depression impairs intuition

Posted comment on ´Impaired intuition in patients with major depressive disorder` by C Remmers, S Topolinski, DE Dietrich, and J Michalak published in British Journal of Clinical Psychology 2015 Jun;54(2):200-13. doi: 10.1111/bjc.12069. Epub 2014 Oct 11.

Remmers and colleagues investigated whether people suffering with a major depressive disorder (MDD) exhibited impaired intuition that would affect decision-making capability. Twenty nine depressed patients and 27 controls took the Judgment of Semantic Coherence Task test, which is a language based test involving the presentation of three words that may or may not be linked by a fourth word. The participant was given three and a half seconds to say whether they thought the words were linked or not, and if affirmative, a further eight seconds to state the linking word. Participants were allowed to confirm the presence of a linking word, but not give it and this was described as intuition. Remmers and colleagues found that it was this group with correct intuitive responses that was lower in their depressed subject group. Since, the number of correct responses and no responses were similar for both subject groups, unequal motivational or attentional levels could be ruled out. Remmers and colleagues studies also showed that the depressed group demonstrated higher levels of rumination (brooding).

Remmers and colleagues work is interesting because depression is considered to be related to conscious cognitive dysfunctions, but this study shows that unconscious/subconscious ones are also affected. This observation implies that the physiological effects seen with depression impact on intuition and this supports my views on the mechanisms involved in conscious and subconscious brain memory input, storage and recall. Remmers and colleagues experiment was designed so that in the first three and a half seconds the subject experiences visual input and processing of the first word, which requires an effective visual input system and attentional mechanisms. In my version of the brain memory mechanisms, the immediate subconscious recognition of the word is achieved by the recall without processing mechanism and requires binding of event features and firing of the appropriate storage neuronal cell assembly (sNCA), and since an emotional signal is also recalled, emotional tag re-activation. The signal from the latter is probably ignored unless the event or in this case word is linked with fear. The rapid input of the second word requires an attentional shift and visual input and processing mechanisms. Again, binding of features and sNCA firing occurs, but there is also subconscious activation of extended sNCA links ie. Neuronal cells representing the links connecting this word/event with other words/events with the same/similar characteristics, categories etc. in the hope that a link with the first word is present. The processes for the third word follow the previous two and at the end there is conscious awareness whether the three words are linked, or not.
Some of the physiological changes observed with depression appear according to Remmers and colleagues to impact on the brain memory mechanisms required to bring about this recall without processing and monitoring for associations between the events. It is likely that for these stages the decreased 5-HT and noradrenaline neurotransmitter levels, the smaller hippocampus with its decreased level of neurogenesis and the change in prefrontal cortex function all reported in depression are major causes of the change in the cognitive functions observed. The hippocampus has, according to my version of the brain memory mechanisms, two important brain memory functions: it confers timing and synchronicity on firing and it has an important role in the emotional system (in this case, ignored unless the words initiate a fear response). The hippocampus is required for new memories because it confers synchronicity on memory event features, but it is also required for memory reactivation (Frankland, Fried) leading to patterns in the cortex and stabilization of the connections between the hippocampus and cortex (Frankland) and hence, here subconscious word recognition. Noradrenaline signaling in the hippocampus by norepinephrine is said to be important for the retrieval of intermediate term memory (Zhang) and hence, in depression where there is a reported decrease in the serotonin and noradrenaline neurotransmitters as well as smaller hippocampus size, then retrieval of words would be affected. The hippocampus is also said to be involved in the maintenance of multiple items (hippocampal dependent working memory -Axmacher) and matching of probe stimulus (word 3) and goal state (word 1,2) (Duncan) which is required in the subconscious matching of the three words in the early stage of the experiment. It is also known that only new synapses act and so normally neurogenesis would counteract the increase in neuronal stimulation (Meshi, Bischofburger, Toni, Kee), but in depressed patients decreased hippocampal neurogenesis is observed, hence having an effect on memory storage and reactivation. Hence, even in the first three and half seconds of the experiment the physiological changes to the hippocampus observed in depression have a significant effect on the informational input, recall and matching mechanisms required for successful execution of the experiment.
The physiological effect of depression on the prefrontal cortex may also play a role in the decreased intuition observed in the early stage of this experiment. Prefrontal cortical functioning in memory mechanisms involves the release of dopamine, whether by dopamine agonists or serotonin. Since a lower level of serotonin is observed in depression then it is likely that the dopamine levels in this brain area are also negatively affected and hence, affecting the overall functioning of the area. The prefrontal cortex is said to have roles in information memory formation and recall, working memory (Sakurai) with repeated retrieval of target memories leading to decreased activity (Kuhl), and in encoding and retrieval of emotional memories (Labar), a process requiring the mitogen PK/ERK pathway (Leam). Connectivity between the medial temporal lobe and the prefrontal cortex is required in the transfer of information from past experiences to novel ones (Zeitharma), important for word recognition and processing in these early stages.
After the first stage when the subject has eight seconds to report the linking word, the brain memory processes involved shift to a conscious recall with processing type mechanism according to my views on the mechanisms involved in brain memory. The attentional system switches between the three words and there is conscious recall with processing to establish exactly the similarity between the words. This stage relies on merging activated neuronal groupings, a monitoring system thought to be located in the cingulate cortex and possibly a decision-making mechanism involving the prefrontal cortex. This may be required if there is more than one instance of linking between the words or where the link may be more tenuous. An overactive prefrontal cortex as reported in depression may affect this process since a change in the right inferior area may change Evans and Stenovitch´s decision-making system 2 (slow, sequential, central, working memory based); may affect the dorsal lateral area which is more active in reasoning (D’Esposito); may affect the ventral medial area involved in the comparison of event values (Wunderlich) for example. The prefrontal cortex also plays a role in maintaining attention (increased activity in the dorsal lateral region when actions are selected and initiated – Spence and Firth) and any alterations in the 5HT and dopamine levels in this brain area can lead to changes in attention (Scholes). Hence, the second stage of the experiment where there is conscious cognitive functioning is also affected in depressed subjects.
Therefore, the physiological effects on brain areas observed in depression have effects on cognitive functioning both conscious and unconscious and this was shown in the experiments carried out by Remmers and colleagues.

Since we´re talking about the topic……
….would a repeat of this experiment with depressed subjects who have been administered an anti-inflammatory drug eg. etanercept for three months show an effect on intuition since it has been reported that Alzheimer patients have exhibited an improvement in memory capability?
….can it be assumed that an increased level of stress hormones which leads to a hippocampal effect and decreased neurogenesis (Gould) would also exhibit the same effect on intuition as depression has?
….it has been shown that there is specificity of areas in the prefrontal cortex and hippocampus for particular cognitive functions and therefore, would accurate imaging of the both areas during this experiment locate areas particularly linked with intuition or switches in function ie at the three and half second mark?

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