The Brain Electrical Activity - Assignment Example

Question Brain electrical activity is described as slow wave (SWA) when high amplitude power can be measured at low, delta frequency, which rangesbetween only 0.5 and 5 Hz. This means that there is a great number of synchronized neurons in the middle frontal cortex working at low frequency. This correlation results from the finding that deterioration in the middle frontal lobe is directly associated with the level of impairment of SWA during sleep (Anwar, 2013). This is evaluated through a fast Fourier transform (FFT) of the scalp or cortical surface electroencephalography (EEG), which obtains the power distribution across 0 to 80 Hz (Canadian Institutes of Health Resarch, n. d.). Since wake states are characterized by great amounts of cortical neuronal firing rates to facilitate learning and memory, prolonged waking is associated with increased expression of proteins for energy metabolism, cellular stress response and synaptic potentiation (Cirelli and Tononi, 2008). Interestingly, REM sleep is also associated with increased neuronal firing, since it allows the establishment of synaptic connections, especially among infants (Canadian Institutes of Health Resarch, n. d.). On the other hand, sleep at non-rapid eye movement (non-REM) stage is characterized by long periods of decreased sensory responsiveness and muscle tone, as well as the gradual appearance of tonic, global, high-amplitude SWA. This is in contrast to REM, which is much shorter and is characterized by electrical activity similar to waking (Canadian Institutes of Health Resarch, n. d.). Given these differences among wake and sleep states, the non-REM sleep is considered as a rebound from prior wake duration. In addition, SWA is also considered a reliable index of sleep homeostasis, a regulatory process, which controls the accumulation and discharge of sleep need. This is supported by the finding that EEG SWA during non-REM is relative to the number of hours spent awake, such that the normal amounts of SWA during the rest phase is reduced by naps and increased by sleep deprivation (Dijk, 2009). SWA is also seen to be important in brain plasticity, as its enhancement during sleep increases the overnight task improvement (Landsness, et al., 2009). Moreover, slow waves in the frontal brain strengthen memories (Anwar, 2013). SWA is influenced by the interplay of neurotransmitters, ontogenesis and aging, such that a decrease in the activity of arousal centers increases SWA. In fact, cholinergic, noradrenergic, serotonergic, dopaminergic, and histaminergic systems are less active in high-SWA, non-REM than in low-SWA, wake states (Tononi and Cirelli, 2006). On the other hand, the amplitude of non-REM SWA is very low in infancy, rapidly increases just before reaching adolescence, and sharply declines in adulthood, reaching its lowest value in senescence (Feinberg and Campbell, 2009). Indeed, this can be correlated to the differences among infants, adolescence and the elderly in terms of the amount of brain activity. Taking into consideration all of these evidence, it seems to be that the increase in the amount of neurons operating at low frequency allows the brain to recuperate after the wake state. Thus, to recuperate from a prolonged wake state in which the brain was exposed to increased metabolism and greater cellular stress, more neurons take a break and operate at delta frequency. This is seen in EEG as higher SWA values. Question 2: Beginning in 1995, Milner and Goodale have proposed two major endpoints of the projections coming from the primary visual area (V1), inferior temporal (IT) and posterior parietal (PP) cortices. In the macaque monkey, the V1-IT processing of the visual input was observed to pass ventrally along the brain, while the VI-PP pathway was seen to proceed dorsally. Further research by Ungerleider and Miskin in 1982 showed that lesions of the IT cortex resulted to deficits in the monkey’s discrimination between objects, but did not bump into obstacles or misjudge distances during landmark tasks. Despite weeks of training IT-lesioned monkeys, they still fail on discriminating patterns, even if they were able to catch flying objects within their cages. On the other hand, lesions of the PP cortex produced deficits in the conduct of landmark tasks, but did not affect discrimination learning. Also, Gallese, et al. (1997) had observed that monkeys with PP lesions were unable of accurately grasping objects, failing to shape and orient their hands or fingers to pick up the item. This is because the ventral and dorsal streams are different in terms of function. Neurons in the ventral stream are tuned to the features of objects, allowing categorical specificity in some. These cells are minimally influenced by motor behavior, but are significantly modulated by how often the visual stimulus has been presented and whether or not it can be associated with reward. Meanwhile, some neurons in the PP cortex were seen to be activated by visual stimuli only when the primate had to do something in response to the stimulus. In fact, as demonstrated by Kawashima, et al. (1996), PP neurons are important in guiding the movements of the eyes and the movements of the hands. The findings in monkeys were also found translatable in humans. Those with IT deficits manifest with visual form agnosia, in which the non-blind person is unable to recognize faces or objects, identify shapes visually. In a study on one patient, the perceptual report of an object’s orientation did not accurately describe the actual orientation. However, the patient was able to easily insert her hand into a slot. There was also a more accurate grip scaling among IT-deficient, PP-patent samples as compared to IT-patent, PP-deficient participants. However, the ability of those with visual form agnosia in grip scaling is lost when there was delay between the stimulus and the response, even for just two seconds (Milner and Goodale, 1998). On the other hand, those with impairment of the dorsal stream suffer from optic ataxia, or difficulty in accurately reaching in space to pick up objects. Similar to the monkeys with PP lesions described above, humans with optic ataxia made errors in hand rotation to allow their hand to enter a large oriented slot. There was also deficient grip scaling during reach out exercises. Despite these difficulties, they were able to give verbal reports as to the orientation and location of the objects they tried to grasp. This is because the patient cannot recreate in her imagination an object that she failed to perceive in the first place (Milner and Goodale, 1998). Question 3: The brain is able to provide a response appropriate to the type of stimulus by the presence of different somatosensory pathways, each of which is activated only by a particular stimulus. The signals from the activated receptor travel through the particular somatosensory pathway to which it is linked to. For example, emotional information, such as sharp pain, which includes cutting and heat pain, or thermal stimulus, non-painful changes in temperature, applied onto the body and face, as detected by free nerve endings, results to the activation of the neospinothalamic pathway (NSTP) and spinal trigeminal pathway (STP), respectively. On the other hand, discriminative touch, which includes fine, crude, deep, vibratory, fluttering or skin indenting touch, or proprioception, that is sensation of positional changes, from the body and face, as sensed by Meissner’s corpuscles, Ruffini endings and Pacinian corpuscles, is sent to the brain via the medial lemniscus pathway (MLP) and main sensory trigeminal pathway (MSTP), respectively (Dougherty, n. d.). The signals from the mechanoreceptors pass through the spinal cord or trigeminal nerve, depending on whether the receptor is located at the body or the face. The axons of the gracile and cuneate nuclei of the MLP decussate in the medulla, while the axons of the posterior marginal nucleus of the NSTP cross-over at the level of the spinal cord. The spinal trigeminal axons decussate upon leaving the nucleus that is located at the medulla and the lower pons. Similarly, the main sensory trigeminal axons cross-over the other side upon leaving the nucleus, which is at the mid pons. There is little mixing among these pathways, allowing the person to differentiate among, pain, cold, discriminative touch and proprioception, as well as to localize where the stimulus was applied (Dougherty, n. d.). From the brain stem or the spinal cord, the signals pass through the thalamus, from where information flows predominantly to the cerebral cortex. Upon reaching the cerebral cortex, the primary somatosensory cortex, composed of the postcentral gyrus and posterior paracentral lobule of the parietal lobe, is responsible for the initial stage of cortical processing. At this point, discriminative touch and proprioception at the same area can be integrated to allow the brain to respond to them. Interestingly, the location of a neuron in the cortex is related to its receptive field, such that adjoining areas of the body are represented by adjoining areas of the cortex. However, the neural maps of the body and face are not isomorphic representations of each other. In fact, they appear quite distorted because although the receptive fields of hands and face are relatively smaller compared to others (such as the back), a greater number of neurons represent the hands or face. From the primary somatosensory cortex, signal is forwarded to the secondary somatosensory cortex, the motor cortex and the posterior parietal cortex. The secondary somatosensory cortex is special in that it sends impulse to the insula, allowing learning and memory from the sensation. As part of the limbic system, the insula allows a person to elicit particular emotions from the experienced stimulus (Dougherty, n. d.). References Anwar, Y., 2013. Poor sleep in old age prevents the brain from storing memories. [online] Available at: < http://newscenter.berkeley.edu/2013/01/28/sleep-memory/> [Accessed 30 January 2013] Canadian Institutes of Health Research, n. d. The Different Types of Sleep. [online] Available at: < http://thebrain.mcgill.ca/flash/a/a_11/a_11_p/a_11_p_cyc/a_11_p_cyc.html> [Accessed 30 January 2013] Cirelli C, Tononi G. 2008. Is sleep essential? PLoS Biol 6, p. e216. Dijk, D. J., 2009. Regulation and functional correlates of slow wave sleep. J Clin Sleep Med, 5, pp. S6–S15. Dougherty, P., n. d. Chapter 5: Somatosensory Processes. [online] Available at: . [Accessed 30 January 2013] Feinberg, I. and Campbell, I. G., 2009. Sleep EEG changes during adolescence: an index of a fundamental brain reorganization. Brain Cogn, 72, pp. 56–65. Landsness, E. C., Crupi, D., Hulse, B. K., Peterson, M. J., Huber, R., Ansari, H. M., Coen, M., Cirelli, C., Benca, R. M., Ghilardi, M. F., and Tononi, G., 2009. Sleep-dependent improvement in visuomotor learning: a causal role for slow waves. 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