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Discussion forum

There is more than imitation Kenneth M. Heilman Department of Neurology, University of Florida College of Medicine, and The Malcom Randall Veteran’s Affairs Medical Center, Gainesville, FL, USA

Both Derek Denny-Brown and Norman Geschwind were strongly interested in apraxic disorders of the upper limb and having been trained by both of these leaders during my neurology residency I also became interested in these disorders. Shortly after completing my training I joined the faculty at the University of Florida and was asked to give a lecture at a course. I decided to speak about limb apraxia. After I was introduced and the topic of my lecture was announced two physicians who were sitting in front of the auditorium got up from their seats and one said to the other “Apraxia? Did you ever have a patient complain about apraxia?” The other physician said, “No, but I think there are one or two neurologists who do research on this. Let’s get something to drink”. Then these two physicians left the lecture hall. Unfortunately, these physicians did not get the opportunity to learn that the upper limb apraxic disorders are common and terribly disabling. Apraxic disorders can be caused by a variety of different diseases and are commonly associated with disorders including stroke, Alzheimer’s disease, and Parkinson’s disease. Fortunately, interest and research in these disorders have increased. For example, when I searched PubMed for papers published under the heading of “limb apraxia” during the decade between 1970 and 1979 there were a total of 15 papers listed. However, in just the year of 2013 there were more than 30 papers listed. Hopefully, Goldenberg’s clearly written book “Apraxia” will allow more clinicians to better recognize and understand these disorders as well as stimulate more research. Good papers and books, however, also stimulate controversy. In the pre´cis Goldenberg wrote, “Chapters are devoted to core manifestations of apraxia, that is, imitation of gestures, use of single tools and objects and production of communicative gestures on command”. Goldenberg developed and has strongly promoted assessing patients with a test

of gesture imitation (Goldenberg, 1995). If patients have a degradation of what Liepmann called movement formula (Liepmann, 1920) and we call visuokinesthetic movement representations (VKMR) (Heilman & Rothi, 2012), when tested for apraxia by using imitation or viewing tools they are provided with visual cues that may decrease the sensitivity of these tests for detecting apraxia. In addition, having patients perform transitive movements is a more sensitive test than having them perform intransitive or communicative gestures. Thus, the most sensitive test for ideomotor apraxia is having patients pantomime transitive actions to command. When patients attempt to imitate a gesture, they must perform a movement analyses on this visual input, which may be mediated by visual association areas such as MT (V5) and this decoded information must be able to access the patient’s VKMR. Thus, patients with impaired visual movement analysis or impaired access to the VKMR may be impaired at imitation but not be impaired when pantomiming to command, a task that does not require visual analysis. For example, Ochipa et al. (Ochipa, Rothi, & Heilman, 1994) reported a patient who could not correctly imitate a gesture but performed normally to command. In addition patients may have an impaired ability to access the VKMR, but be able to recognize a hand-arm posture as an object and thus be able to a name a viewed pantomime, but be unable to imitate the movements since they have a selective deficit at accessing VKMR. There may also be patients who have problems pantomiming in response to viewed objects such as toolimplements, because they may have a degradation of object recognition units or an inability of these object recognition unit representations from accessing the VKMR. Thus, when assessing patients for apraxia, the patients should be tested by having them pantomime to commands, having them imitate, as well as having them pantomime in response to seeing

E-mail address: [email protected]. http://dx.doi.org/10.1016/j.cortex.2014.01.022 0010-9452/ª 2014 Published by Elsevier Ltd.

Please cite this article in press as: Heilman, K. M., There is more than imitation, Cortex (2014), http://dx.doi.org/10.1016/ j.cortex.2014.01.022

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objects upon which tool work (e.g., nail), seeing the actual tools and even actually holding tools. In addition, to learning if patients have a degradation of the their VPMRs, as well as the sensory systems that access these movement representation, versus a deficit in these patients’ ability to implement-motor program despite having intact VPMR representations, patients should also be tested for their ability to perceive correctly performed from incorrectly performed transitive paradigms (Heilman, Rothi, & Valenstein, 1982). When training with Norman Geschwind, he would ask me if a patient was apraxic. I found that sometimes when I thought a patient made an apraxic error he thought the pantomime was normal and vice versa. Thus several decades ago we studied the types of errors made by patients with ideomotor apraxia (Poizner, Mack, Verfaellie, Rothi, & Heilman, 1990). We noted that patients with ideomotor apraxia primarily make three major types of errors: 1) postural errors where patients make an incorrect posture or internal configuration of their hand and arm; 2) improper joint movements (egocentric movement errors) and 3) allocentric spatial errors, such that the action is not correctly directed to the real or imaginary object upon which the tool would interact. Just as the visual system can be dichotomized into ‘where’ and ‘what’ systems, perhaps there are also independent representations for the elements of a transitive gesture. For example, since posture depends on the type of tool that is being held, the representational network that programs posture may receive more information from the ventral ‘what’ visual association areas and the representational network that programs the allocentric direction of the movements may receive more information from the dorsal ‘where’ visual stream. In addition, whereas we have previously demonstrated that patients with different diseases may make different forms of apraxic errors (Merians et al., 1999), the relationships between different diseases and error types should also be further investigated. In his book, Goldenberg only briefly mentions limb-kinetic apraxia (LKA), a loss of deftness with a decrease in the ability to correctly perform independent but coordinated finger movements (Heilman & Rothi, 2012). In 1975, I reported that when patients with a left hemisphere stroke and apraxia performed a tapping test with their left hand, these patients performance was impaired (Heilman, 1975). The tapping test primarily assesses patients’ ability to rapidly perform flexion and extension movements of the forefinger. Although these patients’ left hemisphere lesions appeared to impair left hand deftness, a test that assesses the ability of patients to perform precise, but independent and coordinated finger movements of several fingers may be a more sensitive test. Thus, using a coin rotation test, we demonstrated that not only is the right hand of right handed people more deft than the left, but that lesions of the left hemisphere are more likely to induce a loss of deftness of left hand (LKA) than vice versa (Hanna-Pladdy, Mendoza, Apostolos, & Heilman, 2002). While the premotor cortex (Brodmann’s area 6) may be important in the programing the firing pattern of the neurons in the motor cortex and dysfunction of this area may induce LKA, Lawrence and

Kuypers (Lawrence & Kuypers, 1968) demonstrated that damage of the corticospinal pathway in monkeys causes a loss of the ability to perform independent deft finger movements. Whereas the corticospinal system has both contralateral and ipsilateral projections the ipsilateral projection are more often directed to the motor neurons that control proximal than distal movements suggesting that the left hemisphere dominance for controlling deftness even of the left hand may be mediated by interhemispheric connectivity. This postulate was supported by the recent observation. Recently, we reported a man who post-operatively was found to have a lesion of the mesial portion of his corpus callosum and an assessment of praxis revealed that he had both an LKA and ideomotor apraxia of his left but not his right hand (Acosta, Bennett, & Heilman, 2013). There are many diseases that cause a loss of hand-finger deftness including Parkinson’s disease, strokes and corticobasal degeneration. Since this loss of deftness may even impair a patient’s ability to perform activities of daily living such as buttoning garments research that is directed to learning how to rehabilitate this condition is imperative.

references

Acosta, L. M., Bennett, J. A., & Heilman, K. M. (2013 Aug 23). Callosal disconnection and limb-kinetic apraxia. Neurocase (Epub ahead of print). PMID: 23972140. Goldenberg, G. (1995). Imitating gestures and manipulating a mannikin e the representation of the human body in ideomotor apraxia. Neuropsychologia, 33(1), 63e72. Hanna-Pladdy, B., Mendoza, J. E., Apostolos, G. T., & Heilman, K. M. (2002 Nov). Lateralised motor control: hemispheric damage and the loss of deftness. Journal of Neurology Neurosurgery and Psychiatry, 73(5), 574e577. Heilman, K. M. (1975 Sep). A tapping test in apraxia. Cortex, 11(3), 259e263. Heilman, K. M., & Rothi, L. J. G. (2012). Apraxia. In K. M. Heilman, & E. Valenstein (Eds.), Clinical neuropsychology (4th ed.) (pp. 214e237). New York: Oxford University Press. Heilman, K. M., Rothi, L. J., & Valenstein, E. (1982 Apr). Two forms of ideomotor apraxia. Neurology, 32(4), 342e346. Lawrence, D. G., & Kuypers, H. G. J. M. (1968). The functional organization of the motor system in the monkey. Brain, 91, 1e36. Liepmann, H. (1920). Apraxia. Ergebnisse Geschichte der Medizin, 1, 516e543. Merians, A. S., Clark, M., Poizner, H., Jacobs, D. H., Adair, J. C., Macauley, B., et al. (1999 Jul). Apraxia differs in corticobasal degeneration and left-parietal stroke: a case study. Brain and Cognition, 40(2), 314e335. Ochipa, C., Rothi, L. J., & Heilman, K. M. (1994). Conduction apraxia. Journal of Neurology Neurosurgery and Psychiatry, 10, 1241e1244. Poizner, H., Mack, L., Verfaellie, M., Rothi, L. J. G., & Heilman, K. M. (1990). Three dimensional computer graphic analysis of apraxia. Brain, 113, 85e101.

Received 27 January 2014 Accepted 29 January 2014

Please cite this article in press as: Heilman, K. M., There is more than imitation, Cortex (2014), http://dx.doi.org/10.1016/ j.cortex.2014.01.022

There is more than imitation.

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