Questions and Answers
Which of the following is a common symptom of transverse myelitis?
Transverse myelitis can only occur as a result of autoimmune conditions.
False
Name one notable pathogen associated with peri-infectious causes of transverse myelitis.
Dengue virus
Transverse myelitis can result in __________ weakness due to anterior gray horn damage.
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Match the cytokine with its effect in transverse myelitis:
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Which diagnostic method is the first line for detecting transverse myelitis?
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Autoimmune causes of transverse myelitis are primarily associated with multiple sclerosis.
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What type of dysfunction can lead to fecal incontinence in patients with transverse myelitis?
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The involvement of T cells in transverse myelitis leads to the release of __________.
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Which of the following is not categorized as a cause of transverse myelitis?
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What is the first-line treatment for transverse myelitis?
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Transverse myelitis primarily affects the lumbar spinal cord.
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What procedure is used to analyze cerebrospinal fluid in transverse myelitis?
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_________ is a second-line treatment for transverse myelitis in cases unresponsive to corticosteroids.
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Which of the following drugs inhibits the transcription of pro-inflammatory cytokines?
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Early diagnosis and intervention are unnecessary for improving outcomes in transverse myelitis.
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Name one cytokine that mycophenolate aims to decrease.
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Corticosteroids are used to manage __________ causes related to transverse myelitis.
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Match the treatments with their intent:
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What is a common outcome for patients with transverse myelitis?
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What is the main role of T cells in the pathophysiology of transverse myelitis?
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Which of the following cytokines is known to be released by T cells during transverse myelitis?
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What type of immune response is primarily associated with the peri-infectious causes of transverse myelitis?
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What symptom might be observed in patients due to involvement of the dorsal column in transverse myelitis?
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What is the primary aim of using high-dose corticosteroids in the treatment of transverse myelitis?
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In addition to multiple sclerosis, which condition is commonly associated with autoimmune causes of transverse myelitis?
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Which of the following pathogens is NOT a known cause of peri-infectious transverse myelitis?
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Which of the following treatments is classified as second-line for transverse myelitis?
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What is the primary role of plasmapheresis in the management of transverse myelitis?
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What effect do cytokines have in the inflammatory process of transverse myelitis?
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Which imaging technique is considered the first-line diagnostic tool for transverse myelitis?
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Which medication is used to inhibit the transcription of pro-inflammatory cytokines in transverse myelitis?
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What is a significant potential outcome of transverse myelitis based on the affected spinal cord segments?
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What is the primary focus during acute treatment of transverse myelitis?
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What is a significant benefit of early diagnosis and intervention in transverse myelitis?
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Which is NOT a focus of long-term management strategies for transverse myelitis?
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What is a potential cause of transverse myelitis that is classified as idiopathic?
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What main effect do cytokines released by T cells have in the context of transverse myelitis?
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Which symptom might be present due to dysfunction in the spinal cerebellar tracts associated with transverse myelitis?
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Which cytokine is NOT commonly released by T cells in the context of transverse myelitis?
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In the diagnosis of transverse myelitis, which MRI sequence is specifically indicated?
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What is a common outcome related to the autonomic dysfunction seen in transverse myelitis?
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Which of the following is NOT considered a peri-infectious cause of transverse myelitis?
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In severe cases of transverse myelitis, which symptoms may arise from damage to the anterior gray horn?
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What is the primary therapeutic focus during the acute treatment of transverse myelitis?
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Which long-term management option aims to inhibit pro-inflammatory cytokines?
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What is a significant potential outcome of transverse myelitis depending on the affected spinal cord segments?
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What role does rituximab play in the treatment of transverse myelitis?
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In the management of transverse myelitis, plasmapheresis is primarily utilized for what purpose?
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Why is early diagnosis and intervention crucial in transverse myelitis?
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Which of the following cytokines does mycophenolate aim to decrease the levels of?
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What is the effect of corticosteroids in the context of infectious causes related to transverse myelitis?
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What is the primary goal of using plasmapheresis in the treatment of transverse myelitis?
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Which drug is commonly used as a first-line treatment for transverse myelitis?
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What role does mycophenolate play in the management of transverse myelitis?
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What is a notable consequence of transverse myelitis depending on the spinal cord segments affected?
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Which cytokines does mycophenolate aim to decrease in relation to transverse myelitis?
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How does rituximab contribute to the treatment of transverse myelitis?
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What is a critical aspect of long-term management strategies for patients with transverse myelitis?
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Why is early diagnosis and intervention important in transverse myelitis?
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What type of immune response is generally responsible for peri-infectious transverse myelitis?
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Which cytokine is involved in increasing capillary permeability during the inflammatory response in transverse myelitis?
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Which symptom is associated with upper motor neuron involvement due to transverse myelitis?
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What is the effect of cytokines released by T cells in the context of transverse myelitis?
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In transverse myelitis, which diagnostic imaging technique is most often used as the first line to confirm the condition?
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What is a potential trigger for autoimmune-related transverse myelitis aside from multiple sclerosis?
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Which symptom is indicative of involvement in the spinal thalamic tracts due to transverse myelitis?
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What is a characteristic feature of the idiopathic causes of transverse myelitis?
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What is the main function of cytokines produced by T cells in transverse myelitis?
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Which of the following is a notable peri-infectious pathogen associated with transverse myelitis?
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In acute cases of transverse myelitis, which symptom indicates involvement of the corticospinal tract?
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Transverse myelitis can occur idiopathically. What does 'idiopathic' mean in this context?
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During the diagnostic process for transverse myelitis, what is the primary imaging method utilized?
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Which cytokine is primarily associated with increasing capillary permeability in the context of transverse myelitis?
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What kind of treatment approach is typically employed for autoimmune-related transverse myelitis?
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What underlying mechanism primarily leads to the demyelination observed in transverse myelitis?
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Which treatment is primarily used for managing autoimmune causes of transverse myelitis in the long term?
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What is the primary goal of conducting a lumbar puncture in suspected cases of transverse myelitis?
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What principal mechanism does mycophenolate utilize to affect inflammation in transverse myelitis?
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Which of the following is a second-line treatment option for transverse myelitis when corticosteroids are ineffective?
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In acute transverse myelitis treatment, what is the primary focus during the early management phase?
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Which of the following describes a significant risk if transverse myelitis is not diagnosed and treated early?
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What is the role of plasmapheresis in the context of transverse myelitis?
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What consequence can arise from damage to specific spinal cord segments due to transverse myelitis?
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Which of the following best describes the role of T cells in the pathophysiology of transverse myelitis?
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Which of the following symptoms is correlated with upper motor neuron damage in transverse myelitis?
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Which approach is vital for the initial diagnosis of transverse myelitis?
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What is a primary consequence of increased capillary permeability due to cytokine release in transverse myelitis?
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Which pathogen is specifically noted as a peri-infectious cause of transverse myelitis?
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What type of immune response commonly leads to transverse myelitis as an autoimmune condition?
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Which of the following effects is NOT attributed to cytokines produced during transverse myelitis?
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In severe cases of transverse myelitis, which symptom may develop from damage to the anterior gray horn?
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What is the main goal of high-dose corticosteroids in the treatment of transverse myelitis?
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Which treatment option clears abnormal proteins from the blood in patients with transverse myelitis?
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What is a pivotal role of mycophenolate in the management of transverse myelitis?
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What potential complication can arise from transverse myelitis related to the affected spinal cord segments?
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Which of the following statements is true regarding the long-term management strategies for transverse myelitis?
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Which treatment serves as a second-line option in cases of transverse myelitis that are unresponsive to corticosteroids?
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Which of the following cytokines is targeted by mycophenolate to decrease inflammation in transverse myelitis?
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What is the key reason early diagnosis and intervention are emphasized in managing transverse myelitis?
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Study Notes
Transverse Myelitis Overview
- Transverse myelitis involves inflammation and demyelination of spinal cord axons.
- Causes are categorized into three groups: peri-infectious, autoimmune, and idiopathic.
Etiology
-
Peri-infectious Causes:
- Immune response to pathogens leads to central nervous system damage.
- Notable pathogens include:
- Dengue virus
- Herpes virus
- Mycoplasma pneumoniae (bacterial infection)
- Schistosomiasis (parasite related to liver fluke)
-
Autoimmune Causes:
- Associated with multiple sclerosis.
- Can occur alongside acute disseminating encephalomyelitis (ADEM), particularly in children.
-
Idiopathic Causes:
- Presence of transverse myelitis without identifiable cause.
Pathophysiology
- Involvement of T cells crossing the blood-brain barrier.
- T cells release cytokines such as interleukin-1, interleukin-6, TNF-alpha, and interferon-gamma.
- Effects of cytokines:
- Increase cell adhesion molecules, promoting white blood cell adhesion.
- Induce vasodilation, enhancing blood flow and leukocyte recruitment.
- Raise capillary permeability, allowing white blood cells and proteins to exit vessels.
- Activate macrophages, increasing phagocytic activity.
Clinical Features
-
Common Symptoms:
- Autonomic dysfunction leading to urinary and fecal incontinence.
- Depending on spinal cord involvement:
- Loss of dorsal column sensations (light touch, proprioception).
- Upper motor neuron symptoms from corticospinal tract involvement (spasticity, hyperactive reflexes).
- Changes in pain and temperature sensation from damaged spinal thalamic tracts.
- Ataxia from compromised spinal cerebellar tracts.
-
Severe Cases:
- May exhibit lower motor neuron symptoms from anterior gray horn damage (flaccid weakness, decreased tone, fasciculations).
Diagnosis
-
First Line Diagnostic:
- MRI of the spinal cord, using T1 and T2 imaging with and without contrast.
- Most commonly affected area is thoracic spinal cord.
-
Additional Test:
- Lumbar puncture for cerebrospinal fluid analysis, looking for pleocytosis (increased white blood cell count).
Treatment
-
First-Line Treatment:
- High-dose corticosteroids to reduce inflammation and limit demyelination.
-
Second-Line Treatment:
- Plasmapheresis for cases unresponsive to corticosteroids or when contraindicated; clears abnormal proteins from the blood.
Important Notes
- Transverse myelitis can lead to significant neurological deficits depending on the affected spinal cord segments.
- Early diagnosis and intervention are crucial for improving outcomes.### Transverse Myelitis Treatment Overview
- Acute treatment involves processing blood through a chamber and tubing, allowing for clearing of harmful proteins and antibodies.
- Donor plasma or solutions like saline with albumin are reinfused to restore circulation, reducing immune response.
Pharmacological Interventions
-
Mycophenolate:
- Inhibits transcription of specific genes that produce pro-inflammatory cytokines.
- Aims to decrease levels of interleukin-1, interleukin-6, and tumor necrosis factor-alpha among other cytokines.
-
Rituximab:
- Targets immune cells including T helper cells, macrophages, and B cells to modulate immune response.
- Enhances the activity of regulatory T cells, promoting anti-inflammatory effects and reducing further neural damage.
Long-term Management Strategies
- Emphasis on mycophenolate and rituximab for chronic treatment following acute episodes.
- Corticosteroids effectively manage infectious causes related to transverse myelitis, often without the need for antibiotics or antiparasitic medications.
Key Points to Remember
- Acute therapies primarily focus on plasmapheresis.
- Mycophenolate and rituximab serve as pivotal long-term management options.
- Managing immune response is crucial to prevent further injury, demyelination, and axonal destruction in transverse myelitis.
Transverse Myelitis Overview
- Involves inflammation and demyelination of spinal cord axons, affecting neurological function.
- Causes are classified into three groups: peri-infectious, autoimmune, and idiopathic.
Etiology
-
Peri-infectious Causes:
- Immune response to various pathogens can damage the central nervous system.
- Notable pathogens include Dengue virus, Herpes virus, Mycoplasma pneumoniae, and Schistosomiasis.
-
Autoimmune Causes:
- Associated with multiple sclerosis and may accompany acute disseminating encephalomyelitis (ADEM), especially in children.
-
Idiopathic Causes:
- Occurs without any identifiable factors.
Pathophysiology
- T cells cross the blood-brain barrier and release pro-inflammatory cytokines, such as interleukin-1, interleukin-6, TNF-alpha, and interferon-gamma.
- Cytokines enhance white blood cell adhesion, induce vasodilation, increase capillary permeability, and activate macrophages, leading to further inflammation and damage.
Clinical Features
-
Common Symptoms:
- Autonomic dysfunction can result in urinary and fecal incontinence.
- Symptoms vary based on spinal cord involvement:
- Loss of sensations such as light touch and proprioception due to dorsal column damage.
- Upper motor neuron symptoms include spasticity and hyperactive reflexes from corticospinal tract damage.
- Altered pain and temperature sensation from spinal thalamic tract damage.
- Ataxia may occur from compromised spinal cerebellar tracts.
-
Severe Cases:
- Can show lower motor neuron symptoms from anterior gray horn damage, leading to flaccid weakness and decreased muscle tone.
Diagnosis
-
First-Line Diagnostic:
- MRI of the spinal cord is essential, particularly T1 and T2 imaging with and without contrast; thoracic spinal cord is the most affected area.
-
Additional Test:
- Lumbar puncture for cerebrospinal fluid analysis reveals pleocytosis (increased white blood cell count).
Treatment
-
First-Line Treatment:
- High-dose corticosteroids reduce inflammation and limit demyelination.
-
Second-Line Treatment:
- Plasmapheresis is used for cases resistant to corticosteroids or when corticosteroids are contraindicated.
Important Notes
- Timely diagnosis and intervention are critical for minimizing neurological deficits.
- Long-term outcomes can be significantly affected by the speed and effectiveness of treatment.
Transverse Myelitis Treatment Overview
- Acute treatment involves utilizing plasmapheresis, clearing harmful proteins and antibodies from the blood, followed by reinfusion of donor plasma or saline with albumin.
Pharmacological Interventions
-
Mycophenolate:
- Inhibits transcription of genes that produce pro-inflammatory cytokines, reducing interleukin-1, interleukin-6, and TNF-alpha levels.
-
Rituximab:
- Targets immune cells to modulate the immune response while enhancing regulatory T cell activity for anti-inflammatory effects.
Long-term Management Strategies
- Focus on mycophenolate and rituximab for chronic treatment post-acute episodes.
- Corticosteroids are effective against infections related to transverse myelitis, often minimizing the need for additional antibiotics or antiparasitic treatments.
Key Points to Remember
- Acute therapies rely heavily on plasmapheresis.
- Mycophenolate and rituximab play crucial roles in long-term management.
- Controlling immune response is vital to prevent continued demyelination and axonal damage in transverse myelitis.
Transverse Myelitis Overview
- Involves inflammation and demyelination of spinal cord axons, affecting neurological function.
- Causes are classified into three groups: peri-infectious, autoimmune, and idiopathic.
Etiology
-
Peri-infectious Causes:
- Immune response to various pathogens can damage the central nervous system.
- Notable pathogens include Dengue virus, Herpes virus, Mycoplasma pneumoniae, and Schistosomiasis.
-
Autoimmune Causes:
- Associated with multiple sclerosis and may accompany acute disseminating encephalomyelitis (ADEM), especially in children.
-
Idiopathic Causes:
- Occurs without any identifiable factors.
Pathophysiology
- T cells cross the blood-brain barrier and release pro-inflammatory cytokines, such as interleukin-1, interleukin-6, TNF-alpha, and interferon-gamma.
- Cytokines enhance white blood cell adhesion, induce vasodilation, increase capillary permeability, and activate macrophages, leading to further inflammation and damage.
Clinical Features
-
Common Symptoms:
- Autonomic dysfunction can result in urinary and fecal incontinence.
- Symptoms vary based on spinal cord involvement:
- Loss of sensations such as light touch and proprioception due to dorsal column damage.
- Upper motor neuron symptoms include spasticity and hyperactive reflexes from corticospinal tract damage.
- Altered pain and temperature sensation from spinal thalamic tract damage.
- Ataxia may occur from compromised spinal cerebellar tracts.
-
Severe Cases:
- Can show lower motor neuron symptoms from anterior gray horn damage, leading to flaccid weakness and decreased muscle tone.
Diagnosis
-
First-Line Diagnostic:
- MRI of the spinal cord is essential, particularly T1 and T2 imaging with and without contrast; thoracic spinal cord is the most affected area.
-
Additional Test:
- Lumbar puncture for cerebrospinal fluid analysis reveals pleocytosis (increased white blood cell count).
Treatment
-
First-Line Treatment:
- High-dose corticosteroids reduce inflammation and limit demyelination.
-
Second-Line Treatment:
- Plasmapheresis is used for cases resistant to corticosteroids or when corticosteroids are contraindicated.
Important Notes
- Timely diagnosis and intervention are critical for minimizing neurological deficits.
- Long-term outcomes can be significantly affected by the speed and effectiveness of treatment.
Transverse Myelitis Treatment Overview
- Acute treatment involves utilizing plasmapheresis, clearing harmful proteins and antibodies from the blood, followed by reinfusion of donor plasma or saline with albumin.
Pharmacological Interventions
-
Mycophenolate:
- Inhibits transcription of genes that produce pro-inflammatory cytokines, reducing interleukin-1, interleukin-6, and TNF-alpha levels.
-
Rituximab:
- Targets immune cells to modulate the immune response while enhancing regulatory T cell activity for anti-inflammatory effects.
Long-term Management Strategies
- Focus on mycophenolate and rituximab for chronic treatment post-acute episodes.
- Corticosteroids are effective against infections related to transverse myelitis, often minimizing the need for additional antibiotics or antiparasitic treatments.
Key Points to Remember
- Acute therapies rely heavily on plasmapheresis.
- Mycophenolate and rituximab play crucial roles in long-term management.
- Controlling immune response is vital to prevent continued demyelination and axonal damage in transverse myelitis.
Transverse Myelitis Overview
- Involves inflammation and demyelination of spinal cord axons, affecting neurological function.
- Causes are classified into three groups: peri-infectious, autoimmune, and idiopathic.
Etiology
-
Peri-infectious Causes:
- Immune response to various pathogens can damage the central nervous system.
- Notable pathogens include Dengue virus, Herpes virus, Mycoplasma pneumoniae, and Schistosomiasis.
-
Autoimmune Causes:
- Associated with multiple sclerosis and may accompany acute disseminating encephalomyelitis (ADEM), especially in children.
-
Idiopathic Causes:
- Occurs without any identifiable factors.
Pathophysiology
- T cells cross the blood-brain barrier and release pro-inflammatory cytokines, such as interleukin-1, interleukin-6, TNF-alpha, and interferon-gamma.
- Cytokines enhance white blood cell adhesion, induce vasodilation, increase capillary permeability, and activate macrophages, leading to further inflammation and damage.
Clinical Features
-
Common Symptoms:
- Autonomic dysfunction can result in urinary and fecal incontinence.
- Symptoms vary based on spinal cord involvement:
- Loss of sensations such as light touch and proprioception due to dorsal column damage.
- Upper motor neuron symptoms include spasticity and hyperactive reflexes from corticospinal tract damage.
- Altered pain and temperature sensation from spinal thalamic tract damage.
- Ataxia may occur from compromised spinal cerebellar tracts.
-
Severe Cases:
- Can show lower motor neuron symptoms from anterior gray horn damage, leading to flaccid weakness and decreased muscle tone.
Diagnosis
-
First-Line Diagnostic:
- MRI of the spinal cord is essential, particularly T1 and T2 imaging with and without contrast; thoracic spinal cord is the most affected area.
-
Additional Test:
- Lumbar puncture for cerebrospinal fluid analysis reveals pleocytosis (increased white blood cell count).
Treatment
-
First-Line Treatment:
- High-dose corticosteroids reduce inflammation and limit demyelination.
-
Second-Line Treatment:
- Plasmapheresis is used for cases resistant to corticosteroids or when corticosteroids are contraindicated.
Important Notes
- Timely diagnosis and intervention are critical for minimizing neurological deficits.
- Long-term outcomes can be significantly affected by the speed and effectiveness of treatment.
Transverse Myelitis Treatment Overview
- Acute treatment involves utilizing plasmapheresis, clearing harmful proteins and antibodies from the blood, followed by reinfusion of donor plasma or saline with albumin.
Pharmacological Interventions
-
Mycophenolate:
- Inhibits transcription of genes that produce pro-inflammatory cytokines, reducing interleukin-1, interleukin-6, and TNF-alpha levels.
-
Rituximab:
- Targets immune cells to modulate the immune response while enhancing regulatory T cell activity for anti-inflammatory effects.
Long-term Management Strategies
- Focus on mycophenolate and rituximab for chronic treatment post-acute episodes.
- Corticosteroids are effective against infections related to transverse myelitis, often minimizing the need for additional antibiotics or antiparasitic treatments.
Key Points to Remember
- Acute therapies rely heavily on plasmapheresis.
- Mycophenolate and rituximab play crucial roles in long-term management.
- Controlling immune response is vital to prevent continued demyelination and axonal damage in transverse myelitis.
Transverse Myelitis Overview
- Involves inflammation and demyelination of spinal cord axons, affecting neurological function.
- Causes are classified into three groups: peri-infectious, autoimmune, and idiopathic.
Etiology
-
Peri-infectious Causes:
- Immune response to various pathogens can damage the central nervous system.
- Notable pathogens include Dengue virus, Herpes virus, Mycoplasma pneumoniae, and Schistosomiasis.
-
Autoimmune Causes:
- Associated with multiple sclerosis and may accompany acute disseminating encephalomyelitis (ADEM), especially in children.
-
Idiopathic Causes:
- Occurs without any identifiable factors.
Pathophysiology
- T cells cross the blood-brain barrier and release pro-inflammatory cytokines, such as interleukin-1, interleukin-6, TNF-alpha, and interferon-gamma.
- Cytokines enhance white blood cell adhesion, induce vasodilation, increase capillary permeability, and activate macrophages, leading to further inflammation and damage.
Clinical Features
-
Common Symptoms:
- Autonomic dysfunction can result in urinary and fecal incontinence.
- Symptoms vary based on spinal cord involvement:
- Loss of sensations such as light touch and proprioception due to dorsal column damage.
- Upper motor neuron symptoms include spasticity and hyperactive reflexes from corticospinal tract damage.
- Altered pain and temperature sensation from spinal thalamic tract damage.
- Ataxia may occur from compromised spinal cerebellar tracts.
-
Severe Cases:
- Can show lower motor neuron symptoms from anterior gray horn damage, leading to flaccid weakness and decreased muscle tone.
Diagnosis
-
First-Line Diagnostic:
- MRI of the spinal cord is essential, particularly T1 and T2 imaging with and without contrast; thoracic spinal cord is the most affected area.
-
Additional Test:
- Lumbar puncture for cerebrospinal fluid analysis reveals pleocytosis (increased white blood cell count).
Treatment
-
First-Line Treatment:
- High-dose corticosteroids reduce inflammation and limit demyelination.
-
Second-Line Treatment:
- Plasmapheresis is used for cases resistant to corticosteroids or when corticosteroids are contraindicated.
Important Notes
- Timely diagnosis and intervention are critical for minimizing neurological deficits.
- Long-term outcomes can be significantly affected by the speed and effectiveness of treatment.
Transverse Myelitis Treatment Overview
- Acute treatment involves utilizing plasmapheresis, clearing harmful proteins and antibodies from the blood, followed by reinfusion of donor plasma or saline with albumin.
Pharmacological Interventions
-
Mycophenolate:
- Inhibits transcription of genes that produce pro-inflammatory cytokines, reducing interleukin-1, interleukin-6, and TNF-alpha levels.
-
Rituximab:
- Targets immune cells to modulate the immune response while enhancing regulatory T cell activity for anti-inflammatory effects.
Long-term Management Strategies
- Focus on mycophenolate and rituximab for chronic treatment post-acute episodes.
- Corticosteroids are effective against infections related to transverse myelitis, often minimizing the need for additional antibiotics or antiparasitic treatments.
Key Points to Remember
- Acute therapies rely heavily on plasmapheresis.
- Mycophenolate and rituximab play crucial roles in long-term management.
- Controlling immune response is vital to prevent continued demyelination and axonal damage in transverse myelitis.
Transverse Myelitis Overview
- Involves inflammation and demyelination of spinal cord axons, affecting neurological function.
- Causes are classified into three groups: peri-infectious, autoimmune, and idiopathic.
Etiology
-
Peri-infectious Causes:
- Immune response to various pathogens can damage the central nervous system.
- Notable pathogens include Dengue virus, Herpes virus, Mycoplasma pneumoniae, and Schistosomiasis.
-
Autoimmune Causes:
- Associated with multiple sclerosis and may accompany acute disseminating encephalomyelitis (ADEM), especially in children.
-
Idiopathic Causes:
- Occurs without any identifiable factors.
Pathophysiology
- T cells cross the blood-brain barrier and release pro-inflammatory cytokines, such as interleukin-1, interleukin-6, TNF-alpha, and interferon-gamma.
- Cytokines enhance white blood cell adhesion, induce vasodilation, increase capillary permeability, and activate macrophages, leading to further inflammation and damage.
Clinical Features
-
Common Symptoms:
- Autonomic dysfunction can result in urinary and fecal incontinence.
- Symptoms vary based on spinal cord involvement:
- Loss of sensations such as light touch and proprioception due to dorsal column damage.
- Upper motor neuron symptoms include spasticity and hyperactive reflexes from corticospinal tract damage.
- Altered pain and temperature sensation from spinal thalamic tract damage.
- Ataxia may occur from compromised spinal cerebellar tracts.
-
Severe Cases:
- Can show lower motor neuron symptoms from anterior gray horn damage, leading to flaccid weakness and decreased muscle tone.
Diagnosis
-
First-Line Diagnostic:
- MRI of the spinal cord is essential, particularly T1 and T2 imaging with and without contrast; thoracic spinal cord is the most affected area.
-
Additional Test:
- Lumbar puncture for cerebrospinal fluid analysis reveals pleocytosis (increased white blood cell count).
Treatment
-
First-Line Treatment:
- High-dose corticosteroids reduce inflammation and limit demyelination.
-
Second-Line Treatment:
- Plasmapheresis is used for cases resistant to corticosteroids or when corticosteroids are contraindicated.
Important Notes
- Timely diagnosis and intervention are critical for minimizing neurological deficits.
- Long-term outcomes can be significantly affected by the speed and effectiveness of treatment.
Transverse Myelitis Treatment Overview
- Acute treatment involves utilizing plasmapheresis, clearing harmful proteins and antibodies from the blood, followed by reinfusion of donor plasma or saline with albumin.
Pharmacological Interventions
-
Mycophenolate:
- Inhibits transcription of genes that produce pro-inflammatory cytokines, reducing interleukin-1, interleukin-6, and TNF-alpha levels.
-
Rituximab:
- Targets immune cells to modulate the immune response while enhancing regulatory T cell activity for anti-inflammatory effects.
Long-term Management Strategies
- Focus on mycophenolate and rituximab for chronic treatment post-acute episodes.
- Corticosteroids are effective against infections related to transverse myelitis, often minimizing the need for additional antibiotics or antiparasitic treatments.
Key Points to Remember
- Acute therapies rely heavily on plasmapheresis.
- Mycophenolate and rituximab play crucial roles in long-term management.
- Controlling immune response is vital to prevent continued demyelination and axonal damage in transverse myelitis.
Transverse Myelitis Overview
- Involves inflammation and demyelination of spinal cord axons, affecting neurological function.
- Causes are classified into three groups: peri-infectious, autoimmune, and idiopathic.
Etiology
-
Peri-infectious Causes:
- Immune response to various pathogens can damage the central nervous system.
- Notable pathogens include Dengue virus, Herpes virus, Mycoplasma pneumoniae, and Schistosomiasis.
-
Autoimmune Causes:
- Associated with multiple sclerosis and may accompany acute disseminating encephalomyelitis (ADEM), especially in children.
-
Idiopathic Causes:
- Occurs without any identifiable factors.
Pathophysiology
- T cells cross the blood-brain barrier and release pro-inflammatory cytokines, such as interleukin-1, interleukin-6, TNF-alpha, and interferon-gamma.
- Cytokines enhance white blood cell adhesion, induce vasodilation, increase capillary permeability, and activate macrophages, leading to further inflammation and damage.
Clinical Features
-
Common Symptoms:
- Autonomic dysfunction can result in urinary and fecal incontinence.
- Symptoms vary based on spinal cord involvement:
- Loss of sensations such as light touch and proprioception due to dorsal column damage.
- Upper motor neuron symptoms include spasticity and hyperactive reflexes from corticospinal tract damage.
- Altered pain and temperature sensation from spinal thalamic tract damage.
- Ataxia may occur from compromised spinal cerebellar tracts.
-
Severe Cases:
- Can show lower motor neuron symptoms from anterior gray horn damage, leading to flaccid weakness and decreased muscle tone.
Diagnosis
-
First-Line Diagnostic:
- MRI of the spinal cord is essential, particularly T1 and T2 imaging with and without contrast; thoracic spinal cord is the most affected area.
-
Additional Test:
- Lumbar puncture for cerebrospinal fluid analysis reveals pleocytosis (increased white blood cell count).
Treatment
-
First-Line Treatment:
- High-dose corticosteroids reduce inflammation and limit demyelination.
-
Second-Line Treatment:
- Plasmapheresis is used for cases resistant to corticosteroids or when corticosteroids are contraindicated.
Important Notes
- Timely diagnosis and intervention are critical for minimizing neurological deficits.
- Long-term outcomes can be significantly affected by the speed and effectiveness of treatment.
Transverse Myelitis Treatment Overview
- Acute treatment involves utilizing plasmapheresis, clearing harmful proteins and antibodies from the blood, followed by reinfusion of donor plasma or saline with albumin.
Pharmacological Interventions
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Mycophenolate:
- Inhibits transcription of genes that produce pro-inflammatory cytokines, reducing interleukin-1, interleukin-6, and TNF-alpha levels.
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Rituximab:
- Targets immune cells to modulate the immune response while enhancing regulatory T cell activity for anti-inflammatory effects.
Long-term Management Strategies
- Focus on mycophenolate and rituximab for chronic treatment post-acute episodes.
- Corticosteroids are effective against infections related to transverse myelitis, often minimizing the need for additional antibiotics or antiparasitic treatments.
Key Points to Remember
- Acute therapies rely heavily on plasmapheresis.
- Mycophenolate and rituximab play crucial roles in long-term management.
- Controlling immune response is vital to prevent continued demyelination and axonal damage in transverse myelitis.
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Description
This quiz covers the overview of transverse myelitis, including its causes and pathophysiology. It explores peri-infectious, autoimmune, and idiopathic factors contributing to the condition, along with the immune responses involved. Test your understanding of how this neurological disorder affects the spinal cord!
