Telencephalon

The Parkinson's-Reversing Breakthrough

Cure for Parkinson Disease

Get Instant Access

Two large parts of the telencephalon have important roles in motor control: the cerebral cortex and the basal ganglia. Of course, the function of both structures extends beyond motor control, but this article addresses only that role.

a. Cerebral Cortex The number of functionally distinct motor cortical fields remains unknown. One heuristically useful view of the frontal cortex divides it into three main parts: the primary motor cortex, a group of areas collectively known as nonprimary motor cortex, and the prefrontal cortex (Fig. 2). The first two components can be referred to collectively as the motor cortex, although this term is sometimes used as a synonym for primary motor cortex.

The primary motor cortex (abbreviated M1) corresponds approximately to Brodmann's area 4. It lies in the anterior bank of the central sulcus and contains a topographic representation of the musculature. Most textbooks depict this topography in the form of a homunculus (i.e., a projection of the body onto the cortical surface). Such pictures have validity only at the most superficial level. They correctly imply that the medial part of M1 contains the leg and foot representation, that a more lateral part includes the arm and hand representations, and that an even more lateral part has the face, tongue, and mouth representation. However, at any finer level of detail, the homunculus presents an inaccurate image of M1's organization. Instead, Ml consists of a mosaic of

Figure 2 Motor areas of the human brain plotted onto a highly simplified sketch of the cerebral hemispheres. The lateral surface of the left hemisphere is shown below the medial surface of the right hemisphere. Rostral is to the left; dorsal is up. The dashed line indicates the fundus of the central sulcus, showing that the primary motor cortex is located mainly within the rostral (anterior) back of that sulcus. Ce, central sulcus; CMAs, cingulate motor areas; FEF, frontal eye field; Ml, primary motor cortex; PF, prefrontal cortex; PMd, dorsal premotor cortex; PMv, ventral premotor cortex; PPC, posterior parietal cortex; SEF, supplementary eye field; pSMA, presupplementary motor area; SMA, supplementary motor area.

Figure 2 Motor areas of the human brain plotted onto a highly simplified sketch of the cerebral hemispheres. The lateral surface of the left hemisphere is shown below the medial surface of the right hemisphere. Rostral is to the left; dorsal is up. The dashed line indicates the fundus of the central sulcus, showing that the primary motor cortex is located mainly within the rostral (anterior) back of that sulcus. Ce, central sulcus; CMAs, cingulate motor areas; FEF, frontal eye field; Ml, primary motor cortex; PF, prefrontal cortex; PMd, dorsal premotor cortex; PMv, ventral premotor cortex; PPC, posterior parietal cortex; SEF, supplementary eye field; pSMA, presupplementary motor area; SMA, supplementary motor area.

broadly overlapping muscle representations, with each part of the body represented repeatedly. The functions of M1 are discussed in Section III.

By current estimates, there are about a dozen nonprimary motor areas. Many of these fields occupy parts of Brodmann's area 6. However, parts of areas 8 and 24, the latter also known as anterior cingulate cortex, also contain nonprimary motor areas. A medial group of areas includes the well-known supplementary motor area (SMA), an area immediately anterior to it (the pre-SMA), and two or more cingulate motor areas. A lateral group of areas, often termed simply the premotor cortex (PM), can be divided into separate dorsal and ventral components, and these two divisions can be subdivided further into rostral and caudal parts. At least two eye-movement fields, the frontal eye field, and the supplementary eye field, have been identified. Finer subdivisions and combinations of these regions have been proposed and may have some validity. The functions of these areas are discussed in Sections III and V.B.

The primary and nonprimary motor areas project to the other components of the motor system, at virtually all levels of the neural axis (Fig. 1). The cortical output system, often called the corticofugal system, arises exclusively from layer 5 and includes a direct projection to the spinal cord (the corticospinal system). Some motor areas, especially M1, have monosynaptic excitatory connections with alpha motor neurons. Accordingly, the oxymoron "upper motor neuron'' has been applied to M1's corticospinal neurons. However, Ml exerts its influence over genuine motor neurons in large measure through relatively indirect pathways, and its synapses on spinal interneurons vastly outnumber those on motor neurons. Corticosp-inal axons accumulate in large bundles traversing the internal capsule, cerebral peduncle, pyramidal tract, and corticospinal tract on the way from the telence-phalon to the spinal cord. Because corticospinal axons run through the pyramidal tract, the term pyramidal motor system is sometimes applied to it. However, many fiber systems coexist within the pyramidal tract, such as neurons projecting to the dorsal column nuclei and other targets in the brain stem. Thus, the corticospinal and pyramidal motor systems do not correspond exactly. Additional outputs from the motor cortex include massive projections to the basal ganglia, the red nucleus, the cerebellum (via the basilar pontine nuclei), and the reticulospinal system.

b. Basal Ganglia Long considered part of the so-called extrapyramidal motor system, much of the motor output from the basal ganglia depends, ultimately, on the pyramidal tract. Accordingly, the concept of an extrapyramidal motor system has been largely abandoned. The striatum is the basal ganglia's input structure, encompassing the putamen, caudate nucleus, nucleus accumbens, and other regions within the ventral forebrain. Likewise, the pallidum is the basal ganglia's output structure, including not only the globus pallidus but also the substantia nigra pars reticulata (Fig. 1) and additional parts of the ventral forebrain. The pallidum sends GABAergic inhibitory projections to the brain stem and thalamus. These thalamic nuclei connect to nearly the entire frontal lobe as well as additional areas, such as the inferior temporal contex and the posterior papietal cortex.

The major excitatory inputs to the striatum come from the cerebral cortex (including the hippocampus) and the intralaminar complex of thalamic nuclei. A major input arises from the dopaminergic cells of the midbrain, located in the substantia nigra pars compacta and the adjacent ventral tegmental area. Degeneration of the striatum results in Huntington's disease, whereas degeneration of the dopaminergic neurons causes Parkinson's disease.

Much attention has recently focused on the modular organization of cortical and basal ganglia interconnections. This trend accords with the recognition of other important modules in the motor system, such as CPGs, reflex circuits, and cortical-cerebellar modules. The cortical-basal ganglionic modules, often called "loops," consist of cortical, striatal, pallidal, and thalamic elements that form, at least in principle, a recurrent excitatory pathway. This circuit includes the so-called "direct pathway,'' striatal output neurons (technically, medium spiny neurons) that project directly to the pallidal projection neurons (Fig. 1), including those in the internal segment of the globus pallidus (GPi). Another part of the basal ganglia, the "indirect pathway,'' begins with projections from the striatum to the external segment of the globus pallidus (GPe). These neurons influence the subthalamic nucleus and pallidum, in turn (Fig. 1).

This sketch of the basal ganglia has heuristic value in understanding Parkinson's disease and other consequences of basal ganglia dysfunction. However, the reader should recognize that it represents a coarse oversimplification. Many other features of its anatomy are important to basal ganglia physiology. The subthalamic nucleus, for example, excites not just GPi but also GPe; the GPe sends inhibitory inputs "back" to the striatum; and the motor cortex sends a direct, excitatory projection to the subthalamic nu cleus. Furthermore, in addition to dopaminergic inputs, serotonergic inputs arise from the raphe nucleus, and there are a large variety of intrinsic neurons using other neurotransmitters, including acetylcholine.

c. Parkinson's Disease According to one current view, dopamine acts to support activation of the direct pathway's striatal neurons but to suppress those of the indirect pathway. Accordingly, the direct pathway's inhibitory influence over GPi might wane in the absence of dopamine. This decrease in inhibition from the striatal direct-output pathway would lead to GPi neurons having greater activity and therefore greater inhibitory output to the thalamus. The indirect pathway may also contribute to greater inhibition of the thalamus. This increased inhibitory influence on recurrent cortical-thalamic modules may cause the slowing of movement (technically, bradykinesia) that is a symptom of Parkinson's disease.

Was this article helpful?

0 0
Breaking Bulimia

Breaking Bulimia

We have all been there: turning to the refrigerator if feeling lonely or bored or indulging in seconds or thirds if strained. But if you suffer from bulimia, the from time to time urge to overeat is more like an obsession.

Get My Free Ebook


Post a comment