Etiology of Bipolar Disorder

The Biological Model

A. Anatomical Research

    Hauser and colleagues researched the anatomical differences between Bipolar I and Bipolar II Disorders using Magnetic Resonance Imaging to measure temporal lobe and ventricular structures in the brain, postulating that bipolar I patients would demonstrate significantly smaller temporal lobe and hippocampal structures in comparison to bipolar II and control subjects (Hauser, et al., 2000).  The results of their study did not support their hypothesis that bipolar I patients would have smaller temporal lobe and hippocampal structures than bipolar II or control subjects, but a significant gender effect was revealed for left and right temporal lobes and left and right hippocampus.  The volumes of both structures were larger in males.  Bipolar I diagnosis was correlated with left hemisphere ventricular enlargement and increased lateral ventricle to cerebrum area ratio.
    Researchers are currently researching working memory and attention in Bipolar Disorder patients versus healthy controls using Functional Magnetic Resonance Imaging (fMRI).  These studies are ongoing, and an example of images displaying differences in brain functioning between Bipolar and non-Bipolar groups can be viewed via the The Imaging Research Center Web site.

B. Neurotransmitter Research

    Several Neurotransmitter substances have been linked to Mood Disorders.  The  Catecholemene Hypothesis, which focused primarily on Norepinephrine, stated that depression was caused by too little Norepinephrine, and mania was caused by an overabundance of Norepinephrine.  The amount of Norepinephrine in the brain was measured by the presence of a Norepinephrine metabolite (MHPG) in urine samples, however only about 25% of MHPG is derived from Norepinephrine metabolism in the brain (Zuckerman, 1998).  While depletion of Serotonin may help to account for depressive symptoms, Dopamine may be linked to manic arousal.

The Diathesis Stress Model

    A  popular etiological model, the Diathesis Stress model maintains that a person is predisposed to a diagnosis (a diathesis) and the diagnosis is brought out by some stressful life event (a stress).  For Bipolar I and Bipolar II, the diathesis stress model builds the predisposition to be one of a person who is hyperactive, sensation seeking, and impulsive in temperament, with a biological tendency towards some type of Monoamine Dysregulation.  With the introduction of a stress to this system, the individual can develop Bipolar I or Bipolar II Disorder (Zuckerman, 1998).
 
 


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