3)

Along the thorax and abdomen, the dermatomes are evenly spaced segments stacked up on top of each other, and each is supplied by a different spinal nerve. The dermatomes along the arms and legs differ from the pattern of the trunk dermatomes, because they run longitudinally along the limbs. The general [1] pattern is similar in all people, but significant variations exist in dermatome maps from person to person. Clinical significance Dermatomes are useful to help localize neurologic levels, particularly in radiculopathy. Effacement or encroachment of a spinal nerve may or may not exhibit symptoms in the dermatomic area covered by the compressed nerve roots in addition to weakness, or deep tendon reflex loss. Viruses that infect spinal nerves, such as herpes zoster infections (shingles), can reveal their origin by showing up as a painful dermatomic area. Herpes zoster, a virus that can be dormant in the dorsal root ganglion, migrates along the spinal nerve to affect only the area of skin served by that nerve.

4) Spinal Cord Level Numbering System The spinal nerves carry information to and from different levels (segments) in the spinal cord. Both the nerves and the segments in the spinal cord are numbered in a similar way to the vertebrae. The point at which the spinal cord ends is called the conus medullaris, and is the terminal end of the spinal cord. It occurs near lumbar nerves L1 and L2. After the spinal cord terminates, the spinal nerves continue as a bundle of nerves called the cauda equina. The upper end of the conus medullaris is usually not well defined. There are 31 pairs of spinal nerves which branch off from the spinal cord. In the cervical region of the spinal cord, the spinal nerves exit above the vertebrae. A change occurs with the C7 vertebra however, where the C8 spinal nerve exits the vertebra below the C7 vertebra. Therefore, there is an 8th cervical spinal nerve even though there is no 8th cervical vertebra. From the 1st thoracic vertebra downwards, all spinal nerves exit below their equivalent numbered vertebrae. The spinal nerves which leave the spinal cord are numbered according to the vertebra at which they exit the spinal column. So, the spinal nerve T4, exits the spinal column through the foramen in the 4th thoracic vertebra. The spinal nerve L5 leaves the spinal cord from the conus medullaris, and travels along the cauda equina until it exits the 5th lumbar vertebra. The level of the spinal cord segments do not relate exactly to the level of the vertebral bodies i.e. damage to the bone at a particular level e.g. L5 vertebrae does not necessarily mean damage to the spinal cord at the same spinal nerve level. Spinal Cord Nerve Levels

5) Treatment Treatment of SCI begins before the patient is admitted to the hospital. Paramedics or other emergency medical services personnel carefully immobilize the entire spine at the scene of the accident. In the emergency department, this immobilization is continued while more immediate life-threatening problems are identified and addressed. If the patient must undergo emergency surgery because of trauma to the abdomen, chest, or another area, immobilization and alignment of the spine are maintained during the operation. Intensive Care Unit Treatment

If a patient has a SCI, he or she will usually be admitted to an intensive care unit (ICU). For many injuries of the cervical spine, traction may be indicated to help bring the spine into proper alignment. Standard ICU care, including maintaining a stable blood pressure, monitoring cardiovascular function, ensuring adequate ventilation and lung function, and preventing and promptly treating infection and other complications, is essential so that SCI patients can achieve the best possible outcome. Steroid Therapy Methylprednisolone, a steroid drug, became available as a treatment for acute SCI in 1990 when a multicenter clinical trial showed better neurological change scores in patients who were given the drug within the first eight hours of injury. These studies have been criticized in part because this increase in scores has never been shown to translate into better functional outcomes for patients. This area remains controversial. Perhaps clinicians should consider methylprednisolone infusion if its potential benefits are felt to outweigh the risks of potential associated complications. Surgery Occasionally, a surgeon may wish to take a patient to the operating room immediately if the spinal cord appears to be compressed by a herniated disc, blood clot, or other lesion. This is most commonly done for patients with an incomplete SCI or with progressive neurological deterioration. Even if surgery cannot reverse damage to the spinal cord, surgery may be needed to stabilize the spine to prevent future pain or deformity. The surgeon will decide which procedure will provide the greatest benefit to the patient. Outcome Persons with neurologically complete tetraplegia are at high risk for secondary medical complications. The percentages of complications for individuals with neurologically complete tetraplegia have been reported as follows:

60.3 percent developed pneumonia 52.8 percent developed pressure ulcers 16.4 percent developed deep vein thrombosis 5.2 percent developed a pulmonary embolism 2.2 percent developed a postoperative wound infection

Pressure ulcers are the most frequently observed complications, beginning at 15 percent during the first year postinjury and steadily increasing thereafter. The most common pressure ulcer location is the sacrum, the site of one third of all reported ulcers. Source: National Spinal Cord Injury Statistical Center, University of Alabama at Birmingham, Annual Statistical Report, June 2004

Neurological Improvement Recovery of function depends upon the severity of the initial injury. Unfortunately, those who sustain a complete SCI are unlikely to regain function below the level of injury. However, if there is some degree of improvement, it usually evidences itself within the first few days after the accident. Incomplete injuries usually show some degree of improvement over time, but this varies with the type of injury. Although full recovery may be unlikely in most cases, some patients may be able to improve at least enough to ambulate and to control bowel and bladder function. Patients with anterior cord syndrome tend to do poorly, but many of those with Brown-Sequard syndrome can expect to reach these goals. Patients with central cord syndrome often recover to the point of being ambulatory and controlling bowel and bladder function, but they often are not able to perform detailed or intricate work with their hands. Once a patient is stabilized, care and treatment focuses on supportive care and rehabilitation. Family members, nurses, or specially trained aides all may provide supportive care. This care might include helping the patient bathe, dress, change positions to prevent bedsores, and other assistance. Rehabilitation often includes physical therapy, occupational therapy, and counseling for emotional support. The services may initially be provided while the patient is hospitalized. Following hospitalization, some patients are admitted to a rehabilitation facility. Other patients can continue rehab on an outpatient basis and/or at home. 6) Brown-Squard syndrome is an incomplete spinal cord lesion characterized by a clinical picture reflecting hemisection of the spinal cord, often in the cervical cord region. (See Presentation.) Patients with Brown-Squard syndrome suffer from ipsilateral upper motor neuron paralysis and loss of proprioception, as well as contralateral loss of pain and temperature sensation. A zone of partial preservation or segmental ipsilateral lower motor neuron weakness and analgesia may be noted. Loss of ipsilateral autonomic function can result in Horner syndrome. (See Etiology, Presentation, and Workup.) As an incomplete spinal cord syndrome, the clinical presentation of Brown-Squard syndrome may range from mild to severe neurologic deficit.

Brown-Squard syndrome results from damage to or loss of ascending and descending spinal cord tracts on 1 side of the spinal cord. Scattered petechial hemorrhages develop in the gray matter and enlarge and coalesce by 1 hour postinjury. Subsequent development of hemorrhagic necrosis occurs within 2436 hours. White matter shows petechial hemorrhage at 3-4 hours. Myelinated fibers and long tracts show extensive structural damage. Traumatic causes

Brown-Squard syndrome can be caused by any mechanism resulting in damage to 1 side of the spinal cord. Multiple causes of Brown-Squard syndrome have been described in the literature. The most common cause remains traumatic injury, often a penetrating mechanism, such as a stab or gunshot wound or a unilateral facet fracture and dislocation due to a motor vehicle accident or fall.[2, 3] More unusual etiologies that have been reported include assault with a pen, removal of a cerebrospinal fluid drainage catheter after thoracic aortic surgery, and injury from a blowgun dart. [4] Traumatic injury may also be the result of blunt trauma or pressure contusion. Nontraumatic causes Numerous nontraumatic causes of Brown-Squard syndrome have also been reported, including the following:

Tumor (primary or metastatic) Multiple sclerosis Disk herniation[5] Cervical spondylosis Herniation of the spinal cord through a dural defect (idiopathic or posttraumatic) Epidural hematoma Vertebral artery dissection Transverse myelitis Radiation Type II decompression sickness Intravenous drug use Tuberculosis Ossification of the ligamentum flavum[6] Meningitis Empyema Herpes zoster Herpes simplex Syphilis

Ischemia Hemorrhage - Including spinal subdural/epidural and hematomyelia

Prognosis for significant motor recovery in Brown-Squard syndrome is good.[10]One half to two thirds of the 1-year motor recovery occurs within the first 1-2 months following injury. Recovery then slows but continues for 3-6 months and has been documented to progress for up to 2 years following injury. The most common pattern of recovery includes the following [11] : Recovery of the ipsilateral proximal extensor muscles prior to that of the ipsilateral distal flexors Recovery from weakness in the extremity with sensory loss before recovery occurs in the opposite extremity Recovery of voluntary motor strength and a functional gait within 1-6 months A retrospective review by Pollard and Apple of 412 patients with traumatic, incomplete cervical SCIs found that the most important prognostic variable relating to neurologic recovery was completeness of the lesion. If the cervical spinal cord lesion is incomplete, such as central cord or Brown-Squard syndrome, younger patients with have a more favorable prognosis for recovery. Recovery in the study was not linked to high-dose steroid administration, early surgical intervention on a routine basis, or surgical decompression in patients with stenosis who were without fracture. (Other studies, however, have demonstrated improved outcomes for patients with traumatic SCIs who were given high-dose steroids early in the clinical course.[12] ) Surgical treatment of stenosis with myelopathy or incomplete spinal cord injury, including Brown-Squard syndrome, has been shown to halt progressive loss of neurological function.[13] Studies suggest that spared descending motor axons in the contralateral cord may mediate much of the motor recovery. Most individuals with incomplete injuries at the time of initial examination recover the ability to ambulate.