Thursday, August 28, 2008

The Orienting Response Part I

The Orienting Response in Health and Disease


Description
History
Physiology
Modalities—visual, acoustic, somatosensory, motor
Neurochemistry
Anatomy
Lesions
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
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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).
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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.

Thursday, July 31, 2008

Nosology and terms associated with "alien hand syndrome"

taken from Biran I, Chatterjee A. Alien hand syndrome, Arch Neurol 61:292-294, 2004

Categories--3 broad
1) terms implying a conflict of will of hands or opposition of one hand to other (intermanual conflict, diagonistic apraxia, agonistic apraxia)
2) terms implying aberrant movements, stimulus boundedness of hands (compulsive manipulation of tools, anarchic hand, magnetic apraxia)
3) terms describing the subjective reaction to limb (autocriticism, interhemspheric autocriticism, strange hand sign)

original credit for "la main etrangere" Brion and Jedynak, 1972(rev Neurologie (Paris) 126:257-266, describing patients with callosotomy

first revision Wilson et al.Neurology 1977 27:708-715 to "the stranger's hand sign" leading to Bogen's "Alien hand"(se 3rd edition Heilman and Valenstein).

Historically descriptions of the syndrome previously were described by Liepmann ad Goldstein. Akelaitis introduced "diagonistic dyspraxia" in 1940s. Gazzaniga , Bogen and Sperry wrote about it in 1962 in split brain patients. Rebeiz wrote about it in his eponymic syndrome, also called corticobasal ganglionic degeneration, in his seminal article in the late 1960s. Patients with this condition would be more likely to have type 2 above.


Denny-Brown described "repellant" and"magnetic" apraxia in patients with parietal and frontal lesions, and explained them in terms of approach and avoidance behaviors. Magnetic apraxia involves compulsive grasping, repellant apraxia may involve levitation and hyperextension of wrist showing an exaggerated posture.

Wednesday, July 23, 2008

Neuroendocine aspects of behavioral neurology


(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.

Outline for Behavioral Neurology Review

I History of
II Physiology
III Neurochemistry.endocrinology
IV White Matter Tracts
V Symmetry of hemispheres
VI Learning/memory

Tuesday, July 22, 2008

Pharmacology of the orienting response


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.

Nadeau on conduction aphasia-- model


See other post on c.a also. Material summarized from Nadeau SE et al, eds. Aphasia and Language theory to practice Guilford Press 2000.

Nadeau begin with a model for phonology. A semantic concept is translated into the articulatory hierarchy. Eventually it reaches the articulatory motor representations at the bottom of the hierarchy. When hearing, a word is translated upwards along the acoustic hierarchy from a pattern of sound sequences upwards finally to a concept representation.

Articulatory word forms are sequences of phonemes devoid of meaning that correspond to words. Morphemes are the major subsegment of words. For example, "passed" has a stem, pass linked to the essential meaning of the word and and affix ed, Affixes can be inflectional or derivational and modify the meaning of the word. Words also are made of syllables that are made of phonemes. Eg., the syllable "bot" is made of onset b, rhyme ot that itself has a nucleus or peak o and coda t. A joint phoneme is a string of phonemes that stick together like "str" in "stream." All phonemes are described by 16 distinctive features. These include vowel to consonant (/a/ to /k/), to nasal (/d/ to /n/), acute to grave (/d/ to /b/), diffuse to compact (/d/ to /g/), voice (/t/ to /d/), to continuant (/p/ to /f/), mellow to stridor (theta/ to /s/)/ . The diffference between phonemes are measured by the number of distinctive features that separate them, the paradigmatic distance ((Lecours and Lhermitte, 1969). For example, the pairs above are one distinctive uit apart, /p/ and /m/ are 2 apart ( nasality and voice), and /d and /f/ are 3 apart ( voice, acute to grave, and continuance). Nadeau can't say based on data whether acoustic processing hierarchy conforms to his model. Articulatory processing is also affected by grammar, parsing (segmenting phonemic stream into words), prosody, and phonetic modification. Phonemes are coarticulated, and phonological processor is substrate for memory as well as language.Procesing is 2 way.

In the auditory processor, the definitive method for assessing integrity is lexical decision, whether or not a heard sound is a word.

The concept representation interacts with and interfaces with other prcoessors (graphemic, eg.).

The acoustic-articulatory link translates sounds into articulatory representations. This is a system and not a discrete bundle. The optimal probe of the integrity of the path are phonetic discrimination (are /gat/ and /gap/ same of different) and rhyme judgment. The phoneme instantiating acoustic-articulatory linkage is similar, but instantiates patterns of neural activity corresponding to phonemes and can be best tested with nonword repetition.

Higher level functions that are involved and important are phonological and lexical-semantic working memory.

Nadeau postulates 3 types of conduction aphasia. Repetition conduction aphasia (rare) is caused by complete destruction of lower level acoustic-articulatory linkage and the higher level phoneme instantiating route. Naming and spontaneous language are normal, no phonemic paraphasic errors occur, there is poor phonetic discrimination, poor auditory short term momemory, impaired repetition due to disconnection and memory impairment.

Reproduction conduction aphasia is due to partial damage to higher level phoneme instantiating acoustic -articulatory linkage. There is relatively normal naming and spontaneous language, good phonetic discrimination, spared auditory short term memory, and severely impaired repetition due to phonemic mis-selection. Prototype is patient of Bub (1987).

Phonological aphasia is due to damage to phonological articulatory hierarchy and sparing of acoustic-articulatory links. It has phonemic paraphasias, normal repetition, and normal discrimination and auditory verbal memory. Most cases are combinations of reproduction and phonological types.

Conduction aphasia Goodglass and his critics

Harold Goodglass in "Understanding Aphasia" (Academic Press, 1993) expresses the correlation with "afferent motor aphasia" (Luria) and central aphasia (Goldstein). The aphasia is fluent with consistent errors, especially phonemic paraphasias (tangling, transposing, substituting/insertion extra phonemes, stutterlike blocking). Errors may preferentially affect nouns/key words rather than grammatical forms, or resemble Wernicke's aphasia with syntactically disordered speech and attempts to repair syntax. Repetition is poor especially polysyllabic words. Auditory and even reading comprehension is relatively remarkably preserved. This feature differentiates from Wernicke's aphasia. Patients lack neologistic speech seen in Wernicke's aphasia and can correct errors offline (Shuren et al.). Mild cases may have paraphrase errors.

The anatomy may involve the supramarginal gyrus, compatible with Geschwind, or other lesions along the Sylvian fissure. Lesion extent is restricted though. K. Goldstein attributed central aphasia to an insular lesion (1948). Damasio and Damasio (1989) Neuroanatomy and Neuropsychological Disorders. Neuroimaging procedures and problmes, New York, Oxford Press) rejected disconnection, and attributed the disorder to a disruption of the perception and short term storage of phoneme strings and their assembly for production (blogger question: Did the Damasios give a hat tip to Luria???). They further stated the cortex and not the white matter had to be involved.

Nadeau reviews the anatomy of conduction aphasia and believes it to be partly reconciliable with the Wernicke-Geschwind model, with a center for auditory images in area 22 is linked to posterior inferior frontal lobe (Broca's area) via the arcuate fasciculus. Nadeau contends there is a two part language cortex, with one part extending from area 22 variably backwards into area 40, and that an anterior area extending variably from Broca's area to areas 4 and 6. There is substantial individual variability. fMRI and cortical stim studies (Ojemann and others) show distributed and hierarchical processes in 2 distributed systems but not necessarily disconnection.

There are white matter tracts between the two areas, and also WITHIN them. Acoustic representations within the STG (Howard et al, 1992, Brain 115: 1769-1782). The connectivity between the two areas could be direct or indirect, and be individually variable. Nadeau defines the anatomy of conduction aphasia as including, variably, the supramarginal gyrus, the posterior part of Wernicke's area, the angular gyrus and possibly the extreme capsule and insula. Nadeau thinks of it as a limited form of Wernicke's aphasia with better lexical access and more preserved acoustic hierarchy. He cites this as the view of Sigmund Freud.

Nadeau's views of PDP processing are elaborated extensively but omitted here.

Psycholinguistic accounts include Dubois et al. (1964) Etude neurolinguistique de l'aphasie de conduction. Neuropsychologia 2, 9-44. They noted worse repetition with longer sylables and witgh "negating prefixes" that confronted the speaker with a "high information decision at the end of the prefix" . In contrast, the anomic aphasics did well on negating prefixes but not with lexical selection. Pate et al (1987) Specifying the locus of impairment in conduction aphasia, Language and Cognitve processes 2:43-81, found identical pholonogical strings were harder to repeat if one word than if 2 words (murderous v. murder us). Geschwind noted difficulties with functor loaded sentences ("no if ands ands or buts") but Goodglass believes that is not reliable.

Warrington, Logue and Pratt (1972) Neuropsycologia 9:377-387 and Warrington and Shallice (1969) Brain 92:885-896 proposed decreased auditory short term memory as a feature of conduction aphasia (again the question: was there a hat tip to Luria for this "new" finding?). Their view was what Nadeau later called "repetition conduction aphasia." (see separate blog entry). That view was disputed by Strub and Gardner 1974 (Brain and Language) . Tzortzis and Albert (1974) and subsequent studies by Goodglass found "invariable" impaired auditory spans that is not adequate to explain the deficit; the persistent auditory trace allows attempts at self correction. The term "reproduction conduction aphasia" refers to the classical form of the disorder with problems beyond auditory memory impairment, encompassing equal impairments of oral reading and naming. Kohn (1984, Brain and Language) emphasized the phonlogical link between successive attempts and target words and considers the problem "post-lexical" ie. after achievement of phonological representation of the word, but before its motor realization, due to a breakdown of "prearticulatory programming" similar to Dubois.

Nadeau described 3 types of conduction aphasia from the literature. Please see separate entry regarding.



Tuesday, July 15, 2008

LuriaL hemispheric interaction

Luria AR, Simernitskaya EG. Interhemispheric relations and the functions of the minor hemisphere. Neuropsychologia 1977; 15:175-178.

Proposes active, intentional memorizing is done by the dominant hemisphere, whereas involuntary or incidental memory depends on the nondominant hemisphere. Relates it to the idea of "figure" and "background" of K Goldstein.

Subjects were tested on their ability to memorize a list of 2-3 syllable words (intentional memorizing) v. counting the letters "k" in words and incidentally recalling words.

Idea was criticized in a note Rothenberg S, Gross K, Comments on the note byu Luria and Simernitskaya. Neuropsychologia 1978l 16: 367. They suggested there were baseline differences among groups.

Physiology of neglect syndrome

Hat tip to Kim Meador, AAN notes from 2000 course on physiology of cognition

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 Neurology 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).

Modern physiology of orienting response

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.

links for MMSE, FAST and MoCA

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FAST (stages of Alzheimers




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Sunday, July 13, 2008

Internal (inner) speech

Sokolov et al. studied the activity of the tongue and lip muscles in planning speech and found that alterations in this muscular activity correlated with difficulties with internal speech or planning of speech.

from Luria The Working Brain. Luria described the transition from general plan to narration requiring the recoding of a plan into speech, with a role played by internal speech, which has a "predicative" nature. This linear scheme of a sentence" is obliterated in patients with lesions in the inferior postfrontal zones of the left hemisphere. Patients cannot express the scheme, but may be able to do so if given cards indicating the pertinent parts of the sentence and asked to arrange them in order (Leontiev).

Vygotsky (Luria's mentor and the not originator of the concept of inner speech) was a silent stage of sentence formation between a preverbal intent to communicate and a fully formed message. It has a simplified syntax as in a message to oneself. It allows a transition from inner concepts to formal syntax. Developmentally, a child received names for symbols externally, helping to develop its mental functions. Acquisition of language then become internal to the individual in late childhood, and becomes the means by which theindividual regulates his/her own behavior. Pavlov ostensibly admitted that certain cerebral processes were not conditioned and excluded from his analysis of reflexes.

Luria also wrote (1970) that one must condense a heard message into inner speech in order to deal with its syntax. That may explain impaired comprehension of syntax in agrammatics.

Friday, July 11, 2008

Seeing trees but not the forest: limited perception of large configurations in PD

Barrett AM, Crucian GP, Schwartz Rm Nallamshetty H, Heilman KM.  Neurology 2001; 56:724-729.

The authors discuss the attentional "floodlight" v. "spotlight" and note that some patients with neglect lack the floodlight as do patients with dopamine deficit. Subjects with PD and controls were shown large and small letters but PD subjects had trouble naming the large letters consistent with the theory of attentional floodlight abnormality in PD.  Patients who had undergone pallidotomy did markedly better on the floodlight task.  The latter raised the possibility that the problem was not dopaminergic per se, but thalamic activation of the frontal cortex, since pallidotomy reduces inhibition ofthe thalamus.

Sunday, July 6, 2008

EN Sokolov, and the Conditioned Reflex (orienting response)


AN Sokolov Perception and the Conditioned Reflex (1958).

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 (intensity, duration, frequency, etc.). It correlates with a generalized physiologic reaction. A basic property is habituation, 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 noed that tongue and lip activities were active during "inner speech" and wa a physiological index for indicating mental planning.

Correlation of psychological with physiologic variables is absent in contemporary Soviet research.

Nikolay Bernshtein (1896-1966) And Petr Anokhin (1896-1974)

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 moment 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.

Vygotsky and Pavlov


Vygotsky rejected strict reflexology of Bekhterev, CR of Pavlov, behaviorism of Watson. CR cannot explain higher cortical processes such as language. Instead of stimulus-response, he proposed stimulus -means. Buridano's donkey was an example given -- a donkey between 2 sacks of flour, instead of choosing either, starves of indecision. This is because the 2 stimuli produce "equal and opposite reactions."

Pavlov- CNS Conceptual nervous system

Ivan Pavlov (1849-1936) differentiated himself from boh 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 Priz 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."

Bekhterev 1857-1927



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.

Psychophysiological theories sechenov

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 are controlled by the cortex. The higher cerebral reflexes and the lower spinal reflexes each were decomposed into their single elements, and analyzed. Sechenov's students, the Petersburg (Leningrad) school, 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).

2 kinds of motor perseveration in massive injury of the frontal lobes


Luria AR Brain 88:1-10 1965.



Luria's highest fame includes techniques devised to parse frontal lobe defects. Luria described motor perseveration with preserved intention and switching, but pathological inertia which he calls "efferent" perseveration of the motor periphery.

The second type is pathological inertia of the program of action. The initiated program becomes inert adn the patient cannot switch task but is stuck on the first. Syndrome is typically superimposed on aspontaneity. This is called inertia of a a previously recorded programme of action.

The first type is due to massive frontal injury extending to the subcortex.

Russian neurolinguistics post Luria

Authors discuss parts of the lexicon, "Kernel, peripheral and individualistic features". Word fluency did not distinguish aphasia types. Perseverations were more common in anterior groups, semantization index decreased in all groups. Both cortical and subcortical lesions did not change the nominal lexicon, but did change the structure of verbs, with de-individualization. In aphasia more than PD , the individual parts of verbs disappear.

The kernel lexicon is primarily based on the frequency and time of appearance of the words in childhood. Also, personal reflection in the words based on personal scholarship, etc. are common, but these are especially reduced in all groups, ie relatively preserved kernel lexicon but reduced personalized lexicon.

In left handers who speak Russian, conduction and transcortical aphasia is commoner, whereas motor and acoustic-gnostic aphasia is commoner in right handers with left hemisphere lesions.

Russian Neuropsychology of memory after Luria


Luria discusses "interhemispheric interactions" with a variety of pupils collaborating.

The right hemisphere is slower in information processing and less able to regulate one's mental activity. The right hemisphere analyzes perceptive features but not semiotic features (phonetic and semantic) of stimuli. The left hemisphere does the opposite. (Meerson and Zalman, Russsian). Cognitive deficits of the left hemisphere are more evident with cortical lesions, whereas subdominant syndromes appear after subcortical lesions of the right hemisphere ( Moskovichyute LK, Simernitskaya EG, Smirnov NA, Filatov YF (1982) On the role of the corpus callosum in organization of higher cortical functions. in Tsetkova LS, Zeigarnik BV eds. AR Luria and Modern Psychology (in Russian) Moscow Unviersity Press, Moscow, 143-150.). Modality specific (visual, tactile or acoustic) disturbances of interhemispheric interaction and the dyscopia-dysgraphia syndrome (ability to write only with the right hand and draw only with the left one) occur after partial dissection of the corpus callosum but only the posterior part (Moskovichyute et al, 1982 IBID). Left hemisphere lesions were more pronounced but also rehabbed better, possibly due to greater plasticity of the left hemisphere (IBID) or due to a transformation of the interhemispheric interaction (Krotkova).

A different idea is that the right hemisphere is involved in elementary, involuntary and automatized mnestic activity, whereas the left hemisphere is responsible for complex, voluntarymemorizing (Simernitskaya, 1978) [blogger note: Luria published a letter to this effect in Neuropsychologia around 1973, whereupon a reply criticized his methodology and finding].

Separately-- I have to find the citation for this again-- Luria proposes the left hemisphere reads consonants, the right vowels. Also Glozman claims left hemisphere lesions cause more retroactive inhibition, that right hemisphere ones cause proactive inhibition. The left does selectivity and and activity of memorizing, the right ensures retention of item order and plasticity and flexibility of memorizing.

Saturday, July 5, 2008

Luria on anomia


AR Luria. Towards the mechanisms of naming disturbance. Neuropsychologia 1973; 11:417-421.

Naming difficulties can be attributed to defective phonematic perception of articulatory control, among . He refers to "amnesic aphasia" as an archaic concept associating a sound with an object image. However, he states that objects are "coded" thereby acquiring meaning. Either an image oo relevant semantic connections must be activated and connected to an auditory form. Abstract ideas are coded and also can be named. However, the "law of force" of Pavlov, leading to failure to differentiate strong and weak connections, lead to inhibitory states. Blocking of traces of psychological events, which is "easily achieved by a nervous system with normal level of plasticity" becomes severely deranged in pathological states. Pathological inertia, or perseveration hinders the normal selectivity of psychological processes.

Anomia can occur due to sensorimotor modaltiy specific processes at input, or selectivity at a higher level. Selection of phonemes is impaired, leading to "alienation of word meaning" typical of sensory aphasia. Alternatively, articulatory phonemes cannot be accessed normally. Luria states that anomia may be visual agnostic (with trouble completing pictures, for example) or a higher order problem of word choice. A third area is fluent sequential organization of speech choices, or "syntagmatic disorganization." There is a derangement of"inner speech" andof "linear scheme of phrase."

Luria: Visual agnosia explained through physiology

AR Luria Disorders of"simultaneous perception in a case of bilateral occipito-parietal brain injury. Brain 82:437-449 year?

Luria notes explanations in literature should but do not include the physiologic. He cites a case discussion by Pavlov in 1935 that the "occipital lobe is inhibited to such a degree that it cannot endure two simultaneous stimulations." The occipital lobe has a "low tonus of excitation" and can concentrate only on one point at a time. There is not a notion of space, and the patient feels lost. Luria takes off on the "restriction of attention in physiological terms" and discusses the deficit in terms of excessive cortical inhibition, leading to failure to synthesize excitation under complex stimulation.

The patient had signs of optic ataxia and simultanagnosia.Writing was poor but improved with the eyes closed. One interesting experiment (no 9 on this patient) the patient could see the rectangle formed by 6 dots but with the instruction to count the dots, had difficulty. Concentration on one detail led to loss of the whole. The injection of caffeine (.05-.1 gram) led to much better results. The improvement lasted about 35 minutes. It helppd tachistoscopic presentation and perception of two or more figures and helped oculomotor scanning.

Friday, July 4, 2008

Luria: The influence of Pavlov and Vygotsky

Hatfield FM. Analysis and remediationof aphasia in the USSR: the contribution of AR Luria. J Speech and Hrg Disorders46: 338-47, 1981.

[blogger note: these notes on article are not considered close to a complete discussion of subject. readers take note of the point]

Luria credits Sechenov(1863) and Pavlov with physiological studies of localization of cerebral function. Pavlov's explanation of localization of function (1949) is the cornerstone of Luria's explanationas well. Anokhin also was involved in the idea of "functional systems." Centers and complete equipotentiality of cortex are rejected. Author described a "Hegelian" synthesis of debate between localizationists and antilocalizationists.

The writing debate and "Exner's center" was specifically rejected and subjected to detailed elaboration of a functional system for writing. Sechenov/Pavlov "reflexes" were so called because they "reflected" the outside world.

Luria uses Pavlov's idea of "cortical analyzers" which are primary sensory projection areas in the cortex. The "second signalling system" referred to the first signalling system, which were conditioned reflexes including verbal symbols. The acquisition of speech was the second system, and a new and the highest regulator of human behavior. Pavlov believed, according to Luria, that the "laws of conditioning are quite different in animals and man."

On a personal level, Pavlov is said to have rebuked Luria after his first book, after which Luria was "purged" and did not publish again for well over a decade. When he did publish, some of his material was anti-Pavlovian.

Vygotsky:

Luria's mentor, wrote that thought and language were successively higher levels of consciousness, and based in social origin. Inner speech is egocentric speech, which might include shorthand, condensed and predicative. It is the basis of thought.

Author reviews Luria's classifiction of aphasias and tests of cortical function. Author stresses Luria's involvement and training in psychology, neurology, medicine, linguisitcs and founding involvement in neurolinguistics and neuropsychology. He was among the first to include phonemics, syntax, Jakobsen's schema, differential destructionof the "linguistics context" and the "linguistic code." He borrows from Chomsky with the model of deep and surface syntactic structures.

Luria Neuropsychological studies in the USSR A Review Part II

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 voluntary 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 can be 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 reorganize, and step by step sequence of neuropsychological methods.

Luria: Part I. cont. Speech


again from 1973 article op cit.

The primary defect in "sensory aphasia" in in phonematic hearing, disturbance of perception of basic units of acoustic speech sounds leading to problems with naming,writing, etc. This contrasts with the classical view of these areas as crucial for "understanding speech." Similary motor aphasia, classically thought to be the center for motor images of a word, is incomplete and lacks the notion of a system of afferents to provide control of complex motor efferents. 2 types of motor aphasia exist. Posterior inferior lesions cause deafferentation with patients unable to find "articulemes" and is similar to "disintegration of speech" described by Alajouanine et al. Lesions of the posterior third frontal convolution (Broca's area) allows articulation but not transitions or "kinetic melodies" andis called an "efferentor kinetic motor aphasia."

Semantic aphasia is originally attributed to Henry Head and involves tertiary tempero-parieto-occipital zones and is associated with loss of understanding of complex grammatical structures with loss of computation, spatial orientation,and constructional praxis. Luria posits 2 forms of grammatical structures with one due to spatial lesions,the other spared.

Dynamic aphasia is similar to transcortical motor aphasia andaspontaneity of speech. Lesions of anterior speech areas spare naming and repetition but greatly affect spontaneous fluent propositional speech. Inner speech and predicative function is affected (cites Vygotsky and Luria et al, 1968). The "linear scheme of the phrase" and"deep grammaticalstructure" is affected.

Luria "Neuropsychological studies in the USSR" Perception


op cit. still part I. Neuropsychology of perception

Luria stresses perception depends not just on afferents to primary visual cortex,but on selection of decisive cues about which objects seen are significant. Perception depends greatly on inputs from secondary visual areas, parietal and frontal inputs that are important for visual coding. Searching activities are crucial in formation of visual images in children. Sechenov is cited as showing ocular movements play a role similar to the searching movements of the hand.

Hubel and Wiesel showed the primary visual zone has neurons responsive to specific pieces of visual information such as shape, brightness, etc. Lesions lead to spatial disorganization of perceptions. Lesions of secondary areas lead to ability only to see separate details of an perceived object that Luria calls "amorphosynthesis" wherein they see only separate details of the image but can'tsynthesize it into a whole. The amount of "visual noise " in the background can affect perception. Lesions of the tertiary zones (occipito-parietal) cause Balint's syndrome involving simultanagnosia and impaired searching in space. Lesions of posterior eye fields lead to problems in passive eye searching, and lesions of the anterior premotor eye fields lead to problems in active eye searching.

Luria: Neuropsychological Studies in the USSR, A Review


AR Luria (Part I) Proc Nat Acad Sci USA 70:959-964 1973
(Part II) IBID 70:4 1278-83 1973

Definition of the central problem of neuropsychology: "localization of functions in the brain cortex"

Luria proposes radically revising the concept of "function" and "localization." Every behavioral function is "really a functional system" with feedback for control of the behavior and feedforward to establish plans and programs which is decisive for the elaboration of complex behaviors. Functional systems (as opposed to reflex circles) was formulated by Russians Anokhinand Bernstein and Pribham. A "new" physiology of activity (not reactivity) is based on coordinated functions (or constellations) of cerebral zones which have some overlap. Rather than localizing a cerebral function, n,'s try to discover how a functional system is distributed in different parts of the brain. However, lesions of different functional zones lead to deterioration of different functions. Luria stresses the importance of "double dissociations"the idea of which he credits to
Teuber. Certain zones that contain a specific"factor" of psychological "qualification" disturb the functional zone.

Luria proposes the temporal zone is decisive in acoustic analysis of speech sounds, perception of words and writing, but not computation or maps. Parietal zones associate with spatial analysis. Studying "qualifications of the system"leads to discovery of "factors"

Luria states that the "ideation center" that creates "motor schemes" that are superimposed on the "sensation of movement" ie praxis centers, "does not yet have a physiologic reality." NA Bernstein proposed a rule of the "impossibility of regulation of movements only by efferent impulses" and required that afferent influences give constant information about the changing positions of joints and flexibility of muscles. These "afferent fields" are organized from primitive (spinal cord) to high level (cortical) sensory systems. These afferent fields provide stable "afferent corrections" of motor acts and at first they are "secondary" or passive movements, later they become "primary type of correctionss" with feed forward mechanisms. The feed forward organization of flexible movements provides what Anokhin called the "acceptor of action." Lesions of the postcentral gyrus cause "afferent paresis" of "afferent ataxia" as first described by Foerster (1936).Inferoparietal or parietooccipital zones of the "spatial afferent fields"cause a "spatial apraxia" with confusion of the vertical, horizontal and sagittal planes. Lesions of the premotor areas cause a loss of fluid shifts from one movement to another with breakdown of the "kinetic melodies" of movement. Involvement of the subcortex causes a pathological inertia of movement with motor perseverations. Prefrontal lesions cause a loss of goal linked actions and their replacement with inert stereotypes or incorrect imitations.

Monday, June 30, 2008

AR Luria and history of Russian Neuropsychology

JM Glozman J Hist Neurosci 16:168-180, 2007. Author discusses neglected field of Russian contributions, many of which preceded German and French contemporaries. A few examples:

Tarnovsky (1867) proposed in an 80 page paper a comprehensive model for organizing aphasic syndromes. He ?pioneered the notion of separating "the localization of function from the localization of the defect." Kojevnikov (1874) preceded Wernicke in publishing "sensory aphasia" due to left temporal injury. Rodossky (1872)connected deficits of sound articulation and comprehension of speech, and "inner speech" and writing disorders. He also noted the emotional reaction of aphasics to their speech.

Contributions to the study of memory were made by Korsakoff (1890) related to medial temporal lobes by Bekhterev in 1907, 50 years before Scoville and Milner.

Lurian period drew on the reflexology of Bekhterev, and Freud. Luria and his mentor Vygotsky rejected the notion that Pavlovian ideas could explain complex processes such as speech, attention, planning. They based their neuropsychology on the principle that higher functions consist of factors that can be parsed, and that functions could not be localized so much as factors comprising the function?.

Astvatsaturov (MI, 1908) proposed in 1908 that amnesia for nouns in revealed after motor center disturbances while amnesia for verbs is due to Wernicke area lesions."

Saturday, June 28, 2008

Denny-Brown's view of the basal ganglia



His views are outlined (and portended) in the book entitled "The Basal Ganglia and their relation to disorders of movements" (single author, D Denny-Brown, Oxford University Press, 1962).

Subcortex and Apraxia


The following are taken from articles in Brain and Cognition 40:1999 special issue.

Merians AS et al. Patient with aphasia due to corticobasal degeneration did better pantomiming to command than using an actual tool. This contrasts to apraxic patients with left parietal damage who pantomime worse but do better with actual tool. Authors speculate that apraxia in CBD is due to SMA/convesity/premotor areas not parietal (or putamen). They differentiated convexity premotor and SMA premotor cortices. SMA lesions cause apraxia but it implements internally generated programs (projecting from parietal). The CBD patient did not have that much trouble with internally generated programs.

Jacobs et al. studied the same CBD patient as Merians et al., plus two others and evaluated neuropsychologically extensively. They noted adequate gesture comprehension, poor production, a tendency to gesture better with eyes open than closed, normal tests of memory and other basic neuropsychological tests, impaired learned and novel gesture production, impaired gesture imitation. Cortical sensory loss may be important. The network responsible may include the CN/PUT, SMA, convexity and inferior parietal lobule.

Saturday, June 7, 2008

Japanese aphasia and agrammatism

Kudo T, Tateishi M. Sensitivity to functors in Japanese aphasics. Neuropsychologia 20:641-651, 1982.

Notes: on Japanese language. In Japanese, one can reverse the word order (OSV= object-subject-verb or SOV) and unlike English, does not change the meaning to passive. A case particle is always placed after a nominal (subject or object) and in Japanese the case particle denotes the role of each word (subject or object). (Japanese is termed an "agglutinative" language).

Various theories exist about gradations of syntactic damage in aphasics and aphasia types. The Japanese language model for studying aphasics allows, for example, one to "control" for abnormal comprehension due to word order because word order does not affect comprehension. Fujita et al. (Jap J Jogoped Phoniatr 18:6-13, Japanese & Communic Disorders Res 6:151-161 in Japanese) proposed aphasics could be classified into 4 groups based on strategies of sentence comprehension, namely, 1) not decoding sentences at all 2) decoding by semantic constraint, 3) decoding by word order and 4) decoding by case particles.

The authors examined whether Japanese aphasics sensitivity to comprehension due to imbedded functors were due to the sentence types in which the functors were embedded, due to informational value and whether different aphasic types had different sensitivity to functors.

The task was in 64 sentence with various factors (inverted word order, not inverted, active, passive ) truth was assessed re pictorial accompanying. 42 aphasics and ten controls were run. Broca's patients had difficulty with truth decisions and could do so only with lexical meanings, ignoring syntactice structure. They had severe trouble with detecting incorrect functors. All aphasics had trouble with reversibility, that is they did worse with nonreversible than reversible sentences. Therefore all apahsics, Brocas plus Wernickes had trouble with functors.

Central or conduction aphasia in a Japanese patient


Yamadori A, Ikumura G. Cortex 1975; 11:73-82.

Notes on Japanese language: the basic unit of Japanese similar to a syllable is called a haku. All haku (unlike syllables) have equal temporal duration. A kanji can have any number of haku, but a kana always has one haku. There are 46 kana characters for 46 basic haku. Using diacritical marks all 112 kana can be transcribed with 46 kana. Word length is proportional to the number of haku.

The patient had fluent speech and good understanding but had verbal paraphasias and anomias. Repetition was poor. Written comprehension was good in silent reading but worse in aloud reading. Copying words and sentences was without error.

Repetition was worse with increasing number of syllables. Naming was worse with increasing number of syllables. Cueing did not help. Kana was read better than kanji (but recall that kana only has one haku and so word length was shorter). In writing, word length was an issue with more errors with longer words. That the patient had superior transcription of kanji than kana (due to absent phonology when writing) and superior oral reading of kana was expected (kana has less haku).

The authors thought the problem was the stability of the acoustic word image and not in concept (blogger note: a Luria idea). However the author credits Saussure (1916) and Dubois (1964) that conduction aphasia is "an efferent disturbance." The ability to represent a distinct acoustic image is lost in the first phase of the motor encoding process. They criticize the term "conduction" aphasia noting errors of naming, oral reading and dictation. The authors suggest "central" aphasia as used by Goldstein (1948) and Conrad (1948). "anomia has never been considered as an integral part, except by Conrad"

Notes: alternative explanations of conduction aphasia include disconnection of the motor speech area from Wernicke's area (Wernicke; Geschwind; Benson); degradation of the concept formation (Goldstein; Conrad, Hacaen); disturbed receptive function (Lieppmann and Pappenheim, 1915) and disturbed auditory short term memory(Warrington and Shallice).

References:
Benson DF, Sheremata WA, Bouchard R, Segarra JM, Price JM, Geschwind N. Conduction aphasia Arch Neurol 1973; 28: 339-346.

Conrad K. Strukturanalysen birnpathologischer Falle. Zum problem der leitungsaphasie. Dtsc Z Nervenheilk 159:188-228.

Dubois J, Hacaen H, Angelergues R et al. Etude neurolinguistique de l'aphasie de conduction. Neuropsychologia 2:944 (1964).

Geschwind.. disconnection syndromes etc.

Goldstein K. Language and language disturbances New York, Grune and Stratton, 1948.

Sasanuma S , Fujimora O (1971). Selective impairment of phonetic and non-phonetic transcripton of words in Japanese aphasic patients: kana v. kanji in visual recognition and writing. Cortex &: 1-18.

ibid. An analysis of writing errors in Japanese aphasic patients. Kanji v. kana words. Cortex 8:265-282 (1972) note-- see other post.

Warrington EK , Shallice T (1969). The selective impairment of auditory verbal short-term memory Brain 92: 885-896.

Korean aphasia: Hangul and Hanja reading

Kwon M, Kim JS, Lee JH et al. Double dissociation of Hangul and Hanja reading in Korean patients with stroke. Eur Neurol 2005; 54:199-203.

Korean has an phonogram (Hangul) /ideogram (Hanja) reading system analagous to kana/kanji in Japanese. Unlike Japanese, the Korean system does not depend nearly as much on ideograms. Also in Japanese, the same ideogram can be read phonologically or according to its meaning, which is not the case in Korean. Authors report a double dissociation as one showed more impairment in Hanjul adn the other showed the opposite. Blogger note: does Korean offer a purer model for dissociation of phonologic and orthographic routes since ideograms cannot be read phonologically? Need to check with Korean contacts.

Monday, June 2, 2008

Out of body experience v. depersonalization

Ridder DD, Laere KV, Dupont P, et al. Visualizing out-of-body experience in the brain. NEJM 2007; 357:1829-33.

Glossary
autoscopy- the impression of seeing one's own body from an elevated and distanced visuospatial persepctive.

depersonalization-- the subjective experience of unreality and detachment from the self

disembodiment-- an experience in which the self is perceived as being outside the body

out of body experience-- a brief subjective episode of disembodiment, with or without autoscopy.

Out of body experience was repeatedly elicited with stimulation of the posterior STG on the RIGHT in a subject in whom electrodes had been placed to suppress tinnitus. Brain activation on PET scanning occurred on the right at the junction of the SMG and the angular gyrus and the STG gyrus /sulcus on the right. There also was activation in the right precuneus and posterior thalamus extending into the superior vermis.

Such patients may have a transient inability to integrate the visual, tactile, proprioceptive and vestibular information that converges at the site. These events occur in near death experiences, in epilepsy, migraine, and by electrical stimulation of the temperoparietal junction on the right side in epileptics.

The authors note the right SMG processes vestibular information for head and body orientation in space. The area may embody an internal map of self-perception.

In contrast, during depersonalization and derealization, metabolic activity occurs in the inferior parietal cortex (area 7B) so that mislocalization in space is a slightly more dorsal lesion. The anterior cingulum usually coactivates with the angular gyrus, and precuneus during reflective self-awareness (Cavanna AE and Trimble MR. The precuneus: a review of its functional analtomy and behavioral correlates. Brain 2006; 129:564-583). Penfield found patients with floating feelings with stimulation of the right temporoparietal junction, and Blanke et al (Nature 2002; 419:269-270) found the stimulation target for autoscopy was more posterior at the occipital side of the angular gyrus. Caloric stimulation can also produce a feeling of detachment from the suroundings in healthy subjects and those with vestibular disorders (Sang FY et al. 2006; JNNP;77:760-766).
Th authors bring up that epileptics with atrophy might have altered brain connections or coactivation of two areas that are normally not coactivated.

This article concludes with a hypothesis that disembodiment is mediated by the coactivation of the small area at the junction of the angular and SMG and STG/sulcus. Activation of the posterior part of the superior temporal cortex with its map of self perception, results in altered self-perception. They aren't sure if this is what happens in near death experiences.

Sunday, June 1, 2008

Chinese aphasia

Overall there is a paucity of information and this article will be updated as I find more references. Much of this information is taken from an old book chapter "Aphasia in Chinese speakers" by Chen Ya-Huang in Chopra JS, Jagannathan K, Sawhney IMS, eds. Modern Trends in Neurology, New Delhi, Churchill-Livingstone, 1991. Other references are taken largely secondhand.

Chinese of course uses orthographic symbols to represent words. Whereas there is little or no difference in clinical characterisitcs of Brocas/Wernicke's aphasias in Chinese, several debates have emerged due to the nature of the written language.

Chinese words are monosyllabic, often, and simple tone differences may cause homophones to have different meanings. Since tone is processed by the right hemisphere, which hemisphere mediates processing of tone in Chinese, which is connected to meaning? H. Cohen et al. (Neuropsychologia, 1989; 27:241-5) studied Chinese and French Canadian subjects, and found that on dichotic listening tasks, both groups had a right ear superiority for consonant-vowel syllables, and a left ear superiority for non linguistic melodies and triple tones. However, Baudoin-Chial showed that in French subjects there is left hemisphere processing for Chinese consonant words, and right hemisphere processing for Chinese tone words; however among Chinese subjects there was no dominance for either task (J Neurolinguitics 1986; 2: 189-200).

Among Chinese left hemisphere-damaged nonfluent aphasics, a tonal production deficit exists that is "qualitatively and quantitatively equivalent" to an inability to produce consonants (Packard, Brain and Language 29:212-223). With right hemisphere damage, Chinese subjects become aprosodic but maintain tonal defferentiation for words (Hughes CP et al. Arch Neurol , 1983). In other words, when tone has a linguistic meaning, the left hemisphere processes it.

Chinese grammar is not built-in to words that do not have transitivity, inflections for tense, gender or plural markers on nouns. Subject-verb-object word order is like other languages and is maintained in Broca's and Wernicke's aphasics. Reading errors in Wernicke's aphasia include phoneme substitution, tone changes, morphological errors, and neologisms, with global reading errors and no differences based on the complexity of the logogram, part of speech, concreteness. Broca's errors are mostly phonologic or unclassifiable. Action naming is preferntially affected in Broca's aphasics (Tzeng and Chen, 1988, AAN poster).

Reading of orthographs is delayed among patients with Chinese word-form dyslexia or occipital strokes (author, unpublished). They found that activating an orthograph also activated semantically connected lexigraphs in the same orthographic string. In a case of alexia without agraphia, Chinese aphasics read out component radicles of the orthograph and then piece the radicles together into a single orthograph, even though that method is not normally used in reading. Reading stimulus activates similar orthographs (simlar morphologically, semantically, or phonologically).

Homophones can be constructed by putting together two real orthographs, and nonwords by putting together two normally unrelated orthographs. In Broca's, patients read bisyllabic real words better than homophones, while Wernicke's aphasics did not show homophone superiority to nonwords. The author has two potential explanations, see text.

Dysgraphia in Chinese in Broca's aphasics usually consist of visual errors wherein subjects write normal Chinese orthographs with either missing or excessive strokes. This compares to Western language in which errors use acceptable letter constraints, but make errors of compound or multiple letters rather than omission or substitution. Evidence suggest Chinese use all 3 routes, visual, semantic and phonologic.

Studies have shown equivalent, overwhelming left hemisphere dominance for speech in Chinese undergoing WADA tests or stimulation (Hung CC et al. , J Neurolinguistics, 1985: 1: 143-164) and Rapport RL, Tan CT and Whitaker HA, Brain and Lang 1983; 18: 342-366). Studies show a right hemisphere superiority for processing Chinese or Kanji logographs and a left hemisphere superiority for kana or syllabic symbols in Japanese. However, the studies that show a right hemisphere superiority in RECOGNIZING orthographs show a left hemisphere superiority for processing them semantically (semantic decision of relatedness) ( Tzeng OJL et al. 1979, Nature 282: 499-501; and Hossain R et al., Neuropsychologia1989; 27: 7-5-712; CK LEong et al, Brain and Lang, 1985). Crossed aphasia has not been found in higher rates among Chinese patients.

The Neuropsychology of handwriting

Patients with Parkinson's disease have a tendency to micrographia, that is small handwriting that is technically and qualitatively correct in major instances. Micrographia tends to improve with the withdrawal of visual feedback (eyes closed condition) and worsens with withholding of dopaminergic drugs. Moreover, with continuation of the task, micrographia becomes worse. It is worse in copying than free writing paradigm and improved with external cues (such as lined paper). Patients have worse micrographia with worse external attentional demands. Only one report exists of macrographia, in autism.


Ondo WG, Satija P. Withdrawal of visual feedback improves micrographia in Parkinson's disease. Mov Disorder 2007; 31: 2130-2131.

Van Gemmert AW, Adler CH, Stelmach GE. Parkinson's disease patients undershoot target size in handwriting and similar tasks. J Neurol Neurosurg Psychiatry. 2003 ; 74:1502-8.

Teulings HL, Contreras-Vidal JL, Stelmach GE, Adler CH. Adaptation of handwriting size under distorted visual feedback in patients with Parkinson's disease and elderly and young controls.
J Neurol Neurosurg Psychiatry. 2002 Mar;72(3):315-24.

Kim EJ, Lee BH, Park KC, Lee WY, Na DL. Micrographia on free writing versus copying tasks in idiopathic Parkinson's disease.
Parkinsonism Relat Disord. 2005 Jan;11(1):57-63.

Contreras-Vidal JL, Teulings HL, Stelmach GE, Adler CH. Adaptation to changes in vertical display gain during handwriting in Parkinson's disease patients, elderly and young controls.
Parkinsonism Relat Disord. 2002 Dec;9(2):77-84.

Tucha O, Mecklinger L, Thome J, Reiter A, Alders GL, Sartor H, Naumann M, Lange KW.
Kinematic analysis of dopaminergic effects on skilled handwriting movements in Parkinson's disease.J Neural Transm. 2006 May;113(5):609-23.

Oliveira RM, Gurd JM, Nixon P, Marshall JC, Passingham RE. Micrographia in Parkinson's disease: the effect of providing external cues.
J Neurol Neurosurg Psychiatry. 1997 Oct;63(4):429-33.

Van Gemmert AW, Teulings HL, Stelmach GE.The influence of mental and motor load on handwriting movements in parkinsonian patients. Acta Psychol (Amst). 1998 Nov;100(1-2):161-75.

Van Gemmert AW, Teulings HL, Stelmach GE.Parkinsonian patients reduce their stroke size with increased processing demands.

Beversdorf DQ, Anderson JM, Manning SE, Anderson SL, Nordgren RE, Felopulos GJ, Bauman ML. Brief report: macrographia in high-functioning adults with autism spectrum disorder. J Autism Dev Disord. 2001 Feb;31(1):97-101.
Brain Cogn. 2001 Dec;47(3):504-12.

Thursday, May 29, 2008

Japanese aphasia: Gogi, kanji, kana, kuku

Gogi, or word meaning aphasia, refers to selective impairment of kanji pprocessing. Kanji is text from ideographs as opposed to kana, which is phonologic writing, with a 1:1 correspondence between sound and script for each mora or syllable. Gogi aphasia was first described by Imura T (Aphasia: characteristic symptoms in Japanese. Psychiatria et Neurologia Japonica 47: 196-218 1943). Gogi aphasic patients have preservation of kana processing, difficulty in comprehension, in the retrieval of content words (ie lexical items), and fluent oral repetition. One author compares it to the mixed form of transcortical aphasia (Goldstein K, Die transcortikalen aphasien. Fishcer, Jena, 1917), to Luria's semantic aphasia, or Geschwind, Quadfasel and Segarra's isolation of the speech area. A patient reported by Sasanuma and Monoi (after a traumatic hemorrhage) (Neurology 1975) could repeat without comprehension. He did poorly on sentencite comprehension, auditory comprehension but had preserved comprehension of numbers. He had fluent speech with normal prosody and loss of content words. He made numerous "unrelated" errors on confrontation naming. He pwherformed at 95 % on the Controlled Oral Word Association Test (Japanese version). He produced well formed but semantically empty sentences, and could repeat orally normally. Reading was impaired in kanji and kana in term s of comprehension, but he could read most kana words aloud but not kanji. Japanese on and kun reading of kanji requires semantic knowledge to read. Also, Japanese text does not have word boundaries except semanticallepy deduced by kana and kanji words, so one has to rely on semantics to know the correct boundaries (which take the place of commas, periods and spaces in English). Gogi aphasics who lack comprehension place pauses at the wrong loci eg in the middle of a morpheme. Writing was impaired in both kana and kanji with kanji worse. Writing to dictation in kana was relatively preserved, whereas kanji was awful. Kanji errors were made in which kanji chthe aracters which are ideograms were treated as though they were phonetic with phonetic errors in substitutions made. Number concept and calculation was preserved. Reviewing the literature, all but one of six cases spared "parietal" signs such as angular gyrus symptoms, constructional apraxia, or visuomotor impairment. The author posits impairment of kana processing, in contrast as being in Broca's area, whereas Gogi aphasia may represent impaired second or third temporal gyri or underlying white matter but sparing the "Wernicke-Broca" complex(Neurology 25: 627-632, 1975).

Kuku is a mnemonic rhyme by which Japanese learn the multiplication tables via ther auditory route. Patients with impaired kuku learning relearned multiplication tables using the visual route. (Kashiwagi et al. Neduropsychologia 1987).


For those English speakers who want to impress your audiences when you give a lecture, kana is further divided into katakan (imported words) and hiragana (nonimported or native words). Generally there is no difference in performance in the two types.

Another article analyzed error types in kana and kanji . Patients with kanji aphasia had "word (graphical) confusion" whereas kana aphasics had "phonologic confusion." However there were significantly less vowel errors than consonant errors in kana, and those vowel errors that occurred also had a substitution error in the preceding consonant. Patients with kana aphasia typically had apraxia of speech (80%) whereas patients with kanji aphasia did not. (Sasanuma S, Fujimura O. An analysis of writing errors in Japanese aphasic patients: kanji v. kana words).

Yet another article compared writing Arabic numerals, kani and kana in brain damaged patients (Tamara I, Kikuchi S, OtsukiM, Tashiro K. Cognitive Neuroscience and Neuropsychology Neuroreport 14:861-865, 2003). 4 patients with Gerstmann's syndrome and 4 with Wernicke's aphasia were studied. Wernicke's aphasics could write Arabic numerals, but Gerstmann's patients could write kanji numbers better than Arabic numbers. The authors speculate that Arabic numerals are somesthetic and linked to concept of number processing and bypass phonological analysis.

Sugishita M, Otomo K, Kabe S, Yunoki K. A critical appraisalof neuropsychological correlates of Japanese ideogram (kanji) and phonogram (kana) reading (Brain 1992; 115:1563-1585) looked at 23 patients with Broca aphasia, 13 Wernicke's and 7 with alexia and agraphia and did not find a relationship between aphasia pattern and lesion site, contrary to previous smallcase series.

Saturday, May 24, 2008

Introduction to Luria


I have just read two and a half books of the half dozen or so I bought written by Alexander Romanovich Luria. Luria expands behavioral neurology well beyond what "classical" behavioral neurology. Whereas here we have been captive to anatomy and classical syndromes, Luria incorporates much more discussion of unknown Russian authors, known but underestimated Russian neurophysiologists, Pavlovian theory, developmental neurology, cross cultural neurology, politics, and evolutionary neurology. Need I add that Luria does discuss all the classical Western behaviorists from the time of Wernicke and before, and adds more bedside examination devices than I knew existed? The next few blogs will discuss this giant of neurology who happened to live in the Soviet Union. As a tidbit, the epilog written in "The Making of a Mind" takes us through the political contexts of the twists and turns in Luria's fascinating career, including purges, and makes sense of events that have caused some to label him as a "Soviet" neuropsychologist.

Interhemispheric relations and the functions of the minor hemisphere

Luria AR , Simernitskaya EG. Neuropsychologia 1977; 15: 175-178.

The authors propose a novel theory of brain reorganization wherein active, intentional memorization is governed by the dominant hemisphere, and involuntary or incidental memory depends upon the nondominant hemisphere. They introduce their relucatance to divide the hemispheres into verbal and nonverbal realm, but to further parse. He quotes Goldstein (1948) regarding the dedifferentiation of figure and background, and Bernstein NA (M0scow, 1948 in Russian) for the disorganization of movement.

The subjects were given lists of 10 unrelated 2 and 3 syllable words and asked to memorize them. The percentage retrieved was an indication of voluntary memory. In the second experiment subjects were asked to count the number of words with the letter K or thenumber of letters in the series. Then, retrieval was assessed as a measure of passive memory. The subjects were fifteen patients with left hemisphere lesions, fifteen with right hemisphere lesions, and fifteen normal controls (college students). The results showed that left hemisphere lesions were particularly impaired on active memorizing, whereas the right hemisphere patients were severely impaired on passive memorization. The right hemisphere lesion group showed catastrophic results on passive memorization. The authors speculate the findings indicated the concentration of attention on the conscious non memory task blocked the retrieval of background traces.

Caplan B (Hemispheric dominance for intentional and automatic processes: a test of the Luria and Simernitskaya hypotheses Neuropsychologia 22:247 1984) proposes the results were more consistent with material specific deficits following unilateral lesions.

Luria's frontal lobe syndrome: psychological and anatomical considerations

Canavan AGM, Janota I, Schurr PH. JNNP 1985; 48: 1049-1053. Authors cast doubt on Luria's "frontal lobe syndrome" except in cases of more global cerebral dysfunction.

Complexmotor function in humans: validating and extending the postulates pf Alexandr R. Luria

Bhimani AA, Hlustik P, Small SL, Solodkin A. Cog Behav Neurol 2006; 19:11-20.

The authors use functional imaging to elaborate the neural circuitry of 3 of Luria's motor tests, modified for convenience with fMRI. The fist-palm-edge test, modified to fist, scissors, gun test, activated M1, S1 and the Supplementary motor area. The hand imitation task activated the right more than the left IFC (inferior frontal cortex) , as well as S1 and PL. The piano key task activated the SMA, pre SMA and LPMCd (lateral premotor cortex).

In the discussion the authors noted the contralateral M! activated without fail during movement, but ipsilateral activation was seen for simple movements. The paino key task had LESS ipsilateral M! activation than did fist-scissors-gun. (Familiarity diminished activation, and all subjects had typing experience per authors). However all 3 tasks had some ipsilateral activation. S1 activation was thought necessary to the requirement for proprioception activation. PL (parietal lobe) was extensively activated for the hand imitation task, as in other studies the area is shown tobe important for visuomotor transformation (Luria, Higher Cortical Functions), mental imagery rotation (Bonda et al. J Neurophysiol, 1996), and mechanisms of imitation (Iacoboni M et al. Science 1999; 286:2526-2528).
HI task is thought by Rizolatti to be part of the continuum of learning language through imitation (Trends in Neurosci 1998). The deficit was for static not dynamic HI which may be separately affected. Left preference was not seen, unlike cases in literature (Poizner et al.) nor in PK task perhaps due to familiarity. The piano key task had more activation of the pre SMA, perhaps due to self pacing.

The cerebellar cortex was crucially activated in all 3 tasks. Activation however, was generally ipsilateral.

Monday, May 19, 2008

Hallucinations and related conditions

from S Tekin and JL Cummings, Clinical Neuropsychology, fourth edition, ed by Heilman KM and Valenstein E, chapter 17. An overview of semiology and terminology:

Unusual syndromes

Hallucinations with eye disorders: trauma, cataracts, macular degeneration, choroidal revascularization, retinal detachment, retinal traction, central retinal vein occlusion, and serous retinopathy. Moore's lighting streaks are vertical bands of light in temporal fields during eye movements. Saccades may cause flick phosphenes which are streaks of light in the central visual field. Photopsias are light with geometric structure. Phantom vision may occur after visual loss or enucleation. Hallucinations are rare after visual loss in the young.

The Charles Bonnet syndrome are visual hallucinations in normal elderly usually due to deprivation often with insight, usually pleasant formed images lasting for a few seconds to all day and disappearing with eye closure. Age, poor vision and binocular vision loss are risk factors. They are worse in demented patients and can be precipitated by beta blockers.

Entopic phenomena are actual visual phenomena, not hallucinations, occurring due to particles in the vitreous, macular edema or elements of one's own retinal circulation (Scheere's phenomena). Vitreous deposits (floaters) occur as amoeba shaped or shadow like forms.

Optic neuritis or compressive ischemic optic neuropathy may cause unformed visual hallucinations, including phosphenes, which occur in dim lighting often with horizontal saccades. Sudden sounds can cause auditory visual synesthesia.

Peduncular hallucinosis as part of the top of the basilar syndrome are vivid and full of motion including small (Lilliputian) people, animals, or kaleidoscopic views of landscapes. They occur in the evening or night and last a few seconds or minutes over days to weeks. Visual acuity and fields are normal. They are pleasant. Associations are abnormal SWS, impaired EOM's, and abnormal balance between serotonin and dopaminergic stimulation.

Release hallucinations occur with homonymous hemianopsia in 13 % of such patients, and consist of complex visual patterns, colored patterns or formed images in the area of the defect, and last minutes to hours. The "picture within a picture " sign was described in someone with a right parietal lesion, who saw people "milling around" only in the lower left quadrantanopic field.

Epileptic hallucinations are brief and stereotyped and in the occipital cortex are usually unformed, consisting of colored lights, weaving patterns, zig-zag lights, spots or amaurosis. Complex or formed visual hallucinations usually originate in the parietal or temporal association cortex. Epileptic hallucinations usually occur in one quadrant or hemifield and may be associated with motion, often rapid motion contralateral to the seizure focus. Headache may follow a seizure.

Migraines cause unformed flashes of light, or color, scintillating scotomas and zig zag lines called "fortification spectra." Reproductions of self or body parts in external space are called autoscopic phenomena. Migraine fortification spectra tend to be linear and black and white and last longer than epileptic phenomena, which tend to be multicolored circular or spheroid patterns.
Migraine visual phenomena tend to move across one fourth or one half the visual field and to grow in size as they do. Blurring of part or all of the field with scintillating lights around a scotoma is more common than fortification spectra.

Narcoleptics have hypnagogic and hypnopompic hallucinations which may be formed or unformed and associated with sleep paralysis.

In Parkinson's disease, hallucination are realistic nonthreatening images of people or animals and may be treatment associated. In Lewy body dementia hallucinations (by definition) occur in the first year.

Hallucinations in AD are as high as 67 % in facilities (much lower at home) and are associated with aggressive behavior. Such patients may also have visual processing deficits.

In DT's, patients usually see animals but may see Lilliputian hallucinations.

LSD usually causes visual hallucinations exacerbated by eye closure, geometric colors or audiovisual synesthesia. In general hallucinosis correlates with serotoninergicity. Other drugs include PCP, mescaline, cocaine, and meth (ecstasy) cause hallucinations.

Eidetic imagery is vivid internal imagery expressed onto the outside.

In depression, hallucinations are mood congruent, whereas in schizophrenia they are not.

Musical hallucinations occur in deafness, encephalitis, epilepsy, , and temporal lobe lesions.

Tactile hallucinations occur after amputations including children born without limbs. If they have the feeling of amputated limbs moving they are called kinesthetic hallucinations.Formication hallucinations (of bugs crawling) occur in DT's, schizophrenia, complex partial seizures, the use of hallucinogens, or if unilateral,with thalamic or parietal lesions.They also can be paraneoplastic in origin.

Narcoleptics may experience auditory hallucinations such as collections of sounds or melodies or tactile ones such as pinching, rubbing, light touching, or feeling above the bed and seeing one's own body below. They are complex and realistic.

Olfactory hallucinations may be part of an aura or complex partial seizure, and emanate from the olfactory bulb, posterior medial frontal cortex, olfactory cortex, uncus or anterior temporal lobe.

Gustatory hallucinations are especially common with uncinate gyrus seizures with a bitter, sweet, salty or tobacco like metallic or indescribable strange taste. They occur in 4 % of TLE, and parietal opercula seizures. Visceral hallucinations are common in TLE.

Drugs can cause hallucinations. Notably, digoxin can cause a yellow green tinge and sildafenil a blue tinged hallucination.

Monday, May 12, 2008

Regional frontal injuries cause distinct impairments in cognitive control


Alexander MP, Stuss DT, Picton T el al. Neurology 2007; 68: 1515-1523. 42 patients and 38 CS performed a modified Stroop test. Lesions in the left ventrolateral area produced errors of commission (ie utilization behavior) whereas lesions of the right ant cing, SMA, pre SMA or DL area caused a slowed reaction time (errors of omission).

Comment- a wonderful example of an advanced ablation paradigm article that is current, parcelling out frontal lobe function.

Aphasia: progress in the last quarter of a century

Hillis AE. Neurology 2007; 69: 200-213. (Views and reviews).
Summary: Dax, Broca and Wernicke made observations that Geschwind then summarized and reclassified in the 1960's. His BDAE held throught the CT/ MRI era.

In the 1980s, PET, fMRI and MEEG revolutionized our thinking. They showed bilateral involvement during language tasks, although the left hemisphere has more activation. These activated areas include remote locales such as inferior and anterior temporal cortex and basal ganglia and thalamus. The cognitive processes involved in language tasks in increasingly complex models were mapped out, involving PDP systems, linguistics, mathematics, and neuroscience. Third, analysis of dementia allowed analysis of semantic dementia after lobar degeneration, which does not occur after stroke.

Minutiae discovered include the constant finding of activation of the midfusiform area during reading, and the left midfusiform area during naming and other lexical tasks. Inhibition with cortical stimulation among presurgical epileptic patients of this area or the posterior basal temporal area disrupts kanji (represents meanings not sounds) and picture naming (semantic to phonologic conversions are necessary) but not comprehension of kana (sounds of words), copying or tool use (Usui, Brain 2003). Infarction of this area caused impaired oral reading and naming.

Classic aphasiology is reviewed. In Broca's aphasia, "nonfluency"can refer to decreased length of phrases, impaired melodies and articulatory agility, decreased words per minute, or agrammatism. Most patients have islands of preserved fluency especially of overlearned speech. This confounds classification. Comprehension of complex forms or noncanonical phrases (eg. passive voice) or comparisons of word order or meaning are damaged (Is a horse larger than a dog?) as is spelling of familiar words, and use of phonics to spell unfamiliar words. She criticizes the argument htat a single underlying impairment can cause Broca's syndrome, but allows that it is a vascular syndrome. She also discusses the conundrum of Broca's area lesion causing speech apraxia, and warns against excessive inflexibility in "localization," since individuals vary in their makeup. Hypoperfusion of surrounding tissue without infarction is another source of error.

Wernicke's aphasia consists of fluent jargons, neologisms, and lack of awareness of the deficit. Melody is preserved. Writing parallels speech (meaningless). It relates to posterior division of the MCA .

ACA lesions cause TCM aphasia (or watershed strokes between ACA and MCA).

Conduction aphasia has fluent accurate spontaneous speech with phonemic paraphasias, with conduit 'approche. Author rebuts Geschwind that the arcuate fasciculus is important, citing lesions in SMG or deep parietal white matter and on lesion studies showing lack of reliability of arcuate fasciculus lesions causing conduction aphasia.

Author discusses pure alexia and takes the classic disconnection explanation, emphasizing the co-occurrence with optic aphasia and the similarity of the neurologic lesions. She discusses semantic errors in such patients noting that they are partial.
Hillis discusses aphasia secondly, from the pov of the distributed semantic networks implied in addition to the previously described vascular syndromes. These account for category selectivity in naming, eg.

Treatment is discussed briefly, but author notes that intense treatment 4 days per week for a short time is more effective than spread out sessions over alonger period (Bhogal, Stroke, 2003).