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Dr. Milind Deogaonkar Epidemiology of spinal cord injury: Accidents are the fourth most common cause of death in the USA after heart disease, cancer and stroke. The incidence accounts for 50 deaths per 1,00,000 population each year. 3% of these are a direct result of spinal cord injury from trauma. The incidence is 5 times greater in males than in females. While in the absence of a national spinal cord injury registry in India, the exact incidence is not known, the cervical cord remains the most common site of involvement. The commonest causes of injury are motor vehicle, accidents, falls, assault and sports related injuries. Clinical Presentation: The symptoms of the patient range from mild local site pain to quadriplegia and death. This depends of the severity of the injury and on the level of involvement. Involvement above DI spinal segment may show feature of upper limb involvement while involvement below will not. Involvement of the conus presents predominantly with bowel and bladder involvement. Pyramidal tract involvement presents with varying degrees of spasticity and motor weakness on the ipsilateral side of the body. Spinothalamic tract involvement presents with sensory loss to coarse touch, pain and temperature of the contralateral side of the body while posterior column impairment with loss of proprioceptive input from the ipsilateral body parts. Involvement of segments above C4 leads to respiratory compromise. Patients may also present with varying degrees of autonomic dysfunction of Horner's syndrome due to interruption of intermediomedial and intermediolateral columns of the cord. Several well-defined syndromes have been described in connection with cord injury. a. Brown Sequard syndrome: Presentation of ipsilateral pyramidal and posterior column impairment and contralateral hemisensory loss-manifestation of cord hemisection. b. Central Cord Syndrome: Weakness of upper limb more than lower limbs with or without suspended, disseminated sensory loss - a manifestation of damage to the central areas of the cervical cord common in whiplash injuries. c. Conus Syndrome: Loss of perineal sensation with varying degrees of sphincter dysfunction - a manifestation of damage to the terminal cord common in thoraco-lumber fracture dislocations. Concepts in the spinal stability: Since the spinal cord is covered on all sides by the bony spinal canal, cord injury is in almost all cases accompanied by and usually a consequence of vertebral injury. The vertebral column itself consisting of 33 separate bony elements does not move as a single piece but rather movement occurs to varying degrees between separate elements, the culmination of which helps to achieve the whole range of motion. In some places e.g. the cervical spine, stability has been sacrificed for increasing mobility. The reverse occurs in the thoracic spine. Dennis has propounded a 3-column theory of stability wherein disruption of 2 columns is supposed to lead to the development of instability and requires stabilization. Punjabi and White have enumerated criteria of spinal stability and an unstable spine entails the risk of furthering neurological injury. Pathophysiology of spinal cord injury: Experiment and clinical studies on spinal cord injury noted that there was a spectrum of pathologic appearances that evolved over the initial days following injury. This led to the concept that the injury process was a result of both primary and secondary insults. When the primary injury was not amenable to any pharmacological intervention, the effects of secondary insult could be mitigated if treatment was started early enough. Primary mechanism of cord injury can be due to four kinds of mechanical forces. a. Impact with persisting compression e. g. fractures, dislocations, and disc herniations. b. Impact with no persisting compression e. g. hyperextersion injuries. c. Distraction e. g. hyperflexion injuries. d. Laceration/ Transection: Penetrating injuries, fracture dislocation Secondary injury mechanisms that may be involved are: a. Systemic shock: Profound hypotension, and bradycardia (often lasting for days) follows cord injury and there may be a compromise of an already damaged cord. b. Local microcirculatory damage: may be due to mechanical disruption of capillaries, hemorrhage, thrombosis and loss of autoregulation. c. Biochemical damage: may occur due to excitotoxin release (glutamate), free radical production, arachidonic acid release, lipid peroxidation, eicosanoid production, cytokines and electrolyte shifts. All these factors (along with edema) lead to loss of energy producing ability with consequent loss of impulse transmission, cell swelling, membrane, lysis and cell death. Pathological changes: The pathological changes following cord injury are most profound in the central gray matter of the cord, which is softer and has more vascularity. Macroscopically an acutely injured cord shows features of cord swelling, central hemorrhages, remote venous hemorrhage and infractions. Microscopically there is evidence of axonal injury with swelling, giant axons, organelle accumulation and granular dissolution. Myelin sheath injuries lead to formation of periaxonal spaces and numerous microglia and macrophages can also be seen at the injury site. In the chronic phase there is evidence of central cavitation, Posttraumatic syrinx formation, arachnoiditis, and cord atrophy. Microscopic examination normally shows gliosis, siderosis and a persistant subpial rim of axons. Management of spinal cord injury: Initial treatment of patients with cord injury focuses on two aspects - preventing further damage and resuscitation. Immobilization with a hard cervical collar (in case of cervical spine injuries) and care in transportation of patient is of paramount importance if the spine is unstable. Resuscitation is aimed at airway maintenance, adequate oxygen saturation of peripheral blood, restoring blood pressure to acceptable limits, preventing bradycardia, done simultaneously to prevent any ischemic damage to the already compromised cord. Methyl prednisolone has been shown by the NASCIS-II trail to be significantly beneficial in causing favorable neurological outcome if administered early enough (within 8 hours) of the primary insult. The recommended dose is 30mg/kg bolus to be administered over 15 minutes and after a 45-minute pause 5.4 mg/kg/hr over the next 23 hours. Only one other regimen (involving GMI ganglioside) has been shown to be effective. Investigation protocols are designed to demonstrate site of injury and neural compression if any. For the former usually a good quality skiagram (in both AP and lateral planes) suffices, while for the latter magnetic resonance imaging (MRI) in both sagittal and axial planes of the involved area in T1 and T2 sequences is done. X-rays are useful to demonstrate fractures, dislocations and instability while the MR imaging is useful to show cord compression, contusions are edema. In special situations thin section CT scans or flexion/ extension views of the spine are required. The timing and goals of surgical intervention were subject to much debate. The goals of surgery include dural decompression, prevention of tethering and spinal stabilization. The type of surgery performed (anterior vs. posterior), distraction forces during surgery, preoperative grade all influence the outcome. While anterior decompression has proven to be better than a posterior approach and stabilization with fusion gives definite benefits in an unstable spine, till now no clear consensus on timing of surgery has emerged with proponents of both early and late intervention claiming advantages. Management also encompasses aggressive nursing programs including turning (to prevent decubitus ulcers), pulmonary care, deep venous thrombosis prophylaxis, management of orthostatic hypotension, limb edema and nutrition supplementation. Regular physiotherapy instituted early in the course of illness keeps muscles supple, delays wasting, prevents contractures and allows for better functional recovery should reinnveration occur. Functional restoration is also achieved by life techniques like biofeedback, instructions regarding ambulation and transfer, wheelchair considerations (including altering the environment to suit the patient), braces and reconstructive surgery. Devices like implantable pumps (to reduce spasticity), diaphragmatic pacers (to render a patient ventilator free) are also a part of a comprehensive rehabilitation programme. Outcome of patients with spinal cord injury: The main determinant of outcome is the patient's neurological grade at the time of admission with patients having complete motor and sensory myelopathy showing the worst prognosis. Other predictive factors include rectal tone status, admission blood pressure and pulse status, reflexes, and medical and surgical management since injury. The time course of recovery is also prolonged and recovery itself often incomplete. Taking all grades and locations into considerations a study concluded that while the majority of cases improved within a year, even at 3 years post injury 23.3% continue to improve whereas 7.1% deteriorated. The trend continued in the 5th year post injury also with 12.5% and 5.5% respectively showing further improvement and late deterioration. Hence prolonged rehabilitation at a comprehensive spinal rehabilitation center is the management of spinal cord injuries. |
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