What is the term that relates to the minimum amount of stimulation that people can detect on a sensory channel?

Sensory stimulation

Sensory stimuli, experiences, and emotions continuously influence brain structure. The rationale for using sensory stimulation with the aim of promoting plasticity and recovering consciousness in patients with DOCs comes from protocols of environmental enrichment that, as previously described, are associated with positive biologic and behavioral effects in experimental conditions. The assumptions of this approach lie in the concept that environmental changes after a severe brain injury manifest as virtual isolation of the patient (for example, during an intensive care unit stay) and have potentially detrimental effects on his/her recovery. However, there are significant differences between the environmental enrichment adopted in animal models and sensory stimulation, essentially depending on the fact that the first creates the conditions for a high level of behavioral interactions, whereas the second requires that specific stimuli be actively administered. There is no consensus on what stimuli should be used, but it is generally accepted that stimuli with emotional salience and autobiographic content may be more effective in promoting consciousness recovery (Abbate et al., 2014). Studies with different techniques suggest that seeing the patient's own face or familiar faces (Sharon et al., 2013; Bagnato et al., 2015) or listening to the patient's own name (Kempny et al., 2018) may lead to more effective activation of specific brain areas rather than stimuli without autobiographic content, especially in patients who are in an MCS. Similarly, a patient's preferred flavor or smell is generally used for stimulation rather than generic flavors or smells. A recent study showed that sensory stimulation based mainly on autobiographic content (a picture of the patient's closest family member; his/her favorite music, flavor and smell; and nonspecific tactile stimulation of the arms) may lead to some improvements in responsiveness in patients with MCS but not in patients with UWS (Cheng et al., 2018). Because the awareness of one's own experiences and personality (self-awareness) and the awareness of the external world (perceptual awareness) involve different cortical areas (Tacikowski et al., 2017), sensory stimulation programs should include stimuli with both autobiographic and non-autobiographic content to maximize the chances of achieving cortical activation and plastic changes. Despite the encouraging theoretical premises, the current evidence for the use of sensory stimulation in patients with DOCs is still low, and no standardized procedures are widely accepted. The increasing diffusion of virtual reality systems for cognitive rehabilitation will likely facilitate the adoption of new and more standardized programs of sensory stimulation in patients with DOCs over the coming years.

1.4.1 Sensory

A sensory stimulus or property of a stimulus can be used as a substitute for the original sensation. Damage to visual cortex in rats makes them blind to form and pattern perception yet they are still capable of detecting primitive visual experiences such as brightness and contour. As a result, such rats appear to be able to solve discriminations for orientation (e. g., horizontal vs. vertical black and white stripes) because they can make use of local brightness and contour cues to solve the problem. In extreme conditions where the rats are prevented from using these local cues, they can no longer ‘solve’ the orientation problem, and thus they are blind. The goal for a therapist would be to design conditions where a problem can be solved in multiple ways. For example, persons who are red–green color blind can learn to drive by noting the position of the active light on a traffic signal.

Relationship of interictal GSW discharges with sleep phasic events

Another interesting aspect is the strong link of GSW activity with phasic events in superficial NREM sleep.

If sensory stimuli applied in NREM sleep – usually in stage 2 – elicit GSW discharge, this is linked with the “synchronization type” (K-complexes, spindles, and delta waves) reaction and never with the “desynchronization type” (decrease in amplitude and increase in frequency response), identical with the phase d'activation transitoire of the Strasburg group (Halász, 1991a; Halász et al., 2004a).

The association of GSW activity with synchronization-type oscillations in NREM sleep was further confirmed by studies based on the CAP phenomenon. The occurrence of GSW discharges in patients with IGE was shown to be linked to the synchronized part (containing slow waves, K-complexes) of the CAP oscillation (linked to the so-called A phase) (Terzano et al., 2000). Later, once the A phase had been separated into A1, A2, and A3 types (Parrino et al., 2000), further studies showed a strong link to A1 phase but not to the A3 phase (Halász et al., 2002b).

6.01.1.5 Stimulus Transduction by Sensory Endings

Once sensory stimuli have sufficiently activated a sensory neuron, the outcome is an action potential that is electrochemically similar to that in any other neuron, although the shape of the axon potential may differ across fiber types (Dijouhri, L. et al., 1998; Koerber, H. R., and Woodbury, C. J. 2002. As in any other neuron, the generation of an action potential depends upon sufficiently depolarizing the membrane to a threshold level at a site located at the beginning of the axon (Gardner, E. and Martin, J., 2000). In a typical neuron, the impulse-generating zone is located where the axon is attached to the cell body (the axon hillock). The threshold depolarization is achieved at this site through the spatiotemporal integration of excitatory and inhibitory graded responses generated by numerous synapses on the dendrites and the cell body. In general, the excitatory synaptic mechanisms open sodium channels to permit depolarization, whereas inhibitory synaptic mechanisms cause a countering hyperpolarization by activating potassium channels. In a primary sensory neuron, the impulse-generating zone is at the transition between the sensory ending and the beginning of the axon, and the threshold depolarization is achieved by activating ion channels in the sensory ending. Thus, the specific stimulus detection property of primary sensory neurons is dependent on the location (local tissue environment), structure, and chemistry of its sensory ending.

Abstract

Memories for sensory stimuli underlie many of the cognitive processes we rely on, from interacting with dynamic environments to communication. Several indicators suggest that auditory memory capabilities differ from well-established norms for visual memory. Our findings suggest strong similarities and differences exist in behavioral and neuronal processing of auditory and visual stimuli. We explore working and recognition memory using an auditory delayed matching-to-sample task in rhesus macaques with superior temporal gyrus and prefrontal cortex neuronal recordings. The results suggest that many of the same neural mechanisms are expressed during auditory and visual recognition memory (e.g., enhancement or suppression for matching stimuli). However, retention interval activity for auditory stimuli is not robust in analogous regions compared with tasks using visual stimuli, but is stronger in primary auditory cortex. These variances may contribute to differences in modality memories.

Emotion from Memory and Imagination

Besides external sensory stimuli, imagination of personal memories (Damasio et al., 2000) or fictive scenarios (Kassam et al., 2013) associated with emotional events recruits distributed brain areas that are implicated in processing interoceptive and somatic information as well as motivational signals, such as the insula, somatosensory cortices, OFC and ventromedial prefrontal cortex (vmPFC), posterior and anterior cingulate, striatum, and other subcortical structures in brain stem or hypothalamus. These activations demonstrate an important role in the experiential component of emotions (i.e., feeling states), which can be generated even without external inputs. Reliving different emotions produces partly segregated activation patterns, for example, increases in subgenual cingulate for happiness and sadness but decreases in the mPFC and increases in the dorsal ACC for fear and anger (Damasio et al., 2000), while there is substantial overlap in the anterior insula (aINS) across many emotion types. This overlap accords with a central role for the aINS in both current and predicted feeling states (Haddad et al., 2009; but see Damasio, Damasio, & Tranel, 2013).

Scenario-based elicitation allows studying more complex emotions beyond basic categories, particularly related to social and moral values such as pride, guilt, shame, embarrassment, and indignation (moral disgust). Such emotions consistently activate the dorsomedial prefrontal cortex, temporoparietal junction (TPJ), STS, and temporal pole regions, thought to subtend theory of mind and social knowledge. Accordingly, social emotions require the anticipation of thoughts and intentions of people, whenever they are the cause or target of positive or negative actions from others (Kedia, Berthoz, Wessa, Hilton, & Martinot, 2008; Moll et al., 2005; Takahashi et al., 2004, 2008; Wagner, N'Diaye, Ethofer, & Vuilleumier, 2011). In addition, selective increases occur in the lateral OFC for guilt (Wagner et al., 2011) or indignation (Moll et al., 2005) relative to other negative emotions such as sadness or physical disgust, respectively. The lateral OFC also activates in self-reflective emotions associated with social rejection (Eisenberger, Lieberman, & Williams, 2003) and regret (Coricelli et al., 2005), suggesting a more general involvement in negative feeling states that guide social behavior and decision making (Rilling, King-Casas, & Sanfey, 2008). These data converge with neuropsychological observations that damage or dysfunction affecting the OFC/vmPFC may cause severe disturbances in moral behavior and psychopathy (Damasio, 1994).

6.11.2 Sensory Detection

The detection of sensory stimuli is among the simplest perceptual experiences and is a prerequisite for any further sensory processing. A fundamental problem posed by the sensory detection tasks is that repeated presentation of a near-threshold stimulus might unpredictably fail or succeed in producing a sensory percept. Where in the brain are the neuronal correlates of these varying perceptual judgments? Pioneering studies on the neuronal correlates of sensory detection showed that in the case of vibrotactile stimuli the responses of S1 neurons account for the measured psychophysical accuracy (Mountcastle, V. B. et al., 1969). However, direct comparisons between S1 responses and detection performance was not directly addressed and, therefore, it is not clear whether the activity of S1 accounts for the variability of the behavioral responses. Psychophysical performance was measured in human observers and S1 recordings were made in anesthetized monkeys.

Taste detection and intensity evaluation

Detection of a sensory stimulus is the first step in the cascade of perceptual processes. Gustatory sensitivity or the detection threshold for a substance indicate the lowest concentration of the substance that is necessary to be detected above chance level. Studies in animals and humans show that lesions in structures rostral to the taste regions in the brainstem, i.e., the AIFO area but also the amygdala, affect taste sensitivity (Small et al., 1997; Small, 2006).

The insula/operculum region is also essential for gustatory intensity perception or evaluation. Although increasing intensity of taste stimulation will lead to an increase in activation in areas involved in all processing steps, the intensity–response curves of gustatory neurons in this area best fit the slopes of actual intensity estimates in the case of humans. Further, lesions in left or right AIFO lead to an ipsilateral decrease in intensity ratings (Pritchard et al., 1999); however, when compared to healthy controls, it becomes evident that taste intensity ratings did not decrease on the ipsilateral side, but rather increased on the contralateral side. Thus, the lesion in AIFO is considered to lead to a release of contralateral inhibition (Small, 2006). Further, amygdala activation is likely driven by intensity irrespective of the valence of the taste stimulation (Small et al., 2003).

Stimulus Evoked Responses

Brief presentations of sensory stimuli elicit a sequence of responses in the chain of specialized cortical and subcortical areas that process sensory information. In the primate visual system, over three dozen areas have been identified that are involved in the processing of visual information. Other sensory modalities such as auditory and somatosensory systems involve smaller numbers of areas and less cortical real estate but still employ distributed processing strategies.

In order to enhance the consistent aspects of the sensory response while suppressing the contribution of other physiological processes or environmental noise, most investigators employ averaging of temporal sequences time-locked to the stimulus. In this sort of evoked response paradigm, individual stimuli are typically presented in isolation. Different examples of a class of stimuli are often presented in a random sequence. The interstimulus interval typically is varied within some limits to minimize habituation and thwart the generation of temporal expectations by the subject; such effects can influence the amplitude and timing of certain components of the response. The time course of the electrophysiological response to a single stimulus ranges from tens of milliseconds to a few hundred. Thus, by presenting stimuli at intervals of 500 ms or more, it is possible to examine the entire time course of the response with little or no overlap from preceding or subsequent responses. Fig. 5 illustrates an example of some of the techniques used for visualizing a somatosensory evoked response.

Cortical Function during Movement

Although responses to sensory stimuli are sculpted during active use, certain similarities remain to what is seen in the quiescent condition. It is well known that the way neuronal responses under anesthesia often differ from those that can be observed during active behavior. As already noted, active areas of the somatosensory cortex depend on how and when the cortex receives input. To a certain extent, so does the extent of the region activated by a given stimulus. There are limits, however. When a portion of somatosensory cortex is deprived of functional innervation from the periphery for an extended period of time, that deprived region often can be shown to respond to inputs that were not originally there. Whether this is due to functional unmasking of inputs that were previously suppressed or the establishment of new connections to take the place of older ones is a subject of debate. What is true is that the somatosensory cortex rarely if ever reorganizes whereby new representations spring up in deprived areas that used to represent other major body parts. It seems that the line between body parts is not often crossed and may be a reflection of the intrinsic cortical connections underlying functional sensory representations.

When the activity of somatosensory cortical neurons is observed during purposeful movements, several things begin to become clear. Active movement is accompanied by the enhancement of some neurons and the suppression of others. These enhancements and suppressions vary over short time scales, of the order of tens of milliseconds, and are consistent from movement to movement if conditions remain the same. Many factors seem to influence whether somatosensory cortical neurons respond to sensory inputs. These include whether the inputs are useful in determining which type of movements should be made, whether the inputs may distract and thus compete for valuable cognitive resources needed to initiate desired behaviors, and whether inputs may get in the way of monitoring the execution of behaviors that have been initiated. As a result, for example, neurons activated by an input during the decision phase of a behavior may no longer respond as well, if at all, during the initial part of that behavior even though the activating stimulus is still present. Many have suggested that the parts of the brain that generate behaviors also send a copy of the generation signal (efference copy) to other brain regions. The purpose of this signal may be to inform the other regions that what is to come is self-generated, to cancel inputs that result from the behaviors themselves, or to establish a template against which feedback from behaviors can be compared to see if things are going according to plan. These centrally generated signals appear to alter somatosensory cortical neuronal responses to both central and peripheral inputs. The existence of these signals has been postulated, but proving unequivocally that they exist has been somewhat difficult. Theories behind them provide intriguing insights into the way the nervous system works when it is working.