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Obsessive Compulsive Disorder Case Study Ppt Sample

In a previous article we reviewed a range of treatments that are used to help clients suffering from obsessive-compulsive disorder (OCD). In this edition we showcase the case study of Darcy [fictional name], who worked with a psychologist to address the symptoms and history of her OCD.

Marian, a psychologist who specialised in anxiety disorders, closed the file and put it into the filing cabinet with a smile on her face. This time she had the satisfaction of filing it into the “Work Completed” files, for she had just today celebrated the final session with a very long-term client: Darcy Dawson. They’d come through a lot together, Darcy and Marian, during the twelve years of Darcy’s treatment for Obsessive-Compulsive Disorder, and they had had a particularly strong therapeutic alliance.

Marian reflected on the symptoms and history which had brought Darcy into her practice.

Obsessions at age nine

Now 37, Darcy reckoned that she had begun having obsessions around age nine, soon after her beloved grandma had died. Already grieving the loss of the person she was closest to in life, Darcy experienced further alienation – and resultant anxiety — when her father relocated the family from the small town in Victoria where they lived to Melbourne. Adjusting to big-city life wasn’t easy for someone as anxious as Darcy, and she soon found that she was obsessing. She had fears of being hit by a speeding car if she stepped off the kerb. She feared that the new friends she began to develop in Melbourne would be kidnapped by bad people. And she was terrified that, if she didn’t do an elaborate prayer routine at night, all manner of terrible things would befall her family.

The prayer routine, relatively simple at first, grew to gigantic proportions, containing many rules and restrictions. Darcy believed that she had to repeat each family member’s full name 15 times, say a sentence that asked for each person to be kept safe, promise God that she would improve herself, clap her hands 20 times for each person, kneel down and get up 5 times, and then put her hands into a prayer position while bowing. She “had” to do this routine at least 10 times each night, and if she made a mistake anywhere along the way, she had to start totally over again from the beginning, or else something bad would happen to her parents or little brother. Once she went flying to her mother’s side in the kitchen, tears streaming down her face, because she couldn’t get her “prayers” right. Darcy was certain that she was a huge disappointment to God and everybody.

Just like Granddad

Marian had asked Darcy if her parents were similar at all, and Darcy couldn’t think of many ways in which they were. Then she remembered something. “Ah,” she said, “my parents aren’t having these awful thoughts like me, but I remember my mum often telling me, ‘You’re just like your grandfather.’” Darcy’s grandfather had died when she was only five, so she didn’t have strong recollections of him, but there were two images that she always remembered about him: Grandfather standing by the kitchen sink in their farmhouse, washing his hands – always washing his hands. And if they decided to take a walk around the farm, he would take a seeming eternity to check that all the windows and doors were locked, even though they were on good terms with everyone within a ten-mile radius!

Obsessions and compulsions worsen through Uni

Marian had felt huge compassion for Darcy as she outlined the course that the disorder had taken. While the intrusive thoughts waxed during high-stress times and waned when Darcy felt relatively stable, there was nevertheless a general broadening of the obsessions – and resultant compulsion to do certain repetitive acts – throughout Darcy’s growing-up years. In high school, for instance, Darcy began to have an aversion to looking at any woman with a scoop-neck top on, going so far as to grab a glass and pretend to be holding it high up near her lips (as if to drink) if she had to talk to someone dressed in any but the most conservative top. In that way, she felt, she would be blocked from seeing what she should not see and thus sinning. Short skirts were also a problem, as Darcy feared that she was looking at people in inappropriate ways, and was offensive.

If anyone at a party crossed their legs while she was looking at them, Darcy assumed that they had done that because they were offended by her having glanced at them; she feared that they would think she was looking at their crotch area. She prayed constantly for forgiveness, but ended up ceasing hugs to family and friends because she felt like a hypocrite. Of course, not feeling that she could/should touch anyone made for huge social problems, and dating anyone became impossible: a huge punishment for a friendly extravert like Darcy. She petitioned God relentlessly, asking to be a better, less sinful person. It did not seem to help.

When Darcy began University, the experience was defined by a series of irrational obsessions. She would worry incessantly about having written something offensive on an email or an assignment. Walking around campus, she would pick up rubbish: papers that she had never seen before; she would worry that she might have written something on one of them. She feared that she would accidentally hurt one of her fellow students by something that she might do or say. By this time Darcy was repeating certain phrases over and over again to ward off disaster. She was amazed that she was getting through school at all (she often made straight A’s), because her rampant perfectionism caused her to take at least twice as long as other students to complete assignments, and she still wasn’t happy then. The anxiety and depression were overwhelming Darcy to the point where she recognised that she could barely function and something needed to change.

The Uni psychologist says, “You’re fine”

Marian shook her head in amazement as she recalled how Darcy’s first attempts to find out what was wrong with her had been fruitless; all the health professionals had completely missed the OCD! Upon first coming to Marian, Darcy had recounted how getting along to the University psychologist in her senior year was a “non-event”. He had asked a few questions, chatted to her about her schoolwork, told her she was basically fine, and then told her to go see a psychiatrist, who merely prescribed a sleeping pill. Darcy had taken this, as instructed, because the intrusive thoughts in her mind often did keep her from sleeping, but when she was awake she still had the thoughts and the horrible compulsion to perform the anxiety-alleviating acts: routines which now occupied several hours each day. Moreover, Darcy’s parents still didn’t believe that anything was wrong with her; they even found it funny that she was “quirky” like her grandfather.

Age 25: Treatment begins

Darcy was to graduate and spend another three years being held prisoner by her out-of-control mind before a chance meeting of her mother with a specialist in OCD at a conference. The specialist didn’t live in Melbourne, but – by incredible coincidence – he had a highly recommended colleague who did: Marian. Marian recalled with some fondness how Darcy had sat in her office during the first session, shedding tears of joy at being truly “seen”: both as a person and in her disorder. When Marian had issued the magical words, “Obsessive-Compulsive Disorder”, Darcy had been surprised – after all, her sense of OCD was people who continually washed their hands – but she also felt like she had just been given the key to her prison. Her treatment began soon after.

Marian worked intensively with Darcy at first, and then steadily. She helped Darcy get onto an even keel emotionally first by raising her serotonin levels (which had been quite low). Marian then began the laborious process of helping Darcy to change her habits of thinking: the assumptions that she made, the irrationalities that controlled her behaviour, and the intrusive obsessions that seemed to take over her life. Marian helped Darcy to see the importance of an exercise regimen, a good diet, and a stillness practice. Darcy joined an online support group, and Marian and Darcy enlisted the help of Darcy’s family and a few close friends. Partway through the therapy, Darcy was even able to come off the medications: a goal she had long sought, because she had married a “wonderful” man and they wanted to start a family.

Epilogue

At 37, Darcy is a happy and fulfilled person, with a solid marriage and an eight-year-old daughter. She believes that she worries about her “like a normal mother”, rather than in the obsessional way she used to pray in order to protect her family from imagined harm. She still petitions God, as she is active in her church, but now the petitions are free of the superstitious routines she used to perform, and she is quick to be thankful for her many blessings.

Unwanted thoughts still come to her, but now she has tools to focus elsewhere, and when the intrusive thoughts come, Darcy knows how to keep them from causing her to repeat irrational acts in a compulsive way. She knows that she will probably always be managing her disorder, as there is no cure for OCD. But the difference now is that she controls it, rather than having it control her. As far as Darcy is concerned, Marian gave her back her life.

Marian smiled again as she recalled Darcy’s journey and her original fear of being a “disappointment to God and everyone”. Indeed, Marian felt blessed to have had Darcy as a client.

This article is an extract of the upcoming Mental Health Academy “OCD and OCPD Case Studies” CPD course. Click here for a full list of currently available MHA continuing professional development courses.

There is an increasing body of literature implicating structural white matter abnormalities in obsessive-compulsive disorder (OCD). Diffusion tensor imaging studies in OCD-affected adults13 and children4 have demonstrated white matter composition abnormalities, albeit with some variability of findings. Candidate gene studies have implicated genes involved in both the development and structural integrity of the myelin sheath.5,6 Moreover, a growing body of research provides evidence that OCD is a complex genetic disorder in which both inborn genetic vulnerability and environmental factors play important etiologic roles.7

The variability of OCD neuroimaging findings may be at least partially accounted for by the fact that this is a phenotypically heterogeneous disorder.8 A recent imaging study has demonstrated that different symptom dimensions within OCD may be associated with distinct neural networks.9 It is likely that the etiology of OCD is also multifactorial. The new clinical criteria developed for pediatric acute-onset neuropsychiatric syndrome (PANS)10 address some of this etiologic heterogeneity by defining a distinct group of children who have an abrupt onset of OCD after either an infectious trigger or an environmental trigger.

Acute disseminated encephalomyelitis (ADEM) is a disorder that shares some similar features with PANS. Consensus definition11 describes ADEM as a clinical event of presumed inflammatory or demyelinating etiology with acute or subacute onset that affects multiple areas of the central nervous system. Patients have encephalopathy, variable neurologic deficits, and MRI features compatible with inflammatory demyelination.

Here we describe a case that, to the best of our knowledge, is the first report of subacute-onset OCD in a child with ADEM.

Case Report

A 12-year-old boy was referred to a pediatric OCD subspecialty clinic for evaluation of obsessive compulsive symptoms. He was born after an uncomplicated pregnancy at full term. He was delivered via forceps due to fetal distress and a nuchal cord. He was initially cyanosed but did not require resuscitation or demonstrate symptoms of neurologic dysfunction. He was developmentally normal except for mild fine motor and articulation difficulties and advanced language skills. There were no notable concerns related to attention, behavior, anxiety, mood, or learning previous to the illness described below. With respect to family history, a maternal great uncle and the maternal grandmother had OCD, both parents had reading difficulties, a maternal cousin had schizophrenia, and a paternal grandfather had bipolar disorder.

At 6 years of age, he presented with diplopia, headache, irritability, lethargy, and sleep disturbance that was preceded by a 2-week history of conjunctivitis and pain and joint swelling, diagnosed as postinfectious arthritis. The neurologic examination at presentation demonstrated an altered level of consciousness with alternating drowsiness and irritability, bilateral sixth nerve palsies, and bilateral papilledema. He was afebrile and the systemic examination was normal.

MRI of the brain initially showed no abnormalities. At lumbar puncture, the opening pressure of cerebrospinal fluid (CSF) was elevated at 45 cm H2O. CSF examination showed 31 white blood cells (82% lymphocytes), 16 red blood cells, protein 0.46 g/L, glucose 2.8 mmol/L, and lactate 1.3 mmol/L. Gram stain and culture of CSF were negative. An extensive infectious and rheumatologic work-up was negative. Repeat brain MRI 1 month later demonstrated an area of increased T2-weighted signal in the white matter of the left frontal lobe near the genu of the corpus callosum and a smaller area of increased T2 signal in the white matter of the right frontal lobe (Fig 1). There was no enhancement with gadolinium.

FIGURE 1

T2-weighted cranial MRI, axial slices. A, Normal MRIs of the frontal lobes on initial MRI. B, Arrows indicate areas of T2 hyperintensity in the left and right frontal lobes 1 month after presentation. C, Arrows indicate decreased size of T2 hyperintense areas at 1 year follow-up.

A diagnosis of ADEM was made, he was treated with high-dose methylprednisone, and his neurologic symptoms resolved. An MRI 1 year later showed that the white matter lesions were both smaller.

This patient was closely followed neurologically and had no recurrence of symptoms indicating demyelination. After his illness, he had poor attention, distractibility, and worsening of his fine motor difficulties. Neuropsychological testing performed 8 months after diagnosis using the Wechsler Intelligence Scale for Children, 4th edition, demonstrated average intellectual function overall, but with coding and symbol search subtests and processing speed index on the second percentile. The Wechsler Individual Achievement test, 2nd edition, identified below average scores in word reading, reading comprehension, math reasoning, and spelling. The Behavior Rating Inventory of Executive Function revealed more executive problems. His language and visual spatial skills were in the average range, but fine motor skills using the Purdue Pegboard were reduced. Given the absence of cognitive difficulties before his illness, no formal baseline neuropsychological testing results are available for comparison.

Follow-up neuropsychological evaluation at the age of 10 years revealed improved overall intellectual function, increasing to the 63rd percentile from the 32nd percentile. However, he had significant persisting deficits in processing speed and working memory. Academically, he continued to meet diagnostic criteria for a mathematics learning disorder. He had intermittent motor tics and also met clinical criteria for diagnoses of generalized anxiety disorder and attention deficit hyperactivity disorder.

In addition to the above, the patient experienced a subacute onset of OCD symptoms within 1 month of being hospitalized for ADEM. At that time, the school expressed concern that he was spending excessive time washing his hands. He expressed a fear of germs and becoming sick, which was decreased by hand-washing. The OCD symptoms continued for 2 months, then decreased somewhat and waxed and waned until 11 years of age, when they worsened significantly. His contamination fears, focused on contracting a serious illness such as Salmonella, led to food intake restriction at school and contributed to a 30-pound weight loss. He re-engaged in excessive hand washing, doing so up to 18 times daily, which resulted in skin irritation and chronic redness. Moreover, he did not want to swallow his saliva.

At the time of initial assessment for OCD, the patient presented as a cooperative 12-year-old. He was casually dressed and there were no noted movement abnormalities. His speech was normal in rate and rhythm, and mood was somewhat anxious with a congruent affect. His thought content was notable for obsessions. He had difficulty in maintaining attention throughout the assessment. On the Children’s Yale-Brown Obsessive Compulsive Scale, he scored in the moderate range with scores of 8/20 for obsessions and 14/20 for compulsions for a total score of 22/40. This patient was started on a selective serotonin reuptake inhibitor and scheduled for cognitive behavioral therapy, the 2 evidence-based therapies for children with OCD.12,13 Currently, his obsessive compulsive symptoms are significantly improved on sertraline and by using cognitive behavioral strategies.

This presentation of new-onset obsessive compulsive symptoms meeting criteria for OCD after an episode of ADEM raises important questions about the etiology of both of these disorders.

It is possible that the findings observed in our patient are an example of a previously unreported pathophysiologic pathway to developing OCD. This is consistent with current research demonstrating structural white matter changes in patients with OCD. The etiology of white matter changes is likely to be multifactorial, with evidence from a recent twin study finding that different white matter abnormality regions are associated with environmental versus genetic risk loading for obsessive compulsive symptoms.14 This patient had neuroimaging findings demonstrating focal white matter changes in his anterior frontal lobes, regions that have been implicated in OCD in the orbitofrontal striatal model.15

This patient’s symptom presentation provides suggestive evidence that demyelinating injury may lead to the development of OCD. This theory is supported by an additional line of research, in which increased OCD risk has been reported in patients with multiple sclerosis,16,17 another disorder involving demyelination. A recent Canadian study estimated the lifetime prevalence of OCD in patients with multiple sclerosis to be 8.6%,18 which is significantly higher than general population lifetime prevalence rates of 1% to 2%.19

It is also possible that this presentation satisfies diagnostic criteria for PANS. The family gave a history of a subacute rather than an abrupt onset of symptoms, given that the OCD symptoms were not noticed during hospitalization. To fulfill the diagnostic criteria for PANS,10 there should be an abrupt, dramatic onset of symptoms. There should also be concurrent presence of additional neuropsychiatric symptoms. The patient’s school difficulties and behavioral changes such as being irritable and easily frustrated could satisfy this second criterion, however these features are also commonly seen in patients after ADEM. If this is a case of PANS, it would seem that PANS and ADEM had a unitary trigger in this patient. Because both PANS and ADEM are presumed to have a precipitant causing the patient to develop psychiatric or neurologic symptoms, it is possible that similar environmental, or, as in this case, infectious triggers could produce these similar phenomena.

Despite the suggestive evidence that ADEM and OCD onset were not independently occurring events for this patient, there are alternate explanations that require consideration. This patient has a family history of OCD, thus increasing his vulnerability to OCD. It is possible that this patient’s OCD is unrelated to the ADEM episode and is simply due to his genetic predisposition, given the heritability estimates of 45% to 65% for the child-onset form of the disorder.20 However, it more likely supports the model of OCD as a complex genetic disorder in which an environmental trigger, in the context of genetic vulnerability, results in the onset of illness.

This case is important because it is the first report of OCD occurring after ADEM. This presentation is consistent with our understanding of OCD as a disease involving the frontal cortical white matter tracts and may indicate a potential pathway for the development of OCD or a shared trigger for the development of PANS and ADEM.

Footnotes

  • Address correspondence to S. Evelyn Stewart, MD, Pediatric OCD Program, A3-118 938 West 28th Ave, Vancouver BC, V5Z 4H4. E-mail: evelyn.stewart{at}ubc.ca
  • Dr Muir conceptualized the case report and wrote the initial manuscript; Dr McKenney conducted the detailed psychiatric history; Dr Connolly is this patient’s neurologist from initial diagnosis and contributed the neurologic data and critically reviewed and revised the manuscript; Dr Stewart conceptualized the case report and critically reviewed and revised the manuscript; and all authors approved the final manuscript as submitted.

  • FINANCIAL DISCLOSURE: The authors have indicated they have no financial relationships relevant to this article to disclose.

  • FUNDING: This project was conducted with assistance from a Michael Smith Foundation Health Research award to Dr Stewart.

  • POTENTIAL CONFLICT OF INTEREST: The authors have indicated they have no potential conflicts of interest to disclose.

References

  • Copyright © 2013 by the American Academy of Pediatrics