Neurophysiology and Pathophysiology of Mood Disorders - Assignment Example

Principles of Psychopharmacology Principles of Psychopharmacology Neurophysiology and Pathophysiology of Mood Disorders Mood disorders such as bipolar and unipolar disorders have a neurophysiological foundation within the brain of the affected individual. Mood disorders result from physiological abnormality in neuro circuits within the glopus pallidus and lateral ventricles of the brain (Marchand & Yurgelun-Todd, 2010). These disorders have also been linked to an abnormal gene which predisposes individuals to psychosis.

The episodes of depression and mania which characterize bipolar mood disorder have been traced to abnormalities in the sodium ATPase pump within the mitochondria of the associated brain cells (Vollenweider & Kometer, 2010). Unipolar mood is as a result of either poor firing of neurons or hyperactivity in neuron firing. On the other hand, episodes of hypersensitivity and depressed firing of brain neurons cause bipolar mood disorder (Marchand & Yurgelun-Todd, 2010). The modern thinking on the pathophysiology of mood disorders is aligned toward the belief that most of the mental disorders into which patients are given prescription drugs are of unknown etiology and as a result of this, general treatment approaches are used to mood disorders regardless of the unique neurophysiological basis.

Psychopharmacology of Mood disorders The Brain disabling theory as postulated by Peter Breggin is a significant contribution into the understanding of the pharmacokinetics and pharmacodynamics of psychiatric drugs (Moncrieff, 2007). The brain dysfunction which the treatment of bipolar and unipolar mood disorders aim to attain justified by the need to deactivate the episodes of mania which characterize mood disorders. Mood stabilizers are the pharmacological drugs which are used in therapy of people with the bipolar mood disorder (Vollenweider & Kometer, 2010).

The pharmacodynamics of mood stabilizers in the treatment of bipolar mood disorder includes revering abnormal neural firing. Mania in bipolar mood disorder is suppressed by the pharmacokinetic activity of mood stabilizers of acting on the sodium ATPase pump. These drugs act on the pump by attaching to their receptors within the pump and either inhibiting hyperactivity or enhancing the depressed activity of the pump (Marchand & Yurgelun-Todd, 2010). This illustrates how the drugs act to stabilize the mood of the patient.

On the other hand, the pharmacokinetics and pharmacodynamics of mood stabilizers in unipolar mood disorder depends on the sodium ATPase pump activity. When the pump is hyperactive it is depressed and reactivated in depressive cases of unipolar mood disorder. The goal of treatment Psychiatrists normally employ both pharmacological therapy and behavioral therapy as approaches of treatment of bipolar and unipolar mood disorders. The goal of the treatment includes impairment of brain functions when there is mania.

This impairment include application of therapeutic approaches such as group and individual therapy sessions in which individuals are allowed to learn to control their emotional responses and behaviors such as euphoria and indifference (Moncrieff, 2007). Nonetheless, it is necessary to note that the response which people demonstrate to the various forms of therapy varies. The response to therapy by patients with mood disorders is either physiological or psychological (Marchand & Yurgelun-Todd, 2010).

Pharmacological treatment is usually applied after attempts by psychiatrist to modulate the psychological response of the patient to various stimuli in the environment. The goal of pharmacological treatment is to suppress the negative symptoms of psychosis by preventing mood lapses. Dose-Response Relationships and Drug-Receptor Interactions Lithium carbonate which is the commonly used to treat mood disorders interacts with receptors on the sodium ATPase pump of brain neurons and prevents hyperactivity in firing and thus treats the maniac symptoms which are associated with mood disorders (Vollenweider & Kometer, 2010).

Sufficient doses of lithium have demonstrated inhibiting action on manic symptoms. As a result of its antipsychotic action, lithium has been used to reduce the risk of self harm such as suicidal tendencies among maniac patients (Marchand & Yurgelun-Todd, 2010). Carbamazepine is commonly used to treat bipolar mood disorder. However it is less effective than lithium in the prevention of lapses of the disorder (Vollenweider & Kometer, 2010). Psychiatrists may prescribe antidepressants in the treatment of psychotic disorders but the direct pharmacokinetic action of the mood stabilizers on the sodium ATPase pump makes them more effective in the treatment of mood disorders.

However it is necessary to note that there are pharmacological side effects which are associated with anti-psychotic drugs such as mood stabilizers. These include poor judgment and general loss of cognitive orientation (Moncrieff, 2007). These symptoms result from the need of the physiological functioning of the brain to compensate the changes which are associated with the inoculation of a foreign substance. Therefore, psychiatrists must aspect possible physical and psychological changes in behavior which emanate from the treatment of mood disorders.

References Moncrieff, J. (2007). Understanding Psychotropic Drug Action: The Contribution of the Brain-Disabling Theory. Ethical Human Psychology & Psychiatry, 9(3), 170-179. Marchand, W. R., & Yurgelun-Todd, D. (2010). Striatal structure and function in mood disorders: a comprehensive review. Bipolar Disorders, 12(8), 764-785. Vollenweider, F. X., & Kometer, M. (2010). The neurobiology of psychedelic drugs: implications for the treatment of mood disorders. Nature Reviews Neuroscience, 11(9), 642-651