Acute Traumatic Central Cord Syndrome Research Articles

Predictors of outcome in acute traumatic central cord syndrome due to spinal stenosis

the objective of this study was to elucidate the relationship between admission demographic data, validated injury severity measures on imaging studies, and clinical indicators on the American Spinal Injury Association (ASIA) motor score, Functional Independence Measure (FIM), manual dexterity, and dysesthetic pain at least 12 months after surgery for acute traumatic central cord syndrome (ATCCS) due to spinal stenosis. over a 100-month period (January 2000 to April 2008), of 211 patients treated for ATCCS, 59 cases were due to spinal stenosis, and these patients underwent surgical decompression. Five of these patients died, 2 were lost to follow-up, 10 were not eligible for the study, and the remaining 42 were followed for at least 12 months. in the cohort of 42 patients, mean age was 58.3 years, 83% of the patients were men, and 52.4% of the accidents were due to falls. Mean admission ASIA motor score was 63.8 (upper extremities score, 25.8 and lower extremities score, 39.8), the spinal cord was most frequently compressed at skeletal segments C3-4 and C4-5 (71%), mean midsagittal diameter at the point of maximum compression was 5.6 mm, maximum canal compromise (MCC) was 50.5%, maximum spinal cord compression was 16.5%, and length of parenchymal damage on T2-weighted MR imaging was 29.4 mm. Time after injury until surgery was within 24 hours in 9 patients, 24-48 hours in 10 patients, and more than 48 hours in 23 patients. At the 1-year follow-up, the mean ASIA motor score was 94.1 (upper extremities score, 45.7 and lower extremities score, 47.6), FIM was 111.1, manual dexterity was 64.4% of baseline, and pain level was 3.5. Stepwise regression analysis of 10 independent variables indicated significant relationships between ASIA motor score at follow-up and admission ASIA motor score (p = 0.003), MCC (p = 0.02), and midsagittal diameter (p = 0.02); FIM and admission ASIA motor score (p = 0.03), MCC (p = 0.02), and age (p = 0.02); manual dexterity and admission ASIA motor score (p = 0.0002) and length of parenchymal damage on T2-weighted MR imaging (p = 0.002); and pain level and age (p = 0.02) and length of parenchymal lesion on T2-weighted MR imaging (p = 0.04). the main indicators of long-term ASIA motor score, FIM, manual dexterity, and dysesthetic pain were admission ASIA motor score, midsagittal diameter, MCC, length of parenchymal damage on T2-weighted MR imaging, and age, but different domains of outcome were determined by different predictors.

The Urgency of Surgical Decompression in Acute Central Cord Injuries With Spondylosis and Without Instability

Systematic review, ambispective analysis of observational data. To make recommendations as to whether or not urgent surgical decompression is ever indicated as the optimal treatment for enhancing neurologic recovery in a patient with acute central cord injury without fracture or instability. There are currently no standards regarding the role and timing of decompression in acute traumatic central cord syndrome. In the setting of TCCS without spinal column instability, much controversy exists. We have performed a thorough literature search based on the following question: "Is there a role for urgent (within 24 hours from injury to surgery) surgical decompression in acute central cord syndrome without fracture or instability specifically to enhance neurologic recovery?" Data including patient demographics, mechanism of injury, comorbidities, neurologic status, and surgical treatment was analyzed from a multicenter STSG observational database. Outcome measured included ASIA Motor Score, ASIA Grade, Functional Independence Measure (FIM) Score, SF-36, Sphincter Disturbance, and Ambulatory status. Measures were recorded on admission, discharge, 6 months and 1 year. At 12-month follow-up, early surgery resulted in a 6.31 point greater improvement in total motor score than did the late surgery group, with a P = 0.0358. At 6-month follow-up, early surgery result in higher chance of improvement in ASIA Grade than late surgery, with an odds ratio = 3.39, while at 12-month follow-up early surgery resulted in a higher chance of improvement in ASIA Grade, with an odds ratio of 2.81. Patients who were operated on within 24 hours had 7.79 U more improvement in FIM Total Score than late surgery at 6 month follow-up, with P = 0.0474. The consensus of experts following review of relevant and examination of observational dataset concluded that it is reasonable and safe to consider early surgical decompression in patients with profound neurologic deficit (ASIA = C) and persistent spinal cord compression due to developmental cervical spinal canal stenosis without fracture or instability. Those with less severe deficit (ASIA = D) can be treated with initial observation with surgery potentially at a later date depending on the extent and temporal profile of the patients neurologic recovery.

Central cord syndrome in Ireland: the effect of age on clinical outcome

Central cord syndrome is an incomplete spinal cord injury first described by Schneider et al. (J Neurosurg 11:546-547, 1954). The typical neurological deficit is symmetrical incomplete quadriplegia affecting the upper more than the lower limbs; sensory impairment is variable and urinary retention is common. Records of all patients with acute traumatic central cord syndrome admitted to the National Spinal Injuries Unit from 1999 to 2007 were compiled from a prospectively collected computerized spinal database. Data recorded included patient demographic profile, mechanism of injury, initial neurological deficit, treatment instituted, complications of treatment, and final neurological status. A total of 50 patients with acute traumatic central cord syndrome were identified accounting for 6.2% of all admissions to the spinal injuries unit. There were 42 men and 8 women. The mean age was 56.1 years with a range of 41-88 years. We stratified patients according to age at injury to determine the effect of age on clinical outcome. There were 13 patients <50 years of age, 24 aged 50-70, and 13 aged >70 years. The mean follow-up time was 42.2 months. More than one-third of patients were intoxicated with alcohol at the time of the injury. Both upper and lower limb motor scores and total sensory scores improved in all age groups. Absolute and relative improvements were greatest in patients <50 years of age. Sphincter disturbance was documented in 42% of all the patients on admission. At follow up 12% of patients had residual disturbance. At final follow up none of the patients under 70 years of age had residual sphincter disturbance while 60% of those aged >70 years group had. Both of these results reached statistical significance. In conclusion, central cord syndrome is a common cause of acute traumatic neurological deficit, with alcohol intoxication being a common confounder at the time of injury. The clinical outcomes are significantly worse in patients aged 70 years or older.

Acute central cord syndrome with bodybuilder sign

We describe a 81-year-old man who after falling face forward and hyperextending his neck suffer an acute cervical spinal cord injury consistent with acute traumatic central cord syndrome (ATCCS) who developed a peculiar posture with arm abduction at the shoulders and flexion at the elbows and wrists resembling the pose of a bodybuilder.

Central cord injury: pathophysiology, management, and outcomes

Cervical spinal trauma can result in a heterogeneous collection of spinal cord injury syndromes. Acute traumatic central cord syndrome is a common category of which no uniform consensus on the etiology, pathophysiology, and treatment exists. To evaluate and review potential pathophysiology, current treatment options, and management of central cord injuries. Comprehensive literature review and clinical experience. A systematic review of Medline for articles related to central cord and spinal cord injury was conducted up to and including journal articles published in September 2005. Central cord injuries is a clinical definition which is composed of a heterogeneous population for which medical management and surgical decompression and stabilization provide improved neurologic recovery.

Pathophysiology of acute traumatic central cord syndrome based on the mechanical features of the spinal cord white and gray matter

Pathophysiology of acute traumatic central cord syndrome based on the mechanical features of the spinal cord white and gray matter

Acute traumatic central cord syndrome—experience using surgical decompression with open-door expansile cervical laminoplasty

Background Open-door expansile cervical laminoplasty (ODECL) is an effective surgical technique in the treatment of multilevel cervical spondylotic myelopathy. In the present study, we reviewed the safety and short-term neurological outcome after expansile cervical laminoplasty in the treatment of acute central cord syndrome. Methods We retrospectively reviewed our database over a 3-year period (January 1997-January 2001) and identified 69 surgically treated cervical spinal cord injuries, including 29 cases of acute traumatic central cord syndrome (ATCCS). Fifteen of these patients underwent expansile cervical laminoplasty, whereas 14 did not because of radiographic evidence of sagittal instability. We collected data on the preoperative and the immediate postoperative and 3-month neurological examinations. Neurological function was assessed using the Asia Spinal Injury Association (ASIA) grading system. We also reviewed the occurrence of complications and short-term radiological stability after the index procedure. Results The median age was 56 years. All patients had hyperextension injuries with underlying cervical spondylosis and stenosis in the absence of overt fracture or instability. The average delay from injury to surgery was 3 days. The preoperative ASIA grade scale was grade C, 8 patients, and grade D, 7 patients. There were no cases of immediate postoperative deterioration or at 3 months follow-up. Neurological outcome: 71.4% (10/14) of patients improved 1 ASIA grade when examined 3 months post injury. Conclusions Surgical intervention consisting of ODECL can be safely applied in the subset of patients with ATCCS without instability who have significant cervical spondylosis/stenosis. Open-door expansile cervical laminoplasty is a safe, low-morbidity, decompressive procedure, and in our patients did not produce neurological deterioration.

Surgery for acute subaxial traumatic central cord syndrome without fracture or dislocation

Twenty-two patients with subaxial acute traumatic central cord syndrome (CCS) without fracture or dislocation who underwent surgery between 1995 and 2002 were reviewed, retrospectively. There were 13 males and nine females ranging in age from 24 to 84 years (mean 61.2). Falls were the most common injury (68%), followed by motor vehicle accidents (32%). All patients had dynamic cervical lateral radiographs and magnetic resonance imaging (MRI). Cord compression was present in all cases and cervical instability in 11. Associated pathology included disc herniation in seven patients, cervical spondylosis (CS) in 11 and ossification of the posterior longitudinal ligament (OPLL) in four. Anterior decompression and fusion was performed in 12 patients with 1- or 2-level lesions. Posterior decompression and fusion was performed for multilevel lesions in 11 patients, including one patient who required re-operation. The interval between injury and surgery ranged from 1 to 37 days (mean 8.0). Postoperatively, all patients improved clinically. We conclude that surgical management of subaxial acute traumatic CCS without fracture or dislocation improved neurological status and prevented delayed neurological deterioration in our patients.

Acute traumatic central cord syndrome: magnetic resonance imaging and clinical observations.

Acute traumatic central cord syndrome has been classically thought to be caused by a hemorrhage that primarily affects the central part of the spinal cord and that destroys the axons of the inner part of the corticospinal tract devoted to the motor control of the hands. Some authors, however, have proposed that its pathogenesis is based on the destruction of the motor neurons supplying the muscles of the hand. To test the validity of these two theories, the authors retrospectively studied the magnetic resonance (MR) images obtained in 18 cases of acute traumatic central cord syndrome (ATCCS) to assess the presence of intramedullary blood and to define the distribution of the abnormal signal intensities in the cervical spinal cord. The authors used the American Spinal Injury Association (ASIA) motor scale to assess upper- and lower-limb deficits and to evaluate its metameric distribution. The abnormal intramedullary signal was then compared with the distribution of the motor deficit. All MR imaging sessions performed in the acute stage revealed a hyperintense signal on T2-weighted sequences without any signal change suggesting the presence of intramedullary blood. The localization of this signal was distributed predominantly from the C3-4 to the C5-6 disc levels. The mean ASIA motor score was 74.3 of 100, with an unequal representation between the upper and lower limbs (32 of 50 compared with 42.3 of 50, respectively). The metameric distribution of the deficit was also unequal, with a major deficit in hand function (C8-T1) compared with the more proximal cord segments (5.2 of 10 compared with 7.8 of 10, respectively). This demonstrates the absence of any correlation between the hyperintense signal and the motor deficit distribution. Acute traumatic central cord syndrome cannot be explained by the injury to the gray matter at the level of motor neurons supplying the hand muscles. In agreement with recently published data, the results of this series confirm the absence of intramedullary hemorrhage and corroborate the hypothesis that ATCCS may be explained by the impairment of the corticospinal tract, which can be affected globally.

Acute traumatic central cord syndrome: MRI-pathological correlations.

The acute traumatic central cord syndrome (ATCCS) is commonly stated to result from an injury which affects primarily the center of the spinal cord and is frequently hemorrhagic. To test the validity of this widely disseminated hypothesis, the magnetic resonance images [MRI] of 11 consecutive cases of ATCCS caused by closed injury to the spine were analyzed and correlated with the gross pathological and histological features of 3 cervical spinal cords obtained at post mortem from patients with ATCCS, including 2 of patients studied by MRI. The MRI studies were performed acutely (18 h to 2 days after injury) in 7 patients and subacutely (3-10 days after injury) in 4. Ten of the 11 patients had pre-existing spondylosis and/or canal stenosis. The 11th suffered a cervical fracture. All patients exhibited hyperintense signal within the parenchyma of the cervical spinal cord on gradient echo MRI. None showed MRI features characteristic of hemorrhage on T1-weighted spin echo or T2-weighted gradient echo studies. Gross and histological examination of the necropsy specimens showed no evidence of blood or blood products within the cord parenchyma: the primary finding was diffuse disruption of axons, especially within the lateral columns of the cervical cord in the region occupied by the corticospinal tracts. The central gray matter was intact. In patients with ATCCS, the predominant loss of motor function in the distal muscles of the upper limbs may reflect the importance of the corticospinal tract for hand and finger function in the primate. In this study, the MRI and pathological observations indicate that ATCCS is predominantly a white matter injury and that intramedullary hemorrhage is not a necessary feature of the syndrome; indeed, it is probably an uncommon event in ATCCS. We suggest that the most common mechanism of injury in ATCCS may be direct compression of the cervical spinal cord by buckling of the ligamenta flava into an already narrowed cervical spinal canal; this would explain the predominance of axonal injury in the white matter of the lateral columns.

A reappraisal of acute traumatic central cord syndrome.

A review of 77 patients with traumatic central cord syndrome revealed that atypical variations are more common than the existing literature suggests and that these may be seen in a wide variety of acute injuries to the cervical spine. In general the outcome is good; a favourable prognosis on admission is suggested by good hand function, hyperpathia, Lhermitte's sign and normal perianal sensation. The study has highlighted the value of regular muscle charting and has cast doubt on previous neuroanatomical assumptions about the syndrome.

FRACTURES, DISLOCATIONS, AND FRACTURE-DISLOCATIONS OF THE SPINE

Over 1000 patients with traumatic paraplegia or tetraplegia and many more with fractures and dislocations of the spine without damage to the central nervous system have been observed and treated at the Sheffield Spinal Injuries Centre. The vertebral lesions with or without injury to the spinal cord or nerve roots have been classified on the basis of the clinical and roentgenographic findings into five groups: 1. Pure flexion which causes a wedge fracture which is stable. 2. Flexion-rotation which produces an unstable fracture-dislocation with rupture of tue posterior ligament complex, separation of the spinous processes, a slice fracture near the upper border of the lower vertebra, and dislocation of the lower articular processes of the upper vertebra. 3. Extension which causes rupture of the intervertebral disc and the anterior common ligament along with avulsion of a small bone fragment from the anterior border of the dislocated vertebra. The dislocation almost always reduces spontaneously and is stable in flexion. 4. Vertebral compression which results in a fracture of the end plate as the nucleus of the intervertebral disc is forced into the vertebral body and causes it to burst with outward displacement of fragments of the body. Since the ligaments remain intact this comminuted fracture is stable. 5. Shearing which results in forward displacement of the whole vertebra and an unstable fracture of the articular processes or pedicles. Accurate diagnosis and prognosis of the neurological lesion depend on knowledge of the anatomy of the spinal cord and nerve roots, a careful neurological examination shortly after the original injury and repeated examinations thereafter, comparison of the level of spinal injury with the level of paraplegia or tetraplegia, differentiation between paraplegia and tetraplegia of immediate and delayed onset, and the appropriate therapy of the various types and levels of lesion. Simple wedge fractures were treated by bed rest for two to three weeks, mobilization of the back, and ambulation with a back support. Rotational fracture-dislocations in the cervical, thoracolumbar, or lumbar spine were almost invariably associated with tetraplegia or paraplegia. Cervical fracture-dislocations with or without tetraplegia were treated by skull-caliper traction. Thoracolumbar or lumbar fracture-dislocations without paraplegia were treated on a plaster bed for twelve weeks followed by a back support for a few weeks. The thoracolumbar fracture-dislocations with paraplegia were never treated by the plaster bed method but rather by open reduction of the dislocation, and maintenance of the reduction by internal fixation with double plating of the spinous processes. Spontaneous fusion was sufficiently advanced after eight to twelve weeks to get the patient out of bed. If the plates cut out of the bone after twelve weeks, they were removed. Patients with loss of sensation resulting from paraplegia or tetraplegia were turned every two hours to avoid pressure sores. Extension dislocations in the cervical spine, if they had reduced spontaneously, were fitted with a collar to hold the head and neck in sligh flexion for a period of eight to twelve weeks. For dislocations in this region which had not reduced spontaneously, manual manipulation under endotracheal anesthesia was employed. Reduction was maintained by skull tongs applied prior to manipulation. If after four weeks there was roentgenographic evidence of new bone indicating Spontaneous fusion, traction was continued for four to six weeks more followed by a neck collar for an additional six weeks. If new bone did not appear on the roentgenograms after four weeks, anterior fusion was performed followed by skull traction for an additional eight weeks. Vertical compression burst fractures in the cervical spine were treated by skull traction for six weeks followed by a neck collar. In the lumbar spine, burst fractures without paraplegia were treated by immobilization in a plaster bed for eight to twelve weeks followed by back support. The plaster bed was never used in burst fractures with paraplegia. Shear fractures were always associated with complete paraplegia. These fractures were usually stable and did not require operative reduction except when the displacement was great.