RAS: Reticular activating system

Image and Location

Schematic drawing of the reticular activating system

The reticular activating system (RAS) consists of neuronal networks originating in brainstem regions that project upward to the subthalamic nucleus and from there to many cortical and subcortical brain structures as indicated by arrows. The RAS is responsible for maintaining conscious activity and is very sensitive to hypnotics and general anesthetic.

Musacchio, J. (2012). Contradictions. Springer Praxis Books. musacchio2012qualiaandconsciousness.springer.pdf

The dynamic core—the reticular activating system, thalamus and cortex

The reticular activating system, thalamus and cortex constitute a “dynamic core;” lesions to these structures remove the possibility of conscious experience (Edelman and Tononi, 2000). The reticular activating system is responsible for arousal and for governing the waking/sleeping transition (Magoun, 1952). The thalamus plays a central role in the dynamic core. It is the “switchboard” of action potentials from the sensory and motor systems to the cortex. Afferents from the reticular activating system project to the thalamus and then up to the cortex (Steriade, 1996). These circuits shift attention levels and lead to desynchronized EEG and gamma activity (Steriade, 1995).

Travis, F. (2012). Core and Matrix Thalamic Nuclei: Parallel Circuits Involved in Content of Experience and General Wakefulness. Neuroquantology, 10(2), 144-149. travis2012wakefulness.neuroquantology.pdf

Role of RAS

Personality and RAS

Eysenck (1967) suggested that behavioral differences between introverts and extraverts are caused by variability in cortical arousal. According to his theory introverts are chronically more cortically aroused than extraverts. Therefore, introverts exhibit an inherent drive to compensate for this high cortical arousal or overactive reticulo-thalamo-cortical pathways. In contrast, extraverts require more external stimulation than introverts, because they have lower cortical arousal. According to Eysenck cortical arousal can be produced from the reticular formation and from the visceral brain (e.g., hypothalamus, hippocampus, amygdala, cingulum, and septum). It is assumed that introverts have lower thresholds in the ascending reticularactivatingsystems (ARAS) than extraverts, whereas unstable subjects (scoring high on neuroticism) are hypothesized to have lower thresholds in the visceral brain than stable subjects (scoring low on neuroticism (Eysenck, 1967).

Schaefer, M. et al. (2012). Touch and personality: Extraversion predicts somatosensory brain response. Neuroimage, 62(1), 432–438. schaefer2012touchandpersonality.neuroimage..pdf

Migraine and RAS, Limbic system

Historical and cultural references have long given psychosocial factors prominence in our conceptualization of migraine. Rafaelli and Menon may have been the first to suggest, in 1975, that much of “chronic headache or migraine” could be explained by limbic system dysfunction. They suggested specific anatomic localization of migraine symptoms and phenomena, especially to the hypothalamus (hormonal triggers), reticular activating system (sleep), and the limbic system in general (emotional features). Without specifying the limbic system, Lance wrote: “. . . we believe that there is an upstream projection from brainstem monoaminergic nuclei to the cortex that can regulate blood flow, and downstream projection that plays an important part in the descending pain control system.” Salloway and White included migraine in the differential diagnosis of “paroxysmal limbic disorders.” More recently, Schoenen suggested that inhibitory serotonergic afferents from the raphe magnus nucleus were influenced by excitatory input from the periaqueductal grey and “other limbic structures.” O'Carroll has argued eloquently for the importance of considering limbic factors in our understanding and treatment of migraine.

Factors influencing pain perception and the neural basis for endogenous pain modulation, placebo and nocebo effects. (a, b) Schematic illustration of key brain regions involved in generating a pain experience and core brain regions that comprise the cognitive and descending pain modulatory networks (a) and a description of the various factors that influence the pain experience listed in the text boxes (b). The hippocampal region is important for amplifying pain experiences during nocebo or increased anxiety. © Schematic illustration indicating where endogenous opioid and dopamine neurotransmission occurs in the human brain during placebo analgesia. For some brain regions (NAc), there is a bidirectional response of both opioid and dopamine release that produces either placebo (increased release) or nocebo (decreased release) effects. Amy = amygdala; CCK = cholecystokinin; CNS = central nervous system; dlPFC = dorsolateral prefrontal cortex; Hipp = hippocampus; Hypo = hypothalamus; mACC = midanterior cingulate cortex; NAc = nucleus accumbens; OFC = orbito-frontal cortex; PAG = periaqueductal gray; rACC = rostral anterior cingulate cortex; RVM = rostral ventral medulla; Sl = primary somatosensory cortex; S2 = secondary somatosensory cortex; vlPFC = ventrolateral prefrontal cortex; vmPFC = ventromedial prefrontal cortex. (used with permission from Tracey I. Getting the pain you expect.).

Proposed pathways of neurolimbic model of migraine. The concept of periaqueductal gray (PAG) as “migraine generator” is expanded to a neurolimbic pain network. Brainstem pain-modulating circuits have bidirectional connections with the limbic system (anterior cingulate cortex, amygdala, insula, orbito-frontal cortex [OFC] and prefrontal cortex [PFC], hypothalamus), and tonically influence migraine expression. Cortical hyperexcitability (shown in occipital cortex) is also influenced by brainstem circuits. See text for detailed description of interrelationships. ACC = anterior cingulate cortex; RVM = rostral ventral medulla; SSN = superior salivatory nucleus.

Maizels, M. et al. (2012). Beyond Neurovascular: Migraine as a Dysfunctional Neurolimbic Pain Networkh. Headache. maizels2012migraine.headache.pdf

Gulf War Illness and RAS (ERP study)

An exaggerated response to emotional stimuli is one of the several symptoms widely reported by veterans of the 1991 Persian Gulf War. Many have attributed these symptoms to post-war stress; others have attributed the symptoms to deployment-related exposures and associated damage to cholinergic, dopaminergic, and white matter systems. We collected event-related potential (ERP) data from 20 veterans meeting Haley criteria for Gulf War Syndromes 1–3 and from 8 matched Gulf War veteran controls, who were deployed but not symptomatic, while they performed an auditory three-condition oddball task with gunshot and lion roar sounds as the distractor stimuli. Reports of hyperarousal from the ill veterans were significantly greater than those from the control veterans; different ERP profiles emerged to account for their hyperarousability. Syndromes 2 and 3, who have previously shown brainstem abnormalities, show significantly stronger auditory P1 amplitudes, purported to indicate compromised cholinergic inhibitory gating in the reticularactivatingsystem. Syndromes 1 and 2, who have previously shown basal ganglia dysfunction, show significantly weaker P3a response to distractor stimuli, purported to indicate dysfunction of the dopaminergic contribution to their ability to inhibit distraction by irrelevant stimuli. All three syndrome groups showed an attenuated P3b to target stimuli, which could be secondary to both cholinergic and dopaminergic contributions or disruption of white matter integrity.

Tillman, G. (In press). Event-related potential patterns associated with hyperarousal in Gulf War illness syndrome groups. Neurotoxicology. http://www.sciencedirect.com/science/article/pii/S0161813X12001337

Consciousness and RAS

All Consciousness Is Endogenous

The “state” of consciousness as a whole is generated in the upper brainstem. We have known this for many years. A mere decade after the death of Freud, Moruzzi and Magoun [42] first demonstrated that global consciousness, in the sense measured by EEG activation, is generated not by exteroceptive stimuli but endogenously, in a part of the upper brainstem then called the “reticular activating system”. This was quickly confirmed by Penfield and Jasper, who recognized in absence attacks (mentioned above) “a unique opportunity to study the neuronal substratum of consciousness”. Their extensive studies led them to the conclusion that obliteration of consciousness could only be reliably evoked by restricted damage to such upper brainstem sites (which they termed the “centrencephalic system”). They were also impressed by the fact that removal of large expanses of cortex under local anaesthetic, even total hemispherectomy, had limited effects on consciousness. Cortical removal did not interrupt the presence of the conscious “self”, of conscious being, it merely deprived the patient of “certain forms of information”. Lesions in the region of the upper brainstem, by contrast, totally and rapidly destroyed consciousness, just as the absence seizures did. These observations demonstrated a point of fundamental importance: all consciousness ultimately derives from upper brainstem sources. Contrary to LeDoux and the other corticocentric theorists: all the cortical varieties of consciousness depend upon the integrity of these subcortical structures, not the other way round. This in not to deny that higher cortical regions add much to consciousness. Of course they do. But the evolutionary “roots” of consciousness are to be found elsewhere, and they are probably affective.

Solms, M. (2012). The “Id” Knows More than the “Ego” Admits: Neuropsychoanalytic and Primal Consciousness Perspectives on the Interface Between Affective and Cognitive Neuroscience. Brain Sciences, 2(2), 147-175. solms2012idego.brainsciences.pdf


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Most important references

Fields, H. L. (2000). Pain modulation: expectation, opioid analgesia and virtual pain.Progress in brain research, 122, 245-253.

Maizels, M. et al. (2012). Beyond Neurovascular: Migraine as a Dysfunctional Neurolimbic Pain Networkh. Headache.

Musacchio, J. (2012). Contradictions. Springer Praxis Books.

Schaefer, M. et al. (2012). Touch and personality: Extraversion predicts somatosensory brain response. Neuroimage, 62(1), 432–438.

Tillman, G. (In press). Event-related potential patterns associated with hyperarousal in Gulf War illness syndrome groups. Neurotoxicology.

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Last modified: 2017/05/13 02:15