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Major depression is a mood disorder that affects nearly 7% of the American population and is the most common cause of disability worldwide. Standard treatment typically involves antidepressant medication alone, although a combination of antidepressant medication and psychological treatment, such as psychotherapy or cognitive-behavioral therapy, is often more effective. However, because depression has genetic, environmental, and psychological contributing factors, treatment can be challenging. Approximately 10% of those suffering from depression have treatment-resistant depression (TRD) that does not respond to standard treatment.A number of treatment options for those with TRD target the functioning of the nervous system. Deep-brain stimulation (DBS) , which is used to treat Parkinson disease, has also been investigated as a treatment for TRD. DBS involves implanting a device in the brain that sends electrical impulses to a specific area. Although the mechanism by which DBS alleviates depressive symptoms is unclear, neurostimulation provided by DBS is thought to disrupt dysfunctional patterns of electrical activity in local areas and connected brain regions.A meta-analysis reviewed the data from several studies that used different brain regions as DBS targets in the treatment of TRD. Table 1 shows the percentage of TRD patients who underwent DBS and showed clinical responsiveness and remission of depression. Clinical response was defined as a 50% reduction in scores on a measure of depression. Various scales were used in the studies, including different versions of the Hamilton Depression Rating Scale (HDRS) and Montgomery-Asberg Depression Rating Scale (MADRS) . Remission of depression was defined as a score that fell below a predetermined threshold.Table 1 Percentage of TRD Patients Who Showed Clinical Response and Remission With DBS Treatment

-Which of the following is true regarding two classes of drugs commonly used to treat depression, selective serotonin reuptake inhibitors (SSRIs) and monoamine oxidase inhibitors (MAOIs) ?

Question

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Major depression is a mood disorder that affects nearly 7% of the American population and is the most common cause of disability worldwide. Standard treatment typically involves antidepressant medication alone, although a combination of antidepressant medication and psychological treatment, such as psychotherapy or cognitive-behavioral therapy, is often more effective. However, because depression has genetic, environmental, and psychological contributing factors, treatment can be challenging. Approximately 10% of those suffering from depression have treatment-resistant depression (TRD) that does not respond to standard treatment.A number of treatment options for those with TRD target the functioning of the nervous system. Deep-brain stimulation (DBS) , which is used to treat Parkinson disease, has also been investigated as a treatment for TRD. DBS involves implanting a device in the brain that sends electrical impulses to a specific area. Although the mechanism by which DBS alleviates depressive symptoms is unclear, neurostimulation provided by DBS is thought to disrupt dysfunctional patterns of electrical activity in local areas and connected brain regions.A meta-analysis reviewed the data from several studies that used different brain regions as DBS targets in the treatment of TRD. Table 1 shows the percentage of TRD patients who underwent DBS and showed clinical responsiveness and remission of depression. Clinical response was defined as a 50% reduction in scores on a measure of depression. Various scales were used in the studies, including different versions of the Hamilton Depression Rating Scale (HDRS) and Montgomery-Asberg Depression Rating Scale (MADRS) . Remission of depression was defined as a score that fell below a predetermined threshold.Table 1 Percentage of TRD Patients Who Showed Clinical Response and Remission With DBS Treatment

-Which of the following is true regarding two classes of drugs commonly used to treat depression, selective serotonin reuptake inhibitors (SSRIs) and monoamine oxidase inhibitors (MAOIs) ?

Quizplus · Accepted Answer

11ecba2d_0c76_591e_a3bf_0f21fa403665_MD0008_00 Depression symptoms appear to be related to decreased levels of the monoamine neurotransmitters serotonin, dopamine, and norepinephrine in the central nervous system (monoamine hypothesis). Many antidepressant medications increase the concentration or prolong the function of one or more of these neurotransmitters at the synaptic cleft. These drugs usually function via one of four general mechanisms: Increasing production of neurotransmitters within the presynaptic neuron Promoting release of neurotransmitters from the axon terminal into the synaptic cleft Blocking reabsorption (reuptake) of neurotransmitters into the presynaptic neuron Decreasing breakdown of neurotransmitters within the presynaptic neuron For instance, MAOIs inhibit monoamine oxidase, an enzyme attached to the mitochondria in axon terminals that catalyzes the oxidation (breakdown) of monoamines such as serotonin, dopamine, and norepinephrine. This enzyme functions in the presynaptic neuron to recycle monoamines that have been removed from the synaptic cleft. Inhibition of monoamine oxidase therefore increases the concentrations of monoamines in the axon terminal and eventually within the synaptic cleft. SSRIs belong to another class of antidepressants that selectively block the reabsorption (reuptake) of serotonin into the presynaptic neuron, thereby prolonging the presence of serotonin in the synaptic cleft. (Choice A) Neither SSRIs nor MAOIs directly stimulate the release of serotonin or other monoamines. However, some drugs, such as serotonin-releasing agents and amphetamines, promote the release of neurotransmitters to increase the activity of these in the synaptic cleft. (Choice B) Reuptake inhibitors such as SSRIs block the uptake of neurotransmitters into the pre-synaptic cleft, where they were originally synthesized and released. (Choice D) Promoting uptake of serotonin would decrease the concentration of serotonin in the synaptic cleft, likely exacerbating the symptoms of depression. Educational objective: Antidepressants increase the function of one or more neurotransmitters within the synaptic cleft. This is often done by increasing the production of neurotransmitters, promoting their release, blocking their reuptake, or decreasing their breakdown within the presynaptic neuron. One class of drugs, MAOIs, inhibits the enzyme monoamine oxidase, decreasing the breakdown of serotonin, dopamine, and epinephrine.

Passage Major Depression Is a Mood Disorder That Affects Nearly 7