Imaging Studies:
Simple radiography showed pronounced demineralization of the skeleton MEMBER who becomes severely affected with diseaseprogression. Articular erosions are not present. Demineralizationbegins at the ends of bones and progresses until it becomessmooth.
Scanning scintigraphy is positive in 50% of patients. The study isuseful in the early stages of the disease. Items are abnormal latestages, with increased joint and periarticular capture. This findingis not specific reflex sympathetic dystrophy but cause suspicion.
The differential diagnosis is made with the following conditions:acute nerve injury, cellulitis, septic arthritis, upper limb occlusivedisease, median neuropathy, neurosarcoidoza, diabeticneuropathy, alcoholic neuropathy, toxic neuropathy, cauzalgia,insuficeinta pressure chronic peripheral nerve compression,plexopatii, flebotromboza, rheumatologic diseases.
Wednesday, June 1, 2011
Reflex Sympathetic Dystrophy
Reflex sympathetic dystrophy or complex regional pain syndrome is a clinical syndrome with variable and unknown causes evolution characterized by pain, swelling and vasomotor dysfunction of the extremities. The condition is often the result of trauma or surgery.
It is estimated that 5% of the population that has suffered trauma to the upper extremity reflex sympathetic dystrophy develops.Extremity immobilization can trigger disease. Without prophylactic measures, active physical therapy, reflex sympathetic dystrophy develops in 20% of people with stroke hemiplegia. The disease does not cause mortality.
The disease affects mainly women of 25-55 years. It is precipitated by trauma or surgery and affects the upper and lower extremities. The pain is accompanied by edema, vasomotor changes, sudomotorii, motor and trophic. It extends to other areas of the body. Multiple pharmacological and pharmacological interventions fail many times. Interfere with the profession, sleeping, moblitatea and personal care. Remissions and relapses are frequent.
80% of patients with this disease shows complete relief of pain and associated symptoms in 18 months. Some patients do not regress spontaneously and are cured by treatment. 50-80% of patients experience pain or disability limit secondary movements.Long duration of symptoms, this trophic changes associated with adverse prognosis and disability.Disease is associated with negligible mortality, although morbidity is extremely high. Despite good results after sympathetic blockade, and mobilization techniques, limb weakness is seen in 50% of patients.
Pathogenesis of reflex sympathetic dystrophyIt is not known. Three conditions are considered important in its development, including persistent painful lesions, succeptibilitatea predisposition to develop disease and an abnormal sympathetic reflex. Succeptibilitate factors are unknown and may include genetic predisposition in some patients a tendency towards increased sympathetic activity. This includes cold hands, hyperhidrosis, or history of seizures.
Healthy individuals presents a sympathetic response to injury, the vasoconstriction to prevent blood loss and swelling. This initial response is rapidly replaced by vasodilation and increased capillary permeability, allowing tissue repair.In patients with reflex sympathetic dystrophy, this sympathetic response continues. The reasons for maintaining sympathetic reflex are unknown but are related to dysfunction of the central regulation painful stimuli. This lack of control is mediated by neurons in the spinal cord. Prolonged ischemia caused by vasoconstriction causes pain setting that promotes the release of a sympathetic reflex arc and vasospasm. This is accompanied by local response to trauma with the release of substantial amounts of proinflammatory mediators such as histamine, serotonin and bradykinin. End result is a swollen, painful nonfunctionala.
Causes and risk factors:Reflex sympathetic dystrophy is posttraumatic or postsurgical and can occur on previously healthy end without known trigger.
Traumatic causes:-Laceration, abrasion, venipunctie, intramuscular injections-Gunshot wounds, neck and shoulder injuries-Traumatic acute carpal tunnel syndrome-Thoracic trauma, fracture or dislocation of the spine.
Postsurgical cases:Carpal-tunnel release, tooth extraction-Rib resection and repair of fractures-Postartroscopie.
Local and general diseases:-Nerve compression syndromes, arthritis, tissue ischemia-Stenosing tenosynovitis, myocardial infarction-Stroke, Pancoast tumorPancreatic-cancer, herpes zoster.
Possible risk factors:-Persistent mechanical irritation of peripheral nervesIncomplete regeneration of peripheral nerves-Abnormal neurotransmitter-activityNutritional deprivation secondary-abnormal arteriovenous shuntsGenetic predisposition or family-Cigarette-smoking, schizophrenia or depression.
Signs and symptomsThe three clinical stages of reflex sympathetic dystrophy are: acute, subacute and chronic. Acute form evolves around three months.Burning pain is one of the first symptoms initially limited function.Swelling, redness, vasomotor instability that worsens with cold extremities, hyperhidrosis are common. Demineralization of the skeleton is determined by the lack of limb use. If the process is not stopped or reversed in the acute phase, the condition can progress to the subacute stage, evolving nine months. The patient developed persistent pain and swelling fixed end, which was reversible during the acute phase. Redness acute stage is replaced by the pallor and cyanosis, or hyperhidrosis, or dry skin.Progressive loss of function, cause pain and fibrosis with chronic inflammation of joints. Lead to distortion from the cameraman finger flexion. The skin and subcutaneous tissues begin to atrophy.Bone demineralization is pronounced.
If the process continues, chronic phase develops in a year after onset. This stage may develop several years or may be permanent. The pain is more variable during this period. Continue undiminished or decreasing. Edema tends to resolve over time, leaving fibrosis around the joints. The skin is dry, pale, cold and bright. Flexion and extension are absent. Marked loss of function and stiffness, and osteoporosis is extreme. The upper extremity is manifested by frozen shoulder and hand in paw.
Reflex sympathetic dystrophy affecting the hands, wrist, shoulder, ankle and foot. Symptomatic disease is a condition of the extremities. Dystrophy is recognized and accepted best if the regional distribution affects the upper extremity involving the distal forearm, wrist, hands and occasionally the arm and shoulder. At the lower end are particularly affected foot and ankle.
Physical examination:Reflex sympathetic dystrophy usually affects only one extremity. It is bilateral in 25% of cases, but more prominent on one side.
Pain:-Constant and disproportionate to the injury-May be exacerbated by environmental factors such as noise and stress, bright lights, touch, active movement, passive-Is described as burning, like a knife as a pressure or sfisiietoare-Starts locally but can progress to the entire extremity.
Increased sympathetic activity:-Hyperhidrosis-Cold hands, pale-History of frequent seizures.
Edema:-Is the most frequently detected and the physical element is always disproportionate to the severity of the lesion-Pain, swelling and color changes may be more prominent in the early stages of addiction-Edema worsen than improve and extend beyond the region initially affectedGrows as a swelling-brown, which progresses to fibrosis nepruriginos intense joint.
Stiffness is severe and debilitating for the patient.
Skin discoloration:-Stage of the disease varies-May be cyanotic, dusty, pale or red skin can lead to hypopigmentation-Starts as redness or interphalangeal metacarpofalangiana and increases the whole deal.
Abnormal skin hydration:Wet-skin-hyperhidrosisLate-dry-skin.
Sensitivity is located initially but progressed to generalized form.Sensitivity is articular and periarticular. Patients and shows allodinia hiperpatie (mild pain on pressure).Skin and subcutaneous fat atrophy is overdue.
It is estimated that 5% of the population that has suffered trauma to the upper extremity reflex sympathetic dystrophy develops.Extremity immobilization can trigger disease. Without prophylactic measures, active physical therapy, reflex sympathetic dystrophy develops in 20% of people with stroke hemiplegia. The disease does not cause mortality.
The disease affects mainly women of 25-55 years. It is precipitated by trauma or surgery and affects the upper and lower extremities. The pain is accompanied by edema, vasomotor changes, sudomotorii, motor and trophic. It extends to other areas of the body. Multiple pharmacological and pharmacological interventions fail many times. Interfere with the profession, sleeping, moblitatea and personal care. Remissions and relapses are frequent.
80% of patients with this disease shows complete relief of pain and associated symptoms in 18 months. Some patients do not regress spontaneously and are cured by treatment. 50-80% of patients experience pain or disability limit secondary movements.Long duration of symptoms, this trophic changes associated with adverse prognosis and disability.Disease is associated with negligible mortality, although morbidity is extremely high. Despite good results after sympathetic blockade, and mobilization techniques, limb weakness is seen in 50% of patients.
Pathogenesis of reflex sympathetic dystrophyIt is not known. Three conditions are considered important in its development, including persistent painful lesions, succeptibilitatea predisposition to develop disease and an abnormal sympathetic reflex. Succeptibilitate factors are unknown and may include genetic predisposition in some patients a tendency towards increased sympathetic activity. This includes cold hands, hyperhidrosis, or history of seizures.
Healthy individuals presents a sympathetic response to injury, the vasoconstriction to prevent blood loss and swelling. This initial response is rapidly replaced by vasodilation and increased capillary permeability, allowing tissue repair.In patients with reflex sympathetic dystrophy, this sympathetic response continues. The reasons for maintaining sympathetic reflex are unknown but are related to dysfunction of the central regulation painful stimuli. This lack of control is mediated by neurons in the spinal cord. Prolonged ischemia caused by vasoconstriction causes pain setting that promotes the release of a sympathetic reflex arc and vasospasm. This is accompanied by local response to trauma with the release of substantial amounts of proinflammatory mediators such as histamine, serotonin and bradykinin. End result is a swollen, painful nonfunctionala.
Causes and risk factors:Reflex sympathetic dystrophy is posttraumatic or postsurgical and can occur on previously healthy end without known trigger.
Traumatic causes:-Laceration, abrasion, venipunctie, intramuscular injections-Gunshot wounds, neck and shoulder injuries-Traumatic acute carpal tunnel syndrome-Thoracic trauma, fracture or dislocation of the spine.
Postsurgical cases:Carpal-tunnel release, tooth extraction-Rib resection and repair of fractures-Postartroscopie.
Local and general diseases:-Nerve compression syndromes, arthritis, tissue ischemia-Stenosing tenosynovitis, myocardial infarction-Stroke, Pancoast tumorPancreatic-cancer, herpes zoster.
Possible risk factors:-Persistent mechanical irritation of peripheral nervesIncomplete regeneration of peripheral nerves-Abnormal neurotransmitter-activityNutritional deprivation secondary-abnormal arteriovenous shuntsGenetic predisposition or family-Cigarette-smoking, schizophrenia or depression.
Signs and symptomsThe three clinical stages of reflex sympathetic dystrophy are: acute, subacute and chronic. Acute form evolves around three months.Burning pain is one of the first symptoms initially limited function.Swelling, redness, vasomotor instability that worsens with cold extremities, hyperhidrosis are common. Demineralization of the skeleton is determined by the lack of limb use. If the process is not stopped or reversed in the acute phase, the condition can progress to the subacute stage, evolving nine months. The patient developed persistent pain and swelling fixed end, which was reversible during the acute phase. Redness acute stage is replaced by the pallor and cyanosis, or hyperhidrosis, or dry skin.Progressive loss of function, cause pain and fibrosis with chronic inflammation of joints. Lead to distortion from the cameraman finger flexion. The skin and subcutaneous tissues begin to atrophy.Bone demineralization is pronounced.
If the process continues, chronic phase develops in a year after onset. This stage may develop several years or may be permanent. The pain is more variable during this period. Continue undiminished or decreasing. Edema tends to resolve over time, leaving fibrosis around the joints. The skin is dry, pale, cold and bright. Flexion and extension are absent. Marked loss of function and stiffness, and osteoporosis is extreme. The upper extremity is manifested by frozen shoulder and hand in paw.
Reflex sympathetic dystrophy affecting the hands, wrist, shoulder, ankle and foot. Symptomatic disease is a condition of the extremities. Dystrophy is recognized and accepted best if the regional distribution affects the upper extremity involving the distal forearm, wrist, hands and occasionally the arm and shoulder. At the lower end are particularly affected foot and ankle.
Physical examination:Reflex sympathetic dystrophy usually affects only one extremity. It is bilateral in 25% of cases, but more prominent on one side.
Pain:-Constant and disproportionate to the injury-May be exacerbated by environmental factors such as noise and stress, bright lights, touch, active movement, passive-Is described as burning, like a knife as a pressure or sfisiietoare-Starts locally but can progress to the entire extremity.
Increased sympathetic activity:-Hyperhidrosis-Cold hands, pale-History of frequent seizures.
Edema:-Is the most frequently detected and the physical element is always disproportionate to the severity of the lesion-Pain, swelling and color changes may be more prominent in the early stages of addiction-Edema worsen than improve and extend beyond the region initially affectedGrows as a swelling-brown, which progresses to fibrosis nepruriginos intense joint.
Stiffness is severe and debilitating for the patient.
Skin discoloration:-Stage of the disease varies-May be cyanotic, dusty, pale or red skin can lead to hypopigmentation-Starts as redness or interphalangeal metacarpofalangiana and increases the whole deal.
Abnormal skin hydration:Wet-skin-hyperhidrosisLate-dry-skin.
Sensitivity is located initially but progressed to generalized form.Sensitivity is articular and periarticular. Patients and shows allodinia hiperpatie (mild pain on pressure).Skin and subcutaneous fat atrophy is overdue.
Monday, May 30, 2011
Muscular dystrophy - Diagnosis
The first step in diagnosis is to the patient's physical examinationto highlight the characteristic signs of muscular dystrophy.
Laboratory analysis consists in the concentration of creatineresearch, a chemical released in the process of necrosis(destruction) of cells. An increased concentration of creatine allowsdiagnosis of muscular dystrophy.
For diagnosis of Duchenne myopathy may be investigated and the level of dystrophin in muscle. A very low level of this protein willindicate the presence of DMD.
Muscle biopsy is the best method of diagnosis. During thismedical procedure, is take a sample of tissue for examinationunder a microscope. In the case of muscular dystrophy, willhighlight microscopic muscle fiber degeneration. As the disease,muscle tissue necrosis (dead) will be replaced by connectivetissue or fat.
Muscle functioning can be verified with electromyography (EMG) -test that measures electrical activity of muscles.
Laboratory analysis consists in the concentration of creatineresearch, a chemical released in the process of necrosis(destruction) of cells. An increased concentration of creatine allowsdiagnosis of muscular dystrophy.
For diagnosis of Duchenne myopathy may be investigated and the level of dystrophin in muscle. A very low level of this protein willindicate the presence of DMD.
Muscle biopsy is the best method of diagnosis. During thismedical procedure, is take a sample of tissue for examinationunder a microscope. In the case of muscular dystrophy, willhighlight microscopic muscle fiber degeneration. As the disease,muscle tissue necrosis (dead) will be replaced by connectivetissue or fat.
Muscle functioning can be verified with electromyography (EMG) -test that measures electrical activity of muscles.
Muscular dystrophy - Signs and symptoms
Generally, symptoms occur before age 5.
Children who suffer from muscular dystrophy have trouble walking, climbing stairs, lifting arms overhead or lifting from the ground.Normally, muscle atrophy affects basin first, then reaches shoulder muscles. As the weakening of the muscles, they grow in size by replacing fat with muscle fibers (pseudohipertrofie).
In some forms of muscular dystrophy, the disease becomes debilitating in adolescence, the patient was immobilized in a wheelchair. Note the changes of the spine (scoliosis). Pneumonia and other respiratory diseases are common due to malfunctioning of the respiratory muscles.
General symptoms and signs of muscular dystrophies are:
- Muscle weakness
- Coordination slips
- Progressive sinvaliditate
Signs and symptoms vary depending on the specific type of muscular dystrophy in question. Each type differs in terms of onset, muscle groups affected and the disease.
Duchenne muscular dystrophy: the onset of symptoms generally occurs between 3 and 5 years. As a result of lower limb muscle atrophy, children have a tendency of falling and difficulty in lifting off the ground. As weight loss, muscle fibers grow in size due to the replacement of muscle tissue or fat necrosis (pseudohipertrofie).Using a wheelchair becomes necessary to 12 years. Some patients have scoliosis, mental retardation or suffer from heart failure.
Becker muscular dystrophy - the symptoms are comparable with those of Duchenne myopathy, but begins between 5 and 15 years are less marked.
Myotonic dystrophy - myotonic characterized by (abnormally prolonged muscle contractions difficulties in decontractare).Debuts at five years, affecting mainly the hands and tongue. Facial muscles may also be affected, and neck muscles, toes and ankle.Atrophy of the muscles involved in speech and swallowing difficulties in performing these acts trains. Impaired diaphragm cause breathing difficulties.
Muscular dystrophy belt - symptoms begins in late childhood or early adulthood. It is characterized by muscle atrophy in shoulders and hips, and breathing difficulties in case of reaching the diaphragm. It may be accompanied by heart failure or arrhythmia.
Facio-scapular-humeral dystrophy or (Landouzy-Dejerine dystrophy) - is characterized by affecting the facial muscles, so patients can not smile, whistle, or close your eyes.
Children who suffer from muscular dystrophy have trouble walking, climbing stairs, lifting arms overhead or lifting from the ground.Normally, muscle atrophy affects basin first, then reaches shoulder muscles. As the weakening of the muscles, they grow in size by replacing fat with muscle fibers (pseudohipertrofie).
In some forms of muscular dystrophy, the disease becomes debilitating in adolescence, the patient was immobilized in a wheelchair. Note the changes of the spine (scoliosis). Pneumonia and other respiratory diseases are common due to malfunctioning of the respiratory muscles.
General symptoms and signs of muscular dystrophies are:
- Muscle weakness
- Coordination slips
- Progressive sinvaliditate
Signs and symptoms vary depending on the specific type of muscular dystrophy in question. Each type differs in terms of onset, muscle groups affected and the disease.
Duchenne muscular dystrophy: the onset of symptoms generally occurs between 3 and 5 years. As a result of lower limb muscle atrophy, children have a tendency of falling and difficulty in lifting off the ground. As weight loss, muscle fibers grow in size due to the replacement of muscle tissue or fat necrosis (pseudohipertrofie).Using a wheelchair becomes necessary to 12 years. Some patients have scoliosis, mental retardation or suffer from heart failure.
Becker muscular dystrophy - the symptoms are comparable with those of Duchenne myopathy, but begins between 5 and 15 years are less marked.
Myotonic dystrophy - myotonic characterized by (abnormally prolonged muscle contractions difficulties in decontractare).Debuts at five years, affecting mainly the hands and tongue. Facial muscles may also be affected, and neck muscles, toes and ankle.Atrophy of the muscles involved in speech and swallowing difficulties in performing these acts trains. Impaired diaphragm cause breathing difficulties.
Muscular dystrophy belt - symptoms begins in late childhood or early adulthood. It is characterized by muscle atrophy in shoulders and hips, and breathing difficulties in case of reaching the diaphragm. It may be accompanied by heart failure or arrhythmia.
Facio-scapular-humeral dystrophy or (Landouzy-Dejerine dystrophy) - is characterized by affecting the facial muscles, so patients can not smile, whistle, or close your eyes.
Emery-Dreifuss muscular dystrophy
Emery-Dreifuss muscular dystrophy is a disease transmitted byautosomal dominant, recessive (rarely) or X-linked. The incidenceis not known. Women can be carriers, but only men can beaffected with the clinical forms of X-linked transmission. GeneEmery-Dreifuss dystrophy involved in coding for a protein callednuclear membranes emerina.
Amyotrophy (muscle atrophy) and weakness may occur before the age of 20 years, usually affecting the arm muscles (biceps, triceps)and more rarely, the muscles of the legs. Emery-Dreifuss dystrophycan affect the heart, involving paralysis fibrillation, conduction abnormalities (atrioventricular block), cardiomyopathy (damage toheart muscle) and an increased risk of sudden death.
Diagnosis is based on clinical data, age of onset, family historyand are supported by the slight increase in the level of serumcreatinine by electromyography and muscle biopsy. DNA testsconfirm the diagnosis.
Treatment aims to prevent contractures. Using a pacemaker(pacemaker) is indicated in patients with conduction disturbances(AV block).
Amyotrophy (muscle atrophy) and weakness may occur before the age of 20 years, usually affecting the arm muscles (biceps, triceps)and more rarely, the muscles of the legs. Emery-Dreifuss dystrophycan affect the heart, involving paralysis fibrillation, conduction abnormalities (atrioventricular block), cardiomyopathy (damage toheart muscle) and an increased risk of sudden death.
Diagnosis is based on clinical data, age of onset, family historyand are supported by the slight increase in the level of serumcreatinine by electromyography and muscle biopsy. DNA testsconfirm the diagnosis.
Treatment aims to prevent contractures. Using a pacemaker(pacemaker) is indicated in patients with conduction disturbances(AV block).
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