Fourth Translation: Motor Movement
Henderson, L.A.
Background:
After a spinal cord injury (SCI) the loss of somatosensory information to higher cortical levels results in the reorganization of the primary somatosensory cortex (SI). The question which this research asks is whether after a SCI in humans is the functional reorganization a result of physical changes in brain anatomy or a reflection of unmasking-silent existing dormant synapses? This is an important question; because if changes in the silent synapses occurred that would mean the thalamus would affect cortical anatomy of after SCI and possibly affect the treatment after SCI as well!
First let’s review the anatomy of the sensory and motor mechanisms. The cortex contains regions of motor and sensory functional areas; this includes the primary motor area (MI) of the frontal lobe which contains motor neurons in the neocortex areas that are dedicated to skeletal muscles. Representations of theses areas are reflected in the homunculus. We can see that the part of the cortex is organized for motor control of our body by areas; for example near the upper part of the cortex contains neurons which send motor information for the leg and foot. The primary sensory area (SI) in the parietal lobe receives sensory information from the peripheral nervous system by ascending spinal tracts which are first sent to the thalamus and then routed to the appropriate areas of the cortex. Again the homunculus represents areas of the brain which receives sensory information from specific areas of the body and is sent to specific areas of the cortex.
The thalamus is the main mediator for relaying sensory information to the cortex. The thalamocortical connections consist of axonal fibers to the cortex. The thalamus sends or receives information from other important neural structures as well; the cerebellum, basal ganglia, visual and hearing axons. Once sensory information has been received to these areas of the cortex (SI), this information is then sent to the posterior multimodal areas of the brain for interpretation. This system interprets sensory information and sends it to the anterior multimodal area for motor planning and motor production.
Theory:
10 years ago scientists researched the thalamocortical projection in monkeys with chronic arm injuries and amputations. Microelectrode recordings showed large reorganization of the missing limb SI representation, and revealed normal thalamocortical connections were intact. This means that the sensory information relayed by the thalamus was unchanged but anatomical changes took place in the cortex where the sensory information was delivered. In addition, significant cortical SI reorganization took place as well. The axonal connections of the thalamus were intact but were not able to reach the thalamus from the spinal level of injury. This meant that these connections were lost and no longer connected to higher cortical levels.
Findings:
Researchers used MRI scans to assess cortical changes in the S1 functional areas after thoracic T1-T12 SCI and in control subjects upon stimulation of the lower extremity. They also tested for anatomical changes in the SI reorganization between movements of the little finger in the cortex. They were able to track axonal fibers between the thalamus and brain maps or cortical representation in the neocortex for functional areas of the brain in the SI regions. Their findings showed a significant decrease in S1 cortical representation of the lower extremities in these regions. In addition, the surrounding intact cortical areas increased and invaded the non innervated S1 cortically deprived area. This was supported by the increased areas for the little finger in SCI participants. They found that in human cortical reorganization was the result of changes in cortical anatomy from an increase in axonal sprouting in this region. No changes in the axonal connections from the thalamus were supported. Which means any latent synapse was not recruited for the reorganization of the cortical or thalamic connections to the neocortex.
Clinical Applications:
This is an important finding which indicates that sensory afferent input after SCI will not affect sensory connections to the thalamus but the cortical anatomy which is intact and connected to spinothalamic pathways will eventually take over the space vacated by the loss of S1 representation reflected in SCI somatosensory areas. I have seen therapist brushing limbs affected by SCI in the hopes sensory impulses would affect areas lost by SCI, but in the light of this research this modality would not affect this condition. It has no clinical validity. As a SCI patient adapts to a new body and learns how to balance new skills their cortical representations below the level of spinal cord injury will be lost and the intact levels will increase in the cortex.
Take Home Point:
I have worked with SCI patients and it is difficult for these individuals to deal with the loss of motor and sensory function. After a SCI the spinal cord and nervous system goes into “spinal shock” do to swelling and axonal shut down. This phenomenon is not well understood and takes time for this condition to resolve. The level of function and spinal cord functional return may take up to two years until the edema and swelling in the spinal cord has resolved. There is a waiting period to see what the individual will receive in finial motor and sensory function.
The hope of walking again never dies and the hope for a cure is never lost. The individual needs support from their family and most importantly from others who have had the same experience to understand what they are going through and to provide emotional support.
The spinal cord remains a mysterious area of the central nervous system. We ask ourselves, how a pregnant woman with a SCI can give birth without the input of the lower body muscles. Why do complete SCI individuals report some sensory input at times from the area below their injury? There are connections which we can not explain and there is much to learn from this area. I love the spinal cord because of its complexity and its ability to transmit vast amounts of information. With out it life is not possible.
Mary Groves, M.S. Anatomy, OTR/L
Glossary:
Corticalspinal track: motor spinal tracks which originate in the cortex M1 and send motor information to the spinal cord and specific muscles of the body.
Spinothalamic track: sensory tracks which originate in the peripheral nervous system and ascend the spinal cord synapse in the thalamus and continue to the sensory cortex S1.
Thalamus: a two lobe structure located in the medial portion of each hemisphere, responsible for relaying sensory information from the spinothalamic tracks.
Homunculus: Cortical representation of each body part’s motor and sensory function. Sensory homunculus is located in the post central gyrus or SS1. Motor homunculus is located in the pre central gyrus or MM1
.
Third Translations: Motor Movement
Jung, J., Cai, W., Lee, H. K., Pellegatta, M., Shin, Y. K., Jang, S.Y., Suh, D.J., Wrabetz, L., Feltri, M. L., & Park, H. T. (2011). Actin Polymerization is Essential for Myelin Sheath Fragmentation during Wallerian Degeneration. The Journal of Neuroscience, 31, 6, 2009-2015.
Background:
The mechanics of a peripheral nerve injury involves the transection or damage of the axon and loss of transmission of the neurons afferent or efferent information to its destination. The Schwann cell is the main insulator and protective glial cell of the peripheral nervous system (PNS). The Schwann cell is a remarkable supportive cell of the PNS; it is a flat like cell which wraps its plasma membrane around an individual segment of the axon of a neuron. Its myelin substance creates insulation for the rapid transmissions of nerve impulses and creates an environment for the neuron’s axon to be nourished and protected.
Wallerian degeneration (WD) is a process of axonal degeneration after a sever injury to the peripheral nerves. Wallerian degeneration (WD) after a peripheral nerve injury precedes axonal degeneration and decomposition of the myelin sheath. The process of demyelination of the Schwann cells begins with the myelin sheath breaking into small ovoid-like structures. Molecular changes occur with the deregulation of the myelin gene expression as well. Without myelin protection the axon begins to decompose and neuron death may follow.
Theory:
The morphology of the Schwann cell is important to maintaining cytoskeleton structures of the cell which is the maintenance of the cell’s shape. Actin is the main protein which affects this cytoskeleton structures, without this molecule the shape is altered. Shape is everything in the microscopic world. It dictates how molecules will adhere to each other, or how substances will or not bid to each other. Schmidt-Lantermann incisures are an area of the Schwann cell where the ends of the cell divide into irregular portions. It’s as if the petty coats of the cell were hanging out. They look like small clefts instead of the rounded ends of the Nodes of Ranvier which we are more familiar with as part of the cell structure. RhoGTPases is the major signaling molecule in axon sorting and myelination in the development of the PNS.
Findings:
Results of this study suggests that actin polymerization in the Schwann cells following a nerve injury may involve RhoGTPases signaling molecules. The expression of these molecules directly affects the Schmidt-Lantermann incisures first. This may be a weaker portion of the Schwann cell and susceptible to degeneration at the start of WD versus the typical Schwann cell structure. Who knew that the structural endings of the Schwann cell typical or atypical would have an effect on WD! As WD proceeds, the Schwann cells form small-ovoid like structures and the protective myelin degenerates. Soon the axon may begin to die off and the transmission properties of the axon miss fires and gives false information.
 |
| Schmidt-Lantermann incisures |
Clinical Applications:
After a PNS injury the percentage rate for recovery is high after an injury in this region. The growth rate of axons is one inch a month. If some one had a radial nerve injury three inches from the triceps muscle it would typically take three months to regain function of the muscle and the nerve. When I am working with a patient I am always thinking of what is going on a cellular level. What is happing to the axon, the neuron, the molecules which affect the metabolic functions because this is where recover is affected. Now I will think of the Schmidt-Lantermann incisures the small cleft like petty coats hanging out of some of the Schwann cells. If someone is under going WD the start of this process is beginning at theses structures. The ability to affect the deregulation of WD with pharmaceuticals may be a future treatment for WD. But as therapists what can we do? Protect the area from further damage by compensatory strategies; promote health through nutrition, rest, and emotional support. Our greatest ally is the regenerative properties of the Schwann cell to bring about neurological return and function.
Take Home Point:
I love the peripheral nervous system especially the Schwann cell. It’s my favorite cell in the peripheral nervous system because of its insulating ability and the regenerative properties of this cell. I love the way it wraps around the axon and hugs it like a very small jelly-role. Because of the Schwann cell our PNS can transmit rapid efferent impulses to our muscles and afferent information to the spinal cord. If we had a support cell like the Schwann cell in our central nervous system (CNS) we would be able to recover from spinal cord injuries much better than we can today. Think of it, spinal cord injury patients would be able to walk in two years after an injury! C- 5 injury patients would be able to dress and cut their food again and walk out side without a wheel chair! If only we had the Schwann cell in the CNS.
Mary Groves, M.S. Anatomy, OTR/L
Glossary:
Glial cell: supportive cells of the central and peripheral nervous system.
Myelin: insulating material composed of lipid (fat) proteins. Schwann cells contain lipid material.
Polymerization: molecules forming long chains, to react or cause to react with similar molecules to from a polymer.
Second Translation:Motor Movement
Hou, Z., Lei, H., Hong, S., Sun, B., Fang, K., Lin, X., Liu, M., Yew, D.T. W., and Liu, S. (2010). Functional changes in the frontal cortex in Parkinson’s disease using a rat model. Journal of Clinical Neuroscience, Vol. 17, 628-633.
Background:
Research on Parkinson’s disease (PD) has focused on the pathological process mostly in the Nigrostriatal system. This article investigates the involvement of the frontal lobe of the cortex and the affects of Parkinson’s disease. PD is a progressively debilitating disease which involves the lost of dopamine production in the substantia nigra located in the midbrain. PD leads to loss of motor control, tremors, and in some cases cognitive dysfunction. Functional imaging has been used to confirm metabolic and functional disorder in PD patients but these studies have been unable to identify the mechanisms of pathological changes of the frontal cortex.
Theory:
Primary Motor control involves the frontal lobes but the basal ganglia, cerebellum, thalamus and dopamine serve to modulate gross motor movements. These structures communicate with each other through neural pathways. A pathological change of the substantia nigra produces tremors, gait disturbances, and affects cognitive functions as well. Studies of PD have primarily concentrated on the Nigrostriatal system and the loss of production of dopamine. It is important to understand the clinical and pathological changes of PD to better treat our clients.
Findings:
This study is one of the first to investigate the affects of PD on the frontal cortices. 6-Hydroxy-dopamine and ascorbic acid was used to produce loss of dopaminergic neurons in the substantia nigra in rats. Electron microscopy, 1 H-MRS analysis, and immunohistochemistry analysis were used to examine metabolic and structural changes within the frontal cortices of a Parkinson’s disease-model rat brain. Synaptic changes in the frontal cortex of the PD- model rats were notably decreased on the lesion side of the rat brain compared to the non-lesioned side. A decrease in mitochondria production was noted as well in neurons of affected PD- model rat brains. Changes in presynaptic and postsynaptic membrane structures were noticed. The densities of these structures were reduced or not visible. The number of synaptic vesicles in the synaptic bouton decreased as well. Metabolic changes were detected in the form of decreased glucose metabolism in the frontal cortex of PD patients in a recent study. Decrease blood flow to the supplementary motor area and frontal cortex was detected.
Clinical Applications:
So, what does this mean if the presynaptic and postsynaptic membranes are decreased in the PD frontal cortices or if the mitochondria population decreases in the neuron? This tells a story of the nervous system deprived of not only dopamine but the processes of PD affecting the frontal cortices to connect primary motor control with pathways which in the process affects smooth motor movement. If basic neural circuitry is disrupted by decreasing synaptic connections in the frontal cortex this will have a profound effect on motor control. Diminished mitochondrial production means decreased energy production for the basic process of neuron function. We must remember neurons are high energy cells and to function at their peak requires a high production out put by mitochondria especially at the terminal boutons to release neurotransmitters.
I always ask myself questions on what pathways or process are involved with a function and try to name them. Now I will a question what is going on in the frontal cortex of a person with PD. It is not enough to only think of the substantia nigra and the loss of dopamine production. Some how the mechanisms of PD are affecting the terminal boutons and the pre- and post synaptic neurons but we do not know the process. How will we connect these pathways to help our clients?
Take Home Point:
My Uncle Bill had Parkinson’s disease. I was a young at the time and had not become an OT yet and I did not understand what was happening to him. Before he died, I visited him at his home, and he was bed bound by then, and I did not know what to say or do for him. All I could do was hold his hand. We talked and I noticed his hands did not trembled as much when we held hands. Now when I work with PD clients I always think of my uncle Bill, I know the process of PD and know I will think of the changes in the frontal cortex which affects this condition. But as with my uncle, I remember my clients are human beings and if we can provide human contact through holding a hand or an arm we are connecting our hearts and our own nervous system to communicate on a level which is basic and direct. When we as occupational therapist go on to talk to our clients about adaptive equipment or compensatory techniques we must continue to connect to our clients by our own nervous system through touch, our hearts, and our mind. That is the true strength of our profession; we know how to make the important connections which makes our work meaningful to our clients.
Glossary:
Dopamine-a monoamine neurotransmitter, a principal neurotransmitter concerned with mood, memory, and motor modulation. Dopamine is produced only in one area of the nervous system, substantia nigra of the midbrain.
Immunohistochemistry- is a method of using chemical, antigen antibody, and histological processes involved in testing various chemical changes in tissue.
Nigrostriatal system- a neural pathway which includes the substantia nigra and the corpus striatum for dopaminergic production.
Substantia Nigra- the gray matter of the midbrain, is concerned with muscle tone and connected to the cerebral cortex, spinal cord, hypothalamus, and basal nuclei.
Bernard, J. A., Taylor
Background:
Are you right handed or left handed? This article discusses the neuroanatomical organization of the brain for handedness and the differences in motor control. But let’s go back to basics first; the motor area of our brain (frontal lobe) in both hemispheres contains motor neurons which send information for movement to the muscles of our body. If you are right handed this means the motor control for your right hand is in the left hemisphere of your brain. If you are left- handed the motor control for your left hand is in the right hemisphere of your brain. The cortical spinal tracts send these motor messages from the right or left hemisphere down through the internal capsule of the brain to the brainstem and at the decussation of the pyramids this pathway crosses over to the contralateral side of the body. So, if you are right-handed the motor response starts in your left primary motor area (M1) of the left hemisphere à crosses over to the right side of the brainstem down the spinal cord and out to the right brachial plexus and to your right hand, and you begin to feed yourself with your right hand or shave your legs with your right hand.What this article suggests is that the connections (interhemispheric) between the right and a left hemisphere affect motor speed and control. Besides the cortical spinal tracks there are other influences for motor control as well. The major connection between the two hemispheres is the corpus callosum. This is a massive group of axons which cross over from one hemisphere to the other hemisphere. It is the communication highway for the two hemispheres and our brain’s way of communication between these two structures.
Theory:
Research suggests that the neuroanatomical organization of the corpus callosum may indicate that left- and right- handedness may be different. The anatomical organization of the brain has been linked to motor performance as well; left handed persons on average have faster and more accurate interhemispheric transmission than right handed persons. This means that if you are left-handed the axons which connect from the right side of your brain have much faster synaptic speed. If you were in a gun fight you may have the advantage with a quicker draw. Or in a hotdog eating contest you would be able to grab that hotdog much faster and stuff it into your mouth. Studies have also found that right- and left- handers have different activation patterns in the primary motor cortex (M1). Right handed brains have more asymmetrical activation patterns where left-handed brains have more bilateral activity in a one handed task. The literature on the corpus callosum has been mixed but it has been suggested the difference in the size of this structure may contribute to the speed of interhemispheric communication. The corpus callosum in left- and mixed-handed people tends to be larger, especially in the midsagittal area of the where the sensory and motor cortex connects. There is a direct association to handedness for motor organization, interhemispheric exchanges, speed, and structural size of the corpus callosum.
Findings:
This study examined forty-eight participants and used a Transcranial Magnetic Stimulator (TMS) to record the speed of interhemispheric communication between the hemispheres. They also used a battery of tests to measure the differences of speed and dexterity between right- and left- handed individuals; The Purdue Pegboard, Edinburgh Handedness Inventory, Tapping Circles and Tapping Squares from the Hand Dominance Test. Motor-evoke potentials (MEPs) were recorded on the right or left first dorsal interosseous muscle for the Tapping tests which provided data on the resting motor threshold. This provided data on the speed of a motor response. Their findings supported the suggestion that strongly left handed individuals have faster transfer from dominant to the non-dominant hemisphere. This means their corpus callosum is faster. The contralateral motor representations in (M1) were related to interhemispheric communication which demonstrates a strong connection to the use of the hand other than the cortical spinal tracts. There was also a suggestion that the degree of handedness is associated with cortical motor areas and the interhemispheric connections.
Clinical Applications:
First of all, I would never consider changing a child’s handedness because the neuroanatomical organization is in place. The change would not only cause motor problems but may also cause behavioral problems as well. Some societies consider left-handedness as evil, one of the words for left is sinisterly which has references to sinister. Working with predominantly right or left handed persons we will have to think about the hardwired connections which they have developed and consider the effect on the communications between the two hemispheres.
The body is a great place and we are still finding new information on how it works. We learned in OT school that the main movers of our muscles are the descending motor pathways but considering this article other neurological connections are at play for speed of hand movement and dexterity. Our corpus callosum is important for these functions. I have always liked this structure; I liked the idea that there is this big hunk of axonal connections between our hemispheres. If you ever have dissected a human brain, the corpus callosum is like a big floppy hinge holding the hemispheres together. Once you divide this structure, you can see the medial side of the brain and it is a wonderland. You can see the thalamus, lateral ventricles, Cingulate gyrus, and hypothalamus just to name a few of the structures in this aspect of the brain.
Take Home Point:
When I work with a person who has right hemiparesis and is predominantly right handed, I have often wondered how this is affecting their brain and their motor control. I have asked myself “is this making motor return more difficult?” Not only is the motor area damaged from a stroke but the communication between hemispheres may be impaired as well. If they are right-handed the communication speed may be slower because of dominant handedness. Does this affect learning motor movements as well? Many questions to ask ourselves when working with individuals, handedness is an aspect to consider as well.
Glossary:
Axon- a process of the neuron which transmits impulses away from the cell body
Primary motor area- area of the frontal lobe which contains motor neurons
dedicated to specific areas of the body. Often referred as M1 in the
Precentral gyrus.
