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Frontiers in Psychology 2024
PubMed: 38868354
DOI: 10.3389/fpsyg.2024.1408797 -
PCN Reports : Psychiatry and Clinical... Sep 2023Nocturnal eating behavior in patients with sleep-related eating disorder (SRED) is difficult to control and can become chronic, causing weight gain and psychological...
BACKGROUND
Nocturnal eating behavior in patients with sleep-related eating disorder (SRED) is difficult to control and can become chronic, causing weight gain and psychological distress. Here, we report a case of SRED comorbid with major depressive disorder successfully treated by switching from brotizolam to suvorexant, that is, from a benzodiazepine to an orexin receptor antagonist.
CASE PRESENTATION
A 25-year-old woman complained of night snacking with partial/complete amnesia and sleepwalking for 1 year. She had a diagnosis of major depressive disorder at age 20 and was on paroxetine and brotizolam for depression and insomnia. At 24 years of age, she experienced her second depressive episode, then her amnestic nocturnal eating became prominent. Even after improvement in depressive symptoms, she experienced uncontrollable nocturnal eating episodes every 2 days, resulting in weight gain of over 10 kg. After a partial amnestic eating episode following an awakening from stage N2 sleep was confirmed through video polysomnography, she was diagnosed with SRED. Considering her strong desire to resolve involuntary eating, we instructed her to discontinue brotizolam and start suvorexant. Subsequently, her nocturnal eating completely disappeared. She experienced rebound insomnia, which improved within 1 month. She was then continued on 10 mg of suvorexant and has not experienced nocturnal eating for 2 years.
CONCLUSION
This case highlights the importance of discontinuing benzodiazepines in the treatment of SRED, but also suggests the potential benefit of orexin receptor antagonists in the treatment of SRED. The efficacy of orexin receptor antagonists in idiopathic SRED should be tested in future studies.
PubMed: 38867814
DOI: 10.1002/pcn5.123 -
Bio Systems Jun 2024A thermodynamic model for memory formation is proposed. Key points include: 1) Any thought or consciousness corresponds to a thermodynamic system of nerve cells. 2) The...
A thermodynamic model for memory formation is proposed. Key points include: 1) Any thought or consciousness corresponds to a thermodynamic system of nerve cells. 2) The system concept of nerve cells can only be described by thermodynamics of condensed matter. 3) The memory structure is logically associated with the system structure or the normal structure of biology. 4) The development of our thoughts is processed irreversibly, and numerous states or thoughts can be generated. 5) Memory formation results from the reorganization and change of cellular structures (or memory structures), which are related to nerve cell skeleton and membrane. Their alteration can change the excitability of nerve cells and the pathway of neural impulse conduction. 6) Amnesia results from the loss of thermodynamic stability of the memory structure, which can be achieved by different ways. Some related phenomena and facts are discussed. The analysis shows that thermodynamics can account for the basic properties of memory.
PubMed: 38866100
DOI: 10.1016/j.biosystems.2024.105247 -
BioRxiv : the Preprint Server For... May 2024Cerebral Cavernous Malformations (CCMs) are neurovascular abnormalities in the central nervous system (CNS) caused by loss of function mutations in KRIT1 (CCM1), CCM2,...
BACKGROUND
Cerebral Cavernous Malformations (CCMs) are neurovascular abnormalities in the central nervous system (CNS) caused by loss of function mutations in KRIT1 (CCM1), CCM2, or PDCD10 (CCM3) genes. One of the most common symptoms in CCM patients is associated with motor disability, weakness, seizures, stress, and anxiety, and the extent of the symptom or symptoms may be due to the location of the lesion within the CNS or whether multiple lesions are present. Previous studies have primarily focused on understanding the pathology of CCM using animal models. However, more research has yet to explore the potential impact of CCM lesions on behavioral deficits in animal models, including effects on short-term and long-term memory, motor coordination, and function.
METHODS
We used the accelerating RotaRod test to assess motor and coordination deficits. We also used the open field test to assess locomotor activity and pathology-related behavior and Pavlovian fear conditioning to assess short-and long-term memory deficits. Our behavioral studies were complemented by proteomics, histology, immunofluorescence, and imaging techniques. We found that neuroinflammation is crucial in behavioral deficits in male and female mice with neurovascular CCM lesions ( ).
RESULTS
Functional behavior tests in male and female mice revealed that CCM lesions cause sudden motor coordination deficits associated with the manifestation of profound neuroinflammatory lesions. Our findings indicate that maturation of CCM lesions in mice also experienced a significant change in short- and long-term memory compared to their littermate controls, mice. Proteomic experiments reveal that as CCM lesions mature, there is an increase in pathways associated with inflammation, coagulation, and angiogenesis, and a decrease in pathways associated with learning and plasticity. Therefore, our study shows that mice display a wide range of behavioral deficits due to significant lesion formation in their central nervous system and that signaling pathways associated with neuroinflammation and learning impact behavioral outcomes.
CONCLUSIONS
Our study found that CCM animal models exhibited behavioral impairments such as decreased motor coordination and amnesia. These impairments were associated with the maturation of CCM lesions that displayed a neuroinflammatory pattern.
PubMed: 38853989
DOI: 10.1101/2024.05.29.596485 -
Brain Research Bulletin Aug 2024Tongue coating affects cognition, and cognitive decline at early stage also showed relations to functional and structural remodeling of superior temporal sulcus (STS) in...
Tongue coating affects cognition, and cognitive decline at early stage also showed relations to functional and structural remodeling of superior temporal sulcus (STS) in amnestic mild cognitive impairment (aMCI). The potential correlation between disparate cognitive manifestations in aMCI patients with different tongue coatings, and corresponding mechanisms of STS remodeling remains uncharted. In this case-control study, aMCI patients were divided into thin coating (n = 18) and thick coating (n = 21) groups. All participants underwent neuropsychological evaluations and multimodal magnetic resonance imaging. Group comparisons were conducted in clinical assessments and neuroimaging measures of banks of the STS (bankssts). Generalized linear models were constructed to explore relationships between neuroimaging measures and cognition. aMCI patients in the thick coating group exhibited significantly poorer immediate and delayed recall and slower information processing speed (IPS) (P < 0.05), and decreased functional connectivity (FC) of bilateral bankssts with frontoparietal cortices (P < 0.05, AlphaSim corrected) compared to the thin coating group. It was found notable correlations between cognition encompassing recall and IPS, and FC of bilateral bankssts with frontoparietal cortices (P < 0.05, Bonferroni's correction), as well as interaction effects of group × regional homogeneity (ReHo) of right bankssts on the first immediate recall (P < 0.05, Bonferroni's correction). aMCI patients with thick coating exhibited poor cognitive performance, which might be attributed to decreased FC seeding from bankssts. Our findings strengthen the understanding of brain reorganization of STS via which tongue coating status impacts cognition in patients with aMCI.
Topics: Humans; Cognitive Dysfunction; Male; Female; Aged; Temporal Lobe; Magnetic Resonance Imaging; Tongue; Case-Control Studies; Middle Aged; Neuropsychological Tests; Amnesia; Mental Recall
PubMed: 38844172
DOI: 10.1016/j.brainresbull.2024.110995 -
PloS One 2024A large body of evidence has shown that treatments that interfere with memory consolidation become ineffective when animals are subjected to an intense learning...
A large body of evidence has shown that treatments that interfere with memory consolidation become ineffective when animals are subjected to an intense learning experience; this effect has been observed after systemic and local administration of amnestic drugs into several brain areas, including the striatum. However, the effects of amnestic treatments on the process of extinction after intense training have not been studied. Previous research demonstrated increased spinogenesis in the dorsomedial striatum, but not in the dorsolateral striatum after intense training, indicating that the dorsomedial striatum is involved in the protective effect of intense training. To investigate this issue, male Wistar rats, previously trained with low, moderate, or high levels of foot shock, were used to study the effect of tetrodotoxin inactivation of dorsomedial striatum on memory consolidation and subsequent extinction of inhibitory avoidance. Performance of the task was evaluated during seven extinction sessions. Tetrodotoxin produced a marked deficit of memory consolidation of inhibitory avoidance trained with low and moderate intensities of foot shock, but normal consolidation occurred when a relatively high foot shock was used. The protective effect of intense training was long-lasting, as evidenced by the high resistance to extinction exhibited throughout the extinction sessions. We discuss the possibility that increased dendritic spinogenesis in dorsomedial striatum may underly this protective effect, and how this mechanism may be related to the resilient memory typical of post-traumatic stress disorder (PTSD).
Topics: Animals; Male; Rats, Wistar; Extinction, Psychological; Rats; Avoidance Learning; Corpus Striatum; Tetrodotoxin; Memory Consolidation; Amnesia; Electroshock
PubMed: 38843228
DOI: 10.1371/journal.pone.0305066 -
Brain and Behavior Jun 2024Visual attention-related processes that underlie visual search behavior are impaired in both the early stages of Alzheimer's disease (AD) and amnestic mild cognitive...
BACKGROUND
Visual attention-related processes that underlie visual search behavior are impaired in both the early stages of Alzheimer's disease (AD) and amnestic mild cognitive impairment (aMCI), which is considered a risk factor for AD. Although traditional computer-based array tasks have been used to investigate visual search, information on the visual search patterns of AD and MCI patients in real-world environments is limited.
AIM
The objective of this study was to evaluate the differences in visual search behaviors among individuals with AD, aMCI, and healthy controls (HCs) in real-world scenes.
MATERIALS AND METHODS
A total of 92 participants were enrolled, including 28 with AD, 32 with aMCI, and 32 HCs. During the visual search task, participants were instructed to look at a single target object amid distractors, and their eye movements were recorded.
RESULTS
The results indicate that patients with AD made more fixations on distractors and fewer fixations on the target, compared to patients with aMCI and HC groups. Additionally, AD patients had longer fixation durations on distractors and spent less time looking at the target than both patients with aMCI and HCs.
DISCUSSION
These findings suggest that visual search behavior is impaired in patients with AD and can be distinguished from aMCI and healthy individuals. For future studies, it is important to longitudinally monitor visual search behavior in the progression from aMCI to AD.
CONCLUSION
Our study holds significance in elucidating the interplay between impairments in attention, visual processes, and other underlying cognitive processes, which contribute to the functional decline observed in individuals with AD and aMCI.
Topics: Humans; Alzheimer Disease; Cognitive Dysfunction; Female; Male; Aged; Attention; Visual Perception; Amnesia; Eye Movements; Aged, 80 and over; Middle Aged
PubMed: 38841742
DOI: 10.1002/brb3.3567 -
BMC Nephrology Jun 2024Long-term enzyme replacement therapy (ERT) may improve prognosis in the patients with Fabry disease (FD), however, detail psychosocial burden has not been focused on...
BACKGROUND
Long-term enzyme replacement therapy (ERT) may improve prognosis in the patients with Fabry disease (FD), however, detail psychosocial burden has not been focused on long life expectancy. We experienced a male case of FD under ERT, he was placed on hemodialysis and presented rapidly progressive cognitive function.
CASE PRESENTATION
A 51-year-old male patient with FD has been receiving ERT from age of 38 years. Hemodialysis was initiated at the age of 47 years. The patient experienced several attacks of cerebral infarction, and brain images demonstrated wide-spread asymptomatic ischemic lesions. His behavior became problematic at the age of 51 years. He often exhibited restlessness during hemodialysis sessions and failure to communicate effectively. The patient experienced impairment of attention and executive function, topographical disorientation, and amnesia. Consequently, it was necessary for medical staff and family members to monitor his behavior for safe extracorporeal circulation and daily life activities. Annual standardized neuropsychiatric testing revealed worsening of cognitive performance.
CONCLUSIONS
Despite treating with long-term ERT, it is necessary to determine the psychosocial burden derived from the progression of cognitive impairment in patients with FD undergoing hemodialysis.
Topics: Humans; Male; Fabry Disease; Renal Dialysis; Middle Aged; Cognitive Dysfunction; Enzyme Replacement Therapy; Disease Progression; Cost of Illness
PubMed: 38831308
DOI: 10.1186/s12882-024-03624-9 -
Scientific Reports Jun 2024
PubMed: 38830872
DOI: 10.1038/s41598-024-62399-z -
Cureus May 2024Transient global amnesia (TGA) is an uncommon neurologic disorder that consists of a sudden and temporary loss of memory, both present and past. Its causes and risk...
Transient global amnesia (TGA) is an uncommon neurologic disorder that consists of a sudden and temporary loss of memory, both present and past. Its causes and risk factors are not well known. We describe a case of a 58-year-old woman who was brought to the emergency department (ED) with sudden onset loss of memory and disorientation after a dive in the ocean. She presented memory deficits with incapacity to retain new memories and amnesia for the previous 24 hours. All exams ordered were normal, including computed tomography of the brain and laboratory analysis. After six hours of close monitoring in the ED, she gradually started to retain short-term memories and was discharged after 48 hours with no memory or other deficits. The diagnosis of TGA was made based on the clinical presentation and the patient's rapid improvement. Follow-up neurology consultation and further testing did not demonstrate any evidence to exclude this diagnosis. Further research is needed on this topic to allow the identification of risk factors and causes to prevent it.
PubMed: 38826884
DOI: 10.7759/cureus.59603