by Ian Osborn
BRAIN TRAUMA AND OCD
Direct damage to the basal ganglia can be another cause of OCD. In one reported case, a previously healthy fifty-six-year-old woman with no history of nervous or psychiatric problems was hospitalized following a stroke. For two days she recovered well; then she developed the urge to count things over and over: lines on the wall, dots in the ceiling, and stitches in her hospital gown. She couldn’t stop. A psychiatrist was consulted for treatment of OCD. Several dozen similar cases of brain injury leading to sudden OCD—some involving head trauma, others carbon monoxide poisoning—have been studied. In each instance, X rays, CAT scans, and MRI studies of the brain have shown that the physical injury was limited to the basal ganglia.
Minor brain damage, often caused by childhood infections, birth injury, or genetic factors, is also statistically correlated with the development of OCD. Such subtle brain injuries are usually recognized by the presence of neurological “soft signs,” minor abnormalities affecting movement, coordination, and sensation. In a 1990 study, thirty-four of forty-one patients with severe OCD were found unable to rapidly point their fingers back and forth from one object to another in a normally coordinated manner, whereas only nine in the control group showed the abnormality. OCD patients are also more likely than others to have slight deficiencies in memory and in planning and organizational skills, as demonstrated by neuropsychological testing. OCD patients also often show minor irregularities in vision.
In sum, sufficient evidence has now accumulated that no unbiased observer can seriously doubt that OCD is a true medical disorder. Does this mean that only physical processes are involved in the cause of OCD? Obviously not. Consider again the example of coronary artery disease. Its direct, or proximal, cause is the biochemical abnormality referred to as atherosclerosis. However, many factors contribute to the development of this abnormality, including elevated cholesterol, high blood pressure, and psychological stress. These, in turn, are affected to varying degrees by a person’s genetic makeup, the genes they were born with. In considering the root causes of OCD, genetics and stress are especially important.
THE GENETICS OF OCD
Our understanding of how our genetic makeup interacts with the environment in which we live has grown immensely over the last twenty years. To grasp the implications of the genetic model for OCD, a few basic principles should be kept in mind. It is well known that a person inherits one set of genes from the mother and another from the father. Together, these two join in the formation of a cell, which then starts dividing. With each division, the genes form exact replicas of themselves. The cells, on the other hand, begin to turn out differently.
It has been clear for several decades now that the reason for this type of cell differentiation is that only a small portion of the gene serves as the architectural template for each cell. What has recently been discovered is that the part of the gene that serves as a template is regulated by signals from the outside world. We now know that the genetic plans are not, as many people have thought, fixed and unchanging. Rather, they are regulated, fine-tuned, by experience.
The part of the gene that regulates eyesight, for example, is uncovered shortly after birth, ready to go to work as a blueprint for the visual system. Yet, animal studies show that in order for sight to develop there is a critical period during which perceptions from the outside must start coming in through the eye. If an animal is left in darkness during this interval, the gene controlling vision is covered up, and the opportunity to develop sight is forever lost. A more complicated illustration: Suppose a person is genetically coded to be timid but is raised in a turbulent household where he is continually exposed to dangerous, unpredictable situations. In this case, the plans for timidity languish, and other half-hidden blueprints for aggression and decisiveness are opened up. A person who starts with an inclination to timidity will not necessarily end up that way. Genetic inclinations are adjusted by feedback from life circumstances.
Of the evidence that proves OCD to have a strong genetic influence, family studies are most prominent. Although research of this type cannot provide the absolute final word on genetic cause—that will have to wait for the identification of a specific OCD gene—the results from these studies are already very convincing.
Over a dozen reliable studies, for example, show that on average, if a person has OCD, the chance that a parent, child, brother, or sister will develop the problem is 10–25 percent—much higher than OCD’s overall lifetime incidence of 1–2 percent. In a well-controlled 1995 study, investigators from Yale and Brown universities interviewed all the available parents, siblings, and children of 100 OCD patients, finding that fully 10 percent of these relatives had definite OCD, and another 8 percent had possible OCD. Reviewing all the studies in this area, a team of scientists from four American universities recently concluded that of all anxiety disorders, OCD and panic disorder are the two that run most strongly families.
The results of such family studies, admittedly, can be misleading. Environmental problems such as neglect and abuse, which can run in families for generations, might drive people to obsessions. In order to establish genetic cause with greater certainty, scientists study pairs of twins.
The key to twin studies is the fundamental difference between identical and fraternal twins. Identicals, formed at the union of one sperm and one ovum, have matching genes. They’re clones of each other. Fraternals, on the other hand, result from different sperms meeting different ovums—they’re no more alike genetically than ordinary brothers and sisters. To find out whether a trait is genetic, researchers determine how often it is shared by pairs of identical twins, then they compare that to how often it is shared by fraternals. When a trait is found more often in both identicals than in both fraternals, the discrepancy proves some degree of genetic cause.
In Huntington’s disease, the causative factor is a single mutant gene. If one identical twin is affected with Huntington’s, the other will be affected, too; among fraternals, the disease is shared only 50 percent of the time. Huntington’s is rare—a 100 percent genetic illness. Compare it to generalized anxiety disorder, a broad term for excessive nervousness and worry. Here the incidence in identical twins equals that in fraternals exactly; such anxiety is not genetic at all. Or consider, again, coronary artery disease. A recent study in Norway found that if one identical twin has CAD, the chance of the other twin having CAD is 66 percent, whereas if one fraternal twin has CAD, the chance of the other twin having the disease is 25 percent. CAD, then, is one of many diseases that are partially genetic in origin.
In the case of obsessive-compulsive disorder, ten different studies have reported on a total of fifty-one OCD patients with identical twins; thirty-two of those twins were found to also have OCD (63 percent), while 19 (37 percent) did not. One of the best studies in this area was a 1982 trial that located fifteen OCD patients who had identical twins and another fifteen with fraternals; on interviewing the siblings, 87 percent of the identicals were found to have OCD, while for the fraternal twins that figure was 47 percent. In sum, the results indicate that OCD is a partially genetic disease with a heritability factor that is, in fact, very similar to that of CAD. David Fogelson, psychiatrist at UCLA’s Neuropsychiatric Institute, has concluded: “A good guess is that OCD is 60 percent genetically caused.”
In order to appreciate the scope of the genetic influence in OCD, it is helpful to note that the personality factors associated with OCD—timidity, introspection, and a tendency to depression—have been shown themselves to be genetic to varying degrees. Timidity has been well researched. Tests show that even in the first year of life, the fear of strangers develops more similarly among identical twins than fraternals. Harvard psychologist Jerome Kagan, the world’s expert in this area, has followed infants’ levels of fearfulness from birth to adulthood, finding that although environment does play a part, timidity is, in fact, a largely inherited trait. Introversion is also strongly genetic, as the English psychologist Hans Eysenk
first suggested in the 1950s. A 1992 report by Heath and co-workers in St. Louis on 2000 twins concluded that genetic factors account for 73 percent of the variance in introversion. The tendency to develop severe depression also has a strong genetic component.
Other personality traits that predispose to OCD are also thought to be partially genetic. Robert Cloninger, whose biochemically based personality theory was discussed in Chapter 3, views the traits of novelty seeking, harm avoidance, and reward dependence as independent, genetic factors that lead to OCD. A 1996 article in Nature Genetics has supported this view, reporting the discovery in both Israel and the United States of a specific gene that regulates the trait of novelty seeking.
One important result of the genetic research on OCD, however, is often overlooked. In pointing out percentages of genetic influence, these studies also demonstrate that a large part of the cause of OCD is, indeed, environmental. Heritability of 60 percent still leaves 40 percent for life experiences. This 40 percent may determine whether or not the disorder becomes severe.
STRESS AS A TRIGGER OF OCD
Experts agree that stress plays an important role in the development of OCD. Thus far, seven studies have addressed this issue, with the best work coming from India, where Sumant Khanna and co-workers compared patients with recently developed OCD to a matched control group. In the year prior to developing the illness, the OCD patients experienced more than twice as many stressful events as the control group, particularly episodes of sickness and death in their families.
Stress may lead to OCD by a number of mechanisms. As discussed in Chapter 8, researchers have demonstrated that traumatic experiences must be replayed again and again in our minds until they are processed—matched and integrated with previous life experiences. It is probable that the repeated appearance of minor post-traumatic thoughts secondary to life stresses can start a vulnerable person on the way to experiencing true obsessions.
Researchers have also found that the physiologic state of anxiety itself may lead to obsessions. Studies by Colin MacLeod and co-workers in Australia have demonstrated that highly anxious students have more trouble than others ignoring various types of threats, a finding that has been confirmed by half a dozen other investigators. MacLeod concludes that when we are anxious, an automatic mechanism of the mind opens the door to increased numbers of intrusive, worrisome thoughts.
The important role of life experiences in the development of OCD was certainly true in my own case. My obsessions and compulsions started during my first year of medical school and ceased to be a significant problem once I was finished with the late nights of studying and the long days under scrutiny. A friend provided me with still another example of the effect of stress on the development of obsessions. Soon after her husband died, she began developing for the first time in her life a number of compulsive behaviors: She checked her doors and appliances many times a day to make sure they were safe and frequently had to leave work and run home to see about the electric blanket. She knew this checking was unnecessary and it bothered her, but she could not control it until a year had passed after her husband’s death. In a group for grieving widows, she found that three of the other six women had also developed minor compulsions.
In the cases of my patients, the pattern is similar. I find that their obsessions usually come along—commonly accompanied by other symptoms of anxiety, such as loss of sleep, nervousness, and exhaustion—when health, marital, and job problems pile up.
It is when a person is highly stressed, dealing with life’s more acute difficulties and challenges, that he or she is most likely be hit by self-tormenting thoughts.
The research reviewed in this chapter demonstrates beyond a doubt that OCD is a biological, medical brain disorder with both genetic and environmental determinates. It is worth re-emphasizing that although OCD’s symptoms are directly caused by biochemical brain changes, that does not mean that OCD is merely a matter of biochemistry. Attitudes, behaviors, and life events play a major role. More than biological factors must be addressed.
One current concern of vital interest to OCD sufferers and their advocates is parity in insurance coverage. If OCD is a medical condition, shouldnt it be insured in full? Fearing the high cost of coverage, insurance companies have been dragging their feet on this issue for years, but there is reason for cautious optimism. In 1997 the state legislature of Colorado passed a health insurance parity bill mandating that every policy provide coverage for the treatment of biologically based mental illness that is no less extensive than the coverage provided for any other physical illness. The bill pertains specifically to four psychiatric disorders, one of which is OCD. Similar bills have been introduced in twenty-six other states, and a parity amendment has been introduced to the Kassebaum–Kennedy health insurance legislation of 1997 by U.S. senators Wellstone and Domenici.
10
FROM HYPOCHONDRIASIS
TO SEXUAL ADDICTIONS:
OBSESSIVE-COMPULSIVE
SPECTRUM DISORDERS
As recent discoveries from many different areas of brain research have greatly expanded our knowledge of OCD, interest has been kindled in syndromes that bear similarities to OCD, usually referred to as “OCD-related” or “OC spectrum” disorders. All manifest themselves in either intrusive thoughts that resemble obsessions or repetitive behaviors akin to compulsions. For the most part, these disorders are not especially well understood, and how closely they actually resemble OCD is controversial. Some appear to be quite similar to OCD; they may even be the same disorder. Others, however, seem fundamentally different.
Two of these syndromes, in particular, can appear almost identical to OCD: hypochondriasis (unfounded preoccupations with medical illnesses), and body dysmorphic disorder (preoccupations with deformed appearance). It is quite possible that in the future some cases of both of these will be considered as OCD. Two other syndromes show essential similarities to OCD but also have significant differences: trichotillomania (pathological hair pulling), and anorexia nervosa. Then there are a number of disorders involving a loss of impulse control, such as impulsive stealing and sexual addictions, which are also often included in the OC spectrum.
HYPOCHONDRIASIS
In 1724, the eminent physician Daniel Turner, author of the first English textbook on dermatology, recorded a case of a man with the irrational fear of having syphilis. Dermatologists of that era were keenly interested in syphilis, then the most dreaded of all diseases, because lesions of the skin were often its presenting symptom.
Dr. Turner recounts being visited one evening by “a tradesman in good business, of a thoughtful temper … who sat down and fell into tears, wringing his hands.” The patient had been going from doctor to doctor complaining of a multitude of aches and pains, fearful that he had contracted syphilis. Unable to feel reassured by doctors who told him he had no serious disease, he had seen a number of charlatans, who treated him with strong doses of laxatives and salivants (medications that cause the mouth to water copiously). Subsequently, he misinterpreted the powerful side effects of these drugs, such as nausea and dizziness, as further proof that he did, indeed, have a grave illness. A vicious cycle of anxiety-related complaints and iatrogenic symptoms was in motion.
On examining the patient, Dr. Turner determined that although the tradesman complained of symptoms of his “head, his nose, and all parts of his body,” he had absolutely none of the characteristic symptoms of syphilis. Furthermore, he had not been to a prostitute, then considered the most likely source for contracting the disease. “I now plainly perceived it was all a delusion,” Dr. Turner relates. “I told him he had been abused not by a girl, but by his quack doctors; and that he was free entirely from any such disease, and stood in no need of my assistance.”
Despite such an excellent consultation (we present-day physicians should be so honest and direct), the patient continued to seek out different doctors and to go downhill. Eventually he became bedridden and developed the idea that, since advanced syph
ilis can cause the loss of body parts, his nose might fall off. At that time he called again for Dr. Turner, and while holding tightly onto his nose, angrily told him: “You never would believe I had the distemper, but it is now apparent, for my nose, if I were not to support it, would drop off this instant.”
Dr. Turner relates that he reassured the patient of the integrity of his nose by means of a dramatic demonstration: “Ordering a candle to be brought near, with much difficulty I persuaded him to take away his fingers, when immediately with my own fingers taking fast hold thereof, I raised his head from the pillow, and saying never a word, I let the same drop down again.” When the patient saw that his nose was not in Dr. Turner’s fingers, but rather still on his face, he became “convinced of his mistake.”
But soon the insight gained was lost and his worries returned in full. Dr. Turner then had a talk with the family: “I called his wife aside … and advised her to provide some place for him where he might be kept out of harm’s way.” Following this advice, the patient and his family moved to a country village. His condition improved somewhat, yet he continued to be disabled by his fear of illness. He spent a great deal of time, Dr. Turner notes, examining his nose in front of a mirror.
In discussing the case, Dr. Turner points out the distinguishing feature of hypochondriacs: Despite being free of disease they cannot be convinced that they are well. He also issues the warning that because these patients seem satisfied only when being tried on a new course of medication, they are easy prey for quack doctors.
In the eighteenth century this malady was diagnosed, like OCD, as a type of melancholia, or depression. Now it is classified as a separate disorder. In the current diagnostic manual of American psychiatry (DSM-IV), hypochondriasis is defined as an intense preoccupation with having a serious illness that persists despite medical reassurance. It is estimated that from 5 to 9 percent of patients seen by family doctors suffer from the condition, and perhaps, up to 2 percent of the general population.