Thoracic and Lumbar Spine and Spinal Cord Injuries (Advances in Neurotraumatology)

Free download. Book file PDF easily for everyone and every device. You can download and read online Thoracic and Lumbar Spine and Spinal Cord Injuries (Advances in Neurotraumatology) file PDF Book only if you are registered here. And also you can download or read online all Book PDF file that related with Thoracic and Lumbar Spine and Spinal Cord Injuries (Advances in Neurotraumatology) book. Happy reading Thoracic and Lumbar Spine and Spinal Cord Injuries (Advances in Neurotraumatology) Bookeveryone. Download file Free Book PDF Thoracic and Lumbar Spine and Spinal Cord Injuries (Advances in Neurotraumatology) at Complete PDF Library. This Book have some digital formats such us :paperbook, ebook, kindle, epub, fb2 and another formats. Here is The CompletePDF Book Library. It's free to register here to get Book file PDF Thoracic and Lumbar Spine and Spinal Cord Injuries (Advances in Neurotraumatology) Pocket Guide.

CT also has advantages over plain x-rays in assessing the patency of the spinal canal. CT also provides some assessment of the paravertebral soft tissues and perhaps of the spinal cord as well but is inferior in that regard to magnetic resonance imaging MRI. When MRI is available, myelography is rarely if ever used, but remains an alternative in combination with CT when an MRI cannot be performed, and spinal canal compromise is suspected.

The chief advantage of MRI is that it provides a detailed image of the spinal cord, as well as, spinal ligaments, intervertebral discs, and paraspinal soft tissues that is superior to CT and is more sensitive for detecting epidural hematoma. Nonetheless, if the patient's clinical status permits, an MRI can provide valuable information that complements CT regarding the extent and mechanism of spinal cord injury, which can influence treatment and prognosis. It originated prior to the use of MRI and but it is often defined as the presence of neurologic deficits in the absence of bony injury on a complete, technically adequate, plain x-ray series or CT scan.

Because an MRI provides superior imaging of the spinal cord, it can detect injuries to the cord that exist despite the apparent absence of bony abnormalities. A common explanation for this phenomenon is transient ligamentous deformation with spontaneous reduction. This injury pattern is more common in children who have weak paraspinal muscles, elastic spinal ligaments, lax soft tissues, disc prolapse and cervical sponylosis which fail to protect the spinal cord from force but has also been described in adults.

Other possible mechanisms for SCIWORA include radiographically occult intervertebral disc herniation, epidural or intramedullary hemorrhage, fibrocartilaginous emboli from an intervertebral disc that has ruptured into the radicular artery, and traumatic aortic dissection with spinal cord infarction. MRI is invaluable for the diagnosis of these conditions. Clinicians should suspect a cervical ligamentous injury in the injured patient who has persistent severe pain or paresthesias or focal neurologic findings e.

Such injuries may be unstable, although they are rarely associated with permanent neurologic damage. Patients with TSCI require intensive medical care and continuous monitoring of vital signs, cardiac rhythm, arterial oxygenation, and neurologic signs in the intensive care unit ICU. A careful neurologic assessment for associated head injury is compulsory. Neurogenic shock refers to hypotension, usually with bradycardia, attributed to interruption of autonomic pathways in the spinal cord causing decreased vascular resistance.

Patients with TSCI may also suffer from hemodynamic shock related to blood loss and other complications. An adequate blood pressure is believed to be critical in maintaining adequate perfusion to the injured spinal cord and thereby limiting secondary ischemic injury. Guidelines currently recommend maintaining mean arterial pressures of at least 85 to 90 mmHg, using intravenous fluids, transfusion, and pharmacologic vasopressors as needed.

Patients with multiple injuries often receive large amounts of intravenous fluids usually an isotonic crystalloid solution to a maximum of 2 L for various reasons. Excess fluids cause further cord swelling and increased damage and places the patient at increased risk for acute respiratory distress syndrome ARDS. Bradycardia may require external pacing or administration of a tropine. Autonomic dysreflexia is usually a later complication of TSCI, but may appear in the hospital setting, requiring acute management. Aspiration and pulmonary complications are the most frequent category of complications during acute hospitalization after TSCI which contribute substantively to early morbidity and mortality and both are related to the level of neurologic injury.

Weakness of the diaphragm and chest wall muscles leads to impaired clearance of secretions, ineffective cough, atelectasis, and hypoventilation. Signs of impending respiratory failure, such as increased respiratory rate, declining forced vital capacity, rising pCO2, or falling pO2, indicate urgent intubation and ventilation with positive pressure support.

Rapid-sequence intubation with in-line spinal immobilization is the preferred method of intubation when an airway is urgently required. If time is not an issue, intubation over a flexible fiberoptic scope may be a safer, effective option. Tracheostomy is performed within 7 to 10 days, unless extubation is imminent. All patients should receive prophylactic treatment. Use of either low-dose unfractionated heparin therapy or pneumatic compression stockings as monotherapy is considered inadequate protection , but combination therapy with these two approaches may be considered an alternative to LMW heparin.

Inferior vena cava filters should be inserted for patients for whom anticoagulation is contraindicated. When using opiates with potential sedating properties, the need for pain control must be balanced with the need for ongoing clinical assessment, particularly in patients with concomitant head injury.

Pain is often reduced by realignment and stabilization of the cervical fracture by surgery or external orthosis. Pressure sores are most common on the buttocks and heels and can develop quickly within hours in immobilized patients. Initially, an indwelling urinary catheter must be placed to avoid bladder distension, to monitor urine output and to decompress the neurogenic bladder. Rarely, inotropic support with dopamine or norepinephrine is required and should be reserved for patients who have decreased urinary output despite adequate fluid resuscitation.

Three or four days after injury, intermittent catheterization should be substituted, as this reduces the incidence of bladder infections. Urologic evaluation with regular follow-up is recommended for all patients after SCI. Patients with TSCIs, particularly those that affect the cervical cord, are at high risk for stress ulceration. Bowel motility may be silent for a few days to weeks after TSCI. Placement of a nasogastric NG tube is essential to prevent aspiration. Aspiration pneumonitis is a serious complication in the patient with a spinal cord injury with compromised respiratory function.

Antiemetics should be used aggressively. Patients should be monitored for bowel sounds and bowel emptying and should not ingest food or liquid until motility is restored. Prevent hypothermia. Patients with a cervical spinal cord injury may lack vasomotor control and cannot sweat below the lesion. Their temperature may vary with the environment and needs to be maintained. There is limited evidence that glucocorticoid therapy improves neurologic outcomes in patients with acute TSCI, and such therapy is not endorsed by major society guidelines.

Methylprednisolone is the only treatment that has been suggested in clinical trials to improve neurologic outcomes in patients with acute, nonpenetrating TSCI. However, the evidence is limited, and its use is debated. In , based upon the available evidence, the American Association of Neurological Surgeons and Congress of Neurological Surgeons stated that the use of glucocorticoids in acute spinal cord injury is not recommended. There are little data regarding the use of methylprednisolone with penetrating spinal cord injuries since retrospective studies suggest a higher rate of complications and no evidence of benefit.

Similarly, the results of NASCIS II and III studies may not apply to individuals with multisystem trauma, in whom the risk of complications is likely higher than those with isolated spinal cord injury. Patients with TSCI require urgent neurosurgical consultation to manage efforts at decompression and stabilization. There are currently no standards regarding the role, timing, and method of vertebral decompression in acute spinal cord injury. This technique involves use of longitudinal traction using skull tongs or a halo headpiece.

An initial weight of 5 to 15 pounds is applied. This is increased in five-pound increments, taking lateral x-rays after each increment is applied. The more rostral the dislocation, the less weight is used, usually about three to five pounds per vertebral level. While weights up to 70 pounds are sometimes used, it is suggested that after 35 pounds is applied, patients be observed for at least an hour with repeat cervical spine x-rays before the weight is cautiously increased further.

Administration of a muscle relaxant or analgesic, such as diazepam or meperidine, may help facilitate reduction. For cervical spine fracture with subluxation, closed reduction methods are a treatment option. Indications for cervical spine surgery include significant cord compression with neurologic deficits, especially those that are progressive, that are not amenable or do not respond to closed reduction, or an unstable vertebral fracture or dislocation. Most penetrating injuries require surgical exploration to ensure that there are no foreign bodies imbedded in the tissue, and to clean the wound to prevent infection.

Defining surgical indications for closed thoracolumbar fractures has been somewhat more challenging, in part because of difficulties defining spinal instability in these lesions. The timing of surgical intervention is not defined and remains somewhat controversial. Most clinicians consider deteriorating neurologic function after incomplete TSCI to be an indication to perform surgery as early as possible if there are no contraindications e. A report of an expert panel concurred with this approach. Not all surgical cases require decompression, and not all decompression cases require instrumentation and fusion.

The technical aspects of the surgery are tailored to the individual case. In the case of a cervical fracture with a cervical spinal cord injury, the anesthesiologist usually performs a fiberoptic intubation, done with the patient awake to reduce any further cord injury that potentially could be caused by a regular intubation with neck movement and extension.

Anesthetists are also usually involved in the postoperative care of patients with TSCI. Many strategies are being investigated as potential treatments of acute TSCI 29 but are not currently recommended. Severe systemic injuries, traumatic brain injury, and medical comorbidity also increase mortality. Rates of motor score improvements are also related to the initial severity and level of injury. Most recovery in patients with incomplete TSCI takes place in the first six months.

Joan Hutton, fell backwards while stepping out of the bathtub following her shower hitting her back on the side of the tub.

Denies LOC. Patient was able to crawl to the phone and call Upon arrival in the emergency department, EMS reports:. GCS: Temp: afebrile. HR: , sinus tachycardia without ectopy. RR: , rapid, shallow. You observe: Patient is on a backboard with a semi-rigid cervical collar in place. Patient alert, oriented, cooperative. Associated findings include mild osteopenia and chronic fracture of the left 3rd, 4th, 5th, and 6th ribs. All laboratory tests WNL. All vital signs WNL. HR , NSR without ectopy. TSCI is a problem that largely affects young male adults because of motor vehicle accidents, falls, or violence.

Blunt trauma, particularly motor vehicle collisions, accounts for most spinal column injuries. Elderly patients who fall are also at increased risk. Most TSCI occurs with injury to the vertebral column, producing mechanical compression or distortion of the spinal cord with secondary injuries resulting from ischemic, inflammatory, and other mechanisms. The cervical spine is the most commonly injured part of the spinal column. Within the cervical spine, the most common sites of injury are around the second cervical vertebra C2, or axis or in the region of C5, C6, and C7.

Associated injury of the spinal cord or possibly the brain due to vascular compromise are critical clinical considerations and must be investigated immediately. In the absence of apparent spinal cord or brain injury, the degree of fracture stability is the most important feature of any spinal column injury. Differences in the structure and location of the cervical and thoracolumbar portions of the spinal column lead to different types of injuries, although there is some overlap.

The cervical spinal column is susceptible to a wide range of fractures, dislocations, and ligamentous injuries. Compression fractures are the most common injury of the thoracolumbar spinal column. The neurologic injury produced by TSCI is classified according to the spinal cord level and the severity of neurologic deficits. Half of TSCIs involve the cervical spinal cord and produce quadriparesis or quadriplegia.

Anesthetic considerations in acute spinal cord trauma Dooney N, Dagal A - Int J Crit Illn Inj Sci

The initial evaluation and management of patients with TSCI in the field and emergency department focuses on the ABCDs airway, breathing, circulation, and disability , evaluating the extent of traumatic injuries, and immobilizing the potentially injured spinal column. Patients with acute TSCI require admission to an ICU for monitoring and treatment of potential acute, life-threatening complications, including cardiovascular instability and respiratory failure. Because the neurologic benefits are uncertain, glucocorticoid therapy is NOT recommended in cases when there are clear risks associated with such therapy, such as penetrating injury, multisystem trauma, moderate to severe traumatic brain injury, and other comorbid conditions associated with risk of complications from glucocorticoid therapy.

In other patients who present within eight hours of isolated, nonpenetrating TSCI, administration of intravenous methylprednisolone can be considered with knowledge of potential risks and uncertain benefits. Braddom R. Physical medicine and rehabilitation. Alzheimer's and Dementia. How much does CEUfast cost? How soon do I get my certificate? You are not currently logged in. Please log in to CEUfast to enable the course progress and auto resume features.

This course is applicable for the following professions:. CEUFast Inc. The Planning Committee and Authors do not have any conflict of interest. Spinal Cord Injuries: Traumatic. Earn Certificate. Options Back Earn Certificate Print. Time Remaining:. Nursing Assistants from California, only. You must read the material on this page before you can take the test. The California Department of Public Health, Training Program Review Unit has determined that is the only way to prove that you actually spent the time to read the course.

Outcomes This course describes injuries to the cervical, thoracic, and lumbosacral spinal column, including fractures, dislocations, and subluxations of the vertebrae, and injuries to the spinal ligaments. Objectives Upon completion of this course, the participant will be able to: Describe the epidemiology underlying traumatic spinal cord injuries TSCIs including etiology and risk factors. Differentiate between the cervical and the thoracic and lumbar TL spinal column injury classifications.

Differentiate between the initial evaluation and treatment of the suspected acute SCI patient at the scene of the trauma and the continuation of care in the emergency department. Describe the clinical management of the suspected acute SCI patient in terms of prevention of further injury and prevention of complications.

Epidemiology Spinal cord injury SCI has become epidemic in modern society. Acts of violence primarily gunshot wounds : Soldiers deployed in armed conflicts also have a substantial risk of TSCI. Since that time, the average age has increased in the United States to 37 years in , presumably as a reflection of the aging population. These conditions include 1,19 : Cervical spondylosis Atlantoaxial instability Congenital conditions, e. Anatomy The human spine consists of 33 bony vertebrae: 7 cervical, 12 thoracic, 5 lumbar, 5 sacral fused , and 4 coccygeal usually fused.

Figure 1 Spine Anatomy Overview. Physiology of the Spinal Cord The vertebral column and the spinal cord within it is divided into cervical, thoracic, lumbar, sacral, and coccygeal regions. The cervical region of the cord gives rise to eight cervical nerves C1-C8. The thoracic region gives rise to twelve thoracic nerves T1-T The lumbar region gives rise to five lumbar nerves L1-L5. The sacral region gives rise to five sacral nerves S1-S5. The coccygeal region gives rise to one coccygeal nerve. The spinal cord expansion that corresponds to the arms is called the cervical enlargement and includes spinal segments C5-T1.

The expansion that corresponds to the legs is called the lumbar enlargement and includes spinal segments L2-S3. Longitudinal Organization of the Spinal Cord The spinal cord is divided longitudinally into four regions : Cervical Thoracic Lumbar Sacral The spinal cord extends from the base of the skull and terminates near the lower margin of the first lumbar vertebral body L1. The C1 through C8 spinal cord segments lie between the C1 through C7 vertebral levels. The C1 through C7 nerve roots emerge above their respective vertebrae.

What is a Spinal Cord Injury?

The C8 nerve root emerges between the C7 and T1 vertebral bodies. The remaining nerve roots emerge below their respective vertebrae. The T1 through T12 cord segments lie between T1 through T8. The five lumbar cord segments are situated at the T9 through T11 vertebral levels. The S1 through S5 segments lie between T12 to L1.

Cervical Cord The first cervical vertebra the atlas and the second cervical vertebra the axis , upon which the atlas pivots, support the head at the atlanto-occiput junction.

Why Don't We Have a Cure for Spinal Cord Injury?

Cervical spinal segments innervate the skin and musculature of the upper extremity and diaphragm: C3 through C5 innervate the diaphragm, the chief muscle of inspiration, via the phrenic nerve C4 through C7 innervate the shoulder and arm musculature C6 through C8 innervate the forearm extensors and flexors C8 through T1 innervate the hand musculature. Thoracic Cord The thoracic vertebral segments are defined by those that have an attached rib.

Lumbosacral Cord The lumbosacral spinal cord contains the segments that innervate the muscles and dermatomes of the lower extremity, as well as, the buttocks and anal regions. L2 and L3 mediate hip flexion L3 and L4 mediate knee extension L4 and L5 mediate ankle dorsiflexion and hip extension L5 and S1 mediate knee flexion S1 and S2 mediate ankle plantar flexion Sacral nerve roots also provide parasympathetic innervation of pelvic and abdominal organs. Cauda Equina In adults, the spinal cord ends at the level of the first or second lumbar vertebral bodies.

Mechanisms of Injury Spinal column injury may result in spinal cord or brain injury through many mechanisms: 23 Transection Penetrating or massive blunt trauma resulting in spinal column injury may transect all or part of the spinal cord. Less severe trauma may have similar neurologic effects by displacing bony fragments into the spinal canal or through disk herniation. Compression When elderly patients with cervical osteoarthritis and spondylosis forcibly extend their neck, the spinal cord may be compressed between an arthritically enlarged anterior vertebral ridge and a posteriorly located hypertrophied ligamentum flavum.

Injuries that produce blood within the spinal canal can also compress the spinal cord. Contusion Contusions of the spinal cord can occur from bony dislocations, subluxations, or fracture fragments. Vascular Compromise When there is a discrepancy between a clinically apparent neurologic deficit and the known level of spinal column injury primary vascular damage to the spinal cord should be suspected. In addition, many spinal fracture patterns are closely associated with vertebral artery injuries, which can cause stroke and permanent disability if diagnosis and appropriate interventions are delayed.

Injuries of concern include fractures associated with displacement into the transverse foramen, fractures involving both the atlas C1 and axis C2 , fractures involving the transverse foramen, and subluxation of two or more adjacent cervical vertebral levels. Pathophysiology The primary injury refers to the immediate effect of trauma which includes forces of compression, contusion, and shear injury to the spinal cord.

Cervical Spinal Column Injury. Cervical Spinal Column Injury Classification Acute cervical spinal column injury may be classified according to the stability of the injury, its location, or the mechanism flexion, flexion-rotation, extension, and vertical compression Table 1. Atlanto-Occipital Dislocation Pure flexion injuries involving the atlas C1 and the axis C2 can cause an unstable atlanto-occipital or atlanto-axial joint dislocation, with or without an associated odontoid fracture.

Atlanto-Axial Dislocation Rotary atlanto-axial dislocation is an unstable injury, caused by a flexion-rotation mechanism, best visualized on open-mouth odontoid x-rays or CT scan. Figure 6 Cervical Vertebrae Dislocation. C1 Atlas Fracture Burst Jefferson Fracture The Jefferson fracture of C1 is highly unstable and occurs when a vertical compression force is transmitted through the occipital condyles to the lateral masses of the atlas. Posterior Arch A posterior neural arch fracture of C1 results from compression of the posterior elements between the occiput and the spinous process of C2 during forced neck extension.

C2 Axis Pedicle Fractures Traumatic Spondylolysis of C2 so-called "Hangman's Fracture" Traumatic spondylolysis of C2 is an unstable injury that occurs when the cervicocranium the skull, atlas, and axis functioning as a unit is thrown into extreme hyperextension because of abrupt deceleration i. Fractures can occur: Above the transverse ligaments type I Type I fractures are stable. At the base of the odontoid process most common where it attaches to C2 type II. Type II odontoid fractures are the most common type.

Anterior Wedge Fracture Forceful, extreme flexion of the cervical spine can compress the anterior portion of a vertebral body, creating an anterior wedge fracture. Flexion Teardrop Fracture A flexion teardrop fracture results when severe flexion and compression cause one vertebral body to collide with the body below, leading to anterior displacement of a wedge-shaped fragment resembling a teardrop of the antero-inferior portion of the superior vertebra.

Extension Teardrop Fracture An extension teardrop fracture occurs when abrupt neck extension causes the anterior longitudinal ligament to pull the antero-inferior corner from the remainder of the vertebral body, producing a triangular-shaped fragment. Spinous Process Fractures The clay shoveler's fracture, an isolated fracture of one of the spinous processes of the lower cervical vertebrae, is a stable injury. It derives its name from its occurrence in clay miners during the s.

Today, this fracture is more commonly seen following direct trauma to the spinous process and after motor vehicle crashes involving sudden deceleration that result in forced neck flexion. Burst Fractures Vertical compression injuries occur in the cervical and lumbar regions when axial loads are exerted on the spine. Laminar Fractures Most laminar fractures of the cervical spine are associated with other fractures, such as burst fractures or fracture dislocations, which usually determine the stability of the injury. Facet Dislocations Bilateral Bilateral facet dislocations occur when flexion forces extend anteriorly, causing disruption of the annulus fibrosus of the intervertebral disc and the anterior longitudinal ligament, resulting in extreme instability.

The inferior articulating facets of the upper vertebra pass over the superior facets of the lower vertebra, resulting in anterior displacement of the spine. Complete spinal cord injury most often results. On x-ray, the displacement will appear to be greater than one half of the AP diameter of the lower vertebral body with the superior facets anterior to the inferior facets, which is best seen on the lateral view.

Unilateral Unilateral facet dislocations involve flexion and rotation. Rotation occurs around one of the facet joints. Dislocation occurs at the contralateral facet joint, with the superior facet moving over the inferior facet, and coming to rest within the intervertebral foramen. On a lateral plain x-ray, the two lateral masses of the dislocated vertebrae may partially overlap giving the appearance of a bow tie radiologists may refer to a bowtie or double diamond sign.

Since the dislocated articular mass is locked in place, this is a stable injury despite posterior ligament complex disruption. Spinal cord injury rarely occurs following isolated unilateral facet dislocation. However, associated fractures of the facet or surrounding structures can create instability. Thoracic and Lumbar Spinal Injury TL Spinal Column Injury Classification In contrast to the two-column scheme for cervical spinal column injury, a three-column scheme may be used to describe injuries of the thoracic and lumbar TL spinal column.

The anterior column includes the: Anterior longitudinal ligament Annulus fibrosus Anterior half of the vertebral body The middle column includes the: Posterior longitudinal ligament Posterior annulus fibrosus Posterior half of the vertebral body The posterior column includes the: Supraspinous ligaments Interspinous ligaments Facet joint capsule According to the three-column scheme, stability is based upon the integrity of two of the three spinal columns.

Figure 8 Thoracic Compression Fracture. Figure 9 Burst Fracture. Translational Spinal Column Injury Massive direct trauma to the back can cause failure of all three columns of the TL spine resulting in translational injuries. Figure 10 Dislocation. Clinical Presentation A patient with a spinal cord injury typically has pain at the site of the spinal fracture. No motor or sensory function is preserved in the sacral segments S B Sensory incomplete. Sensory but not motor function is preserved below the neurologic level and includes the sacral segments light touch or pin prick at S or deep anal pressure AND no motor function is preserved more than three levels below the motor level on either side of the body.

C Motor incomplete. D Motor incomplete. E Normal. Sensation and motor function are graded as normal in all segments and the patient had prior deficits. Incomplete Injury In incomplete injuries ASIA grades B through D , there are various degrees of motor function in muscles controlled by levels of the spinal cord caudal to the injury.

Central Cord Syndrome An acute central cord syndrome, characterized by disproportionately greater motor impairment in upper compared with lower extremities, bladder dysfunction, and a variable degree of sensory loss below the level of injury, is described after relatively mild trauma in the setting of preexisting cervical spondylosis.

Anterior Cord Syndrome Lesions affecting the anterior or ventral two-thirds of the spinal cord, sparing the dorsal columns, usually reflect injury to the anterior spinal artery. Transient Paralysis and Spinal Shock Immediately after a spinal cord injury, there may be a physiological loss of all spinal cord function caudal to the level of the injury, with flaccid paralysis, anesthesia, absent bowel and bladder control, and loss of reflex activity. Initial Evaluation and Treatment. During the secondary survey ascertaining a detailed history from the trauma patient if possible or from other information sources such as prehospital personnel, family members or other victims.

Complete physical examination Additional radiologic and special diagnostic studies Ongoing monitoring of vital signs including heart rate, blood pressure, respiratory status usually via capnography or pulse oximetry , and temperature. Interventions should include: Placement of ECG leads attached to a cardiac monitor to evaluate real-time heart rate and rhythm. If indicated and possible, an arterial line should be inserted to allow for real-time blood pressure monitoring and for the many laboratory draws that are inevitable following major trauma.

Continuous pulse oximetry should persist on an area of sufficient blood flow to give an accurate reading to monitor oxygen saturation. The most important treatment consideration in the patient with a high cervical cord injury is to maintain adequate oxygenation and perfusion of the injured spinal cord. Interventions may include: Administration of supplemental oxygen Hypoxia in the face of cord injury can adversely affect neurologic outcome.

Arterial oxygenation via arterial blood gases should be monitored and supplemental oxygen adjusted as needed. The modified jaw thrust and insertion of an oral airway when indicated. Intubation and respiratory mechanical support Approximately one-third of patients with cervical injuries require intubation within the first 24 hours.

If time is not an issue, intubation over a flexible fiberoptic laryngoscope may be a safer, effective option. Drawing and monitoring laboratory studies Type and Crossmatch The most important lab study. This should be completed within 20 minutes of receipt of the blood sample. Arterial Blood Gases Useful in the initial assessment period although their use for serial monitoring has declined since the introduction of continuous pulse oximetry. Baseline Hemoglobin or Hematocrit Useful on arrival, with the understanding that in acute hemorrhage, a fall in hematocrit may not be apparent until autogenous mobilization of extravascular fluid or administration of IV resuscitation fluids begins.

Urine Drug Screens for drugs of abuse and Blood Alcohol Levels Commonly ordered in trauma centers to identify correctable causes of decreased level of consciousness. A recent review from the data of the National Trauma Data Bank of the United States reveals a disturbing decline in substance use screening despite the importance of substance use as a contribution to injury. Early hyperglycemia has been linked to an increased risk of infectious complications and mortality after injury. Interventions may include: Elevation of the legs Head-dependent position Blood replacement Vasoactive agents Until spinal injury has been ruled out, immobilization of the neck and body must be maintained.

Imaging Patients with suspected TSCI because of neck pain or neurologic deficits and all trauma victims with impaired alertness or potentially distracting systemic injuries require continued immobilization until imaging studies exclude an unstable spine injury.

Login to your account

Plain X-ray Plain x-rays provide a rapid assessment of alignment, fractures, and soft tissue swelling and are, in general, the first method of assessment of TSCI. Computed Tomography CT Helical CT scanning with coronal and sagittal reconstructions may replace plain x-rays for screening assessment in centers in which it is readily available. Myelography When MRI is available, myelography is rarely if ever used, but remains an alternative in combination with CT when an MRI cannot be performed, and spinal canal compromise is suspected.

MRI is contraindicated in the setting of a cardiac pacemaker and metallic foreign bodies. Life support equipment may be incompatible with the performance of an MRI as the patient is enclosed during the study, which can pose some risk for monitoring vital signs and for maintaining an airway. In some medical centers, an MRI is not always available because of resource and personnel issues.

Medical Care Patients with TSCI require intensive medical care and continuous monitoring of vital signs, cardiac rhythm, arterial oxygenation, and neurologic signs in the intensive care unit ICU. Assess for: The presence of amnesia External signs of head injury or basilar skull fracture Focal neurologic deficits Associated alcohol intoxication or drug abuse A history of loss of consciousness Cardiovascular Complications Neurogenic shock refers to hypotension, usually with bradycardia, attributed to interruption of autonomic pathways in the spinal cord causing decreased vascular resistance.

Aspiration and Pulmonary Complications Aspiration and pulmonary complications are the most frequent category of complications during acute hospitalization after TSCI which contribute substantively to early morbidity and mortality and both are related to the level of neurologic injury. Other Medical Complications Pain control When using opiates with potential sedating properties, the need for pain control must be balanced with the need for ongoing clinical assessment, particularly in patients with concomitant head injury. Pressure sores Pressure sores are most common on the buttocks and heels and can develop quickly within hours in immobilized patients.

After spinal stabilization, the patient should be turned side to side log-rolled everyone to two hours to avoid pressure sores. Rotating beds designed for the patient with spinal cord injury should be used in the interim, if available. Urinary catheterization Initially, an indwelling urinary catheter must be placed to avoid bladder distension, to monitor urine output and to decompress the neurogenic bladder.

Interventions may include: Place the patient in a warm ambient room Administer warmed IV fluids Cover the patient with warm blankets Functional recovery Occupational and physiotherapy should be started as soon as possible. Psychological counseling is also best offered to patients and relatives as early as possible. Glucocorticoids There is limited evidence that glucocorticoid therapy improves neurologic outcomes in patients with acute TSCI, and such therapy is not endorsed by major society guidelines. Contraindications to the use of glucocorticoids include: Methylprednisolone has been associated with increased mortality in patients with moderate to severe traumatic brain injury TBI.

Decompression and Stabilization Patients with TSCI require urgent neurosurgical consultation to manage efforts at decompression and stabilization. Thoracic and lumbar fractures do not respond to closed treatment methods. Surgical Care Goals for surgical intervention in TSCI include: Stabilization of the spine Reduction of dislocations and decompression of neural elements Indications for cervical spine surgery include significant cord compression with neurologic deficits, especially those that are progressive, that are not amenable or do not respond to closed reduction, or an unstable vertebral fracture or dislocation.

Investigational Treatments Many strategies are being investigated as potential treatments of acute TSCI 29 but are not currently recommended. Computer access by tongue, breath, voice controls. Weight shifts with power tilt and recline chair. Mouth stick use. Operate power chair with tongue, chin, or breath controller. C5 Drink from cup, feed with static splints and setup. Dressing upper body possible. Side-to-side weight shifts. Propel chair with hand rim projections short distances on smooth surfaces.

Power chair with hand controller. C6 Feed, dress upper body with setup. Dressing lower body possible. Forward weight shifts. Bed mobility with equipment. Recovery of function is first apparent within days after injury as a result of recuperation from spinal shock. Some degree of remyelination within the spinal cord can occur and may have a clinical impact.

Remyelination can occur in two different ways. The first is by Schwann cells, which are myelinating cells normally found in the peripheral nervous system, but after an injury they are able to migrate directly into the spinal cord, where they can myelinate regrowing axons Bunge and Wood, Awareness of the role of Schwann cells has spawned an entire new line of research on therapies involving the transplantation of a variety of cell types see Chapter 5.

The second means of possible remyelination is by oligodendrocyte precursor cells. Mature oligodendrocytes cannot divide or migrate. Yet, imma-. It bears remembering, however, that oligodendrocyte precursor cells can also mature into oligodendrocytes that do the opposite: inhibit axon regrowth through the release of inhibitory substances see above. What triggers their development into inhibitory cells versus beneficial cells is not yet known.

It is also possible that demyelinated axons within the injured spinal cord may reorganize at the molecular level to acquire the ability to conduct nerve impulses without myelin insulation. This type of recovery is known to occur not only in animal models but also in humans with multiple sclerosis, in whom demyelinated spinal cord axons produce additional sodium channels to support impulse conduction after damage to the myelin Craner et al.

Limited regrowth of axons and sprouting of new branches from the tips of existing axons to form new synapses are part of yet another mechanism of functional recovery Raineteau and Schwab, The fact that limited regrowth and sprouting do occur reveals that axons possess the capacity for some degree of regrowth, a capacity that can be cultivated with better knowledge of what governs it.

Numerous studies with animals have demonstrated the ways in which axonal regrowth from central neurons can be improved, particularly across the area of injury. Research indicates that, after injury, the surviving cells continue to produce certain molecules and release them into the extracellular milieu that bathes the sprouting axons. Some of the molecules are growth factors—members of a family of molecules called neurotrophins Raineteau and Schwab, Others are guidance molecules that guide axons to their destination Walsh and Doherty, ; Willson et al. This area of research is still in its early phases, and much of the information on axonal guidance gained to date involves the developing nervous system.

Research is needed to determine if the same or similar mechanisms are involved in axon guidance following injury in the adult CNS. No daily activity can be taken for granted for someone with a spinal cord injury. A range of functions—getting out of bed, walking, dressing, eating, controlling the bladder and the bowel, and breathing—can be severely compromised, and their loss has a staggering effect. To develop the technological or medical means to restore function and to improve quality of life, it is vital to understand the neurological basis of dysfunction. The initiation and regulation of movements require a complex set of events that integrate information from many regions of the brain, brain stem, and spinal cord Figure When an action potential is generated in the brain, it travels along axons and down the spinal cord via the corticospinal tract to the motor neurons at speeds upwards of meters per second, resulting in contraction of a muscle and a movement.

However, before it reaches the motor neurons, the information is modulated by neurons found in the basal ganglia, cerebellum, and brain stem. When the signals finally reach the motor neurons, these specialized nerve cells provide the final conduit for the transmission of the signals to muscles throughout the body, stimulating muscles to contract.

Thus, an injury or disruption to the motor pathways leading to and from the brain could cause a patient to lose motor function. The circuitry between the primary motor cortex and the motor neurons of the ventral horn of the spinal cord is very complex. Many regions of the CNS, including the basal ganglia, cerebellum, and brain stem, help regulate movements Figure The degree of cortical control varies depending on the motor function.

For example, movement of the fingers requires more integration from the brain than gross movement of the legs, which relies more on circuitry confined to the spinal cord. The majority of the signals from the brain are transmitted along bundles of axons that make up the corticospinal tract, which connects the primary motor cortex in the brain to the motor neurons in the ventral horn of the spinal cord. The motor neurons in turn transmit the information from the ventral horn directly to the muscle.

Motor control of most other body parts involves additional circuitry, or connections, between the primary motor cortex and the motor neurons. Signals are transmitted either from the primary motor cortex to intermediate layers within the spinal cord to modulate the tone or reflex gain and to cause direct contraction of the muscles or through intermediate processing stages in the midbrain or pons of the brain stem.

In addition to regulating voluntary movements, neurons in the descending motor tracts traveling from the brain down to the spinal cord are also responsible for regulating the smooth muscles of internal organs. Control of movements involves a complex network of connections. Signals commanding the initiation of a movement are generated in the primary motor cortex of the brain. These signals are modulated before they reach the muscle. They are modulated through an intricate circuit in the basal ganglia and thalamus, which regulate the initiation of movements and help coordinate movements.

Information from muscle contractions is also transmitted back to the brain through sensory receptors. This information is also used to provide feedback and to modify the movements. Critical feedback from sensory nerve endings located on muscles is transferred to the spinal cord via the sensory roots and dorsal horn to the brain, resulting in involuntary modulation of movements. This component of the sensory system is called proprioception.

It is responsible for immediately varying the degree of muscle contraction in response to incoming. When individuals lose their proprioception, they are unable to freely move and interact comfortably with the external environment see Box This sensory information bypasses ascending information to the brain and is conveyed directly to lower motor neurons, resulting in involuntary or reflex movements. Experiments performed by Shik, Severin, and Orlovsky in the s provided evidence of a central pattern generator CPG , which is a complex circuit of neurons responsible for coordinated rhythmic muscle activity, such as locomotion Shik et al.

In these experiments, the brain stem of a cat was transected so that no information could travel from the brain to the spinal cord. Surprisingly, following this surgery, cats were still able to stand on their own and could be induced to walk Box Similar results have been observed in rats and mice that have had their spinal cords transected.

Therefore, it was concluded that the CPG is located in the spinal cord of these animals and does not require input from the brain. If the CPG is located in the spinal cord and does not require any input from the brain, why is it that most individuals with spinal cord injuries and a complete transection of the spinal cord cannot walk? The function and control of the CPG in Old World primates and humans may be different from those in animals that walk on four feet, like cats and dogs i.

Humans and other bipeds may have more cortical dominance integrated into the locomotor circuitry than quadrapeds Fulton and Keller, , which may explain why the recovery of rhythmic locomotor activity is not commonly observed in primates and humans with complete spinal cord injuries Kuhn, ; Bussel et al.

However, because of the limitations of performing invasive experiments with primates and humans, it is difficult to verify the significance of the cortical circuitry. The complexity of the cortical regulation of the CPG in humans and primates compared with that in cats and rodents demonstrates a potential area of concern for the translation of the results from experiments performed with laboratory animals to humans. Spasticity is a state of increased muscular tone, often with heightened stretch reflexes.

In severe cases, spasticity causes chronic pain, flexion. At the turn of the 20th century, Charles Scott Sherrington and T. Graham Brown published two seminal papers that demonstrated the capacity of the spinal cord in cats and dogs to generate rhythmic motor activity Brown, Later, in the s, further insight was garnered when the work of three Russian scientists, M. Shik, F. Severin, and G. Orlovsky, and one Swedish scientist, Sten Griller, showed that when a portion of the brain stem of a cat was cut across the middle—thus severing any connections between the brain and the spinal cord—the cat was still capable of standing.

Furthermore, if a specific region of the brain stem was stimulated, the cats could be induced to walk on a treadmill, and alternating bursts of muscle activity could be recorded in extensors and flexors in conjunction with walking Shik et al. These series of experiments led to the conclusion that each limb is controlled by a central pattern generator CPG in the spinal cord, which controls rhythmic motor activity, including walking.

Shik and colleagues experimented with a cat whose brain stem was severed but that was still able to walk on a treadmill when a specific region of the brain stem was stimulated. The top of the figure shows the brain and the spinal cord. The muscle activity recorded from the flexors and extensors demonstrates that they are contracting and relaxing at opposite times from each other, consistent with normal function. Copyright by Sinauer Associates, Inc. Muscle spasticity frequently occurs after spinal cord injuries, with one study finding 78 percent of individuals experiencing spasticity after they were discharged from the hospital Maynard et al.

The precise causes of muscle spasticity are not well understood. Most studies point to the greater excitability of motor neurons, with several possible causes Burchiel and Hsu, One is thought to be decreased inhibitory input from the brain to spinal cord motor neurons through direct or indirect via spinal cord interneuron connections.

Some of those neurons are inhibitory, whereas others are excitatory.

Guide Thoracic and Lumbar Spine and Spinal Cord Injuries (Advances in Neurotraumatology)

A single motor neuron can receive a direct or an indirect input from several regions of the brain and from sensory neurons. The array of inputs is critical for the modulation and fine-tuning of motor neuron control of muscles. If inhibitory input to the motor neuron is destroyed or reduced as a result of a spinal cord injury, the balance weighs in favor of heightened excitability and firing of motor neurons. The spasticity that occurs with a spinal cord injury may also be produced by other mechanisms.

One is a by-product of injury-induced sprouting. The new synapses formed by surviving axons see below may be too excitatory in nature. They might arise from motor pathways that descend from the brain, from ascending sensory pathways, or from the many synapses between the interneurons that form an intricate local circuitry within the spinal cord. Continual sensory feedback from muscles such as for the detection of muscle length is indispensable for the production of graded movements.

If stretch reflexes are altered in individuals with spinal cord injuries, the lack of appropriate feedback may lead to spastic muscle contractions. Spasticity may also be produced by pathological alterations in the electrical properties of the motor neurons themselves, including changes in sodium channel type, number, and distribution Hiersemenzel et al. Pain is a common and debilitating outcome of spinal cord injuries. Most studies find that 60 to 80 percent of individuals report chronic pain after a spinal cord injury. More precise estimates have been hindered by a.

Decubitus ulcers, or pressure ulcers, of the skin form over bony parts of the body, usually from prolonged pressure in patients and individuals who are not able to move around easily. The lack of definitions was addressed in with the release of a proposed scheme by the International Association for the Study of Pain for characterization of the pain associated with spinal cord injuries.

The impact of chronic pain may be so great—deterioration of quality of life, ability to function, self-image, and care delivery—that depression and thoughts of suicide are common Cairns et al. The new classification system organizes spinal cord injury pain under two broad categories—nociceptive and neuropathic—along with five subclassifications each of which has further clinical subtypes and possible pathologies; see Table Nociceptive pain arises from an external source e.

The two types of nociceptive pain—musculoskeletal and visceral—were reported by 59 and 5 percent of patients, respectively, in the prospective trial cited above Siddall et al. Of the three types of neuropathic pain, 41 percent of patients reported at-level neuropathic pain, whereas 34 percent reported below-level neuropathic pain Siddall et al. Nociceptive pain is the dull and aching pains that one encounters when a limb is broken or when one has lower back pain.

Painful stimuli are registered by specialized sensory cells known as nociceptors. Nociceptors, which are intact with this type of pain, respond to local damage to nonneural tissues e. Neuropathic pain, on the other hand, is produced by direct damage to neural tissue. It is described as a sharp, shooting, burning, or electrical type of pain. Sensory neurons and pathways undergo physiological alterations; they may become exquisitely sensitive, firing off impulses out of proportion to the stimulus hyperesthesia or even without an external trigger whatsoever.

They may register the light touch of a feather as an unpleasant burning sensation dysesthesia instead of a pleasant one. Nociceptive pain and neuropathic pain have distinct causes and, as a result, distinct treatments. Because nociceptive pain arises from tissue damage and not from nerve pathology, it is often treated with standard therapies, most commonly physical therapy, various pain medications, and surgical therapy. Neuropathic pain is more difficult to treat, partly because its mechanisms are still being uncovered. The distinction between the two types of pain, however, is not always clear-cut Bryce and Ragnarsson, Over time, nociceptive pain can lead to the sensitization of spinal.

Sensitization represents an increased response to a standard stimulus, and it is manifest as hypersensitivity to pain Woolf and Mannion, Much of what is known about the pathophysiology of the pain that occurs after a spinal cord injury comes from studies with a host of animal models of different types of injuries. Although much remains to be learned, some of the intensively studied mechanisms underlying spinal cord pain include the following Yezierski, :.

Neurotransmitters and neuromodulators commonly involved in excitatory pain pathways include glutamate, substance P, aspartate, galinin, brain-derived neurotrophic factor, and calcitonin gene-related peptide. Many of these mechanisms also apply to other pain conditions not associated with spinal cord injuries Woolf and Mannion, Multiple areas of the cerebral cortex process pain information relayed there by a certain tract in the spinal cord, which receives its information from incoming peripheral nerves. The brain, in turn, modulates the incoming messages through several descending pathways from nuclei in the midbrain, including the periaqueductal gray.

Three common types of bladder dysfunction accompany spinal cord injuries, depending on the level of the injury Kaplan et al. Understanding of the types of dysfunction first requires some understanding of the anatomy of the bladder and its control by the spinal cord and the brain. Two main muscle groups surrounding the bladder control urination: the detrusor muscle, which controls bladder contraction, and the external sphincter muscles at the base of the bladder, which control bladder outflow.

The two muscles normally work reciprocal to one another: the detrusor muscle contracts while the sphincter muscles relax, allowing urine to flow from the bladder. Because each is fed by separate nerves, their coordination—i. That portion of the brain sends its axons to the sacral region of the spinal cord S2 and S3 , which also receives sensory input from the bladder via the pelvic nerve about bladder distention.

When the pelvic nerve conveys the message that the bladder is full, the information is relayed up to the pons, which then coordinates the motor messages necessary to empty the bladder. This process is called the voiding reflex. In individuals with complete spinal cord injuries above the level of the sacral cord, disruption of the pathway from the spinal cord to the brain can lead to bladder problems related to the lack of coordination between the detrusor and the sphincter muscles see below.

If the sacral cord or the cauda equina is injured directly, the bladder detrusor muscle becomes flaccid—a condition known as areflexia. The detrusor muscle loses its ability to. Large volumes of urine overfill the bladder and back up to the kidneys Kaplan et al. Two common types of bladder conditions occur in individuals with spinal cord injuries at levels above the sacral cord. The first is detrusor hyperreflexia, in which the bladder is overreactive. As the bladder fills with small volumes of urine, the detrusor muscle contracts prematurely, causing frequent urination.

Research with animals suggests that part of the pathological process occurs in the sensory nerves coming from the bladder. Sensory fibers normally carrying other types of information actually switch their functioning: they become sensitive to bladder distention and trigger bladder detrusor contraction de Groat, This form of sensory plasticity is mediated by changes in electrical properties of C fibers, a particular type of sensory neuron Yoshimura, Less is known about the biological basis of the second type of bladder dysfunction, detrusor-sphincter dyssynergia.

This condition is marked by involuntary contractions of the sphincter muscles, which prevent urine from leaving the bladder. It can occur with the loss of the reciprocal relationship between detrusor muscle contraction and sphincter muscle relaxation. One hypothesis is that the condition is related to the reduced activity of the neurotransmitter nitric oxide in sphincter muscles. Nitric oxide is involved in relaxation of the sphincter. Reduced levels would therefore increase sphincter contraction Mamas et al. Detrusor-sphincter dyssynergia can also arise from lesions to the pontine reticular nucleus and the reticular formation Sakakibara et al.

Bowel dysfunction frequently occurs after a spinal cord injury because the brain and spinal cord have major roles in stool elimination. Although the movement of feces down the length of the bowel is partly controlled by independent neurocircuits that reside within the bowel, 4 the brain and spinal cord are essential for voluntary control over defecation.

Loss of bowel function is so deeply distressing and embarrassing to individuals with spinal cord injuries that it affects their social interactions and their willingness to engage in sexual activities. The impact of a spinal cord injury on voluntary control of the bowel is known as neurogenic bowel. Neurogenic bowel comes in two types—reflexic and areflexic—depending on the location of the injury. When the bowel wall is stretched, the local neurocircuits cause the muscles above the stretched area to constrict, whereas those below the stretched area are induced to relax, thus propelling feces down the bowel toward the anus.

Reflexic bowel brings constipation and an inability to defecate by conscious effort. The anal sphincter muscle remains tight and can be stimulated manually to induce defecation. Areflexic bowel, or lower motor neuron bowel, results from injuries at or below the sacral cord. It also causes constipation and incontinence. The anal sphincter becomes so flaccid that it is incapable of being manually stimulated to induce defecation.

Both types of neurogenic bowel carry the risk of serious complications, including bowel obstruction, colorectal distention, and a life-threatening rise in blood pressure triggered by a distended bladder or bowel. Many aspects of human sexuality are under reflexive control by various centers in the spinal cord, most frequently in the sacral and in the thoracic and lumbar regions.

The site and extent of injury are thus key determinants of sexual function. Several brain regions—most notably, the limbic system and the hypothalamus—also contribute to sexual function by exerting some degree of control over neuronal centers located in the spinal cord, especially sexual drive or inhibition. A large proportion of men and women with spinal cord injuries report reduced sexual desire Alexander et al.

Male infertility appears to be the result of abnormalities in semen, especially low sperm motility and viability and increased numbers of leukocytes Randall et al. For men, the sexual response includes three separate functions: erection, ejaculation, and orgasm. Erection has two descriptive types, both of which are controlled by distinct spinal cord reflexes. Psychogenic or mentally induced erection is controlled by the T11 to L2 segments of the spinal cord, whereas reflexogenic erections are mediated by the sacral cord. Ejaculation is a more complex process, with two stages mediated by the region from T10 to S4, which controls certain sympathetic, parasympathetic, and somatic nerves.

A physiological component of an orgasm is rhythmic pelvic floor contractions and other smooth-muscle contractions mediated by sacral regions of the spinal cord. The experience of orgasm as pleasurable depends on processing and interpretation by the brain. Damage to the relevant spinal cord centers or disruption of connections to the brain can thus lead to various types of sexual dysfunction.

For women, the sexual response depends on arousal and orgasm. Sexual arousal involves vaginal lubrication; swelling of the clitoris; and increases. Vaginal lubrication has two types, psychogenic or reflexive, which are controlled by the regions of the spinal cord from T10 to L2 and S2 to S5, respectively. Orgasm has been directly investigated in laboratory-based studies with women with spinal cord injuries.

Overall, only 52 percent of women with spinal cord injuries were able to stimulate themselves to orgasm, regardless of the nature of their injury Sipski, Women with injuries of the sacral cord were significantly less likely to reach orgasm than women with spinal cord injuries at other, higher levels. Researchers therefore postulate that an intact sacral reflex is necessary for orgasm Sipski, ; Benevento and Sipski, Although much progress has been made, especially in the past 25 years, in understanding the basic biology of the nervous system and the complex pathways in the pathophysiology of spinal cord injuries that involve the immune, vascular, and nervous systems, much remains to be learned.

As emphasized in the following chapters, this basic research is the underpinning of progress that will be made in developing therapeutic interventions. Many research avenues remain to be examined to understand the biochemical mechanisms responsible for spinal cord injuries and thus the targets for the development of therapeutic interventions.

Research is needed on the processes involved in cellular death and the immediate sequelae of apoptotic and necrotic cell death. The molecular mechanisms that promote and inhibit axonal regeneration need to be further explored, as do the molecular mechanisms that direct axons to their appropriate targets and regulate the formation and maintenance of appropriate and functional synaptic connections and circuitry. Moving this research forward involves opportunities and challenges that are not isolated to spinal cord injury research. Rather, this research has far-reaching potential to both inform and be informed by many other fields of research and the efforts that are under way to examine other neurological diseases and conditions.

Axonal elongation in peripheral and central nervous system transplants. Advances in Cell Neurobiology 3: Sexual activities, desire, and satisfaction in males pre- and post-spinal cord injury. Archives of Sexual Behavior 22 3 : Anderson AJ. Mechanisms and pathways of inflammatory responses in CNS trauma: Spinal cord injury. Journal of Spinal Cord Medicine 25 2 : Ultrastructural evidence for arteriolar vasospasm after spinal cord trauma. Neurosurgery 39 4 : Chicago: American Spinal Injury Association. Inflammation, degeneration and regeneration in the injured spinal cord: Insights from DNA microarrays.

Trends in Neurosciences 26 10 : Review of current evidence for apoptosis after spinal cord injury. Journal of Neurotrauma 17 10 : Neurogenic bladder, neurogenic bowel, and sexual dysfunction in people with spinal cord injury. Physical Therapy 82 6 : Brown TG. On the nature of fundamental activity of the nervous centers; together with an analysis of the conditioning of rhythmic activity in procession, and a theory of the evolution of function in the nervous system. Journal of Physiology Bryce TN, Ragnarsson K.

Pain management in persons with spinal cord disorders. Spinal Cord Medicine: Principles and Practice. New York: Demos Medical Publishing. Transplantation of Schwann cells and olfactory ensheathing cells to promote regeneration in the CNS. Textbook of Neural Repair and Rehabilitation. Observations on the pathology of human spinal cord injury.

A review and classification of 22 new cases with details from a case of chronic cord compression with extensive focal demyelination. Advances in Neurology Observations on the pathology of several types of human spinal cord injury, with emphasis on the astrocyte response to penetrating injuries. Pain and spasticity after spinal cord injury: Mechanisms and treatment. Spine 26 24 Suppl : S Evidence for a spinal stepping generator in man. Paraplegia 34 2 : Caceci T, El-Shafey S. Fenbendazole improves pathological and functional recovery following traumatic spinal cord injury.

Endoplasmic reticulum stress response in the rat contusive spinal cord injury model-susceptibility in specific cell types. Give progesterone a chance. Longitudinal assessment of white matter pathology in the injured mouse spinal cord through ultra-high field Anti-interleukin-6 receptor antibody reduces neuropathic pain following spinal cord injury in mice. Restoring endoplasmic reticulum homeostasis improves functional recovery after spinal cord injury. Elena B. Okon , Femke Streijger , Jae H. Lee , Lisa M. Anderson , Amy K. Russell , and Brian K. Simon G.

Sjovold , Stephen F. Mattucci , Anthony M. Choo , Jie Liu , Marcel F. Dvorak , Brian K. Kwon , Wolfram Tetzlaff , and Thomas R. Host reaction to poly 2-hydroxyethyl methacrylate scaffolds in a small spinal cord injury model. Animal models of axon regeneration after spinal cord injury. Peripheral nerve alterations after spinal cord injury in the adult rat.

Megan Ryan Detloff , Rodel E. Wade , and John D. Johongir M. Muradov and Theo Hagg. Thrombospondin-4 contributes to spinal cord injury-induced changes in nociception. Rolipram promotes functional recovery after contusive thoracic spinal cord injury in rats. Jae H. Lee , Claire F. Jones , Elena B. Jennifer N. Dulin , Meredith L. Moore , and Raymond J. Genome-wide gene expression profiling of stress response in a spinal cord clip compression injury model.

Joint-specific changes in locomotor complexity in the absence of muscle atrophy following incomplete spinal cord injury. Improved rat spinal cord injury model using spinal cord compression by percutaneous method. Blockade of interleukin-6 signaling inhibits the classic pathway and promotes an alternative pathway of macrophage activation after spinal cord injury in mice. Ward and Charles H. Molecular and cellular mechanisms underlying the role of blood vessels in spinal cord injury and repair.

  • The Invention of the Palestinians [The Revised Edition].
  • Incidence and mortality;
  • Extreme Blushing;
  • Bibliographic Information.
  • Requiescat;

Alterations in chondroitin sulfate proteoglycan expression occur both at and far from the site of spinal contusion injury. Respiratory function following bilateral mid-cervical contusion injury in the adult rat. Age-related differences in cellular and molecular profiles of inflammatory responses after spinal cord injury.

  • The Good War: NATO and the Liberal Conscience in Afghanistan.
  • Spinal Cord Injury;
  • Get PDF Thoracic and Lumbar Spine and Spinal Cord Injuries (Advances in Neurotraumatology);

Multiple drug delivery hydrogel system for spinal cord injury repair strategies. Scott A. Myers , William H. DeVries , Mark J. Gruenthal , Kariena R. Andres , Theo Hagg , and Scott R. Independent evaluation of the effects of glibenclamide on reducing progressive hemorrhagic necrosis after cervical spinal cord injury. Replication and reproducibility in spinal cord injury research.

Translational spinal cord injury research. Induction of angiopoietin-2 after spinal cord injury. New approach for graded compression spinal cord injuries in Rhesus macaque: method feasibility and preliminary observations. Grafted human-induced pluripotent stem-cell-derived neurospheres promote motor functional recovery after spinal cord injury in mice. Attenuating the endoplasmic reticulum stress response improves functional recovery after spinal cord injury.

Synergistic effects of galectin-1 and reactive astrocytes on functional recovery after contusive spinal cord injury. Peter E. Batchelor , Nicole F. Kerr , Amy M. Gatt , Susan F. Wills , Tara K. Sidon , and David W. CD47 knockout mice exhibit improved recovery from spinal cord injury. Calcium channel alphadelta-1 protein upregulation in dorsal spinal cord mediates spinal cord injury-induced neuropathic pain states. Impact speed does not determine severity of spinal cord injury in mice with fixed impact displacement.

Activating Notch signaling post-SCI modulates angiogenesis in penumbral vascular beds but does not improve hindlimb locomotor recovery. Experimental spinal cord injury in rats diminishes vagally-mediated gastric responses to cholecystokinin-8s. Animal Models of Central Neuropathic Pain. Raman spectroscopic investigation of spinal cord injury in a rat model. Juan J. Herrera , Laura M. Kelly A. Functional recovery after transplantation of bone marrow-derived human mesenchymal stromal cells in a rat model of spinal cord injury. Automatic segmentation of rodent spinal cord diffusion MR images.

Predifferentiated embryonic stem cells promote functional recovery after spinal cord compressive injury. Task-specificity vs. Aquaporins in spinal cord injury: the janus face of aquaporin 4. Repetetive hindlimb movement using intermittent adaptive neuromuscular electrical stimulation in an incomplete spinal cord injury rodent model. Involvement of ERK2 in traumatic spinal cord injury. Herrera , Ricky J. Haywood-Watson , and Raymond J.

Aberrant sensory responses are dependent on lesion severity after spinal cord contusion injury in mice. Quantitative analysis of cellular inflammation after traumatic spinal cord injury: evidence for a multiphasic inflammatory response in the acute to chronic environment. Anshu Chen , Melanie L. Chemokine expression in the white matter spinal cord precursor niche after force-defined spinal cord contusion injuries in adult rats. Biomechanical Aspects of Spinal Cord Injury. Bilateral cervical contusion spinal cord injury in rats. Methylprednisolone fails to improve functional and histological outcome following spinal cord injury in rats.

Exacerbation of spinal cord injury due to static compression occurring early after onset. Gemma E. Rooney , Siobhan S. Windebank , and Frank P. Neuromuscular stimulation therapy after incomplete spinal cord injury promotes recovery of interlimb coordination during locomotion. Bayly , and Sheng-Kwei Song. Kimberly M. Carrico , Radhika Vaishnav , and Edward D. Herrera , Olivera Nesic , and Ponnada A. Chirag B. Patel , David M. Sundberg , Tessy Chacko , and Ponnada A.

Modeling spinal cord contusion, dislocation, and distraction: Characterization of vertebral clamps, injury severities, and node of Ranvier deformations. Combinatorial strategies with Schwann cell transplantation to improve repair of the injured spinal cord. Time-course of recovery of gastric emptying and motility in rats with experimental spinal cord injury. Laura E.

Spinal Cord Injuries: Traumatic

Crystal M. Simon , Shan Sharif , Richard P. Tan , and Michelle C. Treadmill training enhances the recovery of normal stepping patterns in spinal cord contused rats. Pharmacological evidence for a role of peroxynitrite in the pathophysiology of spinal cord injury. A simple, inexpensive and easily reproducible model of spinal cord injury in mice: Morphological and functional assessment. Rachel L. Burke , William H. Magnuson , Scott R. Whittemore , and Christopher B. Neuroproteomic Methods in Spinal Cord Injury. Spinal Cord Injury: experimental animal models and relation to human therapy.

Yi Ping Zhang , Darlene A. Burke , Lisa B. Shields , Sergey Y. Smith , Richard L. Benton , William H. Glial precursor cell transplantation therapy for neurotrauma and multiple sclerosis. Secondary pathology following contusion, dislocation, and distraction spinal cord injuries. A comparison of two-dimensional and three-dimensional techniques for the determination of hindlimb kinematics during treadmill locomotion in rats following spinal cord injury.

Microdialysis in central nervous system disorders and their treatment. Jason T. Dynamics of the inflammatory response after murine spinal cord injury revealed by flow cytometry. Small mammal MRI imaging in spinal cord injury: A novel practical technique for using a 1. Rolipram attenuates acute oligodendrocyte death in the adult rat ventrolateral funiculus following contusive cervical spinal cord injury. Glutamate-induced losses of oligodendrocytes and neurons and activation of caspase-3 in the rat spinal cord. Mehdorn , and Janka Held-Feindt. Models of experimental spinal cord injury: Translational relevance and impact.

Rangaswamyrao Ravikumar , Melanie L. McEwen , and Joe E.