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Solitary osteochondroma of the lumbar spine with cord compression: a case report.

Solitary osteochondromas are usually of little significance. However, if they are located near neurologic structures, they may cause irritation due to compression. Spinal cord compression is a rare but potentially catastrophic manifestation of solitary osteochondromas. As far as can be ascertained, a solitary osteochondroma in the lumbar region with spinal cord compression has not been reported in Taiwan. This article includes the treatment of an 11-year-old girl with osteochondromas which was complicated by the late development of kyphoscoliosis and a review of the literature.

Child↗

Massive hemorrhagic necrosis of the spinal cord in metastatic cord compression.

A fusiform longitudinal hemorrhagic necrosis of the spinal cord is described in a patient with spinal cord compression caused by metastases from an adenocarcinoma of the prostate. The lesion extended from the D3 down to L2 level with maximal involvement of the D7-D8 segments. The shape, location, and distribution of the lesion and its prominent hemorrhagic component corresponded to Jellinger's category of cylindrical liquefaction necrosis, probably due to venous obstruction. The multiple thrombi found in epidural veins supported such a pathogenic mechanism, which although extremely rare has been reported previously in five cases.

Adenocarcinoma↗

Surgical decompression of anterior and posterior malignant epidural tumors compressing the spinal cord: a prospective study.

Of 167 episodes of spinal epidural neoplastic compression, 86 were treated by operation. The surgical approach was prospectively selected according to the location of the tumor in the spinal canal. Decompression was achieved by 61 vertebral body resections (VBRs) and by 25 laminectomies. The indications for operation were: neurological relapse after previous radiotherapy, the need to make a tissue diagnosis, a radioresistant tumor, and neurological deterioration during radiotherapy. Before VBR, 28% (17 of 61) were still able to walk, 51% (31 of 61) were parAparetic, and 21% (13 of 61) were paraplegic. Bowel and bladder dysfunction was present in 49% (30 of 61). After VBR, the outcome of only 57 procedures was available for evaluation because of the postoperative death of 4 patients. Eighty per cent (46 of 57) were able to walk, 18% (10 of 57) were paraparetic, and 2% (1 of 57) were paraplegic. Ninety-three per cent had normal sphincter control. Before laminectomy, 8% (2 of 25) were ambulatory, 84% (21 of 25) were paraparetic, and 8% (2 of 25) were paraplegic. Bowel and bladder dysfunction was present in 76% (19 of 25). After laminectomy, only 23 procedures were evaluated because of the postoperative death of 2 patients. Thirty-nine per cent (9 of 23) were ambulatory, 35% (8 of 23) were paraparetic, and 26% (6 of 23) were paraplegic. Fifty-seven per cent regained normal sphincter control. The operative mortality was 7% (4 of 61) in VBR and 8% (2 of 25) in laminectomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Primary spinal epidural Burkitt's lymphoma.

Three Japanese children suffered from symptoms of spinal cord compression, and myelography demonstrated extradural masses compressing the spinal cord at different levels. Decompressive laminectomy revealed epidural tumors which were resected as completely as possible. Histologic pictures of the tumors showed Burkitt's lymphoma, and the diagnosis of primary epidural Burkitt's lymphoma with clinical stage A was made in each case after postoperative examination. Though postoperative radiotherapy and systemic chemotherapy were administered to all patients, they only survived for a short period of time.

Burkitt Lymphoma↗

Compression of spinal cord caused by spinal deformation in a cat.

An 8-month-old cat with bilateral hindlimb paresis was admitted. Radiography revealed a curvature of the thoracic spine and a partial deformation of thoracolumbar vertebrae (dorsal extrusion of the cranial and caudal edges). Compression of the spinal cord (T9-L1 and L6-7) was found by myelography. Medicinal treatment did not yield the desired result. Hemilaminectomy and laminectomy were done to relieve pressure on the spinal cord leading to improved gait. It is, however, not clear whether this syndrome was primarily caused by metabolic or genetic factors.

Animals↗

[A case of epidural lipomatosis presenting spinal ataxia].

A 41-year-old man was doing well until July 1989, when he noted numbness over soles, followed 4 months later by difficulty in walking. These symptoms were progressively getting worse, and he was admitted to our department on June 12, 1990. General physical examination was unremarkable. Neurologically cranial nerves were intact except old right, traumatic strabismus. Muscle tone and deep tendon reflexes were normal throughout, but bilateral Babinski and Chaddock reflexes were present. Mild weakness of lower extremities were found on muscle testing (4/5). In sensory system, superficial sensory disturbance below T10 was seen, and markedly diminished vibration and position senses of lower extremities were noted. Cerebellar test was intact, although unsteadiness was found on heel-shin test. Romberg sign was definitely positive. His gait was wide-based and ataxic. Laboratory data showed no abnormalities in CBC, chemistry, urinalysis, serological tests and endocrinological examinations. Spinal MRI (Siemens 1.5 Tesla) showed abnormal deposition of epidural fatty tissues compressing spinal cord with flattening of cord from T4 to T8. Spinal ataxia as compressive myelopathy due to epidural lipomatosis was considered and he underwent laminectomy from T4 to T8 with improvement in walking. Epidural lipomatosis is an unusual cause of spinal cord compression, presenting compressive myelopathy, radiculopathy, cauda equina syndrome, intermittent claudication, or back pain. Most of cases were associated with long-term administration of adrenocortical steroid hormone, or underlying diseases, except only 3 cases including ours. This is the first case of spinal epidural lipomatosis presenting progressive gait disturbance due to spinal ataxia.

Adult↗

Compression of rat spinal cord in vitro: effects of ethanol on recovery of axonal conduction.

The effect of ethanol on recovery of neural conduction after spinal cord compression was evaluated in an isolated rat spinal cord preparation. Controlled compression of 50 to 75 percent of the cord cross-section was delivered using a piezoelectric translator. Postcompression compound action potential (CAP) amplitude, latency, and refractory periods were measured relative to pre-compression values. Recovery of CAP's was compared for spinal cords exposed to ethanol in vitro (100 mg/dl bath concentration, started one hour prior to compression) versus those maintained in normal artificial CSF. The in vitro effects of ethanol were evaluated on spinal cords from rats maintained on a normal diet and from those repeatedly intoxicated with ethanol for 15 days prior to the acute experiment. Compression of the cord resulted in an immediate 68% decrease in CAP peak amplitude and an increase in latency (171%) and refractory period (256%). In normal bathing medium, CAP amplitude recovered to 83% of pre-compression values 180 minutes after compression. The addition of ethanol to the artificial CSF did not directly affect CAP parameters, but combined with compression, CAP amplitude recovered to only 42% of pre-compression values 180 minutes after impact (p less than .01). Recovery was less affected by acute ethanol exposure in cords from ethanol pretreated animals. CAP amplitude recovered to 83% of pre-compression levels and was not different from compression-only recovery (p less than 0.10). The data suggest that direct effects of ethanol on axonal membranes may affect the sensitivity of axons to mechanical trauma or their capacity to recover normal function. Since spinal cords from repeatedly exposed animals are less sensitive to the acute effects of ethanol, ethanol may be acting to "fluidize" the axonal membrane.

Alcoholic Intoxication↗

Magnetic resonance imaging features of extradural hematomas associated with intervertebral disc herniation in a dog.

Myelography and magnetic resonance imaging (MRI) were performed on a 4-year-old neutered female Rottweiler with bilateral pelvic limb paresis. On the myelogram, there was extradural spinal cord compression at the level of the T11-12 intervertebral disc. Inadvertent placement of epidural contrast medium also allowed identification of a 1-cm circular filling defect in the epidural space dorsal to the compressed spinal cord. MRI showed partial loss of the nucleus pulposus signal of the T11-12 disc, a focal signal void within the vertebral canal at T11 compatible with a free disc fragment, and extradural masses compressing the spinal cord at T10-11 and T11-12. Hemorrhage within the masses was confirmed on T2*-weighted images. A mixture of hematoma and mineralized disc material was found at surgery, and there was no histopathologic evidence of neoplasia. In this article, the appearance on MRI of hemorrhage associated with intervertebral disc herniation is discussed.

Animals↗