A 76-year-old woman with a spinal subdural hematoma (SDH) was presented with severe back pain without headache. Magnetic resonance imaging (MRI) performed 4 days after onset showed SDH extending from Th2 to L3. She was diagnosed with spontaneous SDH without neurological manifestation, and conservative treatment was selected. Transient disturbance of orientation appeared 7 days after onset. Small subarachnoid hemorrhage (SAH) was detected on head CT, and strict antihypertensive therapy was started. Symptoms changed for the better. Back pain disappeared 4 weeks after onset. On follow-up MRI at 6 months after onset, the SDH had been resolved spontaneously. Although adhesive arachnoiditis was observed at Th4-6, the recurrence of clinical symptoms was not observed at one year and a half after onset. Spinal subdural space is almost avascular; a hematoma in a subdural space is considered to come from a subarachnoid space when it is a lot. A hemorrhage in subarachnoid space was flushed by cerebral spinal fluid; hematoma or arachnoiditis was not formed in general. In our case, hemorrhage was a lot and expansion of SDH was large enough to cause cranial SAH and arachnoiditis. But longitudinally expanded SDH did not show neurological manifestation and resolved spontaneously in our case.
We describe a technique for computed tomographic (CT) fluoroscopy-guided celiac artery or superior mesenteric artery (SMA) catheterization for use with CT hepatic arteriography or CT arterial portography, respectively. Patients underwent conventional hepatic angiography to define the anatomy and to place a catheter within the celiac artery or the SMA. Subsequently, the catheter was repositioned in the target vessels under CT fluoroscopy. Our success rate was 94%.
We report the case of a 51-year-old female with rapid neurological deterioration as an initial presentation of non-Hodgkin's lymphoma. Paraplegia occurred suddenly after a 4-day history of weakness and numbness of the lower extremity. MRI revealed a dorsal epidural mass from T10 to T11 that compressed the spinal cord. There was neither bone destruction nor a paravertebral mass. Emergency decompressive laminectomy and tumor resection were performed. Histological analysis of the surgical specimen indicated diffuse large B cell lymphoma. The clinical stage was IV on CT and complete remission was achieved by subsequent chemotherapy. Spinal cord compression occurs in the course of non-Hodgkin's lymphoma in 0.1% -6.5% of cases, but this situation usually develops in the late phase with bone destruction and/or a paravertebral mass. Cord compression and especially the severe symptoms such as paraplegia are rare as the initial presentation of lymphoma.
Synovial osteochondromatosis is a rare, benign condition of unknown etiology in which the synovium undergoes metaplasia, leading to cartilaginous nodules that ultimately break free, mineralize, and even ossify. The most commonly involved joint is the knee. Typically, radiographs can be diagnostic and mineralized nodules are pathognomonic. In as many as one-third of cases, however, no calcification or ossification of the cartilage occurs in the early stage of the disease because mineralization is time-dependent. In such cases, gadolinium-enhanced MRI can be useful. Unmineralized nodules are typically peripherally enhanced because they are attached to and derive a vascular supply from the synovium. We experienced an unmineralized case of synovial osteochondromatosis of the right knee joint, in which imaging diagnosis was difficult. Neither calcification nor ossification was observed, but all nodules were released from the synovium as loose bodies and there was no vascular supply. Therefore, MRI did not show a typical appearance. These findings suggest that synovial osteochondromatosis should be considered as a differential diagnosis in a case in which unmineralized loose bodies without a synovial lesion are found in an imaging examination.
Septic arthritis of the shoulder is uncommon in the immunocompetent patient with no previous risk factors for joint infection. We treated an immunocompetent patient who developed septic arthritis of the shoulder after suprascapular nerve block for pain due to rotator cuff tear. An 80-year-old man with no underlying disease visited a nearby orthopedics clinic with complaint of left shoulder joint pain. Left suprascapular nerve block was performed, but the pain gradually aggravated. On the day after the block, he had a fever of 39˚C and came to our department. On examination, enlargement and tenderness were present at the injection site. Cellulitis at the site was suspected. He was admitted and administration of a cephem antibiotic was started. Pain subsequently decreased. Magnetic resonance imaging (MRI) performed 4 days after hospitalization showed massive effusion close to the injection site. The effusion spread into the joint cavity through the tear site of the supraspinatus. Septic arthritis of the shoulder was strongly suspected, open irrigation and debridement were performed 11 days after hospitalization. After surgery, pain immediately improved. In our case the extra-articular infection caused by suprascapular nerve block considered to spread into the shoulder joint cavity through the site of rotator cuff tear, although there have been no reports of such cases. This case suggests the possibility that patients with rotator cuff tear may easily develop septic arthritis because extra-articular infection may spread into the joint cavity through the site of tear.
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