The concept of “relational memory” is very cool. It is a form of complex brain function joining associations together :
Relational memory is the ability to remember arbitrary associations between objects or events. These memories include things related by location, order, and context. Lesions of the medial temporal lobe (MTL) cause severe relational memory impairments suggesting that the MTL plays an important role in the formation of relational memories. Lesions to the hippocampus, the final output of the MTL, also causes relational memory impairments.
Relational memory in the early stage of psychotic bipolar disorder
Rachel A McKinney 1, Suzanne N Avery 2, Kristan Armstrong 1, Jennifer Urbano Blackford 3, Neil D Woodward 1, Stephan Heckers 1 Psychiatry Res. 2020 Dec;294:113508. doi: 10.1016/j.psychres.2020.113508. Epub 2020 Oct 11. PMID: 33096436 PMCID: PMC7809627 DOI: 10.1016/j.psychres.2020.113508
Relational memory is impaired in psychotic disorders. In non-affective psychotic disorders, relational memory deficits are present in the early stage of illness and become more pronounced in the chronic stage. Previous studies have demonstrated cognitive deficits in early-stage psychotic bipolar disorder, but it is unclear whether relational memory is impaired. We examined relational memory using a face-scene binding task in early-stage psychotic bipolar disorder patients (n = 33) and compared their performance with healthy control (n = 40) and early-stage non-affective psychosis participants (n = 40). During training, participants learned to associate faces with background scenes. During testing, participants viewed a scene overlaid by three faces and were asked to recall the matching face. Relational memory was assessed indirectly using eye movements and explicitly using forced-choice recognition. Preferential viewing of the matching face, as captured by overall proportion of viewing and viewing across time, was significantly lower in psychotic bipolar disorder than in the healthy control group. However, preferential viewing of the matching face in psychotic bipolar disorder was significantly better than in non-affective psychosis. These findings provide novel evidence that relational memory in patients with early-stage psychotic bipolar disorder is intermediate between healthy control and early-stage non-affective psychosis subjects.
Keywords: Affective psychosis; Early psychosis; Eye movements; Hippocampus; Non-affective psychosis; associative memory; first episode.
Paula would define the very essence of her attack of bipolar depression as loss of relational memory involved retrograde memory loss. This loss of relational memory was accompanied by cognitive impairment and psychomotor retardation. Paula became aware that she lost the ability to converse with people she knew well; she did not remember how she used to behave when being around them, she did not know what she usually said, whether she smiled or not, when to pause, how long to pause, etc…it was so strange. .Paula was aware that her mind was blank when talking to people she knew. Her reaction to this realization was normal, Paula was internally appalled by her lack of knowledge and her lack of memory, and her loss of social skill, Paula was embarrassed at how dull and stupid she seemed, she was shocked that this was happening to her and she tried her best to act normal even though she no longer knew what normal was. Mostly she pretended to listen and said very little.
When she realized that she also did not remember how to do her work, while she was trying to do her work, she was appalled, embarrassed, felt stupid, and felt very guilty because she knew she was letting her students down and was not at her best…she simply was “not” there and she was a witness to this horror. And she did not know what to do [she did nothing] and she did not know what to say [she said nothing] and she was very pathetic and she knew it.
She was not able to say any of this, but she was still able to respond to focused questions; such as…
**** .have you lost your memory? she would have said yes. but no one asked a focused question and she could not answer a general question because she could not organize her thoughts or explain. Paula needed people who had a functioning mind to ask her questions about her memory.
Instead, people responded to her shame and embarrassment by feeling shame and embarrassment for her and avoided asking anything and simply assumed she was having a bad day , instead of suddenly having a bad memory – because she had lost her mind. People assumed that Paula was distracted, that she was not paying attention and that was completely untrue; Paula was paying a lot of attention to her blank mind devoid of facts and general information about the people around her; Paula could not fail to pay attention to this because this blankness was obvious to her every second of every minute of every hour of every day [and night] as she tried her best to do her best.
Is there evidence of hippocampal atrophy in major depression and bipolar depression? The answer seems to be yes.
“Chronic stress and hypersecretion of cortisol in mood disorders can exert neurotoxic effects on the hippocampus [Reference Surget, Tanti, Leonardo, Laugeray, Rainer and Touma8]. Hippocampal atrophy is one of the most consistent neuroimaging finding in MDD [Reference Cole, Costafreda, McGuffin and Fu11]. Although less consistent than results in MDD, numerous structural MRI studies have reported hippocampal volume losses in BD [Reference Otten and Meeter12]. Moreover, illness duration and number of mood episodes were reported to be correlated with degree of hippocampal volume reduction in MDD [Reference McKinnon, Yucel, Nazarov and MacQueen13] and BD [Reference Javadapour, Malhi, Ivanovski, Chen, Wen and Sachdev14].” Han, K., Kim, A., Kang, W., Kang, Y., Kang, J., Won, E., . . . Ham, B. (2019). Hippocampal subfield volumes in major depressive disorder and bipolar disorder. European Psychiatry, 57, 70-77. doi:10.1016/j.eurpsy.2019.01.016
Paula experienced chronic stress while she was partially amnesic and cognitively impaired. This sensation of distress was separate from her altered mental status. Paula was short of breathe and could not speak more than 2-3 words . Paula could not verbalize her shortness of breath and it was not visible to the eye because she also had a depressed rate of breathing.
A quick survey of her vital signs showed that the chronic stress was due to some level of ventilatory failure and [most likely] reduced minute ventilation and her lack of physical ability to raise her respiratory rate [already depressed at baseline] during a severe respiratory challenge. [she had been sick with a number of viruses before her amnesic attack.].
Dr Emile Kraepelin [1926 Manic depressive Insanity Chapter 3, Bodily Signs] also found abnormal respiratory rates at baseline at rest in his manic depressive unmedicated patients; he mentioned depressed rates of ventilation in the depressed stage of the syndrome and what sounds like Cheyne-Stokes ventilation in mania. The ventilatory system consists mostly of skeletal muscle and includes muscles and nerve fibres of the neck, torso and tummy.
Paula and I think that she has a respiratory defect due to hypotonia of the respiratory skeletal muscles . She most likely suffered some injury when she was born, hypotonic and barely alive, needing resuscitation, and transfusion. It is apparently easy to damage muscle when it is hypotonic and resistant to stretch. Paula survived and developed normally, albeit with abnormal and depressed ventilation which is adequate most of the time due to a large enough tidal volume. [We have had her tested when healthy].
The mood component in bipolar illness may be a result of some level of either reversible brain hypoxia and/or reversible hypercapnia and/or reversible rising of the intracranial pressure due to the cerebral vasodilation effects of C02 [a normal product of cell metabolism and one that the body is very used to dealing with].
This would make bipolar illness a reversible dementia [an encephalopathy] or a lengthy attack of delirium [all psychomotor subtypes].
Cognitive impairment and retrograde amnesia and a defective ventilatory system under stress [infection, inflammation, undernourishment, exposure, etc..] would explain why the patient suffers so much and why they are not “themselves”; they have “forgotten” how to be themselves and are at a loss to be able to verbalize such a strange impairment.
More and more research is once again showing what Kraepelin’s research showed long ago , that memory and cognition is impaired during bipolar attacks. This is not mentioned in the Diagnosis handbook of Psychiatry, the DSM 5.
This is why Kraepelin called manic depressive illness a insanity; he did not consider it a full fledged dementia because 1] attacks lifted spontaneously, even after decades- long attacks and because the motor manifestations were the same as a delirium with its altered mental status, but lasted much longer than a usual attack of delirium and unlike delirium, it did not result in death as often. [maybe because the patients with manic depressive insanity were much younger, between the ages of 20 and 30, at the age of their first attack.
Scientists and doctors understood, even back then, that exacerbation of chronic ventilatory failure would lead to decompensation and to hypercapnia and reversible disfunction of the brain and of the mind [and could be very unpleasant to experience but also could lead to intoxication – euphoria, confabulation, irritability- due to the mixed up ratio’s of these vital gases.
We think that Kraepelin [knowledgeable in medicine and physiology and physiological psychology and botany and evolutionary thinking and zoology and biology and math and scientific methods] thought that all this would be obvious to anyone who is a doctor, and would not think that he would have to spell it out to other professionals. He assumed that doctors treating patients with this syndrome would know all this, especially if they knew about his methods and the findings in his studies.
He was wrong. He should have included a chapter in gas exchange, cellular respiration and acid base balance of the blood, of the tissues and of the cells and how ventilatory muscle defects could threaten the function of the brain, the mind and the rest of the organs and how metabolic dysfunction becomes obvious upon measuring the vital signs, especially the baseline respiratory rate at rest.
Despite Paula’s doctors, we managed to understand that Paula could recover 100 percent of her mind, as long as we monitored the effects of any and all treatment on her memory and baseline cognitive status. [We think that it would have taken less than 10 years for her to regain her baseline memory and mind, if we had been able to get her supportive medical help to ease her breathing but no one listed to us, then and now.] It would be an easy hypothesis to check out…..
And this is why Paula and I are able to discuss this fascinating subject every morning over breakfast.