STUDY - Technical - New Dacian's Medicine
Spasms,
Cramps and Regular Muscle Weakness
(2)
Translation Draft
Let's get on with the muscle diseases. Myotonia is the repetitive depolarization of muscle cells that can produce muscle contractions that lead to muscle stiffness and impaired relaxation.
Myotonia is usually painless, but can be a handicap by interfering with fine hand movements and slowing down movement. Myotonic dystrophy is the most common condition associated with myotonia, although other manifestations of the disease such as cataracts and muscle weakness are usually much more symptomatic.
A similar condition, proximal myotonic myopathy (MMP), is associated with muscle pain. Congenital myotonia and congenital paramyotonia are much rarer, but much more disabling in terms of the severity of myotonic phenomena.
Myotonia often worsens in the cold and characteristically diminishes as a result of repeated muscle activity. Congenital myotonia is found in both the dominant and recessive forms. Myotonia occurs by the existence of defects in the functioning of chlorine channels, but may also be the result of defects in the functioning of the sodium channel.
One such disorder is congenital paramyotonia, which is characterized by paradoxical myotonia (myotonia which worsens through repeated activity). These patients also have episodic, cold-induced muscle weakness. Myotonia can often be removed by quinine, phenytoin or mexiletin.
Muscle contraction is the painful shortening of the muscle, without association with the depolarization of the muscle membrane. It can occur in conditions where there is a metabolic defect that limits the production of phosphates that store increased energy, for example in myophosphorylase deficiency.
Contracts are precipitated by exertion, are usually painful and cause muscle damage (generalized muscle contraction can produce myoglobinuria in sufficient quantity to precipitate renal failure).
The use of the term contracture causes confusion, because the same word is used to describe the limitation of joint movements following the shortening of muscle tendons, which occurs in rheumatic disorders, cerebral palsy or chronic myopathy.
Muscle stiffness in metabolic contracts may occur in malignant hyperthema syndrome, usually associated with general anesthesia. In neuroleptic malignant syndrome, muscle stiffness is the consequence of CNS hyperactivity and the intense electrical activity that exists in the muscles.
Next comes pain, neuralgia and muscle tenderness. Muscle pain does not always involve a pathological condition at this level. Joint and bone damage frequently causes muscle pain and may create confusion about the anatomical location of symptoms due to the association of moderate atrophy and muscle weakness.
Also, pain that comes from the suffering of over-adjacent subcutaneous tissues or fascists and tendons can also be irradiated to the muscles. In addition, the pathology of the main peripheral nerves or their intramuscular branches can produce both pain and muscle weakness. Muscle pain can be a major symptom in inflammatory, metabolic, endocrine and toxic myopathy.
Muscle trauma occurs mainly due to sustained activity, even in performance athletes, through the possibility of the production of muscle or tendon ruptures that temporarily generate acute muscle pain, inflammation and tenderness.
The rupture of the tendons of the muscles, for example, the biceps or gastrocnemian, produces obvious muscle shortening. Many of these ruptures are resolved without the intake of surgery, but lead to an abnormal, excavated appearance of the muscles.
The difference of almost pleasant sensations of pain and muscular fatigue following an intense activity of strong but normal pain, which follows over-demanding activities, is done only by the degree of intensity.
Such symptoms are often associated with paraclinical highlighting of deep muscle damage, including increased serum enzymes (creatinkinase), MRI focal edema and muscle necrosis extended to biopsy. Myoglobinuria can also occur. Certain types of exercise predispose to muscle pain and necrosis: short periods of muscle contraction during its elongation (eccentric contractions) and prolonged effort, such as that of marathon runners.
The moment such symptoms become abnormal is not certain. Many patients experience painful phenomena in moderate activities. Such muscle pain, which occurs during exercise, is also characteristic of metabolic muscle diseases, such as carnitine-palmitoil-transferase deficiency (patients with partial dystrophin deficiency may experience stress-induced recurrent myalgia).
The total lack of this protein produces Duchenne muscular dystrophy. Deficiencies in glycolysis enzymes are more commonly associated with contractures. Most patients with muscle pain during and after physical exertion do not have an identifiable abnormality.
Let's move on to diffuse myalgia now. Muscle pain in the absence of muscle weakness can occur in acute infections with influenza and coxsackie viruses. Fibrosis, fibromyalgia and fibromyositis are synonymous with a condition associated with muscle pain and tenderness and adjacent connective tissues.
Focal sensitivity trigger points can be identified and systemic symptoms such as fatigue, insomnia and depression may frequently be present. Although patients identify painful inflammation, histological examination does not reveal muscle or connective tissue abnormalities.
Symptoms may respond in part to amitriptyline or nonsteroidal anti-inflammatory drugs, but the disease tends to be chronic without remissions. Sometimes a supportive psychological treatment is useful. Patients whose symptoms persist for months or years are often suspected of depression, without being able to specify whether depression is the cause or result of symptoms.
Rheumatic polymyalgia occurs in patients over 50 years of age and is characterized by stiffness and pain in the shoulder and hip muscles. Despite painful symptoms localized muscle, there is compelling evidence in favor of the existence of proximal inflammatory arthritis (there are frequently fluid overflows in the joints of the knee or other peripheral joints).
Patients develop a deep muscle atrophy over time through underuse and accuse muscle weakness, thus raising the problem of possible polymyositis. However, serum levels of creatikinase are usually normal and muscle biopsy highlights atrophy without demonstrating necrosis or muscle inflammation.
The rate of sedimentation of hematoids is increased in most patients, and temporal arthritis may be present. Treatment with non-steroidal anti-inflammatory drugs is indicated, except for patients with temporal arteritis who benefit from prednisone corticotherapy.
If patients with rheumatic polymyalgia do not respond to non-steroidal anti-inflammatory treatment, low doses of prednisone may be required. Myalgias are also common in other rheumatic conditions, including rheumatoid arthritis, systemic lupus erythematosus, node polyarteritis, scleroderma and mixed connective tissue syndrome. Patients with polymyositis or dermatomyositis may experience myalgia, although in most cases muscle pain is lacking.
Accusations of muscle pain and fatigue are among the most common symptoms offered by the patient. Deciding whether such patients require extensive diagnostic tests can usually be made through history, clinical examination and routine blood samples.
It's time for episodic muscle weakness. The term weakness is often used by patients to describe decreased vitality or loss of "energy". Even a very careful anamnesis cannot make a clear distinction between a real or subjective symptomatology. The most useful strategy is to ask the patient to determine whether there is a discrete decrease in functionality and to specify the circumstances in which the symptomatology occurs.
Muscle weakness, real or not, may be due to CNS or peripheral disorders. Weakness in CNS disorders, such as transient cerebral ischemia, is usually associated with changes in consciousness or cognitive reflexes, increased muscle tone and stretching muscle reflexes, often even with sensory impairment. Most neuromuscular causes of intermittent weakness are associated with normal mental function, but with a muscle tone and diminished stretching reflexes.
The most common muscle weakness is episodic asthenia. Patients who describe intermittent "weakness", but in reality are fatiguability, suffer from asthenia, which can differ from true weakness by the fact that patients do not lack the ability to make an order, but rather cannot perform it repetitively.
Asthenia is an important problem for many patients with severe kidney, liver, heart or lung disease. Their examination confirms that they can perform all functional activities at least once, such as: do a full squat, climb the stairs, get up from the chair. Fatigue is also characteristic for relatively selective CNS impairment in descending motor pathways, where signs of neurological abnormalities may be minimal.
Fatigue that worsens through activity is characteristic of chronic fatigue syndrome. Intermittent weakness due to peripheral neuromuscular disorders can occur by sudden changes in peripheral nerve function, intermittent muscle dysfunction, alteration of muscle electrophysiological properties through blood electrolyte abnormalities, genetic disorders of muscle ion channels and intermittent blocking of neuromuscular transmission.
Blocking peripheral nerve conduction through certain uncommon peripheral neuropathies sometimes attracts recurrent weakness. Hereditary predisposition to pressure paralysis, also called tomaculous neuropathy due to the salami-like appearance of myelin to nerve biopsy, is a condition characterized by sudden paralysis when compressing a peripheral nerve.
The condition is autosomal dominant and occurs in many families due to an abnormality of the peripheral myelin protein. Paralysis is usually self-limiting and lasts for days to weeks. Other types of peripheral neuropathies also predispose to the development of reversible compression neuropathies.
Another cause of weakness is impaired transmission in the neuromuscular plaque. Myasthenia gravis, especially at onset, is characterized by transient weakness. The cranial muscles are usually the first to be affected and result in diplopia, palpebral ptosis, dysphagia and dysartria. rarely, weakness in the limbs can be the debut sign of myasthenia gravis and, in the absence of symptomatology of damage to the cranial muscles, diagnosis can be delayed for months.
Diurnal variations in muscle strength are typical, with worsening weakness throughout the day. Other conditions at this uncommon level, such as Lambert-Eaton syndrome, may also experience intermittent muscle weakness.
Transitional weakness may also cause intermittent electrolyte disturbances. Transient variations in serum potassium are associated with severe impairments of muscle strength. Although periodic primary paralysis (periodic hyper and hypokaliemal paralysis) are the first to be considered in a patient with abnormal serum potassium and weakness, other causes of serum potassium changes are frequently found behind episodes of weakness.
Periodic familial paralysis rarely begins after the age of 30 (other causes are involved in elderly patients). Periodic hypokaliemypal paralysis may occur in hyperthyroid patients. Episodic muscle weakness due to hypokalemia may occur during renal or gastrointestinal potassium loss.
Hyperkaliemic weakness usually occurs when chronic renal or adrenal disease is installed. Other electrolyte disturbances may result in intermittent weakness as an initial clinical sign of a severe metabolic abnormality. Correcting metabolic imbalance improves muscle weakness.
Since I mentioned metabolism, I can say a little bit about muscle metabolic diseases. Certain rare defects in the use of glycogen and lipids affect the production of energy at the muscle level and generate intermittent weakness, usually accompanied by muscle pain and the highlighting of muscle damage.
Carnitine-palmitoil-transferase deficiency is one of these conditions. Mitochondrial damage, such as cytochrome-oxidase deficiency, can produce severe stress intolerance with fatigue and weakness associated with lactic acidosis. Pain and muscle damage rarely occur.
I'll finish with other conditions involved in the manifestation of episodic weakness. Recurrent bouts of "weakness" often occur in patients with hyperventilation syndrome. Such patients have normal muscle strength when examined.
Similarly, recurrent hypoglycaemic episodes are associated with a subjective feeling of weakness, although hypoglycaemia rarely produces such a symptom. CNS disorders can cause generalized weakness without altering consciousness. The liptomy seizures resulting from the damage to motor airways in the brain stem produce sudden para or tetraparesis, which usually lasts only a few seconds.
Patients with narcolepsy may experience sudden loss of muscle tone and strength during cataleptic episodes. An impairment of the reticulated activator system is responsible for these episodes, as well as for the paralysis in sleep that occurs during the sleep or awakening of narcoleptic patients.
I'm ready! Have a good day!!
Let's get on with the muscle diseases. Myotonia is the repetitive depolarization of muscle cells that can produce muscle contractions that lead to muscle stiffness and impaired relaxation.
Myotonia is usually painless, but can be a handicap by interfering with fine hand movements and slowing down movement. Myotonic dystrophy is the most common condition associated with myotonia, although other manifestations of the disease such as cataracts and muscle weakness are usually much more symptomatic.
A similar condition, proximal myotonic myopathy (MMP), is associated with muscle pain. Congenital myotonia and congenital paramyotonia are much rarer, but much more disabling in terms of the severity of myotonic phenomena.
Myotonia often worsens in the cold and characteristically diminishes as a result of repeated muscle activity. Congenital myotonia is found in both the dominant and recessive forms. Myotonia occurs by the existence of defects in the functioning of chlorine channels, but may also be the result of defects in the functioning of the sodium channel.
One such disorder is congenital paramyotonia, which is characterized by paradoxical myotonia (myotonia which worsens through repeated activity). These patients also have episodic, cold-induced muscle weakness. Myotonia can often be removed by quinine, phenytoin or mexiletin.
Muscle contraction is the painful shortening of the muscle, without association with the depolarization of the muscle membrane. It can occur in conditions where there is a metabolic defect that limits the production of phosphates that store increased energy, for example in myophosphorylase deficiency.
Contracts are precipitated by exertion, are usually painful and cause muscle damage (generalized muscle contraction can produce myoglobinuria in sufficient quantity to precipitate renal failure).
The use of the term contracture causes confusion, because the same word is used to describe the limitation of joint movements following the shortening of muscle tendons, which occurs in rheumatic disorders, cerebral palsy or chronic myopathy.
Muscle stiffness in metabolic contracts may occur in malignant hyperthema syndrome, usually associated with general anesthesia. In neuroleptic malignant syndrome, muscle stiffness is the consequence of CNS hyperactivity and the intense electrical activity that exists in the muscles.
Next comes pain, neuralgia and muscle tenderness. Muscle pain does not always involve a pathological condition at this level. Joint and bone damage frequently causes muscle pain and may create confusion about the anatomical location of symptoms due to the association of moderate atrophy and muscle weakness.
Also, pain that comes from the suffering of over-adjacent subcutaneous tissues or fascists and tendons can also be irradiated to the muscles. In addition, the pathology of the main peripheral nerves or their intramuscular branches can produce both pain and muscle weakness. Muscle pain can be a major symptom in inflammatory, metabolic, endocrine and toxic myopathy.
Muscle trauma occurs mainly due to sustained activity, even in performance athletes, through the possibility of the production of muscle or tendon ruptures that temporarily generate acute muscle pain, inflammation and tenderness.
The rupture of the tendons of the muscles, for example, the biceps or gastrocnemian, produces obvious muscle shortening. Many of these ruptures are resolved without the intake of surgery, but lead to an abnormal, excavated appearance of the muscles.
The difference of almost pleasant sensations of pain and muscular fatigue following an intense activity of strong but normal pain, which follows over-demanding activities, is done only by the degree of intensity.
Such symptoms are often associated with paraclinical highlighting of deep muscle damage, including increased serum enzymes (creatinkinase), MRI focal edema and muscle necrosis extended to biopsy. Myoglobinuria can also occur. Certain types of exercise predispose to muscle pain and necrosis: short periods of muscle contraction during its elongation (eccentric contractions) and prolonged effort, such as that of marathon runners.
The moment such symptoms become abnormal is not certain. Many patients experience painful phenomena in moderate activities. Such muscle pain, which occurs during exercise, is also characteristic of metabolic muscle diseases, such as carnitine-palmitoil-transferase deficiency (patients with partial dystrophin deficiency may experience stress-induced recurrent myalgia).
The total lack of this protein produces Duchenne muscular dystrophy. Deficiencies in glycolysis enzymes are more commonly associated with contractures. Most patients with muscle pain during and after physical exertion do not have an identifiable abnormality.
Let's move on to diffuse myalgia now. Muscle pain in the absence of muscle weakness can occur in acute infections with influenza and coxsackie viruses. Fibrosis, fibromyalgia and fibromyositis are synonymous with a condition associated with muscle pain and tenderness and adjacent connective tissues.
Focal sensitivity trigger points can be identified and systemic symptoms such as fatigue, insomnia and depression may frequently be present. Although patients identify painful inflammation, histological examination does not reveal muscle or connective tissue abnormalities.
Symptoms may respond in part to amitriptyline or nonsteroidal anti-inflammatory drugs, but the disease tends to be chronic without remissions. Sometimes a supportive psychological treatment is useful. Patients whose symptoms persist for months or years are often suspected of depression, without being able to specify whether depression is the cause or result of symptoms.
Rheumatic polymyalgia occurs in patients over 50 years of age and is characterized by stiffness and pain in the shoulder and hip muscles. Despite painful symptoms localized muscle, there is compelling evidence in favor of the existence of proximal inflammatory arthritis (there are frequently fluid overflows in the joints of the knee or other peripheral joints).
Patients develop a deep muscle atrophy over time through underuse and accuse muscle weakness, thus raising the problem of possible polymyositis. However, serum levels of creatikinase are usually normal and muscle biopsy highlights atrophy without demonstrating necrosis or muscle inflammation.
The rate of sedimentation of hematoids is increased in most patients, and temporal arthritis may be present. Treatment with non-steroidal anti-inflammatory drugs is indicated, except for patients with temporal arteritis who benefit from prednisone corticotherapy.
If patients with rheumatic polymyalgia do not respond to non-steroidal anti-inflammatory treatment, low doses of prednisone may be required. Myalgias are also common in other rheumatic conditions, including rheumatoid arthritis, systemic lupus erythematosus, node polyarteritis, scleroderma and mixed connective tissue syndrome. Patients with polymyositis or dermatomyositis may experience myalgia, although in most cases muscle pain is lacking.
Accusations of muscle pain and fatigue are among the most common symptoms offered by the patient. Deciding whether such patients require extensive diagnostic tests can usually be made through history, clinical examination and routine blood samples.
It's time for episodic muscle weakness. The term weakness is often used by patients to describe decreased vitality or loss of "energy". Even a very careful anamnesis cannot make a clear distinction between a real or subjective symptomatology. The most useful strategy is to ask the patient to determine whether there is a discrete decrease in functionality and to specify the circumstances in which the symptomatology occurs.
Muscle weakness, real or not, may be due to CNS or peripheral disorders. Weakness in CNS disorders, such as transient cerebral ischemia, is usually associated with changes in consciousness or cognitive reflexes, increased muscle tone and stretching muscle reflexes, often even with sensory impairment. Most neuromuscular causes of intermittent weakness are associated with normal mental function, but with a muscle tone and diminished stretching reflexes.
The most common muscle weakness is episodic asthenia. Patients who describe intermittent "weakness", but in reality are fatiguability, suffer from asthenia, which can differ from true weakness by the fact that patients do not lack the ability to make an order, but rather cannot perform it repetitively.
Asthenia is an important problem for many patients with severe kidney, liver, heart or lung disease. Their examination confirms that they can perform all functional activities at least once, such as: do a full squat, climb the stairs, get up from the chair. Fatigue is also characteristic for relatively selective CNS impairment in descending motor pathways, where signs of neurological abnormalities may be minimal.
Fatigue that worsens through activity is characteristic of chronic fatigue syndrome. Intermittent weakness due to peripheral neuromuscular disorders can occur by sudden changes in peripheral nerve function, intermittent muscle dysfunction, alteration of muscle electrophysiological properties through blood electrolyte abnormalities, genetic disorders of muscle ion channels and intermittent blocking of neuromuscular transmission.
Blocking peripheral nerve conduction through certain uncommon peripheral neuropathies sometimes attracts recurrent weakness. Hereditary predisposition to pressure paralysis, also called tomaculous neuropathy due to the salami-like appearance of myelin to nerve biopsy, is a condition characterized by sudden paralysis when compressing a peripheral nerve.
The condition is autosomal dominant and occurs in many families due to an abnormality of the peripheral myelin protein. Paralysis is usually self-limiting and lasts for days to weeks. Other types of peripheral neuropathies also predispose to the development of reversible compression neuropathies.
Another cause of weakness is impaired transmission in the neuromuscular plaque. Myasthenia gravis, especially at onset, is characterized by transient weakness. The cranial muscles are usually the first to be affected and result in diplopia, palpebral ptosis, dysphagia and dysartria. rarely, weakness in the limbs can be the debut sign of myasthenia gravis and, in the absence of symptomatology of damage to the cranial muscles, diagnosis can be delayed for months.
Diurnal variations in muscle strength are typical, with worsening weakness throughout the day. Other conditions at this uncommon level, such as Lambert-Eaton syndrome, may also experience intermittent muscle weakness.
Transitional weakness may also cause intermittent electrolyte disturbances. Transient variations in serum potassium are associated with severe impairments of muscle strength. Although periodic primary paralysis (periodic hyper and hypokaliemal paralysis) are the first to be considered in a patient with abnormal serum potassium and weakness, other causes of serum potassium changes are frequently found behind episodes of weakness.
Periodic familial paralysis rarely begins after the age of 30 (other causes are involved in elderly patients). Periodic hypokaliemypal paralysis may occur in hyperthyroid patients. Episodic muscle weakness due to hypokalemia may occur during renal or gastrointestinal potassium loss.
Hyperkaliemic weakness usually occurs when chronic renal or adrenal disease is installed. Other electrolyte disturbances may result in intermittent weakness as an initial clinical sign of a severe metabolic abnormality. Correcting metabolic imbalance improves muscle weakness.
Since I mentioned metabolism, I can say a little bit about muscle metabolic diseases. Certain rare defects in the use of glycogen and lipids affect the production of energy at the muscle level and generate intermittent weakness, usually accompanied by muscle pain and the highlighting of muscle damage.
Carnitine-palmitoil-transferase deficiency is one of these conditions. Mitochondrial damage, such as cytochrome-oxidase deficiency, can produce severe stress intolerance with fatigue and weakness associated with lactic acidosis. Pain and muscle damage rarely occur.
I'll finish with other conditions involved in the manifestation of episodic weakness. Recurrent bouts of "weakness" often occur in patients with hyperventilation syndrome. Such patients have normal muscle strength when examined.
Similarly, recurrent hypoglycaemic episodes are associated with a subjective feeling of weakness, although hypoglycaemia rarely produces such a symptom. CNS disorders can cause generalized weakness without altering consciousness. The liptomy seizures resulting from the damage to motor airways in the brain stem produce sudden para or tetraparesis, which usually lasts only a few seconds.
Patients with narcolepsy may experience sudden loss of muscle tone and strength during cataleptic episodes. An impairment of the reticulated activator system is responsible for these episodes, as well as for the paralysis in sleep that occurs during the sleep or awakening of narcoleptic patients.
I'm ready! Have a good day!!
Dorin, Merticaru