a previously healthy 36-year - old man presented with slowly progressive spastic paraparesis , impairment of vibration , and pain perception below the upper trunk associated with constipation , urinary difficulty , and sexual dysfunction . he had experienced lower abdominal pain and vomiting 7 months before the onset of these symptoms , and subsequently noticed a tingling sensation in the right leg and voiding difficulties . the neurologic examination performed at the time of his first visit to our clinic was compatible with a spinal cord lesion : there was bilateral hypesthesia below the t10 level , hyperactive knee and ankle jerks , and extensor plantar responses . t2-weighted magnetic resonance imaging ( mri ) of the spine showed a lesion with a high signal intensity and mild swelling that was not enhanced after the administration of contrast material in the cervical spinal cord ( fig . 1 ) . the cerebrospinal fluid ( csf ) was clear and colorless with 5 white blood cells/l , and the cells were mostly lymphocytes . electrophoresis of csf was negative for the oligoclonal band , and the igg index was within the normal range . the laboratory findings for rheumatoid factor , antinuclear antibody , antineutrophil cytoplasmic antibodies , cryoglobulinemia , hepatitis b and c , and human immunodeficiency virus were negative . the erythrocyte sedimentation rate and c - reactive protein and complement levels ( c3 , c4 , and ch50 ) were normal . the results for the visual evoked potential and brain mri were negative . the patient was treated with steroid pulse therapy under a diagnosis of transverse myelitis . he complained of intermittent chest discomfort when subsequently visiting our clinic , but electrocardiography , cardiac enzymes , and echocardiography findings were normal . the first steroid pulse therapy provided temporary relief from bilateral hypesthesia and paresthesia , but he still experienced spastic paraparesis with painful tonic spasm and bladder dysfunction including recurrent urinary tract infection and nonspecific anterior chest tenderness , especially in the costochondral joint area . another two cycles of steroid pulse therapy were administered during the 2 years following the first treatment due to progression of sensory and motor symptoms . follow - up spine mri after the second steroid pulse therapy revealed recurrence of intramedullary myelopathy ( fig . two years after the onset of myelopathy , he developed painful swelling of his costochondral joints and both knees . a tc methylene diphosphonate bone scan showed markedly increased uptake in the left costomanubrial junction and the first rib ( fig . pelvis radiographs showed ankylosis of bilateral hip joints and poorly delineated bilateral sacroiliac joints ( fig . he subsequently displayed multiple pustular skin eruptions on the palms of the hands , soles of the feet , elbows , trunk ( fig . administration of methotrexate and sulfasalazine markedly reduced the patient 's arthralgia and neurologic symptoms , which were stabilized by maintenance therapy with methotrexate and prednisolone . the spondyloarthropathies comprise a diverse group of inflammatory arthritis conditions that share certain genetic predisposing factors and clinical features . recent studies have provided insight into distinct pathogenetic mechanisms underlying ankylosing spondylitis and reactive arthritis that arise from a complex interplay between genetic factors ( including hla - b27 ) and environmental factors.2 the pathogenesis of reiter 's syndrome may involve molecular mimicry between bacterial fragments in synovial fluid and the hla - b27 molecule . most ( 70 - 80% ) patients with reiter 's syndrome are positive for hla - b27 , as compared with only 6% of the general population . the arthritis may be perpetuated by the induction of cytotoxic t lymphocytes by microbial fragments in the joints , but these cytotoxic t lymphocytes have specificity for hla - b27-positive cells . the presence of hla - b27 may allow stronger or persistent microbial invasion.3 reactive arthritis usually has a self - limited course of 3 to 12 months , but up to 50% of patients experience recurrent bouts of arthritis , and 15% to 30% of them develop chronic symptoms of the disease.4 extra - articular manifestations such as ocular inflammation , enteritis , mucocutaneous lesions , urethritis , and ( rarely ) carditis provide essential support for a diagnosis of reactive arthritis . however , neurological complications are rare.5 there have been only a few case reports of polyneuropathy , cranial nerve palsy , or myelopathy in reiter 's syndrome.6,7 whilst there were gastrointestinal symptoms in this case , stool examinations provided no laboratory evidence of preceding infection . the patient visited our clinic at 7 months after the onset of the first symptoms . the high dose of steroids administered might have inhibited a systemic inflammatory reaction . according to a previous report , approximately only 60% of such cases have evidence of previous infection detected either by serology or by cultures from urogenital or stool samples.8 nonsteroid anti - inflammatory drugs ( nsaids ) and sulfasalazine are effective treatments for reactive arthritis , and methotrexate can also be beneficial.9 our patient did not respond to nsaids , but methotrexate and sulfasalazine relieved his neurological symptoms and arthralgia , making them stable during a 5-year follow - up . the association between reactive arthritis and   cervical myelopathy was not clear in this patient , but there were some features suggesting reiter 's syndrome as a cause of the myelitis . first , the gastrointestinal symptoms that appeared before the development of cervical myelopathy might have reflected a preceding infection that initiated an autoimmune reaction , which led to myelitis and systemic inflammation . initial urinary tract infection and costochondral tenderness at the time of the first attack of myelitis might be indicative of reiter 's syndrome . second , despite the application of steroid pulse therapy , recurrences of progressive myelopathy associated with systemic symptoms of the skin and joints , and the positivity for hla - b27 suggest other causes of myelitis . third , both neurological symptoms and the arthritis that was resistant to the steroid pulse therapy did not recur after sulfasalazine and methotrexate treatment . in conclusion , reiter 's syndrome should be considered in the differential diagnosis of cases of progressive myelopathy with multiple arthritis , urethritis , and skin lesions .
reiter 's syndrome belongs to the family of spondyloarthropathies that usually present with a triad of arthritis , urethritis , and uveitis . 
 the diagnostic criteria include clinical , radiological , and genetic findings , and the response to treatment . 
 nervous system involvement in reiter 's syndrome is extremely rare . 
 we report here on a 36-year - old man who initially presented with progressive cervical myelopathy and was diagnosed as reiter 's syndrome 2 years later . 
 the myelopathy was stable after treatment with methotrexate and sulfasalazine . 
 this case suggests that reiter 's syndrome can present as progressive myelopathy and should be considered in the differential diagnosis of treatable myelopathies .