The Orienting Response in Health and Disease
Modalities—visual, acoustic, somatosensory, motor
Neglect syndrome extinction, anosognosia, impersistence,
The orienting response is the initial reaction of an organism to a stimulus. The response is based on the strength and physical attributes of the signal such as brightness, hue and contour or higher order features such as complexity, novelty, and significance. The response consists of a large number of muscular, skeletal, autonomic and central nervous system responses that are triggered reflexively after encountering the stimulus.
The orienting response declines in strength over time and after repeated exposures. This diminution in the strength of the response is known as habituation. Habituation involves an inhibition of amplification of the orienting response through the reticular formation. The capacity to habituate allows the organism to shift attention away to other items of importance or interest. Past exposures to the same or related stimuli create an expectancy for future exposure. Small changes in the stimulus after a delay may then trigger a new, heightened orienting response called sensitization, with heightened amplification of the response through reticular activation (groves and Thompson, 1970). Movement of an object that has served as a stimulus or small changes in its physical appearance may trigger a new, heightened orienting response.
Habituation leads to the diminution of the size of the orienting response. The rate of habituation is determined by the same factors that affect the response, including novelty, information content, complexity, and intensity. Habituation allows an organism to respond to new stimuli (shift attention or set). Habituation helps an organism resist distraction, and the introduction of distraction during habituation increases the likelihood of a phasic orienting response ( Waters, McDonald and Koresko, 1977). Amphetamines… the reticular formation.
While any type of stimulus can trigger an orienting response, humans display relatively stronger responses to visually complex shapes, including patterned stimuli and human facial features, from infancy (Fantz, 1958, 1965). Novelty is an important determining factor in the occurrence of the orienting response, possibly due to a mismatch between the incoming stimulus and an existing neuronal template of the external world, a view that has been called the “neuronal model” (Sokolov 1969).
Orienting responses of a primitive sort appear in nonmammalian organisms, which may consist of membrane permeability changes (Kandel 1982).
Stimulus variation is “fundamental” to the elicitation of the response, including changes in the sensory modality or auditory tone of presentation, changes in the stimulus intensity and duration, and stimulus omission (Siddle et al., 1983). However, the factors affect the response differentially. Stimulus intensity increases produce higher amplitude physiologic responses with decreased and slower habituation. Stimulus duration does not affect the amplitude of the response (Raskin et al., 1969). Interstimulus interval is proportional to the size of the stimulus and inversely proportional to the rate of habituation. Long intervals between stimuli (greater than 120-240 sec) may prevent habituation (Schaub, 1965).
Factors that may result in an enhancement of the orienting response and a diminution of the habituation response include not just novelty, but increasing task stimuli complexity, as well as a verbal task demand that stimuli be “learned” in preparation for a future recognition test (Verbaten et al, 1979). The orienting response is a nonspecific response related to readiness and expectancy of stimulus selection. During conditioning (learning), the physiologic response becomes more specific with an increased activation to the conditioned stimulus, but less expectancy response (Ohman, 1983). Thus the orienting response may be associated not just with novelty but with higher order conditioning and learning.
Features of the orienting response include head turning, autonomic sympathetic responses including sweating, papillary dilatation, peripheral vasoconstriction, central vasodilatation, changes in heart rate, and EEG desynchronization (Kimmel et al., 1979). The electrodermal response, measured through changes in skin resistance and sweating, correlates well with the response including habituation and is often used to define the response. The heart rate decelerates and the blood pressure diminishes with the orienting response, unlike the startle response or the defensive response during which the heart rate accelerates and the blood pressure increases; however, otherwise the orienting response resembles the startle and defensive responses. The orienting response occurs during stimulus onset or offset, whereas the startle/defensive reactions occur only during onset, and tend to habituate more rapidly than the orienting response (Jackson, 1974). An important difference is that the defensive response occurs only in relation to high amplitude stimuli and is not changed by ambient differences and changes in information at lower amplitudes (Graham, 1973).
Lacey (1959, 1967) proposed that during the orienting response, during the period of sensory intake, the heart rate decelerates, whereas during subsequently, during preparation for a motoric response, the heart rate activates.
The orienting response represents an organism’s registration of/confrontation with a stimulus, rather than processing of it (Sokolov,? 1976). Cohen (1993) writes that “the orienting response provides a behavioral index of attention.” However, Cohen (1993) has suggested the difficulty of defining a truly novel and/or important stimulus and differentiating them from ambient environmental noise.
History of the Orienting Response:
The orienting response was described by Pavlov but elaborated by Sokolov. It is a reaction to a new or unexpected stimulus or to change in parameters such as intensity, duration, frequency, etc.). It correlates with a generalized physiologic reaction. A basic property is habituation, and it disappears with repeated presentation. It can be seen in EEG, EMG, GSR, psychogalvanic response etc. Sokolov showed that the orienting response is not analysis of a stimulus, but confrontation of it. If a representation of the stimulus is formed, and subsequent presentations "match" the response habituates. If there is discordance, the response reappears. Thus the nervous system has to have an imprint of the external world (that is subject to continuous revision). OS Vinogradov, did further experiments and found that neurons in the hippocampus and other subcortical nuclei would compare stimuli to past traces. Sokolov also noted that tongue and lip activities were active during "inner speech" and was a physiological index for indicating mental planning.
The orienting reaction, as measured by GSR and suppression of alpha rhythm of the EEG, cannot be stabilized by verbal stimuli in patients with frontal lobe lesions. In ordinary individuals, verbal stimuli can prevent the habituation response and thereby prevent the orienting response from disappearing. Conversely , patients with lesions in the posterior sensory cortex have normal habituation of the OR (Homskaya, 1966). Stimuli that would increase the amplitude of visual evoked potentials in normals failed to do so in patients with frontal lobe damage (Simernitskaya and Homskaya, 1966; Simernitskaya, 1970). Animal models of frontal lobe damage also show changes in the OR (Grueninger et al., 1965, Kimble et al., 1965).
Orienting responses are impaired after human dorsolateral (Heilman and Valenstein, 1972) and cingulate gyrus lesions (Watson et al., 1973), as indicated by hypoarousal, spatial neglect, and hypomobility of the neglected side contralateral to the lesion. CM Fisher described the “intermittent interruption of behavior” following ACA stroke (1968).
Neglect, which often includes unilateral hypokinesia and lack of arousal responses, can be seen with lesions of the arcuate region in primates (Kennard and Ectors, 1938, Welch and Stuteville, 1958), in the parietal association areas (Heilman et al, 1971), and lesions of the thalamus, hypothalamus and midbrain (Marshall and Teitelbaum, 1974; Marshall et al, 1971, Segara and Angelo 1970, Watson et al., 1974.
Cohen RA. The Neuropsychology of Attention. (New York, Plenum Press, 1993).
Kennard MA and Ectors L. (1938). Forced circling movements in monkeys following lesions of the frontal lobes. J Neurophysiol 1:45-54.
Welch K and Stuteville P (1958). Experimental production of neglect in monkeys. Brain 81:341-347.
Fantz RL. (1958) Pattern vision in young infants. Psychol Recod 8:43-48.
Fantz RL. (1965) Visual perception from birth as shown by pattern selectivity. Annals of the New York Academy of Sciences, 118:793-814.
Homskaya ED. (1966) Vegetative components of the orienting reflex to indifferent and significant stimuli in patients with lesions of the frontal lobes. In Frontal Lobes and Regulation of Psychological Processes, AR Luria and ED Homskaya (eds), Moscow, Moscow University Press.
Simernitskaya EG and Homskaya ED (1966) Changes in evoked potential to significant stimuli in normal subjects and in lesions of the frontal lobes. In Frontal Lobes and Regulation of Psychological Processes, AR Luria and ED Homskaya (eds), Moscow, Moscow University Press.
Simernitskaya EG (1970) Evoked potentials as an indicator of the active process. Moscow, Moscow University Press.
Fisher CM. (1968) Intermittent interruption of behavior. Trans Am Neurol Assoc 93:209-210.
Graham FK (1973) Habituation and dishabituation of responses innervated by the autonomic nervous system. In Peke HVS, Herz MJ (eds.) Habituation: volume 1: Behavioral studies pp.163-218. New York, Academic Press.
Graham FK, Clifton RK (1966). Heart rate change as a component of the orienting response. Psychological Bulletin 65:305-320.
Graham FK (1979). Distinguishing among orienting, defense and startle reactions. In Kimmel HD, van Olst EH, Orlebeke JF (eds.) The orienting reflex in humans (pp137-167) Hillsdale, New Jersey, Erlbaum.
Groves PM, Thompson RF (1970) Habituation: a dual process theory. Psychological review 77:419-450.
Grueninger WE, Kimble DP, Grueninger J, Ledvine SE (1965) GSR and corticosteroid response in monkeys with frontal ablations. Neuropsychologia 3:205-216.
Heilman KM, Pandya DN, Karol EA, Geschwind N. Auditory inattention. Arch Neurol 1971 24:323-325.
Heilman KM and Valenstein E. Frontal lobe neglect in man. Neurology 22:660-664, 1972.
Jackson JC. Amplitude and habituation of the orienting reflex as a function of stimulus intensity. Psychophysiology 11: 647-659.
Kandel ER and Scwartz JH (1982) Molecular biology of memory. Modulation of transmitter release. Science 218:433-443.
Kimble DP, Bagshaw MH, Pribham KH (1965). The GSR of monkeys during orienting and habituation after selective partial ablations of the cingulated and frontal cortex. Neuropsychologia 3: 121-128.
Kimmel H. Van Olst EH, Orlebeke JF (eds.) The orienting reflex in humans. Hillsdale, New Jersey, Erlbaum.
Lacey JI (1959) Psychophysiological approaches to the evaluation of psychotherapeutic process and outcome. In Rubinstein EA, Parloff MB (eds.). Research in psychotherapy, pp160-208, Washington, D.C>, American Psychological Association.
Lacey, JI, (1967). Somatic response patterning and stress: some revisions in activation theory. In Appley MH and Trumbull R (eds.) Psychological stress: isues in research. New York, Appleton-Century-Crofts.
Marshall JF and Teitelbaum P (1974). Further analysis of sensory inattention following lateral hypothalamic damage in rats J Comp Physiol Psychol. 86:375-395.
Marshall JF, Turner BH and Teitelbaum P (1971) Sensory neglect produced by lateral hypothalamic damage Science 174: 523-525.
Ohman A. (1983). The orienting response during Pavlovian conditioning. In Siddle D (ed.) Orienting and habituation. Perspectives in human research. Pp.315-370. New York, Wiley.
Raskin DC, Kotses H, and Bever J (1969). Autonomic indicators of orienting and defensive reflexes. J Exper Pscyhol 80:423-433.
Schaub RE (1965). The effect of interstimulus interval of GSR adaptation. Psychonomic Science 2: 361-362.
Segarra J and Angelo J (1970). Anatomical determinanants of behavioral change. In Behavioral change in cerebrovascular disease, AL Benton (ed.) New York, Harper and Row.
Siddle DAT and Spinks JA (1979). Orienting response and information processing: some theoretical and empirical problems. In Kimmel HD, Van Olst EH, Orlebeke JF (eds.). The Orienting reflex in humans. Hillsdale, New Jersey, Erlbaum.
Siddle D, Stephenson D, Spinks JA (1983). Elicitation and habituation of the orienting response. In Siddle D (ed.) Orienting and habituation: perspectives in human research (pp. 109-182) New York, Wiley.
Sokolov EN. The modeling properties of the nervous system. In Cole M, and Maltzman I (eds.). A handbook of contemporary Soviet psychology. (pp.671-704). New York, Basic Books, 1969.
Stephenson D (1982). Habituation and systemic desensitization. Unpublished doctoral dissertation, University of Southamptom.
Verbaten MN, Woestenburg JC and Sjouw W (1979). The influence of visual information on habituation of the electrodermal and visual orienting reaction. Biological Psychiatry, 8: 189-201.
Waters WF, McDonald DG, Koresko RO (1977). Habituation of the orienting response: agating mechanism subserving selective attention. Psychophyiology 14(3) 228-236.
Watson RT, Heilman KM, Cauthen JC, King FA (1973). Neglect after cingulectomy. Neurology 23:1003-1007.
Watson RT, Heilman KM, Miller BD, King FA. (1974). Neglect after mesencephalic reticular formation lesions. Neurology 24:294-298.
(from McNamara and Albert, Clinical Neuropsychology (Valenstein and Heilman, eds.) fourth edition. Acetylcholine activity is greater in the left human brain as measured by CAT (Amaducci 1981) in temporal lobes and globus pallidus (Glick et al. 1982). Orbitofrontal also received ACH projections. Dopamine is represented most in the corpus striatum (nigrostriatal tract), the cingulate gyrus (mesolimbic system), and the SMA and prefrontal areas (from ventral tegmental area). Only trace DA is found in occipital area, with the most in motor and premotor areas. D1 receptors on pyramidal cells of layer 3 of the cortex and striate modulate glutaminergic receptors through "triads" wherein DA affects neuronal firing patterns. DA (and NE) runs in an a-p plane. NE projects from locus ceruleus (LC) to whole forebrain with collaterals to somatosensory and motor cortex (all 6 layers) and less to temporal and primary visual cortex. The prefrontal area provides the only afferents back to LC and disinhibit firing of LC and impair regulation. DA and ACH act in concert to affect cognition. Clonidine and physostigmine affect memory in aged monkeys more than either drug alone. DA blockade can be reversed by cholinergic depletion and cholinergic blockade can be reversed by DA depletion. Memory fields in cortex correspnding to D1 receptor projection fields include the sulcus principalis of the monkey and are crucial in delayed response task. These responses are highly dependent on DA concentrations available and with that aspect of working memory. Clonidine improves performance in DR task after lesioning prefrontal cortex, as well as antergograde memory in patients with Korsakoffs syndrome.
(from McNamara and Albert, Clinical Neuropsychology (Valenstein and Heilman, eds.) fourth edition. Hat tip to Kim Meador, AAN notes from 2000 course on physiology of cognition
var pageTracker = _gat._getTracker("UA-3639768-40");
Contralesional visual P3 event related potential is consistently abnormal among patients with visual neglect (increased latency and decreased amplitude). (L'Hermitte et al. Arch Neurol 1985 42:567-573). Monkeys with lesion induced neglect have normal early but abnormal late components on the SEP (N2 and P3) (Watson RT et al. Neurology 1986; 36:636-640 and Watson RT et al. Arch Neurol 1977; 34: 224-227). In humans, SEP reliably differentiates those with extinction/tactile neglect/tactile joint sense. (Maugiere et al. Paris Rev Neurol 1987; 143:643-656). VEP's are normal is visual neglect patients who have no conscious knowledge of visual stimulation (Vallar et al. Neurology 1991; 41: 1918-1921). A delay does occur in steady state visual VEP's in contralesional field of neglect patients, especially at high but not low frequencies (Spinelli et al. Neuroreport, 1996) and consistent with loss of contrast sensitivity in neglected field (Angellini et al. 1998 COrtex) and worse in left lower field implying vertical as well as horizontal neglect. VEP and blood flow both improve with direction of head/gaze to right (Nadeau et al. JNNP 1997). PET scan studies of tactile extinction were performed (Remy et al Neurolohy 1999). Left hand stimuli activated SII regions, but not right SM1 region. Bilateral stimuli showed suppression of right SM! but also both SII regions. Compensation is inhibited by overstimulation of both sides. In healthy humans, PET shows selective activation of right prefrontal and parietal cortex irrespective of side stimulated on somatosensory and visual vigilance tasks. Amphetamines decrease habituation in the midbrain, to already detected stimuli thereby increasing vigilance (Cite).
Lesions of the DL frontal cortex modulate the locus ceruleus (LC) and the DLF may be the only cortical afferent to the LC. Clonidine enhances anterograde memory in Korsakoff's patients. Suppression of LC firing suppresses background cortical activity, enhancing stimulus evoked activity, enhancing the signal to noise ratio. The LC is activated by novel stimuli. Lesions of the PFC inhibit attentional switching by impairing afferents to the LC. Clonidine or ritalin, that activate prefrontal cortex through the LC should improve attentional function.
Also called "novelty detection." Novelty detection is crucial for learning and for cognitive flexibility. Novel events are better remembered (von Restorff H 1933). Molecular links of novelty are established to the short arm of chromosome 11 and the D4 receptor gene. Structural network encompasses the dorsolateral prefrontal cortex, temporoparietal junction, hippocampus and cingululate gyrus. Physiological detection is accomplished with an "oddball"task eg. P300 stimulus, MEEG and ERP. Maximal amplitude occurs over the parietal area of scalp. Frontal activation increases with task difficulty. Human lesions typically show inferior parietal, superior temporal, thalamic and cingulate activation. Involuntary and voluntary attention to novelty have different physiologies. The (involuntary) P300 (P3a) has a frontoscalp distribution, peaks in 50 msec (earlier) and habituates over 5-10 presentations. P3a recordings show activation of multiple areas. The hippocampal recorded (voluntary) ERP, like the scalp P3b, does not habituate over repeated presentation of stimulus. Conversely, the hippocampal novelty ERP like the P3a scalp recording, rapidly habituates. The P3a is thought to be a CNS marker of the orienting response. Prefrontal lesions differentially reduce P3a but not P3b. Patients with orbitofrontal damage have an orthogonal response with a heightened p3a amplitude, perhaps correlating with increased startle and and labile behavior. Moreover with prefrontal damage, p3a response is muted over the entire hemisphere. This supports a modulating role for prefrontal cortex over the rest of the hemisphere. The hippocampus is involved in novelty mismatch (Sokolov and Vinogradova). The artery of Uchimara irrigates the hippocampus, especially the posterior part. Patients have normal parietal p3b but abnormal frontal p3a associated with novelty. ERP recordings suggest the prefrontal cortex processes the initial novelty detection and then alerts the hippocampus which fires afterwards. The fibers alerting the hippocampus may traverse the retrosplenial cortex. fMRI as of (old data) depended upon field strength and technique to show the changes seen by other techniques. Norepinephrine may also be important in novelty detection. See post on pharmacotherapy with NE for orienting response. Selected references Benjamin J , Li L, Patterson BD et al. Population and familial association between the D$ dopamine receptor gene and measures of novelty seeking. Nature Genetics 12: 81-84. Chao LL, Knight RT. Human prefrontal lesions increase distractibility to irrelevant sensory inputs. Neuroreport 6:1605-1610. 1995. Ibid. 1998. Contribution of human DL prefrontal cortex ti delay performance. J COgn Neuroscience 10:167-177. Courchesne E. Hillyard SAm Galambos R 1975. Stimulus novelty task relevance and the visual evoked potential in man. EEG Clin Neurophys 39: 131-143. Picton TW 1995. The P300 wave of the human event related potential. J Clin Neurophysiol 9: 456-479. Woods DL , Knight RT. 1986. Electrophysiological evidence of increased distractibility after dorsolateral prefrontal lesions. Neurology 36; 212-216.
AN Sokolov Perception and the Conditioned Reflex (1958). Correlation of psychological with physiologic variables is absent in contemporary Soviet research
AN Sokolov Perception and the COnditioned Reflex (1958).
Bernshtein authored theoretical principles of a new physiology "of activity" as opposed to "of reactions." Every action has a reaction which would be a new stimulus and so on, leading to a "dynamic physiology" that Luria also accepted. Behavior must be plastic and depend on modifications and adjustments In place of a rigid reflex arc, Bernshtein postulated a "reflex ring" with continuous adjustments and corrections. picture p. 93. Petr Anokhin,a student of Bernshtein, elaborated direct physiologic investigation of CR's, eg. in the 1950's by hosting the first EEG conference in the USSR. His work, Biology and Neurophysiology of the Conditioned Reflex (1968) is considered the most important Pavlovian elaboration post Pavlov. His afferent synthesis hypothesis proposes a key momennt when the organic needs of the individual ("dominant motive") are confronted with environmental situation and preceding experience (memory) to elicit a behavior. The CR is inserted into functional organization. So to satisfy hunger, a precise sequence of processes occurs. Author states that today CR is seen as only one process not the only process.
Ivan Pavlov (1849-1936) differentiated himself from both Sechenov and Western physiology and psychiatry. He began as a digestive physiologist for 25 years, studying salivation "psychologic salivation" with various physiologic techniques and won the Nobel Prize in 1904. His trespass into psychology was deemed risky by colleagues and was criticized. BF Skinner in 1938 The Behavior of Organisms interpreted Pavlov in a way that was accepted by Konorski and Hebb. The conditioned reflex is mediated by a complex S-R (stimulus-response) with processes of modulation including excitation, inhibition and reciprocal induction. The modulatory processes of the brain were not observed but were deduced from the S-R. The central nervous system therefore was more virtual than real, and Skinner termed Pavlov's CNS as the "Conceptual Nervous System." Skinner noted that Sherrington had deduced the spinal synapse long before it was actually described, and Pavlov hoped to do analagously with the CNS. The S-R was explained in behavioral terms , but also in neuroconceptual terms and on a third level, on neuronal terms (after observing the physiology). For example, in behavioral terms, the strength of a reflex could be reduced by presenting a second stimulus related to the effector involved. In neuroconceptual terms, the second stimulus coming by different afferents inhibits the conductivity of the impulses specific to the effector. In neuronal terms, the actual pathways are described. On a conceptual level, the importance is that the neuroconceptual models predct that eventually the entire behavior will be explained physiologically. Pavlov was misunderstood, but stated clearly that "it was not our aim to interpret the activity of the hemispheres in terms of the elementary functions of the nervous system." Soviets misunderstood his ideas as applying to all behaviors. Western sources criticised him as well. Konorski and Hebb later accepted Pavlovian models as the models that they were. Konoski chronologically divides Pavlov's life into periods. From 1901-1910, Pavlov elaborated phenomena of the conditioned reflex such as external inhibition, generalization, differentiation. 1910-1920, Pavlov introduced laws of dynamics of cortical processes such as irradiation, concentration, reciprocal induction. From 1920 on, Pavlov focused on processes of excitation and inhibition, types of nervous system and neurosis. The reflex arc is a means by which animals adapt to their environments. Pavloc said investigation of the higher centers ought to be faithful to the same methods used in the lower systems. The conditioned reflex ensures the survival of the individual. Reflexes are derived from the "innate organization" of the nervous system. Instincts are complex systems of unconditioned reflexes. Conditional (conditioned, acquired) reflexes are formed by connections between centers for conditioned reflexes and centers for unconditioned reflexes. Conditioned reflexes can be suppressed, or inhibited, externally (passively or unconditioned) by something that suppresses the formation of the reflex, or internally (or actively) . It can be experimentally extinguished by withholding the conditioned stimulus. There may be a post inhibitory effect afterwards in which other CR are inhibited from being formed. Stimuli similar to the conditioned reflex can cause excitation (generalization of the stimulus). If only one class of the stimuli are reinforced and others are not, there is differentiation of the CR. The signalling action of the reinforced stimulus (duration, intensity, action, etc.) are reinforced, and other stimuli are inhibited. Inhibition of delay occurs if the stimulus is produced a few seconds after the conditioned stimulus, then the action occurs a few seconds later as well. Transmarginal inhibition occurs if some feature of the CS eg intensity, fatigues the nervous system and prevents the formation of the normal CR. The dynamics of the reflex are interactions between excitatory and inhibitory processes. Expansion of excitation to adjacent parts of the nervous system is called irradiation, and then focus at the point where it continues to have an action is called concentration. These 2 functions depends on characteristics of the stimulus especially intensity. In sleep, inhibition irradiates through the CNS and dominates the "equilibrium." The law of reciprocal induction refers to the fact that around an area of excitation there is a zone of inhibition (negative induction), and vice-versa (positive induction forms around an area of inhibition). The analyzer is the functional unit of the receptor and cortical projections that analyse a stimulus. Pavlov counted five sensory analyzers, plus a motor analyzer. The cortex was an analyzer-synthesizer without specific specialization. The analyzers all communicated with each other, but communicated best to other analyzers in close proximity. Pavlov rejected therefore the idea current in neurology of cortical centers, and of physiologists such as Bekhterev that cortical centers existed. Pavlov thought CR operated through subcortical centers. Pavlov used lesion studies to "show" the "diffuse" nature of the cortical analyzer which was the "law of equivalence of all the parts of the hemispheres from the functional point of view." In the last period of his life, Pavlov studied the principal properties of the nervous system, including the strength of the excitation and inhibition, the mobility, and the equilibrium between the two. Strength was the ability to react strongly to a CR, the mobility referred to adaptability to different types of stimuli, and equilibrium was whether there was an equal capacity to deliver positive or negative reflexes. Subjects could be typed into strong subjects (easy to form CR) and weak subjects (hard to form CR) and by balanced (equivalent ability to form positive or negative reflexes) or unbalanced. The latter if inert, could never form CR, if mobile they could adapt and perhaps be able to do so. For a number of years in the USSR, the Pavlovian precepts were accepted in an orthodox manner, uncritically. Later, Westerners and USSR scientists such as Konorski explored them critically. In 1949, Donald Hebb published The Organization of Behavior that discussed the use of physiological models for behavior processes. His concepts of "cell assemblies" borrowed heavily from Pavlov. His book was influenced by Lorente de No's work on reverberating circuitry. Integration of behaviorism and neurophysiology continued with Pribham "neurobehaviorism" and Razran "brain-behaviorism."
The reductionist reflexology of Vladimir M Bekhterev differed from Sechenov. It was not just physiological and psychological but also biological and social. It did not penetrate well into Sechenov/Pavlov labs. Only Bekhterev was truly reflexology in classical Soviet nosology. Bekhterev was a neurologist and psychiatrist who was aware of the German localizationists. He discussed innate and acquired reflexes (which Pavlov called conditioned reflexes). For example, a shock to a dog's leg preceded by a noise would eventually lead to the noise causing the shock. The associative reflex was, according to Bekhterev due to the formation of a connection between two cortical center. His idea appeared simple, and even though Pavlovian ideas were similar, the Pavlovian model was more sophisticated and better accepted. Vygotsky wrote in 1930 that the most important application of reflexology was in the early infantile period"genetic reflexology." Genetic research would permit the study by developmental factors of what factors in personality are social by nature. Ultimately Bekhterev's reflexology was reducing psychology to a chain of reflexes and a schema of higher cortical connections. It fell out of favor for the most part by the mid 19830's.
post from mecacci l, brain and history 1979 Sechenov wrote Reflexes of the brain (1863), Studies of Physiology (1884-1898) and Elements of Thought (1878, 1903). He argued psychological processes reduced to physiologic processes. It derived from German physiologists such as Ernst Brucke, who reduced psychology to chemistry and physics. He also includes Sigmund Exner (outline of a physiological interpretation of psychological phenomena, 1894), Freud (Project for a scientific psychology for neurologists, 1895) and others. In Reflexes, originally titled "An Attempt to explain physiologically the origin of psychological phenomena" the brain is broken down into a machine. The complex human brain has actions that pass from involuntary to voluntary then to psychological. The latter is a series of reflexes that are integrated. What Sechenov did is to move the functional/structural analysis from spinal cord to the brain. p.6 schema stimulus and effector. The reflex apparatus updates itself constantly. Simple reflexes include movement of the leg of a decapitated frog, neonatal suck, and later in ontogeny, walking which is increasingly automatic. Emotional reflexes are triggered by stimuli such as thirst or hunger. Psychological reflexes have a psychological factor that relate to the external world. In man, emotion may intensify behavior, or thought may inhibit them. External factors are always the origin of the psychological processes. Centers in the mesencephalon and medulla inhibit reflexes chemically based on context and past experience, and controlled by the cortex. The higher cerebral reflexes and the lower spinal reflexe each were decomposed into their single elements, and analyzed. Sechenov's students, the Petersburg (Leningrad) schoo, applied it to neuromuscular function. They outlined precise rules by which , studied in the muscle prep, excitatory and inhibitory processes established themselves. "Principle of dominance" Students Tarkhnishvili in 1890 studied gavanic skin response. Danilevsky in 1891 stated the study of electrical phenomena of the brain can be an instrument for the investigation of material processes which are he substrate of subjective psychological processes (beginning of psychophysics).
var pageTracker = _gat._getTracker("UA-3639768-40");
op cit 1973. Activation and attention. Luria cites the importance of the brainstem/reticular activating system ascending systems, but wonders about descending systems. Luria cites importance of "frontal" zones in producing "expectancy waves" or contingent negative waves) . EEG, GSR, EP and others by Sokolov (orienting reflex) and Homskaya et al. were important. In general, verbal instructions to mobilize attention (counting, etc.) led to higher eeg frequency including patients with posterior lesions. Patients with frontal lesions, esp. mesial and basal could not evoke these changes. Luria emphasizes not only frontal lesions, but also the role of verbal instruction. Consciousness: Vygotsky showed aoluntary organization of conscious actions have a social origin and cannot be understood just by biological growth. It begins with childhood, when adults begin actions that children learn and finish. After children achieve speech, they give themselves instructions and inner speech is a well developed and important mental act. Frontal lesions that do not affect sensory, motor, or speechfunctions cause deterioration of complex functions that involve internalor external speech. Goal driven behavior is replaced by impulsive or echopraxic movements. Pribham and Anokhin showed impaired complex reaction times. Testing os accomplished through contrasting program motor tasks. Memory: Cites Scoville and Milner the Papez circuit Long discussion not included Rehabiliation Loss of function occurs but so does inhibition of function (diaschisis or functional asynapsia). The latter canbe treated pharmacologically as done on ww I veterans and in children with cerebral palsy. Luria cites Russian sources for overproduction of cholinesterase can be overcome with prostigmine and other antichlinesterase drugs. If the whole functional system is damaged, rehab training should involve the "planned reorganization of functional systems." Doing so requires a careful psychological qualification of the deficit, ways to reorganiza, and step by step sequence of orthopsychological methods.