Patients With Symptoms Of Obsessive Compulsive Disorder example essay topic

Obsessive-Compulsive Disorder Introduction Obsessive-Compulsive disorder (OCD), although still unrecognized by most people, affects about six million Americans (Neziroglu and Yaryura-Tobias, 1991). This paper is written to give others a feel of OCD by explaining what it is, how to distiungiush it from other disorders, the way it effects their lives, the theories behind it, and its treatment. What is OCD? Obsessive-compulsive disorder is a frequent, chronic, costly, and disabling disorder that presents in several medical settings, but is under-recognised and under treated (Stein, 2002).

OCD is a disease of the brain manifested by intrusive, unwanted, and persistent thoughts that cannot be rejected and keep coming back over and over again (Neziroglu and Yaryura-Tobias, 1991.) OCD ranks fifth among the major psychiatric illnesses, with approximately 2.6% of the population suffering from OCD for at least six months (Yaryura-Tobias, Anderson, & Neziroglu, 2000). Obsessive-compulsive disorder is viewed as a good example of a neuropsychiatric disorder, mediated by pathology in specific neuronal circuits, and responsive to specific pharmacotherapeutic and psychotherapeutic interventions (Stein, 2002). Obsessive-compulsive disorder was once considered a rare condition, but is now viewed as not only one of the more prevalent psychiatric disorders, but also one of the most disabling medical disorders (Stein, 2002). It is regarded as a neuropsychiatric disorder mediated by specific neuronal circuitry and closely related to neurological conditions such as Tourette's syndrome and Sydenham's chorea (Stein, 2002). Obsessive-compulsive disorder is characterised by intrusive thoughts or images (obsessions), which increase anxiety, and by repetitive or ritualistic actions (compulsions), which decrease anxiety (Stein, 2002). Obsessions are defined as recurrent and persistent distressing thoughts, impulses or images, not due to real-life worries alone, that cannot be suppressed or ignored by these patients and that are perceived by them as originating from within their own minds (Shusta, 1999).

An obsession is a passive experience: it happens to the person. A person may be engaged in some activity, like reading a book or driving a car, when the obsession intrudes into their consciousness disrupting their normal thinking or behavior (Silva & Rachman, 1998). Compulsions are defined as repetitive behaviors or mental acts that the person feels driven to (Shusta, 1999). The behaviour is not an end in itself, but is usually intended to prevent some event or situation (Silva & Rachman, 1998).

No pleasure is derived from carrying it out, although it provides a release of tension or a feeling of relief in the short term (Silva & Rachman, 1998). Distiungishing OCD from other disorders Obsessions and compulsions should not be confused with the inflexible character traits that comprise obsessive-compulsive personality disorder (Stein, 2002). Obsessive-compulsive or stereotypic symptoms are an intrinsic component of many disorders, including autism, Tourette's syndrome, and frontal lobe lesions (Stein, 2002). Patients with symptoms of obsessive-compulsive disorder but a family history of Tourette's can have neurobiological dysfunction more similar to Tourette's than to primary obsessive-compulsive disorder (Stein, 2002). Some disorders have such closely related habits that it is unclear which disorder is really taking place. Dan Stein writes: Although the distinction between axis I (eg, a syndrome such as obsessive-compulsive disorder) and II (eg, a personality disorder such as obsessive-compulsive personality disorder) disorders is unclear at times, the obsessions and compulsions of obsessive-compulsive disorder differ qualitatively from obsessive-compulsive personality traits such as perfectionism and over conscientiousness.

Similarly, despite the occasional overlap, the symptoms of obsessive-compulsive disorder differ clearly from the fears and worries seen in other anxiety disorders, from the actions characteristic of mood disorders, and from the delusions of psychotic disorders (Stein, 2002). Some disorders will overlap with one another. Disorders that overlap with obsessive-compulsive disorder are postulated to lie on an obsessive-compulsive disorder spectrum of conditions (Stein, 2002). Freud postulated that there was a spectrum from obsessive-compulsive personality to obsessive-compulsive neurosis to psychosis (Stein, 2002). More recently, attempts to characterize the obsessive-compulsive disorder spectrum have emphasised neurobiological findings, including neuro genetic approaches in which obsessive-compulsive disorder might be related to Tourette's, pharmacotherapeutic dissection approaches that emphasise the range of disorders that respond selectively to serotonin reuptake inhibitors, and neuroanatomical approaches that postulate a spectrum of striatal disorders (Stein, 2002). Another approach has been to highlight the distinction between compulsive and impulsive disorders (Stein, 2002).

Compulsive disorders such as body dysmorphic disorder are characterised by exaggerated harm concerns, impulsive disorders involve underestimation of risk, and some disorders such as Tourette's have both compulsive and impulsive features (Stein, 2002). OCD's effect on life The most frequent symptoms in obsessive-compulsive disorder are contamination concerns with consequent washing, or concerns about harm to self or others with consequent checking (Stein, 2002). To be clinically significant, symptoms of obsessive-compulsive disorder must be accompanied by marked distress and dysfunction (Stein, 2002). Subclinical obsessive-compulsive symptoms are not uncommon, and are seen during the course of normal development (Stein, 2002). Patients with obsessive-compulsive disorder, however, can cause substantial impairment, including severely affected quality of life (Stein, 2002). Patients with OCD may also have to face pharmacotherapy and behavioral instructions.

One notes that these patients were far more consistent and compliant with pharmacotherapy than they were with behavioral instructions. Although no definitive statement can be made about this difference in compliance, it is our hypothesis that complying with medications requires far less of an investment of time and effort than does compliance with behavior therapy (Yaryura-Tobias, Anderson, & Neziroglu, 2000). Symptoms of OCD can differ in people depending on many different factors or things that go on in there life. Dan Stein explains one way in which they can differ: Symptoms do, however, differ in patients with and without tics, perhaps pointing to psychobiological differences. Although patients generally recognise the excessiveness of their symptoms, their insight is varied and some are judged as having poor insight. Lack of insight in obsessive-compulsive disorder symptoms might be associated with frontal lesions.

Patients with obsessional slowness could have another type of obsessive-compulsive disorder characterised by a greater degree of neurological impairment. (Stein, 2002). Brain organicity may cause personality disorders conducive to anancastic thinking and behavior, irritability, mental or physical hyperkinesia, or other changes observed in abstract thinking (Goldstein, 1951). Theories of what causes OCD There are a wide variety of theories of what causes OCD. One of the first was the connection between OCD and organic lesion was first postulated by Ga delius in 1896, who implied cerebral cortical and subcortical damage existed in patients (Yaryura-Tobias, Anderson, & Neziroglu, 2000). The earliest indication that obsessive-compulsive disorder is mediated by specific neuronal circuits probably came from work showing an association between post encephalitis parkinsonian and obsessive-compulsive symptoms together with striatal lesions (Stein, 2002).

Advances in brain imaging have, however, provided the most persuasive neuroanatomical data for obsessive-compulsive disorder. In some studies, structural imaging has shown abnormalities such as decreased volume or increased grey matter density in cortico-striatal-thalamic-cortical circuits (Stein, 2002). In another article, about OCD and handwriting, nearly a year before Stein made nearly the same remark stating that brain imaging and other studies have shown the involvement of cortico-striatal-thalamic-cortical (CSTC) circuits in OCD (Stein, 2001). The researchers found that OCD patients have significant impairments in certain features of handwriting, such as a lower peak velocity (a measure of bradykinesia), micrograph ia, and shortened acceleration phase per stroke and that these impairments correlate with severity of OCD symptoms (Stein, 2001). Functional imaging has consistently shown that obsessive-compulsive disorder is characterised by increased activity in orbitofrontal cortex, cingulate, and striatum at rest, and especially during exposure to feared stimuli (Stein, 2002).

Other regions of the brain might also play a part in obsessive-compulsive disorder (Stein, 2002). For example, temporal dysfunction has been associated with obsessive-compulsive disorder and there is some evidence of amygdala involvement in obsessive-compulsive disorder (Stein, 2002). One cortico-striatal- thalamic-cortical neurotransmitter system that could be especially important in mediation of obsessive-compulsive disorder in some patients is dopamine (Stein, 2002). Early work suggesting that obsessive-compulsive disorder has a familial component has been confirmed by more recent rigorous studies in which investigators used structured diagnostic interviews of pro bands and controls (Stein, 2002). Stein go further into his view of CSTC breaking it down into three observational steps of how CSTC circuits cause OCD. Perhaps obsessive-compulsive disorder results from an inability to inhibit procedural strategies mediated by cortico-striatal-thalamic-cortical circuits from intruding into consciousness.

Such a view is consistent with three observations. First, the limited number of symptom themes in obsessive-compulsive disorder and their apparent evolutionary importance. Second, dysfunction of cortico-striatal-thalamic-cortical circuits in obsessive-compulsive disorder, with activation of temporal rather than striatal regions during implicit cognition. And third, the role of the serotonin system in cortico-striatal-thalamic-cortical circuits, since the serotonin system is thought to play an important part in mediation of inhibitory processes (Stein, 2002).

There is a confluence of thought that implicates defined pathways or connections between prefrontal lobes, cingulate gyr i, basal ganglia and thalamus as being involved with obsessive compulsive disorder (Anton, 2000). Brain imaging studies on patients with obsessive compulsive disorder show reduced pre-frontal lobe activity and enhanced basal ganglia activity (Anton, 2000). At the University of Florida, a study may settle once and for all the question of whether common strep infections are linked to OCD or tics in some children (TB & Outbreaks Week, 2002). Researchers say that a possible link between strep and OCD has prompted the UF and the U.S. M ational Institute of Mental Health to discover whether these infections in children are truly linked (TB & Outbreaks Week, 2002).

Treatment and Therapies Although acute episodes of obsessive-compulsive disorder have been documented, the illness is generally chronic (Stein, 2002). Furthermore, obsessive-compulsive disorder is associated with substantial direct and indirect costs, which are compounded by an absence of recognition, and by under diagnosis and inappropriate treatment (Stein, 2002). Few investigators have done fixed-dose studies of serotonin reuptake inhibitors in obsessive-compulsive disorder, and these have not always yielded similar conclusions. Nevertheless, a general impression, supported by clinical consensus, is that a serotonin reuptake inhibitor trial of long duration (10-12 weeks) and high dose (increasing gradually, at 2-4 weekly intervals, to maximum recommended dose) should be prescribed (Stein, 2002). Although response to treatment does not necessarily imply remission of symptoms, it could be associated with a large improvement in quality of life (Stein, 2002). The best evidence for augmentation of serotonin reuptake inhibitors is for low doses of dopamine blockers; earlier work was undertaken with traditional neuroleptic's and more recent work has confirmed the value of better tolerated new generation antipsychotic agents in adults (Stein, 2002).

A recent study about several months ago showed a way of treatment. The study group implanted subthalamic electrodes to alleviate parkinsonian symptoms in two patients who had Parkinson's disease and a history of severe OCD (Mallet, 2002). Parkinsonian disability improved postoperatively in both patients and 2 weeks after the procedure, their complusions had disappeared and obsessive symptoms improved (58% improvement for one patient and 64% for the other on the Yale-Brown obsessive complusive scale) (Mallet, 2002). Because the electrodes were implanted medially to the lateral hypothalamus, which is known to regulate emotions, they couldn't exclude the possibility that stimulation of the lateral hypothalamus contributed to the change in their patients' behaviours (Mallet, 2002). However, even though the intensity of the stimulation was moderate and not applied directly to the lateral hypothalamus, they believe that the improvement of OCD symptoms in their patients was probably mediated by the subthalamic nucleus (Mallet, 2002).

Psychoanalytical treatment for obsessive-compulsive neurosis was suggested by Freud, and for a long time was thought to be an effective approach to management (Stein, 2002). However, despite the contribution of investigators in delineation of the characteristics and psychology of obsessive-compulsive disorder, at present, insufficient data support use of psychoanalytical treatment (Stein, 2002). Behavioural therapy was the first psychotherapy for which careful empirical support was obtained, and is useful in obsessive-compulsive disorder in adults and children (Stein, 2002). Cognitive interventions might also have a role in treatment of obsessive-compulsive disorder (Stein, 2002). Consensus ratings suggested that several belief domains are important in obsessive-compulsive disorder, including inflated responsibility; over importance of thoughts; excessive concern about the importance of controlling thoughts; and overestimation of threat (Stein, 2002). In practice, a cognitive-behavioural approach is often used, administered individually or in groups, with the contexts ranging from self-help computer instruction through to treatment in an intensive care unit (Stein, 2002).

Because symptoms of obsessive-compulsive disorder can greatly affect the patient's family, assessment of such an effect and inclusion of the patient's partner or family in development of a treatment strategy would seem appropriate in some cases (Stein, 2002). Unfortunately, few investigators have assessed how best to sequence or combine pharmacotherapy and psychotherapy for obsessive-compulsive disorder (Stein, 2002). Combinations of antidepressants have been useful in some studies of adults (controlled) and children (uncontrolled). Various augmenting agents from other classes (eg, lithium, buspirone, pindolol, inositol) have also been assessed in controlled trials of adult obsessive-compulsive disorder, but to date, findings have been negative or inconsistent. In patients resistant to treatment, several monotherapy and augmentation approaches can be considered, but to date perhaps most data support use of intravenous clomipramine in adults (Stein, 2002). With all these different forms of treatment and therapies still some are treatment refractory.

Though pharmacological and / or behavioral interventions have proven highly effective, 20 to 30% of the obsessive-compulsive disorder (OCD) population is treatment refractory (Yaryura-Tobias, Anderson, & Neziroglu, 2000). Although it is certainly premature to make any causal statements about the relationship between brain abnormalities and treatment-resistant OCD patients, clinicians will want to explore the possibility of organic involvement if they see patients who are indifferent to their illness, are treatment resistant, lack motivation, have rigid and concrete thinking, are non anxious, or are non depressed (Yaryura-Tobias, Anderson, & Neziroglu, 2000). Unfortunately, many patients with OCD fail to respond to clomipramine or SSRI therapy (Shusta, 1999). Various permutations of psychotherapy and pharmacotherapy have been used, some with considerable success (Shusta, 1999). Conclusion OCD is a very serious disorder that is becoming more and more open to the American public. It is not to be taken lightly.

Although many treatments and therapies are out there nothing is one hundred percent prove to work yet. This disease headers the six million people that suffer from it and I hope this paper opens the eyes of others to this disease. Work Cities Anton, Raymond F. (2000) Obsessive-compulsive aspects of craving: development of the Obsessive Compulsive Drinking Scale. Addiction, 08/10/2000, Vol. 95 Issue 8 supp 2, (pp. 211) Goldstein, K. (1951).

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Successful Treatment of Refractory Obsessive-Compulsive Disorder. American Journal of Psychotherapy, Summer 99, Vol. 53 Issue 3, (pp. 377). Silva, Padma l de & Rachman, Stanley (1998). Obsessive-Compulsive Disorder The Facts. Oxford: Oxford University Press. Stein, Dan J. (2001) Handwriting and obsessive-compulsive disorder.

Lancet, 8/18/2001, Vol. 358 Issue 9281, (pp. 524). Stein, Dan J. (2002) Obsessive-compulsive disorder. Lancet. 8/3/2002, Vol. 360 Issue 9330, (pp. 397). UF researchers probe possible strep link. (2002) TB & Outbreaks Week, 11/19/2002, (pp. 19).

Yaryura-Tobias, Jose A. ; Anderson, Mark C. ; Neziroglu, Fugen A. (2000) Organicity in Obsessive-Compulsive Disorder. Behavior Modification, Sep 2000, Vol. 24 Issue 4, (pp. 553).