Control of movement

0. Introduction:
This is some problem-based learning work I did a while ago. Unfortunately, voluntary movement depends on the integration of several non-voluntary mechanisms so the material I had to cover seemed pretty complex to me. I thought I might as well share my work here instead of wasting it, but I am no neuro-physiologist so please do not expect any rocket science.

1. Sensation:
In order to move in a controlled manner it is first necessary to be aware of one’s position is space. There are various sensory mechanisms in pace for this.

1.1. Vision: the importance of vision for position awareness only becomes clear in the absence of visual and tactile cues. Examples of this are being deep under water (divers are trained to blow and follow bubbles in emergencies when they are unable to tell the difference between up and down) or being buried in snow (clearing an air pocket and spitting into it will show you the direction of gravity). The physiology of sight will not be addressed here but points to note are that binocular vision helps us judge distance and visual data is received by the lateral geniculate nucleus of the thalamus and then relayed to the visual cortex of the brain for processing.[1]

1.2. Vestibular system (in the inner ear): [1]
· semicircular canals detect angular acceleration: fluid from the canals flows through a widening (ampulla) which contains a gelatinous mass (cupula) embedded with cilia from sensory cells.
· utricles (fluid-filled chamber between the semicircular cannals and saccule) detect horizontal (if a person is standing) linear acceleration: cilia covered with a gelatinous substance impregnated with heavy calcium carbonate crystals (otoliths).
· saccules (fluid-filled chamber between the utricle and cochlea) detect vertical (if a person is standing) linear acceleration: cilia covered with a gelatinous substance impregnated with heavy calcium carbonate crystals (otoliths).

1.3. Mechanoreceptors (touch): [1] if you sit on the edge of your chair so that one buttock is on the chair while the other is hanging off the side, the lack of pressure on one buttock is the reason you are aware that you are in danger of falling off the chair.

1.4. Nociceptors (pain): [1] If you bear weight excessively through one of your ischial tuberosities, pain may inspire you to shift your weight to the other one.

1.5. Proprioceptors (body position):
· Muscle Spindles (stretch):[1] muscle spindles contain sensors for a) how far and b) how quickly muscles are being stretched.
· Golgi Tendon Organs (tension):[1] detect tension (force) at musculotendonous junctions.
· Joint mechanoreceptors: fire during specific ranges of movement (in feline models [2])

2. Motor response to stimuli:
Sensory information is processed at and responses are generated at various functional levels of the nervous system.

2.1. Reflexes: are the simplest level of movement control. Examples of this include:
· Muscles contracting automatically when their muscle spindles are stretched.[3] Examples of this include the knee jerk and ankle jerk tests. These are the simplest reflexes because they involve only one synapse (monosynaptic). All other reflexes are polysynaptic [1].
· Muscles relaxing automatically when their golgi tendon organs detect tension of a magnitude that might damage the muscle.[3]
Simple reflexes are mediated in the spinal cord by the reflex arc. This basically involves a sensory neuron running to the spinal cord and either connecting to a motor neurone (monosynaptic reflex) or to inter-neurones that either stimulate or inhibit motor neurones (polysynaptic). The motor neurones connect to muscle fibers where they stimulate contraction.
Why are reflexes important for voluntary movement? Reflexes play a role in co-ordination of movement. Examples of this include:
· When muscle spindles are stimulated the antagonist muscles are automatically inhibited. This is why clonus (shaking) does not occur when the knee jerk or ankle jerk reflex are tested.
· When muscle spindles are stimulated synergistic muscles may be activated.

2.2. Central pattern generators
Simple movement patterns such as gross flexion or extension are generated from the spinal cord. Interplay between these patterns at the spinal level can produce complex movements without regulation from the brain:
· The crossed extensor reflex occurs when nociceptors in one foot are sufficiently stimulated. The motor response generated is flexion of the threatened lower limb with extension of the opposite lower limb. This reflex is partially responsible for enabling a person to lift a painful foot while standing on the other leg.[1]
The term ‘central pattern generators’ is used to describe how complex systems within the spinal cord can generate rhythmical patterns of movement such as those required for walking without regulation from the brain [4]. Impulses from the brain selectively promote or inhibit these movement patterns to produce controlled movement.

2.3. Roles of the brain:
Looking at the functions of different brain parts and applying the theory of evolution, we may assume that the human brain evolved anatomically upwards and outwards; the brainstem generally regulates physiological functions necessary for viability, the midbrain is involved with gross processing of sensory information and gross responses, while the cerebrum is responsible for higher awareness and reasoning.

2.3.1. Sub-cortical influences on movement:
Sensory information is mostly relayed from the spinal cord to the thalamus (touch via the anterior spinothalamic tract [10], pain and temperature via the lateral spinothalamic tract [10]) and from there to other appropriate areas of the brain:

2.3.1.1. Brainstem: The brainstem contains the pons, medulla and midbrain. The brainstem coordinates neck and eye movements via the medial longitudinal fasiculus and tectospinal tracts[12]. The reticular formation in the brainstem regulates the muscle tone necessary for posture via the reticulospinal tract[9]. The red nucleus in the midbrain is thought to influence gross flexion and extension via the rubrospinal tract[13] and the vestibular nuclei stimulate increased extensor activity via the vestibulospinal tract[14]. If you attempted to walk using your spinal central pattern generators alone you would fall over as soon as you stepped on an uneven surface. You would also fall over if you exhibited a crossed extensor reflex (see section 2.2.) without postural compensations regulated by your brainstem. Similarly sitting with just one buttock on your chair while the other hangs over the edge, you would fall off your chair unless the muscle tone in the unsupported side of your trunk increased automatically. The brainstem therefore regulates postural control under the influence of the cerebellum and cerebrum.

2.3.1.2. The basal ganglia: are a group of sub-cortical nuclei involved in the initiation and inhibition of movement through their influence on the brainstem and spinal cord[8]. Disorders of the basal ganglia are anecdotally associated with uncontrolled movements (such as tics[5]) collectively known as dyskinesias[6]. A lack of dopamine supply to the basal ganglia is responsible for the difficulties with starting and stopping movements that people with Parksinson’s disease experience[6].

2.3.1.3. The cerebellum: is an area posterior to the brainstem. It plays a role in refinement of movement using sensory feedback[1]. Proprioceptive information is relayed to the cerebellum via the spinocerebellar tracts [11]. Smooth grading of movement depends on the sequential recruitment of motor units within muscle to match the amount of force required [1]. Damage to the cerebellum leads a condition known as ataxia, characterised by poor balance and loss of accuracy of movement [7]. The cerebellum does not connect directly to the spinal cord but influences movement via connections to the brainstem nuclei.
· I once prepared myself for an army course that involved running long planks 20-30 feet high by walking on the top beam of a set of swings in a playground. Even though the beam was less than 10 feet high and I could easily walk along such a beam if it was on the floor, my lower limbs shook uncontrollably due to my fear of heights. Perhaps this shaking was because I was trying to use my motor cerebral cortex to do a job much better suited to my brainstem and cerebellum (trying to consciously control balance). My theory is totally unsubstantiated, but if it is true, it contribute to the increased falls risk associated with fear of falling.

2.3.2. Cortical influences on movement:
The outer-most part of the brain is called the cerebral cortex. This is thought to be the home of our conscious awareness of movement. Parts of the cortex are specifically for our awareness of sensation and others are for conscious control of movement. The cortex communicates with the spinal cord via upper motor neurons collectively termed the anterior and lateral corticospinal tracts[1]. It also communicates with brainstem nuclei via the corticobulbar tract to control movements of the head and neck[1].

3. Limitations
Some of the data gathered for this work was from animal studies and may have limited validity for humans. Assumptions about neurological function have mostly been made by studying function when parts of the nervous system have been removed or impaired either experimentally or by pathology. As the functional relationships between different neuro-anatomical structures are complex, functional deficits noted once a structure has been removed may not accurately mark all of the functions of the removed structure. One could therefore argue that much of the text above is based on assumption!

References
1.Vander A.J., Sherman J.H., Luciano D.S. (1994) Human Physiology. 6th edition. McGraw Hill: New York.
2. Cohen L.A. (1955) Activity of knee joint proprioceptors recorded from the posterior articular nerve. Yale Journal Of Biology And Medicine. 28(6): 225-232
3. Tortora G.J., Derrickson B. (2007) Principles of Anatomy and Physiology. 11th edition. John Wiley & Sons: Hoboken
4. Lacquaniti F., Grasso R., Zago M. (1999) Motor Patterns in Walking. News In Physiological Science 14: 168-174
5. Saba P.S., Dastur K., Reza Raji M.R., Keshavan M.S., Katerji M.K. (1998) Obsessive-compulsive disorder, Tourette’s syndrome, and basal ganglia pathology on MRI Journal Of Neuropsychiatry 10(1): 116
6. Moyer J.T., Danish S.F. (2007) Stimulation-induced dyskinesias inform basal ganglia models and the mechanisms of deep brain stimulation. The Journal of Neuroscience, 27(8):1799 –1800
7. Hartree N. (2008) Cerebellar Ataxia. http://www.patient.co.uk/showdoc/40001724/ accessed 14:53 15/2/2008
8. Takakusaki K., Saitoh K., Harada H., Kashiwayanagi M. (2004) Role of basal ganglia–brainstem pathways in the control of motor behaviors. Neuroscience Research 50: 137–151
9. Magoun H.W. (1950) Caudal and cephalic influences of the brain stem reticular formation. Physiological Reviews. 30(4):459-474
10. Takahashi S., Yamada T., Ishii K., Saito H., Tanji H., Kobayashi T., Soma Y., Sakamoto K. (1992) MRI of anterior spinal artery syndrome of the cervical spinal cord. Neuroradiology 35:25-29
11. Poppele R.E.,·Rankin A., Eian J. (2003) Dorsal spinocerebellar tract neurons respond to contralateral limb stepping. Experimental Brain Research. 149:361–370
12. Hendelman W.J. (2000) Atlas of Functional Neuroanatomy. CRC Press Inc: Klagenfurt
13. McDougal D., Lieshout D.V., Harting J. (2006) Red Nucleus ("The Ruber") http://www.neuroanatomy.wisc.edu/virtualbrain/BrainStem/22Ruber.html accessed 20:27 15/2/2008
14. McDougal D., Lieshout D.V., Harting J. (2006) Vestibular Nuclei And Abducens Nucleus http://www.neuroanatomy.wisc.edu/virtualbrain/BrainStem/13VNAN.html accessed 20:46 15/2/2008