Memory Consolidation In Patients Research Articles

Closed-loop auditory stimulation of slow-wave sleep in chronic insomnia: a pilot study.

Insomnia is a prevalent and disabling condition whose treatment is not always effective. This pilot study explores the feasibility and effects of closed-loop auditory stimulation (CLAS) as a potential non-invasive intervention to improve sleep, its subjective quality, and memory consolidation in patients with insomnia. A total of 27 patients with chronic insomnia underwent a crossover, sham-controlled study with 2 nights of either CLAS or sham stimulation. Polysomnography was used to record sleep parameters, while questionnaires and a word-pair memory task were administered to assess subjective sleep quality and memory consolidation. The initial analyses included 17 patients who completed the study, met the inclusion criteria, and received CLAS. From those, 10 (58%) received only a small number of stimuli. In the remaining seven (41%) patients with sufficient CLAS, we evaluated the acute and whole-night effect on sleep. CLAS led to a significant immediate increase in slow oscillation (0.5-1 Hz) amplitude and activity, and reduced delta (1-4 Hz) and sigma/sleep spindle (12-15 Hz) activity during slow-wave sleep across the whole night. All these fundamental sleep rhythms are implicated in sleep-dependent memory consolidation. Yet, CLAS did not change sleep-dependent memory consolidation or sleep macrostructure characteristics, number of arousals, or subjective perception of sleep quality. Results showed CLAS to be feasible in patients with insomnia. However, a high variance in the efficacy of our automated stimulation approach suggests that further research is needed to optimise stimulation protocols to better unlock potential CLAS benefits for sleep structure and subjective sleep quality in such clinical settings.

Does epileptic activity impair sleep-related memory consolidation in epilepsy? A critical and systematic review.

People with epilepsy often complain about disturbed sleep and cognitive impairment. Beyond seizures, the occurrence of interictal epileptic activity during sleep is also increasingly recognized to negatively impact cognitive functioning, including memory processes. The aim of this study was to critically review the effect of interictal epileptic activity on sleep-related memory consolidation. PubMed and PsychINFO databases were systematically searched to identify experimental studies that investigated sleep-related memory consolidation and the relationships between sleep-related epileptic activity and memory in adults and children with epilepsy. This review also highlights hypotheses regarding the potential pathophysiological mechanisms. A total of 261 studies were identified; 27 of these met selection criteria. Only 13 studies prospectively assessed the effect of sleep on memory in epilepsy. Most studies reported no alteration of sleep-related memory consolidation in patients, with either similar retention levels following a period containing sleep (n = 5) or improved memory performance postsleep (n = 4). Two studies in children with epilepsy found impaired sleep-related memory consolidation. Ten studies, of which 6 were in childhood epilepsy syndromes, reported a debilitating effect of sleep-related epileptic activity on memory functioning. Conclusions from existing studies were hampered by small sample sizes, heterogeneous patient groups, and variations in memory assessment techniques. Overall, results to date preclude any definitive conclusions on the alteration of sleep-related memory consolidation in epilepsy. We discuss methodological considerations specific to people with epilepsy and provide suggestions on how to best investigate the relationship between epileptic activity, sleep, and memory consolidation in future studies. Latreille V, Schiller K, Peter-Derex L, Frauscher B. Does epilepticimpair sleep-related memory consolidation in epilepsy? A critical and systematic review. J Clin Sleep Med. 2022;18(10):2481-2495.

Dysfunctional Overnight Memory Consolidation in Patients with Schizophrenia in Comparison to Healthy Controls: Disturbed Slow-Wave Sleep as Contributing Factor?

Introduction: Memory deficiency has been shown in schizophrenia patients, but results on the role of sleep parameters in overnight consolidation of associative verbal memory are still missing. Therefore, the aim of our study was to elucidate underlying processes of impaired sleep-related consolidation of associative word pairs in schizophrenia including standard sleep parameters as well as sleep spindle counts and spectral analysis. Methods: Eighteen stably medicated schizophrenia patients and 24 healthy age-matched controls performed an associative declarative memory task before and after polysomnographic recordings. Part of the participants expected verbal associative memory testing in the morning, while the others did not. Furthermore, participants filled in self-rating questionnaires of schizophrenia-typical experiences (Eppendorf Schizophrenia Inventory [ESI] and Psychotic Symptom Rating Scale). Results: Schizophrenia patients performed worse in verbal declarative memory in the evening as well as in overnight consolidation (morning compared to evening performance). While duration of slow-wave sleep was nearly comparable between groups, schizophrenia patients showed lower sleep spindle count, reduced delta power during slow-wave sleep, and reduced spindle power during the slow oscillation (SO) up-state. In healthy but not in schizophrenia patients, a linear relationship between overnight memory consolidation and slow-wave sleep duration as well as delta power was evident. No significant effect with respect to the expectation of memory retrieval was evident in our data. Additionally, we observed a negative linear relationship between total number of sleep spindles and ESI score in healthy participants. Discussion/Conclusion: As expected, schizophrenia patients showed deficient overnight verbal declarative memory consolidation as compared to healthy controls. Reduced sleep spindles, delta power, and spindle power during the SO up-state may link sleep and memory deficiency in schizophrenia. Additionally, the absence of a linear relationship between sleep-related memory consolidation and slow-wave sleep as well as delta power suggests further functional impairments in schizophrenia. Note that this conclusion is based on observational data. Future studies should investigate if stimulation of delta waves during sleep could improve memory performance and thereby quality of life in schizophrenia.

Memory-relevant nap sleep physiology in healthy and pathological aging.

Aging is associated with detrimental changes in sleep physiology, a process accelerated in Alzheimer's disease. Fine-tuned temporal interactions of non-rapid eye movement slow oscillations and spindles were shown to be particularly important for memory consolidation, and to deteriorate in healthy older adults. Whether this oscillatory interaction further decline in early stages of Alzheimer's disease such as mild cognitive impairment has not been investigated to date, but may have important therapeutic implications. Here, we assessed differences in sleep architecture and memory-relevant slow oscillation, sleep spindles and their functional coupling during a 90-min nap between healthy young and older adults, and in older patients with mild cognitive impairment. Furthermore, associations of nap-sleep characteristics with sleep-dependent memory performance change were evaluated. We found significant differences between young and older healthy adults, and between young adults and patients with mild cognitive impairment, but not between healthy older adults and patients for several sleep metrics, including slow oscillation-spindle coupling. Moreover, sleep-dependent retention of verbal memories was significantly higher in young healthy adults versus older adults with and without mild cognitive impairment, but no difference between the two older groups was observed. Associations with sleep metrics were only found for pre-nap memory performances. In conclusion, our results indicate changes in nap sleep physiology and sleep-related memory consolidation in older adults with and without mild cognitive impairment. Thus, interventions targeted at improving sleep physiology may help to reduce memory decline in both groups, but our study does not indicate additional benefits for patients with mild cognitive impairment. Effects of Brain Stimulation During Daytime Nap on Memory Consolidation in Younger, Healthy Subjects: https://clinicaltrials.gov/ct2/show/NCT01840865; NCT01840865. Effects of Brain Stimulation During a Daytime Nap on Memory Consolidation in Older Adults; https://clinicaltrials.gov/ct2/show/study/NCT01840839?term=01840839&draw=2&rank=1; NCT01840839. Effects of Brain Stimulation During a Daytime Nap on Memory Consolidation in Patients With Mild Cognitive Impairment; https://clinicaltrials.gov/ct2/show/NCT01782365?term=01782365&draw=2&rank=1; NCT01782365.

Distributed slow-wave dynamics during sleep predict memory consolidation and its impairment in schizophrenia

The slow waves (SW) of non-rapid eye movement (NREM) sleep reflect neocortical components of network activity during sleep-dependent information processing; their disruption may therefore impair memory consolidation. Here, we quantify sleep-dependent consolidation of motor sequence memory, alongside sleep EEG-derived SW properties and synchronisation, and SW–spindle coupling in 21 patients suffering from schizophrenia and 19 healthy volunteers. Impaired memory consolidation in patients culminated in an overnight improvement in motor sequence task performance of only 1.6%, compared with 15% in controls. During sleep after learning, SW amplitudes and densities were comparable in healthy controls and patients. However, healthy controls showed a significant 45% increase in frontal-to-occipital SW coherence during sleep after motor learning in comparison with a baseline night (baseline: 0.22 ± 0.05, learning: 0.32 ± 0.05); patient EEG failed to show this increase (baseline: 0.22 ± 0.04, learning: 0.19 ± 0.04). The experience-dependent nesting of spindles in SW was similarly disrupted in patients: frontal-to-occipital SW–spindle phase-amplitude coupling (PAC) significantly increased after learning in healthy controls (modulation index baseline: 0.17 ± 0.02, learning: 0.22 ± 0.02) but not in patients (baseline: 0.13 ± 0.02, learning: 0.14 ± 0.02). Partial least-squares regression modelling of coherence and PAC data from all electrode pairs confirmed distributed SW coherence and SW–spindle coordination as superior predictors of overnight memory consolidation in healthy controls but not in patients. Quantifying the full repertoire of NREM EEG oscillations and their long-range covariance therefore presents learning-dependent changes in distributed SW and spindle coordination as fingerprints of impaired cognition in schizophrenia.

The effects and relevance of sleep on memory consolidation in patients with stable paranoid schizophrenia

Objective To explore the memory function and the effects of sleep on memory consolidation in patients with stable paranoid schizophrenia. Method Sixty patients with stable paranoid schizophrenia were randomly assigned into research group(n=30) and control group(n=30).30 healthy people were raised as a healthy control group.The polysomnography (PSG) was used for 10 hours of sleep monitoring in the research group and the healthy control group and the multiple memory assessment scale(MMAS) was used to test the subjects memory before and after the sleep monitoring.Control group performed memory tests in equal length daytime.Pre-test and post-memory measurements were compared. Results The pre-memory test of three groups had significant statistical differences (F(2, 87)=31.40, 39.89; P 0.05) .But compared with the control group, auditory verbal memory conservation rate((62.64±9.06)% vs (43.00±9.73)%, P<0.01), recognition accuracy rate ((69.11±11.04)% vs (61.78±11.67)%, P<0.05), picture memory conservation rate((71.20±14.95)% vs (58.72±16.19)%, P<0.01), recognition accuracy rate ((86.89±8.02)% vs (78.89±12.63)%, P<0.01) of the research group showed statistical significance differences (P<0.05). Both N2 (r=0.377, P<0.05) and REM(r=0.436, P<0.05) had positive correlation with recognition accuracy rate of auditory verbal memory in research group. Conclusion Stable paranoid schizophrenic patients have poorer memory function(auditory verbal words memory recall, picture memory recall) than healthy people.Sleep promotes the consolidation of memory in patients with schizophrenia.Both N2 and REM of patients with stable paranoid schizophrenic have positive correlation with recognition accuracy rate of auditory verbal memory. Key words: Paranoid; Schizophrenia; Sleep; Memory consolidation

Promoting Sleep Oscillations and Their Functional Coupling by Transcranial Stimulation Enhances Memory Consolidation in Mild Cognitive Impairment.

Alzheimer's disease (AD) not only involves loss of memory functions, but also prominent deterioration of sleep physiology, which is already evident at the stage of mild cognitive impairment (MCI). Cortical slow oscillations (SO; 0.5-1 Hz) and thalamocortical spindle activity (12-15 Hz) during sleep, and their temporal coordination, are considered critical for memory formation. We investigated the potential of slow oscillatory transcranial direct current stimulation (so-tDCS), applied during a daytime nap in a sleep-state-dependent manner, to modulate these activity patterns and sleep-related memory consolidation in nine male and seven female human patients with MCI. Stimulation significantly increased overall SO and spindle power, amplified spindle power during SO up-phases, and led to stronger synchronization between SO and spindle power fluctuations in EEG recordings. Moreover, visual declarative memory was improved by so-tDCS compared with sham stimulation and was associated with stronger synchronization. These findings indicate a well-tolerated therapeutic approach for disordered sleep physiology and memory deficits in MCI patients and advance our understanding of offline memory consolidation.SIGNIFICANCE STATEMENT In the light of increasing evidence that sleep disruption is crucially involved in the progression of Alzheimer's disease (AD), sleep appears as a promising treatment target in this pathology, particularly to counteract memory decline. This study demonstrates the potential of a noninvasive brain stimulation method during sleep in patients with mild cognitive impairment (MCI), a precursor of AD, and advances our understanding of its mechanism. We provide first time evidence that slow oscillatory transcranial stimulation amplifies the functional cross-frequency coupling between memory-relevant brain oscillations and improves visual memory consolidation in patients with MCI.

Hypothetical neurochemical mechanisms of paradoxical sleep deficiency in Alzheimer’s disease

Based on the known experimental data on the specific morphological and neurochemical changes in the neural circuits involved in the occurrence of paradoxical sleep (REM sleep) that are observed in Alzheimer’s disease (AD) and our analysis of the effects of neuromodulators on the functioning of these circuits we propose that REM sleep deficiency in AD is caused by the following mechanisms: (1) the activity of the lateral geniculate body and occipital cortex is not sufficient to generate the ponto-geniculo-occipital (PGO) waves that are specific for REM sleep due to lower activity of cholinergic cells of the pedunculopontine and laterodorsal tegmental nuclei (PPN and LDTN) and lower density of cholinergic receptors; (2) because of reduced activity of cholinergic neurons of the PPN and LDN on GABAergic interneurons projecting to noradrenergic and serotonergic cells, the activity of the latter cannot be completely inhibited, as should occur during REM sleep; (3) the concentration of melanin-concentrating hormone is not sufficient for sleep due to the decreased activity of cholinergic cells of the basal forebrain nucleus, which excite neurons that produce this hormone; and (4) the activity of histaminergic cells increases and the activity of neurons that release melanin-concentrating hormone decreases due to the increased orexin level. Our analysis shows that common use of drugs that increase the acetylcholine concentration in patients with AD may result in increased activity of orexinergic cells and this must prevent the occurrence of REM sleep. We hypothesize that microstimulation of PPN may improve the occurrence of REM sleep because it should decrease the activity of serotoninergic, noradrenergic, and histaminergic cells and promote the generation of PGO waves and hippocampal theta activity. This treatment may improve the conditions for memory consolidation in patients with AD. Such microstimulation should be applied at night according to a special protocol.

Sleep-dependent memory consolidation in the epilepsy monitoring unit: A pilot study.

We sought to examine whether patients with focal epilepsy exhibit sleep dependent memory consolidation, whether memory retention rates correlated with particular aspects of sleep physiology, and how the process was affected by seizures. We prospectively recruited patients with focal epilepsy and assessed declarative memory using a task consisting of 15 pairs of colored pictures on a 5×6 grid. Patients were tested 12h after training, once after 12h of wakefulness and once after 12h that included sleep. EMG chin electrodes were placed to enable sleep scoring. The number and density of sleep spindles were assessed using a wavelet-based algorithm. Eleven patients were analyzed age 21-56years. The percentage memory retention over 12h of wakefulness was 62.7% and over 12h which included sleep 83.6% (p=0.04). Performance on overnight testing correlated with the duration of slow wave sleep (SWS) (r=+0.63, p<0.05). Three patients had seizures during the day, and 3 had nocturnal seizures. Day-time seizures did not affect retention rates, while those patients who had night time seizures had a drop in retention from an average of 92% to 60.5%. There is evidence of sleep dependent memory consolidation in patients with epilepsy which mostly correlates with the amount of SWS. Our preliminary findings suggest that nocturnal seizures likely disrupt sleep dependent memory consolidation. Findings highlight the importance of SWS in sleep dependent memory consolidation and the adverse impact of nocturnal seizures on this process.

Slow sleep spindle and procedural memory consolidation in patients with major depressive disorder.

IntroductionEvidence has accumulated, which indicates that, in healthy individuals, sleep enhances procedural memory consolidation, and that sleep spindle activity modulates this process. However, whether sleep-dependent procedural memory consolidation occurs in patients medicated for major depressive disorder remains unclear, as are the pharmacological and physiological mechanisms that underlie this process.MethodsHealthy control participants (n=17) and patients medicated for major depressive disorder (n=11) were recruited and subjected to a finger-tapping motor sequence test (MST; nondominant hand) paradigm to compare the averaged scores of different learning phases (presleep, postsleep, and overnight improvement). Participants’ brain activity was recorded during sleep with 16 electroencephalography channels (between MSTs). Sleep scoring and frequency analyses were performed on the electroencephalography data. Additionally, we evaluated sleep spindle activity, which divided the spindles into fast-frequency spindle activity (12.5–16 Hz) and slow-frequency spindle activity (10.5–12.5 Hz).ResultSleep-dependent motor memory consolidation in patients with depression was impaired in comparison with that in control participants. In patients with depression, age correlated negatively with overnight improvement. The duration of slow-wave sleep correlated with the magnitude of motor memory consolidation in patients with depression, but not in healthy controls. Slow-frequency spindle activity was associated with reduction in the magnitude of motor memory consolidation in both groups.ConclusionBecause the changes in slow-frequency spindle activity affected the thalamocortical network dysfunction in patients medicated for depression, dysregulated spindle generation may impair sleep-dependent memory consolidation. Our findings may help to elucidate the cognitive deficits that occur in patients with major depression both in the waking state and during sleep.

Sleep-dependent memory consolidation and its implications for psychiatry.

Both sleep disturbance and memory impairment are very common in psychiatric disorders. Since sleep has been shown to play a role in the process of transferring newly acquired information into long-term memory, i.e., consolidation, it is important to highlight this link in the context of psychiatric disorders. Along these lines, after providing a brief overview of healthy human sleep, current neurobiological models on sleep-dependent memory consolidation and resultant opportunities to manipulate the memory consolidation process, recent findings on sleep disturbances and sleep-dependent memory consolidation in patients with insomnia, major depression, schizophrenia, and post-traumatic stress disorder are systematically reviewed. Furthermore, possible underlying neuropathologies and their implications on therapeutic strategies are discussed. This review aims at sensitizing the reader for recognizing sleep disturbances as a potential contributor to cognitive deficits in several disorders, a fact which is often overlooked up to date.

Impairment of sleep-related memory consolidation in schizophrenia: relevance of sleep spindles?

ObjectivesDeficits in declarative memory performance are among the most severe neuropsychological impairments in schizophrenia and contribute to poor clinical outcomes. The importance of sleep for brain plasticity and memory consolidation is widely accepted, and sleep spindles seem to play an important role in these processes. The aim of this study was to test the associations of sleep spindles and picture memory consolidation in patients with schizophrenia and healthy controls. MethodsWe studied 16 patients with schizophrenia on stable antipsychotic medication (mean age ± standard deviation, 29.4 ± 6.4 years) and 16 healthy controls matched for age and educational level. Sleep was recorded and scored according to American Academy of Sleep Medicine (AASM) standard criteria. We performed a picture recognition paradigm and compared recognition performance for neutral and emotional pictures in sleep and wake conditions. ResultsRecognition accuracy was better in healthy controls than in patients with schizophrenia in the sleep and wake conditions. However, the memory-promoting effect of sleep was significantly lower in schizophrenia patients than in controls. Sleep spindle activity was reduced in patients, and sleep spindle density was correlated with sleep-associated facilitation of recognition accuracy for neutral pictures. ConclusionReduced sleep spindles seem to play an important role as a possible mechanism or biomarker for impaired sleep-related memory consolidation in patients with schizophrenia, and are a new target for treatment to improve memory functions and clinical outcomes in these patients.

Untreated Sleep-Disordered Breathing: Links to Aging-Related Decline in Sleep-Dependent Memory Consolidation

BackgroundIncreasing age is associated with a decline in cognition and motor skills, while at the same time exacerbating one's risk of developing obstructive sleep apnea (OSA). OSA-related cognitive deficits are highly prevalent and can affect various memory systems including overnight memory consolidation on a motor sequence task.Thus, the aim of our study was to examine the effect of aging on sleep-dependent motor memory consolidation in patients with and without OSA.MethodsWe studied 44 patients (19–68 years) who had been referred by a physician for a baseline polysomnography (PSG) evaluation. Based on their PSG, patients were assigned either to the OSA group (AHI>5/h), or control (Non-OSA) group (AHI<5/h).All subjects performed the Psychomotor Vigilance Task (PVT) and the Motor Sequence Learning Task (MST) in the evening and again in the morning after their PSG.ResultsDespite similar learning in the evening, OSA subjects showed significantly less overnight improvement on the MST, both for immediate (OSA −2.7%±2.8% vs. controls 12.2%±3.5%; p = 0.002) and plateau improvement (OSA 4.9%±2.3% vs. controls 21.1%±4.0%; p = 0.001). Within the OSA group, there was a significant negative correlation between overnight MST improvement and age (r2 = 0.3; p = 0.01), an effect that was not observed in the Non-OSA group (r2 = 0.08; p = 0.23)ConclusionsConsistent with previous research, healthy sleepers demonstrated a higher degree of sleep-dependent overnight improvement on the MST, an effect not mitigated by increasing age. However, the presence of untreated obstructive sleep apnea is associated with an aging-related cognitive deficit, otherwise not present in individuals without OSA. As other research has linked the presence of OSA to a higher likelihood of developing dementia, future studies are necessary to examine if the inhibition of memory consolidation is tied to the onset of neurodegenerative disease.

Noradrenergic blockade and memory in patients with major depression and healthy participants

Patients with major depressive disorder (MDD) often suffer from impaired declarative, episodic and working memory. Further, MDD is associated with alterations in the noradrenergic system. There is evidence that presynaptic α2 receptors that inhibit release of noradrenaline are upregulated in MDD. Results from our recent study demonstrated that increasing noradrenergic activity by blocking the α2 receptor with yohimbine leads to stronger memory consolidation in MDD patients. In the current study, we further examined the role of noradrenaline on memory in MDD by administering clonidine that activates presynaptic α2 receptors and thereby globally suppresses the noradrenergic output. In a placebo-controlled, within-subject crossover design, 20 patients with MDD and 20 healthy controls received either 0.15 mg of clonidine or placebo orally before memory testing. A word list paradigm (memory consolidation), an autobiographical memory test (retrieval) and a working memory test were applied. Salivary alpha-amylase and blood pressure were measured. Across groups, clonidine decreased blood pressure and alpha-amylase. Clonidine impaired memory consolidation (word list learning) in depressed patients and controls. Memory retrieval and working memory were not affected by clonidine. Reducing noradrenergic activity had a specific effect on memory consolidation in patients with MDD and healthy controls. The underlying mechanisms need further scrutiny.

Decreased nocturnal growth hormone secretion and sleep fragmentation in combat-related posttraumatic stress disorder; potential predictors of impaired memory consolidation

Healthy sleep facilitates the consolidation of newly acquired memories. Although patients with posttraumatic stress disorder (PTSD) often complain of sleep disturbances and memory deficits, the interrelatedness of these symptoms is not well understood. Sleep may be disturbed in PTSD by increased awakenings during sleep, which has been associated with decreased growth hormone (GH) secretion. We conducted a controlled study in which we assessed sleep fragmentation, nocturnal secretion of GH, and memory consolidation in patients with PTSD. While sleep EEG was being monitored, 13 veterans with PTSD, 15 trauma controls (TC) and 15 healthy controls (HC) slept with an iv catheter, through which blood was collected every 20 min from 23:00 h to 08:00 h. Declarative memory encoding was assessed with the 15 word task before sleep, and consolidation was assessed the next morning by a free recall. Sleep was more fragmented in patients with PTSD, with more awakenings in the first half of the night (p<0.05). Plasma levels of GH during the night were significantly decreased in PTSD compared with HC (p<0.05). Furthermore, GH secretion and awakenings were independent predictors for delayed recall, which was lower in PTSD compared to HC (p<0.05). These data show that PTSD is associated with increased awakenings during sleep and decreased nocturnal GH secretion. Furthermore, decreased GH secretion may be related to sleep fragmentation and both variables may exert a negative effect on sleep dependent memory consolidation.

Off-line memory consolidation impairments in multiple sclerosis patients receiving high-dose corticosteroid treatment mirror consolidation impairments in depression

Sleep supports the consolidation of procedural memory, however patients with major depression show impaired motor memory performance after a night of sleep. It was hypothesized that this impairment is related to hypothalamic-pituitary-adrenal (HPA) axis dysfunction. We tested if high-dose administration of corticosteroids impairs off-line motor memory consolidation in patients with multiple sclerosis (MS). Nine patients with MS receiving high-dose corticosteroid therapy (methylprednisolone) and nine MS patients receiving alternative therapy (mitoxantrone) were assessed using a sequential finger tapping task before and after a night with polysomnography. In addition, nine patients with major depression (MD) receiving antidepressants and nine healthy controls were assessed. Although the four groups did not differ in practice-dependent learning, healthy subjects and MS patients receiving mitoxantrone showed markedly overnight-improvements in tapping performance of 17% and 24% while MS patients receiving high-dose corticosteroid therapy and depressed patients showed -9% and -10% overnight decrease. MS patients with and without corticosteroid therapy did not differ in their amount of REM sleep, nor did MD patients and healthy controls. In addition, we did not find any correlation between REM sleep and memory consolidation. Our results show that a strong intervention into the HPA system like in MS high-dose corticosteroid therapy impairs off-line motor memory consolidation comparable to the impairments seen in depressed patients. We propose therefore that depression-related changes in plasma corticosteroid levels rather than in sleep per se underlie off-line memory consolidation impairments in MD.

Sleep-related memory consolidation in patients with borderline personality disorder

Previous research suggests that sleep quality may be reduced in Borderline Personality disorder (BPD) patients. As recent findings point to the importance of sleep for memory consolidation, sleep-related memory consolidation was investigated in 15 BPD patients (mean age=26.1±6.1, all female) and 15 healthy controls (mean age=25.6±6.8, all female). Before and after the study night, declarative and procedural memory tasks were carried out. Sleep was recorded by a portable sleep recording device (QUISI®) in n=9 patients and n=12 healthy controls. No significant group differences were found regarding percentage of overnight improvement in the declarative and procedural memory tasks, nor were any significant differences observed in sleep characteristics. BPD patients showed a significant correlation between overnight declarative memory improvement and total sleep time (rsp=.733; p<.05) as well as number of NREM/REM cycles (rsp=.877; p<.01). Moreover, overnight procedural memory improvement in number of errors was significantly associated with REM latency (rsp=-.783; p<.05), a significant association was also found between overnight improvement in performance time and number of NREM/REM cycles (rsp=.953; p<.001). Present findings indicate that sleep-related memory consolidation is intact in BPD patients, with total sleep time, number of NREM/REM cycles and REM latency being of particular importance.

Numb ears in resurrection: Great auricular nerve injury in hanging attempt

<h3>Abstract</h3> <h3>Introduction</h3> Current analysis approaches of accelerometry data use sum score measures which do not provide insight in activity patterns over 24 hours, and thus do not adequately depict circadian activity patterns. Here, we used a functional approach to analyze accelerometer data that models activity pattern and circadian rhythm. As a test case, we demonstrated its application in patients with mild cognitive impairment (MCI) and age-matched healthy older volunteers (HOV). Moreover, we assessed the impact of chronotype on distribution of activity data. <h3>Methods</h3> Data of two studies were pooled for this analysis. Following baseline cognitive assessment participants were provided with accelerometers for seven consecutive days. A function on scalar regression (FoSR) approach was used to analyze 24 hours accelerometer data. In a second step, analyses were controlled for chronotype using the German version of the morningness-eveningness questionnaire (d-MEQ). <h3>Results</h3> Information on 47 HOV (mean age 66 SD 6 years) and 13 patients with MCI (mean age 69, SD 8 years) were available for this analysis. MCI patients displayed slightly higher activity in the morning hours as compared to HOV (maximum relative activity at 7:35 am: 75.6%, 95% CI 2.6 to 200.4%, p = 0.031). After controlling for d-MEQ, disturbed activity patterns were found in MCI of intermediate or evening chronotype, compared to HOV, i.e., MCI presented with higher activities in the morning hours (peak at 8:40 am: 357.6%, 95% CI 92.9 to 985.1, <i>p</i> &lt; 0.001) and early afternoon hours (peak at 1:40 pm: 401.8%, 95% CI 63.9 to 1436.4, <i>p</i> &lt; 0.001). <h3>Discussion</h3> Using a novel approach of FoSR, we found timeframes with higher activity levels in MCI patients compared to HOV which were not evident if sum scores of amount of activity were used. In addition, we found that previously described activity patterns as a function of chronotype swere altered in MCI patients, possibly indicating that changes in circadian rhythmicity in neurodegenerative disease are detectable using easy-to-administer accelerometry. <h3>Clinical Trials</h3> Effects of Brain Stimulation During Nocturnal Sleep on Memory Consolidation in Patients With Mild Cognitive Impairments, https://clinicaltrials.gov/ct2/show/NCT01782391?term=NCT01782391&amp;rank=1, ClinicalTrial.gov identifier: NCT01782391 Effects of Brain Stimulation During a Daytime Nap on Memory Consolidation in Patients With Mild Cognitive Impairment, https://clinicaltrials.gov/ct2/show/NCT01782365?term=NCT01782365&amp;rank=1, ClinicalTrial.gov identifier: NCT01782365

REM sleep, dreaming, and procedural memory

In this commentary the “incredibly robust” evidence for the relationship between sleep and procedural memory is questioned; inconsistencies in the existing data are pointed out. In addition, some suggestions about extending research are made, for example, studying REM sleep augmentation or memory consolidation in patients with sleep disorders. Last, the possibility of a relationship between dreaming and memory processes is discussed.