Acute atraumatic neurologic dysfunction in an otherwise healthy college football player is an extremely rare and worrisome event. Every physician knows how devastating permanent neurological damage can be in a young athlete. Physical and emotional morbidity can be great with a sudden drastic change in lifestyle. In this paper we discuss an athlete who presented just before game time with an acute neurologic event. We also discuss the differential diagnosis, work-up, and management of this rare but serious condition. Informed consent was obtained.
A 19-yr-old white male with no significant past medical history was evaluated in the athletic training room just before game time for right-sided (upper and lower extremity) heaviness, weakness, and paraesthesia. He stated that he had experienced the onset of mild numbness and tingling earlier that day. During the evaluation the patient reported new onset of symptoms involving the left lower extremity as well. The athlete denied history of drug abuse, significant remote or recent trauma to neck or back, sexually transmitted diseases, heavy metal exposure including the use of "moonshine," animal or insect bites, or recent travels. He did report a recent upper respiratory illness. A brief initial examination revealed stable vital signs, cranial nerves 2-12 intact, definite weakness of the right upper and lower extremity, and absent reflexes. An ambulance was called to transport the athlete to a tertiary care center because of concern about a possible cerebral vascular event or Guillain-Barré syndrome.
On evaluation in the emergency room, he complained of progressive numbness and weakness in all four extremities. He was also unable to urinate, and catheterization of the bladder revealed 800 cc of retained urine. Vital signs were stable on initial presentation, but shortly thereafter the patient began to experience difficulty with respiration. Head, ears, eyes, nose, throat, neck, lungs, heart, and abdominal exam proved no significant abnormalities. Neurologic exam revealed the cranial nerves to be intact. Motor function was impaired throughout all four extremities (left upper extremities: all 3/5, right upper extremities: 3/5 for the deltoid, biceps, wrist extensors and 0/5 for the triceps, finger extensors/flexors, interossei, left lower extremities: all 3/5, right lower extremities: all 0/5). The patient was able to shrug his shoulders and had full neck range of motion. Sensory examination showed partial impairment (R > L) to about the T4 level. Reflexes were absent throughout and bilateral Babinski signs were noted. There were no fasciculations.
Initial laboratory and diagnostic studies showed no significant abnormalities. These included a complete blood count, electrolytes, liver function test, erythrocyte sedimentation rate, arterial blood gas, PT/PTT, urinary analysis, and urine toxicology screen. Radiographs of the chest, cervical spine, thoracic spine, and lumbar spine were negative. Also, a CT scan of the head proved to be unremarkable. A lumbar puncture was performed. The opening pressure was within normal range and the cerebral spinal fluid (CSF) appeared to be clear. Preliminary report of the CSF showed 19 RBC·CU mm−1, 0 WBC·CU mm−1, glucose of 81 mg·dL−1, and protein of 41 mg·dL−1.
The patient was admitted to the neurologic intensive care unit with the presumptive diagnosis of a transverse myelitis and was then placed on empiric steroids. Vital capacity and arterial blood gases were serially measured. His respiratory status progressively deteriorated but he never required intubation. The lowest recorded vital capacity was 1.9 L. A magnetic resonance imaging (MRI) of the head, thoracic, and cervical spine revealed no significant findings. The MRI of the head with contrast showed punctate enhancement areas in the brainstem, right cerebellar hemisphere, and the right and left periventricular white matter. These were of unknown significance. A follow-up MRI a few days later, however, showed no abnormalities. Other laboratory studies were negative. These included cultures of the CSF for bacteria, fungus, and tuberculosis, viral studies (including enterovirus, cytomegalovirus, Epstein-Barr virus, HIV), antinuclear antibody profile, blood cultures, mycoplasma titers, serum and CSF for Veneral Disease Research Laboratory, CSF for oligoclonal bands, heavy metal screen, urine porphyrin, and serum immunoelectrophoresis.
The patient's condition stabilized and by day five he had some improvement in function of the left side. A physiatrist was consulted and bedside physical therapy was initiated. During the evaluation by the physiatrist the patient was noted to have symptomatic orthostasis on the tilt table test. The patient was subsequently transferred to the rehabilitation unit and stayed for 2 months. He regained bowel function after 6 wk and bladder control after 3 months. He did require the use of a wheelchair for approximately 5 months.
At 1 yr from the initial event the patient can ambulate without assistive devices. He has regained full motor function on the left side although he still has significant deficits on the right side (triceps 0/5, wrist flexors 5/5, finger flexors 4/5, finger extensors 0/5, hamstrings 4/5, quadriceps 5/5, toe extension 3/5, calf 5/5). The patient still complains of bilateral sensory deficits. He has decreased sensation of the left arm extending into the fourth and fifth digit. He also notes numbness involving the right arm and left leg. Reflexes of the bilateral lower extremities and left arm are now present. Reflexes are absent in the right triceps, biceps, and brachioradialis. He plans on returning to college in the fall and hopes to return to football in the future.
Transverse myelitis is a spinal cord type syndrome that is not caused by macrotrauma. It may result from a wide variety of causes (see Table 1). The pathogenesis remains unknown, but demyelination may be the pathologic event. It may be acute, developing over hours to several days, or subacute, developing over 1 to 2 wk. Berman et al. (2) suggested diagnostic criteria for this syndrome: 1) acutely developing paraparesis affecting motor and sensory systems as well as sphincters, 2) spinal segmental level of sensory disturbance, 3) stable nonprogressive course, 4) no evidence of spinal cord compression, and 5) absence of other neurologic disease (excluding syphilis, severe back trauma, malignancy, or encephalitis). Quadriplegia is rare since only 10% of patients have involvement of the cervical cord (1). Urinary retention, often associated with constipation, is present in many patients. Deep tendon reflexes can be either spastic or absent in the case of spinal shock. This is a phenomenon characterized by absence of reflexes and loss of control of vasomotor tone, profuse sweating, and piloerection below the level of the lesion. This makes it difficult to differentiate transverse myelitis from a peripheral nerve lesion such as Guillain-Barré syndrome. Berman also found two peaks of incidence in their population, one at 10-19 yr of age and the other over 40 yr of age. Those who had slower onset of symptoms and for whom improvement began earlier generally had the greatest likelihood of recovering (2). Patients who presented with spinal shock had less likelihood of a good outcome. The incidence has been suggested to be anywhere from 1.34 cases per million population per year in Israel (4) to 4.6 cases per million per year in a case series from New Mexico (5). The differential diagnosis in the nonstructural types of this syndrome includes systemic lupus erythematous, toxins, syphilis, neoplasm, radiation myelopathy, tick paralysis, multiple sclerosis, parainfectious (mycoplasma, ECHO virus, EBV, HIV, CMV) and postvaccinial events. A preceding upper respiratory illness is present in approximately 38% of the reported cases (2-7). Despite the many known causes of transverse myelitis, one-third are labeled idiopathic. Patients may identify a minor antecedent traumatic event.
Laboratory examinations should be rather extensive. If there is an antecedent infectious process, a complete blood count and cultures (viral, fungal, bacterial, and tuberculosis) of all body fluids should be obtained. Hepatitis panel, syphilis testing, Lyme, chlamydia, and mycoplasma titers should all be drawn. Appropriate rheumatologic tests include antibody anti-nuclear, rheumatoid factor, and erythrocyte sedimentation rate. The CSF examination is often nonspecific but remains an essential part of the evaluation. It may reveal a leukocytosis of primarily lymphocytes and/or increased protein. Ruling out neurosyphilis requires a CSF VDRL. Also, testing for oligoclonal bands in the CSF is extremely helpful. If present, this often indicates the possibility of multiple sclerosis (MS). This condition may also be identified by a cranial MRI showing the characteristic plaques to be present. Other helpful ancillary tests to help make the diagnosis of MS include abnormal visual evoked response (VER) and brainstem auditory evoked response (BAER). MS is apparently the cause of transverse myelitis in about 7% of cases according to recent medical literature (2-7). Extramedullary cord compression by spinal epidural abscess or tumor, herniated disk, spondylosis, hematoma, or fracture must be ruled out by appropriate MRI evaluation of the spinal cord. Findings in the spinal cord in patients with transverse myelitis are nonspecific and variable. These findings may include low intensity signal lesions on T1 weighted imaging, which may or may not enhance with gadolinium, and possibly cord swelling (8). Treatment is supportive although any treatable cause needs to be identified, i.e., infection. Steroids are not proven to be of benefit and, because of the rarity of acute transverse myelitis, a controlled study to evaluate the benefits is not feasible. However, steroids are always administered unless contraindicated since there are no other effective treatments and certain subgroups of patients, i.e., those with multiple sclerosis and systemic lupus erythematosus, may exhibit a good response to early administration of large doses of intravenous steroids (9).
This athlete presented just before game time and was initially evaluated in the athletic training room. His symptoms developed rapidly. Guillain-Barré syndrome, cerebral vascular accident, and remote trauma caused by slipped facet or cervical vertebral fracture were considered in our differential diagnosis. Transverse myelitis was added to this after a thorough neurologic exam was performed. Most of the possible etiologies were ruled out by a thorough history and physical exam. No identifiable agent was ever recovered; therefore, in essence, this case should have been labeled idiopathic transverse myelitis. We believe, however, that parainfectious transverse myelitis would be appropriate since the athlete was a reliable historian and did give a good account of a viral syndrome about 10 d before presentation.
We have presented a case of acute transverse myelitis probably caused by an infectious agent in a college football player and have seen the detrimental consequences. He hopes to return to athletics in the future. No previous cases of atraumatic transverse myelitis has been reported in the sports medicine literature. However, two cases should be noted. A 15-yr-old recreational baseball player who fell while playing baseball ruptured the nucleus pulposus which apparently then entered the venous sinusoids and thrombosed the spinal arteries and veins causing a fatal spinal cord infarction (10). Also, a layperson's travel magazine featured a story of a young female cyclist who overcame and adapted to the great disability caused by acute transverse myelitis (11). She is now apparently a world-renowned wheelchair racer.
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