In this article, we argue that motor and cognitive processes are functionally related and most likely share a similar evolutionary history. This is supported by clinical and neural data showing that some brain regions integrate both motor and cognitive functions. In addition, we also argue that cognitive processes coincide with complex motor output. Further, we also review data that support the converse notion that motor processes can contribute to cognitive function, as found by many rehabilitation and aerobic exercise training programs. Support is provided for motor and cognitive processes possessing dynamic bidirectional influences on each other.

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 associated with frontal lobes. The basal ganglia, which regulate motor control, are also crucial elements in the circuits that confer human reasoning and adaptive function. The basal ganglia are key elements in the control of reward-based learning, sequencing, discrete elements that constitute a complete motor act, and cognitive function. Imaging studies of intact human subjects and electrophysiologic and tracer studies of the brains and behavior of other species confirm these findings. We know that the relation between the basal ganglia and the cerebral cortical region allows for connections organized into discrete circuits. Rather than serving as a means for widespread cortical areas to gain access to the motor system, these loops reciprocally interconnect a large and diverse set of cerebral cortical areas with the basal ganglia. Neuronal activity within the basal ganglia associated with motor areas of the cerebral cortex is highly correlated with parameters of movement. Neuronal activity within the basal ganglia and cerebellar loops associated with the prefrontal cortex is related to the aspects of cognitive function. Thus, individual loops appear to be involved in distinct behavioral functions. Damage to the basal ganglia of circuits with motor areas of the cortex leads to motor symptoms, whereas damage to the subcortical components of circuits with non-motor areas of the cortex causes higher-order deficits. In this report, we review some of the anatomic, physiologic, and behavioral findings that have contributed to a reappraisal of function concerning the basal ganglia and cerebellar loops with the cerebral cortex and apply it in clinical applications to attention deficit/hyperactivity disorder (ADHD) with biomechanics and a discussion of retention of primitive reflexes being highly associated with the condition.

New information about the basal ganglia and cerebellar connections with the cerebral cortex has prompted a reevaluation of the role of the basal ganglia in cognition. We know that the relation between the basal ganglia and the cerebral cortical region allows for connections organized into discrete circuits. Rather than serving as a means for widespread cortical areas to gain access to the motor system, these loops reciprocally interconnect a large and diverse set of cerebral cortical areas with the basal ganglia. The properties of neurons within the basal ganglia or cerebellar components of these circuits resemble the properties of neurons within the cortical areas subserved by these loops. For example, neuronal activity within the basal ganglia and cerebellar loops with motor areas of the cerebral cortex is highly correlated with parameters of movement, whereas neuronal activity within the basal ganglia and cerebellar loops with areas of the prefrontal cortex is more related to the aspects of cognitive function. Thus, individual loops appear to be involved in distinct behavioral functions. Studies of the basal ganglia and cerebellar pathology support this conclusion. Damage to the basal ganglia or cerebellar components of circuits with motor areas of the cortex leads to motor symptoms, whereas damage to the subcortical components of circuits with nonmotor areas of the cortex causes higher-order deficits. In this report, we review some of the new anatomic, physiologic, and behavioral findings that have contributed to a reappraisal of function concerning the basal ganglia and cerebellar loops with the cerebral cortex and apply it in clinical applications to obsessive-compulsive disorder, Tourette's syndrome, and attention-deficit/hyperactivity disorder as examples of how compromise at different points in the system may yield similar but different clinical results.

Cortical Visual Impairment (CVI) is a condition of bilateral visual loss due to injury of visual areas in the brain without significant eye or anterior visual pathway impairment. Perinatal hypoxic ischemic encephalopathy (HIE) and postnatal anoxia are frequent etiologies of CVI and tend to result in more extensive gray and white matter injury affecting optic radiations and visual cortex. Often these children have other significant neurological disabilities and seizures as well. This article provides an analysis of a clinical database of children with CVI evaluated between January 1996 and March 2003. The results of an intensive visual stimulation program were retrospectively examined. Criteria were set to extract a fairly homogeneous group of 21 children with CVI due to perinatal HIE or postnatal anoxia who had extensive gray and white matter injury and multiple neurological deficits; 20 of 21 (95%) had symptomatic epilepsy as well. Subjects entered the study with responses ranging from just a pupillary light reflex to rudimentary perception of outline. Each subject underwent an at-home treatment program. Twenty of 21 children (95%) manifested significant improvement after 4 to 13 months on the program. Results indicate that even in this challenging group, there may be considerable neuroplasticity in visual systems leading to reintegration and visual recovery.