Dr.JEEJA.S, M.D.Hom (Repertory), M.D.Hom (HOMOEOPATHIC PHYLOSOPHY)
Tutor, Department of Organon of Medicine, Govt.Homoeopathic Medical College, Thiruvananthapuram, Kerala.
- Skeletal muscles are controlled by alpha motor neurons whose cell bodies are located in the ventral column of the spinal cord.
- They release acetylcholine at the neuromuscluar junction
- This results in muscle contraction or shortening which can produce limb movement
- Frontal lobe controls motor function
- Prefrontal – plans, obtains feedback, adapts responses to the environment Three types of muscle (smooth, cardiac, & skeletal)
- Premotor – area in which control of more complex motor acts are developed (i.e. language)
- Precentral gyrus – Area of spatial distribution of muscles in the body
- Subcortical system essential for carrying out basic motor functions
- All information decends to the motor neuron pool in spinal cord
- Here information is integrated by spatial and temporal summation and action potentials traverse the motor neuron to reach the muscle fibers.
|. Upper Motor Neuron|
|In order to reach the muscles, motor commands generated in the central nervous system must travel down upper motor neurons and synapse with lower motor neurons.
Upper motor neurons are a type of first order neuron. They are unable to leave the central nervous system. The pyramidal tract is a very important upper motor neuron tract. The extrapyramidal tract also consists of upper motor neurons, and is multi synaptic.
As upper motor neurons must remain inside the neuraxis, they synapse with neurons of another type called lower motor neurons which can carry messages to the muscles of the rest of the body
- Definition: motor system with cell bodies in cortex & axons terminating directly on the motor neuron pool.
- Betz cells in motor cortex make up only 3% of this tract.
- Thought to be voluntary motor system while extrapyramidal is involuntary
- Involved in instigating, terminating, and altering movement.
- Functions to relate behavior to environment by use of sensory feedback.
- Precentral gyrus controls individual movements
- Premotor region (plan & integration of sequences of movements)
- Motor homunculus — Organization inverted — head at bottom
- Motor cortex area conforms to innervation ratio
- Muscle vs. movement localization controversy
Cortico-spinal and Cortico-bulbar path:
- Axons arise from motor areas of neocortex
- Called the Pyramidal tract
- Pass through the Coronal radiata
- Through the Cerebral peduncles
- Decussation (cross) — in brain stem — 80%
- Forms Lateral Corticospinal tract
- Uncrossed fibers form the ventral corticospinal tract
- Axons originate – cortex terminate -spinal cord:
- In (motor neuron pool)
- Directly on visceral motor neurons
- Mostly on accessory cells medial to tract
- Connecting neurons — necessary where fiber must mediate excitor and inhibitor function
- Two synapses
- One bypassed with repeated stimulation
- Corticobulbar tract
The basal ganglia and cerebellum are large collections of nuclei that modify movement on a minute-to-minute basis. Motor cortex sends information to both, and both structures send information right back to cortex via the thalamus. (Remember, to get to cortex you must go through thalamus.) The output of the cerebellum is excitatory, while the basal ganglia are inhibitory. The balance between these two systems allows for smooth, coordinated movement, and a disturbance in either system will show up as movement disorders.
The basal ganglia:
What are the basal ganglia? The name is confusing, as generally a ganglion is a collection of cell bodies outside the central nervous system. Blame the early anatomists. The basal ganglia are a collection of nuclei deep to the white matter of cerebral cortex. The name includes: caudate, putamen, nucleus accumbens, globus pallidus, substantia nigra, subthalamic nucleus, and historically the claustrum and the amygdala. However, the claustrum and the amygdala do not really deal with movement, nor are they interconnected with the rest of the basal ganglia, so they have been dropped from this section. Other groupings you may hear are the striatum (caudate + putamen + nucleus accumbens), the corpus striatum (striatum + globus pallidus), or the lenticular nucleus (putamen + globus pallidus), but these groupings obviously get confusing very quickly, so we will try to avoid them.
The anatomy of these structures should be a review from the “coronal and horizontal sections” lab. Here once again are the basal ganglia as they appear when stained for myelin:
|rostral section:||middle section:|
An alternate stain is the acetylcholinesterase (AChE) stain. This technique stains for the enzyme that degrades acetylcholine (ACh), a major neurotransmitter. Areas which use ACh generally stain darkly. Here is a section through monkey brain, stained for AChE.
You can see that the caudate and putamen are stained, while the globus pallidus remains fairly pale. This emphasizes their different functions and connections. And those are…?
Different functions and connections:
The relationships between the nuclei of the basal ganglia are by no means completely understood. When dealing with the brain, you may sometimes be tempted to think that everything is connected to everything else. Take heart, some fairly simple generalizations and schematics can be drawn.
The caudate and putamen receive most of the input from cerebral cortex; in this sense they are the doorway into the basal ganglia. There are some regional differences: for example, medial caudate and nucleus accumbens receive their input from frontal cortex and limbic areas, and are implicated more in thinking and schizophrenia than in moving and motion disorders. The caudate and putamen are reciprocally interconnected with the substantia nigra, but send most of their output to the globus pallidus (see diagram below).
The substantia nigra can be divided into two parts: the substantia nigra pars compacta (SNpc) and the substantia nigra pars reticulata (SNpr). The SNpc receives input from the caudate and putamen, and sends information right back. The SNpr also receives input from the caudate and putamen, but sends it outside the basal ganglia to control head and eye movements. The SNpc is the more famous of the two, as it produces dopamine, which is critical for normal movement. The SNpc degenerates in Parkinson’s disease, but the condition can be treated by giving oral dopamine precursors.
The globus pallidus can also be divided into two parts: the globus pallidus externa (GPe) and the globus pallidus interna (GPi). Both receive input from the caudate and putamen, and both are in communication with the subthalamic nucleus. It is the GPi, however, that sends the major inhibitory output from the basal ganglia back to thalamus. The GPi also sends a few projections to an area of midbrain (the PPPA), presumably to assist in postural control.
This schematic summarizes the connections of the basal ganglia as described above.
Although there are many different neurotransmitters used within the basal ganglia (principally ACh, GABA, and dopamine), the overall effect on thalamus is inhibitory. The function of the basal ganglia is often described in terms of a “brake hypothesis”. To sit still, you must put the brakes on all movements except those reflexes that maintain an upright posture. To move, you must apply a brake to some postural reflexes, and release the brake on voluntary movement. In such a complicated system, it is apparent that small disturbances can throw the whole system out of whack, often in unpredictable ways. The deficits tend to fall into one of two categories: the presence of extraneous unwanted movements or an absence or difficulty with intended movements.
This system is involved in automatic motor movements, and in gross rather than fine movement. It works with the autonomic nervous system to help with posture and muscle tone and has more influence over midline structures than those in the periphery. Facial expression is one important communicative behavior that is mediated by the extrapyramidal tract. This is the reason that some Parkinson’s patients have little facial expression. In contrast to the pyramidal tract, the extrapyramidal tract is an indirect, multisynaptic tract.
Components of the extrapyramidal tract include the basal ganglia, the red nucleus, the substantia nigra, the reticular formation and the cerebellum. All of these structures send information to the lower motor neurons.
Some sources, including the text by Love and Webb, 1992, consider the basal ganglia to be the sole constituent of the extrapyramidal system, saying that the other structures listed above synapse with the extrapyramidal tract but are not part of it.
The basal ganglia acts to inhibit the release phenomenon, or the rapid firing of motor neurons. It is aided in this function by the substantia nigra of the midbrain. The muscles most often affected by this inhibitory functions are those controlling the head, the hands, and the fingers.
Releasing hemiballismus amidal Tract
The neurotransmitters involved in the inhibitory function of the basal ganglia include dopamine, which is produced by the substantia nigra, acetylcholine, and GABA (gamma amino butyric acid), which is a glutamate. Dopamine is an especially powerful inhibitor.
Extrapyramidal Projections to Lower Motor Neurons
The extrapyramidal tract has an important role in motor movement. It has projections that carry autonomic motor impulses to voluntary muscles in the body, including the muscles for speech and swallowing. During speech, muscles are receiving input from both the pyramidal and extrapyramidal systems. it is involved in gross motor movement rather than fine. It is responsible for facial expression such as sadness, irony and happiness.
The rubrospinal tract passes through the red nucleus. The cerebellum sends messages to the spinal nerves along this tract. Information flows from the superior cerebellar peduncle to the red nucleus and finally to the spinal nerves. This information is very important for somatic motor, or skeletal muscle control and the regulation of muscle tone for posture. Facilitate the motor activity of flexor muscle and inhibit the activity of extensor muscles.
The reticulospinal tract runs from the reticular nuclei of the pons and medulla to the spinal nerves. It is involved in somatic motor control like the rubrospinal tract and also plays an important role in the control of autonomic functions. Facilitate or inhibit voluntary and reflex motor activity.
The tectospinal tract has points of origin throughout the brain stem, but especially in the midbrain area, and ends in the spinal nerves. It is involved in the control of neck muscles. Postural reflex in response to visual and auditary stimuli.
The vestibulospinal tract runs from the vestibular nuclei located in the lower pons and medulla to the spinal nerves. It is involved in balance.
The olivo spinal tract regulate motor activity
(Note that all of these tracts receive input from the cerebellum.)
The Extra-Pyramidal Tracts (and Basal Ganglia):
Deep to the cortex of each cerebral hemisphere are located several massive nuclei forming the basal ganglia. This structure, also known as the corpus striatum, is composed of the caudate nucleus and the putamen. In turn, the putamen and globus pallidus form together the lentiform nucleus.
The basal ganglia establish feedback loop-like connections with the different motor areas of the cortex. The cortex projects fibers to the basal ganglia, which then project to the thalamus (ventro-lateral and ventro-anterior nuclei), which project back to the cortex. The basal ganglia establish also several connections with other nuclei such as the substantia nigra and the subthalamus. This network of interconnections forms the extra-pyramidal system.
A complete understanding of the role of these structures has not yet been fully established. It is known that damage of any of these different structures can result in:
the generation of a variety of involuntary movements
Lesions of the basal ganglia:
Lesions in specific nuclei tend to produce characteristic deficits. One well-known disorder is Parkinson’s disease, which is the slow and steady loss of dopaminergic neurons in SNpc. An instant Parkinson-like syndrome will result if these neurons are damaged. This happened several years ago to an unfortunate group of people who took some home-brewed Demerol in search of a high. It was contaminated by a very nasty byproduct, MPTP ,which selectively zapped the SNpc neurons. The three symptoms usually associated with Parkinson’s are tremor, rigidity, and bradykinesia. The tremor is most apparent at rest. Rigidity is a result of simultaneous contraction of flexors and extensors, which tends to lock up the limbs. Bradykinesia, or “slow movement”, is a difficulty initiating voluntary movement, as though the brake cannot be released.
Huntington’s disease, or chorea, is a hereditary disease of unwanted movements. It results from degeneration of the caudate and putamen, and produces continuous dance-like movements of the face and limbs. A related disorder is hemiballismus, flailing movements of one arm and leg, which is caused by damage (i.e., stroke) of the subthalamic nucleus.
Extrapyramidal Diseases and Syndromes Affecting Communication/Swallowing
Lesions in the extrapyramidal tract cause various types of diskinesias or disorders of involuntary movement.
The problems most commonly affecting the extrapyramidal tract include degenerative diseases, encephalitis, and tumors.
Parkinson’s Disease, which is a degenerative disease, is probably the most frequently occurring illness that results from extrapyramidal tract lesions. It occurs when the dopaminergic neurons of the substantia nigra are destroyed. Its symptoms include:
Festinating movements, especially a festinating gait. (Festinating movements are movements which become increasingly rapid and uncontrolled).
Mask-like facial expression
Diseases associated specifically with lesions of the basal ganglia include Huntington’s Chorea and Sydenham’s Chorea. The term “chorea” comes from the Greek “khoros” which means dance. Both of these diseases are associated with jerky, uncontrolled movements of the limbs. Sydenham’s chorea was probably the cause of the malady that was known as St. Vitus’ Dance during the middle ages. Huntington’s Chorea is an inherited degenerative disease. Sydenham’s tends to clear up spontaneously.
Essential Tremor Syndrome, which is associated with Spastic Dysphonia may also be the result of basal ganglia lesions.
Lesions of the basal ganglia will also cause hyperkinetic dysarthria.
- Note that not only is the definition of the extrapyramidal system controversial, but also many sources say that it is very difficult to make functional distinctions between the extrapyramidal and pyramidal systems. When upper motor neuron lesions occur, it is sometimes difficult to determine which tract has been damaged.
- Substantia nigra loss
LOWER MOTOR NEURON Lower motor neurons, or second order neurons are cranial and spinal nerves. The cell bodies of these neurons are located in the brain stem, but their axons can leave the central nervous system and synapse with the muscles of the body
Lower motor connecting the brainstem and spinal cord to muscle fibers, bringing the nerve impulses from the upper motor neurons out to the muscles. The lower motor neuron’s axon goes through a foramen and terminates on an effector (muscle).
In the spinal cord, the axons of the upper motor neuron connect (most of them via interneurons, but to a lesser extent also via direct synapses) with the lower motor neurons (LMNs), located in the ventral horn of the spinal cord.
In the brain stem, the lower motor neurons are located in the motor cranial nerve nuclei (occulomotor, trochlear, motor nucleus of the trigeminal nerve, abducens, facial, accessory, hypoglossal). The lower motor neuron axons leave the brain stem via motor cranial nerves and the spinal cord via anterior roots of the spinal nerves respectively, end-up at the neuromuscular plate and provide motor innervation for voluntary muscles.
Lower motor neurons, or second order neurons are cranial and spinal nerves. The cell bodies of these neurons are located in the brain stem, but their axons can leave the central nervous system and synapse with the muscles of the body.
All lower motor neurons are either spinal or cranial nerves. All spinal nerves have a lower motor neuron component as they are mixed nerves. However, not all cranial nerves have lower motor neuron components. Some of the cranial nerves contain only sensory fibers and therefore cannot be classified as lower motor neurons. For example, CN I, the olfactory nerve, CN II the optic nerve, and CN VIII, the auditory nerve, do not have motor components.
The axons of lower motor neurons are a type of motor fibers. Lower motor neurons are classified based on the type of muscle fiber they innervate:
- Alpha motor neurons (α-MNs) innervate extrafusal muscle fibers, the most numerous type of muscle fiber and the one most involved in muscle contraction.
- Gamma motor neurons (γ-MNs) innervate intrafusal muscle fibers, which are involved with muscle spindles and the sense of body position.
Glutamate released from the upper motor neurons triggers depolarization in the lower motor neurons in the anterior horn which in turn causes an action potential to propagate the length of the axon to the neuromuscular junction where acetylcholine is released to carry the signal across the synaptic cleft to the postsynaptic receptors of the muscle cell membrane, signaling the muscle to contract.
Consequences of lesions
Damage to lower motor neurons (lower motor neurone lesions) is indicated by abnormal EMG potentials, fasciculation, fibrillation, paralysis, weakening of muscles, and neurogenic atrophy of skeletal muscle.