Triggers and Characteristics of Brain Zaps According to the Findings of an Internet Questionnaire.

Objective: To build on the findings of our prior study of spontaneous posts made about brain zaps on a popular lay mental health website using questions specifically targeting brain zaps in a web-based questionnaire.Methods: 3,141 responses were examined from an online questionnaire made available between June 2016 and February 2018. The questions probed the specifics of the medications taken, the temporal characteristics of medication taken, the symptoms associated with the brain zaps, the specifics of the "zap" experience itself, and their effect on quality of life. Special attention was paid to gathering data regarding the triggers of brain zaps, because in our previous study, eye movements triggering brain zaps emerged as an unexpected finding. As this was a convenience sample, qualitative analysis was primarily performed, except regarding the interaction between the half-life of antidepressants and the time to the onset of the first brain zaps, for which the numerical data appeared to be specific enough to allow such analyses.Results: The data from the targeted questionnaire showed a pattern of responses that was very similar to that obtained from analysis of the spontaneous posts. These data include the types of medications taken, the length of time these medications were taken before the onset of the zaps, the length of the zaps, the feeling quality of the zaps, and the effect of gradual versus sudden discontinuation on their onset and presence. Lateral eye movement as a trigger emerged with even more clarity than in the previous study. The positive correlation between the time from onset of the brain zaps and the half-life of the drugs strongly suggests that brain zaps are indeed associated with antidepressant discontinuation.Conclusions: Brain zaps remain a barely examined and poorly understood symptom of antidepressant discontinuation. Further studies are needed from both a prevention and treatment perspective. There is now an even stronger indication that brain zaps are typically triggered by lateral eye movements, which may open avenues for investigating this process.

In-Home Sleep Recordings in Military Veterans With Posttraumatic Stress Disorder Reveal Less REM and Deep Sleep <1 Hz.

Veterans with posttraumatic stress disorder (PTSD) often report suboptimal sleep quality, often described as lack of restfulness for unknown reasons. These experiences are sometimes difficult to objectively quantify in sleep lab assessments. Here, we used a streamlined sleep assessment tool to record in-home 2-channel electroencephalogram (EEG) with concurrent collection of electrodermal activity (EDA) and acceleration. Data from a single forehead channel were transformed into a whole-night spectrogram, and sleep stages were classified using a fully automated algorithm. For this study, 71 control subjects and 60 military-related PTSD subjects were analyzed for percentage of time spent in Light, Hi Deep (1-3 Hz), Lo Deep (<1 Hz), and rapid eye movement (REM) sleep stages, as well as sleep efficiency and fragmentation. The results showed a significant tendency for PTSD sleepers to spend a smaller percentage of the night in REM (p < 0.0001) and Lo Deep (p = 0.001) sleep, while spending a larger percentage of the night in Hi Deep (p < 0.0001) sleep. The percentage of combined Hi+Lo Deep sleep did not differ between groups. All sleepers usually showed EDA peaks during Lo, but not Hi, Deep sleep; however, PTSD sleepers were more likely to lack EDA peaks altogether, which usually coincided with a lack of Lo Deep sleep. Linear regressions with all subjects showed that a decreased percentage of REM sleep in PTSD sleepers was accounted for by age, prazosin, SSRIs and SNRIs (p < 0.02), while decreased Lo Deep and increased Hi Deep in the PTSD group could not be accounted for by any factor in this study (p < 0.005). Linear regression models with only the PTSD group showed that decreased REM correlated with self-reported depression, as measured with the Depression, Anxiety, and Stress Scales (DASS; p < 0.00001). DASS anxiety was associated with increased REM time (p < 0.0001). This study shows altered sleep patterns in sleepers with PTSD that can be partially accounted for by age and medication use; however, differences in deep sleep related to PTSD could not be linked to any known factor. With several medications [prazosin, selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs); p < 0.03], as well as SSRIs were associated with less sleep efficiency (b = -3.3 ± 0.95; p = 0.0005) and more sleep fragmentation (b = -1.7 ± 0.51; p = 0.0009). Anti-psychotics were associated with less sleep efficiency (b = -4.9 ± 1.4; p = 0.0004). Sleep efficiency was negatively impacted by SSRIs, antipsychotic medications, and depression (p < 0.008). Increased sleep fragmentation was associated with SSRIs, SNRIs, and anxiety (p < 0.009), while prazosin and antipsychotic medications correlated with decreased sleep fragmentation (p < 0.05).

Brain Zaps: An Underappreciated Symptom of Antidepressant Discontinuation.

OBJECTIVE: To describe the characteristics of the electrical phenomena of antidepressant discontinuation syndrome known as brain zaps and their effect on quality of life. METHODS: We examined 595 unsolicited posts made by individuals frequenting a popular lay mental health website. The site was accessed between December 13, 2014, and December 12, 2016, and its content was saved in a text document. The posts had been accumulating on the site since December 2014. These posts were analyzed and separated into 648 separate statements regarding antidepressant intake. Of the statements, 378 contained reference to symptoms experienced in the context of antidepressant discontinuation. These posts were further analyzed for specifics of the medications involved, temporal characteristics of the medication intake, associated symptoms, specifics of the "zap" experience itself, and effect of the zaps on quality of life. As this was a convenience sample, only qualitative analysis was performed. RESULTS: Venlafaxine and paroxetine were reported more frequently, and fluoxetine less frequently, in the sample compared to their frequency of prescription in clinical practice. This finding mirrors the frequency distribution of all withdrawal effects versus antidepressant prescriptions written as reported in the literature. The most likely cause of brain zaps was abrupt discontinuation of the medication, but gradual tapering had only a partial mitigating effect. An unexpected finding was the frequent association of brain zaps with lateral eye movements. The presence of brain zaps was typically transitory, but in a small number of cases it caused significant disability lasting for months or years with no treatment available. Patients' inability to obtain effective help from prescribers and the perceived lack of interest in this symptom on the part of the medical profession risks fueling antipsychiatry attitudes among patients. CONCLUSIONS: Brain zaps are a poorly understood symptom of antidepressant discontinuation, which require further study for both better prevention and treatment. The apparent association of brain zaps with lateral eye movements may open avenues for investigation of this process.

Visualization of Whole-Night Sleep EEG From 2-Channel Mobile Recording Device Reveals Distinct Deep Sleep Stages with Differential Electrodermal Activity.

Brain activity during sleep is a powerful marker of overall health, but sleep lab testing is prohibitively expensive and only indicated for major sleep disorders. This report demonstrates that mobile 2-channel in-home electroencephalogram (EEG) recording devices provided sufficient information to detect and visualize sleep EEG. Displaying whole-night sleep EEG in a spectral display allowed for quick assessment of general sleep stability, cycle lengths, stage lengths, dominant frequencies and other indices of sleep quality. By visualizing spectral data down to 0.1 Hz, a differentiation emerged between slow-wave sleep with dominant frequency between 0.1-1 Hz or 1-3 Hz, but rarely both. Thus, we present here the new designations, Hi and Lo Deep sleep, according to the frequency range with dominant power. Simultaneously recorded electrodermal activity (EDA) was primarily associated with Lo Deep and very rarely with Hi Deep or any other stage. Therefore, Hi and Lo Deep sleep appear to be physiologically distinct states that may serve unique functions during sleep. We developed an algorithm to classify five stages (Awake, Light, Hi Deep, Lo Deep and rapid eye movement (REM)) using a Hidden Markov Model (HMM), model fitting with the expectation-maximization (EM) algorithm, and estimation of the most likely sleep state sequence by the Viterbi algorithm. The resulting automatically generated sleep hypnogram can help clinicians interpret the spectral display and help researchers computationally quantify sleep stages across participants. In conclusion, this study demonstrates the feasibility of in-home sleep EEG collection, a rapid and informative sleep report format, and novel deep sleep designations accounting for spectral and physiological differences.

Combat veterans with comorbid PTSD and mild TBI exhibit a greater inhibitory processing ERP from the dorsal anterior cingulate cortex.

Posttraumatic stress disorder (PTSD) is common among combat personnel with mild traumatic brain injury (mTBI). While patients with either PTSD or mTBI share abnormal activation of multiple frontal brain areas, anterior cingulate cortex (ACC) activity during inhibitory processing may be particularly affected by PTSD. To further test this hypothesis, we recorded electroencephalography from 32 combat veterans with mTBI-17 of whom were also comorbid for PTSD (mTBI+PTSD) and 15 without PTSD (mTBI-only). Subjects performed the Stop Task, a validated inhibitory control task requiring inhibition of initiated motor responses. We observed a larger inhibitory processing eventrelated potential (ERP) in veterans with mTBI+PTSD, including greater N200 negativity. Furthermore, greater N200 negativity correlated with greater PTSD severity. This correlation was most dependent on contributions from the dorsal ACC. Support vector machine analysis demonstrated that N200 and P300 amplitudes objectively classified veterans into mTBI-only or mTBI+PTSD groups with 79.4% accuracy. Our results support a model where, in combat veterans with mTBI, larger ERPs from cingulate areas are associated with greater PTSD severity and likely related to difficulty controlling ongoing brain processes, including trauma-related thoughts and feelings.

Combat veterans with PTSD after mild TBI exhibit greater ERPs from posterior-medial cortical areas while appraising facial features.

Posttraumatic stress disorder (PTSD) worsens prognosis following mild traumatic brain injury (mTBI). Combat personnel with histories of mTBI exhibit abnormal activation of distributed brain networks-including emotion processing and default mode networks. How developing PTSD further affects these abnormalities has not been directly examined. We recorded electroencephalography in combat veterans with histories of mTBI, but without active PTSD (mTBI only, n=16) and combat veterans who developed PTSD after mTBI (mTBI+PTSD, n=16)-during the Reading the Mind in the Eyes Test (RMET), a validated test of empathy requiring emotional appraisal of facial features. Task-related event related potentials (ERPs) were identified, decomposed using independent component analysis (ICA) and localized anatomically using dipole modeling. We observed larger emotional face processing ERPs in veterans with mTBI+PTSD, including greater N300 negativity. Furthermore, greater N300 negativity correlated with greater PTSD severity, especially avoidance/numbing and hyperarousal symptom clusters. This correlation was dependent on contributions from the precuneus and posterior cingulate cortex (PCC). Our results support a model where, in combat veterans with histories of mTBI, larger ERPs from over-active posterior-medial cortical areas may be specific to PTSD, and is likely related to negative self-referential activity.

Mapping single-trial EEG records on the cortical surface through a spatiotemporal modality.

Event-related potentials (ERPs) induced by visual perception and cognitive tasks have been extensively studied in neuropsychological experiments. ERP activities time-locked to stimulus presentation and task performance are often observed separately at individual scalp channels based on averaged time series across epochs and experimental subjects. An analysis using averaged EEG dynamics could discount information regarding interdependency between ongoing EEG and salient ERP features. Advanced tools such as independent component analysis (ICA) have been developed for decomposing collections of single-trial EEG records into separate features. Those features (or independent components) can then be mapped onto the cortical surface using source localization algorithms to visualize brain activation maps and to study between-subject consistency. In this study, we propose a statistical framework for estimating the time course of spatiotemporally independent EEG components simultaneously with their cortical distributions. Within this framework, we implemented Bayesian spatiotemporal analysis for imaging the sources of EEG features on the cortical surface. The framework allows researchers to include prior knowledge regarding spatial locations as well as spatiotemporal independence of different EEG sources. The use of the Electromagnetic Spatiotemporal ICA (EMSICA) method is illustrated by mapping event-related EEG dynamics induced by events in a visual two-back continuous performance task. The proposed method successfully identified several interesting components with plausible corresponding cortical activation topographies, including processes contributing to the late positive complex (LPC) located in central parietal, frontal midline, and anterior cingulate cortex, to atypical mu rhythms associated with the precentral gyrus, and to the central posterior alpha activity in the precuneus.

Reduced G(i) and G(o) protein function in the rat nucleus accumbens attenuates sensorimotor gating deficits.

Prepulse inhibition of the acoustic startle response (PPI) is a cross-species measure of sensorimotor gating, which is severely disrupted in patients with schizophrenia. PPI deficits can be produced in experimental animals by administration of selective D(2)-like dopamine receptor agonists in the nucleus accumbens (NAc). G proteins coupled to these receptors reportedly are altered in the NAc of patients with schizophrenia. Therefore, we sought to determine whether experimental inactivation of intracellular G proteins in the NAc alters PPI. In adult male Sprague-Dawley rats, baseline PPI was determined by presenting acoustic pulse stimuli (120 dB) alone or preceded 100 ms earlier by prepulse stimuli (3, 6 or 12 dB above 70 dB ambient noise). PPI disruption was assessed in the presence of quinpirole (0.0, 0.05, 0.1, 0.5 mg/kg, sc), and pertussis toxin (PTX; 0.05 microg/side) was then infused into the NAc bilaterally. Ten days later, quinpirole-mediated disruption of PPI was significantly reduced; neither PTX alone, nor heat-inactivated PTX had any effect on quinpirole-induced PPI reductions. PPI was significantly higher after PTX infusion upon moderate quinpirole challenge, suggesting that D(2)-like receptors were less effective. PTX treatment significantly reduced basal and dopamine-stimulated [35S]GTPgammaS binding in the NAc core and shell, and reduced G(i)(alpha) protein immunoreactivity in the NAc. The results suggest that PPI disruption mediated by D(2)-like receptor activation in the NAc depends on coupling to G(i) and G(o) proteins, alteration of which could cause sensorimotor gating deficits in schizophrenia.