Neurotransmission OCD and the Psychotropic

Neurotransmission OCD and the Psychotropic Treatment

Neurotransmission Psychotropic OCD

Neurotransmission OCD and the Psychotropic Treatment of OCD

This review briefly explains neurotransmission and then moves on to discuss how neurotransmission abnormalities have been linked to psychological disorders, more specifically Obsessive Compulsive Disorder (OCD). The work reviews literature beginning with a few secondary sources to define terms and provide a basic explanation of neurotransmission and OCD and will then delve into a deeper analysis of primary research associated with psychotropic treatment of OCD as it applies to the biological processes of neurotransmission abnormalities and corrections via pharmacological means.

Literature Review

The basics of neurotransmission have offered science a window into the development of a better understanding of the biological basis for several psychological disturbances and disorders, including but certainly not limited to Obsessive Compulsive Disorder. A very basic synopsis of neurotransmission is that neurons and their synapses or receiver cells transmit messages via a chemical or electrical means traveling from one cell synapse to another through the gap between the two or more synapse locations. Every action and reaction of the body both conscious and unconscious is dictated by how these neurotransmissions occur in the neural networks that take messages from the body to the brain and back to the response mechanisms in a cyclical manner. The chemicals which dictate this complex set of communications are referred to as neurotransmitters and the functioning of neurotransmitters as well as the whole linked chain of neurons and synapse configurations is often observed as impaired in a biological way in patients with psychological disorders.

Chemical neurotransmission occurs at chemical synapses. At chemical synapses, the presynaptic neuron and the postsynaptic neuron are physically separated by the fluid-filled synaptic cleft. The arrival of an action potential in the presynaptic neuron causes it to release neurotransmitter. Neurotransmitter diffuses across the cleft and binds to receptors on ion channels. This causes the ion channels to open. The influx of ions causes a synaptic potential in the postsynaptic neuron. Chemical neurotransmission requires neurotransmitters to act as chemical messengers linking an action potential in one neuron with a synaptic potential in another. (Shufflebeam, 2008, The Mind Project Glossary: Chemical Synapse)

The initial view of the connectivity of the core neurotransmission and psychological disorders has since been labeled simplistic, yet they are still fundamentally associated with the understanding of and research about OCD and other biologically-based psychological disorders.

The earliest theories of the biological basis of various psychological disorders suggested dysfunction of CNS systems subserved by key neurotransmitters: norepinephrine (NE), serotonin (5-hydroxytryptamine or 5-HT), and dopamine (DA). & #8230; Dysregulation of NE, 5-HT, and DA systems, individually or in combination, also was believed to be more broadly associated with psychopathological states of depression, anxiety, mania, and psychosis…(Howland, 2005, p. 109)

Yet, it is also clear that even the basic neurotransmitter alterations using pharmacological means has an effect on many psychological disorders including OCD, and though these simple explanations are now known to be much more complex most pharmacological research and intervention acts upon a small rather than large set of neurotransmitters and can be fundamentally affective for the treatment of OCD and other anxiety disorders.

…the first effective pharmacological treatments for depression and anxiety (tricyclic and monoamine oxidase inhibitor antidepressant drugs) were shown to have effects that enhanced NE and/or 5-HT neurotransmission, and the first effective pharmacological treatments for mania and psychosis (antipsychotic drugs such as chlorpromazine) were shown to block DA neurotransmission. (Howland, 2005, p. 109)

OCD itself is classified as an anxiety disorder, among several others for a comprehensive definition one must consider that the disorder can be marked by obsessions (recurrent and persistent ideas, thoughts, or images) and/or compulsions (repetitive behaviors performed according to certain rules or in a stereotyped fashion) and either or both often seriously impair the function of an individual.

… obsessions or compulsions cause marked distress or significantly interfere with the patient's function. Symptomatically, both compulsivity and impulsivity have in common the inability to inhibit or delay repetitive behaviors. The difference between the two lies in the driving foci. In compulsivity, it is the need to decrease the discomfort associated with rituals, and in impulsivity, it is the need for the maximization of pleasure. & #8230; however, & #8230;not all compulsions reduce anxiety. In more impulsive patients, there is also an additional component of the rituals being pleasurable, albeit with associated guilt after the behavior is carried out. In individuals with OC-related disorders, features of both compulsivity and impulsivity may be observed. Clearly, compulsivity and impulsivity are not mutually exclusive, and individuals may have one set of behaviors driven by the need to reduce anxiety, and another set of behaviors driven to obtain pleasure. This could be due to differential dysregulation of serotonin (5-HT) pathways in different brain areas in these patients, but more research needs to investigate this possibility. (Goodman, Rudorfer, & Maser, 2000, p. 4)

OCD can often be effectively be aided by psychotropic treatment that effect neurotransmission, mostly of the most basic and first discovered neurotransmitters, norepinephrine, serotonin and dopamine. Most often serotonin is the treated mechanistic neurotransmitter.

Selective serotonin reuptake inhibitors (SSRIs) such as fluvoxamine (Luvox), fluoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft) are popular first-line therapy because of their low side effects and benefits (Table 4). They produce a 30% to 60% reduction in obsessive compulsive symptoms that is meaningful to the patient… (Valente, 2002, p. 125)

Unlike many other psychological disorders pharmacological means are a first line treatment and no alternative treatments, i.e. nonbiological treatments are recommended until after pharmacological drug treatment has helped develop a baseline of effectiveness. At this point effectiveness of symptom reduction is evaluated and drug treatment can be altered or alternatives added to treatment. This as well as the understandings of the disorder lend credence to the idea that OCD is very much considered a biological disorder, having a great deal to do with neurotransmission abnormalities and dysfunctions. The accepted efficacy for treatment of OCD and anxiety disorders in general is a combined pharmacotherapy with other non-biological alternatives. (Otto, Smits & Reese, Spring 2006) Challenges to this protocol, by the removal or reduction of pharmacological interventions (SSRI) being replaced with behavioral therapy alone have proved ineffective. (Ravizza, Barzega, Bellino, Bogetto & Maina, 1996, pp. 167-173)

SSRI drug therapy has a fundamental efficacy rate of about 75% in patients with OCD. Additionally, the clinical evidence suggests that early onset OCD in children and adolescents might not prove pervasive over a lifetime and often treatment can be discontinued after a period of 1-2 years. (Thomas, November 2000, p. 176) SSRIs are considered the most pharmacologically affective medications with regard to long-term treatment of OCD, as well. Again this is stressed in pervasive adult cases of the disorder.

Patients in phase 1 acute treatment receiving 40 mg/day or 60 mg/day of paroxetine improved significantly (p < .05) more than those receiving placebo; the mean reduction in Yale-Brown Obsessive-Compulsive Scale score was 25% on 40 mg/day of paroxetine and 29% on 60 mg/day compared with 13% on placebo. During phase 3, long-term treatment, a greater proportion of placebo- (59%) than paroxetine-treated (38%) patients relapsed. Paroxetine was well tolerated at all doses, with no significant increase in frequency of adverse events during long-term compared with short-term therapy. Greater adverse events in the placebo than in the paroxetine group in phase 3 probably represent a discontinuation effect. CONCLUSION: Paroxetine doses of 40 mg/day and 60 mg/day (but not 20 mg/day) are effective in treating acute obsessive-compulsive disorder. Long-term treatment with paroxetine is effective and safe, decreases the rate of relapse, and lengthens the time to relapse. (Hollander, Allen, Steiner, Wheadon, Oakes, & Burnham, Spetember 2003, p. 1113)

Patients who are contraindicated for treatment with SSRI have been tried on medications in the class of Risperidone, with some positive effects, though once again adverse effects need to be monitored as they occur in some cases. (Stein, Bouwer, Hawkridge & Emsley, March 1997, p. 119-122) Augmentation or replacement of SSRI or SUI (Seratonin uptake inhibitors) has also been tried again with patients who have contraindication or prove resistant to treatment with SSRI alone. Drugs like lithium and buspirone that enhance 5-HT neurotransmission have been tried to augment SSRI in resistant patients with OCD, but this has proven ineffective.

In addition another class of drugs, the dopamine antagonists have proven effective for some patients with complicated OCD and other tick disorders. Ticks or physical impulse disorders are common in conjunction with OCD, especially in adults with persistent OCD. (McDougle, Goodman & Price, March 1995) The addition of drugs that enhance serotonin (5-HT) neurotransmission, such as lithium and buspirone, to ongoing treatment in SUI-refractory patients has generally proved to be an ineffective strategy. The addition of dopamine antagonists to the regimens of SUI-resistant patients appears to be a useful approach for OCD patients with a comorbid chronic tic disorder (e.g., Tourette's syndrome) and possibly for those with concurrent psychotic spectrum disorders. These drug response data suggest that both the 5-HT and dopamine systems may be involved in the treatment, and possibly the pathophysiology, of specific subtypes of OCD.

Discussion

Though a great deal more is known about neurotransmission today than was known at the beginning of the research associated with the initial biological discoveries of neurotransmitters and the neurotransmission process there is still a great deal to be discovered. Neurotransmission disorganization and impairment is clearly identified as a pervasive aspect of many psychological disorders. This is particularly true of the anxiety disorders and OCD. There is no doubt that increased understanding of the various mechanisms of OCD and normal neurotransmission will add to a greater research understanding of the biological causalities and modalities of OCD.

Though the most simplistic and earliest neurotransmission disturbance theories have been largely discounted the research has created ample evidence of disturbances in neurotransmission function (in more complex terms) as the root cause of several psychological disorders including various forms of anxiety disorders the subgroup which OCD falls into.