STUDY - Technical - New Dacian's Medicine
Muscle
Weakness, Abnormal Movements and Imbalance
(1)
Translation Draft
Motor dysfunction can result from weakness, disordered movements, ataxia, imbalance and other disorders in the initiation or coordination of movement.
Muscle weakness is a decrease in the normal strength of one or more muscles. Patients may use different terms to describe how one or more specific examples of weakness feel should be highlighted during anamnesis. Increased fatigue or limitation of movement due to pain are commonly confused with weakness by patients. Increased fatigue is the inability to perform a sustained activity that should be normal for a person of the same age, sex and weight.
Weakness is commonly described by severity and distribution. Paralysis and the suffix "-plegia" indicate weakness that is so severe that it is complete or almost complete. "Paresis" refers to weakness that is mild. The prefix "hemi-" refers to one half of the body, "para-" to both legs, and "quadri-" to all four limbs.
Recognition of the modified tone is important for locating the cause of the weakness. The tone is the resistance of a muscle to passive stretching. The abnormalities of the central nervous system that cause weakness generally produce spasticity, an increase in tone due to central motor neuron disease. Spasticity depends on velocity, has a sudden relaxation after reaching its maximum (the phenomenon of "briceag") and predominantly affects the antigravity muscles (for example, the flexors of the upper limb more than the extensors and extensors of the lower limb more than the flexors).
Spasticity is distinct from stiffness and paratony, two other types of increased tone. Rigidity is the increased tone that is present in all kinds of motion (a "lead tube" or "plastic" stiffness) and affects flexors and extensors equally. In some patients, stiffness is a tooth wheel type, i.e. it is accentuated by the voluntary movement of the contralateral limb (consolidation). Rigidity occurs in certain extrapyramidal conditions.
Paratonia, which we also refer to as resistance to passive movements (gegenhalten), is the increased tone that varies irregularly in a manner that may seem related to the degree of relaxation, is present throughout all kinds of movement and affects flexors and extensors equally. Paratonia usually results from frontal lobe disease. Low tone (flascity) or normal tonus weakness occurs in motor unit disorders, i.e. a single peripheral motor neuron and all the muscle fibers that they irritate.
Three basic types of weakness can usually be recognized on the basis of signs (atrophy, fasciculations, tone, distribution of affection, tendinous reflexes and Babinski sign): 1. of central motor neuron, 2. of peripheral motor neuron and 3. Myopathy. So, as can be seen, one type results from the pathology of the central motor neuron and the other two from the disorders of the motor unit (peripheral motor neuron and myopathic weakness). Fasciculations and the early presence of atrophy help to distinguish the weakness of the peripheral (neurogenic) motor neuron from the myopathic neuron. A fasciculation is a visible or palpable spasm of a single muscle due to the spontaneous discharge of a motor unit. Neurogenic weakness also produces a more prominent hypotonia and a greater depression of tendon reflexes than myopathic impairment.
Weakness due to the central neuron is a type of disability resulting from disorders of the central motor neurons or their axons in the cerebral context, the white cortical substance, the internal capsule, the brain stem or the spinal cord. Central motor neurons have cellular bodies in the V layer of the cerebral cortex, most of which are contained in the primary motor cortex (precentral gyrus or area 4 Brodmann) and in the premotor and additional motor cortex (area 6). A significant minority is in the primary sensory cortex (areas 3, 1 and 2) and the upper parietal lobe (areas 5 and 7). The central motor neurons in the primary motor cortex are organized somatotonic.
Those who activate the facial muscles are at the lower end of the precentral gyrus, those who activate the arm and hand muscles are higher in this gyrus and those who activate the leg muscles are in the paracentral lobe on the medial surface of the cerebral hemispheres. The somatotopic organization of central motor neurons is also preserved in other motor cortical areas (e.g. premotor and additional motor cortexes). The axons of central motor neurons descend through the subcortical white substance and through the posterior limb of the internal capsule. Those axons that comprise the pyramidal or corticospinal system descend through the brain stem into the cerebral peduncles of the mesencephalus, at the base of the bridge and into the medullary pyramids.
At the cervicomedular junction, most pyramidal axons intersect in the contralateral corticospinal tract of the lateral medullary cord, but 10 to 30% remain ipsilateral in the anterior medullary cord. Pyramid neurons include both large corticomotor neurons and smaller corticospinal neurons.
Corticomotor neurons are glutamatergic and make direct monosynaptic connections with peripheral motor neurons. They very densely irritate the peripheral motor neurons of the hand muscles and are involved in the execution of learned, fine movements. Corticospinal neurons are also glutamatergic, but synapse with neurons in the posterior horn and interneurons in the intermediate area of the spinal cord to facilitate cortical initiated movements. Corticobulbar neurons are central motor neurons that are similar to corticospinal neurons, but irritate the motor core of the brain stem. Corticobulbar neurons, although analogous as function and often designated as pyramidal in general contexts are not a strict part of the pyramid system as their axons never cross the medullary pyramids. Bulbospinal central motor neurons influence strength and tone, but are not part of the pyramidal system. Corticorubral, reticular, corticopontin and other cerebral cortex-trunk beams constitute the activities of the peripheral motor neuron, indirectly through these paths.
Cortical neurons influence the red nucleus and upper colic of the mesencephalus and vestibular nuclei, the lower olivar nucleus and the reticulated formation of the bridge and marrow. The descending ventromedial bulbospinal beams originate in the mesencephalic tectum (tectospinal beam), lateral and medial vestibular nuclei (vestibulospinal beam) and the reticulated formation (reticulospinal fasciculation). These bundles influence the axial and proximal muscles and are involved in maintaining limb and torso movements. The descending ventrolateral bulbospinal beams, which originate predominantly in the magnoliallet portion of the red nucleus (rubrospinal beam) influence the distal muscles of the limbs. The bulbospinal system is sometimes designated as the extrapyramidal system of the upper motor neuron.
The pyramidal and bulbospinal pathways contribute to maintaining within normal limits the force, tone, coordination and gait. Clinical lesions generally affect both pyramidal and bulbospinal pathways and are rarely purely pyramidal. Purely pyramidal lesions in animals produce an acute contralateral flaccid hemiplegia that respects the face and is associated with an extensor plantar response (Babinski), the strength being regained in weeks to months and spasticity and hyperreflexia do not occur. In humans, in weakness due to the central motor neuron, the development of spasticity and hyperreflection has been reported in rare cases of pure pyramidal bilateral infarction.
Central motor neuron lesions produce weakness through low activation of peripheral motor neurons, which irritate muscles in one or more regions of the body. Weakness due to the central motor neuron always targets more than one muscle group and rarely affects all muscles in a limb.
In general, distal muscle groups are affected more severely than proximal ones and axial movements are preserved if the lesion is not severe and bilateral. In corticobulbar damage, weakness is observed only in the face and tongue (extraocular, upper facial, pharyngeal and jaw muscles are almost always unaffected. In bilateral corticobulbar lesions, pseudobulbar paralysis frequently occurs, in which dysarcria, dysphagia, dysphonia and emotional lability accompany bilateral facial weakness. The spastic tone accompanies the damage of the central motor neuron if it is not acute. Acute injuries under the large hole usually produce spinal shock if the weakness is severe. During spinal shock, tendinous reflexes are absent and the tone is flasc. Subsequent spasticity occurs in days to weeks.
The lesions of the central motor neuron also cause incoordination, which is manifested by slow, coarse movements, for which normal rhythmicity is maintained. Finger-toe and heel-knee-tibia movements are achieved slowly but appropriately. The lack of coordination is more evident in rapidly repeated movements, such as the slight beating of the index on the font.
Let's move now to weakness due to the peripheral motor neuron. This type results from the disorders of the cellular bodies of the lower motor neurons in the motor fluids of the brain stem and from the anterior horn of the spinal cord, or from the dysfunction of the axons of these neurons on their path to the skeletal muscle. Peripheral motor neurons are divided into alpha and gamma types. Gamma motor neurons are smaller than alpha motor neurons and irritate the intrafusal muscle fibers of the muscle zone. Activation of the gamma motor neuron increases tension in muscle zones and facilitates stretching reflexes and other local reflex mechanisms, which activate the muscle through alpha motor neurons. Each muscle is innervated by several alpha motor neurons (usually a few hundred).
Each alpha motor neuron activates several extrafusal muscle fibers, several hundred for a limb's muscles and axial muscles or less than 20 for extraocular muscles by releasing acetylcholine. The axons of peripheral motor neurons leave the brain stem through certain cranial nerves and spinal cord through their anterior roots. The anterior roots merge with the posterior ones at the level of the intervertebral hole to form the spinal nerves. For the innervation of the limb muscles, a few adjacent spinal nerves fuse to form plexuses, before dividing into peripheral nerves. Most peripheral nerves branch out once or more as they irritate different muscles. Each alpha motor axon gives multiple branches even before it reaches the numerous muscle fibers that it irritates.
The alpha motor neuron receives excitatory, glutamatergic direct impulses from corticomotor neurons and related primary muscle zones. Alpha and gamma motor neurons also receive direct or indirect excitatory impulses from other descending pathways of central motor neurons, sensory segmentation impulses and interneuronal impulses. Alpha motor neurons in the spinal cord receive direct postsynaptic inhibitory impulses from Renshaw cellular interneurons, which release glycine. Other interneurons produce presynaptic inhibition of the neurons of the hind horns by releasing aminobutyric gamma acid (GABA), which indirectly inhibits alpha and gamma motor neurons.
Other descending pathways of central motor neurons and sensory segmentation impulses also produce direct or indirect inhibition of alpha and gamma motor neurons. When the balance of the descending impulses of the central and segmental motor neurons is on the excitation side, the totality of the peripheral motor neurons that irritate a muscle is activated in an orderly manner. Peripheral motor neurons with the smallest cellular bodies are activated first. At increased effort, these motor units discharge quickly and larger motor units are then gradually recruited. At maximum effort, all peripheral motor neuron reserves are activated to produce maximum power.
Peripheral motor weakness is caused by a decrease in the number of motor units that can be activated, due to a loss of alpha motor neurons or the interruption of their connections to the muscle. With the decrease in the number of motor units, fewer muscle fibers are activated at total effort and the maximum power is reduced. Loss of gamma motor neurons does not cause weakness, but decreases tension in the muscle zones.
Muscle tone and tendinous reflexes depend on gamma motor neurons, muscle spindles, their related fibers and alpha motor neurons. A slight hit of the tendon stretches the muscle zones and activates the fibers related to the primary spindle. They stimulate monosynaptic alpha motor neurons in the spinal cord by releasing glutamate. Active alpha motor neurons produce a short muscle contraction, which is the familiar tendinous reflex. The loss of the impulses of the gamma motor neurons to the intrafusal muscle fibers decreases both the continuous discharges of the related spindles (which increase muscle tone) and the phase discharges of the related spindles in response to stretching (which produces the tendinous reflex).
When a motor unit is affected, especially in the diseases of the anterior horn neurons, it can spontaneously discharge, producing a fasciculation, without normal recruitment. These small, isolated spasms can be seen in a normal manner. These small, isolated spasms can be seen or felt clinically or recorded by electromyography (EMG). When alpha motor neurons or their axons degenerate, denervated muscle fibers spontaneously discharge, in a manner that cannot be seen or felt, but that can be recorded with EMG.
These small, singular discharges of muscle fibers are called fibrillation potentials. Recruitment of outstanding motor units can be estimated with EMG. if significant impairment of the peripheral motor neuron is present, the recruitment of motor units is delayed or reduced, meaning that fewer motor units than normal are activated at a given discharge frequency. This contrasts with weakness due to the central motor neuron, in which a normal number of motor units are activated at a given frequency, but in which the maximum discharge frequency is low.
You guys, I'm stopping here! I still have some of this medical-technical-anatomical stuff to implement-... etc. But at most one more post. I'm sorry, but all these details will have their purpose later. Thank you for your understanding!
Motor dysfunction can result from weakness, disordered movements, ataxia, imbalance and other disorders in the initiation or coordination of movement.
Muscle weakness is a decrease in the normal strength of one or more muscles. Patients may use different terms to describe how one or more specific examples of weakness feel should be highlighted during anamnesis. Increased fatigue or limitation of movement due to pain are commonly confused with weakness by patients. Increased fatigue is the inability to perform a sustained activity that should be normal for a person of the same age, sex and weight.
Weakness is commonly described by severity and distribution. Paralysis and the suffix "-plegia" indicate weakness that is so severe that it is complete or almost complete. "Paresis" refers to weakness that is mild. The prefix "hemi-" refers to one half of the body, "para-" to both legs, and "quadri-" to all four limbs.
Recognition of the modified tone is important for locating the cause of the weakness. The tone is the resistance of a muscle to passive stretching. The abnormalities of the central nervous system that cause weakness generally produce spasticity, an increase in tone due to central motor neuron disease. Spasticity depends on velocity, has a sudden relaxation after reaching its maximum (the phenomenon of "briceag") and predominantly affects the antigravity muscles (for example, the flexors of the upper limb more than the extensors and extensors of the lower limb more than the flexors).
Spasticity is distinct from stiffness and paratony, two other types of increased tone. Rigidity is the increased tone that is present in all kinds of motion (a "lead tube" or "plastic" stiffness) and affects flexors and extensors equally. In some patients, stiffness is a tooth wheel type, i.e. it is accentuated by the voluntary movement of the contralateral limb (consolidation). Rigidity occurs in certain extrapyramidal conditions.
Paratonia, which we also refer to as resistance to passive movements (gegenhalten), is the increased tone that varies irregularly in a manner that may seem related to the degree of relaxation, is present throughout all kinds of movement and affects flexors and extensors equally. Paratonia usually results from frontal lobe disease. Low tone (flascity) or normal tonus weakness occurs in motor unit disorders, i.e. a single peripheral motor neuron and all the muscle fibers that they irritate.
Three basic types of weakness can usually be recognized on the basis of signs (atrophy, fasciculations, tone, distribution of affection, tendinous reflexes and Babinski sign): 1. of central motor neuron, 2. of peripheral motor neuron and 3. Myopathy. So, as can be seen, one type results from the pathology of the central motor neuron and the other two from the disorders of the motor unit (peripheral motor neuron and myopathic weakness). Fasciculations and the early presence of atrophy help to distinguish the weakness of the peripheral (neurogenic) motor neuron from the myopathic neuron. A fasciculation is a visible or palpable spasm of a single muscle due to the spontaneous discharge of a motor unit. Neurogenic weakness also produces a more prominent hypotonia and a greater depression of tendon reflexes than myopathic impairment.
Weakness due to the central neuron is a type of disability resulting from disorders of the central motor neurons or their axons in the cerebral context, the white cortical substance, the internal capsule, the brain stem or the spinal cord. Central motor neurons have cellular bodies in the V layer of the cerebral cortex, most of which are contained in the primary motor cortex (precentral gyrus or area 4 Brodmann) and in the premotor and additional motor cortex (area 6). A significant minority is in the primary sensory cortex (areas 3, 1 and 2) and the upper parietal lobe (areas 5 and 7). The central motor neurons in the primary motor cortex are organized somatotonic.
Those who activate the facial muscles are at the lower end of the precentral gyrus, those who activate the arm and hand muscles are higher in this gyrus and those who activate the leg muscles are in the paracentral lobe on the medial surface of the cerebral hemispheres. The somatotopic organization of central motor neurons is also preserved in other motor cortical areas (e.g. premotor and additional motor cortexes). The axons of central motor neurons descend through the subcortical white substance and through the posterior limb of the internal capsule. Those axons that comprise the pyramidal or corticospinal system descend through the brain stem into the cerebral peduncles of the mesencephalus, at the base of the bridge and into the medullary pyramids.
At the cervicomedular junction, most pyramidal axons intersect in the contralateral corticospinal tract of the lateral medullary cord, but 10 to 30% remain ipsilateral in the anterior medullary cord. Pyramid neurons include both large corticomotor neurons and smaller corticospinal neurons.
Corticomotor neurons are glutamatergic and make direct monosynaptic connections with peripheral motor neurons. They very densely irritate the peripheral motor neurons of the hand muscles and are involved in the execution of learned, fine movements. Corticospinal neurons are also glutamatergic, but synapse with neurons in the posterior horn and interneurons in the intermediate area of the spinal cord to facilitate cortical initiated movements. Corticobulbar neurons are central motor neurons that are similar to corticospinal neurons, but irritate the motor core of the brain stem. Corticobulbar neurons, although analogous as function and often designated as pyramidal in general contexts are not a strict part of the pyramid system as their axons never cross the medullary pyramids. Bulbospinal central motor neurons influence strength and tone, but are not part of the pyramidal system. Corticorubral, reticular, corticopontin and other cerebral cortex-trunk beams constitute the activities of the peripheral motor neuron, indirectly through these paths.
Cortical neurons influence the red nucleus and upper colic of the mesencephalus and vestibular nuclei, the lower olivar nucleus and the reticulated formation of the bridge and marrow. The descending ventromedial bulbospinal beams originate in the mesencephalic tectum (tectospinal beam), lateral and medial vestibular nuclei (vestibulospinal beam) and the reticulated formation (reticulospinal fasciculation). These bundles influence the axial and proximal muscles and are involved in maintaining limb and torso movements. The descending ventrolateral bulbospinal beams, which originate predominantly in the magnoliallet portion of the red nucleus (rubrospinal beam) influence the distal muscles of the limbs. The bulbospinal system is sometimes designated as the extrapyramidal system of the upper motor neuron.
The pyramidal and bulbospinal pathways contribute to maintaining within normal limits the force, tone, coordination and gait. Clinical lesions generally affect both pyramidal and bulbospinal pathways and are rarely purely pyramidal. Purely pyramidal lesions in animals produce an acute contralateral flaccid hemiplegia that respects the face and is associated with an extensor plantar response (Babinski), the strength being regained in weeks to months and spasticity and hyperreflexia do not occur. In humans, in weakness due to the central motor neuron, the development of spasticity and hyperreflection has been reported in rare cases of pure pyramidal bilateral infarction.
Central motor neuron lesions produce weakness through low activation of peripheral motor neurons, which irritate muscles in one or more regions of the body. Weakness due to the central motor neuron always targets more than one muscle group and rarely affects all muscles in a limb.
In general, distal muscle groups are affected more severely than proximal ones and axial movements are preserved if the lesion is not severe and bilateral. In corticobulbar damage, weakness is observed only in the face and tongue (extraocular, upper facial, pharyngeal and jaw muscles are almost always unaffected. In bilateral corticobulbar lesions, pseudobulbar paralysis frequently occurs, in which dysarcria, dysphagia, dysphonia and emotional lability accompany bilateral facial weakness. The spastic tone accompanies the damage of the central motor neuron if it is not acute. Acute injuries under the large hole usually produce spinal shock if the weakness is severe. During spinal shock, tendinous reflexes are absent and the tone is flasc. Subsequent spasticity occurs in days to weeks.
The lesions of the central motor neuron also cause incoordination, which is manifested by slow, coarse movements, for which normal rhythmicity is maintained. Finger-toe and heel-knee-tibia movements are achieved slowly but appropriately. The lack of coordination is more evident in rapidly repeated movements, such as the slight beating of the index on the font.
Let's move now to weakness due to the peripheral motor neuron. This type results from the disorders of the cellular bodies of the lower motor neurons in the motor fluids of the brain stem and from the anterior horn of the spinal cord, or from the dysfunction of the axons of these neurons on their path to the skeletal muscle. Peripheral motor neurons are divided into alpha and gamma types. Gamma motor neurons are smaller than alpha motor neurons and irritate the intrafusal muscle fibers of the muscle zone. Activation of the gamma motor neuron increases tension in muscle zones and facilitates stretching reflexes and other local reflex mechanisms, which activate the muscle through alpha motor neurons. Each muscle is innervated by several alpha motor neurons (usually a few hundred).
Each alpha motor neuron activates several extrafusal muscle fibers, several hundred for a limb's muscles and axial muscles or less than 20 for extraocular muscles by releasing acetylcholine. The axons of peripheral motor neurons leave the brain stem through certain cranial nerves and spinal cord through their anterior roots. The anterior roots merge with the posterior ones at the level of the intervertebral hole to form the spinal nerves. For the innervation of the limb muscles, a few adjacent spinal nerves fuse to form plexuses, before dividing into peripheral nerves. Most peripheral nerves branch out once or more as they irritate different muscles. Each alpha motor axon gives multiple branches even before it reaches the numerous muscle fibers that it irritates.
The alpha motor neuron receives excitatory, glutamatergic direct impulses from corticomotor neurons and related primary muscle zones. Alpha and gamma motor neurons also receive direct or indirect excitatory impulses from other descending pathways of central motor neurons, sensory segmentation impulses and interneuronal impulses. Alpha motor neurons in the spinal cord receive direct postsynaptic inhibitory impulses from Renshaw cellular interneurons, which release glycine. Other interneurons produce presynaptic inhibition of the neurons of the hind horns by releasing aminobutyric gamma acid (GABA), which indirectly inhibits alpha and gamma motor neurons.
Other descending pathways of central motor neurons and sensory segmentation impulses also produce direct or indirect inhibition of alpha and gamma motor neurons. When the balance of the descending impulses of the central and segmental motor neurons is on the excitation side, the totality of the peripheral motor neurons that irritate a muscle is activated in an orderly manner. Peripheral motor neurons with the smallest cellular bodies are activated first. At increased effort, these motor units discharge quickly and larger motor units are then gradually recruited. At maximum effort, all peripheral motor neuron reserves are activated to produce maximum power.
Peripheral motor weakness is caused by a decrease in the number of motor units that can be activated, due to a loss of alpha motor neurons or the interruption of their connections to the muscle. With the decrease in the number of motor units, fewer muscle fibers are activated at total effort and the maximum power is reduced. Loss of gamma motor neurons does not cause weakness, but decreases tension in the muscle zones.
Muscle tone and tendinous reflexes depend on gamma motor neurons, muscle spindles, their related fibers and alpha motor neurons. A slight hit of the tendon stretches the muscle zones and activates the fibers related to the primary spindle. They stimulate monosynaptic alpha motor neurons in the spinal cord by releasing glutamate. Active alpha motor neurons produce a short muscle contraction, which is the familiar tendinous reflex. The loss of the impulses of the gamma motor neurons to the intrafusal muscle fibers decreases both the continuous discharges of the related spindles (which increase muscle tone) and the phase discharges of the related spindles in response to stretching (which produces the tendinous reflex).
When a motor unit is affected, especially in the diseases of the anterior horn neurons, it can spontaneously discharge, producing a fasciculation, without normal recruitment. These small, isolated spasms can be seen in a normal manner. These small, isolated spasms can be seen or felt clinically or recorded by electromyography (EMG). When alpha motor neurons or their axons degenerate, denervated muscle fibers spontaneously discharge, in a manner that cannot be seen or felt, but that can be recorded with EMG.
These small, singular discharges of muscle fibers are called fibrillation potentials. Recruitment of outstanding motor units can be estimated with EMG. if significant impairment of the peripheral motor neuron is present, the recruitment of motor units is delayed or reduced, meaning that fewer motor units than normal are activated at a given discharge frequency. This contrasts with weakness due to the central motor neuron, in which a normal number of motor units are activated at a given frequency, but in which the maximum discharge frequency is low.
You guys, I'm stopping here! I still have some of this medical-technical-anatomical stuff to implement-... etc. But at most one more post. I'm sorry, but all these details will have their purpose later. Thank you for your understanding!
Have
a good day!
Dorin, Merticaru