Controlled study of 50-Hz repetitive transcranial magnetic stimulation for the treatment of Parkinson disease.

OBJECTIVE: To investigate the safety and efficacy of 50-Hz repetitive transcranial magnetic stimulation (rTMS) in the treatment of motor symptoms in Parkinson disease (PD). BACKGROUND: Progression of PD is characterized by the emergence of motor deficits that gradually respond less to dopaminergic therapy. rTMS has shown promising results in improving gait, a major cause of disability, and may provide a therapeutic alternative. Prior controlled studies suggest that an increase in stimulation frequency might enhance therapeutic efficacy. METHODS: In this randomized, double blind, sham-controlled study, the authors investigated the safety and efficacy of 50-Hz rTMS of the motor cortices in 8 sessions over 2 weeks. Assessment of safety and clinical efficacy over a 1-month period included timed tests of gait and bradykinesia, Unified Parkinson's Disease Rating Scale (UPDRS), and additional clinical, neurophysiological, and neuropsychological parameters. In addition, the safety of 50-Hz rTMS was tested with electromyography-electroencephalogram (EMG-EEG) monitoring during and after stimulation. RESULTS: The authors investigated 26 patients with mild to moderate PD: 13 received 50-Hz rTMS and 13 sham stimulation. The 50-Hz rTMS did not improve gait, bradykinesia, and global and motor UPDRS, but there appeared a short-lived "on"-state improvement in activities of daily living (UPDRS II). The 50-Hz rTMS lengthened the cortical silent period, but other neurophysiological and neuropsychological measures remained unchanged. EMG/EEG recorded no pathological increase of cortical excitability or epileptic activity. There were no adverse effects. CONCLUSION: It appears that 50-Hz rTMS of the motor cortices is safe, but it fails to improve motor performance and functional status in PD. Prolonged stimulation or other techniques with rTMS might be more efficacious but need to be established in future research.

Early processing in the human lateral occipital complex is highly responsive to illusory contours but not to salient regions.

Human electrophysiological studies support a model whereby sensitivity to so-called illusory contour stimuli is first seen within the lateral occipital complex. A challenge to this model posits that the lateral occipital complex is a general site for crude region-based segmentation, based on findings of equivalent hemodynamic activations in the lateral occipital complex to illusory contour and so-called salient region stimuli, a stimulus class that lacks the classic bounding contours of illusory contours. Using high-density electrical mapping of visual evoked potentials, we show that early lateral occipital cortex activity is substantially stronger to illusory contour than to salient region stimuli, whereas later lateral occipital complex activity is stronger to salient region than to illusory contour stimuli. Our results suggest that equivalent hemodynamic activity to illusory contour and salient region stimuli probably reflects temporally integrated responses, a result of the poor temporal resolution of hemodynamic imaging. The temporal precision of visual evoked potentials is critical for establishing viable models of completion processes and visual scene analysis. We propose that crude spatial segmentation analyses, which are insensitive to illusory contours, occur first within dorsal visual regions, not the lateral occipital complex, and that initial illusory contour sensitivity is a function of the lateral occipital complex.

Successful surgical resection in non-lesional operculo-insular epilepsy without intracranial monitoring.

Pre-operative assessment and surgical management of patients with non-lesional extratemporal epilepsy remain challenging due to a lack of precise localisation of the epileptic zone. In most cases, invasive recording with depth or subdural electrodes is required. Here, we describe the case of 6.5-year-old girl who underwent comprehensive non-invasive phase I video-EEG investigation for drug-resistant epilepsy, including electric source and nuclear imaging. Left operculo-insular epilepsy was diagnosed. Post-operatively, she developed aphasia which resolved within one year, corroborating the notion of enhanced language plasticity in children. The patient remained seizure-free for more than three years.

Mutism and Amnesia following High-Voltage Electrical Injury: Psychogenic Symptomatology Triggered by Organic Dysfunction?

Background: Mutism and dense retrograde amnesia are found both in organic and dissociative contexts. Moreover, dissociative symptoms may be modulated by right prefrontal activity. A single case, M.R., developed left hemiparesis, mutism and retrograde amnesia after a high-voltage electric shock without evidence of lasting brain lesions. M.R. suddenly recovered from his mutism following a mild brain trauma 2 years later. Methods: M.R.'s neuropsychological pattern and anatomoclinical correlations were studied through (i) language and memory assessment to characterize his deficits, (ii) functional neuroimaging during a standard language paradigm, and (iii) assessment of frontal and left insular connectivity through diffusion tractography imaging and transcranial magnetic stimulation. A control evaluation was repeated after recovery. Findings: M.R. recovered from the left hemiparesis within 90 days of the accident, which indicated a transient right brain impairment. One year later, neurobehavioral, language and memory evaluations strongly suggested a dissociative component in the mutism and retrograde amnesia. Investigations (including MRI, fMRI, diffusion tensor imaging, EEG and r-TMS) were normal. Twenty-seven months after the electrical injury, M.R. had a very mild head injury which was followed by a rapid recovery of speech. However, the retrograde amnesia persisted. Discussion: This case indicates an interaction of both organic and dissociative mechanisms in order to explain the patient's symptoms. The study also illustrates dissociation in the time course of the two different dissociative symptoms in the same patient.

Plastic brain mechanisms for attaining auditory temporal order judgment proficiency.

Accurate perception of the order of occurrence of sensory information is critical for the building up of coherent representations of the external world from ongoing flows of sensory inputs. While some psychophysical evidence reports that performance on temporal perception can improve, the underlying neural mechanisms remain unresolved. Using electrical neuroimaging analyses of auditory evoked potentials (AEPs), we identified the brain dynamics and mechanism supporting improvements in auditory temporal order judgment (TOJ) during the course of the first vs. latter half of the experiment. Training-induced changes in brain activity were first evident 43-76 ms post stimulus onset and followed from topographic, rather than pure strength, AEP modulations. Improvements in auditory TOJ accuracy thus followed from changes in the configuration of the underlying brain networks during the initial stages of sensory processing. Source estimations revealed an increase in the lateralization of initially bilateral posterior sylvian region (PSR) responses at the beginning of the experiment to left-hemisphere dominance at its end. Further supporting the critical role of left and right PSR in auditory TOJ proficiency, as the experiment progressed, responses in the left and right PSR went from being correlated to un-correlated. These collective findings provide insights on the neurophysiologic mechanism and plasticity of temporal processing of sounds and are consistent with models based on spike timing dependent plasticity.

Neurophysiological origin of human brain asymmetry for speech and language.

The physiological basis of human cerebral asymmetry for language remains mysterious. We have used simultaneous physiological and anatomical measurements to investigate the issue. Concentrating on neural oscillatory activity in speech-specific frequency bands and exploring interactions between gestural (motor) and auditory-evoked activity, we find, in the absence of language-related processing, that left auditory, somatosensory, articulatory motor, and inferior parietal cortices show specific, lateralized, speech-related physiological properties. With the addition of ecologically valid audiovisual stimulation, activity in auditory cortex synchronizes with left-dominant input from the motor cortex at frequencies corresponding to syllabic, but not phonemic, speech rhythms. Our results support theories of language lateralization that posit a major role for intrinsic, hardwired perceptuomotor processing in syllabic parsing and are compatible both with the evolutionary view that speech arose from a combination of syllable-sized vocalizations and meaningful hand gestures and with developmental observations suggesting phonemic analysis is a developmentally acquired process.

A temporal hierarchy for conspecific vocalization discrimination in humans.

The ability to discriminate conspecific vocalizations is observed across species and early during development. However, its neurophysiologic mechanism remains controversial, particularly regarding whether it involves specialized processes with dedicated neural machinery. We identified spatiotemporal brain mechanisms for conspecific vocalization discrimination in humans by applying electrical neuroimaging analyses to auditory evoked potentials (AEPs) in response to acoustically and psychophysically controlled nonverbal human and animal vocalizations as well as sounds of man-made objects. AEP strength modulations in the absence of topographic modulations are suggestive of statistically indistinguishable brain networks. First, responses were significantly stronger, but topographically indistinguishable to human versus animal vocalizations starting at 169-219 ms after stimulus onset and within regions of the right superior temporal sulcus and superior temporal gyrus. This effect correlated with another AEP strength modulation occurring at 291-357 ms that was localized within the left inferior prefrontal and precentral gyri. Temporally segregated and spatially distributed stages of vocalization discrimination are thus functionally coupled and demonstrate how conventional views of functional specialization must incorporate network dynamics. Second, vocalization discrimination is not subject to facilitated processing in time, but instead lags more general categorization by approximately 100 ms, indicative of hierarchical processing during object discrimination. Third, although differences between human and animal vocalizations persisted when analyses were performed at a single-object level or extended to include additional (man-made) sound categories, at no latency were responses to human vocalizations stronger than those to all other categories. Vocalization discrimination transpires at times synchronous with that of face discrimination but is not functionally specialized.

A comparison of electrophysiological changes during the sleep onset period of psychophysiological insomniacs, psychiatric insomniacs and normal sleepers

The EEG of the sleep onset period of psychophysiological insomniacs, psychiatric insomniacs and controls was compared using power spectral analysis (FFT). Eighteen drug-free subjects were equally divided into three groups according to their responses in the Brock Sleep and Insomnia Questionnaire, the Minnesota Multiphasic Personality Inventory and the Sleep Disorders Questionnaire. Group 1 consisted of psychophysiological insomniacs, group 2 included insomniacs with an indication of psychiatric disturbances, and group 3 was a control group. EEG, EOG and EMG were recorded for two consecutive nights. Power spectral analysis (FFT) of EEG at C4 from the sleep onset period (defined as lights out to the first five minutes of stage 2) was performed on all standard frequency bands, delta: .5-4 Hz; theta: 4-8 Hz; alpha: 8-12 Hz; sigma: 12-15 Hz beta: 15-25 Hz. Psychophysiological insomniacs had less alpha during wakefulness than the other two groups and did not show the dramatic drop in alpha across the sleep onset period, which characterizes normal sleep. They also had less delta, especially during stage 2 on night 2. They also showed less delta in the last quartile of the chronological analysis of the sleep onset period. Psychiatric insomniacs showed lower relative beta power values overall while psychophysiological insomniacs showed higher relative beta power values during wakefulness. This microanalysis 11 confirms that the sleep onset period is generally similar for psychiatric insomniacs and normal sleepers. This may be due to the sample of psychiatric insomniacs being heterogeneous or may reflect a sleep onset system that is essentially intact. Psychophysiological insomniacs have higher cortical arousal during the sleep onset period than do the psychiatric insomniacs and the controls. Clear differences in the sleep onset period of psychophysiological insomniacs exist. The dramatic changes in power values in these two groups are not seen in the psychophysiological insomniacs, which may make the discrimination between wakefulness and sleep more difficult.

The role of daytime napping in sleepiness and cognitive function in 24-70 year olds /

Daytime napping improves well-being and performance for young adults. The benefits of napping in older adults should be investigated because they have fragmented nocturnal sleep, cognitive declines, and more opportunity to nap. In addition, experience with napping might influence the benefits of napping. Study 1 examined the role of experience with napping in young adults. Habitual (n = 23) and non-habitual nappers (n = 16) were randomly assigned to a 20-minute nap or a 20- minute reading condition. Both groups slept the same according to macro architecture. However, microarchitecture showed greater theta, alpha, and beta power during Stage 1, and greater delta, alpha, and sigma power during Stage 2 for habitual nappers, for the most part indicating better sleep. Both groups felt less sleepy after the nap. P2 latency, reflecting information processing, decreased after the nap for habitual nappers, and after the control condition for non-habitual nappers. In sum, both groups who slept felt better, but only the habitual nappers who napped gained a benefit in terms of information processing. Based on this outcome, experience with napping was investigated in Study 2. Study 2 examined the extent to which daytime napping enhanced cognition in older adults, especially frontal lobe function. Cognitive deficits in older adults may be due to sleep loss and age-related decline in brain functioning. Longer naps were expected to provide greater improvement, particularly for older adults, by reducing sleep pressure. Thirty-two adults, aged 24-70 years, participated in a repeated measures dose-response manipulation of sleep pressure. Twenty- and sixty-minute naps were compared to a no-nap condition in three age groups. Mood, subjective sleepiness, reaction time, working memory, 11 novelty detection, and waking electro physiological measures were taken before and after each condition. EEG was also recorded during each nap or rest condition. Napping reduced subjective sleepiness, improved working memory (serial addition / subtraction task), and improved attention (reduced P2 amplitude). Physiological sleepiness (i.e., waking theta power) increased following the control condition, and decreased after the longer nap. Increased beta power after the short nap, and seen with older adults overall, may have reflected increased mental effort. Older adults had longer latencies and smaller amplitudes for several event-related potential components, and higher beta and gamma power. Following the longer nap, gamma power decreased for older adults, but increased for young adults. Beta and gamma power may represent enhanced alertness or mental effort. In addition, Nl amplitude showed that benefits depend on the preceding nap length as well as age. Since the middle group had smaller Nl amplitudes following the short nap and rest condition, it is possible that they needed a longer nap to maintain alertness. Older adults did not show improvements to Nl amplitude following any condition; they may have needed a nap longer than 60 minutes to gain benefits to attention or early information processing. Sleep characteristics were not related to benefits of napping. Experience with napping was also investigated. Subjective data confirmed habitual nappers were happier to nap, while non-habitual nappers were happier to stay awake, reflecting self-identified napping habits. Non-habitual nappers were sleepier after a nap, and had faster brain activity (i.e., heightened vigilance) at sleep onset. These reasons may explain why non-habitual nappers choose not to nap.

Subjective, behavioural and electrophysiological measurements of the time-course and intensity of sleep inertia after a full night of sleep /

Several recent studies have described the period of impaired alertness and performance known as sleep inertia that occurs upon awakening from a full night of sleep. They report that sleep inertia dissipates in a saturating exponential manner, the exact time course being task dependent, but generally persisting for one to two hours. A number of factors, including sleep architecture, sleep depth and circadian variables are also thought to affect the duration and intensity. The present study sought to replicate their findings for subjective alertness and reaction time and also to examine electrophysiological changes through the use of event-related potentials (ERPs). Secondly, several sleep parameters were examined for potential effects on the initial intensity of sleep inertia. Ten participants spent two consecutive nights and subsequent mornings in the sleep lab. Sleep architecture was recorded for a fiiU nocturnal episode of sleep based on participants' habitual sleep patterns. Subjective alertness and performance was measured for a 90-minute period after awakening. Alertness was measured every five minutes using the Stanford Sleepiness Scale (SSS) and a visual analogue scale (VAS) of sleepiness. An auditory tone also served as the target stimulus for an oddball task designed to examine the NlOO and P300 components ofthe ERP waveform. The five-minute oddball task was presented at 15-minute intervals over the initial 90-minutes after awakening to obtain six measures of average RT and amplitude and latency for NlOO and P300. Standard polysomnographic recording were used to obtain digital EEG and describe the night of sleep. Power spectral analyses (FFT) were used to calculate slow wave activity (SWA) as a measure of sleep depth for the whole night, 90-minutes before awakening and five minutes before awakening.

The effects of simple procedural, cognitive procedural and declarative learning on sleep /

Sleep spindles have been found to increase following an intense period of learning on a combination of motor tasks. It is not clear whether these changes are task specific, or a result of learning in general. The current study investigated changes in sleep spindles and spectral power following learning on cognitive procedural (C-PM), simple procedural (S-PM) or declarative (DM) learning tasks. It was hypothesized that S-PM learning would result in increases in Sigma power during Non-REM sleep, whereas C-PM and DM learning would not affect Sigma power. It was also hypothesized that DM learning would increase Theta power during REM sleep, whereas S-PM and C-PM learning would not affect Theta power. Thirty-six participants spent three consecutive nights in the sleep laboratory. Baseline polysomnographic recordings were collected on night 2. Participants were randomly assigned to one of four conditions: C-PM, S-PM, DM or control (C). Memory task training occurred on night 3 followed by polysomnographic recording. Re-testing on respective memory tasks occurred one-week following training. EEG was sampled at 256Hz from 16 sites during sleep. Artifact-free EEG from each sleep stage was submitted to power spectral analysis. The C-PM group made significantly fewer errors, the DM group recalled more, and the S-PM improved on performance from test to re-test. There was a significant night by group interaction for the duration of Stage 2 sleep. Independent t-tests revealed that the S-PM group had significantly more Stage 2 sleep on the test night than the C group. The C-PM and the DM group did not differ from controls in the duration of Stage 2 sleep on test night. There was no significant change in the duration of slow wave sleep (SWS) or REM sleep. Sleep spindle density (spindles/minute) increased significantly from baseline to test night following S-PM learning, but not for C-PM, DM or C groups. This is the first study to have shown that the same pattern of results was found for spindles in SWS. Low Sigma power (12-14Hz) increased significantly during SWS following S-PM learning but not for C-PM, DM or C groups. This effect was maximal at Cz, and the largest increase in Sigma power was at Oz. It was also found that Theta power increased significantly during REM sleep following DM learning, but not for S-PM, C-PM or C groups. This effect was maximal at Cz and the largest change in Theta power was observed at Cz. These findings are consistent with the previous research that simple procedural learning is consolidated during Stage 2 sleep, and provide additional data to suggest that sleep spindles across all non-REM stages and not just Stage 2 sleep may be a mechanism for brain plasticity. This study also provides the first evidence to suggest that Theta activity during REM sleep is involved in memory consolidation.

Sleep and information processing in individuals who have sustained a traumatic brain injury

Individuals who have sustained a traumatic brain injury (TBI) often complain of t roubl e sleeping and daytime fatigue but little is known about the neurophysiological underpinnings of the s e sleep difficulties. The fragile sleep of thos e with a TBI was predicted to be characterized by impairments in gating, hyperarousal and a breakdown in sleep homeostatic mechanisms. To test these hypotheses, 20 individuals with a TBI (18- 64 years old, 10 men) and 20 age-matched controls (18-61 years old, 9 men) took part in a comprehensive investigation of their sleep. While TBI participants were not recruited based on sleep complaint, the fmal sample was comprised of individuals with a variety of sleep complaints, across a range of injury severities. Rigorous screening procedures were used to reduce potential confounds (e.g., medication). Sleep and waking data were recorded with a 20-channel montage on three consecutive nights. Results showed dysregulation in sleep/wake mechanisms. The sleep of individuals with a TBI was less efficient than that of controls, as measured by sleep architecture variables. There was a clear breakdown in both spontaneous and evoked K-complexes in those with a TBI. Greater injury severities were associated with reductions in spindle density, though sleep spindles in slow wave sleep were longer for individuals with TBI than controls. Quantitative EEG revealed an impairment in sleep homeostatic mechanisms during sleep in the TBI group. As well, results showed the presence of hyper arousal based on quantitative EEG during sleep. In wakefulness, quantitative EEG showed a clear dissociation in arousal level between TBls with complaints of insomnia and TBls with daytime fatigue. In addition, ERPs indicated that the experience of hyper arousal in persons with a TBI was supported by neural evidence, particularly in wakefulness and Stage 2 sleep, and especially for those with insomnia symptoms. ERPs during sleep suggested that individuals with a TBI experienced impairments in information processing and sensory gating. Whereas neuropsychological testing and subjective data confirmed predicted deficits in the waking function of those with a TBI, particularly for those with more severe injuries, there were few group differences on laboratory computer-based tasks. Finally, the use of correlation analyses confirmed distinct sleep-wake relationships for each group. In sum, the mechanisms contributing to sleep disruption in TBI are particular to this condition, and unique neurobiological mechanisms predict the experience of insomnia versus daytime fatigue following a TBI. An understanding of how sleep becomes disrupted after a TBI is important to directing future research and neurorehabilitation.

Electrophysiological constituents of the P100 and N170 ERP complex: De-constructing of face processing using independent component analysis and robust estimation.

The initial timing of face-specific effects in event-related potentials (ERPs) is a point of contention in face processing research. Although effects during the time of the N170 are robust in the literature, inconsistent effects during the time of the P100 challenge the interpretation of the N170 as being the initial face-specific ERP effect. The interpretation of the early P100 effects are often attributed to low-level differences between face stimuli and a host of other image categories. Research using sophisticated controls for low-level stimulus characteristics (Rousselet, Husk, Bennett, & Sekuler, 2008) report robust face effects starting at around 130 ms following stimulus onset. The present study examines the independent components (ICs) of the P100 and N170 complex in the context of a minimally controlled low-level stimulus set and a clear P100 effect for faces versus houses at the scalp. Results indicate that four ICs account for the ERPs to faces and houses in the first 200ms following stimulus onset. The IC that accounts for the majority of the scalp N170 (icNla) begins dissociating stimulus conditions at approximately 130 ms, closely replicating the scalp results of Rousselet et al. (2008). The scalp effects at the time of the P100 are accounted for by two constituent ICs (icP1a and icP1b). The IC that projects the greatest voltage at the scalp during the P100 (icP1a) shows a face-minus-house effect over the period of the P100 that is less robust than the N 170 effect of icN 1 a when measured as the average of single subject differential activation robustness. The second constituent process of the P100 (icP1b), although projecting a smaller voltage to the scalp than icP1a, shows a more robust effect for the face-minus-house contrast starting prior to 100 ms following stimulus onset. Further, the effect expressed by icP1 b takes the form of a larger negative projection to medial occipital sites for houses over faces partially canceling the larger projection of icP1a, thereby enhancing the face positivity at this time. These findings have three main implications for ERP research on face processing: First, the ICs that constitute the face-minus-house P100 effect are independent from the ICs that constitute the N170 effect. This suggests that the P100 effect and the N170 effect are anatomically independent. Second, the timing of the N170 effect can be recovered from scalp ERPs that have spatio-temporally overlapping effects possibly associated with low-level stimulus characteristics. This unmixing of the EEG signals may reduce the need for highly constrained stimulus sets, a characteristic that is not always desirable for a topic that is highly coupled to ecological validity. Third, by unmixing the constituent processes of the EEG signals new analysis strategies are made available. In particular the exploration of the relationship between cortical processes over the period of the P100 and N170 ERP complex (and beyond) may provide previously unaccessible answers to questions such as: Is the face effect a special relationship between low-level and high-level processes along the visual stream?

Electrophysiological investigations of the timing of face processing

As important social stimuli, faces playa critical role in our lives. Much of our interaction with other people depends on our ability to recognize faces accurately. It has been proposed that face processing consists of different stages and interacts with other systems (Bruce & Young, 1986). At a perceptual level, the initial two stages, namely structural encoding and face recognition, are particularly relevant and are the focus of this dissertation. Event-related potentials (ERPs) are averaged EEG signals time-locked to a particular event (such as the presentation of a face). With their excellent temporal resolution, ERPs can provide important timing information about neural processes. Previous research has identified several ERP components that are especially related to face processing, including the N 170, the P2 and the N250. Their nature with respect to the stages of face processing is still unclear, and is examined in Studies 1 and 2. In Study 1, participants made gender decisions on a large set of female faces interspersed with a few male faces. The ERP responses to facial characteristics of the female faces indicated that the N 170 amplitude from each side of the head was affected by information from eye region and by facial layout: the right N 170 was affected by eye color and by face width, while the left N 170 was affected by eye size and by the relation between the sizes of the top and bottom parts of a face. In contrast, the P100 and the N250 components were largely unaffected by facial characteristics. These results thus provided direct evidence for the link between the N 170 and structural encoding of faces. In Study 2, focusing on the face recognition stage, we manipulated face identity strength by morphing individual faces to an "average" face. Participants performed a face identification task. The effect of face identity strength was found on the late P2 and the N250 components: as identity strength decreased from an individual face to the "average" face, the late P2 increased and the N250 decreased. In contrast, the P100, the N170 and the early P2 components were not affected by face identity strength. These results suggest that face recognition occurs after 200 ms, but not earlier. Finally, because faces are often associated with social information, we investigated in Study 3 how group membership might affect ERP responses to faces. After participants learned in- and out-group memberships of the face stimuli based on arbitrarily assigned nationality and university affiliation, we found that the N170 latency differentiated in-group and out-group faces, taking longer to process the latter. In comparison, without group memberships, there was no difference in N170 latency among the faces. This dissertation provides evidence that at a neural level, structural encoding of faces, indexed by the N170, occurs within 200 ms. Face recognition, indexed by the late P2 and the N250, occurs shortly afterwards between 200 and 300 ms. Social cognitive factors can also influence face processing. The effect is already evident as early as 130-200 ms at the structural encoding stage.

The Role of Sleep in the Selective Reconsolidation of Declarative Memories

While sleep has been shown to be involved in memory consolidation and the selective enhancement of newly acquired memories of future relevance (Wilhelm, et al., 2011), limited research has investigated the role of sleep or future relevance in processes of memory reconsolidation. The current research employed a list-method directed forgetting procedure in which participants learned two lists of syllable pairs on Night 1 and received directed forgetting instructions on Night 2. On Night 2, one group (Labile; n = 15) received a memory reactivation treatment consisting of reminders designed to return memories of the learned lists to a labile state. A second group (Stable, n = 16) received similar reminders designed to leave memories of the learned lists in their stable state. No differences in forgetting were found across the two lists or groups. However, a negative correlation between frontal delta (1 – 4 Hz) electroencephalographic (EEG) power during Early Stage 2 non-rapid eye movement (NREM) sleep and forgetting of to-beremembered material was found exclusively in the Labile group (r = -.61, p < .05). Further, central theta (4 – 8 Hz ) EEG power during rapid eye movement (REM) sleep was found to correlate with directed forgetting exclusively in the Labile group (r = .81, p < .001) and total forgetting in the Stable group (r = .50, p < .05). These observed relationships support the proposed hypothesis suggesting that sleep processes are involved in the reconsolidation of labile memories, and that this reconsolidation may be selective for memories of future relevance. A role for sleep in the beneficial reprocessing of memories through the selective reconsolidation of labile memories in NREM sleep and the weakening of memories in REM sleep is discussed.