Neurotransmission OCD and the Psychotropic essay

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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.

…this research has revealed the staggering complexity of integrated CNS response systems. & #8230; include the identification of dozens of additional peptide and amino acid neurotransmitters, recognition that neurons can express receptors for several different types of neurotransmitters (enabling direct "cross -- talk" between various neuronal systems), and elucidation of intracellular mechanisms of gene transduction. (Howland, 2005, p. 110)

More tailored drug research that effects newly discovered neurotransmitters as well as the interactions of the other two major neurotransmitters (secondary to Serotonin) will likely be added to the pharmacopeias of available drug treatments for OCD as more research becomes available on OCD and its specific neurotransmitter dysfunctions. Pharmacological treatment for the most part demonstrates most effectively in patients with OCD when SSRIs are used and prove effective.

Secondary disorders as well as other contraindications, such as age below 18 are fundamentally contraindicative of SSRI treatment and some patients where SSRI is contraindicated are simply non-responsive to this drug treatment regimen. Studies on augmentation are limited, and need additional long and short-term development. Ultimately OCD is considered a biologic disorder with only limited environmental causation. For this reason pharmacology is the primary and sometimes singular treatment modality though like a lot of other psychological disorders behavioral or alternative treatments augment psychotropic intervention. In other words behavioral treatment is rarely if ever a feasible alternative to pharmacological treatment of OCD.

Continued discoveries and treatment options, in the form of new and ever expanding lists of psychotropic and anti-depressant drugs including new multi-neurotransmitter affective drugs will likely begin to be researched as alternative drug treatments in OCD. Adding to the research associated with neurotransmission and vice versa.

Trycyclic antidepressants, monoamine oxidase (MAO) inhibitors, and most antipsychotic drugs have been used in the past to alter neurotransmission in anxiety/OCD patients but have been nearly completely abandoned as a result of the many side effects these early developed drugs produce as well as only limited positive treatment outcomes. (Goodman, Rudorfer, & Maser, 2000, p. 31)

Challenges to clinicians may develop as a result of the fact that OCD often exhibits and impairs function in childhood and adolescence and SSRI and other anti-depressant medications have been linked to a small number of cases of suicidal ideations in these populations. Clinicians and parents must carefully weigh concerns of symptoms vs. potential alternative psychotic outcomes. (Liebowitz et.al. December 2002, p. 1433)

References

Goodman, W.K., Rudorfer, M.V., & Maser, J.D. (Eds.). (2000). Obsessive-compulsive disorder contemporary issues in treatment. Mahwah, NJ: Lawrence Erlbaum Associates.

Hollander, E. Allen, A. Steiner, M. Wheadon, D.E. Oakes, R. Burnham, D.B. (September 2003) Acute and long-term treatment and prevention of relapse of obsessive-compulsive disorder with paroxetine. Journal of Clinical Psychiatry 64(9) 1113-1121.

Howland, R.H. (2005). Chapter 6 Biological bases of psychopathology. In Psychopathology: Foundations for a Contemporary Understanding, Maddux, J.E. & Winstead, B.A. (Eds.) (pp. 109-119). Mahwah, NJ: Lawrence Erlbaum Associates.

Liebowitz, M.R. Turner, S.M. Piacentini, J. Beidel, D.C. Clarvit, S.R. Davies, S.O. Graae, F. Jaffer, M. Lin, S. Sallee, F.R. Schmidt, A.B. Simpson, H.B. (December 2002) Fluoxetine in Children and Adolescents With OCD: A Placebo-Controlled Trial Journal of the American Academy of Child & Adolescent Psychiatry 41(12) 1431-1438.

McDougle, C.J. Goodman, W.K. & Price, L.H. (March 1995) Dopamine antagonists in tic-related and psychotic spectrum obsessive compulsive disorder. Journal of Clinical Psychiatry 55 Supplement 24-31.

Otto, M.W. Smits, J.A.J. Reese, H.E. (Spring 2006) Combined psychotherapy and pharmacotherapy for mood and anxiety disorders in adults: review and analysis Focus APA 4. 204-214.

Ravizza L, Barzega G, Bellino S, Bogetto F, Maina G. (1996) Drug treatment of obsessive-compulsive disorder (OCD): long-term trial with clomipramine and selective serotonin reuptake inhibitors (SSRIs). Psychopharmacological Bulletin 32 (1), 167-173.

Shufflebeam, R. (2008) Neurons, synapses, action potentials, and neurotransmission

Consortium on Cognitive Science Instruction/The Mind Project [Online]. Available http://www.mind.ilstu.edu/curriculum/neurons_intro/neurons_intro.php [2009 July, 20]

Stein, D.J. Bouwer, C. Hawkridge, S. Emsley, R.A. (March 1997) Risperidone augmentation of serotonin reuptake inhibitors in obsessive-compulsive and related disorders. Journal of Clinical Psychiatry 58(3) 119-122.

Thomas, P.H. (November 2000) Obsessive-compulsive…[continue]

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