Excitation of the indirect pathway has the net effect of inhibiting thalamic neurons rendering them unable to excite motor cortex neurons.
The normal functioning of the basal ganglia apparently involves a proper balance between the activity of these two pathways. One hypothesis is that the direct pathway selectively facilitates certain motor or cognitive programs in the cerebral cortex that are adaptive for the present task, whereas the indirect pathway simultaneously inhibits the execution of competing motor programs.
An upset of the balance between the direct and indirect pathways results in the motor dysfunctions that characterize the extrapyramidal syndrome see below. Direct pathway. Although the connectivity patterns of the direct and indirect pathways are relatively straightforward, the predominance of inhibitory connections in the system can make an understanding of the functional circuitry complicated and non-intuitive Figure 4.
Solid lines represent direct pathway and dashed lines represent indirect pathway. The output from GPi is common to both pathways. Green lines represent excitatory connections and red lines represent inhibitory connections. Click on individual pathway names to view each pathway in isolation.
The direct pathway starts with cells in the striatum that make inhibitory connections with cells in the GPint. The GPint cells in turn make inhibitory connections on cells in the thalamus. Thus, the firing of GPint neurons inhibits the thalamus, making the thalamus less likely to excite the neocortex.
When the direct pathway striatal neurons fire, however, they inhibit the activity of the GPint neurons. This inhibition releases the thalamic neurons from inhibition i. Indirect pathway. The indirect pathway starts with a different set of cells in the striatum. These neurons make inhibitory connections to the external segment of the globus pallidus GPext. The GPext neurons make inhibitory connections to cells in the subthalamic nucleus, which in turn make excitatory connections to cells in the GPint.
Remember that the subthalamic-GPint pathway is the only purely excitatory pathway within the intrinsic basal ganglia circuitry. As we saw before, the GPint neurons make inhibitory connections on the thalamic neurons. To see the net effects of activation of the indirect pathway, let us work backwards from the GPint. When the GPint cells are active, they inhibit thalamic neurons, thus making cortex less active. When the subthalamic neurons are firing, they increase the firing rate of GPint neurons, thus increasing the net inhibition on cortex.
Firing of the GPext neurons inhibits the subthalamic neurons, thus making the GPint neurons less active and disinhibiting the thalamus. However, when the indirect pathway striatal neurons are active, they inhibit the GPext neurons, thus disinhibiting the subthalamic neurons. With the subthalamic neurons free to fire, the GPint neurons inhibit the thalamus, thereby producing a net inhibition on the motor cortex.
Thus, as a result of the complex sequences of excitation, inhibition, and disinhibition, the net effect of the cortex exciting the direct pathway is to further excite the cortex positive feedback loop , whereas the net effect of cortex exciting the indirect pathway is to inhibit the cortex negative feedback loop. Presumably, the function of the basal ganglia is related to a proper balance between these two pathways. Motor cortex neurons have to excite the proper direct pathway neurons to further increase their own firing, and they have to excite the proper indirect pathways neurons that will inhibit other motor cortex neurons that are not adaptive for the task at hand see below.
An important pathway in the modulation of the direct and indirect pathways is the dopaminergic, nigrostriatal projection from the substantia nigra pars compacta to the striatum Figure 4. Direct pathway striatal neurons have D1 dopamine receptors, which depolarize the cell in response to dopamine. In contrast, indirect pathway striatal neurons have D2 dopamine receptors, which hyperpolarize the cell in response to dopamine.
The nigrostriatal pathway thus has the dual effect of exciting the direct pathway while simultaneously inhibiting the indirect pathway.
Because of this dual effect, excitation of the nigrostriatal pathway has the net effect of exciting cortex by two routes, by exciting the direct pathway which itself has a net excitatory effect on cortex and inhibiting the indirect pathway thereby disinhibiting the net inhibitory effect of the indirect pathway on cortex. The function of the basal ganglia in motor control is not understood in detail.
It appears that the basal ganglia is involved in the enabling of practiced motor acts and in gating the initiation of voluntary movements by modulating motor programs stored in the motor cortex and elsewhere in the motor hierarchy Figure 4. Thus, voluntary movements are not initiated in the basal ganglia they are initiated in the cortex ; however, proper functioning of the basal ganglia appears to be necessary in order for the motor cortex to relay the appropriate motor commands to the lower levels of the hierarchy.
The proper motor programs are selected based on the desired motor output relayed from cortex. Note that the complex circuits of the direct and indirect pathways are schematically diagramed as single neurons for clarity of illustration. Recall that the major output from the basal ganglia is an inhibitory connection from the GPint or SNr to the thalamus or superior colliculus.
Studies of eye movements in monkeys have shed light on the function of the basal ganglia loop. Normally, the SNr neurons are tonically active, suppressing the output of the collicular neurons that control saccadic eye movements. When the direct pathway striatal neurons are excited by the cortical frontal eye fields, the SNr neurons are momentarily inhibited, releasing the collicular neurons from inhibition.
This allows the appropriate collicular neurons to signal the target of the eye movement, allowing the monkey to change its gaze to a new location. The movement was initiated in the frontal eye fields; however, the proper activation of the eye movement required that collicular neurons be released from the inhibition of the basal ganglia. What is the function of the tonic inhibitory output of the basal ganglia?
Recall from the Motor Cortex chapter that stimulating the motor cortex of monkeys at various locations results in stereotyped sequences of movements, such as bringing the hand to the mouth or adopting a defensive posture.
It is important that only one motor program be active at a given time, however, such that one motor act e. It is thought that the basal ganglia is normally active in suppressing inappropriate motor programs, and that activation of the direct pathway temporarily releases one motor program from inhibition, enabling it to be executed by the organism.
Thus, the basal ganglia act as a gate that enables the execution of automatic programs in the hierarchy. A If a reward occurs unexpectedly, the dopaminergic neuron fires briskly. The investigators observed, in those with incomplete pattern, a trend toward delayed acquisition of independent walking. Teitelbaum et al. They noted that in the children they reviewed, some had reflexes that persisted too long in infancy, whereas others first appeared much later than they should.
The asymmetric tonic neck reflex is one reflex that they noted may persist too long in autism. A normal child, lying on its back and wanting to roll over onto its front, soon learns that this can be readily accomplished if first the head, then the shoulders, and finally the hips are swiveled in the same direction.
If the timing of this sequence is correct, the supine-prone transition requires a minimum of effort. Autistic infants appear to experience considerable difficulty in learning this simple motor sequence. Indeed, the sequence does not even occur in their failed attempts. Instead, they awkwardly arch their backs and ultimately fall into the desired position. When a new motor pattern is being acquired, both the means and the ends will be coded in currently active patterns of neuronal signals.
And there must be interactions between these patterns because the goal will influence the route through muscular hyper- space by which it is to be achieved. The PFC probably dictates patterns of elementary muscular sequences, but it must be borne in mind that the sophistication of the latter will depend upon what the individual has already learned.
A ballet dancer would regard as an elementary motor pattern a muscular sequence, which the novice would find quite difficult. The most spectacular feature to evolve thus far has been that seen in the mammals, and it permitted acquisition, during a creature's own lifetime, of novel context-specific reflexes, especially those relying on sequences of muscular movements.
This mechanism makes heavy demands on the neural circuitry, because it requires an attentional mechanism. And because attention must, perforce, be an active process, there has to be feedback from the muscles, carrying information about their current state, including their current rate of change of state. Without such information, anticipation would be impossible, and without anticipation there could be no meaningful adjudication and decision as to the most appropriate way of continuing an on-going movement.
Without such a mechanism, novel context-specific reflexes could not be acquired. The fascinating thing is that access to such on-line information mediates consciousness, the gist of which is the ability to know that one knows. The ability to know that one knows is referred to by psychologists as first-order embedding.
Higher embedding, such as that exemplified by knowing that one knows that one knows, merely depends upon the ability to hold things in separate patches of neuronal activity in working memory. This manifests itself in a creature's intelligence, which also dictates its ability to consolidate existing schemata into a new schema.
When we know that we know, the muscular apparatus is not only monitoring its own state, it is monitoring the monitoring. The basal ganglia are important for initiating motor movements, but not for determining the detailed properties of those movements. We have elsewhere described how abnormal motor development can accurately be used as a marker to predict autism and other developmental disorders in later development Leisman, Many authors have noted a relationship between incoordination and clumsiness, especially of posture and gait, and autism as well as with other neurodevelopmental disorders.
The type of gait and motor disturbance has been compared mostly to those that are either basal ganglionic and most commonly cerebellar in origin Nayate et al.
In fact, practically all children in this spectrum have some degree of motor incoordination. The type of incoordination is also usually of the same type primarily involving the muscles that control gait and posture or gross motor activity.
Sometimes to a lesser degree, we find fine motor coordination also affected. Postural sway during quiet stance is often assumed to be a resultant sum of internal noises generated in the postural control system carrying little useful information Ishida and Imai, ; Fitzpatrick et al.
This suggests that a small and slow sway as a part of the postural control during quiet stance might be important to provide updated and appropriate sensory information helpful to standing balance and it is certainly cognitively mediated Gatev et al.
Body sway is a kinematic term and can be derived from the sum of forces and moments acting on the human body. Many studies have shown that when various sensory systems are systematically manipulated, body sway is affected Masani et al.
For example, absence of visual input has been shown to result in an increase in body sway Sarabon et al. Thus, postural sway can be analyzed neurologically as well as biomechanically Melillo and Leisman, and the combination of both aspects can contribute to a more comprehensive understanding of the processes involved when maintaining body balance in general and the relationship between the basal ganglia and the frontal cortex in particular in developmental disorders.
Before viewing the biomechanical considerations, let us first define some basic biomechanical notions represented in Figure 4. Figure 4. Summary of biomechanical principles. Body center-of-mass COM —is the location where all of the mass of the system could be considered to be located.
For a solid body it is often possible to replace the entire mass of the body with a point mass equal to that of the body's mass. This point mass is located at the center of mass. COG—the resultant force of all of small attractive forces of the mass particles of which the body is composed is the body's weight, and the location at which the resultant force is assumed to act.
Ground reaction force vector GRF —the resultant of a pressure distribution under the foot or feet. Base of support BoS , is defined as the possible range of the COP, which is loosely equal to the area below and between the feet in two-feet standing Winter et al. The most simplified biomechanical model assumes the human as one rigid body, where the COM is located at the waist, a pivot axis at the ankle, and a COP where the GRF vector acts.
The assumptions used in the presented model are those of the inverted pendulum model of human standing balance Winter and Eng, : 1 The balance problem can be completely described by the movement of the whole-body COM, 2 the distance l from the axis of rotation to the COM remains constant, and 3 the excursions of the COM are small with respect to l. Where small body movements cause acceleration of the COM, a radial acceleration exists leading to priority of equilibrium control during almost all motor tasks including quiet standing aimed at reposition the COG over the COP Gatev et al.
The muscles around the ankle and hip joints work continuously as the human body struggles to maintain balance. One can see that as long as the COP is kept beyond the COM position, with respect to the rotation center at the ankle, the body is accelerated back to the upright position. A major problem for human standing posture is the high center of gravity COG maintained over a relatively small base of support.
In attempting to understand motor mechanisms involved in the development of balance, research on postural control has focused mainly on two types of study: a balance with respect to external conditions, b postural adjustments to anticipated internal disturbances of balance. Unexpected external disturbances reveal centrally programmed patterns of postural responses. Afferent feedback also influences posture when the initial setting is disturbed.
The second type of disturbance reveals feed-forward postural adjustments for review, Dietz, By feed-forward, we mean that the controller predicts an external input or behaves using higher-order processing rather than simple negative feedback of a variable Gatev et al.
Studies of the postural responses to unexpected small and slow external disturbances in the antero-posterior direction found that most people reposition the COG by swaying as a flexible inverted pendulum primarily about the ankles with little hip or knee motion.
The choice of a postural strategy to disturbance was found to depend on the available appropriate sensory information Nashner et al.
Locomotion is fundamental for an optimal child development. The ability to smoothly and adequately navigate through the environment enables the child to interact with the environment.
ADHD and autistic spectrum individuals have reported significant motor difficulties, both fine and gross Melillo and Leisman, According to Patla et al.
The bipedal walking pattern that humans have adopted over time constitutes an elegant way to meet these requirements in an efficient and economic way. Several findings with respect to motor control in children with DCD and ADHD, however, indicate that they could have problems to meet some of these constraints related to neuromuscular control. Raynor observed decreased muscular strength and power in children with DCD, accompanied by increased levels of co-activation in a unilateral knee flexion hand extension task.
Similar neuromuscular problems, indicating difficulties with the selective muscle control necessary for rhythmic coordination, were found in a unilateral tapping task by Lundy-Ekman et al. Likewise Volman and Geuze showed that these rhythmic coordination difficulties of children with DCD are not restricted to the control of unilateral tapping.
By means of a bimanual flexion-extension paradigm they found that relative phase stability of children with DCD was less stable than in controls. From studies where upright stance was perturbed by means of a sudden displacement of a moveable platform it was concluded that the balance recovery strategy of children with DCD was different Williams, Their strategy was characterized by a top-down muscular activation pattern compared to the distal-proximal pattern displayed by children without DCD, which was argued to be more efficient.
In stance, the projection of the center of mass has to be kept within the borders of the base of support, in order to maintain balance. For locomotor balance however, one must achieve a compromise between the forward propulsion of the body, which involves a highly destabilizing force, and the need to maintain the overall stability Winter and Eng, Taking into account this complexity with respect to the control of posture during locomotion it can be hypothesized that the balance problems experienced by children with DCD might be a limiting factor for their locomotor activity.
So far, descriptions of the gait pattern of children with DCD are limited to some qualitative observations. Larkin and Hoare have notified for example poor head control, bent arms in a guard position, jerky limb to limb transitions, excessive hip flexion, pronounced asymmetry, wide base of support, short steps, foot strike with flat foot and toe-walking. This index is based on a comparison of four spatio-temporal gait parameters time of opposite toe-off, single stance time, total stance time, and step length with reference parameters of the San Diego database Sutherland, From their calculations Woodruff et al.
This one-dimensional measure of walking performance is useful for classifying and evaluation of gait performance in clinical practice; however, it does not explain the nature or source of atypical gait see Figure 5. In addition, comparison of gait variables with a reference population without controlling for stature or leg length and body weight might obscure deviations and lead to imprudent conclusions, since the walking pattern is highly dependent on anthropometrical characteristics Therefore, in order to gain insight into the gait pattern of children Hof, ; Stansfield et al.
Figure 5. Stick-figures of the body configuration at initial FS left and TO right. Feet with broken lines are the contralateral feet. Figure 6. The horizontal broken line indicates the cut-off value 2. Different studies report balance testing included a disruption of sensory signals. During dynamic posturography ADHD-participants showed mild balance problems, which correlated with findings in cerebellar children.
ADHD children showed abnormalities in a backward walking task and minor abnormalities in the paced stepping test. They did not differ in treadmill walking from the controls. These findings support the notion that cerebellar dysfunction may contribute to the postural deficits seen in ADHD children. However, the observed abnormalities were minor. It needs to be examined whether balance problems become more pronounced in ADHD children exhibiting more prominent signs of clumsiness.
In the past, motor clumsiness had been viewed as a neurological rather than as a psychiatric disorder. Motor control problems were first noted in what were then called minimal brain dysfunction syndromes or MBD. Several studies by Denckla and others Denckla and Rudel, ; Denckla et al. Minor developmental deviations were reported to consist of dyscoordination, fine motor deviations, choreiform movements, and abnormalities of muscle tone.
Researches that have dealt with these minor neural developmental deviations tend to look at motor dysfunction as a sign of neurological disorder that may be associated with other problems such as language and perception dysfunction.
In Asperger's syndrome, it has been noted that individual's have significant degrees of motor incoordination. Wing and Attwood noted that posture, gait, and gesture incoordination were most often seen in Asperger's syndrome and that children with classic autism seem not to have the same degree of balancing and gross motor skill deficits. However, it was also noted that the agility and gross motor skills in children with autism seem to decrease as they get older and may eventually present in similar or at the same level as Asperger's syndrome.
Gillberg and Gillberg also reported clumsiness to be almost universal among children that they had examined for Asperger's syndrome. The other associated symptoms noted consisted of severe impairment and social interaction difficulties, preoccupation with a topic, reliance on routines, pedantic language, comprehension, and dysfunction of nonverbal communication. In subsequent work, Gillberg included clumsiness as an essential diagnostic feature of Asperger's syndrome.
Klin et al. They further noted that all 21 Asperger's cases showed gross motor skill deficits, but 19 of these also had impairment in manual dexterity, which seems to suggest that poor coordination was a general characteristic of Asperger's. With studies like these, many researches have noted dysfunction of fine motor coordinative skills as a feature of autistic spectrum disorders.
Walker et al. Vilensky et al. Hallett et al. Using a computer assisted video kinematic technique; they found that gait was atypical in these individuals. The authors noted that the overall clinical findings were consistent with a cerebellar rather than a basal ganglionic dysfunction. Kohen-Raz et al. These objective measures were obtained using a computerized posturographic technique. It has been also noted that the pattern of atypical postures in children with autism is more consistent with a mesocortical or cerebellar rather than vestibular pathology.
Numerous investigators Howard et al. Makris et al. They noted that ADHD is hypothesized to be due, in part, to structural defects in brain networks influencing cognitive, affective, and motor behaviors Leisman et al.
Although the literature on fiber tracts is limited in ADHD, Makris and colleagues note that gray matter abnormalities suggest that white matter connections may be altered selectively in neural systems.
A prior study, Ashtari et al. In this study of adults the authors hypothesized that fiber pathways subserving attention and executive functions would be altered.
Relative to controls, the fractional anisotropy FA values were significantly smaller in both regions of interest in the right hemisphere, in contrast to a control region the fornix , indicating an alteration of anatomical connections within the attention and EF cerebral systems in adults with childhood ADHD. Researchers at Stanford University have observed that in children with ADHD, also known as childhood hyperkinetic disorder Wing and Attwood, frontal-subcortical connections are disrupted by subcortical dysfunction showing decreased glucose consumption in frontal cortex, and decrease nigrostriatal D2 receptor uptake ratios The Stanford study used functional MRI to image the brains of boys between the ages of 8 and 13 while playing a mental game.
Ten of the boys were diagnosed with ADHD and six were considered normal. When the boys were tested there appeared to be a clear difference in the activity of the basal ganglia with the boys with ADHD having less activity in that area than the control subjects. After administering methylphenidate, the participants were scanned again and it was found that boys with ADHD had increased activity in the basal ganglia whereas the normal boys had decreased activity in the basal ganglia.
Interestingly, the drug improved the performance of both groups to the same extent. This may be a similar finding as the PET scans on patients with hyperactivity disorder, where normal appearing frontal metabolism existed with decreased caudate and putamen metabolism Gillberg and Gillberg, Methylphenidate, a dopamine reuptake inhibitor, may increase function in a previously dysfunctional basal ganglia whereas raising dopamine levels in normal individuals would most likely result in decreased activity of the basal ganglia to prevent overproduction of dopamine.
The previously dysfunctional basal ganglia would have most likely resulted in decreased frontal metabolism with increased thalamo-cortical firing; this would result in decreased cognitive function with increased hyperkinetic hyperactive behavior.
Increasing dopamine levels may increase frontal metabolism due to increased activity of the striatum with decreased firing of the globus pallidus thereby inhibiting thalamo-cortical firing decreases which in turn decreases hyperkinetic behavior. This would make sense based on the findings of fMRI before and after, and the fact that both groups showed equal improvement in performance. Etiological theories suggest a deficit in cortico-striatal circuits, particularly those components modulated by dopamine and therefore discussed in comparison with the other basal ganglia related disorders in the paper.
Teicher et al. Daily treatment with methylphenidate significantly changed the T2 relaxation times in the putamen of children with ADHD. There was a similar but non-significant trend in the right caudate. Converging evidence implies the involvement of dopaminergic fronto-striatal circuitry in ADHD.
Anatomical imaging studies using MRI have demonstrated subtle reductions in volume in regions of the basal ganglia and prefrontal cortex Castellanos et al. Cognitive functioning is mildly impaired in this disorder Seymour et al.
In particular, cognitive control, the ability to inhibit inappropriate thoughts and actions, is also affected and therefore we are again dealing with a disorder of inhibition.
Several studies have shown that this impairment is related to the reduction in volume in fronto-striatal regions Sergeant et al. Durston et al. Volumetric abnormalities have also been associated with the basal ganglia and in turn with ADHD.
Qiu et al. The basal ganglia caudate, putamen, globus pallidus were manually delineated on magnetic resonance imaging from typically developing children and children with ADHD. LDDMM mappings from 35 typically developing children were used to generate basal ganglia templates. These investigators found that boys with ADHD showed significantly smaller basal ganglia volumes compared with typically developing boys, and LDDMM revealed the groups remarkably differed in basal ganglia shapes.
Volume compression was seen bilaterally in the caudate head and body and anterior putamen as well as in the left anterior globus pallidus and right ventral putamen. Volume expansion was most pronounced in the posterior putamen. They concluded that the shape compression pattern of basal ganglia in ADHD suggests an atypical brain development involving multiple frontal-subcortical control loops, including circuits with premotor, oculomotor, and prefrontal cortices.
Aaron et al. Their paper was not about the problems of ADHD individuals per se but a thorough analysis of the neurophysiology of stopping. They hand indicated that sensory information about a stop signal is relayed to the prefrontal cortex, where the stopping command must be generated.
They collected the evidence together indicating that the right inferior frontal cortex IFC is a critical region for stop signal response inhibition Chambers et al. The Go process is likely generated by premotor areas that project via the direct pathway of the basal ganglia through striatum, pallidum, and thalamus , eventually exciting primary motor cortex and generating cortico-spinal volleys to the relevant effector each interacting with the globus pallidus Aaron and Poldrack, The Stop process could activate the globus pallidus via a projection from the STN.
As seen in Figures 7A—C , high resolution fMRI has shown activation of a midbrain region, consistent with the STN, when subjects successfully stop their responses Aaron and Poldrack, , and diffusion tractography shows that this STN region is directly connected to the right IFC via a white matter tract Aaron et al.
Two recent studies identified a third critical node for the stopping process in the dorso-medial frontal cortex, including the pre-supplementary motor area Floden and Stuss, Figure 7. A The interactive race model between Go and Stop processes. The parameters were estimated by fitting the model to thousands of behavioral trials from a monkey neurophysiology study. B Schematic of fronto-basal-ganglia circuitry for Going and Stopping. The Go process is generated by premotor cortex, which excites striatum and inhibits globus pallidus, removing inhibition from thalamus and exciting motor cortex see text for details.
The stopping process could be generated by IFC leading to activation of the subthalamic nucleus, increasing broad excitation of pallidum and inhibiting thalamocortical output, reducing activation in motor cortex.
D Regions of the rat brain implicated in behavioral stopping. Stopping is significantly impaired following excitotoxic lesions within the regions highlighted in red, whereas lesions within the gray-colored regions have no effect on stopping. Balance deficits, motor planning, motor coordination and perceptual-motor problems associated with other developmental disorders are, as we have noted, present with individuals with ADHD Kaplan et al.
As we had noted earlier, there have been attempts to assume a single underlying disorder such as atypical brain development because of the high level of comorbidity between learning, attention, developmental coordination, and behavioral disorders Kaplan et al.
The contribution of sensory organs to posture has been the object of much inquiry and for good reason. A malfunction in any of the three primary sensory subsystems visual, vestibular, or somatosensory can compromise integrative function and as a result limit adaptability of posture. A lack of optimal postural control limits the development of sensory strategies, anticipatory mechanisms, internal representations, neuromuscular synergies, and adaptive mechanisms Shumway-Cook and Woolacott, Inadequate input and the inability to integrate and prioritize information from different sources result in instability, poor motor planning, poor coordination, and perceptual motor problems.
Although posture dysfunction among children with ADHD may not be easily identified, research indicates that balance is compromised with this population Zang et al. Posture and balance are accomplished through several mechanisms acting together to maintain orientation and stability Shumway-Cook and Woolacott, Both the sensory and motor systems, along with the biomechanical properties of the organism provide the foundation for posture control Palmeri et al.
Self-organizing properties of motor behavior evident in other biological and natural systems are evident in the developing human as well Kamm et al. Various subcomponents within the individual, the task at hand, and the environment all interact to determine the movement that emerges, with no a priori determination of which system is the primary control parameter.
Unlike hierarchical theories of motor control that adhere to a prescriptive system of generating behavior i. Gravity, musculoskeletal properties, motion dependent torques and all other changing dynamical contexts, which can include the environment e.
In postural terms, early forms of coordinative units that allow infants to interact with the environment necessitate reflexes. Through development, more complex forms of control emerge such as anticipatory postural responses e. Subsequently voluntary motor control is available or possible as temporarily organized units or components within the organism perform at optimized levels.
This includes sensory, perceptual and motor functions that collectively allow highly adaptive responses. Dysfunction may arise because a subcomponent of the system is not functioning to its capacity, thus acting as a weak link. Children with ADHD interact with their environment but not in a consistent fashion as the typical population, perhaps due to a less than adequate sensory apparatus as suggested Zang et al.
The weakest component of the system serves as the control parameter in this case and determines the integrity of the coordinative unit. Neural circuits linking activity in anatomically segregated populations of neurons in subcortical structures and the neocortex throughout the human brain regulate complex behaviors such as walking, talking, language comprehension and other cognitive functions including those associated with frontal lobes.
Many neocortical and subcortical regions support the cortical-striatal-cortical circuits that confer various aspects of language ability, for example. However, many of these structures also form part of the neural circuits regulating other aspects of behavior. For example, the basal ganglia, which regulate motor control, are also crucial elements in the circuits that confer human linguistic ability and reasoning.
The cerebellum, traditionally associated with motor control, is active in motor learning. The basal ganglia are also key elements in reward-based learning.
Data from studies individuals with Tourette's syndrome, Obsessive-Compulsive Disorder as well as with Broca's aphasia, Parkinson's disease, hypoxia, focal brain damage, and from comparative studies of the brains and behavior of other species, demonstrate that the basal ganglia sequence the discrete elements that constitute a complete motor act, syntactic process, or thought process.
That applies with as much force to the human brain and the neural bases of cognition as it does to the human foot or jaw. The converse follows: the mark of evolution on the brains of human beings and other species provides insight into the evolution of the brain bases of human language. The neural substrate that regulated motor control in the common ancestor of apes and humans most likely was modified to enhance cognitive and linguistic ability.
Language and cognition played a central role in this process. However, the process that ultimately resulted in the human brain may have started when our earliest hominid ancestors began to walk. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Aaron, A. Converging evidence for a fronto-basal-ganglia network for inhibitory control of action and cognition.
Cortical and subcortical contributions to stop signal response inhibition: role of the subthalamic nucleus. Alexander, G. Parallel organization of functionally segregated circuits linking basal ganglia and cortex. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. Ashtari, M. Beiser, D. Model of cortical-basal ganglionic processing: encoding the serial order of sensory events. Pubmed Abstract Pubmed Full Text. Broadbent, D.
Perception and Communication. Oxford: Oxford University Press. CrossRef Full Text. The functional anatomy of basal ganglia disorders. Trends Neurosci. Alexander, G. Parallel organization of functionally segregated circuits linking basal ganglia and cortex. Aron, A. The neural basis of inhibition in cognitive control.
Neuroscientist 13, — Baradaran, N. Parkinson's disease rigidity: relation to brain connectivity and motor performance. Bar-Gad, I. Information processing, dimensionality reduction and reinforcement learning in the basal ganglia. Bassett, D. Small-world brain networks. Neuroscientist 12, — Cognitive fitness of cost-efficient brain functional networks.
Dynamic reconfiguration of human brain networks during learning. Bellec, P. The pipeline system for Octave and Matlab PSOM : a lightweight scripting framework and execution engine for scientific workflows. Biswal, B. Functional connectivity in the motor cortex of resting human brain using echo-planar MRI. Bogacz, R. The basal ganglia and cortex implement optimal decision making between alternative actions. Neural Comput. Bullmore, E. Complex brain networks: graph theoretical analysis of structural and functional systems.
Buxton, R. A model for the coupling between cerebral blood flow and oxygen metabolism during neural stimulation. Blood Flow Metab. Calzavara, R. Relationship between the corticostriatal terminals from areas 9 and 46, and those from area 8A, dorsal and rostral premotor cortex and area 24c: an anatomical substrate for cognition to action.
Cao, H. Altered brain activation and connectivity in early Parkinson disease tactile perception. AJNR Am. Carbonell, F. Dopamine precursor depletion impairs structure and efficiency of resting state brain functional networks. Neuropharmacology 84, 90— Chang, C. Temporal dynamics of basal ganglia response and connectivity during verbal working memory.
Neuroimage 34, — Cisek, P. Neural mechanisms for interacting with a world full of action choices. Cui, G. Concurrent activation of striatal direct and indirect pathways during action initiation. Nature , — Dosenbach, N. A dual-networks architecture of top-down control. Trends Cogn. Distinct brain networks for adaptive and stable task control in humans. Draganski, B. Evidence for segregated and integrative connectivity patterns in the human Basal Ganglia.
Ebisch, S. Long-range functional interactions of anterior insula and medial frontal cortex are differently modulated by visuospatial and inductive reasoning tasks. Neuroimage 78, — Fox, M. The human brain is intrinsically organized into dynamic, anticorrelated functional networks. Francois-Brosseau, F. Basal ganglia and frontal involvement in self-generated and externally-triggered finger movements in the dominant and non-dominant hand.
Georgiou, N. An evaluation of the role of internal cues in the pathogenesis of parkinsonian hypokinesia. Brain Pt 6 ,— Gottlich, M. Altered resting state brain networks in Parkinson's disease. Greicius, M. Functional connectivity in the resting brain: a network analysis of the default mode hypothesis. Haber, S. The primate basal ganglia: parallel and integrative networks. Hagmann, P. Mapping the structural core of human cerebral cortex. PLoS Biol.
He, Y. Graph theoretical modeling of brain connectivity. Hoehn, M. Parkinsonism: onset, progression and mortality. Neurology 17, — Howe, M. Prolonged dopamine signalling in striatum signals proximity and value of distant rewards.
Huettel, S. Dynamic and strategic aspects of executive processing. Brain Res. Hughes, A. What features improve the accuracy of clinical diagnosis in Parkinson's disease: a clinicopathologic study. Neurology 42, — Isomura, Y. Reward-modulated motor information in identified striatum neurons. Jacobson, S.
Neuroanatomy for the Neuroscientist. New York, NY: Springer. Joshua, M. The dynamics of dopamine in control of motor behavior. Kiesel, A. Control and interference in task switching—a review.
Kitzbichler, M. Cognitive effort drives workspace configuration of human brain functional networks. Lago-Fernandez, L. Fast response and temporal coherent oscillations in small-world networks. Latora, V. Efficient behavior of small-world networks. Leh, S. The connectivity of the human pulvinar: a diffusion tensor imaging tractography study. Imaging Fronto-striatal connections in the human brain: a probabilistic diffusion tractography study.
Lehericy, S. Cortex 14, — Lewis, S. Cognitive impairments in early Parkinson's disease are accompanied by reductions in activity in frontostriatal neural circuitry. Pubmed Abstract Pubmed Full Text. Litvan, I. Differential memory and executive functions in demented patients with Parkinson's and Alzheimer's disease. Mars, R.
Short-latency influence of medial frontal cortex on primary motor cortex during action selection under conflict. Martinu, K. Levodopa influences striatal activity but does not affect cortical hyper-activity in Parkinson's disease.
Masuda, N. Global and local synchrony of coupled neurons in small-world networks. McFarland, N. Thalamic relay nuclei of the basal ganglia form both reciprocal and nonreciprocal cortical connections, linking multiple frontal cortical areas.
McHaffie, J. Subcortical loops through the basal ganglia. Monchi, O. Neural bases of set-shifting deficits in Parkinson's disease. Cortical activity in Parkinson's disease during executive processing depends on striatal involvement. Brain , — Wisconsin Card Sorting revisited: distinct neural circuits participating in different stages of the task identified by event-related functional magnetic resonance imaging.
Nagano-Saito, A. Effect of mild cognitive impairment on the patterns of neural activity in early Parkinson's disease. Aging 35, — Dopamine depletion impairs frontostriatal functional connectivity during a set-shifting task. Nathaniel-James, D. The role of the dorsolateral prefrontal cortex: evidence from the effects of contextual constraint in a sentence completion task. Neuroimage 16, —
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