Thalamus consciousness

Maintenance of these frequencies relies on the degree of depolarisation of the thalamic neurons (Jahnsen and Elinas 1985) and this, in turn, depends on the nature and intensity of their afferent inputs. The NspRTN and other thalamic nuclei receive reciprocal inputs from the cortex and it is possible that it is the ensuing oscillations in neuronal activity in this circuit between the cortex and thalamus that give rise to the sleep spindle waves in stages 2-4. In fact, it has been suggested that the stronger and clearer these oscillations become, the more likely it is that there will be loss of consciousness. 

A global view of consciousness is that it is generated throughout the entire brain, as a result of synchronisation of relevant neural networks. Specific systems or regions—for example the cerebral cortex, brainstem reticular formation and thalamic nuclei—may be key anatomical integrators. Areas with the most widespread interconnections are pivotal, and on this basis the cortex and thalamus are more relevant than cerebellum and striatum for example. Frontal cortex for example connects with every other brain region, both in terms of input and output, with 80% of such connections accounted for by cortico-cortical connections. Thalamic intralaminar nuclei are, in conjunction with the reticular nucleus, reciprocally connected to all cortical areas. By contrast the cerebellum has very few output pathways and striatal-cortical input is (via the thalamus) confined to frontal lobe. 

Of the different sensory modalities, olfaction does not appear to feature in reports of the effects of plant hallucinogens. Since olfaction is the one sense not relayed through the thalamus, this brain area is likely to be central to the changes in consciousness described. Many target receptors implicated, e.g. muscarinic, 5-HT2, D2, D3 and opiate, are present in this thalamic nuclei the human brain. 

In both waking and dreaming, consciousness depends on the physiological condition of the upper brain. More specifically, the brain stem must continually activate the billions of brain cells that constitute the cerebral cortex and thalamus if we are to be fully aware (waking) or even partially so (dreaming). Here is how thalamocortical activation is brought about. 

The contention that the thalamocortical system is essential to the synchronous activation of the forebrain and hence to consciousness is supported by the loss of consciousness in subjects with disease destruction of the thalamus and by the capacity to restore consciousness by activating the thalamocortical system if that system (and of course, the cortex) is intact. The case of Karen Ann Quinlan is well known her profound coma was caused by a very small, restricted thalamic lesion and was irreversible because the thalamocortical system could not be activated by any known means. 

The reticular formation is also located in the midbrain and brainstem. The reticular formation is comprised of a collection of neurons that extend from the reticular substance of the upper spinal cord through the midbrain and the thalamus. The reticular formation monitors and controls consciousness and is also important in regulating the amount of arousal or alertness in the cerebral cortex. Consequently, CNS drugs that affect the arousal state of the individual tend to exert their effects on the reticular formation. Sedative-hypnotics and general anesthetics tend to decrease activity in the reticular formation, whereas certain CNS stimulants (caffeine, amphetamines) may increase arousal through a stimulatory effect on reticular formation neurons. 

Other structures in this area make up the limbic system which is directly linked to the olfactory system. Areas called the septal nuclei and amygdala contain regions often called the pleasure centres, with the hippocampus concerned with motivational memory. Projections from the cerebral cortex connect with the thalamus, hypothalamus and posterior pituitary gland. The network of connections between all these different areas of the brain is highly complex. The role of the limbic system is significant in autonomic (involuntary or non-conscious) reactions that are implicated with emotional responses including fear, rage and motivation. 

Small thalamic lesions may cause a pure sensory stroke or sensorimotor stroke, sometimes with ataxia in the same limbs (Schmahmann 2003). However, other deficits may occur in isolation, or in combination depending on which thalamic nuclei are involved. These include paralysis of upward gaze, small pupils, apathy, depressed consciousness, hypersomnolence, disorientation, visual hallucinations, aphasia and impairment of verbal memory attributable to the left thalamus, and visuospatial dysfunction attributable to the right thalamus. Occlusion of a single small branch of the proximal posterior cerebral artery can cause bilateral paramedian thalamic infarction with severe retrograde and anterograde amnesia. 

The time delay between sensory signaling and the subjective conscious perception of sensation which has so carefully been demonstrated by neurosurgeon Benjamin Li bet and other experimenters may also have a simpler explanation than those proposed so far. Li bet and others have shown that a pin-prick of the finger, for example, transmits a signal to the cortex of the brain via the thalamus, which arrives in a few thousandths of a second. All sensory signaling except olfaction is similarly transmitted first to the thalamus which acts as a sort of relay-station distributing the signals to the appropriate domains of the cortex. Yet conscious perception of the pin-prick can by various experimental techniques be shown to be delayed by up to a half-second, while "cerebral neuronal adequacy" is achieved. 

The reticular activating system (RAS) is a network of neural pathways extending from the brain stem to the thalamus and other parts of the limbic system. It plays a role in controlling arousal and awareness. Sensory neurons from peripheral sensory receptors feed into the RAS, which appears to filter sensory messages going to the cerebral cortex, so that some sensory information reaches conscious awareness and some does not. 

Meprobamate exerts a unique combination of actions on the central nervous system. These actions are so much those that would be theoretically expected of a tranquillizer that it is surprising that they are not produced by other depressants of the nervous system and that meprobamate is not a more powerful psychotropic agent. It weakly stimulates the ascending reticular system and does not depress the cortex (thus the level of consciousness is unimpaired) but it does selectively depress the thalamus and it inhibits artificially evoked seizure discharges in the limbic system (thus reducing emotional tension). Although it is possible to specify the physiological systems on which meprobamate acts, it is not yet possible to translate this information into terms of the neurohumoral systems involved. 

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