Transverse myelitis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Transverse myelitis is a neurological disorder caused by an inflammatory process of the grey and white matter of the spinal cord, and can cause axonal demyelination.

Axonal demyelination arises idiopathically following infections or vaccination, or due to multiple sclerosis. One major theory of the cause is that an immune-mediated inflammation is present as the result of exposure to a viral antigen. The lesions are inflammatory, and involve the spinal cord on both sides.

Prognosis for complete recovery is generally poor. Recovery from transverse myelitis usually begins between weeks 2 and 12 following onset and may continue for up to 2 years in some patients, many of whom are left with considerable disabilities. Some patients show no signs of recovery whatsoever.

Blood tests may be performed to rule out various disorders such as systemic lupus erythematosus, HIV infection, vitamin B12 deficiency, and many others A blood test for NMO, called NMO-IgG, is also necessary. In some patients with transverse myelitis, the cerebrospinal fluid that bathes the spinal cord and brain contains more protein than usual and an increased number of leukocytes (white blood cells). A spinal tap may be performed to obtain fluid to study these factors, exclude infections, and to look for markers of diseases such as MS.

If an MRI is not possible (for example, if the patient has a pacemaker), physicians may consider other diagnostic tests such as computed tomography (CT) of the spine with or without myelography, which involves injecting a dye into the sac that surrounds the spinal cord.

It is often difficult to distinguish between a patient with an idiopathic form of transverse myelitis and one who has an underlying condition, physicians must first eliminate potentially treatable causes of the condition. when a spinal cord problem is suspected, physicians seek first to rule out structural lesions (damaged or abnormally functioning areas) that could cause spinal cord compression or otherwise affects its function. Such potential lesions include tumors, herniated or slipped discs, stenosis (narrowing of the canal that holds the spinal cord), abscesses, and abnormal collections of blood vessels. To rule out such lesions and check for inflammation of the spinal cord, patients often undergo magnetic resonance imaging (MRI), a procedure that provides a picture of the brain and spinal cord. The spinal cord MRI will almost always confirm the presence of a lesion within the spinal cord, whereas the brain MRI may provide clues to other underlying causes, especially MS.

Treatments are designed to reduce spinal cord inflammation and manage and alleviate symptoms. Initial therapy includes prescription of anti-inflammatorycorticosteroid therapy soon after the diagnosis is made in order to decrease inflammation and hopefully improve the chances and speed of neurological recovery. In severe cases that do not appear to respond to corticosteroid treatment, other therapies such as plasma exchange or drug therapies may be used to try to salvage neurological function. Later, if patients begin to recover limb control,physical therapy begins to help improve muscle strength,coordination, and range of motion.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

Transverse myelitis was first discovered by Dr. Suchett-Kaye, an English neurologist at St. Charles Hospital in London, utilized the term “acute transverse myelitis” in 1948. Cases of “acute myelitis” have been described earlier as cases of “acute myelitis” that have been described in association with or after infection and smallpox vaccination.

• Transverse myelitis was first discovered by Dr. Suchett-Kaye, an English neurologist at St. Charles Hospital in London, utilized the term “acute transverse myelitis” in 1948.^[1]

• Cases of “acute myelitis” have been described earlier as cases of “acute myelitis” that have been described in association with or after infection and smallpox vaccination.^[2]

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

There is no established system for the classification of transverse myelitis.

There is no established system for the classification of transverse myelitis.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

• In the pathogenesis of transverse myelitis, a variety of immunological mechanisms may cause pathological substrate and dysfunction of neural cells within the spinal cord.

• Transverse myelitis is the result of progressive demyelination and axonal loss in addition to gray matter involvement, necrosis and cavitation.
• It is understood that infections may cause transverse myelitis by:
  • Direct tissue damage
  • Immune-mediated infection-triggered tissue damage
• Multiple sclerosis is the other cause to the transverse myelitis and it sometimes transverse myelitis can appear as the first symptom of Multiple sclerosis.
• Acute partial transverse myelitis may be predictive of a subsequent diagnosis of multiple sclerosis in children.
• Invariable histopathological findings of transverse myelitis include:
  • Perivascular spread of monocytes
  • Focal areas of lymphocytes infiltrating
  • Astroglial and microglial activation

• Other histopathological findings of transverse myelitis include:
  • Infiltration of CD4⁺ and CD8⁺ T-lymphocytes
  • Typically preservation of the subpial parenchyma suggesting ischemia as the ultimate cause of the cord lesions in transverse myelitis

Conditions that may cause transverse myelitis include:

• Various infectionsin 30% to 60% of the cases:
  • Herpesviridae
  • Enteroviruses
  • Influenza viruses
  • Adenoviruses
  • Coxsackieviruses
  • Enteric cytopathogenic human orphan (ECHO) virus
  • Hepatitis A virus
  • Lymphocytic choriomeningitis virus (LCMV)
  • Mumps virus
  • Measles virus
  • Rubella virus
  • Poliovirus
  • Rubeola virus
  • Dengue virus
  • Russian spring-summer encephalitis virus
  • Varicella virus
  • Mycoplasma pneumonia bacteria
  • Legionella pneumonia bacteria
  • Pulmonary tuberculosis
  • Borrelia (Lyme disease)
  • Listeria
  • Bartonella (cat scratch disease)
• Vaccination
  • About 30% of pediatric cases are preceded with immunizations within one month of disease onset

Infections can cause transverse myelitis through two main mechanisms:

1. Direct tissue damage
2. Immune-mediated infection-triggered tissue damage which may be due to: Molecular mimicry or superantigen effect

• This immune response may be caused either by T-cell mediated immune response or by antibody-mediated immune response.

A non-microbial related immune dysfunction by the presence of autoantibodies has been also proposed in the immunopathogenesis of transverse myelitis.

In the spinal fluid of patients with transverse myelitis, Interleukin 6 (IL-6) levels were also markedly elevated.

• The lesions in acute transverse myelitis are invariably limited to the spinal cord.^[1][2]
• There is no involvement of other structures in the central nervous system.^[1]
• The spinal cord involvement in patients with transverse myelitis is usually central, uniform and symmetric but in patients with multiple sclerosis it typically affects the spinal cord in a patchy way and the lesions are usually peripheral.

• In the pathogenesis of transverse myelitis, a variety of immunological mechanisms may cause pathological substrate and dysfunction of neural cells within the spinal cord.^[3]

• Transverse myelitis is the result of progressive demyelination and axonal loss in addition to gray matter involvement, necrosis and cavitation.^[1]
• It is understood that infections may cause transverse myelitis by: ^[1]
  • Direct tissue damage
  • Immune-mediated infection-triggered tissue damage
• Multiple sclerosis is the other cause to the transverse myelitis and it sometimes transverse myelitis can appear as the first symptom of Multiple sclerosis.^[1]
• Acute partial transverse myelitis may be predictive of a subsequent diagnosis of multiple sclerosis in children.^[4]
• Invariable histopathological findings of transverse myelitis include:^[1]
  • Perivascular spread of monocytes
  • Focal areas of lymphocytes infiltrating
  • Astroglial and microglial activation

• Other histopathological findings of transverse myelitis include:^[1][5]
  • Infiltration of CD4⁺ and CD8⁺ T-lymphocytes
  • Typically preservation of the subpial parenchyma suggesting ischemia as the ultimate cause of the cord lesions in transverse myelitis

Conditions that may cause transverse myelitis include:

• Various infectionsin 30% to 60% of the cases:^{[1][6][7][8][9][10][11][12][13][14]}
  • Herpesviridae
  • Enteroviruses
  • Influenza viruses
  • Adenoviruses
  • Coxsackieviruses
  • Enteric cytopathogenic human orphan (ECHO) virus
  • Hepatitis A virus
  • Lymphocytic choriomeningitis virus (LCMV)
  • Mumps virus
  • Measles virus
  • Rubella virus
  • Poliovirus
  • Rubeola virus
  • Dengue virus
  • Russian spring-summer encephalitis virus
  • Varicella virus
  • Mycoplasma pneumonia bacteria
  • Legionella pneumonia bacteria
  • Pulmonary tuberculosis
  • Borrelia (Lyme disease)
  • Listeria
  • Bartonella (cat scratch disease)
• Vaccination^[1][15]
  • About 30% of pediatric cases are preceded with immunizations within one month of disease onset

Infections can cause transverse myelitis through two main mechanisms:^[1][14][16]

1. Direct tissue damage
2. Immune-mediated infection-triggered tissue damage which may be due to: Molecular mimicry or superantigen effect

• This immune response may be caused either by T-cell mediated immune response or by antibody-mediated immune response.

A non-microbial related immune dysfunction by the presence of autoantibodies has been also proposed in the immunopathogenesis of transverse myelitis.^{[1][17][18][19]}

In the spinal fluid of patients with transverse myelitis, Interleukin 6 (IL-6) levels were also markedly elevated.^[1][8][20]

Conditions associated with transverse myelitis include:^{[21][22][1][3][23]}

• Various infections
• Systemic autoimmune diseases like:
  • Lupus erythematosus
  • Sjögren’s syndrome
  • Sarcoidosis
  • Optic neuritis
  • multiple sclerosis

Findings on microscopic histopathological analysis of transverse myelitis include:^[24][25]

• Perivascular lymphocytic infiltrates
• Axonal injury
• Necrosis and demyelination

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

• Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. There are no life-threatening causes of disease name, however complications resulting from untreated disease name is common.
• Life-threatening causes of [symptom/manifestation] include [cause1], [cause2], and [cause3].
• [Cause] is a life-threatening cause of [disease].

Common causes of myelitis include may include:

• Various infectionsin in 30% to 60% of the cases:^{[1][2][3][4][5][6][7][8][9][10]}
  • Herpesviridae
  • Enteroviruses
  • Influenza viruses
  • Adenoviruses
  • Coxsackieviruses
  • Enteric cytopathogenic human orphan (ECHO) virus
  • Hepatitis A virus
  • Lymphocytic choriomeningitis virus (LCMV)
  • Mumps virus
  • Measles virus
  • Rubella virus
  • Poliovirus
  • Rubeola virus
  • Dengue virus
  • Russian spring-summer encephalitis virus
  • Varicella virus
  • Mycoplasma pneumonia bacteria
  • Legionella pneumonia bacteria
  • Pulmonary tuberculosis
  • Borrelia (Lyme disease)
  • Listeria
  • Bartonella (cat scratch disease)
• Vaccination^[1][11]
  • About 30% of pediatric cases are preceded with immunizations within one month of disease onset
• [Condition

OR

• [Disease name] is caused by an infection with [pathogen name].
• [Pathogen name] is caused by [pathogen name].

Less common causes of [disease name] include:

• [Cause1]
• [Cause2]
• [Cause3]

• [Disease name] is caused by a mutation in the [gene name] gene.

List the causes of the disease in alphabetical order:

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Tarek Nafee, M.D. [2] Mohamadmostafa Jahansouz M.D.[3] Syed Musadiq Ali M.B.B.S.[4]

Transverse myelitis must be differentiated from other diseases that cause hypotonia, muscle weakness, or paralysis such as: Adult botulism, infant botulism, Guillian-Barre syndrome, Eaton Lambert syndrome, myasthenia gravis, electrolyte disturbance, organophosphate toxicity, tick paralysis, stroketetrodotoxin poisoning, poliomyelitis, neurosyphilis, muscular dystrophy, multiple sclerosis exacerbation, amyotrophic lateral sclerosis and inflammatory myopathy.

Transverse myelitis must be differentiated from other diseases that may cause hypotonia, muscle weakness, or paralysis:^{[1][1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16]}

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

• The incidence/prevalence of transverse myelitis is approximately [number range] per 100,000 individuals worldwide.
• In [year], the incidence/prevalence of [disease name] was estimated to be [number range] cases per 100,000 individuals worldwide.

• The incidence/prevalence of [disease name] is approximately [number range] per 100,000 individuals worldwide.
• In [year], the incidence/prevalence of [disease name] was estimated to be [number range] cases per 100,000 individuals worldwide.
• The prevalence of [disease/malignancy] is estimated to be [number] cases annually.

• In [year], the incidence of [disease name] is approximately [number range] per 100,000 individuals with a case-fatality rate/mortality rate of [number range]%.
• The case-fatality rate/mortality rate of [disease name] is approximately [number range].

• Patients of all age groups may develop [disease name].
• The incidence of [disease name] increases with age; the median age at diagnosis is [#] years.
• [Disease name] commonly affects individuals younger than/older than [number of years] years of age.
• [Chronic disease name] is usually first diagnosed among [age group].
• [Acute disease name] commonly affects [age group].

• There is no racial predilection to [disease name].
• [Disease name] usually affects individuals of the [race 1] race. [Race 2] individuals are less likely to develop [disease name].

• [Disease name] affects men and women equally.
• [Gender 1] are more commonly affected by [disease name] than [gender 2]. The [gender 1] to [gender 2] ratio is approximately [number > 1] to 1.

• The majority of [disease name] cases are reported in [geographical region].

• [Disease name] is a common/rare disease that tends to affect [patient population 1] and [patient population 2].

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

There are no established risk factors for [disease name].

OR

The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].

OR

Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].

• Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.
• Common risk factors in the development of [disease name] include:
  • [Risk factor 1]
  • [Risk factor 2]
  • [Risk factor 3]

• Less common risk factors in the development of [disease name] include:
  • [Risk factor 1]
  • [Risk factor 2]
  • [Risk factor 3]

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamadmostafa Jahansouz M.D.[2]

There is insufficient evidence to recommend routine screening for transverse myelitis.

Template:WH Template:WS

Please help WikiDoc by adding more content here. It’s easy! Click here to learn about editing.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Prognosis for complete recovery is generally poor. Recovery from transverse myelitis usually begins between weeks 2 and 12 following onset and may continue for up to 2 years in some patients, many of whom are left with considerable disabilities. Some patients show no signs of recovery whatsoever.

Recovery from transverse myelitis usually begins within 2 to 12 weeks of the onset of symptoms and may continue for up to 2 years. However, if there is no improvement within the first 3 to 6 months, significant recovery is unlikely. About one-third of people affected with transverse myelitis experience good or full recovery from their symptoms; they regain the ability to walk normally and experience minimal urinary or bowel effects and paresthesias. Another one-third show only fair recovery and are left with significant deficits such as spastic gait, sensory dysfunction, and prominent urinary urgency or incontinence. The remaining one-third show no recovery at all, remaining wheelchair-bound or bedridden with marked dependence on others for basic functions of daily living. Unfortunately, making predictions about individual cases is difficult. However, research has shown that a rapid onset of symptoms generally results in poorer recovery outcomes.

The majority of people with this disorder experience only one episode although in rare cases recurrent or relapsing transverse myelitis does occur. Some patients recover completely, then experience a relapse. Others begin to recover, then suffer worsening of symptoms before recovery continues. In all cases of relapse, physicians will evaluate possible underlying causes such as MS, NMO, or systemic lupus erythematosus since most people who experience relapse have an identifiable underlying disorder. People with a recurrent relapsing disorder will usually require some type of ongoing therapy that modulates or suppresses the immune system. The propose of such therapies is to reduce the chance of future relapses.

Template:WH Template:WS