Acute Spinal Cord Compression

Multiple myeloma presenting with acute bony spinal cord compression and mechanical instability successfully managed nonoperatively

An evidence-based analysis of published radiologic criteria for assessing spinal canal compromise and cord compression in patients with acute cervical spinal cord injury. This study was conducted to determine whether literature-based guidelines could be established for accurate and objective assessment of spinal canal compromise and spinal cord compression after cervical spinal cord injury. Before conducting multicenter trials to determine the efficacy of surgical decompression in cervical spinal cord injury, reliable and objective radiographic criteria to define and quantify spinal cord compression must be established. A computer-based search of the published English, German, and French language literature from 1966 through 1997 was performed using MEDLINE (U.S. National Library of Medicine database) to identify studies in which cervical spinal canal and cord size were radiographically assessed in a quantitative manner. Thirty-seven references were included for critical analysis. Most studies dealt with degenerative disease, spondylosis, and stenosis; only 13 included patients with acute cervical spinal cord injury. Standard lateral radiographs were the most frequent imaging method used (23 studies). T1- and T2-weighted magnetic resonance imaging were used to assess spinal cord compression in only 7 and 4 studies, respectively. Spinal cord size or compression were not precisely measured in any of the cervical trauma studies. Interobserver or intraobserver reliability of the radiologic measurements was assessed in only 7 (19%) of the 37 studies. To date, there are few quantitative, reliable radiologic outcome measures for assessing spinal canal compromise or cord compression in patients with acute cervical spinal cord injury.

A multicenter, retrospective study using computed tomographic and magnetic resonance imaging data to establish quantitative, reliable criteria of canal compromise and cord compression in patients with cervical spinal cord injury. To develop and validate a radiologic assessment tool of spinal canal compromise and cord compression in cervical spinal cord injury for use in clinical trials. There are few quantitative, reliable criteria for radiologic measurement of cervical spinal canal compromise or cord compression after acute spinal cord injury. The study included 71 patients (55 men, 16 women; mean age, 39.7 +/- 18.7 years) with acute cervical spinal cord injury. Causes of spinal cord injury included motor vehicle accidents (n = 36), falls (n = 20), water-related injuries (n = 8), sports (n = 5), assault (n = 1), and farm accidents (n = 1). Canal compromise was measured on computed tomographic scan and T1- and T2-weighted magnetic resonance imaging, and cord compression at the level of maximum injury was measured on T1- and T2-weighted magnetic resonance imaging. All films were assessed by two independent observers. There was a strong correlation of canal compromise and/or cord compression measurements between axial and midsagittal computed tomography, and between axial and midsagittal T2-weighted magnetic resonance imaging. Spinal canal compromise assessed by computed tomography showed a significant although moderate correlation with spinal cord compression assessed by T1- and T2-weighted magnetic resonance imaging. Virtually all patients with canal compromise of 25% or more on computed tomographic scan had evidence of some degree of cord compression on magnetic resonance imaging, but a large number of patients with less than 25% canal compromise on computed tomographic scan also had evidence on magnetic resonance imaging of cord compression. In patients with cervical spinal cord injury, the midsagittal T1- and T2-weighted magnetic resonance imaging provides an objective, quantifiable, and reliable assessment of spinal cord compression that cannot be adequately assessed by computed tomography alone.

Acute dorsal compression of the spinal cord was applied to adult cats, and magnetic resonance signal intensity, spinal cord evoked potentials, and morphologic changes of the spinal cord were examined after 5 hours. The present study investigated the correlation of magnetic resonance signal intensity with spinal cord evoked potentials and spinal cord morphology after 5 hours of spinal cord compression in cats. Neurologic prognosis of the injury might be predicted by an analysis of magnetic resonance signal intensity pattern. Little information is available on relationships between magnetic resonance images and functional or morphologic damage of spinal cord in acute animal experiments. Acute dorsal compression of the spinal cord was performed in 24 anesthetized cats. After laminectomy, the L2 segment was compressed for 5 hours. Spinal cord evoked potentials were recorded by electrodes placed in the epidural space at L4, and the spinal cord was stimulated at T12. The animals were divided into four groups based on changes in the amplitude of spinal cord evoked potentials. Immediately after compression for 5 hours, magnetic resonance images were obtained. Signal intensity of the spinal cord was measured on sagittal midline images. Morphologic changes were assessed. Spinal compression significantly increased the signal intensity of the L1, L2, and L3 segments on T2-weighted and proton density-weighted images. The increase in signal intensity was remarkable in the animals whose spinal cord evoked potentials were reduced greatly (< 40% of the control group). Histologically, edema was present in the high intensity area on T2-weighted and proton density-weighted images. In summary, the present study documents that spinal compression causes tissue edema, which produces high signal intensity on magnetic resonance imaging. The magnetic resonance signal intensity is correlated closely with decreased amplitude of spinal cord evoked potentials.

Objective To explore the clinicopathological features, imaging features and treatment of spinal cord myeloma in patients with spinal cord compression as the first symptom. Methods The retrospective cross-sectional study was conducted which the clinical data of five patients with spinal myeloid sarcoma confirmed by bone marrow aspiration and pathology from January 2014 to December 2017 in Changzheng Hospital. There were 3 males and 2 females, aged from 15 to 54 years old. the tumors were located in 3 cases of thoracic vertebrae and 2 cases of lumbar vertebrae. Four cases were treated with open surgery. After discharge, they were treated with chemotherapy and hematological tumors according to bone marrow puncture and pathological results. Another patient underwent conservative treatment (anti-inflammatory analgesia, nutritional support, chemotherapy, etc.). The observation items were analysed. Results All the 5 patients had a low back pain, three of them had a lower limbs weakness, and one of them was accompanied by paralysis of both lower limbs. X-ray examination showed no abnormal findings. CT and MRI showed bone destruction or soft tissue shadow. Bone marrow aspiration and postoperative pathological examination showed that five cases were leukemia including four acute myeloid leukemia(AML)and one chronic myeloid leukemia(CML). All patients' preoperative symptoms were relieved after treatment. All patients were followed up. One patient underwent IA regimen chemotherapy for five courses, and was treated with allogeneic hematopoietic stem cell transplantation. It had been followed up for 28 months after surgery and still in good condition without tumor recurrence. The other four patients relapsed after chemotherapy, all died of infection, and the survival period was from 5 to 26.5 months. Conclusions Spinal cord compression caused by myeloid sarcoma as an initial symptom is rare. The imaging manifestations of the myeloid sarcoma are lack of specificity and and it is easy to be misdiagnosed. Bone marrow aspiration and pathological examination can confirm the diagnosis. When the symptoms of spinal cord compression occur, it is recommended to perform early tumor decompression. The allogeneic hematopoietic stem cell transplantation and systemic chemotherapy should be performed after surgery. Key words: Sarcoma, myeloid; Leukemia; Spinal compression; Diagnosis; Treatment outcome

Spinal cord compression secondary to spinal extradural myeloid sarcoma in acute myeloid leukaemia: A case report and literature review

Acute spinal cord injury was induced by a clip compression model in rats to approximate spinal cord injury encountered in spinal surgery. Spinal somatosensory-evoked potential neuromonitoring was used to study the electrophysiologic change. To compare and correlate changes in evoked potential after acute compression at different core temperatures with postoperative neurologic function and histologic change, to evaluate current intraoperative neuromonitoring warning criteria for neural damage, and to confirm the protective effect of hypothermia in acute spinal cord compression injury by electrophysiologic, histologic, and clinical observation. With the increase in aggressive correction of spinal deformities, and the invasiveness of surgical instruments, the incidence of neurologic complication appears to have increased despite the availability of sensitive intraoperative neuromonitoring techniques designed to alert surgeons to impending neural damage. Many reasons have been given for the frequent failures of neuromonitoring, but the influence of temperature-a very important and frequently encountered factor-on evoked potential has not been well documented. Specifically, decrease in amplitude and elongation of latency seem not to have been sufficiently taken into account when intraoperative neuromonitoring levels were interpreted and when acceptable intraoperative warning criteria were determined. Experimental acute spinal cord injury was induced in rats by clip compression for two different intervals and at three different core temperatures. Spinal somatosensory-evoked potential, elicited by stimulating the median nerve and recorded from the cervical interspinous C2-C3, was monitored immediately before and after compression, and at 15-minute intervals for 1 hour. Spinal somatosensory-evoked potential change is almost parallel to temperature-based amplitude reduction and latency elongation. Significant neurologic damage induced by acute compression of the cervical spinal cord produced a degree of effect on the amplitude of spinal somatosensory-evoked potential in normothermic conditions that differed from the effect in moderately hypothermic conditions. Using the same electromonitoring criteria,moderately hypothermic groups showed a significantly higher false-negative rate statistically (35%) than normothermic groups (10%). Systemic cooling may protect against the detrimental effects of aggressive spinal surgical procedures. There is still not enough published information available to establish statistically and ethically acceptable intraoperative neuromonitoring warning and intervention criteria conclusively. Therefore, an urgent need exists for further investigation. Although a reduction of more than 50% in evoked potential still seems acceptable as an indicator of impending neural function loss, maintenance of more than 50% of baseline evoked potential is no guarantee of normal postoperative neural function, especially at lower than normal temperatures.

Managing Nontraumatic Acute Back Pain

Background and Objectives: Metastatic spinal cord compression represents a substantial risk to patients, given its potential for spinal cord and/or nerve root compression, which can result in severe morbidity. This study aims to evaluate the effectiveness of a diagnostic-therapeutic algorithm developed at our hospital to mitigate the devastating consequences of spinal cord compression in patients with vertebral metastases. Materials and Methods: The algorithm, implemented in our practice in January 2022, is based on collective clinical experience and involves collaboration between emergency room physicians, oncologists, spine surgeons, neuroradiologists, radiation oncologists, and oncologists. To minimize potential confounding effects from the COVID-19 pandemic, data from the years 2019 and 2021 (pre-protocol) were collected and compared with data from the years 2022 and 2023 (post-protocol), excluding the year 2020. Results: From January 2022 to December 2023, 488 oncological patients were assessed, with 45 presenting with urgency due to suspected spinal cord compression. Out of these, 44 patients underwent surgical procedures, with 25 performed in emergency settings and 19 cases in elective settings. Comparatively, in 2019 and 2021, 419 oncological patients were evaluated, with 28 presenting with urgency for suspected spinal cord compression. Of these, 17 underwent surgical procedures, with 10 performed in emergency scenarios and 7 in elective scenarios. Comparing the pre-protocol period (years 2019 and 2021) to the post-protocol period (years 2022 and 2023), intrahospital consultations (commonly patients neurologically compromised) for spine metastasis decreased (105 vs. 82), while outpatient consultations increased remarkably (59 vs. 124). Discussion: Accurate interpretation of symptoms within the context of metastatic involvement is crucial for patients with a history of malignancy, whether presenting in the emergency room or oncology department. Even in the absence of a cancer history, careful interpretation of pain characteristics and clinical signs is crucial for diagnosing vertebral metastasis with incipient or current spinal cord compression. Early surgical or radiation intervention is emphasized as it provides the best chance to prevent deficits or improve neurological status. Preliminary findings suggest a notable increase in both the number of patients diagnosed with suspected spinal cord compression and the proportion undergoing surgical intervention following the implementation of the multidisciplinary protocol. The reduced number of intrahospital consultations (commonly patients neurologically compromised) and the increased number of visits of outpatients with vertebral metastases indicate a heightened awareness of the issue, leading to earlier identification and intervention before neurological worsening necessitating hospitalization. Conclusions: A comprehensive treatment planning approach is essential, and our multidisciplinary algorithm is a valuable tool for optimizing patient outcomes. The protocol shows potential in improving timely management of spinal cord compression in oncological patients. Further analysis of the factors driving these changes is warranted. Limitations: This study has limitations, including potential biases from the retrospective nature of data collection and the exclusion of 2020 data due to COVID-19 impact. To enhance the robustness of our results, long-term studies are required. Moreover, the single-center study design may limit the validity of the findings. Further multicenter studies would be beneficial for validating our results and exploring underlying factors in detail.

Vertebral hemangioma is common, benign lesion that occurs mostly in the body of vertebral bones and is mostly asymptomatic although they may occasionally extend into the posterior elements. An isolated location in the neural arch of vertebrae is extremely rare. An acute spinal cord compression by an exceptional hemangioma involving spinous process of the seventh thoracic vertebra and respecting vertebral body in a 40-year-old woman is reported. On magnetic resonance imaging of the spine, the lesion was hypointense on T1-weighted image, hyperintense on T2-weited image, and enhancing avidly, causing compression of spinal cord. Our case is exceptional by the rapidly character of symptom installation and by atypical and elective involvement of spinous process.

Axonal injury was examined in 18 human cases of acute spinal cord compression using amyloid precursor protein as a marker of AI. To topographically map and semiquantitate axonal injury in spinal cord compression of sufficient severity to produce para- or quadriplegia. Amyloid precursor protein is carried along the axon by fast axoplasmic transport and has been extensively used as a marker of traumatic axonal injury. The study group comprised 18 cases of spinal cord compression (17 due to fracture dislocation of the vertebral column and 1 iatrogenic compression from Harrington rods) and two normal control. All the cords were examined according to a standard protocol, and at least 10 segmental levels were immunostained using a monoclonal antibody to amyloid precursor protein and immunopositive AI was semiquantitated using a grading system to provide the axonal injury severity score (AISS). The focal injury at the site of cord compression (haemorrhage, haemorrhagic necrosis, ischaemic necrosis) was also semiquantitated to provide the focal injury area score (FIAS). AI occurring around the site of focal compression (focal axonal injury severity score or FAISS) was distinguished from AI distant to the focal injury (nonfocal axonal injury severity score or NFAISS). All 18 cases showed widespread amyloid precursor protein immunoreactive axonal injury and the AISS ranged from 28 to 60%. In all cases, the FAISS was greater than the NFAISS and there was a statistically significant relationship between the AISS and the FIAS. Acute spinal cord compression of sufficient severity to produce permanent paralysis causes widespread axonal damage that is maximal at the site of compression but also present throughout the length of the cord in segments far distant from the site of the focal injury.

Acute spinal cord compression with myelopathy is a neurologic emergency. Recognition of spinal cord compression, timely imaging, and treatment are important to restore and preserve neurologic function. This chapter reviews the causes and clinical approach to spinal cord compression. Traumatic and nontraumatic causes of spinal cord compression are addressed together because of their overlapping symptoms and management. The chapter concludes with a brief discussion of peripheral nerve injury.

Acute balloon compression of the thoracic spinal cord for 15, 7, 5, 3, and 1 minute in monkeys caused immediate disappearance of the spinal evoked response and complete focal ischemia of the compressed segment in all animals. Only the animals in the 1-minute group, however, demonstrated return of the evoked response. These data, coupled with data from previous experiments of slow balloon compression of the spinal cord and spinal cord ischemia, suggest that the major pathological substrate for neural dysfunction after balloon compression of the spinal cord, be it acute or slow, is physical injury of the neural membrane, irrespective of blood flow changes. These findings also suggest that the ability of that membrane to recover is related to rapidity and length of time of compression. Focal changes in blood flow do not appear to be significant in this mechanism.

We studied MR images of the spine in a consecutive series of 100 patients with acute compression of the spinal cord due to metastases. All patients had documented neurological deficit and histologically proven carcinoma. MRI was used to localise bony metastatic involvement and soft-tissue impingement of the cord. A systematic method of documenting metastatic involvement is described. A total of 43 patients had compression at multiple levels; 160 vertebral levels were studied. In 120 vertebrae (75%), anterior, lateral and posterior bony elements were involved. Soft-tissue impingement of the spinal cord often involved more than one quadrant of its circumference. In 69 vertebrae (43%) there was concomitant anterior and posterior compression. Isolated involvement of a vertebral body was observed in only six vertebrae (3.8%). We have shown that in most cases of acute compression of the spinal cord due to metastases there is coexisting involvement of both anterior and posterior structures.

Primary hepatocellular carcinoma (HCC) ranks as the most lethal malignancy in Taiwan. Its initial presentation as acute spinal cord compression from epidural metastasis is rare. Because of newer treatment modalities and better control of the primary tumor, the mean survival has increased, making early diagnosis and detection of distant metastases of utmost importance. The authors describe a 60-year-old man presented with a sudden onset of bilateral lower limb weakness and a sensory level at T8. Plain film of the thoracic spine was normal. Magnetic resonance imaging of the thoracic spine showed a large intraspinal epidural tumor at T6 level causing spinal cord compression. A diagnosis of HCC with epidural metastasis was made after surgical removal of the tumor mass.