Member Questions and Answers from Joanne Lynn, MD

The following information is offered as a general response to questions related to Transverse Myelitis and is not to be construed as a specific medical recommendation for any individual. This information is based on the information provided in a brief question and is without the benefit of a complete history or an examination. Any decisions regarding diagnosis or treatment should be made in consultation with your physician who is best suited to make appropriate medical recommendations for you.

1. How do illnesses, such as colds, fever and flu impact TM?

There are two ways to interpret this question. The first possible relationship is that viral illnesses are well known precipitants of post-infectious TM. Somehow the viral infection sets off an autoimmune response directed at the spinal cord with resultant inflammation and injury within spinal cord tissue. Recurrent transverse myelitis has been reported; therefore, there is a very small theoretical risk that viral infection might set off a recurrence of post-infectious TM. However, this is very small and it is more likely that worsening of symptoms with a cold or fever would occur by the mechanism described in the next paragraph.

The other way to interpret this question is how do colds, fever and flu impact upon the patient with a past episode of TM who is now stable with residual neurologic problems from spinal cord injury. We know from studies of people with multiple sclerosis that fever may have profound effects on neurologic function in areas of the brain and spinal cord with demyelination (injury to the myelin or insulation material wrapped around nerve fibers). In normal myelinated nerves, small increases in temperature will speed up conduction of electrical nerve impulses. However, an increase in temperature such as a fever may cause failure (or block) of conduction of nerve impulses in demyelinated nerve fibers. In fact, decades ago before MRIs and other sophisticated tests, MS was often diagnosed with the aid of the "hot bath test". The patient was placed in a hot bath to raise body temperature and then reexamined to see if new neurologic problems developed. It is commonplace for a person with MS who is walking with a cane to become temporarily paralyzed in the legs if they develop a high fever. This phenomenon is not specific for MS but may occur in any injury to the central nervous system and especially when there is prominent demyelination as there often is in TM.

This means that a person with TM may experience a worsening of lower extremity weakness or numbness, etc. when they have a fever. People who have experienced this worsening with fever should try to bring fever down with Tylenol or aspirin if there are no contraindications to taking these agents and get with their physician to determine what is causing the fever. A worsening of neurologic function in the setting of a fever is usually not a new episode of transverse myelitis just the result of the stress of the fever on a neurologic system without the usual reserves to tolerate the stress.

2. For how long can the healing process continue and in what degrees?

Again, there are few good studies that report on the healing process and outcome in large numbers of people with TM. Berman et al reported that out of 59 patients with TM, 22 had good recovery, 20 had fair recovery and 14 had poor recovery. They observed that recovery usually began within 4 weeks to 3 months after the onset of symptoms. If no signs of improvement were seen within 3 months, significant recovery was unlikely to occur.

Reference:
Berman M, Feldman S, Alter M, et al. Acute transverse myelitis: incidence and etiological considerations. Neurology 1981;31:966.

3. Is there a way to prevent this (TM) from happening again, i.e., diet, stress reduction, vitamins, etc.?

For most people, the cause of TM is unknown or idiopathic. Therefore, there is no evidence available that diet, stress reduction or vitamins would decrease the risk of an exacerbation of TM. Of course, there is much that we do not know about the immune system. There are some studies that suggest that stress may have adverse effects on the immune system. However, it is virtually impossible to construct a stress-free life that is rich and fulfilling. For that reason, it would seem prudent for those with TM to follow the same recommendations for a healthy life-style that are given for all: adequate rest, regular exercise, a good diet, moderation in alcohol intake, no smoking, etc. There is no dietary or vitamin supplement that has been proven to heal nervous system injury so beware those who promote expensive regimens.

4. So many people who have TM complain about fatigue. What possible explanations are there for this symptom?

Fatigue is one of the most common complaints in clinical medicine. The cause of abnormal fatigue is poorly understood in most clinical conditions. The only ways that we have to measure fatigue are through subjective rating scales in which the person reports how fatigued he or she is. There are several different types of fatigue, which include 1) a sense of low energy, 2) abnormal mental fatigue, 3) fatigability in physical activities, 4) delayed recovery after fatiguing exercise. There are very few studies on fatigue and TM, so we should look at what is known or hypothesized about fatigue in other diseases that injure the spinal cord such as MS, spinal cord trauma, and degenerative diseases of the spinal cord. The types of fatigue that would be most expected to occur in a person with TM would be the third and fourth types. With injury to the spinal cord, there is a breakdown in the pathway for nervous system activation of muscles. In order to move your right toe, upper motor neuron cells in the motor cortex on the left side of the brain must be activated and send a signal through nerve fibers along a pathway which crosses to the right side in the brainstem and then courses down through the spinal cord to the lower levels of the spinal cord. These fibers make connections with lower motor neurons in the spinal cord, which then send fibers to the muscle. These fibers spritz out chemicals that travel short distances to the muscle fibers and cause them to contract.

One theory about motor fatigue in spinal cord injury is that it is due to an increase in energy demands caused by the inefficiency that is caused by weakness. What this means is that if your legs are weak, you have to work harder than a person with normal strength to walk and this requires more oxygen consumption and more work for your heart and lungs. Some studies suggest that this increased inefficiency is especially present if you have significant spasticity (or abnormally increased muscle tone) which must be fought against to move a limb. Some studies have suggested that the muscles themselves function poorly after an upper motor neuron injury with weak muscle contraction and quick fatigue.

Another possible contribution to fatigue is the fact that nerve fibers within the spinal cord that have been injured do not transmit electrical signals as well as normal fibers. One type of injury is demyelination. Nerve fibers are normally surrounded by an insulation material known as myelin. In inflammatory conditions such as TM and MS, the myelin is injured. This may lead to a type of "short-circuiting" of electrical flow across channels which results in weakened nerve firing and thus fatigue.

Another contribution to fatigue may be that people with significant leg weakness may become deconditioned and have poor physical fitness. That part of fatigue might be lessened by physical training and physical therapy.

There is no cure for fatigue. Even though the mechanism of fatigue is not well understood, there are several measures that may be tried. Rest and conservation of energy for those times when it is most needed are important strategies. Fatiguing tasks should be performed in the morning before fatigue sets in for most people with TM. It is sometimes helpful to analyze daily routines to see if tasks are performed efficiently. Moderate physical exercise and condition will result in gradual benefits for most.

Several medications have been tried for fatigue in MS; they could also be tried for people with TM. Amantadine is an antiviral medication that has been shown to have some benefits for fatigue in MS. It is given in doses of 100 mg in the morning and the afternoon and is tolerated well by most people. Pemoline is another stimulant that has been used with some success for fatigue in MS. Of course, other illnesses that might cause fatigue should be considered such as hypothyroidism, sleep disturbances of various kinds, depression and others.

References:
Miller RG, Green AT, Moussavi RS et al. Excessive muscular fatigue in patients with spastic paraparesis. Neurology 40:1271, 1990.

Olgiati R, Jacquet J and Prampero PE. Energy cost of walking and exertional dyspnea in multiple sclerosis. Am. Rev. Respir. Dis. 134:1005,1986.

5. Are there eye problems or vision problems that can occur as a symptom of having TM?

No. By definition TM is a disorder of the spinal cord and cannot affect vision. Vision is affected by disorders of the eye, optic nerve, or optic pathways that radiate to the visual cortex that is located in the back of the brain (occipital lobe). However, there is a disorder that is related to TM named acute disseminated encephalomyelitis (ADEM). This is a monophasic inflammation of white matter in multiple areas of the central nervous system including brain, brainstem, optic nerves and spinal cord. It is triggered by the same things as post-infectious/post-vaccinal transverse myelitis. Some researchers propose that TM is just a form fruste (a partial form in which not all of the elements of the syndrome are present) or isolated, limited form of ADEM. So it is possible that one might develop an acute problem with spinal cord, vision or eye movement abnormalities as part of the same process. Spinal cord and optic nerve demyelination may also occur simultaneously or in close temporal relationship in one form of multiple sclerosis known as Devic's syndrome.

There are many other nervous system disorders that might affect vision. If there is a disturbance of vision, obviously this should be evaluated by an ophthalmologist. It is difficult in this setting to review all of the possible problems with vision. Briefly, double vision or diplopia suggests a disorder of the brainstem that is directly above the spinal cord and links the spinal cord with the rest of the brain or with the nerves or muscles that move the eyes. One cause of loss of vision in one eye is inflammation of the optic nerve that brings messages from the retina of that eye back to the brain. If either of these things should occur, then this suggests an underlying process that is affecting several levels of the nervous system, not just the spinal cord. Some possibilities might be multiple sclerosis, sarcoidosis, systemic lupus erythematosis, infections, vitamin B12 deficiency, or less likely, cancer.

6. Should a person with TM be concerned about receiving a flu vaccination or any other type of vaccination?

This is a difficult question. The reason is that acute disseminated encephalomyelitis (ADEM) or TM may occur as an immune response to vaccination. ADEM is a monophasic inflammatory disease of white matter of the central nervous system (brain and spinal cord). Epidemiology of ADEM and, to some degree, TM is discussed in the chapter by Tselis and Lisak referenced below. ADEM and TM can occur after immunization with vaccines against measles, diphtheria/tetanus, rubella and pertussis. But when you consider the very large number of vaccinations given against these diseases and the small incidence of ADEM/TM that occurs, many would think that the incidence is rare enough to suggest a coincidence rather than causality. They discuss reports of ADEM after influenza shots.

Given these uncertainties, the only possible answer is that one must weigh the potential risks versus the benefits. One moderate view would be that vaccination should certainly be avoided during any phase of active worsening and in those in whom the initial episode of TM followed an influenza vaccination by a short period of time. Certainly, the benefits of influenza vaccination probably exceed the small risks in people who have significant risk factors for death or severe illness from the flu (e.g., severe emphysema or other lung disease, etc.).

Reference:

Acute Disseminated Encephalomyelitis. Tselis AC and Lisak RP in Antel J, Birnbaum G and Hartung H. Clinical Immunology. Malden MA: Blackwell Science, Inc., 1998. Pp118-119.

7. Should a person who has been diagnosed with TM who experiences recurring symptoms or an intensification of existing symptoms be tested for MS?

Recurrent idiopathic transverse myelitis has been reported (Tippett 1991) and does not necessarily mean that there is underlying MS. However, recurrent exacerbations of myelopathy or spinal cord dysfunction should prompt reevaluation. Myelitis due to an underlying autoimmune disease is more likely to recur than idiopathic transverse myelitis. This would include systemic lupus erythematosis, Sjogren's syndrome, or multiple sclerosis. Relentlessly progressive spinal cord dysfunction should prompt consideration of a spinal cord mass lesion such as tumor or abscess, MS, or a paraneoplastic disorder (immune attacks on the spinal cord related to an underlying cancer).

Other neurologic symptoms occurring after the initial spinal cord attack that might suggest multiple sclerosis or another underlying inflammatory central nervous system disease would include visual loss, double vision, trouble with speech or swallowing, vertigo or seizures.

In most follow-up studies of people who present with transverse myelitis, the majority do not develop MS. However, if there are abnormal lesions in the white matter of the brain, the risk of subsequently developing MS is increased. Those with myelitis who have total paralysis of both legs (complete TM) are more unlikely to develop MS than those who had incomplete TM (weakness or sensory loss without complete paralysis).

References:
Tippett DS, Fishman PS, Panitch HS. Relapsing transverse myelitis. Neurology 1991;41:703-706.

Christensen PB, Wermuth L, Hinge HH, Bomers K. Clinical course and long-term prognosis of acute transverse myelopathy. Acta Neurol Scand 1990;81:431-435.

Ropper AH, Poskanzer DC. The prognosis of acute and subacute traumatic myelopathy based on early signs and symptoms. Ann Neurol 1978;4:51-59.

Ford B, Tampieri D, Francis G. Long-term follow-up of acute transverse myelopathy. Neurology. 1992;42:250-252.

Miller DH, Ormerod IEC, Rudge P, et al. The early risk of multiple sclerosis following isolated acute syndromes of the brainstem and spinal cord. Ann Neurol. 1989;26:635-639.