STUDY - Technical - New Dacian's Medicine
Spasms,
Cramps and Regular Muscle Weakness
(1)
Translation Draft
Spontaneous musculo-articular discomfort or following physical exertion is usually benign and does not have the significance of neuromuscular disorders.
Spontaneous musculo-articular discomfort or following physical exertion is usually benign and does not have the significance of neuromuscular disorders.
However,
this type of symptoms may provide suggestive clues for
debilitating conditions that are long undiagnosed.
Terms like pain, spasm and cramp are frequently used incorrectly by patients when describing the symptomatology of the muscular system, they substitute one term for another. Other terms such as neuralgia, weight and stiffness are also commonly used and usually provide little useful information about the location of the condition. Clinically, the notion of spasm means a paroxysmal, spontaneous, prolonged and painful contradiction of one or more muscles. Muscle pain may be associated with fatigue (asthenia) or weakness.
Spasms are abnormal muscle movements that can occur through abnormalities in electrical activity in the central nervous system (CNS), mediated by motor neurons or that occur even in motor neurons or muscle fiber. It is difficult to establish the exact origin of abnormal motor activity, using only clinical data.
In general, movements originating in the CNS affect an entire part of the body, a limb or a muscle group. Central diseases can be rhythmic or intermittent, with those occurring at the peripheral level usually random. Electroencephalogram (EEG) may highlight changes in cortical activity in pathology with CNS etiology. Electromyogram (EMG) is less useful because it reflects motor changes of varied etiology. However, highlighting a basic nerve or muscle fiber condition on EMG may be useful for diagnosis.
Intermittent, arrhythmic movements of the entire limb, torso or a facial portion may occur within epilepsy or through myoclonia. Spasms in flexion and extension of an entire part of the body or lower limbs occur by the disappearance of motor inhibition within the CNS. Segmental myoclonia is the result of focal disorders in the brain stem or spinal cord, which cause abnormal discharges of the groups of motor neurons. Localized vascular disorders, tumors or other lesions may be involved.
Let's talk about abnormal facial movements now. Hemifacial spasms occur through the paroxysmal activity of the facial nerve, sometimes triggered by pressure exerted by a torchy blood vessel, located adjacent to where the facial nerve leaves the brain stem. Hemifacial spasm usually occurs in muscles adjacent to the eyeball, but it can also involve or spread throughout the face.
Symptoms are often intermittent and intensify when the patient uses facial muscles, for example, during speech. Hemifacial spasm is painless but embarrassing, especially for people who work in public. Because it is more intense and severe when the patient is under stress, it can be misdiagnosed as tic.
Injuries at the pontocerebelous angle can sometimes produce similar manifestations. Neuroradiological investigation is indicated in patients with hemifacial spasm. Injecting botulinum toxin into the affected muscles removes spasm for up to 3 months and surgical exploration and isolation of the facial nerve from the adjacent vessel is often curative.
Facial tics are stereotypical facial movements, e.g. blinking, turning the head, grimaces, which are under voluntary control, but can only be suppressed with effort and anxiety on the part of the subject. Some tics are so common that they are considered mannerisms, such as the act of excessive "dreging" of the voice.
An example is the repeated raising of the eyebrows by contraction of the frontal muscles. Certain hereditary motor disorders, such as Gilles de la Tourette syndrome, are characterized by multiple tics. Tics can usually be controlled by neuroleptic medication.
Facial sinkinesis occurs as part of the aberrant regeneration of the facial nerve, following damage to the facial nerve from Bell's palsy or other facial lesions. Nearly 50% of patients recovering from Bell's palsy experience such movements. An example is mandibulal sinkinesis in which voluntary movements of the lower part of the face produce the contraction of the orbicular of the eye, with unilateral closure of the eye.
Trigeminal neuralgia (painful ticks) is characterized by short, paroxysmal, lancinating pain in one half of the face. Although the affected portion of the nerve is almost exclusively sensory, the severity of the pain produces involuntary contractions of the facial muscles (hence the name of tic). Abnormal movements do not occur in the absence of pain. Facial myokimia refers to the presence of almost continuous pulsations in the facial muscles.
Although it is usually benign, it can occur through pontine lesions, such as neoplasia or multiple sclerosis. Facial or limb myokimia occurs in association with episodic ataxia in the genetic defects of the potassium channels of the nerves. Similar movements occur in motor neuron disorders, such as amyotrophic lateral sclerosis.
Let's get to the motor abnormalities of the limbs! When the muscles are totally relaxed, no movement should be felt. The diseases of motor neurons or their proximal axons are frequently associated with fasciculations, representing the spontaneous discharge of an entire motor unit. Fasciculations are visible on inspection or perceived by the patient in the form of tremors or intramuscular pulsations.
They sometimes occur in healthy people, and in the absence of muscle weakness have no pathological significance. Fasciculations are a normal phenomenon when they occur in an incomplete relaxed muscle and are frequently observed at rest in the calves of normal individuals. Miotimia, consisting of numerous repetitive fasciculations, can also occur in the muscles of the limbs, creating the sensation of crispness.
It disappears through neuromuscular blockage, thus demonstrating that the initiation of movements is done in the anterior medullary horns or in the peripheral nerves. In patients with long-lasting muscle denervation and then reinervation, the dimensions of the motor unit increase and the fasciculations can be so strong that movements of the limbs, especially the fingers, occur called minipolymioclonus.
Certain conditions are characterized by a tendency to move limbs. Akatisia or muscle agitation occurs in Parkinson's disease and other damage to the basal ganglia, including medicinal ones. Restless leg syndrome is a feeling of muscle discomfort, commonly in the legs and thighs, which is usually found in middle-aged women.
Patients feel the need to move their legs to remove the disturbing sensation. This syndrome is common in uremia and may occur in other neuropathies, suggesting that discomfort is secondary to a basic neuropathy. It may also be familial, and in-depth studies have failed to highlight in these cases the existence of neuropathy.
The feeling of agitation may be accompanied by myoclonic muscle contractions. These myoclonic seizures are similar to myoclonus revealed in normal people who pass the REM phase of sleep. These forms of muscle spasms and myoclons are somewhat similar to a group of unusual syndromes of scare or hyperexplex, characterized by sudden contraction of the limbs and occasionally of the torso muscles.
Sudden noise or touching can cause the patient to jump or suddenly move an extremity of the body. Hyperexplexes occur through mutations in the glycine receptor.
Sustained muscle contractions often have causes that are difficult to differentiate between central and peripheral. Abnormal muscle contractions accompanied by increased muscle tone usually occur through CNS damage.
Thus, the decrease or disappearance of CNS inhibition may produce pathological muscle contractions characteristic of spasticity, rigidity or "paratonic" stiffness. In most cases there are other signs of CNS damage. Damage to the basal ganglia, most commonly hereditary, can cause dystonia.
Abnormal muscle contractions can also occur through repeated depolarization of the motor unit components: motor neuron, peripheral axons of neurons, neuromuscular junction or muscle fibers. Contractions in the absence of electrical activity can occur by affecting the contractile muscular system.
It follows motor neuron disorders. The term used by patients to describe a painful and involuntary muscle contraction of a single muscle or muscle group is a cramp. Muscle cramps occur by spontaneous depolarization of cell groups in the anterior medullary horns, followed by contraction of several motor units.
EMG records show that motor unit fibers generate contractions with a frequency of up to 300 per second, much higher than in the case of voluntary contractions. Cramps frequently occur in the legs in the elderly and, when severe, are followed by residual sensitivity and necrosis of muscle fibers, including increased serum creatikinase.
The cramps of the calf muscles are so common that they are considered physiological, but when generalized they can signal chronic disorders of the motoneurons, for example amyotrophic lateral sclerosis. Cramps may be an unpleasant manifestation in pregnancy in patients with electrolyte disorders (hyponatry) and in hemodialysis patients. When recurrent and localized in a single muscle group, it suggests damage to the nerve roots.
However, in many situations, it is impossible to determine the cause of cramps. Benign cramps usually occur at night and can disappear when administered quinine sulfate. Other causes of contractions originating in motor neurons are tetanus and "man-rigid" syndrome. In both conditions a loss of inhibitory neuronal adhesions in the anterior medullary horns, can produce repeated stimulation of motor neurons, with the appearance of severe, painful muscle contractions.
Antibodies to glutamic acid decarboxylase are often present in human-rigid syndrome, this condition being likely to respond to plasmapheresis. A similar clinical picture may be found in acute strychnine poisoning. Diazepam relieves these spasms but, in the doses needed to remove contractions, produces respiratory depression.
I'm going to finish this post with peripheral nerve disorders. Tetania is characterized by the predominant contraction of the distal muscles, especially the hand (carpal spasm) and the foot (pedal spasm), but laryngospasm can also occur. Tetanus is the result of increased excitability of peripheral nerves.
Muscle contractions are initially painless but, if sustained, can cause muscle damage and pain. Severe tetanus can affect the spinal muscles with the production of opistotonus. Tetania usually has hypocalcemic etiology, but it can also occur through hypomagnesemia or severe respiratory alkalosis.
Idiopathic calcemic normo tetanus, spasmophilia, is both hereditary and acquired. The acquired form is similar to Isaac syndrome (neuromyotonia), in which the hyperexcitability of peripheral neurons produces cramps and muscle contractions. These patients respond positively to plasmapheresis, the condition probably being mediated by IgC antichannel antichannel nerve membranation autoantibodies.
Terms like pain, spasm and cramp are frequently used incorrectly by patients when describing the symptomatology of the muscular system, they substitute one term for another. Other terms such as neuralgia, weight and stiffness are also commonly used and usually provide little useful information about the location of the condition. Clinically, the notion of spasm means a paroxysmal, spontaneous, prolonged and painful contradiction of one or more muscles. Muscle pain may be associated with fatigue (asthenia) or weakness.
Spasms are abnormal muscle movements that can occur through abnormalities in electrical activity in the central nervous system (CNS), mediated by motor neurons or that occur even in motor neurons or muscle fiber. It is difficult to establish the exact origin of abnormal motor activity, using only clinical data.
In general, movements originating in the CNS affect an entire part of the body, a limb or a muscle group. Central diseases can be rhythmic or intermittent, with those occurring at the peripheral level usually random. Electroencephalogram (EEG) may highlight changes in cortical activity in pathology with CNS etiology. Electromyogram (EMG) is less useful because it reflects motor changes of varied etiology. However, highlighting a basic nerve or muscle fiber condition on EMG may be useful for diagnosis.
Intermittent, arrhythmic movements of the entire limb, torso or a facial portion may occur within epilepsy or through myoclonia. Spasms in flexion and extension of an entire part of the body or lower limbs occur by the disappearance of motor inhibition within the CNS. Segmental myoclonia is the result of focal disorders in the brain stem or spinal cord, which cause abnormal discharges of the groups of motor neurons. Localized vascular disorders, tumors or other lesions may be involved.
Let's talk about abnormal facial movements now. Hemifacial spasms occur through the paroxysmal activity of the facial nerve, sometimes triggered by pressure exerted by a torchy blood vessel, located adjacent to where the facial nerve leaves the brain stem. Hemifacial spasm usually occurs in muscles adjacent to the eyeball, but it can also involve or spread throughout the face.
Symptoms are often intermittent and intensify when the patient uses facial muscles, for example, during speech. Hemifacial spasm is painless but embarrassing, especially for people who work in public. Because it is more intense and severe when the patient is under stress, it can be misdiagnosed as tic.
Injuries at the pontocerebelous angle can sometimes produce similar manifestations. Neuroradiological investigation is indicated in patients with hemifacial spasm. Injecting botulinum toxin into the affected muscles removes spasm for up to 3 months and surgical exploration and isolation of the facial nerve from the adjacent vessel is often curative.
Facial tics are stereotypical facial movements, e.g. blinking, turning the head, grimaces, which are under voluntary control, but can only be suppressed with effort and anxiety on the part of the subject. Some tics are so common that they are considered mannerisms, such as the act of excessive "dreging" of the voice.
An example is the repeated raising of the eyebrows by contraction of the frontal muscles. Certain hereditary motor disorders, such as Gilles de la Tourette syndrome, are characterized by multiple tics. Tics can usually be controlled by neuroleptic medication.
Facial sinkinesis occurs as part of the aberrant regeneration of the facial nerve, following damage to the facial nerve from Bell's palsy or other facial lesions. Nearly 50% of patients recovering from Bell's palsy experience such movements. An example is mandibulal sinkinesis in which voluntary movements of the lower part of the face produce the contraction of the orbicular of the eye, with unilateral closure of the eye.
Trigeminal neuralgia (painful ticks) is characterized by short, paroxysmal, lancinating pain in one half of the face. Although the affected portion of the nerve is almost exclusively sensory, the severity of the pain produces involuntary contractions of the facial muscles (hence the name of tic). Abnormal movements do not occur in the absence of pain. Facial myokimia refers to the presence of almost continuous pulsations in the facial muscles.
Although it is usually benign, it can occur through pontine lesions, such as neoplasia or multiple sclerosis. Facial or limb myokimia occurs in association with episodic ataxia in the genetic defects of the potassium channels of the nerves. Similar movements occur in motor neuron disorders, such as amyotrophic lateral sclerosis.
Let's get to the motor abnormalities of the limbs! When the muscles are totally relaxed, no movement should be felt. The diseases of motor neurons or their proximal axons are frequently associated with fasciculations, representing the spontaneous discharge of an entire motor unit. Fasciculations are visible on inspection or perceived by the patient in the form of tremors or intramuscular pulsations.
They sometimes occur in healthy people, and in the absence of muscle weakness have no pathological significance. Fasciculations are a normal phenomenon when they occur in an incomplete relaxed muscle and are frequently observed at rest in the calves of normal individuals. Miotimia, consisting of numerous repetitive fasciculations, can also occur in the muscles of the limbs, creating the sensation of crispness.
It disappears through neuromuscular blockage, thus demonstrating that the initiation of movements is done in the anterior medullary horns or in the peripheral nerves. In patients with long-lasting muscle denervation and then reinervation, the dimensions of the motor unit increase and the fasciculations can be so strong that movements of the limbs, especially the fingers, occur called minipolymioclonus.
Certain conditions are characterized by a tendency to move limbs. Akatisia or muscle agitation occurs in Parkinson's disease and other damage to the basal ganglia, including medicinal ones. Restless leg syndrome is a feeling of muscle discomfort, commonly in the legs and thighs, which is usually found in middle-aged women.
Patients feel the need to move their legs to remove the disturbing sensation. This syndrome is common in uremia and may occur in other neuropathies, suggesting that discomfort is secondary to a basic neuropathy. It may also be familial, and in-depth studies have failed to highlight in these cases the existence of neuropathy.
The feeling of agitation may be accompanied by myoclonic muscle contractions. These myoclonic seizures are similar to myoclonus revealed in normal people who pass the REM phase of sleep. These forms of muscle spasms and myoclons are somewhat similar to a group of unusual syndromes of scare or hyperexplex, characterized by sudden contraction of the limbs and occasionally of the torso muscles.
Sudden noise or touching can cause the patient to jump or suddenly move an extremity of the body. Hyperexplexes occur through mutations in the glycine receptor.
Sustained muscle contractions often have causes that are difficult to differentiate between central and peripheral. Abnormal muscle contractions accompanied by increased muscle tone usually occur through CNS damage.
Thus, the decrease or disappearance of CNS inhibition may produce pathological muscle contractions characteristic of spasticity, rigidity or "paratonic" stiffness. In most cases there are other signs of CNS damage. Damage to the basal ganglia, most commonly hereditary, can cause dystonia.
Abnormal muscle contractions can also occur through repeated depolarization of the motor unit components: motor neuron, peripheral axons of neurons, neuromuscular junction or muscle fibers. Contractions in the absence of electrical activity can occur by affecting the contractile muscular system.
It follows motor neuron disorders. The term used by patients to describe a painful and involuntary muscle contraction of a single muscle or muscle group is a cramp. Muscle cramps occur by spontaneous depolarization of cell groups in the anterior medullary horns, followed by contraction of several motor units.
EMG records show that motor unit fibers generate contractions with a frequency of up to 300 per second, much higher than in the case of voluntary contractions. Cramps frequently occur in the legs in the elderly and, when severe, are followed by residual sensitivity and necrosis of muscle fibers, including increased serum creatikinase.
The cramps of the calf muscles are so common that they are considered physiological, but when generalized they can signal chronic disorders of the motoneurons, for example amyotrophic lateral sclerosis. Cramps may be an unpleasant manifestation in pregnancy in patients with electrolyte disorders (hyponatry) and in hemodialysis patients. When recurrent and localized in a single muscle group, it suggests damage to the nerve roots.
However, in many situations, it is impossible to determine the cause of cramps. Benign cramps usually occur at night and can disappear when administered quinine sulfate. Other causes of contractions originating in motor neurons are tetanus and "man-rigid" syndrome. In both conditions a loss of inhibitory neuronal adhesions in the anterior medullary horns, can produce repeated stimulation of motor neurons, with the appearance of severe, painful muscle contractions.
Antibodies to glutamic acid decarboxylase are often present in human-rigid syndrome, this condition being likely to respond to plasmapheresis. A similar clinical picture may be found in acute strychnine poisoning. Diazepam relieves these spasms but, in the doses needed to remove contractions, produces respiratory depression.
I'm going to finish this post with peripheral nerve disorders. Tetania is characterized by the predominant contraction of the distal muscles, especially the hand (carpal spasm) and the foot (pedal spasm), but laryngospasm can also occur. Tetanus is the result of increased excitability of peripheral nerves.
Muscle contractions are initially painless but, if sustained, can cause muscle damage and pain. Severe tetanus can affect the spinal muscles with the production of opistotonus. Tetania usually has hypocalcemic etiology, but it can also occur through hypomagnesemia or severe respiratory alkalosis.
Idiopathic calcemic normo tetanus, spasmophilia, is both hereditary and acquired. The acquired form is similar to Isaac syndrome (neuromyotonia), in which the hyperexcitability of peripheral neurons produces cramps and muscle contractions. These patients respond positively to plasmapheresis, the condition probably being mediated by IgC antichannel antichannel nerve membranation autoantibodies.
Have
a good day, everyone!
Dorin, Merticaru