STUDY - Technical - New Dacian's Medicine
Muscle
Weakness, Abnormal Movements and Imbalance
(2)
Translation Draft
To continue the small and rather boring stage of description required for this post with the weakness of the myopic type. This type of weakness is caused by disorders within the motor unit that target muscle fibers or neuromuscular junctions.
There are two types of muscle fibers. Type I muscle fibers, rich in mitochondria and oxidative enzymes, which produce a relatively low force but have low energy needs, which can be supplemented by continuous aerobic metabolism. They perform sustained postural movements that do not require strength.
Type II muscle fibers are rich in glycolytic enzymes and can produce relatively high force, but have increased energy needs that cannot be substituted for long by continuous aerobic metabolism. Thus, these units can be activated maximum only for short periods of time, to produce movements involving a large force.
For voluntary progressive movements, type I muscle fibers are activated most early in recruitment. For each muscle fiber, if the terminal nerve presynapticly releases a normal number of acetylcholine molecules and a sufficient number of postsynaptic acetylcholine receptors are "opened", the terminal plaque reaches the threshold and thus generates a potential for action that spreads along the membrane of the muscle fiber and into the transverse tubular system. This electrical excitation activates intracellular events that produce an energy-dependent contraction of the muscle fiber (excitement-contraction coupling).
Myopathic weakness is caused by a decrease in the number or contractile force of muscle fibers activated within the motor unit. In muscular dystrophies, inflammatory myopathy or myopathy with muscle fiber necrosis, a low number of muscle fibers survives within many motor units.
As demonstrated with EMG, the size of the action potential of each motor unit is low, so motor units must be recruited faster than normal to produce the force required for a particular movement. Diseases of neuromuscular junctions produce weakness in a similar manner, although the loss of muscle fibers in a motor unit is functional rather than real.
Furthermore, the number of activated muscle fibers may vary over time, depending on the resting state of the neuromuscular junctions. Some myopathy causes weakness by loss of contractile strength of muscle fibers. These may not affect the size of the motor unit's action potential and are detected by the discrepancy between electrical activity and muscle strength.
Non-paralytic disorders of movement are other disorders of movement that do not cause weakness. Those that are classified as motion dysfunctions or as imbalances and ataxia are a distinct group that I will expose later. Others are caused by conditions in the initiation or integration of movement.
Such dysfunctions are caused by diseases that affect the cerebral hemispheres without causing obvious weakness of the central motor neuron. Many functional movements require integrated coordination from many muscle groups.
For example, let's look at a simple move, like catching a ball. The initial movement is the flexion of the font and fingers of a hand, with the opposition of the font and the little finger. This requires contraction of different muscles, including the superficial digital flexor, the deep digital flexor, the long flexor of the font, the short flexor of the font, the opponent of the font and the opponent of the little finger.
These first muscles that perform this action are called agonists. In order for the grip to be smooth and strong, the font and finger extenders must relax at the same speed with which the flexors contract. Muscles that behave in a way that are freely opposed to agonists are called antagonists. A secondary action of the flexors of the font and finger is to flex the wrist.
Since wrist flexion tends to weaken the flexion of the fingers, if both occur, activating the wrist extenders helps to move the grip. Muscles that produce such complementary movements are called synergistic muscles. Finally, the arm must be held in a stable position as the catch begins, so that the ball is not dropped before it is securely caught. Muscles that stabilize the position of the arm are called fixers.
The coordination of the activity by agonists, antagonists, synergists and fixers is regulated by a hierarchy on three levels of motor control. The lowest level is mediated by segmentation reflexes in the spinal cord. These reflexes stimulate agonists and mutually inhibit antagonists. Spinal segments also control rhythmic types of motion involving more than one pair of agonists and antagonists.
For example, the lombosacrate marrow contains the basic programming for cyclic movements in steps, which involves synergistic activation of different muscle groups over time. The intermediate level of control is mediated by bulbospinal descending pathways, which integrate visual, proprioceptive and vestibular feedback for the execution of an action.
For example, the locomotor center in the mesencephalus is required to modify cyclic movements in stages, so that the balance is maintained and the movement continues to occur. The highest level of control is mediated by the cerebral cortex. The overlap of this higher level of control is necessary for activities, such as walking, to be directed by a goal.
Precise movements, which are learned and perfected through practice, are also initiated and controlled by the motor cortex. Although only agonists are activated directly during a complete sequence of actions, such as playing the piano, sequential activation of different groups of agonists for each note or string is part of a learned motor program.
Moreover, the practice of these actions also involves impulses from the basal ganglia and cerebellar hemispheres, in order to facilitate agonists, synergists and fixers and to inhibit unwanted antagonists.
Apraxia is a condition of initiation and planning of movement. Unilateral apraxia of the right hand may be caused/ due to a lesion of the left frontal lobe (especially anterior or lower), left temporoparietal region (especially supramarginal gyrus) or their connections.
Left body apraxia is caused by lesions of these regions of the right hemisphere or by lesions in the calos body, which disconnect the right temporoparietal or frontal regions from those on the left. Bilateral apraxia is commonly due to bilateral lesions of the frontal lobe or bilateral hemispheric diffuse diseases.
All right, I'm done with the descriptions for now. Now we can move on to diagnostic approach and differential diagnosis for frequent clinical presentations of muscle weakness.
I'll start with the clinical assessment of weakness. When there is a discrepancy between the anamnesis data and the physical examination, it usually occurs because the patient is weak, while the symptoms are actually due to other causes, such as incoordination. The appropriate approach to weakness requires that the mode of onset, carefuldefinition of the distribution and associated traits, in order to identify the responsible anatomical lesion and probable etiology.
The force can be examined in different ways. Direct testing is commonly used to determine whether weakness is present and assess its distribution. The patient is asked to push or pull in a certain direction, against the resistance opposed by the evaluator, and the force of each muscle group is graduated from 0 to 10 (or to 5, depending on the assessment model approached).
A second method is indirect testing by observing performance at a task such as holding out arms. This is especially useful in detecting light, asymmetrical, central motor neuron weakness by observing a downward motion with the protrusion of the forearm on one side. A third method is functional testing involving quantitatively measured activities.
Frequent tests include recording the number of knee bends or climbs on a stool or seat, or the timing of how long the arms can be held in abstraction at 90 degrees. Functional tests for weakness consume time and any weakness is difficult to locate in a specific muscle or group of muscles, however it provides reproducible data to assess changes in patient status over time.
Other essential data of motor examination include muscle mass assessment, examination for fasciculations and estimation of tone in the four limbs. The presence of beams is most easily determined by observing relaxed limbs, which are illuminated from the back. Fasciculations can also be palpated as irregular spasms of low amplitude within the muscle.
The tone is evaluated by the passive movement of each limb in different joints and at several different speeds. In the clinical context of weakness, the tone may be spastic or low. The presence of stiffness in the toothed wheel, lead tube or proton suggests unparalytic damage to movement.
Hemiparesis results from a central motor neuron lesion over the middle cervical marrow, with most lesions causing hemiparesis being located above foramen magnum. the more precise location of the lesion is achieved by recognizing the associated signs.
Language impairment, sensory cortical disorders, cognitive impairment, visual-spatial integration impairment, apraxia and seizures identify a cortical lesion. The homonymous defects of the field of vision reflect either a cortical or a subcortical hemispheric lesion.
A hemiparesis of the face, arm or leg without associated signs indicates a small, discrete lesion in the posterior limb of the inner capsule, in the cerebral peduncle or at the top of the bridge. Some brain stem lesions produce classic manifestations of ipsilateral cranial nerve signs and contralateral hemiparesis (commonly referred to as "cross-paralysis"). The absence of signs of cranial nerve or facial weakness suggests that hemiparesis is due to injury in the upper cervical marrow, especially if it is associated with loss of ipsilateral proprioceptivity and contralateral loss of sense of pain and temperature (Brown-Sequard syndrome). However, most spinal cord injuries cause quadriparesis or paraparesis.
Acute hemiparesis usually has a vascular pathogenesis. Less common, bleeding can occur in primary or metastatic brain tumours or in rupture of normal vessels due to trauma (trauma may be common in patients who are on anticoagulant treatment or in the elderly).
Rarer possibilities include an inflammatory focal lesion of multiple sclerosis or sarcoidosis, or an acute bacterial abscess. The diagnostic approach starts immediately with a computed tomography (CT) of the brain and subsequent decisions are based on its outcome. If the TC of the brain is normal and it's not likely an ischemic stroke, nuclear magnetic resonance (NMR) of the brain or cervical spine may be required.
Subacute hemiparesis has a long differential diagnosis. Subacute subdural hematoma is a common cause of hemiparesis that develops in days to a few weeks, requiring prompt treatment, especially in elderly patients or those on anticoagulant treatment, even in the absence of a history of trauma.
Possibilities of infection include cerebral bacterial abscesses, fungal granulomas or meningitis and parasitic infection. Weakness in primary and metastatic malignant neoplasms may evolve from days to weeks, AIDS may present with subacute hemiparesis given by toxoplasmosis or primary lymphoma of the central nervous system. Non-infectious inflammatory processes, such as multiple sclerosis or, less commonly, sarcoidosis, are additional considerations. In the diagnostic approach, if cerebral MRI is normal, cervical spine MRI may be required.
Chronic hemiparesis develops in months (opposite that which develops acutely and then persists for months) is usually due to a benign histological neoplasm, an integral arteriovenous malformation, a chronic subdural hematone or a degenerative disease. The initial diagnostic test is frequently a brain MRI, especially if clinical data suggest the pathology of the brain stem. If cerebral MRI is normal, there are less likely possibilities to consider a magnum foramen lesion or upper cervical spine.
We've got other opinions to discuss... But that's in tomorrow's post...
To continue the small and rather boring stage of description required for this post with the weakness of the myopic type. This type of weakness is caused by disorders within the motor unit that target muscle fibers or neuromuscular junctions.
There are two types of muscle fibers. Type I muscle fibers, rich in mitochondria and oxidative enzymes, which produce a relatively low force but have low energy needs, which can be supplemented by continuous aerobic metabolism. They perform sustained postural movements that do not require strength.
Type II muscle fibers are rich in glycolytic enzymes and can produce relatively high force, but have increased energy needs that cannot be substituted for long by continuous aerobic metabolism. Thus, these units can be activated maximum only for short periods of time, to produce movements involving a large force.
For voluntary progressive movements, type I muscle fibers are activated most early in recruitment. For each muscle fiber, if the terminal nerve presynapticly releases a normal number of acetylcholine molecules and a sufficient number of postsynaptic acetylcholine receptors are "opened", the terminal plaque reaches the threshold and thus generates a potential for action that spreads along the membrane of the muscle fiber and into the transverse tubular system. This electrical excitation activates intracellular events that produce an energy-dependent contraction of the muscle fiber (excitement-contraction coupling).
Myopathic weakness is caused by a decrease in the number or contractile force of muscle fibers activated within the motor unit. In muscular dystrophies, inflammatory myopathy or myopathy with muscle fiber necrosis, a low number of muscle fibers survives within many motor units.
As demonstrated with EMG, the size of the action potential of each motor unit is low, so motor units must be recruited faster than normal to produce the force required for a particular movement. Diseases of neuromuscular junctions produce weakness in a similar manner, although the loss of muscle fibers in a motor unit is functional rather than real.
Furthermore, the number of activated muscle fibers may vary over time, depending on the resting state of the neuromuscular junctions. Some myopathy causes weakness by loss of contractile strength of muscle fibers. These may not affect the size of the motor unit's action potential and are detected by the discrepancy between electrical activity and muscle strength.
Non-paralytic disorders of movement are other disorders of movement that do not cause weakness. Those that are classified as motion dysfunctions or as imbalances and ataxia are a distinct group that I will expose later. Others are caused by conditions in the initiation or integration of movement.
Such dysfunctions are caused by diseases that affect the cerebral hemispheres without causing obvious weakness of the central motor neuron. Many functional movements require integrated coordination from many muscle groups.
For example, let's look at a simple move, like catching a ball. The initial movement is the flexion of the font and fingers of a hand, with the opposition of the font and the little finger. This requires contraction of different muscles, including the superficial digital flexor, the deep digital flexor, the long flexor of the font, the short flexor of the font, the opponent of the font and the opponent of the little finger.
These first muscles that perform this action are called agonists. In order for the grip to be smooth and strong, the font and finger extenders must relax at the same speed with which the flexors contract. Muscles that behave in a way that are freely opposed to agonists are called antagonists. A secondary action of the flexors of the font and finger is to flex the wrist.
Since wrist flexion tends to weaken the flexion of the fingers, if both occur, activating the wrist extenders helps to move the grip. Muscles that produce such complementary movements are called synergistic muscles. Finally, the arm must be held in a stable position as the catch begins, so that the ball is not dropped before it is securely caught. Muscles that stabilize the position of the arm are called fixers.
The coordination of the activity by agonists, antagonists, synergists and fixers is regulated by a hierarchy on three levels of motor control. The lowest level is mediated by segmentation reflexes in the spinal cord. These reflexes stimulate agonists and mutually inhibit antagonists. Spinal segments also control rhythmic types of motion involving more than one pair of agonists and antagonists.
For example, the lombosacrate marrow contains the basic programming for cyclic movements in steps, which involves synergistic activation of different muscle groups over time. The intermediate level of control is mediated by bulbospinal descending pathways, which integrate visual, proprioceptive and vestibular feedback for the execution of an action.
For example, the locomotor center in the mesencephalus is required to modify cyclic movements in stages, so that the balance is maintained and the movement continues to occur. The highest level of control is mediated by the cerebral cortex. The overlap of this higher level of control is necessary for activities, such as walking, to be directed by a goal.
Precise movements, which are learned and perfected through practice, are also initiated and controlled by the motor cortex. Although only agonists are activated directly during a complete sequence of actions, such as playing the piano, sequential activation of different groups of agonists for each note or string is part of a learned motor program.
Moreover, the practice of these actions also involves impulses from the basal ganglia and cerebellar hemispheres, in order to facilitate agonists, synergists and fixers and to inhibit unwanted antagonists.
Apraxia is a condition of initiation and planning of movement. Unilateral apraxia of the right hand may be caused/ due to a lesion of the left frontal lobe (especially anterior or lower), left temporoparietal region (especially supramarginal gyrus) or their connections.
Left body apraxia is caused by lesions of these regions of the right hemisphere or by lesions in the calos body, which disconnect the right temporoparietal or frontal regions from those on the left. Bilateral apraxia is commonly due to bilateral lesions of the frontal lobe or bilateral hemispheric diffuse diseases.
All right, I'm done with the descriptions for now. Now we can move on to diagnostic approach and differential diagnosis for frequent clinical presentations of muscle weakness.
I'll start with the clinical assessment of weakness. When there is a discrepancy between the anamnesis data and the physical examination, it usually occurs because the patient is weak, while the symptoms are actually due to other causes, such as incoordination. The appropriate approach to weakness requires that the mode of onset, carefuldefinition of the distribution and associated traits, in order to identify the responsible anatomical lesion and probable etiology.
The force can be examined in different ways. Direct testing is commonly used to determine whether weakness is present and assess its distribution. The patient is asked to push or pull in a certain direction, against the resistance opposed by the evaluator, and the force of each muscle group is graduated from 0 to 10 (or to 5, depending on the assessment model approached).
A second method is indirect testing by observing performance at a task such as holding out arms. This is especially useful in detecting light, asymmetrical, central motor neuron weakness by observing a downward motion with the protrusion of the forearm on one side. A third method is functional testing involving quantitatively measured activities.
Frequent tests include recording the number of knee bends or climbs on a stool or seat, or the timing of how long the arms can be held in abstraction at 90 degrees. Functional tests for weakness consume time and any weakness is difficult to locate in a specific muscle or group of muscles, however it provides reproducible data to assess changes in patient status over time.
Other essential data of motor examination include muscle mass assessment, examination for fasciculations and estimation of tone in the four limbs. The presence of beams is most easily determined by observing relaxed limbs, which are illuminated from the back. Fasciculations can also be palpated as irregular spasms of low amplitude within the muscle.
The tone is evaluated by the passive movement of each limb in different joints and at several different speeds. In the clinical context of weakness, the tone may be spastic or low. The presence of stiffness in the toothed wheel, lead tube or proton suggests unparalytic damage to movement.
Hemiparesis results from a central motor neuron lesion over the middle cervical marrow, with most lesions causing hemiparesis being located above foramen magnum. the more precise location of the lesion is achieved by recognizing the associated signs.
Language impairment, sensory cortical disorders, cognitive impairment, visual-spatial integration impairment, apraxia and seizures identify a cortical lesion. The homonymous defects of the field of vision reflect either a cortical or a subcortical hemispheric lesion.
A hemiparesis of the face, arm or leg without associated signs indicates a small, discrete lesion in the posterior limb of the inner capsule, in the cerebral peduncle or at the top of the bridge. Some brain stem lesions produce classic manifestations of ipsilateral cranial nerve signs and contralateral hemiparesis (commonly referred to as "cross-paralysis"). The absence of signs of cranial nerve or facial weakness suggests that hemiparesis is due to injury in the upper cervical marrow, especially if it is associated with loss of ipsilateral proprioceptivity and contralateral loss of sense of pain and temperature (Brown-Sequard syndrome). However, most spinal cord injuries cause quadriparesis or paraparesis.
Acute hemiparesis usually has a vascular pathogenesis. Less common, bleeding can occur in primary or metastatic brain tumours or in rupture of normal vessels due to trauma (trauma may be common in patients who are on anticoagulant treatment or in the elderly).
Rarer possibilities include an inflammatory focal lesion of multiple sclerosis or sarcoidosis, or an acute bacterial abscess. The diagnostic approach starts immediately with a computed tomography (CT) of the brain and subsequent decisions are based on its outcome. If the TC of the brain is normal and it's not likely an ischemic stroke, nuclear magnetic resonance (NMR) of the brain or cervical spine may be required.
Subacute hemiparesis has a long differential diagnosis. Subacute subdural hematoma is a common cause of hemiparesis that develops in days to a few weeks, requiring prompt treatment, especially in elderly patients or those on anticoagulant treatment, even in the absence of a history of trauma.
Possibilities of infection include cerebral bacterial abscesses, fungal granulomas or meningitis and parasitic infection. Weakness in primary and metastatic malignant neoplasms may evolve from days to weeks, AIDS may present with subacute hemiparesis given by toxoplasmosis or primary lymphoma of the central nervous system. Non-infectious inflammatory processes, such as multiple sclerosis or, less commonly, sarcoidosis, are additional considerations. In the diagnostic approach, if cerebral MRI is normal, cervical spine MRI may be required.
Chronic hemiparesis develops in months (opposite that which develops acutely and then persists for months) is usually due to a benign histological neoplasm, an integral arteriovenous malformation, a chronic subdural hematone or a degenerative disease. The initial diagnostic test is frequently a brain MRI, especially if clinical data suggest the pathology of the brain stem. If cerebral MRI is normal, there are less likely possibilities to consider a magnum foramen lesion or upper cervical spine.
We've got other opinions to discuss... But that's in tomorrow's post...
Have
a good day, everyone!
Dorin, Merticaru