Transverse myelitis is a demyelinating and immune-mediated inflammatory disorder of the spinal cord, the part of the central nervous system that sends impulses from the brain to nerves in the body. This inflammation can cause damage to the ensheathing nerve cell fiber myelin, with resultant neurological dysfunction including weakness, sensory impairments, and autonomic problems including the bowel and bladder.[rx, rx, rx] The spinal cord also carries sensory information back to the brain. The term myelitis refers to inflammation of the spinal cord; transverse refers to the pattern of changes in sensation—there is often a band-like sensation across the trunk of the body, with sensory changes below. Symptoms may develop suddenly (over a period of hours) or over days or weeks and include:
- pain
- sensory problems
- weakness in the legs and possibly arms, and
- bladder and bowel problems.
Transverse myelitis can affect people of any age, gender, or race. It does not appear to be genetic or run in families. The disorder typically occurs between ages 10 and 19 years and 30 and 39 years.
Although some people recover from transverse myelitis with minor or no residual problems, the healing process may take months to years. Most people with transverse myelitis have at least partial recovery, with most recovery taking place within the first 3 months after the attack. Others may suffer permanent impairments that affect their ability to perform ordinary tasks of daily living. Some individuals will have only one episode of transverse myelitis; other individuals may have a recurrence, especially if an underlying illness caused the disorder. There is no cure for transverse myelitis, but there are treatments to prevent or minimize permanent neurological deficits.
What causes transverse myelitis?
The exact cause of transverse myelitis and extensive damage to the bundles
of nerve fibers of the spinal cord is unknown in many cases. Cases in which a cause cannot be identified are called idiopathic. Viral, bacterial, and fungal infections affecting the spinal cord may cause the disorder.
A number of conditions appear to cause transverse myelitis, including:
- Immune system disorders appear to play an important role in causing damage to the spinal cord. Such disorders are:
- an aquaporin-4 autoantibody associated neuromyelitis optic. Neuromyelitis Optica is a disorder that affects the eye nerves and spinal cord. Aquaporin-4 is a channel on the cell membrane that lets water enter the cell and helps maintain the chemical balance for processes to take place within the central nervous system. An antibody is a protein that binds to foreign substances that can attack the host organism.
- multiple sclerosis, a disorder in which immune system cells that normally protect us from viruses, bacteria, and unhealthy cells mistakenly attack the protective coating of myelin in the brain, optic nerves, and spinal cord
- the post-infectious or post-vaccine autoimmune phenomenon, in which the body’s immune system mistakenly attacks the body’s own tissue while responding to the infection or, less commonly, a vaccine
- an abnormal immune response to underlying cancer that damages the nervous system; or
- other antibody-mediated conditions that are still being discovered.
- Viral infections including herpes viruses such as varicella-zoster (the virus that causes chickenpox and shingles), herpes simplex, cytomegalovirus, and Epstein-Barr; flaviviruses such as West Nile and Zika; influenza, echovirus, hepatitis B, mumps, measles, and rubella. It is often difficult to know whether a direct viral infection or a post-infectious response causes transverse myelitis.
- Bacterial infections such as syphilis, tuberculosis, actinomyces, pertussis, tetanus, diphtheria, and Lyme disease. Bacterial skin infections, middle-ear infections, campylobacter jejuni gastroenteritis, and mycoplasma bacterial pneumonia have also been associated with the condition.
- Fungal infections in the spinal cord, including aspergillus, Blastomyces, coccidioides, and cryptococcus.
- Parasites, including toxoplasmosis, cysticercosis, schistosomiasis, and angtiostrongyloides.
- Other inflammatory disorders that can affect the spinal cord, such as sarcoidosis, systemic lupus erythematosus, Sjogren’s syndrome, mixed connective tissue disease, scleroderma, and Bechet’s syndrome.
- Vascular disorders such as arteriovenous malformation, dural arterial-venous fistula, intra-spinal cavernous malformations, or disk embolism.
or
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a.Multiple sclerosis
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b.NMO
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c.ADEM
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a.SLE
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b.SS
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c.Antiphospholipid syndrome
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d.Behçet disease
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e.Vogt-Koyanagi Harada disease
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f.Ankylosing spondylitis
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g.Mixed connective tissue disease
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h.Others: systemic sclerosis, anti-Jo-1 antibody, urticarial vasculitis, psoriatic arthritis, perinuclear ANCA systemic vasculitis, graft-versus-host disease, common variable immunodeficiency, celiac disease
- a.Viral: hepatitis A, hepatitis B, hepatitis C, hepatitis E, measles, mumps, rubella, varicella-zoster, Epstein-Barr, cytomegalovirus, herpes simplex, influenza A/B, lymphocytic choriomeningitis virus, chikungunya, Hanta virus, HIV, human T-cell lymphotropic virus, human herpesvirus 6, Japanese encephalitis, Murray Valley encephalitis, St. Louis encephalitis, tick-borne encephalitis, vaccnia. Rocky Mountain spotted fever, dengue virus, enterovirus 71, coxsackievirus A and B, West Nile virus, parvovirus B19, human corona virus, and echovirus
- b.Bacterial: Mycoplasma pneumoniae, Campylobacter jejuni, Borrelia burgdorferi, Acinetobacter baumanii, Coxiella burnetii, Bartonella henselae, Chlamydia psittaci, Leptospira, Chlamydia pneumoniae. Legionella pneumonia, Orientia tsutsugamushi (scrub typhus). Salmonella paratyphi B, Mycobacterium tuberculosis, Treponema pallidum, Brucellosis melitensis, and groups A and B strep to cocci
- c.Fungal: Actinomyces, Blastomyces, Coccidioides, Aspergillus, Cryptococcus, and Cladophialophora bantiana
- d.Parasitic: Toxocara species. Schistosoma species, Gnasthostoma spinigerum, Echinococcus granulosus, Taenia solium, Toxoplasma gondii, Acanthamoeba species, Paragonimus westermani, and Trypanosoma brucei
- a.Anti-Ri (ANNA-2) antibody
- b.CRMP-5-lgG antibody
- c.Anti-amphiphysin IgG antibody
- d.Anti-GAD65 antibody
- e.NMDAR antibody
- a.Tumor necrosis factor-alpha inhibitors
In some people, transverse myelitis represents the first symptom of an autoimmune or immune-mediated disease such as multiple sclerosis or neuromyelitis optica.“Partial” myelitis—affecting only a portion of the cord cross-section—is more characteristic of multiple sclerosis. Neuromyelitis Optica is much more likely as an underlying condition when the myelitis is “complete” (causing severe paralysis and numbness on both sides of the spinal cord). Myelitis attacks with neuromyelitis optica spectrum disorder (NMOSD) tend to be more severe and are associated with less recovery than attacks with multiple sclerosis.
What are the symptoms of transverse myelitis?
Transverse myelitis may be either acute(developing over hours to several days) or subacute(usually developing over one to four weeks).
The segment of the spinal cord at which the damage occurs determines which parts of the body are affected. Damage at one segment will affect function at that level and below. In individuals with transverse myelitis, myelin damage most often occurs in nerves in the upper back.
Four classic features of transverse myelitis are:
- Weakness of the legs and arms. People with transverse myelitis may have weakness in the legs that progresses rapidly. If the myelitis affects the upper spinal cord it affects the arms as well. Individuals may develop paraparesis(partial paralysis of the legs) that may progress to paraplegia(complete paralysis of the legs), requiring the person to use a wheelchair.
- Pain. Initial symptoms usually include lower back pain or sharp, shooting sensations that radiate down the legs or arms or around the torso.
- Sensory alterations. Transverse myelitis can cause paresthesias(abnormal sensations such as burning, tickling, pricking, numbness, coldness, or tingling) in the legs and sensory loss. Abnormal sensations in the torso and genital region are common.
- Bowel and bladder dysfunction. Common symptoms include an increased frequency or urge to use the toilet, incontinence, and constipation.
Many individuals also report experiencing muscle spasms, a general feeling of discomfort, headache, fever, and loss of appetite, while some people experience respiratory problems. Other symptoms may include sexual dysfunction and depression and anxiety caused by lifestyle changes, stress, and chronic pain.
or
Symptoms of transverse myelitis may develop within a few hours or days. Or, they may develop over 1 to 4 weeks. Symptoms can quickly become severe. Symptoms tend to occur at or below the damaged area of the spinal cord. Both sides of the body are often affected, but sometimes only one side is affected. Symptoms include:
Abnormal sensations
- Numbness
- Pricking
- Tingling
- Coldness
- Burning
- Sensitivity to touch or temperature
Bowel and bladder symptoms
- Constipation
- Frequent need to urinate
- Difficulty holding urine
- Urine leakage (incontinence)
Pain
- Sharp or blunt
- May start in your lower back
- May shoot down your arms and legs or wrap around your trunk or chest
Muscle weakness
- Loss of balance
- Difficulty walking (stumbling or dragging your feet)
- Partial loss of function, which may develop into paralysis
Sexual dysfunction
- Difficulty having an orgasm (men and women)
- Erectile dysfunction in men
Other symptoms can include loss of appetite, fever, and respiratory problems. Depression and anxiety can occur as a result of dealing with chronic pain and illness.
How is transverse myelitis diagnosed?
Motor symptoms may vary depending on the level of the spinal cord involved. Upper cervical lesions (C1-C5) may affect all four extremities. Additionally, if the lesion affects the phrenic nerve (C3, C4, C5), it could lead to diaphragmatic dysfunction and respiratory failure.
Lesions in the lower cervical levels (C5-T1) many develop upper and lower motor neuron signs in the upper extremities and exclusive upper motor neuron signs in the lower extremities. Cervical lesions account for approximately 20% of cases.
Lesions in the thoracic region (T1-T12) may cause both upper and lower motor neuron signs in the lower extremities. The thoracic region is the most commonly affected in TM cases (70%).
Lesions in the lumbosacral regions (L1-S5) may cause both upper and lower motor neuron signs in the lower extremities. Lumbar lesions account for approximately 10% of cases.
Sensory symptoms generally affect the level of the lesion or one of the levels above or below the lesion.
Back pain in the corresponding area of the lesion may also be present.[rx]
To diagnose transverse myelitis, a compressive cord lesion must be excluded first. Exclusion is usually performed by magnetic resonance imaging (MRI). This is followed by a confirmation of inflammation either by a gadolinium-enhanced MRI or lumbar puncture (LP). A set of diagnostic criteria was developed but is generally reserved for research purposes as not all features are required to make the diagnosis in a clinical setting.[rx]
Diagnostic criteria include:
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Sensory, motor, or autonomic dysfunction originating from the spinal cord
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T2 hyperintense signal changes on MRI
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No evidence of a compressive lesion
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Bilateral signs/symptoms.
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Clearly defined sensory level.
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Evidence of inflammatory process demonstrated by gadolinium enhancement on MRI, cerebrospinal fluid (CSF) analysis showing pleocytosis, or elevated immunoglobulin G (IgG) index.
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Progression to nadir between 4 hours and 21 days
Most important of the above criteria are the first 3.
When considering TM as a possible diagnosis, it is recommended the following investigative analyses be performed:[rx]
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MRI of the entire spine with and without gadolinium contrast to differentiate compressive vs. non-compressive lesions.
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Brain MRI with and without gadolinium contrast to evaluate for evidence of brain lesions.
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LP for CSF analysis including cell count with differential, protein, glucose, the Venereal Disease Research Laboratory (VDRL) test, oligoclonal bands, immunoglobulin G (IgG) index, and cytology.
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Serum anti-aquaporin-4 (APQ-4)-IgG autoantibodies, anti-myelin oligodendrocyte glycoprotein (MOG) autoantibodies, B12 level, methylmalonic acid, serum antinuclear antibodies (ANA), Ro/SSA, and La/SSB autoantibodies, syphilis serologies, HIV antibodies, TSH and viral etiology tests as applicable.
Patients with evidence of longitudinally extensive spinal cord lesions additionally will require the following additional studies:[rx]
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Serum erythrocytes sedimentation rate (ESR), C-reactive protein (CRP), ANA, antibodies to extractable nuclear antigens, rheumatoid factor, antiphospholipid antibodies, and antineutrophil cytoplasmic antibodies (ANCA)
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Computed tomography (CT) of the chest to evaluate for evidence of sarcoidosis.
Additional testing may be performed in the appropriate clinical setting.
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Neuro-ophthalmologic evaluation
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Paraneoplastic evaluation
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Infectious serologic and CSF studies
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Nasopharyngeal swab for enteroviral PCR
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Serum copper and ceruloplasmin (copper deficiency may mimic TM)
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Serum vitamin B12 and vitamin E levels
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Spinal angiogram
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Prothrombotic evaluation
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Salivary gland biopsy
Physicians diagnose transverse myelitis by taking a medical history and performing a thorough neurological examination. Tests that can indicate a diagnosis of transverse myelitis and rule out or evaluate underlying causes include:
- Magnetic resonance imaging(MRI) produces a cross-sectional view or three-dimensional image of tissues, including the brain and spinal cord. A spinal MRI will almost always confirm the presence of a lesion within the spinal cord, whereas a brain MRI may provide clues to other underlying causes, especially MS. In some instances, computed tomography (CT) may be used to detect inflammation.
- Blood tests may be performed to rule out various disorders, including HIV infection and vitamin B12 deficiency. Blood is tested for the presence of autoantibodies (anti- aquaporin-4, anti-myelin oligodendrocyte) and antibodies associated with cancer (paraneoplastic antibodies). The presence of autoantibodies (proteins produced by cells of the immune system) is linked to autoimmune disorders and point to a definite cause of transverse myelitis.
- Lumbar puncture and spinal fluid analysis (also called a spinal tap) can identify more protein than usual in some people with transverse myelitis and an increased number of white blood cells (leukocytes) that help the body fight infections.
If none of these tests suggests a specific cause, the person is presumed to have idiopathic transverse myelitis.
How is transverse myelitis treated?
Non-Pharmacological
Common neurological deficits resulting from transverse myelitis include incontinence, chronic pain, and severe weakness, spasticity, or paralysis. In some cases, these may be permanent. Individuals with lasting or permanent neurological defects from transverse myelitis typically consult with a range of rehabilitation specialists, which may include physiatrists, physical therapists, occupational therapists, vocational therapists, and mental health care professionals.
- Physical therapy – can help retain muscle strength and flexibility, improve coordination, reduce spasticity, regain greater control over bladder and bowel function, and increase joint movement. Individuals are also taught to use assistive devices such as wheelchairs, canes, or braces.
- Occupational therapy – teaches people new ways to maintain or rebuild their independence by participating in meaningful, self-directed, everyday tasks such as bathing, dressing, preparing meals, and house cleaning.
- Vocational therapy – involves offering instructions to help people develop and promote work skills, identify potential employers, and assist in job searches. Vocational therapists act as mediators between employees and employers to secure reasonable workplace accommodations.
- Psychotherapy – for people living with permanent includes strategies and tools to deal with stress and a wide range of emotions and behaviors.
Medication
Treatments are designed to address infections that may cause the disorder, reduce spinal cord inflammation, and manage and alleviate symptoms.
Initial treatments and management of the complications of transverse myelitis include:
- Intravenous corticosteroid drugs – may decrease swelling and inflammation in the spine and reduce immune system activity. Such drugs may include methylprednisolone or dexamethasone. These medications may also be given to reduce subsequent attacks of transverse myelitis in individuals with underlying disorders.
- Plasma exchange therapy – (plasmapheresis) may be used for people who don’t respond well to intravenous steroids. Plasmapheresis is a procedure that reduces immune system activity by removing plasma (the fluid in which blood cells and antibodies are suspended) and replacing it with special fluids, thus removing the antibodies and other proteins thought to be causing the inflammatory reaction.
- Intravenous immunoglobulin (IVIG) – is a treatment thought to reset the immune system. IVIG is a highly concentrated injection of antibodies pooled from many healthy donors that bind to the antibodies that may cause the disorder and remove them from circulation.
- Pain medicines – that can lessen muscle pain include acetaminophen, ibuprofen, and naproxen. Nerve pain may be treated with certain antidepressant drugs (such as duloxetine), muscle relaxants (such as baclofen, tizanidine, or cyclobenzaprine), and anticonvulsant drugs (such as gabapentin or pregabalin).
- Antiviral medications – may help individuals who have a viral infection of the spinal cord.
- Medications can treat other symptoms and complications – including incontinence, painful muscle contractions called tonic spasms, stiffness, sexual dysfunction, and depression.
Following initial therapy, it is a critical part to keep the person’s body functioning during the recovery period. This may require placing the person on a respirator in the uncommon scenario where breathing is significantly affected.
Management of Neuromyelitis Optica
| Medication | Use | Typical dose | Evidence |
|---|---|---|---|
| High dose IV methylprednisolone | Acute | 1 gm IV daily for 5 days with or without a taper | Observational studies |
| Plasma exchange | Acute as a rescue therapy | 5 exchanges (each exchange 250 ml) over 5-10 days | Randomized trials in TM patients |
| Rituximab | Maintenance | 1 gm (or 375 mg/m2) IV every 1-2 weeks for 2-4 weeks then redoes based on CD19 count (typically every 6-8 month) for ≤ 2 years | Several open label and retrospective clinical trials |
| Azathioprine | Maintenance | 2 mg/kg PO divided BID (typically 100 mg BID) for ≤2 years | Observational studies |
| Mycophenolate | Maintenance | 1-3 gm PO daily divided BID or TID for ≤2 years | Retrospective trial |
| Methotrexate | Maintenance | 5-15 mg PO weekly for ≤2 years | Open label trial |
| Mitoxantrone | Maintenance | 12 mg/m2 every 3 months (maximum dose 140 mg/m2) | Open label trial |
| Cyclophosphamide | Maintenance | 0.5-1.5 mg/m2 (typically 1 gm) IV every month until absolute lymphocyte count<1000/mm3 (typically 6 cycles) or immunoablative dose of 200 mg/kg divided over 4 days | Open label trial |
| IVIG | Maintenance | 2 gm/kg induction followed by 0.4-0.5 gm/kg every month | Case series |
Management options for addressing long term mobility issues following transverse myelitis
| Therapy/Device/Concept | Description | References |
|---|---|---|
| Conventional therapy | Focuses on compensatory strategies for nonremediable neurologic deficits. Focuses on strengthening muscles above the level of the lesion, and unaffected muscles below the level of the lesion. |
|
| Activity-based therapy | Interventions that provide activation of the neuromuscular system below the level of lesion with the goal of retraining the nervous system to recover a specific motor task. | 451 |
| Ankle-foot orthoses (AFOs) | AFOs can support the weakened musculature around the ankle. AFOs address excess plantar flexion during initial contact, stabilize the ankle for effective push-off during late stance, and prevent toe-drag during swing. |
452 |
| Functional electrical stimulator devices | Can reduce toe drag, circumduction, pelvic obliquity, and genu recurvatum, improving energy efficiency and facilitating safety and walking duration. Long-term use results in stable improvements of walking performance that persist even when the device is turned off. Adherent use of a dorsiflexion assist device may enhance the fidelity of activation of motor cortical regions and the descending corticospinal connections that control the swing phase of ambulation. |
286, 453, 454 |
| Robot-assisted gait training | Different systems are commercially available, including the “Lokomat,” the “LokoHelp,” and the “Gait trainer.” | 455 |
| Neuromuscular electrical stimulation (NMES) | Helpful in improving interlimb coordination during locomotion | 456 |
| Dalframpridine | Dalframpridine is the extended-release, oral form of 4-aminopyridine approved by the Food and Drug Administration that has been shown to improve the walking ability in patients with multiple sclerosis by improving conduction along demyelinated axons. |
Management options for spasticity in patients with transverse myelitis
| Management Strategy | Comment |
|---|---|
| Nonpharmacologic measures | Physical therapy, stretching exercises, orthotics, and aquatic therapy Useful for mild cases. |
| Pharmacologic therapy | Baclofen Tizanadine Dantrolene (must monitor liver function tests) Anticonvulsants Benzodiazepines Anticonvulsants and benzodiazepines are useful for paroxysmal tonic spasms. Sedation may limit the use of the above-mentioned drugs. |
| Botolinum neurotoxin | Particularly useful for nonambulatory patients with severe adductor spasms that complicate adequate perineal hygiene. |
| Intrathecal baclofen (ITB) | May be used when oral medications cause too much sedation. Patients must be carefully evaluated before ITB use because of serious risks associated with baclofen withdrawal. |
Managing the urinary dysfunction following transverse myelitis
| Treatment Options | Comments | |
|---|---|---|
| Detrusor hyperreflexia (failure to store) |
|
Common side effects include dry mouth and constipation. Contraindicated in patients with angle-closure glaucoma and mechanical bladder outlet obstruction. Nonselective agents should be used cautiously, if at all, in patients with cognitive dysfunction. |
|
||
| Detrusor-sphincter dyssynergia |
|
Alpha antagonists may cause hypotension, tachycardia, and bladder incontinence, particularly in those patients with coincident bladder spasms. CIC should be considered if postvoid residual volume exceeds 100 mL. Patients with sacral nerve stimulators cannot undergo MRIs. Indwelling Foley catheters are contraindicated in females. |
| Frequent urinary tract infections | Appropriate antibiotics Prophylactic antibiotic therapy Cranberry preparations Vitamin C supplementation |
Cystoscopic evaluation may be needed to look for bladder trabeculations that serve as a nidus for infections. |
| Painful bladder spasms | Pharmacotherapy Timed voiding Neuromodulation |
Pharmacotherapy: baclofen, benzodiazepines, hyoscine butylbromide, gabapentin and cannabinoids. |
| Nocturia | Behavioral measures Pelvic floor exercises Imipramine Desmopressin (DDAVP) Bladder rehabilitation |
Avoid alcoholic and caffeinated beverages after 5 pm, to limit fluid intake in the evening, to avoid any fluids 2 h before bedtime and to void before going to bed. |
Management of gastrointestinal dysfunction in patients with transverse myelitis
| Problem | Management Strategies |
|---|---|
| Gastroparesis | Stop drugs that inhibit gastrointestinal motility (eg, narcotics, calcium channel blockers, anticholinergics). Consultation with a gastroenterologist for endoscopy, gastric emptying studies, and investigations to characterize the nature of dysmotility. Gastric decompression with a nasogastric tube, bowel rest, intravenous fluids, and proton-pump inhibitors or gastric H2-receptor blockers should be considered. Prokinetic agents (eg, metoclopramide, macrolide antibiotics, bethanecol or pyridostigmine) may be used. Tardive dyskinesia is a risk of metoclopramide use. Gastric electrical stimulation (Enterra therapy) and endoscopic injection of botulinum neurotoxin may be of potential benefit. In refractory cases, surgical interventions like pyloroplasty may be needed. |
| Constipation | General measures: high-fiber diet, bulking agents, increased fluid intake (at least 2 L daily), physical exercise, and establishing a regular toileting routine (best accomplished after breakfast to take advantage of the gastrocolic response, which peaks about 30 minutes after eating). Stimulant or osmotic laxatives (senna and bisacodyl) can be titrated to produce a satisfactory response (without producing liquid stool). Osmotic laxatives, although effective, can produce liquid stool with subsequent incontinence. Rectal stimulants have a predictable time of response. Begin with a glycerine suppository, progressing to bisacodyl, sodium citrate micro-enema, and ultimately a phosphate enema. Biofeedback may help, particularly in pelvic floor incoordination. Neostigmine in combination with glycopyrrolate has been shown to be effective. 4-aminopyridine may improve constipation. Digital stimulation of the anal canal serves to manually disimpact the rectum. Abdominal massage may be helpful. For refractory cases: colostomy, neuromodulation, Malone Antegrade Continence Enema. Transanal irrigation (TAI). |
| Fecal incontinence | Mild and infrequent: loperamide, codeine phosphate. Antidiarrheal drugs should be used with caution if incontinence and constipation coexist, and periodic checks for impaction may be required. Fecal impaction is a common complication and patients experience anorexia, nausea, and spurious diarrhea (liquid stool passing around the blockage). Biofeedback is another useful tool. Anal plugs or pads may be needed. Severe cases: surgical intervention (eg, dynamic graciloplasty, artificial bowel sphincter, and sacral nerve stimulation). TAI |
Management strategies for sexual dysfunction in patients with transverse myelitis
| Problem | Management Strategies |
|---|---|
| Reduced libido | Stop any offending medication (particularly selective serotonin reuptake inhibitors). Consider using bupropion. Check free testosterone levels (in both men and women) – testosterone replacement therapy for deficient states. |
| Erectile dysfunction | Phosphodiesterase 5 inhibitors (sildenafil, tadalafil, and vardenafil). If unresponsive to oral agents, intracavernosal alprostadil injection, intraurethral alprostadil pellet, penile tension rings, vacuum devices, implantable penile prostheses, and sacral neuromodulation (Sacral Anterior Root Stimulator Implants) may be considered. |
| Ejaculatory dysfunction (affecting fertility) | Strong afferent stimulation and intense activation of the autonomic nervous system is needed to trigger the ejaculatory reflex. Penile vibratory stimulation (PVS) is the first line of treatment. Midodrine may be used as an adjunct to PVS in men who failed PVS alone. Rectal probe electro-ejaculation may be used but frequently results in retrograde ejaculation and may cause significant discomfort. Surgical techniques for sperm retrieval (eg, Brindley reservoir, microsurgical aspiration of spermatozoa from the vas deferens, or testicular biopsy) may also be considered if other measures fail. |
| Female orgasmic dysfunction | Manual and vibratory clitoral stimulation (eg, Eroscillator). Clitoral vacuum suction device (Eros) is approved by the Food and Drug Administration for female orgasmic dysfunction. |
| Lubrication dysfunction | Lubricants Topical estrogen Clitoral vacuum suction device (Eros) Estrogen replacement therapy |
Prevention of future transverse myelitis episodes
Multiple sclerosis and neuromyelitis optica typically require long-term treatment to modify the immune system response. Treatment of MS with immunomodulatory or immunosuppressant medications such as alemtuzumab, dimethyl fumarate, fingolimod, glatiramer acetate, interferon-beta, natalizumab, or teriflunomide may be needed.
Immunosuppressant treatments are used for neuromyelitis optica spectrum disorder and recurrent episodes of transverse myelitis that are not caused by multiple sclerosis. They are aimed at preventing future myelitis attacks (or attacks at other sites) and include steroid-sparing drugs such as mycophenolate mofetil, azathioprine, and rituximab.
What research is being done?
The mission of is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. NINDS is a component of the National Institutes of Health, the leading supporter of biomedical research in the world.
NINDS researchers are working to better understand how the immune system destroys or attacks the nerve-insulating substance called myelin in autoimmune diseases or disorders. Other work focuses on strategies to repair demyelinated spinal cords, including approaches using cell transplantation. This research may lead to a greater understanding of the mechanisms responsible for damaging myelin and may ultimately provide a means to prevent and treat transverse myelitis.
Glial cell studies. Glia, or neuroglia, are non-neuronal cells (they do not provide electrical impulses) in the nervous system that form myelin and provide support and protection for neurons. Oligodendrocyte progenitor cells (OPCs) are stem cells that generate myelin-producing oligodendrocytes, a type of glial cell. NINDS-funded scientists are studying cellular mechanisms that control the generation and maturation of OPCs to allow remyelination, which could be an effective therapy for transverse myelitis and spinal cord injury. Other NINDS-funded investigators are focusing on mechanisms and interventions designed to increase oligodendrocyte proliferation and remyelination after spinal cord injury.
Astrocytes are another type of glial cell. The aquaporin-4 IgG antibody binds to astrocytes, which has led to an increased interest in its role in transverse myelitis of neuromyelitis optica spectrum disorder (NMOSD). The antibody appears to cause myelitis in NMOSD by activating other components of the immune system, resulting in injury to the spinal cord. Many studies are trying to better understand the role of astrocytes in autoimmune diseases.
Genetic studies. NINDS-funded scientists hope to develop a better understanding of the molecular control of central nervous system myelination and remyelination by studying the theBrg1(Brahma-related) gene that appears to be involved in oligodendrocyte myelination. The long-term objective of this research is to develop drugs that modulate the activity ofBrg1and other genes to promote myelination and remyelination.
Animal models. NINDS funds research using animal models of spinal cord injury aimed at replacing or regenerating spinal cord nerve cells. The ultimate goals of these studies are to develop interventions for the regeneration or remyelination of spared nerve fibers in humans and to restore function to paralyzed individuals.
Neuroimaging with MRI. Research funded by aims to develop and implement new MRI techniques to quantitatively assess the relationship between spinal cord pathology and neurological dysfunction in MS. This new approach may assess changes in lesions and myelin in MS and possibly transverse myelitis. Other NIH-funded researchers plan to develop MRI methodologies to non-invasively detect and characterize networks to identify the extent of injury to the spinal cord and to monitor the progression of recovery after injury. These techniques may aid in earlier detection of transverse myelitis and other neurological disorders such as MS.
Brain-machine interfaces and prosthetic devices. Scientists are developing brain-machine interfaces and neural prostheses to help people with spinal cord damage regain functions by bypassing the injury site. These sophisticated electrical and mechanical devices connect with the nervous system to supplement or replace lost motor and sensory function.
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