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After recalling the historical background of treatment of Pott disease paraplegia, seven cases of tuberculous medullary compression treated by triple antibiotic therapy, corticosteroids and cast immobilization are reported. The diagnostic, etiologic and prognostic criteria which indicate the initiation and continuation of such treatment are defined.
The study design was to decrease the damage of spinal cord on the experimentally induced acute spinal cord injury in rats. The objective of this study was to evaluate whether recombinant human erythropoietin (rHu-EPO) and methylprednisolone (MPSS) improve neurological function and histopathological changes if systemically administered after traumatic spinal cord injury. This study included 48 rats that underwent experimental SCI. Forty-eight animals were randomly divided into six groups. Animals constituted a moderate compression of 0.6 N that was produced by application of an aneurysm clip at level T3 for 1 min. rHu-EPO (1,000 and 3,000 U (Unit) per kg of body weight i.p.) and MPSS (30 mg/kg) were administered 5 min after injury, and control group was saline treated. (1) Control group (n=8), (2) MPSS group (n=8), (3) rHu-EPO 1,000 U group (n=8), (4) MPSS + rHu-EPO 1,000 U group (n=8), (5) rHu-EPO 3,000 U group (n=8), and (6) MPSS + rHu-EPO 3,000 U group (n=8). The neurological function and histopathology were evaluated at 24 and 72 h. According to the neurological functional test scores significant improvements between the control group and the other groups that had taken medical treatment were observed (P<0.001). Histopathologically severe ischemic findings were observed in the control group. A significant decrease in ischemic damage was detected in MPSS + rHu-EPO 3,000 U group (P<0.001). The most significant neurological functional and histopathological improvements were observed after systemical administration of MPSS + rHu-EPO 3,000 U and rHu-EPO 3,000 U. Furthermore, the MPSS + rHu-EPO 3,000 U group provides the most improved neurological functional and histopathological recovery.
One hundred sixty-six patients presented to a cancer center with malignant spinal cord compression (SCC) proven by magnetic resonance imaging (MRI). The majority of patients (92%) were treated with radiotherapy. Changes in functional capability over time were assessed using performance (PS) and neurological status (NS). Over the course of treatment, there was no significant change in PS or NS. The median survival from confirmation of SCC was 82 days (range 1-1349 days). Survival was significantly better for those presenting with good functional status. One hundred thirteen patients (68%) were discharged from hospital; 88 (78%) were discharged home, 11% were sent to another hospital, 4% were transferred to a rehabilitation unit, and 5% went to a hospice. Fifty-three patients (32%) died before discharge. The confirmation that PS and NS have prognostic significance in the functional outcome of patients with SCC may prove helpful in decisions regarding care planning for individual patients with SCC who are discharged from hospital.
BACKGROUND: Primary epidural non-Hodgkin lymphoma (NHL) is a rare but devastating event in pediatric oncology. Spinal cord compression due to an epidural mass from NHL, although it presents as a localized problem, in fact, is a systemic disease. Over the last 3 decades, aggressive systemic treatments with central nervous system prophylaxis have been designed with improving results. PROCEDURE: We reviewed the 20-year experience of the treatment of NHL with the LSA2-L2 protocol in our institution. Among 256 patients treated, five presented with primary epidural mass. Clinical features, treatment, and outcome of those five patients are presented. RESULTS: Three patients out of five responded favorably, and after a median follow-up of 10 years, they are cured. After presenting with paraplegia, functional and neurological recoveries were excellent. Of the patients who failed treatment, relapse occurred early, either during the treatment or right after completion of therapy. The relapses were within the central nervous system as well as systemic. CONCLUSIONS: Patients with primary epidural NHL presented with long histories of persistent back pain. Plain films of the spine were useless. All patients were diagnosed when neurologic damage had already been established. However, when the epidural NHL is treated aggressively with systemic chemotherapy and vigorous rehabilitation, the prognosis for complete neurological recovery and cure of the lymphoma is encouraging.
STUDY DESIGN: A case is reported in which a patient had acute paraplegia with sensory loss caused by a spontaneous epidural hematoma that was ascribed to bleeding of pre-existing myeloma lesions of the thoracic vertebrae. OBJECTIVES: To highlight the causes of secondary epidural hematomas with special attention to pre-existing vertebral or epidural lesions. SUMMARY OF BACKGROUND DATA: There are no apparent previous reports of epidural spinal hematomas ascribed to underlying malignant diseases. Benign dysplasia, such as hemangioma or Paget's disease, has been implicated in a few cases. METHODS: A case of spontaneous dorsal epidural hematoma is reported in a patient followed up for plasma cell myeloma with osteolytic lesions in the lower thoracic spine. There was no history of major trauma or coagulation disorders. Complete loss of motor and sensory function in both lower limbs was noted, with sphincter dysfunction. Magnetic resonance imaging of the thoracic spine showed a large posterolateral epidural hematoma responsible for spinal cord compression. RESULTS: The patient failed to improve despite surgical decompression within 6 hours of symptom onset. He died 13 days later of refractory bacterial pneumonia. A large epidural hematoma adjacent to myelomatous lesions of the thoracic vertebrae was found at autopsy. CONCLUSIONS: This is the first reported case of spontaneous epidural hematoma ascribed to underlying malignant disease, with confirmation of the diagnosis by postmortem examination. Possible mechanisms include tumor-related epidural inflammation and fragility of epidural venous plexuses.
Thalassemia is a common hematological disease in Southeast Asia. Extramedullary hematopoiesis is common sequelae in thalassemic patients but extramedullary hematopoiesis in the spinal epidural space that leads to paraparesis in pregnancy is very rare. We managed a thalassemic patient with extramedullary hematopoiesis and spinal cord compression during pregnancy. The diagnosis was made on clinical features and magnetic resonance imaging (MRI) showing a paravertebral mass infiltrating the epidural space. She was treated successfully with repeated blood transfusions until delivery. Fetal growth restriction was found but otherwise the fetus was clinically normal. She had an uneventful recovery when she was seen 6 weeks after delivery.
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Symptomatic arachnoid cysts of the spine are uncommon in children and have only rarely been reported to occur extradurally. The authors report a case of multiple extradural spinal arachnoid cysts in a 9-year-old child who presented with signs of spinal cord compression. The extent of the disease, which affected the thoracic, lumbar, and sacral spine, and the number of independent cysts make this case unique and suggest an underlying defect in the dura of the spinal canal that is predisposed to the formation of cysts. The investigations of choice, surgical planning, and surgical technique are considered. The literature is reviewed and mechanisms of cyst formation discussed.
Protein gene product 9.5 (PGP 9.5) is a neuron-specific protein which acts as a ubiquitin carboxyl-terminal hydrolase. It facilitates the conversion of polyubiquitin to monoubiquitin, which can be reused for another catalytic cycle. Monoubiquitin plays an important role in degrading abnormal and denatured proteins. Previously, we have reported that ubiquitin-like immunoreactivity is expressed in axonal swellings following compression trauma to the rat thoracic cord. It was characterized by fast occurrence, progressive increase and gradual disappearance over a period of 9 days. The expression of PGP 9.5 has now been studied in the same material. Control rats showed a weak PGP 9.5 immunoreactivity in the nerve cell bodies of the cord. Except for the corticospinal tracts, the axons of other longitudinal tracts were weakly stained. Accumulation of PGP 9.5 immunoreactivity occurred in expanded axons at the site of compression already 4 h after trauma. They became more frequent in number 1 and 4 days after injury and remained so over the entire observation period of 9 days. The labelled axons were randomly distributed in the longitudinal tracts, but were never found in the corticospinal tracts. The extent of immunoreactivity was related to the degree of impact on the cord. Compression injury thus induces accumulation of both ubiquitin and PGP 9.5 immunoreactivity in axonal expansions. The injured axons may have a mechanism for degradation of proteins by the ubiquitin-mediated proteolytic pathway and another mechanism for effective ubiquitin regenerative cycling by the action of PGP 9.5.
Proprioceptive loss, paresthesias, and atrophy of the hands can occur with disorders afflicting the upper cervical spinal cord. The diagnosis might be erroneous, because compression in this region might produce signs and symptoms that seem to originate in the lower cervical cord. This article reviews the clinical presentation and radiographic data of a consecutive series of 11 patients who presented between 1992 and 1994 with an extradural lesion above the C4 level. Each patient had a characteristic syndrome of finger and hand dysesthesia, hand atrophy, and occipital or cervical pain. These complaints usually preceded the development of spasticity and gait disturbance. Initial diagnoses included brachial plexopathy, shoulder dysfunction, viral syndrome, and cervical spondylosis at a lower segment. Cervical spondylosis or a herniated disc was the most common pathogenesis. The most commonly involved level was C3-C4. Nine patients underwent a surgical procedure; eight showed significant postoperative improvement (mean time of follow-up examination, 9.7 mo; follow-up range, 1-24 mo). One patient was lost to follow-up. Although the pathophysiology of these findings is unknown, theories include anterior spinal artery ischemia, venous obstruction, and differential decussation of the forelimb and hindlimb fibers of the corticospinal tract. Recognition of this syndrome might prevent inappropriate operative intervention in patients with coexisting pathological conditions of the lower cervical spinal cord.
Retroperitoneal fibrosis is a rare disorder in which the abnormal fibrotic tissue compresses retroperitoneal organs. In the majority of patients no obvious cause can be found, hence the name idiopathic retroperitoneal fibrosis. The process can also arise from other anatomic areas, suggesting a multifocal origin. We report a case of dorsal epidural compression in a 63-year-old patient harboring idiopathic retroperitoneal fibrosis. A magnetic resonance imaging scan revealed the precise location of the lesion. It is suggested that retroperitoneal fibrosis should be considered in the differential diagnosis of epidural spinal cord compression.
An unusual case of congenital generalized fibromatosis in which involvement of the spinal dura mater was accompanied by flaccid paralysis in the lower limbs is presented.