Acute Spinal Cord Compression, Spinal Cord Trauma, and Peripheral Neural Injury

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

Background: Spinal cord compression is a formidable complication of advanced cancer, and clinicians of copious specialities often have to encounter significant complex challenges in terms of diagnosis, management, and prognosis. Metastatic lesions from cancer are a common cause of spinal cord compression, affecting a substantial portion of oncology patients, and only in the US has the percentage risen to 10%. Acute metastasis-correlated spinal cord compression poses a considerable clinical challenge, necessitating timely diagnosis and intervention to prevent neurological deficits. Clinical presentation is often non-specific, emphasizing the importance of thorough evaluation and appropriate differential diagnosis. Diagnostic workup involves various imaging modalities and laboratory studies to confirm the diagnosis and assess the extent of compression. Treatment strategies focus on pain management and preserving spinal cord function without significantly increasing patient life expectancy, while multidisciplinary approaches are often required for optimal outcomes. Prognosis depends on several factors, highlighting the importance of early intervention. We provide an up-to-date overview of acute spinal cord compression in metastases, accentuating the importance of comprehensive management strategies. Objectives: This paper extensively explores the pathophysiology, clinical presentation, diagnostic strategies, treatment modalities, and prognosis associated with spinal cord metastases. Materials and Methods: A systematic literature review was conducted in accordance with the PRISMA guidelines. Conclusions: We aim to help healthcare professionals make informed clinical decisions when treating patients with spinal cord metastases by synthesizing current evidence and clinical insights.

Background: Intervertebral disc disease is a usual neurological disorder in dogs, which the spinal cord is compressed by intervertebral disc extrusion or protrusion. Fibrocartilaginous embolic myelopathy isan acute infarction disease of spinal cord caused by fibrocartilaginous emboli histologically identical to the nucleus pulposus of intervertebral discs. The aim of this report is present two cases of fibrocartilaginous embolic myelopathy in dogs with intervertebral disc disease.Cases: Two dogs - dachshund breed - were referred to the Veterinary Medical Teaching Hospital of the UFSM. In the first case, the dog was three years old and the owner described complete inability to move the pelvic limbs. The neurological examination revealed paraplegia, postural reactions deficits, normal spinal reflexes and muscle tonus in the hind limbs, pain on palpation in T12-T11 region and loss of deep pain in hind limbs. In the other case, the dog was seven years old and the owner described partial inability to move four limbs. The neurological examination revealed non-ambulatory tetraparesis, postural reactions deficit, normal spinal reflexes in four limbs and pain on palpation in cervical spine. In both cases, the presumptive diagnosis was intervertebral disc disease and surgical treatment was indicated. The dog with thoracolumbar injury died during the anesthesia and the dog with cervical injury was euthanized, after decision of owner. During the necropsy was observed intervertebral disc extrusion between L1-L2 vertebrae in a dog and between C3-C4 vertebrae in the other case with cartilaginous fragments in the spinal canal. Histopathology revealed marked diffuse necrosis with multifocal hemorrhage and cartilaginous emboli.Discussion: Fibrocartilaginous embolic myelopathy is commonly reported in large and giant breed dogs, though also occur in small and medium-sized breeds of dogs. One hypothesis is the pulpous nucleus remains soft for a longer period in large breed dogs, empowering to infiltration in the spinal cord vessels. The intervertebral disc extrusion occurs predominantly in dogs with age between three and six years old, in the cervical, thoracolumbar (T11-L3) and lumbar regions. Chondroid or fibroid degeneration of the intervertebral disc is the most common cause of spinal cord compression in small animals. In chondrodistrophic breed dogs is frequently chondroid degeneration, which the nucleus pulposus moves into the spinal canal through rupture of the annulus fibrosus (extrusion or Hansen type I), causing acute spinal cord compression. The prevalence of fibrocartilaginous embolism in adult and old dogs increase the possibility of predisposing factors, facilitating the injection intravascular of nucleus pulposus material. One of the most accepted theories about the mechanism of fibrocartilaginous emboli into the vessels is due to increase of inside discal pressure and liberation of fibrocartilaginous emboli from nucleus pulposus into the vertebral artery for retrograde flow, reaching the spinal cord by blood flow. The simultaneous occurrence of intervertebral disc disease and the infarction of spinal cord in the proximate region accentuate the hypothesis that the etiology of fibrocartilaginous embolic myelopathy is mechanical into the vessels of the spinal cord.Keywords: neurology, spinal cord, intervertebral disc disease, dogs.

Epidural hematoma is a rare cause of spinal cord compression, which usually provokes severe neurological deficits. It is presumed to originate from venous or, more probably, arterial bleeding. Thrombocytopenia and other disorders of coagulation may precipitate the onset of epidural hematoma and facilitate the evolution of the disease. We report the case of a patient suffering from a non-Hodgkin's lymphoma with severe thrombocytopenia during a MACOP-B schedule, who presented with a spontaneous cervical epidural hematoma. We discuss the etiopathological aspects, diagnosis, and treatment of this rare cause of acute cervical spinal cord compression.

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

Acute idiopathic spinal subdural hematoma: What to do in an emergency?

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.

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

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 compression of the spinal cord is a devastating but treatable disorder. Diseases that cause acute spinal cord compression constitute a special category because they originate in the spinal column and narrow the spinal canal. This review addresses the disorders that account for most instances of acute spinal cord compression: trauma, tumor, epidural abscess, and epidural hematoma. The pathophysiological features and management of these disorders are similar to those of other acute and serious spinal conditions. The medical context of spinal cord compression determines the diagnosis and directs treatment. Traumatic cord compression is often self-evident. Cord compression in patients with . . .

Two children presented with acute spinal cord compression by primary and metastatic intraspinal mesenchymal chondrosarcoma, a rare pediatric malignancy. Patients with the primary intraspinal tumor usually present early and often respond well to combined surgery, irradiation and chemotherapy. Patients with intraspinal metastases present late in the course of their disease and their prognoses are poor.

Systematic review and meta-analysis. To perform a systematic review of the clinical symptoms, radiographic findings, and outcomes after spinal decompression in B-cell lymphoma. B-cell lymphoma is a potential cause of spinal cord compression that presents ambiguously with nonspecific symptoms and variable imaging findings. Surgical decompression is a mainstay for both diagnosis and management, especially in patients with acute neurological deficits; however, the efficacy of surgical intervention compared with nonoperative management is still unclear. The databases of Medline, PubMed, and the Cochrane Database of Systemic Reviews were queried for all articles reporting spinal B-cell lymphoma. Data on presenting symptoms, treatments, survival outcomes, and histologic markers were extracted. Using the R software "survival" package, we generated bivariate and multivariate Cox survival regression models and Kaplan-Meier curves. In total, 65 studies were included with 72 patients diagnosed with spinal B-cell lymphoma. The mean age was 56.22 (interquartile range: 45.00-70.25) with 68% of patients being males and 4.2% of patients being immunocompromised. Back pain was the most common symptom (74%), whereas B symptoms and cauda equina symptoms were present in 6% and 29%, respectively. The average duration of symptoms before presentation was 3.81 months (interquartile range: 0.45-3.25). The most common location was the thoracic spine (53%), with most lesions being hyperintense (28%) on T2 magnetic resonance imaging. Surgical resection was performed in 83% of patients. Symptoms improved in 91% of patients after surgery and in 80% of patients treated nonoperatively. For all 72 patients, the overall survival at 1 and 5 years was 85% (95% CI: 0.749-0.953; n = 72) and 66% (95% CI: 0.512-0.847; n = 72), respectively. Although surgery is usually offered in patients with acute spinal cord compression from B-cell lymphoma, chemotherapy and radiation alone offer a hopeful alternative to achieve symptomatic relief, particularly in patients who are unable to undergo surgery.

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.

Background:Spontaneous epidural hematoma arising from the ligamentum flavum is a rare cause of acute spinal cord compression. There are only four reports in the cervical spine literature, and all were managed with surgery. Here, we describe an acute case of a spontaneous epidural hematoma arising from the ligamentum flavum in the cervical spine successfully managed without surgery.Case Description:A 69-year-old woman with a cervical spine epidural hematoma contained within the ligamentum flavum presented with paroxysmal neck pain and stiffness without a history of trauma. The magnetic resonance imaging (MRI) revealed a posterolateral epidural hematoma contained within the ligamentum flavum. As the patient was intact, she was managed conservatively with cervical orthosis. Three months later, she was symptom-free, and the hematoma resolved on the follow-up MRI study.Conclusion:Spontaneous epidural hematoma arising from ligamentum flavum is a rare cause of spinal cord compression. Previous reports have described success with surgical decompression. However, initial observation and conservative management may be successful as illustrated in this case.

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.