Fluctuations In Awareness Research Articles

Clinical Presentation, Diagnosis, and Pathogenesis of Dementia With Lewy Bodies

Dementia with Lewy bodies is a neurodegenerative disorder typified by progressive cognitive decline with associated visual hallucinations, fluctuations in awareness, parkinsonism, and rapid eye movement sleep behavior disorder. The diagnosis can be difficult to make and requires a detailed interview, identification of characteristic signs on neurological examination, and diagnostic testing when atypical features are present. This article delves into the salient features of the disorder, highlighting the neuropsychiatric spectrum of clinical manifestations, emerging disease biomarkers, and the role of ancillary studies in the diagnosis. [ Psychiatr Ann. 2022;52(10):398–403.]

Awareness for People With Alzheimer's Disease: Profiles and Weekly Trajectories.

Objective: To understand awareness and fluctuations of awareness in Alzheimer’s disease (AD), it is fruitful to consider the objects of awareness, e.g., cognitive functioning or recognition of the disease, as well as the mechanisms and modes of expression underlying awareness. With a holistic and discourse-centered approach, we aimed to identify different awareness profiles and test whether these profiles were stable or whether transitions from one profile to another occurred over short time intervals.Methods: Twenty-eight residents of nursing homes with a diagnosis of AD participated in four semistructured interviews at biweekly intervals. These interviews were cluster analyzed to determine profiles of awareness. A Markov chain was applied to model their fluctuation.Results: Five awareness profiles were observed that differed in terms of objects and underlying processes. Awareness proved to be quite stable for four of the five profiles. Interindividual variability in awareness was also observed through numerous different trajectories that were identified.Discussion: Self-awareness and disease awareness are characterized by profiles that vary subtly between individuals. Fluctuations in awareness underscore the need to employ assessment intervals that closely reflect daily life in institutions.

Cognitive Interference in the Context of Daily Stressors, Daily Awareness of Age-Related Change, and General Aging Attitudes.

Previous diary work indicates that older people experience more intrusive and unwanted thoughts (i.e., cognitive interference) on days with stressors. We examined additional predictors of daily cognitive interference to enhance understanding of the psychological context surrounding this link. We specifically focused on factors related to subjective experiences of aging based on studies that have related higher stress and impairments in cognition such as executive control processes (working memory) to negative age stereotypes. Consistent with these findings, we generally expected stronger stress effects on cognitive interference when daily self-perceptions of aging (i.e., within-person fluctuations in awareness of age-related losses [AARC losses]) and general aging attitudes (i.e., individual differences in attitudes toward own aging [ATOA]) were more negative. Participants (n = 91; aged 60-80) on Amazon's Mechanical Turk completed surveys on 9 consecutive days, reporting on their ATOA (Day 1) as well as their stressors, AARC losses, and cognitive interference (Days 2-9). Multilevel models showed that people reported more cognitive interference on days with more AARC losses. Individuals with positive ATOA also experienced less cognitive interference on days with more stressors, whereas those with negative ATOA experienced more. Both individual differences and fluctuating daily perceptions of aging appear to be important for older adults' cognitive interference. Consistent with other work, positive ATOA protected against daily stressor effects. Further elucidating these relationships can increase understanding of and facilitate efforts to improve (daily) cognitive experiences in older adults.

Limbic encephalitis as the presenting feature of sjögren syndrome

Autoimmune encephalitis associated with serum and intrathecal antibodies against intracellular and surface neuronal antigens of the limbic system neuropiles, and several neuropsychiatric and neurocognitive disorders have shared mechanisms of origin. Sicca syndrome is present in only 50% of patients with neurologic involvement. However, limbic encephalitis (LE) has been recognized on occasion as a feature of Sjogren’s syndrome (SS). A 40-years-old male patient presented with sudden development of headache, episodic memory failure, focal cognitive epileptic and generalized seizures, fever, complex visual hallucinations, fluctuations in awareness. Neurological examination showed drowsiness, as well as high freceuncy generalized tremor at rest. MRI showed an area of increased signal on fluid-attenuated inversion recovery (FLAIR) sequence bilaterally in the temporal lobe. CSF analysis showed a high protein level; viral screening and bacterial cultures, paraneoplastic antibody panel, anti NMDA were negative, EEG showed bilateral temporal focal slowing, PET scan was negative for malignancy, Anti Ro / SSA and anti La / SSB antibodies were elevated, Schirmer test was positive for reduced tear production and minor salivary gland biopsy demonstrated focal lymphocytic sialadenitis. Treatment with azathioprine and prednisone was started as well as rituximab every 6 months with marked improvement shown by lack of seizure recurrence; However, episodic memory failure remained. Recognizing the association between MRI temporal lobe lesions and LE should prompt further evaluation for paraneoplastic and autoantibody-related entities, including SS. This is the first case where the association of neuropsychiatric symptoms is described between LE and SS.

Eye dominance alternations in binocular rivalry do not require visual awareness.

Binocular rivalry provides a valuable means to study how sensory processing gives rise to subjective experiences because it involves a changing percept without any change in the visual stimulus. An important question, however, is whether visual awareness is necessary for binocular rivalry to emerge. To address this question, we presented conflicting random dot motion stimuli in the two eyes at luminance contrasts around perceptual threshold. We asked subjects to report continuously, via button presses, if they noticed any kind of motion in the display (be it coherent or not) and indicate which direction of motion they thought was dominant at any given instant even if they were unaware of any motion in the display. We biased the competition between the two dichoptic stimuli by changing the motion coherence in one eye while keeping it fixed in the other to test if this induced predictable changes in rivalry dynamics. We also probed the strength of the interocular suppression. Our data show that binocular rivalry continues even if subjects claim complete absence of visual motion awareness. This remarkable dissociation between visually guided behavior and visual awareness resembles the dissociation seen in other phenomena, such as blindsight and visual masking. Fluctuations in awareness that did occur were temporally linked to the dominance switches in a manner that is consistent with adaptation reciprocal-inhibition models of binocular rivalry.

Making Waves in the Stream of Consciousness: Entraining Oscillations in EEG Alpha and Fluctuations in Visual Awareness with Rhythmic Visual Stimulation

Rhythmic events are common in our sensory world. Temporal regularities could be used to predict the timing of upcoming events, thus facilitating their processing. Indeed, cognitive theories have long posited the existence of internal oscillators whose timing can be entrained to ongoing periodic stimuli in the environment as a mechanism of temporal attention. Recently, recordings from primate brains have shown electrophysiological evidence for these hypothesized internal oscillations. We hypothesized that rhythmic visual stimuli can entrain ongoing neural oscillations in humans, locking the timing of the excitability cycles they represent and thus enhancing processing of subsequently predictable stimuli. Here we report evidence for entrainment of neural oscillations by predictable periodic stimuli in the alpha frequency band and show for the first time that the phase of existing brain oscillations cannot only be modified in response to rhythmic visual stimulation but that the resulting phase-locked fluctuations in excitability lead to concomitant fluctuations in visual awareness in humans. This entrainment effect was dependent on both the amount of spontaneous alpha power before the experiment and the level of 12-Hz oscillation before each trial and could not be explained by evoked activity. Rhythmic fluctuations in awareness elicited by entrainment of ongoing neural excitability cycles support a proposed role for alpha oscillations as a pulsed inhibition of cortical activity. Furthermore, these data provide evidence for the quantized nature of our conscious experience and reveal a powerful mechanism by which temporal attention as well as perceptual snapshots can be manipulated and controlled.

Neural Correlates of Motion-induced Blindness in the Human Brain

Motion-induced blindness (MIB) is a visual phenomenon in which highly salient visual targets spontaneously disappear from visual awareness (and subsequently reappear) when superimposed on a moving background of distracters. Such fluctuations in awareness of the targets, although they remain physically present, provide an ideal paradigm to study the neural correlates of visual awareness. Existing behavioral data on MIB are consistent both with a role for structures early in visual processing and with involvement of high-level visual processes. To further investigate this issue, we used high field functional MRI to investigate signals in human low-level visual cortex and motion-sensitive area V5/MT while participants reported disappearance and reappearance of an MIB target. Surprisingly, perceptual invisibility of the target was coupled to an increase in activity in low-level visual cortex plus area V5/MT compared with when the target was visible. This increase was largest in retinotopic regions representing the target location. One possibility is that our findings result from an active process of completion of the field of distracters that acts locally in the visual cortex, coupled to a more global process that facilitates invisibility in general visual cortex. Our findings show that the earliest anatomical stages of human visual cortical processing are implicated in MIB, as with other forms of bistable perception.

Neural correlates of motion-induced blindness in the human brain

Motion-induced blindness (MIB) is a visual phenomenon in which highly salient visual targets spontaneously disappear from visual awareness (and subsequently reappear) when superimposed on a moving background of distracters. Such fluctuations in awareness of the targets, although they remain physically present, provide an ideal paradigm to study the neural correlates of visual awareness. Existing behavioral data on MIB are consistent both with a role for structures early in visual processing and with involvement of high-level visual processes. To further investigate this issue, we used high field functional MRI to investigate signals in human low-level visual cortex and motion-sensitive area V5/MT while participants reported disappearance and reappearance of an MIB target. Surprisingly, perceptual invisibility of the target was coupled to an increase in activity in low-level visual cortex plus area V5/MT compared with when the target was visible. This increase was largest in retinotopic regions representing the target location. One possibility is that our findings result from an active process of completion of the field of distracters that acts locally in the visual cortex, coupled to a more global process that facilitates invisibility in general visual cortex. Our findings show that the earliest anatomical stages of human visual cortical processing are implicated in MIB, as with other forms of bistable perception.

Exacerbation of Lewy bodies dementia due to memantine

Lewy body dementia (DLB) is common but frequently misdiagnosed as Alzheimer's disease plus delirium or parkinsonism. DRUGS USED IN THIS DISORDER CAN CAUSE EXACERBATIONS: neuroleptic medication is relatively contraindicated because some patients show severe neuroleptic sensitivity, antiparkinsonian medication has the potential to exacerbate psychotic symptoms, and even cholinesterase inhibitors, while relatively safe, have provoked adverse responses in some DLB patients. There are few data available about the use of memantine in DLB. A 74-year-old man was diagnosed with Alzheimer disease and parkinsonism. After memantine was started he developed severe fluctuations in awareness, visual hallucinations, agitation, and worsened parkinsonism. When he was evaluated thoroughly, the diagnosis was revised to Lewy body dementia, leading to changes in treatment that were associated with dramatic improvement in the patient's mental status. In our patient, motor and cognitive symptoms worsened with memantine treatment; these resolved after memantine was discontinued.

Le pouvoir des malades. L'Association française contre les myopathies et la Recherche: École des Mines, coll.Sciences économiques et sociales , 1999, 181 p., 199 F.

Anosognosia for hemiplegia has seen a century of almost continuous research, yet a definitive understanding of its mechanism remains elusive. Essentially, anosognosic patients hold quasi-delusional beliefs about their paralysed limbs, in spite of all the contrary evidence, repeated questioning, and logical argument. We review a range of findings suggesting that emotion and motivation play an important role in anosognosia. We conclude that anosognosia involves (amongst other things) a process of psychological defence. This conclusion stems from a wide variety of clinical and experimental investigations, including data on implicit awareness of deficit, fluctuations in awareness over time, and dramatic effects upon awareness of psychological interventions such as psychotherapy, reframing of the emotional consequences of the paralysis, and first versus third person perspectival manipulations. In addition, we review and refute the (eight) arguments historically raised against the ‘defence’ hypothesis, including the claim that a defence-based account cannot explain the lateralised nature of the disorder. We argue that damage to a well-established right-lateralised emotion regulation system, with links to psychological processes that appear to underpin allocentric spatial cognition, plays a key role in anosognosia (at least in some patients). We conclude with a discussion of implications for clinical practice.

Methodology of psychosomatic research.

Anosognosia for hemiplegia has seen a century of almost continuous research, yet a definitive understanding of its mechanism remains elusive. Essentially, anosognosic patients hold quasi-delusional beliefs about their paralysed limbs, in spite of all the contrary evidence, repeated questioning, and logical argument. We review a range of findings suggesting that emotion and motivation play an important role in anosognosia. We conclude that anosognosia involves (amongst other things) a process of psychological defence. This conclusion stems from a wide variety of clinical and experimental investigations, including data on implicit awareness of deficit, fluctuations in awareness over time, and dramatic effects upon awareness of psychological interventions such as psychotherapy, reframing of the emotional consequences of the paralysis, and first versus third person perspectival manipulations. In addition, we review and refute the (eight) arguments historically raised against the ‘defence’ hypothesis, including the claim that a defence-based account cannot explain the lateralised nature of the disorder. We argue that damage to a well-established right-lateralised emotion regulation system, with links to psychological processes that appear to underpin allocentric spatial cognition, plays a key role in anosognosia (at least in some patients). We conclude with a discussion of implications for clinical practice.