Int. J., Vol. x, No. x, 200x 1 Biometry of electromechanical and artificial neural network models of arm gait in Huntington’s disease patient O.O.E. Ajibola, V.O.S. Olunloyo and O. Ibidapo-Obe Department of Systems Engineering, University of Lagos Akoka, Yaba, Lagos, 234(01) Nigeria. ABSTRACT In 1837, George Huntington described Huntington’s disease (HD) as an heirloom which had unleashed untold suffering on people in the dim past. Huntington’s disease is a neurodegenerative disease which has been traced to mutant alleles in the short arm of chromosome 4. Since the etiology of the disease is not clearly understood, the question of cure is not addressable at the moment but management of HD presentations is addressable. To this end, this paper is directed towards management of chorea, a major presentation of HD. Earlier attempts made by our study group have given birth to two distinct models designed to facilitate an electroconvulsive therapy for the ailment. In this work however, we have done a comparative analysis of both models in order to promote a better understanding of HD, and concluded that even though the electromechanical model may not completely capture the gait disorder, both models have the capability of forming a strong basis for the design of a management model for the phenomenon. Keywords: chorea, Huntington’s disease, electromechanical model, artificial neural network model, arm gait, graphical analysis 1. INTRODUCTION A major presentation of Huntington’s disease (HD) is the choreiform movements called chorea that forms a major symptom of the disease. Although there are other symptoms of HD, existing literature pointed in the direction of chorea whenever a common denominator symptom is being considered. Unlike other presentations of the disease which may be detected only on close observation, a glance at HD patient reveals chorea, a devastating presentation that constitute a debacle to happiness in the life of the patient. To this end, we have directed our effort in this paper towards the promotion of a better understanding of these unwanted movements that have constituted great barrier to day to day activities of HD sufferer. In the past, several works have been done in the area of modeling of the dynamics of human linkages. For instance, in the works of Amirabdollahian, F. et al (2002), Flash, T. et al (2001), Flash, T. and Hogan, N. (1985), Rai, J.K. et al (2009), and Zhang, Y. (2009), motion related analyses were cleverly done with different sets of authors choosing a unique path of the body of the study of biomechanics with special emphasis on human linkages. Although these authors considered motions without recur to their causes, they have made no small contributions to the study of motion-related diseases especially the neurodegenerative diseases such as the Parkinson’s disease and the Huntington’s disease. Banaie, M. et al (2008), described the gait in Huntington’s disease by a schematic model which did a chronological analysis of post-synaptic potentiation that culminates in choreiform movements, the form of gait in Huntington’s disease. In Yashar, S. et al (2007), both the inhibitory and excitatory potentiation were captured in Hill functions using varying level of GABAergic precipitations in their analyses. In this paper, we have only considered the two models namely: electromechanical model by Ibidapo-Obe, O. et al (2010) and artificial neural network simulation model by Ajibola, O.O.E. et al (2010) and the comparison of the two models were done using statistical tool. 2. ELECTROMECHANICAL MODEL ANN SIMULATION MODEL VERSUS In Ibidapo-Obe, O. et al (2010), the electromechanical model for the arm gait in HD was proposed. The model was based on the interactions between both the inhibitory and the excitatory postsynaptic potentials in the postsynaptic membrane of HD sufferer. According to the paper, the process which leads to the precipitation of jerk in HD began with the release of acetylcholine (Ach) into the synaptic cleft as a result of a nerve action potential that invades the presynaptic terminal. The Ach diffuses across the synaptic cleft and combines with receptors on the postjunctional membrane. The resultant increase in Na + and K+ permeabilities depolarizes the postsynaptic membrane triggering an action potential in the muscle cell which produces an impulse in the form of muscular contraction in the muscle cell. Invariably, the jerk produced depends on the electromotive force (emf) produced by the EPSP. The rate of change in emf is a function of the magnitude of jerk produced among other factors, Ibidapo-Obe, O. et al (2010). And the governing equation for the gait (i.e. jerk) is defined by: 2 2 d3y 1 d 3 x RT C o exp E ln dt 2 3 dt 3 nF C i C dt (1) yt t xt (2) Subject to: heat sources and pulses in the theory of heat conduction, to mention but a few. At this juncture, we introduce the point action. Let us imagine that a sudden excitation is administered to a system. Suppose the excitation is denoted by d x which has a a nonzero value over the infinitesimal interval I * a , a , but is zero otherwise. The total impulse impact to the system is thus defined by: Where Ci and Co are the concentration of ions both inside and outside the neuron; T is the absolute temperature; n is the charge on the ion; the Faraday constant, F is the magnitude of the charge per mole of electrons; R is the universal gas constant. The graph of the electromechanical equation (1) is a parabolic smooth curve which is a derivation of the experimental evidential model of jerk as presented by Flash and Hogan in their paper entitled “The coordinate of arm movements: an experimentally confirmed mathematical model”, Flash and Hogan, (2005), and corroborated by Chuanasa, J. et al, (2010). Figure 1 is the graphical analyses of equation (1) as contained in O. Ibidapo-Obe et al for three distinct patients with slightly different thresholds. I aa x a dx 1 x x a, , 0, 1 (3) The value of I is a measure of the strength of the sudden excitation. Defining the integral of any continuous and bounded function f in terms of the unit impulse function and applying the mean value theorem of the integral calculus, then; x f xdx f (4) defines the excitation graphed by f for every point a , a , Ajibola, O.O.E. (2008). Figure 2: The graph of Dirac delta function I t . Figure 1: The graphical analysis of arm gait in HD patient Curled from: http://en.wikipedia.org/wiki/File: Dirac_function_approximation.gif In physics and in engineering, mathematical consideration of such a staccato motion as jerk inevitably deal with the notion of "point actions", that is, actions which are highly localized in space and/or time. These include point forces and couples in solid mechanics, impulsive forces in rigid body dynamics, point masses in gravitational field theory, point charges and multi-poles in electrostatics, and point However, jerk is the total impulse impart produced by the cumulative excitatory post-synaptic potentiation, and potentiated by the failure of the inhibitory post-synaptic potentiation track in the body system thus exacerbating a point action that is described by the Dirac delta function and by extension, by equation (4). The implication of equation (4) is that the function f is an enhancement of the Dirac delta function in equation (3) over the domain D t 0 t , t 0 t of its definition. It suffices to claim therefore that the jerk takes the shape of the points traced by Artificial Neural Networks (ANN) is an information processing paradigm that is inspired by the way biological nervous systems, such as the brain, process information. An ANN is composed of a large number of highly interconnected parallel processing elements called neurons. The neurons work in unison to solve specific class of problems through repetitive learning process, modifying the inference rules following arrival of new information thereby adjusting to the synaptic connections that exist between the neurons much like the biological systems. Hypothetically, a neural network is made up of very simple computational units (or neurodes). An artificial neuron is an eclectic simulation of biological neuron, and it consists of its own dendrites, synapses, cell body and axon terminals. It receives stimulation from nearby cells, or from its environment, and generates a modified nerve signal, Ajibola, O.O.E. et al (2010). The architectural system underlying human cognitive performance is functionally modular, Long, D.L. et al (1998). An ANN system is composed of a number of dedicated processing components each of which contains knowledge that is specific to the operations it performs and this knowledge is available only to the component responsible for these operations. In addition, the partial results of operations that are specific to one component are unavailable to other components. An ANN has remarkable ability to derive meaning from complicated or imprecise data used to extract patterns, and detect trends that are too complicated to be noticed by either human or known computer techniques. In the words of Long, D.L. et al (1998), a trained ANN can be thought of as an “expert” that can provide projections when given new situations of interest using the outcomes from primary information to provide adequate answer to “if what” questions that may arise from the new situations in the category of information it has been given to analyse. Other advantages of ANN include the ability to learn how to do tasks based on the data given for training or initial experience. An ANN can create its own representation of the information it receives during learning time, organise same and carry out computations in parallel, using special hardware devices designed and manufactured to take advantage of this capability. Even though partial destruction of a network may lead to the corresponding degradation of performance, some network capabilities may be retained even with major network damage. As a result of the aforementioned advantages of ANN, the arm gait in Huntington’s disease patient was captured in an Artificial Neural Network (ANN) simulation model, Ajibola, O.O.E. et al (2010). In the paper titled: Artificial neural network simulation model of arm gait in Huntington’s disease patient, the jerk was simulated based on the primary data used for the electromagnetic model for the same presentation so as to establish leverage between the two models. The learning rate of 0.0004 was used to train the ANN with an error tolerance of 0.0002. The number of cycles used for its training is 500 while the ANN architecture of 17 18 1 was used. The artificial neural network analysis was done in computer C++ programming language environment. To ascertain high efficiency, the C++ program from which the results for the ANN training procedure were obtained was based both on the source and derived data from where epoch values of Table 1 were obtained. However, Figure 3 represents the graph of the deprocessed data for the ANN simulation model, Ajibola, O.O.E, (2010). Figure 4: The graph of ANN Analysis of Arm gait of HD Patient GRAPH OF CRISP MODEL VS ANN MODEL 4 3.5 EXCITATORY POST-SYNAPTIC POTENTIAL BUILD-UP the Dirac delta function t as described by Figure 2 as t 0 . But a jerk requires a build-up of excitatory postsynaptic potentiation (EPSP) to a threshold level after which excessive EPSP produced results in the staccato nature of the gait (i.e. jerk) much like orgasm is attained during sexual intercourse, after which the process terminates abruptly. To that extent, the Dirac delta function of Figure (2) and by extension Figure (1), and consequently equation (1) failed to capture the jerk in the arm of HD patient. The Dirac function may only approximate the jerk as a 0 . It is the recognition of this fact that exacerbated our exploit of the Artificial Neural Network paradigm. 3 2.5 2 CRISP ANN 1.5 1 0.5 0 1 4 7 10 13 16 19 22 25 28 31 34 -0.5 TIME IN MSEC 3. STOCHASTIC ANALYSIS OF BOTH MODELS Of important in this work is the comparative analysis of the mathematical models we have developed for the arm gait in HD patient in our earlier papers namely: the electromechanical model from “On equation of arm gait of Huntington’s disease patient”, Ibidapo-Obe, O. et al (2010) and ANN model from “artificial neural network simulation of arm gait of Huntington’s disease patient”, Ajibola, O.O.E. et al (2010). A veritable tool for measuring the degree of agreement between two set of data arising from scientific experiments reside entirely in a body of knowledge called statistics. In analyzing our models, we have adopted statistical tools to establish the relationship between the two models in order that we may make an enduring assertion as regards their relationship with the choreiform movements that characterizes HD. In this paper, we have applied regression analysis, using a measure of correlation of the graph of the two models in our attempt to summarize the relationship between the two mathematical models. And where applicable, Microsoft excel statistical tool was applied for numerical computations to facilitate our argument. The summary of data which serve as the basis for our analysis as contained in the paper by Ajibola, O.O.E et al (2010) and augmented with the data for our regression line (in red) is presented in Table 1. Figure 5: The Scatter diagram/Regression line for the data from both models Table 1: Data from Electromechanical and ANN models with the Regression Line EPOCH 0 10 20 30 40 50 60 70 80 90 100 110 120 130 140 150 160 170 180 190 200 210 220 230 240 250 260 270 280 290 300 310 320 330 CRISP 0 0.154582 0.308486 0.461202 0.612217 0.761006 0.907089 1.049966 1.189172 1.324243 1.45474 1.580243 1.700331 1.814628 1.922773 2.024421 2.119241 2.206961 2.287297 2.360008 2.424899 2.481789 2.530528 2.571012 2.603179 2.626985 2.64243 2.649559 2.648462 2.639275 2.622163 2.597351 2.565126 2.525803 ANN 0 -0.06304 -0.05758 0.021569 0.136378 0.275615 0.435387 0.584056 0.735779 0.891097 1.047544 1.204307 1.357654 1.508385 1.654963 1.795944 1.930563 2.058157 2.177237 2.287022 2.386293 2.473638 2.548048 2.607585 2.650445 2.67428 2.67565 2.649545 2.590686 2.709225 3.239446 3.34505 3.363036 3.223094 Y 0 0.154581 0.308484 0.461200 0.612214 0.761002 0.907084 1.049960 1.189166 1.324236 1.454732 1.580235 1.700322 1.814618 1.922763 2.024410 2.119230 2.206949 2.287285 2.359995 2.424886 2.481776 2.530515 2.570998 2.603165 2.626971 2.642416 2.649545 2.654629 2.697206 2.776512 2.891504 3.040851 3.223094 And the graphical analysis is as presented in Figure 5: In Figure 5, both the scatter diagram and the regression line have been presented as line diagrams to facilitate easy comparison. The freehand method was used for the regression line since it is adequate for the purpose of this analysis. The regression line is completely described by its slope and the intercept on the y-axis. For ease of analysis the line has been partitioned into two segments labelled AB and BC. The segment AB with positive slope is an indication that there is an agreement between the two models while the segment BC has negative slope representing a dispersal of the two graphs from each other. The determination of the level of agreement or otherwise between two sets of data is a statistical measure of their correlation coefficient defined by: Corr X , Y where Cov X , Y Cov X , Y s X sY (5) iN 1 X i X Yi Y N 1 (6) Using the Microsoft Excel Statistical tool, the correlation coefficient of the two graphs along segment AB of Figure 5 is CorrAB X , Y 0.989329 this is a confirmation of a strong agreement between the two models. Relating this to the post-synaptic potentiation that produces the arm gait, this part of the graphs, Figure 6, represents the excitatory precipitation of jerk at the level of threshold and our statistical analysis shows that the two models both represent this phenomenon adequately within the interval under consideration (i.e. to the point of threshold). This is evident from Figure 6 where the behavior of the two models is graphed from the point of initiation of the excitatory process to the threshold of the jerk. Figure 6: The excitatory precipitation at the level threshold of jerk of Any point above the threshold line, especially after point B, will contribute to the gait in one way or the other whereas every point below the threshold line will not. It is therefore clear from the figure that one of the models (i.e. the ANN model) completely captured the phenomenon as it reflects the jerk. 4. However, a correlation coefficient CorrBC X , Y 0.75494 indicates that there is a strong disagreement between the two graphs from point B. This may mean one of the following: None of the two graphs captured the arm gait phenomenon One of the two graphs captured the arm gait phenomenon The instrument used in this analysis can be found in Figure 7. The blue curve (series 1) is the graph of the electromechanical model, the red (series 2) of ANN simulation model while the green straight line (series 3) stands for the threshold. Figure 7: Relating Both Models with Arm Gait Phenomenon DISCUSSION A survey of opinions from patients of Huntington’s disease is revealing. The presence of depression in the list of the symptoms of HD is more of a product of the discovery by patients that they belong to HD family. And one of the causes of the patients’ withdrawal from the public is the presence of the choreiform movements which distinguishes the patients among their friends and colleagues. In this work we have forged ahead to do a statistical analysis of both methods we proposed earlier namely, the electromechanical model and the artificial neural network simulation model all in our attempt to promote a better understanding of chorea, a major presentation of this devastating ailment. Clinical consideration of biomechanics of HD patients opined that the GABAergic pathway in the affected patients might have been malfunctioning causing inadequacy in the supply of inhibitory neurotransmitters that is required to support the inhibitory post-synaptic potentiation (IPSP) needed to match the excitatory post synaptic potentiation (EPSP) which pathway is assume to perform at optimum level. It is believed that it is not impossible that the GABAergic pathways in HD patients might have been constricted much like a near rupture rusted narrow water iron pipe at advanced stage of the disease causing the dopaminergic pathways to produce excessive EPSP thus precipitating jerk at will. However, the graphical analysis in Figure 7 revealed that although the electromechanical model did not capture the jerk phenomenon completely, the strong agreement between the two graphs shows that both graphs provide adequate representation of the process of chemical build-up that precipitates the staccato movement (the jerk) to the point of threshold and therefore both models are adequate to propose a model for the management of the phenomenon since what we seek to eliminate is the jerk. It is therefore enough to introduce a damper that neutralizes the excitatory neurotransmitter produce in excess of IPSP at the threshold of the jerk. It is believed that this work has contributed to a better understanding of chorea and as such can serve as a basis which is strong enough to attempt to propose a management model for the phenomenon with any of the two models as pedestal. 5. CONCLUSION AND FUTURE WORK The paper is a major leap from our preliminary exploration in the modeling of chorea that constitutes major impediment to day-to-day activities of HD patient. In this paper we have attempted to provide a strong pedestal for proposing a dependable model for the management of the physiological presentation of HD that has debased the personality of the patient by carrying out a comparative analysis of the electromechanical model and the artificial neural network model using statistical tool. The essence of this paper is to determine the strength of each of the models when used as a basis for proposing a model for the electroconvulsive therapy for the arm gait phenomenon in HD. In the near future we hope to design a model for the management of the physiological presentation called chorea based on the electromechanical model and subsequently, the artificial neural network model. REFERENCES Ajibola, O.O.E, (2008); A model for the management of neurodegenerative diseases: the case of Huntington’s disease. A thesis submitted to the School of Postgraduate Studies, University of Lagos, Lagos, Nigeria, for the award of PhD in Systems Engineering. Ajibola, O.O.E., Olunloyo, V.O.S. and Ibidapo-Obe, O. (2011); Artificial neural network simulation of arm gait in Huntington’s disease Patient. Int. J. of Biomechatronics and Biomedical Robotics. Vol. 1, No. 3, pp. 133-140. Albright, S.C., Winston, W.L. and Zappe, C. (2006); Data analysis and decision making with Microsoft Excel. Thompson South-Western, USA. Amirabdollahian, F., Loureiro, R and Harwin, W.; A case study on the effects of haptic interface on human arm movements with implications for rehabilitation robotics. Department of Cybernetics, Reading University, Reading RG6 6AY. Banaie, M., Sarbaz, Y., Gharibzadeh, S. and Towhidkhah, F. (2008); Huntington’s disease: Modeling the gait disorder and proposing novel treatment. Journal of Theoretical Biology 254: 361-367. Chuanasa, J. and Songschon, S. (2010); Arm movement recorder. Energy Researching Journal. 1(2): pp. 126-130. De Tommaso, M., De Carlo. F., Difruscolo, O., Massafra, R, Sciruicchio, V. and Bellotti, R (2003); Detection of subclinical brain electrical activity changes in Huntington’s disease using artificial neural networks. Clinical Neurophysiology. 114: pp. 1237-1245. Dingwell, J.B., Mah, C.D. and Mussa-Ivaldi (2004); Experimentally confirmed mathematical model for human control of a non-rigid object. Journal of Neurophysiology 91: 1158-1170. Flash, T, and Hogan, N. (1985); The coordinate of arm movements: an experimentally confirmed mathematical model. Journal of Neuroscience 5: 1688-1703. Huntington, G. (2003); On chorea. Journal of Neuropsychiatry Clinical Neuroscience. 15: 109-112. Originally appeared in The Medical and Surgical Reporter; A Weekly Journal (Pniladelphia: S.W. Butler) vol. 26, no. 15 (April 13, 1872) pp. 317-321. Ibidapo-Obe, O., Ajibola, O.O.E. and Olunloyo, V.O.S. (2010); On equation of arm gait of Huntington’s disease patient. International Journal of Biometry. Vol. 2, No. 1 pp.53-70. Lanska, D.J. (2000); George Huntington (1850-1916) and Hereditary Chorea. Journal of the History of the Neurosciences. Vol. 9, No. 1, pp. 76-89(14). Long, D.L. Parks, R.W. and Levine, D.S. (1998); An introduction to neural network modeling, merits, limitations, and controversies. Fundamentals of Neural Network Modeling: Neurophysiology and Cognitive Neuroscience. The MIT Press, London, England. Pp. 332. Rai, J.K., Tewari, R.P. and Chandra, D. (2009); Hybrid control strategy for robotic leg prosthesis using artificial gait synthesis. International Journal of Biomechatronics and Biomedical Robotics. 1(1): pp. 4450. Sarbaz, Y., Banaie, M. and Gharibzadeh, S. (2007); A computational model for the Huntington’s disease. Medical Hypotheses 68: 1154-1158. Shi-Hua, L., and Xiao-Juang, L. (2004); Huntingtin and its role in neuronal degeneration. The Neuroscientist 10:467-475. Smith, M.A. and Shadmehr, R. (2005); Intact ability to learn internal models of arm dynamics in Huntington’s disease but not cerebellar degeneration. Journal of Neurophysiology 93: 2809-2821. Wolpert, D.M., Ghahramani, Z., and Jordan, M.I. (1995); An arm trajectories planned in kinematic or dynamic coordinates? An adaptation study. Experimental Brain Research. 103(3): pp. 460470. Yashar, S, Banaie, M., Gharibzadeh, S. (2007); A computational model for the Huntington’s disease. Medical Hypothesis. Vol. 68: pp. 11541158. Zhang, Y. (2009); Estimation of upper limb muscle forces by biomechanical simulation model. International Journal of Biomechatronics and Biomedical Robotics. 1(1): pp. 17-20.
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