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Post-Traumatic Stress Disorder and Deception
Published in Harold V. Hall, Joseph G. Poirier, Detecting Malingering and Deception, 2020
Harold V. Hall, Joseph G. Poirier
The CNS activity of abused and non-abused children, measured by the impact of acoustic startle tones on EEG-evoked potentials, reflected significant differences between the two groups (McPherson, Newton, Ackerman, Oglesby, & Dykman, 1997). Essentially, the children with PTSD had greater EEG intensity gradients compared with the non-abused subjects. Auditory-evoked EEG potentials were recorded with male Vietnam combat veterans with PTSD (Gillette et al., 1997). Diminished EEG latencies were significantly correlated with the intensity of re-experiencing symptoms, e.g., nightmares and flashbacks. The authors suggested that the finding was supportive of a “sensory gating effect at the brainstem level,” and that the suppression effect may similarly influence other psychophysiological measures. In a study employing magnetic resonance imaging, Gurvits, Shenton, Hokama, and Ohta (1996) observed that both right and left hippocampi were significantly smaller in subjects with PTSD compared with combat control and normal subjects. There were no significant differences in intracranial cavity, whole brain, ventricles, brain ratio, or amygdala. The two combat groups did evidence increased subarachnoid cerebrospinal fluid. The authors suggested that since hippocampal volume was directly correlated with combat, traumatic stress might cause damage to the hippocampus.
Mesolimbic Interactions with Mesopontine Modulation of Locomotion
Published in Peter W. Kalivas, Charles D. Barnes, Limbic Motor Circuits and Neuropsychiatry, 2019
Robert D. Skinner, E. Garcia-Rill
Deficits in sensory gating also have been reported. In a paired stimuli paradigm, schizophrenic patients do not inhibit the response to the second stimulus under conditions in which normal subjects do inhibit such responses.186–188 Because the PPN appears to generate the auditory evoked P1 wave, these data are suggestive of enhanced activity in this nucleus in schizophrenia. Recently, we reported that the brain stems of schizophrenic patients have on average twice as many PPN neurons as those of normal controls or of psychiatric (non-schizophrenic) controls.189 Even though these findings appear to be holding up with the addition of more brains to this study, caution is necessary because this is a small sample (7–8 brains in each group) and the population of schizophrenic patients was limited to extremely chronic (>30 years of institutionalization), fairly intractable cases.
Neuropharmacologic considerations in the treatment of vegetative state and minimally conscious state following brain injury
Published in Mark J. Ashley, David A. Hovda, Traumatic Brain Injury, 2017
Dorsal projections from the brain stem ARAS reach the thalamus. The thalamus serves as the main relay and filtering station for ascending sensory information. Without the thalamus, most sensory input would not reach the cortex. Activation of the thalamic nuclei by cholinergic and glutaminergic fibers of the ARAS facilitates transmission of sensory input to higher cortical regions. The thalamic nuclei have both afferent and efferent connections with the cerebral cortex and brain stem. The thalamic reticular nucleus, in particular, is involved in the process of sensory gating. Gating of the stream of sensory data allows attention to be selectively focused on some aspects of sensory input and not others. The ascending pathways from the thalamus to the primary sensory areas of the cerebral cortex are predominantly glutaminergic. From the primary sensory areas, collateral connections proceed to the sensory association areas, where information is processed, interpreted, and consciously experienced.
EEG reveals deficits in sensory gating and cognitive processing in asymptomatic adults with a history of concussion
Published in Brain Injury, 2022
Anthony Tapper, W. Richard Staines, Ewa Niechwiej-Szwedo
Relatively fewer studies have investigated sensory ERPs in individuals with a history of concussion. For example, the P50 and N100 are two sensory ERPs elicited following an auditory stimulus and may reflect a multistage sensory gating process that protects higher-order cognitive areas from being bombarded with sensory stimuli (18–21). The sensory gating process entails selection of incoming relevant information and/or suppression of irrelevant stimuli (22). Studies examining sensory ERPs during the auditory oddball task in individuals with a history of concussion have yielded mixed results (3,6,9–12). For instance, some studies reported smaller N100 ERP amplitudes in groups with previous concussion compared to controls (9–12); in contrast, other studies reported no differences between groups (3,6). The mixed findings could arise due to different analytic procedures as studies reporting no N100 amplitude differences only analyzed target trials whereas those showing smaller amplitudes in participants with concussion compared target to non-target trials. This is particularly important because sensory gating is often calculated using the difference between target and non-target ERP amplitudes; thus, studies reporting smaller N100 amplitudes could reflect poorer target facilitation, non-target inhibition or a combination of the two.
Discriminating schizophrenia disease progression using a P50 sensory gating task with dense-array EEG, clinical assessments, and cognitive tests
Published in Expert Review of Neurotherapeutics, 2019
Yu Luo, Jicong Zhang, Changming Wang, Xiaohui Zhao, Qi Chang, Hua Wang, Chuanyue Wang
Smoking can affect P50 sensory gating in patients with schizophrenia. For example, previous research showed that cigarette smoking could normalize the impairment of auditory sensory gating in patients with schizophrenia [45]. Moreover, the α7 nicotinic acetylcholine receptor agonist, tropisetron was proved to be helpful for the treatment of cognitive deficits in schizophrenia, and the administration of tropisetron could significantly improve auditory sensory gating P50 deficits in patients with schizophrenia [46].All smokers were therefore not included in the present study. As expected, significant P50 suppression was only found in HCs, which was consistent with the results of previous studies [23,24,28,29]. Among the four groups, patients with FESZ had the worst P50 suppression whether this variable was quantified by the P50 suppression ratio (S2/S1) or the amplitude difference score (S1−S2). Poor P50 suppression was also evident among UHR and HR individuals, and UHR individuals showed worse P50 suppression than HR individuals. The P50 suppression ratio is commonly used to evaluate sensory gating. Large values of the P50 suppression ratio reflect poor inhibition capacity and sensory gating deficits. Moreover, we found that patients with FESZ had the lowest P50 response amplitude for the S1 stimulus, and HCs had the highest; the P50 amplitudes of UHR and HR individuals were between those of patients with FESZ and HCs. In contrast, the opposite was true for the P50 amplitude for the S2 stimulus (FESZ>UHR>HR>HC). Only the P50 suppression ratio and P50 amplitude were significantly different among the four groups, whereas the S1 amplitude and S2 amplitude did not significantly differ among the four groups. The findings indicate that the P50 suppression ratio and P50 amplitude may act as indicators of sensory gating deficits in patients with schizophrenia and individuals with psychosis risk.
Maternal overnutrition leads to cognitive and neurochemical abnormalities in C57BL/6 mice
Published in Nutritional Neuroscience, 2019
Christian Wolfrum, Daria Peleg-Raibstein
In the clinic, sensory gating deficits are measured employing PPI. Alterations in PPI are found in different neuropsychiatric disorders including anxiety disorders, major depression, obsessive-compulsive disorders, and schizophrenia.40 PPI is measured under similar conditions in both human and animals. Thus, this phenomenon is often employed in animal studies to investigate the neuronal underlying mechanisms of different neuropsychiatric disorders.41 In the last decade, PPI was linked with cognitive functions.42–46 There are no published reports thus far that have associated PPI in the offspring as a function of maternal HFD exposure. The brain circuits regulating PPI include projections from the hippocampus to the striatum and prefrontal cortex.47 Our observations, in several independent cohorts of HFD offspring tracked longitudinally demonstrate a potentiation of PPI. This phenomenon emerged only at adulthood. The magnitude of augmentation of the startle was significant in all prepulse intensities and across all pulse intensities. The potentiation of sensory-motor gating in these offspring may be a consequence of reduced striatal dopamine signaling. We have observed in a previous study abnormalities in dopamine-related behaviors in our HFD offspring at adulthood, such as enhanced sensitivity to drugs of abuse (amphetamine, cocaine, and alcohol). These behavioral abnormalities were coupled with reduced striatal dopamine transmission, enhanced striatal dopamine D2 receptor levels as well as reduced tyrosine hydroxylase (TH) positive cells compared to control offspring.39 PPI abnormalities in HFD offspring emerged in adulthood and remained in the aged adult group but were not present when animals were tested in the peripubertal age. Interestingly, we have previously found that HFD offspring did not show any difference in amphetamine-induced locomotor activity during adolescence and this effect emerged only in adulthood.39 It may imply that the PPI potentiation may be due to reduced striatal dopamine signaling in the HFD offspring. These findings are consistent with pharmacological studies showing that PPI is mediated by the mesolimbic dopamine system.48 More specifically, dopamine agonists, such as amphetamine and apomorphine, lead to disruption of PPI in normal animals and this effect appears to be mediated mainly by dopamine D2 receptors.41 In contrast, dopamine antagonists, such as neuroleptic drugs, lead to facilitation of PPI by decreasing dopamine transmission.41,49 In an animal model of Parkinson’s disease it was shown that increased PPI was evident only in adulthood after the mice exhibit progressive loss of dopamine signaling.50 A similar result of enhanced PPI in the adult offspring was reported employing another developmental manipulation, prenatal exposure of methamphetamine.51