Juxtafacet Cyst of the Lumbar Spine. Clinical, Radiological and Therapeutic Aspects in 28 Cases

OBJECT: A consecutive series of 28 "operated" juxtafacet cysts is reported. We emphasize the clinical and radiological aspects leading to diagnosis. We also discuss the results of the surgical treatment. MATERIAL AND METHODS: Medical information and radiological studies involving 28 patients were analyzed. Each patient has been operated on by decompressive laminectomy and resection of the cyst. The diagnosis was always confirmed by a pathological examination. The cyst most frequently occurred at the L4-L5 level (n = 18), and seldom at the L5-S1 (n - 6) or L3-L4 (n - 4) levels. RESULTS: The differential diagnosis from other pathological causes responsible for a radicular compression could not be done by physical examination. Spine X-rays or myelogram were nonspecific. Computed Tomography or CT-myelography could help in the diagnosis but MR imaging was the most sensitive. In our series, the respective sensitivities of these techniques are 56, 42 and 77%. The preoperative diagnosis was correct in 18 patients (64%). The cyst was sometimes adherent to the underlying dura, then significantly increasing the risk of dural tear and spinal fluid leak, especially when located at L3-L4 level. Surgical ablation lead to a complete recovery or an important improvement in 26 patients. CONCLUSIONS: The diagnosis of the juxtafacet cyst of the lumbar spine is better achieved by MRI. Surgery is the gold standard treatment, safe and long-term effective. When a total cyst removal with an internal facetectomy are performed, recurrence is exceptional

Pseudotumoral Medullary Syndrome Manifesting a Probably Beginning Multiple Sclerosis. Clinical, Radiological and Neuropathological Correlations

A 19-y old sportsman was admitted because he complained of ascending paresthesia since two weeks, muscular strength diminution in both arms, then respiratory difficulties without fever. Clinical examination confirmed an asymmetric bilateral pyramidal syndrome affecting the four limbs, a hyposensitive level up to C5, without meningeal symptoms. MRI detected a widening of the cervical (C2-C5) spinal cord, with gadolinium enhancement. CSF demonstrated lymphocytic pleocytosis and total protein of 530 mg/l with an oligoclonal IgG pattern. With a diagnosis of multiple sclerosis, a corticoid therapy was started but without clinical improvement. Six weeks later, a new MRI revealed an increased enlargement of the cervical spinal cord suggesting a tumoral process. No tumor could be detected at neurosurgery. Biopsy specimen (from C3-C4) demonstrated an inflammatory demyelinating disease with astrocytic hypertrophy. Electron microscopy confirmed the active demyelinating disorder with persistently denuded axons. Several macrophages were observed, but no lymphocytic invasion. Astrocytes were prominent in some areas with "en plaque" gliosis. MRI failed to discover any other demyelinating lesions. Further clinical evaluation was inconspicuous, the patient regaining full activities after 6 months. MRI after 9 months demonstrated no spinal cord lesion. This observation contributes to suggest the influence of the blood-brain barrier breakdown on the occurrence of clinical and radiological signs of new lesions in suspected multiple sclerosis

Acute traumatic central cord syndrome: magnetic resonance imaging and clinical observations

Object. Acute traumatic central cord syndrome has been classically thought to be caused by a hemorrhage that primarily affects the central part of the spinal cord and that destroys the axons of the inner part of the corticospinal tract devoted to the motor control of the hands. Some authors, however, have proposed that its pathogenesis is based on the destruction of the motor neurons supplying the muscles of the hand. To test the validity of these two theories, the authors retrospectively studied the magnetic resonance (MR) images obtained in 18 cases of acute traumatic central cord syndrome (ATCCS) to assess the presence of intramedullary blood and to define the distribution of the abnormal signal intensities in the cervical spinal cord. Methods. The authors used the American Spinal Injury Association (ASIA) motor scale to assess upper- and lower-limb deficits and to evaluate its metameric distribution. The abnormal intramedullary signal was then compared with the distribution of the motor deficit. All MR imaging sessions performed in the acute stage revealed a hyperintense signal on T-2-weighted sequences without any signal change suggesting the presence of intramedullary blood. The localization of this signal was distributed predominantly from the C3-4 to the C5-6 disc levels. The mean ASIA motor score was 74.3 of 100, with an unequal representation between the upper and lower limbs (32 of 50 compared with 42.3 of 50, respectively). The metameric distribution of the deficit was also unequal, with a major deficit in hand function (C8-T1) compared with the more proximal cord segments (5.2 of 10 compared with 7.8 of 10, respectively). This demonstrates the absence of any correlation between the hyperintense signal and the motor deficit distribution. Conclusions. Acute traumatic central cord syndrome cannot be explained by the injury to the gray matter at the level of motor neurons supplying the hand muscles. In agreement with recently published data, the results of this series confirm the absence of intramedullary hemorrhage and corroborate the hypothesis that ATCCS may be explained by the impairment of the corticospinal tract, which can be affected globally