Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic inflammation of multiple joints. Genetic and environmental factors contribute to disease development. RA is associated with elevated inflammatory markers like ESR and CRP. Early diagnosis and treatment with DMARDs can reduce joint damage. Osteoarthritis (OA) is the most common form of arthritis. It is a degenerative joint disease characterized by cartilage breakdown in the joints. Risk factors include age, obesity, trauma, and genetic predisposition. OA shows asymmetric joint involvement and symptoms are typically worse in the evening. Treatment focuses on weight loss, braces, and conservative measures to reduce joint stress.
Central post-stroke pain (CPSP) is a chronic neuropathic pain syndrome that can develop after a stroke and affect the body areas corresponding to the damaged brain region. CPSP is characterized by burning, aching pain and abnormal skin sensations and occurs in 1-12% of stroke patients. The pathophysiology likely involves changes in thalamic and cortical processing of sensory information after damage to brain areas involved in temperature and pain signaling. Treatment involves medications like antidepressants and anticonvulsants, as well as neurostimulation therapies for refractory cases, with varying success rates.
Trigeminal neuralgia is a chronic pain condition that affects the trigeminal nerve, which carries sensation from the face. It causes sudden, severe facial pain that feels like electric shocks. It is more common in older women, with onset typically between 50-70 years old. The pain is usually unilateral and affects one or more branches of the trigeminal nerve. Carbamazepine is usually the first-line treatment, though its effectiveness may decrease over time. For some patients, microvascular decompression surgery can provide long-term relief by decompressing the trigeminal nerve root where it enters the brainstem. Trigeminal neuralgia has no cure but proper diagnosis and management can help patients achieve a good
Reducing spasticity and pain after stroke to improve functionaditya romadhon
1. Spasticity is a common condition after stroke that causes abnormal muscle tone and stiffness. It can lead to pain and contractures.
2. Damage to upper motor neurons disrupts communication between the brain and spinal cord, resulting in net disinhibition of spinal reflexes causing spasticity.
3. Spasticity has both neural and non-neural components. Soft tissue changes like fibrosis can contribute to passive muscle stiffness.
The document provides an overview of incomplete spinal cord injuries. Some key points:
- Spinal cord injuries can range from complete to incomplete, depending on the severity and location of the lesion in the spinal cord. Incomplete injuries result in partial preservation of motor or sensory function below the injury level.
- The American Spinal Injury Association (ASIA) scoring system is used to clinically classify spinal cord injuries based on motor and sensory function. Injuries are classified on a scale from A (complete injury) to D (near normal function).
- Recovery from incomplete injuries is possible, though most occurs within the first year as spontaneous recovery plateaus. Sensory preservation is a predictor of potential motor recovery.
The term Spinal Cord Injury is used to refer to neurological damage of the spinal cord
Any lesion involving the spinal cord result a syndrome called a “myelopathy”
Spinal cord injuries are defined as complete or incomplete according to the International Standards for the Neurological Classifification of SCI and the American Spinal Injuries Association Impairment Scale (AIS)
Complete lesions are defifined as AIS A, and incomplete lesions are defifined as AIS B, AIS C, AIS D or AIS E (Harvey, 2016)
Neuropathic pain is chronic, severe pain that occurs as a result of damage or dysfunction in the nervous system. It is characterized by allodynia (pain from normally non-painful stimuli) and hyperalgesia (exaggerated pain response). Neuropathic pain can be caused by mechanical nerve injury, metabolic diseases like diabetes, viral infections, inflammation, ischemia, or multiple neurotransmitter system dysfunctions. The mechanisms of neuropathic pain involve peripheral and central sensitization, uncontrolled neuronal firing, glial cell activation, loss of endogenous inhibitory pathways, and neuroplastic changes in the brain.
Myofascial pain is a common condition caused by trigger points in muscles that produce pain and motor and autonomic symptoms. Trigger points are focal areas of tenderness caused by hypercontracted muscle tissue. Myofascial pain syndrome is characterized by localized pain that differs from fibromyalgia which causes widespread pain. Trigger points are classified as active or latent based on whether they cause spontaneous pain. Diagnosis involves palpation to identify taut bands and tender spots. Treatment includes non-invasive techniques like stretching, massage, and dry needling as well as invasive techniques like injections.
Peripheral and central sensitization can cause pain hypersensitivity. Peripheral sensitization occurs when tissue damage and inflammation reduce the threshold and increase responsiveness of peripheral nerve endings, causing them to fire in response to normally non-painful stimuli. Central sensitization manifests as hyperalgesia and allodynia due to changes in the dorsal horn neurons of the spinal cord that cause non-painful stimuli to be interpreted as painful. Repetitive firing of C fibers can cause wind up, where increasing amounts of glutamate are released with each stimulus, further depolarizing dorsal horn neurons. Together, peripheral and central sensitization are responsible for hypersensitivity states like hyperalgesia and allodynia.
Central post-stroke pain (CPSP) is a chronic neuropathic pain syndrome that can develop after a stroke and affect the body areas corresponding to the damaged brain region. CPSP is characterized by burning, aching pain and abnormal skin sensations and occurs in 1-12% of stroke patients. The pathophysiology likely involves changes in thalamic and cortical processing of sensory information after damage to brain areas involved in temperature and pain signaling. Treatment involves medications like antidepressants and anticonvulsants, as well as neurostimulation therapies for refractory cases, with varying success rates.
Trigeminal neuralgia is a chronic pain condition that affects the trigeminal nerve, which carries sensation from the face. It causes sudden, severe facial pain that feels like electric shocks. It is more common in older women, with onset typically between 50-70 years old. The pain is usually unilateral and affects one or more branches of the trigeminal nerve. Carbamazepine is usually the first-line treatment, though its effectiveness may decrease over time. For some patients, microvascular decompression surgery can provide long-term relief by decompressing the trigeminal nerve root where it enters the brainstem. Trigeminal neuralgia has no cure but proper diagnosis and management can help patients achieve a good
Reducing spasticity and pain after stroke to improve functionaditya romadhon
1. Spasticity is a common condition after stroke that causes abnormal muscle tone and stiffness. It can lead to pain and contractures.
2. Damage to upper motor neurons disrupts communication between the brain and spinal cord, resulting in net disinhibition of spinal reflexes causing spasticity.
3. Spasticity has both neural and non-neural components. Soft tissue changes like fibrosis can contribute to passive muscle stiffness.
The document provides an overview of incomplete spinal cord injuries. Some key points:
- Spinal cord injuries can range from complete to incomplete, depending on the severity and location of the lesion in the spinal cord. Incomplete injuries result in partial preservation of motor or sensory function below the injury level.
- The American Spinal Injury Association (ASIA) scoring system is used to clinically classify spinal cord injuries based on motor and sensory function. Injuries are classified on a scale from A (complete injury) to D (near normal function).
- Recovery from incomplete injuries is possible, though most occurs within the first year as spontaneous recovery plateaus. Sensory preservation is a predictor of potential motor recovery.
The term Spinal Cord Injury is used to refer to neurological damage of the spinal cord
Any lesion involving the spinal cord result a syndrome called a “myelopathy”
Spinal cord injuries are defined as complete or incomplete according to the International Standards for the Neurological Classifification of SCI and the American Spinal Injuries Association Impairment Scale (AIS)
Complete lesions are defifined as AIS A, and incomplete lesions are defifined as AIS B, AIS C, AIS D or AIS E (Harvey, 2016)
Neuropathic pain is chronic, severe pain that occurs as a result of damage or dysfunction in the nervous system. It is characterized by allodynia (pain from normally non-painful stimuli) and hyperalgesia (exaggerated pain response). Neuropathic pain can be caused by mechanical nerve injury, metabolic diseases like diabetes, viral infections, inflammation, ischemia, or multiple neurotransmitter system dysfunctions. The mechanisms of neuropathic pain involve peripheral and central sensitization, uncontrolled neuronal firing, glial cell activation, loss of endogenous inhibitory pathways, and neuroplastic changes in the brain.
Myofascial pain is a common condition caused by trigger points in muscles that produce pain and motor and autonomic symptoms. Trigger points are focal areas of tenderness caused by hypercontracted muscle tissue. Myofascial pain syndrome is characterized by localized pain that differs from fibromyalgia which causes widespread pain. Trigger points are classified as active or latent based on whether they cause spontaneous pain. Diagnosis involves palpation to identify taut bands and tender spots. Treatment includes non-invasive techniques like stretching, massage, and dry needling as well as invasive techniques like injections.
Peripheral and central sensitization can cause pain hypersensitivity. Peripheral sensitization occurs when tissue damage and inflammation reduce the threshold and increase responsiveness of peripheral nerve endings, causing them to fire in response to normally non-painful stimuli. Central sensitization manifests as hyperalgesia and allodynia due to changes in the dorsal horn neurons of the spinal cord that cause non-painful stimuli to be interpreted as painful. Repetitive firing of C fibers can cause wind up, where increasing amounts of glutamate are released with each stimulus, further depolarizing dorsal horn neurons. Together, peripheral and central sensitization are responsible for hypersensitivity states like hyperalgesia and allodynia.
Acquired neuromyotonia is an inflammatory disorder characterized by abnormal nerve impulses from peripheral nerves that cause continuous muscle fiber activity and symptoms like muscle stiffness, cramping and weakness. It has several potential causes including an unknown acquired cause, paraneoplastic syndrome related to cancer, or a hereditary form. Diagnosis involves identifying continuous muscle contractions and abnormal electrical muscle activity on electromyography. Treatment focuses on using anti-convulsant drugs to stop abnormal nerve impulses or plasma exchange to provide short-term relief from symptoms.
This document discusses radial tunnel syndrome, which is caused by compression of the posterior interosseous nerve (PIN) as it passes through the radial tunnel of the forearm. The PIN originates from the radial nerve and innervates several muscles of the forearm and hand. Radial tunnel syndrome commonly affects those who participate in racquet sports or activities involving repetitive pronation and supination. Patients experience pain in the lateral forearm without motor weakness. Diagnosis is based on physical exam findings of tenderness over the radial tunnel and pain with resisted wrist and finger motions.
Trigger points are hyperirritable spots within taut bands of muscle that are painful on compression and can cause referred pain patterns. They are commonly caused by overload, injury, lack of exercise, or poor posture in sedentary individuals between 27-55 years old. Trigger points have two types - active points that cause pain at rest and latent points that cause pain with direct pressure or muscle contraction. Electrotherapy can stimulate the body's endogenous opiate system to relieve pain by using low frequency stimulation below 10 Hz with long pulse durations to activate areas of the brain and spinal cord that inhibit nociception.
This document discusses carpal tunnel syndrome, which is caused by compression of the median nerve as it passes through the carpal tunnel of the wrist. It can cause numbness, tingling, and weakness in the hand. The presentation outlines the causes, clinical features, diagnosis, and treatment options for carpal tunnel syndrome, which include wrist splints, oral anti-inflammatory medications, local steroid injections, and carpal tunnel release surgery if conservative measures fail. The document provides details on physical exam findings and special tests like Tinel's and Phalen's maneuvers used to diagnose carpal tunnel syndrome.
electrodiagnostics for pmr - dr henry prakashmrinal joshi
This document provides an overview of electrodiagnosis techniques including NCV/EMG. It discusses using these tests to assess sensory and motor function as well as evaluate conditions like radiculopathy, neuropathy, and myopathy. Specific techniques are described like analyzing CMAPs and SNAPs to identify denervation, conduction block, and demyelination. EMG techniques like evaluating spontaneous activity, insertional activity, and motor unit action potentials are covered to assess muscle health and innervation. The document provides details on interpreting electrodiagnostic results to localize issues and characterize conditions as acute vs chronic.
This document discusses myasthenia gravis (MG), a neuromuscular disease causing muscle weakness and fatigue. It begins by defining MG and describing its symptoms, which include weakness of the eyes, face, neck and limbs that worsens throughout the day. It then covers diagnosis of MG using tests like the edrophonium test and repetitive nerve stimulation. Treatment options are also outlined including medications, plasmapheresis and IVIG. The document emphasizes that physiotherapy can benefit MG patients by improving strength, mobility and cardiovascular fitness. A variety of exercises are recommended like aerobics, strength training and swimming, aimed at enhancing daily function while avoiding overexertion.
This document discusses neuropathic pain, including its causes, evaluation, and treatment approaches. Some key points covered include:
- Neuropathic pain can originate from the central or peripheral nervous systems and have various etiologies such as metabolic issues, trauma, compression, autoimmune conditions, or genetics.
- Evaluation involves taking a pain history including characteristics of the pain and examining for sensory and motor dysfunction, as well as potentially ordering imaging or lab tests.
- Treatment approaches include interventional procedures like spinal cord stimulation as well as pharmacologic options like anticonvulsants, benzodiazepines, antidepressants, antiarrhythmics, corticosteroids, baclofen, and capsaicin
Myasthenia gravis is an autoimmune disease that causes muscle weakness. It is caused by antibodies that block signals from nerves to muscles. The main symptoms are drooping eyelids, blurred vision, difficulty speaking and swallowing, and weakness in the limbs. Diagnosis involves tests like tensilon tests, EMGs, and checking for antibodies against acetylcholine receptors or related proteins. Treatment focuses on medications to enhance nerve signaling, immunosuppressants, and sometimes surgery to remove the thymus gland. Crises can occur where weakness suddenly worsens and ventilator support may be needed.
The document discusses pain transduction, transmission, and modulation. It begins by describing sensory receptors including nociceptors, which detect potentially harmful stimuli and transduce them into neural signals. Nociceptive fibers called Aδ and C fibers transmit these signals to the spinal cord. Transduction involves converting stimuli into neural signals, transmission moves these signals through the nervous system, and modulation regulates signal strength. The spinothalamic tract then relays nociceptive information from the spinal cord to the thalamus and cortex, allowing the perception of pain.
This document summarizes several chronic pain conditions and their treatments. It discusses myofascial pain, intercostal neuralgia, postherpetic neuralgia, complex regional pain syndrome types I and II, cancer pain, and various procedures to treat them. These procedures include trigger point injections, transcutaneous electrical nerve stimulation, spinal cord stimulation, peripheral nerve stimulation, neurolytic blocks, sympathetic nerve blocks, regional anesthesia techniques, and drug therapies. The document provides details on anatomy, signs and symptoms, and techniques for specific procedures to manage chronic pain conditions.
This document discusses spinal cord injuries, including their definition, causes, and common syndromes. The most common cause of traumatic spinal cord injury is motor vehicle accidents, while non-traumatic causes include cervical spondylosis and tumors. Diagnostic tests include x-rays, CT scans, and MRIs. Treatment involves high-dose corticosteroids, respiratory therapy, and surgical procedures like decompression laminectomy to relieve pressure on the spinal cord and nerve roots. Complications can include blood clots, infections, skin breakdown, incontinence, and chronic pain.
This document discusses the management of spasticity after stroke. It defines spasticity as increased muscle tone and exaggerated reflexes caused by hyper-excitability of stretch reflexes after damage to upper motor neurons. Stroke patients can develop spasticity, which has disadvantages like reduced mobility and pain. Treatment options include positioning, oral medications like baclofen and tizanidine, botulinum toxin injections, and intrathecal baclofen for severe cases. Baclofen and botulinum toxin have evidence for improving spasticity, while botulinum toxin may also aid rehabilitation; however, medications often have side effects.
Myofascial pain syndrome is characterized by painful muscle trigger points that cause pain in the affected muscle and potentially other referred pain in distant areas. Trigger points form due to muscle injury or overuse and maintain a contracted knot within the muscle via a positive feedback loop. Examination involves identifying a taut band within the muscle and locating the most tender point, which may elicit a local twitch response when pressed. Diagnosis is based on identifying a trigger point and reproducing the patient's pain. Treatment involves education, medications, and non-pharmacological therapies like exercise, massage, and dry needling of trigger points.
Nerve compression syndrome, also known as entrapment neuropathy, is caused by direct pressure on a single nerve from external forces or the body itself. It results in symptoms like pain, tingling, numbness, and muscle weakness in the affected body part. Diagnosis involves identifying the compressed nerve based on symptoms and confirming with nerve conduction studies. Treatment ranges from conservative options like splints, NSAIDs, and steroid injections to surgery to relieve nerve pressure. Common types of nerve compression syndromes are carpal tunnel syndrome affecting the median nerve and cubital tunnel syndrome affecting the ulnar nerve.
Spasticity is a motor disorder characterized by velocity-dependent increase in muscle tone and exaggerated reflexes resulting from hyper-excitability of the stretch reflexes as part of the upper motor neuron syndrome. It is caused by interruption of descending inhibitory pathways and alteration of central inhibitory commands leading to rearrangement of spinal cord circuitry and peripheral changes in the muscle over time. Spasticity is not a single symptom but part of a movement disorder defined by features like hypertonia, abnormal reflexes, dystonia, resistance to movement, and abnormal posturing affecting coordination and mobility. A multifaceted approach is needed for management including prevention, physiotherapy, pharmacological and surgical interventions to address both neural and non-neural factors.
1. Spasticity is a motor disorder characterized by increased muscle tone and exaggerated reflexes caused by hyper-excitability of the stretch reflex due to loss of inhibitory pathways in the spinal cord.
2. The pathophysiology of spasticity involves denervation supersensitivity, axonal sprouting, and loss of descending inhibition resulting in disinhibition of segmental reflexes. Changes in muscle properties also contribute to increased tone.
3. Spasticity is assessed using measures of physiology like reflexes, muscle tone, and stiffness scales; measures of voluntary movement; and functional measures of activities and quality of life.
The document discusses molecular mechanisms of pain and summarizes recent research from the Bogomoletz Institute of Physiology in Kiev, Ukraine. It covers classification of pain, measurements used to study pain, sensory pathways involved in pain transmission, ion channels and receptors implicated in pain such as ASICs, P2X receptors, T-type calcium channels and TRPV1. Recent findings from studies of knockout mice and modulators of ion channels suggest these molecular targets hold promise for developing new pain treatments.
Rheumatoid arthritis is an autoimmune disorder that primarily affects the joints, causing pain, swelling, stiffness, and decreased range of motion. It is caused by a combination of genetic and environmental factors which trigger an immune response against tissues in the joints. Symptoms progress from early inflammatory changes in the synovium to destruction of cartilage and bone in the joint. While there is no cure, treatment aims to reduce inflammation and slow joint damage through medications like NSAIDs, DMARDs, steroids, and biologics. Surgery may be used in advanced cases to repair or replace severely damaged joints.
Rheumatoid arthritis and osteoarthritis are common forms of arthritis. Rheumatoid arthritis is a systemic inflammatory disease that affects the joints and other organs, causing progressive joint deformity if not treated early. It can be a potentially fatal illness with increased risks of infections, renal impairment and cardiovascular disease. Osteoarthritis is the most common joint disorder and affects older individuals, particularly the weight-bearing joints like the hips and knees. It involves the breakdown of cartilage and bone within a joint. Management of both conditions involves conservative measures as well as medications aimed at reducing pain and inflammation.
The document summarizes connective tissue diseases and rheumatoid arthritis. It discusses that connective tissue diseases include common disorders like rheumatoid arthritis and osteoarthritis as well as rare conditions like systemic lupus erythematosus. Diagnostic studies for connective tissue diseases include blood tests, x-rays, and biopsies. Rheumatoid arthritis is a chronic inflammatory disease that affects the synovial joints and can lead to joint deformity and damage. Management of rheumatoid arthritis involves pharmacological therapies like NSAIDs and DMARDs as well as nonpharmacological treatments like physical therapy.
Acquired neuromyotonia is an inflammatory disorder characterized by abnormal nerve impulses from peripheral nerves that cause continuous muscle fiber activity and symptoms like muscle stiffness, cramping and weakness. It has several potential causes including an unknown acquired cause, paraneoplastic syndrome related to cancer, or a hereditary form. Diagnosis involves identifying continuous muscle contractions and abnormal electrical muscle activity on electromyography. Treatment focuses on using anti-convulsant drugs to stop abnormal nerve impulses or plasma exchange to provide short-term relief from symptoms.
This document discusses radial tunnel syndrome, which is caused by compression of the posterior interosseous nerve (PIN) as it passes through the radial tunnel of the forearm. The PIN originates from the radial nerve and innervates several muscles of the forearm and hand. Radial tunnel syndrome commonly affects those who participate in racquet sports or activities involving repetitive pronation and supination. Patients experience pain in the lateral forearm without motor weakness. Diagnosis is based on physical exam findings of tenderness over the radial tunnel and pain with resisted wrist and finger motions.
Trigger points are hyperirritable spots within taut bands of muscle that are painful on compression and can cause referred pain patterns. They are commonly caused by overload, injury, lack of exercise, or poor posture in sedentary individuals between 27-55 years old. Trigger points have two types - active points that cause pain at rest and latent points that cause pain with direct pressure or muscle contraction. Electrotherapy can stimulate the body's endogenous opiate system to relieve pain by using low frequency stimulation below 10 Hz with long pulse durations to activate areas of the brain and spinal cord that inhibit nociception.
This document discusses carpal tunnel syndrome, which is caused by compression of the median nerve as it passes through the carpal tunnel of the wrist. It can cause numbness, tingling, and weakness in the hand. The presentation outlines the causes, clinical features, diagnosis, and treatment options for carpal tunnel syndrome, which include wrist splints, oral anti-inflammatory medications, local steroid injections, and carpal tunnel release surgery if conservative measures fail. The document provides details on physical exam findings and special tests like Tinel's and Phalen's maneuvers used to diagnose carpal tunnel syndrome.
electrodiagnostics for pmr - dr henry prakashmrinal joshi
This document provides an overview of electrodiagnosis techniques including NCV/EMG. It discusses using these tests to assess sensory and motor function as well as evaluate conditions like radiculopathy, neuropathy, and myopathy. Specific techniques are described like analyzing CMAPs and SNAPs to identify denervation, conduction block, and demyelination. EMG techniques like evaluating spontaneous activity, insertional activity, and motor unit action potentials are covered to assess muscle health and innervation. The document provides details on interpreting electrodiagnostic results to localize issues and characterize conditions as acute vs chronic.
This document discusses myasthenia gravis (MG), a neuromuscular disease causing muscle weakness and fatigue. It begins by defining MG and describing its symptoms, which include weakness of the eyes, face, neck and limbs that worsens throughout the day. It then covers diagnosis of MG using tests like the edrophonium test and repetitive nerve stimulation. Treatment options are also outlined including medications, plasmapheresis and IVIG. The document emphasizes that physiotherapy can benefit MG patients by improving strength, mobility and cardiovascular fitness. A variety of exercises are recommended like aerobics, strength training and swimming, aimed at enhancing daily function while avoiding overexertion.
This document discusses neuropathic pain, including its causes, evaluation, and treatment approaches. Some key points covered include:
- Neuropathic pain can originate from the central or peripheral nervous systems and have various etiologies such as metabolic issues, trauma, compression, autoimmune conditions, or genetics.
- Evaluation involves taking a pain history including characteristics of the pain and examining for sensory and motor dysfunction, as well as potentially ordering imaging or lab tests.
- Treatment approaches include interventional procedures like spinal cord stimulation as well as pharmacologic options like anticonvulsants, benzodiazepines, antidepressants, antiarrhythmics, corticosteroids, baclofen, and capsaicin
Myasthenia gravis is an autoimmune disease that causes muscle weakness. It is caused by antibodies that block signals from nerves to muscles. The main symptoms are drooping eyelids, blurred vision, difficulty speaking and swallowing, and weakness in the limbs. Diagnosis involves tests like tensilon tests, EMGs, and checking for antibodies against acetylcholine receptors or related proteins. Treatment focuses on medications to enhance nerve signaling, immunosuppressants, and sometimes surgery to remove the thymus gland. Crises can occur where weakness suddenly worsens and ventilator support may be needed.
The document discusses pain transduction, transmission, and modulation. It begins by describing sensory receptors including nociceptors, which detect potentially harmful stimuli and transduce them into neural signals. Nociceptive fibers called Aδ and C fibers transmit these signals to the spinal cord. Transduction involves converting stimuli into neural signals, transmission moves these signals through the nervous system, and modulation regulates signal strength. The spinothalamic tract then relays nociceptive information from the spinal cord to the thalamus and cortex, allowing the perception of pain.
This document summarizes several chronic pain conditions and their treatments. It discusses myofascial pain, intercostal neuralgia, postherpetic neuralgia, complex regional pain syndrome types I and II, cancer pain, and various procedures to treat them. These procedures include trigger point injections, transcutaneous electrical nerve stimulation, spinal cord stimulation, peripheral nerve stimulation, neurolytic blocks, sympathetic nerve blocks, regional anesthesia techniques, and drug therapies. The document provides details on anatomy, signs and symptoms, and techniques for specific procedures to manage chronic pain conditions.
This document discusses spinal cord injuries, including their definition, causes, and common syndromes. The most common cause of traumatic spinal cord injury is motor vehicle accidents, while non-traumatic causes include cervical spondylosis and tumors. Diagnostic tests include x-rays, CT scans, and MRIs. Treatment involves high-dose corticosteroids, respiratory therapy, and surgical procedures like decompression laminectomy to relieve pressure on the spinal cord and nerve roots. Complications can include blood clots, infections, skin breakdown, incontinence, and chronic pain.
This document discusses the management of spasticity after stroke. It defines spasticity as increased muscle tone and exaggerated reflexes caused by hyper-excitability of stretch reflexes after damage to upper motor neurons. Stroke patients can develop spasticity, which has disadvantages like reduced mobility and pain. Treatment options include positioning, oral medications like baclofen and tizanidine, botulinum toxin injections, and intrathecal baclofen for severe cases. Baclofen and botulinum toxin have evidence for improving spasticity, while botulinum toxin may also aid rehabilitation; however, medications often have side effects.
Myofascial pain syndrome is characterized by painful muscle trigger points that cause pain in the affected muscle and potentially other referred pain in distant areas. Trigger points form due to muscle injury or overuse and maintain a contracted knot within the muscle via a positive feedback loop. Examination involves identifying a taut band within the muscle and locating the most tender point, which may elicit a local twitch response when pressed. Diagnosis is based on identifying a trigger point and reproducing the patient's pain. Treatment involves education, medications, and non-pharmacological therapies like exercise, massage, and dry needling of trigger points.
Nerve compression syndrome, also known as entrapment neuropathy, is caused by direct pressure on a single nerve from external forces or the body itself. It results in symptoms like pain, tingling, numbness, and muscle weakness in the affected body part. Diagnosis involves identifying the compressed nerve based on symptoms and confirming with nerve conduction studies. Treatment ranges from conservative options like splints, NSAIDs, and steroid injections to surgery to relieve nerve pressure. Common types of nerve compression syndromes are carpal tunnel syndrome affecting the median nerve and cubital tunnel syndrome affecting the ulnar nerve.
Spasticity is a motor disorder characterized by velocity-dependent increase in muscle tone and exaggerated reflexes resulting from hyper-excitability of the stretch reflexes as part of the upper motor neuron syndrome. It is caused by interruption of descending inhibitory pathways and alteration of central inhibitory commands leading to rearrangement of spinal cord circuitry and peripheral changes in the muscle over time. Spasticity is not a single symptom but part of a movement disorder defined by features like hypertonia, abnormal reflexes, dystonia, resistance to movement, and abnormal posturing affecting coordination and mobility. A multifaceted approach is needed for management including prevention, physiotherapy, pharmacological and surgical interventions to address both neural and non-neural factors.
1. Spasticity is a motor disorder characterized by increased muscle tone and exaggerated reflexes caused by hyper-excitability of the stretch reflex due to loss of inhibitory pathways in the spinal cord.
2. The pathophysiology of spasticity involves denervation supersensitivity, axonal sprouting, and loss of descending inhibition resulting in disinhibition of segmental reflexes. Changes in muscle properties also contribute to increased tone.
3. Spasticity is assessed using measures of physiology like reflexes, muscle tone, and stiffness scales; measures of voluntary movement; and functional measures of activities and quality of life.
The document discusses molecular mechanisms of pain and summarizes recent research from the Bogomoletz Institute of Physiology in Kiev, Ukraine. It covers classification of pain, measurements used to study pain, sensory pathways involved in pain transmission, ion channels and receptors implicated in pain such as ASICs, P2X receptors, T-type calcium channels and TRPV1. Recent findings from studies of knockout mice and modulators of ion channels suggest these molecular targets hold promise for developing new pain treatments.
Rheumatoid arthritis is an autoimmune disorder that primarily affects the joints, causing pain, swelling, stiffness, and decreased range of motion. It is caused by a combination of genetic and environmental factors which trigger an immune response against tissues in the joints. Symptoms progress from early inflammatory changes in the synovium to destruction of cartilage and bone in the joint. While there is no cure, treatment aims to reduce inflammation and slow joint damage through medications like NSAIDs, DMARDs, steroids, and biologics. Surgery may be used in advanced cases to repair or replace severely damaged joints.
Rheumatoid arthritis and osteoarthritis are common forms of arthritis. Rheumatoid arthritis is a systemic inflammatory disease that affects the joints and other organs, causing progressive joint deformity if not treated early. It can be a potentially fatal illness with increased risks of infections, renal impairment and cardiovascular disease. Osteoarthritis is the most common joint disorder and affects older individuals, particularly the weight-bearing joints like the hips and knees. It involves the breakdown of cartilage and bone within a joint. Management of both conditions involves conservative measures as well as medications aimed at reducing pain and inflammation.
The document summarizes connective tissue diseases and rheumatoid arthritis. It discusses that connective tissue diseases include common disorders like rheumatoid arthritis and osteoarthritis as well as rare conditions like systemic lupus erythematosus. Diagnostic studies for connective tissue diseases include blood tests, x-rays, and biopsies. Rheumatoid arthritis is a chronic inflammatory disease that affects the synovial joints and can lead to joint deformity and damage. Management of rheumatoid arthritis involves pharmacological therapies like NSAIDs and DMARDs as well as nonpharmacological treatments like physical therapy.
Rheumatoid arthritis is a chronic inflammatory disease that causes pain, stiffness, and swelling in the joints. It occurs when the immune system mistakenly attacks the joints, causing the synovial membrane to become inflamed. Over time, this can cause cartilage and bone damage and limit function. Treatment focuses on reducing inflammation, managing symptoms, and preventing further joint damage through medications, surgery, and lifestyle changes. While there is no cure, proper treatment can help improve quality of life by reducing pain and disability.
Rheumatoid arthritis is a chronic autoimmune disease that causes inflammation of connective tissues, primarily in the joints. It affects about 1% of the population worldwide and occurs 2-4 times more often in women. While the specific causes are unknown, risk factors include age, sex, genetics, smoking, and obesity. Symptoms include pain, stiffness, swelling, and tenderness in multiple joints as well as fatigue and weight loss. Treatment focuses on education, exercise, medications to reduce inflammation and slow disease progression, and surgery in severe cases. Nursing care involves pain management, education on the disease and treatments, and demonstrating techniques to maintain independence.
SEMINAR PRESENTATION ON RHEUMATOID ARTHRITIS.pptxmrcopyxerox
This presentation summarizes rheumatoid arthritis (RA). RA is an autoimmune disease where the immune system attacks healthy cells in the body, causing inflammation in joints. It most commonly affects the hands, wrists and knees. While its exact cause is unknown, RA is believed to have genetic and environmental risk factors. Symptoms include tender, warm, swollen joints and stiffness. RA is diagnosed through evaluating symptoms, physical exams, x-rays and lab tests. Treatments include medications like DMARDs and biologics to reduce inflammation and slow disease progression, as well as supportive therapies.
Rheumatoid arthritis is a chronic autoimmune disease that causes inflammation of the synovial joints, resulting in pain, stiffness, and swelling. It affects around 1% of the population worldwide. The cause is unknown but is believed to involve genetic and environmental factors. Diagnosis is based on symptoms, blood tests for rheumatoid factor and CRP levels, and x-ray evidence of joint damage. Treatment aims to reduce inflammation and prevent further joint destruction, using medications like NSAIDs, DMARDs, corticosteroids, and biologics. Surgery may be required in advanced cases to repair damaged joints.
This document discusses rheumatoid arthritis (RA), an autoimmune disease where the immune system attacks the synovium lining the joints, causing pain, swelling, and inflammation. It covers signs and symptoms of RA like joint stiffness and pain. Risk factors include genetics and gender, with most cases occurring between ages 35-50. Treatment involves NSAIDs, DMARDs, corticosteroids, biologics, and JAK inhibitors to reduce inflammation and slow disease progression. The pathology involves cytokines and immune cells that promote inflammation, and diagnosis is based on symptoms, physical exam, blood tests, and x-rays.
The document discusses biologic therapies for rheumatological conditions. It provides information on TNF antagonists that are approved for treating diseases like rheumatoid arthritis, spondyloarthropathies, and psoriasis. It discusses the mechanisms of action, pharmacokinetics, administration, and safety monitoring of TNF inhibitors like infliximab, etanercept, and adalimumab. The document also summarizes clinical trial data on the effectiveness of TNF inhibitors for conditions like Crohn's disease and ankylosing spondylitis.
Rheumatoid arthritis is a chronic autoimmune disease that causes inflammation and destruction of joints. It has no cure and negatively impacts quality of life through debilitating symptoms. The disease process involves an abnormal immune response and development of inflammatory cells and antibodies that attack joints. Common symptoms include pain, swelling, stiffness, and loss of function in small and large joints. Treatment focuses on managing symptoms, preventing joint damage, and slowing disease progression through exercise, diet, medications like NSAIDs, DMARDs, and biologics, and self-care strategies. Nurses help patients cope with the disease through education, pain management, exercise, mobility aids, and monitoring for potential complications of treatment.
This document discusses rheumatoid arthritis (RA), a chronic inflammatory disease characterized by joint inflammation and damage. The clinical presentation of RA involves symmetric joint pain, swelling, and morning stiffness. The pathogenesis involves an immune response involving T cells, B cells, and cytokines like TNF-alpha that promote inflammation. Disease activity is the main driver of joint damage and disability in RA. Treatment involves conventional disease-modifying antirheumatic drugs (DMARDs) and biologic agents to reduce inflammation, prevent further joint destruction, and improve function.
Rheumatoid arthritis is an autoimmune disease characterized by chronic inflammation of the joints which can lead to joint damage and physical disability. It is a progressive disease affecting the synovial lining of peripheral joints, causing symmetrical inflammation and potentially deforming polyarthritis. Symptoms include tender swollen joints, morning stiffness lasting hours, fatigue, and rheumatoid nodules under the skin. Treatment focuses on relieving pain, reducing inflammation, protecting joints, maintaining function, and controlling systemic effects through use of drugs like NSAIDs, DMARDs, biologics, glucocorticoids, and surgery.
This document provides an overview of rheumatoid arthritis (RA). It defines RA as a long-term autoimmune disorder that primarily affects the joints, causing swollen and painful joints, most commonly in the wrists and hands. It discusses the epidemiology, etiology, pathophysiology, clinical manifestations, diagnosis, and treatment of RA. The treatment section explains the main categories of drugs used to manage RA, including NSAIDs, DMARDs, glucocorticoids, and biological therapies that target cytokines like TNF-alpha and IL-1.
Rheumatoid arthritis is an autoimmune disease that causes chronic inflammation of the joints and surrounding tissues. It can affect multiple organs and is considered a systemic illness. The cause is unknown but is believed to involve genetic susceptibility and environmental triggers activating an immune response. Treatment involves medications to reduce inflammation and slow joint damage, physical therapy, exercise and lifestyle changes, and sometimes surgery. The goals are to relieve pain, reduce inflammation, prevent further joint damage, and improve quality of life.
Rheumatoid arthritis is a chronic autoimmune disease that causes inflammation of the joints and can damage bone and cartilage. It progresses through four stages, from initial attack of joint tissue by the immune system to potential fusing of joints. Symptoms include joint swelling, stiffness, and tenderness. Diagnosis involves blood tests to check for rheumatoid factor and C-reactive protein levels. Treatment aims to reduce inflammation and prevent further joint damage through lifestyle changes, medications like disease-modifying antirheumatic drugs and biologics, and sometimes surgery.
This document provides historical background on spondyloarthropathies and discusses key aspects of these conditions. It describes how spondyloarthropathies were recognized as a distinct group of inflammatory arthritis in the 1960s. It also outlines that spondyloarthropathies are characterized by inflammatory back pain, asymmetric peripheral arthritis, enthesitis, and specific organ involvement. Ankylosing spondylitis is discussed in more detail, including its etiology being a combination of genetic and environmental factors like the presence of the HLA-B27 gene. Diagnosis and clinical features of ankylosing spondylitis are also summarized.
A case presentation on juvenile idiopathic arthritisDr. Tanvir
This document provides an overview of juvenile idiopathic arthritis (JIA), including its etiology, pathophysiology, classification, clinical manifestations, diagnosis, complications, treatment, and follow up. JIA is the most common chronic rheumatic illness in children, characterized by synovitis and inflammation of peripheral joints. While its exact cause is unknown, it involves both genetic and environmental factors. Treatment involves a multidisciplinary approach including medications like NSAIDs, DMARDs, steroids, and biologics, as well as physiotherapy, with the goals of relieving symptoms, slowing disease progression, and preserving joint function.
Rheumatoid arthritis is an autoimmune disease that causes inflammation of the joints. It is characterized by joint pain, swelling, and stiffness, especially in the hands, feet, and wrists. If left untreated, it can cause permanent joint damage and deformity. The disease is caused by an abnormal immune response that leads to inflammation within the joints. Genetics and environmental factors such as smoking increase the risk. Treatment involves medications such as DMARDs and biologics to reduce inflammation and prevent further joint damage. Early diagnosis and treatment improves long-term prognosis and can help prevent disability.
This document provides information on rheumatoid arthritis (RA), including its presentation, pathogenesis, diagnostic criteria, management, and complications. Some key points:
- RA is a chronic inflammatory disease that primarily affects the joints in a symmetrical pattern. It has an unknown cause but is associated with certain genetic factors.
- Diagnosis is based on symptoms lasting over 6 weeks involving at least 3 joint areas. Serological markers and imaging can help with diagnosis. Untreated, it can lead to long-term joint damage and disability.
- Management involves early use of disease-modifying antirheumatic drugs (DMARDs) like methotrexate to reduce inflammation and prevent joint damage. Biologics may be
Similar to Systemic inflamatory rheumatoid arthritis & non inflamatory osteoarthritis (20)
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Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
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O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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2. Systemic inflammatory rheumatoid disease
doi:10.1093/rheumatology/kes113
Environmental factors, such as smoking and infection, may also influence the development rate of progression and severity of RA
The HLA complex helps the immune system distinguish the body's own proteins from proteins made by foreign invaders such as viruses
and bacteria
Gene provides instructions for making a protein that plays a critical role in the immune system
Recent findings suggest a genetic basis for disease development, expressing two HLA-DRB1, it is part of a family of genes called the
human leukocyte antigen (HLA) complex
The exact cause of RA remains unknown (idiopathic), but genetic and environmental influences clearly participate.
Dysregulated adaptive immunity can precede the clinical manifestation joint disease for many years
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by the progressive chronic inflammation of multiple joints
3. Early rheumathoid arthritis
The earliest event in RA pathogenesis is activation of the innate
immune response, which includes the activation of dendritic cells by
exogenous material and autologous antigens
Humans are exposed to millions of potential pathogens daily, through
contact, ingestion, and inhalation
Our ability to avoid infection depends in part on the adaptive immune
system, which remembers previous encounters with specific pathogens
and destroys them when they attack again
Adaptive immune responses, however, are slow to develop on first
exposure to a new pathogen as specific clones of B and T cells have to
become activated and expand (take a week)
Therefore, during the first critical hours and days of exposure to a new
pathogen, we rely on our innate immune system to protect us from
infection.
4. Early diagnosis-progressif treatment
Early diagnosis is
considered as the key
improvement index for
the most desirable
outcomes
Reduced joint
destruction
Less radiologic
progression
No functional
disability
Disease modifying
antirheumatic drugs
(DMARD)
Early diagnosis
remains challenging
as it relies heavily on
the clinical
information gathered
from the patient’s
history and physical
examination
supported by blood
tests, and imaging
analysis.
5. With poorly controlled or severe
disease
There is risk that extra-articular
manifestations such as keratitis,
pulmonary
granulomas,pericarditis/pleuritis,
small vessel vasculitis, and other
non specific extra-articular
symptoms will develop
While there is currently no cure
for RA, the treatment strategy
aims to expedite diagnosis and
rapidly achieve a low disease
activity state (LDAS)
Universally applied
pharmacologic therapy with non-
steroidal anti-inflammatory drugs
(NSAIDs) and corticosteroids have
proven effective in relieving
stiffness and pain
https://doi.org/10.1038/s41413-018-0016-9
6. Pathophysiology
The hallmark of rheumatoid
arthritis is synovitis
Synovitis caused by the influx
of mononuclear cells (T cells,
B cells, plasma cells, dendritic
cells, macrophages and mast
cells) or local activation (FLS)
The synovial lining then
becomes hyperplastic, and the
synovial membrane expands
large component of cell
activity that generates and
perpetuates inflammation
(pannus), its contains
numerous cytokines and
proteases
Cytokines (esp. TNF-α and
IL-1) and proteolytic
enzymes
Destruction of articular
cartilage
Cytokines produced by pro-
inflammatory effector T-cells
increase bone resorption by
osteoclasts
Bone reabsorption
(erosion/destruction)
7. Joints
Fibrous : synarthroses, minimal
to none ROM, no cartilage
(sutures of the skull)
Fibrocartilagenous :
amphiarthroses, limited ROM,
cartilage (pubic symphysis, sacro-
iliac, intervertebral)
Synovial :
diarthrosis, wide
ROM, cartilage and
ligaments (most of
extremity joints,
atlanto axial, costo-
vertebral, temporo
mandibular)
8. Articular manifestations
Chronic disease (>6 weeks
of symptoms)
Systemic inflammatory
Cardinal sign of
inflammation
Erythrocyte sedimentation
rate (ESR) and C-reactive
protein (CRP) are markers
of inflammatory conditions
increases also WBC >2000
cells/mm3
Symetrical joints
involvement (autoimmune
disease)
Polyarticular (>5 joints)
Stiffness predominate (>1
hour-morning stiffness)
improves with activity
Pain worse in the morning
but improves with activity
(better in the evening)
11. Treatment of rheumatoid arthritis
Surgical for advance disease
only
Medication
Non-steroidal anti-inflammatory
drugs (NSAIDs) = for
symptomatic relief only, they do
not modify the disease nor alter
disease progression
Disease modifying
antirheumatic drugs (DMARD)
are immunosuppressive and
immunomodulatory
agents (synthetic & biological),
it’s the core of RA therapy
Immunosupressants including
steroids
12. Physiotherapy management
TENS is generally a short-acting therapy (6–24 hours), and the most beneficial frequency is 70 Hz, it also has a high placebo effect
Electrostimulation is used in patients with RA to relieve pain. Transcutaneous electrical nerve stimulation (TENS) therapy is the most
commonly used method
With temperatures of 30° Celsius or lower, effects of these enzymes are negligibly small. Normal intra-articular temperature is 33° Celsius,
whereas it may rise up to 36° Celsius in patients with RA
Levels of destructive enzymes such as collagenase, elastase, hyaluronidase, and protease are affected by the temperature of local joints
Cartilage-destroying enzymes are produced within the inflamed joints of patients with RA
Cold application is preferred in active joints where intra-articular heat increase is undesired
By using heat, analgesia is accomplished, muscle spasm relieved, and elasticity of periarticular structures obtained. Heat can be used before
exercise for maximum benefit
Physiotherapy modalities are commonly used in the treatment of RA, include cold/hot applications, electrical stimulation, and hydrotherapy
Kavuncu V, Evcik D. Physiotherapy in rheumatoid arthritis. MedGenMed. 2004 May 17;6(2):3.
PMID: 15266230; PMCID: PMC1395797.
13. Non-Inflammatory Osteoarthritis
Knee osteoarthritis is characterized by structural modifications to primarily articular cartilage and the subchondral bone but also Hoffa’s fat pad,
synovia, ligaments and muscles, leading to the concept of observing OA as a WHOLE JOINT DISEASE
On the biochemical level, OA is characterized by uncontrolled production of matrix-degrading enzymes, including aggrecanases (a disintegrin and metallo
protease with trombospondine motifs (ADAMTSs)) and matrix metalloproteinases (MMPs), which result in the destruction of cartilage matrix
Its incidence increases with age, and thus this degenerative disease is a major problem in ageing populations.
This degenerative and progressive joint disease affects around 250 million people worldwide
The disease is characterized by a progressive degradation of articular cartilage leading to loss of joint mobility and function accompanied by chronic pain
Osteoarthritis (OA) is the most common form of arthritis and one of the leading causes of disability
doi:10.3390/genes11080854
15. Cellular and biochemical has been
driven by biomechanical stimulation,
it is not systemic inflammatory
disease “itis”
Information on SF WCC was
available in 55 subjects. An increase
in white cell count category (< 100,
101–250 and > 250–1,000 cells/mm3)
was associated with an increase in
synovial tissue volume (p = 0.028)
and with other MRI-based measures
of disease severity
(doi:10.1002/art.39829)
Effect entire joint as well as
subchondral bone not only cartilage
loss
Many patients has x-ray changes
associated with OA, however they
are asymptomatic
16. Osteoarthritis Risk Factors
Non modifiable :
Age, Sex
(female>Male),
Genetic
Modifiable :
Obesity,
Occupational,
Trauma,
Malalignment
18. Articular Cartilage
Articular cartilage (AC) is avascular, alymphatic, and aneural tissue with
chondrocytes as the only cell type in the cartilage tissue
Besides chondrocytes, AC is formed by the extracellular matrix (ECM),
which is composed of water (more than 70%) and organic components
such as collagen, aggrecan, proteoglycans, glycosaminoglycans and
glycoproteins
All cartilage components are synthesized by chondrocytes,which play a
key role in maintaining the cartilaginous environment by balancing the
production of ECM components (degrading enzymes, providing minimal
and balanced turnover between anabolic and catabolic processes)
AC metabolism is stimulated by mechanical loading, detected by
mechanoreceptors on the cell surface
Through the process of mechanotransduction, mechanical signals
modulate the biochemical activity of chondrocytes, inducing the
biosynthesis of molecules to preserve the integrity of the tissue.
doi:10.3390/genes11080854
19. Resulting in the depletion of matrix components and, due to lack of AC regenerative capacity, leads to irreversible destruction, thus
making it the most apparent triggering cause of OA
Conversely, excessive mechanical loading leads to a quantitative imbalance between anabolic and catabolic activity
The importance of proper mechanical loading is demonstrated by the fact that insuficient biomechanical stimuli, such as
immobilization, can lead to reduced thickness (>10%) and softening of AC in the knee joint, in the absence of normal joint loading
Furthermore, biomechanical stimulus generated by dynamic compression during moderate exercise can reduce the synthesis of
proteolytic enzymes, regulate the metabolic balance, and prevent the progression of cartilage damage
The activation of these mechanoreceptors initiates intracellular signaling cascades, leading to the tissue remodeling process.
20. Cartilage extracellular matrix changes
Cartilage matrix changes in osteoarthritis defined by degradation of proteoglycans and cleavage of type II collagen fibres by matrix degrading
enzymes ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) and MMPs (matrix metalloproteinases)
21.
22.
23. Chondrocytes changes in OA
Chondrocyte injured
(nature “genetic factor” and
nurture “environment-
biomechanical factors”)
Chondrocyte proliferation
secrete matrix
metalloproteinases,
inflammatory mediators,
collagenase, protease leads
to matrix remodeling
Secondary inflammation in
synovium and subchondral
bone
Significant loss of cartilage
due to chondrocytes dies
and significant changes of
subchondral bone
(osteophytes)
Its a cartilage loss and
bone growth
24. Local Pathological Process
The histopathological scoring of synovitis in synovium obtained from OA patients during total knee arthroplasty showed a
significant correlation between synovitis and pain intensity (Eitner et al., 2017).
A positive relationship between inflammatory changes in the joint and pain was also shown in recent MRI studies, pain in knee OA
fluctuates with changes of bone marrow lesions and synovitis, when bone marrow lesions become smaller, the pain is reduced, and
the risk of frequent pain decreases.
E.g., knee pain occurred in a higher proportion of OA patients with Kellgren/Lawrence (K/L) grade 4 than of OA patients with K/L
grades 2 and 3
Some studies reported associations between the structural damage of the joint (cartilage and bone) and pain (Malfait and
Schnitzer, 2013), frequent pain displayed greater rates of medial cartilage loss (Eckstein et al., 2011), osteophytes were strongly
associated with knee pain (Kaukinen et al., 2016).
A systematic literature search of Bedson and Croft (2008) showed that 15%–76% of the patients with knee pain had radiographic
indications of OA
doi: 10.3389/fnmol.2017.00349
25. BML are patterns from magnetic resonance images (MRI) that have been linked with pain and cartilage
degeneration.
However, earlier bony changes, such as Bone Marrow Lesions (BML detected by MRI), are a relatively recent
discovery and their potential utility in predicting OA progression
Changes in subchondral bone (sclerosis) at late stages of OA, identifiable by plain film X-ray, have long been
recognized as a hallmark of OA
26. Bone Marrow Lession
The MRI signal that defines
BMLs may represent physical
damage (microdamage), or a
response to such damage in
the subchondral bone
From a mechanical
perspective, microdamage can
be generated by a single
(monotonic) significant
loading event, or by multiple
(up to millions) cycles at
lower magnitudes
These lesions occur in areas
where there is increased
stress
There is already evidence
that BMLs are strongly
related to OA
Their presence increases the
risk of cartilage loss,
likelihood of OA progression,
and of development of knee
pain
DOI:https://doi.org/10.1016/j.joca.2012.08.020
27. Synovitis
Locally, all of these components can induce hydrolytic enzymes resulting in cartilage breakdown
secondary to proteoglycan and collagen destruction.
In OA, the synovial fluid has been found to contain multiple inflammatory mediators including
plasma proteins, prostaglandins (PGE2), leukotrienes, cytokines, growth factors, nitric oxide
It can be present in early stages of the disease but is more prevalent towards the more advanced
stages and can be related with severity
Synovitis is an infiltration of inflammatory cells into the synovium (a common finding of OA)
28.
29. Osteoarthritis is a biomechanical
disease
doi:10.4414/smw.2012.13583
Pathomechanics
of
osteoarthritis
Cartilage
degradation
Subchondral
bone changes
Decrease joint
congruency
Malalignment
Increased
mechanical
stress
Ligament
derangements
Muscular
impairments
OA is regarded
as a whole joint
disease
31. Conservative osteoarthritis treatment
Diet and weight loss are important therapeutic measures, because they result in a direct reduction of load exerted on
the knee during locomotion
Valgus knee braces and gait modifications with a toe-out gait have been shown to reduce knee adduction moment
significantly (doi: 10.1002/1529-0131(200008)13:4<191::aid-anr3>3.0.co;2-c)
The use of lateral wedge insoles in patients with OA led to a immediate reduction of pain during walking and a
reduction of the knee adduction moment (torque) by 4–14% (doi: 10.1136/bmj.d2912)
Barefoot walking has been shown to reduce the knee adduction moment by 7–13% compared to normal shoes and up to
23% compared to high-heeled shoes in healthy women (doi: 10.1016/S0140-6736(00)04312-9 & doi: 10.1002/art.22123 )
Conservative treatment strategies include footwear interventions, braces, gait modifications, muscle strengthening and
weight loss