Fact Sheet

Transverse
Myelitis

TM

Revised 4/12/2021 | This information sheet has been reviewed and approved by members of SRNA’s
Medical and Scientific Council.
TM Fact Sheet 2

Myelitis roughly translates to “spinal cord inflammation”,

which can result from an infection or inflammatory cause. The
term transverse myelitis (TM) has been adopted to describe
inflammation of the spinal cord due to a misdirected immune
response, resulting in varying degrees of weakness, sensory
alterations, and autonomic dysfunction (the part of the nervous
system that controls involuntary activity, such as the heart,
breathing, the digestive system, and reflexes). Reports describing
TM date back to the 1880s, but the first known use of “transverse
myelitis” is in 1931, where it was used to describe inflammatory
changes across the anatomical “transverse” plane seen on
autopsy. The Transverse Myelitis Consortium Working Group
provided a framework to delineate TM from non-inflammatory
spinal cord disorders in 2002.1

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TM Fact Sheet 3

Epidemiology

TM has a conservatively estimated incidence of between 1 and 8 new cases per

million per year, or approximately 1,400 new cases each year in the US.2-6 Although
this disease affects people of all ages, there are peaks between the ages of 10
to 19 years and 30 to 39 years.4-6 In addition, approximately 25% of cases are in
children.7 There is no gender or familial association with TM.8 In 75-90% of cases
TM is monophasic, yet a small percentage experience recurrent disease, especially
if there is a predisposing underlying illness.9-11

Signs and Symptoms

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. TM generally presents with rapidly
progressing muscle weakness or paralysis, beginning with the legs and potentially moving
to the arms with varying degrees of severity.12-14 The arms are involved in a minority of
cases and this is dependent upon the level of spinal cord involvement.12-14 Sensation is
diminished below the level of spinal cord involvement in the majority of individuals.12 Pain
(ascertained as appreciation of pinprick by the neurologist) and temperature sensation
are generally diminished and appreciation of vibration (as caused by a tuning fork) and
joint position sense may also be decreased. Many report a tight banding or girdle-like
sensation around the trunk, and that area may be very sensitive to touch.12

In most cases, a sensory level is documented, most commonly in the mid-thoracic

region in adults or the cervical region in children.7 Pain in the back, extremities, or
abdomen is also common while paresthesias (e.g., tingling, numbness, burning
sensations) are typical in adults.12 Sexual dysfunction is also the result of sensory
and autonomic involvement.12,15-17 Increased urinary urgency, bowel or bladder
incontinence, difficulty or inability to void, and incomplete evacuation of bowel or
constipation are other characteristic autonomic symptoms.15-16 Spasticity and fatigue
are other symptoms common to transverse myelitis. Additionally, depression is often
documented in TM patients and must be treated to prevent devastating consequences.

In some cases, symptoms progress over hours whereas in other instances, the
presentation is over days. Neurologic function tends to decline during the 4-21-day
acute phase, while 80% of cases reach their maximal deficit within 10 days of symptom
onset.1,18 At its worst point, 50% of individuals have lost all movements of their legs,
80-94% experience numbness, paresthesias or banding or girdling, and almost all
have some degree of bladder dysfunction.12

Diagnosis

Diagnosis of TM is based on clinical features, imaging, and laboratory findings.

Clinical characteristics of spinal cord injury are bilateral signs and/or symptoms of
sensory, motor or autonomic dysfunction attributable to the spinal cord or a clearly
defined sensory level. Evaluation for signs of inflammation to distinguish TM from

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... Diagnosis

other spinal cord disorders typically involves a magnetic resonance imaging (MRI) of
the spine with contrast and spinal fluid analysis (which requires a lumbar puncture).19

If a myelopathy is suspected based on history and physical examination, a gadolinium-

enhanced magnetic resonance imaging (MRI) of the spinal cord is first obtained to
assess if there is a compressive or inflammatory (gadolinium enhancing) lesion, as
signs and symptoms can overlap. It is essential to rule out compressive myelopathy
(compression of the spinal cord), which can be caused by a tumor, herniated disc,
stenosis (a narrowed canal for the cord), hematoma or abscess. Identifying these
disorders is critical since immobilization to prevent further injury and early surgery to
remove the compression may sometimes reverse neurologic injury to the spinal cord.19

Lumbar puncture is used to look for surrogate markers of inflammation in the

cerebrospinal fluid (CSF). These include elevated white cell counts, elevated protein
or other markers such as oligoclonal bands. While these markers are supportive of
TM, it should be noted that they are not present in all individuals.19

A series of blood tests are often recommended for patients with spinal cord disorder
suspicious for TM. This commonly includes testing for aquaporin-4 and myelin
oligodendrocyte glycoprotein (MOG) antibodies, in addition to tests associated with
systemic autoimmune disorders such as systemic lupus erythematosus (SLE) and
Sjögren’s syndrome. If sarcoidosis is suspected based upon history and imaging
characteristics, a CT of the chest may be considered to look for lung findings. Other
common ordered tests include HIV, syphilis, vitamin B12 and copper levels.19

An MRI of the brain is often performed to screen for lesions suggestive of a

demyelinating disorder such as MS, NMOSD, or MOG antibody disease. In patients
with imaging features of TM that are consistent with MS, brain imaging may be
repeated over time to see if characteristic MS lesions develop.19

If none of the tests are suggestive of a specific cause, a diagnosis of idiopathic

transverse myelitis can be made.

Non-inflammatory myelopathies include those caused by arterial or venous ischemia

(blockage), vascular malformations, radiation, fibrocartilaginous embolism or nutritional/
metabolic causes. The work-up for suspected vascular spinal cord disorder may
include angiograms of the spinal cord vessels and blood testing for a predisposition
to developing blood clots.19

Potential Causes There are many disorders that can cause spinal cord inflammation, so TM should be
thought of as a group of disorders, and not a single condition. “Disease-associated
transverse myelitis” refers to TM that occurs in a patient with an identified autoimmune
disorder. Disorders such as neuromyelitis optica spectrum disorder and multiple
sclerosis are common causes of TM and may also cause inflammation in other
parts of the nervous system. Autoimmune disorders targeting other organs, such

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... Diagnosis

as Systemic Lupus Erythematosus,20-22 Sjogren’s syndrome,20,23,24 and sarcoidosis,25,26

are also known to cause TM.

Even after comprehensive medical evaluation, there remains a significant proportion

of individuals with spinal cord inflammation that is without a clear identifiable cause.
This is a condition called “idiopathic transverse myelitis”.19 When a healthcare provider
diagnoses someone with “transverse myelitis”, they are typically referring to idiopathic
TM. Even among those labeled as having idiopathic TM, it is likely that there are
multiple yet-to-be-identified causes for this inflammation.

TM may develop in the setting of a viral or bacterial infection, even if the symptoms
from the infection are mild. Approximately 30-60% of individuals with TM report a febrile
illness (flu-like illness with fever) around the time of neurologic symptoms.4-6,14,27-29
Certain infections, such as polio, enteroviruses, and herpes zoster, can directly infect
the cells of the spinal cord and cause injury.19 In other cases, damage may be mostly
due to the immune system’s response to the infection.19

Experts believe that in many cases, an infection triggers a misdirected immune

response without directly infecting the spinal cord. This is supported by evidence
that infections are an important factor in the development of autoimmune disorders
of different types. Infections may trigger autoimmunity through a variety of ways,
but one mechanism that has significant evidence is called molecular mimicry.13 This
theory postulates that an infectious agent may share a molecule that resembles or
mimics 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, resulting in TM.13

Although a causal relationship has not been established, TM has been rarely reported
following influenza and Hepatitis B vaccinations.13,30-32 One theory suggests that it
is possible that the vaccination may have excited the immune system, similar to
an infection. It is critically important to bear in mind that extensive research has
demonstrated that vaccinations are safe, and the potential link to TM may only be
coincidental or at worst an exceptionally rare complication.

Myelitis related to cancer (called a paraneoplastic syndrome) is quite rare.19,33 When

this occurs, the symptoms usually accrue over a much longer timeline (usually several
months) than is typical of other causes of myelitis. This is thought to occur due to
an immune response to proteins in the cancer cells that are also present on spinal
cord cells, resulting in a misdirected immune response.

Vascular causes are noted because they present with the same problems as transverse
myelitis.34 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 “stroke” of the spinal cord.

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TM Fact Sheet 6

Acute Treatments

It is extremely important to begin treatments as soon as possible after a rare

neuroimmune diagnosis. Treatment in the acute or early stages involves quieting down
the immune system as quickly as possible, before damage is done. Time is critical.

The acute therapies most frequently used to treat an inflammatory attack include: high
dose intravenous steroids (methylprednisolone), Plasmapheresis (Plasma Exchange
or PLEX), Immunoglobulin Therapy (IVIG), and cyclophosphamide.19,35

Intravenous Steroids Intravenous steroid treatment is the first line of therapy often used in acute TM.
Corticosteroids have multiple mechanisms of action including anti-inflammatory
activity, immunosuppressive properties, and antiproliferative actions. Though there
is no randomized double-blind placebo-controlled study that supports this approach,
evidence from related disorders and clinical experience support this treatment. The
standard of care includes intravenous methylprednisolone (30 mg/kg up to 1000
mg daily) or dexamethasone (120 to 200 mg daily for adults) for 3 to 5 days unless
there are compelling reasons to avoid this therapy.19 The decision to offer continued
steroids or to add a new treatment is often based on the clinical course and MRI
appearance at the end of 5 days of steroids.19,34

Plasma Exchange (PLEX) PLEX is often initiated in individuals with motor impairment36 or who show little clinical
improvement after intravenous steroid treatment,37-39 but may also be initiated at first
presentation for those with significant deficits.19 It is often given as five treatments,
each with exchanges of 1.1 to 1.5 plasma volumes, every other day for 10 days.40
PLEX is believed to work in autoimmune CNS diseases through the removal of specific
or nonspecific soluble factors likely to mediate, be responsible for, or contribute to
inflammatory-mediated organ damage. PLEX has been shown to be effective in adults
with TM and other inflammatory disorders of the CNS.

Other Immunomodulatory Treatment If there is continued progression despite intravenous steroid therapy and PLEX,
pulse dose intravenous cyclophosphamide (800–1200 mg/m2) is considered.19
Cyclophosphamide is known to have immunosuppressive properties. From the Johns
Hopkins TM Center experience, it has been reported that PLEX provided an added
benefit to steroids in patients who were not at a disability level of ASIA A and who did
not have a history of autoimmune disease. For those who were classified at a disability
level of ASIA A at their nadir, they showed a significant benefit when given combination
therapy with steroids, PLEX and IV cyclophosphamide.35 Cyclophosphamide should be
administered under the supervision of an experienced oncology team, and caregivers
should monitor the patient carefully for hemorrhagic cystitis and cytopenias.

Another option for treating acute inflammation is intravenous immunoglobulin (IVIG).

Immunoglobulin comes from pooled blood that is donated from thousands of healthy
people. As the name suggests, IVIG is given intravenously. IVIG is generally well-
tolerated. Potential adverse reactions are uncommon, but usually occur during or
immediately after an infusion and include headache, nausea, muscle pain, fever, chills,
chest discomfort, skin and anaphylactic reactions. Reactions after an infusion can be

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... Acute Treatments

more serious and include migraine headaches, aseptic meningitis, renal impairment
and blood clots. Like corticosteroids and PLEX, there are no data confirming the
value of IVIG in the setting of acute events. While most studies support the use of
corticosteroids and/or PLEX in acute demyelinating syndromes, IVIG can be considered
in certain circumstances.

Recurrence of idiopathic TM is rare and warrants a comprehensive evaluation for

known causes of recurrent myelitis. Consultation with a neuroimmunologist should
strongly be considered when recurrence occurs, and immunosuppressive treatments
may be recommended.

Prognosis and Management

The spectrum of recovery from TM is broad, and ranges from no improvement in

symptoms to complete recovery. Some improvement in symptoms can be appreciated
during acute treatment, but may not be appreciable until 1-3 months later. Historical data,
not controlling for treatment, suggested that approximately 1/3 of individuals recover
with little or only minor symptoms, 1/3 are left with a moderate degree of permanent
disability and 1/3 have virtually no recovery and are left severely functionally disabled.
These data, however, predate a number of more aggressive treatment protocols and
are likely inaccurate. In present day experiences the outcomes seem to be better than
this distribution, with most persons with TM showing good to fair recovery. Some
studies have suggested that certain clinical features (rapid progression of symptoms,
back pain) and clinical studies (such as evoked potential tests or markers of injury
in the spinal fluid) are often indicators of a less complete recovery. These markers
are imperfect and do not assume aggressive rehabilitation or treatment strategies.

TM can be the presenting feature of multiple sclerosis. In individuals with acute partial
transverse myelitis and normal brain MRI, about 10-33 percent develop MS over a
five to ten-year period. Those who are ultimately diagnosed with MS are more likely
to have asymmetric clinical findings, predominant sensory symptoms with relative
sparing of motor systems, lesions extending over fewer than 2 spinal segments,
abnormal brain MRI, and oligoclonal bands in the CSF.

Long-Term Care

After the acute phase, rehabilitative care to improve functional skills and prevent
secondary complications of immobility involves both psychological and physical
accommodations. There is very little written in the medical literature specifically
dealing with rehabilitation after TM. However, much has been written regarding
recovery from spinal cord injury (SCI) in general, and this literature applies. The physical
issues include bowel and bladder management, sexual dysfunction, maintenance
of skin integrity, spasticity, activities of daily living (i.e., dressing), mobility, and pain.

It is important to begin occupational and physical therapies early during the course of
recovery to prevent the inactivity-related problems of skin breakdown and soft tissue

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Long-Term Care

contractures that lead to a decreased range of motion. Assessment and fitting for
splints designed to passively maintain an optimal position for limbs that cannot be
actively moved is an important part of the management at this stage.

The long-term management of TM requires attention to a number of issues. These are

the residual effects of any spinal cord injury, including TM. In addition to chronic medical
problems, there are the ongoing issues of ordering the appropriate equipment, reentry
into school, re-socialization into the community, and coping with the psychological
effects of this condition by the patients and their families. During the early recovery
period, family education is essential to develop a strategic plan for dealing with the
challenges to independence following return to the community.

Bladder Function Bladder function is almost always at least transiently impaired in patients with TM.
Immediately after the onset of TM, there is frequently a period of transient loss or
depression of neural activity below the involved spinal cord lesion, referred to as “spinal
shock,” which lasts about 3 weeks. Following this period, two general problems can
affect the bladder. The bladder can become overly sensitive and empty after only
a small amount of urine has collected, or relatively insensitive, causing the bladder
to become over extended and overflow. An overly distended bladder increases the
likelihood of urinary tract infections and, in time, may threaten the health of the kidneys.
Depending on the dysfunction, treatment options include timed voiding, medicines,
external catheters for males (a catheter connected to a condom), padding for women,
intermittent internal self-catheterization, an indwelling catheter or electrical stimulation.
Surgical options may be appropriate for some people. Common bladder problems
include incontinence, frequency, nocturia (frequent urination at night), hesitancy,
and retention. Treating incontinence, frequency, and nocturia is often easier than
treating hesitancy and retention, where clean intermittent urinary catheterizations
are the basic component to success. Working with a good urologist is imperative
to prevent potential serious complications, particularly one who understands spinal
cord disease. Urodynamic testing is necessary to determine urine retention to check
risk for urinary tract infections, particularly if there is a history of UTIs to guide the
urologist in terms of the best management.

Bowel Function Another major area of concern is effective management of bowel function. A common
problem in spinal cord injury is difficulty with evacuation of stool, although fecal
incontinence can also occur. The neurologic pathways for defecation are similar to
those of the bladder. Many lacking voluntary control of the bowel may still be able
to achieve continence by diet, strategic use of stool softeners and fiber, and the
technique of rectal stimulation. Other aids include suppositories, anal irrigation, and
oral medications. A high-fiber diet, adequate and timely fluid intake, and medications to
regulate bowel evacuations are the basic components of success. Regular evaluations
by medical specialists for adjustment of the bowel program are recommended to
prevent potentially serious complications. There are some surgical options, although
this is rarely necessary.

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... Long-Term Care

Sexual Dysfunction Sexual dysfunction involves similar innervation and analogous syndromes as those
found in bladder dysfunction. Treatment of sexual dysfunction should take into account
baseline function before the onset of TM. Of the utmost importance is adequate
education and counseling about the known physical and neurologic changes that TM
has on sexual functioning. Because of the similarities in innervation between sexual and
bladder function, patients with sexual dysfunction should be encouraged to empty their
bladders before sexual stimulation to prevent inopportune incontinence. The mainstays
of treatment of erectile dysfunction in men are inhibitors of cGMP phosphodiesterase,
type 5, which will allow most men with TM to achieve adequate erections for success in
intercourse through a combination of reflex and/or psychogenic mechanisms. Although
less effective in women, these same types of medications have been shown capable
of enhancing a woman’s sexual functioning. The most commonly used oral erectile
dysfunction drugs are Viagra (sildenafil), Levitra (vardenafil), and Cialis (tadalafil).
Although sexual experience is impacted by spinal cord injury, sensual experience
and even orgasm are still possible. Lubricants and aids to erection and ejaculation
(for fertility) are available. Adjustment to altered sexuality is aided by an attitude of
permissive experimentation, as the previous methods and habits may no longer serve.

Skin breakdown occurs if the skin is exposed to pressure for a significant amount of
time, without sensation or the strength to shift position as necessary. Sitting position
should be changed at least every 15 minutes. This can be accomplished by standing,
by lifting the body up while pushing down on armrests, or by just leaning and weight
shifting. Wheelchairs can be supplied with either power mechanisms of recline or tilt-
in-space to redistribute weight bearing. A variety of wheelchair cushions are available
to minimize sitting pressure. Redness that does not blanch when finger pressure is
applied may signal the beginning of a pressure ulcer. Good nutrition, vitamin C, and
avoidance of moisture all contribute to healthy skin. Pressure ulcers are much easier
to prevent than to heal.
Skin Breakdown
Spasticity means stiffness or muscle spasms and is often a very difficult problem to
manage. Some stiffness in our muscles is necessary in order to control our movement,
but when they become too tight, the result can range from slightly bothersome
stiffness (particularly upon wakening) to uncontrollably painful spasms. When the
latter occurs, small triggers such as changes in position, temperature, humidity, or
presence of infections can cause this painful spasticity. The key goal is to remain
flexible with exercise, a daily stretching routine, and a bracing program with splints,
as needed. These splints are commonly used at the ankles, wrists or elbows. Also
recommended are appropriate strengthening programs for the weaker of the spastic
muscles acting on a joint and an aerobic conditioning regimen. These interventions are
Spasticity supported by adjunctive measures that include antispasticity drugs (e.g., diazepam,
baclofen, dantrolene, tizanidine), therapeutic botulinum toxin injections, and serial
casting. In cases where spasticity is severe, a baclofen pump, which provides the
medication directly to the spinal cord, may be considered. The therapeutic goal is to
improve the function of the individual in performing specific activities of daily living
(i.e., feeding, dressing, bathing, hygiene, mobility) by improving the available joint

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... Long-Term Care

range of motion, teaching effective compensatory strategies, and relieving pain. Left
untreated, severe spasticity can lead to shortening of the affected muscle or joint
called contractures, further impacting mobility, rehabilitation, and independence.

Pain Pain is common following transverse myelitis.

Changes in sensation often occur and can manifest as lack of sensation, or numbness,
as well as painful sensations called neuropathic pain. This pain is described in
many different ways, including burning, squeezing, stabbing, or tingling. Having the
sensation of pain means the nerve signal is getting through, but in an inappropriate
way. While this can get better over time, there is a long list of medications to treat
these symptoms. The same medication doesn’t work for everyone, so the trial and
error of finding the right medication can be frustrating. Alternative therapies such as
acupuncture and meditation have also been utilized, with varying success.

While the body is constantly working toward repair, once damage is done to the central
nervous system, there will always be evidence of this damage, usually evidenced on
an MRI. Clinical fluctuations of old symptoms, particularly in the setting of infection,
stress, heat (Uhthoff’s phenomenon), menstrual cycle, or anything that increases
core body temperature or throws the body off of its normal course are also possible.
It is important to note that this is not inflammatory driven and therefore in no way
represents worsening of the condition.

The first step in treating pain effectively is obtaining an accurate diagnosis.

Unfortunately, this can be very difficult. Causes of pain include muscle strain from
using the body in an unaccustomed manner, nerve compression (i.e., compression
of the ulnar nerve at the elbow due to excessive pressure from resting the elbow on
an armrest continuously) or dysfunction of the spinal cord from the damage caused
by the inflammatory attack. Muscle pain might be treated with analgesics, such as
acetaminophen (Tylenol), non-steroidal, anti-inflammatory drugs such as naproxen
or ibuprofen (Naprosyn, Aleve, Motrin), or modalities such as heat or cold. Nerve
compression might be treated with repositioning and padding (i.e., an elbow pad for
an ulnar nerve compression).

Nerve pain can be a significant challenge to find effective treatment. Nerve messages
traveling through the damaged portion of the spinal cord may become scrambled
and misinterpreted by the brain as pain. Besides the treatments listed above,
certain antidepressants such as amitriptyline (Elavil), or anticonvulsants, such as
carbamazepine, phenytoin, or gabapentin (Tegretol, Dilantin, Neurontin) may be
helpful. Stress and depression should also be addressed since these conditions
make pain harder to tolerate.

Depression Individuals with TM should be educated about the effect of TM on mood regulation and
routinely screened for the development of symptoms consistent with clinical depression.
Warning signs that should prompt a complete evaluation for depression include failure

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... Long-Term Care

to progress with rehabilitation and self-care, worsening fixed low mood, pervasive
decreased interest, and/or social and professional withdrawal. A preoccupation with
death or suicidal thoughts constitutes a true psychiatric emergency and should lead to
prompt evaluation and treatment. Depression in TM is similar to the other neurologic
symptoms patients endure, which are mediated by the effects of the immune system
on the brain. Depression is remarkably prevalent in TM, occurring in up to 25% of
those diagnosed at any given time, and is largely independent of the patient’s degree
of physical disability. Depression is not due to personal weakness or the inability to
“cope.” It can have devastating consequences; not only can depression worsen physical
disability (such as fatigue, pain, and decreased concentration) but it can have lethal
consequences. Despite the severity of the clinical presentation of depression in TM,
there is a very robust response to combined aggressive psychopharmacologic and
psychotherapeutic interventions. With appropriate recognition and treatment of TM
depression, complete symptom remission is standard.

During the early recovery period, family education is essential to develop a strategic plan
for dealing with the challenges to independence following a return to home. Ongoing
problems typically include ordering the appropriate equipment, dealing with re-entry
into school, work, and community, and coping with the psychological effects of this
condition on both those diagnosed with TM and their families. Being saddened or
demoralized by the diagnosis of TM is appropriate. The inability to move past this grief
in a reasonable period of time such that it interferes with relationships and functional
living needs to be addressed and treated. Many fear that depression reflects on oneself
as an inadequate ability to cope with their diagnosis and feel weak. But it is not a
personal strength issue, and depression is very much a physiological manifestation
and treatable. Both talking to a psychiatrist/psychologist and medication management
can be beneficial, and some studies indicate a synergistic effect of combining the
two. Depression can rebound and can at times become more resistant to treatment.

Fatigue Fatigue is the lack of mental and/or physical energy. Fatigue can be a direct result
of a disease process (primary fatigue) or an indirect result (secondary fatigue). In
TM, fatigue is more often thought to be a result of secondary fatigue. Examples of
secondary fatigue include fatigue from medications, depression, stress, poor sleep
patterns, infections, or changes in walking, which increase energy requirements.
The key is to try to identify the underlying cause of the fatigue – for example, if one
is not sleeping well because of pain, bladder dysfunction, or depression, this needs
to be identified and addressed; not getting consistent sleep will worsen every other
aspect of TM! If too much energy is exerted due to changes in walking, physical
therapy can help identify better body mechanics that will help conserve energy. When
nothing else can be identified as contributing to fatigue, REST is recommended!
Conserving energy such that activities are planned and paced can allow for these
activities to be more enjoyable rather than stressful. Also, reorganizing home and
office can help to reduce the amount of wasted energy exerted so that energy can
be saved up for activities that are enjoyable. Also, exercise routines incorporated in
the day can actually help build stamina and reduce fatigue in the long-run – it’s also

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... Long-Term Care

a great stress reducer! Pilates, yoga, and swimming are great, but the key is to find
something enjoyable and not overdo it.

Rehabilitation and Activities An appropriate strengthening program and an aerobic conditioning regimen are
of Daily Living recommended. The effects on mobility as a result of TM can vary widely, however,
from paralysis to mild weakness. Either way, physical therapy is instrumental in
returning function. Because physical therapists deal with many different types of
injuries and diseases, it is ideal to work with one who has a particular interest in
spinal cord rehabilitation when possible. Assistive devices may be necessary for
weakness – it can be difficult and oftentimes humbling to take the necessary step of
using an assistive device, but when faced with the alternative of broken hips, heads,
and the downstream effects of lost wages or jobs, it is an important and sometimes
indispensable step in maintaining independence. It is also always very important to
remember to exercise, as tolerated, in order to maintain physical health and stamina.

Individuals with TM may find ordinary tasks such as dressing, bathing, grooming,
and eating very difficult. Many of these obstacles can be mastered with training and
specialized equipment. For example, long handled sponges can make bathing easier
as can grab bars, portable bath seats and hand-held shower heads. For dressing,
elastic shoelaces can eliminate the need to tie shoes while other devices can aid
in donning socks. Occupational therapists are specialists in assessing equipment
needs and helping people with limited function perform activities of daily living. A
home assessment by an experienced professional is often helpful.
Physical therapists assist with mobility. Besides teaching people to walk and transfer
more easily, they can recommend mobility aids. This includes everything from canes
(single point vs. small quad cane vs. large quad cane) to walkers (static vs. rolling
vs. rollator) and braces. For a custom-fabricated orthotic (brace), an orthotist is
necessary. Careful thought should go into deciding whether the brace should be an
ankle-foot orthosis, whether it should be flexible or stiff, and what angle the foot portion
should be in relationship to the calf portion. Some will benefit by a knee-ankle foot
orthosis. Each person should be evaluated individually. The best results occur when
a physician coordinates the team so that the therapists and orthotists are united on
what is to be achieved. The physician best trained to take this role is the physiatrist.

Additional Resources

Myelitis Helpline For questions about our organization and rare neuroimmune disorders, visit the
srna.ngo/helpline Myelitis Helpline, an online tool developed by SRNA.

Resource Library To access up-to-date resources on rare neuroimmune disorders, which include
srna.ngo/resources symposium videos, magazines, podcast recordings, published research summaries,
information sheets and relevant external resources, visit our Resource Library.

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PO Box 826962 email: info@wearesrna.org twitter.com/wearesrna
Philadelphia, PA 19182-6962 website: wearesrna.org instagram.com/wearesrna
TM Fact Sheet 13

References

1 Transverse Myelitis Consortium Working Group. Proposed diagnostic criteria and

nosology of acute transverse myelitis. Neurology. 2002 Aug 27;59(4):499-505. doi:
10.1212/wnl.59.4.499. PMID: 12236201.

2 Berman M, Feldman S, Alter M, Zilber N, Kahana E. Acute transverse myelitis:

incidence and etiologic considerations. Neurology. 1981 Aug;31(8):966-71. doi:
10.1212/wnl.31.8.966. PMID: 7196523.

3 Bhat A, Naguwa S, Cheema G, Gershwin ME. The epidemiology of transverse myelitis.

Autoimmun Rev. 2010 Mar;9(5):A395-9. doi: 10.1016/j.autrev.2009.12.007. Epub
2009 Dec 24. PMID: 20035902.

4 Jeffery DR, Mandler RN, Davis LE. Transverse myelitis. Retrospective analysis
of 33 cases, with differentiation of cases associated with multiple sclerosis
and parainfectious events. Arch Neurol. 1993 May;50(5):532-5. doi: 10.1001/
archneur.1993.00540050074019. PMID: 8489410.

5 Christensen PB, Wermuth L, Hinge HH, Bømers K. Clinical course and long-term
prognosis of acute transverse myelopathy. Acta Neurol Scand. 1990 May;81(5):431-
5. doi: 10.1111/j.1600-0404.1990.tb00990.x. PMID: 2375246.

6 Altrocchi PH. Acute transverse myelopathy. Arch Neurol. 1963 Aug;9:111-9. doi:
10.1001/archneur.1963.00460080021002. PMID: 14048158.

7 Pidcock FS, Krishnan C, Crawford TO, Salorio CF, Trovato M, Kerr DA. Acute transverse
myelitis in childhood: center-based analysis of 47 cases. Neurology. 2007 May
1;68(18):1474-80. doi: 10.1212/01.wnl.0000260609.11357.6f. PMID: 17470749.

8 Scott TF, Frohman EM, De Seze J, Gronseth GS, Weinshenker BG; Therapeutics
and Technology Assessment Subcommittee of American Academy of Neurology.
Evidence-based guideline: clinical evaluation and treatment of transverse myelitis:
report of the Therapeutics and Technology Assessment Subcommittee of the
American Academy of Neurology. Neurology. 2011 Dec 13;77(24):2128-34. doi:
10.1212/WNL.0b013e31823dc535. Epub 2011 Dec 7. PMID: 22156988.

9 Seifert T, Enzinger C, Ropele S, Storch MK, Strasser-Fuchs S, Fazekas F. Relapsing

acute transverse myelitis: a specific entity. Eur J Neurol. 2005 Sep;12(9):681-4. doi:
10.1111/j.1468-1331.2005.01007.x. PMID: 16128868.

10 Kim KK. Idiopathic recurrent transverse myelitis. Arch Neurol. 2003 Sep;60(9):1290-
4. doi: 10.1001/archneur.60.9.1290. PMID: 12975297.

11 Borchers AT, Gershwin ME. Transverse myelitis. Autoimmun Rev. 2012 Jan;11(3):231-
48. doi: 10.1016/j.autrev.2011.05.018. Epub 2011 May 18. PMID: 21621005.

SRNA phone: +1 (855) 380-3330 facebook.com/wearesrna

PO Box 826962 email: info@wearesrna.org twitter.com/wearesrna
Philadelphia, PA 19182-6962 website: wearesrna.org instagram.com/wearesrna
TM Fact Sheet 14

... References

12 Krishnan C, Kaplin AI, Pardo CA, Kerr DA, Keswani SC. Demyelinating disorders:
update on transverse myelitis. Curr Neurol Neurosci Rep. 2006 May;6(3):236-43.
doi: 10.1007/s11910-006-0011-1. PMID: 16635433.

13 Kaplin AI, Krishnan C, Deshpande DM, Pardo CA, Kerr DA. Diagnosis and management
of acute myelopathies. Neurologist. 2005 Jan;11(1):2-18. doi: 10.1097/01.
nrl.0000149975.39201.0b. PMID: 15631640.

14 Ropper AH, Poskanzer DC. The prognosis of acute and subacute transverse
myelopathy based on early signs and symptoms. Ann Neurol. 1978 Jul;4(1):51-9.
doi: 10.1002/ana.410040110. PMID: 697326.

15 Sakakibara R, Hattori T, Yasuda K, Yamanishi T. Micturition disturbance in acute

transverse myelitis. Spinal Cord. 1996 Aug;34(8):481-5. doi: 10.1038/sc.1996.82.
PMID: 8856855.

16 Burns AS, Rivas DA, Ditunno JF. The management of neurogenic bladder and sexual
dysfunction after spinal cord injury. Spine (Phila Pa 1976). 2001 Dec 15;26(24
Suppl):S129-36. doi: 10.1097/00007632-200112151-00022. PMID: 11805620.

17 DasGupta R, Fowler CJ. Sexual and urological dysfunction in multiple sclerosis: better
understanding and improved therapies. Curr Opin Neurol. 2002 Jun;15(3):271-8.
doi: 10.1097/00019052-200206000-00008. PMID: 12045724.

18 Berger JR, Cambi F, Di Rocco A, Farace J. Overview to approach to the patient with
noncompressive myelopathy. Continuum (Minneap Minn) 2005; 11:13.

19 Krishnan C, Greenberg B. Transverse myelitis. In: UpToDate, Dash JF (Ed),

UpToDate, Waltham, MA, 2021.

20 de Seze J, Lanctin C, Lebrun C, Malikova I, Papeix C, Wiertlewski S, Pelletier J, Gout

O, Clerc C, Moreau C, Defer G, Edan G, Dubas F, Vermersch P. Idiopathic acute
transverse myelitis: application of the recent diagnostic criteria. Neurology. 2005
Dec 27;65(12):1950-3. doi: 10.1212/01.wnl.0000188896.48308.26. PMID: 16380618.

21 Lehnhardt FG, Impekoven P, Rubbert A, Burghaus L, Neveling M, Heiss WD, Jacobs

AH. Recurrent longitudinal myelitis as primary manifestation of SLE. Neurology. 2004
Nov 23;63(10):1976. doi: 10.1212/01.wnl.0000140623.47437.b3. PMID: 15557531.

22 Krishnan AV, Halmagyi GM. Acute transverse myelitis in SLE. Neurology. 2004 Jun
8;62(11):2087-. doi: 10.1212/01.wnl.0000123089.25458.90. PMID: 15184619.

23 Anantharaju A, Baluch M, Van Thiel DH. Transverse myelitis occurring in association

with primary biliary cirrhosis and Sjogren's syndrome. Dig Dis Sci. 2003 Apr;48(4):830-
3. doi: 10.1023/a:1022821800714. PMID: 12741480.

SRNA phone: +1 (855) 380-3330 facebook.com/wearesrna

PO Box 826962 email: info@wearesrna.org twitter.com/wearesrna
Philadelphia, PA 19182-6962 website: wearesrna.org instagram.com/wearesrna
TM Fact Sheet 15

... References

24 Rabadi MH, Kundi S, Brett D, Padmanabhan R. Neurological pictures. Primary Sjögren

syndrome presenting as neuromyelitis optica. J Neurol Neurosurg Psychiatry. 2010
Feb;81(2):213-4. doi: 10.1136/jnnp.2009.183913. PMID: 20145030.

25 Flanagan EP, Kaufmann TJ, Krecke KN, Aksamit AJ, Pittock SJ, Keegan BM, Giannini
C, Weinshenker BG. Discriminating long myelitis of neuromyelitis optica from
sarcoidosis. Ann Neurol. 2016 Mar;79(3):437-47. doi: 10.1002/ana.24582. Epub
2016 Feb 12. PMID: 26677112.

26 Scott AM, Yinh J, McAlindon T, Kalish R. Two cases of sarcoidosis presenting as

longitudinally extensive transverse myelitis. Clin Rheumatol. 2018 Oct;37(10):2899-
2905. doi: 10.1007/s10067-018-4144-9. Epub 2018 May 17. PMID: 29770929.

27 Lipton HL, Teasdall RD. Acute transverse myelopathy in adults. A follow-up study.
Arch Neurol. 1973 Apr;28(4):252-7. doi: 10.1001/archneur.1973.00490220060009.
PMID: 4688431.

28 Poulter MO, Payne KB, Steiner JP. Neuroimmunophilins: a novel drug therapy for
the reversal of neurodegenerative disease? Neuroscience. 2004;128(1):1-6. doi:
10.1016/j.neuroscience.2004.06.016. PMID: 15450348.

29 Paine RS, Byers RK. Transverse myelopathy in childhood. AMA Am J Dis Child. 1953
Feb;85(2):151-63. doi: 10.1001/archpedi.1953.02050070160004. PMID: 13007166.
30 Patja A, Paunio M, Kinnunen E, Junttila O, Hovi T, Peltola H. Risk of Guillain-Barré
syndrome after measles-mumps-rubella vaccination. J Pediatr. 2001 Feb;138(2):250-
4. doi: 10.1067/mpd.2001.111165. PMID: 11174624.

31 Schonberger LB, Bregman DJ, Sullivan-Bolyai JZ, Keenlyside RA, Ziegler DW, Retailliau
HF, Eddins DL, Bryan JA. Guillain-Barre syndrome following vaccination in the National
Influenza Immunization Program, United States, 1976--1977. Am J Epidemiol. 1979
Aug;110(2):105-23. doi: 10.1093/oxfordjournals.aje.a112795. PMID: 463869.

32 Baxter R, Lewis E, Goddard K, Fireman B, Bakshi N, DeStefano F, Gee J, Tseng HF,

Naleway AL, Klein NP. Acute Demyelinating Events Following Vaccines: A Case-
Centered Analysis. Clin Infect Dis. 2016 Dec 1;63(11):1456-1462. doi: 10.1093/cid/
ciw607. Epub 2016 Sep 1. PMID: 27585798; PMCID: PMC6708556.

33 Flanagan EP, Keegan BM. Paraneoplastic myelopathy. Neurol Clin. 2013 Feb;31(1):307-
18. doi: 10.1016/j.ncl.2012.09.001. PMID: 23186906.

SRNA phone: +1 (855) 380-3330 facebook.com/wearesrna

PO Box 826962 email: info@wearesrna.org twitter.com/wearesrna
Philadelphia, PA 19182-6962 website: wearesrna.org instagram.com/wearesrna
TM Fact Sheet 16

... References

34 Beh SC, Greenberg BM, Frohman T, Frohman EM. Transverse myelitis. Neurol Clin.
2013 Feb;31(1):79-138. doi: 10.1016/j.ncl.2012.09.008. PMID: 23186897; PMCID:
PMC7132741.

35 Greenberg BM, Thomas KP, Krishnan C, Kaplin AI, Calabresi PA, Kerr DA. Idiopathic
transverse myelitis: corticosteroids, plasma exchange, or cyclophosphamide. Neurology.
2007 May 8;68(19):1614-7. doi: 10.1212/01.wnl.0000260970.63493.c8. PMID: 17485649.

36 Greenberg BM. Treatment of acute transverse myelitis and its early complications.
Continuum (Minneap Minn). 2011 Aug;17(4):733-43. doi: 10.1212/01.
CON.0000403792.36161.f5. PMID: 22810928.

37 Weinshenker BG, O'Brien PC, Petterson TM, Noseworthy JH, Lucchinetti CF, Dodick
DW, Pineda AA, Stevens LN, Rodriguez M. A randomized trial of plasma exchange in
acute central nervous system inflammatory demyelinating disease. Ann Neurol. 1999
Dec;46(6):878-86. doi: 10.1002/1531-8249(199912)46:6<878::aid-ana10>3.0.co;2-q.
PMID: 10589540.

38 Cortese I, Chaudhry V, So YT, Cantor F, Cornblath DR, Rae-Grant A. Evidence-based

guideline update: Plasmapheresis in neurologic disorders: report of the Therapeutics
and Technology Assessment Subcommittee of the American Academy of Neurology.
Neurology. 2011 Jan 18;76(3):294-300. doi: 10.1212/WNL.0b013e318207b1f6.
PMID: 21242498; PMCID: PMC3034395.

39 Bigi S, Banwell B, Yeh EA. Outcomes after early administration of plasma exchange
in pediatric central nervous system inflammatory demyelination. J Child Neurol.
2015 Jun;30(7):874-80. doi: 10.1177/0883073814545883. Epub 2014 Sep 22.
PMID: 25246301.

40 Gwathmey K, Balogun RA, Burns T. Neurologic indications for therapeutic plasma

exchange: an update. J Clin Apher. 2011;26(5):261-8. doi: 10.1002/jca.20298. Epub
2011 Sep 13. PMID: 21915895.

SRNA phone: +1 (855) 380-3330 facebook.com/wearesrna

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