Symptomatic autonomic dysfunction in SCI/D is common in persons with high-level paraplegia and tetraplegia. Orthostatic hypotension and relative hypotension is nearly ubiquitous in those with higher level injuries. Orthostasis occurs as a result of loss of sympathetic tone and systemic loss of vascular resistance. Management includes application of elastic stockings, abdominal binders, adequate hydration, progressive daily head-up tilt, and, at times, administration of salt tablets, midodrine, or fludrocortisone. Autonomic dysreflexia (AD) is a syndrome that affects persons with a neurologic level at T6 level or above, who are unable to vasodilate the splanchnic vascular bed in response to acute hypertension. It is caused by a noxious stimulus below the injury level leading to sudden reflex sympathetic activity. Symptoms of AD include pounding headache; bradycardia; hypertension; profuse sweating; and cutaneous vasodilatation with flushing of the face, neck, and shoulders. Delay in treatment of AD may lead to intracerebral and subarachnoid hemorrhage, stroke, retinal hemorrhage, seizure, cardiac dysrhythmias, and even death. The most important step of acute management of AD is to find and remove the noxious stimulus, of which bladder distension is the most common, causing the problem (6). Other measures include sitting the person upright, loosening tight clothing, and monitoring the blood pressure until the problem resolves. If symptoms are not relieved quickly with the above measures, which should include bladder emptying in the absence of any other easily identified cause, and the systolic blood pressure remains above 150 mmHg, treatment with a rapidly acting and preferably reversible antihypertensive such as topical nitroglycerine should be considered while searching for other sources of noxious stimuli.

Individuals with SCI/D are prone to developing deep vein thrombosis (DVT) secondary to stasis of the venous circulation, hypercoagulability of blood, and intimal vascular injuries. The greatest period of risk is during the first 2 weeks following the injury, with the incidence decreasing thereafter. The majority of persons with SCI/D do not have clinical signs or symptoms such as swelling, warmth, or pain. PE and the postphebitic syndrome are potential sequelae of DVT. Because of the high incidence of DVT and potential fatal outcomes of PE, DVT prophylaxis with low-molecular-weight heparin has been shown to be the most effective of the available options. DVT prophylaxis is typically continued for no longer than 3 months as the risk of further DVT is not thought to be greater than the risk of adverse events due to anticoagulation at that point. Warfarin is generally given for 3 to 6 months after the diagnosis of DVT or PE with a target international normalized ratio goal of between 2 and 3. Inferior vena cava filters are indicated for patients who have a contraindication to anticoagulation or have failed anticoagulation.

Spasticity after UMN SCI/D is characterized by several different features including velocity-dependent increases in tonic stretch reflexes, uninhibited spastic co-contractions of agonist and antagonist muscles, and low-threshold phasic muscle spasms occurring in either a flexor or an extensor pattern. Each of these features may be more or less present in any one person. Furthermore, although spasticity can cause difficulty with mobility, positioning, and comfort, it can also be helpful with ambulating and performing activities of daily living, maintaining muscle bulk, and increasing venous return, depending on which features predominate. Treatments include stretching of spastic muscles; proper wheelchair seating and positioning; splinting and casting; standing; keeping warm; functional electrical stimulation; and medications such as baclofen, various benzodiazepines, and tizanidine. More invasive treatment options for spasticity include intrathecal baclofen administration through an implanted pump; percutaneous nerve or muscle blocks with phenol, alcohol, or botulinum toxin; and rarely surgical rhizotomy.

Pain is a significant problem for many individuals with SCI. Approximately 80% of people with SCI report chronic pain, while approximately one-third report chronic severe pain that interferes with activity and affects quality of life (7). There are two basic types of pain, neuropathic and nociceptive pain. Neuropathic pain is pain arising as a direct consequence of an injury or disease affecting the somatosensory system, whereas nocicpetive pain is pain arising from activation of peripheral nerve endings or sensory receptors that are capable of transducing and encoding noxious stimuli. The International Spinal Cord Injury Pain (ISCIP) Classification organizes SCI pain hierarchically into three tiers (7). The first tier includes the main types of nociceptive and neuropathic pain. The second tier includes subtypes for neuropathic (at level, below level, or other neuropathic pain) and nociceptive (musculoskeletal, visceral, or other nociceptive pain) types, while the third tier is used to specify the primary pain source at the organ level as well as the pathology. Medications used to treat neuropathic pain related to SCI/D include anticonvulsants, antidepressants, and opioids. A significant proportion of the chronic pain reported by persons with SCI/D is due to overuse of the upper extremities. Education, physical training, and adaptive techniques for doing activities should be primary interventions to minimize overuse nociceptive pains of the upper limbs.

Key psychological issues related to SCI/D include adjustment to body structure and function limitations as well as pain, coping, family and caregiver roles, and ultimately the assumption of a new identity. Adjustment is usually gradual and may or may not progress in a linear fashion. The influence of social supports and premorbid coping strategies can either help or hinder the adjustment process. Peers with SCI/D can be invaluable in facilitating a positive adjustment and assumption of a new identity.

MEDICAL KNOWLEDGE

GOALS

Demonstrate knowledge of established evidence-based and evolving biomedical, clinical, epidemiological, and sociobehavioral sciences pertaining to SCI/D, as well as the application of this knowledge to guide holistic patient care.

SCI/D results in temporary and permanent changes to motor, sensory, and/or autonomic function resulting in multibody system dysfunction. Trauma results in approximately 12,000 injuries per year in the United States, of which 4 out of 5 are experienced by men (8). Approximately 42% of the injuries result from motor vehicle crashes, 20% from falls, and 17% from violence (9). Approximately 30% of the injuries cause incomplete tetraplegia, 25% complete paraplegia, 20% incomplete paraplegia, and 20% complete tetraplegia (9). Life expectancy today remains significantly below that expected for persons without SCI. Persons acquiring paraplegia from a traumatic etiology at 20 years of age have a life expectancy shortened by 14 years, while persons acquiring an SCI with ventilator dependency at 40 years of age have a life expectancy shortened by 32 years (9). The leading causes of death after SCI are diseases of the respiratory system accounting for one-fifth of the deaths, of which four-fifths are due to pneumonia (9).

The spinal cord is organized into a series of tracts that carry motor (descending) and sensory (ascending) information; 31 pairs of nerve roots (8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal) extrude from the spinal cord. Each spinal segment has a pair of ventral (motor) and dorsal (sensory) spinal nerve roots. The cervical nerves exit above the corresponding vertebrae and the thoracic and lumbar nerves exit below the corresponding numbered vertebrae.

During embryologic development, the vertebral column elongates more than the spinal cord. Therefore, the spinal cord is shorter than the spinal canal, and the individual spinal cord segments do not line up with the corresponding numbered vertebrae. The spinal cord terminates as a conical structure known as conus medullaris at the L1–L2 intervertebral disk. Below the L1–L2 intervertebral level, the nerve fibers of the cord continue as the cauda equina, named as such because it resembles a horse’s tail.

A cross-sectional view of the spinal cord reveals gray and white matter. The central gray matter is subdivided into two horns on each side called the ventral (anterior) and dorsal (posterior) horns. The dorsal horns contain projections of the cell bodies of sensory fibers from dorsal root ganglia, and the ventral horn contains motor neurons. The peripheral white matter is subdivided into three columns on each side called anterior, lateral, and posterior columns. The posterior column is further subdivided into tracts: fasciculus gracilis located in the medial posterior column and fasciculus cuneatus located in the lateral posterior column relay touch, vibration, and position sense for T7–S5 dermatome and above T7, respectively. This posterior column ascends ipsilaterally and decussates at the medulla. The anterolateral spinothalamic tract, located peripherally in the lateral column, contains fibers that carry information for pain and temperature (laterally) and touch and pressure (anteriorly). This tract decussates within three segments of their origin and ascends contralaterally to the thalamus. The corticospinal tract is located centrally and posteriorly in the lateral column and carries information for voluntary and reflexive movement.

UMNs are corticospinal neurons originating in the cerebral cortex and synapsing in the anterior horn with LMNs. LMNs originate in the anterior horn of the spinal cord and exit via spinal nerves to target muscles. Damage to UMNs leads to spasticity, while damage to the anterior horn cell or nerve roots (LMNs) leads to decreased muscle tone, absent muscle stretch reflexes, and flaccid paralysis.