Acute TM is rare, affecting around 1-8 individuals per million each year. While it can occur at any age, it is most common between 10-19 years of age, and again between 30-39 years of age. Approximately 20% of cases are pediatric. Women are slightly more affected than men. In the United States, there are roughly 1,400 cases diagnosed annually. 

TM can also occur as a symptom of other diseases which damage the myelin sheath, such as multiple sclerosis (MS). When systemic autoimmune disease causes of TM are included in the case count, there are approximately 25 cases per million people each year.

For idiopathic TM, the cause is unknown by definition. However, for most acute TM, the cause is either a previous infection, or systemic autoimmune disease. 

30-60% of cases develop within 30 days after a respiratory or gastrointestinal infection. This has led to the prevailing theory that the cause of TM is an autoimmune response triggered by molecular mimicry. In molecular mimicry, the immune system mistakes a molecule normally found in humans, such as the myelin sheath, for a foreign pathogen such as a virus or bacteria because of structural similarities between two molecules. In doing so, the immune system attacks and damages the myelin sheath. Most commonly, the molecules attacked are myelin basic protein, proteolipid protein, or galactocerebroside, but it is dependent on the triggering infection. A few known triggers include:

• Viruses: Influenza, Varicella Zoster, Herpes Simplex Virus 1/2, Cytomegalovirus, Epstein-Barr Virus, West Nile, COVID-19

• Bacteria: Mycoplasma pneumoniae (walking pneumonia), Borrelia burgdorferi (Lyme Disease), Treponema pallidum (Syphilis), and Mycobacterium tuberculosis (Tuberculosis), Actinomyces israelii (Actinomycosis)

• Fungi: Blastomyces, Aspergillus, Cryptococcus

• Parasites: Toxocara, Schistosoma, Echinococcus, Toxoplasma

It is important to note that only a very small fraction of individuals with these infections ever develop TM, and it is not known why some people develop it and others do not.

TM can also occur as a symptom of a systemic autoimmune disease, such as multiple sclerosis (MS), systemic lupus erythematosus (lupus), or neuromyelitis optica spectrum disorder (NMOSD). In NMOSD triggered cases, often the molecule attacked is aquaporin-4, an important transfer protein found in cells that help manage the immune response of the central nervous system, called astrocytes. 

Rarer causes of TM include vaccines, though the incidence rate is extremely low, estimated at 1-2 cases per million doses given. Extremely rarely, some underlying cancers may also trigger immune responses that result in TM.

Symptoms typically develop very rapidly over a few hours to a few days. Exactly how symptoms manifest is dependent on where in the spinal cord the site of inflammation is located. The majority of cases affect either the thoracic or cervical sections of the spine. Thoracic refers to the middle section of the spine running down your back, and cervical refers to the upper area of the spine, in the neck.

• Pain: Sudden, sharp, or shooting pain in the back, neck, or wrapping around the abdomen (sometimes called a TM band). This is often the first symptom.

• Sensory Changes: Numbness, tingling ("pins and needles"), or burning sensations in the limbs, beginning in the hands and feet and ascending towards the body. Sometimes, only the lower limbs are affected, depending on where in the spinal cord the inflammation is located.

• Motor Weakness: Heavy-feeling limbs and stumbling, which can progress to complete paralysis (paraplegia or quadriplegia).

• Autonomic Dysfunction: Urgent need to urinate, incontinence, and/or severe constipation.

• Respiratory Distress: If the inflammation occurs high up in the spine (near the cervical vertebrae found in the neck), it may affect the diaphragm, which can cause pain while breathing.

Diagnosis focuses on confirming spinal inflammation and ruling out physical compression (like a tumor or slipped disc). Common diagnostic tests include:

• MRI (Magnetic Resonance Imaging): With contrast (gadolinium) to visualize and locate inflammation or lesions within the spinal cord. If the lesion pattern is limited to the area around a single vertebra, this is indicative of idiopathic TM or a symptom of MS. If the pattern expands across multiple vertebrae, this suggests the cause is NMOSD.

• Lumbar Puncture (Spinal Tap): To analyze cerebrospinal fluid (CSF) for elevated white blood cells and proteins indicating an immune response.

• Blood Tests: Used to check for specific autoantibodies or underlying infections.

Treatments for TM include interventions to reduce acute inflammation and alleviate symptoms. For cases of TM that are secondary to another autoimmune disease, long term management and immunosuppression therapies are also utilized. 

Reducing inflammation in the acute phase: the primary goal is to quickly arrest inflammation to prevent permanent nerve damage.

• Intravenous Corticosteroids: High-dose methylprednisolone is the first-line therapy. Steroids help by suppressing the immune response.

• Plasma Exchange Therapy (PLEX): For patients who do not respond to intravenous steroids, PLEX is the next line of defense. This process involves removing the patient's plasma and replacing it with fresh plasma to filter out the harmful antibodies and inflammatory proteins.

• Intravenous Immunoglobulin (IVIG): Often used in pediatric cases or when steroids/PLEX are not an option, IVIG provides pooled donated antibodies that can neutralize the autoantibodies causing disease.

• Cyclophosphamide: In severe cases of TM that do not respond to other treatments (particularly those associated with SLE or NMOSD), high-dose intravenous chemotherapy may be used to provide more aggressive immunosuppression.

Symptom management: Alleviating symptoms is important to improve quality of life. 

• Pain Management: Sharp, shooting nerve pain is often treated with anticonvulsants (Gabapentin, Pregabalin) or sometimes antidepressants (Duloxetine). Common over the counter pain medications like Ibuprofen or Acetaminophen may help with musculoskeletal pain.

• Spasticity Control: Muscle stiffness and spasms are managed with muscle relaxants such as Baclofen, Tizanidine, or Cyclobenzaprine.

• Bladder and Bowel Care: Management may include medications for bladder urgency and incontinence, or intermittent catheterization if urinating is difficult. Fiber and stool softeners are often used to manage constipation.

• Mental Health: Psychotherapy and medications are often necessary to address the anxiety and depression that commonly accompany sudden-onset disability.

• Physical Therapy: Rehabilitation after acute episodes focuses on regaining strength and control of the limbs, with a goal of regaining independence. Robot assisted treadmills can help retrain the spinal cord’s nerve firing pathways to help individuals walk again. Sometimes, weak electrical currents can also be used to stimulate weak or paralyzed muscles.

Long-term management and relapse prevention: for individuals with systemic autoimmune diseases causing TM, long term treatment is needed to help prevent or limit future episodes.

• For individuals with MS, NMOSD, SLE or other autoimmune diseases, there are many pharmaceutical interventions that can be used to prevent recurrent inflammatory attacks including Rituximab, Ocrelizumab, and more.

Prognosis for transverse myelitis is variable. Approximately one third of individuals recover fully and return to normal or near-normal function, experiencing only minor sensory changes. Another third experience some recovery, but are left with moderate disabilities, such as a spastic gait, urinary urgency, and persistent numbness or tingling of the hands and feet. The final third have poor recovery, and may remain permanently paralyzed. While relapse is uncommon, there is a higher risk in individuals who experience TM as a result of a systemic autoimmune disease such as MS, NMSOD, or SLE compared to those who experience idiopathic TM.

The recovery process is slow, but usually begins 2 to 12 weeks after the onset of the episode. Significant progress is often made within 3-6 months, but full recovery can take up to two years or longer. If the individual does not experience some amount of recovery within the first 3 months, there is a poorer long-term prognosis. Cases of TM which onset rapidly within 24 hours are also associated with a less favorable outcome. Continued research into neuroregenerative therapies such as stem cell transplantation and myelin repair remains the most promising path for improving the outlook for those living with permanent effects from TM.

1. Johns Hopkins Medicine. (2026). Transverse myelitis. https://www.hopkinsmedicine.org/health/conditions-and-diseases/transverse-myelitis

2. Mayo Clinic Staff. Transverse myelitis - Symptoms and causes. Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/transverse-myelitis/symptoms-causes/syc-20354726

3. National Institute of Neurological Disorders and Stroke. Transverse myelitis. U.S. Department of Health and Human Services. https://www.ninds.nih.gov/health-information/disorders/transverse-myelitis

4. Oregon Health & Science University. Transverse myelitis. OHSU Brain Institute. https://www.ohsu.edu/brain-institute/transverse-myelitis

5. Simone, C. G., & Emmady, P. D. (2024, May 6). Transverse myelitis. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK559302/