myocardial infarction in 11119 cases and 13648 controls from 52 countries (the INTERHEART study): case-control study

3. Thayer JF, Yamamoto SS, Brosschot JF. 

The relationship of autonomic imbalance, heart rate variability and cardiovascular disease risk factors

Insights into causal pathways for ischemic heart disease: adverse childhood experiences study

9. Jagannathan R, Patel SA, Ali MK, Narayan KMV. 

Global updates on cardiovascular disease mortality trends and attribution of traditional risk factors

12. McCaffery JM, Frasure-Smith N, Dubé MP, et al. 

Common genetic vulnerability to depressive symptoms and coronary artery disease: a review and development of candidate genes related to inflammation and serotonin

How does relapse prevention for depression in patients with coronary heart disease differ from relapse prevention in those with depression alone? That question and more answered.

In May 1997, a young Rwandan girl came to a clinic in Kigali reporting nausea and the feeling of insects crawling on her face. She complained of the strong smell of feces and grew increasingly agitated and fearful, describing vivid images of people trying to kill her at that moment. For months she had vomited at the sight of avocados, and for three years she had been unable to tolerate the sight of rice. 

During the evaluation, she related that her parents and siblings had been murdered in the spring of 1994 and that she had been severely wounded. The perpetrators, thinking she was dead, had thrown her into an open public toilet, where she lay for one week among feces and maggots-white maggots resembling bloated grains of rice-feeding on the avocados that fell on her from a tree above the toilet.

In February 1997, outside Rwanda's capital of Kigali, a roadblock stopped a public bus on the Kigali-Gisenyi road. Armed men ordered the passengers to separate according to ethnic allegiance. The armed men then gunned down those suspected of ties with the current regime and let the other passengers go. In January 1998, Rwandan genocide perpetrators entered a working brewery and murdered 30 workers.

Rwanda's 1994 civil war officially ended in July of that year, but as massacres and episodes of genocide continue to erupt sporadically within and around Rwanda's borders, the many faces of posttraumatic stress disorder (PTSD) continue to surface in dramatic ways. Each April through July, the anniversary of the genocide, the Trauma Clinic in Butare sees a parade of people with severe PTSD. 

In April 1997, more than 30 teenagers from Nyanza Secondary School attended a reburial ceremony of the remains of their relatives who died in 1994. They developed acute emotional reactions such as agitation, seeing vivid images of genocide and weeping for over two days after the ceremony ended. The children fled the scene; the government ordered the school to close. 

The same phenomenon happened in Nyamata in a similar memorial service. Closer investigation by the school faculty and a consulting psychiatrist suggested mass hysteria as the most likely explanation. 

The horrors of the civil war in Rwanda have no match in recent history. Never before have so many civilians (at least 500,000) been killed so rapidly (within 3 months) by hand-to-hand combat, primarily with machetes and short-range firearms. 

The most active perpetrators were young men from rural villages. The majority of them had no prior combat experience and were trained in the militia of the ruling party. The majority of the victims were innocent civilians, often neighbors of the perpetrators, and sometimes friends or extended family members. 

In April 1994, high government authorities initially sanctioned genocide by explicit commands transmitted by word-of-mouth and over the radio. Bishops of the Anglican and Catholic churches did nothing to discourage the killing. In a culture that traditionally accords its leaders high respect, such betrayal defied the public trust. 

Following the genocide, the exodus of refugees was rapid and enormous: Over 2 million refugees fled into Zaire and Tanzania by the end of August 1994, and most remained exiled for over two years. The pervasive effects of the genocide, massacres and refugee exodus have spared no one. Every family has experienced maiming, torture or death; each family has witnessed atrocities, lost a home or a family member to refugee status. Many citizens remain missing. And in the three-and-a-half year wake of these events, no satisfactory explanation has emerged for why such unprecedented genocide and massacres should have happened in Rwanda at this time. 

No one knows how prevalent PTSD is in Rwanda, but according to our recent survey its prevalence may approach 20% in the adult population-much higher than in other war-torn countries.

The sudden, overwhelming trauma afflicting most civilians and the persistence of unpredictable threats four years after the "end" of the war (a period now commonly known as "the insecurity" in Rwanda) have caused an epidemic of PTSD and related psychiatric disorders. And yet only one study of the recent prevalence of psychiatric disorders in Rwanda has been published (Hagengimana, 1997). 

To assess the exposure to trauma and the prevalence of psychiatric disorders, Hagengimana completed a door-to-door community survey in 1996. By interviewing the household members in various neighborhoods in Kigali and several outlying towns, he collected data on a sample of 157 citizens between the ages of 8 and 60. Each subject completed the Kinyarwanda translations of the 

Harvard Trauma Questionnaire and the Standardized Psychiatric Interview

, administered by the investigator as an interview.

Fifty percent (79 out of 157) met DSM-IV criteria for a psychiatric disorder. The most common diagnosis was acute grief reaction (25%), but depression (22%) and PTSD (20%) were also common. The average number of traumatic events during the 1994 war reported by each subject was 15. Four of these events were significantly related to the diagnosis of PTSD: forced isolation, the helpless witnessing of atrocities, rape and loss of parents. Treatment for any of these disorders was rare.

Anecdotal support for the findings of this small pilot study comes from the observations of physicians and nurses working in primary care clinics around the country. Emmanuel Gasakure, M.D., a cardiologist and secretary of the faculty of medicine at the National University of Rwanda in Butare, reports that he continues to see many patients with minor physical complaints who are unable to function due to unnamed psychological distress. 

The growing burden of mental illness in Rwanda remains largely unknown and untreated. The culture and its language, Kinyarwanda, still lack words for common depressive and anxiety syndromes. Only since the 1994 civil war has a word emerged for PTSD: ihahamuka, which means "breathless with frequent fear." 

Substance abuse, particularly alcohol dependence, and smoking has risen dramatically since the war, according to Hagengimana's study. 

Two psychiatrists serve a population of 8 million, so specialty mental health treatment is rare. Mental health treatment is usually delivered in outlying clinics or at Rwanda's only psychiatric hospital (outside Kigali) by a few nurses untrained in psychiatry. Other treatment is delivered through the primary care system and by traditional healers. Psychotropic medications have been ample at the hospital but scarce in the rural clinics, so the incentive to diagnose mental illness remains low where pharmacologic treatments are scarce. 

Public health experts in Rwanda generally agree that the highest risk groups for psychiatric disorders currently are widows, orphans and soldiers. Over 60 cases of PTSD among soldiers have presented to the clinic in Butare, mainly in the form of conversion and dissociative reactions. 

One soldier, referred from the front line, presented with aphonia, pseudoparalysis of the right side of the body and contractions of the right hand, particularly the index finger (his trigger finger). 

Another man, an escort for a top officer in the army, lost his siblings and parents in the 1994 genocide. Although he wants to leave the army, his sense of duty prevents him. In January 1998 he lost his auditory acuity and developed la belle indifference. Audiometry done in the Ear, Nose and Throat (ENT) service was normal. 

Signs of a PTSD epidemic abound in Rwanda, but no one knows the size and severity of the trauma-related psychiatric disorders. The barriers to further study of the prevalence and severity of mental disorders are the same barriers that limit access to care; namely, insufficient medical resources, competing political agendas and inadequate public awareness, both within Rwanda and around the world, of the toll of mental disorders related to the 1994 war. 

Hagengimana A, Mburu J, Kang'ethe R, Ndetei D, Wulsin L (1998), PTSD in Survivors of Rwanda's 1994 War. American Psychiatric Association Annual Meeting. New Research #621.

In May 1997, a young Rwandan girl came to a clinic in Kigali reporting nausea and the feeling of insects crawling on her face. She complained of the strong smell of feces and grew increasingly agitated and fearful, describing vivid images of people trying to kill her at that moment. For months she had vomited at the sight of avocados, and for three years she had been unable to tolerate the sight of rice.