Case record...Idiopathic postinfectious transverse myelitis

1. CASE OF THE WEEK
PROFESSOR YASSER METWALLY
CLINICAL PICTURE
CLINICAL PICTURE
A 35 years old female patient presented with paraplegia with a high dorsal sensory level of acute onset. The
neurological disability occurred 10 days following rabies vaccination.
RADIOLOGICAL FINDINGS
RADIOLOGICAL FINDINGS
Figure 1. MRI study of the cervico-dorsal region showing multisegmental (almost 8 spinal segments) T2
hyperintensity / precontrast T1 hypointensity (representing central cord edema) occupying centrally more than 2/3 of
the cross section of the spinal cord and causing mild spinal cord enlargement at the affected zone.

2. Figure 2. (A, Precontrast MRI T1 image, B MRI T2 image) MRI study of the cervico-dorsal region in a case of acute
idiopathic transverse myelitis showing multisegmental (almost 8 spinal segments) T2 hyperintensity / T1 hypointensity
(representing central cord edema) occupying centrally more than 2/3 of the cross section of the spinal cord and causing
mild spinal cord enlargement at the affected zone. Notice the peripheral enhancement on postcontrast MRI T1 image
(C).
Figure 3. MRI T2 cross sectional images showing central hyperintensity occupying more than 2/3 of the cross sections
of the spinal cord with central dot sign seen on A.

3. Figure 4. MRI pre and post contrast images and MRI T2 images in a case of acute idiopathic transverse myelitis.
Notice the central dot sign in the cross sectional T2 images, also notice that enhancement on the postcontrast MRI T1
image is peripherally located and outside the T2 central hyperintensity.
Figure 5. (A, MRI T2 image and B, postcontrast MRI T1 image) Notice that enhancement on the postcontrast MRI T1
image is peripherally located and outside the T2 central hyperintensity.

4. Figure 6. A case with acute idiopathic transverse myelitis. Notice spinal cord swelling and the MRI T2 central
hyperintensity and the central dot sign. Also notice the involvement of the complete cross section of the spinal cord.
 The MRI picture characteristic of idiopathic transverse myelitis
1. A centrally located multisegmental (3 to 8 spinal segments) MRI T2 hyperintensity that occupies more
than two thirds of the cross-sectional area of the cord is characteristic of transverse myelitis. The MRI T2
hyperintensity commonly shows a slow regression with clinical improvement. The central spinal cord
MRI T2 hyperintensity represents evenly distributed central cord edema. MRI T1 Hypointensity might
be present in the same spinal segments that show T2 hyperintensity although to a lesser extent. The MRI
T2 hyperintensity is central, bilateral, more or less symmetrical and multisegmental.
2. MRI T2 central isointensity, or dot (within and in the core of the MRI T2 hyperintensity) might be
present and is believed to represent central gray matter squeezed by the uniform, evenly distributed
edematous changes of the cord. (central dot sign). It might not be of any clinical significance.
3. Contrast enhancement is commonly focal or peripheral and maximal at or near the segmental MRI T2
hyperintensity. In idiopathic transverse myelitis enhancement is peripheral to the centrally located area
of high T2 signal intensity rather than in the very same area. The prevalence of cord enhancement is
significantly higher in patients with cord expansion.
4. Spinal cord expansion might or might not be present and when present is usually multisegmental and
better appreciated on the sagittal MRI T1 images. Spinal cord expansion tapers smoothly to the normal
cord, and is of lesser extent than the high T2 signal abnormality.
5. Multiple sclerosis plaques (and subsequent T2 hyperintensity) are located peripherally, are less than 2
vertebral segments in length, and occupies less than half the cross-sectional area of the cord. In contrast
to transverse myelitis, enhancement in MS occurs in the same location of high-signal-intensity lesions
seen on T2-weighted images.

5. DIAGNOSIS:
DIAGNOSIS: ACUTE IDIOPATHIC TRANSVERSE MYELITIS
DISCUSSION
DISCUSSION
Transverse myelitis (TM) is a neurologic syndrome caused by inflammation of the spinal cord. TM is uncommon but
not rare. Conservative estimates of incidence per year vary from 1 to 5 per million population (105). The term myelitis
is a nonspecific term for inflammation of the spinal cord; transverse refers to involvement across one level of the spinal
cord. It occurs in both adults and children. You may also hear the term myelopathy, which is a more general term for
any disorder of the spinal cord. The term radiculomyelitis refers to inflammation of the spinal roots as they emerge
from the spinal cord along with inflammation of the spinal cord itself. Myelitis probably rarely occurs without
concomitant involvement of the emerging spinal roots in the inflamed spinal segments and in such a case a
combination of upper and lower motor neuron manifestations is the usual clinical presentation.
 Clinical symptoms
TM symptoms develop rapidly over several hours to several weeks. Approximately 45% of patients worsen maximally
within 24 hours (Ibid.). The spinal cord carries motor nerve fibers to the limbs and trunk and sensory fibers from the
body back to the brain. Inflammation within the spinal cord interrupts these pathways and causes the common
presenting symptoms of TM which include limb weakness, sensory disturbance, bowel and bladder dysfunction, back
pain and radicular pain (pain in the distribution of a single spinal nerve).
Almost all patients will develop leg weakness of varying degrees of severity. The arms are involved in a minority of
cases and this is dependent upon the level of spinal cord involvement. Sensation is diminished below the level of spinal
cord involvement in the majority of patients. Some experience tingling or numbness in the legs. Pain (ascertained as
appreciation of pinprick by the neurologist) and temperature sensation are diminished in the majority of patients.
Appreciation of vibration (as caused by a tuning fork) and joint position sense may also be decreased or spared.
Bladder and bowel sphincter control are disturbed in the majority of patients. Many patients with TM report a tight
banding or girdle-like sensation around the trunk and that area may be very sensitive to touch.
Recovery may be absent, partial or complete and generally begins within 1 to 3 months. Significant recovery is
unlikely, if no improvement occurs by 3 months. Most patients with TM show good to fair recovery. TM is generally a
monophasic illness (one-time occurrence); however, a small percentage of patients may suffer a recurrence, especially
if there is a predisposing underlying illness.
 Causes of transverse myelopathy / myelitis or radiculomyelitis
Transverse myelitis may occur in isolation or in the setting of another illness. When it occurs without apparent
underlying cause, it is referred to as idiopathic. Idiopathic transverse myelitis is assumed to be a result of abnormal
activation of the immune system against the spinal cord. A list of illnesses associated with TM includes:
Table1: Diseases Associated with transverse myelitis transverse myelopathy or radiculomyelitis
 Parainfectious (occurring at the time of and in association with an acute infection or an episode of infection).
 Viral: herpes simplex, herpes zoster, cytomegalovirus, Epstein-Barr virus, enteroviruses (poliomyelitis,
Coxsackie virus, echovirus), human T-cell, leukemia virus, human immunodeficiency virus, influenza, rabies
 Bacterial: Pyogenic, Mycoplasma pneumoniae, Lyme borreliosis, syphilis, tuberculosis, Neuroschistosomiasis
 Postvaccinal (rabies, cowpox)

6.  Systemic autoimmune disease
 Systemic lupus erythematosis and other connective tissue disease
 Sjogren's syndrome
 Sarcoidosis
 Multiple Sclerosis
 Paraneoplastic syndrome
 Vascular
 Thrombosis of spinal arteries
 Vasculitis secondary to heroin abuse
 Spinal arterio-venous malformation
 Antiphospholipid syndrome
 Radiation induced
The cause of idiopathic transverse myelitis is unknown, but most evidence supports an autoimmune process. This
means that the patient's own immune system is abnormally stimulated to attack the spinal cord and cause
inflammation and tissue damage. Examples of autoimmune diseases which are more common include rheumatoid
arthritis, in which the immune system attacks the joints, and multiple sclerosis, in which myelin, the insulating
material for nerve cells in the brain, is the target of autoimmune attack.
TM often develops in the setting of viral and bacterial infections, especially those which may be associated with a rash
(e.g., rubeola, varicella, variola, rubella, influenza, and mumps). Approximately one third of patients with TM report a
febrile illness (flu-like illness with fever) in close temporal relationship to the onset of neurologic symptoms. In some
cases, there is evidence that there is a direct invasion and injury to the cord by the infectious agent itself (especially
poliomyelitis, herpes zoster, and AIDS). A bacterial abscess can also develop around the spinal cord and injure the
cord through compression, bacterial invasion and inflammation.
However, experts believe that in many cases infection causes a derangement of the immune system which leads to an
indirect autoimmune attack on the spinal cord, rather than a direct attack by the organism. One theory to explain this
abnormal activation of the immune system toward human tissue is termed quot;molecular mimicry.quot; This theory
postulates that an infectious agent may share a molecule which resembles or quot;mimicsquot; a molecule in the spinal cord.
When the body mounts an immune response to the invading virus or bacterium, it also responds to the spinal cord
molecule with which it shares structural characteristics. This leads to inflammation and injury within the spinal cord.
Vaccination is well known to carry a risk of the development of acute disseminated encephalomyelitis (ADEM) which
is an acute inflammation of the brain and spinal cord. This was particularly common with the older antirabies vaccine
which was grown in animal spinal cord cultures; the use of the newer antirabies vaccine grown in human tissue culture
has almost eradicated this complication. This is also thought to occur as an immune system response.
Transverse myelitis may be a relatively uncommon manifestation of several autoimmune diseases including systemic
lupus erythematosis (SLE), Sjogren's syndrome, and sarcoidosis. SLE is an autoimmune disease of unknown cause
which affects multiple organs and tissues in the body. Features of this illness include arthralgias (joint pain) and
arthritis (joint inflammation), rashes, kidney inflammation, low blood counts (including white and red blood cells,
platelets), oral ulcers and the presence of abnormal autoantibodies (antibodies which are directed against the person's
own tissues) in the blood. The fully developed syndrome of SLE is easy to recognize; however, this illness may begin
with just one or two signs and is then more difficult to diagnose.

7. Sjogren's syndrome is another autoimmune disease characterized by invasion and infiltration of the tear and salivary
glands by (lymphocytes) white blood cells with resultant decreased production of these fluids. Patients complain of dry
mouth and dry eyes. Several tests can support this diagnosis: the presence of a SS-A antibody in the blood,
ophthalmologic tests that confirm decreased tear production and the demonstration of lymphocytic infiltration in
biopsy specimens of the small salivary glands (a minimally invasive procedure). Neurologic manifestations are unusual
in Sjogren's syndrome, but TM can occur.
Sarcoidosis is a multisystem inflammatory disorder of unknown cause manifested by enlarged lymph nodes, lung
inflammation, various skin lesions, liver and other organ involvement. In the nervous system, various nerves, as well as
the spinal cord, may be involved. Diagnosis is generally confirmed by biopsy demonstrating features of inflammation
typical of sarcoidosis.
Multiple sclerosis is an inflammatory autoimmune disease of the central nervous system (brain and spinal cord) which
results in demyelination or loss of myelin (the insulating material on nerve fibers) with resultant neurologic
dysfunction. A definite diagnosis of MS is not given until a patient has had at least two attacks of demyelination (hence,
multiple) at two different sites in the central nervous system. The spinal cord is frequently affected in multiple sclerosis
and may be the site of involvement of the first attack of MS. This presents the possibility that patients with acute
transverse myelitis could later go on to have a second episode of demyelination and receive a diagnosis of MS.
Just what percentage of patients with a first attack of acute transverse myelitis will go on to develop MS is unclear in
the medical literature, ranging from 15 to 80%; however, the majority of studies show a low risk. We do know that
patients who have abnormal MRI scans of the brain with lesions like those seen in MS are much more likely to go on to
develop MS than those who have normal brain MRIs at the time of their myelitis (between 60 and 90% for those with
abnormal brain scans, less than 20% for those with normal scans in one study). It is also suggested in the medical
literature that patients with quot;completequot; transverse myelitis (which means severe leg paralysis and sensory loss) are
less likely to develop MS than those who had a partial or less severe case. The literature also suggests that patients who
have abnormal antibodies in their spinal fluid, called oligoclonal bands, are at higher risk to develop MS subsequently.
Myelitis related to cancer (paraneoplastic syndrome) is uncommon. There are several reports in the medical literature
of a severe myelitis occurring in association with a malignancy. In addition, there are a growing number of reports of
cases of myelopathy associated with cancer in which the immune system produces an antibody to fight off the cancer
and this cross-reacts with the molecules in the spinal cord neurons. It should be emphasized that this is an unusual
cause of myelitis.
Figure 7. A case with acute idiopathic transverse myelitis. Notice spinal cord swelling and the MRI T2 central
hyperintensity and the central dot sign. Also notice the involvement of the complete cross section of the spinal cord.
Vascular causes are listed because they present with the same problems as transverse myelitis; however this is really a
distinct problem primarily due to inadequate blood flow to the spinal cord instead of actual inflammation. The blood
vessels to the spinal cord can close up with blood clots or atherosclerosis or burst and bleed; this is essentially a
quot;strokequot; of the spinal cord.
Myelopathy as a complication of heroin toxicity commonly has an acute onset often within hours of drug

8. administration (Often related to single dose after period of abstinence ) with weakness (Paraplegia or Quadriplegia)
and urinary retention. Prominent recovery may occur over weeks to months. CSF analysis is usually normal with
occasional pleocytosis or increased protein. The mechanism of disease could be due to hypersensitivity or vasculitis.
Corticosteroids or plasma exchange might be tried for treatment during the acute phase.
MRI examination commonly shows transverse myelitis-like findings with intramedullary T2 hyperintensity and cord
swelling. Enhancement is often patchy, over several levels.
Figure 8. Heroin myelopathy Increased T2 signal (Arrow) in cervical spinal cord
 Diagnosis
The general history and physical examination are first performed, but often do not give clues about the cause of spinal
cord injury. The first concern of the physician who evaluates a patient with complaints and examination suggestive of
a spinal cord disorder is to rule out a mass-occupying lesion which might be compressing the spinal cord. Potential
lesions which might compress the cord include tumor, herniated disc, stenosis (a narrowed canal for the cord), and
abscess. This is important because early surgery to remove the compression may sometimes reverse neurologic injury
to the spinal cord. The easiest test to rule out such a compressive lesion is magnetic resonance imaging of the
appropriate levels of the cord.
Figure 9. MRI T2 showing a case of acute idiopathic transverse
myelitis. Notice cord swelling and the multisegmental, central
increased cord signal intensity at the cervicodorsal region
If the MRI shows no mass lesion outside or within the spinal cord, then the patient with spinal cord dysfunction is

9. thought to have transverse myelitis or vascular problems. The MRI can sometimes show an inflammatory lesion
within the cord. It is difficult to get to the cause of the inflammation, because biopsy is rarely done on the spinal cord
because of the damage this would cause. The physician would next send blood for general bloodwork and studies for
SLE and Sjogren's syndrome, HIV infection, vitamin B12 level to rule out deficiency and a test for syphilis. The next
test which is commonly performed is a lumbar puncture to obtain fluid for studies, including white cell count and
protein to look for inflammation, cultures to look for infections of various types, and tests to examine for abnormal
activation of the immune system (immunoglobulin level and protein electrophoresis). A MRI of the brain is often
performed to screen for lesions suggestive of MS. If none of these tests are suggestive of a specific cause, the patient is
presumed to have idiopathic transverse myelitis or parainfectious transverse myelitis, if there are other symptoms to
suggest an infection.
 The MRI picture characteristic of idiopathic transverse myelitis
1. A centrally located multisegmental (3 to 8 spinal segments) MRI T2 hyperintensity that occupies more
than two thirds of the cross-sectional area of the cord is characteristic of transverse myelitis. The MRI T2
hyperintensity commonly shows a slow regression with clinical improvement. The central spinal cord MRI
T2 hyperintensity represents evenly distributed central cord edema. MRI T1 Hypointensity might be
present in the same spinal segments that show T2 hyperintensity although to a lesser extent. The MRI T2
hyperintensity is central, bilateral, more or less symmetrical and multisegmental.
2. MRI T2 central isointensity, or dot (within and in the core of the MRI T2 hyperintensity) might be present
and is believed to represent central gray matter squeezed by the uniform, evenly distributed edematous
changes of the cord. (central dot sign). It might not be of any clinical significance.
3. Contrast enhancement is commonly focal or peripheral and maximal at or near the segmental MRI T2
hyperintensity. In idiopathic transverse myelitis enhancement is peripheral to the centrally located area of
high T2 signal intensity rather than in the very same area. The prevalence of cord enhancement is
significantly higher in patients with cord expansion.
4. Spinal cord expansion might or might not be present and when present is usually multisegmental and
better appreciated on the sagittal MRI T1 images. Spinal cord expansion tapers smoothly to the normal
cord, and is of lesser extent than the high T2 signal abnormality.
5. Multiple sclerosis plaques (and subsequent T2 hyperintensity) are located peripherally, are less than 2
vertebral segments in length, and occupies less than half the cross-sectional area of the cord. In contrast to
transverse myelitis, enhancement in MS occurs in the same location of high-signal-intensity lesions seen on
T2-weighted images. (See Fig. 9)
Table 2. Differences between idiopathic transverse myelitis and spinal multiple sclerosis
Number
T2 of
Disease entity Contrast element Pathology
hyperintensity segments
involved
Idiopathic transverse Central, 4-8 In transverse myelitis Nonspecific necrosis that affects
myelitis multisegmental enhancement is peripheral to the gray and white matter
centrally located area of high T2 indiscriminately and destroys
signal intensity rather than in axons and cell bodies as well as
the very same area. myelin.
Spinal multiple Peripheral 1-2 In contrast to transverse White matter demyelination
sclerosis myelitis, enhancement in MS only.
occurs in the same location of
high-signal-intensity lesions seen
on T2-weighted images.

10. Figure 10. MRI T1 precontrast (A,B,C,D) and postcontrast (E,F,G) and MRI
T2 image (H) showing a case of acute idiopathic transverse myelitis, notice
cord swelling in the cervico dorsal region with patchy irregular and peripheral
contrast enhancement. Also notice the central T2 hyperintensity. Peripheral
contrast enhancement is outside and peripheral to the central T2
hyperintensity.
MRIs are uninformative in a large number of patients with acute transverse myelitis. There is a relatively good
differentiation on MRI between MS-associated acute transverse myelitis and parainfectious-associated acute
transverse myelitis. Patients with MS-associated acute transverse myelitis show small plaque-like lesions (partial
myelopathy), and those patients with parainfectious acute transverse myelitis show swelling of the spinal cord if they
have abnormalities on MRI.
Figure 11. A case with acute idiopathic transverse myelitis. Notice spinal cord swelling and the MRI T2 central
hyperintensity. Also notice the involvement of the complete cross section of the spinal cord.

11. Figure 12. A case with acute idiopathic transverse myelitis. Notice spinal cord swelling and the MRI T2 central signal
changes. Also notice the involvement of the complete cross section of the spinal cord.
Figure 13. A, Transverse Myelitis. B, Myelitis in ADEM

12. Figure 14. MS-myelitis is more peripheral and more likely
to involve less than half of the cross-sectional cord area.
ACUTE IDIOPATHIC TRANSVERSE MYELITIS
 Introduction
Acute transverse myelitis (ATM) is a group of disorders characterized by focal inflammation of the spinal cord and
resultant neural injury. Acute Transverse Myelitis may be an isolated entity or may occur in the context of multifocal
or even multisystemic disease. It is clear that the pathologic substrate-injury and dysfunction of neural cells within the
spinal cord- may be caused by a variety of immunologic mechanisms. For example, in acute Transverse Myelitis
associated with systemic disease (i.e. systemic lupus erythematosus or sarcoidosis), a vasculitic or granulomatous
process can often be identified. In idiopathic acute Transverse Myelitis, there is an intraparenchymal and/or
perivascular cellular influx into the spinal cord resulting in breakdown of the blood-brain barrier and variable
demyelination and neuronal injury.
There are several critical questions that must be answered before we truly understand acute Transverse Myelitis: 1)
what are the various triggers for the inflammatory process that induces neural injury in the spinal cord; 2) what are
the cellular and humoral factors that induce this neural injury and 3) is there a way to modulate the inflammatory
response in order to improve patient outcome. Although much remains to be elucidated about the causes of acute
Transverse Myelitis, tantalizing clues as to potential immunopathogenic mechanisms in acute Transverse Myelitis and
related inflammatory disorders of the spinal cord have recently emerged. It is the purpose of this review to illustrate
recent discoveries that shed light on this topic, relying when necessary on data from related diseases such as acute
disseminated encephalomyelitis (ADEM), Guillain-Barre syndrome (GBS) and Neuromyelitis Optica (NMO).
Developing further understanding of how the immune system induces neural injury will depend upon confirmation
and extension of these findings and will require multicenter collaborative efforts.
Acute transverse myelitis (ATM) is group of poorly understood inflammatory disorders resulting in neural injury to
the spinal cord. It is unclear what are the triggers and effector mechanisms resulting in neural injury, though
tantalizing clues have emerged. acute Transverse Myelitis exists on a continuum of neuroinflammatory disorders that
also includes Guillain-Barre syndrome (GBS), multiple sclerosis (MS), acute disseminated encephalomyelitis (ADEM)
and Neuromyelitis Optica (NMO). Each of these disorders differs in the spatial and temporal restriction of
inflammation within the nervous system. However, clinical and pathologic studies support the notion that there are
many common features of the inflammation and neural injury. In the current review, we will examine recent evidence
that shed light on the immunopathogenesis of acute Transverse Myelitis and, where applicable, related
neuroinflammatory disorders. These studies point to a variety of humoral and cellular immune derangements that
potentially result in neuronal injury and demyelination. Further advances in understanding the immunopathogenesis
of acute Transverse Myelitis will require controlled studies with epidemiologic and clinical-pathologic correlation. It is
only then that we will be able to establish rational intervention strategies designed to improve the outcome of patients
with acute Transverse Myelitis.
 History of acute transverse myelitis
Several cases of “acute myelitis” were described in 1882, and pathologic analysis revealed that some were due to

13. vascular lesions and others to acute inflammation [1,2] . In 1922 and 1923, physicians in England and Holland became
aware of a rare complication of smallpox vaccination: inflammation of the spinal cord and brain [3] . Given the term
post-vaccinal encephalomyelitis, over 200 cases were reported in those two years alone. Pathologic analyses of fatal
cases revealed inflammatory cells and demyelination.” In 1928, it was first postulated that many cases of acute myelitis
are “post-infectious rather than infectious in cause” since for many patients, the “fever had fallen and the rash had
begun to fade” when the myelitis symptoms began [4] . It was proposed, therefore, that the myelitis was an “allergic”
response to a virus rather than the virus itself that caused the spinal cord damage. It was in 1948 that the term “acute
transverse myelitis” was utilized in reporting a case of fulminant inflammatory myelopathy complicating pneumonia
[5] .
 Diagnosis of acute transverse myelitis
Acute transverse myelitis (ATM) is an inflammatory process affecting a restricted area of the spinal cord. It is
characterized clinically by acutely or subacutely developing symptoms and signs of neurological dysfunction in motor,
sensory and autonomic nerves and nerve tracts of the spinal cord. There is often a clearly defined rostral border of
sensory dysfunction and a spinal MRI and lumbar puncture shows evidence of acute inflammation (CSF culture and
sensitivity should always be carried out to rule out bacterial, fungal, parasitic infections, see table 1). When the
maximal level of deficit is reached, approximately 50% of patients have lost all movements of their legs, virtually all
patients have some degree of bladder dysfunction, and 80-94% of patients have numbness, paresthesias or band like
dysesthesias [6-8,9,10,11] . Autonomic symptoms consist variably of increased urinary urgency, bowel or bladder
incontinence, difficulty voiding, or bowel constipation [12].
MRI characteristics of acute idiopathic transverse myelitis
 Involvement of the whole cross section of the spinal cord. Partial myelopathy (either on clinical examination or on
MRI imaging) should rule out acute idiopathic transverse myelitis.
 The lesion induces swelling of the spinal cord in the involved segments in the acute stage
 The lesion has the following MRI characteristics (see above for MRI characteristics of transverse myelitis)
 A centrally located multisegmental (3 to 8 spinal segments) MRI T2 hyperintensity that occupies more than two
thirds of the cross-sectional area of the cord is characteristic of transverse myelitis. The MRI T2 hyperintensity
commonly shows a slow regression with clinical improvement. The central spinal cord MRI T2 hyperintensity
represents evenly distributed central cord edema. MRI T1 Hypointensity might be present in the same spinal
segments that show T2 hyperintensity although to a lesser extent. The MRI T2 hyperintensity is central, bilateral,
more or less symmetrical and multisegmental.
 MRI T2 central isointensity, or dot (within and in the core of the MRI T2 hyperintensity) might be present and is
believed to represent central gray matter squeezed by the uniform, evenly distributed edematous changes of the
cord. (central dot sign). It might not be of any clinical significance.
 Contrast enhancement is commonly focal or peripheral and maximal at or near the segmental MRI T2
hyperintensity. In idiopathic transverse myelitis enhancement is peripheral to the centrally located area of high
T2 signal intensity rather than in the very same area. The prevalence of cord enhancement is significantly higher
in patients with cord expansion.
 Spinal cord expansion might or might not be present and when present is usually multisegmental and better
appreciated on the sagittal MRI T1 images. Spinal cord expansion tapers smoothly to the normal cord, and is of
lesser extent than the high T2 signal abnormality.
 Multiple sclerosis plaques (and subsequent T2 hyperintensity) are located peripherally, are less than 2 vertebral
segments in length, and occupies less than half the cross-sectional area of the cord. In contrast to transverse
myelitis, enhancement in MS occurs in the same location of high-signal-intensity lesions seen on T2-weighted
images. (See Fig. 9)
 Intramedullary lesions that can simulate acute idiopathic transverse myelitis on clinical background can easily be ruled
out by MRI

14.  In the author experience, acute idiopathic transverse myelitis occurred exclusively in the lower cervical and/or the
upper dorsal spinal cord regions. Evolvement of other regions of the spinal cord should direct the attention to disease -
associated transverse myelopathy. (See table 1)
 Classification of acute transverse myelitis
Recently, a diagnostic and nosology scheme has been proposed which defines acute Transverse Myelitis according to
the inclusion and exclusion criteria set forth in Table 3 [13] . These criteria have attempted to define acute Transverse
Myelitis as a monofocal inflammatory process of the spinal cord and to distinguish it from non-inflammatory
myelopathies (i.e. radiation-induced myelopathy or ischemic vascular myelopathy). It further attempts to distinguish
various etiologies for acute Transverse Myelitis. Thus, two diagnostic categories of “idiopathic acute Transverse
Myelitis” and “disease-associated acute Transverse Myelitis” (i.e. SLE associated acute Transverse Myelitis) are
proposed, provided that other criteria are met. Disease-associated acute Transverse Myelitis is diagnosed when the
patient meets standard criteria for other known inflammatory diseases (e.g. multiple sclerosis, sarcoidosis, systemic
lupus erythematosus, Sjogren’s syndrome) or direct infection of the spinal cord. When an extensive search fails to
determine such a cause, idiopathic acute Transverse Myelitis is defined.
Table 3: Idiopathic acute transverse myelitis criteria
Inclusion criteria
 Development of sensory, motor or autonomic dysfunction attributable to the spinal cord
 Bilateral signs and/or symptoms (though not necessarily symmetric)
 Clearly-defined sensory level
 Exclusion of extra-axial compressive etiology by neuroimaging (MRI)
 Inflammation within the spinal cord demonstrated by CSF pleocytosis or Elevated IgG index or gadolinium
enhancement. If none of the inflammatory criteria is met at symptom onset, repeat MRI and LP evaluation between 2-
7 days following symptom onset meets criteria
 Progression to nadir between 4 hours to 21 days following the onset of symptoms (if patient awakens with symptoms,
symptoms must become more pronounced from point of awakening)
Exclusion criteria
 History of previous radiation to the spine within the past 10 years, history of drug abuse especially heroin
 Clear arterial distribution clinical deficit consistent with thrombosis of the anterior spinal artery
 Abnormal flow voids on the surface of the spinal cord c/w AVM
 *Serologic or clinical evidence of connective tissue disease (sarcoidosis, Behcet’s disease, Sjogren’s syndrome, SLE,
mixed connective tissue disorder etc)
 *CNS manifestations of syphilis, Lyme disease, HIV, HTLV-1, mycoplasma, other viral infection (e.g. HSV-1, HSV-2,
VZV, EBV, CMV, HHV-6, enteroviruses),
 CNS manifestations of vasculitis, schistosomiasis
 *Brain MRI abnormalities suggestive of MS
 *History of clinically apparent optic neuritis
*Do not exclude disease-associated ATM
ACUTE TRANSVERSE MYELITIS / MYELOPATHY IS A TERMINOLOGY THAT HAS NO AETIOLOGICAL
IMPLICATIONS, IT IS SIMPLY A CLINICAL DIAGNOSIS WHICH MEANS COMPLETE TRANS-
SECTIONAL PATHOLOGICAL INVOLVEMENT OF THE SPINAL CORD WITH AN ACUTE ONSET.
ALWAYS LOOK FOR AN AETIOLOGICAL FACTOR. ACUTE IDIOPATHIC TRANSVERSE MYELITIS IS A
DIAGNOSIS BY EXCLUSION.
 Immunopathogenesis of acute transverse myelitis.
The immunopathogenesis of disease-associated acute Transverse Myelitis is varied. For example, pathologic data
confirms that many cases of lupus-associated TM are associated with a CNS vasculitis [14-16] while others may be
associated with thrombotic infarction of the spinal cord [17,18] . Neurosarcoid is often pathologically associated with
non-caseating granulomas within the spinal cord [19] , while TM associated with MS often has perivascular

15. lymphocytic cuffing and mononuclear cell infiltration immunopathogenic and with variable complement and antibody
deposition [20] . Since these diseases have such varied (albeit poorly understood) immunopathogenic and effector
mechanisms, these diseases will not be further discussed here. Rather, the subsequent discussion will focus on findings
potentially related to idiopathic acute Transverse Myelitis.
 Post-vaccination acute transverse myelitis
Several reports of acute Transverse Myelitis following vaccination have been recently published. Indeed, it is widely
reported in neurology texts that acute Transverse Myelitis is a post-vaccination event. One publication reports a case
of post flu vaccine myelitis in which a 42 year-old male with a history of bilateral optic neuritis developed acute
Transverse Myelitis 2 days following an influenza vaccine [21] . A separate study reports a 36 year old male who
developed a progressive and ultimately fatal, inflammatory myelopathy/polyradiculopathy 9 days following a booster
Hepatitis B vaccination [22] . The patient had no fever or systemic illness and did not respond to extensive
immunotherapy. Autopsy evaluation of the spinal cord revealed severe axonal loss with mild demyelination and a
mononuclear infiltrate, predominantly T-lymphocytes in nerve roots and spinal ganglia. The spinal cord had
perivascular and parenchymal lymphocytic cell infiltrates in the grey matter, especially the anterior horns. The
suggestion from these studies is that a vaccination may induce an autoimmune process resulting in acute Transverse
Myelitis. However, it should be noted that extensive data continues to overwhelmingly show that vaccinations are safe
and are not associated with an increased incidence of neurologic complications [23-30] . Therefore, such case reports
must be viewed with caution, as it is entirely possible that two events occurred in close proximity by chance alone.
 Parainfectious acute transverse myelitis
In 30-60% of the idiopathic acute Transverse Myelitis cases, there is an antecedent respiratory, GI or systemic illness
[6-10,31,32] . The term “parainfectious” has been used to suggest that the neurologic injury may be associated with
direct microbial infection and injury as a result of the infection, direct microbial infection with immune-mediated
damage against the agent, or remote infection followed by a systemic response that induces neural injury. An
expanding list of antecedent infections is now recognized, though in the vast majority of these cases, causality cannot
be established. Several of the herpes viruses have been associated with myelitis and are likely due to direct infection of
neural cells within the spinal cord [33-35] . Other agents, such as Listeria monocytogenes may be transported
intraaxonally to neurons in the spinal cord [36] . By using such a strategy, an agent may be able to gain access to a
relatively immune privileged site, avoiding the immune surveillance present in other organs. Such a mechanism may
also explain the limited inflammation to a focal region of the spinal cord seen in some patients with acute Transverse
Myelitis.
Though in these cases, the infectious agent is required within the CNS, other mechanisms of autoimmunity, such as
molecular mimicry and superantigen-mediated disease, require only peripheral immune activation and may account
for other cases of acute Transverse Myelitis.
 Molecular Mimicry
Molecular mimicry as a mechanism to explain an inflammatory nervous system disorder has been best described in
GBS. First referred to as an “acute post-infectious polyneuritis” by W. Osler in 1892, GBS is preceded in 75% of cases
by an acute infection [37-40] . Campylobacter jejuni infection has emerged as the most important antecedent event in
GBS, occurring in up to 41% of cases [41-44] . Human neural tissue contains several subtypes of ganglioside moieties
such as GM1, GM2 and GQ1b within their cell walls [45,46] . A characteristic component of human gangliosides, sialic
acid [47] , is also found as a surface antigen on C. jejuni within its lipopolysaccharide (LPS) outer coat [48] .
Antibodies that cross-react with gangliosides from C. jejuni have been found in serum from patients with GBS [49-51]
and have been shown to bind peripheral nerves, fix complement and impair neural transmission in experimental
conditions that mimic GBS [45,52,53,54] .
Susceptibility to the development of GBS is dependent upon both strain-specific features of the C. jejuni and host
genetic factors. Enterogenic strains of C. jejuni differ from strains likely to induce GBS [44,46,55,56] . However, the
susceptibility to develop GBS also depends on host genetic factors. In a recent study, several members of the same
family became infected with a single strain of C. jejuni, yet only one patient developed a humoral response against the
LPS extract and that patient was the only one to develop GBS [57] . Additionally, recent studies have suggested a
predominance of certain HLA alleles- HLA-B35, HLA-B54, HLA-Cwl and HLA-DQB1*0- in GBS patients, suggesting
a genetic restriction [41,58] .

16. Molecular mimicry in acute Transverse Myelitis may also occur and may be associated with the development of
autoantibodies in response to an antecedent infection. One acute Transverse Myelitis patient developed elevated titers
of lupus anticoagulant IgG, antisulfatide antibodies (1:6400) and anti-GM1 antibodies (1:600 IgG and 1:3200 IgM)
following Enterobium vermicularis (perianal pinworm) infection [59] . Since E. vermicularis has been shown to
contain cardiolipin, ganglioside GM1, and sulfatides within their lipid composition, it was postulated that in the proper
genetic and hormonal background, the infection triggered the pathogenic antibodies. Several additional studies have
suggested how this process could cause neural injury and will be discussed below.
 Microbial superantigen-mediated inflammation
Another link between an antecedent infection and the development of acute Transverse Myelitis may be the fulminant
activation of lymphocytes by microbial superantigens (SAGs). SAGs are microbial peptides that have a unique
capacity to stimulate the immune system and may contribute to a variety of autoimmune diseases. The best-studied
superantigens are staphylococcal enterotoxins A through I, toxic shock syndrome toxin-1 and Streptococcus pyogenes
exotoxin, though many viruses encode superantigens as well [60-63] . SAGs activate T-lymphocytes in a unique
manner compared to conventional antigens: instead of binding to the highly variable peptide groove of the T cell
receptor (TCR), SAGs interact with the more conserved Vb region [64,65-67] . Additionally, unlike conventional
antigens, SAGs are capable of activating T lymphocytes in the absence of co-stimulatory molecules. As a result of these
differences, a single superantigen may activate between 2-20% of circulating T-lymphocytes compared to 0.001-0.01%
with conventional antigens [68-70] . Interestingly, SAGs often cause expansion followed by deletion of T lymphocyte
clones with particular Vß regions resulting in “holes” in the T lymphocyte repertoire for some time following the
activation [64-67,71] . Therefore, patients can often be tested for presumptive evidence of previous superantigen
exposure through TCR Vß usage frequencies.
Stimulation of large numbers of lymphocytes may trigger autoimmune disease by activating autoreactive T-cell clones
[72,73] . In humans, there are multiple reports of expansion of selected Vß families in patients with autoimmune
diseases suggesting a previous superantigen exposure [72,74] . Since this limited expansion was not seen in serum and
non-inflamed tissues, it was proposed that SAG activated previously quiescent autoreactive T cells which then entered
a tissue and were retained in that tissue by repeat exposure to the autoantigen [75] . In the central nervous system,
SAG isolated from Staphlococcus induced paralysis in mice with experimental autoimmune encephalomyelitis (EAE)
through its ability to directly stimulate Vb8-expressing T-cells specific for the MBP peptide Ac1-11 [68,69,76] . In
humans, a patient with ADEM and necrotizing myelopathy was found to have Strep pyogenes SAG-induced T cell
activation against myelin basic protein [77] .
 Humoral derangements
Either of the above processes may result in abnormal immune function with blurred distinction between self and non-
self. The development of abnormal antibodies potentially may then activate other components of the immune system
and/or recruit additional cellular elements to the spinal cord. Recent studies have emphasized distinct autoantibodies
in patients with NMO [78-82] and recurrent acute Transverse Myelitis [83-85] . The high prevalence of various
autoantibodies seen in such patients suggests polyclonal derangement of the immune system.
However, it may not just be autoantibodies, but high levels of even normal circulating antibodies that have a causative
role in acute Transverse Myelitis. A case of acute Transverse Myelitis was described in a patient with extremely high
serum and CSF antibody levels to hepatitis B surface antigen following booster immunization [86] . Such circulating
antibodies may form immune complexes that deposit in focal areas of the spinal cord. Such a mechanism has been
proposed to describe a patient with recurrent TM and high titers of hepatitis B surface antigen [87] . Circulating
immune complexes containing HbsAg were detected in the serum and CSF during the acute phase and the
disappearance of these complexes following treatment correlated with functional recovery.
Several Japanese patients with acute Transverse Myelitis were found to have much higher serum IgE levels than MS
patients or controls (360 vs. 52 vs. 85 U/ml) [88] . Virtually all of the patients in this study had specific serum IgE to
household mites (Dermatophagoides pteronyssinus or Dermatophagoides farinae), while less than 1/3 of MS and
control patients did. One potential mechanism to explain the acute Transverse Myelitis in such patients is the
deposition of IgE with subsequent recruitment of cellular elements. Indeed, biopsy specimens of two acute Transverse
Myelitis patients with elevated total and specific serum IgE revealed antibody deposition within the spinal cord,
perivascular lymphocyte cuffing and infiltration of eosinophils [89] . It was postulated that eosinophils, recruited to the
spinal cord degranulated and induced the neural injury in these patients.

17. Recently, several reports have suggested that elevated prolactin levels occur in some patients with NMO [90,91] . The
elevated prolactin was limited to Asian and black women and correlated with involvement of the optic nerve. It
therefore may be that extension of inflammation to the hypothalamus results in diminished hypothalamic dopamine
and increased pituitary secretion of prolactin. Further, since prolactin is a potent immune stimulant for Th1
responses, it is possible that the enhanced prolactin leads to augmentation of disease activity elsewhere in the neuraxis.
It may even be that autoantibodies initiate a direct injury of neurons. A particular pentapeptide sequence found on
microbial agents is a molecular mimic of dsDNA, and antibodies raised against this sequence react against dsDNA
[92] . This pentapeptide sequence is also present in the extracellular region of the glutamate receptor subunits NR2a
and NR2b, present on neurons in the CNS. dsDNA antibodies recognize glutamate receptors in vitro and in vivo, and
can induce neuronal death. Other studies have shown that the IgG repertoire from active plaque and periplaque
regions in MS brain and from B cells from the CSF of a patient with MS are comprised of anti DNA antibodies [93] .
These antibodies bind to the surface of neuronal cells and oliogdendrocytes. Hence, molecular mimicry may cause the
development of antibodies that interact with neuronal surface proteins and induce neural injury through the
activation of neural pathways.
 Potential treatment options in acute transverse myelitis
There currently is no treatment that has been clearly shown to modulate outcome in patients with acute Transverse
Myelitis. Indeed, with such varied immunopathogenesis, it may be that distinct treatment options need be employed
for different subsets of acute Transverse Myelitis patients. Recent studies that have investigated potential strategies to
modulate neural injury associated with acute Transverse Myelitis will be reviewed.
 Methylprednisolone
Based on the presumptive immunopathogenic mechanisms in acute Transverse Myelitis, several recent studies have
investigated a role for intravenous methylprednisolone (MP) in the acute phase. Both studies evaluated a series of
patients with acute Transverse Myelitis treated with methylprednisolone in open-label studies [94,95,96] . Two of these
studies suggested a role for methylprednisolone in small, open label trials [94,96] , while one suggested no
improvement in outcome [95] . In one study, 12 children with severe acute Transverse Myelitis were treated with MP
and were compared with a historical group of 17 patients. Follow up evaluation revealed the following in the MP vs.
non-MP group: 66% vs. 17.6% walking independently at one month; 54.6 vs. 11.7 % full recovery at one year; and 25
days vs. 120 days median time to independent walking. Subsequently, in a multicenter open label study of 12 children
with severe acute Transverse Myelitis, outcome measures were compared to historical controls and suggested a
beneficial outcome at one month and one year [94] .
However, in a prospective, hospital-based study, outcome evaluations and electrophysiologic studies were used to
evaluate a potential effect of methylprednisolone in 21 acute Transverse Myelitis patients [95] . It was found that
patients in both groups with positive physiologic studies (recordable central conduction time on evoked potential and
absent denervation) improved, while those with negative physiologic studies did not. There was no observed difference
in the outcome due to methylprednisolone both in patients with mild and severe symptoms.
Therefore, there remains uncertainty as to the beneficial effect of steroids in acute Transverse Myelitis, though this
treatment is widely offered to patients in the acute phase. The limitations in these studies - heterogeneous patient
population, small study size, open label and the use of historical control population-necessitate the conclusion that
further definition of a role for steroids in acute Transverse Myelitis will require controlled studies on more defined
patient populations.
 Cyclophosphamide
Several reports have suggested a role for cyclophosphamide and steroids in lupus-associated acute Transverse Myelitis
[97-99] . However, the role for immunomodulatory treatments in other forms of acute Transverse Myelitis remains
unclear.
 Plasma exchange
Plasma exchange (PE) was recently shown to be effective in patients with severe, isolated CNS demyelination
[100,101] . In this randomized, sham-controlled, crossover-design study, 44% of patients with severe inflammatory

18. demyelination who had not responded to steroids improved following plasma exchange. It has been reasoned that the
plasma exchange may remove humoral factors (including antibodies, endotoxins and/or cytokines) contributing to the
inflammation.
 CSF filtration
CSF filtration (CSFF) was recently proposed and investigated for patients with the related monophasic inflammatory
disease GBS [102] . In this study 37 patients were randomized to receive CSFF or plasma exchange during the acute
phase of GBS. CSFF consisted of placement of a spinal catheter then removal of 30-50 cc of CSF via a filter bypass
designed for the elimination of cells, bacteria, endotoxins, immunoglobulins and inflammatory mediators. A filtration
session comprised several such cycles (5-6 times, each of 30-50 cc), repeated daily for 5-15 consecutive days compared
to standard PE regimen for GBS. CSFF showed equal effectiveness compared to PE with fewer complications. The
rationale for this treatment-that cellular or humoral factors in the CSF may be contributing to dysfunction and injury
of peripheral nerves and nerve roots-is even stronger in acute Transverse Myelitis patients in which the inflammation
is largely or entirely within the central nervous system. Therefore, it is worthwhile of further investigation in such
patients.
 Protective Autoimmunity
Though this review has focused on how the immune system may damage the neural system, recent evidence suggests
that in certain situations, the immune system may play a role in recovery from spinal cord injury [103,104] . In these
studies, active or passive immunization of animals against central nervous system antigens resulted in improved
functional status and diminished neuronal death following spinal cord contusion. The benefit was mediated by T
lymphocytes and may indicate that removal of damaged neural tissue facilitates enhanced recovery.
 Conclusion
In summary, emerging evidence suggests that a variety of immune stimuli, through such processes as molecular
mimicry or superantigen-mediated immune activation, may trigger the immune system to injure the nervous system.
Activation of previously quiescent autoreactive T-lymphocytes or the generation of humoral derangements may be
effector mechanisms in this process. Several recent studies have highlighted the importance of specific immune system
components in inducing neural injury: IgE and hypereosinophilia, autoantibodies, complement fixation, and
deposition of immune complexes within the spinal cord. It is our current challenge to define clinical, genetic and
serologic characteristics which predict this pathologic heterogeneity. Only then can rational, targeted therapies be
envisioned.
Before diagnosis of acute idiopathic transverse myelitis, you should consider the following points (see table 1)
 Try to rule out disease - associated transverse myelopathy that might have a clinical picture similar to the clinical
picture of acute idiopathic transverse myelitis
 MRI should be carries out to rule out non- inflammatory causes of acute myelopathy such as ischemic, arterial,
venous, watershed or arteriovenous malformation, arteriovenous fistula, radiation myelopathy, tumor infiltration
or intramedullary inflammatory process with abscess formation.
 CSF culture and sensitivity should always be carried out to rule out bacterial, fungal, parasitic infections, always
consider early inflammatory myelopathy with early false negative result (repeat Lumbar culture in 2-7 days)
 Serological evidence of collagen disease, vasculitis, should be looked for (see table 1)
 Diseases like antiphospholipid syndrome, sarcoidosis, bilharziasis etc. should be ruled out (see table 1)
 Demyelinating diseases like multiple sclerosis, acute disseminated encephalomyelitis, or neuromyelitis optica
should be ruled out by brain MRI

19. SUMMARY
SUMMARY
Over the past decade, researchers and clinicians have gained new insights into the core of demyelinating diseases of the
spinal cord, and much progress has been made in the management of these diseases. Although we are starting to
uncover some of the structural and physiologic substrates of demyelination of the CNS, we are far from understanding
what causes many of these demyelinating disorders and how to prevent their progression. With further development of
new techniques, such as DTI and more potent MR units, spinal cord diseases may be distinguished from each other,
and effective therapeutic strategies may be initiated before any cord damage occurs (Fig. 17).
In particular MRI is very helpful in differentiation between Spinal multiple sclerosis and transverse myelitis In the
series reported by Choi et al, [59] the centrally located MRI T2 high signal intensity occupied more than two thirds of
the cross-sectional area of the cord in transverse myelitis. In multiple sclerosis, plaques are usually located
peripherally and occupy less than half the cross-sectional area of the cord. The central isointensity, or dot (commonly
seen in transverse myelitis), represents central gray matter squeezed by the uniform, evenly distributed oedematous
changes of the cord. Choi and colleagues [59] have demonstrated the role of contrast media in differentiating
transverse myelitis from multiple sclerosis. In transverse myelitis, enhancement is in the periphery of a centrally
located area of high T2 weighted images. In multiple sclerosis, the lesions show enhancement in the central zone of
peripherally located high signal intensity on T2 weighted images. [74]
In conclusion, certain MRI characteristics help in differentiating acute transverse myelitis from spinal form of
multiple sclerosis. These include: 1) centrally located high intensity signal extending over 3 to 4 segments and
occupying more than two thirds of the cord cross-sectional area and 2) peripheral contrast enhancement of high
intensity signal.

20. Figure 15. Differential diagnoses of intramedullary lesions based on their location at the cross-sectional area of the
cord. (A) MS: Dorsally located wedge-shaped lesion involving less then two thirds of the cross-sectional area of the
spinal cord seen on axial T2-Wi MR image. (B) Poliomyelitis: Bilateral enhancing anterior nerve roots demonstrated
on postcontrast T1-Wi MR image. (C) Vacuolar myelopathy: Bilateral, symmetrical, high-signal-intensity abnormality
located dorsally in the spinal cord in an HIV-positive patient. DD: Subacute combined degeneration. (D) ATM: On
axial T2-Wi, a high-signal-intensity lesion involving more than two thirds of cross-sectional area of the spinal cord is
observed. (E) Herpes-simplex-virus myelitis: Postcontrast T1-Wi axial MR image showing nodular enhancing lesion
located in the lateral part of the cervical spinal cord. DD: active MS plaque. (F) Spinal cord infarction: Swelling of the
anterior parts of the spinal cord is shown on axial T2-Wi MR images, indicating vulnerability of the anterior portions
of the spinal cord to ischemia.
 Addendum
 A new version of this PDF file (with a new case) is uploaded in my web site every week (every Saturday and
remains available till Friday.)

21.  To download the current version follow the link quot;http://pdf.yassermetwally.com/case.pdfquot;.
 You can also download the current version from my web site at quot;http://yassermetwally.comquot;.
 To download the software version of the publication (crow.exe) follow the link:
http://neurology.yassermetwally.com/crow.zip
 The case is also presented as a short case in PDF format, to download the short case follow the link:
http://pdf.yassermetwally.com/short.pdf
 At the end of each year, all the publications are compiled on a single CD-ROM, please contact the author to know
more details.
 Screen resolution is better set at 1024*768 pixel screen area for optimum display.
 For an archive of the previously reported cases go to www.yassermetwally.net, then under pages in the right
panel, scroll down and click on the text entry quot;downloadable case records in PDF formatquot;
REFERENCES
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such a mechanism, Listeria causes a focal encephalitis or Myelitis depending on the route of entry.
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24. 49 Gregson NA, Rees JH, Hughes RA. Reactivity of serum IgG anti-GM1 ganglioside antibodies with the
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51 Hao Q, Saida T, Kuroki S, Nishimura M, Nukina M, Obayashi H et al. Antibodies to gangliosides and
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52 Goodyear CS, O'Hanlon GM, Plomp JJ, Wagner ER, Morrison I, Veitch J et al. Monoclonal antibodies raised
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53 Plomp JJ, Molenaar PC, O'Hanlon GM, Jacobs BC, Veitch J, Daha MR et al. Miller Fisher anti-GQ1b antibodies:
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An important study which shows how autoantibodies, generated through a molecular mimicry mechanism, have the
potential to diminish neuronal conduction
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