Echopraxia: Difference between revisions
No edit summary |
No edit summary |
||
| Line 17: | Line 17: | ||
==Causes and Pathophysiology== |
==Causes and Pathophysiology== |
||
When learning a new action, the parietal lobe of the brain is responsible for directly observing the action and its spatial configuration. The premotor cortex of the frontal lobe encodes how that action is being conducted. A healthy brain can differentiate between seeing and doing. Damage to the frontal lobe could be responsible for combining the two and causing echopraxia. |
When learning a new action, the parietal lobe of the brain is responsible for directly observing the action and its spatial configuration. The premotor cortex of the frontal lobe encodes how that action is being conducted. A healthy brain can differentiate between seeing and doing. Damage to the frontal lobe could be responsible for combining the two and causing echopraxia. |
||
| ⚫ | Frontal lobe damage may affect the [[mirror neuron system]], a group of neurons in the F5 region of the brain.<ref name=pmid16540574>{{cite journal | author = Aziz-Zadeh, L., Koski, L., Mazziotta, J., Iacoboni, M. | title = Lateralization of the human mirror neuron system | journal = The Journal of Neuroscience | pages = 2964–70 | year = 2006 | pmid = 16540574}}</ref> These neurons fire action potentials when an action is observed, as well as when the action is being performed. They are primarily located in the [[inferior frontal gyrus]] and the inferior lobule of the [[parietal lobe]]. When an action is being observed or executed, the path begins at the occipital cortex, where the brain processes the visual input. The action then progresses to the [[superior temporal sulcus]], which plays an important role in perception of biological movements.<ref name=pmid22727762>{{cite journal | author = Vander Wyk, B. C., Voos, A., Pelphrey, K. A. | title = Action representation in the superior temporal sulcus in children and adults: an fMRI study | journal = Developmental Cognitive Neuroscience | volume = 2 | issue = 4 | pages = 409–16 | year = 2012 | pmid = 22727762}}</ref> The parietal cortex is then able to map the action. Finally, the action passes through the [[inferior frontal gyrus]] and ends at the primary cortex.<ref name=pmid16540574/> Damage to any of these components could cause echopraxia. |
||
[[File:Frontal lobe animation.gif|thumb|Frontal lobe animation]] |
[[File:Frontal lobe animation.gif|thumb|Frontal lobe animation]] |
||
| ⚫ | Frontal lobe damage may affect the [[mirror neuron system]], a group of neurons in the F5 region of the brain.<ref name=pmid16540574>{{cite journal | author = Aziz-Zadeh, L., Koski, L., Mazziotta, J., Iacoboni, M. | title = Lateralization of the human mirror neuron system | journal = The Journal of Neuroscience | pages = 2964–70 | year = 2006 | pmid = 16540574}}</ref> These neurons fire action potentials when an action is observed, as well as when the action is being performed. They are primarily located in the [[inferior frontal gyrus]] and the inferior lobule of the [[parietal lobe]]. When an action is being observed or executed, the path begins at the occipital cortex, where the brain processes the visual input. The action then progresses to the [[superior temporal sulcus]], which plays an important role in perception of biological movements.<ref name=pmid22727762>{{cite journal | author = Vander Wyk, B. C., Voos, A., Pelphrey, K. A. | title = Action representation in the superior temporal sulcus in children and adults: an fMRI study | journal = Developmental Cognitive Neuroscience | volume = 2 | issue = 4 | pages = 409–16 | year = 2012 | pmid = 22727762}}</ref> The parietal cortex is then able to map the action. Finally, the action passes through the [[inferior frontal gyrus]] and ends at the primary cortex.<ref name=pmid16540574/> Damage to any of these components could cause echopraxia. |
||
==Diagnosis== |
==Diagnosis== |
||
Revision as of 05:21, 28 November 2012
Echopraxia, a type of tic disorder, is the involuntary repetition of another person’s movements.[1] Rather than being an independent condition that can be diagnosed, echopraxia is a a disorder which often accompanies other neurological disorders with tic symptoms. Imitation and emulation of physical and verbal actions are critical to early development. However, when these behaviors become reactions rather than a means for learning, they are considered echophenomena. Echopraxia has been observed in patients with frontal lobe damage, but the exact cause is currently unknown. Patients with Gilles de la Tourette Syndrome, Schizophrenia, and Latah exhibit echopraxia; however, the reason for the link between echopraxia and these disorders is undetermined. Echopraxia is closely related to echolalia, the involuntary repetition of another person’s words or word phrases.[2] Although no medical treatments are available, psychological counseling may help patients who exhibit echophenomena in some cases. The effects of therapy vary depending on the initial cause of echopraxia.
Eponym
Echopraxia is sometimes grouped with echolalia, and referred to as echophenomena.
Etymology
Echopraxia, termed in 1904, is derived from Ancient Greek: "ekho" + "praxis", meaning action.[3]
Signs and Symptoms
Echopraxia is typically classified by the uncontrollable mirroring of an observed action. Imitated actions are not limited to a specific type. Imitation can be divided into two types: imitative learning and automatic imitation. Imitative learning occurs when a person consciously mimics an observed action in order to learn the mechanism behind that action and perform it himself or herself. According to Jean Piaget, this is essential to the sensorimotor stage.[4] Imitative learning continues to develop as a person ages, and is important as new skills are available to learn. For example, a person may learn to hit a nail with a hammer by watching his or her parent hammering nails. Automatic imitation on the other hand, occurs without a person's consent.[1] Babies begin copying movements soon after birth. It is not possible to diagnose echopraxia at this age, because it is difficult to differentiate between imitative learning and automatic imitation. This normally begins diminishing around the age of 3 years old. If the imitative behavior continues to be present, it is considered echopraxia. Automatic behavior is occasionally present in healthy adults. For instance, when a person observes someone yawning, he or she immediately does the same. These behaviors are not considered echopraxia.
Case Studies
Case #1: A 52-year old man was reported to his local Department of Forensic Medicine in 2007 for inappropriate behavior in public, including echopraxia and echolalia. He had been diagnosed with Tourette's Syndrome at the age of 20. He experienced involuntary screaming and cursing. He noted imitative behaviors such as undressing and hitting objects and people when these actions were observed. The man worked as a professional bus driver for 25 years, but was dismissed because of his behaviors. He was analyzed for a potential for criminal actions due to his condition.[5]
Case #2: A 55-year old man reported meaningless repetition of syllables and actions to the local neurology department. He had no medical history other than chronic alcohol abuse, but he did suffer head trauma 6 years prior to his admission. He did not lose consciousness or suffer aphasia at the time of the incident; however, he began to suffer seizures 7 months prior to admission to the clinic. Brain magnetic resonance imaging revealed frontal lobe damage, which was thought to be the cause of his echopraxia and echolalia.[2]
Causes and Pathophysiology
When learning a new action, the parietal lobe of the brain is responsible for directly observing the action and its spatial configuration. The premotor cortex of the frontal lobe encodes how that action is being conducted. A healthy brain can differentiate between seeing and doing. Damage to the frontal lobe could be responsible for combining the two and causing echopraxia.
Frontal lobe damage may affect the mirror neuron system, a group of neurons in the F5 region of the brain.[6] These neurons fire action potentials when an action is observed, as well as when the action is being performed. They are primarily located in the inferior frontal gyrus and the inferior lobule of the parietal lobe. When an action is being observed or executed, the path begins at the occipital cortex, where the brain processes the visual input. The action then progresses to the superior temporal sulcus, which plays an important role in perception of biological movements.[7] The parietal cortex is then able to map the action. Finally, the action passes through the inferior frontal gyrus and ends at the primary cortex.[6] Damage to any of these components could cause echopraxia.
Diagnosis
Echopraxia not diagnosed by formal testing. It is easier to distinguish in individuals over the age of 5 years old. Because younger children frequently imitate others' actions, it is difficult to define echopraxia in them. Older individuals easily notice echopraxia, because their behaviors in relation to prior behaviors can be differentiated. They report feeling an uncontrollable urge to perform an action after seeing it being performed.
Treatment
Therapeutic Treatment
Therapeutic treatment has an effect on general tic disorders in some cases. If repairable problems contribute to the cause of the tic, such as family, school, or health problems, therapeutic treatment is more likely to be successful. There is evidence which supports a problem being resolved and the tic diminishing.[1]
Stress-induced Tic Suppression
There have been instances reported where severe stress suppresses the tic. For example, Oliver Sacks has written about a surgeon and amateur pilot with severe Tourette Syndrome who was successful because his tics disappeared in the operating room and on a plane.[8] However, this is not an effective means of treating tics as they re-appear in non-stressful situations.
Echopraxia in Neurological Disorders
Echophenomena are frequently observed in organic disorders, which are described as affecting the physiology or structure of an organ.[6] Patients with these disorders typically experience increased sensitivity to external stimuli, which makes them more susceptible to acquiring tics. The exact reason for the link between echopraxia and the following neurological disorders is unknown. Possible mechanisms, as follows, have been suggested.
Gilles de la Tourette Syndrome
Tourette Syndrome, the most most severely expressed tic disorder, is characterized by multiple motor tics and at least one vocal tic.[5] Echophenomena is expressed in 21-46% of patients with Tourette Syndrome.[6] These patients typically experience increased sensitivity to external stimuli, which makes them more susceptible to acquiring tics.[9]
Schizophrenia
Approximately 30% of patients with Schizophrenia exhibit catatonic Schrizphrenia, which is characterized by echopraxia and echolalia. Some studies have shown that Schizophrenia is associated with decreased inhibition and increased arousal in the nervous system.[6] A proposed mechanism for echopraxia in Schizophrenia is related to disinhibition, arousal, and the mirror neuron system. Dysfunction of the anterior cingulate cortex, where cognitive and motor processes converge, is common in patients with Schizophrenia. This dysfunction could cause movements to pass throughthe inferior frontal gyrus and automatically be repeated.[6]
Latah
Echopraxia is a common characteristic in individuals affected with Latah, a condition in South Asia triggered by the startle reflex. Patients with Latah perform exaggerated actions when startled.[10]
See also
External links
References
- ^ a b c Pridmore, S., Brüne, M., Ahmadi, J., Dale, J. (2008). "Echopraxia in schizophrenia: possible mechanisms". The Royal Australian and New Zealand College of Psychiatrists: 565–71. PMID 18612859.
{{cite journal}}: CS1 maint: multiple names: authors list (link) Cite error: The named reference "pmid18612859" was defined multiple times with different content (see the help page). - ^ a b Cho, Y., Han, S., Song, S., Lee, B., Heo, K. (2009). "Palilalia, echolalia, and echopraxia-palipraxia as ictal manifestations in a patient with left frontal lobe epilepsy". Epilepsia: 1616–19. PMID 19175395.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ "Online Etymology Dictionary".
- ^ Cook, R., Press, C., Dickinson, A., Heyes, C. (2010). "Acquisition of automatic imitation is sensitive to sensorimotor contingency". Journal of Experimental Psychology: 840–52. PMID 20695703.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ a b Gullucayir, S., Asirdizer, M., Yavuz, S., Zeyfeoglu, Y., Ulucay, T. (2010). "Criminal and Legal Responsibilities in Tourette's Syndrome". Israel Journal of Psychiatry and Related Sciences. 46 (3): 221–5. PMID 20039524.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ a b c d e f Aziz-Zadeh, L., Koski, L., Mazziotta, J., Iacoboni, M. (2006). "Lateralization of the human mirror neuron system". The Journal of Neuroscience: 2964–70. PMID 16540574.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Vander Wyk, B. C., Voos, A., Pelphrey, K. A. (2012). "Action representation in the superior temporal sulcus in children and adults: an fMRI study". Developmental Cognitive Neuroscience. 2 (4): 409–16. PMID 22727762.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Sacks, Oliver (1995). An Anthropologist on Mars.
- ^ Jonas, M., Thomalla, G., Biermann-Ruben, K., Siebner, H. R., Müller-Vahl, K., Baümer, T., Gerloff, C., Schnitzler, A., Orth, M., Münchao, A. (2010). "Imitation in patients with Gilles de la Tourette syndrome--a behavioral study". Movement Disorders. 25 (8): 991–9. PMID 20535824.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Tanner, C. M., Chamberland, J. (2001). "Latah in Jakarta, Indonesia". Movement Disorders. 16 (3): 526–9. PMID 11391750.
{{cite journal}}: CS1 maint: multiple names: authors list (link)