Depression: Neurobiological and Neuropsychological Models

A correlation of Neurobiological and Neuropsychological cognitive model toward Depression

Abstract

Depression is a chronic illness that has stirred centuries of debate regarding its mechanism. Notwithstanding the sharp contrast among theories that have been proposed to explain the underlying source of depression from different perspectives, all of them accept the fact that it affects body, mood and even thoughts of individuals and as World Health organization predicted, it is expected to be the second mental disorder by 2020. The most compelling models regarding the source of depression and its treatment in this realm are Monoamine model and cognitive model. Monoamine model claims that depression has a biological source and it is caused by neurochemical imbalance in individuals, whereas base on cognitive model impaired information processing and negative biases are the key factors in the development of depression. The present paper attempts to assert the missing point in each of these theories and propose an explanation about the mechanism and treatment from two similar perspectives: Cognitive Neurobiological and Cognitive Neuropsychological, which work as a combination of Monoamine and Cognitive model. Both of these models categorize biases based on two pathways: Bottom- Up and Top- Down processing. With the help of cognitive Neuropsychological model, it is shown how negative affective processing can be the main core of depression, while Neurobiological model will show how hyper activation and hypo activation in different brain regions can develop depression. Therefore, a correlation of both models can explain underlying source of depression and thus can be used for modifying depression symptoms.

Definition:

Depression is a universal mental disorder that has been growing at an alarming rate. It will be the second mental disorder by 2020; most people will be affected by depression in their lives either directly or indirectly, through a friend or family member. It is a severe and even painful disorder that will influence almost all aspects of sufferer’s life. Most people misdiagnose depression as feeling down, but depression is not a sign of weakness and is not the same as passing blue mood. According to UK medical reference, depression will be identified and categorized base on its symptoms, which is called ICD10 clinical criteria of depression and depends on the number of symptoms, types of depression, can be diagnosed. Symptoms are:

• Persistent sadness or low mood
• Loss of interests or pleasure
• Fatigue or low energy
• Disturbed sleep
• Poor concentration or indecisiveness
• Low self-confidence
• Poor or increased appetite
• Suicidal thoughts or acts
• Agitation or slowing of movements
• Guilt or self-blame

If an individual suffer from 4 of these symptoms most of the time for at least 2 weeks, he/she will be diagnosed with mild depression, and with 5 to 6 of symptoms he/she suffer from moderate depression and in dangerous cases or severe depression, depressed person has more than 6 symptoms.

Models of depression:

A significant number of studies have been trying to reveal the mechanism of depression from different perspectives. Among the biologically based theories, the most reliable model that arguing reasonably about underlying source of depression and proposing acceptable treatment is Monoamine model. Monoamines are neurotransmitters and neuromodulators that include serotonin, dopamine, norepinephrine, and epinephrine. The basic concept is that neurotransmitter imbalance within the brain is the main core of depression and neurotransmitters can be balanced again by using antidepressant medication. Type of antidepressant medication depends on severity of symptoms; for patients suffering from dysphoria (low mood) SSRIs or norepinephrine reuptake inhibitors can be used, while anhedonia patients (ones with the loss of energy and enjoyment of life) should be treated with norepinephrine and dopamine enhancing drugs (SNRIs). Despite their immediate effects at the synaptic level, in approximately 40% of the cases, they are ineffective in the short time and 30% of patients will suffer from depression within 12 months after recovery. This result suggests that depression is not only the cause of chemical imbalance and psychological factors play an important role in its development. On the other hand, the most prominent and empirically based model of psychological factors of depression is cognitive model proposed by Aaron Beck in 1976. This model claims that negative affective biases, which are negative biases in perception, attention, emotional processing, thoughts and rumination and even memory, will affect individual’s information processing and lack of cognitive control over these negative biases are the main cores of depression. According to this model, depressed people are likely to experience different phenomena such as: negative cognitive triad, think negatively about themselves, their future and even the world; positive blockade, blocking positive information, inhibitory deficits, inability to disengage from negative stimuli. The model defined depression like an infinite loop, which receive feedback from its components:

Figure 1: cognitive model of depression

Beck claimed that by the help of cognitive behavioral therapy (CBT) and behavioral activation therapy (BA) negative biases and negative schemata of depressed people can be modified, however the reality was far from his thought and CBT and BA failed to cure depression, therefore scientists try to find a better explanation and treatment. Based on Beck’s cognitive model, two models have been proposed by researchers: Cognitive Neurobiological and Cognitive Neuropsychological model, which are built on the assumption that negative bottom-up and top-down biases are vital in development of depression.

Cognitive neuropsychological model:

This model was proposed in 2011 and is a combination of Monoamine model and Cognitive model. From neuropsychological perspective environmental factors, genetic factors and personality can change the function of monoamine neurotransmitters; this neurotransmitter imbalance causes negative affective processing biases, which is the impairment of information processing especially in emotional and reward processing and play the main role in development and treatment of depression; and finally the negative affective processing will cause negative schemata in depressed people. In comparison to healthy individuals, who process information in positive way, in depressed people the negative affective processing will change this automatic process more negatively.

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The difference between Neuropsychological model and cognitive model is in the formation of negative schemata; based on cognitive model negative schemata are a result of early hostile life experience and they influencing the information processing, while cognitive psychological model claims that negative schemata are not the direct result of life experience, instead they are caused by negative information processing biases. Neuropsychological model categorized negative biases proposed by cognitive model into two groups: Bottom- up biases and Top-down biases.

Bottom-up biases:

Negative biases that give rise to formation of negative schemata are called bottom-up biases and consist of perceptual biases especially negative emotional perception, negative thoughts and rumination and reward- punishment processing biases. Generally, healthy individual perceive positive information or less negative information from environment, while depression makes sufferers to perceive more negative information from a stimulus faster and filter out the positive information. In a study done by Persad and Polivy in 1993, they observed individuals with depression have difficulty when they were shown facial emotion; paucity in identification, perception and even sensation of facial emotion was common in these patients. A series of experiments were conducted as a support for this finding and in nearly all of them biases toward negative part of stimuli is reported. For example in another study, researchers found a reduced sensitivity toward happy faces, but an extreme sensitivity to sad faces. There is also neuroimaging evidence that support their result. There is a known pathway in perceiving information, which consists of Thalamus (responsible for the distribution of afferent signals), the Dorsal Anterior Cingulate Cortex (region that relays top-down cognitive control from the Dorsolateral Prefrontal Cortex) and the Subgenual Cingulate Cortex (a region that integrates emotional feedback from the limbic system and projects to higher-order cognitive structures). Information from environment will pass through this pathway from Thalamus to Amygdala, which is responsible for detecting emotion and finally with the help of Dorsolateral Prefrontal Cortex Amygdala activity will be controlled in order to not to perceive only negative information. Depressed individuals seem to have a longer and more intense Thalamus and Amygdala activity as a response to negative stimuli. They also showed greater activity in Subgenual Cingulate Cortex, which is a region connecting limbic activity to higher cortical level (Prefrontal Cortex), whereas regions that are responsible for cognitive control, Dorsolateral Prefrontal Cortex and Anterior Cingulate Cortex, showed a reduction in perceptional processing, which means less cognitive control over Amygdala and Thalamus, therefore more negative stimuli will be perceived.

Figure 2: negative perceptional biases

How we perceive emotion will determine how we think about our environmental events and ourselves. As currently said, depression will induce perception and as a result will alter individual’s thoughts in a negative way. Since Individuals are more likely to discern negative information, it is highly probable that their life events, especially ones that are related to their failure, determine their perspective toward themselves; they suffer from lack of self-steem, since they think they are useless, which gradually will cause more negative perception and more negative thoughts. This situation is like an infinite loop and is called rumination. Different brain regions involve in this process, which again prove lack of cognitive control in depression. As previously discussed, hyperactivity in the Amygdala and Hippocampus increase activity of Subgenual Cingulate Cortex (SCC), which is a connection between lower structural and cognitive part of brain and higher ones, therefore, Medial Prefrontal cortex (MPFC), a specific region that is in charge for internal representation of self, will be activated as a response negative information that is received from SCC. Beside the hyperactivation in these parts, there is hypoactivation in higher levels, especially in Dorsolateral Prefrontal Cortex and Ventrolateral Prefrontal Cortex, cognitive control regions; this reduction causes less control over Amygdala and Hippocampus and result in more negative perceptuational biases.

Figure 3: negative thoughts and rumination

After this finding researchers went further and tried to determine how depression affects the reward and punishment process. Interestingly they indicate an exaggeration in negative performance feedback, while a reduction in reward seeking behavior. Neuroimaging evidence revealed an increased activity in the Amygdala as a response to negative situation and decrease activation in the Amygdala, Striatal regions, prefrontal cortex, Nuscleus Accumbens and Dorsal Anterior Cingulate Cortex as a response to reward. This evidence supports the claim that was made earlier with respect to impairment cognitive control in depressed individuals.

Top-down biases:

These types of biases are negative biases that bolster the existence of depressive state and are composed of emotional attention and emotional memory. Not all the information we perceive from environment will be processed; only those that are attended will be selected for further processing. This selecting process in healthy individual is more in favor of positive stimuli, which means greater Rostral Anterior Cingulate Cortex (ACC) activity when they successfully inhibit attention to positive stimuli, while in depressed individual this area cannot be activated in response to positive stimuli and are unable them to disengage their attention from negative stimuli. Disengagement attention requires a top-down mediation from high-level cortical regions, which in depression these regions cannot work properly. Moreover, depressed individuals suffer from lack of selecting and guiding their attention toward positive information and as a result they attend to more negative stimuli. Neuroimaging studies reveled 4 brain regions that are responsible for the whole process of attention: Ventrolateral Prefrontal Cortex (VLPFC; associated with control over stimulus selection), Dorsolateral Prefrontal Cortex (DLPFC) and Anterior Cingulate Cortex (ACC; associated with disengagement functioning), Superior Parietal Cortex (SPC; associated with shifts in gaze). Depression will affect the activity in these regions: Prefrontal Cortex, especially Perigenual ACC, including Brodmann areas 24, 25, and 32, which will cause negative attentional biases; reduced activity in the right VLPFC, therefore they are less likely to guide their attention toward positive stimuli; decreased activity in right DLPFC and right SPC, which cause an impaired disengagement from negative stimuli; greater activation in ACC when successfully inhibiting attention to negative stimuli and less activity as a response to positive stimuli.

Figure 4: negative attentional biases

Various researchers claimed that depressed individuals prefer to remember their failure or negative events rather than their success. Their argument is base on the result of differnet tasks in which depressed individuals showed biases in remembering negative stimulus, not for positive materials. They suggest that since these patients are highly probable to perceive and attend negatively, they are more likely to encoding and recalling negative information. Thanks to neuroimaging studies, their claim was proved. As we might know hippocampus is an essential region for episodic memory and is connected to amygdala and as already discussed Amygdala’s activity is increased toward negative stimuli, which lead to increase activity in Hippocampus as well as Caudate and Putamen, regions for implicit memory and skill learning, in negative situation and as result will bolster the recall probability of negative information.

Figure 5: negative memory biases

According to cognitive model, negative schemata are the most responsible source for developing depression. Base on Neurobiological model, there is a circuit that involve in forming belief and representation of individual’s life, environment and even themselves. The elements of this circuit are: Medial Prefrontal Cortex that is a higher cortical level responsible for internal representation, Anterior Cingulate Cortex that is an intermediate level and a connector between limbic area and Prefrontal Cortex, and finally Amygdala, a lower structural level which detect and process emotion. The high activation in this circuit will cause the maintenance of depression state.

Individuals at risk of depression

According to cognitive neuropsychological model, we can predict the risk factors of depression and we might be able to prevent its development. The most important factors are: neuroticism, genetic factors and recovered depressed individuals. Neuroticism, which is a personality trait, characterized by anxiety, moodiness, worry, envy and jealousy, is most well-established risk factors for depression in non depressed people, however negative attentional biases are not found in them and it suggest that they only suffer form a bottom-up biases. Fortunately since they do not have the top down biases, their biases might be diminished by help of antidepressant drugs that influence bottom-up biases directly. As well as neurotic individuals, relative of depressed individual are in high risk of depression, since they tend to score higher on measures of neuroticism. Moreover, they show a greater activity in Amygdala as well as a reduced Ventral Striatal responsiveness to reward and less efficient activation of Parietal and Temporal networks during working memory performance. All together prove the existence of risk of depression in these individuals. Last vulnerable individuals are those who recently recovered from depression. They have behavioral biases toward negative stimuli as well as abnormal activity in Amygdala. All of these vulnerable individuals exhibit bottom-up biases that are similar to depressed people.

Conclusion

Neuropsychological model and neurobiological model are proposed base on cognitive model and believe that different biases will cause and help the depression state in both depressed people and individuals at risk of depression. According to them, depression is a sequential process that is caused by two pathways: Bottom-up and Top-down biases. Bottom-up biases will influence the lower cognitive and structural level of brain and is the main cause of generating depression, while Top- down affect the higher level and is responsible for maintaining the depressed state. By help of antidepressed drugs, the bottom up biases (perceptional, toghts biases) of depression will be modified and by help of CBT and BT, the top down biases ( attentional and memory biases) will be remit gradually . Figures below are used to show development of depression base on two models.

Figure 6: cognitive neurobiological model

In this figure the whole process of depression is shown as a loop and as can be seen each step will get feedback to each other, even depressive symptoms will influence the Schema activation, which make the whole system stronger. The blue boxes are brain regions that are described as bottom-up biases, while gray boxes are more higher structural levels or top-down biases, which are responsible for cognitive control.

Figure 7: cognitive neuropsychological model:

As can be seen the environment event or genetic factors or personality will cause an imbalance in monoamine transmitters, this change cause negative affective biases (perceptual biases), bottom-up biases and lack of cognitive control over these biases, which is a result of environmental trigger as well as bottom-up biases will increase the chance of depression by generating dysfunctional negative schemata; dysfunctional negative schemata will causes more severe and higher level of biases (top-down biases). Green boxes are treatments that can be use for each step.