Part 1: Image-Mapped Tutorial
Part 2: Matching Self-Test:
33a |
33b |
33c
Part 3: Multiple-Choice Self-Test
1 - Cerebral Hemisphere
A number of structures within the cerebral hemispheres contribute to the extrapyramidal control of movement. Diffuse regions of the cerebral cortex, the basal ganglia nuclei, the ventral anterior and ventrolateral thalamic nuclei, and the subthalamic nucleus all contribute to the extrapyramidal system. One route by which these regions ultimately affect movement is via projections to the red nucleus and the reticular formation located in the midbrain and the medulla and vestibular nuclei located in the medulla. In addition to these descending projections, some extrapyramidal structures affect movement via ascending projections to the motor cortex.
The connections between the cerebral cortex, the basal ganglia, and the thalamus play a major role in the extrapyramidal system. Association cortical regions of the frontal, parietal, and temporal lobes project to the caudate nucleus of the basal ganglia, whereas the primary motor and somatosensory cortical regions project to the putamen of the basal ganglia. The caudate and putamen both then convey information to the globus pallidus of the basal ganglia. The globus pallidus then sends information to the motor cortex via the ventral anterior and ventrolateral nuclei of the thalamus. This series of connections completes a communication loop that has both excitatory and inhibitory components. In general, the basal ganglia monitor somatosensory information coming from the somatosensory cortex and the movements being planned and executed by the motor cortex. These nuclei then influence the adjustment of ongoing movement both via indirect projects to the motor cortex and direct projections to motor nuclei of the ventromedial system of the thalamus.
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The basal ganglia do not specify the forces needed to execute specific movements nor do they initiate movements, but rather they facilitate the use of motor programs located elsewhere for the automatic performance of previously learned motor acts (Mauk, 2000a & 2000b; Parent, 1996). They prepare for these motor acts and adjust them on an ongoing basis to meet the requirements of the particular context under which the act is executed. For example, the basal ganglia would make the adjustments to the motor program used to write your name, as would be necessary for performing this action on a piece of paper as well as the larger scale needed for a classroom to view on a blackboard.
Scaling the intensity of motor programs to fit the task requirements is a job for the motor loop of the basal ganglia. This motor loop scales the amplitudes of motor movements in the execution of high-level motor plans by comparing commands for movement from the cortex with proprioceptive feedback from the movement in progress. Thus, the assembly of motor programs is under the control of the complex loop involving the basal ganglia. Finally, the basal ganglia are connected to the limbic system. This basal ganglia-limbic loop enables motor programs to be implemented in relation to emotional and motivational drive states.
Two types of deficits emerge with dysfunction of the basal ganglia, dyskinesia and akinesia. Dyskinesia is characterized by the occurrence of abnormal involuntary movements. These include rhythmic tremors at rest, athetosis or slow writhing movements of the fingers and hands, chorea or abrupt movements of the limbs and facial muscles, and ballismus or violent flailing movements. Hemiballismus is a severe form of involuntary movement that occurs contralateral to a lesion of the subthalamic nucleus. Tardive dyskinesia involves abnormal involuntary movements especially of the face and tongue. It is caused by long-term treatment with anti-psychotic medication used to reduce dopamine function. Akinesia is characterized by abnormal involuntary postures. These include rigidity or movements that are cogwheel or ratchet like in nature and dystonia or persistent and distorted positions of the body. In general, the various symptoms associated with dyskinesia and akinesia are caused by disruption in specific neurotransmitter systems, in particular the dopamine and GABA (gamma amino butyric acid) systems.
Parkinson's disease is associated with the loss of dopamine cells in the substantia nigra and locus coeruleus of the brain stem, degeneration of the nigrostriatal pathway, and the depletion of dopamine in the brain. The output of basal ganglia is increased in response to the decrease in dopamine function. Parkinson's disease is characterized by numerous symptoms including rhythmic tremors, cogwheel rigidity, akinesia or poor movement initiation, and bradykinesia or slow movement. Motor programs are intact, but are used inappropriately.
Huntington's disease is associated with the loss of GABAergic neurons projecting to the globus pallidus. This reduction in GABAergic activity results in a release of the inhibitory effects of the subthalamic nucleus. Disinhibition of the subthalamic nucleus results in a reduction of output from the basal ganglia. The normal effect of the basal ganglia on movement is inhibitory. Therefore, disinhibition of the motor loop is facilitated by Huntington's disease. This facilitation is associated with chorea, decreased muscle tone, and eventually dementia.
The standard therapy for Parkinson's disease is the drug levodopa, a precursor molecule for the production of the depleted dopamine. There are, however, side effects to this drug treatment and its effects wear off over time. More recently developed treatments for Parkinson's disease offer promise. Medications that may prevent the deterioration of dopamine neurons offer some hope. Those tested include anti-oxidants (tocopherol) and monoamine oxidase B inhibitors (deprenyl). Both seem to have the ability to slow the progression of deterioration associated with Parkinson's disease. Gene therapy or genetic engineering has also been researched. In this technique, viral or natural host cells are used to add functioning genes to the brain. A strategy used in animal models involves an injection into skin cells of the gene that produces the enzyme that converts the amino acid tyrosine into dopamine (tyrosine hydroxylase). These cells are then injected in deficient brain regions. Surgical interventions are sometimes used in late-stage cases of Parkinson's disease. Pallidotomy, or destruction of a region of the globus pallidus, may help to restore the imbalance between inhibitory and excitatory influences. The reduction of inhibitory activity in this region may counteract the excessive inhibition of movement initiation caused by this disease. Thalamotomy (destruction of the ventrolateral and ventral medial thalamic nuclei) may be more effective in reducing tremor. The results of such surgical procedures have indicated that current models of basal ganglia function are inadequate, and have suggested fruitful areas for future research. Transplantation or implantation of fetal, dopamine-producing cells into the brain has yielded moderate results. Although this approach shows some promise (with a reduction of symptoms and improved response to medication), its effectiveness is limited by the poor survival rate of the grafted cells. In addition, the use of fetal tissue has raised complicated ethical questions.
| References |
Mauk. M.D. (2000a, March 12). Lecture 38 - Basal Ganglia. Retrieved May 3, 2000 from the World Wide Web: http://nba5.med.uth.tmc.edu/academic/neuroscience/lectures/section_3/lecture38_10.htm
Mauk. M.D. (2000b, March 12). Lecture 40 - The Integrated Motor System and Disorders of the Motor System. Retrieved May 3, 2000 from the World Wide Web: http://nba5.med.uth.tmc.edu/academic/neuroscience/lectures/section_3/lecture40_03.htm
Parent, A. (1996). Carpenter's human neuroanatomy (9th ed.). London: Williams & Wilkins.