Time-Dispersive Eects in the J.

Gonzalos Research on Cerebral Dynamics

Isabel Gonzalo1 and Miguel A. Porras2
Departamento de Optica. Facultad de Ciencias F sicas. Universidad Complutense de Madrid. Ciudad Universitaria s/n. 28040-Madrid. Spain igonzalo@eucmax.sim.ucm.es 2 Departamento de F sica Aplicada. ETSIM. Universidad Politcnica de Madrid. e Rios Rosas 21. 28003-Madrid. Spain
1

Abstract. In the present work, certain aspects, restricted to the visual system, of the J. Gonzalos research, are interpreted according to a simple linear theory of time-dispersion applied to the dynamic cerebral system, characterized by its excitability and its reaction velocity.

Introduction

As exposed in previous work [8]-[12], J. Gonzalo characterized what he termed the central syndrome associated to a unilateral lesion in the parieto-occipital cortex, equidistant from the visual, tactile and auditory projection areas (central lesion). The projections paths are untouched while rather unspecic central cerebral mass is lost, producing a decit in the cerebral excitability. In the central syndrome all sensory systems are involved, in all their functions and with symmetric bilaterality. As was explained previously [8]-[11], the decit in the excitability produces a diminution in the reaction (response) velocity of the cerebral system leading to an allometric dissociation or desynchronization of sensory qualities (normally united in perception) according to their excitability demands. Concerning the visual system, for instance, when the illumination of a vertical white arrow diminishes, the perception of the arrow is at rst upright and well-dened; next the arrow is perceived to be more and more rotated, becoming at the same time smaller, and losing its form and colors in a well dened order. The sensorial perception thus splits into components; several functions appear, as the direction function which gives place to the striking phenomenon of the inverted vision: about 160 degrees in patient M under low stimulation (systematically studied for the rst time by J. Gonzalo [7,8]). The importance of this type of involvement (central syndrome) lies in the fact that the change in the nervous excitability can reveal the dynamics of the cerebral cortex, the organization of the sensorial structures and a continuity from the simplest sensorial function to the more complex ones, according to the nervous excitability and following a physiological order. The cerebral system follows the same organization plan and the same physiological laws as in the normal case but in a smaller scale [9]. J. Gonzalos contribution to the knowledge of the brain
J. Mira and A. Prieto (Eds.): IWANN 2001, LNCS 2084, pp. 150157, 2001. c Springer-Verlag Berlin Heidelberg 2001

Time-Dispersive Eects in the J. Gonzalos Research

151

is connected with the research of other authors, e.g., [6] [13]-[16] [20]-[23], and was considered [1]-[4] [18] accurate, rich in physiological data and clinical proofs, as well as theoretically elaborated. His research appears to be related to recent approaches in cerebral dynamics in which integrative and adaptative aspects are involved, e.g., [5,17,22]. In the present work we deal with the excitability and the reaction velocity of the cerebral system. It is then suitable to study cases with dierent magnitude of central syndrome since their cerebral systems are slower in dierent degree from the normal case. We show that the simple mathematical theory of linear timedispersion can describe some manifestations of the central syndrome. This simple model can also account for the phenomenon of summation [8,9]. The slowness of the cerebral system in the central syndrome makes the cerebral excitation to dissipate slowly, confering the system with temporal summation capability (iterative aptitude). There is also intersensorial summation or facilitation, that is, the perception in a sensory system (e.g., visual) can be improved by stimulating other sensory systems. In particular is very noticeable the reinforcement or facilitation obtained by strong muscular contraction (very pronounced in case M). Unlike the summation by iteration, this type of summation modies the system essentially, and makes the cerebral system more rapid and excitable, i.e., supplies in part the neural mass lost in the central lesion [8,9]. This eect is greater as the decit (the lesion) is greater, but is null in a normal case.

The Model

In the theory of dynamical systems, a system is said to be time-dispersive if its response at a time t depends not only on the stimulus at that time, but also at all previous times, t t. Thus, if we consider an stimulus S(t ) acting on the cerebral system, the excitation E(t) produced at time t in the cerebral system is determined by the stimulus at times t t. In the linear case, the excitation can be expressed by E(t) =
t

(t, t )S(t )dt =

( )S(t )d,

(1)

where = tt , is related to the capability of the system to be excited and will be called excitation permeability. The quantity can also be interpreted as the excitation produced by a delta pulse stimulus, i.e., E (t) = 0 ( )(t )d = (t). A simple form of , which accounts for the presumed dispersive behaviour, is ( ) = 0 ea . (2) With this choice, a delta pulse stimulus results in a sudden growth of the excitation up to 0 followed by the exponential temporal decay ea , where a is related to the velocity of the system. For Eq. (1), we then have E(t) =
0

0 ea S(t )d.

(3)

152

I. Gonzalo and M.A. Porras

For the case of a constant stimulus S during the time interval [0,t], the excitation at time t can evaluated from Eq. (3), to be E(t) = 0 S
t 0

ea d =

0 S(1 eat ). a

(4)

Threshold Curves of Nervous Excitation

We examine now, in the framework of the above model, some of the basic physiological data of the visual system obtained by J. Gonzalo [8,9]. (a) We rst chose the fundamental threshold curves stimulus-time (also known as strength-duration curves) of the nervous excitation by electrical stimulation of retina with capacitor discharge (cathode on eyelid). As shown in Fig.1(a), the data were taken for the normal case N, patient M (very pronounced central syndrome), the same patient under strong muscular contraction (40 Kg held in each hand), i.e., under reinforcement, and for patient T with less intense central syndrome (smaller central lesion). The main source of errors are related to the experimental diculties to obtain the data [8], especially for patient M, and for long times in all cases. Each point of the curves represents, for a given electrical intensity I = V /R (expressed indirectly in volts V ), the needed time t = RC (expressed in microfarads) during which the intensity must act to obtain minimum luminous sensation. V is the potential applied, R is a constant resistance and C is the capacity of the capacitor. These curves can be explained from the above model if a few reasonable assumptions are made. We assume that the stimulus just on the retina is proportional to the electrical intensity, i.e., S = G(V /R), G being a constant, and that the cerebral excitation threshold Eth necessary to have a particular sensorial function (minimum luminous sensation) is the same for the patient with central syndrome (functional depression) and for the normal man. The threshold can be reached by dierent ways, e.g., by low intensity during long time or higher intensity during shorter time. The corresponding values S and t are related by Eq. (4) for E = Eth constant, that is, S= 1 aEth . 0 1 eat (5)

What is expected to be dierent for patients with central lesions with respect to a normal case is the value of the permeability 0 and the reaction velocity a of the cerebral system. To make a direct comparison between Eq. (5) and experimental data, we rewrite Eq. (5) as V = 1 B R aEth G 0 1 eaR106 c 1 eAc (6)

where c is given in microfarads, A aR106 and B (REth /G)(a/0 ). The tted curves given by Eq. (6) are shown in Fig. 1(a). The obtained values to the best tting are, BN = 2, AN = 2 for normal case; BT = 11.5, AT = 1.3 for case

Time-Dispersive Eects in the J. Gonzalos Research

153

T; BMr = 14.5, AMr = 0.7 for case M reinforced; and BM = 22, AM = 0.48 for M inactive. Patient M under reinforcement (that supplies in part the lesion) has an active cerebral system intermediate between M inactive and T. We see that, when the decit in the active central cerebral mass grows, the reaction velocity a decreases: aT /aN = 0.65, aM r /aN = 0.35, aM /aN = 0.24, and the excitation permeability 0 also decreases: 0T /0N = 0.17, 0M r /0N = 0.14, 0M /0N = 0.09, but the ratio a/0 increases signicantly: (a/0 )T /(a/0 )N = 5.91, (a/0 )Mr /(a/0 )N = 7, (a/0 )M /(a/0 )N = 12.

(a)

(b)

Fig. 1. Threshold curves stimulus-time. (a) Electrical stimulation of retina: For a given intensity I = V /R, the time necessary t = R106 c to obtain minimum luminous sensation, for normal case (N) and patients with central lesions (T and M) [8,9] (see the text). (b) Two perception levels (40o and 180o ) of the direction function for case M, right eye. For each level, time necessary to illuminate with an intensity I an upright test arrow in order to be perceived as rotated a certain angle [8,9] (see the text).

(b) Here we consider also threshold curves stimulus-time, but for dierent perception levels of a particular sensorial function perceived by the same observer (patient M, right eye). In order to illustrate an striking phenomenon we chose the direction function explained in the preceding section. Dierent perception levels correspond to dierent degrees of rotation under which a vertical upright white test arrow is perceived, according to the intensity of illumination of the arrow. Under low stimulation (illumination), the arrow is perceived as very turned, almost inverted in patient M , but under high illumination (and then greater cerebral excitation), the image becomes upright. From detailed studies of visual, tactile and auditory inversion, it was proposed [8,9] that the perception originated in the projection area is inverted and constricted, but is then magnied and reinverted, i.e., elaborated or integrated, in the whole cortex, and particularly in the central zone. The reinversion of the arrow made by the cerebral system was called direction function and reaches its maximum value (180 degrees) when the image is seen upright. Each point of Fig. 1(b) represents the time necessary to illuminate the test arrow with an intensity I, in order to be perceived as turned 140 degrees (180 140 = 40 degrees of direction function), or in order to be perceived upright (180

154

I. Gonzalo and M.A. Porras

degrees of direction function). We consider that the stimulus S on the cerebral system is S = KI, K being a constant factor. From the theoretical Eq. (5) we then obtain, 1 aEth D I= , (7) 0 K 1 eat 1 eat where D aEth /(0 K) and Eth is here the threshold or required excitation for a given level of perception (40o or 180o ). The tting of Eq. (7) to the experimental data leads to D40 = 1.3, a40 = 0.09 and D180 = 10.6, a180 = 0.088. It is reasonable to assume that the dierent values of D are due to dierent values of Eth only, the factor (a/0 ) being considered to be the same, in a rst approximation, for the dierent sensorial perception levels of a given sensorial function, as it can be seen in the next case (c). We can then assert that for the most elaboratedperception (maximum of the direction function), the required excitation (180) (40) Eth is greater than for the less elaborated perception Eth . In addition, since a180 a40 , we can deduce from the above assumption that 180 40 . 0 0 This suggests that each sensorial function (direction in this case) is characterized by the values of a and 0 .

(c)

(d)

Fig. 2. (c) Perceived direction of the upright test arrow for each value of the intensity I illuminating the arrow for indenite time (case M, right eye) [8,9]. (d) Threshold curve for patient M in similar experience as in Fig. 1(a): For a given electrical intensity (given indirectly by V ), the number of stimuli (each one of duration of the order of milliseconds and spaced 1/12 seconds) necessary to perceive minimum luminous sensation [8,9].

(c) We continue with patient M, right eye. Figure 2(c) shows the maximum value reached by the direction function (perceived direction of the upright test arrow) for each value of the the intensity I illuminating the arrow for indenite time, i.e., t . The experimental data were obtained by switching on the illumination I and waiting for long time enough for the image that the patient sees to become stable. From our model, Eq. (4), we obtain the excitation at t as E = 0 S. If we assume that the perception (sensation) of a sensorial a function F (here the direction function) is proportional to the logarithm of the cerebral excitation, we obtain the Fechner law, well-known in normal cases, 0 S 0 QI F = Z log E = Z log = Z log Z log(Y I), (8) a a

Time-Dispersive Eects in the J. Gonzalos Research

155

where Z and Q are constants (we consider that S is proportional to the intensity, S = QI) and Y Q0 /a is constant if (0 /a) can be considered as a constant. In fact, the tting of Eq. (8) to the data (curve of Fig. 2(c)) is good enough with the values Z = 54, Y = 90, to consider that the logarithm law describes satisfactorily the sensorial growth versus the stimulus, and that the ratio 0 /a can be considered constant for a given sensorial function of a given cerebral system. For other data in the case of patient T for example, or in the case of other sensorial functions, the behaviour is similar.

Iterative Aptitude

As shown in Sec. 2, the cerebral excitation for a single short stimulus has an exponential decay. If a second stimulus arrives before the excitation has completely fallen down, there is an eect of summation in the cerebral excitation. The same can be said for a train of impulse stimuli, so that it is possible to achieve the threshold to produce a sensorial perception despite a single one is unable to do it. The iterative aptitude is then more pronounced as the cerebral system is slower, i.e., as the central lesion is greater [8,9]. In Fig. 2(d) this property was shown [8,9] in a similar experience as in Fig. 1(a), except that in horizontal axis we have the number of stimuli. Each one has a duration t0 = R C of the order of milliseconds (C = 1.5 106 farads and R of the order of several thousand ohms), and the time between successive stimuli is T = 1/12 s. Let us now consider that S(t) is a train of stimuli, as illustrate in the inset of Fig. 2(d), which can be expressed as

S(t) = S
n=0

[(t nT ) (t nT t0 )] ,

(9)

where (t) is the Heaviside step function, and S is a constant. Evaluation of Eq. (1) with Eq. (9) yields E(t) =

0 S f (t) g(t)eat , a

(10)

where f (t) n=0 [(t nT ) (t nT t0 )] , g(t) n=0 [(t nT )eanT (t nT t0 )ea(nT +t0 ) ]. The patient has received N = 1, 2, ... complete stimuli at t = (N 1)T + t0 . As in the case (a) of Sec. 3, S = G(V /R ), and E(t) = Eth for each experimental point. Then, from Eq. (10) and B (R Eth /G)(a/0 ) we can write B V = (11) f (t) g(t)eat for the relation voltage-number of impulses to have minimum luminous sensation. The tting to the data of patient M inactive, right eye, yields B = 0.55 and a = 1.65. From the available data it is not possible to know the value of R , thus, it is not possible to know the exact value of t0 . However, in contrast to case (a) of Sec. 3, without iteration, here we can neglect t0 compared to (N 1)T in the expression of t, so that the value of a can be obtained from the tting.

156

I. Gonzalo and M.A. Porras

Conclusions

We have shown that it is possible to model the temporal dynamics of simple sensorial functions as a rst-order linear time-dispersive system, having, as a rst approach, a response 0 ea to a short impulse stimulus. The reaction velocity a and the permeability to the excitation 0 of the cerebral system decrease when the decit in the active central cerebral mass, or central lesion, grows, but the ratio a/0 increases signicantly. For a given active cerebral system, the ratio a/0 can be considered to be a constant for each sensorial function. Even we can suggest that a and 0 are two constants that characterize the sensorial function. The fact that the sensorial perception is related to the logarithm of the stimulus also in pathological cases was already found by J. Gonzalo, and here it is expressed in the framework of the model employed. It allows to conrm that the perception is proportional to the logarithm of the cerebral excitation, at least in the range of the data analyzed. The model can also describe the iterative aptitude, and the value of a can be deduced from it. This simple model can then be considered as a rst approach to the mathematical description of some aspects of the cerebral dynamics studied by J. Gonzalo. The model can be improved in several ways: the excitation permeability ( ) of Eq. (2) can be replaced by a more realistic function; the macroscopic magnitudes a and 0 should be related to the neural mass and its microscopic structure (quantity of neurons, conexions); changes in the value of (a/0 ) for dierent sensorial functions must be analyzed; and intersensorial summation is expected to be described by including spatial dispersion.

References
1. de Ajuriaguerra J. et Hcaen H.: Le Cortex Cerebral. Etude Neuro-psychoe pathologique, Masson, Paris 1949. 2. Bender M.B. and Teuber H.L.:Neuro-ophthalmology in: Progress in Neurology and Psychiatry, Ed. Spiegel E.A., III , Chap. 8, 163-182 (1948) 3. Critchley Mc.D.: The Parietal lobes, Arnold, London 1953. 4. Delgado Garc A.G.: Modelos Neurocibernticos de Dinmica Cerebral, Ph.D. Thea e a sis. E.T.S. de Ingenieros de Telecomunicacin. U.P.M. Madrid 1978. o 5. Engel A.K. et al.: Temporal coding in the visual cortex: new vistas on integration in the nervous system, TINS, 15, 6, 218-226 (1992). 6. Gelb A. and Goldstein K.: Psychologische Analysen hirnpathologischer Flle. a Barth, Leipzig 1920. Psychologische Analysen hirnpathologischer Flle auf Grund a Untersuchungen Hirnverletzter: VII Ueber Gesichtsfeldbefunde bei abnormer Ermdbarkeit des Auges (sog. Ringskotome), Albrecht v. Graefes Arch. Ophthal., u 109, 387-403 (1922). 7. Gonzalo J. Investigaciones sobre Dinmica Cerebral. La accin dinmica en el sisa o a tema nervioso. Estructuras sensoriales por sincronizacin cerebral, Memory como municated to Consejo Superior de Investigaciones Cient cas, Madrid 1941. 8. Gonzalo J.: Investigaciones sobre la nueva dinmica cerebral. La actividad cerebral a en funcin de las condiciones dinmicas de la excitabilidad nerviosa, Publ. C.S.I.C., o a Instituto S. Ramn y Cajal. Vol. I: Optic functions, 342 pp., Madrid 1945. Vol. II: o Tactile functions, 435 pp., Madrid 1950.

Time-Dispersive Eects in the J. Gonzalos Research

157

9. Gonzalo J.: Las funciones cerebrales humanas seg n nuevos datos y bases u siolgicas. Una introduccin a los estudios de Dinmica Cerebral, Trabajos del o o a Instituto Cajal de Investigaciones Biolgicas, C.S.I.C., Vol. XLIV, 95-157 (1952). o 10. Gonzalo I. and Gonzalo A.: Functional gradients in cerebral dynamics: The J. Gonzalo theories of the sensorial cortex in Brain Processes, theories, and models. An international conference in honor of W.S. McCulloch 25 years after his death, 78-87, Moreno-D R. and Mira-Mira J. (Eds.), The MIT Press, Cambridge, Masaz sachusetts 1996. 11. Gonzalo I.: Allometry in the Justo Gonzalos Model of the Sensorial Cortex, Lecture Notes in Computer Science, 124, Proceedings of the International WorkConferenceon on Articial and Natural Neural Networks, Lanzarote, Canary Islands, Spain, June 1997, Mira J., Moreno-D R. and Cabestany J. (Eds.), az Springer-Verlag, Berlin 1997. 12. Gonzalo I.: Spatial Inversion and Facilitation in the J. Gonzalos Research of the Sensorial Cortex, Lecture Notes in Computer Science, 1606, Proceedings of the International Work-Conferenceon on Articial and Natural Neural Networks, Alicante, Spain, June 1999, Vol. I, Mira J., and Snchez-Andrs J.V. (Eds.), Springera e Verlag, Berlin 1999. 13. Khler W.: Gestalt Psychology, Liveright, New York 1929. Dynamics in Psychology, o Liveright, New York 1940. 14. Lapique L.: Lexcitabilit en Fonction du Temps, Hermann et Cie., Paris 1926. e 15. Lashley K.S.: Brain mechanisms and intelligence, Univ. of Chicago Press, Chicago 1929. Integrative functions of the cerebral cortex, Psychol. Rev., 13, 1-42 (1933). Studies of cerebral function in learning, Comp. Psychol. Monogr., 11 (2), 5-40 (1935). Functional determinants of cerebral localization, Arch. Neurol. Psychiat. (Chicago), 30, 371-387 (1937). The problem of cerebral organization in vision, Biol. Symp., 7, 301-322 (1942). 16. Luria A.R.: Restoration of Function after Brain Injury, Pergamon Press, Oxford 1963. Traumatic Aphasia, Mouton, Paris 1970. 17. Llins R.R.: The intrinsic electrophysiological properties of mammalian neurons: a Insights into central nervous system function, Science, 242, 1654-1664 (1988). 18. Mira J., Delgado A.E. and Moreno-Diaz R.: The fuzzy paradigm for knowledge representation in cerebral dynamics, Fuzzy Sets and Systems, 23, 315-330 (1987). 19. Mira J., Delgado A.E., Manjarrs A., Ros S. and Alvarez J.R.: Cooperative proe cesses at the symbolic level in cerebral dynamics: reliability and fault tolerance in Brain Processes, theories, and models. An international conference in honor of W.S. McCulloch 25 years after his death, 244-255, Moreno-D R. and Mira-Mira az J. (Eds.), The MIT Press, Cambridge, Massachusetts 1996. 20. Piron H.: La connaissance sensorielle et les probl`mes de la vision, Hermann, Paris e e 1936. Physiologie de la vision in Trait dophtalmologie, Masson, Paris 1939. e 21. Ptzl O.:Die optish-agnostichen Strungen in Handbuch der Psychiatrie, Aschafo o fenburg, Wien 1928. 22. Rakic D. and Singer W. (Eds): Neurobiology of Neocortex, Wiley, 1988. 23. Ramn y Cajal S.: Histologia del sistema nervioso del hombre y de los vertebrados, o Vol. II, Madrid 1899.