Why Cant You Tickle Yourself - Essay Example

Why can’t you tickle yourself? Psychobiological explanation s All human beings used to experience tickling since a very early age. Firstly, when parents tickle their children, and then children tickle each other during games; grownups also experience tickling when tickle their lovers, - whatever the age is a body response stays the same. While making ones who are tickled laugh and squirm against their will, the ones who tickle get powers to cause either pleasure or pain to tickled persons. Yet no one can tickle oneself for some reason, and it makes tickling an outstanding reflex, and a curious activity. Having psychobiological consequences, tickling as well appears to have the same psychobiological origin for most of the human beings. The aim of this paper is too look, why we can’t tickle ourselves, using explanations from psychobiological studies. Generally, tickling can be described as executed on a human skin tactile action, which leads to a general excitement, accompanied by laughter and reflex movements. Provine (2004) describes tickling as a social activity, and even as a form of communication, and suppose that originally tickling had a warning function. Scholar proposes that as a neurobiological mechanism, tickling might be an evolved form of a defensive reflex once needed to protect a body surface from external dangerous moving stimuli for example, small insects or parasites (Provine, 2004). Therefore, when tickled, humans are remained about a possible externally coming danger. In this way, a phenomenon why one parts of human body are more ticklish than others is explained: the most ticklish body areas are also the most vulnerable ones. Despite tickling starts from a tactile action on a body surface, stimulating effectors under the top layer of human skin as for example temperature may also do, tickling is a more complex reflex then any others (Provine, 2004). To form a response on a perceived tickling, nerve endings send electrical signals to the brain, and to know what happens next, a variety of studies appeared on tickling, exploring the phenomenon. Blakemore et al. (1999) were ones of the first to define specific brain areas, mostly activated when tickling, using MRI and FMRI (functional magnetic resonance imaging). Scientists defined, that the most responsible for tickling (as well as for other tactile stimulus) brain areas are the somatosensory cortex and anterior cingulate cortex, - the areas, which are originally responsible for analyzing a tactile activity and for pleasurable feelings (Blakemore et al., 1999). During a more recent FMRI study made by Wattendorf et al. (2013, 3) on tickling, “Activity was also recorded in the frontal operculum, the thalamus, the putamen/ pallidum, the hypothalamus (bilaterally), the anterior and posterior lobe of the right cerebellum, and the PAG”. In this way, the brain reaction studies using MRI and FMRI were helpful for scientists in predicting and confirming the routine of tickling process. Blakemore et al. (2000) describe the aforward model, earlier hypothesized by Frith on tickling. The brain is always trying to predict the sensory consequence of a tactile movement, despite it’s a self-produced touch or external action. Central nervous system explores either a central monitor, or “forward model” to “mimic aspects of the external world” and make a relation between action and its possible outcome (Blakemore et al. 2000, 11). A sense of a self-produced tickling is known to the brain due to a previous constant experience of self-sensing, and efferent copy on known sensation is formed. Actual sensation from receptors is coming by nerves to the brain (afference), and meats a predicted sensation (efference). In case of self-sensing, the brain correctly predicts coming sensation “on the basis of motor commands”, and a very little “or no sensory discrepancy” would be a result from comparing a predicted sensation with actually sensed one as there’s no much difference the brain finds between efference and afference (Blakemore et al. 2000, 11). Therefore, tickling was commonly viewed either as a predictive mechanism (when the brain makes a motor command based on previous experience efferent copy first), or as a result of the received sensation, a postdictive mechanism (when brain firstly receives afference from actual sensation, and then compares it to efferent copy) (Gross, 2006). Nowadays, most scientists argue for a predictive mechanism as it would also explain, why humans may response in a similar way (with laughter and reflex movements) already on intension of tickling, despite a tactile contact never happens (Bays et al, 2006) (Blakemore et al., 2000). Whatever the mechanism is, Provine (2004) says humans normally develop a cancellation reaction on self-produced tickling stimuli, because they get used to own touches. “In the absence of such cancellation, we would be constantly tickling ourselves by accident” (Provine 2004, 217). The existence of cancellation reaction was proved by FMRI examine on neural responses from tickling. Blakemore et al. (1999) study confirmed that somatosensory cortex indeed, demonstrates less activity associated with movement when a self-produced tickling, comparing to external tickling. At the same time, the brain cannot predict an external tickling sensory consequence with the same accuracy, because the brain hasn’t experience it so constantly to make a correct efferent copy (Blakemore et al., 2000). The brain finds no correspondence between given motor commands and afference, actually coming from the most vulnerable areas. New sensation is recognized as a danger, and the brain commands to demonstrate defensive reactions: the reflex defensive movements and laughter as a typical defensive reaction. Therefore, Blakemore et al. (2000) made a prediction that a lack of awareness about a self-produced tickling would cause the same reaction as on an external tickling. Among all humans, they are mentally ill people who commonly have a damaged awareness, and among them, specifically schizophrenics are ones who most common report on tactile hallucinations (Berrios, 1982). Despite a schizophrenic mental disorder affects about 1% of a general Earth population, a deep neuropathology of schizophrenia is still not fully discovered (Shenton et al., 2001). Yet scientific studies report a lot of data on schizophrenia disease progress, accompanied symptoms and brain damage. Among most common symptoms are hallucinations presented at least for six months (Harrison, 1999). Specifically, schizophrenics are known to hear strange voices (auditory hallucinations), and often report of small animals on their skin and believe the sensations are real (tactile hallucinations) (Berrios, 1982). Berrios (1982) says, those false sensations are real for schizophrenics due to the disorder among sensed perceptions and the brain. Already when first describing schizophrenic disease, Kraepelin and Bleuler believed brain abnormalities to be ultimately linked to the etiology of schizophrenia, and that external factors have important role in symptomatic (Shenton et al., 2001). The first computer assisted tomography (CT) was used to study brain damaged caused by schizophrenia, yet only MRI and FMRI allowed a better observing of abnormalities: the most consistently schizophrenia damages the temporal lobe, including the amygdala-hippocampal complex, and parahippocampal gyrus (Kotrala and Weinberger, 1995). Other functional studies also indicate a poor activity in the frontal lobe, - the brain area responsible for interconnectivity (neural networks linking) (Shenton et. al., 2001). Additionally, schizophrenia causes damage to the subcortical region, specifically, cerebellum and thalamus (Harrison, 1999). Other words schizophrenia hits almost the same areas which, according to Blakemore et al. (1999) and Wattendorf et al. (2013) findings the normal brain activates to recognize ticking as a self-produced tactile movement, and as the result, to cancel a psychobiological defensive response. Blakemore et al. (2000) predicted, that due to specifics of brain damage during the disease, schizophrenics may only be aware of a tactile sensation, while not recognizing this sensation as a self-produced. Basing own hypothesis on a forward model for tickling, scientists proposed that schizophrenics may be enabling to relate a well-known tactile sensation (efferent copy) to actual sensation (afference). Then brain gives a false interpretation of a self-produced sensation and doesn’t cancel a defensive reaction. In this way, schizophrenics may tickle themselves accidently without knowing (Berrios, 1982). Taking into account earlier computational, neurophysiological and functional neuroimaging data Blakemore et al. (2000) specifically investigated the somatosensory cortex and the cerebellum when producing a self vs. externally tickling among schizophrenics, comparing to results of healthy experimental group. The results from FMRI study Blakemore et al. (2000) received confirmed predictions scientists had made. All experimental groups demonstrated increasing activity in the somatosensory cortex and the anterior cingulate gyrus when external tickling (Blakemore et al. 2000, 14). Yet schizophrenics were demonstrating abnormal awareness about a self-produced tickling too. The brain activity never decreased comparing to external tickling, therefore a self-produced tickling was experienced by schizophrenics with a greater intense than among a healthy experimental group (Blakemore et al., 2000). Blakemore et al. (2000) expressed a possibility that neural mechanisms associated with a forward model operate abnormally for schizophrenics, failing to cancel a defensive reaction on self-produced tickling. Inability to tickle oneself appears to be a normal reaction, meaning the brain’s working well, successfully predicting actual sensation through comparing efferent copy to afferent tactile sensation, cancelling a defensive reaction. Such cancellation relieves healthy humans from a constant self-stimulated squirming and laughing from accidental tickling. Meanwhile, ones suffering from tactile hallucinations (for example, schizophrenics) may tickle themselves accidentally, and falsely recognize actual sensation as externally produced danger. The reason is that damage schizophrenia causes to specific areas of the brain, which at the same time, appear to be areas healthy brain needs to compare afferent sensation and efferent copy, recognize tickling and cancel a defensive reaction, if self-produced. The nature of tickling now seems less mysterious due to a technical progress in magnetic resonance imaging. References Bays, P.M., Flanagan, J.R. and Wolpert, D.M. (2006). Attenuation of Self-Generated Tactile Sensations Is Predictive, not Postdictive. PLoS Biol , 4(2). http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.0040028 Berrios, G. (1982). Tactile hallucinations: conceptual and historical aspects. Journal of Neurology, Neurosurgery, and Psychiatry, n. 45, 285-293. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC491362/pdf/jnnpsyc00048-0011.pdf Blakemore, S. J., Wolpert, D. M. and Frith, C. D. (1999). The Cerebellum Contributes to Somatosensory Cortical Activity during Self-Produced Tactile Stimulation. NeuroImage, n. 10, 448-459. http://learning.eng.cam.ac.uk/pub/Public/Wolpert/Publications/BlaWolFri99.pdf Blakemore, S. J., Wolpert, D. M. and Frith, C. D. (2000). Why can’t you tickle yourself? NeuroReport, vol. 11, n. 11, 11-16. http://m.tutis.ca/NeuroMD/L9Touch/tickle.pdf Gross, L. (2006). Self-Generated Touch: A Neural Perspective. PLoS Biol, 4(2). http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.0040048 Harrison, P. J. (1999). The neuropathology of schizophrenia. A critical review of the data and their interpretation. Brain, n. 122, 593-624. http://brain.oxfordjournals.org/content/brain/122/4/593.full.pdf Iritani, S. (2013). What happens in the brain of schizophrenia patients?: An investigation from the viewpoint of neuropathology. Nagoya J. Med. Sci., n. 75, 11-28. http://www.med.nagoya-u.ac.jp/medlib/nagoya_j_med_sci/7512/02_Iritani.pdf Kotrla, K. J. and Weinberger, D, R. (1995). Brain imaging in schizophrenia. Annu. Rev. Med., n. 46, 113-122. http://www.unm.edu/~atlab/papers/others/Kotrla-Weinberger95.pdf Provine, R. R. (2004). Laughing, tickling, and evolution of speech and self. Current Directions in Psychological Science, vol. 13, n. 6, 215-218. www.researchgate.net/profile/Robert_Provine/publication/228699037_Laughing_tickling_and_the_evolution_of_speech_and_self/links/004635282667b4ea05000000.pdf Shenton et al. (2001). A review of MRI findings in schizophrenia. Schizophr Res, n. 49(1-2), 1-52. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2812015/pdf/nihms166514.pdf Wattendorf et al. (2013). Exploration of the Neural Correlates of Ticklish Laughter by Functional Magnetic Resonance Imaging. Cerebral Cortex. http://cercor.oxfordjournals.org/content/early/2012/04/15/cercor.bhs094.full.pdf+html Read More