Analysis of spinal cord evoked potential and locomotor function during acute spinal cord compression in cats.

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

Spinal cord evoked potentials and peripheral nerve evoked potentials after spinal cord stimulation were recorded under acute spinal cord compression in 19 cats. To investigate the effects of acute compression upon grey matter and white matter by comparing both potentials. We compared peripheral nerve evoked potentials, recorded at the biceps brachii branch of the musculocutaneous nerve, with descending spinal cord evoked potentials, recorded from the lumbar spinal cord, by stimulation to the C2 level, under compression of the C6 segment. The amplitude of both potentials decreased with increased compression. The second wave of peripheral nerve evoked potentials, which are motor fibre action potentials, decreased sooner than those of the spinal cord evoked potentials. These findings indicate that peripheral nerve evoked potentials are sensitive to acute damage of the segmented compression. This suggests that grey matter is more vulnerable to compression than white matter.

To explore the effect and underlying mechanism of decompression(DE)combined with Governor Vessel(GV)electro-acupuncture(EA) on rats with acute severe upper cervical spinal cord compression injury. Thirty SPF rats were randomly divided into 5 groups(control group A, B and experiment group C, D, E), 6 rats in each group. The model of acute severe upper cervical spinal cord compression injury were made by forcing a balloon catheter put in atlas pillow clearance. The group A was blank one, the group B put balloon catheter in atlas pillow clearance without forcing, and the group C, D, E sustained compressed for 48 h. The group C received electric acupuncture intervention, selecting the Baihui and Dazhui point, having the continuous wave and frequency of 2 Hz, with the treatment time of 15 min and continuous treatment for 14 d; the group D received methylprednisolone intervention, injected by caudal vein; the group E did not received any intervention again. The arterial blood and injured spinal cord tissue of all the rats were obtained after 14 days' treatment, and BBB score was used to evaluate the change of each group hind limbs motor function, the contents of platelet activating factor(PAF) in injured spinal cord tissue and blood serum were assess by ELISA method; the Caspase-9 expression for each group after 14 days' treatment was assess by Western blot method. BBB scores were(21.000±0.000) points at the 6 time points, that was, 1 h, 48 h after forcing in control group, 24 h, 3 d, 7 d, 14 d after treating in experiment group; the score of experimental groups (group C, D, E) were always lower than control groups(group A, B); compared with group E, group C and D were significantly higher(P<0.05); and there was no significant difference between group C and group D(P>0.05). The results of PAF by ELISA method to measure:the concentration of serum PAF, there was no statistical difference among group A, B, D, E (P>0.05), group C was lower than the other groups (P<0.05); the concentration of tissue PAF, there was no significant difference between group A and group B(P>0.05), group D was significantly higher than that of group A, B, and C(P<0.05), group E was the highest one than that of the other groups(P<0.05). Western blot med tests showed that the Caspase-9 protein expression in group A and B was similar (P>0.05), group C was higher than that of group A and B(P<0.05), group D was higher than group A, B and C(P<0.05), group E was the highest than that of group A, B, C and D (P<0.05). Decompression and Governor Vessel electro-acupuncture on acute severe upper cervical spinal cord compression injury had a better effect compare with decompression and methylprednisolone or simple decompression only, its mechanism may be related to lower the PAF levels and downregulating Caspase-9 protein expression in spinal injury tissue.

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.

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 . . .

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

The conventional method of using Conductive Evoked Spinal Cord Potentials (hereinafter abbreviated C-ESCP) to monitor the spinal cord function during surgery on the cervical or thoraco-lumbar region is the recording of ascending spinal cord potentials, and it is not possible to detect dysfunctions of motor pathways or grey matter of the spinal cord at an early stage. To improve this status, we have reported since 1987 on action potentials recorded in the median nerve after a stimulus to the upper cervical spinal cord as a new monitoring method (Descending Segmental Evoked Spinal Cord Potentials; hereinafter abbreviated DS-ESCP), especially on the origin of the potentials and the conductive pathways1,2. In the present study, we have compared the changes in the potentials and pathological findings in cases of acute posterior compression of the spinal cord in order to check this method for its reliability.

Acute Spinal Cord Compression: CQI Framework Increases Resource Efficiency While Promoting Delivery of High-Quality Care

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.

Experiments were conducted to determine the therapeutic value of subarachnoid perfusion of the traumatized dog spinal cord with the fluorocarbon, Fluosol-DA (20%). Control dogs without lesions, but which had durotomy, subarachnoid catheter placement, and saline irrigation for 4 hours, did not have any residual neurological deficit. A series of 41 dogs underwent an acute spinal cord compression using an epidural balloon inflated to a pressure of 160 mm Hg and maintained for 1 hour. Treatment included durotomy only (11 dogs), durotomy with saline perfusion at room temperature (15 dogs), and durotomy with oxygenated Fluosol-DA perfusion at room temperature (15 dogs). The dogs underwent daily grading of neurological status for a 60-day period. Dogs undergoing perfusion of the spinal cord with either saline or oxygenated Fluosol-DA had significantly improved motor recovery (p less than 0.004) compared with dogs undergoing durotomy only. Perfusion with oxygenated Fluosol-DA resulted in significantly better motor recovery (p less than 0.05) than did perfusion with normal saline. Microscopic examination of the traumatized spinal cords failed to reveal a substantial difference between the three groups. However, dogs with better functional results tended to have less destruction of the white matter. Hemorrhagic necrosis of the central gray matter was consistently observed in all traumatized spinal cords.

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.

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.

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.

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.

Hématome sous-dural aigu intrarachidien non traumatique étendu