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In a developmental study conducted by Geller and his colleagues (2001), OCD in childhood and adolescence was male preponderant and associated with a higher frequency of aggression/catastrophe obsessions, hoarding and saving compulsions, multiple obsessions and compulsions, and poor insight compared with adult OCD. Sexual and religious obsessions were selectively more prevalent in adolescents compared with either children or adults. Children with OCD had higher rates of Tourette’s disorder and separation anxiety disorder than older age groups, but mood disorders were similarly high in both adolescents and adults with OCD. Adults with OCD also had higher rates of substance use and eating disorders than either children or adolescents. This study indicated that age specific correlates with different types of OCD.
DSM Diagnosis Criteria of OCD (DSM-IV-TR, 2000)
A. The Person Exhibits Either Obsessions or Compulsions
Obsessions are indicated by the following:
The person has recurrent and persistent thoughts, impulses, or images that are experienced, at some time during the disturbance, as intrusive and inappropriate and that cause marked anxiety or distress
The thoughts, impulses, or images are not simply excessive worries about real-life problems
The person attempts to ignore or suppress such thoughts, impulses, or images or to neutralize them with some other thought or action
The person recognizes that the obsessional thoughts, impulses, or images are a product of his or her own mind (not imposed from without as in thought insertion)
Compulsions are indicated by the following:
The person has repetitive behaviors (eg, hand washing, ordering, checking) or mental acts (eg, praying, counting, repeating words silently) that the person feels driven to perform in response to an obsession or according to rules that must be applied rigidly
The behaviors or mental acts are aimed at preventing some dreaded event or situation; however, these behaviors or mental acts either are not connected in a realistic way with what they are designed to neutralize or prevent or are clearly excessive.
B. At some point during the course of the disorder, the person has recognized that the obsessions or compulsions are excessive or unreasonable. (Note: this does not apply to children.)
C. The obsessions or compulsions cause marked distress, are time consuming (take more than 1 hour a day), or significantly interfere with the person’s normal routine, occupational/academic functioning, or usual social activities or relationships.
D. If another axis I disorder is present, the content of the obsessions or compulsions is not restricted to it (e.g., preoccupation with drugs in the presence of a substance abuse disorder).
E. The disturbance is not due to the direct physiologic effects of a substance (e.g., drug abuse, a medication) or a general medical condition.
Sign and Symptoms of OCD
Most people with obsessive-compulsive disorder (OCD) have both obsessions and compulsions, but some people experience just one or the other (Help Guide, 2010).
Common obsessive thoughts in OCD include (Help Guide, 2010):
Fear of being contaminated by germs or dirt or contaminating others.
Fear of causing harm to yourself or others.
Intrusive sexually explicit or violent thoughts and images.
Excessive focus on religious or moral ideas.
Fear of losing or not having things you might need.
Order and symmetry: the idea that everything must line up “just right.”
Superstitions; excessive attention to something considered lucky or unlucky.
Common compulsive behaviors in OCD include (Help Guide, 2010):
Excessive double-checking of things, such as locks, appliances, and switches.
Repeatedly checking in on loved ones to make sure they’re safe.
Counting, tapping, repeating certain words, or doing other senseless things to reduce anxiety.
Spending a lot of time washing or cleaning.
Ordering, evening out, or arranging things “just so.”
Praying excessively or engaging in rituals triggered by religious fear.
Accumulating “junk” such as old newspapers, magazines, and empty food containers, or other things you don’t have a use for.
ETIOLOGY
Biological Aspects of OCD
Family and twin studies
Family studies have demonstrated an increased prevalence of obsessive-compulsive disorder in the first degree relatives of patients as compared to controls (Hettema, Neale, Kendler, as cited inTaberner et al., 2009). Studies of OCD patients and their families have established a 10% prevalence of OCD in first degree relatives (Brynes, 2009). One American study (as cited in Anxiety Care, 2011) suggested that up to 30% of teenagers with OCD had a member of the immediate family with the problem or with obsessive symptoms. However, a two years study carried out by Black (2003, as cited in Waite & Williams, 2009) demonstrated that although the children of parents with OCD were likely to go on to develop an emotional disorder, it was not particularly likely to be OCD. In studies of twins, there is a 63% concordance rate for OCD in identical twins (Brynes, 2009). Twin studies suggested a higher concordance rate in monozygotic as compared to dizygotic twins (Samuels & Nestadt, 1997; Eley, Bolton, O’Connor, Perrin, Smith, & Plomin, 2003). Because MZ twins share 100% of their genes and DZ twins share 50% of their genes on average, the concordance rate for a genetically influenced disorder is expected to be higher for MZ twins than for DZ twins (Shih, Belmonte, & Zandi, 2004).
Brain structure and chemistry
Positron emission tomography (PET) studies measuring resting glucose metabolism have reported hyperactivity in the inferior frontal and anterior cingulate cortices, striatum, and thalamus in patients with OCD (Saxena et al., as cited in Busatto et al., 2001).Researcher believed that OCD may be developed by the “abnormal metabolic activity” in the orbitofrontal cortes, the anterior cingulate, and the caudate nucleus (Dejdar, 2002). The interaction between these different parts is called a “cortico-basal ganglia network” (Dejdar, 2002). Dejdar described that “these cortico-basal ganglia interactions make up a neural system that is crucial in the acquisition of habits and also establishing a fixed routine of performing those habits, which in turn connected to the typical behaviors of OCD where people maintain certain obsessive habits and continue to perform those habits”.
Study by Lewin, Storch, Adkins, Murphy, & Geffken (2005) supported the neurochemical etiology involving a functional disturbance in the frontal-limbic-basal ganglia system as well as thalamic and cortical neurostructural abnormalities. “It is hypothesized that if cortical regions are dysfunctional in patients with OCD, then conscious mechanisms must be used to accomplish what would occur automatically in an unimpaired brain” (Sturm, 2008). As a result, inappropriate or obsessive thoughts repeatedly intrude and conscious thought processes suppress them, facilitated by accompanying ritualistic behaviors (Neel, Stevens, & Stewart, as cited in Sturm, 2008).
There is a strong connection between basal ganglia and OCD. Several studies have implicated that basal ganglia is active during the learning or execution of sequential behavior (Brown, 1997; Graybiel, 1998). Graybiel (1998) explained that the chunking functions of the basal ganglia helps people to focus. Chunking refers to the organization of information into specific associated groups (Dolan DNA learning center, n.d.). This happened when the dopamine released in the basal ganglia system communicates with the brain areas in the prefrontal cortex to allow people to pay attention to critical tasks, ignoring distracting information (Dolan DNA learning center, n.d.). In an experiment by Graybiel, she hypothesized that the basal ganglia system helps the cortex to chunk learning into habits and routines to help the brain quickly access stored information. The experiment of Graybiel was done on training the rats on maze tasks and records the firing groups of neurons in the striatum as the rats learn, forget, and then relearn the task. When the rats get used to the maze, lots of cells in motor striatum tend to fire at the beginning and the end of the run instead of the whole thing. This happened because the basal ganglia has chunked the behavior. The symptoms of OCD included repetitive, intrusive thoughts and compulsions which lead to ritualistic behaviors such as washing, counting and checking. These behaviors according to Graybiel involved sequential acts and they are performed as chunks, unitized and driven by the extraordinary imperative of urges and compulsions that the patient recognizes as abnormal and out of the person’s control. As the result, OCD patients showed over focused attention to irrelevant stimuli.
In OCD patients, an abnormal activation of the striatum has been observed. A clearer view is illustrated by a charity organization, Anxiety Care (2011). The organization explained that the thalamus is involved in sensory perception processes and caudate nucleus, a component within basal ganglia work to sort sensory information and filter thoughts. When these messages are being misinterpreted or misfiring, which mean that the normal electrical activity in the brain is being disrupted by the overactive electrical dischargers, it will causes the problem of communication between nerve cells. This will affect and confused the thinking part of the brain to respond chemically to a threat perceived by the primitive part of the brain as if the danger is real. “In effect, the caudate nucleus is letting unnecessary thoughts and impulses through to the cortex where the thoughts and emotions combine; and an over active cingulate nucleus at the brain’s centre, which helps shift attention from one thought or behavior to another, becomes over active and gets stuck on certain behaviors, thoughts or ideas. The cingulate is that part of the brain which tells the OCD sufferer that something terrible will happen if the compulsions are not carried out” (Anxiety Care, 2011).
Besides that, some researchers have suggested that OCD results from the imbalance of the neurotransmitter in the brain which is known as serotonin (Pauls, Mundo, & Kennedy, 2002). A study by Stengler-Wenzke, Muller, Angermeyer, Sabri and Hesse (2004) revealed that there is a significant reduction of serotonin transporter availability in the midbrain and upper brainstem in OCD patients. The reduction of serotonin transporter availability may reflect a reduced number of serotonergic neurons that may result in low level of serotonin. Serotonin is responsible for transporting impulses to and away from the nerves (Dejdar, 2006). The physiological activity of serotonin starts from the brainstem in groups of brain cells called raphe nucleus (“Function of Serotonin”, 2009). Serotonin brain cells then spread to various regions of the central nervous system by branching out throughout the brain(“Function of Serotonin”, 2009).
In a case reported by Cohen, Angladette, Benoit, and Pierrot-Deseilligny (1999), a 59-year-old man developed obsessive-compulsive disorder symptoms after his head injury. The magnetic resonance imaging (MRI) brain scans showed a small contusion in the right orbitofrontal region. In the similar case, the single-photon emission CT (SPECT) showed greatly reduced blood flow in the orbitofrontal region of the 59-year-old man with OCD (Cohen et al., 1999). A study by Busatto et al. (2001) supported the findings as their research found reduced right cerebral blood flow in the right orbitofrontal cortex in OCD patients as compared with the healthy control group. Paulmann, Seifert, and Kotz (2009) explained that the orbitofrontal cortex is linked to a variety of cognitive and emotional functions. Gray, Braver, and Raichle (as cited in Bracha & Brown, 2009) mentioned that emotion and cognition conjointly and equally contribute to the control of thought and behavior. Additionally, Pessoa (as cited in Bracha & Brown, 2009) added that emotions and cognition not only strongly interact in the brain, but they are often integrated so that they jointly contribute to behavior. Hence, impairment of orbitofrontal cortex contributed to the intrusive thoughts and bizarre behavior of OCD patients (Swinson, Antony, Rachman, Richter, 1998).In particular, lesions of the human orbitofrontal cortex lead to large-scale changes in social and emotional behavior (Paulmann, Seifert, and Kotz, 2009). For example, patients with orbitofrontal lesions are reported to suffer from deficits in affective decision-making (Hornak, as cited in Paulmann, Seifert, and Kotz, 2009). Consistently, Swinson and his colleagues (1998) stated that OCD patients have difficulties in decision making.
Psychological Aspects of OCD
According to Salkovskis, Shafran, Rachman, and Freeston (1999), there are five mechanisms for the development of inflated responsibility which are critical for the development of OCD. Inflated responsibility refers to an excessive sense of personal responsibility related to unwanted or upsetting thoughts (Abramowitz, Deacon, Woods, & Tolin, 2004).
The first mechanism is being given too much of responsibility. A child or adolescent, who assumed responsibility during early age due to incompetent parenting, might believe that they are responsible for the negative consequences over which they have little or no control. This is related to the parental communications, where the child is scapegoated for negative occurrences whether or not they are in fact responsible. Through this type of upbringing, Salkovskis et al. stated that “the child will develop and accept a wide sense of responsibility and are inclined to translate it into a high degree of conscientiousness, marked by a dedication to work and an acute sense of social obligations.”
The second mechanism in influencing a person to be OCD is the exposure to rigid or extreme codes of conduct. Strict behavioral codes being instilled by schools, authorities or religion will lead to the development and the reinforcement of attitudes about responsibility. In the study by Abramowitz et al., they found evidence that religion and other cultural influences affect the presentation of OCD symptoms. Rasmussin and Tsuang (as cited in Abramowitz et al., 2004) observed that strictly religious patients often had religious themes to their obsessional thoughts and compulsive rituals. An early study by Khanna and Channabasavanna (as cited in Abramowitz et al., 2004) noted a large portion of symptoms related to contamination and washing among Hindus with OCD, and commented that Indian culture emphasizes on the issues of purity and cleanliness.
The third mechanism for the development of inflated responsibility is being given too little responsibility. The responsibility is withheld from the child by the parents. Worries are prominent in the family system and the parents are likely to be excessively anxious and fearful themselves, they will be overprotected toward their child. This will thus convey a sense that danger is around the corner to the child. When growing up, the child will have difficulty in leaving home and being independent; he or she is unprepared to cope with the dangers that the child believe to have in the world outside. Salkovskis et al. further mentioned that leaving home is usually marked by the emergence of OCD symptoms in the child. The lack of preparation to deal with the world outside will frighten the child and leads to the development of anxiousness in the child.
The fourth route to the development of an inflated sense of responsibility is the sudden critical incidents that happened where a person’s action or inaction contributed to serious misfortune. An example illustrated by Salkocskis et al. on a young doctor who gave the wrong prescription to the patients. Although it did not have any adverse effects on the patient, the young doctor was reprimanded intensely by his senior supervisor. Since then, he developed repetitive checking on the prescription and spent an inordinate amount of time in checking the details of each prescription.
Another factor that contributed to the exaggerated sense of responsibility occurred from an incident that is in fact coincidental but the person erroneously assumed that their thoughts, actions or inactions contributed to a serious misfortune. This happened though the learning experiences, for example, when a child angrily wishes an adult dead; soon afterwards the adult, by unfortunate coincidence, actually dies (Salkocskis et al., 1999). The child will think that it is his fault and he has caused the death but actually it was just a coincidence. Salkocskis et al. described that people who are prone to the cognitive bias of thought-action fusion are the ones who are most likely to experience inflations of responsibility and thus contribute to the origins of OCD.
PHYSIOLOGICAL TREATMENT
Medication
Selective serotonin reuptake inhibitor
The pathogenesis of OCD has been linked to abnormal serotonin levels. Drugs which increase levels of serotonin in the brain have been shown to improve symptoms of OCD. Selective serotonin reuptake inhibitors (SSRIs) are the most commonly prescribed antidepressants to deal with OCD (Taylor, 2009). SSRIs included citalopram, fluoxetine, fluvoxamine, paroxetine and sertraline (Taylor, 2009). Taylor in his study discussed that SSRIs ease the anxious feeling of OCD patients by affecting the neurotransmitters of the brain that used to communicate between brain cells. SSRIs block the reuptake or re-absorption of the neurotransmitter serotonin in the brain. Changing the balance of serotonin seems to help brain cells send and receive chemical messages, which in turn boosts patient’s mood. Taylor explained that SSRIs are called selective because they seem to primarily affect serotonin, not other neurotransmitters. Side effects of SSRIs included nausea, headaches and insomnia (Taylor, 2009).
In evaluating the safety and effectiveness of sertraline in children and adolescents, Cook et al. (2001) ran a study in United States. Their research indicated that long-term sertraline treatment was well tolerated and effective in the treatment of childhood and adolescent OCD. In consistent with the result of sertraline, studies has showed that fluoxetine, citalopram and fluvoxamine were well tolerate and effective in treating children and adolescent with OCD (Liebowitz et al., 2002; Riddle et al., 2001). Nonetheless, six adverse events occurred significantly more frequently in fluoxetine patients who experienced palpitations, weight loss, drowsiness, tremors, nightmares, and muscle aches (Riddle et al., 2001).
Escitalopram, another type of SSRI has been examined by researchers in Malaysia in treating OCD patients (Hatim et al., 2008). The research reviewed that the risk of relapse for those treated with placebo appeared to be four times that of those treated with escitalopram. Moreover, the study suggested that escitalopram is well tolerated in Malaysian patients with OCD. No serious adverse event was reported throughout the study. A few milder side effects have been reported by the patients, such as dizziness, hypertension, delayed ejaculation, and throat tightness. The sample of the study, however, may be too small to yield broad generalizations.
Serotonin norepinephrine reuptake inhibitor
Serotonin norepinephrine reuptake inhibitor (SNRI) such as venlafaxine has been used to manage OCD. Researchers found that venlafaxine may be beneficial to individuals with OCD, including those who have not responded to prior SSRI trials (Hollander, Friedberg, Wasserman, Allen, Birnbaum, & Koran, 2003SNRI works by inhibiting the reuptake of the neurotransmitters serotonin and norepinephrine (Donaldson, 2010). As low serotonin is associated with OCD, SNRI function to increase the amount of two neurotransmitters, serotonin and norepinephrine, and thus enhance the neuronal activity of the brain. The side effects of SNRI included nausea, restlessness, sexual dysfunctions, insomnia, and increased blood pressure (Bandelow, 2008).
Tricyclic antidepressants
One of the effective tricyclic antidepressants (TCAs) that have been using to treat OCD is clomipramine. It was one of the first anti-obsession drugs prescribed in the 1960s, but is less prescribed now due to their unpleasant side effects (Goodman, 2011). The side effects of this drug included dry mouth, constipation, urinary retention, sexual dysfunction, weight gain, seizures, and cardiac side effects (Bandelow, 2008). Bandelow added that TCAs should be avoided in patients who are considered to be at risk of suicide, due to their potential cardiac and central nervous system toxicity after overdose. In general, the side effects of TCAs are more adverse than SSRIs. Therefore, it is usually recommended when the treatment with SSRI’s have failed (Taylor, 2009).
Neurosurgical treatment
More than 10% of OCD patients remain incapacitated despite rigorously involving in medication trials and intensive behavior therapy (Kim et al., 2003). Several neurosurgical procedures have been used in OCD for treating such refractory patients. Cingulotomy is among the neurosurgical methods to deal with OCD. Cingulotomy defined by Carlson (2008) as “the surgical destruction of the cingulum bundle, which connects the prefrontal cortex with the limbic system; helps to reduce intense anxiety and the symptoms of obsessive-compulsive disorder” (p. 489). Anterior cingulotomy targets the anterior cingulate cortex and the fibers of the cingulum has been recently reported as being effective and safe (Dougherty, as cited in Kim et al., 2003). Study by Kim et al. (2003) aimed to to investigate OCD symptom improvements and to evaluate any cognitive changes and adverse effects after cingulotomy. Their study found no evidence of cognitive dysfunction including intelligence, memory and executive function after cingulotomy compared with preoperative performances. In addition, seizure, urinary problems, chronic pain and suicide were not reported and other adverse effects, such as headache, insomnia and weight changes did not continue for more than 3 months. Taken together, they suggested that cingulotomy could be safe in terms of cognitive and other side-effects.
Furthermore, deep brain stimulation (DBS), a procedure in which surgically implanted electrodes stimulate localized brain structures, has also been reported to be effective in patients with OCD when the anterior limb of internal capsule was targeted (Nuttin et al., as cited in Cannistraro et al., 2007). Deep brain stimulation surgery involves the placement of tiny implantable electrodes into abnormally functioning areas of the brain through burr holes in the skull; then a neurostimulator, which is commonly implanted near the collarbone; an insulated wire that connects the electrode to the neurostimulator (Brown University, 2003). The electrodes emit pulses of electrical stimulation to block abnormal brain activity that can cause obsessions, moods, and anxieties associated with psychiatric disorders (Brown University, 2003). A study conducted by Gabriels, Cosyns, Nuttin, Demeulemeester, & Gybels (2003) concluded that deep brain stimulation may have important therapeutic benefits on psychopathology in OCD and no harmful side-effects were detected during follow-up up to 33 months (see Appendix A, for case study). However, Greenberg, Rauch, and Haber (2010) stated that hemorrhages on device insertion may have long-lasting or permanent consequences, although relatively rare. Infection represents another significant risk (Greenberg et al., 2010). On the other hand, Greenberg and his colleagues added that the great appeal of DBS in comparison with lesions is that it permits focal, adjustable, and reversible modulation of the brain. Specifically, various combinations of electrodes can be activated, at adjustable polarity, intensity, and frequency; DBS thus permits flexible neuromodulation. The great clinical advantage of this is that parameters can be optimized for individual patients. In cases in which no beneficial settings can be identified despite extensive efforts, the electrodes can be inactivated, and the devices may be removed (Greenberg et al., 2010).
DISCUSSION & CONCLUSION
Overdose
TCAs have been revealed to be lethal in overdose (Bandelow, 2008). These drugs should be avoided in patients who are considered to be at risk of suicide, due to their potential cardiac and central nervous system toxicity after overdose (Bandelow, 2008). Although the benefit of SSRI and SNRI is that they are relatively safe in overdose (Bandelow, 2008), the issues of associating SNRI with other substances need to be highlighted. During 2010, Donaldson revealed that overdose with SNRIs has commonly occurred in combination with alcohol and/or other drugs. The adverse event of combining alcohol with SNRI medication include electrocardiogram changes, sinus and ventricular tachycardia, bradycardia, hypotension (low blood pressure), altered level of consciousness (from somnolence to coma), rhabdomyolysis, seizures, vertigo, liver necrosis, and death have been reported. Besides that, Donaldson emphasized that SNRI medications should not be taken by patients also taking monoamine oxidase inhibitors (MAOIs). This can lead to increased serotonin levels and cause serotonin syndrome which is a rare, but serious and potentially life-threatening condition unfortunately often mistaken for a viral illness, anxiety, neurological disorder or worsening psychiatric condition). Therefore, it is vital to address the adverse events of drug overdose and the combination with other substances.
Relapse
Relapse and remission is common in OCD and many patients will never be free of the disease (Taylor, 2009). Earlier study in 1973 by Capstick (as cited in Ravizza, 1998) stated that ‘if the SSRI is withdrawn or reduced too quickly, the patient is able to relate the time of onset of the recurrence of the obsessions, usually 36 to 48 hours after the former dose’. In a follow-up study of 15 patients with OCD who responded to clomipramine, Thoren et al. (as cited in Ravizza, 1998) reported that 6 patients who had stopped taking the drug had a recurrence of their symptoms within a few weeks of discontinuation. A research group by Ravizza et al., 1996, the group completed a 2-year, open-label follow-up study of 130 patients with OCD who had previously responded to 6 months’ treatment with clomipramine, fluoxetine or fluvoxamine. At the end of the 2 years of follow-up, the relapse rate was 77 to 85% among those patients who discontinued pharmacotherapy.
Implication
Most research related to the physiological treatment has been studied for not more than five years. Therefore, the effects of long term treatment have yet to be observed. However, when the discontinuation of treatment is discussed, researchers indicated several relapse problems and adverse events. A study stated that response to selective serotonin reuptake inhibitors (SSRIs) may be influenced by body weight, age, sex, and genetic makeup, and therefore can vary between individuals of different ethnic populations (Hatim et al., 2008). Malaysia as a multi-cultural and multi-ethnic country, the use of treatment in patient with OCD should be wise and well considered. The lack of physiological treatment in Malaysia is the major limitation for the implication of treatment toward Malaysian.
On the issue of unresponsive to treatment, researcher found the benefits of switching between venlafaxine and paroxetine for OCD. In 2004, the Brown University reported that 56% of patients who were not responding to venlafaxine benefited from a switch to paroxetine; 19% of patients who were not responding to paroxetine benefited from a switch to venlafaxine.Despite the evidence that clomipramine and selective serotonin reuptake inhibitors (SSRIs) are effective in the pharmacology management of obsessive-compulsive disorder (OCD), between 40% and 60% of the patients suffering from it show only a partial or no symptom improvement (Marazziti et al., 2008). Therefore, Marazziti and his group conducted a research to examine the effectiveness of combined treatment by associating clomipramine and citalopram in the treatment of OCD. The study found that combination treatment is effective and well-tolerated for OCD patients, and much more effective than treating patients with single drug, such as SSRI or TCA. In prescribing medication for the OCD patients in Malaysia, the doctor should inform the possible side effects of the medication to the patients. The adverse events that would occur in combination of substances should be stressed and patients should be education on the appropriate dosage and time to consume the medication.
Limitations on the use of medications include unwillingness of approximately 25% of OCD patients to take medications which they view, globally, as a form of contamination (Greist, 1998); side effects that interfere with comfortable use of medications; and continuing costs of medications that are necessary to prevent relapse associated with discontinuation.
Besides physiological treatment, psychotherapy has been recommended to deal with OCD. The consensus guidelines produced by the American Psychiatric Association (2000) suggested that cognitive, behavioral therapy (CBT) was the first choice treatment for children and young people. Waite and Williams (2009) mentioned that CBT alone or in combination with medication appears to be more effective and less likely to lead to relapse. More recently, National Institute for Health and Clinical Excellence (2011) described a stepped care model beginning with self-help materials for mild cases through CBT, medication and finally combined treatments. The Malaysian Psychiatric Association reviewed a research being done by Saxena et al. (2009) indicated the effectiveness of CBT on brain glucose metabolism in OCD. They discovered significant changes in brain activity solely as the result of four weeks of intensive cognitive-behavioral therapy in ten OCD patients. Reduction of thalamic activity, decreases in glucose metabolism has been observed after the intervention. However, the study also showed a significant increase in activity in an area of the brain called the right dorsal anterior cingulate cortex, a region involved in reappraisal and suppression of negative emotions.
The major constraints on the use of CBT include patient unwillingness to invest the time and energy. This may be due to patient’s fear that their anxiety will be too great when they expose themselves to their triggers.
As the conclusion, there are several causes of OCD which involved both biological and psychological aspects. In introducing the treatment or intervention method, several factors have to be considered especially in Malaysia, a multi-cultural country. The treatment option should be chosen individually for each patient. None of the medications are permanent cures and their effectiveness fluctuates from person to person. SSRI medications have the least side effects and are generally just as effective as or even more effective than any of the other medications. The neurosurgery may be a merit consideration for the tiny minority of patients who are incapacitated by OCD and unresponsive to serotonin reuptake inhibitors and behavior therapy. However, deep brain stimulation surgery has been used in Malaysia to treat Parkinson’s patients and little is known for OCD patients in Malaysia. Finally, a combination of treatment by using psychotherapy and physiotherapy may be considered as mind and behavior are interrelated.
